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Pharm Exam 3 > Antiparkinsonian Drugs > Flashcards

Antiparkinsonian Drugs Flashcards

1
Q

what is the pathology of neurodegenerative disorders?

A

aggregation of misfolded proteins

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2
Q

What happens to the CNS in Parkinsons disease (PD) and huntingtons disease (HD)?

A

loss of dopaminergic neurons in basal ganglia leads to altered movement control

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3
Q

What happens to the CNS in alzheimers disease (AL)?

A

loss of hippocampal and cortical neurons results in impaired memory formation and cognitive deficits

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4
Q

What happens to the CNS in amyotrophic lateral sclerosis (ALS)?

A

degeneration of cortical and spinal motor neurons results in muscular weakness

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5
Q

parkinsons aggregates are called?

A

intracytoplasmic aggregates

specifically: lewis bodies - alpha synuclein

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6
Q

alzheimers aggregates are called?

A

Beta-amyloid plaques and intracytoplasmic neurofibrillary tangles

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7
Q

huntingtons aggregates are called?

A

intranuclear inlusions - huningtin protein

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8
Q

prion aggregates are called?

A

extracellular amyloid plaques

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9
Q

amyotrophic lateral sclerosis (ALS) aggregates are called?

A

Lou garrigs disease(sp?) intracytoplasmic aggregates

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10
Q

Areas of brain affected by parkinson’s?

A 
basal ganglia
AND!
brainstem
hippocampus
cerebral cortex

= many non-motor effects too (memory impairment, affective disorders aka anxiety and depression, sleep disorders, personality changes, sensory complaints or pain, autonomic dysfucntions aka sex, sweat, choking, BP issues… etc)

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11
Q

4 cardinal signs of parkinsons:

A

1) bradykinesia - slowness of execution of movement
2) muscle rigidity
3) resting tremor - goes away with voluntary movement
4) postural instability - cant remain in upright posture

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12
Q

Specific area of basal ganglia that is affected in parkinsons?

What does this look like histologically?

A

**degeneration/loss of dopa neurons in the Substantia nigra that project to Stiratum (putamen and caudate nucleus)

Substantia nigra LOOSES ITS PIGMENT - not dark colored as usually is

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13
Q

Loss of dopa input into striatum results/is accompanied with what?

A
  • less/no dopa input = inc Ach activity pathways in basal ganglia
  • more Ach in basal ganglia dec ability of basal ganglia to modify motor cortex mediated muscle contraction and activation (slower movement, tight muscles, resting tremor, joint rigidity)
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14
Q

How/factors to development of Parkinsons?

A
  • Not exactly knows
    1) genetic factors: gene mutations = overproduction and abnormal accumulation of proteins
  • -> alpha synuclein accumulation forms LEWY BODIES = increased production of free radicals = neuronal function impaired = neuron death

2) Environmental toxins - toxin such as MPTP

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15
Q

Parkinson treatment strategy - general idea?

A

no cure of PD but we can greatly improve motor function and alleviate symptoms

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16
Q

Options for PA Tx:

A

1) DA replacement straight up (DA cant cross BBB though)
2) DA receptor agonists
3) L-DOPA degredation inh
4) Increase in DA release
5) anti-ACH agents

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17
Q

Dopamine replacement drug name?

A

Levodopa -L-DOPA

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18
Q

** Most common drug used to treat PD?

A

L-DOPA

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19
Q

Why not use DOPA instead of Levodopa?

A

DOPA cant cross BBB.

L-DOPA uses AA transporter and is converted into DOPA and NE in the brain by dopa-carboxylase

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20
Q

**What does L-DOPA do well?

A

improves bradykinesia and rigidity rather well = better overall function

  • 1/3 dont respond to drug
  • 1/3 cant tolerate the drug
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21
Q

**Downside to using L-DOPA?

A

benefits to Tx diminish after 3-4 years of therapy = less responsive to the drug

22
Q

Levodopa is usually given with what other drug? WHY?

A
  • levodopa + Carbidopa
  • L-DOPA is lost to peripheral metabolsim by COMT and MAO
  • -> Carbidopa is an inhibitor of dopa-decarboxylase in the periphery ==> inh degredation of L-DOPA
23
Q

MOA for Carbidopa? What is the MOA

A

dopa-decarboxylase

blocks the enzyme that degrades L-DOPA in the periphery so that L-DOPA is able to make it to the brain

24
Q

*L-DOPA adverse effects?

A
  • **1) dyskinesia - more with longer use - involuntary movements/tics
  • *a) Time and dose dependent
  • *b) various DA mediate effects (involuntary movements like tics and tremors)
  • choreiform movements
  • athetosis
  • ballismus
  • dystonia
  • **2) Response Fluctuations
  • *a) Wearing off reactions and end of dose failure
  • *b) on-off phenomenon - abrupt loss of effect
    c) progressive decay
  • *d) Drug holiday - stop taking drug for some time to improve response fluctuation problems
  • *3) GI disturabance - anorexia, N and V
  • *4) cardiovascular
    a) postural hypotension
    b) Tachycardia and other cardiac dysrhythmias
  • *5) Beh disturbances
    a) depression/anxiety
    b) insomnia (sudden sleepiness)
    c) Agitation and confusion
    d) Delusions/hallucinations/nightmares
    e) Psychotic reactions -impulse control/psychosis
    f) hypersexuality
25
Q

What is a drug holiday?

A

Doctors tell PD patients to stop taking their meds to improve response fluctuations

26
Q

***Levodopa - drug interactions:

A
  • ***1) pyridoxine (B6)
    2) MAO-A inh (antidepressants)= hypertension
    3) antipsychotics - DA receptor blockade
    4) protein rich meals - competition for GI and BBB absorption (AA transport)
    5) anticholinergics
27
Q

***Most common Levodopa drug interaction:

A

pyridoxine B6

28
Q

Dopamine Receptor agonists: list the drugs

Where agonized?

A
  • *-pramipexole
  • *-ropinirole
  • apomotrphine - subcutaneous!

agonist to receptors in the striatum

29
Q

Treatment drug for levodopa induced dyskinesia?

A

apomorphine - subcutaneous route

30
Q

**Benefit over using DA receptor agonist over L-DOPA?

A

lower incidence of the response fluctuations and dyskinesias over long term L-DOPA use

31
Q

*Mild/initial form of PD - which drug?

A

give DA receptor agonists - pramipexole or ropinirole

32
Q

**DA receptor agonist MOA?

A

-agonist at D2 receptors in striatum

33
Q

**DA receptor agonist - side effects?

A
  • GI - most common: anorexia, nausea, vomiting, constipation
  • cardiovascular - postural Hypotension
  • dyskinesias (not as bad as LDOPA)
  • beh/mental disturbance
  • headache
  • potential problems with impulse control disorders - gambling, sexual activity, shopping
34
Q

MAO-B inhibitors - list the drugs?

A

rasagiline

selegiline

35
Q

MAO-B inh-MOA

A

rasagiline
selegiline

inh MAO-B selectively at low doses = dec breakdown of

At high doses inh MAO-A

36
Q

**How to use MAO-B inhibitors?

A

Adjunct to L-DOPA especially in patients with declining or fluctuating response to L-DOPA

37
Q

**MAO-B inhibitor - adverse effects?

A
  • GI upset-DOES NOT display the “wine and cheese” interaction
  • serotonin syndrome - if given with SSRI (antidepressants)
38
Q

Catechol-O-methyltransferase (COMT) inhibitors - list the drugs:

A
  • entacapone

- tolcapone

39
Q

COMT drug MOA?

A

inhibit COMT = decreased peripheral metabolism of L-DOPA

40
Q

When to use COMT inh?

A

adjunct with L-DOPA when patients have response fluctuations

41
Q

**Why is entacapone the preferred COMT inh?

A

no hepatotoxicity

42
Q

Adverse effects for COMT inh?

Specific adverse effect for Tolcapone drug?

A

-inc l-dopa toxicity, nausea, dyskinesias, confusion

Tolcapone=acute hepatic failure (hepatotoxicity)

43
Q

Increased DA release Drugs?

A

amantadine

44
Q

What was amantadine originally used for?

A

used as antiviral but antiparkinsonian properties discovered on accident

45
Q

Compared to L-DOPA how good is amantadine?

A

Less efficacious bc short duration of action and short lived therapeutic effectiveness (some to 12 months)

46
Q

Main adverse effect with amatadine?

A
  • inc DA release drug

- livdeo reticularis = blotchy reddened pattern, usually on the legs, clears with in 1 month after stoppage

47
Q

Anticholinergic agents for PD tx - list drugs?

A
  • benzotropine

- trihexyphenidyl

48
Q

MOA for anticholinergic agents for PD?

A

antagonist at M receptors in basal ganglia

49
Q

anticholinergic agents for PD - positive effects?

A

reduces tremor and rigidity but little effect on bradykinesia

50
Q

Anticholinergic agent for PD - adverse effects:

A

antimuscarinic effects:

  • urinary retention
  • dry mouth
  • mydriasis and blurred vision
  • constipation
  • sedation
  • confusion
  • toxic psychosis

Pharm Exam 3 (11 decks)

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