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RESIDENCY > PsychoPharm > Flashcards

PsychoPharm Flashcards

1
Q

What is volume transmission;

A
  • No synaptic connection needed to pass message bc the NT released from presynaptic neuron diffuses out toward other synpases in its diffusion radius.
  • Can also be used in autoregulation.
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2
Q

Monoamines:

-includes which neurotransmitters?

A

catecholamines (END), histamine, tryptamines (serotonin, melatonin).

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3
Q

What are the 3 main reuptake transporters?

-other one that we have a drug for?

A

SERT, NET, DAT

-GABA xporter = GAT1

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4
Q

Which substances do NOT have reuptake inhibitors?

-name 2

A

histamine, neuropeptides

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5
Q

How do inverse agonists decrease baseline enzyme activity?

A

turn off constitutive activity of enzyme.

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6
Q

Olanzapine:

  • two most common side effects, in order:
  • how common?
A
  1. Weight Gain - problematic

2. Sedation - common

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7
Q

Olanzapine

-usual dose:

A

10-20 mg/day

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8
Q

Olanzapine:

  • Is OD lethal?
  • OD side effects:
A
  • rarely lethal in monotherapy

- sedation and slurred speech

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9
Q

Citalopram

-brand name?

A

celexa

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10
Q

Citalopram

-unique s/e is sedation, why?

A

mild anti-histamine properties, may contribute to sedation or fatigue in some patients.

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11
Q

who is more vulnerable to possible activating effects of SSRIs?

A

Undiagnosed bipolar or psychotic disorders

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12
Q

Citalopram

-usual dosage range?

A

20-40mg/day

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13
Q

Escitalopram

-brand name?

A

Lexapro

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14
Q

Mirtazapine

-mechanism of action:

A 
Boost neurotransmitters serotonin and
norepinephrine/noradrenaline
• Blocks alpha 2 adrenergic presynaptic
receptor, thereby increasing norepinephrine
neurotransmission
• Blocks alpha 2 adrenergic presynaptic
receptor on serotonin neurons
(heteroreceptors), thereby increasing
serotonin neurotransmission
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15
Q

Mirtazapine

-how does it cause sedation?

A

anti-histamine

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16
Q

Mirtazapine

  • dosage?
  • best dosage for sedation?
A

15-45mg qHS

-break the 15 in half and give 7.5 mg for best sedative effects.

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17
Q

“neurolepsis”

-classically what does it mean?

A

an extreme form of slowness or absence of motor movements as well as behavioral indifference in experimental animals.
-in humans: psychomotor slowing, emotional quieting, and affective indifference.

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18
Q

Shared pharmacological property of conventional antipsychotics:

A

D2 antagonism (in mesolimbic pathway = quells positive symptoms of psychosis).

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19
Q

How much D2 blocking do you need in mesolimbic pathway for anti-psychotic effect?

A

80% receptor blockage.

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20
Q

EPS: what % of D2 receptor blockade do you need in dorsal striatum to get EPS?

A

80%

21
Q

What % of D2 receptor blockade do you need in pituitary to get hyper-PRL?

A

80%

22
Q

Conventional antipsychotics

-amount the drug blocks D2 receptors in different dopamine pathways?

A

same number blocked in all brain areas

  • this is why there are so many side effects.
  • “high cost of doing business.”
23
Q

Consequence of blocking D2 receptors in nucleus accumbens? (mesolimbic pathway)

A

This is reward center - so blocking D2 receptors here can quell positive symptoms but also cause anhedonia, apathetic, amotivational - particularly with socialization. A state very similar to negative Sxs of schizophrenia.

  • thus using conventional antipsychotics can treat positive Sxs but worsen negative Sxs of schizophrenia.
  • potential reason for drug abuse in schizois - need high the drug to get anything out of that reward system thats being blocked.
24
Q

high or low density of D2 receptors in cortex?

A

low D2 density in cortex

25
Q

Schizos

-too much or too little dopamine in mesocortical pathway?

A

already too low
-which is why blocking D2 receptors here (even tho you have low D2 receptor density in cortex) can worsen negative cognitive Sxs of schizo.

26
Q

1 year conventional anti-psychotic use

-% chance of TD?

A

5-25%

-25% in elderly.

27
Q

How to predict who will be more likely to get TD?

A

Patients who develop EPS early in treatment may be twice as likely to develop TD if treatment with a conventional antipsychotic is continued chronically.

28
Q

D2 blockers and decreased bone density

-whats the relation

A

low dopamine = high PRL

  • high PRL inhibits GNrH
  • low GNrh = low estrogen
29
Q

Conventional anti-psychotics

-what are the main 4 receptors they block?

A

D2, M1, alpha-1, H1

30
Q

Relationship between dopamine and ACh in nigrostriatal pathway?

A

Dopamine normally inhibits acetylcholine release from postsynaptic nigrostriatal cholinergic neurons, thus suppressing acetylcholine activity there.

31
Q

Atypical anti-psychotics

-which major receptors does it block?

A

5HT2a and D2

32
Q

Clinical difference btwn SGA and conventional antipsychotics?

A

equal positive symptom antipsychotic actions, but low extrapyramidal symptoms and less hyperprolactinemia compared to conventional antipsychotics.

33
Q

What receptors are main action of SGA?

A

D2 antagonism with serotonin 5HT2A antagonism

34
Q

Serotonin

-which MAO degrades it?

A

MAO-A

35
Q

5HT2a receptors:

-pre or post synaptic?

A

-post synaptic

-

36
Q

5HT2a receptors:

-where are they excitatory?

A
  • corticol pyramidal neurons - and therefore enhance downstream glutamate release.
  • glutamate regulates downstream dopamine release so 5HT2a has a downstream effect on dopamine release.
37
Q

5HT2a receptors:

-relationship with dopamine release?

A
  • they are excitatory on corticol pyramidal neurons - and therefore enhance downstream glutamate release.
  • glutamate regulates downstream dopamine release so 5HT2a has a downstream effect on dopamine release.
38
Q

5HT2A receptors are brakes on dopamine release in the

striatum

A

Stimulating 5HT2a receptor (w/serotonin) on corticol pyramidal cells (cortex) hypothetically blocks downstream dopamine release in striatum.
-5HT2a stimulation in cortex = less dopamine released in striatum.

39
Q

5HT2a relationship w/dopamine release in striatum

-how does it lead to less EPS?

A
  • 5HT2a stimulation in cortex = less dopamine released in striatum.
  • so blocking 5HT2a means more release of dopamine in striatum which means less EPS!
40
Q

Lithium

- side effects

A
  • GI symptoms (n/v, dyspepsia, diarrhea)
  • weight gain, hair loss, acne, tremor, decreased cognition, incoordination.
  • thyroid, kidney
41
Q

Anti-convulsants w/proven efficacy in Bipolar Disorder:

A

Valproic acid
carbamazepine
lamotrigine

42
Q

proposed mechanism of valproate?

A
  1. diminish voltage gated sodium channel flow leading to less glutamate release (excitatory).
  2. enhances GABA relase
43
Q

valproate:

which is more proven, treating acute mania or prophylaxis of recurrence?

A

proven to treat acute mania more so than maintenance

44
Q

valproate

most common side effects?

A

hair loss, weight gain, sedation

- w/long term use, liver/pancreatic effects, fetal abnormalities (neural tube defects), amenorrhea, polycystic ovaries.

45
Q

Best anti-convulsant for bipolar depression?

A

lamotrigine

46
Q

Carbamazepine

  • 2 biggest side effects:
  • okay in pregnancy?
A

bone marrow suppression, sedation, cyto p450 induction

- can cause neural tube defects

47
Q

Is lamotrigine approved for bipolar mania?

A

no, takes too long to titrate up

48
Q

oxcarbazepine (trileptal)

  • metabolite of tegretal?
  • advantages over tegretal?
  • disadvantages?
A

not a metabolite, but same proposed mechanism

  • less bone marrow suppression, less sedation, and less P450 induction
  • not FDA approved as mood stabilizer, but people use it anyway.
49
Q

combo of lamotrigine and valproate

-what to watch out for?

A

need to reduce lamotrigine dose by half sometimes

RESIDENCY (5 decks)

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