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Pharmacology > Pharm 9.1 > Flashcards

Pharm 9.1 Flashcards

1
Q

norepinephrin is an

A

adrinergic neurotransmitter (except in sweat glands)

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2
Q

Epinephrine is hormone secreted by

A

the adrenal madula

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3
Q

Dopamine a neurotransmitter is found in

A

the basal ganglia, limbic system, CTZ, and anterior pituitary

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4
Q

difference btw norepinephrine and epiephrine

A

NE is an NT secreted by neurons and does not act on beta 2 rec, Epi is a hormone secreted by adrenal medulla and acts on all recptros (low dose acts on beta rec)

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5
Q

Epinephrine, norepinephrine, and dopamine (catecholamines) synthesized form

A

tyrosine

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6
Q

what is the rate limiting step in the synthesis of catecholamines

A

tyrosine hydroxylase

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7
Q

Fates of NE

A

binds alpha 1 rec post synaptically, binds alpha 2 rec presynaptically for auto inhibition, gets metabalized by MAO in axoplasm and COMT in snapse, reuptake back into primary neuron

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8
Q

tyrosine to dopamine happens in

A

axoplasm

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9
Q

dopamine is stored in

A

vesicles to prevent degredation

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10
Q

dopamine to NE in

A

vesicles

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11
Q

transport of dopamien into vesicles is inhibited by

A

reserpine

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12
Q

release of NT from axon termila is caused by

A

influx of ca causing fusion of the vesicle with the cell membrane

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13
Q

release of catecholamine vesicle is blocked by

A

guanethidine and bretylium

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14
Q

reuptake of catecholamines is inhibited by

A

cocain and imipramine

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15
Q

where is dopamine beta hydroxylase

A

dopamine beta hydroxilase is in vesicles to convert dopamine to NE

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16
Q

how is Ne coverted to Epi

A

by PNMT (phenylethanolamine N methyltransferase) only in the adrenal medulla bc epinephrine is important in flight, fright, fight

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17
Q

granules take up dopamine from the

A

cytoplasme

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18
Q

conversion of dopamine to NE occurs in granules by

A

dopamine beta hydroxylase

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19
Q

where are the granules

A

in the adrenergic termina (NE is stored in them)

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20
Q

how are NE and other catecholamines released

A

exocytosis in response to stimulatory signal

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21
Q

indirectly acting amines like tyramine and amphetamines induce

A

release of NE by displacing it from the nerve endings

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22
Q

efficient mechanism of release of NE

A

uptake of Ca

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23
Q

the most important mechanism for the ermination of the NE action

A

axonal uptake–>i.e. reuptake

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24
Q

what ihibits reuptake

A

cocaine and imipramine

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25
Q

NE can bind all receptors EXCEPT

A

BETA 2

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26
Q

metabolism of NE occurs by two enzyme systmes

A

MAO and COMT

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27
Q

MAO

A

monoamine oxidase

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28
Q

COMT

A

catechol-O-methyl transferase

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29
Q

NE is acted upon by MAO in the

A

axoplasm

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30
Q

COMT acts on NE when

A

NE it diffuses out in circulation, mainly in the liver and in the blood stream

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31
Q

MAO-A is present

A

in the nerve/liver mainly or anywhere

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32
Q

MAO-A metabolizes

A

NE, 5HT, tyramine

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33
Q

MAO-A inhibitors

A

Phenelzine, Tyranylcypromine (antidepressants)

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34
Q

MAO-B is present in the

A

Brain

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35
Q

MAO-B metabolizes preferentially

A

dopamine

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36
Q

MAO-B inhibitor

A

Selegiline (antiparkinson)

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37
Q

COMT inhibitors

A

Tolcapone, Entacapone

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38
Q

Tolcapone is

A

long acting

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39
Q

Entacapone is

A

Short acting

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40
Q

major metabolites excreted in the urine are

A

VMA (Vanillyl mandelic acid), metanephrine, and dihydroxy mandelic acid

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41
Q

when do you see an increase in adrenergic metabolites

A

pheochromocytoma - tumor of adrenal gland

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42
Q

does metabolism play a significant role in the termination of action of NE?

A

NO

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43
Q

what inteferes with the synthesis of catecholamines by intefering with tyrosine hydrolase

A

Metyrosine

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44
Q

what causes a blockade of storage in granule or granular uptake of catecholamines

A

Reserpine

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45
Q

what causes Displacement of NE from vesicles

A

amphetamine, tyramine (indirect sympathomimetic agents)

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46
Q

what causes Prevention of release of catecholamines

A

bertylium, guanethidine

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47
Q

wht causes block of reuptake at nerve terminal of chatecholamines

A

cocaine and imipramine

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48
Q

adrenergic receptors

A

alpha beta dopamine

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49
Q

aplpha receptors

A

alpha 1 (usually post synaptic) , alpha 2 (usually pre synaptic)

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50
Q

beta receptors

A

beta 1, 2, 3

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51
Q

dopamine receptors

A

D1, D2

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52
Q

type of receptors that adrenergic receptors are

A

g-proteins coupled receptors

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53
Q

adrenergic receptors act by either

A

increasing or decreasing syn of cAMP OR through IP3, DAG, and Ca2+ as second messengers

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54
Q

alpha 1 is a

A

Gq - inc PLC –> inc IP3, DAG, Ca2+

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55
Q

alpha 2 is a

A

Gi - dec Adenylyl cyclase –> dec cAMP

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56
Q

beta1/2 and D1 receptors are

A

Gs - inc Adenylyl cyclase –> inc cAMP

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57
Q

alpha 1 subtypes

A

A B D

58
Q

alpha 2 subtypes

A

A B C

59
Q

where do you find the alpha 1 subtype

A

SM of urethra – use drugs targetting this recptors in obstructions in BPH

60
Q

alpha 1 on

A

eye (radial/dialator) muscle, Arterioles (skin, viscera), Veins, Bladder trigone and sphincter, Male sex organs, Liver, Kidney

61
Q

alpha 1 in eye/dialator muscle

A

contraction - mydriasis

62
Q

alpha 1 in the arterioles (skin, viscera)

A

contraction - incTPR - inc diastolic pressure - inc afterload –want to shunt blood away from the skin and viscera and more available for the heart

63
Q

alpha 1 in the veins

A

contraction - inc venous return - inc preload

64
Q

alpha 1 bladder trigone and sphincter

A

contraction - urinary retension

65
Q

alpha 1 in male sex organs

A

vas deferens - ejaculation

66
Q

alpha 1 in liver

A

inc glycogenolysis

67
Q

alpha 1 in kidney

A

dec renin release

68
Q

alpha 2 receptors are found in

A

prejunctional nerve terminals, platelets, pancrease

69
Q

alpha 2 in prejunctional never terminals

A

dec transmitter release and NE synthesis

70
Q

alpha 2 in platelets

A

aggregation - makes sense bc in fight or flight you want to prevent bleeding out

71
Q

alpha 2 in pancreas

A

dec insuline secretion

72
Q

beta 1 in the

A

heart, Kidney

73
Q

beta 1 in the SA node

A

inc HR - positive chronotropy

74
Q

beta 1 in the AV node

A

inc conduction velocitiy (positive dromotropy)

75
Q

beta 1 in artiral and ventricular muscle

A

in force of contraction (positive inotropy), conduction velocity, CO and oxygen consumption

76
Q

beta 1 in His-Purkinje

A

inc automaticity and conduction velocity

77
Q

beta 1 in Kidney

A

inc renin release

78
Q

beta 2 in the

A

blood vessels, uterus, bronchioles, skeletal muscle, liver, pancres

79
Q

beta 2 in the blood vessels

A

vasodialation - dec TPR - dec diastolic pressure - dec afterload

80
Q

beta 2 in the uterus

A

relaxation

81
Q

beta 2 in the bronchioles

A

dialation

82
Q

beta 2 in the skeletal muscle

A

inc glycogenolysis - contractility (tremor)

83
Q

beta 2 in the liver

A

inc glycogenolysis

84
Q

beta 2 in the pancreas

A

inc insuline secretion

85
Q

what receptor is most important for glycogenolysis

A

beta 2 then alpha 1

86
Q

D1 peripheral receptor actos on

A

renal, mesenteric, coronary vasculature, causing vasodialation, inc renal blood flow, inc GFR, inc Na secretion(natriuresis)

87
Q

slective agonist of Alpha 1 receptors - alpha 1 mimetics

A

phenylephrine, methoxamine

88
Q

selective antagonist of alpha 1 receptors

A

prazosin, doxazosin, tamsulosin (on alpha 1A)

89
Q

alpha 2 receptor agonsit

A

clonidine, guanfancine, methyldopa

90
Q

alpha 2 antagonist

A

yohimibine

91
Q

beta receptors

A

beta 1, 2, 3

92
Q

beta 1 rec

A

on heart

93
Q

beta 2 on

A

SM

94
Q

beta 3 on

A

fat cells (adipocytes)

95
Q

selective beta 1 agonist

A

dobutamine

96
Q

slective beta 1 antagonist

A

atenolol, metoprolol

97
Q

beta 2 receptors are mostly

A

not innervated

98
Q

selective beta 2 agonsit

A

albuterol (salbutamol), salmenterol (longer acting), terbutaline

99
Q

selective beta 2 antagonist

A

butoxamine

100
Q

why would a beta 2 antaganist be used

A

treat bronchospasm (w/ butoxamine) bc remember beta 2 dialate, they are the enemies of alpha 1 that constrict

101
Q

classification of adrenergic drugs

A

direct, indirect, mixed

102
Q

direct actiong adrenergic drugs

A

epinephrine, norepinephrine, phenylephrine (beta 1), albuterol (beta 2)

103
Q

indirect acting adrenergic drugs

A

acts by releasing NE, Tyramine, Amphetamine

104
Q

Mixed acting adrenergic drugs

A

Ephedrine, Phenylpropanolamine (not on market bc caued stroke after it was in cough mixture)

105
Q

naturally occuring catecholamines includes

A

epinephrine, norepinephrine, dopamine

106
Q

catecholamines sturcture

A

catechol moiety and an ethylamine side chain

107
Q

catecholamines are rapidly inactivated by

A

MAO and COMT (inactivation starts from the gut)

108
Q

the catecholamine epinephrine acts on

A

alpha 1, alpha 2, beta 1, beta 2

109
Q

the catecholamine norepinephrine acts on

A

alpha 1, alpha 2, beta 1

110
Q

the catecholamine isproterenol acts on

A

beta 1, beta2, like epinephrine on steroides bc it vasodialates and decreases heart rate? And there is a reflex tachycardia

111
Q

the catecholamine dobutamine acts on

A

beta 1

112
Q

the catecholamine dopamine acts on

A

D1 ( beta 1 and alpha 1 at high doses)

113
Q

the non-catecholamines that work on alpha 1 only

A

oxymetazolin, phenylephrine, methoxamine

114
Q

non catecholamines that work on beta 2 only

A

albuterol, pirbuterol, terbutaline, salmeterol, formeterol

115
Q

non catecholamines that acts more on beta 2 than beta 1

A

metaproterenol

116
Q

non catecholamines that work on alpha and beta

A

ephedrine, psuedoephedrine

117
Q

action of alpha 1 agonists

A

inc TPR, inc BP, potential reflex bradycardia, no change in pulse pressure

118
Q

when could you use an alpha 1 agonist

A

tachycardia

119
Q

action of beta 2 agonists

A

beta 1 actions increase HR, SV, CO, and pulse pressure, beta 2 actions decrease TPR and BP, overall increase/widening in pulsepressure

120
Q

normal SV is

A

70 ml/beat

121
Q

Epinephrine is a potent activator of

A

alpha and beta adrenergic receptors and have prominent cardiovascular effects

122
Q

Epinephrine is involved in the sympathetic

A

fight flight fright

123
Q

epinephrine on beta 1 receptors in CVS

A

inc rate of depolarization in cardiac myocytes, inc inotropy, inc chronotropy, inc CO, inc in BP

124
Q

how does activating beta 1 receptors in CVS lead to faster depolarization

A

cardiac myocytes always leak out potassium, but activation of beta 1 receptors closes the potassium gates faster, depolarizing the SA-AV purkinje, increasing the rate of contraction and heart reate

125
Q

when is activating beta 1 receptors important

A

asystole (no contraction)

126
Q

epinephrine on alpha 1 receptors in CVS

A

at high dose causes vasoconstriction (vasopressor effect) via alpha 1, but at low does epi causes vasodialation (vasodepressor effect) via beta 2, produces a biphasic response

127
Q

biphasic response

A

different effect based on dose

128
Q

Dale’s vasomotor reversal (Epinephrine Reversal)

A

when alpha 1 receptors are blocked, epinephrine will produce hypotension because of unmasking of beta 2 receptor activation

129
Q

low dose epiniephrine

A

beta 1 and beta 2 stimulation

130
Q

high dose epinephrine

A

alpha 1, beta 1(beta2) stimulation —but beta 2 effect is masked

131
Q

high dose epinephrine on alpha 1

A

inc TPR, inc BP, potential reflex bradycarida

132
Q

high dose epinephrine on beta 1

A

inc HR, inc SV, inc CO, inc pulse pressure

133
Q

high dose epinephrine on beta 2

A

dec TPR, dec BP —> masked at the high dose

134
Q

epinephrine on beta 2 receptors in Respiratory system

A

bronchodialation

135
Q

alpha 2 receptors work by

A

stimulating Gi path, decreasing cAMP, stimulating nitric oxide release

136
Q

anaphylaxis

A

bronchospasm + anaphylactic shock or low BP

137
Q

how is Epinephrine used in anaphylaxis

A

beta 2 action decreases bronchospasm increasing partial pressure of O2; alpha 1 action increases CO, systolic BP, pulse pressure, tissue perfusion; decrease in eosinophil count reducing anaphylatoxin release

138
Q

Gs

A

increases cAMP that inhibits MLCK (myosin light chain kinase)

139
Q

Epinephrine metabolic effect

A

hyperglycemia, lipolysis

140
Q

hyperglycemia by epinephrine

A

inc glycogenolysis in muscle and liver (beta 2), inc in gluconeogenesis (due to inc release of glucagon -( beta 2), dec insulin secretion (alpha 2)

141
Q

lipolysis by epinephrine

A

beta 3 - inc cAMP in adipose tissue stimulating hormone sensitive lipase, leading to hydrolysis of TGs to FFA and glycerol

Pharmacology (15 decks)

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