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Kaplan: CNS Pharmacology > Drugs Used in Parkinson Disease and Psychosis > Flashcards

Drugs Used in Parkinson Disease and Psychosis Flashcards

1
Q

Describe where the Nigrostriatal tract starts and ends. Also described what is released from it that may be related to management of Parkinsons.

A

Cell bodies in substantial nigra project to striatum and release DA which is inhibitory on GABA ergic neurons

In Parkinson disease loss of DA leads to excessive ACH activity

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2
Q

Describe projection of mesolimbic mesocortical tract.

A

cell bodies in midbrain project to cerebrocortical and limbic structures

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3
Q

Compare DA receptor antagonists to DA agonists as it relates to Parkinsons.

A

DA receptor antagonists > pseudo-Parkinsonism (reversible)
DA agonists may cause dyskinesia

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4
Q

Mesolimbic regulation is associated with what conditions?

A

DA increase in these pathways is associated with psychotic disorders and addiction

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5
Q

DA antagonists at mesolimbic pathway may lead to what condition?

A

dec. in cognitive function

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6
Q

Describe the Tuberoinfundibular pathway.

A

cell bodies in hypothalamus project to anterior pituitary and release DA > dec. prolactin

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7
Q

Compare DA agonists and antagonists and their effects on prolactin on the body as well as implications? (DA agonist use and DA antagonist effects)

A

DA agonists are used in hyperprolactinemic states

DA antagonists may cause endocrine dysfunction (gynecomastia and amenorrhea/galactorrhea

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8
Q

What are the effects on GnRH, FSH, and LH when there is increased prolactin?

A

dec. GnRH > dec FSH and LH > amenorrhea

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9
Q

How does activation of DA receptors trigger emesis?

A

they are found in CTZ (chemoreceptor trigger zone) or AP area postrema when it is triggered vomiting may occur

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10
Q

D2 receptors are coupled to what G protein?

A

Gi

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11
Q

Which D2 receptor is for nigrostriatal pathway?

A

D2A

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12
Q

Which D2 receptor is for mesolimbic pathway

A

D2C

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13
Q

What is the pharmacologic strategy for treating Parkinsons

A

restore normal dopamine and decrease ACh activity

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14
Q

Levodopa is a prodrug converted to dopamine by what enzyme?

A

AAAD aromatic amino acid decarboxylse or dopa decarboxylase

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15
Q

What drug is levodopa given that increases activity in CNS?

A

carbidopa

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16
Q

What are the S/E of Levodopa

A

dyskinesias, “on-off” effects, psychosis, hypotension, vomiting

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17
Q

What enzyme converts L-dopa to 3-O-methyldopa a partial agonist at dopamine receptors?

A

COMT catechol- O- methyltransferase

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18
Q

What drugs inhibit COMT to enhance levodopa uptake and efficacy?

A

tolcapone and entacapone

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19
Q

Tolcapone is toxic to what organ in the body?

A

hepatotoxic (liver)

20
Q

Selegeline indication?

A

initial treatment and adjunct to levodopa

21
Q

S/E of Selegiline?

A

dyskinesias, psychosis, insomnia

22
Q

Selegiline is metabolized to what?

A

amphetamine

23
Q

What are some dopamine receptor agonists used for hyperprolactinemia and acromegaly?

A

bromocriptine

24
Q

How is Amantadine used in the treatment of Parkinsons? MOA? What type of drug is it?

A

blocks muscarinic receptors and inc. dopamine release

antiviral

25
Q

What is the dopamine hypotheses?

A

states symptoms arise because of excessive dopaminergic activity in the mesolimbic system

26
Q

MOA to take in treating schizophrenia?

A

blockade of DA receptors
blockade of 5HT2 receptors

27
Q

What are uses for antipsychotic drugs?

A

Treatment of:

schizophrenia and schizoaffective states
BPD
Tourette syndrome and Huntington disease
Drug or radiation emesis

28
Q

S/E from antipsychotic drugs?

A

dyskinesias. *extrapyraidal symptoms” EPS

  • dysphoria
  • endocrine dysfunction
    increased prolactin
    NMS (neuroleptic malignant syndrome)
    Temperature reg problems
    Eating disorders (weight gain
  • tachycardia and decreased seizure threshold from (muscarinic blockade)
  • hypotension from alpha blockade
29
Q

Acute EPS and management?

A

psedoparkinsonism, dystonia, akathisia (management: antimuscarinic drugs)

30
Q

What is Chronic EPS and management?

A

dyskinesia (management: discontinuation switch to atypical antipsychotics

31
Q

How would you treat NMS?

A

Dantrolene and bromocriptine

32
Q

Bromocriptine MOA?

A

D2 agonist

33
Q

What are 2 D2 agonist that are ergot alkaloid derivatives that can be used for initial treatment of Parkinsons?

A

Pramipexole and Ropinrole

34
Q

Suffix to remember the typical antispsychotics

A

“zines”
basically haloperidol and the zines

35
Q

Name some typical antipsychoitcs

A

chlorpromazine
thioridazine
fluphenazine
haloperidol

36
Q

What is the suffix association for atypical antipsychotics?

A

“idones”
“ apines”

37
Q

Important S/E to remember for thioridazine?

A

cardiotoxicity (torsades “quinidine like”)
retinal deposits

38
Q

Name the atypical antipsychotics.

A

clozapine, olanzapine, quetiapine, risperidone, ziprasidone, aripiprazole

39
Q

Which antipsychotic is most commonly linked to NMS?

A

haloperidol

40
Q

Clozapine MOA?

A

blocks D2c and 5HT2 receptors

41
Q

MOA olanzapine.

A

blocks 5HT2 receptors and DA receptors

42
Q

MOA of risperidone.

A

blocks 5HT2 receptors and D2 antagonist

43
Q

MOA Aripiprazole

A

Partial agonist of D2 receptor and blocks 5HT2 receptor

44
Q

S/E clozapine

A

agranulocytosis,
weight gain
increased salivation (wet pillow syndrome)
seizures

45
Q

Olanzapine benefit in treating schizo?

A

improves negative symptoms

46
Q

Risperidone benefit in treating schizophrenia?

A

improve negative symptoms

47
Q

S/E of use of risperidone?

A

increases prolactin

Kaplan: CNS Pharmacology (8 decks)

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