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pharmacology Flashcards

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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
what is botulism
caused by botulism toxin decreases rease of ACh causing paralysis
26
what can botulinum toxin be used to treat
over active muscles
27
what is Myasthenia gravis
autoimmune reduced number of nAChRs muscle weakness causes reduced amplitude of EPP
28
what are curare like compounds
competitive antagonists of nAChRs, reduces EPP to below threshold for muscle AP generation
29
where are curare like compounds used
in surgery to produce reversible paralysis
30
examples of curare like compounds
vesuronium and atracurium
31
what is pain
an unpleasant sensory and emotional experience associated with actual tissue damage or described in terms of such damage
32
what type of pain is nociceptive pain
adaptive
33
what type of pain is inflammatory pain
adaptive
34
what type of pain is pathological pain
maladaptive
35
whta re niciceptors activated by
intense stimuli
36
examples of intense stimuli
thermal mechanical and chemical
37
what are nociceptors
adaptives
38
what do nociceptors have
a high threshold
39
what d nociceptors serve as
an early warning system to detenct and minimise contact with damaging stimuli
40
wha do nociceptors cause
pain, autonomic response and withdrawal reflex
41
what type of pain is inflammatory pain
inflammatory and protective
42
what is inflammatory pain caused by
activation of immune system in injury or infection
43
what type of pain does inflammatory pain cause
sponteneous and hypersensitivity
44
what promotes repair in inflammatory pain
low threshold and tenderness
45
how is inflammatory pain protective
assists in healing of a damaged body part by discouraging physcial contact and movement
46
what type of pain has no protective function
pathological (maladaptive pain)
47
what are the types of pathological pain
neuropathic and dystfunctional
48
what type of pain does pathological pain cause
sponteneous pain and pain hypersensitivity
49
what causes neuropathic pain
nerual lesion, positive negative symptoms and peripheral nerve damage
50
what type of pain causes dysfunctional pain
spontaneous pain and pain hypersensitivity
51
what are the 2 types of nociceptor
A and C fibres
52
what are the A fibres used for
first or fast high intensity pain
53
what are C fibres used for
second less intense pain
54
what functions do peptidergic C fibres have
efferent and afferent functions
55
what is released in from free nerve endings in neurogenic inflammation
peptides (S and CGRP)
56
why are peptides released from free nerve endings in neurogenic inflammation
due to tissue damage or inflammatory mediators
57
what does Sp cause
vasodilation, release of histamine and sensitise surrounding nociceptors
58
what does CGRP cause
vasodilation
59
what does the release of peptides lead to
hyperalgesia and allodynia
60
what is hyperalgesia
increased sensitivity to pain
61
what is allodynia
triggering of pain sensation from stimuli whcih doesnt normally cause pain
62
neuropathic pain perceptive
shooting numbness
63
examples of dysfuncional pain conditiosn
fibromyalgia, IBS, tension headache, temporomandibular joint disease, interstitiyal cystitis
64
what is not effective in pathological pain
simple analgesics
65
how to treat pathological pain
anti depressants and anti epileptics
66
what can be felt as referred pain
deep or visceral pain
67
what pain is not usually referred
pain originating in superficial structures is not referred
68
step 1 pain
paractamol, NSAIDs
69
step 2 pain
codeine
70
step 3 pain
morphine
71
NSAID examples
ibuprofen, naproxen, dclofenca, indomethacin, etodolac, celecoxib
72
indications for NSAIDs
inflammatory arthritis, mechanical MSK pain, pleuritic/[ericardial pain
73
potential side effects of NSAIDs
dyspepsia, oesophagi's, gastritis, peptic ulcer, small/large bowel ulceration, renal impairment, increased CVS events, fluid retention, wheeze, rash
74
newly diagnosed RA what is the best treatment
methotrexate
75
when ti start DMARDs in RA
within 3 months of symptoms
76
DMARDs of choice
MTX, SPX
77
is methotrexate safe in pregnancy
no
78
adverse affects of DMARDs
thrombocytopenia, hepatitis, pneumonitis, rash/mouth ulcers, nausea and diarrhoea
79
what to prescribe along with methotrexate
folic acid
80
SE of sulfalazien
neutropenia
81
SE of HCQ
retinopathy
82
what are biologics
drugs used to target specific parts of the immune system affected in inflammatory arthritis
83
what is more effective than DMARDs
biologics
84
what are anti TNF used in
RA, PA, AS
85
examples of anti TNF
etanercey, adalimumab, certolizumab, infliximab, golimumab
86
what is rituximab
monoclonal antibody against B cells
87
what does tocilizumab do
inhibits IL6
88
how to treat acute flare of gout
NSAIDs, corchincine and steroids
89
se of corchinicne
diarrhoea
90
gout prophylaxis
allopurinol, febuxatsat, uricosurics
91
what is allopurinol
xanthate oxidase inhibitor
92
se of allopurinol
rash, boen marrow toxicity
93
what is febuxastst
xanthine oxidase inhibitor
94
who to not give febustat to
people with heart disease
95
adverse effects of corticosteroids
centripetal obesity, muscle wasting, skin atrophy, osteoporosis, diabetes, hypertension, cataract glaucoma, immune suppression, renal suppression

MSK (19 decks)

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