Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CV > Week 1: Hypertension > Flashcards

Week 1: Hypertension Flashcards

1
Q

Relate cardiac output, resistance, and blood pressure.

A

CO = BP/SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Relate cardiac output, heart rate, and stroke volume.

A

CO = HR*SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is renin released from?

A

Released from granular cells in the juxtaglomerular apparatus in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

Decreased resistance in afferent arteriole

Increased renin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

List two side effects of beta blockers.

A

Fatigue (due to reduced CO)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which beta blocker is cardioselective?

A

Metoprolol (beta-1 only)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which beta blockers are non-cardioselective?

A

Propanolol (beta-1 and beta-2)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which beta blocker is a partial agonist?

A

Acebutolol (partial agonist at beta-1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the effect of dihydropyridines. Give a prototoype.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Give an example of a thiazide diuretic.
Hydrochlorothiazide
26
What type of drug is furosemide? What target does it act on?
Furosemide (Lasix) is a loop diuretic | Loop diuretics inhibit NKCC2 symporters in the TAL of the Loop of Henle
27
What type of drug is spironolactone?
K+ sparing diuretic | Aldosterone antagonist
28
What accounts for the non-proportional effect of diuretics on blood pressure?
Likely some vasodilatory effect
29
Describe the effects of ACE inhibitors. Give a prototype.
``` Inhibit vasoconstriction Inhibit aldosterone secretion Inhibit NaCl (H2O) reabsorption Increase vasodilation (via bradykinin) Prototype: ramipril ```
30
What antihypertensive drug may delay onset of diabetic nephropathy? How?
ACE inhibitors | Vasodilates efferent arteriole, resulting in decreased intraglomerular pressure
31
List the side effects of ACE inhibitors.
Cough (via bradykinin) Angioedema Hyperkalemia (reduced aldosterone) Renal dysfunction (over-reduction of efferent arteriole pressure)
32
Describe the effects of angiotensin receptor blockers. Give a prototype.
``` Inhibit vasoconstriction Inhibit aldosterone secretion Inhibit NaCl (H2O) reabsorption Prototype: losartan ```
33
Why might ARBs be less potent hypotensive agents than ACE inhibitors?
No vasodilatory effect via bradykinin.
34
What major advantage do ARBs have over ACE inhibitors?
Reduced incidence of cough and angioedema (no increase in bradykinin)
35
What receptor does losartan antagonize?
AT1
36
What type of drug is aliskiren?
Renin inhibitor
37
What advantage might renin inhibitors have over ARBs and ACE inhibitors?
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
Is combination therapy with ARBs, ACE inhibitors, and renin inhibitors recommended?
No - caution against inhibiting multiple points in RAS
39
What is the mechanism of action of aldosterone antagonists (anti-mineralocorticoids)? Give a prototype.
Blocks aldosterone effect at mineralocorticoid receptor, inhibiting Na+ reabsorption in the collecting duct Prototype: spironolactone
40
What is the effect of alpha antagonists? Give a prototype. What is a common side effect?
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
What type of drug is hydralazine? What is a common side effect?
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
What is the mechanism of action of clonidine? What are its effects and side effects?
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
What type of drug is bosentan?
Endothelin antagonist
44
What type of drug is omepatrilat?
Vasopeptidase inhibitor
45
Why might ARBs be less potent hypotensive agents than ACE inhibitors?
No vasodilatory effect via bradykinin.
46
What major advantage do ARBs have over ACE inhibitors?
Reduced incidence of cough and angioedema (no increase in bradykinin)
47
What receptor does losartan antagonize?
AT1
48
What type of drug is aliskiren?
Renin inhibitor
49
What advantage might renin inhibitors have over ARBs and ACE inhibitors?
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
Is combination therapy with ARBs, ACE inhibitors, and renin inhibitors recommended?
No - caution against inhibiting multiple points in RAS
51
What is the mechanism of action of aldosterone antagonists (anti-mineralocorticoids)? Give a prototype.
Blocks aldosterone effect at mineralocorticoid receptor, inhibiting Na+ reabsorption in the collecting duct Prototype: spironolactone
52
What is the effect of alpha antagonists? Give a prototype. What is a common side effect?
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
What type of drug is hydralazine? What is a common side effect?
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
What is the mechanism of action of clonidine? What are its effects and side effects?
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
What type of drug is bosentan?
Endothelin antagonist
56
What type of drug is omepatrilat?
Vasopeptidase inhibitor

CV (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions