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MOD 1 Quiz 1 > Antihypertensive drugs > Flashcards

Antihypertensive drugs Flashcards

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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

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2
Q

Short term regulate BP?

A

baroreceptor reflex

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3
Q

Long term regulate of BP?

A

Kidney, Renin-Angiotensin-Aldosterone System

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4
Q

RAAS?

A

Renin increases ANG II, cause vasoconstriction which raises BP

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

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5
Q

Diuretic acute antihypertensive?

A

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

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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

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7
Q

How do diuretics enhance the effects of other drugs?

A

some drugs cause Na retention, this causes release

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8
Q

Most potent diuretic?

A

Loop

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9
Q

Most useful diuretic to treat hypertension?

A

thaizide, first line therapy

Decrease CV events and mortality

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10
Q

When use loop diuretics for hypertension?

A

reduced renal function

severe hypertension when drugs that retain Na are being used

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11
Q

disadvantage to treat hypertension with loop?

A

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

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12
Q

Effect of thiazide and loop on serum K levels?

A

decrease

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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

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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

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15
Q

Use Esmolol to treat chronic hypertension?

A

no because its an IV drug

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16
Q

Propranolol antihypertensive? (heart)

A

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

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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

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18
Q

Propranolol on kidney?

A

decrease renin, decrease ang II, decrease aldosterone

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19
Q

Propranolol on CNS?

A

decrease sympathetic discharge

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20
Q

Not use a beta blocker?

A

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

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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
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22
Q

long term therapy beta blockers?

A

up regulate of receptors, rebound hypertension

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23
Q

Verapamil is?

A

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

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24
Q

Nifedipine is?

A

calcium channel blocker, works only on vascular smooth muscle
dihydropyridine

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25
CCB effect on vasculature?
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
26
If PVR decreases what happens to the heart? BP?
reflex tachy | BP goes down
27
Will there be reflex tachy with verapamil?
no, decrease cardiac output, decrease HR, decrease conduction, decrease force of contraction, no change in PVR
28
First line therapy for hypertension with a compelling indication?
Calcium channel blockers
29
Adverse effects of Verapamil and diliazem?
sinus bradycadria, AV block, exacerbation of heart failure or pulmonary edema
30
Dihydropyridines adverse effects?
Will lower PVR but will cause reflex tachy
31
What will cause nidedipine induced peripheral edema?
increase in hydrostatic pressure in the precapillary sphincter
32
useful agent to combat the nidedipine induced peripheral edema?
ACE inhibitor
33
Angiotensin II effects?
Adrenal- aldosterone release- Na and H2O (increase volume, increase BP) Arterioles/venules- vasoconstriction (increase PVR ,increase BP) facilitate sympathetic activity (increase BP)
34
Ang II on blood pressure?
rise BP
35
Ang II effects?
hypertrophy/hyperplaisa of vascular smooth muscle cell, mesagnial cells, cardiac myocytes, cardiac fibroblasts mycocyte apoptosis, inflammatory mediator, helps regulate GFR
36
block effects of Ang II?
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
Antihypertensive actions of ACE inhibitors?
decrease ang II, increase bradykinin dilate arterioles decrease PVR
38
Decrease Ang II does what?
decrease aldosterone, decrease sympathetic activity
39
Why does ACE inhibitor not cause large drop in aldosterone levels?
other things sim aldosterone release
40
ACEI MOA?
decrease PVR | small effect HR, CO and blood volume
41
ACEI clinical use?
first line for hypertension with compelling indication
42
Acute MI/ ACEI?
administer within 24 hrs post MI to decrease mortality
43
If BP is low, give ACEI?
no
44
ACEI and diabetic nephropathy?
benificial by decreasing bp and benificial without hypertension too
45
primary cause of kidney failure?
diabetes
46
Ang II mainly changes what arteriole in the kidney?
the efferent arteriole, cause dilation cause intraglomerular hydrostatic pressure to decrease less damage, decrease proteinuria
47
Adverse effect ACEI?
Functional renal insufficiency
48
Predisposing conditions for functional renal insufficiency?
``` microvascular renal disease renal artery stenosis and a solitary kidney bilateral renal artery stenosis dehydration heart failure nonsteroidal antiinflammatory drug use ```
49
How to maintain GFR with renal artery stenosis?
Ang II, constrict efferent arteriole, increase glomerular hydrostatic pressure, maintain GFR
50
Large decrease in GFR does what to serum creatinine?
go way up, esp in bilateral renal artery stenosis
51
Diabetes mellitus and kidney disease?
give right amount ACEI, renoprotective | give too much, bad for kidneys
52
ACEI adverse?
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
Contraindications ACEI?
prior history angioedema
54
Absolute contraindications ACEI?
bilateral renal artery stenosis renal artery stenosis in sole kidney teratogenic in 2nd/3rd trimester
55
ARB?
only blocks the ang II receptor
56
Aliskiren?
Renin inhibitor, only inhibit bradykinin
57
ACEI vs ARB/Aliskiren?
ACEI been around longer, prevent destruction of bradykinin ARBS/Aliskiren- don't affect bradykinin
58
Ang II receptor antagonist MOA?
AT1 receptor anagonists blocks effects of Ang II | alternative to patients who cannot tolerate ACE inhibitors
59
adverse effects ARB?
renal insufficiency, hypotension, hyperkalemia, bilateral renal artery stenosis (contraindicated) angioedema, low incidence of cough
60
Aliskiren?
inhibit renin similar to ACEI/ ARB (theurpeutic and side effects) no effect on bradykinin monotherapy or in combo with other agents
61
Contraindication of use a beta blocker?
2nd/3rd degree AV block Active asthma RP interval > 0.24
62
other Adverse effects of CCB?
Constipation (Flushing, headache, dizziness, peripheral edema)
63
Clinical use of Angiotensin II receptor antagonist (ARB)?
alternative agent in patient that can not tolerate ACE inhibitors
64
Clinical use of Aliskiren?
Hypertension ( mono or combines)

MOD 1 Quiz 1 (15 decks)

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