CVS: Anti-hypertensives Flashcards

1
Q

Name a K+ channel blocker that can be used for hypertension.

A

Minoxidil

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2
Q

What is the MOA of minoxidil?

A

It is a K+ channel opener.

Opening of K+ channels, results in Ca2+ not being able to enter the cell and form a Ca++-calmodulin complex. MLCK not activated, so contraction of heart muscles cannot happen.

Works only to vasodilate arterioles NOT VEINS.

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3
Q

What kind of hypertension is minoxidil used to treat?

A

Severe to malignant HT.

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4
Q

Side effects of minoxidil include…

A
  1. Reflex sympathetic stimulation

2. Sodium and fluid retention

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5
Q

Name 4 ACE inhibitors.

A

Captopril
Enalapril
Ramipril
Lisinopril

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6
Q

What are ACE inhibitors used for?

A
  1. Hypertension
  2. Cardiac failure
  3. Post-MI
  4. Renal insufficiency
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7
Q

Adverse effects of ACE inhibitors include…

A
  1. Severe hypotension
  2. Acute renal failure
  3. HyperK
  4. Angioedema (due to increased bradykinin)
  5. Dry cough (due to increased bradykinin)
  6. Damage fetal renal system (so NOT for preg)
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8
Q

What is the MOA of ACE inhibitors?

A

Blocks ACE

Prevents formation of Angiotensin II =

  1. Lowers sympathetic activity
  2. Lowers Tubular NaCI resorption/K+ excretion and H2O retention
  3. Lowers aldosterone and ADH
  4. Lowers arteriolar vasoconstriction
  5. Inhibit bradykinin (releases NO and PG -> vasodilate) degradation
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9
Q

What are 2 contraindications for ACE-I?

A
  1. Pregnancy (teratogenic)
  2. Bilateral renal artery stenosis*

*To be sure, monitor for hyperK, and creatinine. If creatinine increases >30% -> likely renal artery stenosis

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10
Q

Name 6 ARBs (angiotensin II type 1 receptor blockers).

A
  1. Losartan
  2. Valsartan
  3. Candesartan
  4. Eprosartan
  5. Irbesartan
  6. Telmesartan
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11
Q

What is the MOA of ARBs?

A

Blocks angiotensin receptors. Similar effect as ACE-I but different mechanism.

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12
Q

ARB vs ACE-I?

A

ARB has no effects on bradykinin. It is more selective for angiotensin actions.

Therefore. will lead to less dry cough and angioedema.

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13
Q

Concerns for ARBs?

A

Prolonged inhibition of angiotensin II type ONE receptor will increase circulating angiotensin II -> increased angiotensin II type TWO receptor -> vasodilation.

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14
Q

Drug-drug interactions to take note of?

A
  1. If have asthma or diabetes, NO B BLOCKER
  2. If have CHF, NO CA2+ BLOCKER
  3. If pregnant, no ACE-I OR IRB.
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15
Q

What is the MOA of calcium channel blockers?

A

Block Ca channels predominantly in cardiac and smooth muscles -> same as K+ explanation

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16
Q

Concerns for calcium channel blockers?

A

Excessive cardiac depression: cardiac arrest, bradycardia, AV block, HF

Smooth muscle related: relaxation leading to flushing, dizziness, nausea, constipation, peripheral edema

17
Q

Name 3 loop diuretics.

A

Sulfonamides: Furosemide, Bumetamide, Torsemide

Ethacrynic acid (if sulfur allergy)

18
Q

What is the MOA of loop diuretics?

A

Selectively inhibit the luminal Na+/K+/2Cl- transporter in the thick ascending limb of Henle’s loop.

Will cause an increase in Mg2+ and Ca2+ excretion.

Reduce renal PG synthesis. NSAIDs interfere with this process by reducing PG synthesis more.

Furosemide increases renal blood flow.

19
Q

Concerns for loop diuretics?

A
  1. Hypokalemic metabolic alkalosis
  2. Ototoxicity
  3. Hyperuricemia (gout due to hypovolemia assoc. w. enhanced resorption of uric acid)
  4. Hypomagnesemia
20
Q

What is the MOA of aliskirin?

A

Inhibit renin. Taken orally with a short duration of action.

21
Q

What is the MOA of alpha-1-blockers?

A

α1-Receptors mediate contraction and hypertrophic growth of smooth muscle cells
Hence it inhibits vascular smooth muscle contraction

22
Q

When should alpha-1-blockers be taken?

A

Give at bed time for first dose, small dosing

First dose effect: marked postural hypotension

23
Q

Name an alpha-1-blocker.

A

Prazosin

24
Q

First line for DM + HTN?

A

ACEI