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MM Pharmacology > Pharmacology Synopses 2 > Flashcards

Pharmacology Synopses 2 Flashcards

1
Q

Acetyl CoA + Choline via choline acetyl transferase

A

Ach

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2
Q

ratelimiting step in Ach formation

A

availability of choline

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3
Q

excitation by increasing Na+ and K+ conductances

A

Ach in skeletal muscle

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4
Q

excitation by increasing Na+ conductances

A

Ach in smooth muscle

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5
Q

inhibition (slowing heartbeat) by increasing K+ conductances

A

Ach in cardiac muscle

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6
Q

Acetylcholinesterase

A

hydrolyzes Ach at postsynaptic membrane

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7
Q

Butyrocholine esterase

A

metabolizes Ach analogs in blood and liver

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8
Q

250 kDa multimeric glycoprotein, related to other ionopore receptors (GABAa)

A

nicotinic Ach receptor

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9
Q

80 kDa monomeric glycoprotein, related to G-protein coupled receptors like beta-adrenergic

A

muscarinic Ach receptor

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10
Q

skeletal muscle neuromuscular junction receptor type

A

Ach nicotinic

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11
Q

main preganglionic to postganglionic synapses receptor type

A

Ach nicotinic

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12
Q

all parasympathetic postganglionic cells

A

Ach, muscarinic

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13
Q

____ are primary agents for autonomic ganglia, ____ are only effective as adjuncts

A

nicotinic, muscarinic

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14
Q

parasympathetic effects: eye

A

miosis (constriction of pupil)

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15
Q

parasympathetic effects:heart

A

decrease in heart rate

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16
Q

parasympathetic effects: GI tract

A

increase motility and tone

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17
Q

parasympathetic effects: bladder

A

contraction

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18
Q

parasympathetic effects: glands (sweat, lacrimal, nasopharyngeal, etc)

A

increased secretion (*sweat glands receive cholinergic sympathetic innervation)

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19
Q

parasympathetic effects: adrenal medulla

A

none, but receives direct Ach nicotinic pre-ganglionic innervation

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20
Q

tissues without nerves, but with muscarinic receptors (many vascular beds)

A

Ach causes vasodilation

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21
Q

autonomic effects of parasympathetic system, CNS (if passes blood-brain barrier), slow modulatory electrophysiological effects

A

muscarinic Ach receptor

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22
Q

autonomic ganglia and skeletal muscle, symapthetics & parasympathetics, fast electrophysiological effects

A

nicotinic Ach receptor

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23
Q

comes from adrenal medulla chromaffin cells, 10-20% of amines secreted

A

norepinephrine

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24
Q

comes from adrenal medulla chromaffin cells, 80-90% of amines secreted

A

epinephrin

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25
Q

50% of catecholamine content of CNS mammals, interneurons in some sympathetic ganglia

A

dopamine

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26
Q

rate limiting step in catecholamine production

A

tyrosine to DOPA via tyrosine hydroxylase

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27
Q

Pumps 90% norepi into storage vesicles

A

vesicular monoamine transporter (VMAT-2)

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28
Q

norepi in axoplasm does what?

A

regulates synthesis

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29
Q

takes most NE released from nerves back up into the synaptic terminal

A

norepinephrine transporter (NET). NET also transports DA and E.

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30
Q

Cocaine and imipramine (tricyclic antidepressant) inhibit

A

NET

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31
Q

take synaptic NE into other cells

A

OCTs (organic cation transporters)

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32
Q

metabolize NE in other cells

A

COMT (catechol-O-methyltransferase)

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33
Q

members of g-protein-linked receptor family, 7 transmembrane passes

A

adrenergic receptors

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34
Q

Alpha 1 tissues

A

vascular smooth muscle, liver

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35
Q

Alpha 1 responses

A

contraction in vascular smooth muscle, glycogenolysis and gluconeogenesis in liver

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36
Q

Alpha 2 tissues

A

Nerve terminals, vascular smooth muscle

37
Q

Alpha 2 responses

A

decreased release of NE in terminals, contraction in vascular smooth muscles

38
Q

Beta 1 tissues

39
Q

Beta 1 responses

A

increases force and rate of contraction, AV nodal conduction velocity

40
Q

Beta 2 tissues

A

smooth muscle (VASCULAR, bronchial, GI and GU), liver

41
Q

Beta 2 responses

A

relaxation in smooth muscle, glycogenolysis and gluconeogenesis in liver

42
Q

act at sympathetic and parasympathetic ganglia, skeletal muscle and perhaps CNS

A

nicotinic agonists (and antagonists)

43
Q

structural similarity to Ach allows binding and blocking of AchE

A

anticholinesterase mode of action

44
Q

Anti-ACHEs act

A

at both nicotinic and muscarinic cites

45
Q

autonomic effects in order of appearance by dose of muscarinic antagonists

A
  1. decreased salivation and sweating. 2. pupil dilation and heart rate increase 3. inhibit micturition, decrease gut motility 4. inhibit gastric secretion
46
Q

CNS effects of muscarinic antagonists

A

scopolamine causes drowsiness, amnesia, etc. in clinical doses, excitement, restlessness and hallucination in higher doses. atropine has none

47
Q

subtype specific: M1

A

brain (cognition)

48
Q

subtype specific: M2

49
Q

subtype specific: M3

50
Q

subtype specific: M1/3

A

salivary glands

51
Q

subtype specific M2/3

A

GI tract and bladder

52
Q

Epinephrin stimulates which receptors

A

All adrenergic!

53
Q

Give epi how?

A

IM or SC, since PO gets degraded in the GI tract by MAO or COMT.

54
Q

IV epi is dangerous to hypertensive and hyperthyroid because

A

increases BP (via alpha 1) → cerebral hemorrhage, and increases HR (via beta 1) leads to arrhythmia

55
Q

reflex brachycardia pronounced with NORepi why?

A

no beta 2 means no skeletal vasodilation to counteract splanchnic vasoconstriction of alpha 1: increased blood pressure

56
Q

Are MASTs broken down by COMT?

A

No. That is why they have a longer half-life

57
Q

Tyramine (from wine and cheese) + MAO inhibitor

A

hypertensive crisis due to release of NE stores.

58
Q

amphetamine, methamphetamine, and cocaine

A

block NE reuptake

59
Q

reliance on stored NE causes ____ with meth, tyramine and amphetamine

A

tachyphylaxis

60
Q

epi reversal

A

give epi with alpha antagonists, so only beta effects are agonized.

61
Q

responsible for BP increase upon standing

A

Alpha 1, so you’ll faint if it is inhibited

62
Q

blocks alpha 2 only, increases sympathetic tone, HR and BP

A

Yohimbine (opposite of clonidine)

63
Q

SA node location

A

at the junction of the SVC and right atrium

64
Q

the only way the impulse can get to the ventricle

A

through AV node and His bundle

65
Q

After His, impulse enters ___ and propagates through ventricles

A

Purkinje cells

66
Q

Does SA node have resting potential?

A

No. Self-excites.

67
Q

sinus node has special pacemaker cells that pass current from out to in, creating

A

funny current

68
Q

Like SA, AV node depolarizes due to

A

inward Ca current

69
Q

Ca current is slow, allowing what

A

atria to empty into ventricles before ventricles contract

70
Q

What causes contraction?

A

Inward Ca current (Ca–>SR–>releases Ca–>contraction)

71
Q

P on EKG

A

atrial polarization

72
Q

QRS on EKG

A

ventricular depolarization

73
Q

T on EKG

A

repolarization

74
Q

innervate sinus node, atria, and are not in ventricles

A

parasympathetics

75
Q

four ways to change heart rate

A

level of max diastolic potential, rate of funny current, change threshold potential, change slope of pacemaker current via SA node

76
Q

sympathetic (adrenergic to beta 1) effects on SA node

A

increases slope of funny current, membrane depolarizes faster, HR increases

77
Q

parasympathetic effects on SA node

A

decrease pacemaker current, slow down rate of polarization, decrease HR

78
Q

sympathetics on AV node

A

increase inward Ca current, increase nodal action potential, faster conduction

79
Q

parasympathetics on AV node

A

decrease AV nodal action potential, slower conductoin

80
Q

P w/o QRS

A

AV block, extreme parasympathetic activation

81
Q

sympathetics enhance inward pacemaker current ____ than they do in the sinus node

82
Q

parasympathetics don’t work on ventricular rhythms, but

A

they can work on atrial tachycardia

83
Q

who can change stroke volume?

A

sympathetics, increase SV. Paras don’t affect ventricular muscle

84
Q

what can weaken contractions but act of the atria only?

85
Q

Cardiac output equation

A

CO = SV * HR

86
Q

blood pressure equation

A

BP = SV *TPR

87
Q

mean arterial pressure equation

88
Q

systolic PP

A

during contraction

89
Q

diastolic PP

A

during relaxation

MM Pharmacology (5 decks)

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