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Pharm Test 2 > Cardiac Pt 2 > Flashcards

Cardiac Pt 2 Flashcards

1
Q

What do antiangial drugs treat

A

Symptoms cause by inadequate coronary blood flow associated with vasospasms/stress/exercise/athersclerosis

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2
Q

Examples of antiangials and MOA

A

Propranolol- beta antagonist that decreases cardiac output. Decreases the work of the heart and decreases myocardial anoxia

Nitroglycerin- stimulates NO production, induces coronary vasodilation and increases oxygen delivery to the myocardium

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3
Q

Why is sublingual forms of nitroglycerin ineffective when swallowed?

A

High first pass effect. Better to bypass the stomach

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4
Q

Treatment for cardiac arrest

A

Epinephrine or isoproterenol are b1 agonist in cardiac tissue increase sns activity of SA node that can induce myocardial systole (contractions)

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5
Q

What reduces the spread of necrosis from myocardial infarctions

A

Treat with fibrolytic drugs that dissolve blood clots.

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6
Q

Which drugs serve as enzymes that catalyze plasmin formation within a clot that leads to fibrolysis

A

Tissue plasminogen activator (tpa), streptokinase, urokinase

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7
Q

Flow of plasminogen to reduce anoxia and spread of necrosis

A

Plasminogen to plasmin, catalyzes the depolymerization (scaffolding) of fibrin network within a clot, fibrolysis, reinstates blood flow, and reduce anoxia and spread of necrosis

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8
Q

Amiodarone

A

Class iii potassium channel blocker. Used to control a fib and v tach caused by ectopic foci (pacemakers outside of SA node) aka beat is being made outside of SA node. its effects are mediated by inhibition of sodium and calcium channels

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9
Q

The direction of ion movement across membranes during an action potential is influenced by what?

A

The concentration gradients of ions and membrane permeability

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10
Q

Phase 0 cardiac action potential

A

Fast sodium channels open and rapid influx of sodium. Rapid depolarization (systole)

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11
Q

Phase 1 cardiac action potential

A

Sodium channels close, potassium channels start to open.

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12
Q

Phase 2 cardiac action potential

A

Calcium channels open, potassium channels are still open

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13
Q

Phase 3 cardiac action potential

A

Calcium channels close, potassium still open

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14
Q

Phase 4 cardiac action potential

A

Potassium channels finally close.

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15
Q

Amiodarone toxic side effects

A

Lung fibrosis, thyroid damage (amio has iodine), liver damage

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16
Q

What happens when the enzyme that break down bradykinin is inhibited by the ace inhibitor

A

Bradykinin accumulates along the respiratory airway and stimulates an inflammatory like condition that makes a chronic cough

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17
Q

Good side effect of accumulation of bradykinin

A

Stimulates myocardial fibrolysis that reduces progression of cardiac remodeling which prolongs the life of patients with cardiac failure

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18
Q

What are first line treatments of patients with symptoms of fluid overload

A

Diuretics (thiazide/loop) combined with ace and arb

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19
Q

Tolvaptan

A

Oral vasopressin (antidiuretic hormone) antagonist that is used to treat hyponatremia/hypervolemia is secondary to end stage heart failure

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20
Q

Why do you need to be careful with dosing for metoprolol in heart failure

A

May block heart too much that can make heart failure worse

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21
Q

Ivabradine

A

Selectively inhibits a unique sodium potassium ion channel in the SA node of the heart that reduces pacemaker activity and lowers heart rate

22
Q

Digoxin and other cardiac glycosides

A

Produce a positive inotropic effect on the myocardium which increases cardiac output that helps tissue perfusion

23
Q

Entresto combo med

A

Neprilysin inhibitor (sacubitril) *it is not ace inhibitor * and angiotensin ii receptor blocker ARB (valsartan)

24
Q

Neprilysin is an enzyme that breaks down what

A

Natriuretic peptides like ANP

25
Q

Potent natriuretic and vasodilators properties, Inhibit rass, reduce sympathetic drive, have antiproliferative and antihypertrophic effects

A

Natriuretic peptides have

26
Q

Hdl

A

Good cholesterol - removed cholesterol from the walls

27
Q

LDL

A

Bad, cling onto arteries walls

28
Q

Do we make cholesterol endogenously?

A

Yes through acetyl CoA. Cholesterol used to make steroids

29
Q

Exogenous cholesterol is from what?

A

Diet- animal proteins

30
Q

Hyperlipidemia is associated to which cholesterol

A

LDL

31
Q

Hyperlipidemia is associated to which cholesterol

A

LDL

32
Q

Lovastatin

A

Hepatic 3 hydroxy 3 methyl glutarate (HMG) coenzyme e reductase inhibitor which suppresses lipoprotein synthesis

33
Q

Inhibits hepatic triglyceride synthesis thus suppressing lipoprotein synthesis

A

Gemfibrozil

34
Q

Inhibits hepatic triglyceride synthesis thus suppressing lipoprotein synthesis (increases production of hdls that activate reverse cholesterol transport from peripheral vascular beds )

A

Gemfibrozil

35
Q

Niacin

A

Triglyceride lipase inhibitor in adipose tissue that reduces hepatic triglyceride synthesis and lipoprotein synthesis

36
Q

Ion exchange resin that binds to bile salts and results in their elimination through the feces. Hepatic production of cholesterol is diverted from production of lipoproteins to bile salts

A

Cholestryamine

37
Q

Ezetimibe

A

Inhibitor of cholesterol transport protein, blocks absorption of dietary cholesterol and cholesterol that enters the entrohepatic circulation

38
Q

Why might the combo of ezetimibe and simvastatin be expected to have a great effect on blood levels of ldl then a mono therapy with a hmg-coa reductase inhibitor?

A

Working on two different systems.

39
Q

Evolocumab (repatha)

A

Enzyme inhibitor of proprotein convertase subtitlisin/kexin type 9 ( PCSK9) that controls destruction of LDL receptors ( LDLRs) on many tissues including the liver

40
Q

What hyperactive gene causes hypercholesterolemia that leads to early death from CAD

A

PCSK9

41
Q

Circulating PCSK9 proteins bind to and control the destruction of ______ that arises in the uptake and metabolism of ____ _____ in the liver

A

LDL receptors (LDLRs)
LDL cholesterol

42
Q

Aspirin

A

Inhibits cyclooxygenase ( COX) which reduces thromboxane production (reduce platelet adhesion)

43
Q

ADP receptor antagonist on platelets

A

Clopidogrel (plavix)

44
Q

Tirofiban

A

Serves as an antagonist to the GPIIb/IIIa platelet receptor which blocks platelet binding to fibrinogen in an area of platelet plug formation

45
Q

Protease activated receptors (par-1) mediate thrombins effects on platelet aggregation.

______ is a selective inhibitor of par-1 on platelets

A

Vorapaxar (zontivity)

46
Q

How is intrinsic pathway activated ?

A

Internal damaged tissues ex. sepsis, inflammation

47
Q

How is extrinsic pathway activated

A

A trauma ex, fall; injury

48
Q

Warfarin facts

A

Inhibits vitamin k depending clotting factors. (Inhibits 7 on extrinsic, 9, 10 on intrinsic) Onset time is delayed, limit vitamin k rich foods, need blood testing inr/pr, dose adjusted to blood test, antidote is available

49
Q

Dabigatran

A

Reversible inhibition of thrombin, onset time is rapid (hours), few food drugs interactions, no blood testing, fixed dose, less bleeding

50
Q

Fibrolytic drugs like TPA are known _____ ______ . They are used to dissolve ______ blood clots

A

Clot busters, Pre-formed

51
Q

Heparin

A

Inhibit the functions of the clotting cascade in the blood which prevents blood clot formation, treats pulmonary embolisms, DVT

Pharm Test 2 (5 decks)

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