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150 Cards in this Set

  • Front
  • Back
classes of Rx for HTN (4)
2) sympathopleggics (b blocker, alpha1, central agents)
3) direct vasodilators
hydralazine and minoxidil must be given with what to tx HTN
beta blockers to prevent reflex tachycardia
(these are direct vasodilators)
a direct acting vasodilator for HTN
SE: CN toxicity
besides b blockers what sympathoplegics are used for HTN
central: clonidine, methyldopa
inhib NE rel: reserpine, guanethidine
nicotinic Ach R antagonist=hexamethonium
acetazolamide, mech, where acts
- carbonic anhydrase causing NaHCO3 diuresis, act PCT
use acetazolamide (besides HTN)
urinary alkalinization, metabolic alkalosis, altitude sickness, glaucoma
toxicity of acetazolamide
hyper Cl metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
how acetazolamide affect acid/base of body
causes systemic acidosis (gets rid of alkaline)
furosemide actions
sulfa loop diuretic
1) inhibit Na/K/Cl TAL
2) abolishes hypertonicity of medulla
3) increases Ca excretion
toxicity furosemide
OH DANG: ototoxicity, hypokalemia, dehydration, allergy (ssulfa), nephritis (interstitial), gout
ethacrynic acid, type Rx, use
phenoxyacetic acid derivative acts like furosemide but NOT sulfa. use diuresis in those allergic to sulfa
hydrochlorothiazide, mech, where acts
thiazide diuretic - DCT Na reabsorb, decr Ca excretion
summary 3 most impt diuretics
1) loop-Na/K/Cl of TAL, lose Ca
2) thiazide-(-)Na reabsorb DCT, hold onto Ca
3)spironolactone-competit aldosterone R antagonist in CD
which diuretic for Ca kidney stone
thiazide (holds onto Ca, less Ca in urine)
mannitol use
shock, Rx OD, to decrease ICP/IOP
toxicity mannitol, contraindications
pulmonary edema, dehydration
CI: anuria, CHF
toxicity hydrochlorothiazide
hypoK metab alkalosis, low Na, hyperGLUC (Glycemia, Lipidemia, uricemia, calcemia)
also sulfa allergy
name K sparing diuretics
Spironolactone, triamterene, amiloride, eplereone
mech spironolactone
competitive aldosterone R antagonist in CD
toxicity spironolactone
hyperK, gynecomastia, antiandrogen
amiloride, use, mech
K sparing diuretic, blocks Na in CD
triamterene, use, mech
K sparing diuretic, blocks Na in CD
vasodilator arterioles>veins (afterload reduction)
mech hydralazine
incr cGMP causes s.m. relaxation
toxicity hydralazine
compensatory tachycardia (give w b blocker), fluid retention, Lupus-like
mech of CCB
block voltage dependent L type Ca channels of cardiac and smooth muscle, reduce contractility
compare 3 CCBs effect heart, vascul
verapamil works greatest on heart least on sm m, nifedipine opposite, diltiazem is inbetween
toxicities CCB
cardiac depression, edema, flushing dizziness, constipation
verapamil/dilt: bradycardia, AV block
how tx nephrogenic DI
mech ACEI
inhibit ACE
-decr AII
-prevent inactiv bradykinin (vasodilator)
but renin increases
toxicity ACEI
CAPTOPRIL + hyperkalemia
cough, angioedema, proteinuria, taste changes, hypOtension, Preg, Rash, Increased renin, Lower angII.
isosorbide dinitrate, mech
veins > or < arteries?
a longer acting nitroglycerin, vasodilate by releasing NO, causing incr cGMP and sm m relaxation.
dilates veins>>arteries
use isosorbide dinitrate
(also NG) angina and pul edema
toxicity isosorbide dinitrate
tachycardia, hypotension, HA,
[[Monday disease-industrial exposure dev tolerance during week, Mon get tachycardic, dizzy, HA]]
how nitrates v. b blocker mainly tx angina
nitrates mostly affect preload, b blocker mostly affects afterload
5 ways to reduce myocardial O2 consumption
1) EDV
2) BP
3) contractility
4) HR
5) ejection time
how do nitrates affect
1) EDV
2) BP
3) contractility
4) HR
5) ejection time
(decr preload)
1) decr EDV
2) decr BP
3) incr contractility (reflex)
4) incr HR (reflex)
5) decr ejection time
NET: decr MVO2
how do nitrates and b-blockers given together affect
1) EDV
2) BP
3) contractility
4) HR
5) ejection time
1) - EDV
2) decr BP
3) - contractility
4) decr HR
5) - ejection time
NET big decr MVO2
how do b-blockers affect
1) EDV
2) BP
3) contractility
4) HR
5) ejection time
1) incr EDV
2) decr BP
3) decr contractility
4) decr HR
5) incr ejection time
NET decr MVO2
how do indiv CCB compare to b blocker/ nitrates in tx HTN
nifedipine like nitrate, verapamil like b blocker
compare digoxin and digitoxin
digitoxin has grtr bioavail, much grtr t1/2 (168hrs) bc 70% protein bound, digoxin excreted in urine, digitoxin in biliary (no need adjust in RF)
beware toxicity digoxin in the cases of:
RF, hypoK, quinidine (decreases dig clrnc, displaces digoxin from tissue bind sites)
toxicity digoxin
N/V/diarrhea, blurry yellow vision, arrhythmia
mech digoxin
inhibit Na/K/ATPase but ultimately Na/Ca anitport - reulting in incr intracell Ca
antidote dig toxicity
normalize K, lidocaine, cardiac pacer, anti dig Fab
use dig
CHF, A fib (decr conduction AV node
how dig affect EKG
incr PR, decr QT, scooping of ST, T wave inversion
1st generation H1 blocker
1st generation H1 blocker
1st generation H1 blocker
2nd generation H1 blocker
2nd generation H1 blocker
name 1st gen H1 blockers
diphenhydramine, dimenhydrinate, chlorpheniramine
name 2nd gen H1 blockers
loratadine, fexofenadine, desloratadine
toxicity 1st gen H1
sedation, antimuscarinic, anti alpha adrenergic
toxicity 2nd gen H1
less sedation, antimuscarinic, anti alpha adrenergic
use of H1 blocker
allergy, motion sickness, sleep aid
(2nd gen just allergy)
neutrophil chemotactic agent
bronchoconstriction, contraction sm m, incr vascular perm
(along with D4, E4)
inhibits platelet aggreg and incr vasodilation
which Rx inhibit leukotrienes
zafirlukast, montelukast
affects thromboxane
-incr plat aggreg
-incr vascular tone
-incr bronchial tone
affects prostaglandins
-incr uterine tone
-decr vascular tone
-decr bronchial tone
affect prostacyclin
decr plt aggreg, vascular tone, bronchial tone, uterine tone
where do steroids work
inhibit phospholipase A2 and protein syn leading to COX
leukotrienes are derived from what
inhibits lipoxygenase
classes asthma drugs
2) b2 agonist
3) muscarinic antag
4) cromolyn
5) methylxanthine (theophylline)
6) anti-leukotrienes
salmeterol, use, SE
long acting b2 for prophylaxis in asthma,
SE: tremor, arrhythmia
theophylline, mech, SE
mech: inhibit phosphodiesterase incr cAMP causing bronchodilation
SE: cardiotoxicity, neurotoxicity with narrow therapeutic index
ex muscarinic antagonist used in asthma
cromolyn, mech, use, SE
prevents rel mediators from mast cells.
use: only prophylaxis (not acute)
SE: rare
steroid often used in asthma
name 2, give mech action steroids for asthma
beclomethasone, prednisone
mech: inhibits syn of all cytokines. inactivates NFkB (t factor for TNFa).
1st line for CHRONIC ASTHMA
name antiluekotrienes and mech
Zileuton-5-lipoxygenase inhibitor blocks conversion arachidonic acid to leukotrienes
Zafirlukast, montelukast-block leukotriene R
describe early and late response in asthma and tx
early response= bronchoconstriction, tx b agonist, muscarinic antag, theophylline
late response=inflamm/bronchial hyperreactivity, tx steroids
compare/contrast b agonist, theophylline MOA
both act to increase cAMP to cause bronchoconstriction, b agonist incr AC, theophylline - PDE (which degrades cAMP)
compare/contrast where asthma Rx act on pathway causing symptoms
cromolyn and steroids prevent mediator release, the others block mediators effects
name H2 blockers (4)
cimetidine, ranitidine, famotidine, nizatidine
SE cimetidine
1) inhibit P450
2) anti androgen
3) incr creatinine
SE H2 blockers
minimal beside cimetidine
cimetidine SE:
1) inhibit P450
2) anti androgen
3) incr creatinine
use H2 blockers
PUD, gastritis, mild GERD
name PPI (2)
omeprazole, lansoprazole
mech PPI
irreversibly inhibit H/K/ATPase in parietal cells
use PPI (and how differ from H2 blocker)
PUD, gastritis, GERD, ZE
(H2 don't use for ZE)
name 2 anti-ulcer agents
bismuth, sucralfate
sucralfate, MOA
bind to ulver base and allow HCO3 to reestablich pH gradient--cannot be used with antacids of H2 blockers bc need acid to polymerize
misoprostol, type Rx, use (3)
PGE1 analog (increase production and sxn gastric mucous barrier).
use: prevent NSAID induced PUD, maintain PDA, induce labor
SE misoprostol
diarrhea, abortifacient
infliximab, mech, use
monoclonal Ab TNFa,
use: Crohns, RA
infliximab toxicity
respir infxn, F, hypotension
sulfsalazine, mech, use
combo of sulfapyridine (antibacterial) and mesalamine (anti inflamm)
use: UC, Crohns
toxicity sulfsalazine
malaise, N, sulfonamide toxicity
SE calcium carbonate antacid use
hypercalcermia, rebound acid increase
SE for ALL antacid over use
SE AlOH antacid overuse
constipation, hypophosphatemia
advantages of LMWH
-better bioavail
-(2-4)x t1/2
-no lab monitoring
BUT not easily reversible
mech heparin
how monitor?
activates antithrombin III, decr thrombin and Xa
Heparin, intrinsic "HIT"
PT think:
warfarin, extrinsic "wet pet"
lab monitor LMWH
factor Xa (not usu necessary)
heparin use
immed anticoag (PE, stroke, angina, MI, DVT)
can be used in preg (doesn't cross placenta)
reversal of heparin, mech
protamine sulfate positively charged binds negative heparin
toxicity heparin
bleeding, thrombocytopenia/HIT, drug-drug interactions
mech Warfarin
monitor by
interferes syn and gamma carboxylation vit K factors II, VII, IX, X, prot C, S
compare contrast warfarin and heparin: structure
heparin: large anionic, acidic polymer
warfarin: small lipid soluble
compare contrast warfarin and heparin: site action
hep: blood
warfarin: liver
compare contrast warfarin and heparin: onset
hep: rapid
warf: slow (limited by t1/2 of factors)
use warfarin
chronic anticoag, cannot be used in preg (crosses placenta)
toxicity warfarin
bleeding, teratogen, drug-drug interactions
compare contrast warfarin and heparin: reversal
hep: protamine sulfate
warf: IV vit K, FFP
on initial starting of warfarin...
start with heparin, bc warfarin can initially cause pro-coag state bc Prot C has shortest 1/2 life, is affected before the others
mech of thrombolytics
acitvate plasmin (major fibrinolytic ensyme), tPA specifically targets fibrin bound plasminogen
what directly opposes thrombolytics
aminocarpoic acid which inhibits fibrinolysis
contraindications thrombolytics
bleeding, hx intracranial bleed, recent sx, severe HTN
name thrombolytics
streptokinase, urokinase, tPA (alteplase), APSAC (anistreplase)
does ASA affect PT, PTT?
toxicity ASA
ulcer, bleeding, Reye's syndrome, tinnitus, hypervent
inhibits plat aggreg by irrev blocking ADP R, inhibits fibrinogen binding by preventing gpIIb/IIIa expression
inhibits plat aggreg by irrev blocking ADP R, inhibits fibrinogen binding by preventing gpIIb/IIIa expression,
binds gp R IIa/IIIb on activated platelets
toxicity clopidogrel, ticlopidine
neutropenia (ticlodipine)
toxicity abciximab
bleeding, thrombocytopenia
summarize anti coag agents
-ASA via COX - TXA2
-ADP R blockers (clopidogrel, ticlopidine)
-gpIIb/IIIa R blocker (abciximab)
leuprolide, mech, use
GnRH analog agonist when pulsatile, antagonist when continous
1) infertility (pulse),
2) prostate ca (cont),
3) uterine fibroids
toxicity leuprolide
antiandrogen, N/V
propylthiouracil, mech, use
inhibit organification and coupling thyroid H syn, decr peripheral conversion T4 to T3
use: hyperthyroidism
methimazole, mech, use
inhibit organification and coupling thyroid H syn
use: hyperthyroidism
toxicity methimazole
rash, aplastic anemia, agranulocytosis (rare)
note: same SE as for PTU
toxicity PTU
rash, aplastic anemia, agranulocytosis (rare)
(same SE as methimazole)
name antiandrogens and use (4)
finasteride (5a reductase inhib, BPH, baldness)
flutamide (inhib androgens at testost R, prostate ca)
ketoconazole, spironolactone (inhib steroid syn, used polycistic ovarian syn to prevent hirsutism)
inhib steroid syn used polycystic ovarian syn to prevent hirsutism
name glucocorticoids (5)
hydrocortisone, prednisone, dexamethasone, beclomethasone, *triamcinolone
5a reductase inhib,
use: BPH, baldness
inhib androgens at testost R,
use: prostate ca
use steroids
addison's, inflamm, immune suppression, asthma
toxicity steroids
iatrogenic Cushing-buffalo hump, moon facies, truncal obesity, mscl wasting, thin skin, bruising, osteo, adrenocortical atrophy, PUD
tx erectile dysfxn (3), mech
sildenafil, vardenafil, tadafil
mech: - cGMP PDE causing incr cGMP, sm m relax in corpus cavernosum, incr BF, erection
toxicity sildenafil
HA, flushing, dyspepsia, blue-green vision
**risk hypotension w nitrates
clomiphene, mech, use
partial agonist at estrogen R in pituitary, preventing feedback inhib cause incr rel LH, FSH
use: infertility
toxicity clomiphene
hot flashes, ovarian enlargement, multiple preg, visual
mifepristone, mech, use
competit inhib progestins at progesterone R
use: abortion
AKA RU-486
toxicity mifepristone
heavy bleeding, N/V, anorexia, abd pain
tx acute gout
NSAIDs, often indomethacin
colchicine, mech, use
depolymerizes microtubules - leuko chemotaxis and degranulo,
use: acute gout, but not commonly used 2/2 SE (esp GI when given orally)
probenecid, mech, use
- uric acid (also inhib sxn PCN),
use: chronic gout
complication probenacid
inhib sxn PCN
allopurinol, mech, use (2)
inhibits xanthine oxidase (conversion xanthine to uric acid)
use: chronic gout, tumor lysis syndrome
advantages, disadvantages OCP
+: reliable, decr endomet and ovarian ca, decr ectopic preg and pelvic infxn
-: daily, no protection STDs, incr TG, hypercoag, wgt gain, N, depression, HTN