Brainscape's Knowledge GenomeTM

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


See full index

Pharm > Week 3 (Midterm) (Adrenergic) > Flashcards

Week 3 (Midterm) (Adrenergic) Flashcards

1
Q

Organs of the somatic system

A

skeletal muscle

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

Function of the somatic system

A

Voluntary movement

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

Receptor for the somatic system

A

Cholinergic (Nicotinic)

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

Sympathetic organs

A

heart, bronchiole, vascular smooth muscle

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

What type of receptor are nicotinic receptors?

A

Na+ gated channels

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

Receptor for sympathetic system

A

Adrenergic

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

What type of receptor are adrenergic receptors?

A

G-protein coupled, binds NE, Epi

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

Alpha-1, binds which G?

A

Gq

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

Alpha-1, agonistic response?

A

↑ BP (constricts smooth muscle)

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

Alpha-2, binds which G?

A

Gi

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

Alpha-2, agonistic response?

A

↓ BP, centrally (vasodilation)

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

Beta-1, binds which G?

A

Gs

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

Beta-1, agonistic response?

A

↑HR, ↑cardiac contractility

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

Beta-2, binds which G?

A

Gs

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

B-2, agonistic response?

A

bronchodilation, ↓BP (dilates arterioles), relaxation of uterus

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

Neurotransmitter for pre-ganglionic neurons?

A

ACh (somatic, sympathetic and parasympathetic)

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

Organs for parasympathetic system

A

heart, GI tract smooth muscle

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

Receptor for parasympathetic system

A

Cholinergic (muscarinic)

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

What type of receptor is muscarinic?

A

G-Protein

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

M1 and M3 bind which G?

A

Gq

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

M1 and M3 site?

A

(vasodilation) endothelium of vasculature, autonomic ganglia, gastric parietal cells, exocrine glands, smooth muscle

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

M2 and M4, which G?

A

Gi

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

M2 and M4, site?

A

SA, AV nodal cells, CNS

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

What is the exception to short preganglionic in the sympathetic system?

A

adrenal medula

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

What are the 4 cranial nerves involved in parasympathetic functions?

A

3, 7, 9, 10

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

Adrenergic pre-ganglionic neurons secrete:

A

ACh (receptor is nicotinic)

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

Adrenergic post-ganglionic neurons secrete:

A

NE (receptor is adrenergic)

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

Where does NE go to Epi?

A

In the adrenal medulla

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

Step 1: Tyrosine to _____

A

L-DOPA

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

Step 1: Tyrosine to L-DOPA (Enzyme)

A

Tyrosine hydroxylase

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

Step 1: Tyrosine to L-DOPA (inhibited by)

A

metyrosine and NE

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

What is the rate limiting step in synthesizing NE?

A

Tyrosine –> L-DOPA

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

What is metyrosine used to treat?

A

pheochromocytoma

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

Step 2: L-DOPA to _____

A

Dopamine

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

Step 2: L-DOPA to Dopamine (Enzyme)

A

AAAD

L-DOPA decarboxylase

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

Step 2: L-DOPA to Dopamine (inhibited by)

A

Carbidopa

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

Breakdown of Dopamine enzyme

A

MAO-B

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

MAO-B inhibitor

A

Deprenyl

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

Step 3: Dopamine to ____

A

NE

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

Step 3: Dopamine to NE (enzyme)

A

Dopamine Beta-hydroxylase

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

Step 3: Dopamine to NE (inhibited by)

A

Copper chelators i.e. Disulfiram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Step 4: NE to Epi (enzyme)

A

PNMT

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

Carbidopa and parkinson’s

A

Given to build-up L-DOPA in plasma, which can cross the BBB to be converted to dopamine

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

Amantadine and parkinson’s

A

Stimulates release of dopamine in vesicles

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

MPTP

A

Heroine substitute metabolized by MAO-B into toxin –> presents like PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What inhibits the release of catecholamines?

A

Adrenergics (a2) attached to Gi subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Catecholamines are taken back up by:

A

Sodium channels (uptake-1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Catecholamines are broken down by:

A

COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Reserpine and BBB

A

Crosses the BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Reserpine and action

A

permanent inhibition of amine-H+ for catecholamine packaging into vesicles; action duration much longer than plasma half-life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Reserpine and effect

A

Deplete catecholamine stores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Reserpine and use

A

Hypertension

53
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Reserpine and side effects

A

Depression, parkinsonism, gynecomastia

54
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Clonidine action

A

alpha-2 agonist –> inhibits release of catecholamine vesicles

55
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Clonidine effect

A

decreased catecholamines in synapse

56
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Clonidine use

A

hypertension

57
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Clonidine side effects

A

dry mouth, drowsiness (somnolence)

58
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Metyrosine action

A

inhibits tyrosine

59
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Metyrosine effect

A

no neurotransmitter stored

60
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Metyrosine use

A

pheochromocytoma

61
Q

INDIRECT CATECHOLAMINE ANTAGONISTS:

Metyrosine side effects

A

Hypotension, sedation

62
Q

INDIRECT CATECHOLAMINE AGONISTS:

Guanethdine/Guanadrel action

A

inhibits release of packaged catecholamine stores by inhibitig vesicle fusion; competitive inhibition of Uptake-1

63
Q

INDIRECT CATECHOLAMINE AGONISTS:

Guanethdine/Guanadrel effect

A

depletes catecholamine stores by inhibiting vesicle fusion

64
Q

INDIRECT CATECHOLAMINE AGONISTS:

Guanethdine/Guanadrel use

A

Hypertension (obsolete)

65
Q

INDIRECT CATECHOLAMINE AGONISTS:

Guanethdine/Guanadrel side effects

A

Postural hypotension; hypertension on first administration

66
Q

Which has a longer half-life? Guanethidine or Guanadrel?

A

Guanethidine

67
Q

INDIRECT CATECHOLAMINE AGONISTS:

Tyramine action

A

Displaces catecholamines out of nerve terminal; competitive inhibition of uptake-1

68
Q

INDIRECT CATECHOLAMINE AGONISTS:

Tyramine Effect

A

↑ catecholamine in synapse

69
Q

INDIRECT CATECHOLAMINE AGONISTS:

Tyramine side effects

A

“cheese syndrome”, hypertensive crisis, hypertension, vasoconstriction, tachycardia

70
Q

What is tyramine metabolized by?

71
Q

INDIRECT CATECHOLAMINE AGONISTS:

Amphetamines /Ephedrine/ Pseudoephedrine action

A

Displaces catecholamines out of nerve terminal; competitive inhibition of uptake-1

72
Q

INDIRECT CATECHOLAMINE AGONISTS:

Amphetamines /Ephedrine/ Pseudoephedrine effect

A

↑ catecholamine in synapse (indirect release of catecholamines)

73
Q

INDIRECT CATECHOLAMINE AGONISTS:

Amphetamines /Ephedrine/ Pseudoephedrine use

A

Amphetamine: stimulant, ↑ wakefulness, appetite suppressant, and recreational drug

Ephedrine: decongestant

74
Q

INDIRECT CATECHOLAMINE AGONISTS:

Amphetamines /Ephedrine/ Pseudoephedrine side effects

A

hyperactivity, dilated pupils, ED, ↑BR and HR, sweating, hypertension, insomnia, dependence

75
Q

INDIRECT CATECHOLAMINE AGONISTS:

Tricyclic Anti-Depressents and BBB

A

Crosses BBB

76
Q

INDIRECT CATECHOLAMINE AGONISTS:

Tricyclic Anti-Depressents action

A

inhibits uptake-1

77
Q

INDIRECT CATECHOLAMINE AGONISTS:

Tricyclic Anti-Depressents effect

A

increase catecholamine in synapse

78
Q

INDIRECT CATECHOLAMINE AGONISTS:

Tricyclic Anti-Depressents use

A

depression

79
Q

INDIRECT CATECHOLAMINE AGONISTS:

Tricyclic Anti-Depressents side effects

A

sudden death

80
Q

INDIRECT CATECHOLAMINE AGONISTS:

Cocaine action

A

CNS: inhibits Uptake-1

PNS: inhibits Na+ channels

81
Q

INDIRECT CATECHOLAMINE AGONISTS:

Cocaine effect

A

increased catecholamine in synapse; prevents neuronal excitation

82
Q

INDIRECT CATECHOLAMINE AGONISTS:

Cocaine use

A

local anesthetic, recreational drug

83
Q

INDIRECT CATECHOLAMINE AGONISTS:

Cocaine side effects

A

euphoria, increased HR and BP, convulsions, dependence

84
Q

Epinephrine (adrenaline) Mechanism

A

α1, α2, β1, β2 agonist (even split between α and β)

85
Q

Epinephrine Use

A

cardiac arrest, correct low cardiac output, anaphylaxis, added to local anesthetics

86
Q

Epinephrine SE

A

hypertension*, vasoconstriction, tachycardia, ventricular dysrhythmias

87
Q

Norepinephrine mechanism

A

predominantly α1 and α2 agonist; mild β1 agonist

88
Q

Norepinephrine use

A

correct hypotension (critical care setting) - probably mainly via α1 vasoconstriction action

89
Q

Norepinephrine SE

A

hypertension*, vasoconstriction, tachycardia, ventricular dysrhythmias

90
Q

Which causes less hypertension, epi or NE?

A

Epi b/c NE prefers alpha receptors

91
Q

Phenylephrine, Methoxamine mechanism

A

alpha-1 agonist

92
Q

Phenylephrine, methoxamine use

A

Decongestant, pupil dilator, for septic shock or profound hypotension

93
Q

Phenylephrine, methoxamine SE

A

hypertension, reflex bradycardia

94
Q

Clonidine, alpha-methylnoradrenaline mechanism

A

alpha-2 partial agonist

95
Q

Clonidine, alpha-methylnoradrenaline use

A

hypertension, migraine

96
Q

Clonidine, alpha-methylnoradrenaline SE

A

somnolence, orthostatic hypotension, edema, weight gain, rebound hypertension

97
Q

Isoproterenol mechanism

A

Beta-1, beta-2 agonist

98
Q

Isoproterenol use

A

Heart failure, asthma - obsolete

99
Q

Isoproterenol SE

A

Tachycardia, dysrhythmias

100
Q

Dobutamine mechanism

A

Beta-1 agonist

101
Q

Dobutamine use

A

stress test, heart failure, shock

102
Q

Dobutamine SE

A

dysrhythmias

103
Q

Albuterol, terbutaline mechanism

A

beta-2 agonist

104
Q

Albuterol, terbutaline use

A

asthma, pre-term labor (tocolytic anti-contraction)

105
Q

Albuterol, terbutaline SE

A

tachycardia, dysrhythmias, tremor, peripheral vasodilation

106
Q

Phenoxybenzamine, phentolamine mechanism

A

alpha-1, alpha-2 antagonist

107
Q

Phenoxybenzamine, phentolamine use

A

pheochromocytoma (neuroendocrine tumor of adrenal medulla)

108
Q

Phenoxybenzamine, phentolamine SE

A

hypotension, flushing, tachycardia, nasal congestion, impotence

109
Q

Prazosin mechanism

A

alpha-1 antagonist

110
Q

Prazosin use

A

hypertension

111
Q

Prazosin SE

A

hypotension, flushing, tachycardia, nasal congestion, impotence

112
Q

Yohimbine mechanism

A

alpha-2 antagonist

113
Q

Yohimbine use

A

not used clinically

114
Q

Carvedilol mechanism

A

alpha-1, beta-1, beta-2 antagonist

115
Q

Carvedilol use

A

heart failure

116
Q

Carvedilol SE

A

exacerbation of initial heart failure, renal failure

117
Q

Nebivolol mechanism

A

Beta-1 antagonist + vasodilation

118
Q

Nebivolol use

A

hypertension, heart failure

119
Q

Nebivolol SE

A

fatigue, headache

120
Q

Propanolol mechanism

A

beta-1, beta-2 antagonist

121
Q

Propanolol use

A

hypertension, migraine prophylaxis, angina, anxiety tremor, glaucoma

122
Q

Propanolol SE

A

bronchoconstriction, cardiac failure, cold extremities, fatigue, depression, hypoglycemia]

123
Q

Atenolol, metoprolol mechanism

A

Beta-1 antagonist

124
Q

Atenolol, metoprolol use

A

hypertension, arrhythmia, angina at MI

125
Q

Atenolol, metoprolol SE

A

cardiac failure, cold extremities, fatigue, depression, hypoglycemia

126
Q

Prazosin + epinephrine =

A

decreased BP (unopposed alpha-2, beta-2 agonism)

127
Q

Tyramine + MAO-inhibitors =

A

Causes hypertensive crisis

128
Q

Tyramine + MAO-Inhibitors + TCA (imipramine) =

A

TCA blocks Uptake 1 –> no tyramine inside terminal –> no effect

Pharm (9 decks)

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