Brainscape's Knowledge GenomeTM

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


See full index

SBM Pharm term 1 > antihypertensive > Flashcards

antihypertensive Flashcards

1
Q

what are the three main subclasses of diuretics?

A
  • thiazides
  • loop diuretics
  • k sparing diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the four major classes of antihypertensive drugs?

A
  • diuretics
  • inhibitors of the RAA system
  • vasodilators
  • sympatholytic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the two main subtypes of inhibitors of the RAA system?

A
  • ACE inhibitors

- angiotensin receptor blockers

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

what are the two main subtypes of vasodilators?

A
  • direct acting

- calcium entry blockers

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

what are the four major subtypes of sympatholytic antihypertensives?

A
  • CNS
  • autonomic ganglia
  • post-ganglionic neurons
  • block peripheral adrenergic receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what class is hydrochlorothiazide?

A

thiazide diuretic

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

hydrochlorothiazide pharmacodynamics

A

blocks reuptake of Cl and Na from tubular fluid after glomerular filtration

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

how much will hydrochlorothiazide lower BP?

A

10-15mm

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

HCTZ bioavailability

A

70%

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

HCTZ excretion

A

urine, unchanged

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

HCTZ half life

A

short (hours)

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

HCTZ toxicity

A
  • K and Mg depletion
  • Na and Cl depletion
  • metabolic alkalosis
  • volume depletion
  • worsen hyperuricemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HCTZ special considerations

A
  • more side effects in geriatrics
  • pregnancy class D
  • less effective with low GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HCTZ route

A

oral

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

why might chlorthalidone be better than HCTZ?

A
  • greater reduction of SBP
  • better control of SBP at night
  • longer half life (50 hours)
  • 1.5-2x more potent per mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What class is chlorthalidone?

A

thiazide diuretic, same as HCTZ

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

what class is lisinopril?

A

ACE inhibitor, subtype of RAA system inhibitors

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

lisinopril indications

A
  • hypertension/CHF
  • preserve renal function
  • preservation of LV function after MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

lisinopril pharmacodynamics

A
  • inhibits conversion of AT1 to AT2 by ACE
  • diminishes vasoconstriction
  • diminishes stimulation of aldosterone secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

lisinopril excretion

A

urine, unchanged

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

lisinopril timing

A
  • onset 1 hour
  • peak 6 hrs
  • duration 24 hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

lisinopril toxicity

A
  • ortho hypotension
  • caution impaired renal function
  • caution renal artery stenosis
  • caution diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

lisinopril interactions

A
  • NSAIDS may reduce ability to lower BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

lisinopril special considerations

A
  • may wan to discontinue diuretics before use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

lisinopril route

A

oral

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

losartan class

A

ARB, RAA system inhibitor

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

losartan indications

A
  • hypertension

- CHF

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

losartan pharmacodynamics

A

block stimulation of AT1 receptors by angiotensin II, reduce vasoconstriction and production of aldosterone

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

losartan bioavailability

A

F 30%

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

losartan onset/timing

A
  • onset 6 hrs
  • extensive first pass effect
  • active metabolite 40x more potent, much longer half life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

losartan special considerations

A
  • pregnancy
  • caution with diuretics
  • caution with renal stenosis, mitral or aortic stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

losartan route

A

oral

33
Q

nitroprusside class

A

direct vasodilator

34
Q

nitroprusside indications

A
  • severe CHF
  • severe pulmonary hypertension
  • produce hypotension during surgery
35
Q

nitroprusside pharmacodynamics

A
  • direct on vascular smooth muscle of veins and arterioles
  • metabolized to CN- and NO, activates guanylate cyclase, converts GTP and cCMP, leads to vasodilation, cGMP turned to GMP by PDE
36
Q

nitroprusside route

A

IV only, continuous infusion

37
Q

nitroprusside onset/timing

A
  • minutes to onset

- minutes to cessation

38
Q

nitroprusside metabolism

A

CN- metabolite converted to SCN in liver and excreted in urine

39
Q

nitroprusside toxicity

A
  • excessive hypotension
  • metabolic acidosis
  • accumulation of CN- and thiocyanate
  • headache
  • decreased blood flow to brain
40
Q

nitroprusside special considerations

A

monitor very closely to prevent accumulation of CN-

41
Q

hydralazine class

A

direct vasodilator

42
Q

hydralazine indications

A
  • hypertension

- CHF

43
Q

hydralazine pharmacodynamics

A
  • induces endothelium to produce NO, which then passes to the smooth muscle cells and induces production of cGMP
  • minimal venodilating effect
44
Q

contrast hydralazine and nitroprusside

A
  • nitroprusside veno and vasodilates while hydralazine only minimally venodilates
45
Q

hydralazine routes

A

oral, IM, IV

46
Q

hydralazine metabolism

A
  • metabolized extensively in GI mucosa and in liver

- excreted as metabolites in urine

47
Q

hydralazine F

A

40%

48
Q

hydralazine onset vs route

A
  • oral 30 min
  • IV 10 min
  • persists for 2-6 hours
49
Q

hydralazine toxicity

A 
more dangerous in patients with:
- renal disease
- prior stroke
- angina
can cause hyptotension, edema, drug-induced lupus
50
Q

hydralazine special considerations

A

never use as chronic oral monotherapy for treatment of hypertension since edema and reflex tachycardia will result.

51
Q

verapamil class

A

calcium entry blocker (CEB), vasodilator

52
Q

verapamil indications

A
  • hypertension
  • angina
  • arrhythmia
53
Q

verapamil pharmacodynamics

A
  • reduces BP by inhibiting influx of calcium through “slow channels” leading to peripheral arteriolar dilation
  • negative inotropic effect
  • reduces afterload (for angina) to decrease oxygen consumption
  • inhibits spasm of coronary arteries
  • blocks reentry paths through AV node in paroxysmal SVT
54
Q

verapamil absorption speed

A

rapid

55
Q

verapamil F

A

30%

56
Q

verapamil clearance

A

liver and kidney

57
Q

verapamil onset vs route

A

oral - 2hrs

IV - 1-5mins

58
Q

verapamil routes

A

oral, IV

59
Q

verapamil half-life

A

6-12hrs

60
Q

verapamil toxicity

A
  • hypotension
  • AV block
  • worsening CHF
  • bradycardia
61
Q

verapamil interactions

A
  • toxic effect on heart when given with b-blockers
62
Q

verapamil special considerations

A
  • reduce dose if someone has both hepatic and renal disease
63
Q

nifedipine most closely resembles the actions of:

A

verapamil

64
Q

methyldopa class

A

sympatholytic antihypertensive

65
Q

methyldopa pharmacodynamics

A
  • central a2 agonist
  • also competitive inhibitor of L-DOPA decarboxylase which converts L-DOPA into dopamine which subsequently becomes norepinephrine and epinephrine
66
Q

methyldopa indications

A
  • hypertension

- gestational hypertension

67
Q

methyldopa F

A

50%

68
Q

methyldopa half life

A

1-2 hours

69
Q

methyldopa routes

A

oral, IV

70
Q

reserpine class

A

sympatholytic antihypertensive

71
Q

reserpine pharmacodynamics

A

irreversibly blocks vesicular monoamine transporter (VMAT) so presynaptic neurotransmitters can’t be packaged into vesicles for release.

72
Q

reserpine indications

A
  • hypertension

- psychotic symptoms

73
Q

reserpine F

A

50%

74
Q

reserpine metabolism

A

gut/liver

75
Q

reserpine excretion

A

62% feces, 8% urine

76
Q

reserpine half life

A

33 hours, with two phases, first one short, second one long

77
Q

reserpine route

A

oral

78
Q

what two drugs are similar to prazosin? what is their mechanism?

A

terazosin and doxazosin - a1 blockers that lower blood pressure. initially raise heart rate to meet homeostasis but then it adjusts.

SBM Pharm term 1 (9 decks)

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