Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MOD 1 Quiz 1 > Antihypertensive drugs > Flashcards

Antihypertensive drugs Flashcards

1
Q

Formula for BP?

A

CO x PVR
CO=SV x HR
SV= myocardial contractility and venous return
Venous return= blood volume, venous capacitance tone

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

Short term regulate BP?

A

baroreceptor reflex

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

Long term regulate of BP?

A

Kidney, Renin-Angiotensin-Aldosterone System

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

RAAS?

A

Renin increases ANG II, cause vasoconstriction which raises BP

ANG II also increases aldosterone, salt and water retention, raise BP

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

Diuretic acute antihypertensive?

A

increase sodium and water excretion by the kidney, decrease blood volume, decrease CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diuretic chronic antihypertensive?

A

prolonged diuretic use over time CO returns to normal, decrease Na in smooth m cells, decrease PVR

takes about 6-8 weeks

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

How do diuretics enhance the effects of other drugs?

A

some drugs cause Na retention, this causes release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Most potent diuretic?

A

Loop

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

Most useful diuretic to treat hypertension?

A

thaizide, first line therapy

Decrease CV events and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When use loop diuretics for hypertension?

A

reduced renal function

severe hypertension when drugs that retain Na are being used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

disadvantage to treat hypertension with loop?

A

short half life, dont work as well as equally potent dose of a thiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Effect of thiazide and loop on serum K levels?

A

decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

K sparing use for hypertension?

A

to counteract the K loss from loop and thiazides
Spironolactone- use with other agent
Eplerenon- use alone or with other agent

Compelling indication for use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Drugs and new onset diabetes?

A

Diuretics and beta blockers have increased risk
calcium channel blockers neutral or protective
ACE inhibitors and angiotensin receptor antagonists lower risk for new onset diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Use Esmolol to treat chronic hypertension?

A

no because its an IV drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Propranolol antihypertensive? (heart)

A

nonselective beta blocker, decrease heart rate, decrease contractility, decrease cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Some beta blockers have intrinsic sympathomimetic activity?

A

they are partial agonists to beta receptor, activating the receptor but not to full potential as beta agonist

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

Propranolol on kidney?

A

decrease renin, decrease ang II, decrease aldosterone

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

Propranolol on CNS?

A

decrease sympathetic discharge

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

Not use a beta blocker?

A

2nd and 3rd degree AV block, asthma, increased RR interval

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

Adverse effects of beta blockers?

A 
decrease response to exercise
bradycardia
AV conduction abnormalities
beta 2 on smooth muscle in lungs
nightmares, lassitude, mental depression, insomnia (CNS effects) (lipid soluble)
sexual dysfuntion, increase triglycerides and decrease HDL
glucose intolerance
unopposed vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

long term therapy beta blockers?

A

up regulate of receptors, rebound hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Verapamil is?

A

calcium channel blocker, works on smooth m and cardiac muscle
non-dihydropyridines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Nifedipine is?

A

calcium channel blocker, works only on vascular smooth muscle
dihydropyridine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CCB effect on vasculature?

A

Block voltage dependent Ca2+ channels on vascular smooth muscle cells in arteries which is important for contraction (relax smooth m, decreases peripheral resistance), not affect venous beds much

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

If PVR decreases what happens to the heart? BP?

A

reflex tachy

BP goes down

27
Q

Will there be reflex tachy with verapamil?

A

no, decrease cardiac output, decrease HR, decrease conduction, decrease force of contraction, no change in PVR

28
Q

First line therapy for hypertension with a compelling indication?

A

Calcium channel blockers

29
Q

Adverse effects of Verapamil and diliazem?

A

sinus bradycadria, AV block, exacerbation of heart failure or pulmonary edema

30
Q

Dihydropyridines adverse effects?

A

Will lower PVR but will cause reflex tachy

31
Q

What will cause nidedipine induced peripheral edema?

A

increase in hydrostatic pressure in the precapillary sphincter

32
Q

useful agent to combat the nidedipine induced peripheral edema?

A

ACE inhibitor

33
Q

Angiotensin II effects?

A

Adrenal- aldosterone release- Na and H2O (increase volume, increase BP)
Arterioles/venules- vasoconstriction (increase PVR ,increase BP)
facilitate sympathetic activity (increase BP)

34
Q

Ang II on blood pressure?

A

rise BP

35
Q

Ang II effects?

A

hypertrophy/hyperplaisa of vascular smooth muscle cell, mesagnial cells, cardiac myocytes, cardiac fibroblasts
mycocyte apoptosis, inflammatory mediator, helps regulate GFR

36
Q

block effects of Ang II?

A

ACE inhibitor will block angiotensin converting enzyme, Ang I to Ang II conversion (decrease amount of Ang II made)
-will also block inactivation of bradykinin

angiotensin receptor blocker blocks the receptor (decrease effect of Ang II)

renin inhibitor blocks angiotensinogen to ang I

37
Q

Antihypertensive actions of ACE inhibitors?

A

decrease ang II, increase bradykinin
dilate arterioles
decrease PVR

38
Q

Decrease Ang II does what?

A

decrease aldosterone, decrease sympathetic activity

39
Q

Why does ACE inhibitor not cause large drop in aldosterone levels?

A

other things sim aldosterone release

40
Q

ACEI MOA?

A

decrease PVR

small effect HR, CO and blood volume

41
Q

ACEI clinical use?

A

first line for hypertension with compelling indication

42
Q

Acute MI/ ACEI?

A

administer within 24 hrs post MI to decrease mortality

43
Q

If BP is low, give ACEI?

A

no

44
Q

ACEI and diabetic nephropathy?

A

benificial by decreasing bp and benificial without hypertension too

45
Q

primary cause of kidney failure?

A

diabetes

46
Q

Ang II mainly changes what arteriole in the kidney?

A

the efferent arteriole, cause dilation
cause intraglomerular hydrostatic pressure to decrease
less damage, decrease proteinuria

47
Q

Adverse effect ACEI?

A

Functional renal insufficiency

48
Q

Predisposing conditions for functional renal insufficiency?

A 
microvascular renal disease
renal artery stenosis and a solitary kidney
bilateral renal artery stenosis
dehydration
heart failure
nonsteroidal antiinflammatory drug use
49
Q

How to maintain GFR with renal artery stenosis?

A

Ang II, constrict efferent arteriole, increase glomerular hydrostatic pressure, maintain GFR

50
Q

Large decrease in GFR does what to serum creatinine?

A

go way up, esp in bilateral renal artery stenosis

51
Q

Diabetes mellitus and kidney disease?

A

give right amount ACEI, renoprotective

give too much, bad for kidneys

52
Q

ACEI adverse?

A

hypotension (initiation of therapy if volume depleted)
Hyperkalemia- renal insufficiency, combo with K sparing diuretics or K supplements
Hematologic effects
Angioedema (bradykinin, substance P)
Cough (bradykinin, substance P)

53
Q

Contraindications ACEI?

A

prior history angioedema

54
Q

Absolute contraindications ACEI?

A

bilateral renal artery stenosis
renal artery stenosis in sole kidney
teratogenic in 2nd/3rd trimester

55
Q

ARB?

A

only blocks the ang II receptor

56
Q

Aliskiren?

A

Renin inhibitor, only inhibit bradykinin

57
Q

ACEI vs ARB/Aliskiren?

A

ACEI been around longer, prevent destruction of bradykinin

ARBS/Aliskiren- don’t affect bradykinin

58
Q

Ang II receptor antagonist MOA?

A

AT1 receptor anagonists blocks effects of Ang II

alternative to patients who cannot tolerate ACE inhibitors

59
Q

adverse effects ARB?

A

renal insufficiency, hypotension, hyperkalemia, bilateral renal artery stenosis (contraindicated)
angioedema, low incidence of cough

60
Q

Aliskiren?

A

inhibit renin
similar to ACEI/ ARB (theurpeutic and side effects)
no effect on bradykinin
monotherapy or in combo with other agents

61
Q

Contraindication of use a beta blocker?

A

2nd/3rd degree AV block
Active asthma
RP interval > 0.24

62
Q

other Adverse effects of CCB?

A

Constipation (Flushing, headache, dizziness, peripheral edema)

63
Q

Clinical use of Angiotensin II receptor antagonist (ARB)?

A

alternative agent in patient that can not tolerate ACE inhibitors

64
Q

Clinical use of Aliskiren?

A

Hypertension ( mono or combines)

MOD 1 Quiz 1 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions