PsychoPharm Flashcards

(49 cards)

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?

21
Q

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

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
Schizos | -too much or too little dopamine in mesocortical pathway?
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
1 year conventional anti-psychotic use | -% chance of TD?
5-25% | -25% in elderly.
27
How to predict who will be more likely to get TD?
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
D2 blockers and decreased bone density | -whats the relation
low dopamine = high PRL - high PRL inhibits GNrH - low GNrh = low estrogen
29
Conventional anti-psychotics | -what are the main 4 receptors they block?
D2, M1, alpha-1, H1
30
Relationship between dopamine and ACh in nigrostriatal pathway?
Dopamine normally inhibits acetylcholine release from postsynaptic nigrostriatal cholinergic neurons, thus suppressing acetylcholine activity there.
31
Atypical anti-psychotics | -which major receptors does it block?
5HT2a and D2
32
Clinical difference btwn SGA and conventional antipsychotics?
equal positive symptom antipsychotic actions, but low extrapyramidal symptoms and less hyperprolactinemia compared to conventional antipsychotics.
33
What receptors are main action of SGA?
D2 antagonism with serotonin 5HT2A antagonism
34
Serotonin | -which MAO degrades it?
MAO-A
35
5HT2a receptors: | -pre or post synaptic?
-post synaptic | -
36
5HT2a receptors: | -where are they excitatory?
- corticol pyramidal neurons - and therefore enhance downstream glutamate release. * glutamate regulates downstream dopamine release so 5HT2a has a downstream effect on dopamine release.
37
5HT2a receptors: | -relationship with dopamine release?
- 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
5HT2A receptors are brakes on dopamine release in the | striatum
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
5HT2a relationship w/dopamine release in striatum | -how does it lead to less EPS?
- 5HT2a stimulation in cortex = less dopamine released in striatum. - so blocking 5HT2a means more release of dopamine in striatum which means less EPS!
40
Lithium | - side effects
- GI symptoms (n/v, dyspepsia, diarrhea) - weight gain, hair loss, acne, tremor, decreased cognition, incoordination. - thyroid, kidney
41
Anti-convulsants w/proven efficacy in Bipolar Disorder:
Valproic acid carbamazepine lamotrigine
42
proposed mechanism of valproate?
1. diminish voltage gated sodium channel flow leading to less glutamate release (excitatory). 2. enhances GABA relase
43
valproate: | which is more proven, treating acute mania or prophylaxis of recurrence?
proven to treat acute mania more so than maintenance
44
valproate | most common side effects?
hair loss, weight gain, sedation | - w/long term use, liver/pancreatic effects, fetal abnormalities (neural tube defects), amenorrhea, polycystic ovaries.
45
Best anti-convulsant for bipolar depression?
lamotrigine
46
Carbamazepine - 2 biggest side effects: - okay in pregnancy?
bone marrow suppression, sedation, cyto p450 induction | - can cause neural tube defects
47
Is lamotrigine approved for bipolar mania?
no, takes too long to titrate up
48
oxcarbazepine (trileptal) - metabolite of tegretal? - advantages over tegretal? - disadvantages?
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
combo of lamotrigine and valproate | -what to watch out for?
need to reduce lamotrigine dose by half sometimes