Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Psychiatry > Mood Altering Drugs > Flashcards

Mood Altering Drugs Flashcards

1
Q

What drug is a tricyclic antidepressant?

A

amitriptyline

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

What are the 3 SSRIs?

A
  1. sertraline
  2. fluoxeline
  3. paroxetine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the “newer antidepressants”?

A
  1. bupropion
  2. trazodone
  3. duloxetine
  4. venlafaxine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What benzodiazepine is sometimes used as an antidepressant?

A

alprazolam

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

What are the main MAOIs?

A
  1. selegiline

2. tranylcypromine

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

What 4 drugs are used to treat bipolar disorder?

A
  1. lithium
  2. valproate
  3. carbamazepine
  4. atypical anti-psychotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the biogenic amine hypothesis?

How was it derived?

A

Mood disorders are caused by abnormally low levels of monoamines [specifically NE and 5HT].
This theory was derived because reserpine which decreased NE caused depression in some individuals

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

Both TCAs and MAOIs increase the level of neurotransmitters in the synapse. How do they differ in MOA?

A

TCAs prevent reuptake, while MAOIs inhibit degradation

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

What is the mechanism of a1 receptors?

What is the effect on serotonergic neurons?

A

they couple to GPCR that activates PLC which breaks down PIP–>IP3, DAG

IP3–> Ca release
DAG–> activates PKC

On serotonergic neurons, it stimulates firing and enhances 5HT release

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

What is the mechanism of a2 receptors? What is the effect on serotonergic neurons? noradrenergic neurons?

A

they inhibit adenylyl cyclase –> reduced cAMP

presynaptic noradrenergic neurons –> inhibit NE release

synaptic terminal serotonergic–> inhibit 5HT release

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

What is the mechanism of B1 receptors?

A

increase cAMP–> excitatory

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

Where is more than 90% of the body’s 5HT located?

A

Periphery in platelets, mast cells, enterochromaffin cells of GI.

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

In the CNS where is 5HT released?

Where is NE released?

A

both are released from neural projections from the brainstem

NE- locus ceruleus
5HT- raphe nucleus

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

How is serotonin synthesized?

A
  1. tryptophan—tyrosine hydroxylase–> 5-hydroxytryphtophan
  2. decarboxylase –> 5HT
  3. MAO–> HIAA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is dopamine and NE synthesized?

A
  1. tyrosine —tyrosine hydroxylase–>DOPA
  2. decarboxylase–> dopamine
  3. DBH–> NE
  4. MAO–> dihydromandelic acid
  5. VMA–> COMT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the 5HT1a receptor.
Inhibitory or excitatory?
Where in the CNS are they found?
Auto or heteroreceptors?

A

inhibitory causing:

  1. decrease in cAMP
  2. opening of K channels

They are found in:

  1. raphe nuclei where they are autoreceptors for negative feedback
  2. hippocampus, amygdala, frontal cortex as postsynaptic heteroreceptors.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is believed to be the major factor in precipitating serotonin syndrome?

A

activation of 5HT1a heteroreceptors [inhibitory] in the hippocampus, lateral septum, entorhinal, amygdala and frontal cortex

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

Describe 5HT1d receptors.
Is it inhibitory or excitatory?
Auto or heteroreceptors?

A

It depresses cAMP levels when activated.

It is autoreceptors on serotonergic synpapses that provide negative feedback.

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

Describe 5HT2a receptors.
Excitatory or inhibitory?
Where are they found?

A

They activate GCPR, increase PLC–>IP3, DAG–>excitatory

They are found in the hypothalamus and in the periphery [platelet aggregation, smooth muscle contraction]

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

Describe 5HT3 receptors.
How are they distinct from the other serotonin receptors in terms of structure?
Why are they of clinical importance?

A

They are ligand-gated ion channels rather than GPCR.

They are of importance because they are believed to be the cause of the uncomfortable side effects of anti-depressants –>nausea,vomiting from brainstem system

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

What serotonin receptor is responsible for triggering nausea and vomiting response due to increased serotonin due to anti-depressant use?

A

5HT3

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

In synaptic vesicles, there is often peptides co-packaged with neurotransmitters. What are examples of the co-packaged nerotransmitter/neuropeptide pairs?

In these pairs, where do the neurotransmitters come from?

A
  1. NE or Epi with enkaphelins
  2. 5HT with substance P

The neutrotransmitters do NOT come from synthesis in the ER and transport in the golgi
INSTEAD
1. dopamine and 5HT are transported through the synaptic vesicle membrane
2. NE is synthesized in the synaptic vesicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do glutamate and GABA enter synaptic vesicles?

How does this differ from Ach and monoamines?

A

Glut and GABA enter via electrochemical gradient

Ach and monoamines enter via pH gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the principle mechanism of inactivating neurotransmitters after their release?
Because of this, what are the major targets of most currently used antidepressants [and many anxiolytics and stimulants]?

A

Reuptake so presynaptic monoamine transporters are the target

DAT–> dopamine
SERT–> serotonin
NET–> NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What drug/substance inhibits DAT, NET and SERT?
cocaine
26
What is the biological basis for antidepressant action?
After the antidepressant is started, 1. synaptic monoamine levels decrease due to neg feedback on autoreceptors [5HT1a, HT1d] 2. inhibitory autoreceptors gradually get down-regulated and synaptic monoamine again rises 3. post-synaptic excitatory receptors are also down-regulated, but to a lesser degree so you still get desired effects
27
What is the key problem of the bioamine hypothesis for depression?
Antidepressants have immediate effects on synaptic monoamine levels, but therapeutic benefits are not manifested for weeks [2-4]
28
What is the transcriptional regulation model of antidepressants?
Anti-depressants induce increase in neurotransmitter level that activates signal transduction, upregulating factors that trigger synthesis of new proteins. 1. B1 on 5HT4-7 increase cAMP--> activate CREB 2. a1 on 5HT2 increases Ca and PKC --> change gene transcription It is thought that this leads to an increase in BDNF
29
What is the neurotrophic factor hypothesis of antidepressants?
Stress and depression downregulate brain derived neurotrophic factor BDNF causing atrophy of neurons especially in the hippocampus. It is thought that antidepressants inhibit MAPK phosphatase that turns off ERK-P that usually converts to BDNF
30
How does TCA differ from the antipsychotic phenothiazine? | How does this change the function of the drug?
Instead of a Sulfur on the middle ring, it has 2 carbons. This results in the inability to block dopamine receptors but gained ability to block monoamine reuptake
31
What structure is the TCA amitriptyline? What is its preferential function? What happens when it is metabolized?
It is a tertiary amine that blocks the uptake of 5HT preferentially over NE. When it is metabolized it is demethylated and becomes a secondary amine which still has antidepressant effects, but blocks NE preferentially over 5HT and has fewer side effects
32
What is the MOA of TCAs?
They inhibit the reuptake of monoamines after exocytosis to increase the synaptic concentration of NE and 5HT
33
How are TCAs metabolized? What is the half life of most TCAs? What drug interactions are there?
TCAs are metabolized in the liver by P450s and have a typical 1/2 life of about 24 hours. Drug interactions: 1. anti-epileptics because they induce P450s 2. Cimetidine- blocks P450s 3. meperidine, pressors, MAOIs --> lethal HTN 4. TCAs block uptake of tyramine and amphetamine vasopressors
34
The major adverse effects of TCAs come from their ability to do what?
Block muscarinic, H1 histaminic and a-adrenergic receptors. | Tertiary have more side effects than secondary.
35
What are the 5 main adverse effects of TCA?
1. anticholinergic- sedated, constipated, urinary retention, blurred vision, confusion 2. anti a1-adrenergic = orthostatic hypotension 3. cardio effects = widening of QRS interval and slowed cardiac conductance 4. sedation because of H1 effects 5. weight gain = slowed metabolism, craving sweets
36
What are the 4 main uses for TCAs?
1. 70% antidepressant response - not as good as newer drugs 2. OCD - clomipramine bc it blocks 5HT reuptake 3. Nocturnal enuresis - because they cause urinary retention [anticholinergic effect] 4. panic disorder/agoraphobia [SSRIs are better]
37
What is the MOA of SSRIs? | How do they differ from TCAs?
Selective-serotonin reuptake inhibitors [very little effect on NE] They differ from TCAs because they have very little effect on a1, H1 or muscarinic receptors decreasing the side effects.
38
For SSRIs, antidepressant and anxiolytic effects of agents that enhance 5HT neurotransmission are believed to result from stimulation of what receptors? What receptors are most adverse effects linked to?
Anti-depressant, anxiolytic = 5HT1 | Adverse effects = 5HT2, 5HT3
39
How do the SSRIs differ in terms of half-lives? | What is the implication?
Sertraline and paroxetine have a 1 day half life [same as TCAs] Fluoxetine has a 2 day T1/2 but its active metabolites last for 7 days so it takes 4-5 weeks to get to steady state
40
How do the SSRIs differ in terms of drug interactions?
Paroxetine and fluoxetine inhibit P450s decreasing metabolism of TCAs and other anti-psychotics Sertraline has less effect on P450s
41
What drugs should be specifically avoided with ALL SSRIs?
MAOIs because they can cause serotonin syndrome
42
What are the adverse effects of SSRIs due to interaction with: 1. 5HT2 2. 5HT3 3. general effects
1. headache, insomnia, agitation, anxiety, sexual dysfunction 2. nausea, vomiting 3. falls/fractures in elderly, teratogenic effects
43
What is serotonin withdrawal syndrome? | When is the onset and duration?
When the drug is removed, the patient will experience: insomnia, fatigue, dizziness, chills, vomiting diarrhea Onset: several days after cessation of the drug Persistance: 3-4 weeks [except fluoxetine due to long 1/2 life]
44
Which SSRIs have non-linear kinetics?
fluoxetine, paroxetine [due to p450 induction]
45
In addition to depression, what are the other indications for SSRIs?
1. panic disorders 2. bulemia, anorexia 3. OCD 4. PTSD 5. generalized anxiety 6. PMDD [only fluoxetine]
46
What is the MOA of venalfaxine? What is the main use? What is the side effect?
Inhibits reuptake of NE and 5HT without blocking muscarinics, H1 or adrenergics. Behaves like TCA, but without the harsh side effects Main use: treatment of chronic pain Side effect: possible increased BP at high doses. discontinuation insomnia, flu-like symptoms and irritability
47
What is the MOA of duloxetine? What is the main use? What are the side effects?
Like, venlafaxine, it is a 5HT and NE uptake inhibitor. Main use: diabetic neuropathic pain Side effects: less increase in BP than venlafaxine and less rebound symptoms, but there is induction of p450s so warn alcoholic or liver disease patients
48
What is the MOA of trazadone?
1. inhibits 5HT reuptake 2. activates 5HT1a 3. antagonizes 5HT2a It also antagonizes a1-adrenergics and histaminergic receptors [sedation, orthostatic hypotension]
49
What is the MOA of bupropion?
We used to think it was a dopamine uptake blocker, but now we think it blocks NE reuptake by an active metabolite, hydroxybupropion. *only available NDRI -NE, dopamine reuptake inhibitor
50
What is the only known NDRI? What are the uses? What are the negative effects?
Bupropion - it blocks NE and DA It does NOT cause sexual dysfunction like most SSRIs but, it does have a low seizure risk. Uses: 1. antidepressant 2. aid in smoking cessation 3. ADHD Negative effects: 1. slight seizure risk 2. worsens and induces panic in panic disorders
51
What non-SSRI antidepressant can actually WORSEN panic in panic disorders?
Bupropion
52
What benzodiazepine is useful as an anti-depressant, and is used in panic disorders and agoraphobia?
alprazolam
53
What are considered to be the best drugs for "atypical depression" where there is overeating, oversleeping?
MAOIs - tranylcypromine
54
What are the 2 types of MAOs?
``` MAO-A = NE and 5HT MAO-B = dopamine ```
55
What receptor does selegiline act on at low and high doses? | What is the possible negative effect of this drug?
it is a selective MAO-B inhibitor at low doses and can also inhibot MAO-A at high doses. Skin patch delivery allows inhibition of both types MAO in the brain and restricts the inhibition of tyramine degradation in the gut. This leads to a dangerous rxn with cheese.
56
What is the MOA of MAOIs?
MAO enzymes are on the outer surface of mitochondria and oxidize cytoplasmic monoamines [not those amines in synaptic vesicles]. MAOIs increase cytoplasmic amines which can than be transferred into secretory vesicles. They are IRREVERSIBLE
57
What is the pharmacokinetics of MAOIs?
They are irreversible, so their action will persist until the resynthesis of MAO.
58
What are the drug and food interactions with MAOIs?
1. tyramine- cheese and wine. It is metabolized by MAO-A in the liver and gut and since it is blocked, tyramine builts up and causes HTN, headache, chest pain 2. TCA/SSRI that increase 5HT can cause serotonin syndrome which presents similarly to malignant hyperthermia [sweating, diarrhea, myoclonus, hyperthermia, convulsions] 3. Sympathomimetics- enhances the effects of amphetamines, methylphenidate, ephedrine 4. meperidine and DM
59
How long should you wait when switching from an MAOI to another antidepressant? Why?
2 weeks because if MAOI and SSRI/TCA are given together, there is increased risk of serotonin syndrome with changes in mental status, hyperthermia, sweating, diarrhea, myoclonus
60
What are the 4 major adverse effects of MAOIs?
1. orthostatic HTN 2. dizziness, headache, insomnia 3. constipation, dry mouth, blurred vision [antichol] 4. hepatotoxicity
61
What are the therapeutic uses of MAOIs?
second-line drugs that are administered to patients that were refractory to TCA/SSRI treatment
62
What is required for a patient to be considered "responsive" to antidepressants? What is necessary for remission vs. recovery?
50% reduction in symptoms of depression as judged by a psychiatric rating scale Remission is complete loss of all symptoms over a given period. Recovery is loss of all symptoms for 6-12 months.
63
What is likely to increase remission rates for antidepressants?
If the drug affects 5HT and NE pathways
64
After the first recurrence, what is the probability of further recurrence?
50-90% | After 2nd recurrence, there is greater than 90% and the patient should be on medication permanently
65
What has been the standard drug for treatment of bipolar disorder since the 1950s? What are the effects?
Lithium is anti-manic and anti-depressant so it is a "mood stabilizer". It has greater effect on the manic episodes than depressive. It is the most protective drug against suicide
66
What is the MOA of lithium?
The exact mechanism is unclear, but it is thought that it: 1. attenuates phosphoinositide signaling [by inhibiting inositol-1-phosphatase] and decreasing Ca release 2. inhibit activation of PKC Effect takes days to weeks so it is believed that long-term neuronal changes take place
67
What are the pharmacokinetics of lithium? What are the effects of Na on Li? What is the target plasma concentration of Li? How does it vary with age?
It is absorbed rapidly with a peak serum concentration in 3 hrs. If Na is depleted [sweat, vomit, diarrhea] the kidney will absorb more Li in the prox tubule and increase risk of toxicity . Target concentration is 1mEq/l for acute episodes and 0.6-1.2mEq range once the acute episode is cleared. Young adults need more, elderly need less
68
What drugs slow Li excretion and may lead to toxicity?
NSAIDs, diuretics, anything that depletes Na
69
What are the adverse effects of Li?
1. Early GI effects: - nausea, vomiting, diarrhea 2. Chronic renal effects: - nephrogenic diabetes insipidus [kidney doesnt respond to ADH] 3. hypothyroidism 4. weight gain 5. lethargy
70
A bipolar patient taking Lithium develops tremor, spasticity, confusion, slurred speech, convulsion, vomiting. What is the most likely reason and what is treatment?
``` Lithium toxicity due to depleted sodium. You need to: 1. stop giving the drug 2. saline infusion to increase Na 3. hemodialysis ```
71
What drugs are usually used as anti-epileptics but can be anticonvulsants given in bipolar disorder [esp. mixed mania and rapid cycling]?
1. valproic acid -antimanic and given with lithium | 2. carbamazepine
72
What adverse effects are associated with valproic acid?
tremor, sedation, GI upset, hair loss, weight gain, impaired cognition *teratogenic
73
What are the adverse effects of carbamazepine?
LESS cognitive dysfunction than valproic acid, but increased risk of : 1. leukopenia--> aplastic anemia
74
What adverse effect do all three bipolar drugs share?
teratogenic
75
What is thought to be the major cause of manic euphoria in bipolar disorder? What are the implications of this?
dopamine hyperactivity THEREFORE, antipsychotics that block dopamine may be used for tranquilizing effects that take place in hours instead of days like lithium
76
What are the adverse effects of haliperidol?
1. EPS | 2. tardive dyskinesia

Psychiatry (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions