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Pharmacology > Parkison's Disease > Flashcards

Parkison's Disease Flashcards

1
Q

what is the 2nd most prevalent neurodegenerative disorder?

A

parkison’s disease

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2
Q

what are the diff pathogenesis of parkisons?

A
  • impaired degradatio of proteins, intracellular protein accumulation & aggregation, oxidative stress, mitochondrial damage, inflammatory cascades, apoptosis
  • Prion diseaes -> presence of Lewy bodies
  • Genetic factors
  • Environmental & endogenous toxins
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3
Q

what are the 2 parts of substantia nigra & their functions?

A
  • pars reticulata = receives signals from another part of the basal ganglia (stratum)
  • pars compacta = sends messages to the striatium
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4
Q

what is the structure that receives nadequat eamount of nigrate cells which impairs person’s ability to control movement?

A

striatum portion of basal gangli

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5
Q

what is the pathophysiology of parkinons dis?

A
  • loss of dopaminergic neurons in substantia nigra
  • presence of Lewy body
  • Cholinergic & serotenergic deficits
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6
Q

what are important neurotransmitters affected in Parkinsons disease?

A
  • Dopamine
  • Acetylcholine
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7
Q

what will happen if there is no dopamine?

A

excess muscle tone, tremors, & rigidity

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8
Q

when will symptoms of PD show?

A

if there is >60-80% dopamine lost

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9
Q

what are motor & non-motor symptoms of parkinsons disease?

A

Motor symptoms
* resting tumor
* rigidity
* bradykinesia
* postural instability

Non-motor symptoms
* autonomic: GI, urinary, & sexual, orthostatic hypotension, hyperhidrosis
* sleep disorders
* cognitive decline
* sensory problems (pain, visual)
* neuropsychiatric comorbidity (depression, dementia, psychosis)

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10
Q

what are other symptoms of PD?

A
  • “pill-rolling” tremor = repetitive invluntary rubbing of the thumbn and index finger
  • rigidity
  • stooped posture
  • expressionless, mask-like face
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11
Q

what is the tx goal of PD?

A
  • alleviate motor and nonmotor symptoms
  • limit complications
  • slow down, stop, or modify disease progression
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12
Q

what is used to see if there are any improvements in the drug efficacy and symptom control?

A

rating scales: Hoehn & Yahr scale & Unified Parkinson’s disease rating scale

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13
Q

what is the simplest treatment of PD?

A

Dopamine

however, it cannot cross the BBB

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14
Q

what are the different dopamine receptors?

A

D1 reeptors: D1 & D 5
D2 receptors: D2, D3, D4

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15
Q

What happens with stimulation of D2 receptors?

A

Antiparkinsonism

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16
Q

What dopamine receptors are targeted by drugs?

A

D2
D1
D3

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17
Q

What are the 4 pathways for production of Dopamine?

A

Nigostrial pathway
Mesolimbic and mesocortical pathways
Tuberoinfundibular pathway

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18
Q

What are the 4 pathways for production of Dopamine?

A

Nigostrial pathway
Mesolimbic and mesocortical pathways
Tuberoinfundibular pathway

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19
Q

What are the functions of these pathways of Dopamine production?

A
  • Nigostrial pathway = responsible for movement & coordination
  • Mesolimbic & Mesocortical pathway = controls motivation, emotion, desire
  • Tuberoinfundibular pathway = inhibits the secreiton of prolactin
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20
Q

What is the intendd target pathway for Anti-parkinson medication?

A

Nigostrial pathway

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21
Q

what are diff drugs used to tx motor sympotoms in px with parkinsons diseases?

A
  • Levodopa = dopamin precursor
  • Dopamine precursor combination
  • Dopamine receptor agonists
  • Monoamine oxidase B inhibitors
  • COMT inhibitors
  • Anticholinergics
  • Others: Amantadine, Apomorphine
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22
Q

What is the gold std for Parkisons dis?

A

Levodopa

IT CAN CROSS THE BBB

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23
Q

what phenomenon has symptoms of rigidity and hypokinesia improve when they take the med but effects wear of AFTER 1-2 HRS?

A

wearing-off phenomenon

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24
Q

what phenomenon has off periods of marked akinesia alternate over the course of few hrs with on-periods of improve mobility but often marked dyskinesia?

A

On-off phenomenon

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25
Q

what are important AEs of Levodopa?

A
  • dyskinesias (chronic use) -> apomorphine (emergency drug tx for overdose)
  • depression, anxiety, agitation
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26
Q

what are are the clinical uses for Levodopa?

A
  • used during first few yrs
  • motor features of PD, bradykinesia
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27
Q

what are C/Is of Levodopa?

A
  • not for psychotic px
  • peptic ulcer disease
28
Q

what happens to the effects of Levodopa admin from early stages to chronic use?

A
  • early stage = almost complete improvement
  • advanced stage of the disease = partial imprtovement of motor symptoms
  • longer stage = partial improvement with dewveloping dyskinesia
29
Q

what happens if DOPA decarboxylase exits outside the CNS?

A

INC dopamine levels in the rest of the body -> nausea, vomiting, anorexia, and orthostatic hypotension

30
Q

what is the more problematic side effect of L-dopa?

A

can cause tachycardia and arrhythmia

31
Q

what are advantages of Levodopa combinations?

A
  • prevents peripheral side effects (nausea, vomiting)
  • more Levodopa available for use byu the brain
  • GI effects are less bothersome
  • CV effects are reduced
32
Q

what are the diff Levodopa combinations?

A
  • Sinemet (Levodopa + Carbidopa)
  • Stalevo (Levodopa + Carbidopa + Entacapone)
33
Q

what is a DOPA decarboxylase inhibitor of Sinemet?

A

Carbidopa

does not enter CNS

34
Q

What is Entacapone in Stalevo?

A

COMT inhibitor

reduyces metabolism of L-dopa

35
Q

What is Entacapone in Stalevo?

A

COMT inhibitor

reduyces metabolism of L-dopa; prolonging action of the drug

36
Q

what are alternative first line drugs of PD?

A

Dopamine receptor agonsits

37
Q

what are advantages of Dopamine receptor agonists?

A
  • reduced risk of dykinesias & motor fluctuations
  • indicated for those who cannot tolerate high doses of L-dopa
38
Q

what is the MOA of Dopamine receptor agonsits?

A
  • diretly asks on postsynaptic dopamine reeptors
  • no toxic metabolites
  • do not compete
39
Q

what are important AEs of Dopamine receptor agonsits?

A
  • impulse control disorders are enhanced
  • GI: anorexia, nausea, vomiting
  • CV: postural hypotension, painless digital vasospasm
  • Dyskinesias
  • Mental: hallucinations, delusions, impulse control
  • Bromocriptine: nasuea, vomiting, somnolence, pulmonary fibrosis
  • Pergolide: valvular heart disease
40
Q

what are ergot derivatives that can be used in Dopamine receptor agonists?

A

Bromocriptine: D2 agonist
Pergolide: D1 & D2 agonists

41
Q

What are C/Is of Dopamine receptor agonists?

A
  • Ergot derivatives = peripheral vascular disease
  • Pergolide = valvular <3 disease
42
Q

what are diff tx for motor symptoms?

A
  • levodopa
  • levodopa combinations
  • dopamine receptor agonists
  • COMT inhibitors
  • Monoamine oxidase inhibitors
  • acetylcholine blocking agents
  • Amantadine
43
Q

what are the 2 Monoamine oxidase inhibitors used for PD?

A

Selegiline
Rasagiline

44
Q

what are the MOA of Selegiline & Rasagiline?

A
  • retards breakdown of dopamine
  • enhances effect of LD
  • reduce on-off phenomenon
45
Q

what are important AEs?

A
  • Selegiline = insmonia & hallucinations
  • MAO-A or MAO-B = tachycardia, vomiting, headache
46
Q

what drugs are not supposed to be taken w/ MOAIs?

A
  • Meperidine
  • Tramadol
  • Methadone
  • Propoxyphene
  • Cyclobenzaprine
  • St. John’s wort
  • Dectromethorphan
47
Q

What are other COMT inhibitors?

A

Tolcapone
Entacapone

48
Q

what do these COMT inhibitors do?

A
  • prevent peripheral enxyme from degrading L-dopa
  • More L-dopa to get into the brain
  • only Tolcapone can cross BBB
  • given as adjunct
49
Q

what are AEs of COMT Inhibtors?

A
  • dyskinesia
  • nausea
  • confusion
  • diarrhea
  • abdominal pain
  • orthostatic hypotension
  • sleep disturbances
  • orange discoloration of urine
  • Tolcapone
50
Q

what PD drugs are used to improve tremor and rigidity more than bradykinesia?

A

Acetylcholine blocking agents

51
Q

What are the diff Ach Blocking agents?

A

Benzotropine
Biperiden
Trihexyphenidyl HCl

52
Q

what are significant AEs?

A
  • dry mouth
  • blurred vision
  • difficulty with micturition/constipation
53
Q

what is the clinical use of Ach blocking agents?

A

monotherapy later on as adjunct therapy

54
Q

what is an antiviral agent that has potentiate dopaminergic functions that influence synthesis, release and reuptake of dopamine?

A

Amantadine

55
Q

what are important AEs of Amantadine?

A

Restlessness
confusion
irritability
insomnia
depression
hallucinations
confusion
seizures

56
Q

what are other treatment approaches?

A
  • neurosurgery: Pallidotomy & deep brain stimulation
  • neuroprotective therapy
  • gene therapy
  • deep brain stimulation
57
Q

what tx approach involves an implantable device that directly sends elecrtical signals to the basal ganglia and coutneract the signaling in PD?

A

Deep brain stimulation

58
Q

what is used as tx for Dementia?

A

Rivastigmine

59
Q

What is used as tx for Psychosis?

A

Atypical antipsychotics = Clozapine, Quetiapine

DO NOT USE TYPICAL ANTIPSYCHOTICS

60
Q

What is used as tx for Psychosis?

A

Atypical antipsychotics = Clozapine, Quetiapine

DO NOT USE TYPICAL ANTIPSYCHOTICS

61
Q

What is the tx for mood disorders?

A

antidepressants

62
Q

what is the tx for sleep disorders?

A

Melatonin

63
Q

what are txs for Autonomic dysfunction?

A
  • avoid preceipitating factors of orthostatic hypotension (sudden changes in posture, large meals, vasodilators)
64
Q

what are general rules in prescribing levodopa?

A
  • use of this should be delayed until there is signficant disability
  • to delay long-term side effects -> dopamine agonist or a slow-release levodopa
65
Q

what are other anti-PD used if there is functional impairment?

A
  • anticholinergic = for tremors
  • Amantadine = drug-induced dyskinesias
  • Apomorphine = freezing “off” episodes or “on-off” phenomenon
66
Q

what anti-PD is given if age is >60yo or <60yo?

A
  • <60 yo = Dopamine receptor agonists
  • > 60 yo = Levodopa

Pharmacology (19 decks)

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