Cardiology Part 2 Flashcards

1
Q

Organic Nitrates

A

Prodrugs that are converted to nitric oxide (NO) within vascular smooth muscle

Produces general vasodilation -> decreases preload and afterload

Reduces workload on the heart (decreased oxygen demand)

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2
Q

Nitroglycerin (Nitrobid, Nitrostat)

A

Used for acute treatment of anginal attacks. Sublingual administration is preferred in acute attacks due to rapid absorption.

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3
Q

Nitroglycerin protocol for acute chest pain

A

-Dissolve 1 tablet under the tongue
-Wait 5 minutes
-If chest pain is still present, place a 2nd tablet under the tongue
-Call 911
-Wait 5 minutes
-If chest pain is still present, place a 3rd tablet under the tongue
-If chest pain is still present, full myocardial infarction work up should be done

Recommend patient be supine if taking tablets to prevent orthostatic hypotension

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4
Q

Isosorbide dinitrate

A

Used for treatment of acute episodes of angina and for prevention of future attacks, has longer effects

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5
Q

Isosorbide mononitrate

A

Similar to isosorbide dinitirate but longer acting. Given mainly for prevention.

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6
Q

Adverse effects of organic nitrates

A

Headache, dizziness, and orthostatic hypotension

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7
Q

β-Blockers MOA

A

Antagonist to beta 1 receptors on the myocardium
decreases HR and myocardial contraction force
Decreases oxygen demands

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8
Q

β-Blockers adverse effects

A

Nonselective agents may cause bronchoconstriction in patients with asthma. Otherwise, well-tolerated.
Watch for excessive cardiac depression.

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9
Q

Calcium Channel Blockers MOA

A

Blocks calcium entry into vascular smooth muscle (causing vasodilation)

Systemic vasodilation also decreases myocardial oxygen demand

Mediates coronary vasodilation (increases oxygen supply)

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10
Q

Calcium Channel Blockers adverse effects

A

Peripheral vasodilation - headache, flushing, dizziness, orthostatic hypotension

Peripheral edema

Reflex tachycardia (-ipine)

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11
Q

Stable angina

A

myocardial oxygen demand is more than myocardial supply and is typically brought on by exertion. Acute treatment is sublingual nitroglycerin and beta blocker or long acting nitrate for prevention

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12
Q

Variant angina

A

Coronary vasospasm causes a decrease in myocardial oxygen supply. Drug treatment is with calcium channel blocker

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13
Q

Unstable angina

A

Myocardial oxygen supply decreases at the same time oxygen demand increases. Drug therapy further evaluation and a combination of pharmacologic and interventional therapies.

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14
Q

Class I: Sodium Channel Blockers adverse effects

A

Increased arrhythmias
Dizziness
Visual disturbance
Nausea, vomiting, diarrhea

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15
Q

Class II: β-Blockers adverse effects

A

non selective causes increased bronchconstriction, bradycardia, and orthostatic hypotension

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16
Q

Class III: K+ Channel Blockers adverse effects

A

pro-arrhythmic, Amiodarone - pulmonary, thyroid, and liver toxicity

17
Q

Class IV: Calcium Channel Blockers symptoms

A

excessive bradycardia, peripheral vasodilation (dizziness and headache)

18
Q

Digoxin (drug class- digitalis) adverse effects

A

N/D/V, CNS disturbances such as drowsiness, fatigue, confusion, and visual disturbances also can include arrhythmias

19
Q

Phosphodiesterase Inhibitors adverse effects

A

Milrinone,

hypotension and arrhythmias

20
Q

Dobutamine & Dopamine adverse effects

A

hypotension and arrhythmias

21
Q

ACE-I (or) ARBs (or) ARNI adverse effects

A

ACE inhibitors - cough
hypotension and acute kidney injury

22
Q

Loop Diuretics adverse effects

A

volume depletion, electrolyte imbalances which will cause hyponatremia and hypokalemia

23
Q

Vasodilators adverse effects

A

Headache, dizziness
Hypotension & orthostatic hypotension
Reflex tachycardia

24
Q

SGLT2 inhibitors adverse effects

A

UTI
Increased urine output
Genital yeast infection
Weight loss

25
Q

Anticoagulants

A

control the function and synthesis of certain clotting factors, prevent clot formation in the venous system. 4 classes are heparins, warfarin, direct thrombin inhibitors, factor Xa inhibitors (DOACs) which are used to prevent or treat blood clots

26
Q

Heparin Agents

A

potentiates the activity of antithrombin, binds to several clotting factors and renders them inactive. Adverse effects include Heparin-induced thrombocytopenia (HIT)

27
Q

Warfarin

A

Interferes with vitamin K metabolism in the liver and impairs the synthesis of several clotting factors. Needs periodic INR checks and dosing regimens vary patient to patient

28
Q

Direct Thrombin Inhibitors MOA

A

Bind directly to the active site on thrombin and inhibit its ability to convert fibrinogen to fibrin

29
Q

Factor Xa Inhibitors (DOACs)

A

Inhibit factor Xa which is the combination of the intrinsic and extrinsic pathways

30
Q

Adverse effects of anticoagulants

A

Bleeding!

31
Q

Antiplatelets

A

Inhibit abnormal platelet activity and prevent aggregation in arteries

32
Q

Aspirin

A

Limits progression of platelet-induced occlusion thereby reducing the extent of damage to the myocardium in an acute MI. Used for strokes and grafts and valve replacements. Adverse effects are GI irritation, liver, and kidney toxicity

33
Q

P2Y12 Inhibitors

A

Blocks the P2Y12 component on ADP receptor surface on the platelet membrane which decreases platelet aggregation. Used for myocardial infarctions and ischemic stroke

34
Q

Fibrinolytics “lytics”

A

Facilitate destruction of blood clots, used to restablish blood flow through vessels that thrombi have occluded

35
Q

Adverse Effects of Antiplatelets / Fibrinolytics

A

Bleeding!

36
Q

HMG-CoA Reductase Inhibitors (Statins) MOA

A

Inhibit HMG Co-A reductase which catalyzes one of the early steps in cholesterol synthesis
decrease LDLs, decrease triglycerides, increase HDL (modest). Adverse effects are myalgias

37
Q

Fibric Acids (Fibrates)

A

Primarily decreases triglycerides, adverse effects include rhabdomyolysis particularly in combo with other agents