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30 Cards in this Set
- Front
- Back
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FOOSH --> flattening of deltoid mm?
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Axillary nn
anterior dislocation of humerus |
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spiral midshaft fx of humerus?
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Radial nn
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chemotherapeutic whos effective is overcome by N-formyl-tetrahydrofolate?
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Methotrexate
(folinic acid = leucovorin) methotrexate is a folic acid analog that binds & inactivates dihydrofolate reductase |
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what is 5-fluorouracil? MOA?
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pyrimidine analog
primarily inhibits DNA synthesis by inhibition of thymidilate synthetase (after conversion to floxuridine monophosphate) 5-FU binds tetrahydrofolate & thymidylate synthetase in a stable-reaction intermediate form |
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drug that inhibits dihydrofolate reductase?
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methotrexate, it is a folinic acid analog
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what is cytarabine?
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pyrimidine analog antimetabolite
incorporated into DNA leading strand, termination does not affect folate metabolism |
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what is cytarabine?
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pyrimidine analog antimetabolite
much like cytarabine, but is not S-phase specific -likely owing to additional cytotoxic fxns such as inhibition of ribonucleotide reductase |
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what is fludarabine?
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deamination resistant PURINE nucleotide analog
exerts toxicity by many mechanisms -inhibition of DNA polymerase, primase, ligase, & ribonucleotide reductase used for CLL |
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what is MC congenital malformation of heart in Tuner's?
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bicuspid aortic valve
you do get preductal coarctation can get mitral valve prolapse, but thtat's more common in Marfan's/Ehler's Danlos |
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how long after MI until changes become visible on microscopy?
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~4 hours, until then appears nl
4-12 hours - early coag necrosis, edema, hemorrhage, wavy fibers 12-24 hrs - coag necrosis, marginal contraction band necrosis 1-5 days - coag necrosis & neutrophilic infiltrate 5-10 days macrophage phagocytosis 10-14 days - granulation tissue & neovascularization 2 weeks - 2 mos - collagen deposition, scar formation |
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histology of all acute viral hepatitis?
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diffuse ballooning degeneration (hepatocyte swelling)
mononuclear cell infiltrates Councilman bodies (eosinophilic apoptotic hepatocytes) |
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fibrinoid necrosis results from?
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immune complex deposition in walls of blood vessels (vasculitis)
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is pulmonary capillary wedge pressure elevated in ARDS?
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No
one of criteria for ARDS is absence of cardiogenic pulmonary edema |
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what is Polyarteritis nodosa? Histologic features & vessels involved? Organs involved? Characteristic findings?
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segmental, transmural, necrotizing inflammation
medium to small sized arteries in any organ (except lung) Kidneys most often involved Heart, liver, & GI also most often involved SPARES pulmonary arteries & bronchial art inflammation can cause ischemia, infarction, or hemorrhage bead-like aneurysm formation, especially in mesenteric circulation 1/3 of patients get cutaneous manifestations - Livedo reticularis (purplish network patterend) & palpable purpura |
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what is selegiline?
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MAO inhibitor
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what is phenelzine?
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MAO inhibitor, irreversible
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what is sertraline?
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SSRI
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what does psamomma body look like?
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look it up! HIGH YIELD
round, eosinophilic laminar structures core of dense calcification w/surrounding collagen-fiber bundles PINK! meningioma, papillary thyroid carcinoma, serous papillary ovarian adenocarcinoma |
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infiltration of what structure causes nipple inversion?
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infiltration of the suspensory Cooper ligaments
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what are:
etidronate, pamidronate, alendronate, risedronate, zoledronate? |
bisphosphonates
inhibit osteoclastic activity, reduce both formation & resorption of hydroxyapatite used for - malignancy-associated hypercalcemia, paget's dz of bone, postmenopausal osteoperosis |
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what is probenecid?
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it inhibits reabsorption of uric acid in PCT
-useful for CHRONIC gout (urate-lowering therapy) also inhibits secretion of penicillin |
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what is allopurinol? Used for? Interactions?
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inhibits xanthine oxidase, decreasing conversion of xanthine to uric acid
can be used in tx of acute gout (urate-lowering therapy) -don't give w/salicylates! -all but highest doses of salicylates decrease uric acid secretion, (even at high doses doesn't really help) allopurinal is given in cancer too -prevents hyperuricemia from tumor lysis syndrome -increases concentrations of azathioprine & 6-MP (which are both nl metabolized by xanthine oxidase) |
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what is febuxostat?
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inhibits xanthine oxidase
can be used for tx of chronic gout |
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what is colchicine?
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binds & stabilizes tubulin to inhibit polymerization
impairs leukocyte chemotaxis & degranulation GI side effects if given orally |
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how can you tx gout?
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Chronic Gout --> Urate-Lowering Therapy
-Probenecid (inhibt reabsorption of uric acid in PCT) -Allopurinal - inhibit xanthine oxidase (decrease production of uric acid) -Febuxostat - inhibits Xanthine oxidase **don't give salictylates! At low doses they decrease uric acid excretion (even high doses aren't great) Acute -Colchicine - bind & stabilize tubulin, impair leukocyte chemotaxis & degranulation (GI side effects) -NSAIDs (naproxen) |
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anti-TNF therapy - what are the drugs? Used for? Complications?
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Etanercept (TNF-alpha receptor) - RA, psoriasis, ankylosis spondylitis
Infliximab - anti-TNF-alpha antibody - Crohn's, same as above Adalimumab - same as inflix but NOT for crohn's **all can predispose to infection (reactivation of latent TB) b/c TNF blockade prevents activation of macrophages |
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what specific effects does B12 deficiency have on the CNS?
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abnormal myelin synthesis, with degradation of:
1.) Dorsal columns of spinal cord - bilateral loss of position & vibration sense 2.) Lateral corticospinal tracts - UMN signs, spastic paresis, hyperreflexia, pathologic reflexes (babinski) 3.) Axon degeneration of peripheral nn - numbness or paresthesias "subacute combined degeneration" - both ascending (dorsal columns) and descennig (corticospinal tract) pathways |
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tx for invasive aspergillosis?
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amphotericin B
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appearance of dimorphic fungi in human samples?
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they are in YEAST form, in nature they are in mold form
thus biopsy would NOT show hyphae |
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what is metyrapone for?
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used as a stimulation test when suspect an interuption of hypothalamic-pituitary adrenal axis
it BLOCKS cortisol synthesis -INHIBITS enzyme 11-beta-hydroxylase reduces cortisol levels, and ACTH level should rise high ACTH stimulates adrenal gland to produce more deoxycortisol (which does not feedback) 11-deoxycortisol metabolites measured in urine as 17-hydroxy-corticosteroids |
