Brainscape's Knowledge GenomeTM

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


See full index

AFN Pharm 1 > Pharm Exam 3: Anti-Hypertensives 1/2 > Flashcards

Pharm Exam 3: Anti-Hypertensives 1/2 Flashcards

1
Q

________ is the most common CV disease

A

HTN

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

less than ______% of pts with HTN are well controlled

A

50

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

pts with HTN have an increased incidence of what other diseases?

A
  1. renal failure
  2. CAD
  3. heart failure
  4. stroke
  5. dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

T/F: risk of end organ damage is proportional to the extent of HTN

A

True

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

normal BP

A

< 120 / < 80

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

elevated BP (pre-htn)

A

120-129/<80

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

stage 1 htn

A

130-139 or 80-89

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

stage 2 HTN

A

> 140 and/or > 90

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

BP = ______________

A

CO x Peripheral VR

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

________________ accounts for 95% of HTN cases

A

primary

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

what is primary htn?

A

no universally established cause

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

primary htn is aka ___________________

A

essential HTN

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

secondary htn

A

is HTN secondary to other potentially rectifiable conditions/causes

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

common causes of 2ndary htn

A
  1. intrinsic renal dz
  2. renovascular dz (renal artery stenosis)
  3. mineralcorticoid excess
  4. sleep apnea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are uncommon causes of secondary htn

A
  1. pheochromocytoma
  2. glucocorticoid excess
  3. corarctation of the aorta
  4. hyper/hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

causes of perioperative HTN

A
  1. inadequate anesthesia
  2. airway manipulation
  3. hypoxia/hypercarbia
  4. pharmacologic adjuncts
  5. urinary distension
  6. aortic cross clamping
  7. hypervolemia
  8. hypothermia/shivering
  9. tourniquet pain
  10. poor medication compliance
  11. disease related factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are disease related factors that can be etiology of HTN perioperatively

A
  1. pheochromocytoma
  2. hyperthyroid
  3. hyperreflexia
  4. MH
  5. intracranial HTN
  6. renovascular HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what two drugs do we give on induction to blunt the SNS response –> i.e. prevent HTN

A

lidocaine and fentanyl

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

what are your anatomic sites of BP control ?

A
  1. arterioles (AL)
  2. venous capacitance vessels (PL)
  3. heart (HR, CO)
  4. kidney (RAAS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

______________ are your capacitance vessels; while _______________ is your resistance vessels

A

veins; arteries

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

what is your humoral mechanism of blood pressure control

A

RAAS

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

what vascular substances are involved in the regulation of Blood pressure?

A

NO- dilates blood vessels
Endothelin 1 - constricts blood vessels

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

which system is responsible for moment-to-moment regulation of BP

A

baroreceptors

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

what system is responsible for long term regulation of BP

A

kidneys

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

what is the neurogenic control center of BP regulation

A

vasomotor center of the medulla

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

how is local nitrous oxide DIRECTLY released

A

by endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how is local nitrous oxide INDIRECTLY released

A

from sodium nitroprusside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

local NO is created in the _______________ cells and then pushed into ________________

A

endothelial; smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how do sympathoplegics (sympatholytics) function (in general) as anti-htn

A

decrease PVR, decrease Heart fx, increase venous capacitance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how do diuretics (in general) act as anti-htn

A

decrease sodium and blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how do direct vasodilators function in tx of htn

A

decrease PVR by relaxing vascular smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

if you use a vasodilator alone in the tx of HTN why would a diuretic and beta blocker need to be added as well ?

A

VD will cause decrease in PVR –> reflex tachycardia + sodium and water retention.
add beta blocker to prevent tachycardia and add diuretic to prevent salt and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

most patients with moderate to sever htn require __________ or more anti-htn meds

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what anti-htn drugs can be used as initial drug therapy d/t reduction of complications?

A
  1. thiazide diuretics
  2. ACE-I
  3. ARB
  4. CCB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

why are diuretics not commonly used as first line agent in the tx of htn

A

they can increase serum lipid profile and/or impair glucose tolerance –> risk of CAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

_____________ are less effective at reducing cardiovascular event, and are currently not recommended as first line tx for uncomplicated htn

A

beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

you know someone’s HTN is poorly controlled if they are on _______+ anti-hypertensives

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

under what condition can a diuretic be used as the sole agent in htn treatment?

A

mild htn - only need reduction of BP by 10-15 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

which diuretic is the preferred agent as an antihtn agent?

A

thiazide diuretics - specifically chlorthalidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

adverse effects of diuretics

A
  1. hypokalemia
  2. magnesium depletion
  3. impair glucose tolerance
  4. increase serum lipid concentration
  5. increase uric acid –> gout
41
Q

what is the purpose of using a diuretic + a potassium sparing diuretic?

A

reduces blood pressure without causing hypokalemia/hypomagnesmia

42
Q

what is the purpose of using a diuretic + Beta blocker

A

counteracts the water retaining effects of the beta blocker

43
Q

what is the purpose of using ACEI + diuretic

A

thiazide diuretic can activate RAAS, ACE-I will counteract this effect

44
Q

what is the purpose of using ARB + diuretic

A

thiazide diuretic can activate RAAS, ARB will counteract this effect and not cause the dry cough that ACE-I do

45
Q

what are the 2 physiological actions that diuretics do allowing them to fx as anti-htn

A
  1. decrease intravascular volume
  2. cause direct arterial vasodilation
46
Q

under what condition, would a thiazide drugs diuretic effect be less effective

A

with renal insufficiency

47
Q

why are loop diuretics not used as a first line agent for htn

A

short duration of action

48
Q

when is a potassium sparing diuretic useful in the tx of htn

A

htn caused by hyperaldosteronism

49
Q

of pts with primary HTN, _____% have too high plasma renin, and _______% have too low

A

20; 20

50
Q

renin is released when:

A
  1. decreased renal arterial bp
  2. SNS neural stimulation
  3. reduced sodium delivery
  4. increased sodium in the distal renal tubule
51
Q

angiotensin II has ________________ and _____________ activity

A

vasoconstrictor; sodium retaining.

52
Q

angiotensin II and III both stimulate _____________ release

A

Aldosterone

53
Q

drug classes that act on RAAS

A
  1. ACE-I
  2. ARBs
  3. Renin antagonist
  4. aldosterone receptor inhibitors
54
Q

___________ are drugs that do not act on RAAS, but can reduce renin secretion

A

beta blockers

55
Q

what drug is a renin inhibitor

A

aliskiren

56
Q

physiologic response of aliskiren, a renin-inhibitor

A
  1. vasodilation (arterial and venous)
  2. decreases blood volume
  3. decreases SNS
  4. inhibits cardiac and vascular hypertrophy
57
Q

how do ACE-I work?

A
  1. inhibit the enzyme that converts ang I to ang II
  2. stimulates the kallekrein-kinin system by inhibiting the breakdown of bradykinin
58
Q

__________________ do NOT cause reflex SNS activation, therefore they are safe to use in pts with ischemic heart disease.

A

ACE-inhibitors

59
Q

which specific drug do you have to use caution with, when also using a NMBA d/t synergistic effects

A

lisinopril

60
Q

what class of drugs may reduce the incidence of DM in pts with high cardiovascular risk

A

ACE - I

61
Q

what class of anti-htn drugs, is useful in treating patients with CKD, d/t its ability to diminish proteinuria and stabilize renal fx

A

ACE-I

62
Q

all ACE-I are prodrugs except

A

lisinopril

63
Q

what is the most common side effect with ACE-I

A

dry cough

64
Q

what causes the dry cough s/e in 10% of pts on an ACE-I

A

increase in bradykinin (d/t inhibition of bradykinin metabolism)

65
Q

what are the common side effects with ACE-I

A
  1. dry cough
  2. hypotn with hypovolemia
  3. hyperkalemia
  4. angioedema
66
Q

ACE-I are contraindicated with ____________ & ___________

A

pregnancy; bilateral renal artery stenosis

67
Q

why are ACE-I contraindicated with pregnancy

A
  1. fetal hypotension
  2. anuria
  3. renal failure.
68
Q

it is acceptable for Cr to increase up to ____________% while using ACE-I, as long as do not have sudden leaps

A

30%

69
Q

before being put on an ACE-I, baseline Cr must be < _________, and serum K should be less than ________

A

2.5; 5.2

70
Q

what is a common effect of patients with heart failure if put on an ACE-I

A

develop hypotension and worsening renal fx

71
Q

T/F: ACE-I have a relatively low incidence of side effects and are well tolerated

A

true

72
Q

patients with bilateral renal artery stenosis can go into renal failure if __________ is administered

A

ACEI or ARB

73
Q

if you use K+ supplements or K+ sparing diuretics with ACE-I what is the result

A

hyperkalemia

74
Q

what is the effect if you use NSAIDs with ACEI ?

A

block bradykinin-mediated vasodilation

75
Q

what is the only ARB approved for post-myocardial infarction

A

valsartan

76
Q

what drugs inhibit cardiac and vascular remodeling associated with chronic HTN, heart failure, and MI

A

ACEI and ARB

77
Q

physiological response of ARBs for HTN

A
  1. dilate arteries and veins
  2. down regulate SNS activity by blocking the effect of ang II on SNS
  3. promote renal excretion of sodium and water by blocking AngII
78
Q

T/F: s/e are more rare with ACE-I than ARB

A

false; more rare with ARB

79
Q

which drug class has a more complete inhibition of angII - ACEI or ARB?

A

ARB

80
Q

why do ARBs not have as big of a risk with dry cough and/or angioedema when compared to ACEI

A

no effect on bradykinin metabolism

81
Q

if using an ARB, when do hypotensive effects increase?

A

diuretic use
vasodilators
anesthetic drugs

82
Q

if a patient comes in on an ARB, and has intraoperative hypotension, how should you treat it?

A

fluids & vasopressors (esp vasopressin)

83
Q

anesthetic considerations with ARBs

A
  1. hypotensive effects with diuretic use, hypovolemia, VD, and anesthesia
  2. interoperative hypotn tx with fluids and vasopressors (incl vasopressin)
  3. risk of hyperkalemia with potassium containing solutions
  4. increase muscle relaxant effects of non-depolarizing muscle agents
84
Q

contraindications with ARBS

A

pregnancy & Bilateral renal artery stenosis

85
Q

if a patient is unable to tolerate ACE-I, they are often switched to a _________

A

ARB

86
Q

potassium sparing diuretics are aka _____________ and/or ________________

A

aldosterone receptor inhibitors; mineralcorticoid receptor antagonist

87
Q

what are your aldosterone receptor inhibiting drugs

A
  1. eplerenone (inspra)
  2. spirinolactone (aldactone)
88
Q

which diuretic might be useful in a patient with a pericardial effusion

A

aldosterone receptor inhibitors (k-sparin)

89
Q

K - sparing diuretics (aldosterone receptor inhibitors) may cause what electrolyte imbalance?

A

hyperkalemia

90
Q

are vasodilators a good single tx method for htn?

A

no d/t compensatory reflexes –> increased HR, blood volume, sodium

91
Q

if you are using a vasodilator to tx htn, adding a beta blocker will stop what 3 compensatory mechanisms from counteracting the VD?

A
  1. block increased renin release
  2. block increase in HR
  3. block increased cardiac contractility
92
Q

The risk of CV disease doubles for every ____/____ increase in BP.

A

20/10

93
Q

A primary autonomic mechanism that involves sensory input from the carotid sinus and the aorta to the vasomotor center (Neurogenic Control) and output via the PNS and SNS motor nerves.

A

Baroreceptors

94
Q

Activation (Stretch) of these inhibits central sympathetic discharge.

A

Baroreceptors

95
Q

Decreased stretch on the baroreceptors decreases their activity. This leads to a RAPID increase in SNS outflow, leading to:

A

-Increased PVR (via constriction of arterioles)
-Increased CO (via direct stimulation of the heart and constriction of capacitance vessels to increase venous return)

Restoring normal BP

96
Q

What stimulates the release of Renin?

A

-Reduction in renal blood flow (decreased pressure in renal arterioles)
-Sympathetic neural activity (via Beta receptors)

97
Q

What does Angiotensin 2 cause?

A

1) Direct constriction of resistance vessels
2) Stimulation of aldosterone synthesis in the adrenal cortex

98
Q

An arterial dilator used for HTN crisis
-Only IV agent that improves renal perfusion
-D1 agonist
-Dilates peripheral arteries and causes natriuresis
-SE: Reflex tachycardia, increases IOP (beware in glaucoma)

A

Fenoldopam

AFN Pharm 1 (5 decks)

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