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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
Q

NSAID moa

A

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

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26
Q

NSAID indications:

A

chronic inflammatory diseases- arthritis, spondylitis, radiculitis, metastatic bone tumors due to prostaglandin release during bone lysis

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27
Q

NSAID ADR

A

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

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28
Q

NSAID CI

A

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
Q

NSAID drug interxn

A

decrease antihypertensives and diuretics

30
Q

describe the ascending pain pathway (6)

A

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
Q

describe the descending pain pathway(5)

A

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
Q

Acetylsalicylic acid (aspirin) MOA

A

good abs, - soaks through

33
Q

aspirin pk

A

strong binding to plasma proteins-

34
Q

aspirin indications

A

MILD/mod pain, fever, low dose reduces cardiovascular risk due to antiplatelet act. Gout in high doses.

35
Q

aspirin CI

A

pregnancy and breastfeeding-crosses barrier, children causes reye’s syndrome- hepatotoxicity and encephalopathy so paracetamol is given instead-

36
Q

list the weak opiods

A

codeinei phosphas - 10mg, dextropropoxyphene, tramadol

37
Q

list the strong opiods

A

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
Q

guidlines for se of opiods to treat pain

A

ral methods are ideal. Continuous use > as needed. Stable patients are converted to modified release. 2 episodes of breakthrough pain requires increased dose.

39
Q

whats dose dumping

A

Sudden release of a dose in a short amount of time.

40
Q

opiods pharmacokinetics

A

bind to bind to mu kappa and delta receptors mean for morphine, dynorphin and enkaphalin.

41
Q

opiod ADR- Morphine mnemonic

A 
Miosis
Orthostatic hypertension
Respiratory depression
Physical dependence
Hyptertension/Histamine release 
Increasaed ICP
Nausea, vom, constipation
Euphoria
42
Q

morphine pk

A

ORAL ABS, liver metabolism, urine excretion of metabolites morphine 3 glucuronide and m6g(ACTIVE) analgesic. Crosses placental barrier

43
Q

morphine antidote

A

gastric lavage. Nalloxone

44
Q

morpine drug interxn

A

enhanced by neuroleptics

45
Q

codeine pk

A

oral abs, no first pass metabolism, converted to morphine

46
Q

codeine indication

A

antitussive effect

47
Q

codeine adr

A

minimal seadation, nauseas, vomiting and constipation

48
Q

tramadol moa (DUAL)

A

weak opioid receptor agonist. Non selective reuptake inhibition of serotonin and norepinephrine
superior analgesic to codeine

49
Q

tramadol pk

A

excreted active metabolite in urine.

50
Q

tramadol ADR

A

Low abuse potential. Nausea, vom, dizziness, reduce dose in kidney failure

51
Q

how strong is fentanyl

A

100x more potent than morphine but short doa

52
Q

fentanyl ADR

A

less nausea and constipation. Not contraindicated in renal failure. Increaded respiratory depression

53
Q

methadone strength and doa

A

Longer doa than morphine, same strength,

54
Q

methadone indication

A

neuropathic pain

55
Q

methadone adr

A

Decreased tolerance and withdrawal syndrome

56
Q

what occurs with repeated dosing of pethidine

A

Repeated dosing -> accum of toxic met norpethidine. Can be caused by seizures
Shorter doa, lower potency than morphine, spasmolytic.

57
Q

what iis neuropathic pain

A

chronic pain due to damage of the nervous system.

58
Q

which drugs dont work on neuropathic pain

A

unresponsive to nsaid

low respinsiveness to opiods

59
Q

which drugs are effective for neuropathic pain

A

Antidepressants and antiepileptics are potent

60
Q

how do anidepressants releive neuropathic pain

A

inhibits serotonin and norepinephrine uptake.

61
Q

adr’s of tca antidepressants

A

dry mouth, blurred vision, constipation , urinary retention, arrhythmias

62
Q

carbamazapeine is the first choice for what disease

A

trigeminal neuralgia

63
Q

moa of carbamazapine

A

blocks na gated ion channels

64
Q

Adr’s carbamazepine

A

rash, ataxia, nausea, folate deficiency, hyponatremia- liver func and blood count need monitoring.

65
Q

moa of gabapentin

A

Bind to calcium channels on the descending c fibers of the spinal cord.

66
Q

gabapentin indication

A

chronic pain

67
Q

indication of topiramate

A

migrain prophylaxis

68
Q

indication for lamotrigine

A

pain afer stroke

clinical pharm y5 (22 decks)

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