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Pmcol 200 > L15 > Flashcards

L15 Flashcards

1
Q

most common mood disorder in North America

A

Depression

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2
Q

What are the symptoms of depression and what is the guideline for diagnosing depression based on these symptoms?

A

Need five out of nine in a two-week period.

ex: Psychomotor agitation or retardation

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3
Q

Emotions

A 
subjective feelings (anger, fear, sadness, jealousy,
embarrassment, joy) — Limbic System
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4
Q

Motivation:

A

behavior that is purposeful and goal directed —

Mesocorticolimbic dopamine system

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5
Q

Limbic Brain

A

a cortical border
circling the brainstem: “cerebri
limbus” (limbus=border/edge)

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6
Q

Limbic Brain: An evolutionarily ‘old’ ____ that
includes the ___, ____,
__ ___ and ____ gyrus with
connections to the ___ cortex and ____.

A

An evolutionarily ‘old’ neocortex that includes the amygdala, hippocampus,
basal ganglia and cingulate gyrus with connections to the frontal cortex and hypothalamus.

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7
Q

t/f: patients with major depression disorder and health controls were shown images of emotionally evocative facial expression

A

t

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8
Q

Major depression disorder

A

Associated with increased engagement of Limbic regions (amygdala) and decrease engagement of regions involved in motivation (striatum) compared to healthy individuals

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9
Q

changes in brain activity reflect changes in _____
release and/or _____
response

A

changes in brain activity reflect
changes in neurotransmitter
release and/or postsynaptic
response

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10
Q

Neurotransmitter is concentrated within the _____ region may be involved in mediating depression

A

Limbic

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11
Q

monoaminergic neurotransmitters (3)

A

Dopamine, norepinephrine, serotonin

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12
Q

monoaminergic neurotransmitters do/don’t have overlapping synthesis and catabolic pathways

A

do

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13
Q

monoaminergic neurotransmitters do/don’t have a “modulatory” role in the brain,
and are involved in mood, arousal, attention

A

do

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14
Q

alterations in monoaminergic neurotransmitters

are associated with

A

mood disorders

among other things

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15
Q

Depression results from inadequate monoamine neurotransmission (esp. ___ and ____) in the brain

why?

A

Depression results from inadequate monoamine neurotransmission (esp. serotonin and noradrenaline) in the brain

May be due to: last neurotransmitter release, fewer receptors, impaired signal transduction

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16
Q

amine hypothesis:
Originated from serendipitous
observations that manipulation of the
____ system influences depression symptoms (i.e. drugs = ____ and ___)

A

Originated from serendipitous
observations that manipulation of the
monoaminergic system influences depression symptoms (i.e.: Reserpine and ipronazid)

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17
Q

Rezerpine

what % of patients developed symptom

A

Antihypertensive drug that develops symptoms of depression

15%

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18
Q

reserpine depletes
neurons of ____ and ____
transmitters

A

reserpine depletes
neurons of dopamine and norepinephrine
transmitters

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19
Q

ipronazid

MAO inhibition leads to what

A

Anti tubercular drug that alleviates depression by inhibiting monoamine oxidase

leads to increased synaptic concentrations of monoamine neurotransmitters

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20
Q

Drugs that restore monoaminergic levels are only moderately effective in __ - __ % of patients

A

30-50%

21
Q

Inconclusive evidence that ____ and ___ systems are

disrupted in depression

A

Inconclusive evidence that serotonin and noradrenergic systems are
disrupted in depression

22
Q

Antidepressants take _____ before clinical effect is seen, despite
immediate effects on synaptic neurotransmitter levels

A

several weeks

23
Q

depression associated with reduction

glutamatergic signaling in the______

A

cortex

24
Q

• loss of glutamatergic signaling impacts
both ___ and ___ function
leading to ____to noise

also impacts what (4)

A

• loss of glutamatergic signaling impacts
both excitatory and inhibitory function
leading to reduced signal to noise

long-term potentiation, neurotrophics production, synapse formation, Gene transcription (essentially brain remodeling)

25
Q

Monoamine antidepressants increase
synaptic levels of monoamine
neurotransmitters (particularly
____ and ____)

A

Monoamine antidepressants increase
synaptic levels of monoamine
neurotransmitters (particularly
norepinephrine and serotonin)

26
Q

MAO

A 
Monoamine oxidase (MAO) is an enzyme involved in breakdown of amine
neurotransmitters (serotonin,
noradrenaline, and dopamine)
27
Q

t/f: blocking amine neurotransmitter
breakdown (particularly serotonin and
noradrenaline) increase synaptic levels
and can improve move

A

t

28
Q

example of moa inhibitor

A

ipronazid

29
Q

how to avoid tyramine cheese reaction

A

a low tyramine diet

30
Q

tyramine

A 
a sympathomimetic
monoamine (acts like noradrenaline) and
is naturally found in certain foods, such
as aged cheese
also degraded by MAO
31
Q

eating a meal rich in tyramine while taking

an MAO inhibitor can lead to

A

acute hypertension reaction caused by tyramine binding to adrenergic receptors
on blood vessels and in the heart

32
Q

does tyramine have psychoactive effects?

A

no, doesn’t cross blood-brain barrier

33
Q

Selective reuptake inhibitors

A

Inhibit serotonin or noradrenaline transporters, which move neurotransmitter from signups to intracellular space

34
Q

blocking Transporters leads to

A

increase the extracellular concentration of neurotransmitters

35
Q

(SSRIs).

A

selective for SET are
called selective serotonin reuptake
inhibitors

36
Q

SNRI

A

inhibit SET & NET

37
Q

ssri eg

A

fluoxetine

38
Q

Limitations to monoamine antidepressants (3)

A
  1. drugs that restore monoaminergic levels are only moderately effective in 30 to 50% of patients
  2. MAOIs, SSRIs, SNRIs take several weeks before clinical Effect is seen, despite immediate effects on synaptic neurotransmitter levels
  3. lead to side effects such as nausea, indigestion, dizziness, dry mouth, weight loss (since they affect serotonin and noradrenaline level throughout body)
39
Q

ketamine is a noncompetitive ____

receptor antagonist

A

NMDA

40
Q

t/f: ketamine is dissociative anesthetic

A

t

41
Q

how is ketamine a potential anti-depressant

A

depression associated with
reduction in glutamateric
signaling in the cortex

ketamine causes a transient burst
in glutamate resulting from
blockage of NMDA receptors on
GABA interneurons

42
Q

effect of glutamate burst

A

synaptic

remodeling and resetting of glutamate and GABA systems

43
Q

other downstream signaling effects of ketamine

A

(BDNF release, gene

transcription) = long term effects

44
Q

Limitation of ketamine

A

narrow therapeutic index; must be administered intravenously within hospital setting

45
Q

t/f: drugs directly targeting the downstream signalling effect events associated with synaptic remodeling may be a more effective treatment for depression

A

t

46
Q

Decreased secondary messenger (_____, _____, _____) have been reported in brains of patients with major depression at autopsy

A

Inositol, cAMP, CREB

47
Q

rolipram

A

Phosphodiesterase inhibitor that increases cAMP; may be good for depression

48
Q

Depression is a _____genous disease

A

hetero

49
Q

Ketamine effectiveness = ____%, improvement after ___ day(s)

SSRI effectiveness = ___% improvement after ___ weeks

A

25, 1

15, 8

Pmcol 200 (12 decks)

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