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53 Finals > IC14 Pharmaco III (PD, AD) > Flashcards

IC14 Pharmaco III (PD, AD) Flashcards

1
Q

PD definition

A

neurodegenerative disease where nerve cell lose function over time and die, progressive, incurable, increases with age

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2
Q

degeneration of basal ganglion neurons causes

A

decrease dopamine -> PD

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3
Q

degeneration of neuro cortex

A

decrease acetylcholine -> AD

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4
Q

epidemiology of PD

A
  • incidence increases with age
  • avg onset: 60s
  • young onset PD: 21-40yo
  • juvenile onset PD: <20
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5
Q

motor sx of PD

A

TRAP (TRA - cardinal features of PD)
- tremor at rest
- rigidity (cogwheel)
- akinesia/ bradykinesia (slow movement)
- postural instability/ gait disturbances

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6
Q

pathophysiology of PD

A
  1. aggregation of misfolded alpha-synuclein -> form Lewy body
  2. failure to clear Lewy body (contains alpha-synuclein and ubiquitin)
  • Effect: degeneration of dopaminergic neurons with Lewy body inclusion in the substantia nigra -> dysfunction of the nigrostriatal pathway
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7
Q

diagnostic test to confirm PD

A

Lewy body eosinophilic cytoplasmic inclusions in basal ganglia

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8
Q

function of substantia nigra

A

involved in action selection
- basal ganglia normally inhibit a number of motor sx
- substantia nigra mediated release of inhibition -> allows action to occurs

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9
Q

what happen when there is a loss of substantia nigra?

A

no release of inhibition -> hypokinetic state (decreased in motor movements)

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10
Q

how is dopamine synthesised endogenously?

A
  • L-tyrosine -> L-DOPA (tyrosine hydroxylase)
  • L-DOPA -> dopamine (DOPA carboxylase)
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11
Q

Dopamine and L-DOPA which one can pass BBB?

A

Dopamine - cannot pass BBB
L-DOPA - can pass BBB

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12
Q

Drug of choice for PD

A

levodopa (synthetic L-DOPA) + DCI (carbidopa/ benserazide)

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13
Q

Function of DCI

A

peripherally DOPA carboxylase inhibitor -> prevent systemic SE due to excessive dopamine

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14
Q

SE of levodopa

A

short term: N/V/ postural hypotension
long term: motor functions, dyskinesia (does not go away after discontinuation)

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15
Q

eg of COMT inhibitors and MOA

A

entacapone, tolcapone
- MOA: block COMT from breaking down dopamine/ L-DOPA to inactive form -> more levodopa enter brain

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16
Q

can COMT be used as monotx

A

no, must be taken with levodopa

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17
Q

SE of COMT

A

dyskinesia, nausea, diarrhoea, urinary discolouration, visual hallucinations, daytime drowsiness, sleep disturbances
- tolcapone: liver dysfunction

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18
Q

MAO-Bi eg

A

seligiline, rasagiline
- inhibit MAO-B that breakdown dopamine

19
Q

can MAO-Bi be used as a monotx

A

yes for mild PD

20
Q

SE of MAO-Bi

A

heart-burn, loss of appetite, anxiety, palpitation, insomnia, nightmares, visual hallucinations (too much dopamine)

21
Q

dopamine agonist eg and MOA

A

ropinirole, pergolide, pramipexole, rotigotine (patch), apomorphine (SC)
- MOA: act directly on dopamine receptors to reduce sx of PD

22
Q

why is dopamine agonist preferred over levodopa for young onset PD?

A

prevent or delay motor complications with levodopa (eg dyskinesia)

23
Q

SE of dopamine agonsit

A

common: N/V/OH, headache, dizziness, cardiac arrhythmia

  • pergolide ‘ergot’ derivative: peritoneal fibrosis, cardiac valve regurgitation

pramipexole, ropinirole: sedation, somnolence, daytime sleepiness

24
Q

non-dopamine pharmacological approach for PD

A

amantadine and anticholinergics (trihexyphenidyl/benzhexol)

25
Q

MOA of amantadine

A
  • release stored dopamine
  • inhibit presynaptic uptake of catecholamine
  • dopamine agonist
  • NMDA receptor antagonist
26
Q

amantadine place in tx for PD

A
  • monotx or adjunct to levodopa
  • can reduce dyskinesia
27
Q

SE of amantadine

A

cognitive impairment (inability to concentrate), hallucination, insomnia, nightmares, livedo reticularis (venule swelling due to thrombosis)

28
Q

advantages of anticholinergics

A
  • can control tremor, treat sialorrhoea/ drooling
  • used as an adjunct to levodopa to treat tremors in PD
29
Q

SE of anticholinergics

A

dry mouth, sedation, constipation, urinary retention, confusion, hallucinations

30
Q

dementia vs delirium

A

dementia- occurs for at least 6mths
delirium <6mths

31
Q

sx of dementia

A

cognition impairment (at least 2):
- memory
- language
- attention
- problem solving

32
Q

Pathophysiology of AD

A

aggregation of abnormal proteins
1. senile plaques (aggregates of beta-amyloid peptides)
2. neurofibrillary tangles (aggregates of hyperphosphorylated tau proteins)
3. brain atrophy to aggregation at neuro cortex (shrinking of hippocampus)
4. neurodegeneration of neurons at cortex affecting multiple NT (acetylcholine, 5HT, glutamate)

33
Q

what are the neurotransmitters affected in AD. which NT causes clinical features of AD?

A

acetylcholine
5HT
glutamate
- cholinergic deficits causes clinical features of AD

34
Q

difference btw monoaminergic and cholinergic synapse

A

breakdown of acetylcholine occurs in synapse but breakdown of dopamine and 5HT occurs in presynaptic neurons after reuptake

35
Q

goals of tx for AD

A

delay need to institutionalise, improve QOL for both patients and caregivers

36
Q

pharmacological tx for AD

A

AChEI, NMDA receptor antagonist

37
Q

Eg of AChEI and MOA

A

donepezil (best), rivastigmine, galatamine
- MOA: inhibit AChE -> increase ACh in synapse

38
Q

rivastigmine vs galatamine (tested)

A
  • rivastigime: PO, patch, shorter half life, metabolised by kidneys
  • galatamine: PO, longer half life, also act on nicotinic receptors, metabolised by liver
39
Q

SE of AChEI (tested)

A

Cholinergic hyper-activation: N/V/D

less common: (parasympathetic -> rest and digest) muscle cramp, bradycardia, loss of appetite, increase gastric acid secretion

40
Q

which AChEI can be used for moderate AD?

A

donepezil, rivastigmine, galantamine

41
Q

which AChEI can be used for severe AD?

A

donepezil

42
Q

memantine MOA, indication

A

non competitive NMDA receptors antagonist -> block excitotoxicity
- for moderate to severe AD

43
Q

mx of BPSD

A

prescribe the lowest dose possible to alleviate sx and adjust dosage as necessary

53 Finals (10 decks)

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