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79 Cards in this Set

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tyrosine hydroxylase
tyrosine -> DOPA
(-)metyrosine
Dopa Decarboxylase
(aromatic L-aminoacid decarboxylase)
DOPA -> dopamine
(-) carbidopa
Dopamine b hydroxylase
dopamine -> NE
(-) disulfiram (antabase)
momoamine oxidase
breaks down catecholmines to aldehydes
catechol O methyltransferase
NE -> normetanephrine
Unfractioned heparin
indirect thromnin and Xa inhibitor
LMW heparin
Indirect Xa inhibitor
Less variability and monitoring than heparin
slower clearance than heparin
Protamine
tx for heparin overdose
Fondaparinux
pentasaccharide factor Xa inhibitor
Lepirudin
direct thrombin inhibitor
tx HIT
renal clearance
Argatroban
Direct thrombin inhibitor (active site only), tx HIT, liver metab
Bivalrudin
Direct thrombin inhibitor, tx angioplasty, renal clearance
Hirudin
Direct thrombin inhibitor, leech recombinant protein
Warfarin (Coumadin)
Vitamin K antagonist -- ↓post-translational carboxylase, ↓factor 2,7,9,10,C,S, INR
Aspirin
Irreversibly acylates cyclooxygenase, blocking TxA2 synth
Dipyridamole (Persantine)
Inhibits PDE -> ↑cAMP
ASA w/ Dipyridamole (Aggrenox)
good stroke preventing combination
Ticlopidine (Ticlid)
Inhibit ADP platelet activation, more potent
Clopidogrel (Plavix)
Inhibit ADP platelet activation, less potent
Abciximab (Reopro)
GP IIb/IIIa antagonist prevents fibrinogen binding
Ibopamine
ORAL AGENT FOR ↑ CONTRACTILITY
Dopaminergic agonist
Inamrinone (Amrinone)
ORAL AGENTS FOR ↑ CONTRACTILITY
PDE inhibitor ↑cAMP -> ↑CO and ↓SVR, short-term CHF tx, ↑AV cond, ARR, oral ↑toxic
Milrinone (Primacor)
ORAL AGENTS FOR ↑ CONTRACTILITY
Shorter τ (30 min vs 2.5 h), more selective, fewer side fx (e.g. thrombocytopenia, gi, liver, fever)
Pimobendan
ORAL AGENTS FOR ↑ CONTRACTILITY
PDE inhibitor w/ Ca sensitizing properties
Nesiritide
ORAL AGENTS FOR ↑ CONTRACTILITY
Natriuretic peptide
Omapatrilat
ORAL AGENTS FOR ↑ CONTRACTILITY
Neutral endopeptidase inhibitor—blocks both ACE and natriuretic peptide degradation
Digoxin
INHIBITS NAKATPASE -> ↑ CALCIUM; TREAT CHF, ARRHYTHMIAS;

Preferred, Renal excretion, shorter τ (1.6d), SS@1 wk, metabolized by gut bacteria (10%)
Digitoxin
INHIBITS NAKATPASE  ↑ CALCIUM; TREAT CHF, ARRHYTHMIAS;

No 12-OH, Hepatic metab, longer τ (7d), ss@1 mo
Streptokinase (SK)
Plasminogen activator

1° Non-enzymatic protein from streptococci, indirect, antibodies to drugy -> agg
Urokinase (UK)
Plasminogen activator

1° Trypsin-like enzyme, LMW, direct, (-) PAI-1, non-antigenic
Aniosylated Plasminogen Streptokinase Complex (APSAC)
PLASMINOGEN ACTIVATOR

2° SK and human plasminogen complex -> spontaneous deacylation, long τ (60m), IV bolus, Ab
t-PA (Alteplase)
PLASMINOGEN ACTIVATOR

2° Fibrin/clot-specific binding (1000x), glycosylation, short τ (6m), (-) PAI-1
Reteplase
PLASMINOGEN ACTIVATOR

3° t-PA derivative, kringle #2 and protease domain, non-glycosylated, no EGF -> longer τ (15m)
TNK-t-PA (Tenecteplase)
PLASMINOGEN ACTIVATOR

3° no glycosylation, less PAI-1 effect, ↑ fibrin specificity
Amicar (ε-aminocaproic acid)
Tranexamic acid
PLASMINOGEN ACTIVATOR

Antifibrinolytic – inhibits plasmin to stop bleeding
Quinidine
Intermediate recovery (1-5s), ↑ QRS, QT, APD, blocks Na and K channels;

α receptor block and vagal inhibition; ↑[DIG]
Procainamide -> N-acetylprocainamide (NAPA)
Intermediate recovery (1-5s), ↑ QRS, QT, APD, blocks Na and K channels;

Metabolite blocks K channels only, renal dose adjustment, lupus syndrome
Disopyramide
Intermediate recovery (1-5s), ↑ QRS, QT, APD, blocks Na and K channels;

Aggravates CHF and prostatism, effect ↑ with dose
Lidocaine
Fast recovery (<1s), shorten repolarization

IV, ↓ v-fib, ↑ mortality, CNS toxicity, dose adjustment (CHF and liver)
Mexiletine, Tocainide
Fast recovery (<1s), shorten repolarization

Oral ,CNS toxic
Phenytoin
Fast recovery (<1s), shorten repolarization

Anticonvulsant, effective for digitalis intoxication
Flecainide
Slow recovery, marked ↑PR, ↑QRS, ± QT

Very long τ from block, very effective for isolated PVC, RSVT, ↑DIG
Encainide
Slow recovery, marked ↑PR, ↑QRS, ± QT

↑ mortality post-MI, FDA removed
Propafenone
Slow recovery, marked ↑PR, ↑QRS, ± QT

~ Flecainide, Weak ß blocker (↑ at high conc),
Moricizine
Slow recovery, marked ↑PR, ↑QRS, ± QT

Phenothiazine analog, unique, weaker version, multiple metabolites
Esmolol
Ultra short acting (τ = 9m), nonselective ß blocker, good for testing
Amiodarone
K CHANNEL BLOCKERS, ↑ AP DURATION, ↑ QT

Class I,II,III,IV actions, effective most arr, multiple toxic (esp lung), LONG τ (50d), ↑DIG
Bretylium
K CHANNEL BLOCKERS, ↑ AP DURATION, ↑ QT

No longer marketed, still available – biphasic NE effects (↑ then ↓)
Dofetilide
K CHANNEL BLOCKERS, ↑ AP DURATION, ↑ QT

Pure class III, Renal dose adjustment, causes TdP (1-3%)
Sotalol
K CHANNEL BLOCKERS, ↑ AP DURATION, ↑ QT

Non-selective ß blocker, causes TdP
Ibutilide
K CHANNEL BLOCKERS, ↑ AP DURATION, ↑ QT

Acute IV, stop A-flutter (60%) and A-fib (40%), block K, opens Na, Causes TdP (6%)
*N-acetylprocainamide
K CHANNEL BLOCKERS, ↑ AP DURATION, ↑ QT

Might have some class III effects
Verapamil (phenylalkylamine)
CA CHANNEL BLOCKERS, ↓ HR AND ↑ PR

Most potent AV blocking, hypotensive; AVOID: wide-complex tachy,WPW,CHF,AVblock,DIG
Diltiazem (benzothiazepines)
CA CHANNEL BLOCKERS, ↓ HR AND ↑ PR

IV, AV node blocking w/o hypotension, great for A-fib
Adenosine
Purinergic receptor blocker, ultra-short acting AV blocker (seconds) – acute tx, rapid IV, short Sx
Captopril
↑ BRADYKININ, RENIN, ANG I, ↓ANGIOTENSION II

Sulfhydryl, shorter τ, prostaglandin effect
Fosinopril
↑ BRADYKININ, RENIN, ANG I, ↓ANGIOTENSION II

Phosphinyl, L&K
Trandolapril
↑ BRADYKININ, RENIN, ANG I, ↓ANGIOTENSION II

Carboxyl, L&K
Saralasin
ANGIOTENSIN RECEPTOR BLOCKERS, ↑ ANGIOTENSIN II, FETOTOXIC

Original, IV, partial agonist
Losartan -> EXP-3174
ANGIOTENSIN RECEPTOR BLOCKERS, FETOTOXIC

Non-peptide, short τ, normal-high renin levels, uricosuric effect
Mannitol
MOST OF TUBULE: IV VOLUME EXPANSION (FILTERED, NOT REABSORBED)

IV
Acetazolamide (Diamox)
Proximal tubule: ↓NAHCO3 REABSORPTION (METABOLIC ACIDOSIS), SULFONAMIDES

Tx glaucoma
Furosemide (Lasix)
Thick acending loop: NAKCL2 SYMPORT INHIBITOR, MOST POTENT, CA AND MG LOSS

Releases vasodilator prostaglandin from kidneys  ↑ venous capacitance
Ethacrynic Acid (Edecrin)
Thick acending loop: NAKCL2 SYMPORT INHIBITOR, MOST POTENT, CA AND MG LOSS

Non-sulfamide
Hydrochlorothiazide (HCTZ, Esidrex)
DCT: NACL COTRANSPORT INHIBITOR, ↑ GLU,UREA,CA; ↓ K,H,NA

Sulfonamide, hyperuricemia  gout; tx diabetes insipidus
Amiloride
Collecting Tube: NA CHANNEL INHIBITORS, ↓ K EXCRETION; CAREFUL! (ACEI, ↑K, ARF)

Partially absorbed; inhibits NaH antiporter (lumen) and NaK ATPas (basal); tx Liddle’s
Triamterene
Collecting Tube: NA CHANNEL INHIBITORS, ↓ K EXCRETION; CAREFUL! (ACEI, ↑K, ARF)

Well absorbed, renal and metabolism
Spironolactone -> Canrenone
STEROID ANALOGUES COMPETE WITH ALDOSTERONE, BEST FOR CIRRHOSIS

Affects estrogen receptors (gynecomastia), tx Cohn’s
Nifedipine (1,4-dihydropyridine)
↓ CA -> VASODILATION, LONG ACTING, INHIBIT CYP3A4

L channel, ↑ chronotropy and CO, ↑ symp, variable partition coefficients, oral > sublingual
Verapamil (phenylalkylamine)
L channel, ↓ino, chrono, dromotropy, SVT, L isomer more active, PGP inhibition->DIGItoxic
Diltiazem (benzothiazepines)
L channel, ↓ino, chrono, dromotropy, SVT, PGP inhibition->DIGItoxic
Dantrolene
↓ Ca release -> relax muscles, tx malignant hyperthermia
Nitroglycerin (TNG)
Nitrate ester, Sublingual, high clearance (minutes)
IsoSorbide DiNitrate (Isordil)
Nitrate ester, Oral, variable τ of metabolites, intermediate clearance
Isosorbide MonoNitrates (2-IMN > 5-IMN)
Nitrate ester, 100% bioavailable, less variable, low clearance
**Sildenafil (Viagra)
Inhibits cGMP phosphodiesterase V  ↑postural hypotension
Nitroprusside (Nipride)  NO + CN
Spontaneous conversion to NO + CN, Thiocyanate toxicity (tx Na thiosulfate), no light, short τ
Hydralazine (Apresoline)
Arterial vasodilator, tx HT & CHF
Minoxidil (Loniten)
Arterial vasodilator, tx HT