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pharma- mechanisms of action- heamatology,renal,cardio

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summerahmed's version from 2015-06-28 03:55

heamatology

 

Question Answer
heparinactivate antithrombin so decrease factor II AND X. short half life
argatrobaninhibit factor II thrombin directly
bivalirudinrelated to hirudin from leeches inhibit factor II thrombin directly
dabigatraninhibit factor II thrombin directly
enoxaperinLMWH act on factor X, better bioavailability than heparin, longer half life no lab monitoring
dalteparinLMWH act on factor X, better bioavailability than heparin, longer half life no lab monitoring
fondaparinuxLMWH act on factor X, better bioavailability than heparin, longer half life no lab monitoring
warafrinprevent gamma carboxilation of vitamin K ( factor 1972 and protein C,S) affected by polymorphism in the gene of Vitamin K epoxide reductase complex ( VKORC1)
Apixibanbind directly to factor X
Rivaroxibanbind directly to factor X
Alteplase (tPA)directly or indirectly aid the conversion of plasminogen to plasmin which cleaves the thrombin and fibrin clots. increase PT and PTT but no effect on the platelet count.
reteplase (rPA)directly or indirectly aid the conversion of plasminogen to plasmin which cleaves the thrombin and fibrin clots. increase PT and PTT but no effect on the platelet count.
Tenecteplace ( TNK-tPA)directly or indirectly aid the conversion of plasminogen to plasmin which cleaves the thrombin and fibrin clots. increase PT and PTT but no effect on the platelet count.
streptokinase directly or indirectly aid the conversion of plasminogen to plasmin which cleaves the thrombin and fibrin clots. increase PT and PTT but no effect on the platelet count.
Asprincovalent acetylation causing irreiversable inhibition of COX1, COX2 so platelet cannot synthesize new enzyme so effect lasts until new platelets are synthesized so increases bleeding time, decreases TXA2 and prostaglandins.
Clopidogrelirreiversabily inhibit platelet aggregation by blocking ADP receptors and thus prevent glycoproein 11b/111a expression on platelet surface.
prasugrelirreiversabily inhibit platelet aggregation by blocking ADP receptors and thus prevent glycoproein 11b/111a expression on platelet surface.
ticagrelor reiversabily inhibit platelet aggregation by blocking ADP receptors and thus prevent glycoproein 11b/111a expression on platelet surface.
ticlopidineirreiversabily inhibit platelet aggregation by blocking ADP receptors and thus prevent glycoproein 11b/111a expression on platelet surface.
cilostazolephosphodiestrase III inhibitor so increases cAMP resulting in inhibition of platelet aggregation. also a vasodilator
dipyridamolephosphodiestrase III inhibitor so increases cAMP resulting in inhibition of platelet aggregation. also a vasodilator
Abciximab( fab fragments of monoclonal antibodies) prevent platelet aggregation by binding to glycoprotein IIB/IIIa
epifibatideprevent platelet aggregation by binding to glycoprotein IIB/IIIa
tirofibanprevent platelet aggregation by binding to glycoprotein IIB/IIIa
azathioprine, 6 mercaptopurine, 6 thiguanine S phase. purine analogs decrease de novo purine synthesis avtivated by HGPRT. azathioprine is metabolized into 6 MP
CladribineS phase. purine analog. inhibit DNA polymerase and DNA strand break for hairy cell leukeamia
Cytarabine (arabinofuranosyl cytidine)pyrimidine analog inhibit DNA polymerase
5 flourouracilinhibit thymidilate synthase by forming a complex of 5F-dUMP preventing the dTMP from forming.
methotrexatefolic acid analog competitive inhibition of dihydrofolate reductase preventing the conversion of DHF to THF and thus preventing the synthesis of dTMP and DNA synthesis
bleomycinact on G2 free radicals formation that breaks the DNA strands
dactinomycin ( actinomycin D)intercalates into the DNA
doxyrubicingenerate free radicals that intercalates with the DNA strands and break it.
daunirubicingenerate free radicals that intercalates with the DNA strands and break it
dexrazoxaneiron chelating agent that help prevent the dilated cardiomyopathy induced by daunirubicin and doxirubicin.
busulfanwork on G1 cross links the DNA
cyclophosphamidework on G1 cross links the DNA at guanine N-7 require bioactivation by the liver.MESNA prevents the hgic cystitis caused by it
ifsofamidework on G1 cross links the DNA at guanine N-7 require bioactivation by the liver
cramustine (nitrosurea)work at G1. require bioactivation. cross blood brain barrier to the CNS. cross link DNA
lomustine ( nitrosurea)work at G1. require bioactivation. cross blood brain barrier to the CNS. cross link DNA
semustine ( nitrosurea)work at G1. require bioactivation. cross blood brain barrier to the CNS. cross link DNA
streptozocin (nitrosurea) work at G1. require bioactivation. cross blood brain barrier to the CNS. cross link DNA
paclitaxelwork on M phase. hyperstabilize polymerized microtubules so that mitotic spindles cannot break down - anaphase cannot occur-
vincristinevinca alkaloids prevent the polymerization of the microtubules by binding to b-tubulin so prevent the mitotic spindle from forming. M phase arrest.
vinblastine vinca alkaloids prevent the polymerization of the microtubules by binding to b-tubulin so prevent the mitotic spindle from forming. M phase arrest.
cisplatincross link DNA. work on G1
carboplatincross link DNA . work on G1
etoposide teniposideinhibit topoisomerase II so increase DNA degradation. S AND G2 phases
irinotecaninhibit topoisomerase I so prevent DNA unwinding and replication
topotecaninhibit topoisomerase I so prevent DNA unwinding and replication
hydroxyureainhibit riboneucleutide reductase so inhibit DNA synthesis. S phase
amiofostinewith chloride saline to prevent nephrotoxicity by cisplatin and carboplatin
bevacizumabinhibit the angiogenesis because its a monoclonal antibody against VEGF
erlotinibEGFR tyrosine kinase inhibitor . for non small cell lung cancer. causes rash
ImatinibBCR-ABL ( philadelphia chromosome ) tyrosine kinase inhibitor, and c-KIT inhibition for Gi stromal tumors. causes fluid retention
rituximabmonoclonal AB against CD20 so used in most B cell tumors. increase the risk of progressive multifocal leucoencephalopathy
tamoxifen, raloxifenselective estrogen receptor modulator with antagonist effect on breast and agonist on bone. block the binding of estrogen to ER +ve cells
trastazumabmoboclonal ab against HER-2 a tyrosine kinase receptor kill cells expression HER-2 by antibody-dependant cytotoxicity
vemurafenibsmall molecule inhibitor of BRAF oncogen in melanoma
cromolyn sodiumprevent mast cell degranulation for asthma prophylaxis
RhoGAMto rh negative mothers during the thrid trimester
dimercaprol and EDETAfirst line for ttt of lead posining
succimerfor chelation of lead in lead poisining in children
pyridoxine in the ttt of sidroblastic anemia as a cofactor for ALA synthase
uridine monophosphatettt of orotic acidurea and the aneamia it causes
eculizumabterminal complement inhibitor for paroxysmal nocturnal heamogobinuera
hydroxyureafor sickle cell disease to increase HBF concentration
glucose and hemefor acute intermittent porphyria to decrease the ALA synthase
desmopressinfor heamophilia A because it carrys factor VIII and in von willbrand dse
vitamin AAML
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nephrology

Question Answer
mannitolosmotic diueresis increase tubular fluid osmolarity which increases urine flow and decrease intracranial and intraocular pressure
acetazolamidecarbonic anhydrase inhibitor causes self-limited NAHCO3 diuresis and decrease total body HCO3 stores
loop diuretics, furosamide, bumetanide, torsemidesulfonamide, look diuretic inhibit the cotransport system NA/K/CL of the thick ascending limb of loop of henle. abolish hypertonicity from medulla preventing concentration of urine . stimulate PGE to VD affrent arteriole. increase CA excretion. inhibited by NSAIDS
ethacrynic acidphenoxyacetic acid drevative not sulfonamide loop diuretic. same action as furosamide
thiazides, chlorothiazide, hydrochlorothiazideinhibit NACL reabsorption from DCT decreasing the diluting capacity of nephron. decrease CA excretion
K sparing diureticspironolacone and elepranone r competetive aldosterone receptor antagonists in cortical collecting medulla. triametrine and amiloride act at the same part of the tubule by blocking NA channels in the cortical collecting tubule
spironolacone and elepranone competetive aldosterone receptor antagonists in cortical collecting medulla
triametrine and amiloride blocking NA channels in the cortical collecting tubule
ACE inhibitors, captopril, enalapril, lisinopril, ramiprilinhibit ACE decrease AtII so decrease GFR by preventing constriction of effernt arteriole. levels of renin increase as a result of feedback inhibition. inhibition of ACE also prevents inactivation of bradykinin a potent vasodilator
angiotensin II receptor blockerselectively block binding of angiotensin II to AT1 receptor effects similar to ace inhibitor but ARBS dont increase bradykinin
losartan selectively block binding of angiotensin II to AT1 receptor effects similar to ace inhibitor but ARBS dont increase bradykinin
candesartan selectively block binding of angiotensin II to AT1 receptor effects similar to ace inhibitor but ARBS dont increase bradykinin
valsartan selectively block binding of angiotensin II to AT1 receptor effects similar to ace inhibitor but ARBS dont increase bradykinin
aliskerindirect renin inhibitor prevent conversion of angiotensinogen to angiotensin 1
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cardiovascular

Question Answer
ca channel blockers, amlodipine,celvidipine,nicardipine, nifidepine, nimopidine, dihydropyridine, diltiazime, verapamilblock voltage dependent L type CA channel of smooth and cardiac muscles deacreasing the contractility. vascular smooth ms. amlodipine=nifidepine. verapamil on the heart.
hydralazineincreases cGMP leading to smooth ms relaxation. vasodilates the arterioles more than the veins. afterload reduction.
nitroprussideshort acting increase of the cGMP via direct release of NO. can cause cyanide toxicity
fenoldopamdopamine D1 receptor agonist-cronoary,peripheral,renalmsplachnic vasodilation, decreases the blood pressure and increase naturesis
nitrates, nitroglycrine, isosorbide dinitirite, isosorbide mononitratevasodilates by increasing NO in vascular smooth muscle leading to increase cGMP and smooth muscle relaxation dilates veins more than artries. decrease preload
HMG-coA reductase inhibitors, lovastatin,pravastatin,simvastatin,atrovastatin,rosuvastatininhibit the conversion of HMG-coA to mevalonate a cholesterol precursor decrease mortality in CAD ptns
bile acid resins, cholystyramine, colestipol,colesvelamprevent intestinal reabsorption of bile acids liver must use cholesterol to make more
ezetimibeprevent cholesterol absorption at the small intestine brush border
fibrates, gemifibrazole, colifibrate, bezafibrate, fenofibrateupregulate LPL upregulates TG clearance activate PPAR-alpha to induce HDL synthesis
niacin vit B3inhibits lipolysis (hormone sensitive lipase) in adipose tissue reduces hepatic VLDL synthesis
cardiac glycossides, digoxindirect inhibition of NA/K ATPase indirect inhibition NA/CA exchanger increase Ca leading to positive inotropy stimulates vagus nerve to decrease the heart rate
class 1A antiarrythmics:quinidine, porcainamide, disopyramideincreases the AP duration, increase the effective refractory period in ventricular action potential.increase QT interval
class 1B antiarrythmic:lidocaine, mexiletinedecrease AP duration, prefrentially affect ischemic or depolarized purkinjie and ventricular tissue. phynitoin can also fall into this category
class 1C antiarrythmic:flecainamide, propafenonesignificantly porolong ERF in AV node and accessory bypass tracts.no effect on ERF in purkinjie and ventricular fibers. minimal effect on AP duration
class II antiarrythmic b blocker, metoprolol, propranolol, esmolol, atenolol, carvediloldecreases the SA and AV nodal activity by decreasing the cAMP, decrease CA current, suppress abnormal pacemaker by decrease slope of phase 4. AV node particularly sensitive- increase PR interval. esmolol very short acting
class III antiarrythmic K channel blocker, amiodarone, Ibutilide, defotilide, sotalolincrease AP, increase ERF, increase Q-T interval
class IV antiarrythmic CA channel blocker, verapamil, diltiazimdecrease conduction velocity, increase ERP, increase PR interval
Adenosineincrease K out of the cell, hyperpolarizing the cell and decrease Ica . drug of choice in diagnosing and abolishing supraventricular tachycardia. very short acting, 15sec. effects blunted by theophylline and caffiene
Mgeffective in torsade de pointes and digoxin toxicity
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