Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Psychopharmacology > Chapter 6: Mood disorders > Flashcards

Chapter 6: Mood disorders Flashcards

1
Q

DSM5 criteria for major depressive episode

A

depressed mood or apathy and at least 4 of the following:
weight/appetite changes
sleep disturbance
psychomotor agitation/retardation
fatigue
feelings of guilt/worthlessness
suicidal ideation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DSM5 criteria for manic episode

A

elevated or irritable mood and at least 3 of the following:
grandiosity
increased goal-directed activity
risk-taking
decreased need for sleep
easily distracted
talkative/pressured speech
flight of ideas/racing thoughts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

definition of MDD

A

occurrence of at least 1 major depressive episode

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

definition bipolar 1

A

occurrence of at least 1 manic episode

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

definition bipolar 2

A

one+ major depressive episodes and at least one hypomanic episode

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how can unipolar depression turn into bipolar depression

A

unipolar progresses to mixed symptoms which progresses to bipolar symptoms which progress to treatment resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

non-euphoric manic symptoms

A

psychomotor agitation
impulsivity
irritability
racing thoughts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

neurotransmitters involved in depression

A

norepinephrine, dopamine, serotonin, GABA, glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is norepinephrine synthesized

A

tyrosine is transported from blood into brain where tyrosine hydroxylase (TOH) coverts it to DOPA which is then converted into dopamine by DOPA decarboxylase (DDC). Dopamine is converted into norepinephrine by dopamine β-hydroxylase (DBH), which is then packed into synaptic vesicles to await neurotransmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how is the action of norepinephrine terminated

A

reuptake into presynaptic neuron by NET
destroyed by enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

enzymes that destroy norepinephrine and whether they are intra or extracellular

A

MAO (A or B) intracellular (stored in mitochondria)
COMT - extracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the only norepinephrine receptor that can be a presynaptic autoreceptor

A

a2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where are a2 norepinephrine receptors and how do they work

A

axonic - allows norepinephrine release when not bound by monoamine
somatodendritic - when norepinephrine binds to receptor it shuts off neuronal impulse flow which stops the release of the neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the principal inhibitory neurotransmitter in the brain

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how is GABA synthesized

A

GAD (glutamic acid decarboxylase) converts glutamate (amino acid) to GABA which is then transported into vesicles to await neurotransmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

vesicular transporter for GABA

A

VIAAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how is the action of GABA terminated

A

reuptake by GAT
enzyme GABA transaminase converts GABA to an inactive substance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

major postsynaptic GABA receptors and what type of receptors are they

A

GABA A - ligand-gated ion channel
GABA B - G protein-linked receptor
GABA C - ligand-gated ion channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

GABA A isoform subunits

A

a
β
γ
ẟ
ɛ
θ
π

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

action of benzodiazepine-sensitive receptors with a a1 subunit

A

good for sleep, sedative, hypnotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

action of benzodiazepine-sensitive receptors with a a2 subunit

A

good for anxiety

22
Q

“other” GABA A receptor subtypes

A

synaptic
extrasynaptic
benzo-sensitive
benzo-insensitive

23
Q

what is mediated by synaptic and extrasynaptic GABA A receptors

A

synaptic - phasic neurotransmission
extrasynaptic - tonic neurotransmission

24
Q

are benzodiazepines PAMs or NAMs
what has to be present for it to work

A

GABA A PAMs
GABA must be present

25
Q

what counteracts benzodiazepine action

A

flumazenil

26
Q

selectivity of currently available benzodiazepines

A

non-selective for GABA A receptors with different a subunits

27
Q

location of benzodiazepine sensitive/insensitive GABA A receptors

A

sensitive - postsynaptic
insensitive - extrasynaptic

28
Q

monoamine hypothesis of depression

A

depression is d/t a deficiency in monoamine neurotransmission
evidence is lacking for this theory

29
Q

monoamine receptor hypothesis of depression

A

depletion of neurotransmitter causes compensatory upregulation of postsynaptic receptors and this leads to depression

30
Q

if medications cause neurotransmitters to rise immediately, why does it take so long to see clinical effectiveness - hypothetically

A

it takes awhile for the downregulation of receptors to occur

it takes awhile for downstream synthesis of growth factors (BDNF)

31
Q

what is the main function of BDNF

A

promote growth/development of immature neurons

enhance survival/function of adult neurons

help maintain synaptic connections

32
Q

what are a few things that may lead to neuronal cell loss

A

decreased BDNF
HPA axis dysregulation
neuroinflammation

33
Q

what is the relationship between monoamines and BDNF availability

A

monoamines can induce signal transduction cascades that lead to the release of BDNF

34
Q

how does dysregulation of the HPA axis lead to depression

A

when stress causes neurons in the hippocampus to atrophy they no longer inhibit the HPA axis so it becomes overactive leading to elevated levels of glucocorticoid and insensitivity to feedback inhibition

35
Q

how does neuroinflammation lead to loss of synapses and cell death

A

inflammation activates microglia in the brain to release proinflammatory molecules that attract immune cells which disrupts neurotransmission and causes oxidative stress, mitochondrial dysfunction, HPA axis dysfunction, reduction of neurotrophic factor availability, and epigenetic changes to unwanted gene expression which leads to synapse loss and cell death

36
Q

measurements of circadian rhythm that are altered in depression

A

-flattening of daily body-temp cycle
-elevated cortisol secretion in the day
-decreased melatonin secretion at night
-reduction in BDNF and neurogenesis

37
Q

what is one of the most common residual symptoms of depression

A

cognitive dysfunction

38
Q

diffuse dopamine dysfunction drives what type of depressive symptoms

A

symptoms r/t reduction of positive affect

39
Q

diffuse serotonin dysfunction drives what type of depressive symptoms

A

increase in negative affect

40
Q

what depressive symptoms are mediated by the PFC

A

-concentration/interest/pleasure
-mental fatigue
-guilt, suicidality, worthlessness
-mood

41
Q

what depressive symptoms are mediated by the striatum

A

-mental fatigue
-pleasure/interests
-fatigue/energy

42
Q

what depressive symptoms are mediated by the hypothalamus

A

sleep
appetite

43
Q

what depressive symptoms are mediated by the amygdala

A

guilt
suicidality
worthlessness

44
Q

what depressive symptoms are mediated by the spinal cord

A

physical fatigue

45
Q

depressive symptoms mediated by the cerebellum

A

psychomotor

46
Q

manic symptoms mediated by the PFC

A

-racing thoughts
-grandiosity
-distractibility
-pressure speech
-mood
-risk-taking

47
Q

manic symptoms mediated by the basal forebrain

A

decreased need for sleep
increased arousal

48
Q

manic symptoms mediated by the striatum

A

-racing thoughts
-grandiosity
-increased goal-directed behavior
-motor agitation

49
Q

manic symptoms mediated by the thalamus

A

decreased need for sleep
increased arousal

50
Q

manic symptoms mediated by the hypothalamus

A

decreased need for sleep
increased arousal

51
Q

manic symptoms mediated by the amygdala

A

mood

Psychopharmacology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions