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Pharmacology > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

What is Parkinson’s

A

slowly progressive degenerative CNS disorder

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2
Q

Characteristics of Pakinson’s

A

Tremor
Rigidity
Bradykinesia
Postural DIsturbances

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3
Q

Aetiology of primary Parkinson’s

A

Loss of Dopamine-producing neurons in substantia nigra= deficiency of DA in Basal Ganglia.

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4
Q

What is the neurotransmitter imbalance caused by Parkinson’s

A

Too little DA (low inhibitory) and too much ACh (high excitatory)

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5
Q

Cause of Tremors

A

due to involuntary skeletal muscle contractions

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6
Q

When is a tremor at its maximum

A

during rest

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7
Q

Is a tremor present during sleep

A

Nope

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8
Q

How does a tremor start

A

may start in Upper extremity, spread to ipsilateral LL and then to contralateral limb

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9
Q

Cause of rigidity

A

Due to continuous mucle contraction

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10
Q

What is Bradykinesia

A

slowness and poverty of movement

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11
Q

What is Hypokinesia

A

Muscular movements performed with decr. range of motion

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12
Q

Cause of Postural disturbance

A

there is loss of postural reflexes = tendency to fall forward (propulsion) or backward (retropulsion) when center of gravity is displaced

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13
Q

What other symptoms may be seen in Parkinson’s

A

Speech may be affected
Depression: common
Dementia: common

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14
Q

Which Dopaminergic agents are used?

A

DA precursors
DA R agonists
COMT inhibitors
MAO Type B inhibitors

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15
Q

Which are the DA precursor drugs

A

Levodopa

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16
Q

Which are the DA Receptor agonists

A

Bromocriptine
Ropinirole
Pergolide
Pramipexole
Apomorphine

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17
Q

Which are the COMTi drugs

A

Tolcapone
Entacapone

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18
Q

Which are MAO Type B inhibitors

A

Selegiline
Rasagiline

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19
Q

Which Anticholinergic agents are used

A

TBB
Trihexyphenidyl
Benzotrpine
Biperidin???

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20
Q

MOA of Levodopa

A

Is a DA precursor= facilitates synthesis of DA in brain
–> restores Dopaminergic neurotransmission in neostriatum by enhancing DA synthesis in surviving neurons of Substantia nigra

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21
Q

How is Levodopa therapy initiated (dosage)

A

With small doses and gradually increased

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22
Q

How effective is Levodopa therapy

A

not effective
Therapy loses its effectiveness after 2 years of use

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23
Q

Type of Parkinson Levodopa has no effect on

A

Drug-induced Parkinson

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24
Q

Where is Levodopa absorbed

A

in SI

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25
Q

What inactivates Levodopa

A

MAO in SI

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26
Q

Enzyme that converts Levodopa to DA

A

Dopa Decarboxylase.

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27
Q

Distribution of Levodopa

A

95% converted to DA in peripheral tissue; <1% enters brain

28
Q

What interferes with Levodopa transport into CNS

A

ingestion of high protein meals

29
Q

How should Levodopa be taken

A

On an empty stomach (at least 30mins before meals)

30
Q

AE of Levodopa

A

Anorexia
Nausea
Psychiatric disturbances
Incr. HR
Mydriasis
Decr. BP
On-Off effect: rapud fluctuations in clinical state- hypokinesia and rigidity may suddenly worsen then improve
Development of involuntary choreiform movements- usually affecting face and limbs

31
Q

Drugs that improve Levodopa efficacy

A

Carbidopa: peripheral Dopa-decarboxylase inhibitor
Selegiline: MAO-B inhibitor–> inhibits DA degradation in CNS
Rasagiline: irreversibly inhibits MAO-B
Domperidone: Peripheral dopamine antagonist

32
Q

SE of Levodopa+Selegiline

A

HTN crisis
Insomnia

33
Q

Potency of Rasagiline

A

5x more potent than Selegiline

34
Q

SE of Levodopa+Rasagiline

A

Doesn’t cause insomnia

35
Q

MOA of Entacapone

A

Selective reversible inhibitor of COMT
=prevents metabolism of Levodopa to 3-O-methyldopa–>
decr. palsma conc. of 3-O-methyldopa
Incr. central uptake of Levodopa
Incr. conc. of DA in brain

36
Q

What is 3-O-methyldopa

A

A metabolite of Levodopa that competes with Levodopa for active transport into the CNS

37
Q

SE of Entacapone

A

GI upsets
Postural Hypotension
Hallucinations
Sleep disorders

38
Q

SE of Tolcapone

A

Associated with hepatic necrosis

39
Q

MOA of Bromocriptine

A

Is a Dopamine Receptor Antagonist
Is a ergot derivative

40
Q

Cons of Bromocriptine

A

it has many AEs
its very expensive

41
Q

Caution when using Bromocriptine

A

MI or Peripheral Vascular disease

42
Q

When is Bromocriptine used

A

Only for cases that cannot be effectively treated with Levodopa

43
Q

AE of Bromocriptine that occur during first few months of use

A

Nausea
Dizziness
Drowsiness
Postural Hypotension

44
Q

AE of Bromocriptine that occur at high doses over longer periods

A

Dyskinesia
Hallucinations
Confusion
Behavioural Abberations

45
Q

What does Bromocriptine exacerbate

A

Peptic ulcers

46
Q

Common AEs of Bromocriptine

A

Dementia
Depression

47
Q

What is Amantadine

A

An anti-viral agent with moderate anti-Parkinson activity

48
Q

When is Amantidine useful

A

useful as monotherapy for early, mild Parkinsonism
Can be used in combination with Levodopa

49
Q

Effectiveness of Amantidine

A

It loses its effectiveness after several months

50
Q

MOA of Amantidine

A

Releases DA from its stores and inhibits the re-uptake of DA from the synaptic cleft

51
Q

AEs of Amantidine

A

Discolouration of the skin (esp. legs and oedema of ankles)
Pulmonary pleursis
Stops milk production (decr. prolactin)
Acute MI

52
Q

CI of Amantadine

A

PVO
MI
Cardiac vascularity

53
Q

AEs of Amantadine that may occur at high doses

A

Psychotic episodes
Convulsions
Nausea

54
Q

MOA of Anticholinergics (antimuscarinics)

A

competitively antagonize ACh at MR.
They can cross BBB because they are lipphilic

55
Q

Indications of Biperiden

A

Parkinsonism

56
Q

When is an injection of Biperiden useful

A

it can be useful for rapid control of drug-induced acute dystonic reactions

57
Q

AEs of Biperiden

A

Usual Anti-muscarinic effects
Pronounced drowsiness
Urinary retention
Visual disturbance
Aggrevation of glaucoma
Postural hypotension
Euphoria
Aberrations of co-ordination ???

58
Q

What is Orphenadrine

A

Its an anti-histamine with anticholinergic effects

59
Q

When is Orphenadrine used

A

for treatment of mild Parkinsonism
for elderly patients who cannot tolerate the potent parasympatholytic drugs

60
Q

AEs of Orphenadrine

A

Drowsiness
Para-sympatholytic SEs: dry mouth, visual disturbance, urinary retention, constipation
Concurrent intake of alcohol or sedative may cause excessive sedation

61
Q

Uses of Trihexyphenidyl/ Benztropin

A

its used for both idiopathic and drug-induced Parkinsonism.

62
Q

What do Trihexyphenidyl/ Benztropin relieve

A

tremors due to Parkinsonism

63
Q

What do large doses of Trihexyphenidyl/ Benztropin do

A

they induce a feeling of mental well-being and as such is abused for this feeling

64
Q

AES of Trihexyphenidyl/ Benztropin

A

Parasympatholytic SEs: dry mouth, blurred vision, dizziness and nausea occur at beginning of therapy
Elderly: constipation and urinary retention
Tachycardia
Drowsiness

65
Q

CI of Anticholinergics

A

Prostatic Hypertrophy: aggravate urinary retention associated with Prostatic Hypertrophy
Glaucoma: icr. IOR= exacerbate it
GI Obstruction

Pharmacology (50 decks)

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