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53 Finals > IC16 PD > Flashcards

IC16 PD Flashcards

1
Q

cardinal motor sx of PD (LO)

A

TRAP
- Tremor at rest
- Rigidity (cogwheel, leadpipe)
- Akinesia/ bradykinesia
- Postural instability (not cardinal sx)

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2
Q

epidemiology of PD

A

increase with age
decrease with smoking and caffeine

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3
Q

5 non-motor sx of PD (LO)

A
  1. cognitive impairment (depression)
  2. psychiatric sx (depression, psychosis)
  3. sleep disorders
  4. autonomic dysfunction (constipation, decrease GI motility, OH, sialorrhoea)
  5. others (fatigue)
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4
Q

Pathophysiology of PD (LO)

A

misfolded alpha-synuclein aggregate to form Lewy body which:
1. decrease DA transmission
2. causes mitochondrial failure
3. neuroinflammation through activation of microglial

Result: loss of dopaminergic neurons in the substantia nigra -> cause clinical sx of PD

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5
Q

Dx of PD

A

any 2 out of 3 cardinal sx
- Tremor at rest (disappear with movements)
- Rigidity (cogwheel/ leadpipe)
- Akinesia (difficulty getting out of bed/chair, difficulty turning while walking)

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6
Q

Idiopathic PD

A
  • asymmetric sx
  • +’ve response to levodopa
  • postural instability not present initially
  • less rapid progression
  • autonomic dysfunction not present initially
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7
Q

what neuroimaging is used to dx PD?

A

SPECT- DaT scan

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8
Q

Effects of poor motor sx in PD

A
  • unable to perform ADL
  • choking
  • pneumonia/ UTI
  • falls
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9
Q

measuring PD progression

A

Hoehn and Yahr staging, UPDRS

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10
Q

PD timeline

A

20yrs prodrome, dx usually occurs with first motor sx

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11
Q

early/young onset PD

A

slower disease progression, < cognitive decline, early motor sx, dystonia in common initially
- dopamine agonist preferred over levodopa

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12
Q

Goals of tx (LO)

A

manage sx, maintain function and autonomy
- no tx for PD currently

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13
Q

pharmacological treatments (LO)

A
  1. levodopa + DCI
  2. dopamine agonist
  3. MAOBi
  4. COMT
  5. anticholinergics
  6. NMDA antagonist
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14
Q

why is levodopa first line

A

most effective in treating motor sx (bradykinesia, rigidity); less effective for speech, postural reflex and gait disturbances

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15
Q

dopamine cannot be used as tx because…

A

does not cross BBB (only L-DOPA can)

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16
Q

how is levodopa metabolised peripherally?

A

DOPA carboxylase, MAO, COMT
- peripheral dopamine cause N/V/hypotension

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17
Q

how is levodopa absorbed?

A

at proximal part of SI by an active saturable carrier system
- low oral F (increases with DCI)
- abs decrease with high fat or protein meals

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18
Q

eg of DCI, MOA, do they cross BBB?

A

carbidopa, benserazide
- does not cross BBB
- MOA: inhibit peripheral breakdown of levodopa

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19
Q

AE of levodopa

A
  • N/V
  • orthostatic hypotension
  • drowsiness, sudden sleep onset
  • hallucinations, psychosis
  • dyskinesia (within 3-5yrs of initiation)
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20
Q

motor complications of levodopa

A
  1. on-off phenomenon
  2. wearing off effect
  3. dyskinesia
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21
Q

describe on-off phenomenon and mx

A

response/no response to levodopa
- unpredictable, not related to dose/dosing interval
- mx: difficult to control with meds

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22
Q

describe wearing off effect

A

effect of levodopa wanes before end of dosing interval
- mx: increase dosing frequency, use extended release formulations

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23
Q

describe peak dose dyskinesia

A

involuntary, uncontrollable muscle twitching or jerking that occurs at peak dose of levodopa
- mx: add amantadine, use MR levodpa

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24
Q

mx of levodopa motor complications (LO)

A
  1. adjust levodopa dose
  2. change dosing frequency
  3. explore dosage forms (ER)
  4. Adjunct meds: DA, MAO-Bi, COMT
25
Q

Progression of PD and response to levodopa

A
  1. stable phase
  2. wearing off effect
  3. peak dose dyskinesia (when levodopa dose is increased to overcome wearing off effect)
  4. on-off fluctuations at the late stage (appears randomly)
26
Q

Characteristics of sustained released levodopa formulations

A
  • release levodopa slowly over a longer period of time
  • lower F
  • useful to decrease stiffening on waking (usually overnight dose would been reduced when pt wake up)
  • useful to overcome peak dose dyskinesia and wearing off effect
  • do not crush or open capsule
27
Q

levodopa DDI

A
  1. pyridoxine (vit B6) - cofactor for DOPA carboxylase, not an issue of DCI is given
  2. iron - affect absorption (space out)
  3. fat/protein (food, protein powder) - affect absorption (space out)
  4. dopamine antagonist (eg antiemetic - metoclopramide, prochlorperazine; FGA; risperidone)
28
Q

antiemetic of choice in PD

A

domperidone

29
Q

eg of dopamine agonist

A

ropinirole, pramipexole, rotigotine (patch), apomorphine (SC)

30
Q

MOA of dopamine agonist

A

act on D2 receptors in basal ganglia, mimic the action of dopamine

31
Q

PK characteristics of dopamine agonist

A
  • ergot derivative lower F than non-ergot due to first pass metabolism
  • longer half life and duration that levodopa
  • ropinirole: metabolised by liver (caution in liver impairment)
  • pramipexole: excreted largely unchanged in urine (caution in renal failure)
32
Q

AE of dopamine agonist (peripheral and central)

A
  • peripheral: N/V/ orthosatic hypotension, leg edema
  • central: hallucination/psychosis, somnolence, daytime sleepiness, compulsive behaviours (must counsel pt)
  • fibrosis and valvular heart disease (more common in ergot derivative DA)
33
Q

what is the most important counselling point for pt on dopamine agonist?

A

compulsive behaviours (gambling, shopping, eating, hypersexuality)

34
Q

dopamine agonist place in therapy compared to levodpa

A

less motor sx but more hallucination, slp disturbances, leg edema, OH than levodopa
- preferred over levodopa in younger pt

35
Q

indications for dopamine agonist in PD

A
  • monotx for young onset PD
  • adjunct to levodopa for mod-sev PD
  • mx of motor complications caused by levodopa
36
Q

eg of irreversible MAO-Bi, MOA

A

selegiline, rasagiline
- MOA: inhibit breakdown of levodopa and domaine in the brain (central)
- not totally selective for MAO-B

37
Q

MAO-A vs MAO-B

A

MAO-A: peripheral, NA and 5HT
MAO-B: central, dopamine

38
Q

can MAO-Bi be used as monotx

A

yes, in early stage PD

39
Q

what to take note of when taking selegiline

A

metabolised into amphetamines (stimulants) - take second dose late afternoon instead of at night (otherwise cannot sleep)
- effect not seen with rasagiline (not metabolised to amphetamine)

40
Q

MAO-Bi DDI

A
  1. SSRI, SNRI, TCA - washout needed
  2. linezolid
  3. dopamine
  4. dextromethorphan
  5. sympathomimetics: pseudoephedrine
41
Q

MAO-Bi DFI

A

tyramine containing foods (cheese, aged meat, preserved/fermented food)

42
Q

MAO-Bi place in tx

A
  • not as great as DA or levodopa
  • monotx in early stages, adjunct in late stage PD
  • more commonly used in early stages of young onset PD
43
Q

selective reversible COMT inhibitors eg

A

entacapone, tolcapone

44
Q

can COMT be used as monotx

A

no, must be taken together with levodopa
- decreases “off” time with levodopa

45
Q

DDI with COMT

A
  1. iron, Ca
  2. concurrent non-selective MAOi (safe with MAO-Bi)
  3. catecholamine drugs
  4. enhance anticoagulant effect of warfarin
46
Q

SE of COMT inhibitors

A

diarrhoea, urine discoloration (orange)

47
Q

Cautions with COMT inhibitors

A
  • hepatic impairments
  • may cause dyskinesia upon initiating (decrease levodopa dose)
  • potentiates dopaminergic effects (eg OH, N, V)
48
Q

anticholinergics used in PD

A

benztropine, trihexyphenidyl (benzhexol)

49
Q

anticholinergics place in tx for PD

A
  • limited use
  • used to control tremor
  • has anticholinergic SE
50
Q

eg NMDA antagonist used in PD and MOA

A

amantadine
(memantine used in AD)
- MOA: decrease glutamate activity that caused cell death

51
Q

PK of amantadine

A
  • renally excreted
  • can be stimulating (take second dose in afternoon instead of night)
52
Q

amantadine place in tx for PD

A
  • adjunct
  • mx of levodopa induced dyskinesia
53
Q

AE of amantadine

A

nausea, light headedness, insomnia, confusion, hallucinations, livedo reticularis

54
Q

alternative/ complementary medicines

A

co-enzyme Q10, creatine (not proven effective)

55
Q

Drug induced PD (LO): how is it different from idiopathic PD

A
  • sx occurs bilaterally (iPD usually unilateral initially)
  • withdrawal of drugs leads to improvement
  • no resting tremor, acute onset
56
Q

5 drugs that induce PD

A
  1. D2 receptor blockers (FGA, SGA)
  2. Dopamine depleters (valbenzine, tetrabenzine, reserpine)
  3. Dopamine synthesis blocker (methyldopa)
  4. CCB (flunarizine, cinnarizine, diltiazem, verapamil)
  5. valproate
  6. antiemetic (prochlorperazine, metoclopramide)
57
Q

Mx of drug induced PD

A
  • tx: withdraw offending drug
  • may not always be reversible
  • amantadine and anticholinergics may be used
58
Q

Non-pharm

A

physiotherapy, occupational therapy, speech therapy, deep brain stimulation (for advanced PD)

53 Finals (10 decks)

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