Brainscape's Knowledge GenomeTM

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


See full index

Drugs and Behavior > Exam 4: Treatment for Affective Disorders > Flashcards

Exam 4: Treatment for Affective Disorders Flashcards

1
Q

reserpine

A

reduces high blood pressure
induces depression as a side effect
prevents packaging of neurotransmitters into vesicles, leaves in synapse whereMAO can degrade them

it reduces levels of DA, NE and 5-HT

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

serotonin and depression

A

significant influence on sensitivity to pain, emotionality, response to negative consequences or reward

  • having low levels of serotonin does NOT cause depression, except in vulnerable individuals
  • tryptophan challenge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

tryptophan challenge

A

tryptophan is what gets converted into serotonin

if give drink that dec tryptophan in ppl with a history of depression it will cause depression symptoms

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

5-HIAA levels

A

the serotonin metabolite
low levels of 5-HIAA found in postmortem brains of depressed individuals
-low levels associated with 5 fold inc in suicide risk

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

MDD patients have low levels of what in cerebral spinal fluid (spinal tap)

A

5-HT, TPH, 5-HIAA

lowered serotonin is problem in people with depression but does not mean the person will become depressed

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

brains of unmedicated individuals with mood disorders have inc what

A

inc density of postsynaptic 5-HT2 receptors (with hallucinogens too)
this is compensatory response to low serotonergic activity
-more receptors to try to recapture as much serotonin as possible
-antidepressants reduce 5-HT2A receptor binding

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

examples of tricyclic antidepressants

A

amitriptyline, chlorimipramine, imipramine

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

what is NE involved in

A

neuroendocrine function, reward, attention and arousal, response to stress

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

NE and depression

A

dowwn regulation of B-receptors with chronic antidepressant treatment
-takes 7-21 days of treatment to see effects - delay

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

types of antidepressant drugs

A

MAOIs, TCA, second generation antidepressants(SSRIs)

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

nondrug therapies

A 
sleep deprivation
electroconvulsive therapy (shock)
transcranial magnetic stimulation
vagal nerve stimulation
deep brain stimulation

exercise

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

dopamine

A

involved in motivational deficits associated with depression

anhedonia (loss of pleasure)

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

does anxiety or depression come first

A

anxiety

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

anxiety vs depression neurochemistry

A

anxiety = too much serotonin, NE, DA

depression= not enough serotonin, NE< DA

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

anxiety increases SERT…more SERT =

A

less serotonin

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

ROA of antidepressants

A

typically oral
transdermal gel or patch - longer lasting actions
- ex: selegiline: MAOI with transdermal patch

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

Absorption of antidepressants

A

max blood concentrations:

  • TCA: 1-2hrs
  • MAOIs: 2-3hrs
  • SSRIs/SNRIs: 4-8hrs

1st pass metabolism dec bioavailability - oral drugs
-inhibited by alcohol - slows breakdown of drugs

depot binding!!!
-SSRI Fluoxetine has over 95% depot binding - longer time of peak levels in blood, longer half life

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

distribution of antidepressants

A

most cross BBB and placental barrier
concentrate in lungs, liver, kidneys, brain

lipid soluble

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

metabolism of antidepressants

A

inhibition of MAO in liver (normally MAO breaks down dietary tyramine)

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

dietary tyramine

A

formed as byproduct of fermentation in cheeses, meats, pickled products, other foods
people on MAOIs given list of foods they should avoid bc they can cause a dangerous spike in BP

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

what does elevated tyramine do

A

releases higher than normal stores of NE at nerve endings, causing dangerous increases in BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MAOIs inhibit CYP450s

A

effects of alcohol, barbiturates, opiates, aspirin all intensified in presence of MAOIs (enzyme inhibition)
competition for enzymes!

23
Q

side effects of MAOIs

A

changes in BP
sleep disturbances - interesting bc sleep disturbances is problem with depression and this is going to cause it
overeating/weight gain

24
Q

how do most antidepressants increase 5-HT

A

blocking reuptake or inhibiting MAO

-prevent 5-HT breakdown or prevent it from being repackaged

25
Q

acute effects of increased serotonin

A

gives cell more opportunity to activate the 5-HT1A autoreceptor to slow cell firing and reduce synaptic serotonin

26
Q

chronic serotonin treatment results in

A

down regulation of 5-HT1A sutoreceptors and synaptic 5-HT increases

this inc is just initial step, other changes required like hippocampal neurogenesis and functional remodeling of corticolimbic circuits

27
Q

MAOIs increase amount of…

A

serotonin, NE, DA available

28
Q

action of TCAs

A

bind to presynaptic transporter proteins and inhibit reuptake of neurotransmitters - prolongs duration of transmitter action at synapse

diff TCAs have diff NE and 5-HT reuptake blocking potencies

inc in synaptic activity first step but NEED neuronal adaptation

29
Q

side effects of TCAs

A

also block histamine, acetylcholine, and a1 receptors

30
Q

anticholinergic effects of TCAs

A 
dry mouth
constipation
urine retention
dizziness
confusion
impaired memory
blurred vision
31
Q

a1 receptor blockade of TCAs

A

coupled with NE reuptake blocking leads orthostatic hypotension, tachycardia, arrhythmias

  • overdose causes cardiovascular depression, delirium, convulsions, respiratroy depression, coma
  • heart arrythmias can produce ardia arrest
32
Q

histamine receptor blockade - TCAs

A

causes sedation and fatigue that limit the drugs usefulness - positive effect for people with sleep dysfunction
for patients with agitation these side effects help

33
Q

do TCAs have a high or low therapeutic index

A

low!

  • fatalities occur at approximately 10 times the normal dose
  • can also get overdoses if take TCAs with alcohol
34
Q

SSRIs

A

block 5-HT reuptake transporters more than NE transpoters

-used to treat panic and anxiety disorders, OCD, obesity, alcohol use disorder

35
Q

serotonin syndrome

A

SSRIs have potentially life-threatening effects when combines with other serotonergic agonists or drugs that interfere with metabolism of the SSRIs

36
Q

mild symptoms serotonin syndrome

how to manage

A

mydriasis
shivering
sweating
tachycardia

manage: observe for at least 6 hrs and BENZOS

37
Q

moderate symptoms of serotonin syndrome

how to manage

A

altered mental status (agitation, disorientation)
rigidity, tachycardia, hyperthermia
tremor, hypereflexes

manage: hospital
cardiac monitoring, cyproheptadine

38
Q

life threatening symptoms of serotonin syndrome

how to manage

A

delirium, hypertension, hyperthermia, muscle rigidity, tachycardia

manage: ICU, esmolol or nitroprusside, cooling measures, ventilation, SkM paralysis, sedation

39
Q

is it more beneficial to enhance both NE and 5-HT function or just one

A

both

40
Q

mirtazapine

A

antagonist for a2 autoreceptors
inc synaptic NE and a2 heteroreceptors on serotonergic cells
inc 5-HT release

also antagonist for 5-HT2 receptors

41
Q

what is the most effective medication for patients with bipolar disorder

A

lithium carbonate

  • flattens extremes of emotion
  • has no effect on healthy ppl but reduces manic episodes without causing depression or producing sedation
  • effective in dec suicides in bipolar
42
Q

lithium ROA

A

oral

43
Q

absorption and distribution of lithium

A

readily absorbed by GI tract
peak plasma conc 30min-3hr
brain peak conc 18-24 hrs
no depot binding, no 1st pass metabolism

44
Q

metabolism and excretion of lithium

A

NO metabolism
100% excreted unchanged in urine
half life: 18-30 hrs

45
Q

side effects of lithium

A

low therapeutic index
blood levels of lithium must be monitored regularly

mild but can include inc thirst and rination, impaired conc and memory, fatigue, tremor, weight gain

46
Q

lithium pharmacodynamics

A

many system - 5-HT, DA, GABA, glutamate
2nd messenger systems

lithium downregulates NMDA and DA receptors (dec Ca ion influx through NMDA receptors)

lithium enhances 5-HT actions (elevates brain tryptophan, 5-HT, 5-HIAA and inc 5-HT release

lithium inc GABA levels and inc GABA B receptors

47
Q

what does lithium downregulate

A

NMDA and DA receptors

reduces Ca ion influx

48
Q

treatment for bipolar disorder

A

anticonvulsant drugs

-valproate and carbamazepine

49
Q

valproate (depakote)

A

bipolar anticonvulsant treatment

  • inc GABA levels in brain
  • dec glutamate in brain
50
Q

carbamazepine (tegretol)

A

anticonvulsant for bipolar
resembles TCAs and inhibits NE reuptake
-blocks adenosine receptors in sleep

51
Q

addiction and withdrawal

A

no euphoria
little to no abuse liability for SSRIs, TCAs, MAOIs

but can cause physical dependence

52
Q

physical dependence and antidepressants

A

-sudden discontinuation of high dose TCAs - restlessness, anxiety, chills muscle aches, akathisia

53
Q

SSRI withdrawal

A

dizziness, insomnia, fatigue, anxiety, nausea

54
Q

withdrawal from NE targeting drugs

A

heart palpitations, psychiatric symptoms - delusions

Drugs and Behavior (27 decks)

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