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561 > HTN and Arrhythmia > Flashcards

HTN and Arrhythmia Flashcards

1
Q

Name the non-pharmacological strategies to reduce blood pressure

A

-Dietary salt restriction
-Potassium supplementation preferably by dietary modification
-Weight loss
-DASH diet (dietary approaches to stop HTN)
-Exercise - aerobic

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2
Q

ACE inhibitors MOA

A

-prils

-inhibits Ang II formation → decreased vasoconstriction → lower BP
-Inhibits aldosterone secretion → decreases Na and H2O retention → lowers BP
-Prevents remodeling of blood vessels and heart

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3
Q

ACE inhibitors AE

A

-dry cough (common)
-hyperkalemia
-acute kidney damage
-angioedema
-fetotoxic (poisonous for fetus; don’t use these by pregnant women)

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4
Q

ARBs MOA

A

-sartan

-blocks Ang II receptors to prevent vasoconstriction, release aldosterone from adrenal glands
-Same therapeutic effect as ACE inhibitors
-Prevents remodeling of blood vessels and heart

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5
Q

ARBs AE (5)

A

-cough
-angioedema (swelling of deeper layers of skin)
-fetotoxic
-acute kidney damage
-hyperkalemia

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6
Q

Calcium channel blockers MOA

A

-blocks calcium entry into cells of vascular smooth muscle and heart —> decreases BP and work of heart

-Influx of extracellular Ca releases stored Ca from the sarcoplasmic reticulum (SR)
-Increased intracellular calcium concentration binds to calmodulin (a protein), which activates myosin light chain kinase (MLCK)
-Activation of MLCK enables myosin to interact w/ actin to induce contraction

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7
Q

Calcium channel blockers AE (5)

A

-dizziness
-flushing
-headache
-fatigue
-peripheral edema

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8
Q

Common calcium channel blockers (5)

A

verapamil, diltiazem, amlodipine, felodipine, nifedipine

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9
Q

Diuretics MOA

A

act on kidneys to increase excretion of sodium and water

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10
Q

Thiazide diuretics MOA

A

inhibits Na reabsorption (distal convoluted tubule)

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11
Q

Loop diuretics MOA

A

-semide

inhibit Na and chloride reabsorption (loop of Henle)

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12
Q

K+ sparing diuretics MOA

A

prevent secretion of K+, not as good as diuretic but prevents K+ loss (hypokalemia)

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13
Q

Describe phase 0 of the cardiac action potential

A

Phase 0: opening of fast Na channels and rapid depolarization

Na+ goes into cell, changing membrane potential

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14
Q

Describe phase 1 of the cardiac action potential

A

initial rapid repolarization

Closure of fast Na+ channels

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15
Q

Describe phase 2 of the cardiac action potential

A

plateau phase

Balance between inward movement of Ca+ and outward movement of K+

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16
Q

Describe phase 3 of the cardiac action potential

A

repolarization

K+ channels remain open, allows K+ to build up outside the cell, causing the cell to repolarize

17
Q

Describe phase 4 of the cardiac action potential

A

resting phase

18
Q

Subclass IA antiarrhythmic drug MOA

A

moderate blockade of sodium channels; delay repolarization

19
Q

Subclass IA antiarrhythmic drug AE

A

-diarrhea
-nausea
-thrombocytopenia (platelet # too low)
-torsades de pointes (polymorphic vtach)

20
Q

Subclass IB antiarrhythmic drug MOA

A

mild blockade of sodium channels; accelerate repolarization

21
Q

Subclass IB antiarrhythmic drug AE

A

CN effects (drowsiness, seizures), hypoTN

22
Q

Subclass IC antiarrhythmic drug MOA

A

pronounced blockade of sodium channels

23
Q

Subclass IC antiarrhythmic drug AE

A

visual disturbances, dizziness, risk of proarrhythmia

23
Q

Class III (potassium channel blockers) MOA

A

blockade of potassium channels; delay repolarization; also has Class I, II and IV effects

23
Q

Class II (beta blockers) antiarrhythmic drug AE

A

fatigue, bradycardia, hypoTN

23
Q

Class II (beta blockers) antiarrhythmic drug MOA

A

blockade of beta-adrenergic receptors, reducing sympathetic effects

24
Q

Class III (potassium channel blockers) AE

A

Pulmonary toxicity, thyroid dysfunction, hepatotoxicity, corneal deposits

25
Q

Class IV (calcium channel blockers) MOA

A

blockade of calcium channels in cardiac tissue

26
Q

Class IV (calcium channel blockers) AE

A

constipation, hypoTN, bradycardia, heart failure exacerbation

27
Q

PT considerations for anti-hypertensive drugs

A

-monitor BP
-OH
-fatigue and dizziness; gradually progress ex
-intensity: beta blockers blunt HR response to ex
-dehydration w/ diuretics
-electrolyte imbalances w/ diuretics

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