Exam 2 Flashcards

Question

Enalapril

Answer 1

CHF ACE Inhibitor prodrug (liver activation); ↓plasma A-II→↓preload/afterload and indirectly ↑CO + ↑ exercise capacity + ↓pulm/periph congestion; ∅ΔHR; correct high endogenous aldosterone/diuretic hypokalemia (prevent digitalis tox); reduce high aldo myocardial fibrosis; prevent myocardial A-II production → ↓CHF hypertrophy contribution CHF but effects might not be as strong b/c of liver congestion ↓BP too much when used w/ diuretics/antihypertensives; extended therapeutic effects (kyperkalemia, and hypotension); high bradykinin→dry cough (already present w/ CHF) and angioedema (uncommon but very bad); contra for preggos; NO K sparing if hyperkalemia and NO NSAIDs which may block bradykinin-mediated VD

Answer 2

CHF ACE Inhibitor prodrug (liver activation); ↓plasma A-II→↓preload/afterload and indirectly ↑CO + ↑ exercise capacity + ↓pulm/periph congestion; ∅ΔHR; correct high endogenous aldosterone/diuretic hypokalemia (prevent digitalis tox); reduce high aldo myocardial fibrosis; prevent myocardial A-II production → ↓CHF hypertrophy contribution CHF but effects might not be as strong b/c of liver congestion ↓BP too much when used w/ diuretics/antihypertensives; extended therapeutic effects (kyperkalemia, and hypotension); high bradykinin→dry cough (already present w/ CHF) and angioedema (uncommon but very bad); contra for preggos; NO K sparing if hyperkalemia and NO NSAIDs which may block bradykinin-mediated VD

Answer 3

CHF ACE Inhibitor prodrug (liver activation); ↓plasma A-II→↓preload/afterload and indirectly ↑CO + ↑ exercise capacity + ↓pulm/periph congestion; ∅ΔHR; correct high endogenous aldosterone/diuretic hypokalemia (prevent digitalis tox); reduce high aldo myocardial fibrosis; prevent myocardial A-II production → ↓CHF hypertrophy contribution CHF but effects might not be as strong b/c of liver congestion ↓BP too much when used w/ diuretics/antihypertensives; extended therapeutic effects (kyperkalemia, and hypotension); high bradykinin→dry cough (already present w/ CHF) and angioedema (uncommon but very bad); contra for preggos; NO K sparing if hyperkalemia and NO NSAIDs which may block bradykinin-mediated VD

Answer 4

CHF ARB Angiotensin II (AII) antagonist; short HL but active metabolite persists for 1x/24h dose; inactivated by kidney/liver; Block AII receptors; ↓TPR b/c ∅AII mediated VC and aldo synth inhibited which ↓fluid retention → ↓arterial resistance CHF extended therapeutic effects (kyperkalemia, and hypotension); contra for preggos; less bradykinin change .: less chance of dry cough or angioedema; NO K sparing if hyperkalemia and NO NSAIDs which may block bradykinin-mediated VD

Answer 5

CHF ARB Angiotensin II (AII) antagonist; no active metabolite; inactivated by kidney/liver; Block AII receptors; ↓TPR b/c ∅AII mediated VC and aldo synth inhibited which ↓fluid retention → ↓arterial resistance CHF extended therapeutic effects (kyperkalemia, and hypotension); contra for preggos; less bradykinin change .: less chance of dry cough or angioedema; NO K sparing if hyperkalemia and NO NSAIDs which may block bradykinin-mediated VD

Answer 6

CHF ARB Angiotensin II (AII) antagonist; prodrug→GI conversion; inactivated by kidney/liver; Block AII receptors; ↓TPR b/c ∅AII mediated VC and aldo synth inhibited which ↓fluid retention → ↓arterial resistance CHF extended therapeutic effects (kyperkalemia, and hypotension); contra for preggos; less bradykinin change .: less chance of dry cough or angioedema; NO K sparing if hyperkalemia and NO NSAIDs which may block bradykinin-mediated VD

Answer 7

CHF Diuretic - Thiazide sulfa group; secreted in prox. tubule by organic acid sec. mech.; inhibit Na/Cl symport in early distal conv. tubule (NaCl excretion + H2O diuresis); diuretic action independent of acid-base balance; initial ↓CO w/ reflex ↑RAAS to limit BP ∆ → ↓TPR → normal CO but continued anti-HTN effect; ↓ ECF, ↓preload, relieve pulm congestion, ↓periph edema CHF; 1˚ diuretic unless GFR <30 Hypokalemia (mm weakness + leg cramps; sudden cardiac death from ↑ vent. ectopic activity; minimize = small dose from long acting Rx or add K sparing Rx or add RAAS supp Rx or ↓Na/↑K intake) + met. alkalosis (↑K/H excretion in late distal tubule/cortical collecting duct), gout (↓uric acid excr./hyperurecemia/↑uric acid reabsorp.), SJS/TEN (Sulfa), hyperglycemia, ↑LDL/total Cholest./total TAGs

Answer 8

CHF Diuretic - Loop Sulfa deriv.; short half-life, 2-3x/day; bound to plasma proteins, secreted in prox. tubule by organic acid sec. mech.; act on thick asc. limb → block Na/K/2Cl symporter; “High ceiling” b/c of high reabsorp. capacity in thick asc. limb; enhanced Na/K/Cl/K/H/Ca/Mg/NH3 excretion; ↓ ECF, ↓preload, relieve pulm congestion, ↓periph edema CHF; only if unresponsive to thiazide hypotension, hypovolemia, hyponatremia; hypochloremia/hypokalemia + met alkalosis (↓ ECF → ↑NaHCO3 reabsorp. + ↑ NaCl to collecting duct → ↑K/H sec.) .: arrhythmias; gout (↓ uric acid excretion); ototoxicity (reversible; less common furo but ↑ risk w/ amigoglycoside ABX); SJS/TEN

Answer 9

CHF Diuretic - K Sparing Aldo Ant. Liver meta; block aldo receptors and prevent aldo-induced gene transcription, dependent on endogenous aldo levels; ↓Na conductance in lumen → ↓ Na/K ATPase → indirectly ↓ K/H sec; ↓ ECF, ↓preload, relieve pulm congestion, ↓periph edema CHF; in conjunction w/ thiazide/loop to maintain K; esp important to ↓ digitalis tox; help prevent myocardial fibrosis from high aldo Hyperkalemia (arrhythmias/mm weakness), no admin w/ K sparing diuretics (hyperkalemia), caution w/ RAAS blockers (hyperkalemia), antiandrogen effects (gynecomastia, ↓libido, etc)

Answer 10

CHF Diuretic - K Sparing Aldo Ant. Liver meta; block aldo receptors and prevent aldo-induced gene transcription, dependent on endogenous aldo levels; ↓Na conductance in lumen → ↓ Na/K ATPase → indirectly ↓ K/H sec; ↓ ECF, ↓preload, relieve pulm congestion, ↓periph edema CHF; in conjunction w/ thiazide/loop to maintain K; esp important to ↓ digitalis tox; help prevent myocardial fibrosis from high aldo Hyperkalemia (arrhythmias/mm weakness), no admin w/ K sparing diuretics (hyperkalemia), caution w/ RAAS blockers (hyperkalemia)

Answer 11

CHF Direct VD 1˚: ↓Afterload; arterial VD→ inhibit VC from NE/A-II/vasopressin →↓afterload to LV ejection → hemodynamic balance severe, refractory CHF; post acute MI w/ preexisting CHF tachycardia, edema, loss of HTN-tx efficacy; hypotension; lupus-like rxn

Answer 12

CHF Direct VD IV only; 1˚: ↓Preload and ↓Afterload; arterial VD→ inhibit VC from NE/A-II/vasopressin →↓afterload to LV ejection → hemodynamic balance; venodilation → ↑ venous capacitance → ↓preload intensive care only; severe, refractory CHF; post acute MI w/ preexisting CHF rapid action my ↓BP too quickly; significant ↑HR

Answer 13

CHF Direct VD 1˚: ↓Preload; venodilation → ↑ venous capacitance → ↓preload; tolerance w/ longterm use severe, refractory CHF; post acute MI w/ preexisting CHF extension of therapeutic effect (↑VD) → orthostatic hypotension, throbbing HA, reflex ↑HR/Contractility, Na/H2O retention; tolerance w/ continuous exposure, rebound angina w/ abrupt stop; Contra w/ PDE5 inhibitors (viagra) fatal hypotension

Answer 14

CHF Direct VD 1˚: ↓Preload; venodilation → ↑ venous capacitance → ↓preload; tolerance w/ longterm use severe, refractory CHF; post acute MI w/ preexisting CHF extension of therapeutic effect (↑VD) → orthostatic hypotension, throbbing HA, reflex ↑HR/Contractility, Na/H2O retention; tolerance w/ continuous exposure, rebound angina w/ abrupt stop; Contra w/ PDE5 inhibitors (viagra) fatal hypotension

Answer 15

CHF Direct VD IV only; 1˚: ↓Afterload; ↑intracellular cGMP→↓arterial AND venous sm tone → ↓afterload; diuretic action due to natiuretic peptide intensive care only; severe, refractory CHF; post acute MI w/ preexisting CHF rapid action my ↓BP too quickly; significant ↑HR

Answer 16

CHF β-Blocker prevent chronic adverse effects of high endogenous catecholamines on heart esp preventing down reg of β-adrenergic receptor # and fxn, prevent excessive tachy/arrhythmias, and inhibit renin release → inhibit RAAS begin w/ low dose for CHF (high dose detrimental) -

Answer 17

CHF α/β-Blocker prevent chronic adverse effects of high endogenous catecholamines on heart esp preventing down reg of β-adrenergic receptor # and fxn, prevent excessive tachy/arrhythmias, and inhibit renin release → inhibit RAAS; antioxidant + α-blocker begin w/ low dose for CHF (high dose detrimental) -

Answer 18

CHF β-Blocker prevent chronic adverse effects of high endogenous catecholamines on heart esp preventing down reg of β-adrenergic receptor # and fxn, prevent excessive tachy/arrhythmias, and inhibit renin release → inhibit RAAS begin w/ low dose for CHF (high dose detrimental) -

Answer 19

Antiarrhythmic Class IA IV and oral; inhibit Na channels in phase 0 and 4 of APs; in phase 0 → bind to open or inactivated channels (not resting) .: use-dependence (higher degree of block in tissues that depolarize more/high rate w/o interfering normal cells); slow rate of rise in phase 0 → ↓conduction velocity; inhibit phase 3 K channels → ↑AP duration and effective refractory period; “intermediate” phase 0 block; ↑ phase 0 threshold versatile for various arrhythmias, SV/V but little SEs; inhibit ectopic atrial/vent arrhythmias from excessive automaticity; maintain normal rhythm post cardioversion from A.fib; dose 1-2d prior to cardioversion (may revert rhythm w/o shock) arrhythmias (TdP from prolong vent. AP duraiton - prolong QT); N/V/D (common), S/S of cinchonism (α-block + atropine like effect → ↓BP + ↑HR); ↑serum digoxin

Answer 20

Antiarrhythmic Class IA IV and oral; inhibit Na channels in phase 0 and 4 of APs; in phase 0 → bind to open or inactivated channels (not resting) .: use-dependence (higher degree of block in tissues that depolarize more/high rate w/o interfering normal cells); slow rate of rise in phase 0 → ↓conduction velocity; metabolite of procainamide, NAPA (renal elim), inhibits phase 3 K channels → ↑AP duration and effective refractory period; “intermediate” phase 0 block; ↑ phase 0 threshold versatile for various arrhythmias, SV/V but little SEs; inhibit ectopic atrial/vent arrhythmias from excessive automaticity; maintain normal rhythm post cardioversion from A.fib; dose 1-2d prior to cardioversion (may revert rhythm w/o shock) reversible lupus syndrome (less common w/ rapid acetylators); confusion, GI intolerance (LESS than quinidine); LESS α-block + atropine like effect → ↓BP + ↑HR; TdP vent arrhythmias

Answer 21

Antiarrhythmic Class IB IV, extensive 1st pass; inhibit Na channels in phase 0 and 4 of APs; in phase 0 → bind to open or inactivated channels (not resting) .: use-dependence (higher degree of block in tissues that depolarize more/high rate w/o interfering normal cells); LESS inhibition of phase 0 Na channel → LESS slowing effect on rate of rise of phase 0→ LESS of ↓conduction velocity; shorten phase 3 repolarization w/o ↓ phase 0 slope or Δconduction velocity; inhibit late open Na channels → ↓AP duration and ERP (opened more in ischemic conditions); “rapid” phase 0 block; ↑ phase 0 threshold emergency for vent. arrhythmias during MI (or ischemia); suppress vent arrhythmias from automaticity (↓phase 4 slope and ↑ phase 0 threshold); abolishes vent reentry arrhythmias DESPITE ↓AP/↓ERP/↓conduction; stop TdP even w/ ↓AP Wide toxic therapeutic ratio; ∅ impaired vent. contraction (∅ negative inotropic effect); drowsiness, slurred speech, confusion, and convulsions; hyperkalemia→arrhythmias

Answer 22

Antiarrhythmic Class IC oral; inhibit Na channels in phase 0 and 4 of APs; in phase 0 → bind to open or inactivated channels (not resting) .: use-dependence (higher degree of block in tissues that depolarize more/high rate w/o interfering normal cells) ; MARKED inhibition of phase 0 Na channel → MARKED ↓ rate of rise phase 0 → MARKED ↓conduction velocity; little effect on AP duration/ERP b/c inhibition of some K channels and late Na channels; ↑ phase 0 threshold and ↓ phase 4 slope severe arrhythmias unresponsive for other rx negative inotropic effects→aggravate CHF/arrhythmias; Dizzy, blurred vision, HA, N; hyperkalemia→tachy; ↑mortality compared to other rx

Answer 23

Antiarrhythmic Class II β-antagonists; block β-receptors on Ca channels → ↓inward Ca (similar to class IV CCBs); ↓phase 4 depolarization (↓automaticity esp in nodes); ↓phase 0 slope → ↓conduction esp in nodes; ↑AP duration and ↑ERP (like Class IV CCBs); inhibit neural sympathetic input on automaticity and conduction velocity ↓incidence of sudden adrenergic arrhythmia death post MI; tx arrhythmias from ↑ sympathetic neural activity +/- excess catecholamine (even in vent.); a.fib/flutter, AV nodal reentry tachy (prevent SV arrhythmias) suppress DADs from adrenergic stress (even in vent.) CV: bradycardia, reduced exercise ability, easy fatigue, slow AV conduction, and suppress ventricular contraction, rebound HTN w/ sudden withdrawal of TX; bronchoconstriction (inhibit B2 airway receptors); more severe/longer duration induced hypoglycemia (in DM pts); mask hypoglycemia warning signs (tachy but sweating still present); insulin resistance and glc intolereance; hypertriglyceridemia and ↓HDL; hallucinations; avoid combo w/ CCBs (risk of cardiac suppression)

Answer 24

Antiarrhythmic Class II β-antagonists; block β-receptors on Ca channels → ↓inward Ca (similar to class IV CCBs); ↓phase 4 depolarization (↓automaticity esp in nodes); ↓phase 0 slope → ↓conduction esp in nodes; ↑AP duration and ↑ERP (like Class IV CCBs); inhibit neural sympathetic input on automaticity and conduction velocity β1-spec ↓ risk of bronchospasm; partial agonist ↓ risk of too much cardiac suppression; tx arrhythmias from ↑ sympathetic neural activity +/- excess catecholamine (even in vent.); a.fib/flutter, AV nodal reentry tachy (prevent SV arrhythmias) suppress DADs from adrenergic stress (even in vent.) avoid combo w/ CCBs (risk of cardiac suppression)

Answer 25

Antiarrhythmic Class II short acting IV; β-antagonists; block β-receptors on Ca channels → ↓inward Ca (similar to class IV CCBs); ↓phase 4 depolarization (↓automaticity esp in nodes); ↓phase 0 slope → ↓conduction esp in nodes; ↑AP duration and ↑ERP (like Class IV CCBs); inhibit neural sympathetic input on automaticity and conduction velocity use during surgery or emergency; tx arrhythmias from ↑ sympathetic neural activity +/- excess catecholamine (even in vent.); a.fib/flutter, AV nodal reentry tachy (prevent SV arrhythmias) suppress DADs from adrenergic stress (even in vent.) avoid combo w/ CCBs (risk of cardiac suppression)

Answer 26

Antiarrhythmic Class III IV, rapid action; concentrates in tissues→7wk HL; inhibit K channels during AP → ↓ outward K flow → prolong repolarization (phase 3); ↑AP duration/↑ERP w/o Δ to other AP phases; complex 2˚ interactions (similar to all classes); ↓ cardiac cell-cell coupling→↓conduction velocity; contains iodine (similar to thyroxine) severe, refractory SV/V tachyarrhythmias; in pts w/ implantable cardioverter defibrillators (ICD) to control arrhythmias (reduced tachyarrhythmic burden) toxic effects can persist after discontinuation; interstitial pulm fibrosis, dizzy, hyper/hypothryroidsm, blue skin (iodine accumulation); TdP risk from ↑AP duration in vent. but rare

Answer 27

Antiarrhythmic Class III oral/IV; inhibit ONLY K channels during AP → ↓ outward K flow → prolong repolarization (phase 3); ↑AP duration/↑ERP w/o Δ to other AP phases SV arrhythmias (suppression of reentry phenomena); good for A.fib TdP (esp IV @ high dose)

Answer 28

Antiarrhythmic Class IV Oral; extensive liver meta; Block L-type Ca channels→↓inward Ca current→↓phase 0/4 slopes→↓conduction velocity and suppress automaticity; mostly in highly Ca dependent tissues (AV node); ↑AP duration/↑ERP late in phase 3 of AV node (less inward leads to less outward for repolarization) SV > V arrhythmias but good for DADs in both; reentrant SVT involving AV node; protect normal vent rate in A.fib/flutter; make WPW worse w/ a.fib ↓ normal sinus rate and ↓ AV conduction; negative inotropic action; contra: β-blockers

Answer 29

Antiarrhythmic Class IV Oral; Block L-type Ca channels→↓inward Ca current→↓phase 0/4 slopes→↓conduction velocity and suppress automaticity; mostly in highly Ca dependent tissues (AV node); ↑AP duration/↑ERP late in phase 3 of AV node (less inward leads to less outward for repolarization) SV > V arrhythmias but good for DADs in both; reentrant SVT involving AV node; protect normal vent rate in A.fib/flutter; make WPW worse w/ a.fib ↓ normal sinus rate and ↓ AV conduction; negative inotropic action; contra: β-blockers

Answer 30

Antiarrhythmic Misc. Agent IV; short acting (15s); ↓inhibit Ca influx and activate ACh-sens phase 4 K current (hyperpolarization @ rest)→↓conduction velocity and ↓abnormal impulse @ AV node; prolong AV node refractory period IV admin for acute paroxysmal SVT (PVST) from AV node origin or WPW low tox; flushing, SOB, chest pain (bronchospasm)

Answer 31

Antiplatelet Acetylsalicyclic acid oral; irreversible COX inhibitor (COX1 @ low dose and COX1/2 @ high dose) →↓TXA2(platelet)/↓PGI2(endothelial cell) synth Prevent MI/ischemic attacks/ischemic stroke/arterial thrombosis/vein graft occlusion (bypass surgery); 160-325mg/d for antiplatelet tx GI bleed, impaired surgical/mother & fetus hemostasis

Answer 32

``` Antiplatelet Pyrimidine oral; PDE inhibitor → ↑cAMP→inhibit platelet adhension use w/ coumarin; prevent thrombosis hypotension, minimal SEs ```

Answer 33

Antiplatelet Non-peptide antagonist oral; irreversible inhibition of ADP binding to platelet ADP receptor → prevents platelet aggregation (∅ADP mediated GIIb/IIIa activation); ∅PDE inhibition ↓ risk of MI, CVA, vascular death (atherosclerotic events) bleeding

Answer 34

Anticoagulant Sulfated (-) Mucopolysaccharide rapid effect; IV/SubQ NOT IM; Binds antithrombin III→inactivating Factor Xa AND inhibit thrombin → prevent conversion of fibrinogen to fibrin; binds platelets inhibiting fxn +/- aggregating them→thrombocytopenia; monitor tx via aPTT venous/pulm thromboembolism, acute MI (prevent reocclusion), extracorporeal circulation (open heart surg/renal hemodialysis), preggos (instead of oral anticoags), maintain patency of catheters bleeding, thrombocytopenia (Ab formation; acute from heparin effect, mild 2-4d post tx start w/ bovine > porcine, and severe discontinue till platelet # returns), local capillary rupture, hypersensitivity (N/V, lacrimation, HA, pruritis, burning, fever, urticaria, bronchospasm, rhinitis, anaphylaxis; porcine/bovine)

Answer 35

Anticoagulant Cationic (+) LMW Protein IV; rich in arginine/strongly basic; binds heparin forming a salt; instantaneous (lasts 2hr); too much → anticoagulant (prolonging clotting time w/o heparin) severe heparin OD (IV) hypotension, hypersensitivity/anaphylaxis (fish sperm)

Answer 36

Anticoagulant 4-hydroxycoumarin derivative Oral; long HL; liver meta; inhibits vitamin K epoxide reductase → ∅vitamin K→blocks synthesis of Factors: II, VII, IX, X, protein C/S → factors cannot bind Ca→↓thrombin formation and ↓coagulation; effect requires clearance of pre-existing factors (continue heparin when starting warfarin); reverse action: stop Rx and give vit K + fresh frozen plasma (contains factors) Prevent thrombosis w/: non-valvular a.fib, valvular heart dz, prosthetic heart valves, acute venous thrombosis, PE, acute MI, reocclusion w/ coronary bypass, in-dwelling catheters bleeding, HTN, necrotic skin lesions, fetal abnormalities (crosses placenta; use Heparin instead), prolong/intensify: aspirin, salicylates, cyclophosphamides, heparin, indomethacin, tamoxifen, etc; diminish response: azathioprine, barbiturates, corticosteroids, diuretics, penicillins, excessive vit K intake (brussel sprouts, veggies, green tea)

Answer 37

Anticoagulant Recombinant Polypeptide IV; 10min HL; leech derived; inhibit thrombin (1 molecule blocks 1 molecule) anticoag in Heparin-Induced Thrombocytopenia (HIT) bleeding, hypersensitivity; unknown rxn w/ preggos; no antidote

Answer 38

Fibrinolytic Serine Protease IV; 16 min HL; from endothelial/mononuclear cells in kidneys; directly cleaves plasminogen to plasmin thrombolytic, coronary artery thrombosis, MI bleeding, fever

Answer 39

Fibrinolytic Serine Protease IV; 4 min HL; from endothelial cell walls; cleaves plasminogen to plasmin in presence of fibrin thrombolytic, coronary artery thrombosis, MI bleeding, arrhythmias

Answer 40

``` Fibrinolytic Monoamino Carboxylic Acid; lysine Oral/IV; inhibit binding/activation of plasminogen/plasmin to fibrin (inhibit fibrinolysis) overactive fibrinolysis mild tox ```

Answer 41

``` Hemostatics Human Factor from human donors; part of coag cascade (prothrombin to thrombin) Hemophilia A (factor VIII def) few/dose related ```

Answer 42

``` Hemostatics Human Factor part of coag cascade (prothrombin to thrombin) Hemophilia B (factor IX def) few/dose related ```

Answer 43

Hemostatics Synth Vit K Required for synthesis of Factors: II, VII, IX, and X hypoprothrombinemia from coumarins; newborn hemorrhagic dz anaphylaxis (rare)

Answer 44

Anemia Oral/parenteral; component of hemoglobin/myoglobin; stored in ferritin/hemosiderin; requirement: 13mg/kg for males and 21 mg/kg for females; 980 mg for preggos prevent/tx iron deficient microcytic anemias; Oral: male 10mg/d, female 15 mg/d, post-men female 10 mg/d, preggo 30 mg/d, lactation 15 mg/d Parenteral: only if oral tx will not work; IV (test w/ 0.5mL for anaphylaxis prior to first dose) or IM (similar precaution as IV) Oral: GI irritation, N/V/D, constipation, dark stool, hemochromatosis; Tx iron OD w/ deferoxamine Mesylate (iron chelater); avoid taking w/ antacid, tetracyclines, fluoroquinolones (↓abs); Parenteral: anaphylaxis, hypersensitivity (dyspnea, uritcaria, rashes, itching, arthralgia, myalgia, fever), soreness/inflamm @ injection site, brown color @ IM injection site

Answer 45

Anemia ``` Oral/parenteral (not recommended unless malabs); 0.4 mg/d during preggo (↓neural tube defect; spina bifida); cofactor for AA/purine/DNA synthesis and erythropoiesis; liver meta; normal serum = 5-15 ng/mL (< 5ng/mL = folate def. and <2ng/mL → megaloblastic anemia) megaloblastic anemia (sprue, preggos, nutritional anemia); up to 1mg/d non-toxic; contra: pernicious anemia→neural defects; GI (usual in pt w/ 15 mg), CNS (altered sleep, difficulty concentrating, mental depression in pt w/ 15 mg) ```

Answer 46

Anemia ``` 2.2ug/d for preggo; parenteral for pernicious only; Oral if malabsorption NOT present; cofactor for methylmalonyl-CoA mutase, methionine synthase (FFA meta and DNA synth); need intrinsic factor and Ca for abs; stored in liver (5 y to deplete store) megaloblastic anemia (sprue, preggos, nutritional anemia); pernicious anemia (need injection for rest of life); hippies need to take B12 supplement (B12 in meat) Leber’s Dz (optic n atropy), anaphylaxis; pulm edema, CHF, periph vasc thrombosis, itching, feeling of body swelling, pain at injection site ```

Answer 47

Anemia Recombinant Glycoprotein IV/SubQ; erythropoietin; growth/diff of stem cells→erythrocytes Anemia of chronic dz (renal, AZT-tx AIDS, chemo pts); facilitate autologous blood donation prior to surgery flu-like S/S, arthralgia from albumin in Rx prep, HTN (pts w/ renal dz), clotting/seizures/hyperkalemia in dialysis pts

Answer 48

Anemia Recombinant Glycoprotein IV; G-CSF; growth/diff of stem cells→neutrophil lineage; enhance fxn of mature neutrophils (phagocytosis/bactericidal activity) accelerated recovery of neutrophil #; chemotx induced/HIV neutropenia, BM xplant well tolerated (rare SEs)

Answer 49

Anemia Recombinant Glycoprotein IV; GM-CSF; growth/diff of stem cells→granulocytes/MΦ; enhances chmotactic, antifungal, antiparasitic fxn myeloid recovery in cancer pts (lymphoma, leukemia), BM xplant well tolerated (rare SEs)

Answer 50

``` Anemia Recombinant Polypeptide IV; IL-11; growth/diff of stem cells→megakaryocytes/platelets prevent thrombocytopenia in cancer pts well tolerated ```

Exam 2 Flashcards

(74 cards)