Cardio Flashcards

1
Q

Ca Blockers

A

Amlodipine, nomodipine, nifedipine (dyhidropurine)

Diltiazem, verapimil (non-dihydropuridine)

Block voltage gated L-type Ca channels of cardiac and smooth muscle, reduce contractility
Vascular SM- amlodipine and nifedipine
Cardiac- Verapamil

amlodipine and nifedipine- HTN, angina (including prinzmetal), raynaud, isolated systolic HTN
non-dihydropuridine- HTN, angina, A fib
Nimodipine- subarachnoid hemorrhage

can all cause AV block, edema, hyperprolactinemia, constipation

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2
Q

Hydralazine

A
increase cGMP, smooth muscle relaxation
mostly vasodilates arterioles (dec. afterload)
Severe HTN, HTN in pregnancy (w/ mdopa)
give w/ b blocker for reflex tachy
can cause lupus-like syndrome
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3
Q

Nitroprusside

A

HTN emergency
releases NO to increase cGMP
can cause cyanide toxicity

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4
Q

Fenoldopram

A

D1 receptor agonist
coronary, peripheral, renal, splanchnic dilation
decrease BP and increase natriuresis

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5
Q

Nitroglycerine and isosorbide dinitrate

A

increase cGMP
dilate veins more than ateries (dec. preload) (main way reduces pain in angina)
reflex tachy, monday disease in industrial work
lose tolerance over weekend

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6
Q

Statins

A

inhibit HMG-CoA to mevalonate

hepatotoxic, rhabdomyolysis (especially w fibrates and niacin)

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7
Q

niacin

A
decrease LDL and increase HDL
inhibits peripheral lypolysis and VLDL synthesis
Flushed face (give aspirin)
hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)
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8
Q

Bile acid resins

A
Cholestyramine, colestipol, colesevelam
prevents reabsorbion of bile salts
people hate it
decreased fat soluble vitamins
cholesterol gallstones
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9
Q

Ezetimbe

A

blocks cholesterol abs at brush border

causes DIARRHEA

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10
Q

Fibrates

A

Gemfibrozil, clofibrate, bezafibrate
Lowers TGs
upregulates LPL (TG clearance) and activates PPAR-a to induce HDL synthesis a bit
myositis (esp w/ statins)
Cholesterol gallstones (esp w/ bile acid resins)
hepatotoxicity

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11
Q

Digoxin

A

cardiac glycoside
Direct inhibition of Na/KATPase secondarily blocks Na/Ca antiport. More intracellular Ca increases inotropy. stimulates vagus nerve to decrease HR
Use in CHF and A fib (decreased conduction at AV node
ECG- inc PR, dec QT, ST scooping, T inversion
can lead to hypokalemia which is bad
cholinergic- N/V, blurry vision
renal failure decreses excretion
hypokalemia is permissive for dig binding at K binding site
verapamil, amiodarone and quinidine decreases clearance and displaces from tissue binding sites

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12
Q

Class 1 antiarrhythmics in general

A

Na channel blockers
slow or block conduction especially in depolarized cells
decrease phase 0 slope
increase threshold for abnormally firing pacemaker cells

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13
Q

Class 1a antiarrhythmics

A

Disopyramide, quinidine, procainamide
increases AP duration, QT and ERP
use in both atrial and ventricular arrhythmias especially reentrant and ectopic SVT
quinidine- headache and tinnitis
procainamide- SLE like
disopyramide- HF
all thrombocytopenia and torsades de point due to increased QT

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14
Q

Class 1b antiarrhythmics

A

Lidocaine, mexiletine
decreases AP duration
preferentially affects ischemic and depolarized
acute ventricular arrhythmias (esp post MI) and digitalis induced arrhythmias
can cause CN and cardiac depression

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15
Q

Class 1c antiarrhythmics

A

flecainide, propafenone
Significantly prolongs refractory period in AV node, minimal effect on AP duration
SVTs and LAST RESORT in refractory VT
proarrhythmic post MI (contraindicated in structural and ischemic heart disease)

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16
Q

Class 2 antiarrhythmics

A

B blockers
Decrease SA and AV nodal activity by decreases cAMP and Ca
suppresses abnormal pacemakers by decreasing slope of phase 4
AV node particularly sensitive, increases PR
esmolol very short acting
use in SVT to slow ventricular rate
can cause impotence, exacerbate asthma, mask hypoglycemia
metropolol- dyslipidemia
propanolol- exacerbate prinzmetal vasospasm
dont give to cocaine users (a agonist spike)

17
Q

Class 3 antiarrhythmics

A

K channel blockers
Amiodarone, ibutilide, dofetilide, sotalol (AIDS)
increases AP duration, ERP, QT
use when other antiarrhythmics fail
a fib, A and S for V tach
Sotalol- torsades de pointes, high B blockade
ibutilide- torsades de pointes
amiodarone- pulm fibrosis, hepatotoxic, thyroids, blue/grey corneal and skin deposits, photodermatitis and neurologic effects
Test PFT, LFT, TFT when using amiodarone

18
Q

Class 4 antiarrhythmics

A

Ca channel blockers
Verapimil and diltiazem
decreases conduction velocity and increases ERP and PR
Prevent nodal arrhythmias and rate control Afib
constipation and flushing

19
Q

Adenosine

A

Increase K out of cells, hyperpolarizing and decreasing intracellular calcium
drug of choice in diagnosing/abolishing SVT
very short, can cause chest pain. flushing
blocked by theophylline and caffeine
vasodilates coronary arteries, can result in coronary steal
used in imaging to mimic vasodilation seen in exercise

20
Q

Mg2+

A

effective in torsades de pointes and digitoxin toxicity