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MBBS II HNNS > L50 – Anti-depressants > Flashcards

L50 – Anti-depressants Flashcards

1
Q

List 7 signs and symptoms of depression.

A
  1. Feelings of sadness, emptiness, hopelessness
  2. diminished pleasure in life activities
  3. Significant changes in appetite, body weight
  4. Feelings of self-loathing / worthlessness / guilt
  5. Changes in your sleep pattern
  6. Increased anger / irritability
  7. Fatigue / loss of energy
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2
Q

Classify different severity of depression? How to Dx?

A

Major depression disorder:

  • At least 5 that interfere with patient’s ability to function
  • > 2 weeks

Dysthymic disorder (dysthymia)

  • At least 2 sym./signs
  • > 2 years

Minor disorder

  • At least 2 sym/signs
  • about 2 weeks

Dx by clinical interview and tests: Stroop test, Beck Depression inventory, Hamilton depression scale

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3
Q

2 hypothesis in changes in brain chemistry causing depression disorder?

A

Monoamine hypothesis

Neurotropic hypothesis

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4
Q

Outline the monoamine hypothesis

A
  • Depression is caused by low level or a deficit in function of neurotransmitters
  • All antidepressants enhance synaptic availability of serotonin, norepinephrine or dopamine
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5
Q

Shortcomings of monoamine hypothesis

A
  • Many depressed patients do not have alterations in function or levels of monoamines
  • Benefits of monoamine anti-depressants take time to work, feel worse during first week
  • Removal of serotonin precursor doesn’t lead to depression
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6
Q

Outline the neurotrophic hypothesis?

A
  • impaired growth of neurons is associated with depression
  • Loss of volume in hippocampus causes decrease Brain-derived neurotropic factor (BDNF): regulate neural plasticity, neurogenesis, emotions
  • Antidepressants increase BDNF and neuron growth
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7
Q

Shortcomings of neurotrophic hypothesis?

A
  • BDNF knockout mice do not have increase in depressive or anxious behaviors.
  • Social-stressed animals showed increase BDNF levels rather than a decrease
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8
Q

Principal mechanism of all anti-depressive medication?

A

increasing the amount of neurotransmitters in the brain:

  • preventing them being broken down or
  • prevent “reuptake” into the cells

Different anti-depressants affect one or more neurotransmitters to different extent

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9
Q

Which patients are at highest risk to anti-depressive drugs?

A

children, teens, young adults

Increase the risk of suicidality in patients < age 25
» All antidepressants must include FDA black box warning

No risk in older patients >65

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10
Q

What are the ABCDEF anti-depressant withdrawal symptoms?

A 
 A: Agitation, anxiety  
 B: Balance problems, bad dreams  
 C: Concentration problems 
 D: Dizziness, diarrhea, nausea, vomiting  
 E: Electric shock-like sensations  
 F: Flu-like symptoms
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11
Q

How to withdraw anti-depressants?

A

Doses should be gradually reduced over at least a 4-week period

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12
Q

List some other disorders that can be treated with anti-depressants?

A
  • Panic disorder
  • General anxiety disorder
  • PTSD
  • OCD
  • Bulimia
  • Pain disorders
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13
Q

What is the effectiveness of anti-depressants in patients with various severity of depression?

A

Mild to moderate dpression: Nonexistent to negligible difference between placebos and antidepressants

Severe depression: significantly effective

> > should only be given when the risk of untreated depression far outweighs that of antidepressant mediations

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14
Q

Why do anti-depressants work as effectively as placebos in many patients?

A

People’s belief in the power of anti-depressants

> > overcome any actual pharmacological response

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15
Q

List 2 ways to treat depression without using medication?

A
  1. Cognitive –behavioural/ psychotherapy (find out cause): as effective in mild/ moderate depression
  2. Interpersonal therapy (teach communication to improve relationship)
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16
Q

MoA of SSRI? Give 3 examples.

A

Selective serotonin reuptake inhibitor (SSRI): Fluoxetine (Prozac), Fluvoxamine,
Paroxetine

inhibits ~80% activity of serotonin transporter

> > blocks reuptake of serotonin by presynaptic neuron

> > maintains high levels of 5-HT in the synapse

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17
Q

D/D interaction of SSRIs?

A

Fluxoetine + TCA: Fluxoetine = potential inhibitors of CYP2D6 isoenzyme, unpredictable elevations of TCA levels

Fluxoetine + Diltiazem:
Fluxoetine = CYP3A4 inhibitor, use with diltiazem (= calcium channel blocker) cause bradycardia / hypotension

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18
Q

ADR of SSRI?

A

Enhances serotonergic tone / activity throughout the body:

  • Gut = nausea, GI upset, diarrhea
  • CNS:spinal cord and above = diminished sexual function and interest
  • HIS: Inhibits serotonin reuptake into platelets, reduced coagulation, increased risk of bleeding
  • CVS:Inhibits nitric oxide synthase = favors vasoconstriction
19
Q

C/O of SSRI?

A

Inhibits nitric oxide synthase = favors vasoconstriction

Contradicted for pregnant women with hypertension / preeclampsia (can lead to fetal prematurity)

20
Q

Why is SSRI 1st line treatment against other anti-depressants?

A

 Fewest side effects (mild to moderate, transitory) among anti-depressants
 Safety in overdose
 Low cost/ cost effective

21
Q

MoA of NRI, give 2 examples?

A

Binds to noradrenaline transporter on pre-synapse&raquo_space; selectively blocks reuptake of NA
» increases NA concentration in synaptic cleft

 Atomoxetine
 Maprotiline

22
Q

ADR of NRI?

A

 Acts on α receptors on pacemaker cells in heart = increase heart rate and blood pressure

 CNS activation (e.g. insomnia, anxiety, agitation)

23
Q

MoA of SNRI? 2 examples?

A

Serotonin-norepinephrine reuptake inhibitors (SNRI)

 Bupropion
 Mirtazapine

Binds to both serotonin and norepinephrine transporters > blocks serotonin and nonepinephrine reuptake

Low affinity for other receptors, e.g. histamine receptor, mucarinic acetylcholine receptor (unlike TCA)

24
Q

ADR of SNRI?

A

 Have serotonergic adverse affects as serotonin selective reuptake inhibitor

 Have noradrenergic effects as norepinephrine reuptake inhibitor

25
Q

MoA of TCA? Name one

A

Tricyclic antidepressants (TCA): Amitriptyline

Affect the uptake of all 3 neurotransmitters associated with mood:
1. Serotonin: obsessions, compulsions, memory

  1. Norepinephrine: alertness, concentration, energy
  2. Dopamine: pleasure, reward, motivation/drive
26
Q

ADR of TCA?

A

BLurred vision, Drowsiness, Loss of libido

Constipation, dry mouth, Postural hypertension, urinary retention (similar to muscarinic receptor antagonist ADRs)

27
Q

Why is TCA now rarely used?

A

 Poor tolerability
 Difficult to use
 Lethal in overdose
 Serious drug interactions

Nowadays only used in patients who do not response to SSRI

28
Q

Triple MoA of SARI? Name one.

A

Serotonin antagonist-reuptake inhibition (SARI): Trazodone

  1. Antagonizes 5-HT2A receptors (increased receptor number in depression) (= most potent): increases release of neurotransmitter
  2. Blocks serotonin reuptake transporter (SERT) (100-fold less potent)
  3. Agonizes 5-HT1A receptors: Converted into meta-chloro-phenylpiperazine (mCPP) to activates 5-HT2C&raquo_space;> cause downstream activation of 5-HT1A = Anti-depressive
29
Q

ADR of SARI?

A

Agonist actions of serotonin at other subtypes:

 Sexual dysfunction
 Insomnia
 Anxiety

+ desensitization over time

30
Q

MoA of NASA? Name one.

A

α2 adrenoceptor antagonist (NASA): Mianserin

1) Blocks α2 presynaptic autoreceptor (not transporter) (exam)
» remove negative feedback on presynaptic neuron
» enhances noradrenaline release

2) 5-HT2A antagonist

31
Q

ADR of NASA?

A

 Sedation  Dry mouth  Dizziness  Vertigo

32
Q

Classify MAOI (Monoamine oxidase inhibitor) anti-depressants? Give examples of each.

A

Non-selective MAOI:
 Phenelzine
 Tranylcypromine

Selective MAOAI:
 Moclobemide

33
Q

MoA of MAOI (Monoamine oxidase inhibitor)?

A

Inhibit monoamine oxidase: = decrease degradation enzyme of excessive serotonin, norepinephrine, dopamine

2 isoforms:

1) MAOA metabolizes 5-HT, noradrenaline, adrenaline, dopamine, tyramine
2) MAOB metabolizes dopamine, phenylethylamine, tyramine

> > MOAI Increase levels of all 3 major neurotransmitters in synaptic cleft

34
Q

Why is MAOI rarely used?

A

Potentially fatal interaction with certain food and drugs: cause hypertensive crisis, stroke, death

35
Q

Explain the interaction between MAOI and certain foods?

A

MAOI inhibit breakdown of tyramine from food (e.g. avocados, bananas, pineapple, eggplants)

> > accumulated tyramine cause increase release of stored monoamine neurotransmitters (e.g. dopamine, norepinephrine, epinephrine)

> > increases blood pressure and heart rate

> > hypertensive crisis

36
Q

Explain some D/D interactions of MAOI?

A

MAOI + serotonergic agent (SSRI / SNRI / TCA) may lead to serotonin syndrome (life-threatening):

Caused by overstimulation of 5-HT receptors in the brain, potentially lethal

37
Q

Guidelines on switching between MAOI and serotonergic agents?

A

Before starting MAOI, discontinue serotonergic antidepressants for at least 2 weeks

Fluoxetine has long half-life = discontinued for 4-5 weeks

Before starting a serotonergic agent, must discontinue MAOI for at least 2 weeks

38
Q

ADR of MAOI?

A

 Orthostatic hypotension
 Weight gain

 Insomnia, Restlessness
 Confusion

39
Q

MoA of Melatonin receptor agoinst?

A

Acts on:
 Melatonin receptor
 Serotonin receptor (5-HT2C receptors): Does not increase serotonin level, but increases concentrations of dopamine, norepinephrine in brain

40
Q

Name one melatonin receptor agoinst

A

Agomelatine (Valdoxan)

= synthetic melatonin

41
Q

What is the physiological function of melatonin?

A

important for regulating sleep

Released in response to darkness by the pineal gland:
Levels vary according to the circadian rhythm

In tune: helps us sleep and wake

Out of whack: disrupts energy, alertness, mood)

42
Q

ADR of melatonin receptor agonist?

A

Derangement in liver function

requires regular liver function monitoring

43
Q

Which serotonin receptors are acted on by SARI?

A

Serotonin antagonist-reuptake inhibitor (SARI)

Antagonist for 5-HT2A receptor while agonist for 5HT-1A receptor.

It also blocks serotonin reuptake transporter SERT.

44
Q

List some synmptoms of serotonin syndrome caused by MAOI?

A

Minor: Agitation, insomnia, nervousness, BP change, Diarrhea, Akathisia, Mydriasis …

Major: Coma, confusion, fever, tremors, rigidity …

MBBS II HNNS (57 decks)

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