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MSK > pharmacology > Flashcards

pharmacology Flashcards

1
Q

what is skeletal muscle innervated by

A

motor neurons

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2
Q

what is transmitted at the neuromuscular junction of skeletal muscle

A

acetylcholine

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3
Q

some features of the neuromuscular junction of skeletal muscles

A

terminal boiton + surrounding schwann cell, synaptic vesicles, synaptic cleft, end plate region

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4
Q

what chose choline + acetylCoA make

A

Ach

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5
Q

what does calcium binding to vesicle membanes allow

A

it to fuse membrane and release Ach

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6
Q

what does calium binding to vesicle membranes lead to the activation of

A

post junctional nicotinic Ach receptor

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7
Q

what hydrolyses Ach

A

acetylcholinesterase

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8
Q

what are the products of the hydrolysis of Ach

A

choline and acetate

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9
Q

what shape are nicotinic Ach receptors

A

pentameric

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10
Q

when is the nicotinic Ach receptor gate closed

A

in absence of Ach

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11
Q

when does the nicotinic Ach receptor gate open

A

when 2 molecules of Ach bind to exterior

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12
Q

what does the opening of Ach nicotinic receptor cause

A

Na influx and K efflux

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13
Q

at resting potential what has the biggest driving force Na or K

A

Na

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14
Q

what is end plate potential

A

a depolarisation when the influx of Na is greater than the efflux of K

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15
Q

what can reduce the amplitude of EPP

A

drugs or toxins

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16
Q

what does a reduced EPP amplitude mean

A

skeletal muscle paralysis

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17
Q

how does action potential go deep into muscle fibres

A

through T tubules

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18
Q

what does action potential going deep into muscle fibres cause

A

the release of Ca2+ in SR which combines with troponin at bridges to cause contraction

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19
Q

what is the target of therapuetics (anti-cholinesterases)

A

AchE

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20
Q

what do therapeutics that act on AChE fo

A

reversibly block their action and some nerve gases used in warfare can act irreversibly

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21
Q

what is neuromyotonia also known as

A

NMT or Isaacs syndrome

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22
Q

what is neuromytonia

A

antoimmune disease causing reduced K conductance in motor neurones causing hyperexcitability

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23
Q

what is lambert eaton myasthenic syndrome (LEMS)

A

autoimmune, reduced Ca conductance presynaptically - decreased Ach causing muscle weekness

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24
Q

what is LEMS associated with

A

small cell carcinoma of the lung

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25
Q

what is botulism

A

caused by botulism toxin decreases rease of ACh causing paralysis

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26
Q

what can botulinum toxin be used to treat

A

over active muscles

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27
Q

what is Myasthenia gravis

A

autoimmune reduced number of nAChRs muscle weakness causes reduced amplitude of EPP

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28
Q

what are curare like compounds

A

competitive antagonists of nAChRs, reduces EPP to below threshold for muscle AP generation

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29
Q

where are curare like compounds used

A

in surgery to produce reversible paralysis

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30
Q

examples of curare like compounds

A

vesuronium and atracurium

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31
Q

what is pain

A

an unpleasant sensory and emotional experience associated with actual tissue damage or described in terms of such damage

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32
Q

what type of pain is nociceptive pain

A

adaptive

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33
Q

what type of pain is inflammatory pain

A

adaptive

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34
Q

what type of pain is pathological pain

A

maladaptive

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35
Q

whta re niciceptors activated by

A

intense stimuli

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36
Q

examples of intense stimuli

A

thermal mechanical and chemical

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37
Q

what are nociceptors

A

adaptives

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38
Q

what do nociceptors have

A

a high threshold

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39
Q

what d nociceptors serve as

A

an early warning system to detenct and minimise contact with damaging stimuli

40
Q

wha do nociceptors cause

A

pain, autonomic response and withdrawal reflex

41
Q

what type of pain is inflammatory pain

A

inflammatory and protective

42
Q

what is inflammatory pain caused by

A

activation of immune system in injury or infection

43
Q

what type of pain does inflammatory pain cause

A

sponteneous and hypersensitivity

44
Q

what promotes repair in inflammatory pain

A

low threshold and tenderness

45
Q

how is inflammatory pain protective

A

assists in healing of a damaged body part by discouraging physcial contact and movement

46
Q

what type of pain has no protective function

A

pathological (maladaptive pain)

47
Q

what are the types of pathological pain

A

neuropathic and dystfunctional

48
Q

what type of pain does pathological pain cause

A

sponteneous pain and pain hypersensitivity

49
Q

what causes neuropathic pain

A

nerual lesion, positive negative symptoms and peripheral nerve damage

50
Q

what type of pain causes dysfunctional pain

A

spontaneous pain and pain hypersensitivity

51
Q

what are the 2 types of nociceptor

A

A and C fibres

52
Q

what are the A fibres used for

A

first or fast high intensity pain

53
Q

what are C fibres used for

A

second less intense pain

54
Q

what functions do peptidergic C fibres have

A

efferent and afferent functions

55
Q

what is released in from free nerve endings in neurogenic inflammation

A

peptides (S and CGRP)

56
Q

why are peptides released from free nerve endings in neurogenic inflammation

A

due to tissue damage or inflammatory mediators

57
Q

what does Sp cause

A

vasodilation, release of histamine and sensitise surrounding nociceptors

58
Q

what does CGRP cause

A

vasodilation

59
Q

what does the release of peptides lead to

A

hyperalgesia and allodynia

60
Q

what is hyperalgesia

A

increased sensitivity to pain

61
Q

what is allodynia

A

triggering of pain sensation from stimuli whcih doesnt normally cause pain

62
Q

neuropathic pain perceptive

A

shooting numbness

63
Q

examples of dysfuncional pain conditiosn

A

fibromyalgia, IBS, tension headache, temporomandibular joint disease, interstitiyal cystitis

64
Q

what is not effective in pathological pain

A

simple analgesics

65
Q

how to treat pathological pain

A

anti depressants and anti epileptics

66
Q

what can be felt as referred pain

A

deep or visceral pain

67
Q

what pain is not usually referred

A

pain originating in superficial structures is not referred

68
Q

step 1 pain

A

paractamol, NSAIDs

69
Q

step 2 pain

A

codeine

70
Q

step 3 pain

A

morphine

71
Q

NSAID examples

A

ibuprofen, naproxen, dclofenca, indomethacin, etodolac, celecoxib

72
Q

indications for NSAIDs

A

inflammatory arthritis, mechanical MSK pain, pleuritic/[ericardial pain

73
Q

potential side effects of NSAIDs

A

dyspepsia, oesophagi’s, gastritis, peptic ulcer, small/large bowel ulceration, renal impairment, increased CVS events, fluid retention, wheeze, rash

74
Q

newly diagnosed RA what is the best treatment

A

methotrexate

75
Q

when ti start DMARDs in RA

A

within 3 months of symptoms

76
Q

DMARDs of choice

A

MTX, SPX

77
Q

is methotrexate safe in pregnancy

A

no

78
Q

adverse affects of DMARDs

A

thrombocytopenia, hepatitis, pneumonitis, rash/mouth ulcers, nausea and diarrhoea

79
Q

what to prescribe along with methotrexate

A

folic acid

80
Q

SE of sulfalazien

A

neutropenia

81
Q

SE of HCQ

A

retinopathy

82
Q

what are biologics

A

drugs used to target specific parts of the immune system affected in inflammatory arthritis

83
Q

what is more effective than DMARDs

A

biologics

84
Q

what are anti TNF used in

A

RA, PA, AS

85
Q

examples of anti TNF

A

etanercey, adalimumab, certolizumab, infliximab, golimumab

86
Q

what is rituximab

A

monoclonal antibody against B cells

87
Q

what does tocilizumab do

A

inhibits IL6

88
Q

how to treat acute flare of gout

A

NSAIDs, corchincine and steroids

89
Q

se of corchinicne

A

diarrhoea

90
Q

gout prophylaxis

A

allopurinol, febuxatsat, uricosurics

91
Q

what is allopurinol

A

xanthate oxidase inhibitor

92
Q

se of allopurinol

A

rash, boen marrow toxicity

93
Q

what is febuxastst

A

xanthine oxidase inhibitor

94
Q

who to not give febustat to

A

people with heart disease

95
Q

adverse effects of corticosteroids

A

centripetal obesity, muscle wasting, skin atrophy, osteoporosis, diabetes, hypertension, cataract glaucoma, immune suppression, renal suppression

MSK (19 decks)

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