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CVB by Minnie (Madeleine) > SM 133a - Hypertension Pathophysiology and Pharmacology > Flashcards

SM 133a - Hypertension Pathophysiology and Pharmacology Flashcards

1
Q

What is the threshold for medical hypertension treatment if a patient has >10% risk of developing heart disease?

A

Blood pressure should be treated if it is >130 systolic or >80 diastolic

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2
Q

What is the threshold for medical hypertension treatment if a patient has <10% risk of developing heart disease?

A

Blood pressure should be treated if it is >140 systolic or >90 diastolic

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3
Q

Home blood pressure readings over the course of 1 week measure 125/85

Which blood pressure category does this fall into?

A

Stage I Hypertension

(130-139 systolic or 80-89 diastolic)

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4
Q

List the ranges for each category. Note: if systolic and diastolic fall into different categories, go with the higher classification

Normal:

Elevated:

Stage I Hypertension:

Stage II Hypertension:

A

Normal: <120/<80

Elevated: 120-129/<80

Stage I Hypertension: 130-139/80-89

Stage II Hypertension: >140/>90

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5
Q

How many measurements are required to make a diagnosis of hypertension?

A

At least 2

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6
Q

What are the 3 major physiologic determinants of blood pressure?

A

Volume: Stroke volume and total blood volume

Vascular tone

Cardiac Output

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7
Q

List the mechanisms by which Angiotensin II effects blood pressure

A
  • Sympathetic activation
  • Smooth muscle vasoconstriction
  • Decreased bradykinin -> Prevention of vasodilation
  • Na+ and H2O retention
    • By increasing aldosterone in the adrenal cortex
    • By increasing ADH in the brain
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8
Q

What are the 4 options for first-line hypertension treatment?

A
  • Thiazide diuretics
    • Hydrochlorothiazide
  • ACE inhibitors
    • -pril drugs
  • ARBs
    • -sartan drugs
  • Calcium Channel Blockers
    • Verapamil, Diltiazem, Nifedipine
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9
Q

Describe the mechanism and site of action of thiazide drugs

A

Thiazides like hydrochlorothiazide and chlorthalidone block the Na+-Cl- symporter in the distal convoluted tubule

This traps Na+ in the urinary space, leading to increased K+ excretion via Na+/K+ exchanger activity

(Can combine with an ACE inhibitor to preserve K+)

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10
Q

Give 2 examples of thiazide drugs

A

hydrochlorothiazide and chlorthalidone

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11
Q

Describe the mechanism and site of action of furosemide, torsemide, and bumetanide

A

The -(m/n)ide drugs are loop diuretics

They block the Na+-K+-2Cl- symporter in the thick ascending limb of the loop of Henle

This traps these ions in the urinary space, leading to acute volume loss. They are best used for rapid diuresis, while thiazides are better tolerated in the long term

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12
Q

Which diuretics are effective for acute volume loss, but are not recommended for long-term therapy (except in patients who have chronic kidney disease)?

A

Loop duretics: Furosemide, torsemide, and bumetanide

Note: combine with saline if the patient is hypercalcemic

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13
Q

What blood pressure measurements constitute a hypertensive emergency?

A

SBP>180 or DBP >120

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14
Q

List 4 K+ sparing diuretics

A
  • Renal epithelial Na+ channel blockers
    • Triamterene
    • Amiloride
  • Renal epithelial mineralcorticoid receptor blockers
    • Spironolactone
    • Eplerenone
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15
Q

List 3 loop diruetics

Who are these drugs recommended for?

A

Furosemide, torsemide, and bumetanide

Effective for acute volume loss, but are not recommended for long-term therapy (except in patients who have chronic kidney disease)

Note: combine with saline if the patient is hypercalcemic

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16
Q

Which drugs act by blocking the renal epithelial Na+ channels in the late distal tubule and collecting duct?

A

Triamterene

Amiloride

(K+ sparing diuretics)

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17
Q

Describe the mechanism and site of action of Triamterene and Amiloride

A

Triamterene and Amiloride act by blocking the renal epithelial Na+ channels in the late distal tubule and collecting duct of the kidney. They are K+ sparing diuretics

If less Na+ gets into the epithelial cells, less K+ is expelled from them (via decreased activity of the Na+/K+ exchanger)

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18
Q

Describe the mechanism and site of action of spironolactone and eplerenone

A

Spironolactone and eplerenone are aldosterone receptor antagonists. They block mineralcorticoid receptors (aka the aldosterone receptor) on epithelial cells in the late distal tubule and collecting duct of the kidney. They are K+ sparing diuretics

If less Na+ gets into the epithelial cells, less K+ is expelled from them (via decreased activity of the Na+/K+ exchanger)

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19
Q

What drugs would you give to a hypertensive patient despite thiazide therapy who is also hypokalemic?

A

K+ sparing duretic

Tiamterene, amiloride, spironolactone, or eplerenone

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20
Q

Describe the effects of aldosterone on blood pressure

A

Aldosterone acts on the distal nephron to increase blood pressure by promoting Na+ absorption

By promoting the absorption of Na+, K+ and H+ are excreted

21
Q

Describe the mechanism of action of clonidine

A

Clonidine is an adrenergic alpha2 receptor agonist

The alpha2 receptors is located on the presynaptic sympathetic neuron. It usually functions as a feedback mechanism that senses and then downregulates norepinephrine.

Clonidine “artificially” stimualtes the alpha2 receptors, thus inhibiting norepinephrine release and preventing vasoconstriction

22
Q

Which blood pressure medication is an alpha2 adrenergeic receptor agonist?

A

Clonidine

23
Q

Describe the mechanism of action of methyldopa

A

Methyldopa replaces norepinephrine in secretory vescicles of adrenergic neurons.

This blocks central adrenergic outflow through negative feedback mechanisms, thus inhibiting vasoconstriction

24
Q

Which blood pressure medication replaces norepinephrine in secretory vescicles of adrenergic neurons?

A

Methyldopa

25
Q

What are the two major centrally acting blood pressure medications?

A

Methyldopa (replaces norepinephrine in secretory vescicles of adrenergic neurons)

Clonidine (alpha2 adrenergeic receptor agonist)

26
Q

Which blood pressure medications are alpha1 adrenergic receptor blockers?

A

-zosin drugs

Prazosin, Terazosin, Doxazosin

27
Q

Describe the mechanism of action of -zosin drugs (Prazosin, Terazosin, Doxazosin)

A

-zosin drugs are alpha1 receptor blockers

Inhibiting the alpha1 receptor = inhibition of vasoconstriction in response to adrenergic signaling

The result is decreased peripheral vascular resistance

28
Q

List 4 cardioselective beta blockers

Which beta receptors are blocked?

A

Cardioselective = blocks beta1 receptors in the heart

  • Atenolol
  • Metoprolol
  • Carvedilol (also alpha1 blocker)
  • Labetalol
29
Q

Which beta blockers act on beta1 and beta2 receptors?

A

Propanolol

Timolol

30
Q

Which drug is both beta1 and alpha1 adrenergic antagonist?

A

Carvedilol

31
Q

Are beta-blockers conidered first line agents for hypertension?

When are they used?

A

No; they are typically used with other agents (ACE inhibitor, thiazide, ARB, Ca2+ channel blocker), especially if the patient has heart failure

32
Q

List 3 Ca2+ channel blockers that can be used to treat hypertension

A
  • Non-dihydropyridines
    • Veramapil (a Phenylalkylamine)
    • Diltiazem (a Benzothiazepine)
  • Dihydropyridines
    • Nifedipine
33
Q

What precaution should be taken when prescribing non-dihydropyridine drugs?

A

Do not use in conjunction with another agent that lowers heart rate (beta blocker), or in patients with LV systolic dysfunction

34
Q

Describe the mechanism of action of verapamil

A

Verapamil is a non-dihydropyridine Ca2+ channel blocker

It blocks L-type Ca2+ channels in the heart only

Less intracellular Ca2+ = decreased contractility = decreased stroke volume = decreased blood pressure

35
Q

Describe the mechanism of aciton of diltiazem

A

Diltiazem is a non-dihydropyridine Ca2+ channel blocker

It blocks L-type Ca2+ channels in the heart AND vascular smooth muscle. This leads to…

  • Decreased cardiac contractility, leading to decreased BP
  • Decreased constriction in vascular smooth muscle
36
Q

Describe the mechanism of action of nifedipine

A

Nifedipine (and other -dipines) are dihydropyridine Ca2+ channel blocker

They L-type Ca2+ channels in vascular smooth muscle. This leads to decreased constriction in vascular smooth muscle, which decreases peripheral vascular resistance

37
Q

Which Ca2+ channel blocker acts on the heart only?

A

Veramapil (and other phenylalkylamines)

38
Q

Which Ca2+ channel blocker acts on the heart and vascular smooth muscle?

A

Diltiazem (and other Benzothiazepines)

39
Q

Which Ca2+ channel blocker acts on vascular smooth muscle only?

A

Nifedipine (and other dihydropyridines)

40
Q

List 3 hypertension drugs that are peripheral vasodilators

A

Hydralazine, minoxidil, nitroprusside

41
Q

Describe the mechanism of action of hydralazine

A

Peripheral vasodilator

Relaxes arteriolar smooth muscle

42
Q

Describe the mechanism of action of minoxidil

A

Peripheral vasodilator

Activates K+ channels on vascular smooth muscle. This promotes K+ efflux, hyperpolarizing the cell. This prevents contraction and promotes relaxation

43
Q

Describe the mechanism of action of nitroprusside

A

Peripheral vasodilator

Nitroprusside is metabolzed by endothelial cells to nitric oxide, which activates guanyl cyclase to increase cGMP, leading to vasodilation

44
Q

Which drugs should not be prescribed with diltiazem? Why?

A

Beta blockers

Too much decrease in CO due to decreased HR

45
Q

Which drugs should not be prescribed with ACE inhibitors?

Why?

A

Spironolactone, eplerenone, triamterene, amiloride (K+ sparing diuretics)

This would lead to hyperkalemia

46
Q

Which drugs should not be prescribed with nifedipine?

A

Hydralazine

Leads to edema

47
Q

Which drugs should not be prescribed with hydralizine?

A

Nifedipine

Leads to edema

48
Q

What is the mechanism of action of -sartan drugs?

A

-sartan drugs are angiotensin II receptor blockers, also known as ARBs. They block the action of angiotensin II at AT1 to promote vasodilation and Na+ excretion

Note: AT1 may also mediate the progression of atherosclerosis and myocardial remodeling; ARBs may inhibit this as well

CVB by Minnie (Madeleine) (43 decks)

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