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Pharmacology Test 3 > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

What are the two types of hypertension?

A

primary: no known cause
secondary: specific cause (maybe pheochromocytoma of the adrenal gland that produces catecholamines)

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2
Q

What provides acute BP control?

A

baroreceptor, chemoreceptor, atrial stretch reflexes

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3
Q

What provides long-term BP control?

A

RAAS system

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4
Q

What is the most important factor affecting blood pressure?

A

vessel diameter

Ohm’s Law: pressure = flow x resistance

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5
Q

What is the function of arterial baroreceptors?

A

rapid adjustment of BP; protective mechanism to maintain perfusion of brain/heart; buffer rapid deviations in BP from the set-point determined by renal pressure natriuresis

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6
Q

What is the function of chemoreceptors?

A

slow adjustment of BP; BP has to be low enough that your body starts producing byproducts recognized by these receptors (acidosis)

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7
Q

What is the function of the atrial stretch reflex?

A

receptors sensitive to increase in volume; increase HR, dilation of afferent arterioles, decrease ADH and increase ANP

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8
Q

What are endothelial factors involved in BP control? Name the two major factors.

A

factors released by endothelial cells lining the blood vessels
nitric oxide: relaxation
endothelin: constriction

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9
Q

How does NO cause vasodilation?

A

endothelial-derived nitric oxide synthase (eNOS) synthesizes NO from arginine and oxygen; NO diffuses out of cell & acts on smooth muscle; converts cGTP to cGMP which relaxes the vessel

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10
Q

How does endothelin cause vasoconstriction?

A

amino acid peptide released from damaged endothelial cells; prevents bleeding from torn arteries

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11
Q

African Americans are less reactive to which medications?

A

RAAS meds (ACEIs, ARBs)

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12
Q

What are the 4 targets of antihypertensive therapy?

A

fluid balance (Na & water
renin-angiotensin system
central & peripheral SNS control
vascular smooth muscle tone

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13
Q

How do diuretics function overall?

A

deplete body Na stores; reduces blood volume; initially decreases CO; CO returns to normal after 6-8 weeks & PVR declines

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14
Q

How do thiazides work?

A

inhibit Na/Cl transporter in the distal tubule and early collecting duct

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15
Q

How do loop diuretics work?

A

act on Na/K/2Cl transporter in the thick loop of Henle where substantial reabsorption of Na occurs

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16
Q

Which drug types work on the RAAS system?

A

AT1R blockers (ARBs)
ACEIs
renin inhibitor or beta1 adrenergic antagonist

17
Q

How do renin inhibitors work?

A

renin levels are high in HTN pts
beta1 blockers stop production of renin
aliskiren is a direct competitive renin inhibitor

18
Q

How do ACEIs work?

A

inhibit angiotensin I conversion to angiotensin II conversion to aldosterone; inhibit breakdown of bradykinin (increase Na & water excretion, decrease PVR)

19
Q

adverse effects of ACEIs

A

dry cough: bradykinin
hyperkalemia: inhibition of aldosterone secretion
angioedema: substance P
hypotension in presence of hypovolemia

20
Q

How do ARBs work?

A

vasodilate; increase Na & water excretion; reduce plasma volume; decrease cellular hypertrophy; increase plasma renin & renin activity
*don’t affect AT2 that is responsible for remodeling

21
Q

How do beta adrenergic receptor antagonists treat HTN?

A

decrease CO (HR & contractility); decrease renin secretion; decrease central sympathetic outflow; reset baroreceptors

22
Q

function of beta1 receptors

A

cardioselective (increase HR, conduction, contraction, EF); increase renin release by JG cells

23
Q

function of beta2 receptors

A

smooth muscle relaxation; increase renin release by JG cells

24
Q

function of alpha1 receptors

A

vasoconstriction; contraction of smooth muscles

*antagonist drugs cause dilation of arterioles & capacitance veins

25
Q

function of alpha2 receptors

A

inhibits release of NE; indirectly works in CNS

26
Q

mechanism of action of reserpine

A

depletes NE from adrenergic nerve endings; inhibits reuptake of NE; decreases PVR and CO

27
Q

mechanism of action of clonidine & methlydopa

A

decrease sympathetic outflow; increase vagal activity to the heart; decrease PVR & CO

28
Q

mechanism of action of Ca+2 channel blockers

A

block voltage sensitive L-type Ca+2 channels; relax VSM & decrease PVR; decrease MAP (reflex increase sympathetic discharge and HR)

29
Q

mechanism of action of hydralazine

A

requires NO; affects arterioles; decreased PVR/MAP

30
Q

mechanism of action of minoxidil

A

affects arterioles; decreased PVR

31
Q

mechanism of action of nitroprusside

A

direct vasodilator; generates NO which activates guanylyl cyclase and increases cGMP; affects veins & arteries to reduce preload & afterload

32
Q

mechanism of action of nitroglycerin

A

affects veins; generates NO which activates guanylyl cyclase to increase cGMP

33
Q

mechanism of action of epoprostenol

A

direct vasodilator via cAMP; counteracts TXA2

Pharmacology Test 3 (10 decks)

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