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Parkinsons and antipsychotics Flashcards

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1
Q

what is the goal of parkinsons treatment?

A

increase DA and decrease ACh

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2
Q

levadopa mechanism and use

A

central aspect of the treatment. prodrug converted to dopamine by aminoacid decarboxylase. usually administered with carbidopa.

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3
Q

SE of levadopa

A

dyskinesias, on-off effects, psychosis, hypotension, vomit

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4
Q

tolcapone and entacapone

A

inhibit COMT and enhance levodopa uptake.

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5
Q

SE of tolcapone and entacapone

A

hepatotoxic

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6
Q

selegiline mechanism and use

A

MAOb selective inhibitor initial treatment and adjunctive to levodopa.

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7
Q

what is a positive about selegiline

A

there is no tyramine interaction

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8
Q

SE of selegiline

A

dyskinesias, psychosis, insomnia

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9
Q

why does selegiline cause insomnia

A

because it is metabolized into an amphetamine

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10
Q

bromocriptine mechanism and use

A

dopamine receptor agonist used to treat hyperprolactinemia and acromegaly.

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11
Q

SE of bromocriptine

A

dyskinesia and psychosis

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12
Q

benztropine/trihexyphebnidyl/diphenhydramine mechanism

A

decrease the ACh function, they are antimuscarinic.

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13
Q

what are benztropine/trihexyphebnidyl/diphenhydramine good at? and bad at?

A

they decrease tremor and rigidity. but have little effect on bradykinesia.

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14
Q

SE benztropine/trihexyphebnidyl/diphenhydramine

A

atropine like

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15
Q

amantidine mechanism and use

A

antiviral that blocks muscarinic receptors and increases dopamine release.

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16
Q

SE of amantidine

A

atropine like and livedo reticularis (know this most of all)

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17
Q

what are the side effects of antipsychotic drug

A

dyskinesias or extrapyramidal symptoms. acute EPS, TD, dysphoria, endocrine dysfunction (temp regulation issues can cause neuroleptic malignant syndrome), prolactinemia and eating behaviors (weight gain)

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18
Q

what are acute EPS

A

pseudoparkinsonism, dystonia, akathisia (turns into TD)

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19
Q

how do we manage EPS

A

with antimuscarinics such as benztropine or diphenhydramine

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20
Q

chronic EPS does what

A

is tardive dyskinesia. often irreversible. due to the upregulation of the receptors from the blockade

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21
Q

what do we use to the neuroleptic malignant syndrome

A

dantrolene and bromocriptine

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22
Q

chorpromazine

A

typical antipsychotic, m block and alpha block.

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23
Q

SE of chorpromazine

A

EPS, sedation, corneal deposits

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24
Q

thioridizine

A

typical AS, strongest m block and alpha block. this gives it the unique ability to treat its own EPS symptoms giving it less EPS.

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25
SE thioridizine
less EPS, sedation, torsades, retinal deposits, convulsions,
26
fluphenazine
typical AS, little M block and alpha block.
27
SE of fluphenazine
lots of EPS and little sedation
28
haliperidol
typical AS, little M block and alpha block.
29
SE of Haliperidol
lots of EPS, little sedation. likely TD and malignant hypertermia
30
clozapine
atypical with M block and alpha block. blocks D2c and 5HT2 receptors. there is NO reported TD with this drug
31
SE of clozapine
EPS unlikely, sedation is less. increased salivation (serotonin), seizures and weight gain. agranulocytosis need weekly blood tests.
32
what are the three most associated symptoms with antimuscarinics
convulsions, coma, cardiotoxic
33
olanzapine
less m block and alpha block. blocks 5HT2 receptors and improves negative symptoms.
34
SE of olanzapine
less EPS. sedation.
35
aripiprazole
partial agonist of the D2 receptor, blocks 5HT2 receptors. still blocks m and alpha
36
SE of aripiprazole
EPS more likely but not terrible. sedation, but not certain.
37
what is the goal of drugs to treat depression
increase NE and serotonin
38
phenelzine and tranylcypromine
inhibition of MAOa and MAOb. used for atypical depression.
39
what must you watch out for when treating with MAOai
no cheese, etc.
40
interactions for phenelzine and tranylcypromine
increase in NE hypertensive crises increase in BP arrhythmia, excitation and hyperthermia. (drugs to watch for are releasers (tyramine, alpha-agonist, TCA, levodopa)) Serotonin symptoms-sweating, rigidity, myoclonus, hyperthermia, ANS instability, seizures (watch out for SSRIs, TCA, meperidine).
41
amitriptyline/imipramine/clomipramine
these are tricyclic antidepressants. nonspecific blockade of 5HT and NE uptake. use in major depression, panic or phobic disorder, OCDs, neuropathic pain.
42
SE of amitriptyline/imipramine/clomipramine
muscarinic and alpha blockade. (toxicity 3 C's). torsades. QT prolongation
43
what is a specific amitriptyline therapy
neuropathic pain. (same as carbamazepine)
44
what is a specific treatment for imipramine
enuresis
45
what is a specific therapy for clomipramine
OCD
46
interactions for amitriptyline/imipramine/clomipramine
hypertensive crises with MAOi, serotonin syndrome with SSRI, MAOi, meperidine
47
name some SSRIs
fluoxetine, parozetine, sertaline, citalopram, fluvoxamine
48
mechanism of the SSRIs
blockade of the 5HT reuptake.
49
use of the SSRIs
major depression, OCD, bulimia, anxiety disorders, premenstrual syndrome. for anxiety must give with benzo
50
SE for the SSRIs
anxiety, agitation, bruxism, sexual dysfunction (anorgasmia), weight loss.
51
what is a toxicity for the SSRIs
serotonin syndrome
52
what are the drug interactions for the SSRIs
MAOi (serotonin syndrome), meperidine and TCAs.
53
trazadone
sedative associated with cardiac arrhythmias, priapism.
54
venlafaxine
nonselective reuptake blocker devoid of ANS SE.
55
bupropion
dopamine reuptake inhibitor used in smoking sensation.
56
mirtazapine
alpha 2 antagonist. weight gain -used in anorexia.
57
varenicline
partial agonist of the nicotinic receptors. can cause depression.
58
lithium
DOC for bipolar disorder. prevents recycling of PIP2 and drives down cAMP.
59
SE of lithium
narrow therapeutic range, tremor, flu-like symptoms, bad seizures, hypothyroid/goiter, nephrogenic DI (drives down ADH).
60
does lithium do anything to the developing fetus>
yes it is a teratogen. it causes the ebstein anomaly or tricuspid valve malformation
61
risperidone
atypical AS. blocks 5HT2 receptors. improves negative symptoms

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