Cardio Flashcards by Nancy Lan | Brainscape

Q

T-wave inversion
Increase PR
Decrease QT

A

Toxicity for digoxin

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Q

Blurry yellow vision

A

Toxicity for digoxin

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Q

essential HTN

A

ACD

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Q

CHF

A

ABD(K+ sparing)

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Q

DM

A

ABCD

alpha blocker

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Q

nifedipine

A

Work best in vascular, worst in heart
CCB, L-type calcium channels of cardiac and smooth muscle
decrease contractiliy
used in HTN, angina, arrhythmia(not this one), Prinz, raynaud
TOX: cardiac depression:AV block,
edema, flushing,constipation

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Q

verapamil

A

Work worst in vascular, best in heart(ve for ventricle)
CCB, L-type calcium channels of cardiac and smooth muscle
decrease contractiliy
used in HTN, angina, arrhythmia, Prinz, raynaud
TOX: cardiac depression:AV block,
edema, flushing,constipation

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Q

diltiazem

A

Work adverage in vascular, adverage in heart
CCB, L-type calcium channels of cardiac and smooth muscle
decrease contractiliy
used in HTN, angina, arrhythmia(not this one), Prinz, raynaud
TOX: cardiac depression:AV block,
edema, flushing,constipation

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Q

amlodipine

A

Work best in vascular, worst in heart
CCB, L-type calcium channels of cardiac and smooth muscle
decrease contractiliy
used in HTN, angina, arrhythmia(not this one), Prinz, raynaud
TOX: cardiac depression:AV block,
edema, flushing,constipation

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Q

hydralazine

A

increase cGMP–>smooth muscle relaxation, A>V
1st line for HTN in pregnancy with methyldopa
co administer with beta-blocker to prevent tachy
tox: compensatory tachy,
Lupus-like

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Q

nitroprusside

A

malignant HTN
short acting: increase cGMP via direct release of NO,
cause cyanide toxicity

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Q

fenoldopam

A

malignant HTN
D1 receptor agonist: coronary, periperal, renal, splanchic vasodilation
decrease BP and increase natriuresis

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Q

nicardipine

A

CCB

malignant HTN and angina

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Q

clevidipine

A

CCB

malignant HTN and angina

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Q

labetalol

A

beta+alpha blocker

malignant HTN

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Q

nitroglycerin

A

vasodilate by releasing NO in smooth muscle, causing increase in cGMP and smooth muscle relaxation
Dilate V>A, decrease preload
Use: angina, pulmonary edema
TOX: reflex tachy, hypotension, flushing, headache. “Monday disease”, diminished response over repeated use

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Q

isosorbide dinitrate

A

vasodilate by releasing NO in smooth muscle, causing increase in cGMP and smooth muscle relaxation
Dilate V>A, decrease preload
Use: angina, pulmonary edema
TOX: reflex tachy, hypotension, flushing, headache. “Monday disease”, diminished response over repeated use

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Q

lovastatin

A

HMG-CoA reductase inhibitor
decrease LDL, increase HDL, decrease TG
inhibit conversion of HMG-CoA to mevalonate a chol precursor
TOX: hepatotoxicity, increase LFTs,
rhabdomyolysis (increase risk with therapy of gemfibrozil and nicotinic acid)

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Q

provastatin

A

HMG-CoA reductase inhibitor
decrease LDL, increase HDL, decrease TG
inhibit conversion of HMG-CoA to mevalonate a chol precursor
TOX: hepatotoxicity, increase LFTs,
rhabdomyolysis (increase risk with therapy of gemfibrozil and nicotinic acid)

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Q

simvastatin

A

HMG-CoA reductase inhibitor
decrease LDL, increase HDL, decrease TG
inhibit conversion of HMG-CoA to mevalonate a chol precursor
TOX: hepatotoxicity, increase LFTs,
rhabdomyolysis (increase risk with therapy of gemfibrozil and nicotinic acid)

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Q

atorvastatin

A

HMG-CoA reductase inhibitor
decrease LDL, increase HDL, decrease TG
inhibit conversion of HMG-CoA to mevalonate a chol precursor
TOX: hepatotoxicity, increase LFTs,
rhabdomyolysis (increase risk with therapy of gemfibrozil and nicotinic acid)

Q

rosuvastatin

A

HMG-CoA reductase inhibitor
decrease LDL, increase HDL, decrease TG
inhibit conversion of HMG-CoA to mevalonate a chol precursor
TOX: hepatotoxicity, increase LFTs,
rhabdomyolysis (increase risk with therapy of gemfibrozil and nicotinic acid)

Q

Nacin

Vit B3

A

decrease LDL, increase HDL, decrease TG
inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation.
TOX: Red, flushed faces, decreased by aspirin or long term use
hyperglycemia (acanthosis nigrican)
hyperuricemia (exacerbates gout)–>尿糖

Q

cholestyramine

A

bile acid resins
decrease LDL, slight increase in HDL, slight increase in TG
prevent intestinal reabsorption of bile acids; liver must use chol to make more
patients hates it!!!!!!!!!!!!!! taste bad and GI discomfort
decrease absorption of fat-soluble vit. Chol Gall stone

Q

colesevelam

A

bile acid resins
decrease LDL, slight increase in HDL, slight increase in TG
prevent intestinal reabsorption of bile acids; liver must use chol to make more
patients hates it!!!!!!!!!!!!!! taste bad and GI discomfort
decrease absorption of fat-soluble vit. Chol Gall stone

Q

colestipol

A

bile acid resins
decrease LDL, slight increase in HDL, slight increase in TG
prevent intestinal reabsorption of bile acids; liver must use chol to make more
patients hates it!!!!!!!!!!!!!! taste bad and GI discomfort
decrease absorption of fat-soluble vit. Chol Gall stone

Q

ezetimibe

A

Chol absorption blockers
decrease LDL
prevent chol reabsorption at small bowel brush boarder
rare increase in LFTs
diarrhea

Q

gemfibrozil

A

fibrates
decrease LDL, increase HDL, huge decrease TG
up-regulate LPL–>increase TG clearance
TOX: myositis, hepatotoxicity, Chol gall stone

Q

Digoxin

A

inhibition of Na/K/ATPase, indirectly inhibit Na/Ca–>increase Ca
use in: CHF, atrial fibrillation
TOX: cholinergic-N/V, diarrhea, blurry yellow vision
ECG: increase PR, decrease QT, ST scooping, T-wave inversion, AV block
hyperkalemia (poor prognosis)

Q

factor that predisposing digoxin toxic

A

renal failure: excretion
hypokalemia: permissive for digoxin binding at K-binding site
quinidine: decrease clearance
decrease blood level: colestipol(decrease absorption), Glyburide (decrease blood level, DM), pheytoin (increase metabo, seizure) , sulfasalazine(decrease blood level, IBD)

Q

antidote for digoxin

A

K regulation
lisocaine
cardiac pacer
anti-digoxin Fab fragments
Mg2+

Q

quinidine

A

Class IA, hyperK cause increase toxicity
decrease slop of phase 0, increase AP, increase ERP, increase QT
atrial and ventricular, reentry ectopic supraventricular and ventricular
Cinchonism-headache, tinnitus, long QT, torsade, thrombocytopenia

Q

procainamide

A

Class IA, hyperK cause increase toxicity
decrease slop of phase 0, increase AP, increase ERP, increase QT
atrial and ventricular, reentry ectopic supraventricular and ventricular
TOX: SLE-like, long QT, torsade, thrombocytopenia

Q

Disopyramide

A

Class IA, hyperK cause increase toxicity
decrease slop of phase 0, increase AP, increase ERP, increase QT
atrial and ventricular, reentry ectopic supraventricular and ventricular
TOX: heartfailure, long QT, torsade, thrombocytopenia

Q

Lidocaine

A

Class IB, hyperk increase toxicity!
decrease slop of phase 0, decrease AP
used in ischemic or depolarized purkinje and ventricular tissueuseful in acute ventricular arrhythmias(post-MI) and digitalis induced
TOX: local anesthetic, CNS stimulation, depression, cardiovascular depression

Q

Mexiletine

A

Class IB, hyperk increase toxicity!
decrease slop of phase 0, decrease AP
used in ischemic or depolarized purkinje and ventricular tissueuseful in acute ventricular arrhythmias(post-MI) and digitalis induced
TOX: local anesthetic, CNS stimulation, depression, cardiovascular depression

Q

Tocainide

A

Class IB, hyperk increase toxicity!
decrease slop of phase 0, decrease AP
used in ischemic or depolarized purkinje and ventricular tissueuseful in acute ventricular arrhythmias(post-MI) and digitalis induced
TOX: local anesthetic, CNS stimulation, depression, cardiovascular depression

Q

flecainide

A

Class IC
decrease slop of phase 0, no effect on AP duration
ventricular tachy–> to VF and in intractable SVT
LAST RESORT! for pt without structural abnormalities
TOX: proarrhythmic, especially post-MI (CI)
significant prolong refractory in AV

Q

propafenone

A

Class IC
decrease slop of phase 0, no effect on AP duration
ventricular tachy–> to VF and in intractable SVT
LAST RESORT! for pt without structural abnormalities
TOX: proarrhythmic, especially post-MI (CI)
significant prolong refractory in AV

Q

Metoprolol

A

Beta blocker: Decrease SA and AV nodal activity by decrease cAMP, decrease Ca currents, AV particularly sensitive-increase PR
suppress abnormal pace makers by decrease slope of phase 4
Used in Vent tachy, SVT, A Fibrillation and flutter
TOX: impotence exacerbation of asthma, cardiovascular effects (brady, av block, CHF), CNS effects(sedation), mask hypoglycemia,
“DYSLIPIDEMIA”

Q

propranolol

A

Beta blocker: Decrease SA and AV nodal activity by decrease cAMP, decrease Ca currents, AV particularly sensitive-increase PR
suppress abnormal pace makers by decrease slope of phase 4
Used in Vent tachy, SVT, A Fibrillation and flutter
TOX: impotence exacerbation of asthma, cardiovascular effects (brady, av block, CHF), CNS effects(sedation), mask hypoglycemia,
“VASOSPASM in PRINZ angina”

Q

esmolol

A

Beta blocker: Decrease SA and AV nodal activity by decrease cAMP, decrease Ca currents, AV particularly sensitive-increase PR
suppress abnormal pace makers by decrease slope of phase 4
Used in Vent tachy, SVT, A Fibrillation and flutter
TOX: impotence exacerbation of asthma, cardiovascular effects (brady, av block, CHF), CNS effects(sedation), mask hypoglycemia

Q

atenolol

A

Beta blocker: Decrease SA and AV nodal activity by decrease cAMP, decrease Ca currents, AV particularly sensitive-increase PR
suppress abnormal pace makers by decrease slope of phase 4
Used in Vent tachy, SVT, A Fibrillation and flutter
TOX: impotence exacerbation of asthma, cardiovascular effects (brady, av block, CHF), CNS effects(sedation), mask hypoglycemiaa

Q

timolol

A

Beta blocker: Decrease SA and AV nodal activity by decrease cAMP, decrease Ca currents, AV particularly sensitive-increase PR
suppress abnormal pace makers by decrease slope of phase 4
Used in Vent tachy, SVT, A Fibrillation and flutter
TOX: impotence exacerbation of asthma, cardiovascular effects (brady, av block, CHF), CNS effects(sedation), mask hypoglycemiaa

Q

Amiodarone

A

K channel blocker- CHECK PFT, LFT, TFT!
increase AP, increase ERP, used when all other fail, increase QT
TOX: pulmonary fibrosis, hepatotoxic, hypo/hyper thyroid (40% Iod),
corneal depostion, skin deposition(blue/gray)->photodermatitis
neurologic effects, constipation, CV effects(brady, heart block, CHF)
has class I, II, III, IV effects because it alters lipid membrane

Q

Ibutilide

A

K channel blocker-
increase AP, increase ERP, used when all other fail, increase QT
TOX: torsade

Q

dofetilide

A

K channel blocker-
increase AP, increase ERP, used when all other fail, increase QT
TOX:

Q

Soltalol

A

K channel blocker-
increase AP, increase ERP, used when all other fail, increase QT
TOX: torsades, de pointes, excessive beta block

Q

verapamil

A

CCB: decrease conduction velocity
increase ERP increase PR interval.
used in prevention of nodal arrhythmias (SVT)
TOX: constipation, flushing, edema, CV effects(CHF, AV block, sinus node, depression)

Q

dilatiazem

A

CCB: decrease conduction velocity
increase ERP increase PR interval.
used in prevention of nodal arrhythmias (SVT)
TOX: constipation, flushing, edema, CV effects(CHF, AV block, sinus node, depression)

Q

adenosine

A

K out of cells–> hyper polarizing the cell + decrease Ca.
Drug of choice in diagnosis/ abolishing SVT!!!
very short acting
tox: flushing, hypotension, chest pain. effects blocked by theophyllin and caffeine

Q

Mg

A

effective in torsade and digoxin toxicity

MgSO4 also used in eclampsia