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
Class II (beta blockers) antiarrhythmic drug AE
fatigue, bradycardia, hypoTN
23
Class II (beta blockers) antiarrhythmic drug MOA
blockade of beta-adrenergic receptors, reducing sympathetic effects
24
Class III (potassium channel blockers) AE
Pulmonary toxicity, thyroid dysfunction, hepatotoxicity, corneal deposits
25
Class IV (calcium channel blockers) MOA
blockade of calcium channels in cardiac tissue
26
Class IV (calcium channel blockers) AE
constipation, hypoTN, bradycardia, heart failure exacerbation
27
PT considerations for anti-hypertensive drugs
-monitor BP -OH -fatigue and dizziness; gradually progress ex -intensity: beta blockers blunt HR response to ex -dehydration w/ diuretics -electrolyte imbalances w/ diuretics