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clinical pharm y5 > pain > Flashcards

pain Flashcards

1
Q

define pain

A

unpleasant sensory/ emotional experience that can cause tissue injury

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2
Q

what are the types of pain

A

Acute- high intensity, conducted my small myelinated A-delta fibres. Lateral horn spinothalamic .
Chronic- over 6 months, chronic cancer is chronic and acute, non mg is conducted by UNmyelinated c-delta fibres medial smipiniothalamic tractand is low intensity for long duration e.g. radiculitis

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3
Q

Pathway of nociceptive pain (the jitty near the post)

A

transduction
transmission
perception
modulation

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4
Q

what occurs at transduction

A

-conversion of painful stimuli into a action potential 3 types of stimuli thermal, mechanical, chemical. Tissue releases PROSTAGLANDINS, subs P, Serotonin, bradykinin and histamine. Pain impulse travels to cns by neuromediators

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5
Q

describe what occurs at transmission

A

Stimuli is converted into an action potential by influx of na and k ions and processed in the brain
Ascending tracts: neo-spinothalamic( contralateral) paleo and archi spinothalamic (bilat)

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6
Q

what drugs cause modulation of the pain pathway at transmission

A

Local anesthetics and anticonvulsants decrease the ion exchange and decrease transmission

Opioids block neurotransmitter release: glutamate, ach, norepinephrine, serotonin, subs p

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7
Q

what drugs cause modulation of the pain pathway at transduction

A

NSAIDS inhibit COX ->decrease pg ->decrease pain sensation. Corticosteroids inhibit arachidonic acid-> decreased pg, useful in cancer and radiculitis.

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8
Q

describe what occurs at pain perception

A

ccurs in the cortex. Thalamus, sensorimotor cortex, insular cortex,anterior cingulate register the AP as specific pain points in the body
-amygdala and hypothalamus detect intensity

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9
Q

what tract does modulation occur

A

descending tract by serotonin, norepinephrin and enkaphalin at the substantia gelatinosa

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10
Q

types of nociceptive pain:

A

Somatic: well localised. Skin bones fascia meninges peritoneum, pleura and teeth
Visceral: poor loc, even distant. Heart, gut and bladder (ORGANS)

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11
Q

paracetamol moa

A

inhibits cox 3 in brain. Analgesic and antipyretic

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12
Q

paracetamol pk

A

oral abs. Rapid absorp. Tmax is 3 hrs w/ suppositories. Liver metabolism

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13
Q

paracetamol indication

A

mild/mod pain. Headache, muscle etc pregnant women and babies over 3 months

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14
Q

paracetamol ADR

A

no side effects in ti. Hepatotoxicity and renal toxicity at overdose. Liver failure due to excess N ACETYL-P-BENZOQUINONE-IMINE (NAPQI)

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15
Q

paracetamol dose

A

dults- 4g max. 1g Every 6 hrs. Kids. 60mg/kg/24hrs.

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16
Q

paracetamol antidote

A

N-ACETYLCYSTEINE (NAC)

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17
Q

paracetamol CI

A

liver or renal failure.

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18
Q

Metamizole MOA

A

prodrug w/ active metabolites. Analgesic, antipyretic, spasmolytic. Slightly antiinflamm

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19
Q

Metamizole pk

A

oral abs

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20
Q

Metamizole inidication

A

mild/mod- head and toothache, myalgia, neuralgia, chole and nephrolithiasis.

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21
Q

Metamizole CI

A

Ci: avoided in pregs and breastfeeding. Reduced in renal and liver failure. Incresed dose in smokers due to faster metabolism.

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22
Q

Metamizole dose

A

max is 3g. 15yrs n over 1g x3

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23
Q

Metamizole ADR

A

interstitial nephritis, agranulocytosis, allergic reaction in intravenous admin.

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24
Q

classification of NSAIDS

A

Salicylic acid derivatives- aspirin- tab 100mg
Acetic acid derivatives- indomethacin
Oxicam derivatives - meloxicam(selective cox 2) piroxicam
Phenylacetic acid derivatives - diclofenac, aceclofenac
Coxibs- celecoxib- 200mg
Others- nimesulide
Propionic acid derivatives
Ibuprofen- tab 200 mg
Ketoprofen- tab 50mg
Naproxen- tab 250 mg

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25
NSAID moa
inhibit cyclooxygenase 1 and 2 to prevent production of pg thromboxane, prostacyclin. Selective nsaids act on cox 2 only. Aka coxib (celecoxib) Organ effects of PGE2. Gastric mucosa: decrease hcl, increase mucosal protection. Kidney: renal artery dilation to increase blood flow. Platelets: inhibit agg. Mediates pain Cox2 is inflammatory mediator, increases inflamm. Activity of nsaids against cox2 increases with time
26
NSAID indications:
chronic inflammatory diseases- arthritis, spondylitis, radiculitis, metastatic bone tumors due to prostaglandin release during bone lysis
27
NSAID ADR
ulcers, nausea and vom. Less common with coxibs. Nephrotoxicity due to sodium and water retention caused by reduced blood flow from prostaglandin inhibition. Interstitial nephritis. Prolonged bleeding due to decreased thromboxane with is supposed to aggregate platelets Hypersensitivity- asthma- due to increase in leukotrienes due to pg decrease. Leukotrienes cause bronchoconstriction and increased secretion of goblet cells. Coxibs are cox 2 specific so don’t cause asthma
28
NSAID CI
pregnancy- teratogenic in 1st trimester. Close ductus arteriosus in 3rd Liver and kidney failure Elderly, women, smokers, corticosteroid takers are more susceptible to adrs
29
NSAID drug interxn
decrease antihypertensives and diuretics
30
describe the ascending pain pathway (6)
Stimuli releases histamine Sensory nerve fibers respond to histamine, The action potential propagates to 1st order neuron in spinal cord Then goes to 2nd order and crosses Ascends to3rd order neuron in thalamus, anterior cingulate and insular cortex causing perception Amygdala and hypothalamus generates urgency and intensity
31
describe the descending pain pathway(5)
Stimulation of periaqueductal gray matter Activates enkephalin release neurons in the grey matter that send impulse to the raphe nucleus in the midbrain Raphe nucleus releases serotonin and travels to dorsal column And dorsal column enkephalin binds to mu opioid receptors and inhibits reuptake of the same as opioids. Modulation to enhance these effects are opioids and antidepressants
32
Acetylsalicylic acid (aspirin) MOA
good abs, - soaks through
33
aspirin pk
strong binding to plasma proteins-
34
aspirin indications
MILD/mod pain, fever, low dose reduces cardiovascular risk due to antiplatelet act. Gout in high doses.
35
aspirin CI
pregnancy and breastfeeding-crosses barrier, children causes reye’s syndrome- hepatotoxicity and encephalopathy so paracetamol is given instead-
36
list the weak opiods
codeinei phosphas - 10mg, dextropropoxyphene, tramadol
37
list the strong opiods
Morphin hydrochlorid – amp. 1% 1,ml Morphin sulphas – tab. 10; 30; 60; 100 mg, Oxycodone – tab. 10; 20; 40 mg, Methadone, Pethidine – amp. 5 % 2 ml, Fentanyl – amp. 0,005 % 2 ml; transdermal patch
38
guidlines for se of opiods to treat pain
ral methods are ideal. Continuous use > as needed. Stable patients are converted to modified release. 2 episodes of breakthrough pain requires increased dose.
39
whats dose dumping
Sudden release of a dose in a short amount of time.
40
opiods pharmacokinetics
bind to bind to mu kappa and delta receptors mean for morphine, dynorphin and enkaphalin.
41
opiod ADR- Morphine mnemonic
``` Miosis Orthostatic hypertension Respiratory depression Physical dependence Hyptertension/Histamine release Increasaed ICP Nausea, vom, constipation Euphoria ```
42
morphine pk
ORAL ABS, liver metabolism, urine excretion of metabolites morphine 3 glucuronide and m6g(ACTIVE) analgesic. Crosses placental barrier
43
morphine antidote
gastric lavage. Nalloxone
44
morpine drug interxn
enhanced by neuroleptics
45
codeine pk
oral abs, no first pass metabolism, converted to morphine
46
codeine indication
antitussive effect
47
codeine adr
minimal seadation, nauseas, vomiting and constipation
48
tramadol moa (DUAL)
weak opioid receptor agonist. Non selective reuptake inhibition of serotonin and norepinephrine superior analgesic to codeine
49
tramadol pk
excreted active metabolite in urine.
50
tramadol ADR
Low abuse potential. Nausea, vom, dizziness, reduce dose in kidney failure
51
how strong is fentanyl
100x more potent than morphine but short doa
52
fentanyl ADR
less nausea and constipation. Not contraindicated in renal failure. Increaded respiratory depression
53
methadone strength and doa
Longer doa than morphine, same strength,
54
methadone indication
neuropathic pain
55
methadone adr
Decreased tolerance and withdrawal syndrome
56
what occurs with repeated dosing of pethidine
Repeated dosing -> accum of toxic met norpethidine. Can be caused by seizures Shorter doa, lower potency than morphine, spasmolytic.
57
what iis neuropathic pain
chronic pain due to damage of the nervous system.
58
which drugs dont work on neuropathic pain
unresponsive to nsaid | low respinsiveness to opiods
59
which drugs are effective for neuropathic pain
Antidepressants and antiepileptics are potent
60
how do anidepressants releive neuropathic pain
inhibits serotonin and norepinephrine uptake.
61
adr's of tca antidepressants
dry mouth, blurred vision, constipation , urinary retention, arrhythmias
62
carbamazapeine is the first choice for what disease
trigeminal neuralgia
63
moa of carbamazapine
blocks na gated ion channels
64
Adr’s carbamazepine
rash, ataxia, nausea, folate deficiency, hyponatremia- liver func and blood count need monitoring.
65
moa of gabapentin
Bind to calcium channels on the descending c fibers of the spinal cord.
66
gabapentin indication
chronic pain
67
indication of topiramate
migrain prophylaxis
68
indication for lamotrigine
pain afer stroke

clinical pharm y5 (22 decks)

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