Brainscape's Knowledge GenomeTM

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


See full index

Neurology > Pharmacology Antidepressants > Flashcards

Pharmacology Antidepressants Flashcards

1
Q

What is depression

A

Affective disorder with persistently low mood and loss of interest or pleasure in almost all the persons usual activities or pastimes

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

What are the two types of symptoms in depression

A

Emotional symptoms

biological symptoms

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

What are the emotional symptoms of depression

A 
Misery 
Apathy
pessimism 
low self-esteem 
feelings of guilt 
inadequacy 
ugliness 
loss of motivation 
indecisiveness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the biological symptoms of depression

A

Retardation of thoughts and action
loss of libido
sleep disturbance
Loss of appetites

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

You have depressed mood or loss of interest or pleasure if you have five or more of the following symptoms presenting during the same two week periods and represented change from previous States

A

Depressed mood most of the day nearly every day
diminished interest or pleasure in all or almost all activities most of the day

significant weight loss when not dieting or weight gain
increase or decrease appetite
insomnia, hypersomnia
psycho motor agitation or retardation
feelings of worthlessness
excessive or inappropriate guilt nearly every day
diminished ability to think or concentrates or indecisiveness
recurrent thoughts of death
Recurrent suicidal ideation without a specific plan or
Suicide attempt or specific plans for committing suicide

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

What are the different types of depressive disorders

A

Major depressive disorder

persistent depressive disorder dysthymia

disruptive mood dysregulation disorder

premenstrual dysphoric disorder

depressive disorder due to another medical condition

substance medication induced depressive disorder

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

What is major depressive disorder

A

No manic or hypomanic episodes and can be recurrent or single episode

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

What is the persistent depressive disorder

A

No how do faces last longer than major depressive disorder but is not severe enough to be called an episode of major depressive disorder

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

What is the disruptive mood dysregulation disorder

A

Found mostly in children and the modest persistently negative between frequent severe explosions of temper

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

What is the premenstrual dysphoric disorder

A

Occurs a few days before menses

woman experiences symptoms of depression and anxiety

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

What is a depressive disorder due to another medical condition

A

Depressive symptoms due to medical or neurological

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

What is a substance medication induced depressive disorder

A

Depression due to alcohol or other substances leading to intoxication or withdrawal

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

What is responsible for disturbances in depression

A

Brainstem and hypothalamus

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

Part of the brain responsible for appetite and energy changes in depression

A

Hypothalamic areas

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

Part of the brain responsible for anhedonia or mania in depression

A

Limbic structure

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

Part of the brain responsible for anxiety in depression

A

Amygdala

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

Part of brain responsible for alteration in thought content in depression

A

Cortex

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

What is the cortisol neurobiology of depression

A

Stress leads to release of corticotropin releasing factor from hypothalamus

Leads to ACTH hormone released from pituitary gland

Leads to cortisol released from adrenal cortex

Cortisol leads to detrimental gene transcription response which leads to neural apoptosis and neurogenesis inhibition leading to depressive symptoms

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

What is the glutamate neurobiology of depression

A

Stress leads to release of glutamate
Glutamate activates NMDA receptors
NMDA receptors leads to neural apoptosis hence depressive symptoms

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

How does noradrenaline ,serotonin and brain derived neurotrophic factor help in reducing depressive symptoms

A

Noradrenaline activate a2 receptors
serotonin activates 5HT1a receptors
BDNF activate TRKB receptors

They all induce signal transduction pathways which inhibit detrimental gene transcription and promotes beneficial gene transcription response

Leads to inhibition of neural apoptosis and promotion of neurogenesis

Depressive symptoms are inhibited

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

What is the monoamine theory of depression

A

Due to depletion in levels of serotonin norepinephrine and dopamine in CNS

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

What is the neurotrophic hypothesis of depression

A

Neuronal plasticity is key factor in development of depression

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

What are the anti-depressant classes

A 
Tricyclic antidepressant 
monoamine oxidase inhibitors
 selective serotonin reuptake  inhibitors 
serotonin noradrenaline reuptake inhibitors 
noradrenaline reuptake inhibitors 
noradrenaline dopamine inhibitors 
atypical antidepressants 
herbal Saint johns wort 
melatonin receptor agonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Examples of tricyclic antidepressants

A 
Imipramine
Amitriptyline
Trimipramine
Doxepine 
Clomipramine
Nortriptyline
Desipramine
Protriptyline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MOA of TCAs

A

Block reuptake of NA and 5HT by competing at the binding site of protien transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the consequence of 5HT reuptake block

A

Improvement of emotional symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the consequence of NA reuptake block

A

Improvement of biological symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the unwanted effect of tricyclic antidepressants

A

Antimuscarinic effect ( Dry mouth ,blurred vision ,constipation ,urinary retention )

antihistaminergic effect ( sedation ,drowsiness ,difficulty concentrating ,weight gain)

anti-adrenergic alpha1 effect ( postural hypotension)

Sedation, confusion and motor incoordination when non depressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Does TCA at therapeutic dose increase risk of sudden cardiac death, Or lower seizure threshold

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What can TCA cause in overdose

A

Ventricular dysrhythmias with prolongation of QT interval

Life-threatening seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What happens in TCA overdosage

A

Initial effect -> excitement ,delirium ,
convulsions

then-> coma, respiratory depression over days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Are TCAs absorbed well orally ?

A

Yes

33
Q

Do TCAs experience extensive first fast metabolism

A

Yes

34
Q

Half life of TCAs

A

8 to 89

35
Q

dosing of TCAs

A

Once Daily

36
Q

What is the metabolism of TCAs

A

Hydroxylation of tricyclic nucleus

Conjugation of hydroxylated products to glucuronide

37
Q

What drugs can inhibits metabolism of TCAs

A

Antipsychotics
oral contraceptives
some SSRIs

38
Q

What drugs compete with protein binding of TCAs

A

Phenytoin
aspirin
phenothiazines

39
Q

Can TCAs potentiates effects of alcohol and anesthetic agent

A

Yes

40
Q

What happens if you combine TCAs with MAO inhibitors

A

CNS toxicity with hyperpyrexia convulsions and coma

41
Q

Do you have to monitor patient with hypertension when administering TCAs due to toxicity

A

Yes

42
Q

What is the clinical indication for tcas

A 
mood disorders
 anxiety disorders 
eating disorders 
personality disorders 
neurological disorders like ADHD 
Parkinson’s disease 
chronic pain 
neuropathic pain 
Narcolepsy 
insomnia 
pathological crying or laughing
 chronic hiccups 
ciguatera poisoning 
schizophrenia adjunct
fibromyalgia 
headache 
migraine
Smoking cessation
 Tourette’s syndrome
 irritable bowel syndrome 
interstitial cystitis 
nocturnal enuresis
43
Q

Examples of selective serotonin reuptake inhibitors

A 
Fluoxetine 
sertraline 
citalopram 
paroxetine 
fluvoxamine
44
Q

Are SSRIs supported by poeple with cardiac conditions and old people

A

Yes

45
Q

Mechanism of action of SSRIs

A

Inhibition of 5HT reuptake by nurse terminals

desensitization of autoreceptors 5HT1E because of increased serotonin level leads to More serotonin release

46
Q

What are the unwanted effects of SSRIs

A 
Agitation and anxiety in beginning 
insomnia
 nausea 
loose stools 
sexual dysfunction 
decreased libido
 delayed ejaculation
 anorgasmia
47
Q

Why is fluoxetine only given in the morning

A

Because of potential for insomnia

48
Q

Metabolism of fluoxetine

A

Demethylated in the liver and become active metabolites

Inactive metabolites excreted by kidney

49
Q

Should you reduce dose of patients with liver failure taking fluoxetine

A

Yes

50
Q

How long does elimination of fluoxetine take

A

4 to 6 weeks after discontinuation of medication

51
Q

Why should you not give fluoxetine with medication metabolized by cytochrome P4 50 2D6

A

Because inhibits this enzyme

52
Q

Is there some issue with giving fluoxetine with TCAs and type 1C anti-arrhythmic like flecainide and propafenone

A

Yes

53
Q

How do you administer setraline

A

Once a day

In the morning to avoid insomnia

54
Q

Metabolism of sertraline

A

hepatic metabolism so should be reduced in liver disease patient

55
Q

Is sertraline highly bound to protein and hence prevent binding of other medication to protein

A

Yes at 98%

56
Q

If you’re on sertraline and want to start MAOIs what should you do

A

14 day washouts

57
Q

Is sertraline and paroxetine a weak inhibitor of cytochrome P450 2D6

A

Yes So should be attention when giving drugs with narrow therapeutic index metabolized by this route

58
Q

Why should you pay attention when giving paroxetine with warfarin

A

Elimination half-life long 21 hours

highly bound to plasma proteins

59
Q

With which SSRIs is weight gain the most important

A

Paroxetine

60
Q

Which SSRIs has the least effect on the cytochrome P4 50 system and less drug drug interactions

A

Citalopram

61
Q

What is the clinical indication of SSRIs

A 
Major depressive disorder 
anxiety disorders like social anxiety panic disorder  OCD, PTSD
Eating disorders 
depersonalization disorder
 chronic pain
62
Q

What are examples of mono amine oxidase inhibitors hydrazide

A

Phenelzine

Isocarboxazid

63
Q

What are example of monoamine oxidase inhibitors non-hydrazides

A

Tranylcypromine

64
Q

Phenelzine metabolism

A

Acetylated in the liver

Polymorphism

65
Q

What life-threatening threatening events can MAOIs cause

A

Hepatotoxicity

dietary tyramineinduced hypertensive crisis

66
Q

When should you give MAOIs

A

When there is resistant treatment for depression

67
Q

What is the mechanism of action of monoamine oxidase inhibitors like isocarboxazid, phenelzine and tranylcypromine

A

They are irreversible nonselective inhibitors of both MAO-A (NA, HT5, Dopamin) and MAO-B ( dopamine)

68
Q

What are some selective MAO-A inhibitors

A

Clorgyline

Moclobemide

69
Q

What are the adverse effects of MOAIs

A

Hepatotoxicity
Tyramine-induce hypertensive crisis -> increased blood pressure

tremors 
orthostatic hypotension 
ejaculatory delay
 dry mouth 
fatigue 
weight gain
70
Q

What happens if you give over-the-counter cough and cold medication with MAOIs

A

Serious hypertension

71
Q

How long should you wait between switching from MAOIs to another antidepressants

A

2 weeks

72
Q

What is serotonin syndrome

A 
Symptoms occur when coadministrating SSRI with MAOIs
Symptoms like 
Confusion
 elevated or dysphoric mood tremor
 myoclonus  
in coordination 
hyperthermia 
cardiovascular collapse
73
Q

What is the treatment of serotonin syndrome

A

Discontinue serotonergic agents
Treat symptoms
give serotonin antagonist like cyproheptadine or methysergide
Dantrolene

74
Q

What are some example of second generation antidepressant

A

Trazodone
amoxapine
Maprotyline
bupropion

75
Q

What are some example of third generation atypical antidepressant

A

Nefazodone
mirtazapine
venlafaxine
vortioxetine

76
Q

What are examples of serotonin noradrenaline reuptake inhibitors

A 
Venlafaxine
 desvenlafaxine 
duloxetine 
Milnacipran 
Levomilnacipran 
Sibutramine (obesity )
Tramadol (weak agent )
77
Q

Active metabolites of venlafaxine

A

O-desmethyl-venlafaxine

78
Q

Dosage of venlafaxine

A

2x per day

79
Q

Dosage of duloxetine

A

1 per day

Neurology (31 decks)

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