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Neuropharmacology > Parkinsons' disease > Flashcards

Parkinsons' disease Flashcards

1
Q

Pathophysiology of Parkinsons’ Disease

A
  • degeneration of dopaminergic neurons in SNc

-> more cholinergic than dopaminergic input

  • dopaminergic neurons: inhibit GABAnergic output in D2 pathway
  • cholinergic neurons : excitatory effect on D2 pathway
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2
Q

Motor and non motor symptoms of Parkinsons

A

Motor:
- rigidity
- akinesia/ bradykinesia
- flat facies
- tremor at rest

Non motor:
- delusions/ hallucinations
- depression and anxiety
- speech and swallowing problems
- postural hypotension

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3
Q

Why dopamine not used as drug for Parkinsons

A
  1. readily metabolized peripherally
  2. cannot pass thru BBB
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4
Q

Name Levodopa MOA

A
  • precursor of dopamine
    -> increase dopaminergic transmission in nigrostriatal pathway
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5
Q

Name Levodopa CNS effects

A

CNS:
- marked symptomatic improvement in patients (hypokinesia, tremor, rigidity)

  • some may have excitement frank psychosis
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6
Q

Name Levodopa peripheral effects

A
  1. tachycardia
  2. postural hypotension
  3. inhibit prolactin release + increase GH release
  4. enhance GFR
  5. nausea and vomitting (by excitation at chemoreceptor trigger zone)
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7
Q

gastric emptying and levodopa

A
  • slow emptying
    -> less available to penetrate BBB (longer exposure to degrading enzymes)
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8
Q

What competes with levodopa for same carrier

A
  • amino acid
  • compete for carrier for absorption
    -> lower levodopa blood levels when taken with meal
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9
Q

What competes with levodopa for same carrier

A
  • amino acid
  • compete for carrier for absorption
    -> lower levodopa blood levels when taken with meal
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10
Q

Levodopa adverse effects

A
  • nausea, vomitting
  • postural hypotension
  • excessive: psychological disturbance
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11
Q

Cautious use of levodopa needed in

A
  1. elderly
  2. ischemic heart disease
  3. cerebrovascular
  4. psychiatric
  5. hepatic and renal (high first pass in liver)
  6. peptic ulcer (increase risk of bleeding)
  7. glaucoma
  8. gout
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12
Q

Long term effect of Levodopa

A
  1. wearing off - decline in efficacy for same dose
  2. On-off effect: oscillation between state of decreased mobility (off) and when med working and symptoms controlled (on)
  3. peak dose dyskinesia/ dystonic muscle spasm
  4. end of dose akinesia
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13
Q

State two peripheral decarboxylase inhibitor

A
  1. carbidopa
  2. benserazide
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14
Q

Benefits of combination with levodopa

A
  1. prolong levodopa plasma half live -> 1/4 dose reduction
  2. minimize on-off effect
    - more sustained cerebral DA levels and reduced systemic conc.
    -> reduce cardiac complications
  3. minimize nausea and vomitting
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15
Q

Problems not resolved/ accentuated with peripheral decarboxylase inhibitor use

A
  1. involuntary movements more pronounced/ earlier
  2. postural hypotension
  3. excessive daytime sleepiness

-> not used along levodopa if patient develop MARKED involuntary mvmt with its use

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16
Q

SINEMET
MADOPAR

A

SINEMAT: levo + carbidopa

MADOPAR: levo+ berserazide

17
Q

Name four dopaminergic agonis

A
  1. pramipexole
  2. ropinirole
  3. bromocriptine
  4. rotigotine
18
Q

side effects of high dose bromocriptine

A
  1. vomitting
  2. hallucination
  3. hypotension
19
Q

side effects of ropinirole and pramipexole

A
  • behavioural side effects (gambling, impulsive shopping) , sexual overactivity
  • nausea, dizziness
  • hallucintaion
  • postural hypotension
  • daytime sleep -> shd not drive
20
Q

advantage of pramipexole and ropinirole

A
  • fewer GI symptoms
  • slower rate of neuronal degeneration
  • reducing frequency of on off effect
21
Q

Use of ropinirole and pramipexole

A
  • frequently used for monotherapy
  • supplementary drugs to levodopa-carbidopa (in advanced case)
22
Q

Name MAO-B inhibitor

A

Selegiline

23
Q

State MAO-B inhibitor MOA

A
  • selective and irreversible inhibitor
    -> retard intracerebral degradation of DA
    -> increase dopaminergic transmission in nigrostriatal pathway
24
Q

State use of MAO-B inhibitor

A
  • administered with Levodopa
    -> prolongs and enhance levodopa action
    -> decrease wearing off and motor fluctuation
25
Q

Name COMT inhibitors

A
  • Entacapone
    -Tolcapone
26
Q

COMT inhibitors MOA

A
  • selective and reversible inhibitor
  • block peripheral metabolism of levodopa & central metabolism of dopamine
  • prolongs half live of levodopa/ dopamine
    • entacapone acts only in periphery
    • tolcapone prevents peripheral and central metabolism of levodopa
27
Q

Name glutamate/ NMDA receptor antagonist

A

Amantadine

28
Q

State amantadine MOA

A
  1. promotes presynaptic synthesis and release of DA in brain
  2. directly activates dopamine receptors
  3. blocks dopamine reuptake at high doses
29
Q

State side effects of amantadine

A
  1. insomnia, nightmare
  2. restlessness
  3. confusion
  4. anticholinergic effects
    *5. local release of catecholamine
    -> postcapillary vasoconstriction -> bluish discolouration (livedo reticularis) + edema of ankle
  • side effects attenuated when combined with anticholinergics
30
Q

State use of antimuscarinic agents (benztropine and trihexyphenidyl)

A
  1. improve resting tremor and rigidity
  2. good for antipsychotics induced Parkinsonism
  • NOT good for bradykinesia/ patients showing signs of dementia (who may have degeneration of cortical chorlinergics)
31
Q

State undesirable effets of antimuscarinic agents

A
  1. dry mouth
  2. constipation
  3. urinary retention
  4. confusion, dementia
32
Q

Name antimuscarinic agents

A
  • benztropine
    (- trihexyphenidyl)

Neuropharmacology (6 decks)

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