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Pharm II Exam II > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What NT is replaced when treating Parkinsons?

A

Dopamine

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2
Q

Effect of too much DA in mesolimbic area

A

psychosis

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3
Q

L-DOPA mechanism

A
  • provides more precursor for DA
  • only 5% passes BBB
  • need to inc dose after 3-4 years
  • less effective as more neurons die off
  • ineffective in 1/3 of pts
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4
Q

SEs/toxicities of L-DOPA

A
  • Peripheral: nausea, arrhythmias, orthostatic HypoTN

- Central: psychotic sxs, dyskinesias, on-off phenomenon

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5
Q

On-off phenomenon

A
  • variable metabolism
  • on phase: PD sxs are controlled (may have some jerky movements)
  • off phase: PD sxs not controlled (dystonias, twisting movements, unusual posture)
  • reduced by L-AAD and COMT inhibitors
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6
Q

CIs for L-DOPA

A
  • psychosis, melanoma, narrow-angle glaucoma
  • vitamin B6 speeds up peripheral metabolism of L-DOPA (tell pts to avoid it)
  • MAOIs prevent metabolism of DA–> hypertensive crisis
  • D2 blockers antagonize effects of L-DOPA
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7
Q

Carbidopa mechanism

A
  • L-AAD inhibitor

- Inhibit peripheral L-DOPA metabolism by L-AAD –> increase delivery of L-DOPA to CNS

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8
Q

tolcapone/entacapone mechanism

A
  • COMT inhibitor

- Inhibit peripheral L-DOPA metabolism by COMT

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9
Q

Difference between tolcapone and entacapone

A
  • tolcapone passes BBB–> inhibits central and peripheral COMT
  • entacapone doesn’t pass BBB–> inhibits peripheral COMT only
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10
Q

cofactor for L-AAD

A
  • pyroxidine aka vit B6

- pts with Parkinson’s should avoid

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11
Q

what is NOT helped by L-AAD and COMT inhibitors?

A

CNS effects: dyskinesias, psychotomimesis (more DA is available centrally)

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12
Q

SEs of carbidopa, tolcapone, and entacapone

A
  • nausea, orthostatic hypoTN, vivid dreams, confusion, diarrhea
  • tolcapone only: liver toxicity
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13
Q

Selegiline/rasagiline mechanism

A
  • MAO-B inhibitor
  • blocks MAO-B metabolism of central DA
  • MAO-A still intact to handle catecholamines
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14
Q

SEs and CIs for MAO-B inhibitors

A
  • central effects of L-DOPA worsened
  • cannot give with nonselective MAO inhibitor (will cause NE build up–> hypertensive crisis)
  • selegiline metabolites: amphetamine and methamphetamine (sounds fun)
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15
Q

Ropinirole/pramipexole mechanism

A
  • D2 receptor agonist

- easily titratable

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16
Q

Therapeutic effects of ropinirole/pramipexole

A
  • can lower L-DOPA dose
  • less on-off phenom
  • 1st line for younger pts
  • given to pts who have build L-DOPA tolerance
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17
Q

SEs and toxicities of ropinirole/pramipexole

A
  • peripheral: hypoTN, anorexia, nausea, constipation, dyspepsia, reflux esophagitis, bleeding peptic ulcers
  • can be treated with dopamine antagonist that doesn’t cross BBB
  • central: dyskinesias, psychosis, fatigue, somnolence
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18
Q

ropinirole/pramipexole CIs

A
  • psychosis
  • recent MI, peripheral vascular dz (at risk for orthostatic hypoTN)
  • peptic ulcers
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19
Q

Amantidine mechanism

A

-enhances DA release from remaining terminals and inhibits DA reuptake

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20
Q

Amantidine therapeutic effects

A
  • good for initial therapy
  • benefits short-lived
  • reduces bradykinesia, rigidity and tremor (early stages)
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21
Q

Amantidine SEs and toxicities

A
  • restlessness, depression, irritability, insomnia, agitation, excitement, hallucinations, confusion (all mild)
  • OD: acute toxic psychosis
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22
Q

Benztropine mechanism

A

-Muscarinic antagonist/ anticholinergic

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23
Q

therapeutic use of anticholinergics/benztropine

A
  • good in combo with L-DOPA
  • very mild PD (tremor only)
  • doesn’t work as well for bradykinesia
24
Q

SEs of anticholinergics/benztropine

A

central: drowsiness, confusion, inattention, restlessness
peripheral: dry mouth, blurred vision, mydriasis (dilated pupils), urinary retention, n/v

25
Q

CIs of anticholinergics/benztropine

A
  • BPH
  • obstructive GI dz
  • narrow angle glaucoma
26
Q

Psychosis def

A

inability to think coherently or comprehend reality (ex- schizophrenia)

27
Q

Positive schizophrenic sxs

A

hallucinations, delusions, disorganization, formal thought disorder

28
Q

Negative schizophrenic sxs

A

alogia, affective blunting, avolution, asociality, anhedonia, impaired attention

29
Q

DA hypothesis of schizophrenia

A

-untreated schizophrenics have increased D2 receptors in brains
-Antipsychotics block D2 receptors
-Amphetamine, L-DOPA OD–> psychosis
(however, evidence that serotonin and glutamate both play a role)

30
Q

Dopaminergic tracts in the schizophrenic brain

A
  • Mesocorticolimbic projection
  • Nigrostriatal projection
  • Tuberoinfundibular system
  • Medullary-periventricular neurons
  • Dopamine receptors in chemotrigger zone (CTZ)
31
Q

Mesocorticolimbic projection

A
  • Frontal cortex (cortical limb): too little DA–> negative and cognitive sxs
  • Nucleus accumbens (limbic limb): too much DA–> positive sxs
  • arises in the ventral tegmental area (VTA)
32
Q

Nigrostriatal projection

A
  • Substantia nigra to striatum
  • this is what dies in PD
  • foci of extrapyramidal sxs from antipsychotic meds
33
Q

Tuberoinfundibular system

A
  • arcuate nucleus of hypothalamus, terminals in the pituitary
  • D2 block here causes endocrine SEs (elevated prolactin)
34
Q

Medullary-periventricular neurons

A
  • motor nucleus of the vagus
  • controls eating behavior
  • D2 block here causes weight gain
35
Q

Dopamine receptors in chemotrigger zone (CTZ)

A

D2 block here has antiemetic properties

36
Q

Chlorpromazine

A
  • a phenothiazine
  • 1st gen antipsychotic
  • acute txt of psychotic exisode
  • many autonomic effects! slight EPS
  • sedation, alpha1 block (huge risk in elderly!), seizures, sunburns!
37
Q

Haloperidol

A
  • a butyrophenone
  • 1st gen antipsychotic
  • severe EPS
  • lower sedation, less alpha block than phenothiazines/chlorpromazine
  • hyperprolactinemia
  • generic, cheap, IV or injection
38
Q

Atypical or 2nd gen antipsychotics

A
  • clozapine
  • risperidone
  • olanzapine
  • ziprasidone
  • aripiprazole
  • lower EPS than typicals
  • increased ratio of serotonin:D2 receptor blockade
39
Q

Clozapine

A
  • atypical antipsychotic
  • selectively causes DPI only in the mesolimbic pathway–> no EPS!
  • better against negative sxs
  • SEs: risk of agranulocytosis! (2% of pts), wt gain, DM, sedation, anticholinergic effects (esp confusion), seizures
  • need to check WBC ct weekly
40
Q

DPI

A
  • depolarization inactivation

- goal when using antipsychotics

41
Q

EPS

A

extrapyramidal sxs

42
Q

Resperidone

A
  • dose-dependent atypical antipsychotic
  • low risk of EPS as long as dose is low
  • no risk of agranulocytosis
  • alpha1 block, weight gain, elevated prl
43
Q

Olanzapine

A
  • atypical antipsychotic
  • no risk of agranulocytosis
  • serious weight gain, DM, small increase in serum prolactin, anticholonergic effects (esp confusion), sedation, hypoTN,
  • does NOT increase prolactin
  • good for depressive sxs
44
Q

Ziprasidone

A
  • atypical antipsychotic

- temporarily withdrawn from market d/t wide QT intervals, later reintroduced under another name

45
Q

Aripiprazole

A
  • trade name: abilify
  • atypical antipsychotic
  • different mechanism: partial agonist at D2 and 5HT1A receptors, mild antagonist at 5-HT2
  • no DM risk, less effect on prl levels
  • IM available
  • good for depressive sxs
46
Q

SEs of antipsychotics

A
  • CNS early occurring: dystonia, akasthisia (motor restlessness), parkinsonism, neuroleptic malignant syndrome (NMS), sedation, lower seizure threshold
  • CNS late occurring: perioral syndrome (aka Rabbit syndrome), tardive dyskinesia!
  • seizures
  • ANS: orthostatic hypoTN (alpha1 block), reduced sex drive, inability to ejaculate (alpha1 block), anticholinergic effects (dry mouth, blurred vision, constipation, urine retention)
  • Endocrine: increased prolactin, galactorrhea, amenorrhea (exception: olanzepine)
  • Heme: agranulocytosis (check WBCs weekly)
  • Metabolic: wt gain, DM, hyperlipidemia (esp atypicals)
  • Phototoxicity: sunburns (esp phenothiazines/chlorpromazine)
  • Cardiac: prolonged QT interval (ziprasidone)
47
Q

neuroleptic malignant syndrome (NMS)

A
  • catatonia, stupor, fever, unstable BP, myoglobinemia
  • STOP APS IMMEDIATELY
  • may be fatal (10%)
  • occurs w/in weeks, can persist even after stopping APS meds
  • prob due to D2 block in hypothalamus
48
Q

tardive dyskinesia

A
  • late occurring abnormal movements: oral-facial dyskinesias, widespread chorioathetosis, dystonia
  • can occur after mos-yrs of txt
  • 20% of pts
  • due to D2 receptor hypersensitivity
  • prevention is CRUCIAL
  • no txt
49
Q

cause of EPS

A
  • D2 blockers disrupt cholinergic and dopaminergic input balance at the GABA receptor/receiving neuron –> cholinergic signals intensify –> EPS (Parkinson-like sxs/too much inhibitory GABA signalling)
  • treat EPS with anticholinergics
  • prolonged D2 blocks can cause D2 receptor supersensitivity–> tardive dyskinesia (abnl mvmts/too little inhibitory GABA signalling)
  • DO NOT treat with anticholinergic! will make it even worse
50
Q

ADME of APS

A

A: erratic, dec’d by foods, antacids, anticholinergics
D: concentrates in fatty tisses (good for brain), highly protein bound
M: hepatic microsomal system, conjugated by glucuronic acid

51
Q

APS DDIs

A
  • potentiation with CNS depressants, antihypertensives
  • can interfere with dig
  • barbituates enhance metabolism
52
Q

typical vs atypical APS

A
  • atypicals have less EPS
  • atypicals better for negative sxs (exceptionL clozapine)
  • atypicals make you fat
53
Q

APS needed, but pt already has high DM risk?

A

Don’t use clozaine or olanzapine

54
Q

APS for psychosis + depressive sxs?

A

aripiprazole, olanzapine

55
Q

APS with cardiotoxicity risk?

A

phenothiazines (chlorpromazine)

56
Q

alpha block

A
  • orthostatic hypoTN

- especially bad in elderly!

Pharm II Exam II (1 decks)

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