week 4 Flashcards

1
Q

pregnaglionic neurotransmitter for SNS

A

ACH

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2
Q

preganglionic neurotransmitter for PSNS

A

ACH

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3
Q

postganglionic neurotransmitter SNS

A

NE

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4
Q

postganglionic neurotransmitter PSNS

A

ACH

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5
Q

post-ganglionic receptor SNS

A

adrenergic

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6
Q

post-ganglionic receptor PSNS

A

cholinergic

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7
Q

what is acetylcholinesterase

A

enzyme
lives in synapse
inactivates ACH that’s outside a nerve ending

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8
Q

3 types of cholinergic receptors

A

1) muscarinic receptor
2) nicotinic neural receptor
3) nicotinic muscle receptor

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9
Q

where and what target is muscarinic receptor located

A

PSNS

target the smooth and cardiac muscle

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10
Q

where and what target is the nicotinic neural receptor

A

PSNS and SNS
only at ganglion
target smooth and cardiac muscle

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11
Q

where and what target is nicotinic muscle receptors

A

neuromuscular junction - not part of PNS/SNS

target is skeletal muscle cell

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12
Q

2 types of cholinergic drugs

A

1) indirect

2) direct

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13
Q

direct acting, name: action, duration, effects

A

action: direct muscarinic R agonist
duration: until ACHenzyme degrades
effects: increase GI motility and secretions/vasodilation/increase GU activity/miosis/ decrease BP and HR

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14
Q

indirect acting, name: action, duration

A

action: binds to ACHe, inhibiting action
duration: prolonged post-synaptic ACH concentration

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15
Q

types of indirect acting cholinergic drugs

A

1) reversible inhibitors of ACHe

2) irreversible inhibitors of ACHe

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16
Q

duration and primary usage of reversible inhibitors of ACHe

A

short acting
diagnosis and treatment of myasthenia gravis
Alzheimers

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17
Q

duration and primary usage of irreversible inhibitors of ACHe

A

irreversibly bind to ACHe, causing structural change
long acting
primary: chemical warfare, pesticides
low doses: treatment of glaucoma

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18
Q

another name for cholinergic drug

A

Parasympathomimetic

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19
Q

another name for anticholinergic drug

A

parasympatholytic

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20
Q

where do anticholinergic drugs bind

A

muscarinic receptors

21
Q

action of anticholinergic drugs

A

competitive antagonism = compete with ACH for R sites

less binding to Receptors = decrease effectiveness

22
Q

anticholinergic MOA on CVS

A

block vagus nerve action on heart

decrease innervation of the heart: increase SA node firing and increase AV conduction speed

23
Q

anticholinergic MOA on respiratory

A

recall ACH acts to increase secretions in respiratory track, causes bronchoconstriction at high levels
blockage of ACH used preoperatively (decreases secretions) and for asthma

produces bronchodilation

24
Q

anticholinergic MOA on GI

A

drugs decrease motility of GI tract (opposite effect of PSNS)
treatment of IBS

25
What is cholinergic toxicity
excess activation of PSNS
26
how does cholinergic toxicity present
nausea and vomitting, sweating, blurred vision, tremors, bradycardia, hypotension, bronchoconstriction
27
what is a cholinergic crisis
very high doses of ACH
28
cholinergic toxicity signs and symptoms
``` DUMBELLS diarrhea and diaphoresis and abdominal cramping urination miosis bradycardia (muscarinic) and tachycardia (nicotinic) emesis (nausea and vomiting) lacrimination (flow of tears) lethargy salivation ```
29
what does atropine do for cholinergic toxicity
anticholinergic competitive antagonist at muscarinic R antidote for organophosphate poisoning/nerve agents
30
what does pralidoxime do for cholinergic toxicity
reactivates ACHe | usually given with atropine for nerve agent poisoning
31
what is anticholinergic toxicity
excessive blockage of PSNS
32
5 manifestations of anticholinergic toxicity
1) dry mouth 2) urinary retention 3) visual disturbance (excessive dilation) 4)constipation 5) flushing skin reaction = inhibit sweating
33
how is anticholinergic toxicity treated
induced vomiting, gastric lavage
34
what 2 ways do peripherally acting skeletal muscle relaxants act?
1) inhibit muscle contraction at NMJ | 2) inhibit muscle contraction within skeletal muscle fibers
35
what 2 ways do centrally acting skeletal muscle relaxants act?
1) block conduction at spinal cord | 2) prevent impulse from reaching muscle
36
when do we need skeletal muscle relaxants?
1) spastic disease ie// MS and CP 2) SC damage - paraplegia 3) painful muscle overexertion 4) surgical procedures
37
non-depolarizing blockers - peripheral muscle relaxants
combine with Nm but do not stimulate | occupy R sites, preventing ACH from triggering reaction (no depolarization)
38
depolarizing blockers- peripheral muscle relaxants
2 step process 1) succinylcholine attaches to Nm, induces depolarization (fasciculation's) 2) succinylcholine alters Nm - cannot respond to endogenous ACH
39
route, onset, duration and adverse effects for peripheral acting muscle receptors
IV, not well absorbed PO typically onset 3-5min duration: 20-30min (succinylcholine much less) adverse effects: paralysis of respiratory muscles
40
adverse effects of succinylcholine
ventricular arrhythmias some people lack the enzyme to metabolize quickly - effects prolonged, risk for malignant hyperthermia increase in temp, acidosis, electrolyte imbalance = high mortality
41
action of direct acting peripheral muscle relaxants
inhibit skeletal muscle fibre contraction by interfering with calcium release
42
name direct acting skeletal muscle relaxant
dantrolene (dantrium)
43
indication for direct acting skeletal muscle relaxant
treatment of malignant hyperthermia, spastic conditions
44
adverse effects of direct acting skeletal muscle relaxant
dizziness, weakness, fatigue, possible hepatotoxicity
45
how do central acting muscle relaxants work
depress reflex impulse condition within spinal cord no effect on Nm R do not alter skeletal muscle fibers
46
MOA for centrally acting muscle relaxants
enhance inhibition - sedate neurons
47
abuse of central muscle relaxants
CNS sedation | high potential for abuse
48
overdose of central acting muscle relaxants
CNS and vital signs depressed
49
antidotes of central muscle relaxants
flumazenil for benzo OD