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12 Cards in this Set
- Front
- Back
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Acute Poststreptococcal Glomerulonephritis
Nephrotic or nepthritic syndrome? Etiology? Abundance of what cell type is characteristic? Morphology? - Macro - Micro |
Nephritic
Deposition of immune complexes (related to a cleared streptococcal infection) in glomeruli. Neutrophils - Bigger (swollen). Pale w/ red dots on surface. - Uniformly increased cellularity of glomeruli due to prolif. and swelling of endothelial and mesangial cells aswell as by neutrophilic and monocytic inflitrate. Some RBC's present in tubules (hematuria) |
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What is the difference between nephrotic syndrome and nephritic syndrome?
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Both are "clinical complexes" with different composition.
Nephrotic: - Massive proteinuria. Daily loss>3.5g - Hypoalbuminemia (<3g/dL) - Generalized edema - Hyperlipidemia and lipiduria. ----- Cause is damage capillary walls of glomeruli, allowing plasma proteins to filter through. Nephritic: - Hematuria - Oliguria (small amounts of urine) - Azotemia (nitrogen in blood) - HT ------- Cause is injury to glomeruli cells walls due to inflam. |
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Chronic glomerulonephritis
Cause? What may follow? Rate of development? Morphology? - Macro - Micro |
All acute glomerulonephritis can lead to chronic GN, but not at equal rates.
End-stage renal disease, presenting as renal failure. Slow (insidious) - Smaller, red-brown and diffusely granular. - Glomeruli are hyalinized and sclerotic or completely obliterated. The tubules are atrophied. Interstitial lymphocytic infiltrates. |
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What mechanisms are involved in the recognition of allografts?
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- Cell (CD4+) and antibody-mediated hypersensitivity reactions
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GVHD
Mechanism? Types? |
A patient which is to reciece bone marrow from another person must first become immunosupressed. When recieving the bone marrow, the T cells present in the donor marrow recognize the recipient's tissue as "foreing" and react against it.
- Acute -- Days to weeks after transplant -- Epithelial cell necrosis in liver (jaundice), skin (generalized rash) and gut (bloody diarrhea). - Chronic -- Skin lesions resembling those of systemic sclerosis -- Manifestations mimicking other autoimmune disorders. |
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SLE
What type of disease is it? What does it affect? What type of autoantibodies can be found? What is the mechanism of tissue injury? |
Multisystem autoimmune disease
It may affect ANY organ in the body. However, it principally effects - Skin (rash) - Kidneys (lupus nephritis, the worst complication of SLE) - Serosal membranes (serositis) - Joints (arthralgia) - Heart (Libman-Sacks endocarditis (valves)) Many different types, but antinuclear andtibodies (ANA's) seem to be the most important. - Mostly immune complexes (type III hypersensitivity) |
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Polyarteritis Nodosa (PAN)
Characterized by? What, specifically, is affected? Type of hypersensitivity? Morphology? What may it cause? Pathoevolution? Age of onset? |
Necrotizing inflammation id the walls of blood vessels?
Small or medium-sized muscular aa.. Not arterioles, capillaries or venules. Renal and visceral vessels. The pulmonary circulation tends to be spared. Type III Lesions only involve part of the vessel circumference, especially at branching points. - Aneurysms or even rupures - Impaired perfusion - Infarcts - Ischemic atrophy - Hemorrhages in affected vessels. - Acute phase: -- Mixed infiltrate - Later phase: -- Fibrosis of infiltrate -> Thickening of vessel wall. Any age, but usually young. F>M |
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Rheumatic Heart Disease (RHD)
Deifintion? Etiology? Morphology: - Macro - Micro |
The cardiac manifestation of rheumatic fever, associated w/ inflammation of valves, myocardium and pericardium.
RF is an acute, immunologically mediated (hypersensitivity), multisystem inflammatory disease that occurs a few weeks after an episode of group A β-hemolytic streptococcal infection (usually in pharynx). The antibodies cross-react with glycoprotein antigens in heart (and other tissues). - Verrucae (1-2 mm vegetations) along the closing lines of heart valves. Thickening of valve lealets. Commissural fusion and shortening. Thickening and shortening of the cordae tendinae. - Discrete inflammatory lesions calles Aschoff bodies. They have a central necrotic zone infiltrated by T lymphocytes and macrophages. The macrophages are also called Anitschkow cells, and are large and elongated (caterpillar cells). |
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Hashimoto Thyroiditis
Type of disease? Affects which population? Pathogenesis? Clinical features? Morphology: - Macro - Micro |
Autoimmune - autoreactive CD4+ lymphocytes is normally the initiating event.
Mostly women 45-65 (F>M 10:1) but children can also be affected. The thyroid epithelial cells are gradually replaced by mononucler cell infiltration and fibrosis. Painless goiter associated with hypothyroidism. May be preceded by transient thyrotoxicosis (hyperthyroidism) caused by disruption of thyroid follicles, with secondary release of thryoid hormones (hashitoxicosis) - Symmetrically enlarged (mostly) - Parenchymal mononuclear inflitrate (lymphocytes). Well developed germinal centres. Atrophic thyroid follicles lined by a lot of eosinophilic epithelial cells (Hürthle/oxyphil cells). Increased interstital CT. |
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IBS
What types are there? Etiology? Type of infiltrate? |
- Crohn disease
- Ulcerative colitis Unknown. Abnormal local immune response against the normal flora of the gut or against self-antigens of gut epithelium, or both. Initially neutrophils and mononuclear cells later. |
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Crohn Disease
Define. Location? Characterized by? |
A systemic inflammatory disease with predominant GI involvement often accompanied by extra-intestinal complications of immune origin.
- Sharply limited transmural involvement of the bowel. - Presence of noncaseating granulomas - Fistula formation - Skip lesions - Strictures Any portion of the GI tract, from the mouth to the anus but most often involves the terminal ileum. |
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Ulcerative colitis
Define. Characteristic? |
Systemic disorder associated with extra-intestinal manifestations. Begins in rectum and extends proximally in a continous fashion, sometimes involving the entire colon.
- No granulomas - Countinous lesions - Superficial lesions (mucosa and submucosa) - Pseudopolyps (islands of regenerating mucosa) - Toxic megacolon: if ulcer goes deep and infection reaches the muscularis propria. Shutdown of neuromuscular function. - Mononuclear infiltrate - Associated with high risk of cancer. |
