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CV > Week 1: Hypertension > Flashcards

Week 1: Hypertension Flashcards

1
Q

Relate cardiac output, resistance, and blood pressure.

A

CO = BP/SVR

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2
Q

Relate cardiac output, heart rate, and stroke volume.

A

CO = HR*SV

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3
Q

Where in the cardiovascular system are baroreceptors located? What are their innervations?

A

Carotid sinus - glossopharyngeal nerve (IX)
Aortic arch - vagus nerve (X)
Walls of L and R atria at venous entrances - vagus nerve (X)

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4
Q

Describe the physiological effects on the cardiovascular system of increased SNS activity.

A

Increased release of norepinephrine - acts on alpha-1 receptors to cause vasconstriction
Increased release of epinephrine - acts on beta-1 receptors in the heart to increase chronotropy and inotropy

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5
Q

Describe the physiological effects on the cardiovascular system of decreased PNS activity.

A

Reduced release of acetylcholine via muscarinic receptors - heart rate increases (slowing effect decreased)

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6
Q

Describe the effect of increased arginine vasopressin on the cardiovascular system. Where is it released from, and in response to what stimulus?

A

Increases water resorption in kidney distal tubules by activating V2 receptors
Increases vasoconstriction by acting on V1A receptors (only in high concentrations)
Released from posterior pituitary in response to baroreceptors and osmoreceptors

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7
Q

Where is renin released from?

A

Released from granular cells in the juxtaglomerular apparatus in the kidney

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8
Q

What stimuli result in renin release?

A

Increased stretch of afferent arteriolar wall (increased ECFV)
Decreased [Na+] and [Cl-] in the distal tubule, detected by the macula densa
SNS (via beta-1 receptors)
Humoral factors (K+, Ang II, ANPs)

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9
Q

What effect does decreased [Na+] and [Cl-] in the distal tubule have?

A

Decreased resistance in afferent arteriole

Increased renin secretion

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10
Q

What are the effects of angiotensin II?

A 
Vasoconstriction (via AT1 receptor)
Synthesis and secretion of aldosterone
Release of vasopressin
Release of adrenal catecholamines
Increased central sympathetic outflow
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11
Q

Describe the action of endothelin. Where is it released from?

A

Powerful vasoconstrictor - acts on vascular smooth muscle cells via ETA receptor, resulting in calmodulin-mediated activation of MLCK
Synthesized and released from endothelial cells

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12
Q

Describe the action of nitric oxide. Where is it released from?

A

Vasodilator - diffuses into cell, resulting in inactivation (phosphorylation) of MLCK via a protein kinase G mediated pathway
Synthesized and released from endothelial cells

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13
Q

Describe the action of adenosine in coronary blood vessels.

A

Vasodilator in coronary blood vessels - binds to A2A receptors, resulting in MLCK inactivation

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14
Q

List causes of primary hypertension.

A 
No direct cause known
SNS hyperactivity
Abnormal cardiovascular development
RAS activity
Defect in natriuresis
Intracellular sodium and calcium
Exacerbating factors
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15
Q

List causes of secondary hypertension.

A 
Renal disease
Genetic causes
Renal vascular hypertension
Primary hyperaldosteronism
Cushing's syndrome
Pheochromocytoma
Coarctation of the aorta
Pregnancy associated
Estrogen use
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16
Q

List complications of untreated hypertension.

A 
Cerebrovascular disease (stroke)
Coronary artery disease
Left ventricular hypertrophy
Peripheral vascular disease
Abdominal and thoracic aortic aneurysm
Chronic renal failure (chronic kidney disease)
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17
Q

Summarize the mechanism of action and effects of beta blockers and the receptors that are involved.

A

Beta blockers inhibit action of endogenous catecholamines:
Decrease cardiac chronotropy, inotropy (beta-1)
Decrease release of renin from kidneys (beta-1)
Decrease SNS activity (beta-1)

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18
Q

List two side effects of beta blockers.

A

Fatigue (due to reduced CO)

Bronchoconstriction - contraindicated in asthmatics (due to beta-2 antagonism)

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19
Q

Which beta blocker is cardioselective?

A

Metoprolol (beta-1 only)

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20
Q

Which beta blockers are non-cardioselective?

A

Propanolol (beta-1 and beta-2)

Carvedilol (alpha-1, beta-1, and beta-2)

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21
Q

Which beta blocker is a partial agonist?

A

Acebutolol (partial agonist at beta-1)

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22
Q

Describe the effect of dihydropyridines. Give a prototoype.

A

Vasodilation (main effect)
Reduces cardiac chronotropy, inotropy (minor effect)
Prototype: amlodipine

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23
Q

Describe the effect of benzothiazepines. Give a prototype.

A

Vasodilation
Reduces cardiac chronotropy, inotropy
Prototype: diltiazem

24
Q

Describe the effect of phenylalkylamines. Give a prototype.

A

Vasodilation
Reduces cardiac chronotropy, inotropy
Prototype: verapimil

25
Q

Give an example of a thiazide diuretic.

A

Hydrochlorothiazide

26
Q

What type of drug is furosemide? What target does it act on?

A

Furosemide (Lasix) is a loop diuretic

Loop diuretics inhibit NKCC2 symporters in the TAL of the Loop of Henle

27
Q

What type of drug is spironolactone?

A

K+ sparing diuretic

Aldosterone antagonist

28
Q

What accounts for the non-proportional effect of diuretics on blood pressure?

A

Likely some vasodilatory effect

29
Q

Describe the effects of ACE inhibitors. Give a prototype.

A 
Inhibit vasoconstriction
Inhibit aldosterone secretion
Inhibit NaCl (H2O) reabsorption
Increase vasodilation (via bradykinin)
Prototype: ramipril
30
Q

What antihypertensive drug may delay onset of diabetic nephropathy? How?

A

ACE inhibitors

Vasodilates efferent arteriole, resulting in decreased intraglomerular pressure

31
Q

List the side effects of ACE inhibitors.

A

Cough (via bradykinin)
Angioedema
Hyperkalemia (reduced aldosterone)
Renal dysfunction (over-reduction of efferent arteriole pressure)

32
Q

Describe the effects of angiotensin receptor blockers. Give a prototype.

A 
Inhibit vasoconstriction
Inhibit aldosterone secretion
Inhibit NaCl (H2O) reabsorption
Prototype: losartan
33
Q

Why might ARBs be less potent hypotensive agents than ACE inhibitors?

A

No vasodilatory effect via bradykinin.

34
Q

What major advantage do ARBs have over ACE inhibitors?

A

Reduced incidence of cough and angioedema (no increase in bradykinin)

35
Q

What receptor does losartan antagonize?

A

AT1

36
Q

What type of drug is aliskiren?

A

Renin inhibitor

37
Q

What advantage might renin inhibitors have over ARBs and ACE inhibitors?

A

All three drugs produce increased plasma renin concentration (reduced negative feedback of angiotensin II on RAS)
Renin inhibitors potentially block activity of plasma renin (renin has other pathways of effect)

38
Q

Is combination therapy with ARBs, ACE inhibitors, and renin inhibitors recommended?

A

No - caution against inhibiting multiple points in RAS

39
Q

What is the mechanism of action of aldosterone antagonists (anti-mineralocorticoids)? Give a prototype.

A

Blocks aldosterone effect at mineralocorticoid receptor, inhibiting Na+ reabsorption in the collecting duct
Prototype: spironolactone

40
Q

What is the effect of alpha antagonists? Give a prototype. What is a common side effect?

A

Blocks stimulation of alpha-1 receptors, resulting in vasodilation and venodilation
Prototype: prazosin
Not commonly used to treat HTN due to side effect of orthostatic hypotension

41
Q

What type of drug is hydralazine? What is a common side effect?

A

Direct vasodilator - increases cGMP/PKG resulting in MLCK inactivation (phosphorylation) (similar pathway to NO)
Not commonly used to treat HTN due to side effect of reflex tachycardia

42
Q

What is the mechanism of action of clonidine? What are its effects and side effects?

A

Alpha-2 receptor agonist, causing negative feedback on norepinephrine release.
Effects are decreased HR, SV, and SVR; side effects are peripheral hypertension due to alpha-1 receptor agonist activity in periphery.

43
Q

What type of drug is bosentan?

A

Endothelin antagonist

44
Q

What type of drug is omepatrilat?

A

Vasopeptidase inhibitor

45
Q

Why might ARBs be less potent hypotensive agents than ACE inhibitors?

A

No vasodilatory effect via bradykinin.

46
Q

What major advantage do ARBs have over ACE inhibitors?

A

Reduced incidence of cough and angioedema (no increase in bradykinin)

47
Q

What receptor does losartan antagonize?

A

AT1

48
Q

What type of drug is aliskiren?

A

Renin inhibitor

49
Q

What advantage might renin inhibitors have over ARBs and ACE inhibitors?

A

All three drugs produce increased plasma renin concentration (reduced negative feedback of angiotensin II on RAS)
Renin inhibitors potentially block activity of plasma renin (renin has other pathways of effect)

50
Q

Is combination therapy with ARBs, ACE inhibitors, and renin inhibitors recommended?

A

No - caution against inhibiting multiple points in RAS

51
Q

What is the mechanism of action of aldosterone antagonists (anti-mineralocorticoids)? Give a prototype.

A

Blocks aldosterone effect at mineralocorticoid receptor, inhibiting Na+ reabsorption in the collecting duct
Prototype: spironolactone

52
Q

What is the effect of alpha antagonists? Give a prototype. What is a common side effect?

A

Blocks stimulation of alpha-1 receptors, resulting in vasodilation and venodilation
Prototype: prazosin
Not commonly used to treat HTN due to side effect of orthostatic hypotension

53
Q

What type of drug is hydralazine? What is a common side effect?

A

Direct vasodilator - increases cGMP/PKG resulting in MLCK inactivation (phosphorylation) (similar pathway to NO)
Not commonly used to treat HTN due to side effect of reflex tachycardia

54
Q

What is the mechanism of action of clonidine? What are its effects and side effects?

A

Alpha-2 receptor agonist, causing negative feedback on norepinephrine release.
Effects are decreased HR, SV, and SVR; side effects are peripheral hypertension due to alpha-1 receptor agonist activity in periphery.

55
Q

What type of drug is bosentan?

A

Endothelin antagonist

56
Q

What type of drug is omepatrilat?

A

Vasopeptidase inhibitor

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