Drugs for Angina, MI & CVA Flashcards

1
Q

what is atherosclerosis?

A

-presence of plaque within arterial walls

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2
Q

what is plaque and its effects on the vascular system?

A
  • accumulation of fatty, fibrous material that narrows arteries, increases TPR, and reduces vascular elasticity
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3
Q

angina pectoris

A
  • acute chest pain arising from inadequate oxygen supply to the myocardium; steady intense pain that is accompanied with a crushing/constricting sensation
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4
Q

where does angina pectoris pain radiate?

A
  • across the left shoulder, down the left arm, but can move up to the jaw, or across the thoracic region of the back
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5
Q

what are sone signs and symptoms of angina pectoris?

A
  • panic
  • pallor
  • dyspnea
  • diaphoresis
  • tachycardia
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6
Q

what are sone signs and symptoms of angina pectoris?

A
  • panic
  • pallor
  • dyspnea
  • diaphoresis
  • tachycardia
  • elevated BP
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7
Q

what triggers angina pectoris and how long does it last?

A
  • physical exertion or emotional excitement
  • symptoms improve with rest, stress reduction and nitroglycerin
  • 10 to 15 minutes
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8
Q

what are the two types of angina pectoris?

A

stable and unstable

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9
Q

stable angina

A
  • predictable frequency, duration and intensity
  • no associated myocardial damage; relief with rest
  • pain comes from lactic acid build up
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10
Q

unstable angina

A
  • variable intensity, occurs during periods of rest, increased frequency, no associated myocardial damage
  • risk of MI
  • medical emergency
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11
Q

what are non-pharmacological treatments of stable angina pectoris?

A
  • limit alcohol consumption
  • eliminate foods high in cholesterol, saturated fats and sodium
  • control hyperlipidemia
  • control hypertension
  • regular exercise
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12
Q

pharmacological management of stable angina pectoris

A
  • drug therapies reduce myocardial oxygen demand or improve oxygen supply to the myocardium
  • slow heart rate
  • reduce force of cardiac contraction
  • dilate veins
  • dilate arterioles
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13
Q

nitrates mechanism of action

A
  • first line therapy of terminating an angina attack
  • facilitate the formation of nitric acid
  • relax coronary arteries and venous smooth muscle
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14
Q

how do nitrates dilate venous smooth muscle?

A
  • decrease amount of blood returning to the heart
  • decrease cardiac output, workload and oxygen demand
  • risk of hypotension
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15
Q

how do nitrates dilate arterial smooth muscle?

A
  • increases blood flow to myocardium

- improves oxygen supply to myocardium

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16
Q

short acting nitroglycerin and how is it administered?

A
  • used to terminate an angina attack

- tablet and spray; IV, topical and PO

17
Q

what is the protocol with short acting nitroglycerin?

A
  • rest, take drug and wait 5 minutes

- if no improvement take another dose, wait 5 minutes to a max of 3 doses in 15 minutes

18
Q

long acting isosorbide dinitrate

A

-decreases intensity and frequency of angina attacks

19
Q

what is the protocol with isosorbide dinitrate?

A
  • remove patch for 12-16 hours or withhold at night

- slow withdrawal from medications to prevent risk of MI

20
Q

what are some adverse effects for nitrates ?

A
  • throbbing headache, dizziness, weakness, hypotension, reflex tachycardia
21
Q

what are some drug interactions for nitrates?

A
  • drugs for the treatment of erectile dysfunction may cause life threatening hypotension, alcohol
22
Q

beta adrenergic antagonists mechanism of action

A
  • first line therapy for prevention of chronic stable angina attacks
  • reduces cardiac workload, slows heart rate and reduces contractility decreasing oxygen demand
23
Q

caution with beta adrenergic antagonists

A
  • those with asthma, COPD, depression and diabetes
24
Q

what are some adverse effects with beta adrenergic antagonists?

A
  • related to SANS blockade
  • fatigue, weakness, bradycardia, sleep disturbances, hypotension
  • rapid withdrawal worsens angina; reduce over 1-2 weeks
25
Q

calcium channel blockers mechanism of action

A
  • used for prevention of chronic stable angina in clients who cannot tolerate beta blockers
  • decrease myocardial oxygen demand, relax arteriolar smooth muscle lowering blood pressure and decreasing after load, decrease heart rate
26
Q

what are some adverse effects with calcium channel blockers?

A
  • related to effects on cardiac output and smooth muscle
  • dizziness, light-headedness, fatigue, bradycardia, flushing, nausea
  • monitor for hypotension and reflex tachycardia
27
Q

what is a MI and when does it occur?

A
  • a result of advanced coronary artery disease
  • an MI occurs when the coronary artery is completely ischemic
  • myocytes begin to die unless blood supply is restored
  • necrotized tissue release enzyme markers of tissue injury which can be used to confirm MI vs unstable angina
28
Q

what are the goals of therapy with an MI?

A
  • reduce myocardial oxygen demand
  • restore blood supply to the damaged myocardium
  • control dysrhythmias
  • reduce post- MI mortality with anti platelet drugs, and anticoagulant therapy
29
Q

what is a Cerebrovascular Accident (CVA)?

A
  • a stroke

- 80% thrombotic strokes, 20% hemorrhagic strokes

30
Q

what are the warning signs for stroke?

A
  • paralysis on one side
  • vision problems
  • dizziness
  • speech problems
  • headache
31
Q

what are pharmacological managements of thrombotic stroke?

A
  • prevention; lifestyle management, antihypertensive drugs, anti platelet therapy, anticoagulant therapy
  • treatment: thrombolytics; admninistration within 3 hours of brain attack can completely restore function in affected brain areas