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28 Cards in this Set
- Front
- Back
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Which is the least abundant serum Ig? |
IgE (150ng/ml) |
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Which ILs do Th2 cells make to induce B cell IgE production? |
IL-4, IL-13 Present during hypersensitivity type I |
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What cells bind strongly to IgE? |
Mast cell, basophil. Can result in over 12 weeks of binding. |
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What is Virchow's Triad? |
Three broad categories of factors that are thought to contribute to thrombosis: Injury/dysfunction of vascular endothelium, alterations in blood flow (stasis, turbulence), alterations in blood composition (hypercoagulability) |
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Thrombotic microangiopathy: What causes congenital thrombocytopenic purpura? |
Deficiency of ADAMTS13, a plasma enzyme that cleaves vWF |
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Pathogenesis of DIC in sepsis? |
Release of high levels of tissue factor into circulation...among other things |
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What anatomical condition is found in pts with paradoxical emboli? |
Septal defect only thing that can allow emboli to bypass capillary beds/vascular narrowing to cross from systemic to venous circulation |
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What 4 factors determine the severity of ischemia in any affected tissue? |
Speed of onset, presence/quality of collateral perfusion, degree of occlusion, metabolic needs of the tissue. |
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What is hyperemia? Difference between active and passive form? |
Too much blood in an organ, increases its weight. Active: too much flow into organ. Passive: aka congestion, inadequate venous drainage of organ. Generalized passive hyperemia due to heart failure. |
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What characterizes nutmeg liver, a form of hyperemia? |
Darker congested and partially necrotic centrilobular spots surrounded by lighter colored viable parenchyma. |
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Dif between transudate and exudate in edema? |
Trans: low specific gravity, reflects pathology that does not involve increased capillary permeability such as heart failure. Exudate: High spec. grav, high protein, due to capillary permeability (inflammation) |
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Petechiae vs purpura vs ecchymosis? |
Petechiae: small freckle-like hemorrhages, less than 2mm diameter. Purp: purple spots of hemorrhage on skin or mucosa more than 2mm diameterEcc: large diffuse hemorrhagic area |
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Severe hypovolemia happens at what blood volume loss? What signs of shock will be present? |
40% or more, hypotension, tachycardia, oliguria (low urine output), mental confusion |
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What causes "tabby cat heart?" |
Prolonged moderate hypoxia (as in severe anemia) causes fatty change in some myocardicytes, leaving others unaffected, causing yellow and red striping. |
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Myeloma is associated with what type of amyloidosis? |
AL, specifically lambda or kappa light chain |
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What sign is classically pathognomonic for AL amyloidosis? |
Macroglossia |
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Which normal plasma protein is always found within AL amyloidotic plaques? |
Serum amyloid P (SAP), "chaperones" serum proteins |
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Hepcidin binds to ferroportin, blocking and degrading it. Which 3 indicators of iron levels regulate hepcidin expression? |
HFE, transferrin receptor 2 (TfR2), and hemojuvelin (HJV). Mutations in any of these may lead to hemochromatosis. |
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What is the pathogenesis of cell injury in iron-overabundance aka hemochromatosis? |
Fenton reaction: iron catalyzes free-radical creation, leads to lipid peroxidation and/or DNA damage, which can cause hepatocellular carcinoma. |
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Compare metastatic and dystrophic calcification. |
Dystrophic: preferential Ca accumulation in dead/dying tissue (ex atherosclerosis), no serum Ca elevation or Ca metabolism alteration Metastatic: Ca accumulation in normal tissue (ex renal tubular basement membrane) due to excess serum Ca, often from metabolic derangement |
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How does calcification cause inflammation? |
Its crystals (as is the case in other crystal-mediated inflammation) stimulate NLP3, activating inflammasome, producing IL-1B and IL-18 |
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How would you treat acetaminophen (AAP) hepatotoxicity? Why does it work? |
N-acetyl-cysteine, IV, because it is a glutathione precursor. 5% of metabolized AAP is converted to NAPQI, which binds to hepatic protein thiols, causing injury. NAPQI is cleared via conjugation with glutathione. |
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How does AAC-mediated hepatocyte death cause inflammation? |
Spilled DNA activates TLR9, up regulating pro-IL-1B and pro-IL-18, which are cleaved by NLP3 inflammasome. |
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How is silicosis cured? |
It's not. It also increases risk of TB. |
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How do silicosis and asbestosis cause inflammation? |
Activating NLP3 inflammasome. |
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Elevated serum homocysteine indicates what vitamin deficiency? Why? |
B12, used as cofactor of methionine synthase, which uses homocysteine as a substrate. |
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Most common reason for B12 deficiency? |
Pernicious anemia, where autoimmune destruction of gastric parietal cells limits production of intrinsic factor. |
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With C. jejuni, how is "molecular mimicry" a cause of virulence? |
Carbohydrates of C. jejuni resemble gangliosides of peripheral nerves, causing of 30% of Guillain–Barré cases. (CMV causes another 10%) |
