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FINALS - NEURO > pharma > Flashcards

pharma Flashcards

1
Q

what is the analgesic ladder

A
  1. paracetamol +/- NSAIDS // 2. weak opioids eg codeine, tramadol // 3. strong opioids eg morphine, oxy
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2
Q

where is pain processed in the brain

A

cortex, amyglada, thalamus

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3
Q

which brainstem nuclei are excited in descending pain pathway (3)

A

PAG, locus coeruleus, nucleus raphe magnus

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4
Q

which pathways are activated in descending nociceptive pathway

A

serotonergic and enkephalinergic

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5
Q

how does lidocaine or nerve blockers work

A

inactivate sodium channels for ascending nociceptive pathway

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6
Q

how do opioids prevent pain

A

inhibit Ca channels (stop depolarisation) // open K channels to suppress excitation of projection neurones // act in both ascending and descending pathway

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7
Q

what are the 3 opioid receptors and where are they usually found

A

mu (y), delta, kappa // cortex, limbic system + brainstem

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8
Q

SE opioids

A

resp apnoea // orhtostatic hypotension // braducardia // N+V // constipation // euphoria, hallucinations

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9
Q

what are strong opioids

A

morphine, diamorph (heroine), fentanyl (anaesthetics)

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10
Q

what are weaker opioids

A

coedine, buprenorphine, tramadol

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11
Q

what opioid is given in child birth

A

pethidine

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12
Q

what opioid is slow acting and used in chronic pain

A

Buprenorphine

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13
Q

what drug reverses opioid toxicity

A

naloxone (antagonist of mu receptor) // naltrexone or alvimopan

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14
Q

what is the function of COX

A

synthesises phospholipids –> PGE

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15
Q

what is the role of prostaglandin in pain regulation

A

lower nociceptive activation threshold, recruit inflamm mediators

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16
Q

difference between COX 1 and 2

A

COX 1 is systemic but COX2 only at side of injury

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17
Q

mechanism NSAIDs

A

inhibit COX

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18
Q

SE NSAIDs

A

ulcers, COX2 prothrombotic

19
Q

mechanism gabapentin and pregabalin

A

reduce Ca channels upregulated in damaged sensory nerves // decrease NT eg glutamate

20
Q

mechanism TCA

A

recrease reuptake of NA and 5HT which both enhance descending pathway

21
Q

where do 5HT3 antagonists mainly work

A

medulla oblongata

22
Q

examples 5HT3 antagonists

A

ondasetron

23
Q

indication 5HT3

A

chemo nausea

24
Q

SE 5HT3

A

prolonged QT and constipation

25
Q

carbamezepine action

A

blocks Na channels

26
Q

indication carbamezepine

A

AED, bipolar, trigeminal neuralgia

27
Q

mechanism lamotrigene

A

Na channel blocker

28
Q

SE lamotrigine

A

stevens johnson

29
Q

mechanism phenytoin

A

binds to sodium channel + increases refractory period

30
Q

phenytoin effect on p450

A

inducer

31
Q

acute phenytoin SE

A

drunk - dizzy,, nystagmus, diplopia, ataxia

32
Q

chronic SE phenytoin

A

gingivval hyperplasia // peripheral neuropathy // anaemia // lymp

33
Q

idiosyncratic SE phenytoin

A

hepatitis, TENS, aplastic anaemia, baby: cleft palate and heart disease

34
Q

monitoring phenytoin

A

trough levels immediately before dose if: adjustment, toxixity, adherence

35
Q

sodium valproate affect on p450

A

inhibitor

36
Q

mechanism sodium valportate

A

increase GABA

37
Q

SE sodium valproate

A

teratogenic // appetite and weigt gain // ataxia tremor // hepatotoxic // pancreatitis // thrombocytopenia// hypo Na

38
Q

sodium valproate on P450

A

inhibits p450

39
Q

what is levodopa prescribe with

A

decarboxylase inhibitor (e.g. carbidopa or benserazide)

40
Q

SE levodopa

A

dyskinesia // sudden off state // postural hypotension!!! // arrhythmia // N+V // psychosis // red grin on standing

41
Q

indication dopamine agonists

A

parkinsons, prolactinoma, acromegaly

42
Q

examples dopamine agonist

A

bromocriptine, ropinirole, cabergoline, apomorphine

43
Q

SE dopamine agonist

A

N+V // post hypotension // hallucinations // daytime somnolence

44
Q

medical use botox

A

blepharospasm // focal spasticity cerebral palsy // hyperhidrosis // achalasia // spasmodic torticollis

FINALS - NEURO (16 decks)

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