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Pharmacology > Anti-Parkinson Drugs > Flashcards

Anti-Parkinson Drugs Flashcards

1
Q

Cardinal features of Parkinson

A
  • Resting tremor
  • Muscle rigidity (Cogwheel rigidity)
  • Bradykinesia
  • Gait impairment
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2
Q

Etiology of Parkinson

A

Loss of neurons in the Dopaminergic Nigrostriatal pathway

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3
Q

Dopamine Synthesis

A
  • Tyrosine (transported across BBB by System-L in a Na-independent manner)
  • Tyrosine (Tyrosine hydroxylase - RLS) –> DOPA (DOPA Carboxylase) –> Dopamine

Inc Dopamine formation by Inc substrates

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4
Q

Dopamine receptors related to Parkinson

A
  1. D1 Receptors
    - Inc adenylyl cyclase
  2. D2 Receptors
    - Dec adenylyl cyclase
    - Inc K conductance
    - Dec Ca conductance

Treatment of Parkinson is mostly focused on D2 but needs D1 for maximal effect

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5
Q

Dopamine pathways in Brain

A
  1. Nigrostriatal
    - Make focus for PD - Destruction of neurons
  2. Mesolimbic
  3. Mesocortical
  4. Tuberoinfundibular
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6
Q

Pathophysiology of Parkinson Disease

A

NORMAL
GABAergic output from Striatum
- Inhibited by Dopaminergic neuron in Substantia nigra
- Stimulated by Cholinergic neurons

PARKINSON

  • Destruction of Dopaminergic neurons in Nigrostriatal pathway –> Loss of muscle control/ movement
  • 70% neuron loss for symptoms to appears
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7
Q

Aim of Anti-Parkinson Drugs

A
  1. Restoring dopamine in basal ganglia

2. Antagonizing the excitatory effect of cholinergic neurons

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8
Q

Classes of Drugs used to treat Parkinson

A

1 Drugs that restore Dopamine actions

  • Dopamine precursors
  • Dopamine receptor agonists
  • Inhibitors of Dopamine metabolism
  • Amantadine
  1. Acetylcholine Antagonists
    - Antimuscarinics
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9
Q

Dopamine Precursors (Names)

A

Levodopa

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10
Q

Mechanism of Levodopa

A

Levodopa is a precursor for Dopamine

Levodopa is transported into CNS and converted to Dopamine by Dopa-carboxylase (mostly in the periphery)
- Restores dopamine in the Extrapyramidal centers

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11
Q

Why does the effects of Levodopa decrease as the disease progress.

A

As the disease progresses there are less neurons so less Levodopa can be taken up and converted to Dopamine.

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12
Q

Function of Carbidopa

A

Dec the metabolism of Levodopa in the GI tract & periphery tissues –> Inc Levodopa availability to CNS

Levodopa–> GI= 70%, Periphery = 28% & Brain - 2%
Sinemet –> GI = 40%, Periphery = 50% & Brain = 10%

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13
Q

Sinemet

A

Dopa preparation of both Carbidopa & Levodopa in fixed proportions
- 1:10 OR 1:4

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14
Q

Pharmacokinetics of Levodopa

A
  • Rapid absorption in SI
  • Food delays appearance in plasma
  • Some A.a compete w/ drug for absorption from gut
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15
Q

Clinical uses & Response to Levodopa

A

Levodopa/Carbidopa –> DOC for PD treatment

  • Response decrease w/ 3-5 years of therapy
  • Response completely lost overtime due to lost of neurons
  • Does NOT stop PD progression; just helps with symptom management
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16
Q

Adverse effects of Levodopa

A

GI
- Anorexia, Nausea & vomiting

CVS
- Tachycardia, Ventricular extrasystoles & Hypotension

CNS
- Hallucinations (visual & auditory), Dyskinesias, Mood changes, Depression, Anxiety, Agitation & Insomnia

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17
Q

Fluctuations in Response to Levodopa

A
  1. Wearing-Off Reactions
  2. On-Off Phenomenon
    - switch between mobility and immobility in levodopa-treated patients, which occurs as an end-of-dose
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18
Q

Interactions & Contraindications of Levodopa

A

Do NOT give:

  • Psychotic pts/ Concomitant antipsychotic use - worsen symptoms
  • Angle-closure glaucoma - activate D1 receptors in eyes which Inc aqueous humour production & ICP
  • Nonspecific MAOI concomitant use - Hypertensive crisis

MONITOR/

  • Cardiac pts- Arrhythmias
  • Anti-HTN drug use - Orthostatic Hypotension
  • Active peptic ulcer - GI bleeding
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19
Q

Dopamine Receptor Agonist (class & names)

A
  1. Ergot Dopamine Agonists
    - Bromocriptine
  2. Non-ergot Dopamine Agonists
    - Pramipexole
    - Ropinirole
    - Rotigotine

Does NOT require enzymatic conversion - Do NOT depend on the functional capabilities of Nigrostriatal neurons

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20
Q

Bromocriptine

A
  • D2 agonist

- Rarely used now

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21
Q

Pramipexole & Ropinirole

A
  • Initial treatment of PD for younger pts.
  • Well tolerated
  • Less effective than Levodopa in treating motor symptoms; but less likely to cause motor fluctuation & dyskinesia
  • Older pts. are more vulnerable to cognitive AE
22
Q

Rotigotine

A
  • Transdermal formulation - Once-daily use
23
Q

GI Adverse effects of Dopamine Agonists

A
  • Anorexia
  • Nausea & vomiting
  • Constipation
  • Peptic ulcer bleeds
24
Q

CVS Adverse effects of Dopamine Agonists

A
  • Postural hypotension
  • Cardiac arrhythmias
  • Peripheral edema
  • Painless digital vasospasm (Ergot agonists)
25
Q

Motor & Mental Adverse effects of Dopamine Agonists

A
  • Abnormal movements
  • Confusion
  • Hallucinations & Delusions
  • Compulsive behaviors
26
Q

Other Adverse effects of Ergot Dopamine Agonists

A
  • Headache
  • Nasal congestion
  • Inc arousal
  • Pulmonary infiltrates
  • Pleural & retroperitoneal fibrosis
  • Erythromelalgia
27
Q

Other Adverse effects of Non-ergot Dopamine Agonists

A

Uncontrollable Somnolence

- Discontinue use

28
Q

Drug Interactions of Dopamine Agonists

A
  • Antipsychotic drugs antagonize Dopamine - Dec efficacy

- CNS depressants -Inc somnolence & confusion

29
Q

Contraindication of Dopamine agonists

A
  • Hx of psychotic illness
  • Recent MI
  • Active Pectic Ulcer
30
Q

Rescue therapy

A

APOMORPHINE (Non-ergot agonists)

  • Treatment of “off episodes” of akinesis in pts on dopaminergic therapy
  • Pretreatment w/ antiemetic agent TRIMETHOBENZAMIDE
31
Q

Why is Trimethobenzamide used before Apomorphine

A

Apomorphine is an Emetogenic agent so pretreatment with an antiemetic agent is recommended

32
Q

Adverse effects of Apomorphine

A
  • QT prolongation
  • Dyskinesia
  • Drowsiness
  • Sweating
  • Hypotension
33
Q

Inhibitors of Dopamine Metabolism (class & name)

A
  1. MAO Inhibitors
    - Selegiline
    - Rasagiline
  2. COMT Inhibitors
    - Tolcapone
    - Entacapone
34
Q

Selegiline MOA

A

Inhibits MAO-B –> Stops Dopamine breakdown in brain

  • Selective to MAO-B
  • Irreversible
35
Q

Clinical uses of Selegiline

A

Adjunct to Levodopa

- Allows Levodopa dose to be reduced & therefore enhances its effects

36
Q

Metabolism of Selegiline

A

Metabolized to

  • Methamphetamine
  • Amphetamine
37
Q

Adverse effects of Selegiline

A

Insomnia (due to presence of metabolites)

Should NOT be used late evenings

38
Q

Rasagiline

A

MAO-B Inhibitor

- Irreversible

39
Q

MAO-I Drug Interactions

A
  1. MAOI + Serotonergics –> Hypertensive crisis & Serotonin syndrome
  2. MAOI + Sympathomimetic amines –> Severe HTN
40
Q

MOA of COMT Inhibitors

A

NORMAL
- COMT breaks down Levodopa to 3-o-methyl dopa which competes with Levodopa for transport across the intestinal mucosa & BBB

COMT-I prevent the formation of 3-0 methyl dopa

41
Q

Amantadine

A
42
Q

Antimuscarinics (names)

A
  • Benztropine

- Trihexyphenidyl

43
Q

Contraindications of Amantadine

A

CAUTION w/:

  • Hx of seizures
  • Hx of Heart failure
44
Q

Adverse effects of Amantadine

A
  • Restlessness, agitation, confusion & hallucinations
  • Acute toxic psychosis (High- dose)
  • Headache, Heart failure, Orthostatic hypotension, Dry mouth, Urinary retention & GI disturbances
  • Peripheral edema
  • Livedo reticularis - rash that usually clears within a month of drug discontinuation
45
Q

Adverse effects of COMT Inhibitors

A
  • Fulminating Hepatic Necrosis (Tolcapone)
46
Q

Clinical uses of Antimuscarinics

A

ADJUVANT therapy

  • may improve tremor & rigidity
  • little effect on bradykinesia
47
Q

Adverse effects of Antimuscarinics

A
  • Mood changes
  • Xerostomia
  • Pupillary dilation
  • Confusion
  • Hallucinations
  • Urinary retention
48
Q

Contraindications of Antimuscarinics

A
  • Glaucoma
  • Prostatic hypertrophy
  • Pyloric stenosis
49
Q

How to control the Peripheral edema caused by Amantadine?

A

Diuretics

50
Q

Carbidopa

A

Dopa Decarboxylase Inhibitor

  • Does NOT cross the BBB
  • Given in combination w/ Levodopa

Pharmacology (16 decks)

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