Pathology Education Instructional Resource - User contributions [en]

IPLab:Lab 5:Gout

2016-12-05T12:29:23Z

Peter Anderson: /* Study Questions */

== Clinical Summary ==
This patient was diagnosed with gout approximately 20 years ago. At that time, he noted the gradual onset of pain in the left knee, followed by swelling, redness and heat, all of which persisted for approximately one month. Shortly thereafter, he had periodic episodes of hot, painful, swollen joints involving the left knee, left ankle, and both first metatarsophalangeal joints. At this time the patient was hospitalized for evaluation of these arthritides. Serum uric acid values on three separate occasions were 8.0, 9.3, and 8.7 mg/dl. In addition to the presence of the painful swollen joints, a gouty tophus was present on the left arm. The patient was readmitted to the hospital from time to time because of acute exacerbations of gouty arthritis. On the most recent hospital admission, a 3-cm tophus was found over the right elbow, as well as several smaller tophi over the right hand.

== Autopsy Findings ==
The specimen consisted of an elliptically shaped, mottled, yellow-white irregular hard mass, measuring 8.0 x 5.0 x 2.0 cm. in diameter.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab5Gout1.jpg|This is a gross photograph of an index finger from a patient with gout. The finger has been sectioned longitudinally to demonstrate the distal interphalangeal joint. Note the white chalky material within and adjacent to the joint (arrows).
File:IPLab5Gout2.jpg|This is a gross photograph of the elbow of this patient. The subcutaneous nodules (arrows) on this arm are tophi caused by gout.
File:IPLab5Gout3.jpg|This is a low-power photomicrograph of the tophus removed from the elbow of this patient. Note the fibrous connective tissue (1) and the large foci containing the urate crystals (2) surrounded by the intense chronic inflammatory reaction.
File:IPLab5Gout4.jpg|This higher-power photomicrograph of the tophus demonstrates the collections of urate crystals (1) and the inflammatory cells at the edge of these foci (2).
File:IPLab5Gout5.jpg|This is a higher-power photomicrograph of the edge of the tophus. Most of the urate crystals dissolve away during processing. The inflammatory cells at the edge of these foci are clearly visible (arrow).
File:IPLab5Gout6.jpg|This is a high-power photomicrograph of the edge of the tophus. The character of the intense chronic inflammatory cell reaction is evident and note the presence of giant cells within this inflammatory cell reaction (arrows).
File:IPLab5Gout7.jpg|This is a photomicrograph of a tophus that was fixed in alcohol prior to histologic processing. The alcohol fixation preserves the water soluble urate crystals within the tissue. Note the urate crystals visible in this photomicrograph (arrows). Also note the chronic inflammatory reaction in the background.
File:IPLab5Gout8.jpg|This is a gross photograph of a tophus on the great toe of another patient with gout (arrow). The healed surgical incision and the size of this tophus indicate that this was a long-standing problem for this patient.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab5Gout</peir-vm>

== Study Questions ==
* <spoiler text="What are the two types of gout and which is more common?">The main type is primary gout which makes up 90% of all cases. In most cases of primary gout the specific enzyme defect is unknown but there is some enzyme abnormality which leads to hyperuricemia and symptoms of gout. In rare cases the specific enzyme defect is known, but gout symptomatology is the main clinical finding.

In secondary gout the cause of the hyperuricemia is known (e.g. leukemia, renal failure, Lesch-Nyhan syndrome).</spoiler>
* <spoiler text="What are the four stages of gout?"># Asymptomatic hyperuricemia
# Acute gouty arthritis
# Intercritical gout
# Chronic tophaceous gout.</spoiler>
* <spoiler text="Why is gout more severe in peripheral joints?">The decreased temperature accentuates the crystallization of monosodium urate (MSU).</spoiler>
* <spoiler text="What initiates the inflammatory reaction seen in the synovial membrane in gouty arthritis?">MSU crystals are chemotactic and they activate complement. This initiates a cascade of inflammatory events which leads to acute gouty arthritis.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/329958-overview eMedicine Medical Library: Gout and Pseudogout]
* [http://www.aafp.org/afp/1999/0215/p925.html American Academy of Family Physicians: Gout and Hyperuricemia]

=== Journal Articles ===
* Harris MD, Siegel LB, Alloway JA. [http://www.ncbi.nlm.nih.gov/pubmed/10068714 Gout and hyperuricemia]. ''Am Fam Physician'' 1999 Feb 15;59(4):925-34.
* Pittman JR, Bross MH. [http://www.ncbi.nlm.nih.gov/pubmed/10208700 Diagnosis and management of gout]. ''Am Fam Physician'' 1999 Apr 1;59(7):1799-806, 1810.
* Qaseem A, Harris RP, Forciea MA. [http://annals.org/aim/article/2578528/management-acute-recurrent-gout-clinical-practice-guideline-from-american-college Management of Acute and Recurrent Gout]. ''Ann Intern Med'' 2016 Nov 1 10;7326/M16-0570.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/784-gout PEIR Digital Library: Gout Images]

== Related IPLab Cases ==
* [[IPLab:Lab 6:Rheumatoid Arthritis|Lab 6: Rheumatoid Arthritis]]

{{IPLab 5}}

[[Category: IPLab:Lab 5]]

IPLab:Lab 5:Gout

2016-12-05T12:23:11Z

Peter Anderson: /* Study Questions */

== Clinical Summary ==
This patient was diagnosed with gout approximately 20 years ago. At that time, he noted the gradual onset of pain in the left knee, followed by swelling, redness and heat, all of which persisted for approximately one month. Shortly thereafter, he had periodic episodes of hot, painful, swollen joints involving the left knee, left ankle, and both first metatarsophalangeal joints. At this time the patient was hospitalized for evaluation of these arthritides. Serum uric acid values on three separate occasions were 8.0, 9.3, and 8.7 mg/dl. In addition to the presence of the painful swollen joints, a gouty tophus was present on the left arm. The patient was readmitted to the hospital from time to time because of acute exacerbations of gouty arthritis. On the most recent hospital admission, a 3-cm tophus was found over the right elbow, as well as several smaller tophi over the right hand.

== Autopsy Findings ==
The specimen consisted of an elliptically shaped, mottled, yellow-white irregular hard mass, measuring 8.0 x 5.0 x 2.0 cm. in diameter.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab5Gout1.jpg|This is a gross photograph of an index finger from a patient with gout. The finger has been sectioned longitudinally to demonstrate the distal interphalangeal joint. Note the white chalky material within and adjacent to the joint (arrows).
File:IPLab5Gout2.jpg|This is a gross photograph of the elbow of this patient. The subcutaneous nodules (arrows) on this arm are tophi caused by gout.
File:IPLab5Gout3.jpg|This is a low-power photomicrograph of the tophus removed from the elbow of this patient. Note the fibrous connective tissue (1) and the large foci containing the urate crystals (2) surrounded by the intense chronic inflammatory reaction.
File:IPLab5Gout4.jpg|This higher-power photomicrograph of the tophus demonstrates the collections of urate crystals (1) and the inflammatory cells at the edge of these foci (2).
File:IPLab5Gout5.jpg|This is a higher-power photomicrograph of the edge of the tophus. Most of the urate crystals dissolve away during processing. The inflammatory cells at the edge of these foci are clearly visible (arrow).
File:IPLab5Gout6.jpg|This is a high-power photomicrograph of the edge of the tophus. The character of the intense chronic inflammatory cell reaction is evident and note the presence of giant cells within this inflammatory cell reaction (arrows).
File:IPLab5Gout7.jpg|This is a photomicrograph of a tophus that was fixed in alcohol prior to histologic processing. The alcohol fixation preserves the water soluble urate crystals within the tissue. Note the urate crystals visible in this photomicrograph (arrows). Also note the chronic inflammatory reaction in the background.
File:IPLab5Gout8.jpg|This is a gross photograph of a tophus on the great toe of another patient with gout (arrow). The healed surgical incision and the size of this tophus indicate that this was a long-standing problem for this patient.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab5Gout</peir-vm>

== Study Questions ==
* <spoiler text="What are the two types of gout and which is more common?">The main type is primary gout which makes up 90% of all cases. In most cases of primary gout the specific enzyme defect is unknown but there is some enzyme abnormality which leads to hyperuricemia and symptoms of gout. In about 10% of cases cases the enzyme defect is known, but gout symptomatology is the main clinical finding.

In secondary gout the cause of the hyperuricemia is known (e.g. leukemia, renal failure, Lesch-Nyhan syndrome).</spoiler>
* <spoiler text="What are the four stages of gout?"># Asymptomatic hyperuricemia
# Acute gouty arthritis
# Intercritical gout
# Chronic tophaceous gout.</spoiler>
* <spoiler text="Why is gout more severe in peripheral joints?">The decreased temperature accentuates the crystallization of monosodium urate (MSU).</spoiler>
* <spoiler text="What initiates the inflammatory reaction seen in the synovial membrane in gouty arthritis?">MSU crystals are chemotactic and they activate complement. This initiates a cascade of inflammatory events which leads to acute gouty arthritis.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/329958-overview eMedicine Medical Library: Gout and Pseudogout]
* [http://www.aafp.org/afp/1999/0215/p925.html American Academy of Family Physicians: Gout and Hyperuricemia]

=== Journal Articles ===
* Harris MD, Siegel LB, Alloway JA. [http://www.ncbi.nlm.nih.gov/pubmed/10068714 Gout and hyperuricemia]. ''Am Fam Physician'' 1999 Feb 15;59(4):925-34.
* Pittman JR, Bross MH. [http://www.ncbi.nlm.nih.gov/pubmed/10208700 Diagnosis and management of gout]. ''Am Fam Physician'' 1999 Apr 1;59(7):1799-806, 1810.
* Qaseem A, Harris RP, Forciea MA. [http://annals.org/aim/article/2578528/management-acute-recurrent-gout-clinical-practice-guideline-from-american-college Management of Acute and Recurrent Gout]. ''Ann Intern Med'' 2016 Nov 1 10;7326/M16-0570.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/784-gout PEIR Digital Library: Gout Images]

== Related IPLab Cases ==
* [[IPLab:Lab 6:Rheumatoid Arthritis|Lab 6: Rheumatoid Arthritis]]

{{IPLab 5}}

[[Category: IPLab:Lab 5]]

Main Page

2016-11-30T15:52:57Z

Peter Anderson:

<div id="mf-home">
Welcome to the Pathology Education Instructional Resource (PEIR), a web teaching resource and informatics training grounds developed and directed by Seung Park, MD and [https://apps.medicine.uab.edu/facultyDirectory/FacultyData.asp?s_org=392300000&vwAllfacultyPage=1&s_ApptType=Primary&FID=19493 Peter Anderson, DVM, PhD]. Please contact Dr. Anderson directly if you have any interest in contributing and/or editing content.

== PEIR Projects ==
=== Image Libraries ===
* The [{{SERVER}}/library PEIR Digital Library] contains more than 30,000 curated teaching images, and is our flagship project.
* [http://peir-vm.path.uab.edu/ PEIR-VM] is a compehensive teaching repository of whole slide images.

=== Teaching ===
* [[IPLab]] is a comprehensive online course in classic pathology.
* [[Histologic]] is a comprehensive histology manual.
* [[Cytologically Yours]] is an online cytopathology teaching resource for pathology residents and fellows.
* [[This Is Your Brain On Informatics]] consists of the class notes for GBSC703-01D/STP2146: "this is your brain, THIS IS YOUR BRAIN ON INFORMATICS".

__NOGLOSSARY__

Main Page

2016-11-30T15:51:11Z

Peter Anderson:

<div id="mf-home">
Welcome to the Pathology Education Instructional Resource (PEIR), a web teaching resource and informatics training grounds developed and directed by Seung Park, MD and [https://apps.medicine.uab.edu/facultyDirectory/FacultyData.asp?s_org=392300000&vwAllfacultyPage=1&s_ApptType=Primary&FID=19493 Peter Anderson, DVM, PhD]. Please contact one of us directly if you have any interest in contributing and/or editing content.

== PEIR Projects ==
=== Image Libraries ===
* The [{{SERVER}}/library PEIR Digital Library] contains more than 30,000 curated teaching images, and is our flagship project.
* [http://peir-vm.path.uab.edu/ PEIR-VM] is a compehensive teaching repository of whole slide images.

=== Teaching ===
* [[IPLab]] is a comprehensive online course in classic pathology.
* [[Histologic]] is a comprehensive histology manual.
* [[Cytologically Yours]] is an online cytopathology teaching resource for pathology residents and fellows.
* [[This Is Your Brain On Informatics]] consists of the class notes for GBSC703-01D/STP2146: "this is your brain, THIS IS YOUR BRAIN ON INFORMATICS".

__NOGLOSSARY__

IPLab:Lab 9:ARF

2016-11-29T14:52:41Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 21-year-old black male with sickle cell anemia had recurrent attacks of acute rheumatic fever beginning at age 14. Mitral insufficiency and stenosis were present by age 16. On prophylactic antibiotics, the patient had no evidence of recurrence until three weeks before his final admission, when an upper respiratory infection developed. A few weeks later he developed acute migratory polyarthritis. This was associated with rapid deterioration of cardiac function and death.

== Autopsy Findings ==
At autopsy, the heart was enlarged--weighing 675 grams--especially the left atrium. Both the aortic and mitral valves showed fibrosis as well as the fresh, tiny verrucae characteristic of acute rheumatic fever.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9ARF1.jpg|This is a gross photograph of mitral valve demonstrating marked thickening and fibrosis of the valve leaflet. There are also numerous foci of fibrinoid necrosis within the cusps and friable vegetations (verrucae) along the lines of closure (arrows). These irregular, warty projections are found at sites of erosion on the inflamed endocardial surface. The verrucae probably result from the precipitation of fibrin where the leaflets impinge on each other.
File:IPLab9ARF2.jpg|This is a low-power photomicrograph of heart tissue. Little can be seen at this magnification, except that the tissue looks relatively normal.
File:IPLab9ARF3.jpg|This is a higher-power photomicrograph of myocardium showing cellular accumulations--Aschoff bodies (arrows)--within the interstitium of the myocardium. These are found especially around blood vessels.
File:IPLab9ARF4.jpg|This is a higher-power photomicrograph of myocardium containing Aschoff bodies (arrows) within the interstitium.
File:IPLab9ARF5.jpg|This high-power photomicrograph of myocardium shows the cellular detail of an Aschoff body. Aschoff bodies are foci of fibrinoid necrosis surrounded by lymphocytes, macrophages, an occasional plasma cell, and plump “activated” histiocytes called Anitschkow cells or Aschoff cells (arrows). These distinctive cells have abundant amphophilic cytoplasm and central round-to-ovoid nuclei in which the chromatin is disposed in a central, slender, wavy ribbon resembling a caterpillar (hence the designation “caterpillar cells”).
File:IPLab9ARF6.jpg|This high-power photomicrograph of myocardium shows the cellular detail of another Aschoff body. In this case there appears to be a multinucleated Aschoff giant cell (arrow).
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9ARF</peir-vm>

== Study Questions ==
* <spoiler text="What is the etiology of rheumatic myocarditis?">Rheumatic fever is an acute, often recurrent, inflammatory disease that principally affects children following a pharyngeal (but not skin) infection with group A beta-hemolytic streptococci. Evidence strongly suggests that rheumatic fever is the result of an immune response to streptococcal antigens inciting either a cross-reaction to tissue antigens or a streptococcal-induced autoimmune reaction to normal tissue antigens.</spoiler>
* <spoiler text="Would it be possible to culture the causative agent from these lesions on the heart valves?">No. Rheumatic fever is an immune-mediated disease. No organisms can be cultured from the heart valves or from the Aschoff bodies.</spoiler>
* <spoiler text="Is this case an example of acute rheumatic fever?">Yes and no!

This patient has acute ramifications of rheumatic fever (acute valve lesions and Aschoff bodies) but there are also a number of old lesions in the heart suggesting that this patient has had numerous bouts of rheumatic fever over the course of many years.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/236582-overview eMedicine Medical Library: Rheumatic Fever]
* [http://emedicine.medscape.com/article/808945-overview eMedicine Medical Library: Rheumatic Fever in Emergency Medicine]
* [http://emedicine.medscape.com/article/333103-overview eMedicine Medical Library: Acute Rheumatic Fever]
* [http://www.merckmanuals.com/professional/pediatrics/rheumatic_fever/rheumatic_fever.html Merck Manual: Rheumatic Fever]

=== Journal Articles ===
* American Heart Association Committee on Rheumatic Fever. [http://dx.doi.org/10.1161/CIR.0000000000000205 Revision of the Jones Criteria for the Diagnosis of Acute Rheumatic Fever in the Era of Doppler Echocardiography]. ''Circulation'' 2015 April 23; 131:1806-1818.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2153-streptococcus PEIR Digital Library: Streptococcus Images]
* [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html#8 Webpath: Myocarditis]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 1:Fat Necrosis

2016-11-21T18:30:21Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This was a 37-year-old female with chronic renal failure that necessitated a renal transplant. Following transplantation, the patient developed a herpes simplex virus (HSV) infection in her nasal cavity, oral candidiasis, pneumonia, hematuria, pyuria, and gastrointestinal bleeding. Subsequently, the patient became septic and died.

== Autopsy Findings ==
Major findings at autopsy included extensive hemorrhagic bronchopneumonia (Pseudomonas aeruginosa) and multiple ulcers affecting the stomach and esophagus. There was also evidence of disseminated intravascular coagulation (DIC) with multiple hemorrhages present. Firm, whitish foci of necrotic tissue were found in the fat around the pancreas.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab1FatNecrosis1.jpg|This gross photograph shows the intestines and omentum at autopsy. Note the small (5-15 mm in diameter) white nodules on the surface of the omental and mesenteric fat tissue (arrows).
File:IPLab1FatNecrosis2.jpg|This gross photograph of the pancreas from this case shows white nodules (arrows) in the pancreas and the adjacent mesenteric fat tissue.
File:IPLab1FatNecrosis3.jpg|This low-power photomicrograph of the pancreas from this case shows the fat tissue (1) surrounding the pancreas. Note the rim of inflammatory cells (arrows) and the blue areas in the fat adjacent to the pancreas (2).
File:IPLab1FatNecrosis4.jpg|This high-power photomicrograph shows areas of inflammation (1) and fat necrosis (arrows) in the peripancreatic fat tissue (2) of the pancreas from this case.
File:IPLab1FatNecrosis5.jpg|Another high-power photomicrograph shows blue discoloration in the fat tissue in the interlobular spaces (1) of the pancreas.
File:IPLab1FatNecrosis6.jpg|A higher-power photomicrograph of the previous slide contains a small area of fat necrosis (1) in the upper right portion of the image. The fat necrosis is within the fat tissue that is normally found adjacent to the pancreas. The appearance of the pancreatic tissue in this area is somewhat disrupted due to autolysis (the pancreas autolyzes very rapidly after death) but there is some premortem necrosis as well.
File:IPLab1FatNecrosis7.jpg|This is a higher-power photomicrograph of the fat necrosis involving the fat cells in the interlobular spaces (arrow) of the pancreas. Note the blue to purple staining of the calcium deposits within the fat cells.
File:IPLab1FatNecrosis8.jpg|This high-power photomicrograph demonstrates fat necrosis in the interlobular spaces of the pancreas. Note the granular blue-staining calcium deposits (arrows) within the fat cells. The clear areas represent artifact caused by the "washing-out" of fat from cells during tissue processing for histology.
File:IPLab1FatNecrosis9.jpg|This is another high-power photomicrograph demonstrating the calcification (arrows) seen in fat necrosis involving the interlobular spaces of the pancreas.
</gallery>

== Virtual Microscopy ==
=== Pancreatic Fat Necrosis ===
<peir-vm>IPLab1FatNecrosis</peir-vm>

=== Normal Pancreas ===
<peir-vm>UAB-Histology-00154</peir-vm>

== Study Questions ==
* <spoiler text="What is the definition of enzymatic fat necrosis?">Focal areas of destruction of fat tissue resulting from abnormal release of activated lipases.</spoiler>
* <spoiler text="Where else can enzymatic fat necrosis occur besides the pancreas?">Salivary glands.</spoiler>
* <spoiler text="What causes the formation of the white, chalky, nodules that are seen in the fat tissue adjacent to the pancreatic tissue?">Injury to the pancreas (infection, toxins, viruses, trauma, ischemia) causes release of activated pancreatic enzymes which liquefy fat cell membranes. The released lipases split the triglyceride esters contained within the fat cells and these released fatty acids combine with calcium to form the grossly visible chalky white nodules characteristic of fat necrosis.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/775867-overview eMedicine Medical Library: Emergent Management of Pancreatitis]
* [http://www.merckmanuals.com/professional/gastrointestinal_disorders/pancreatitis/acute_pancreatitis.html Merck Manual: Acute Pancreatitis]

=== Journal Articles ===
* Forsmark CE, Vege SS, Wilcox CM. [http://www.nejm.org/doi/full/10.1056/NEJMra1505202 Acute Pericarditis]. ''N Engl J Med" 2016; 375:1972-1981. November 17, 2016.
* LeWinter MM. [http://http://www.nejm.org/doi/full/10.1056/NEJMcp1404070 Acute Pericarditis]. ''NEJM'' 2014 Dec 18;371:2410-2416.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/333-pancreas PEIR Digital Library: Pancreas Images]
* [http://library.med.utah.edu/WebPath/CINJHTML/CINJIDX.html WebPath: Cellular Injury Images]

{{Template:IPLab 1}}

[[Category:IPLab:Lab 1]]

IPLab:Lab 5:Gout

2016-11-04T13:30:21Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This patient was diagnosed with gout approximately 20 years ago. At that time, he noted the gradual onset of pain in the left knee, followed by swelling, redness and heat, all of which persisted for approximately one month. Shortly thereafter, he had periodic episodes of hot, painful, swollen joints involving the left knee, left ankle, and both first metatarsophalangeal joints. At this time the patient was hospitalized for evaluation of these arthritides. Serum uric acid values on three separate occasions were 8.0, 9.3, and 8.7 mg/dl. In addition to the presence of the painful swollen joints, a gouty tophus was present on the left arm. The patient was readmitted to the hospital from time to time because of acute exacerbations of gouty arthritis. On the most recent hospital admission, a 3-cm tophus was found over the right elbow, as well as several smaller tophi over the right hand.

== Autopsy Findings ==
The specimen consisted of an elliptically shaped, mottled, yellow-white irregular hard mass, measuring 8.0 x 5.0 x 2.0 cm. in diameter.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab5Gout1.jpg|This is a gross photograph of an index finger from a patient with gout. The finger has been sectioned longitudinally to demonstrate the distal interphalangeal joint. Note the white chalky material within and adjacent to the joint (arrows).
File:IPLab5Gout2.jpg|This is a gross photograph of the elbow of this patient. The subcutaneous nodules (arrows) on this arm are tophi caused by gout.
File:IPLab5Gout3.jpg|This is a low-power photomicrograph of the tophus removed from the elbow of this patient. Note the fibrous connective tissue (1) and the large foci containing the urate crystals (2) surrounded by the intense chronic inflammatory reaction.
File:IPLab5Gout4.jpg|This higher-power photomicrograph of the tophus demonstrates the collections of urate crystals (1) and the inflammatory cells at the edge of these foci (2).
File:IPLab5Gout5.jpg|This is a higher-power photomicrograph of the edge of the tophus. Most of the urate crystals dissolve away during processing. The inflammatory cells at the edge of these foci are clearly visible (arrow).
File:IPLab5Gout6.jpg|This is a high-power photomicrograph of the edge of the tophus. The character of the intense chronic inflammatory cell reaction is evident and note the presence of giant cells within this inflammatory cell reaction (arrows).
File:IPLab5Gout7.jpg|This is a photomicrograph of a tophus that was fixed in alcohol prior to histologic processing. The alcohol fixation preserves the water soluble urate crystals within the tissue. Note the urate crystals visible in this photomicrograph (arrows). Also note the chronic inflammatory reaction in the background.
File:IPLab5Gout8.jpg|This is a gross photograph of a tophus on the great toe of another patient with gout (arrow). The healed surgical incision and the size of this tophus indicate that this was a long-standing problem for this patient.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab5Gout</peir-vm>

== Study Questions ==
* <spoiler text="What are the two types of gout and which is more common?">The main type is primary gout which makes up 90% of all cases. In most cases of primary gout the enzyme defect is unknown. In rare cases the enzyme defect is known, but gout symptomatology is the main clinical finding.

In secondary gout the cause of the hyperuricemia is known (e.g. leukemia, renal failure, Lesch-Nyhan syndrome).</spoiler>
* <spoiler text="What are the four stages of gout?"># Asymptomatic hyperuricemia
# Acute gouty arthritis
# Intercritical gout
# Chronic tophaceous gout.</spoiler>
* <spoiler text="Why is gout more severe in peripheral joints?">The decreased temperature accentuates the crystallization of monosodium urate (MSU).</spoiler>
* <spoiler text="What initiates the inflammatory reaction seen in the synovial membrane in gouty arthritis?">MSU crystals are chemotactic and they activate complement. This initiates a cascade of inflammatory events which leads to acute gouty arthritis.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/329958-overview eMedicine Medical Library: Gout and Pseudogout]
* [http://www.aafp.org/afp/1999/0215/p925.html American Academy of Family Physicians: Gout and Hyperuricemia]

=== Journal Articles ===
* Harris MD, Siegel LB, Alloway JA. [http://www.ncbi.nlm.nih.gov/pubmed/10068714 Gout and hyperuricemia]. ''Am Fam Physician'' 1999 Feb 15;59(4):925-34.
* Pittman JR, Bross MH. [http://www.ncbi.nlm.nih.gov/pubmed/10208700 Diagnosis and management of gout]. ''Am Fam Physician'' 1999 Apr 1;59(7):1799-806, 1810.
* Qaseem A, Harris RP, Forciea MA. [http://annals.org/aim/article/2578528/management-acute-recurrent-gout-clinical-practice-guideline-from-american-college Management of Acute and Recurrent Gout]. ''Ann Intern Med'' 2016 Nov 1 10;7326/M16-0570.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/784-gout PEIR Digital Library: Gout Images]

== Related IPLab Cases ==
* [[IPLab:Lab 6:Rheumatoid Arthritis|Lab 6: Rheumatoid Arthritis]]

{{IPLab 5}}

[[Category: IPLab:Lab 5]]

File:IPLab1Tuberculosis8b.jpg

2016-10-31T18:55:43Z

Peter Anderson: This is a high-power photomicrograph of Langhans-type multinucleated giant cells (arrows) that are characteristic of tuberculous granulomas. Note the ring of the nuclei in these giant cells.

This is a high-power photomicrograph of Langhans-type multinucleated giant cells (arrows) that are characteristic of tuberculous granulomas. Note the ring of the nuclei in these giant cells.

IPLab:Lab 1:Tuberculosis

2016-10-31T18:52:33Z

Peter Anderson: /* Images */

== Clinical Summary ==
This 70-year-old man was admitted to the hospital with a history of upper abdominal pain, anorexia, nausea, and general malaise, all of approximately three weeks' duration. His hospital stay was characterized by fever and severe respiratory distress. There were multiple densities in the patient's chest x-ray consistent with pneumonia and examination of a stained sputum specimen showed acid fast bacilli. Despite intensive therapy, the patient progressively deteriorated and died 14 days after admission.

== Autopsy Findings ==
It was determined at autopsy that the patient suffered from pulmonary tuberculosis with widespread dissemination throughout the body. The left lung weighed 620 grams and the right lung 1230 grams. These were characterized by marked pulmonary congestion and pulmonary edema. In addition, multiple gray-white nodules ranging from pinpoint size up to 1 cm were diffusely distributed throughout the lung parenchyma.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab1Tuberculosis1.jpg|This is a gross photograph of a cut section of lung from this patient with disseminated tuberculosis. The numerous small white nodules scattered throughout this lung tissue represent individual tuberculosis granulomas. In addition, note the dark areas throughout the lung which represent deposits of anthracotic pigment.
File:IPLab1Tuberculosis2.jpg|This is a closer view of the same section of lung containing multiple white granulomas which are now more easily identified (arrows). These lesions are referred to as miliary tuberculosis. Dark areas of anthracosis are also prominent in this lung.
File:IPLab1Tuberculosis3.jpg|This gross photograph shows hilar lymph nodes from another patient with disseminated tuberculosis. The white, cheesy-appearing nodules (arrows) in the lymph nodes give rise to the descriptive terminology of caseous necrosis. The black pigment in the lymph nodes is anthracotic pigment that has drained from the lungs.
File:IPLab1Tuberculosis4.jpg|This is a low-power photomicrograph of a histology section from the lung of this patient with a chronic history of respiratory disease. Note the multiple eosinophilic nodules (arrows) seen at low power in this section. Other areas of the lung are relatively normal and several bronchi and large vessels can be seen at this low power. The pleural surface of the lung is at the left and the remaining edges are cut edges of the tissue block.
File:IPLab1Tuberculosis5.jpg|This higher-power photomicrograph of the eosinophilic nodules (arrows) illustrates their discreet nature and the surrounding inflammatory response in the remaining normal lung tissue.
File:IPLab1Tuberculosis6.jpg|This photomicrograph shows a single nodule with an amorphous eosinophilic center and accumulations of cells around the outer edge. This is typical of a granuloma associated with tuberculosis in which there is a necrotic center (1) and a rim of lymphocytes, macrophages, and occasional multinucleated giant cells around the periphery.
File:IPLab1Tuberculosis7.jpg|This is a higher-power view of the granuloma with the amorphous eosinophilic material representing caseation necrosis (1), giant cells near the center (2), and inflammatory cells around the periphery.
File:IPLab1Tuberculosis8b.jpg|This is a high-power photomicrograph of Langhans-type multinucleated giant cells (arrows) that are characteristic of tuberculous granulomas. Note the ring of the nuclei in these giant cells.
</gallery>

== Virtual Microscopy ==
=== Lung: Tuberculosis ===
<peir-vm>IPLab1Tuberculosis</peir-vm>

=== Normal Lung ===
<peir-vm>UAB-Histology-00107</peir-vm>

== Study Questions ==
* <spoiler text="From where does the term caseous necrosis originate?">"Caseous" means "cheesy." Grossly, the lesions look white and cheesy.</spoiler>
* <spoiler text="What makes up the caseous core of the lesion in this case?">Amorphous granular debris composed of fragmented, coagulated cells enclosed within a granuloma.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/230802-overview eMedicine Medical Library: Tuberculosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/mycobacteria/tuberculosis_tb.html Merck Manual: Tuberculosis]
* [http://www.cdc.gov/tb/ Centers for Disease Control: Tuberculosis]

=== Journal Articles ===
* Lee MP, Chan JW, Ng KK, Li PC. [http://www.ncbi.nlm.nih.gov/pubmed/11192558 Clinical manifestations of tuberculosis in HIV-infected patients]. ''Respirology'' 2000 Dec;5(4):423-6.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/259-tuberculosis PEIR Digital Library: Tuberculosis Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#4 WebPath: Granulomatous Disease Images]

== Related IPLab Cases ==
* [[IPLab:Lab 3:Tuberculosis|Lab 3: Lung: Tuberculosis]]
* [[IPLab:Lab 6:Tuberculosis|Lab 6: Lung: Tuberculosis]]

{{Template:IPLab 1}}

[[Category:IPLab:Lab 1]]

IPLab:Lab 1:Tuberculosis

2016-10-31T18:48:52Z

Peter Anderson: /* Images */

== Clinical Summary ==
This 70-year-old man was admitted to the hospital with a history of upper abdominal pain, anorexia, nausea, and general malaise, all of approximately three weeks' duration. His hospital stay was characterized by fever and severe respiratory distress. There were multiple densities in the patient's chest x-ray consistent with pneumonia and examination of a stained sputum specimen showed acid fast bacilli. Despite intensive therapy, the patient progressively deteriorated and died 14 days after admission.

== Autopsy Findings ==
It was determined at autopsy that the patient suffered from pulmonary tuberculosis with widespread dissemination throughout the body. The left lung weighed 620 grams and the right lung 1230 grams. These were characterized by marked pulmonary congestion and pulmonary edema. In addition, multiple gray-white nodules ranging from pinpoint size up to 1 cm were diffusely distributed throughout the lung parenchyma.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab1Tuberculosis1.jpg|This is a gross photograph of a cut section of lung from this patient with disseminated tuberculosis. The numerous small white nodules scattered throughout this lung tissue represent individual tuberculosis granulomas. In addition, note the dark areas throughout the lung which represent deposits of anthracotic pigment.
File:IPLab1Tuberculosis2.jpg|This is a closer view of the same section of lung containing multiple white granulomas which are now more easily identified (arrows). These lesions are referred to as miliary tuberculosis. Dark areas of anthracosis are also prominent in this lung.
File:IPLab1Tuberculosis3.jpg|This gross photograph shows hilar lymph nodes from another patient with disseminated tuberculosis. The white, cheesy-appearing nodules (arrows) in the lymph nodes give rise to the descriptive terminology of caseous necrosis. The black pigment in the lymph nodes is anthracotic pigment that has drained from the lungs.
File:IPLab1Tuberculosis4.jpg|This is a low-power photomicrograph of a histology section from the lung of this patient with a chronic history of respiratory disease. Note the multiple eosinophilic nodules (arrows) seen at low power in this section. Other areas of the lung are relatively normal and several bronchi and large vessels can be seen at this low power. The pleural surface of the lung is at the left and the remaining edges are cut edges of the tissue block.
File:IPLab1Tuberculosis5.jpg|This higher-power photomicrograph of the eosinophilic nodules (arrows) illustrates their discreet nature and the surrounding inflammatory response in the remaining normal lung tissue.
File:IPLab1Tuberculosis6.jpg|This photomicrograph shows a single nodule with an amorphous eosinophilic center and accumulations of cells around the outer edge. This is typical of a granuloma associated with tuberculosis in which there is a necrotic center (1) and a rim of lymphocytes, macrophages, and occasional multinucleated giant cells around the periphery.
File:IPLab1Tuberculosis7.jpg|This is a higher-power view of the granuloma with the amorphous eosinophilic material representing caseation necrosis (1), giant cells near the center (2), and inflammatory cells around the periphery.
File:IPLab1Tuberculosis8.jpg|This is a high-power photomicrograph of Langhans-type multinucleated giant cells (arrows) that are characteristic of tuberculous granulomas. Note the ring of the nuclei in these giant cells.
</gallery>

== Virtual Microscopy ==
=== Lung: Tuberculosis ===
<peir-vm>IPLab1Tuberculosis</peir-vm>

=== Normal Lung ===
<peir-vm>UAB-Histology-00107</peir-vm>

== Study Questions ==
* <spoiler text="From where does the term caseous necrosis originate?">"Caseous" means "cheesy." Grossly, the lesions look white and cheesy.</spoiler>
* <spoiler text="What makes up the caseous core of the lesion in this case?">Amorphous granular debris composed of fragmented, coagulated cells enclosed within a granuloma.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/230802-overview eMedicine Medical Library: Tuberculosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/mycobacteria/tuberculosis_tb.html Merck Manual: Tuberculosis]
* [http://www.cdc.gov/tb/ Centers for Disease Control: Tuberculosis]

=== Journal Articles ===
* Lee MP, Chan JW, Ng KK, Li PC. [http://www.ncbi.nlm.nih.gov/pubmed/11192558 Clinical manifestations of tuberculosis in HIV-infected patients]. ''Respirology'' 2000 Dec;5(4):423-6.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/259-tuberculosis PEIR Digital Library: Tuberculosis Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#4 WebPath: Granulomatous Disease Images]

== Related IPLab Cases ==
* [[IPLab:Lab 3:Tuberculosis|Lab 3: Lung: Tuberculosis]]
* [[IPLab:Lab 6:Tuberculosis|Lab 6: Lung: Tuberculosis]]

{{Template:IPLab 1}}

[[Category:IPLab:Lab 1]]

File:IPLab1Tuberculosis8.jpg

2016-10-31T18:42:00Z

Peter Anderson: Peter Anderson uploaded a new version of "File:IPLab1Tuberculosis8.jpg"

This is a high-power photomicrograph of the Langhans-type multinucleated giant cell which is characteristic of tuberculous granulomas (arrow). Note the horseshoe shape of the nuclei in this giant cell. The majority of the cells in the upper left portion of this section are macrophages which provide the major cellular component in a granuloma. Note the smaller number of small blue-staining cells in the peripheral portions of this granuloma to the left of which are lymphocytes.

IPLab:Lab 6:Graves Disease

2016-10-20T13:01:14Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 18-year-old girl presented with complaints of swelling in the neck, weight loss, bulging of the eyes, tremor, decreased heat tolerance, loose stools, and occasional palpitations. Physical examination revealed normal blood pressure, resting tachycardia of 110 beats per minute, mild exophthalmos, eyelid lag, and a diffusely enlarged thyroid gland. Pertinent laboratory findings were thyroxine (T4) level 30.8 mcg/dL, free thyroxine was 2.7 ng/dL, and thyroid stimulating hormone (TSH) was 0.22 mcIU/mL. She was given propylthiouracil until she became nearly euthyroid, at which time a thyroidectomy was done.

== Autopsy Findings ==
The thyroid gland weighed 45 grams. It was beefy red in color and had a homogeneous fleshy consistency.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab6GravesDisease1.jpg|This is a photograph of the thyroid from this case. Note that the gland is enlarged and is dark red.
File:IPLab6GravesDisease2.jpg|This is a low-power photomicrograph of thyroid tissue from this case. The tissue is very cellular with very little colloid.
File:IPLab6GravesDisease3.jpg|This is a higher-power photomicrograph of thyroid. The tissue is very cellular and there is little colloid.
File:IPLab6GravesDisease4.jpg|This is a high-power photomicrograph of thyroid. Note the cellularity of the tissue with marked infolding of the epithelial tissue.
File:IPLab6GravesDisease5.jpg|This is a high-power photomicrograph of thyroid. Note the papillary projections and the moth-eaten appearance of the colloid. This appearance indicates active absorption of the colloid to form thyroglobulin.
File:IPLab6GravesDisease6.jpg|This is a gross photograph of a thyroid from a case of nodular goiter.
File:IPLab6GravesDisease7.jpg|Closer view of cut surface of the thyroid with nodular goiter. Note the multilobular appearance of the tissue.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab6GravesDisease</peir-vm>

== Study Questions ==
* <spoiler text="What is the immunologic mechanism responsible for Graves' disease?">Autoantibodies directed towards the TSH receptor of the thyroid cause stimulation of the thyroid leading to increased secretion of thyroid hormones and growth of the thyroid gland.</spoiler>
* <spoiler text="What role does genetics play in the predisposition to Graves' disease?">* Graves' disease is more common in females than males
* It has been linked to HLA-B8 and DR3 in whites but different haplotypes in Asians
* It has a familial predisposition
* It is more common in patients with other forms of autoimmune thyroid problems (e.g., Hashimoto's thyroiditis)</spoiler>
* <spoiler text="Does Graves' disease predispose to thyroid cancer?">There is little evidence to suggest an increased frequency of thyroid cancer in patients with Graves' disease.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/920283-overview eMedicine Medical Library: Pediatric Graves Disease]
* [http://emedicine.medscape.com/article/767130-overview eMedicine Medical Library: Hyperthyroidism, Thyroid Storm, and Graves Disease]
* [http://emedicine.medscape.com/article/120034-overview eMedicine Medical Library: Goiter]
* [http://emedicine.medscape.com/article/120140-overview eMedicine Medical Library: Diffuse Toxic Goiter]
* [http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/thyroid_disorders/overview_of_thyroid_function.html Merck Manual: Overview of Thyroid Function]
* [http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/thyroid_disorders/hyperthyroidism.html Merck Manual: Hyperthyroidism]

=== Journal Articles ===
* Smith TJ and Hegedüs L. [http://www.nejm.org/doi/full/10.1056/NEJMra1510030 Graves’ Disease]. NEJM 2016 375:1552-1565.
* Fraser T, Green D. [http://www.ncbi.nlm.nih.gov/pubmed/11554873 Weathering the storm: beta-blockade and the potential for disaster in severe hyperthyroidism]. ''Emerg Med (Fremantle)'' 2001 Sep;13(3):376-80.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/15-endocrine/140-thyroid/651-autoimmune_thyroiditis PEIR Digital Library: Autoimmune Thyroiditis Images]
* [http://library.med.utah.edu/WebPath/ENDOHTML/ENDOIDX.html Webpath: Endocrine Pathology]

== Related IPLab Cases ==
* [[IPLab:Lab 6:Hashimoto's Thyroiditis|Lab 6: Thyroid: Hashimoto's Thyroiditis]]
* [[IPLab:Lab 7:Adenoma|Lab 7: Thyroid: Adenoma]]

{{IPLab 6}}

[[Category: IPLab:Lab 6]]

IPLab:Lab 7:Esophagus SCC

2016-09-19T16:42:05Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
Approximately six months prior to admission, this 78-year-old male began having difficulty in swallowing solid food. This difficulty was described as a sticking of the food in his throat and was accompanied by cramping pain which could only be relieved by "coughing up" the ingested food. This dysphagia was accompanied by a twenty-pound weight loss. Following an upper GI series and endoscopic biopsy, the patient was given radiation treatment with considerable improvement. He did well for four months, after which the dysphagia and weight loss increased markedly. He refused operative intervention or further treatment and he died at home two months later.

== Autopsy Findings ==
An autopsy revealed a circumferential fungating mass in the distal third of the esophagus. This mass partially occluded the lumen of the esophagus.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab7EsophSCC1.jpg|This is a gross photograph of the luminal surface of the esophagus with the area of constriction (1). The area protrudes into the lumen. There is also a central area of ulceration (2).
File:IPLab7EsophSCC2.jpg|This low-power photomicrograph of a cross-section through the esophagus at the area of constriction shows extensive infiltration of the esophageal wall with squamous cell carcinoma (arrows).
File:IPLab7EsophSCC3.jpg|This is a high-power photomicrograph demonstrating the normal epithelium undergoing transition to carcinoma (arrows).
File:IPLab7EsophSCC4.jpg|This is a higher-power photomicrograph showing invasive squamous cell carcinoma. Tongues and islands of tumor cells exhibit areas of central necrosis (arrow).
File:IPLab7EsophSCC5.jpg|This is a photomicrograph of bands of tumor cells invading into the adjacent tissues (arrows).
File:IPLab7EsophSCC6.jpg|This is a higher-power photomicrograph of bands of tumor cells (arrows) extending between the muscle bundles.
File:IPLab7EsophSCC7.jpg|This is a high-power photomicrograph of the tumor cells that have invaded the adjacent muscle tissue.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab7EsophSCC</peir-vm>

== Study Questions ==
* <spoiler text="Is squamous cell carcinoma of the esophagus more common in men or in women?">Men. The male-to-female ratio falls in the range of 2:1 to as high as 20:1.</spoiler>
* <spoiler text="What risk factors predispose to squamous cell carcinoma of the esophagus?">* Deficiency of vitamins A, C, riboflavin, thiamine or pyridoxine;
* deficiency of trace metals (zinc or molybdenum);
* fungal contamination of foodstuffs;
* increases in nitrites/nitrates;
* alcohol consumption (hard liquor is worse than beer or wine);
* tobacco use;
* long-standing esophagitis;
* achalasia;
* celiac disease;
* genetic (racial) predisposition.</spoiler>
* <spoiler text="What factors facilitate growth and spread of this tumor?">The rich lymphatic network in the submucosa of the esophagus promotes extensive circumferential and longitudinal spread. Intramural tumor cell clusters are often seen several centimeters away from the main tumor mass. Local extension into adjacent mediastinal structures occurs early and often in this disease and seriously limits the chance of curative resection.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1965430-overview eMedicine Medical Library: Head and Neck Cutaneous Squamous Cell Carcinoma]
* [http://www.merckmanuals.com/professional/dermatologic_disorders/cancers_of_the_skin/overview_of_skin_cancer.html Merck Manual: Overview of Skin Cancer]
* [http://www.merckmanuals.com/professional/dermatologic_disorders/cancers_of_the_skin/squamous_cell_carcinoma.html Merck Manual: Squamous Cell Carcinoma]

=== Journal Articles ===
* Shibata H, Matsubara O. [http://www.ncbi.nlm.nih.gov/pubmed/11472561 Apoptosis as an independent prognostic indicator in squamous cell carcinoma of the esophagus]. ''Pathol Int'' 2001 Jul;51(7):498-503.
* Wu S, Powers S, Zhu W, Hannun YA. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4836858/ Substantial contribution of extrinsic risk factors to cancer development]. ''Nature'' 2016 Jan 7; 529(7584): 43–47.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/254-squamous_cell_carcinoma PEIR Digital Library: Squamous Cell Carcinoma Images]
* [http://library.med.utah.edu/WebPath/NEOHTML/NEOPLIDX.html WebPath: Neoplasia]

== Related IPLab Cases ==
* [[IPLab:Lab 7:Lip SCC|Lab 7: Lip: Squamous Cell Carcinoma]]
* [[IPLab:Lab 7:IDC|Lab 7: Breast: Infiltrating Ductal Carcinoma]]
* [[IPLab:Lab 7:Bronchogenic Carcinoma|Lab 7: Lung: Bronchogenic Carcinoma]]
* [[IPLab:Lab 7:Adenocarcinoma|Lab 7: Colon: Adenocarcinoma]]
* [[IPLab:Lab 7:Metastatic Adenocarcinoma|Lab 7: Lung & Liver: Metastatic Adenocarcinoma]]

{{IPLab 7}}

[[Category: IPLab:Lab 7]]

IPLab:Lab 7:Lip SCC

2016-09-01T18:17:34Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 63-year-old white male had recurrent thickening and scaling of the lower lip for two years. In recent months, it had undergone ulceration and progressive enlargement. The lesion was excised by a wedge resection.

== Autopsy Findings ==
The specimen was triangular in shape; the upper part was covered by mucosa and the lower part by skin. At the junction of the mucosa and skin there was a 2 x 1.4 cm oval shaped superficial lesion which was flat, firm, and had raised borders. The base was orange.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab7LipSCC1.jpg|This is a pre-op photograph of this patient with an ulcerated lesion on his lip (arrow). Also note that the lip is somewhat thickened. The area for surgical excision is delineated by black marker.
File:IPLab7LipSCC2.jpg|This is a low-power photomicrograph of squamous cell carcinoma of the lip. Note focal ulceration (1) and tumor infiltration at the vermilion border (2).
File:IPLab7LipSCC3.jpg|This photomicrograph shows a large area of ulceration (arrow) with underlying congestion and hemorrhage. The area of ulceration is adjacent to an area of tumor infiltration.
File:IPLab7LipSCC4.jpg|This is a higher-power photomicrograph of the well-differentiated squamous cell carcinoma and the inflammatory cell infiltration.
File:IPLab7LipSCC5.jpg|This is a higher-power photomicrograph of infiltrating squamous cell carcinoma and inflammatory cells.
File:IPLab7LipSCC6.jpg|This is a high power photomicrograph of the well-differentiated squamous cell carcinoma. Note the intracytoplasmic keratinization which gives the cells a glassy appearance. The focal accumulations of keratinized cells are called keratin pearls (arrows).
File:IPLab7LipSCC7.jpg|This is a high power photomicrograph of a poorly-differentiated area of tumor. Note the spindle-shaped cells and the irregular pattern of growth.
File:IPLab7LipSCC8.jpg|This is a section of muscle tissue from this biopsy of the lip. Note that the squamous cell carcinoma has infiltrated into the muscle tissue. There are also inflammatory cells within this area of tumor infiltration.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab7LipSCC</peir-vm>

== Study Questions ==
* <spoiler text="What is the most common type of tumor in the oral cavity?">Squamous cell carcinomas make up at least 95% of cancers of the oral cavity (including the tongue). Other tumors include adenocarcinomas (of mucous gland origin), melanomas, various carcinomas, and other rarities. The incidence of oral squamous cell cancers in the United States is about 4% for men and 2% for women.</spoiler>
* <spoiler text="What risk factors are associated with oral squamous cell carcinoma?">Tobacco and alcohol. Nondrinking smokers have a 2- to 4-fold greater risk of developing these cancers than matched control subjects, which increases to 6- to 15-fold with both drinking and smoking. The risk of cancer is quantitatively associated with the amount of smoking and of alcohol consumption. Chewing tobacco and buccal pouches are the highest risk.</spoiler>
* <spoiler text="What is the prognosis with this type of tumor?">The prognosis is best with lip lesions--the 5-year recurrence-free rate approximating 90%--and poorest with tumors in the floor of the mouth and at the base of the tongue--yielding only 20 to 30% 5-year recurrence-free rates. All squamous cell carcinomas of the oral cavity take months to years to progress from carcinoma in situ (after being preceded by leukoplakia) to invasive cancer.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1965430-overview eMedicine Medical Library: Head and Neck Cutaneous Squamous Cell Carcinoma]
* [http://www.merckmanuals.com/professional/dermatologic_disorders/cancers_of_the_skin/overview_of_skin_cancer.html Merck Manual: Overview of Skin Cancer]
* [http://www.merckmanuals.com/professional/dermatologic_disorders/cancers_of_the_skin/squamous_cell_carcinoma.html Merck Manual: Squamous Cell Carcinoma]

=== Journal Articles ===
* Guenthner ST, Hurwitz RM, Buckel LJ, Gray HR. [http://www.ncbi.nlm.nih.gov/pubmed/10459120 Cutaneous squamous cell carcinomas consistently show histologic evidence of in situ changes: a clinicopathologic correlation]. ''J Am Acad Dermatol'' 1999 Sep;41(3 Pt 1):443-8.
* Ling S, Hu Z, Yang Z, Yang F, Li Y, Lin P, Chen K, Dong L, Cao L, Tao Y, Hao L, Chen Q, Gong Q, Wu D, Li W, Zhao W, Tian X, Hao C,Hungate EA, Catenacci DV, Hudson RR, Li WH, Lu X, Wu CI. [http://www.pnas.org/content/112/47/E6496.full.pdf Extremely high genetic diversity in a single tumor points to prevalence of non-Darwinian cell evolution.]. ''Proc Natl Acad Sci U S A'' 2015 Nov 24;112(47):E6496-505.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/254-squamous_cell_carcinoma PEIR Digital Library: Squamous Cell Carcinoma Images]
* [http://library.med.utah.edu/WebPath/NEOHTML/NEOPLIDX.html WebPath: Neoplasia]

== Related IPLab Cases ==
* [[IPLab:Lab 7:Esophagus SCC|Lab 7: Esophagus: Squamous Cell Carcinoma]]
* [[IPLab:Lab 7:IDC|Lab 7: Breast: Infiltrating Ductal Carcinoma]]
* [[IPLab:Lab 7:Bronchogenic Carcinoma|Lab 7: Lung: Bronchogenic Carcinoma]]
* [[IPLab:Lab 7:Adenocarcinoma|Lab 7: Colon: Adenocarcinoma]]
* [[IPLab:Lab 7:Metastatic Adenocarcinoma|Lab 7: Lung & Liver: Metastatic Adenocarcinoma]]

{{IPLab 7}}

[[Category: IPLab:Lab 7]]

IPLab:Lab 1:Fat Necrosis

2016-08-25T14:36:35Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This was a 37-year-old female with chronic renal failure that necessitated a renal transplant. Following transplantation, the patient developed a herpes simplex virus (HSV) infection in her nasal cavity, oral candidiasis, pneumonia, hematuria, pyuria, and gastrointestinal bleeding. Subsequently, the patient became septic and died.

== Autopsy Findings ==
Major findings at autopsy included extensive hemorrhagic bronchopneumonia (Pseudomonas aeruginosa) and multiple ulcers affecting the stomach and esophagus. There was also evidence of disseminated intravascular coagulation (DIC) with multiple hemorrhages present. Firm, whitish foci of necrotic tissue were found in the fat around the pancreas.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab1FatNecrosis1.jpg|This gross photograph shows the intestines and omentum at autopsy. Note the small (5-15 mm in diameter) white nodules on the surface of the omental and mesenteric fat tissue (arrows).
File:IPLab1FatNecrosis2.jpg|This gross photograph of the pancreas from this case shows white nodules (arrows) in the pancreas and the adjacent mesenteric fat tissue.
File:IPLab1FatNecrosis3.jpg|This low-power photomicrograph of the pancreas from this case shows the fat tissue (1) surrounding the pancreas. Note the rim of inflammatory cells (arrows) and the blue areas in the fat adjacent to the pancreas (2).
File:IPLab1FatNecrosis4.jpg|This high-power photomicrograph shows areas of inflammation (1) and fat necrosis (arrows) in the peripancreatic fat tissue (2) of the pancreas from this case.
File:IPLab1FatNecrosis5.jpg|Another high-power photomicrograph shows blue discoloration in the fat tissue in the interlobular spaces (1) of the pancreas.
File:IPLab1FatNecrosis6.jpg|A higher-power photomicrograph of the previous slide contains a small area of fat necrosis (1) in the upper right portion of the image. The fat necrosis is within the fat tissue that is normally found adjacent to the pancreas. The appearance of the pancreatic tissue in this area is somewhat disrupted due to autolysis (the pancreas autolyzes very rapidly after death) but there is some premortem necrosis as well.
File:IPLab1FatNecrosis7.jpg|This is a higher-power photomicrograph of the fat necrosis involving the fat cells in the interlobular spaces (arrow) of the pancreas. Note the blue to purple staining of the calcium deposits within the fat cells.
File:IPLab1FatNecrosis8.jpg|This high-power photomicrograph demonstrates fat necrosis in the interlobular spaces of the pancreas. Note the granular blue-staining calcium deposits (arrows) within the fat cells. The clear areas represent artifact caused by the "washing-out" of fat from cells during tissue processing for histology.
File:IPLab1FatNecrosis9.jpg|This is another high-power photomicrograph demonstrating the calcification (arrows) seen in fat necrosis involving the interlobular spaces of the pancreas.
</gallery>

== Virtual Microscopy ==
=== Pancreatic Fat Necrosis ===
<peir-vm>IPLab1FatNecrosis</peir-vm>

=== Normal Pancreas ===
<peir-vm>UAB-Histology-00154</peir-vm>

== Study Questions ==
* <spoiler text="What is the definition of enzymatic fat necrosis?">Focal areas of destruction of fat tissue resulting from abnormal release of activated lipases.</spoiler>
* <spoiler text="Where else can enzymatic fat necrosis occur besides the pancreas?">Salivary glands.</spoiler>
* <spoiler text="What causes the formation of the white, chalky, nodules that are seen in the fat tissue adjacent to the pancreatic tissue?">Injury to the pancreas (infection, toxins, viruses, trauma, ischemia) causes release of activated pancreatic enzymes which liquefy fat cell membranes. The released lipases split the triglyceride esters contained within the fat cells and these released fatty acids combine with calcium to form the grossly visible chalky white nodules characteristic of fat necrosis.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/775867-overview eMedicine Medical Library: Emergent Management of Pancreatitis]
* [http://www.merckmanuals.com/professional/gastrointestinal_disorders/pancreatitis/acute_pancreatitis.html Merck Manual: Acute Pancreatitis]

=== Journal Articles ===
* Bhatnagar A, Wig J, Vaiphei K, Majumdar S. [http://www.ncbi.nlm.nih.gov/pubmed/11560386 Intracellular cytokines in cells of necrotic tissue from patients with acute pancreatitis]. ''Eur J Surg'' 2001 Jul;167(7):510-7.
* LeWinter MM. [http://http://www.nejm.org/doi/full/10.1056/NEJMcp1404070 Acute Pericarditis]. ''NEJM'' 2014 Dec 18;371:2410-2416.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/333-pancreas PEIR Digital Library: Pancreas Images]
* [http://library.med.utah.edu/WebPath/CINJHTML/CINJIDX.html WebPath: Cellular Injury Images]

{{Template:IPLab 1}}

[[Category:IPLab:Lab 1]]

IPLab:Lab 5:Nodular Intercapillary Glomerulosclerosis

2016-08-25T14:34:22Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 57-year-old white male with a 25-year history of Type I diabetes mellitus (insulin-dependent ) developed an acute myocardial infarction followed by cerebral infarction, pulmonary dysfunction, and renal failure. There was a history of hypertension and proteinuria. Laboratory findings included a BUN and creatinine of 69 mg/dL and 3.3 mg/dL which subsequently rose to 113 and 4.8, respectively. He subsequently died of multisystem failure.

== Autopsy Findings ==
The autopsy showed the expected left ventricular hypertrophy, a large acute myocardial infarction, and a large right cerebral infarction. The pancreas showed amyloidosis of the islets. There was extensive atherosclerosis and arteriolosclerosis. The kidneys were slightly enlarged, weighing 220 and 240 grams respectively, and had rough surfaces, a few cortical scars, and blurring of the corticomedullary junctions.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab5DM1.jpg|This is a gross photograph of the kidneys from this case. Note that there are multiple shrunken regions (old infarcts) (arrows) and the kidneys have a rough granular appearance on the surface, which is caused by multiple small infarcts of small vessels throughout the cortex.
File:IPLab5DM2.jpg|This is a low-power photomicrograph of the kidney from this patient. The section extends from cortex (1) to the medulla (2).
File:IPLab5DM3.jpg|This is a higher-power photomicrograph of the cortical region. In this region there is ischemic obsolescence of glomeruli and one glomerulus with nodular glomerulosclerosis (1). Also note the thickened walls of the blood vessels (2).
File:IPLab5DM4.jpg|This is a high-power photomicrograph of two glomeruli with intercapillary glomerulosclerosis (arrows).
File:IPLab5DM5.jpg|This is a photomicrograph of a glomerulus with nodular glomerulosclerosis (1). Also note the intertubular fibrosis and the changes in the blood vessels (2).
File:IPLab5DM6.jpg|This is a higher-power photomicrograph of a glomerulus with nodular glomerulosclerosis (arrows). These are the classic Kimmelstiel-Wilson lesions ("K-W lesions") seen in diabetics with nodular glomerulosclerosis.
File:IPLab5DM7.jpg|This is a photomicrograph of kidney with a focal exudative lesion in a glomerulus (arrow) and sclerosis, interstitial fibrosis, and congestion.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab5DM</peir-vm>

== Study Questions ==
* <spoiler text="What is another term for nodular glomerulosclerosis?">Kimmelstiel-Wilson disease.</spoiler>
* <spoiler text="What material is found within these sclerotic nodules and what happens to these lesions over time?">The Kimmelstiel-Wilson (K-W) lesions are ovoid or spherical, often laminated, hyaline masses situated in the periphery of the glomerulus. They are usually within the mesangium of the glomeruli. The nodules are composed of lipids and fibrin. As the disease progresses the K-W nodules enlarge until they compress and obliterate the glomerular tuft. Because of these glomerular and arteriolar lesions, the blood flow to the kidney is compromised and the kidney becomes ischemic. This results in tubular atrophy and interstitial fibrosis and leads to a roughened renal cortical surface.</spoiler>
* <spoiler text="What percent of diabetics develop this lesion and what are the functional consequences?">Approximately 15-30% of long term diabetics develop K-W lesions and in most instances it is associated with renal failure.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/117739-overview eMedicine Medical Library: Type 1 Diabetes Mellitus]
* [http://emedicine.medscape.com/article/117853-overview eMedicine Medical Library: Type 2 Diabetes Mellitus]
* [http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/diabetes_mellitus_and_disorders_of_carbohydrate_metabolism/diabetes_mellitus_dm.html Merck Manual: Diabetes Mellitus (DM)]

=== Journal Articles ===
* Herzenberg AM, Holden JK, Singh S, Magil AB. [http://www.ncbi.nlm.nih.gov/pubmed/10469869 Idiopathic nodular glomerulosclerosis]. ''Am J Kidney Dis'' 1999 Sep;34(3):560-4.
* Vinik AI. [http://www.nejm.org/doi/full/10.1056/NEJMcp1503948 Diabetic Sensory and Motor Neuropathy]. ''N Engl J Med" 2016 April 14; 374:1455-1464.
* Kamel KS and Halperin ML. [http://www.nejm.org/doi/full/10.1056/NEJMra1207788 Acid–Base Problems in Diabetic Ketoacidosis]. ''N Engl J Med" 2015 Feb 5;372:546-554.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/137-diabetic_glomerulosclerosis PEIR Digital Library: Diabetic Glomerulosclerosis Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html#3 WebPath: Interstitial Diseases of the Kidney]

== Related IPLab Cases ==
* [[IPLab:Lab 1:Kidney Infarction|Lab 1: Kidney: Infarction (Coagulative Necrosis)]]

{{IPLab 5}}

[[Category: IPLab:Lab 5]]

IPLab:Lab 11:Chagas Disease

2016-08-25T14:31:53Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 12-year-old boy, whose family had recently emigrated from Brazil, presented to the emergency room with a three-day history of malaise, fever, anorexia, and edema of the face and upper extremities. On physical examination the patient had generalized lymphadenopathy and hepatosplenomegaly. The patient was tachycardic and dysgenic with signs of congestive heart failure. A cardiac biopsy was performed which revealed an active myocarditis with leishmanial forms of parasitic organisms within cardiac myocytes. Close examination of peripheral blood smears revealed occasional circulating trypomastigotes. A complement fixation test for antibodies to Trypanosoma cruzi was strongly positive.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab11Chagas1.jpg|This peripheral blood smear from the patient shows two trypomastigotes of Trypanosoma cruzi.
File:IPLab11Chagas2.jpg|This peripheral blood smear from the patient shows a higher power view of a Trypanosoma cruzi trypomastigote. Note the prominent kinetoplast (arrow).
File:IPLab11Chagas3.jpg|This is a low-power photomicrograph of an H & E stained section from the heart biopsy of this patient. Note the organisms within a myocyte (arrow) and the adjacent inflammatory response.
File:IPLab11Chagas4.jpg|This is a higher-power photomicrograph of an H & E stained heart biopsy from this patient. Again, note the organisms within a myocyte (arrow) and the inflammatory response.
File:IPLab11Chagas5.jpg|This is a higher-power photomicrograph of an H & E stained heart biopsy from this patient. At this magnification the organisms within a myocyte (arrows) and the adjacent inflammatory response are more clearly seen. The individual organisms within the myocyte are called amastigotes.
File:IPLab11Chagas6.jpg|This is a higher-power photomicrograph of an H & E stained heart biopsy from this patient. Note the T. cruzi amastigotes (arrows) within this longitudinal section of a myocyte.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab11Chagas</peir-vm>

== Study Questions ==
* <spoiler text="How is Chagas’ disease transmitted?">Reduviid bugs (kissing bugs) bite people while they sleep. The bug defecates on the skin and the infected bug feces is rubbed into the wound. Organisms from the infected feces can also enter the body via mucous membranes. These organisms then circulate via the blood stream to infect cells.</spoiler>
* <spoiler text="This patient had acute Chagas' disease. What would you expect to see in a patient with chronic Chagas' disease?">Chronic Chagas' disease leads to congestive heart failure. These patients commonly have right bundle branch block and/or other arrhythmias. These hearts are dilated and hypertrophied, have areas of fibrosis especially in the apex, and often contain mural thrombi. The myocardium is infiltrated with lymphocytes and macrophages and there is interstitial edema and fibrosis. This inflammatory reaction is most severe around the area of the right bundle branch. Patients may also develop megaesophagus and/or megacolon.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/214581-overview eMedicine Medical Library: Chagas Disease (American Trypanosomiasis)]
* [http://emedicine.medscape.com/article/1000389-overview eMedicine Medical Library: Trypanosomiasis]
* [http://www.merckmanuals.com/professional/infectious_diseases/extraintestinal_protozoa/chagas_disease.html Merck Manual: Chagas Disease]
* [http://www.merckmanuals.com/professional/infectious_diseases/extraintestinal_protozoa/african_trypanosomiasis.html Merck Manual: African Trypanosomiasis]

=== Journal Articles ===
* Bestetti RB. [http://www.ncbi.nlm.nih.gov/pubmed/11422962 Predictors of unfavourable prognosis in chronic Chagas' disease]. ''Trop Med Int Health'' 2001 Jun;6(6):476-83.
* Calzada JE, Nieto A, Beraún Y, Martín J. [http://www.ncbi.nlm.nih.gov/pubmed/11703822 Chemokine receptor CCR5 polymorphisms and Chagas' disease cardiomyopathy]. ''Tissue Antigens'' 2001 Sep;58(3):154-8.
* Bern C. [http://www.nejm.org/doi/full/10.1056/NEJMra1410150 Chagas’ Disease]. ''NEJM'' 2015 July 30;373:456-466.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2166-chagas_disease PEIR Digital Library: Chagas Disease]

{{IPLab 11}}

[[Category: IPLab:Lab 11]]

IPLab:Lab 10:Candidiasis

2016-08-25T14:28:24Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 73-year-old black male was in good health until about three months before his death when he noticed enlarged lymph nodes first in both inguinal regions and later elsewhere. Antileukemic therapy was begun. About two weeks prior to his death the patient presented to the emergency room with uncontrollable epistaxis. On physical examination, the liver was palpable but the spleen was not. The white blood count was below normal and consisted mainly of lymphocytes with many atypical cells. The patient's bone marrow was also found to be heavily loaded with lymphocytes. Platelets were extremely low and remained so despite platelet transfusions. Subsequently, the patient developed pneumonia which progressed until death. Antemortem cultures yielded Candida tropicalis and Pseudomonas aeruginosa.

== Autopsy Findings ==
At autopsy, there was evidence of disseminated candidiasis.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Candidiasis1.jpg|This autopsy photograph of the kidneys demonstrates the multifocal punctate lesions visible on the serosal surface (arrows). Don't confuse these small yellow punctate lesions with the fat that is adherent to the renal capsule.
File:IPLab10Candidiasis2.jpg|This photograph of the cut surface of these kidneys shows that these multifocal punctate lesions are primarily in the cortex (arrows).
File:IPLab10Candidiasis3.jpg|This is a low-power photomicrograph of lymph node with three prominent areas of Candida colonies (arrows). Even at this low magnification, the purple-staining yeast and pseudohyphae can be easily seen. This section was stained with Periodic Acid-Schiff Hematoxylin (PASH ), which stains the cell wall of fungi to make them more easily visible.
File:IPLab10Candidiasis4.jpg|This is a low-power photomicrograph of one of the Candida colonies from this lymph node. The chains of yeast which are termed "pseudohyphae" are apparent at this magnification.
File:IPLab10Candidiasis5.jpg|This higher-power photomicrograph shows the yeasts and pseudohyphae in this focus of Candida organisms.
File:IPLab10Candidiasis6.jpg|This high-power photomicrograph shows the yeasts (1) and pseudohyphae (2).
File:IPLab10Candidiasis7.jpg|This is a low-power photomicrograph of the kidney from this same case. Note the Candida colonies (arrows). The pseudohyphae are evident around the periphery of these colonies even at this low magnification.
File:IPLab10Candidiasis8.jpg|This is a higher-power photomicrograph of a Candida colony in the kidney. Note the pseudohyphae of the Candida organisms.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab10Candidiasis</peir-vm>

== Study Questions ==
* <spoiler text="What is the significance of seeing yeast and hyphae in these histologic tissue sections?">Candida is the only fungus which grows as:
# a yeast form,
# pseudohyphae, and
# true hyphae with septa.

All three of these forms may be present in the same section of tissue.</spoiler>
* <spoiler text="Who is at risk for developing systemic candidiasis?">Neutropenic patients.

Candida species--especially C. albicans--are part of the normal flora of the skin, mouth, and GI tract, and are the most frequent cause of human fungal infections. These infections vary from superficial lesions in healthy persons to disseminated infections in neutropenic patients.

Severe disseminated candidiasis is associated with neutropenia secondary to chronic granulomatous disease, leukemia, anticancer therapy, or immunosuppression after transplantation.

Candida can be introduced into the bloodstream by intravenous lines, catheters, peritoneal dialysis, cardiac surgery, or intravenous drug abuse.</spoiler>
* <spoiler text="What types of infections does Candida cause in humans?">Candida infections can occur in the oral cavity (thrush), vagina, and in the skin--especially in warm moist areas (i.e., between the fingers and toes and in inguinal creases, inframammary folds, and the anogenital region).

Candida esophagitis can occur with nasogastric tube placement.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/781215-overview eMedicine Medical Library: Candidiasis in Emergency Medicine]
* [http://emedicine.medscape.com/article/213853-overview eMedicine Medical Library: Candidiasis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/candidiasis_invasive.html Merck Manual: Candidiasis (Invasive)]

=== Journal Articles ===
* Marr KA, Bowden RA. [http://www.ncbi.nlm.nih.gov/pubmed/11428995 Fungal infections in patients undergoing blood and marrow transplantation]. ''Transpl Infect Dis'' 1999 Dec;1(4):237-46.
* Marr KA, Bowden RA. [http://www.nejm.org/doi/full/10.1056/NEJMra1315399 Invasive Candidiasis]. ''NEJM'' 2015 Oct 8;373:1445-1456.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2156-candidiasis PEIR Digital Library: Candidiasis]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html Webpath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 3:Tuberculosis

2016-08-25T14:25:24Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
Two months prior to admission, this 57-year-old white male underwent a routine physical examination. During the course of the examination, a lesion was found in the upper lobe of the right lung. Initially, the patient was treated for two weeks with ampicillin. He was then admitted to the hospital for further study. All studies including sputum studies for tubercle bacilli, bronchial washings, and bronchoscopy were negative and he was discharged.

Upon re-admission, a review of systems revealed the presence of mild dyspnea on exertion, accompanied by a slightly productive cough. Of interest was the fact that the patient had had a positive PPD test for the past 4 to 5 years, but this had never been evaluated. At this time, physical and laboratory examinations were unremarkable. Radiographic examination of the chest revealed a 2 x 2-cm density in the right lower lung field. A CT scan revealed several small cavities in this area.

== Findings ==
The patient underwent a thoracotomy, at which time a portion of the upper lobe of the right lung was removed. Examination of the cut surface revealed small white nodules measuring up to 0.2 cm in diameter.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab3Tuberculosis1.jpg|This is a gross photograph of a lung containing a nodular lesion at the lung apex (arrows). Note that the lesion appears solid and has a whitish coloration indicating considerable fibrous connective tissue. This is a healed granuloma due to primary tuberculosis in the lung. There are smaller focal lesions adjacent to the major mass. In addition, note the extensive anthracosis in this lung.
File:IPLab3Tuberculosis2.jpg|This low-power photomicrograph of a section of lung reveals multiple large nodules (1) with pale eosinophilic centers surrounded by a rim of blue-staining nuclei. In addition to the large nodules, there are several smaller nodules throughout the slide (2).
File:IPLab3Tuberculosis3.jpg|This is a photomicrograph of a tuberculosis granuloma. Note the central core of caseation necrosis (1) encircled by a rim of epithelioid macrophages and lymphocytes (2). Langhans’ type multinucleated giant cells are also present although they are difficult to see at this power (3).
File:IPLab3Tuberculosis4.jpg|This is a high-power photomicrograph of a granuloma. Note the necrotic core on the right (1), epithelioid macrophages (2), and Langhans’ type giant cells (3) at the periphery of the granuloma. Note also the small lymphocytes characterized by their distinctly blue-staining nuclei. Other cells in the tissue, in addition to the macrophages, include fibroblasts and occasional neutrophils.
File:IPLab3Tuberculosis5.jpg|This high-power photomicrograph of a tuberculosis granuloma demonstrates acid-fast bacilli (arrows).
</gallery>

== Virtual Microscopy ==
=== Lung: Tuberculosis H&E ===
<peir-vm>IPLab3Tuberculosis_HE</peir-vm>

=== Lung: Tuberculosis AFGT ===
<peir-vm>IPLab3Tuberculosis_AFGT</peir-vm>

=== Normal Lung ===
<peir-vm>UAB-Histology-00107</peir-vm>

== Study Questions ==
* <spoiler text="Does everyone with a positive PPD test have TB?">No, it just indicates exposure to a ''Mycobacterium'' species, many of which are non-pathogenic in humans. Those who have received Bacillus Calmette–Guérin (BCG) vaccination, for instance, routinely have a positive PPD test even though they have never been exposed to ''Mycobacterium tuberculosis''.</spoiler>
* <spoiler text="How does this lesion differ from the lesions seen in sarcoid?">These are caseating granulomas with a central region of caseation necrosis and macrophages and lymphocytes around the periphery. Multinucleated, primarily Langhans’ type, giant cells are present within these nodules.</spoiler>
* <spoiler text="What are epithelioid cells?">Epitheliod cells are tissue macrophages that have an epithelium-like appearance.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/230802-overview eMedicine Medical Library: Tuberculosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/mycobacteria/tuberculosis_tb.html Merck Manual: Tuberculosis]

=== Journal Articles ===
* Rodrigues DS, Medeiros EA, Weckx LY, Bonnez W, Salomão R, Kallas EG. [http://www.ncbi.nlm.nih.gov/pubmed/11982602 Immunophenotypic characterization of peripheral T lymphocytes in Mycobacterium tuberculosis infection and disease]. ''Clin Exp Immunol'' 2002 Apr;128(1):149-54.
* Horsburgh CR, Barry CE, Lange C. [http://www.nejm.org/doi/full/10.1056/NEJMra1413919 Treatment of Tuberculosis]. ''NEJM'' 2015 Nov 26;373:2149-2160.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/259-tuberculosis PEIR Digital Library: Tuberculosis]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#4 WebPath: Granulomatous Lung Disease]

== Related IPLab Cases ==
* [[IPLab:Lab 1:Tuberculosis|Lab 1: Lung: Tuberculosis (Caseous Necrosis)]]
* [[IPLab:Lab 6:Tuberculosis|Lab 6: Lung: Tuberculosis]]

{{IPLab 3}}

[[Category: IPLab:Lab 3]]

IPLab:Lab 7:Adenocarcinoma

2016-08-25T14:20:10Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
Approximately four months prior to admission, this 68-year-old male began having "sharp, shooting pains" in the lower abdomen. A barium enema at that time was reported as normal. Two months later, the barium study was repeated because of persistent diarrhea and showed a filling defect in the transverse colon. The patient refused to undergo an exploratory laparotomy. During the week prior to this admission, the patient had recurrent diarrhea, cramping abdominal pain, and marked rectal bleeding. He was hospitalized and required 2500 ml of blood to return his hematocrit to normal. A colectomy was done from the hepatic flexure to the rectosigmoid.

== Autopsy Findings ==
The segment of colon contained numerous polyps and an annular tumor which was 6.7 cm in diameter. Proctoscopic examination of the ascending colon revealed two more polyps which were removed.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab7ColonCA1.jpg|This is a gross photograph of the adenoma from the surgical specimen in this case. Note the large, ulcerated, fungating annular (encircling) carcinoma (1) with areas of hemorrhage (2). Also note the adenomatous polyps (3).
File:IPLab7ColonCA2.jpg|This is a closer view of the previous image demonstrating the raised, annular carcinoma (arrows).
File:IPLab7ColonCA3.jpg|This photomicrograph of the surgical specimen shows the transition between normal mucosa on the left and carcinoma which is invading the wall of the bowel (arrow).
File:IPLab7ColonCA4.jpg|This is a higher-power photomicrograph of the area of transition between the normal (1) and the neoplastic (2) epithelium.
File:IPLab7ColonCA5.jpg|This is a high-power photomicrograph of tumor cells invading the underlying muscularis.
File:IPLab7ColonCA6.jpg|This is a high-power photomicrograph of tumor cells forming glands.
File:IPLab7ColonCA7.jpg|This is a high-power photomicrograph of tumor cells forming glands.
File:IPLab7ColonCA8.jpg|This gross photograph from another case demonstrates an ulcerated adenocarcinoma (arrows) at the rectosigmoid junction.
File:IPLab7ColonCA9.jpg|This is a segment of distal colon from another case. Note the annular tumor that severely compromises the lumen of the colon. There is dilation of the colon proximal to the tumor.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab7ColonCA</peir-vm>

== Study Questions ==
* <spoiler text="What age group usually presents with colon cancer and what factors may predispose to early onset?">The peak incidence for colorectal carcinoma is age 60 to 70 years; fewer than 20% of cases occur under 50 years of age. When colorectal carcinoma is found in a young person, pre-existing ulcerative colitis or one of the polyposis syndromes must be suspected.</spoiler>
* <spoiler text="What is the usual presenting signs or symptoms of a patient with colon cancer?">The clinical presentation depends upon the site of the tumor. Colorectal cancers remain asymptomatic for years. Cecal and right colonic cancers most often lead to fatigue, weakness, and iron-deficiency anemia. These fungating lesions bleed easily and may be discovered at an early stage, provided that the colon is examined thoroughly radiographically and during colonoscopy. Left-sided lesions produce occult bleeding, changes in bowel habit, or crampy left lower quadrant discomfort. In theory, the chance for early discovery and successful removal should be greater with lesions on the left side because these patients usually have prominent disturbances in bowel function, such as melena, diarrhea, and constipation.</spoiler>
* <spoiler text="How does the morphology of colon cancer differ depending upon location?">Almost all colorectal carcinomas begin as in situ lesions within adenomatous polyps; however, they evolve into different morphologic patterns. Tumors in the proximal colon tend to grow as polypoid, fungating masses that extend along one wall of the capacious cecum and ascending colon. Obstruction is uncommon. When carcinomas in the distal colon are discovered, they tend to be annular, encircling lesions that produce so-called napkin-ring constrictions of the bowel. The margins of the napkin ring are classically heaped up, beaded, and firm, and the midregion is ulcerated. The lumen is markedly narrowed, and the proximal bowel may be distended.</spoiler>
* <spoiler text="What predisposing factors lead to colon cancer?">Dietary factors that may predispose to cancer are
# a low fiber diet,
# high intake of refined carbohydrates,
# high fat diet, and
# decreased intake of protective vitamins.
It is thought that reduced fiber content leads to decreased stool bulk, increased fecal transit time in the bowel, and an altered bacterial flora of the intestine. Potentially toxic oxidative byproducts of carbohydrate degradation by bacteria are therefore present in higher concentrations in the small stools and are held in contact with the colonic mucosa for longer periods of time. More recent epidemiologic data have raised some doubt about the importance of fiber in the diet but most nutritionalists still recommend high fiber diet to help prevent colon cancer. Moreover, high fat intake enhances the synthesis of cholesterol and bile acids by the liver, which in turn may be converted into potential carcinogens by intestinal bacteria. Refined diets also contain less vitamins A, C, and E, which may act as oxygen radical scavengers.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/367061-overview eMedicine Medical Library: Imaging in Adenocarcinoma of the Colon]
* [http://emedicine.medscape.com/article/277496-overview eMedicine Medical Library: Colon Adenocarcinoma]
* [http://www.merckmanuals.com/professional/gastrointestinal_disorders/tumors_of_the_gi_tract/colorectal_cancer.html Merck Manual: Colorectal Cancer]

=== Journal Articles ===
* Yuen ST, Wong MP, Chung LP, Chan SY, Cheung N, Ho J, Leung SY. [http://www.ncbi.nlm.nih.gov/pubmed/9543668 Up-regulation of lysozyme production in colonic adenomas and adenocarcinomas]. ''Histopathology'' 1998 Feb;32(2):126-32.
* Strum WB. [http://www.nejm.org/doi/full/10.1056/NEJMra1513581 Colorectal Adenomas]. ''NEJM'' 2016 March 17 374:1065-1075.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/66-colon/112-carcinoma PEIR Digital Library: Colon Carcinoma Images]
* [http://library.med.utah.edu/WebPath/GIHTML/GIIDX.html#10 WebPath: Colon and Appendix]

== Related IPLab Cases ==
* [[IPLab:Lab 7:Metastatic Adenocarcinoma|Lab 7: Lung & Liver: Metastatic Adenocarcinoma]]
* [[IPLab:Lab 7:Lip SCC|Lab 7: Lip: Squamous Cell Carcinoma]]
* [[IPLab:Lab 7:Esophagus SCC|Lab 7: Esophagus: Squamous Cell Carcinoma]]
* [[IPLab:Lab 7:IDC|Lab 7: Breast: Infiltrating Ductal Carcinoma]]
* [[IPLab:Lab 7:Bronchogenic Carcinoma|Lab 7: Lung: Bronchogenic Carcinoma]]

{{IPLab 7}}

[[Category: IPLab:Lab 7]]

IPLab:Lab 5:Nodular Intercapillary Glomerulosclerosis

2016-08-25T14:13:36Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 57-year-old white male with a 25-year history of Type I diabetes mellitus (insulin-dependent ) developed an acute myocardial infarction followed by cerebral infarction, pulmonary dysfunction, and renal failure. There was a history of hypertension and proteinuria. Laboratory findings included a BUN and creatinine of 69 mg/dL and 3.3 mg/dL which subsequently rose to 113 and 4.8, respectively. He subsequently died of multisystem failure.

== Autopsy Findings ==
The autopsy showed the expected left ventricular hypertrophy, a large acute myocardial infarction, and a large right cerebral infarction. The pancreas showed amyloidosis of the islets. There was extensive atherosclerosis and arteriolosclerosis. The kidneys were slightly enlarged, weighing 220 and 240 grams respectively, and had rough surfaces, a few cortical scars, and blurring of the corticomedullary junctions.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab5DM1.jpg|This is a gross photograph of the kidneys from this case. Note that there are multiple shrunken regions (old infarcts) (arrows) and the kidneys have a rough granular appearance on the surface, which is caused by multiple small infarcts of small vessels throughout the cortex.
File:IPLab5DM2.jpg|This is a low-power photomicrograph of the kidney from this patient. The section extends from cortex (1) to the medulla (2).
File:IPLab5DM3.jpg|This is a higher-power photomicrograph of the cortical region. In this region there is ischemic obsolescence of glomeruli and one glomerulus with nodular glomerulosclerosis (1). Also note the thickened walls of the blood vessels (2).
File:IPLab5DM4.jpg|This is a high-power photomicrograph of two glomeruli with intercapillary glomerulosclerosis (arrows).
File:IPLab5DM5.jpg|This is a photomicrograph of a glomerulus with nodular glomerulosclerosis (1). Also note the intertubular fibrosis and the changes in the blood vessels (2).
File:IPLab5DM6.jpg|This is a higher-power photomicrograph of a glomerulus with nodular glomerulosclerosis (arrows). These are the classic Kimmelstiel-Wilson lesions ("K-W lesions") seen in diabetics with nodular glomerulosclerosis.
File:IPLab5DM7.jpg|This is a photomicrograph of kidney with a focal exudative lesion in a glomerulus (arrow) and sclerosis, interstitial fibrosis, and congestion.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab5DM</peir-vm>

== Study Questions ==
* <spoiler text="What is another term for nodular glomerulosclerosis?">Kimmelstiel-Wilson disease.</spoiler>
* <spoiler text="What material is found within these sclerotic nodules and what happens to these lesions over time?">The Kimmelstiel-Wilson (K-W) lesions are ovoid or spherical, often laminated, hyaline masses situated in the periphery of the glomerulus. They are usually within the mesangium of the glomeruli. The nodules are composed of lipids and fibrin. As the disease progresses the K-W nodules enlarge until they compress and obliterate the glomerular tuft. Because of these glomerular and arteriolar lesions, the blood flow to the kidney is compromised and the kidney becomes ischemic. This results in tubular atrophy and interstitial fibrosis and leads to a roughened renal cortical surface.</spoiler>
* <spoiler text="What percent of diabetics develop this lesion and what are the functional consequences?">Approximately 15-30% of long term diabetics develop K-W lesions and in most instances it is associated with renal failure.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/117739-overview eMedicine Medical Library: Type 1 Diabetes Mellitus]
* [http://emedicine.medscape.com/article/117853-overview eMedicine Medical Library: Type 2 Diabetes Mellitus]
* [http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/diabetes_mellitus_and_disorders_of_carbohydrate_metabolism/diabetes_mellitus_dm.html Merck Manual: Diabetes Mellitus (DM)]

=== Journal Articles ===
* Herzenberg AM, Holden JK, Singh S, Magil AB. [http://www.ncbi.nlm.nih.gov/pubmed/10469869 Idiopathic nodular glomerulosclerosis]. ''Am J Kidney Dis'' 1999 Sep;34(3):560-4.
* Vinik AI. [http://www.nejm.org/doi/full/10.1056/NEJMcp1503948 Diabetic Sensory and Motor Neuropathy]. ''N Engl J Med" 2016 April 14; 374:1455-1464.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/137-diabetic_glomerulosclerosis PEIR Digital Library: Diabetic Glomerulosclerosis Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html#3 WebPath: Interstitial Diseases of the Kidney]

== Related IPLab Cases ==
* [[IPLab:Lab 1:Kidney Infarction|Lab 1: Kidney: Infarction (Coagulative Necrosis)]]

{{IPLab 5}}

[[Category: IPLab:Lab 5]]

IPLab:Lab 3:Chronic Peptic Ulcer

2016-08-25T14:09:36Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 56-year-old white female was admitted to the hospital with a six-year history of epigastric pain and burning. This pain was said to be worse at night and on an empty stomach. The patient reported that the pain was relieved by drinking milk. She had also experienced several episodes of hematemesis and melena since the onset of the pain, the last episode occurring 3 weeks prior to admission. The patient described intermittent episodes of colicky pain in the right upper quadrant and right side of the abdomen, frequently radiating to the back and shoulders and often accompanied by "bilious vomiting." Physical examination was noncontributory except for tenderness in the epigastrium and right upper quadrant. An upper GI series showed changes suggestive of a neoplasm. The patient submitted to an abdominal exploration at which time a partial gastrectomy was performed.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab3ChronicPepticUlcer1.jpg|This is a gross photograph of a stomach containing an ulcer. Note the folded pink gastric mucosa that extends up to the edge of the ulcer (arrows).
File:IPLab3ChronicPepticUlcer2.jpg|This is a gross photograph of the ulcer after it has been transected. The edge of the mucosa (1) is better appreciated in this image. Note the thick, fatty tissue (2) which makes up the base of this ulcer (3).
File:IPLab3ChronicPepticUlcer3.jpg|This is a low-power photomicrograph of the transected ulcer. The blue cells on the right hand side of this section are the normal gastric epithelial cells of the mucosa (1). Note the absence of any epithelial cells within the crater of the ulcer (2).
File:IPLab3ChronicPepticUlcer4.jpg|This is a photomicrograph of the margin of the ulcer. Note the intact epithelium on the right side of the section (1) and the ulcerated region without epithelium on the left (2). There are numerous inflammatory cells within this tissue.
File:IPLab3ChronicPepticUlcer5.jpg|This is a medium-power photomicrograph of the base of the ulcer with the fibrinopurulent membrane (1) overlying the ulcerated surface. The ulcerated surface contains granulation tissue and inflammatory cells (2).
File:IPLab3ChronicPepticUlcer6.jpg|This high-power photomicrograph of the ulcer base (arrows) demonstrates the lack of epithelium and the exuberant inflammatory response (1) consisting of primarily of fibrin (and adherent gastric secretions) and PMNs. The surface of the ulcer bed is covered with this fibrinopurulent exudate.
File:IPLab3ChronicPepticUlcer7.jpg|This high-power photomicrograph of the ulcer base demonstrates plump, activated fibroblasts and endothelial cells (arrows) within the granulation tissue that makes up the base of the ulcer. There are inflammatory cells (primarily lymphocytes) within this region as well.
File:IPLab3ChronicPepticUlcer8.jpg|This low-power photomicrograph demonstrates the healing reaction in the base of this ulcer. The base of the ulcer is at the left-hand side of the image and the serosal surface is at the right. Note the fibrous connective tissue within the wall of the stomach and the layer of inflammatory exudate on the surface of the ulcer (arrow).
File:IPLab3ChronicPepticUlcer9.jpg|This high-power photomicrograph demonstrates the granulation tissue within the base of the ulcer.
File:IPLab3ChronicPepticUlcer10.jpg|This is a photomicrograph of the serosal surface (1) from a section of stomach near the ulcer. Note that the inflammatory reaction extends out to the serosa.
File:IPLab3ChronicPepticUlcer11.jpg|This is a trichrome-stained section of tissue demonstrating fibrous connective tissue scar formation (blue color) in this lesion. The surface of the ulcer is at the left-hand side of the image. There is a layer of inflammatory cells and RBCs on the surface of the ulcer.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab3ChronicPepticUlcer</peir-vm>

== Study Questions ==
* <spoiler text="What types of factors may predispose to peptic ulcer formation?">Alcoholic cirrhosis, chronic obstructive airway disease, chronic renal disease, and hyperparathyroidism or any condition which leads to hypercalcemia (calcium stimulates gastrin production).</spoiler>
* <spoiler text="Why is infection with Helicobacter pylori considered to be a significant risk factor for development of peptic ulcers?">''H. pylori'' is found in 90-100% of cases. It is thought that the ''H. pylori'' produce urease, leading to ammonia production and that they also produce a protease that breaks down glycoproteins in the mucus which forms the protective coat on the gastric mucosa.</spoiler>
* <spoiler text="What cells make of the inflammatory reaction at the base of this chronic ulcer?">The base of this chronic ulcer has a granulomatous inflammatory reaction composed of lymphocytes, macrophages, fibroblasts, and endothelial cells. This is in contrast to the acute inflammatory reaction at the surface of the ulcer due to irritation from the acid and gastric contents.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/181753-overview eMedicine Medical Library: Peptic Ulcer Disease]
* [http://www.merckmanuals.com/professional/gastrointestinal_disorders/gastritis_and_peptic_ulcer_disease/gastritis.html Merck Manual: Gastritis and Peptic Ulcer Disease]

=== Journal Articles ===
* Laine L. [http://www.nejm.org/doi/10.1056/NEJMcp1514257 Upper Gastrointestinal Bleeding Due to a Peptic Ulcer.] ''NEJM'' 2016 June 22; 374: 2367-2376.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/122-peptic_ulcer PEIR Digital Library: Peptic Ulcer Images]
* [http://library.med.utah.edu/WebPath/GIHTML/GIIDX.html#2 WebPath: Stomach Pathology]

{{IPLab 3}}

[[Category: IPLab:Lab 3]]

IPLab:Lab 12:Alcoholic Cirrhosis

2016-08-25T13:47:20Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==

This 56-year-old white male came to the emergency room because of weakness, lack of appetite, shortness of breath, abdominal distention, and an altered mental status. He was a known alcoholic who drank approximately one pint of whiskey per day. Physical examination revealed a wasted appearance, icterus, a protuberant abdomen, bilateral gynecomastia, sparse axillary hair, and spider angiomata on his chest. Liver and spleen were not palpable, the testes were atrophic, and the legs showed petechial hemorrhages and 3+ edema. Admission laboratory values revealed a hemoglobin of 9.5 g/dL, an MCV of 106 fL, a platelet count of 97,000/mL, and a prothrombin time of 19.2 seconds. In addition, his albumin was 2.3 g/dL, bilirubin, total 6.5 mg/dL, AST 21.0 U/L, ALT 56 U/L, alkaline phosphatase 180 U/L, and GGT 320 U/L. The patient was treated with thiamine, folate, multivitamins, and vitamin K and an intravenous line was placed to infuse 5% dextrose. An esophagogastroduodenoscopy (EGD) was performed which demonstrated large esophageal varices with evidence of previous bleeding sites. Two days after admission the patient developed a massive hematemesis and his hematocrit dropped to 17%. Emergency EGD showed ruptured esophageal varices. Despite successful sclerotherapy and supportive transfusions, the patient lapsed into coma and died the next day.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab12Alcoholic1.jpg|This is a gross photograph of the liver from this patient. Note the nodular pattern and the areas of greenish discoloration as well as pale tan areas.
File:IPLab12Alcoholic2.jpg|This is a closer view of the liver from this patient. Again note the nodular pattern and the areas of greenish discoloration. These green nodules are actually the viable hepatocytes that are stained green because of bile stasis. The pale areas are the areas of fibrosis.
File:IPLab12Alcoholic3.jpg|This is a low-power photomicrograph of this liver stained with a trichrome stain to highlight the fibrous tissue (arrows). Also note the nodular pattern.
File:IPLab12Alcoholic4.jpg|In this is medium-power photomicrograph of trichrome stained liver the bands of fibrous tissue are seen to form "bridges" between triad areas (arrows); this is called "bridging fibrosis." Also note the fibrous tissue (arrows) and how the hepatocytes are separated into nodules by this fibrous tissue.
File:IPLab12Alcoholic5.jpg|In this high-power photomicrograph of trichrome-stained liver, the bands of fibrous tissue surround the hepatocyte nodules. There is some degeneration and dropout of hepatocytes in this nodule. Also note the increased numbers of bile ducts in the triad area (arrows). Bile duct proliferation is a common feature in many hepatitides.
File:IPLab12Alcoholic6.jpg|This photograph from another autopsy case shows another example of cirrhosis. Note the nodules, the fibrosis, the green coloration and the small size of this cirrhotic liver.
File:IPLab12Alcoholic7.jpg|This photograph was taken during the EGD while the patient was alive. Note the red hyperemic areas (1) and the area of hemorrhage (2).
File:IPLab12Alcoholic8.jpg|This photograph taken at autopsy shows the distal portion of the esophagus and the stomach. The esophageal varices are visible just under the mucosa of the esophagus (arrows). Some of the blood from the ruptured varix can still be seen in the stomach.
File:IPLab12Alcoholic9.jpg|In this closer view of the distal esophagus the ruptured varix is indicated by the probe. Other varices and areas of submucosal hemorrhage can also be appreciated.
File:IPLab12Alcoholic10.jpg|This is a photograph taken from another patient at autopsy to demonstrate numerous esophageal varices in the distal esophagus (arrows). None of these varices have ruptured.
File:IPLab12Alcoholic11.jpg|This photograph taken from still another patient at autopsy demonstrates the esophageal varices in the distal esophagus (arrows). The esophagus was clamped before removing the esophagus from the body in order to trap the blood in these distended varices. It is obvious how easily these thin-walled superficial varices could rupture and bleed.
File:IPLab12Alcoholic12.jpg|This photomicrograph shows the dilated vessel just under the epithelium of the esophagus.
File:IPLab12Alcoholic13.jpg|This photograph of the cerebellum from this patient demonstrates the marked thinning of the anterior portion of the cerebellum (arrows).
File:IPLab12Alcoholic14.jpg|This is another photograph of the cerebellum from this patient demonstrating the marked thinning of the anterior portion of the cerebellum (arrows). This pattern of cerebellar damage is consistent with Wernicke's encephalopathy.
</gallery>

== Study Questions ==
* <spoiler text="How does alcohol cause liver damage?">Initial changes include hepatocellular steatosis. This is caused by altered metabolism with high levels of NADH from lactate dehydrogenase resulting in increased lipid biosynthesis. Mobilization of lipids from peripheral fat stores and decreased lipid acceptor protein synthesis leads to insufficient lipoprotein production.

Alcohol induces free radical production as it is broken down by the microsomal ethanol oxidizing system. Alcohol also impairs microtubular and mitochondrial function and membrane fluidity.

Acetaldehyde, the major ethanol metabolite, can cause lipid peroxidation and acetaldehyde-protein complexes that further inhibit the microtubular system.

Finally, alcohol also induces an immunologic reaction in the liver. This immune-mediated liver damage is thought to result from the expression of neoantigens on hepatocytes possibly due to alcohol-induced alterations in membranes or acetaldehyde binding to proteins leading to neoantigen formation.</spoiler>
* <spoiler text="Why did this patient have a prolonged prothrombin time?">Since most of the clotting factors are produced by the liver, chronic liver damage with loss of liver parenchyma will lead to a reduction in clotting factors. In addition, this patient had bleeding esophageal varices and ascites which could both use up or sequester clotting factors, respectively.</spoiler>
* <spoiler text="What causes esophageal varices in a patient with hepatic cirrhosis?">Hepatic cirrhosis with extensive parenchymal damage and fibrosis results in an increased resistance to portal blood flow. The increased portal pressure leads to increased pressure in the coronary veins of the stomach. This results in increased pressure in the esophageal plexus in the terminal portion of the esophagus as the blood travels through this plexus to empty into the azygous vein. The increased pressure and increased flow of blood through this plexus of thin-walled veins leads to dilation and formation of varices. These varices can then rupture and lead to life-threatening hemorrhage as was seen in this case.

Increased portal pressure also leads to increased pressure in the inferior hemorrhoidal veins and can lead to the formation of anorectal varices.</spoiler>
* <spoiler text="What is the pathogenesis of Wernicke's encephalopathy?">Wernicke's encephalopathy is caused by thiamine (Vitamin B1) deficiency. Chronic alcoholics often have poor diets and alcohol inhibits intestinal absorption of thiamine. Thus, some chronic alcoholics can develop Wernicke's encephalopathy which consists of foci of symmetric discoloration, softening, and punctate hemorrhages in the paraventricular regions of the thalamus and hypothalamus, in the mamillary bodies, around the aqueduct in the midbrain, in the floor of the fourth ventricle and in the anterior cerebellum. There is demyelinization and loss of neuropil. Even after treatment with thiamine, there is significant memory deficit.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/185856-overview eMedicine Medical Library: Cirrhosis]
* [http://emedicine.medscape.com/article/366426-overview eMedicine Medical Library: Cirrhosis Imaging]
* [http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/alcoholic_liver_disease/alcoholic_liver_disease.html Merck Manual: Alcoholic Liver Disease]

=== Journal Articles ===
* Fujimoto J. [http://www.ncbi.nlm.nih.gov/pubmed/10759218 Gene therapy for liver cirrhosis]. ''J Gastroenterol Hepatol'' 2000 Mar;15 Suppl:D33-6.
* Ge PS and Runyon BA [http://www.nejm.org/doi/pdf/10.1056/NEJMra1504367 Treatment of Patients with Cirrhosis]. ''NEJM'' 2016 Aug 25 375(8):767.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/128-cirrhosis PEIR Digital Library: Cirrhosis Images]
* [http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html WebPath: Hepatic Pathology]

== Related IPLab Cases ==
* [[IPLab:Lab 2:Fatty Change and Cirrhosis|Lab 2: Liver: Fatty Change and Cirrhosis]]

{{IPLab 12}}

[[Category: IPLab:Lab 12]]

IPLab:Lab 12:Alcoholic Cirrhosis

2016-08-25T13:44:48Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==

This 56-year-old white male came to the emergency room because of weakness, lack of appetite, shortness of breath, abdominal distention, and an altered mental status. He was a known alcoholic who drank approximately one pint of whiskey per day. Physical examination revealed a wasted appearance, icterus, a protuberant abdomen, bilateral gynecomastia, sparse axillary hair, and spider angiomata on his chest. Liver and spleen were not palpable, the testes were atrophic, and the legs showed petechial hemorrhages and 3+ edema. Admission laboratory values revealed a hemoglobin of 9.5 g/dL, an MCV of 106 fL, a platelet count of 97,000/mL, and a prothrombin time of 19.2 seconds. In addition, his albumin was 2.3 g/dL, bilirubin, total 6.5 mg/dL, AST 21.0 U/L, ALT 56 U/L, alkaline phosphatase 180 U/L, and GGT 320 U/L. The patient was treated with thiamine, folate, multivitamins, and vitamin K and an intravenous line was placed to infuse 5% dextrose. An esophagogastroduodenoscopy (EGD) was performed which demonstrated large esophageal varices with evidence of previous bleeding sites. Two days after admission the patient developed a massive hematemesis and his hematocrit dropped to 17%. Emergency EGD showed ruptured esophageal varices. Despite successful sclerotherapy and supportive transfusions, the patient lapsed into coma and died the next day.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab12Alcoholic1.jpg|This is a gross photograph of the liver from this patient. Note the nodular pattern and the areas of greenish discoloration as well as pale tan areas.
File:IPLab12Alcoholic2.jpg|This is a closer view of the liver from this patient. Again note the nodular pattern and the areas of greenish discoloration. These green nodules are actually the viable hepatocytes that are stained green because of bile stasis. The pale areas are the areas of fibrosis.
File:IPLab12Alcoholic3.jpg|This is a low-power photomicrograph of this liver stained with a trichrome stain to highlight the fibrous tissue (arrows). Also note the nodular pattern.
File:IPLab12Alcoholic4.jpg|In this is medium-power photomicrograph of trichrome stained liver the bands of fibrous tissue are seen to form "bridges" between triad areas (arrows); this is called "bridging fibrosis." Also note the fibrous tissue (arrows) and how the hepatocytes are separated into nodules by this fibrous tissue.
File:IPLab12Alcoholic5.jpg|In this high-power photomicrograph of trichrome-stained liver, the bands of fibrous tissue surround the hepatocyte nodules. There is some degeneration and dropout of hepatocytes in this nodule. Also note the increased numbers of bile ducts in the triad area (arrows). Bile duct proliferation is a common feature in many hepatitides.
File:IPLab12Alcoholic6.jpg|This photograph from another autopsy case shows another example of cirrhosis. Note the nodules, the fibrosis, the green coloration and the small size of this cirrhotic liver.
File:IPLab12Alcoholic7.jpg|This photograph was taken during the EGD while the patient was alive. Note the red hyperemic areas (1) and the area of hemorrhage (2).
File:IPLab12Alcoholic8.jpg|This photograph taken at autopsy shows the distal portion of the esophagus and the stomach. The esophageal varices are visible just under the mucosa of the esophagus (arrows). Some of the blood from the ruptured varix can still be seen in the stomach.
File:IPLab12Alcoholic9.jpg|In this closer view of the distal esophagus the ruptured varix is indicated by the probe. Other varices and areas of submucosal hemorrhage can also be appreciated.
File:IPLab12Alcoholic10.jpg|This is a photograph taken from another patient at autopsy to demonstrate numerous esophageal varices in the distal esophagus (arrows). None of these varices have ruptured.
File:IPLab12Alcoholic11.jpg|This photograph taken from still another patient at autopsy demonstrates the esophageal varices in the distal esophagus (arrows). The esophagus was clamped before removing the esophagus from the body in order to trap the blood in these distended varices. It is obvious how easily these thin-walled superficial varices could rupture and bleed.
File:IPLab12Alcoholic12.jpg|This photomicrograph shows the dilated vessel just under the epithelium of the esophagus.
File:IPLab12Alcoholic13.jpg|This photograph of the cerebellum from this patient demonstrates the marked thinning of the anterior portion of the cerebellum (arrows).
File:IPLab12Alcoholic14.jpg|This is another photograph of the cerebellum from this patient demonstrating the marked thinning of the anterior portion of the cerebellum (arrows). This pattern of cerebellar damage is consistent with Wernicke's encephalopathy.
</gallery>

== Study Questions ==
* <spoiler text="How does alcohol cause liver damage?">Initial changes include hepatocellular steatosis. This is caused by altered metabolism with high levels of NADH from lactate dehydrogenase resulting in increased lipid biosynthesis. Mobilization of lipids from peripheral fat stores and decreased lipid acceptor protein synthesis leads to insufficient lipoprotein production.

Alcohol induces free radical production as it is broken down by the microsomal ethanol oxidizing system. Alcohol also impairs microtubular and mitochondrial function and membrane fluidity.

Acetaldehyde, the major ethanol metabolite, can cause lipid peroxidation and acetaldehyde-protein complexes that further inhibit the microtubular system.

Finally, alcohol also induces an immunologic reaction in the liver. This immune-mediated liver damage is thought to result from the expression of neoantigens on hepatocytes possibly due to alcohol-induced alterations in membranes or acetaldehyde binding to proteins leading to neoantigen formation.</spoiler>
* <spoiler text="Why did this patient have a prolonged prothrombin time?">Since most of the clotting factors are produced by the liver, chronic liver damage with loss of liver parenchyma will lead to a reduction in clotting factors. In addition, this patient had bleeding esophageal varices and ascites which could both use up or sequester clotting factors, respectively.</spoiler>
* <spoiler text="What causes esophageal varices in a patient with hepatic cirrhosis?">Hepatic cirrhosis with extensive parenchymal damage and fibrosis results in an increased resistance to portal blood flow. The increased portal pressure leads to increased pressure in the coronary veins of the stomach. This results in increased pressure in the esophageal plexus in the terminal portion of the esophagus as the blood travels through this plexus to empty into the azygous vein. The increased pressure and increased flow of blood through this plexus of thin-walled veins leads to dilation and formation of varices. These varices can then rupture and lead to life-threatening hemorrhage as was seen in this case.

Increased portal pressure also leads to increased pressure in the inferior hemorrhoidal veins and can lead to the formation of anorectal varices.</spoiler>
* <spoiler text="What is the pathogenesis of Wernicke's encephalopathy?">Wernicke's encephalopathy is caused by thiamine (Vitamin B1) deficiency. Chronic alcoholics often have poor diets and alcohol inhibits intestinal absorption of thiamine. Thus, some chronic alcoholics can develop Wernicke's encephalopathy which consists of foci of symmetric discoloration, softening, and punctate hemorrhages in the paraventricular regions of the thalamus and hypothalamus, in the mamillary bodies, around the aqueduct in the midbrain, in the floor of the fourth ventricle and in the anterior cerebellum. There is demyelinization and loss of neuropil. Even after treatment with thiamine, there is significant memory deficit.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/185856-overview eMedicine Medical Library: Cirrhosis]
* [http://emedicine.medscape.com/article/366426-overview eMedicine Medical Library: Cirrhosis Imaging]
* [http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/alcoholic_liver_disease/alcoholic_liver_disease.html Merck Manual: Alcoholic Liver Disease]

=== Journal Articles ===
* Fujimoto J. [http://www.ncbi.nlm.nih.gov/pubmed/10759218 Gene therapy for liver cirrhosis]. ''J Gastroenterol Hepatol'' 2000 Mar;15 Suppl:D33-6.
* Ge PS and Runyon BA [http://http://www.nejm.org/doi/pdf/10.1056/NEJMra1504367 Treatment of Patients with Cirrhosis]. ''NEJM'' 2016 Aug 25 375(8):767.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/128-cirrhosis PEIR Digital Library: Cirrhosis Images]
* [http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html WebPath: Hepatic Pathology]

== Related IPLab Cases ==
* [[IPLab:Lab 2:Fatty Change and Cirrhosis|Lab 2: Liver: Fatty Change and Cirrhosis]]

{{IPLab 12}}

[[Category: IPLab:Lab 12]]

IPLab:Lab 12:Burns

2016-08-04T13:06:28Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 45-year-old back female was involved in a house fire which killed her husband. Upon admission to a local emergency room she was found to have approximately 80% body surface area burns including 1st, 2nd, and 3rd degree burns. Burns were most severe around the head and neck. The patient was intubated and transferred to a tertiary care center. Upon arrival, the patient had a blood pressure of 71/25 mmHg, a heart rate of 121, and was responsive to deep pain but had few spontaneous movements. Both eyes were swollen shut, her nasal hairs were singed, and carbonaceous deposits were present in her nares, throat, and posterior pharynx. Despite aggressive fluid resuscitation and ventilatory support, she remained hypotensive, and became progressively hypoxemic and hypercapnic until she died approximately eight hours after the fire.

== Autopsy Findings ==
The degree and severity of body surface burns were documented. Carbonaceous material was noted in the throat and posterior pharynx as well as in the trachea and main stem bronchi. The liver was soft, yellow and greasy. Results of premortem blood work showed a blood alcohol level of 147 mg/dL.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab12Burns1.jpg|This photograph taken at autopsy demonstrates the severity of the surface burns on this patient.
File:IPLab12Burns2.jpg|This closer view shows the burned skin peeling off to expose the underlying tissue. The various depths of the burn can be appreciated by the color and character of the underlying tissue.
File:IPLab12Burns3.jpg|This photomicrograph of the burned skin depicts an area of third degree burn. There is some residual epidermis (arrow) but in the majority of this section the epidermis is gone. Also note the severe subcutaneous edema.
File:IPLab12Burns4.jpg|This high-power photomicrograph shows the denuded surface of the skin with thrombosed blood vessels (arrows) and necrosis of the dermis.
File:IPLab12Burns5.jpg|This medium-power photomicrograph of the burned skin demonstrates blister formation. The vessels in the dermis are congested (arrows).
File:IPLab12Burns6.jpg|This high-power photomicrograph of the burned skin shows the blister and the thrombosed vessels in the dermis.
File:IPLab12Burns7.jpg|This photomicrograph of the burned skin depicts an area of first degree burn. Note that there are no blisters and no damage to the dermis. There is mild damage to the superficial epidermis and some hyperemia (arrow).
File:IPLab12Burns8.jpg|This medium-power photomicrograph of the burned skin shows the mild damage to the superficial layers of the epidermis.
File:IPLab12Burns9.jpg|This photograph demonstrates the black carbonaceous material in the trachea.
File:IPLab12Burns10.jpg|This photograph of the lung again shows the black carbonaceous material in the trachea as well as in the main stem bronchi. The lungs are mildly congested and hyperemic. The patient lived for less than 8 hours after the burn injury so there was not enough time to develop a full-blown pneumonia.
File:IPLab12Burns11.jpg|This closer view of the lung shows the black carbonaceous material in the trachea as well as in the main stem bronchi.
File:IPLab12Burns12.jpg|This photomicrograph of the trachea shows sloughing of the tracheal epithelium and the black carbonaceous material contained therein (1). This degree of tracheal epithelial damage is indicative of severe inhalation injury. The tracheal cartilage rings can be seen in cross-section (2).
File:IPLab12Burns13.jpg|The damage to the tracheal epithelium and the black carbonaceous material is present down to the level of the terminal bronchioles.
</gallery>

== Study Questions ==
* <spoiler text="What was the immediate cause of death (COD) in this patient? What other factors played a role in this patient's demise?">The immediate cause of death for this patient is thermal injury involving 80% body surface area. This large body surface area of burn injury is very severe and has a poor prognosis. The gross and microscopic evidence of smoke inhalation and burn injury to the nose, throat and lungs are indicative of severe lung injury. Inhalation injury is seen in over 80% of patients with a burn size of 85% or more of the total body surface area. Carbon monoxide poisoning also contributes to the early death in inhalation injury. The manner of death in this case would have been accidental - unless someone deliberately set the fire.

This additional factor of the severity and the extent of the body surface area burn would likely have lead to death of this patient. Clinical management of a patient with burns this severe would be very difficult. Shock and sepsis are common problems in these patients.</spoiler>
* <spoiler text="What is the significance of the fatty liver and the blood alcohol level noted in this patient?">The fatty liver and the elevated blood alcohol level indicate that this patient was severely incapacitated by alcohol prior to the fire. The patient was likely in an alcoholic stupor when the fire broke out and could not escape.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1278244-overview eMedicine Medical Library: Thermal Burns]
* [http://emedicine.medscape.com/article/769193-overview eMedicine Medical Library: Emergent Management of Thermal Burns]
* [http://www.merckmanuals.com/professional/injuries_poisoning/burns/burns.html Merck Manual: Burns]

=== Journal Articles ===
* Fukuzuka K, Rosenberg JJ, Gaines GC, Edwards CK 3rd, Clare-Salzler M, MacKay SL, Moldawer LL, Copeland EM 3rd, Mozingo DW. [http://www.ncbi.nlm.nih.gov/pubmed/10363899 Caspase-3-dependent organ apoptosis early after burn injury]. ''Ann Surg'' 1999 Jun;229(6):851-8; discussion 858-9.
* Robert L. Sheridan, M.D.[http://www.nejm.org/doi/pdf/10.1056/NEJMra1601128 Fire-Related Inhalation Injury]. ''NEJM'' 2016 Aug;375:464-469.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2171-burn PEIR Digital Library: Burn Images]

{{IPLab 12}}

[[Category: IPLab:Lab 12]]

IPLab:Lab 5:Hemochromatosis

2016-04-21T18:15:46Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 61-year-old female was first admitted to the hospital because of ascites and pedal edema. A liver biopsy revealed a marked intracellular accumulation of iron. The serum iron concentration was reported as 220 mcg/dL. On the basis of these studies, the diagnosis of hemochromatosis was made. It should be noted that the patient also exhibited an abnormal glucose tolerance test at this time (following the ingestion of a test dose of glucose, the blood glucose level rose to 290 mg/dL at one hour and remained at this level for the next three hours). Subsequent to the first admission, the patient was admitted on several occasions for ascites. The patient's last admission was necessitated by the development of symptoms and signs of hepatic failure (hepatic coma) characterized by jaundice and coma.

== Autopsy Findings ==
The liver weighed 820 grams. The cut surface was described as golden-brown in color, having a fine, diffuse nodularity, and being extremely firm in consistency.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab5Hemochromatosis1.jpg|This is a gross photograph of liver (1) and pancreas (2) from this case of hemochromatosis. Note that both of these organs have a dark brown coloration.
File:IPLab5Hemochromatosis2.jpg|This is a gross photograph of a cut section of liver from this case of hemochromatosis. Note that the liver is dark brown. Although hard to appreciate in a photograph, the tissue is also firm (cirrhotic).
File:IPLab5Hemochromatosis3.jpg|This is a low-power micrograph of liver from this patient. Note the nodularity of the tissue (arrows).
File:IPLab5Hemochromatosis4.jpg|This higher-power view of liver from this case demonstrates the nodules and the brown/black pigment within liver parenchymal cells (arrows).
File:IPLab5Hemochromatosis5.jpg|This higher-power photomicrograph demonstrates the increased fibrosis in the periportal area (1) and the pigment accumulation (2).
File:IPLab5Hemochromatosis6.jpg|This trichrome stain of liver section demonstrates the increased fibrous connective tissue in this liver. Note that the liver nodules (1) are surrounded by fibrous connective tissue (2).
File:IPLab5Hemochromatosis7.jpg|This is a low-power view of liver section stained with Prussian blue. Prussian blue reacts with iron in the tissue to give a blue color.
File:IPLab5Hemochromatosis8.jpg|This higher-power view of liver stained with Prussian blue demonstrates the marked accumulation of iron within the parenchymal cells (1) and in the Kupffer cells in the periportal area (2).
File:IPLab5Hemochromatosis9.jpg|This is a gross picture of pancreas from this case. Note the brown discoloration of the tissue.
File:IPLab5Hemochromatosis10.jpg|This is a histologic section of pancreas from this case. It is difficult to appreciate at this magnification, but there is brown pigment in the pancreatic acinar cells. Note the islets of Langerhans (1).
File:IPLab5Hemochromatosis11.jpg|This is a histologic section of pancreas from this case stained for iron (Prussian blue). Note the accumulation of iron in the parenchymal cells (1). There is also iron in the pancreatic islets (2).
</gallery>

== Virtual Microscopy ==
=== H&E ===
===Liver: Hemochromatosis ===
<peir-vm>IPLab5Hemochromatosis_HE</peir-vm>

=== Normal Liver ===
<peir-vm>UAB-Histology-00149</peir-vm>

=== Prussian Blue ===
<peir-vm>IPLab5Hemochromatosis_Prussian_blue</peir-vm>

== Study Questions ==
* <spoiler text="What is the clinical triad associated with hemochromatosis?">Diabetes mellitus, skin pigmentation, and hepatic fibrosis.</spoiler>
* <spoiler text="What are the two main types of hemochromatosis?">Primary or idiopathic hemochromatosis (also called hereditary hemochromatosis - HHC) is an autosomal recessive heritable disorder. The hemochromatosis gene is located on the short arm of chromosome 6, and the associated HLA haplotypes include A3 in 70% of hemochromatosis patients with fewer numbers of patients expressing B7, B14, or Bw35. Males are affected more than females (5 to 7:1) but this earlier and more severe clinical presentation in males is partly due to physiologic iron loss (menstruation, pregnancy) in females which delays iron accumulation. Even though the gene has been isolated and many aspects of the disease are known; the exact mechanism responsible for iron overload in primary hemochromatosis is not known.

The second type of hemochromatosis where the source of iron overload can be explained is called secondary hemochromatosis. Severe anemias due to ineffective erythropoiesis are the most common causes of secondary hemochromatosis. In these anemias the excess iron accumulation results from transfusions and also from compensatory increases in iron absorption. Alcoholic liver disease is also associated with increased iron accumulation in liver cells. Other more obtuse causes of iron overload leading to secondary hemochromatosis include: transfusions of packed RBCs, iron-dextran injections, and long term hemodialysis.</spoiler>
* <spoiler text="Compare and contrast the pathogenesis and clinical features of hemochromatosis and Wilson’s disease.">Hereditary hemochromatosis is an autosomal recessive disorder which results in increased iron absorption and iron induced parenchymal tissue damage. The exact mechanism of this functional defect is unknown. The iron overload leads to ferritin and hemosiderin in the parenchymal tissues of the body; primarily the liver, pancreas, myocardium, endocrine glands, and joints. Iron is a direct hepatotoxin and results in micronodular cirrhosis. Tissue damage and fibrosis is also evident in the pancreas, heart, and endocrine organs. The "bronze diabetes" of hemochromatosis is produced by excess melanin in the skin and by accumulation of hemosiderin in the dermal appendages. The diabetes is caused by destruction of pancreatic islets. Hemosiderin in the joint synovial lining leads to acute synovitis.

Wilson's Disease is also an autosomal recessive disorder that results in the accumulation of toxic levels of copper. Like hemochromatosis, the gene defect has been localized but the exact nature of the genetic defect is unknown. In this disorder, copper absorption and transport to the liver are normal; however, the copper does not get back into the circulation as ceruloplasmin and copper excretion into bile is severely impaired. The accumulation of copper leads primarily to liver, brain and eye damage. The liver develops fatty change and nuclear vacuolization in the setting of acute or chronic hepatitis which later progresses to cirrhosis. Neurologic manifestations include toxic neuronal injury primarily in the basal ganglia. Accumulation of copper in the cornea results in the formation of Kayser-Fleischer rings.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/177216-overview eMedicine Medical Library: Hemochromatosis]
* [http://www.merckmanuals.com/professional/hematology_and_oncology/iron_overload/overview_of_iron_overload.html Merck Manual: Iron Overload: Hemosiderosis and Hemochromatosis]

=== Journal Articles ===
* Powell LW, Seckington RC, Deugnier Y. [http://ac.els-cdn.com/S014067361501315X/1-s2.0-S014067361501315X-main.pdf?_tid=61a0b7de-07d2-11e6-b26f-00000aab0f02&acdnat=1461251264_8f332714107047706b12570ed99cf384 Haemochromatosis]. ''Lancet'' 2016.
* Ayonrinde OT, Milward EA, Chua AC, Trinder D, Olynyk JK. [http://www.ncbi.nlm.nih.gov/pubmed/18712630 Clinical perspectives on hereditary hemochromatosis]. ''Crit Rev Clin Lab Sci'' 2008;45(5):451-84.
* Bassett ML. [http://www.ncbi.nlm.nih.gov/pubmed/11456037 Haemochromatosis: iron still matters]. ''Intern Med J'' 2001 May-Jun;31(4):237-42.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/177-hemochromatosis PEIR Digital Library: Hemochromatosis Images]
* [http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html#3 WebPath: Hepatic Pigmentary Disorders]
* [http://library.med.utah.edu/WebPath/CINJHTML/CINJIDX.html#5 WebPath: Cellular Accumulations]

== Related IPLab Cases ==
* [[IPLab:Lab 13:Biliary Atresia|Lab 13: Liver: Biliary Atresia]]

{{IPLab 5}}

[[Category: IPLab:Lab 5]]

IPLab:Lab 12:Burns

2015-11-20T15:45:36Z

Peter Anderson: /* Study Questions */

== Clinical Summary ==
This 45-year-old back female was involved in a house fire which killed her husband. Upon admission to a local emergency room she was found to have approximately 80% body surface area burns including 1st, 2nd, and 3rd degree burns. Burns were most severe around the head and neck. The patient was intubated and transferred to a tertiary care center. Upon arrival, the patient had a blood pressure of 71/25 mmHg, a heart rate of 121, and was responsive to deep pain but had few spontaneous movements. Both eyes were swollen shut, her nasal hairs were singed, and carbonaceous deposits were present in her nares, throat, and posterior pharynx. Despite aggressive fluid resuscitation and ventilatory support, she remained hypotensive, and became progressively hypoxemic and hypercapnic until she died approximately eight hours after the fire.

== Autopsy Findings ==
The degree and severity of body surface burns were documented. Carbonaceous material was noted in the throat and posterior pharynx as well as in the trachea and main stem bronchi. The liver was soft, yellow and greasy. Results of premortem blood work showed a blood alcohol level of 147 mg/dL.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab12Burns1.jpg|This photograph taken at autopsy demonstrates the severity of the surface burns on this patient.
File:IPLab12Burns2.jpg|This closer view shows the burned skin peeling off to expose the underlying tissue. The various depths of the burn can be appreciated by the color and character of the underlying tissue.
File:IPLab12Burns3.jpg|This photomicrograph of the burned skin depicts an area of third degree burn. There is some residual epidermis (arrow) but in the majority of this section the epidermis is gone. Also note the severe subcutaneous edema.
File:IPLab12Burns4.jpg|This high-power photomicrograph shows the denuded surface of the skin with thrombosed blood vessels (arrows) and necrosis of the dermis.
File:IPLab12Burns5.jpg|This medium-power photomicrograph of the burned skin demonstrates blister formation. The vessels in the dermis are congested (arrows).
File:IPLab12Burns6.jpg|This high-power photomicrograph of the burned skin shows the blister and the thrombosed vessels in the dermis.
File:IPLab12Burns7.jpg|This photomicrograph of the burned skin depicts an area of first degree burn. Note that there are no blisters and no damage to the dermis. There is mild damage to the superficial epidermis and some hyperemia (arrow).
File:IPLab12Burns8.jpg|This medium-power photomicrograph of the burned skin shows the mild damage to the superficial layers of the epidermis.
File:IPLab12Burns9.jpg|This photograph demonstrates the black carbonaceous material in the trachea.
File:IPLab12Burns10.jpg|This photograph of the lung again shows the black carbonaceous material in the trachea as well as in the main stem bronchi. The lungs are mildly congested and hyperemic. The patient lived for less than 8 hours after the burn injury so there was not enough time to develop a full-blown pneumonia.
File:IPLab12Burns11.jpg|This closer view of the lung shows the black carbonaceous material in the trachea as well as in the main stem bronchi.
File:IPLab12Burns12.jpg|This photomicrograph of the trachea shows sloughing of the tracheal epithelium and the black carbonaceous material contained therein (1). This degree of tracheal epithelial damage is indicative of severe inhalation injury. The tracheal cartilage rings can be seen in cross-section (2).
File:IPLab12Burns13.jpg|The damage to the tracheal epithelium and the black carbonaceous material is present down to the level of the terminal bronchioles.
</gallery>

== Study Questions ==
* <spoiler text="What was the immediate cause of death (COD) in this patient? What other factors played a role in this patient's demise?">The immediate cause of death for this patient is thermal injury involving 80% body surface area. This large body surface area of burn injury is very severe and has a poor prognosis. The gross and microscopic evidence of smoke inhalation and burn injury to the nose, throat and lungs are indicative of severe lung injury. Inhalation injury is seen in over 80% of patients with a burn size of 85% or more of the total body surface area. Carbon monoxide poisoning also contributes to the early death in inhalation injury. The manner of death in this case would have been accidental - unless someone deliberately set the fire.

This additional factor of the severity and the extent of the body surface area burn would likely have lead to death of this patient. Clinical management of a patient with burns this severe would be very difficult. Shock and sepsis are common problems in these patients.</spoiler>
* <spoiler text="What is the significance of the fatty liver and the blood alcohol level noted in this patient?">The fatty liver and the elevated blood alcohol level indicate that this patient was severely incapacitated by alcohol prior to the fire. The patient was likely in an alcoholic stupor when the fire broke out and could not escape.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1278244-overview eMedicine Medical Library: Thermal Burns]
* [http://emedicine.medscape.com/article/769193-overview eMedicine Medical Library: Emergent Management of Thermal Burns]
* [http://www.merckmanuals.com/professional/injuries_poisoning/burns/burns.html Merck Manual: Burns]

=== Journal Articles ===
* Fukuzuka K, Rosenberg JJ, Gaines GC, Edwards CK 3rd, Clare-Salzler M, MacKay SL, Moldawer LL, Copeland EM 3rd, Mozingo DW. [http://www.ncbi.nlm.nih.gov/pubmed/10363899 Caspase-3-dependent organ apoptosis early after burn injury]. ''Ann Surg'' 1999 Jun;229(6):851-8; discussion 858-9.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2171-burn PEIR Digital Library: Burn Images]

{{IPLab 12}}

[[Category: IPLab:Lab 12]]

IPLab:Lab 12:Burns

2015-11-20T15:44:05Z

Peter Anderson: /* Study Questions */

== Clinical Summary ==
This 45-year-old back female was involved in a house fire which killed her husband. Upon admission to a local emergency room she was found to have approximately 80% body surface area burns including 1st, 2nd, and 3rd degree burns. Burns were most severe around the head and neck. The patient was intubated and transferred to a tertiary care center. Upon arrival, the patient had a blood pressure of 71/25 mmHg, a heart rate of 121, and was responsive to deep pain but had few spontaneous movements. Both eyes were swollen shut, her nasal hairs were singed, and carbonaceous deposits were present in her nares, throat, and posterior pharynx. Despite aggressive fluid resuscitation and ventilatory support, she remained hypotensive, and became progressively hypoxemic and hypercapnic until she died approximately eight hours after the fire.

== Autopsy Findings ==
The degree and severity of body surface burns were documented. Carbonaceous material was noted in the throat and posterior pharynx as well as in the trachea and main stem bronchi. The liver was soft, yellow and greasy. Results of premortem blood work showed a blood alcohol level of 147 mg/dL.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab12Burns1.jpg|This photograph taken at autopsy demonstrates the severity of the surface burns on this patient.
File:IPLab12Burns2.jpg|This closer view shows the burned skin peeling off to expose the underlying tissue. The various depths of the burn can be appreciated by the color and character of the underlying tissue.
File:IPLab12Burns3.jpg|This photomicrograph of the burned skin depicts an area of third degree burn. There is some residual epidermis (arrow) but in the majority of this section the epidermis is gone. Also note the severe subcutaneous edema.
File:IPLab12Burns4.jpg|This high-power photomicrograph shows the denuded surface of the skin with thrombosed blood vessels (arrows) and necrosis of the dermis.
File:IPLab12Burns5.jpg|This medium-power photomicrograph of the burned skin demonstrates blister formation. The vessels in the dermis are congested (arrows).
File:IPLab12Burns6.jpg|This high-power photomicrograph of the burned skin shows the blister and the thrombosed vessels in the dermis.
File:IPLab12Burns7.jpg|This photomicrograph of the burned skin depicts an area of first degree burn. Note that there are no blisters and no damage to the dermis. There is mild damage to the superficial epidermis and some hyperemia (arrow).
File:IPLab12Burns8.jpg|This medium-power photomicrograph of the burned skin shows the mild damage to the superficial layers of the epidermis.
File:IPLab12Burns9.jpg|This photograph demonstrates the black carbonaceous material in the trachea.
File:IPLab12Burns10.jpg|This photograph of the lung again shows the black carbonaceous material in the trachea as well as in the main stem bronchi. The lungs are mildly congested and hyperemic. The patient lived for less than 8 hours after the burn injury so there was not enough time to develop a full-blown pneumonia.
File:IPLab12Burns11.jpg|This closer view of the lung shows the black carbonaceous material in the trachea as well as in the main stem bronchi.
File:IPLab12Burns12.jpg|This photomicrograph of the trachea shows sloughing of the tracheal epithelium and the black carbonaceous material contained therein (1). This degree of tracheal epithelial damage is indicative of severe inhalation injury. The tracheal cartilage rings can be seen in cross-section (2).
File:IPLab12Burns13.jpg|The damage to the tracheal epithelium and the black carbonaceous material is present down to the level of the terminal bronchioles.
</gallery>

== Study Questions ==
* <spoiler text="What was the immediate cause of death (COD) in this patient? What other factors played a role in this patient's demise?">This patient died of thermal injury involving 80% body surface area. This large body surface area of burn injury is very severe and has a poor prognosis. The gross and microscopic evidence of smoke inhalation and burn injury to the nose, throat and lungs are indicative of severe lung injury. Inhalation injury is seen in over 80% of patients with a burn size of 85% or more of the total body surface area. Carbon monoxide poisoning also contributes to the early death in inhalation injury. The manner of death in this case would have been accidental - unless someone deliberately set the fire.

This additional factor of the severity and the extent of the body surface area burn would likely have lead to death of this patient. Clinical management of a patient with burns this severe would be very difficult. Shock and sepsis are common problems in these patients.</spoiler>
* <spoiler text="What is the significance of the fatty liver and the blood alcohol level noted in this patient?">The fatty liver and the elevated blood alcohol level indicate that this patient was severely incapacitated by alcohol prior to the fire. The patient was likely in an alcoholic stupor when the fire broke out and could not escape.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1278244-overview eMedicine Medical Library: Thermal Burns]
* [http://emedicine.medscape.com/article/769193-overview eMedicine Medical Library: Emergent Management of Thermal Burns]
* [http://www.merckmanuals.com/professional/injuries_poisoning/burns/burns.html Merck Manual: Burns]

=== Journal Articles ===
* Fukuzuka K, Rosenberg JJ, Gaines GC, Edwards CK 3rd, Clare-Salzler M, MacKay SL, Moldawer LL, Copeland EM 3rd, Mozingo DW. [http://www.ncbi.nlm.nih.gov/pubmed/10363899 Caspase-3-dependent organ apoptosis early after burn injury]. ''Ann Surg'' 1999 Jun;229(6):851-8; discussion 858-9.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2171-burn PEIR Digital Library: Burn Images]

{{IPLab 12}}

[[Category: IPLab:Lab 12]]

IPLab:Lab 7:Malignant Melanoma

2015-11-12T14:18:02Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 68-year-old white male had a local excision of a pigmented lesion (melanoma) on the skin of his back. Three years later he became aware of a "lump" in his left axilla. Examination confirmed the presence of a 2.3-cm nodular lesion. Subsequently, the patient underwent a surgical procedure for removal of axillary lymph nodes.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab7Melanoma1.jpg|This is a gross photograph of skin with melanoma. Note the black pigment, multiple satellite nodules, and focal ulceration. Some of the satellite nodules affect the nipple.
File:IPLab7Melanoma2.jpg|This is a gross photograph of lymph nodes almost entirely replaced by black pigment (melanin).
File:IPLab7Melanoma3.jpg|This is a low-power photomicrograph of lymph node that is almost completely replaced/filled with tumor. This lymph node has a capsule (1) and some remaining lymphocytes (2) but the remainder of the node is replaced by tumor cells.
File:IPLab7Melanoma4.jpg|This higher-power photomicrograph shows the remaining portion of lymph node (arrow). The rest of the lymph node is invaded by a neoplasm composed of cells with lighter eosinophilic cytoplasm and pigment.
File:IPLab7Melanoma5.jpg|This is a higher-magnification showing the abundant extracellular melanin (arrows) surrounding the tumor cells. This section of neoplasm shows the numerous cells with abundant cytoplasm and brown pigment within the cytoplasm of some of these cells.
File:IPLab7Melanoma6.jpg|This is a higher magnification showing the abundant extracellular melanin surrounding the tumor cells (brown pigment).
File:IPLab7Melanoma7.jpg|This is a high-power photomicrograph of the main tumor mass with the cells growing as poorly formed nests and sheets of cells. There is little if any pigment in this section.
File:IPLab7Melanoma8.jpg|This is a high-power photomicrograph of the main tumor mass showing the cellular details. The individual melanoma cells contain large nuclei with irregular contours having chromatin clumped at the periphery of the nuclear membrane and prominent red (eosinophilic) nucleoli.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab7Melanoma</peir-vm>

== Study Question ==
* <spoiler text="What are the possible sites of origin for melanomas?">Most melanomas arise in the skin; however, other sites of origin include the oral and anogenital mucosal surfaces, esophagus, meninges, and the eye.</spoiler>
* <spoiler text="What are risk factors for developing melanoma?">Sunlight appears to play an important role in the development of skin malignant melanoma. Lightly pigmented individuals are at higher risk for the development of melanoma than darkly pigmented individuals. Sunlight does not seem to be the only predisposing factor, and the presence of a pre-existing nevus (e.g., a dysplastic nevus), hereditary factors, or even exposure to certain carcinogens may play a role in lesion development and evolution.</spoiler>
* <spoiler text="What role may tumor specific antigens play in development of malignant melanoma?">Approximately 40% of human melanomas express a tumor specific antigen referred to as melanoma antigen-1 (MAGE-1). Molecular analysis has revealed that the gene encoding MAGE-1 is present in normal cells as well as in tumor cells, and there is no evidence that it is mutated in cancer cells. However, as has been seen in some animal tumors, the gene is silent in normal adult cells; whether or not it is expressed during development remains to be determined. CD8+ cytotoxic T cells specific for MAGE-1 can be obtained by culturing tumor cells with patients’ lymphocytes in vitro.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1100753-overview eMedicine Medical Library: Cutaneous Melanoma]
* [http://emedicine.medscape.com/article/280245-overview eMedicine Medical Library: Malignant Melanoma]
* [http://emedicine.medscape.com/article/846566-overview eMedicine Medical Library: Skin Cancer -- Melanoma]
* [http://www.merckmanuals.com/professional/dermatologic_disorders/cancers_of_the_skin/melanoma.html Merck Manual: Melanoma]

=== Journal Articles ===
* Banerjee SS, Harris M. [http://www.ncbi.nlm.nih.gov/pubmed/10792480 Morphological and immunophenotypic variations in malignant melanoma]. ''Histopathology'' 2000 May;36(5):387-402.
* Shain AH, Yeh I, Kovalyshyn I, Sriharan A, Talevich E, Gagnon A, Dummer R, North J, Pincus L, Ruben B, Rickaby W, D’Arrigo C, Robson A, and Bastian BC.[http://www.nejm.org/doi/pdf/10.1056/NEJMoa1502583 The Genetic Evolution of Melanoma from Precursor Lesions]. ''New England Journal of Medicine'' 2015 Nov;373:1926-1936.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2148-melanoma PEIR Digital Library: Melanoma Images]
* [http://library.med.utah.edu/WebPath/NEOHTML/NEOPLIDX.html WebPath: Neoplasia]

{{IPLab 7}}

[[Category: IPLab:Lab 7]]

IPLab:Lab 7:Malignant Melanoma

2015-11-12T14:17:00Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 68-year-old white male had a local excision of a pigmented lesion (melanoma) on the skin of his back. Three years later he became aware of a "lump" in his left axilla. Examination confirmed the presence of a 2.3-cm nodular lesion. Subsequently, the patient underwent a surgical procedure for removal of axillary lymph nodes.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab7Melanoma1.jpg|This is a gross photograph of skin with melanoma. Note the black pigment, multiple satellite nodules, and focal ulceration. Some of the satellite nodules affect the nipple.
File:IPLab7Melanoma2.jpg|This is a gross photograph of lymph nodes almost entirely replaced by black pigment (melanin).
File:IPLab7Melanoma3.jpg|This is a low-power photomicrograph of lymph node that is almost completely replaced/filled with tumor. This lymph node has a capsule (1) and some remaining lymphocytes (2) but the remainder of the node is replaced by tumor cells.
File:IPLab7Melanoma4.jpg|This higher-power photomicrograph shows the remaining portion of lymph node (arrow). The rest of the lymph node is invaded by a neoplasm composed of cells with lighter eosinophilic cytoplasm and pigment.
File:IPLab7Melanoma5.jpg|This is a higher-magnification showing the abundant extracellular melanin (arrows) surrounding the tumor cells. This section of neoplasm shows the numerous cells with abundant cytoplasm and brown pigment within the cytoplasm of some of these cells.
File:IPLab7Melanoma6.jpg|This is a higher magnification showing the abundant extracellular melanin surrounding the tumor cells (brown pigment).
File:IPLab7Melanoma7.jpg|This is a high-power photomicrograph of the main tumor mass with the cells growing as poorly formed nests and sheets of cells. There is little if any pigment in this section.
File:IPLab7Melanoma8.jpg|This is a high-power photomicrograph of the main tumor mass showing the cellular details. The individual melanoma cells contain large nuclei with irregular contours having chromatin clumped at the periphery of the nuclear membrane and prominent red (eosinophilic) nucleoli.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab7Melanoma</peir-vm>

== Study Question ==
* <spoiler text="What are the possible sites of origin for melanomas?">Most melanomas arise in the skin; however, other sites of origin include the oral and anogenital mucosal surfaces, esophagus, meninges, and the eye.</spoiler>
* <spoiler text="What are risk factors for developing melanoma?">Sunlight appears to play an important role in the development of skin malignant melanoma. Lightly pigmented individuals are at higher risk for the development of melanoma than darkly pigmented individuals. Sunlight does not seem to be the only predisposing factor, and the presence of a pre-existing nevus (e.g., a dysplastic nevus), hereditary factors, or even exposure to certain carcinogens may play a role in lesion development and evolution.</spoiler>
* <spoiler text="What role may tumor specific antigens play in development of malignant melanoma?">Approximately 40% of human melanomas express a tumor specific antigen referred to as melanoma antigen-1 (MAGE-1). Molecular analysis has revealed that the gene encoding MAGE-1 is present in normal cells as well as in tumor cells, and there is no evidence that it is mutated in cancer cells. However, as has been seen in some animal tumors, the gene is silent in normal adult cells; whether or not it is expressed during development remains to be determined. CD8+ cytotoxic T cells specific for MAGE-1 can be obtained by culturing tumor cells with patients’ lymphocytes in vitro.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1100753-overview eMedicine Medical Library: Cutaneous Melanoma]
* [http://emedicine.medscape.com/article/280245-overview eMedicine Medical Library: Malignant Melanoma]
* [http://emedicine.medscape.com/article/846566-overview eMedicine Medical Library: Skin Cancer -- Melanoma]
* [http://www.merckmanuals.com/professional/dermatologic_disorders/cancers_of_the_skin/melanoma.html Merck Manual: Melanoma]

=== Journal Articles ===
* Banerjee SS, Harris M. [http://www.ncbi.nlm.nih.gov/pubmed/10792480 Morphological and immunophenotypic variations in malignant melanoma]. ''Histopathology'' 2000 May;36(5):387-402.
* Shain AH, Yeh I, Kovalyshyn I, Sriharan A, Talevich E, Gagnon A, Dummer R, North J, Pincus L, Ruben B, Rickaby W, D’Arrigo C, Robson A, and Bastian BC.[http://https://www.nejm.org/doi/pdf/10.1056/NEJMoa1502583 The Genetic Evolution of Melanoma from Precursor Lesions]. ''New England Journal of Medicine'' 2015 Nov;373:1926-1936.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2148-melanoma PEIR Digital Library: Melanoma Images]
* [http://library.med.utah.edu/WebPath/NEOHTML/NEOPLIDX.html WebPath: Neoplasia]

{{IPLab 7}}

[[Category: IPLab:Lab 7]]

IPLab:Lab 7:Malignant Melanoma

2015-11-12T14:11:49Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 68-year-old white male had a local excision of a pigmented lesion (melanoma) on the skin of his back. Three years later he became aware of a "lump" in his left axilla. Examination confirmed the presence of a 2.3-cm nodular lesion. Subsequently, the patient underwent a surgical procedure for removal of axillary lymph nodes.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab7Melanoma1.jpg|This is a gross photograph of skin with melanoma. Note the black pigment, multiple satellite nodules, and focal ulceration. Some of the satellite nodules affect the nipple.
File:IPLab7Melanoma2.jpg|This is a gross photograph of lymph nodes almost entirely replaced by black pigment (melanin).
File:IPLab7Melanoma3.jpg|This is a low-power photomicrograph of lymph node that is almost completely replaced/filled with tumor. This lymph node has a capsule (1) and some remaining lymphocytes (2) but the remainder of the node is replaced by tumor cells.
File:IPLab7Melanoma4.jpg|This higher-power photomicrograph shows the remaining portion of lymph node (arrow). The rest of the lymph node is invaded by a neoplasm composed of cells with lighter eosinophilic cytoplasm and pigment.
File:IPLab7Melanoma5.jpg|This is a higher-magnification showing the abundant extracellular melanin (arrows) surrounding the tumor cells. This section of neoplasm shows the numerous cells with abundant cytoplasm and brown pigment within the cytoplasm of some of these cells.
File:IPLab7Melanoma6.jpg|This is a higher magnification showing the abundant extracellular melanin surrounding the tumor cells (brown pigment).
File:IPLab7Melanoma7.jpg|This is a high-power photomicrograph of the main tumor mass with the cells growing as poorly formed nests and sheets of cells. There is little if any pigment in this section.
File:IPLab7Melanoma8.jpg|This is a high-power photomicrograph of the main tumor mass showing the cellular details. The individual melanoma cells contain large nuclei with irregular contours having chromatin clumped at the periphery of the nuclear membrane and prominent red (eosinophilic) nucleoli.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab7Melanoma</peir-vm>

== Study Question ==
* <spoiler text="What are the possible sites of origin for melanomas?">Most melanomas arise in the skin; however, other sites of origin include the oral and anogenital mucosal surfaces, esophagus, meninges, and the eye.</spoiler>
* <spoiler text="What are risk factors for developing melanoma?">Sunlight appears to play an important role in the development of skin malignant melanoma. Lightly pigmented individuals are at higher risk for the development of melanoma than darkly pigmented individuals. Sunlight does not seem to be the only predisposing factor, and the presence of a pre-existing nevus (e.g., a dysplastic nevus), hereditary factors, or even exposure to certain carcinogens may play a role in lesion development and evolution.</spoiler>
* <spoiler text="What role may tumor specific antigens play in development of malignant melanoma?">Approximately 40% of human melanomas express a tumor specific antigen referred to as melanoma antigen-1 (MAGE-1). Molecular analysis has revealed that the gene encoding MAGE-1 is present in normal cells as well as in tumor cells, and there is no evidence that it is mutated in cancer cells. However, as has been seen in some animal tumors, the gene is silent in normal adult cells; whether or not it is expressed during development remains to be determined. CD8+ cytotoxic T cells specific for MAGE-1 can be obtained by culturing tumor cells with patients’ lymphocytes in vitro.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1100753-overview eMedicine Medical Library: Cutaneous Melanoma]
* [http://emedicine.medscape.com/article/280245-overview eMedicine Medical Library: Malignant Melanoma]
* [http://emedicine.medscape.com/article/846566-overview eMedicine Medical Library: Skin Cancer -- Melanoma]
* [http://www.merckmanuals.com/professional/dermatologic_disorders/cancers_of_the_skin/melanoma.html Merck Manual: Melanoma]

=== Journal Articles ===
* Banerjee SS, Harris M. [http://www.ncbi.nlm.nih.gov/pubmed/10792480 Morphological and immunophenotypic variations in malignant melanoma]. ''Histopathology'' 2000 May;36(5):387-402.
* Shain AH, Yeh I, Kovalyshyn I, Sriharan A, Talevich E, Gagnon A, Dummer R, North J, Pincus L, Ruben B, Rickaby W, D’Arrigo C, Robson A, and Bastian BC.[http://http://www.nejm.org/doi/pdf/10.1056/NEJMoa1502583 The Genetic Evolution of Melanoma from Precursor Lesions]. ''New England Journal of Medicine'' 2015 Nov;373:1926-1936.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2148-melanoma PEIR Digital Library: Melanoma Images]
* [http://library.med.utah.edu/WebPath/NEOHTML/NEOPLIDX.html WebPath: Neoplasia]

{{IPLab 7}}

[[Category: IPLab:Lab 7]]

IPLab:Lab 2:Fatty Change and Cirrhosis

2015-11-08T21:42:02Z

Peter Anderson: /* Images */

== Clinical Summary ==
This 54-year-old man with a long history of alcohol abuse had been admitted to the hospital numerous times for abdominal pain thought to be due to gastritis or a peptic ulcer. On several occasions his serum amylase level was elevated into the range of 300-500 u/L indicating relapsing or recurrent pancreatitis. Three weeks prior to his demise, the patient began an alcoholic binge. The binge continued until three days prior to the patient's death at which time he developed fever and malaise, prompting him to cease drinking. He was brought to the hospital semi-comatose and with a fever of 105.4°F. Shortly after arriving at the hospital, the patient died from massive pneumonia.

== Autopsy Findings ==
At autopsy, a necrotizing lobar pneumonia was present which contained organisms consistent with Klebsiella pneumoniae. The liver was enlarged--weighing 2700 grams--and had a yellow-orange color. The liver was firm to palpation and the cut surface had a slightly granular appearance suggestive of early cirrhosis. The pancreas showed multiple areas of fibrosis.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2FattyChange1.jpg|This gross photograph of liver tissue illustrates the yellowish color of the liver parenchyma. The yellow color indicates high fat content in this tissue. Compare this with the normal dark red color of liver.
File:IPLab2FattyChange2.jpg|This low-power photomicrograph of liver illustrates a very pale-staining section with a uniform appearance throughout the section.
File:IPLab2FattyChange3.jpg|Another low-power photomicrograph illustrates again the pale, washed-out appearance of this tissue. Notice the numerous holes throughout the tissue. There are accumulations of inflammatory cells (arrows) around portal tracts.
File:IPLab2FattyChange4.jpg|A higher-power photomicrograph illustrates more clearly the inflammatory cells (arrows) around the portal areas.
File:IPLab2FattyChange5.jpg|This higher-power photomicrograph of the centrilobular area gives the appearance of fatty tissue, as indicated by many empty spaces. Very few normal liver cells can be seen in this slide. A few more normal-appearing hepatocytes are present at the left portion of the slide (arrows).
File:IPLab2FattyChange6.jpg|Another view at the same power illustrates the proliferation of bile ducts in the interlobular and perichordal regions (arrows).
File:IPLab2FattyChange7.jpg|A high-power photomicrograph of the liver parenchyma shows that each individual liver cell is filled with a large, clear droplet which represents the space remaining after lipid was dissolved by the dehydration procedure used to embed the tissue. Note that each empty space is surrounded by a thin rim of eosinophilic cytoplasm; in many instances, the hepatocyte nucleus can be seen as well. The red body (arrow) seen within a cell in the center of the slide is an acidophilic body associated with alcoholic hepatitis.
File:IPLab2FattyChange8.jpg|An oil red O stain for fat was performed on a frozen section of this liver tissue. The red droplets represent fat in the tissue which is typical of fatty degeneration in the liver. By using frozen sections the tissues do not have to be dehydrated through alcohol solutions and thus the fat does not get washed out.
File:IPLab2FattyChange9.jpg|This photomicrograph of the liver is from another patient with a history of alcohol use. There are some clear vacuoles indicating fat droplets (1) and there are numerous red-staining granular deposits within the cytoplasm of hepatocytes (3)this is alcoholic hyalin. Alcoholic hyalin is easily distinguished from red blood cells (2) that are also present in this section.
File:IPLab2FattyChange10.jpg|This is a low-power photomicrograph of liver stained with a trichrome stain. In this section, connective tissue stains green (arrows) and hepatic parenchymal cells are red. Note that many of the parenchymal cells have clear spaces indicating fatty degeneration. The proliferation of scar tissue between the liver lobules is the result of cirrhosis.
File:IPLab2FattyChange11.jpg|This gross photograph of liver demonstrates severe nodular cirrhosis. Note the extensive scarring of the capsule and the nodular projections of tissue through the uncut capsule in this tissue. The green color is due to the accumulation of bile pigment.
File:IPLab2FattyChange12.jpg|This is a cut surface of the same tissue seen in the previous slide. Note the marked nodular pattern. The paler-staining areas between the round nodules represent fibrous connective tissue.
</gallery>

== Virtual Microscopy ==
=== Liver: Fatty Change and Cirrhosis ===
<peir-vm>IPLab2FattyChange</peir-vm>

=== Normal Liver ===
<peir-vm>UAB-Histology-00149</peir-vm>

== Study Questions ==
* <spoiler text="What substances have accumulated to produce fatty liver?">Triglycerides</spoiler>
* <spoiler text="What are possible causes of steatosis and which of these may have produced the fatty liver seen in this case?">Steatosis can be caused by:

* toxins
* protein malnutrition
* diabetes mellitus
* obesity
* anoxia

In this case, alcohol abuse (toxin) is the most likely etiologic agent.
</spoiler>
* <spoiler text="What causes hepatocellular steatosis in an alcoholic?">Alcohol induces hepatic steatosis primarily by:

* the shunting of normal substrates away from catabolism and toward biosynthesis due to generation of excess NADH by alcohol dehydrogenase,
* impaired assembly and secretions of lipoproteins,
* and increased peripheral catabolism of fat.

Many other factors also come into play.</spoiler>
* <spoiler text="Is the accumulation of fat in this liver a reversible or an irreversible change?">Reversible</spoiler>

== Additional Resources ==

=== Reference ===

* [http://emedicine.medscape.com/article/185856-overview eMedicine Medical Library: Cirrhosis]
* [http://emedicine.medscape.com/article/170539-overview eMedicine Medical Library: Alcoholic Hepatitis]
* [http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/alcoholic_liver_disease/alcoholic_liver_disease.html Merck Manual: Alcoholic Liver Disease]
* [http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/fibrosis_and_cirrhosis/cirrhosis.html Merck Manual: Cirrhosis]

=== Journal Articles ===
* Satapathy SK, Narayan S, Varma N, Dhiman RK, Varma S, Chawla Y. [http://www.ncbi.nlm.nih.gov/pubmed/11595070 Hyposplenism in alcoholic cirrhosis, facts or artifacts? A comparative analysis with non-alcoholic cirrhosis and extrahepatic portal venous obstruction]. ''J Gastroenterol Hepatol'' 2001 Sep;16(9):1038-43.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/128-cirrhosis PEIR Digital Library: Cirrhosis Images]
* [{{SERVER}}/library/index.php?/tags/231-fatty_change PEIR Digital Library: Fatty Change Images]
* [http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html#2 WebPath: Cirrhosis]

== Related IPLab Cases ==
* [[IPLab:Lab 5:α1 Antitrypsin Deficiency|Lab 5: Lung: α1-Antitrypsin Deficiency]]
* [[IPLab:Lab 11:Schistosomiasis|Lab 11: Schistosomiasis]]
* [[IPLab:Lab 12:Alcoholic Cirrhosis|Lab 12: Liver: Alcoholic Cirrhosis]]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

IPLab:Lab 2:Metaplasia

2015-11-08T21:37:02Z

Peter Anderson: /* Study Questions */

== Clinical Summary ==
This 30-year-old black male was born with a meningocele which was repaired in childhood. Despite repair of the meningocele, this patient continued to have a neurogenic bladder.

Six months previous to this admission, the patient passed a single renal calculus but intravenous pyelogram (IVP) showed left nephrolithiasis (a 1 cm stone in the lower lobe). For 6 months the patient had to be catheterized each day for 6 hours. However, he continued to complain of hesitancy and urgency and suffered occasional urinary tract infections.

On this admission, a culture of the patient's urine specimen grew Gram-negative bacilli (Proteus species). Cystoscopy showed heavy trabeculation of the bladder with early diverticula and the left ureteral orifice showed squamous metaplasia. The lower pole of the left kidney was removed surgically, following which the patient recovered and was discharged on antibiotics.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2Metaplasia1.jpg|This is a low-power photomicrograph showing the full cortical and medullary thickness of the kidney. Note that there is a dilated calyx containing some red blood cells in the center of the section (arrow). The cortex is markedly thin and has severe lesions of degeneration and atrophy, although these are hard to appreciate at this low magnification.
File:IPLab2Metaplasia2.jpg|This high-power photomicrograph demonstrates the transitional epithelium lining the renal calyx (1) and the junction (transition zone) to a thicker hyperplastic epithelium (2). Note the inflammatory cells and increased vascular response in the stromal tissue (3) lying beneath the normal transitional epithelium.
File:IPLab2Metaplasia3.jpg|A higher-power view shows the junction of normal epithelium (1) with hyperplastic transitional epithelium (2). Note the inflammatory cells in the subepithelial tissue.
File:IPLab2Metaplasia4.jpg|This is a higher-power photomicrograph of the junction of normal epithelium (1) with hyperplastic transitional epithelium (2).
File:IPLab2Metaplasia5.jpg|In areas adjacent to the normal transitional epithelium, there are areas of epithelium (arrows) where the epithelial cells have the character of normal squamous epithelium as found in the dermis. However, squamous epithelium is not normal in the renal pelvis. This adaptive change is referred to as squamous metaplasia.
File:IPLab2Metaplasia6.jpg|A high-power photomicrograph of the squamous epithelium shows inflammatory cells in the subepithelial tissue and the formation of keratinized epithelium (arrows).
File:IPLab2Metaplasia7.jpg|This is a photomicrograph of the trachea from a smoker. Note that the columnar ciliated epithelium has been replaced by squamous epithelium.
</gallery>

== Virtual Microscopy ==
=== Kidney: Metaplasia ===
<peir-vm>IPLab2Metaplasia</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is a neurogenic bladder and what complications may result from this condition?">A neurogenic bladder is any condition or dysfunction of the urinary bladder caused by a lesion of the central or peripheral nervous system. Complications primarily include stasis, infection, and stone formation.</spoiler>
* <spoiler text="What factors in this case predisposed to nephrolithiasis?">Stasis and infection.</spoiler>
* <spoiler text="Does this metaplastic process predispose to neoplasia?">No.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/437096-overview eMedicine Medical Library: Nephrolithiasis]
* [http://emedicine.medscape.com/article/453539-overview eMedicine Medical Library: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/urinary_calculi/urinary_calculi.html Merck Manual: Urinary Calculi]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/voiding_disorders/neurogenic_bladder.html Merck Manual: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/approach_to_the_genitourinary_patient/evaluation_of_the_renal_patient.html Merck Manual: Approach to the Genitourinary Patient]

=== Journal Articles ===
* Barbera M, Fitzgerald RC. [http://www.sciencedirect.com/science/article/pii/S1055320709000180 Cellular Mechanisms of Barrett's Esophagus Development]. ''Surg Oncol Clin N Am '' 2009 18:393–410.
* Spechler SJ and Souza RF. [http://www.nejm.org/doi/full/10.1056/NEJMra1314704 Barrett’s Esophagus]. ''N Engl J Med'' 2014 371:836-45.
* Barbera M, Fitzgerald RC. [http://www.biochemsoctrans.org/content/38/2/370 Cellular origin of Barrett’s metaplasia and oesophageal stem cells]. ''Biochem. Soc. Trans'' 2010 38:370–373.
* Mills JC and Sansom OJ. [http://stke.sciencemag.org/content/8/385/re8.full Reserve stem cells: Differentiated cells reprogram to fuel repair, metaplasia, and neoplasia in the adult gastrointestinal tract]. ''Sci. Signal'' 2015 8(385):re8.
* Clouston B and Lawrentschuk N. [http://onlinelibrary.wiley.com/doi/10.1111/bju.12378/full Metaplastic conditions of the bladder]. ''BJU Int''2013 112(Suppl 2):27-31.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/148-bladder/11-urinary PEIR Digital Library: Bladder Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology Images]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

File:IPLab2FattyChange9.jpg

2015-11-05T15:28:11Z

Peter Anderson:

This photomicrograph of the liver is from another patient with a history of alcohol use. There are some clear vacuoles indicating fat droplets (1) and there are numerous red-staining granular deposits within the cytoplasm of hepatocytes (3)--this is alcoholic hyalin. Alcoholic hyalin is easily distinguished from red blood cells (2) that are also present in this section.

IPLab:Lab 4:Atheromatous Emboli

2015-09-17T19:49:52Z

Peter Anderson: /* Virtual Microscopy */

== Clinical Summary ==

This 71-year-old male was admitted to the hospital with dry gangrene of the left great toe. Subsequently, he was found to have a poorly differentiated adenocarcinoma of the left upper lobe of the lung. He developed a perforation of a duodenal ulcer with generalized peritonitis and died five days after admission.

== Autopsy Findings ==

Gross examination of the aorta revealed severe atherosclerosis with extensive mural thrombus formation. Recent infarcts were noted in the spleen and in the left kidney. An old posterior myocardial infarct was noted. The left iliac artery also appeared to be almost totally occluded. A whitish-tan tumor was noted in the apical portion of the left upper lobe of the lung with metastases in the carinal and hilar lymph nodes.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab4AtheromatousEmboli1.jpg|This is a gross photograph of the aorta from this patient opened lengthwise with the luminal surface visible. Note the rough surface with ulcerations and adherent thrombotic material. There is a mild dilation (aneurysm) at the distal aorta just at the bifurcation with an accumulation of thrombus.
File:IPLab4AtheromatousEmboli2.jpg|This is a closer view of the luminal surface of the aorta from the previous image. The rough, ulcerated surface and the thrombotic material can be easily seen in this image.
File:IPLab4AtheromatousEmboli3.jpg|This is a low-power photomicrograph of kidney tissue. Several blood vessels can be identified at the corticomedullary junction (arrows).
File:IPLab4AtheromatousEmboli4.jpg|This higher-power photomicrograph of one of the arcuate arteries reveals a cholesterol embolus. Note the needle-shaped space (arrow) within the lumen of this artery (arrow) which represents the space occupied by the cholesterol crystal that was dissolved away during histologic processing.
File:IPLab4AtheromatousEmboli5.jpg|This is another view of this vessel with an atherosclerotic embolus. Note the cholesterol clefts (1) and thrombotic material (2) that occlude this artery.
File:IPLab4AtheromatousEmboli6.jpg|A mesenteric artery also had an atherosclerotic embolus. Again note the cholesterol clefts and thrombotic material that occlude this artery.
</gallery>

== Virtual Microscopy ==
=== Kidney: Atheromatous Emboli ===
<peir-vm>IPLab4AtheromatousEmboli</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is the cause of atheromatous emboli?">Ulcerated or complex atherosclerotic plaques rupture and release cholesterol and other material into the blood stream. These materials lodge in vessels downstream. Ulceration or rupture of atherosclerotic plaques is part of the normal progression of atherosclerosis.</spoiler>
* <spoiler text="What happens when atherosclerotic material embolizes?">When the atherosclerotic plaque ruptures collagen, cholesterol esters and necrotic material are exposed to the blood stream. This initiates thrombus formation. So, in addition to the cholesterol embolizing to distal vessels, thrombosis is also initiated and can obstruct vessels.</spoiler>
* <spoiler text="What other types of material can embolize and cause clinical problems?">Probably 99% of all emboli are thromboemboli. Other materials that can embolize are: fragments of bone or bone marrow, fat, tumor cells, foreign bodies such as bullets, and bubbles of air or nitrogen.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1950759-overview eMedicine Medical Library: Noncoronary Atherosclerosis]
* [http://emedicine.medscape.com/article/460428-overview eMedicine Medical Library: Cholesterol Embolism]
* [http://www.merckmanuals.com/professional/hematology_and_oncology/thrombotic_disorders/overview_of_thrombotic_disorders.html Merck Manual: Thrombotic Disorders]

=== Journal Articles ===
* Scolari F, Ravani P. [http://www.ncbi.nlm.nih.gov/pubmed/20381857 Atheroembolic renal disease]. ''Lancet'' 2010 May 8;375(9726):1650-60.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/52-kidney PEIR Digital Library: Kidney Images]
* [http://library.med.utah.edu/WebPath/ATHHTML/ATHIDX.html WebPath: Atherosclerosis and Thrombosis]
* [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html WebPath: Cardiovascular Pathology]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology]

== Related IPLab Cases ==
* [[IPLab:Lab 1:Kidney Infarction|Lab 1: Kidney: Infarction (Coagulative Necrosis)]]

{{IPLab 4}}

[[Category: IPLab:Lab 4]]

IPLab:Lab 4:Mural Thrombus

2015-09-17T19:47:25Z

Peter Anderson: /* Virtual Microscopy */

== Clinical Summary ==

This 67-year-old female was transferred to the hospital from a nursing home in a comatose state. Physical findings on examination were compatible with brain stem infarction. On the fourth hospital day, an electrocardiogram revealed changes compatible with anterior myocardial infarction. The patient remained comatose with quadriplegia and expired on the 16th hospital day.

== Autopsy Findings ==

Examination of the brain revealed extensive infarction involving the midbrain and cerebellum with complete occlusion of the upper one-half of the basilar artery; there was also extensive coronary artery atherosclerosis. A large aneurysm of the left ventricle was present; this was filled with mural thrombus. Extensive infarction of the lateral and posterior portions of the left ventricular wall toward the base of the heart was also found.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab4MuralThrombus1.jpg|This is a gross photograph of the heart from this case demonstrating the well-formed thrombus (arrow) tightly attached to the myocardium near the apex of the left ventricle.
File:IPLab4MuralThrombus2.jpg|This is a low-power photomicrograph of the thrombus (1) attached to the myocardium (2).
File:IPLab4MuralThrombus3.jpg|This higher-power photomicrograph shows the border between the thrombus on the right (1) and the endocardium on the left (2). There is a line of inflammatory cells at this interface (arrow).
File:IPLab4MuralThrombus4.jpg|This is a high-power photomicrograph of the border zone between the thrombus (1) and the endocardium (2). In this region there is less inflammation at the border zone.
File:IPLab4MuralThrombus5.jpg|This photomicrograph illustrates the layered effect of the thrombus.
File:IPLab4MuralThrombus6.jpg|This is a higher-power photomicrograph of the thrombus. Note the pale regions which contain primarily platelets (degranulated platelets) with some fibrin (1), and the red areas which contain RBCs, some leukocytes, and fibrin(2).
File:IPLab4MuralThrombus7.jpg|This high-power photomicrograph of thrombus demonstrates more clearly the components of the layers--the pale regions which contain primarily platelets (degranulated platelets) with some fibrin (1), and the red areas which contain RBCs, some leukocytes, and fibrin (2).
</gallery>

== Virtual Microscopy ==
=== Heart:Mural Thrombus ===
<peir-vm>IPLab4MuralThrombus</peir-vm>

=== Normal Heart ===
<peir-vm>IPLab2Hypertrophy_normal_Heart</peir-vm>

== Study Questions ==
* <spoiler text="Why do mural thrombi form on the endocardium of the heart after a myocardial infarction?">The infarct produced necrosis and inflammation. Also, the infarcted ventricular wall is akinetic and/or dyskinetic (bulges outward during systole). Thus, the blood in the ventricle tends to form thrombi on the surface of the infarcted endocardium.</spoiler>
* <spoiler text="List the sequence of events leading to mural thrombus formation.">* Platelets bind to damage endocardium and release ADP, 5-HT, thromboxane and platelet factor 4.
* This results in recruitment of more platelets and more degranulation of platelets with activation of the clotting cascade.
* Thrombin is activated leading to fibrin polymerization.
* This process results in the development of a platelet-fibrin thrombus.</spoiler>
* <spoiler text="What are possible sequelae of these mural thrombi?">The thrombotic material may break off and go to the brain or kidney (the two most likely sites since they get so much blood flow) or any arterial system.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1950759-overview eMedicine Medical Library: Noncoronary Atherosclerosis]
* [http://emedicine.medscape.com/article/155919-overview eMedicine Medical Library: Myocardial Infarction]
* [http://www.merckmanuals.com/professional/hematology_and_oncology/thrombotic_disorders/thrombotic_disorders.html Merck Manual: Thrombotic Disorders]
* [http://www.merckmanuals.com/professional/cardiovascular_disorders/coronary_artery_disease/acute_coronary_syndromes_acs.html Merck Manual: Acute Coronary Syndromes (ACS)]

=== Journal Articles ===
* Diop D, Aghababian RV. [http://www.ncbi.nlm.nih.gov/pubmed/11373977 Definition, classification, and pathophysiology of acute coronary ischemic syndromes]. ''Emerg Med Clin North Am'' 2001 May;19(2):259-67.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/424-mural_thrombus PEIR Digital Library: Mural Thrombus Images]
* [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html#3 WebPath: Myocardial Infarction]
* [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html#2 WebPath: Atherosclerotic Cardiovascular Disease]

== Related IPLab Cases ==
* [[IPLab:Lab 1:Myocardial Infarction|Lab 1: Heart: Myocardial Infarction (Coagulative Necrosis)]]
* [[IPLab:Lab 3:Acute Myocardial Infarction|Lab 3: Heart: Acute Myocardial Infarction]]
* [[IPLab:Lab 3:Healed Myocardial Infarction|Lab 3: Heart: Healed Myocardial Infarction]]
* [[IPLab:Lab 4:Thrombosis|Lab 4: Coronary Artery: Thrombosis]]
* [[IPLab:Lab 4:Pulmonary Congestion and Edema|Lab 4: Lung: Pulmonary Congestion and Edema]]

{{IPLab 4}}

[[Category: IPLab:Lab 4]]

IPLab:Lab 3:Acute Myocardial Infarction

2015-09-17T19:45:16Z

Peter Anderson: /* Virtual Microscopy */

== Clinical Summary ==
This 78-year-old male experienced a posterior myocardial infarction six years prior to this admission. Recently, he had begun to experience occasional angina. Four days prior to death, he experienced anterior chest pain and discomfort which he regarded as not too distressing. However, EKGs showed a classic acute anterior myocardial infarction in addition to the healed posterior infarct. The patient progressively deteriorated with left ventricular failure and died with arrhythmias and pulmonary edema. Pertinent laboratory data are:

# Aspartate Aminotransferase (AST) 60 IU/L.
# Total Creatine Phosphokinase (CPK) 165 IU/L. All of the activity was due to CPK III (MM) isoenzyme fraction; no CPK (MB) activity was detectable.
# Troponin I 38 µg/L.

== Autopsy Findings ==
Examination of the heart showed a healed posterior infarct. The right coronary artery was completely occluded but partially recanalized. The left main coronary artery had severe atherosclerotic stenosis and a thrombus filling the lumen. The entire anterolateral aspect of the left ventricle was soft with variegated areas appearing hyperemic or pale. There was extensive mural thrombosis and reactive pericarditis.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab3AcuteMyocardialInfarction1.jpg|This is a low-power photomicrograph of infarcted heart. There is a layer of surviving myocardial tissue (1) along the epicardium and then a blue line (2) which represents the accumulation of inflammatory cells at the border of the infarct. There is thrombotic material (3) adherent to the endocardial surface.
File:IPLab3AcuteMyocardialInfarction2.jpg|This is a higher-power photomicrograph which shows more clearly the viable tissue along the epicardium (1), the blue line of inflammatory cells (2), and the infarcted myocardium (3).
File:IPLab3AcuteMyocardialInfarction3.jpg|This is a photomicrograph of the edge of the infarct with normal tissue on the left (1). The accumulation of inflammatory cells (2) is at the edge of the infarcted tissue (3).
File:IPLab3AcuteMyocardialInfarction4.jpg|This is a higher-power photomicrograph of the edge of the infarct. The accumulation of inflammatory cells is on the left (1) and the infarcted tissue is on the right (2). Note that intact cells can be seen in the infarct but there are no nuclei.
File:IPLab3AcuteMyocardialInfarction5.jpg|This is a high-power photomicrograph of another area of this section. There are several hypereosinophilic cells within this section (arrows).
File:IPLab3AcuteMyocardialInfarction6.jpg|This is a low-power photomicrograph of a mural thrombus (1) adherent to the endocardial surface (arrows).
File:IPLab3AcuteMyocardialInfarction7.jpg|This is a photomicrograph of the lines of Zahn. Pale areas (1) represent platelets with some fibrin and the darker lines (2) represent RBCs and leukocytes enmeshed in fibrin strands.
</gallery>

== Virtual Microscopy ==
=== Heart: Acute Myocardial Infarction ===
<peir-vm>IPLab3AcuteMyocardialInfarction</peir-vm>

=== Normal Heart ===
<peir-vm>IPLab2Hypertrophy_normal_Heart</peir-vm>

== Study Questions ==
* <spoiler text="Are the serum enzyme results consistent with the time course of this clinical history?">The infarct occurred approximately 4 days prior to death. His CPK-MB levels would be expected to have gone down by now. His AST is slightly elevated and his LDH is moderately elevated with a high LDH1:LDH2 ratio. These findings are consistent with the clinical history.</spoiler>
* <spoiler text="Why do mural thrombi often form in infarcted hearts?">The endocardium is usually the most severely damaged after an arterial occlusion since it is at the end of the circulation of the heart. Thus, with the infarcted tissue in the endocardium there is an acute inflammatory reaction which initiates coagulation and thrombus formation.</spoiler>
* <spoiler text="What is the primary cell type in this inflammatory reaction?">At this stage it is primarily neutrophils, but there area a few macrophages. Usually, neutrophils enter an infarct by 12-24 hours and macrophages enter the lesion by 72 hours post-MI. By 3-7 days the lesion is primarily macrophages and by 10 days there are macrophages, fibroblasts, and endothelial cells (granulation tissue). The healing reaction in this patient may have been slower than normal because of his poor condition.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/155919-overview eMedicine Medical Library: Myocardial Infarction]
* [http://www.merckmanuals.com/professional/cardiovascular_disorders/coronary_artery_disease/acute_coronary_syndromes_acs.html Merck Manual: Acute Coronary Syndromes]

=== Journal Articles ===
* Helft G, Worthley SG. [http://www.ncbi.nlm.nih.gov/pubmed/16352041 Anti-thrombotic, anti-platelet and fibrinolytic therapy: current management of acute myocardial infarction]. ''Heart Lung Circ'' 2001;10(2):68-74.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/43-myocardial_infarct PEIR Digital Library: Myocardial Infarct Images]
* [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html WebPath: Cardiovascular Pathology]

== Related IPLab Cases ==
* [[IPLab:Lab 1:Myocardial Infarction|Lab 1: Heart: Myocardial Infarction (Coagulative Necrosis)]]
* [[IPLab:Lab 3:Healed Myocardial Infarction|Lab 3: Heart: Healed Myocardial Infarction]]
* [[IPLab:Lab 4:Mural Thrombus|Lab 4: Heart: Mural Thrombus]]
* [[IPLab:Lab 4:Thrombosis|Lab 4: Coronary Artery: Thrombosis]]
* [[IPLab:Lab 4:Pulmonary Congestion and Edema|Lab 4: Lung: Pulmonary Congestion and Edema]]

{{IPLab 3}}

[[Category: IPLab:Lab 3]]

IPLab:Lab 3:Sarcoidosis

2015-09-17T19:27:42Z

Peter Anderson: /* Virtual Microscopy */

== Clinical Summary ==
This 33-year-old white female was admitted for evaluation of abnormal findings on a chest x-ray. She was asymptomatic and a physical examination revealed no significant abnormalities. Laboratory results indicated hypercalcemia and elevated gamma globulin. Radiographic examination showed enlarged subcarinal, hilar, and right paratracheal lymph nodes. A right paratracheal lymph node was biopsied. Special stains for acid-fast bacilli and fungi were negative and a diagnosis of sarcoidosis was made.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab3Sarcoidosis1.jpg|This is a low-power photomicrograph of a lymph node. Note the rather pale-pink color of the tissue with dark-staining cells found in only a few scattered areas. These darker cells represent the original lymphocytes of this lymphoid organ.
File:IPLab3Sarcoidosis2.jpg|This photomicrograph of lymph node tissue illustrates a paucity of lymphocytes as well as numerous small, pale-staining nodules (arrows) throughout the tissue.
File:IPLab3Sarcoidosis3.jpg|This is a photomicrograph of the small nodules (arrows) seen in the previous image. Close examination reveals that they are composed of large macrophages (epithelioid macrophages). These small granulomas form multiple series of reaction centers throughout the lymph node. Note the remaining lymphocytes surrounding the granulomas.
File:IPLab3Sarcoidosis4.jpg|This photomicrograph of a single granuloma illustrates the individual macrophages (arrows) which make up the bulk of this tissue. There is an absence of necrosis in the center of the lesions in this case.
File:IPLab3Sarcoidosis5.jpg|This is a photomicrograph of a multinucleated giant cell (1). In the center of this foreign body-containing giant cell there is a small asteroid body (2). There is no functional significance to this asteroid body.
File:IPLab3Sarcoidosis6.jpg|This is a higher-power photomicrograph of an asteroid body (arrow) inside of a multinucleated giant cell.
</gallery>

== Virtual Microscopy ==
=== Lymph Node: Sarcoidosis ===
<peir-vm>IPLab3Sarcoidosis</peir-vm>

=== Lymph Node ===
<peir-vm>UAB-Histology-00035</peir-vm>

== Study Questions ==
* <spoiler text="What is sarcoidosis?">The exact cause of sarcoidosis is unknown. Sarcoidosis is characterized by non-caseating granulomas in many tissues and organs.</spoiler>
* <spoiler text="What is the characteristic phenotype of sarcoid granulomas?">The typical characteristic of a sarcoid granuloma is a non-caseating granuloma which consists of an aggregate of tightly-clustered epitheliod cells, often with Langhans’ or multinucleated giant cells. Occasionally, asteroid bodies may be seen.</spoiler>
* <spoiler text="What are asteroid bodies and are they pathognomonic for sarcoid or are they seen in other diseases?">Asteroid bodies are stellate inclusions within giant cells. They are not pathognomonic for sarcoid; they can be seen in other granulomatous disease processes (e.g., berylliosis).</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/809047-overview eMedicine Medical Library: Acute Complications of Sarcoidosis]
* [http://emedicine.medscape.com/article/301914-overview eMedicine Medical Library: Sarcoidosis]
* [http://emedicine.medscape.com/article/1123970-overview eMedicine Medical Library: Dermatologic Manifestations of Sarcoidosis]
* [http://emedicine.medscape.com/article/1147324-overview eMedicine Medical Library: Neurosarcoidosis]
* [http://www.merckmanuals.com/professional/pulmonary_disorders/sarcoidosis/sarcoidosis.html Merck Manual: Sarcoidosis]

=== Journal Articles ===
* English JC, Patel PJ, Greer KE. [http://www.mdconsult.com/das/article/body/421068364-2/jorg=journal&source=MI&sp=11817316&sid=119276088/N/217466/1.html?issn= Sarcoidosis]. ''J Am Acad Dermatol'' 2001;44:725-43
* Johns CJ, Michele TM. [http://www.ncbi.nlm.nih.gov/pubmed/10195091 The clinical management of sarcoidosis. A 50-year experience at the Johns Hopkins Hospital]. ''Medicine (Baltimore)'' 1999 Mar;78(2):65-111.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/531-sarcoidosis PEIR Digital Library: Sarcoidosis Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#2 WebPath: Granulomatous Disease]

== Related IPLab Cases ==
* [[IPLab:Lab 2:Metastatic Calcification|Lab 2: Lung: Metastatic Calcification]]

{{IPLab 3}}
[[Category: IPLab:Lab 3]]

IPLab:Lab 2:Metaplasia

2015-09-17T18:28:58Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 30-year-old black male was born with a meningocele which was repaired in childhood. Despite repair of the meningocele, this patient continued to have a neurogenic bladder.

Six months previous to this admission, the patient passed a single renal calculus but intravenous pyelogram (IVP) showed left nephrolithiasis (a 1 cm stone in the lower lobe). For 6 months the patient had to be catheterized each day for 6 hours. However, he continued to complain of hesitancy and urgency and suffered occasional urinary tract infections.

On this admission, a culture of the patient's urine specimen grew Gram-negative bacilli (Proteus species). Cystoscopy showed heavy trabeculation of the bladder with early diverticula and the left ureteral orifice showed squamous metaplasia. The lower pole of the left kidney was removed surgically, following which the patient recovered and was discharged on antibiotics.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2Metaplasia1.jpg|This is a low-power photomicrograph showing the full cortical and medullary thickness of the kidney. Note that there is a dilated calyx containing some red blood cells in the center of the section (arrow). The cortex is markedly thin and has severe lesions of degeneration and atrophy, although these are hard to appreciate at this low magnification.
File:IPLab2Metaplasia2.jpg|This high-power photomicrograph demonstrates the transitional epithelium lining the renal calyx (1) and the junction (transition zone) to a thicker hyperplastic epithelium (2). Note the inflammatory cells and increased vascular response in the stromal tissue (3) lying beneath the normal transitional epithelium.
File:IPLab2Metaplasia3.jpg|A higher-power view shows the junction of normal epithelium (1) with hyperplastic transitional epithelium (2). Note the inflammatory cells in the subepithelial tissue.
File:IPLab2Metaplasia4.jpg|This is a higher-power photomicrograph of the junction of normal epithelium (1) with hyperplastic transitional epithelium (2).
File:IPLab2Metaplasia5.jpg|In areas adjacent to the normal transitional epithelium, there are areas of epithelium (arrows) where the epithelial cells have the character of normal squamous epithelium as found in the dermis. However, squamous epithelium is not normal in the renal pelvis. This adaptive change is referred to as squamous metaplasia.
File:IPLab2Metaplasia6.jpg|A high-power photomicrograph of the squamous epithelium shows inflammatory cells in the subepithelial tissue and the formation of keratinized epithelium (arrows).
File:IPLab2Metaplasia7.jpg|This is a photomicrograph of the trachea from a smoker. Note that the columnar ciliated epithelium has been replaced by squamous epithelium.
</gallery>

== Virtual Microscopy ==
=== Kidney: Metaplasia ===
<peir-vm>IPLab2Metaplasia</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is a neurogenic bladder and what complications may result from this condition?">A neurogenic bladder is any condition or dysfunction of the urinary bladder caused by a lesion of the central or peripheral nervous system. Complications primarily include stasis, infection, and stone formation.</spoiler>
* <spoiler text="What factors in this case predisposed to nephrolithiasis?">Stasis and infection.</spoiler>
* <spoiler text="Does this metaplastic process predispose to neoplasia?">Yes.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/437096-overview eMedicine Medical Library: Nephrolithiasis]
* [http://emedicine.medscape.com/article/453539-overview eMedicine Medical Library: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/urinary_calculi/urinary_calculi.html Merck Manual: Urinary Calculi]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/voiding_disorders/neurogenic_bladder.html Merck Manual: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/approach_to_the_genitourinary_patient/evaluation_of_the_renal_patient.html Merck Manual: Approach to the Genitourinary Patient]

=== Journal Articles ===
* Barbera M, Fitzgerald RC. [http://www.sciencedirect.com/science/article/pii/S1055320709000180 Cellular Mechanisms of Barrett's Esophagus Development]. ''Surg Oncol Clin N Am '' 2009 18:393–410.
* Spechler SJ and Souza RF. [http://www.nejm.org/doi/full/10.1056/NEJMra1314704 Barrett’s Esophagus]. ''N Engl J Med'' 2014 371:836-45.
* Barbera M, Fitzgerald RC. [http://www.biochemsoctrans.org/content/38/2/370 Cellular origin of Barrett’s metaplasia and oesophageal stem cells]. ''Biochem. Soc. Trans'' 2010 38:370–373.
* Mills JC and Sansom OJ. [http://stke.sciencemag.org/content/8/385/re8.full Reserve stem cells: Differentiated cells reprogram to fuel repair, metaplasia, and neoplasia in the adult gastrointestinal tract]. ''Sci. Signal'' 2015 8(385):re8.
* Clouston B and Lawrentschuk N. [http://onlinelibrary.wiley.com/doi/10.1111/bju.12378/full Metaplastic conditions of the bladder]. ''BJU Int''2013 112(Suppl 2):27-31.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/148-bladder/11-urinary PEIR Digital Library: Bladder Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology Images]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

IPLab:Lab 2:Metaplasia

2015-09-17T18:20:18Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 30-year-old black male was born with a meningocele which was repaired in childhood. Despite repair of the meningocele, this patient continued to have a neurogenic bladder.

Six months previous to this admission, the patient passed a single renal calculus but intravenous pyelogram (IVP) showed left nephrolithiasis (a 1 cm stone in the lower lobe). For 6 months the patient had to be catheterized each day for 6 hours. However, he continued to complain of hesitancy and urgency and suffered occasional urinary tract infections.

On this admission, a culture of the patient's urine specimen grew Gram-negative bacilli (Proteus species). Cystoscopy showed heavy trabeculation of the bladder with early diverticula and the left ureteral orifice showed squamous metaplasia. The lower pole of the left kidney was removed surgically, following which the patient recovered and was discharged on antibiotics.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2Metaplasia1.jpg|This is a low-power photomicrograph showing the full cortical and medullary thickness of the kidney. Note that there is a dilated calyx containing some red blood cells in the center of the section (arrow). The cortex is markedly thin and has severe lesions of degeneration and atrophy, although these are hard to appreciate at this low magnification.
File:IPLab2Metaplasia2.jpg|This high-power photomicrograph demonstrates the transitional epithelium lining the renal calyx (1) and the junction (transition zone) to a thicker hyperplastic epithelium (2). Note the inflammatory cells and increased vascular response in the stromal tissue (3) lying beneath the normal transitional epithelium.
File:IPLab2Metaplasia3.jpg|A higher-power view shows the junction of normal epithelium (1) with hyperplastic transitional epithelium (2). Note the inflammatory cells in the subepithelial tissue.
File:IPLab2Metaplasia4.jpg|This is a higher-power photomicrograph of the junction of normal epithelium (1) with hyperplastic transitional epithelium (2).
File:IPLab2Metaplasia5.jpg|In areas adjacent to the normal transitional epithelium, there are areas of epithelium (arrows) where the epithelial cells have the character of normal squamous epithelium as found in the dermis. However, squamous epithelium is not normal in the renal pelvis. This adaptive change is referred to as squamous metaplasia.
File:IPLab2Metaplasia6.jpg|A high-power photomicrograph of the squamous epithelium shows inflammatory cells in the subepithelial tissue and the formation of keratinized epithelium (arrows).
File:IPLab2Metaplasia7.jpg|This is a photomicrograph of the trachea from a smoker. Note that the columnar ciliated epithelium has been replaced by squamous epithelium.
</gallery>

== Virtual Microscopy ==
=== Kidney: Metaplasia ===
<peir-vm>IPLab2Metaplasia</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is a neurogenic bladder and what complications may result from this condition?">A neurogenic bladder is any condition or dysfunction of the urinary bladder caused by a lesion of the central or peripheral nervous system. Complications primarily include stasis, infection, and stone formation.</spoiler>
* <spoiler text="What factors in this case predisposed to nephrolithiasis?">Stasis and infection.</spoiler>
* <spoiler text="Does this metaplastic process predispose to neoplasia?">Yes.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/437096-overview eMedicine Medical Library: Nephrolithiasis]
* [http://emedicine.medscape.com/article/453539-overview eMedicine Medical Library: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/urinary_calculi/urinary_calculi.html Merck Manual: Urinary Calculi]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/voiding_disorders/neurogenic_bladder.html Merck Manual: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/approach_to_the_genitourinary_patient/evaluation_of_the_renal_patient.html Merck Manual: Approach to the Genitourinary Patient]

=== Journal Articles ===
* Barbera M, Fitzgerald RC. [http://www.sciencedirect.com/science/article/pii/S1055320709000180 Cellular Mechanisms of Barrett's Esophagus Development]. ''Surg Oncol Clin N Am '' 2009 18:393–410.
* Spechler SJ and Souza RF. [http://www.nejm.org/doi/full/10.1056/NEJMra1314704 Barrett’s Esophagus]. ''N Engl J Med'' 2014;371:836-45.
* Barbera M, Fitzgerald RC. [http://www.biochemsoctrans.org/content/38/2/370 Cellular origin of Barrett’s metaplasia and oesophageal stem cells]. ''Biochem. Soc. Trans'' 2010 38:370–373.
* Mills JC and Sansom OJ. [http://stke.sciencemag.org/content/8/385/re8.full Reserve stem cells: Differentiated cells reprogram to fuel repair, metaplasia, and neoplasia in the adult gastrointestinal tract]. ''Sci. Signal'' 2015 8(385):re8.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/148-bladder/11-urinary PEIR Digital Library: Bladder Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology Images]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

IPLab:Lab 2:Metaplasia

2015-09-17T18:19:42Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 30-year-old black male was born with a meningocele which was repaired in childhood. Despite repair of the meningocele, this patient continued to have a neurogenic bladder.

Six months previous to this admission, the patient passed a single renal calculus but intravenous pyelogram (IVP) showed left nephrolithiasis (a 1 cm stone in the lower lobe). For 6 months the patient had to be catheterized each day for 6 hours. However, he continued to complain of hesitancy and urgency and suffered occasional urinary tract infections.

On this admission, a culture of the patient's urine specimen grew Gram-negative bacilli (Proteus species). Cystoscopy showed heavy trabeculation of the bladder with early diverticula and the left ureteral orifice showed squamous metaplasia. The lower pole of the left kidney was removed surgically, following which the patient recovered and was discharged on antibiotics.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2Metaplasia1.jpg|This is a low-power photomicrograph showing the full cortical and medullary thickness of the kidney. Note that there is a dilated calyx containing some red blood cells in the center of the section (arrow). The cortex is markedly thin and has severe lesions of degeneration and atrophy, although these are hard to appreciate at this low magnification.
File:IPLab2Metaplasia2.jpg|This high-power photomicrograph demonstrates the transitional epithelium lining the renal calyx (1) and the junction (transition zone) to a thicker hyperplastic epithelium (2). Note the inflammatory cells and increased vascular response in the stromal tissue (3) lying beneath the normal transitional epithelium.
File:IPLab2Metaplasia3.jpg|A higher-power view shows the junction of normal epithelium (1) with hyperplastic transitional epithelium (2). Note the inflammatory cells in the subepithelial tissue.
File:IPLab2Metaplasia4.jpg|This is a higher-power photomicrograph of the junction of normal epithelium (1) with hyperplastic transitional epithelium (2).
File:IPLab2Metaplasia5.jpg|In areas adjacent to the normal transitional epithelium, there are areas of epithelium (arrows) where the epithelial cells have the character of normal squamous epithelium as found in the dermis. However, squamous epithelium is not normal in the renal pelvis. This adaptive change is referred to as squamous metaplasia.
File:IPLab2Metaplasia6.jpg|A high-power photomicrograph of the squamous epithelium shows inflammatory cells in the subepithelial tissue and the formation of keratinized epithelium (arrows).
File:IPLab2Metaplasia7.jpg|This is a photomicrograph of the trachea from a smoker. Note that the columnar ciliated epithelium has been replaced by squamous epithelium.
</gallery>

== Virtual Microscopy ==
=== Kidney: Metaplasia ===
<peir-vm>IPLab2Metaplasia</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is a neurogenic bladder and what complications may result from this condition?">A neurogenic bladder is any condition or dysfunction of the urinary bladder caused by a lesion of the central or peripheral nervous system. Complications primarily include stasis, infection, and stone formation.</spoiler>
* <spoiler text="What factors in this case predisposed to nephrolithiasis?">Stasis and infection.</spoiler>
* <spoiler text="Does this metaplastic process predispose to neoplasia?">Yes.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/437096-overview eMedicine Medical Library: Nephrolithiasis]
* [http://emedicine.medscape.com/article/453539-overview eMedicine Medical Library: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/urinary_calculi/urinary_calculi.html Merck Manual: Urinary Calculi]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/voiding_disorders/neurogenic_bladder.html Merck Manual: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/approach_to_the_genitourinary_patient/evaluation_of_the_renal_patient.html Merck Manual: Approach to the Genitourinary Patient]

=== Journal Articles ===
* Barbera M, Fitzgerald RC. [http://www.sciencedirect.com/science/article/pii/S1055320709000180 Cellular Mechanisms of Barrett's Esophagus Development]. ''Surg Oncol Clin N Am '' 2009 18:393–410.
* Spechler SJ and Souza RF. [http://www.nejm.org/doi/full/10.1056/NEJMra1314704 Barrett’s Esophagus]. ''N Engl J Med'' 2014;371:836-45.
* Barbera M, Fitzgerald RC. [http://www.biochemsoctrans.org/content/38/2/370 Cellular origin of Barrett’s metaplasia and oesophageal stem cells]. ''Biochem. Soc. Trans'' 2010 38:370–373.
* Mills JC and Sansom OJ. [http://stke.sciencemag.org/content/8/385/re8.full Reserve stem cells: Differentiated cells reprogram to fuel repair, metaplasia, and neoplasia in the adult gastrointestinal tract]. ''Sci. Signal'' 2015 Vol. 8, Issue 385, pp. re8.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/148-bladder/11-urinary PEIR Digital Library: Bladder Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology Images]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

IPLab:Lab 2:Metaplasia

2015-09-17T18:09:50Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 30-year-old black male was born with a meningocele which was repaired in childhood. Despite repair of the meningocele, this patient continued to have a neurogenic bladder.

Six months previous to this admission, the patient passed a single renal calculus but intravenous pyelogram (IVP) showed left nephrolithiasis (a 1 cm stone in the lower lobe). For 6 months the patient had to be catheterized each day for 6 hours. However, he continued to complain of hesitancy and urgency and suffered occasional urinary tract infections.

On this admission, a culture of the patient's urine specimen grew Gram-negative bacilli (Proteus species). Cystoscopy showed heavy trabeculation of the bladder with early diverticula and the left ureteral orifice showed squamous metaplasia. The lower pole of the left kidney was removed surgically, following which the patient recovered and was discharged on antibiotics.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2Metaplasia1.jpg|This is a low-power photomicrograph showing the full cortical and medullary thickness of the kidney. Note that there is a dilated calyx containing some red blood cells in the center of the section (arrow). The cortex is markedly thin and has severe lesions of degeneration and atrophy, although these are hard to appreciate at this low magnification.
File:IPLab2Metaplasia2.jpg|This high-power photomicrograph demonstrates the transitional epithelium lining the renal calyx (1) and the junction (transition zone) to a thicker hyperplastic epithelium (2). Note the inflammatory cells and increased vascular response in the stromal tissue (3) lying beneath the normal transitional epithelium.
File:IPLab2Metaplasia3.jpg|A higher-power view shows the junction of normal epithelium (1) with hyperplastic transitional epithelium (2). Note the inflammatory cells in the subepithelial tissue.
File:IPLab2Metaplasia4.jpg|This is a higher-power photomicrograph of the junction of normal epithelium (1) with hyperplastic transitional epithelium (2).
File:IPLab2Metaplasia5.jpg|In areas adjacent to the normal transitional epithelium, there are areas of epithelium (arrows) where the epithelial cells have the character of normal squamous epithelium as found in the dermis. However, squamous epithelium is not normal in the renal pelvis. This adaptive change is referred to as squamous metaplasia.
File:IPLab2Metaplasia6.jpg|A high-power photomicrograph of the squamous epithelium shows inflammatory cells in the subepithelial tissue and the formation of keratinized epithelium (arrows).
File:IPLab2Metaplasia7.jpg|This is a photomicrograph of the trachea from a smoker. Note that the columnar ciliated epithelium has been replaced by squamous epithelium.
</gallery>

== Virtual Microscopy ==
=== Kidney: Metaplasia ===
<peir-vm>IPLab2Metaplasia</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is a neurogenic bladder and what complications may result from this condition?">A neurogenic bladder is any condition or dysfunction of the urinary bladder caused by a lesion of the central or peripheral nervous system. Complications primarily include stasis, infection, and stone formation.</spoiler>
* <spoiler text="What factors in this case predisposed to nephrolithiasis?">Stasis and infection.</spoiler>
* <spoiler text="Does this metaplastic process predispose to neoplasia?">Yes.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/437096-overview eMedicine Medical Library: Nephrolithiasis]
* [http://emedicine.medscape.com/article/453539-overview eMedicine Medical Library: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/urinary_calculi/urinary_calculi.html Merck Manual: Urinary Calculi]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/voiding_disorders/neurogenic_bladder.html Merck Manual: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/approach_to_the_genitourinary_patient/evaluation_of_the_renal_patient.html Merck Manual: Approach to the Genitourinary Patient]

=== Journal Articles ===
* Barbera M, Fitzgerald RC. [http://www.sciencedirect.com/science/article/pii/S1055320709000180 Cellular Mechanisms of Barrett's Esophagus Development]. ''Surg Oncol Clin N Am '' 2009 18:393–410.
* Spechler SJ and Souza RF. [http://www.nejm.org/doi/full/10.1056/NEJMra1314704 Barrett’s Esophagus]. ''N Engl J Med'' 2014;371:836-45.
* Barbera M, Fitzgerald RC. [http://www.biochemsoctrans.org/content/38/2/370 Cellular origin of Barrett’s metaplasia and oesophageal stem cells]. ''Biochem. Soc. Trans'' 2010 38:370–373.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/148-bladder/11-urinary PEIR Digital Library: Bladder Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology Images]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

IPLab:Lab 2:Metaplasia

2015-09-17T18:09:24Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 30-year-old black male was born with a meningocele which was repaired in childhood. Despite repair of the meningocele, this patient continued to have a neurogenic bladder.

Six months previous to this admission, the patient passed a single renal calculus but intravenous pyelogram (IVP) showed left nephrolithiasis (a 1 cm stone in the lower lobe). For 6 months the patient had to be catheterized each day for 6 hours. However, he continued to complain of hesitancy and urgency and suffered occasional urinary tract infections.

On this admission, a culture of the patient's urine specimen grew Gram-negative bacilli (Proteus species). Cystoscopy showed heavy trabeculation of the bladder with early diverticula and the left ureteral orifice showed squamous metaplasia. The lower pole of the left kidney was removed surgically, following which the patient recovered and was discharged on antibiotics.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2Metaplasia1.jpg|This is a low-power photomicrograph showing the full cortical and medullary thickness of the kidney. Note that there is a dilated calyx containing some red blood cells in the center of the section (arrow). The cortex is markedly thin and has severe lesions of degeneration and atrophy, although these are hard to appreciate at this low magnification.
File:IPLab2Metaplasia2.jpg|This high-power photomicrograph demonstrates the transitional epithelium lining the renal calyx (1) and the junction (transition zone) to a thicker hyperplastic epithelium (2). Note the inflammatory cells and increased vascular response in the stromal tissue (3) lying beneath the normal transitional epithelium.
File:IPLab2Metaplasia3.jpg|A higher-power view shows the junction of normal epithelium (1) with hyperplastic transitional epithelium (2). Note the inflammatory cells in the subepithelial tissue.
File:IPLab2Metaplasia4.jpg|This is a higher-power photomicrograph of the junction of normal epithelium (1) with hyperplastic transitional epithelium (2).
File:IPLab2Metaplasia5.jpg|In areas adjacent to the normal transitional epithelium, there are areas of epithelium (arrows) where the epithelial cells have the character of normal squamous epithelium as found in the dermis. However, squamous epithelium is not normal in the renal pelvis. This adaptive change is referred to as squamous metaplasia.
File:IPLab2Metaplasia6.jpg|A high-power photomicrograph of the squamous epithelium shows inflammatory cells in the subepithelial tissue and the formation of keratinized epithelium (arrows).
File:IPLab2Metaplasia7.jpg|This is a photomicrograph of the trachea from a smoker. Note that the columnar ciliated epithelium has been replaced by squamous epithelium.
</gallery>

== Virtual Microscopy ==
=== Kidney: Metaplasia ===
<peir-vm>IPLab2Metaplasia</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is a neurogenic bladder and what complications may result from this condition?">A neurogenic bladder is any condition or dysfunction of the urinary bladder caused by a lesion of the central or peripheral nervous system. Complications primarily include stasis, infection, and stone formation.</spoiler>
* <spoiler text="What factors in this case predisposed to nephrolithiasis?">Stasis and infection.</spoiler>
* <spoiler text="Does this metaplastic process predispose to neoplasia?">Yes.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/437096-overview eMedicine Medical Library: Nephrolithiasis]
* [http://emedicine.medscape.com/article/453539-overview eMedicine Medical Library: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/urinary_calculi/urinary_calculi.html Merck Manual: Urinary Calculi]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/voiding_disorders/neurogenic_bladder.html Merck Manual: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/approach_to_the_genitourinary_patient/evaluation_of_the_renal_patient.html Merck Manual: Approach to the Genitourinary Patient]

=== Journal Articles ===
* Barbera M, Fitzgerald RC. [http://www.sciencedirect.com/science/article/pii/S1055320709000180 Cellular Mechanisms of Barrett's Esophagus Development]. ''Surg Oncol Clin N Am '' 2009 18:393–410.
* Spechler SJ and Souza RF. [http://www.nejm.org/doi/full/10.1056/NEJMra1314704 Barrett’s Esophagus]. ''N Engl J Med'' 2014;371:836-45.
* Barbera M, Fitzgerald RC. [http://www.biochemsoctrans.org/content/38/2/370 Cellular origin of Barrett’s metaplasia and
oesophageal stem cells]. ''Biochem. Soc. Trans'' 2010 38:370–373.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/148-bladder/11-urinary PEIR Digital Library: Bladder Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology Images]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

IPLab:Lab 2:Metaplasia

2015-09-17T18:05:42Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 30-year-old black male was born with a meningocele which was repaired in childhood. Despite repair of the meningocele, this patient continued to have a neurogenic bladder.

Six months previous to this admission, the patient passed a single renal calculus but intravenous pyelogram (IVP) showed left nephrolithiasis (a 1 cm stone in the lower lobe). For 6 months the patient had to be catheterized each day for 6 hours. However, he continued to complain of hesitancy and urgency and suffered occasional urinary tract infections.

On this admission, a culture of the patient's urine specimen grew Gram-negative bacilli (Proteus species). Cystoscopy showed heavy trabeculation of the bladder with early diverticula and the left ureteral orifice showed squamous metaplasia. The lower pole of the left kidney was removed surgically, following which the patient recovered and was discharged on antibiotics.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2Metaplasia1.jpg|This is a low-power photomicrograph showing the full cortical and medullary thickness of the kidney. Note that there is a dilated calyx containing some red blood cells in the center of the section (arrow). The cortex is markedly thin and has severe lesions of degeneration and atrophy, although these are hard to appreciate at this low magnification.
File:IPLab2Metaplasia2.jpg|This high-power photomicrograph demonstrates the transitional epithelium lining the renal calyx (1) and the junction (transition zone) to a thicker hyperplastic epithelium (2). Note the inflammatory cells and increased vascular response in the stromal tissue (3) lying beneath the normal transitional epithelium.
File:IPLab2Metaplasia3.jpg|A higher-power view shows the junction of normal epithelium (1) with hyperplastic transitional epithelium (2). Note the inflammatory cells in the subepithelial tissue.
File:IPLab2Metaplasia4.jpg|This is a higher-power photomicrograph of the junction of normal epithelium (1) with hyperplastic transitional epithelium (2).
File:IPLab2Metaplasia5.jpg|In areas adjacent to the normal transitional epithelium, there are areas of epithelium (arrows) where the epithelial cells have the character of normal squamous epithelium as found in the dermis. However, squamous epithelium is not normal in the renal pelvis. This adaptive change is referred to as squamous metaplasia.
File:IPLab2Metaplasia6.jpg|A high-power photomicrograph of the squamous epithelium shows inflammatory cells in the subepithelial tissue and the formation of keratinized epithelium (arrows).
File:IPLab2Metaplasia7.jpg|This is a photomicrograph of the trachea from a smoker. Note that the columnar ciliated epithelium has been replaced by squamous epithelium.
</gallery>

== Virtual Microscopy ==
=== Kidney: Metaplasia ===
<peir-vm>IPLab2Metaplasia</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is a neurogenic bladder and what complications may result from this condition?">A neurogenic bladder is any condition or dysfunction of the urinary bladder caused by a lesion of the central or peripheral nervous system. Complications primarily include stasis, infection, and stone formation.</spoiler>
* <spoiler text="What factors in this case predisposed to nephrolithiasis?">Stasis and infection.</spoiler>
* <spoiler text="Does this metaplastic process predispose to neoplasia?">Yes.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/437096-overview eMedicine Medical Library: Nephrolithiasis]
* [http://emedicine.medscape.com/article/453539-overview eMedicine Medical Library: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/urinary_calculi/urinary_calculi.html Merck Manual: Urinary Calculi]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/voiding_disorders/neurogenic_bladder.html Merck Manual: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/approach_to_the_genitourinary_patient/evaluation_of_the_renal_patient.html Merck Manual: Approach to the Genitourinary Patient]

=== Journal Articles ===
* Barbera M, Fitzgerald RC. [http://www.sciencedirect.com/science/article/pii/S1055320709000180 Cellular Mechanisms of Barrett's Esophagus Development]. ''Surg Oncol Clin N Am '' 2009 18:393–410.
* Spechler SJ and Souza RF. [http://www.nejm.org/doi/full/10.1056/NEJMra1314704 Barrett’s Esophagus]. ''N Engl J Med'' 2014;371:836-45.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/148-bladder/11-urinary PEIR Digital Library: Bladder Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology Images]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

IPLab:Lab 2:Metaplasia

2015-09-17T18:03:17Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 30-year-old black male was born with a meningocele which was repaired in childhood. Despite repair of the meningocele, this patient continued to have a neurogenic bladder.

Six months previous to this admission, the patient passed a single renal calculus but intravenous pyelogram (IVP) showed left nephrolithiasis (a 1 cm stone in the lower lobe). For 6 months the patient had to be catheterized each day for 6 hours. However, he continued to complain of hesitancy and urgency and suffered occasional urinary tract infections.

On this admission, a culture of the patient's urine specimen grew Gram-negative bacilli (Proteus species). Cystoscopy showed heavy trabeculation of the bladder with early diverticula and the left ureteral orifice showed squamous metaplasia. The lower pole of the left kidney was removed surgically, following which the patient recovered and was discharged on antibiotics.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab2Metaplasia1.jpg|This is a low-power photomicrograph showing the full cortical and medullary thickness of the kidney. Note that there is a dilated calyx containing some red blood cells in the center of the section (arrow). The cortex is markedly thin and has severe lesions of degeneration and atrophy, although these are hard to appreciate at this low magnification.
File:IPLab2Metaplasia2.jpg|This high-power photomicrograph demonstrates the transitional epithelium lining the renal calyx (1) and the junction (transition zone) to a thicker hyperplastic epithelium (2). Note the inflammatory cells and increased vascular response in the stromal tissue (3) lying beneath the normal transitional epithelium.
File:IPLab2Metaplasia3.jpg|A higher-power view shows the junction of normal epithelium (1) with hyperplastic transitional epithelium (2). Note the inflammatory cells in the subepithelial tissue.
File:IPLab2Metaplasia4.jpg|This is a higher-power photomicrograph of the junction of normal epithelium (1) with hyperplastic transitional epithelium (2).
File:IPLab2Metaplasia5.jpg|In areas adjacent to the normal transitional epithelium, there are areas of epithelium (arrows) where the epithelial cells have the character of normal squamous epithelium as found in the dermis. However, squamous epithelium is not normal in the renal pelvis. This adaptive change is referred to as squamous metaplasia.
File:IPLab2Metaplasia6.jpg|A high-power photomicrograph of the squamous epithelium shows inflammatory cells in the subepithelial tissue and the formation of keratinized epithelium (arrows).
File:IPLab2Metaplasia7.jpg|This is a photomicrograph of the trachea from a smoker. Note that the columnar ciliated epithelium has been replaced by squamous epithelium.
</gallery>

== Virtual Microscopy ==
=== Kidney: Metaplasia ===
<peir-vm>IPLab2Metaplasia</peir-vm>

=== Normal Kidney ===
<peir-vm>UAB-Histology-00114</peir-vm>

== Study Questions ==
* <spoiler text="What is a neurogenic bladder and what complications may result from this condition?">A neurogenic bladder is any condition or dysfunction of the urinary bladder caused by a lesion of the central or peripheral nervous system. Complications primarily include stasis, infection, and stone formation.</spoiler>
* <spoiler text="What factors in this case predisposed to nephrolithiasis?">Stasis and infection.</spoiler>
* <spoiler text="Does this metaplastic process predispose to neoplasia?">Yes.</spoiler>

== Additional Resources ==

=== Reference ===
* [http://emedicine.medscape.com/article/437096-overview eMedicine Medical Library: Nephrolithiasis]
* [http://emedicine.medscape.com/article/453539-overview eMedicine Medical Library: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/urinary_calculi/urinary_calculi.html Merck Manual: Urinary Calculi]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/voiding_disorders/neurogenic_bladder.html Merck Manual: Neurogenic Bladder]
* [http://www.merckmanuals.com/professional/genitourinary_disorders/approach_to_the_genitourinary_patient/evaluation_of_the_renal_patient.html Merck Manual: Approach to the Genitourinary Patient]

=== Journal Articles ===
* Barbera M, Fitzgerald RC. [http://www.sciencedirect.com/science/article/pii/S1055320709000180 Cellular Mechanisms of Barrett's Esophagus Development]. ''Surg Oncol Clin N Am '' 2009 18:393–410.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/148-bladder/11-urinary PEIR Digital Library: Bladder Images]
* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology Images]

{{IPLab 2}}

[[Category: IPLab:Lab 2]]

IPLab:Lab 12:COPD

2015-09-17T17:57:36Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 64-year-old man was hospitalized because of increasing shortness of breath, cough, increasing sputum production, and fever. The patient had a 75 pack-year history of cigarette smoking. On admission his respiratory rate was 20 breaths per minute and his pulse was 110 bpm. On room air his PaO2 was 46 mm Hg, his PaCO2 was 62 mm Hg, and the pH was 7.26. He was started on 24% O2 and after 6 hours his PaO2 was 52 mm Hg, his PaCO2 was 54 and his pH was 7.30. His hemoglobin was 17.1 g/dL, his PCV was 54%, and his leukocyte count was 15,300 cells/mm³ with 13% bands, 65% PMNs, 15% lymphocytes, 4% monocytes and 3% eosinophils. Chest x-ray showed a narrow heart silhouette, a low, flattened diaphragm, and markedly lucent regions in the upper lung fields suggesting areas of emphysema. An electrocardiogram showed tall P waves and a right axis deviation. The patient was given broad-spectrum antibiotics and was continued on his oral and inhalant bronchodilators and was started on a diuretic. His condition improved but two days after admission he suffered acute respiratory failure and could not be resuscitated.

== Autopsy Findings ==
Pertinent autopsy findings included emphysema with moderate mucous plugging of bronchi. Right ventricular hypertrophy and dilation were also noted.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab12COPD1.jpg|This gross photograph of lung taken at autopsy demonstrates the degree of emphysematous change (arrows). Also note that the rest of the lung is consolidated, indicating a pneumonia.
File:IPLab12COPD2.jpg|This is a higher-power view of the lung showing the emphysematous change.
File:IPLab12COPD3.jpg|This low-power photomicrograph of the lung demonstrates the enlarged air spaces indicative of emphysematous change.
File:IPLab12COPD4.jpg|This higher-power photomicrograph of the lung shows more clearly the enlarged air spaces indicative of emphysematous change.
File:IPLab12COPD5.jpg|This gross photograph of the heart taken at autopsy demonstrates right ventricular hypertrophy and dilatation (arrows).
</gallery>

== Study Questions ==
* <spoiler text="What is COPD and why do cigarette smokers develop it?">Chronic obstructive pulmonary disease is a group of conditions that lead to dyspnea. COPD entails emphysema, chronic bronchitis, bronchiectasis, and asthma. The conditions can occur to varying degrees and there are often complex combinations and severities of each entity. Cigarette smoke and other air pollutants can irritate the lung and lead to increased leukocytes, increased release of elastases, and increased oxidants which inhibit alpha-1 antitrypsin. These and a variety of other factors lead to destruction of the elastic tissue in the lung and result in abnormal lung function and lung damage.</spoiler>
* <spoiler text="What caused the right ventricular hypertrophy and dilatation? What is this called?">The lung damage resulted in pulmonary hypertension which resulted in right ventricular hypertrophy. Over a period of time the increased workload will cause the right ventricle to fail and dilate. This process of right ventricular hypertrophy due to pulmonary hypertension is called cor pulmonale.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/807143-overview eMedicine Medical Library: Chronic Obstructive Pulmonary Disease and Emphysema in Emergency Medicine]
* [http://emedicine.medscape.com/article/297664-overview eMedicine Medical Library: Chronic Obstructive Pulmonary Disease]
* [http://emedicine.medscape.com/article/287555-overview eMedicine Medical Library: Nicotine Addiction]
* [http://www.merckmanuals.com/professional/pulmonary_disorders/chronic_obstructive_pulmonary_disease_and_related_disorders/chronic_obstructive_pulmonary_disease.html Merck Manual: Chronic Obstructive Pulmonary Disease]

=== Journal Articles ===
* Franks TJ, Galvin JR. [http://www.archivesofpathology.org/doi/pdf/10.5858/arpa.2013-0384-RA Smoking-Related Interstitial Lung Disease]. Arch Pathol Lab Med. 2015;139:974–977.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2172-copd PEIR Digital Library: COPD Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#6 WebPath: Obstructive Diseases]

== Related IPLab Cases ==
* [[IPLab:Lab 5:α1 Antitrypsin Deficiency|Lab 5: Lung: α1-Antitrypsin Deficiency]]
* [[IPLab:Lab 10:Cryptococcosis|Lab 10: Lung: Cryptococcosis]]

{{IPLab 12}}

[[Category: IPLab:Lab 12]]

IPLab:Lab 6:Tuberculosis

2015-09-16T19:42:15Z

Peter Anderson: /* Virtual Microscopy */

== Clinical Summary ==
During the course of a routine physical examination two months prior to admission, this 57-year-old white male was noted to have a lesion in the upper lobe of the right lung. Initially, he was treated for two weeks with ampicillin. He was then admitted to an outside hospital for further study. All studies including sputum studies for tubercle bacilli, bronchial washings, and bronchoscopy were negative and he was discharged. Review of systems revealed the presence of mild dyspnea on exertion, accompanied by a slightly productive cough. Of interest was the fact that the patient had been PPD positive for the past 4 to 5 years, but this had never been evaluated. On this hospital admission, physical and laboratory examinations were negative. Radiographic examination of the chest revealed a 2 x 2-cm density in the right lower lung field. Several small cavities were identified in this area on CT scan.

== Autopsy Findings ==
The patient underwent a thoracotomy, at which time a portion of the upper lobe of the right lung was removed. Examination of the cut surface revealed small white nodules measuring up to 0.2 cm in diameter.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab6TB1.jpg|This is a photograph of a section of lung with an apical lesion. This lesion represents an old healed lesion from Mycobacterium tuberculosis infection.
File:IPLab6TB2.jpg|This is a low-power photomicrograph of lung tissue with multiple circumscribed nodules - granulomas (arrows).
File:IPLab6TB3.jpg|This is a higher-power photomicrograph of a TB granuloma. Note the eosinophilic material in the center of this granuloma (caseous necrosis) and the epithelioid macrophages and giant cells around the periphery.
File:IPLab6TB4.jpg|This is a higher-power photomicrograph of a TB granuloma. The area of caseous necrosis is on the left side of the image, there are multinucleated giant cells and epithelioid macrophages throughout the remainder of the tissue.
File:IPLab6TB5.jpg|High-power photomicrograph of a TB granuloma with multinucleated giant cells adjacent to an area of caseous necrosis (to the left).
File:IPLab6TB6.jpg|This is a high-power (oil immersion) photomicrograph of granuloma stained with an acid-fast stain. Mycobacterium tuberculosis bacilli stain red.
</gallery>

== Virtual Microscopy ==
=== Lung: TB H&E ===
<peir-vm>IPLab6TB_HE</peir-vm>

=== Lung: TB AFGT ===
<peir-vm>IPLab6TB_AFGT</peir-vm>

=== Normal Lung ===
<peir-vm>UAB-Histology-00107</peir-vm>

== Study Questions ==
* <spoiler text="What is the Ghon complex?">In primary pulmonary TB you get (1) parenchymal subpleural lesions, often just above or just below the interlobar fissure, and (2) enlarged caseous lymph nodes draining the parenchymal focus (usually the hilar lymph nodes).</spoiler>
* <spoiler text="What factors are responsible for the virulence of M. tuberculosis?">M. tuberculosis has no known exotoxins, endotoxins or histolytic factors. Its pathogenicity is due to the fact that it resists phagocytic killing and sets up a delayed hypersensitivity reaction. Virulent M. tuberculosis organisms have cord factor, sulfatides, LAM, heat shock protein and they activate complement.</spoiler>
* <spoiler text="What is the sequence of events after primary exposure to M. tuberculosis?">The initial infection with M. tuberculosis leads to a T cell-mediated immune response that controls 95% of infections. Alveolar macrophages phagocytose the organisms and then transport them to the hilar lymph nodes. Macrophages cannot kill the mycobacteria so the organisms multiply, lyse the host cell, infect other macrophages, and sometimes disseminate via the blood to other parts of the lung and elsewhere in the body.

After a few weeks, T cell-mediated immunity develops and leads to activation of macrophages so they can kill intracellular mycobacteria via reactive nitrogen intermediates. This process leads to formation of epithelioid cell granulomas and clearance of the mycobacteria. Also, CD8+ suppresser T cells kill macrophages that are infected with mycobacteria, resulting in the formation of caseating granulomas. These processes during the primary infection with M. tuberculosis result in a calcified scar in the lung parenchyma and in the hilar lymph node. This combination is called the Ghon complex.
</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/230802-overview eMedicine Medical Library: Tuberculosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/mycobacteria/tuberculosis_tb.html Merck Manual: Tuberculosis (TB)]

=== Journal Articles ===
* Rodrigues DS, Medeiros EA, Weckx LY, Bonnez W, Salomão R, Kallas EG. [http://www.ncbi.nlm.nih.gov/pubmed/11982602 Immunophenotypic characterization of peripheral T lymphocytes in Mycobacterium tuberculosis infection and disease]. ''Clin Exp Immunol'' 2002 Apr;128(1):149-54.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/259-tuberculosis PEIR Digital Library: Tuberculosis Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#4 WebPath: Granulomatous Diseases]

== Related IPLab Cases ==
* [[IPLab:Lab 1:Tuberculosis|Lab 1: Lung: Tuberculosis (Caseous Necrosis)]]
* [[IPLab:Lab 3:Tuberculosis|Lab 3: Lung: Tuberculosis]]

{{IPLab 6}}

[[Category: IPLab:Lab 6]]

IPLab:Lab 6:Scleroderma

2015-09-16T19:40:28Z

Peter Anderson: /* Virtual Microscopy */

== Clinical Summary ==
This 29-year-old black female had a history of scleroderma involving the lung, kidney, heart, and skin. Her main clinical problems centered on her restrictive lung disease. She was able to live at home with supplemental oxygen but recently she had developed edema, chest pain, weakness, light-headedness, and a loss of appetite. The patient was admitted to the hospital with a working diagnosis of congestive heart failure brought on by her lung disease. Echocardiographic evaluation revealed a pericardial effusion that was tapped. Soon after this procedure her respiratory status degenerated and she required intubation. Despite aggressive supportive treatment for her cardiac and pulmonary problems, she could not be weaned from the ventilator. Two weeks after admission she became febrile and Gram positive cocci were isolated from sputum culture. She was placed on antibiotics but her condition deteriorated and she developed bradycardia followed by electromechanical dissociation (EMD).

== Autopsy Findings ==
Upon opening the thorax there was 600 cc of cloudy serous fluid in each hemithorax and 100 cc of similar fluid in the pericardial sac. The heart weighed 530 grams and there was thickening of both the left and right ventricular walls. The liver weighed 1880 grams and was congested. The spleen weighed 200 grams and was also congested. The combined lung weight was 1875 grams; the lungs were markedly fibrotic with severe emphysema. In addition, dermal thickening was evident throughout the body and the wall of the esophagus was thickened and firm.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab6Scleroderma1.jpg|This is a gross photograph of cut section of the lungs from this patient. Note the extensive fibrosis of the lung parenchyma.
File:IPLab6Scleroderma2.jpg|This is a gross photograph of a cut section of one lung from this patient. Note the extensive fibrosis lower lobe (arrows).
File:IPLab6Scleroderma3.jpg|This is a closer view of the cut section of lung from this patient. Note the extensive fibrosis and the severe emphysematous changes.
File:IPLab6Scleroderma4.jpg|This is a closer view of the cut section of lung from this patient showing the extensive fibrosis and the severe emphysematous change.
File:IPLab6Scleroderma5.jpg|This is a gross photograph of the heart from this case. There is thickening of the left ventricular wall and some thickening of the right ventricle as well.
</gallery>

== Virtual Microscopy ==
=== Lung: Scleroderma ===
<peir-vm>IPLab6Scleroderma</peir-vm>

=== Normal Lung ===
<peir-vm>UAB-Histology-00107</peir-vm>

=== Skin: Scleroderma ===
<peir-vm>IPLab6Scleroderma_Skin</peir-vm>

=== Normal Skin ===
<peir-vm>UAB-Histology-00004</peir-vm>

== Study Questions ==
* <spoiler text="What organs are usually affected in patients with scleroderma (progressive systemic sclerosis, PSS)?">Skin, gastrointestinal tract, kidneys, heart, muscles, and lungs.</spoiler>
* <spoiler text="What are the common clinical ramifications of PSS?">The striking cutaneous involvement is the primary clinical problem in many early cases. Raynaud's phenomenon, dysphagia due to esophageal fibrosis and hypomotility, abdominal pain, and intestinal obstruction are caused by fibrosis and scaring of these tissues. The respiratory problems are caused by pulmonary fibrosis. Chronic pulmonary fibrosis may lead to right-sided heart failure.</spoiler>
* <spoiler text="What is the etiology of PSS?">The exact etiology of PSS is not known. PSS is associated with excessive fibrosis, changes in the microvasculature, and a variety of immunologic abnormalities including T cell and humoral abnormalities that either cause or are caused by cytokines. The antigens that trigger the immune response have not been identified.</spoiler>
* <spoiler text="What is the CREST syndrome?">Some patients with a milder form of PSS may demonstrate the CREST syndrome. CREST stands for calcinosis, Raynaud’s phenomenon, esophageal dysfunction, sclerodactyly, telangiectasia, and the presence of anticentromere antibodies. These patients usually have less skin involvement of skin, and the more serious visceral problems do not develop until later in the course of the disease.
</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/331864-overview eMedicine Medical Library: Scleroderma]
* [http://emedicine.medscape.com/article/1064663-overview eMedicine Medical Library: CREST Syndrome]
* [http://www.merckmanuals.com/professional/musculoskeletal_and_connective_tissue_disorders/autoimmune_rheumatic_disorders/systemic_sclerosis.html Merck Manual: Systemic Sclerosis]

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2144-scleroderma PEIR Digital Library: Scleroderma Images]

== Related IPLab Cases ==
* [[IPLab:Lab 2:Hypertrophy|Lab 2: Heart: Myocardial Hypertrophy]]
* [[IPLab:Lab 5:α1 Antitrypsin Deficiency|Lab 5: Lung: α1-Antitrypsin Deficiency]]

{{IPLab 6}}

[[Category: IPLab:Lab 6]]

IPLab:Lab 4:Thromboembolus

2015-09-16T19:34:18Z

Peter Anderson: /* Virtual Microscopy */

== Clinical Summary ==

This 67-year-old male was hospitalized because of extensive atherosclerotic cardiovascular disease. Following surgery, during which diseased portions of the femoral arteries were bypassed, he developed massive pulmonary embolization and expired.

== Autopsy Findings ==

At autopsy, thrombi were found in the femoral and iliac veins, as well as in the larger pulmonary arteries.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab4Thromboembolus1.jpg|This is a gross photograph of a cut section of lung demonstrating thromboemboli in the pulmonary arteries (arrows).
File:IPLab4Thromboembolus2.jpg|This is a gross photograph of the heart with the main pulmonary artery opened. Note the thromboembolus filling the pulmonary artery (arrows).
File:IPLab4Thromboembolus3.jpg|This is a gross photograph of portions of muscle from the legs including sections of leg veins. Note that the leg veins contain thrombus (arrows).
File:IPLab4Thromboembolus4.jpg|This is a low-power photomicrograph of lung. A large thrombus is lodged at this branch point in the pulmonary artery. Note the hemorrhage and congestion in the surrounding lung parenchyma.
File:IPLab4Thromboembolus5.jpg|This is a photomicrograph of the wall of the pulmonary artery (1) containing the thromboembolus. In this case the artery wall looks normal. If this was a thrombus instead of a thromboembolus, you would expect to see some damage in the artery wall that would have initiated the thrombus. Note the lines of Zahn in the thromboembolus (arrows).
File:IPLab4Thromboembolus6.jpg|This is a low-power photomicrograph of the infarcted lung. The tissue is congested and has a very bland appearance due to coagulation necrosis of the lung parenchyma. You can still see the outlines of the alveoli and the cells that make-up the alveoli but there is almost complete loss of nuclei throughout this section.
File:IPLab4Thromboembolus7.jpg|This is a gross photograph of an infarcted testis. Because of the anatomy of the blood supply to the testis, torsion or the blood vessels often leads to venous occlusion (due to compression of the thin walled veins) but not arterial occlusion. Thus, blood still flows into the testis but it can’t get out! This leads to hypoxia and eventually to hemorrhagic necrosis.
File:IPLab4Thromboembolus8.jpg|This is a gross photograph of cut section of testis from previous image. The tissue is filled with blood.
File:IPLab4Thromboembolus9.jpg|This is a gross photograph of an opened abdomen at autopsy demonstrating loops of infarcted bowel (arrow). Vascular occlusion can lead to ischemic necrosis of the bowel. In this case, a section of bowel herniated through a fibrous connective tissue band and was strangulated, leading to ischemic necrosis.
File:IPLab4Thromboembolus10.jpg|This is a gross photograph of the fibrous band between the uterus and adjacent tissues. This fibrous scar tissue is probably left over from a previous surgery or an infection. A loop of bowel herniated through the opening produced by this fibrous band and became incarcerated leading to the ischemic necrosis seen in the previous image.
</gallery>

== Virtual Microscopy ==
=== Lung: Thromboembolus ===
<peir-vm>IPLab4Thromboembolus</peir-vm>

=== Normal Lung ===
<peir-vm>UAB-Histology-00107</peir-vm>

== Study Questions ==
* <spoiler text="What are the common sources for pulmonary thromboemboli?">Large deep veins of the lower legs: popliteal, femoral, and iliac veins.</spoiler>
* <spoiler text="What are the clinical sequelae of pulmonary thromboemboli?">Most (60-80%) pulmonary thromboemboli are clinically silent. In the remainder of the cases, pulmonary thromboemboli can cause sudden death, acute or chronic cor pulmonale, infarction, or hemorrhage.</spoiler>
* <spoiler text="What is a paradoxical embolism?">When a venous embolus passes through an interatrial or interventricular septal defect and enters the systemic circulation.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/300901-overview eMedicine Medical Library: Pulmonary Embolism]
* [http://emedicine.medscape.com/article/1911303-overview eMedicine Medical Library: Deep Venous Thrombosis]
* [http://emedicine.medscape.com/article/1950759-overview eMedicine Medical Library: Noncoronary Atherosclerosis]
* [http://www.merckmanuals.com/professional/hematology_and_oncology/thrombotic_disorders/overview_of_thrombotic_disorders.html Merck Manual: Thrombotic Disorders]
* [http://www.merckmanuals.com/professional/pulmonary_disorders/pulmonary_embolism/pulmonary_embolism.html Merck Manual: Pulmonary Embolism]
* [http://www.merckmanuals.com/professional/cardiovascular_disorders/peripheral_venous_disorders/deep_venous_thrombosis_dvt.html Merck Manual: Deep Venous Thrombosis]

=== Journal Articles ===
* Garg K. [http://www.ncbi.nlm.nih.gov/pubmed/11813814 CT of pulmonary thromboembolic disease]. ''Radiol Clin North Am'' 2002 Jan;40(1):111-22, ix.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/28-thromboembolus PEIR Digital Library: Thromboembolus Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#7 WebPath: Pulmonary Pathology]

== Related IPLab Cases ==
* [[IPLab:Lab 4:Pulmonary Congestion and Edema|Lab 4: Lung: Pulmonary Congestion and Edema]]

{{IPLab 4}}

[[Category: IPLab:Lab 4]]

IPLab:Lab 4:Pulmonary Congestion and Edema

2015-09-16T19:33:24Z

Peter Anderson: /* Virtual Microscopy */

== Clinical Summary ==

This 69-year-old white male with well-controlled Type I diabetes mellitus (insulin-dependent) presented with upper abdominal and lower chest pain of four hours duration and accompanied by shortness of breath and diaphoresis. An electrocardiogram revealed multiple premature ventricular contractions (PVCs). The hospital course was characterized by recurrent pulmonary edema and oliguria. The terminal event was cardiac arrest.

== Autopsy Findings ==

Significant findings at postmortem examination were old and recent myocardial infarctions and evidence of congestive heart failure. The right and left lungs weighed 950 grams and 750 grams, respectively, and were reddish-brown.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab4PulmonaryCongestion1.jpg|This is a gross photograph of lungs that are distended and red. The reddish coloration of the tissue is due to congestion. Some normal pink lung tissue is seen at the edges of the lungs (arrows).
File:IPLab4PulmonaryCongestion2.jpg|This is a gross photograph of lung demonstrating acute pulmonary congestion and edema. A frothy exudate fills the bronchus (arrow).
File:IPLab4PulmonaryCongestion3.jpg|This gross photograph demonstrates the frothy exudate that is being extruded from the lung tissue.
File:IPLab4PulmonaryCongestion4.jpg|This is a low-power photomicrograph of lung from this case. The lung section has a pale-red color indicating proteinaceous material within the lung.
File:IPLab4PulmonaryCongestion5.jpg|This is a higher-power photomicrograph of lung. The edema fluid within the alveoli is visible at this higher magnification (arrows). The thickened pleura (1) is on the left.
File:IPLab4PulmonaryCongestion6.jpg|This is a higher-power photomicrograph showing edema-filled alveoli in the right portion of this section (arrows).
File:IPLab4PulmonaryCongestion7.jpg|This high-power photomicrograph illustrates the edema fluid within the alveoli (1) and the congestion (RBCs) in the alveolar capillaries (arrows).
</gallery>

== Virtual Microscopy ==
=== Lung: Congestion and Edema ===
<peir-vm>IPLab4PulmonaryCongestion</peir-vm>

=== Normal Lung ===
<peir-vm>UAB-Histology-00107</peir-vm>

== Study Questions ==
* <spoiler text="Name two types of edema fluid.">Inflammatory edema has a higher protein content (specific gravity > 1.020) and is associated with an inflammatory reaction.

Noninflammatory edema is caused by alterations in hemodynamic forces across the capillary wall (hemodynamic edema).</spoiler>
* Define the following:
:* <spoiler text="anasarca">Anasarca: severe and generalized edema which includes marked swelling of the subcutaneous tissues.</spoiler>
:* <spoiler text="hydrothorax">Hydrothorax: fluid build-up in the thorax.</spoiler>
:* <spoiler text="hydropericardium">Hydropericardium: fluid build-up in the pericardial sac.</spoiler>
:* <spoiler text="hydroperitoneum">Hydroperitoneum: fluid accumulation in the abdominal cavity--also referred to as ascites.</spoiler>
* <spoiler text="What is the most common cause of pulmonary edema?">Left-sided heart failure.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/163062-overview eMedicine Medical Library: Heart Failure]
* [http://www.merckmanuals.com/professional/cardiovascular_disorders/heart_failure/heart_failure_hf.html Merck Manual: Heart Failure (HF)]

=== Journal Articles ===
* Welch TD, Yang EH, Reeder GS, Gersh BJ. [http://www.ncbi.nlm.nih.gov/pubmed/22664306 Modern management of acute myocardial infarction]. ''Curr Probl Cardiol'' 2012 Jul;37(7):237-310.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/124-edema/27-lung PEIR Digital Library: Pulmonary Edema Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html WebPath: Lung Pathology]

== Related IPLab Cases ==
* [[IPLab:Lab 1:Myocardial Infarction|Lab 1: Heart: Myocardial Infarction (Coagulative Necrosis)]]
* [[IPLab:Lab 3:Acute Myocardial Infarction|Lab 3: Heart: Acute Myocardial Infarction]]
* [[IPLab:Lab 3:Healed Myocardial Infarction|Lab 3: Heart: Healed Myocardial Infarction]]
* [[IPLab:Lab 4:Mural Thrombus|Lab 4: Heart: Mural Thrombus]]
* [[IPLab:Lab 4:Thrombosis|Lab 4: Coronary Artery: Thrombosis]]

{{IPLab 4}}

[[Category: IPLab:Lab 4]]