Brainscape's Knowledge GenomeTM

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


See full index

Cardiovascular > Misc Sweatman Pharm > Flashcards

Misc Sweatman Pharm Flashcards

Did these quickly as I studied, sorry if some are bizzarre half-thoughts

1
Q

Effects of beta-1 and -2 receptor activation?

A

accelerates SA node, increases contractility, accelerates ectopic pacemakers IN HEART

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

Effects of alpha-1 receptor activation?

A

contract vessels by increasing DAG and IP3, which results in an increase of Ca++

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

What receptors act via NE?

A

alpha 1, alpha 2, beta 1

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

What receptors act via epi?

A

alpha 1, alpha 2, beta 1, beta 2

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

What receptor would you block to treat BPH?

A

alpha 1

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

What class of drugs cause 1st dose orthostatic hypotension? What specific drug is the most prominent?

A

alpha blockers

prazosin

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

Effects of alpha 2 receptors?

A

decrease cAMP production, which blocks further release of NE (feedback inhibition)

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

Effects of alpha-1 antagonists?

A

antagonist circulating NE and epi, which prevents vasoconstriction

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

Effects of alpha-2 antagonists?

A

block feedback inhibition, which increases NE release

increases CO, “tempering” BP lowering

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

Treatment for pheochromocytoma?

A

phenoxybenzamine
phentolamine
(alpha blocker)

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

Why does phenoxybenzamine cause nasal congestion and drowsiness?

A

minor action = blocking histamine, serotonin and ACh

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

What treats hypertensive emergency?

A

phentolamine

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

What is the difference between a small versus a large dose of alpha 2 antagonist?

A

small: increases BP
large: decrease BP (due to periph vasodil)

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

What limits the use of phentolamine in essential HTN?

A

postural hypotension, reflex tach ppt arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q 
Epi causes (increased/decreased) BP); treatment with an alpha blocker will....
Treatment with a beta blocker will...
A

increased BP
decrease BP
no effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q 
NE causes (increased/decreased) BP; treatment with an alpha blocker will....
Treatment with a beta blocker will...
A

increased BP
slight decrease in BP
no effect

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

What drug class affects renin release?

A

B1 agonists (on JG cells)

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

Intrinsic sympathomimetic activity?

A

pure: propranolol

partial:
pindolol

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

Drugs with membrane stabilizing ability?

A

propranolol
cervedilol

class 1 antiarrhythmics

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

How do drugs stabilize membranes?

A

bind/block fast Na channels which are responsible for rapid depol (decrease phase 0 slope)

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

What is intrinsic sympathomimetic activity?

A

activate receptors in the absence of catecholamines

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

What is inverse sympathomimetic activity?

A

selectively bind to inactive form of receptor and behave like competitive antagonists (“off”)

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

B antagonists that block Ca entry:

What does this do?

A

carvedilol
betaxolol

prevents contraction

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

B antagonist that produces NO:

A

nebivolol

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

B antagonists that are also a-1 R antagonists?

A

carvedilol

labetolol

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

B antagonist that has antioxidant activity?

A

carvedilol

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

What results from long term administration of beta blockers?

A

drop in peripheral vasc resistance

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

Beta blocker with no effect on renin? Most effective if elevated renin?

A

pindolol

propranolol

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

What effect does lipid solubility have on antihypertensives?

A

drugs that do NOT penetrate BBB (low sol) are effective anti-HTN

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

Who should NOT take beta blockers?

A

patients with:

  1. compensated HF, acute MI, cardiomeg
  2. AV conduction defects, as these drugs cause bradycardia
  3. bronchospastic disease (due to bronchoconstriction via beta-2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Beta blockers should not be stopped abruptly because:

A

they can exacerbate angina and increase risk of sudden death (receptors are upregulated)

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

Lipophilic beta blockers may cause:

A

CNS depression, causing mental disorders, fatigue, vivid dreams

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

How do beta blockers affect plasma lipids?

A

increase triglycerides

decrease HDL

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

What type of beta blockers reduce cholesterol and LDL?

A

those with intrinsic sympathomimetic activity and cardioselectivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Activation of what receptors mediates lipolysis?

A

alpha1

beta 1, 2, 3

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

What is the effect of using beta blockers post MI?

A

improved mortality

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

Non-CV uses for beta blockers?

A 
tremor
thyrotoxicosis
anxiety
migraines
prevent bleeding from esoph varices
glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Effects of ganglionic blockade on arterioles?

A

vasodilation

hypotension

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

Effects of ganglionic blockade on veins?

A

dilation/pooling

decreased venous return/CO

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

Effects of ganglionic blockade on heart?

A

tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Nicotinic receptors are ______ channels which mediate

A 
post-synaptic ligand gated ion
initial EPSP (caused by Na/K)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

MOA of trimethaphan:

A

competes with ACh for ganglionic receptor binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Causes dry mouth, vision problems, urinary retention, constipation?

A

ganglionic blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

MOA of reserpine:

A

binds to NT storage vesicles and inhibits vesicle transporter VMAT2

=no storage/concentration of dopamine and NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

MOA of clonidine:

A

withdrawal of SNS tone resulting in decreased BP and decreased PVR

46
Q

High, chronic overstimulation of alpha-2 recepors results in:

A

downregulation via beta-arr mediated endocytosis

i.e. during HF

47
Q

Effects of alpha-2-autoreceptors

A

bradycardia

hypotension

48
Q

Activation of central alpha-2-heteroreceptors

A 
sedation
hypothermia
analgesia
bradycardia*
hypotension*

*due to vagal activation

49
Q

Activation of peripheral, vascular alpha 2 receptors causes

A

vasoconstriction

50
Q

Effects of central alpha 2 receptor agonists: (4)

A

decrease plasma renin activity
regression of LV hypertrophy
decreased PVR
decreased BP

51
Q

Side effect of central alpha 2 receptor agonists:

A

salt/water retention (*trx duiretics, too)

52
Q

Chelated by concurrent iron

A

methyldopa

53
Q

Should be given with caution to diabetics

A

beta blockers

mask warning tachycardia (1)
cause hypoglycemia (2)
54
Q

Helpful in blocking reflex tachycardia

A

clonidine (alpha 2 agonists)

55
Q

Adverse effects of central acting alpha 2 agonists

A

somnolence

dry mouth

56
Q

Used to treat HTN in pregnancy?

A

*methyldopa
*labetalol (IV for HTN emergencies)
pindolol/propranolol
HCTZ (recently decided it was ok)

57
Q

Do not give in pregnancy:

A

ACEI
ARBs
reserpine

58
Q

Reserpine’s effects:

A

central and peripheral anti-HTN

59
Q

Side effects of reserpine

A

psychotic depression (suicide)
CNS (sedation, inability to concentrate)
Exacerbation of PUD ulcerative colitis

60
Q

Why are old centrally acting drugs good modern options?

A

cheap

better adverse effect profile

61
Q

alpha blockers end in:
beta blockers end in:
ACEI end in:
ARBs end in:

A
  • in/-ine
  • olol
  • pril
  • artan
62
Q

Treat v-tach:

A
  1. amiodarone
  2. lidocaine
  3. procainamide
63
Q

MOA of class 1 antiarrhythmics:

A

na channel blocker

64
Q

MOA of class 2 antiarrhythmics:

A

beta blocker

65
Q

MOA of class 3 antiarrhythmics:

A

K channel blocker

66
Q

MOA of class 4 antiarrhythmics:

A

Ca channel blocker

67
Q

Effects of local epi?

A

vasoconstriction

68
Q

Direct acting adrenergic agonists stimulate:

A

post-syn receptors

69
Q

Indirect acting adrenergic agonists increase:

A

NE and epi availability

70
Q

Cocaine is a (direct/indirect) adrenergic agonist

A

indirect (blocks reuptake of NE)

71
Q

MAOI’s are (direct/indirect) adrenergic agonists

A

indirect (blocks metabolism of enzymes)

72
Q

Treatment with reserpine results in a loss of (direct/indirect) adrenergic agonist action

73
Q

Epi will ______ CO, _____ HR, ___ contracility and _____BP.

A

increase, increase, increase, increase

74
Q

NE will ____HR, _____CO, ____BP, ____TPR, ____SV

A 
no effect (due to vagus)
no effect/decrease
increase
increase
increase
75
Q

Increases SBP more than DBP; why?

A

Epi

B-2 mediated increase in peripheral resistance

76
Q

Epi causes more vaso-(dilation/constriction); why?

A

dilation

more effect on beta-2 than alpha receptors

77
Q

Where does epi cause vasoconstriction?

A

skin, kidney, veins

78
Q

Small doses of epi may cause:

A

decreased BP (due to differential receptor sensitivity)

79
Q

Where are beta-1 receptors?

A

myocardium, PM, conducting tissues

80
Q

How does epi affect the heart? (4)

A

shortened systole, increased HR, increased CO, increased O2 consumption

81
Q

What is a possible side effect that epi may have on the heart?

82
Q

How does epi affect the kidneys?

A

decreased renal bf by increasing vasc resistance

this will NOT change GFR and will decrease Na/K/CL excretion

83
Q

How does epi affect renin levels?

A

increase due to beta-1 receptors in JGA

84
Q

Can restore cardiac rhythm in patients with cardiac arrest

85
Q

What should be monitored in patients given NE?

86
Q

How do you measure dopamine’s effects?

87
Q

Dopamine acutely benefits patients with:

A

CHF

Renal failure

88
Q

What receptors are activated by dopamine (in order of concentration)?

A

D1 > beta 1 > alpha 1

89
Q

Effects of low dose dopamine?

A

renal, coronary, etc vasodilation

improves GFR

90
Q

Effects of moderate dose dopamine?

A

vasodilation

increased CO

91
Q

Effects of high dose dopamine?

A

increase PVR

renal vasoconstriction

92
Q

Dobutamine will ____HR, ____SV, ____ contractility and ___CO

A

no effect
increase
increase
increase

93
Q

Dobutamine is used to treat:

A

post cardiac surgery
after MI
CHF

94
Q

How does isoproterenol affect BP?

A

decreases DBP (by decreasing PVR)

95
Q

Phenylepherine has a stronger effect on (alpha/beta)

A

alpha

no beta!

96
Q

Effects of phenylepherine:

A

increase BP

REFLEX decrease in HR and CO

97
Q

Side effects of phenylepherine:

A

anxiety
hallucinations/psychosis
HTN
insomnia

98
Q

Ephedrine affects what receptors?

A

alpha and beta

99
Q

Effects of ephedrine:

A

increase HR
increase CO
increase BP

100
Q

Side effects of ephedrine:

A 
increases cardiac workload > angina
ventricular dysfunction
palpitations
s-tach
arrhythmia (*v-fib)
101
Q

the parasympathetic nervous system = ______ receptors

A

muscarinic

102
Q

M2 receptor activation leads to…

A

reduced contractility

SA node deceleration - decreased HR

103
Q

M3 receptor activation leads to…

A

NO synthesis

104
Q

Effects of ACh on CV system:

A

vasodilation
decreased HR
decreased AV node conduction
decreased force of atrial contraction

105
Q

Effects of M2 on cell channels?

A

activate K

inhibit Ca

106
Q

IV ACh results in…

What is a possible negative effect?

A

transient decrease in BP
reflex tachy

bradycardia or AV node conduction block

107
Q

Effects of atropine

A

increase resting HR (no effect or maximal HR)

counteracts vasodilation + BP drop

108
Q

What is an indirect action of atropine?

A

vasodilation of cutaneous vessels (atropine flush)

*this offsets the heat-loss reduction caused by sweating inhibition

109
Q

Prevents cardiac arrest from vagal stimulation

110
Q

How does atropine benefit patients with MI’s?

A

(if inferior or posterior wall)

relieves severe bradycardia or AV block

111
Q

Dobutamine is a:

A

beta agonist with both alpha1 agonist and antagonist activity (cancels out!)

Cardiovascular (31 decks)

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