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Pharmacology III > Depression > Flashcards

Depression Flashcards

1
Q

What is the most common diagnosis associated with psychiatric admission?

A

Depression

One-half of the people that commit suicide have major depression

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2
Q

Are most patients with depression treated?

A

Less than half of depressions are treated

Not seeking care, not getting the right tx

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3
Q

What is the presentation of depressive symptoms?

A
  • Some patients look sad, guilt-ridden, and hopeless
  • Other patients look nervous, and irritable
  • Others complain of somatic problems
  • Psychosis can accompany depression
  • Depression can lead to a dementia-like state
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4
Q

What is more than 2 years of depressed mood of loss of interest but not severe enough to meet MDD?

A

Dysthymia

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5
Q

What is the criteria for major depression?

A 
Five (or more) of the following sx present for a 2-week period:
Depressed mood*
Decrease interest* or pleasure
Change in weight/appetite
Insomnia or hypersomnia
Loss of energy 
Feeling of worthlessness or inappropriate guilt
Decreased concentration
Recurrent thoughts of death
Psychomotor agitation or retardation

*1 of 5 MUST be depressed mood and/or decreased interest

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6
Q

What is Mnemonic depression?

A

SIG E CAPS

S leep disturbance
I nterest loss
G uilt
E nergy loss
C oncentration difficulties
A ppetite disturbance
P sychomotor retardation/ agitation
S uicidality
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7
Q

What are the CV angents/AntiHTN medications that induce depression?

A 
Digitalis products
Clonidine
Methyldopa
Reserpine
Hydralazine
Propranolol
Prazosin
Procainamide
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8
Q

What are the Misc. Agent medications that induce depression?

A

Disulfiram

Antineoplastic agents

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9
Q

What are the CNS medications that induce depression?

A 
Amantadine
L-dopa
Barbiturates
Chloral Hydrate
Haloperidol/Phenothiazines
Alcohol
Amphetamine withdrawal
Alpha interferon
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10
Q

What are the hormones medications that induce depression?

A

Corticosteroids

Progesterone

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11
Q

What are the major CNS causes of depression?

A

Stroke
Alzheimers Disease
MS
Huntington’s Disease

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12
Q

What are the major Endocrine causes of depression?

A

HYPOTHYROIDISM
Cushing’s/Addison’s diseases
Diabetes

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13
Q

What are the major autoimmune causes of depression?

A

RA

Systemic Lupus erthematosis

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14
Q

What are the major cardiovascular causes of depression?

A

Post-MI

CHF

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15
Q

What are the major other causes of depression?

A 
Malignancies
ID
Malnutrition
Narcolepsy
Sleep apnea
Pancreatic disease
Metabolic disturbances
Chronic Pain
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16
Q

What is the pathophysiology of depression?

A

Unknown at present
Genetic predisposition: 40-50% familial linked
Dysregulation of hippocampus and hypothalamic-pituitary-adrenal (HPA) axis
Monoamine hypothesis (DA, NE, 5-HT)
These are how all the meds used to treat depression work so this is incredibly supportive.
Impairment of neurotropic factors (eg., BDNF)
Impairment of brain reward pathways (role of subcortical pathways)
Goes along with monoamine hypothesis.

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17
Q

In the monoamine hypothesis what does depression result from dysregulation of what?

A

Norepinephrine (NE)
Serotonin (5-HT)
Dopamine (DA)

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18
Q

What happens post-synaptic 5-HT, DA, and NE receptors when the amount of these neurotransmitters is decreased?

A

Up-regulation of post-synaptic receptors
Decreased receptor sensitivity
Altered genetic expression

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19
Q

What happens when reserpine is administered for the monoamine hypothesis?

A

Reserpine
Induces depression depletion of monoamines
Depression is reversed by the 5-HT precursor and (less well) by the NE precursor

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20
Q

What is the monoamine hypothesis?

A

Low 5-HT and/or NE in limbic system leads to depression

Increased limbic 5-HT and/or NE can reverse depression

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21
Q

What is involved in the dysregulation of HPA axis?

A 
Hyperactive HPA Axis
Increased CRF
Blunted cortisol supression
May lead to hippocampal toxicity
Increased glucocorticoids may result from severe stress
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22
Q

How does dysregulation of HPA axis work?

A

Hippocampus has negative feedback on the HPA loop
Glucocorticoids trigger this negative feedback

Sustained elevation of glucocorticoids  seen in prolonged and severe stress
Damage the hippocampal neurons
Reduces the negative feedback  “Snowball” effect

Abnormal excessive activation of HPA axis seen in 50% of depressed patients
Corrected with antidepressant treatment

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23
Q

What is a potent regulator of plasticity of adult neurons and glia which is important for survival of neurons?

A

Brain Derived Neurotropic Factor (BDNF)

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24
Q

What is BDNFs role?

A

Acute and chronic stress decreases expression of BDNF
Deficits are seen in hippocampal region of brain in depressed patients
These deficits are alleviated by antidepressant treatment

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25
Q

What is the effect of depression on the hippocampus?

A

Possibly responsible for cognitive symptoms of depression

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26
Q

What is the effect of depression on the nucleus accumbens & Amygdala?

A

Dopaminergic pathway

Deficits may lead to amotivation and anhedonia

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27
Q

What is the effect of depression on the hypothalamus?

A

Mediates numerous functions ie., sleep, appetite, circadian rhythms, interest in sex

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28
Q

What is the goal of Major depressive disorder (MDD)?

A

Reduce the acute symptoms of the depressive episode
Facilitate the patient’s return to premorbid function (prior to illness)
Recovery should be the rule, not the exception!
Prevent further episodes of depression

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29
Q

What are the treatment options for MDD?

A

Selective Serotonin Reuptake Inhibitors (SSRIs)
Tricyclic Antidepressants (TCAs)- anticholinergic SE and are less tolerated.
Bupropion
Venlafaxine
Nefazodone
Mirtazepine
Duloxetine
Monoamine Oxidase Inhibitors (MAOIs)- mainly for PD
Newer agents

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30
Q

What are the selective serotonin reuptake inhibitors (SSRIs)?

A 
Fluoxetine (Prozac)	
Sertraline (Zoloft)
Paroxetine 
Fluvoxamine
Citalpram (Celexa)
Escitalopram (Lexapro)
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31
Q

What is the most commonly prescribed antidepressant?

A

SSRIs

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32
Q

SSRI (fluoxetine, sertraline, paroxetine, fluvoxamine, citalpram, escitalopram)- MOA

A

MOA: Block the reuptake of serotonin

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33
Q

Which is the SSRIs has the longest half life?

A

Fluoxetine

You can stop this abruptly unlike other SSRIs

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34
Q

SSRI (fluoxetine, sertraline, paroxetine, fluvoxamine, citalpram, escitalopram)- Side effects

A 
Nausea
Headache
Sleep disturbances- usually resolved if taking in the morning. 
Changes in weight
Agitation/increased anxiety (initial)- occurs initially
Sexual Dysfunction
Tremor
Sweating
Rare hyponatremia- rarely see this
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35
Q

Which SSRI is more likely to cause sedation, constipation and dry mouth?

A

Paroxetine

36
Q

Does paroxetine CR have less GI side effects that paroxetine IR?

A

Yes

37
Q

Which SSRI is more likely to have GI distress, insomnia, or activation?

A

Sertraline

38
Q

What is the order for risk of discontinuation syndrome from highest to lowest?

A

Paroxetine > sertraline = citalopram = escitalopram > fluoxetine

39
Q

What is involved with antidepressant discontinuation syndrome?

A
  • Flu-like symptoms, malaise
  • Dizziness
  • GI (nausea, diarrhea)
  • Transient changes in mood, affect, appetite, and sleep
  • Electric “shock-like” sensation in upper extremities
  • Vivid dreams/nightmares
  • Poor concentration
40
Q

What are the TCA’s used in depression?

A 
Nortiptyline
Despramine
Protriptyline
Amoxapine
Amitriptyline
Imipramine
Clomipramine
Doxepin
41
Q

What are the secondary amine TCAS?

A

Nortiptyline
Despramine
Protriptyline
Amoxapine

42
Q

What are the tertiary amine TCAs?

A

Amitriptyline
Imipramine
Clomipramine
Doxepin

43
Q

TCA (Nortiptyline, Despramine, Protriptyline, Amoxapine, Amitriptyline, Imipramine, Clomipramine, Doxepin)- MOA

A

Block the reuptake of NE and 5-HT (NE > 5-HT)

44
Q

What TCAs do you need to monitor drug levels?

A

Nortipyline
Despramine
Draw blood sample 12 hours past the last dose

45
Q

TCA (Nortiptyline, Despramine, Protriptyline, Amoxapine, Amitriptyline, Imipramine, Clomipramine, Doxepin)- Side effects

A

Tachycardia
Orthostasis
Weight gain
Sedation
Sexual dysfunction
Anticholinergic effects–Dry mouth, Constipation, Dry eyes, Urinary retention
Cardiac conduction changes– Prolongation of QRS, ST depression, flattened or inverted T waves (Baseline ECG)

46
Q

What side effects are greater in tertiary amine TCAs than in secondary amine TCAs?

A

Anticholinergic effects
Antihistamine effects
Hypotensive effects

47
Q

Mirtazapine (Remeron)- MOA

A

Dual neurotransmitter action:
A potent and direct alpha-2 receptor antagonist
Enhances 5-HT and NE transmission
Blocks 5-HT2 and 3 receptors
Results in enhances 5-HT1 reception
Efficacy comparable to standard antidepressants for the treatment of long and short term depression

48
Q

What is seen less often in mirtazapine as opposed to SSRIs?

A

Less nausea and less sexual dysfunction

49
Q

Mirtazapine- Indications

A

Depression

Comparable efficacy as SSRIS

50
Q

Mirtazapine- pharmacokinetics

A

Dosed once daily at bedtime due to sedation

Soltab (dissolvable tablet) used for patients with default swallowing

51
Q

Mirtazapine- Side effects

A
  • Somnolence (increased risk at lower doses)
  • Dry mouth
  • Constipation
  • Orthostasis
  • Increased appetite->weight gain
52
Q

Venlafaxine (Effexor)- MOA

A

Inhibits reuptake of NE and 5-HT

53
Q

Venlafaxine (Effexor)- side effects

A 
Nausea
Headache
Somnolence
Sexual dysfunction
Insomnia 
Agitation
Increase in DBP (diastolic blood pressure)
	(dose related- if needing to increase too much might need to change patient med)
54
Q

Desvenlafaxine (Pristiq)- MOA

A

Active metabolite for venlafaxine No mechanistic advantage

SHOULD NOT CHOOSE THIS AS AN EXAM ANSWER

55
Q

Should pristiq be chosen as a correct answer on the exam?

A

NO!!!

56
Q

Duloxetine (Cymbalta)- MOA

A

Potent 5-HT NE reuptake inhibitor

57
Q

What else is duloxetine used for besides treating depression?

A

Urinary incontinence and diabetic neuropathic pain

58
Q

Duloxetine (Cymbalta)- Side effects

A 
Insomnia/sedation
NAUSEA, diarrhea, decreased appetite
Sexual dysfunction
Sweating
Urinary hesitancy
Hepatotoxicity- not a huge SE but might want to get AST and ALT
Increase in BP
59
Q

Bupropion (Wellbutrin)- MOA

A

Believed to block reuptake of dopamine and norepinephrine

60
Q

What is considered first line agent for depression?

A

Bupropion along with SSRIs

61
Q

What else can bupropion be used for?

A

Smoking cessation

62
Q

Bupropion (Wellbutrin)- Side effects

A

-Anxiety, agitation
-Headache
-Seizures– Increased risk with higher doses
sweating
-Tremor
-Insomnia
-GI disturbances (anorexia, nausea, constipation)
-Weight loss

63
Q

Nefazodone (Serzone)- MOA

A

Serotonin reuptake inhibitor plus potent 5-HT2 receptor antagonist
Enhanced 5-HT1 neurotransmission through 5-HT2 blockade

64
Q

Nefazodone (Serzone)- indications

A
  • Comparable efficacy for the treatment of depression as standard antidepressants
  • Considered a 2nd or 3rd line agent because of hepatotoxicity risk
  • Associated with improvement in symptoms of poor sleep quality, sleep disturbance, anxiety and agitation in depressed patients
65
Q

Nefazodone (Serzone)- Side effects

A 
Sedation
Orthostasis
Dry mouth
Nausea
Increased appetite
Blurred vision
HEPATOTOXICITY
66
Q

Trazodone (Desyrel)- MOA

A

Blocks 5-HT2A receptors (potently); Blocks 5-HT reuptake less potently
Also has antihistaminic properties → Sedation

67
Q

Monoamine OxidaseInhibitors (MAOIs)- MOA

A

Block the break down of NE, 5-HT, DA, and epinephrine

68
Q

What are the MOA-As?

A 
Epinephrine
Norepinephrine
5-HT (Serotonin)
Dopamine
Tyramine
69
Q

What are the MOA-Bs?

A

Dopamine
Tyramine
benzylamine
phenylethylamine

**NOT USED FOR DEPRESSION

70
Q

What are the mixed irreversible MAOIs?

A

Irreversible: phenelzine, isocarboxazid,

71
Q

What are the mixed reversible MAOIs?

A

Reversible: tranylcypromine

72
Q

Transdermal selegiline

A

Irreversible inhibitor of MAO-B; inhibits A and B in higher doses (>10 mg/day)
Available as a patch 6 mg, 9 mg, and 12 mg

73
Q

MAOIs- side effects

A

Not used as often due to drug-drug and dug-food interactions–Aged, hard cheeses and strongly flavored cheeses contraindicated

SE: orthostasis, dizziness, mydriasis, piloerection, edema, sexual dysfunction, insomnia, weight gain

High risk of serotonin syndrome– Especially when combined with selective serotonin receptor agonists.

High risk of hypertensive crisis

74
Q

MAOIs- Drug interactions

A
  • Other antidepressant medications, including herbals
  • Buspirone
  • Meperidine
  • Dextromethorphan
  • Direct sympathomimetics (e.g., -L-dopa, epinephrine, isoproterenol, norepinephrine)
  • Indirect sympathomimetics (e.g., amphetamines, methylphenidate, phenylpropanolamine, ephedra, pseudoephedrine and tyramine)
  • Cocaine
75
Q

What is an adverse effect due to excessive serotonin in the periphery?

A

Serotonin Syndrome (Toxicity)

76
Q

What are the sx of serotonin syndrome?

A

Neuromuscular hyperactivity
Tremor, myoclonus, hyperreflexia, restlessness

Autonomic hyperactivity
Hyperpyrexia, hypertension, tachycardia

Cognitive/behavioral changes
confusion

77
Q

All antidepressants are considered _______ in efficacy for uncomplicated, unipolar depression?

A

Equal

78
Q

Pharmacotherapy choices for depression should be based on what?

A 
Past response to a medication
Other psychiatric or medical co-morbidity
Potential for drug interaction(s)
Safety
Patient preference
Cost
Family member response to a medication
79
Q

How long does it take for a patient to respond to antidepressents?

A

Most responders will have an onset of response within 4 weeks

80
Q

If there is no response to antidepressants by 4 weeks what should happen?

A

No response at 4 weeks, consider ↑ in dose and waiting another 2-3 weeks

81
Q

If there is no response or minimal response to antidepressants by 8 weeks what should be done?

A

Patients showing minimal to no response should not exceed a trial of 8 weeks

82
Q

Do you need to taper antidepressants?

A

ALL SSRIS, EXCEPT FLX, SHOULD BE TAPERED BEFORE DISCONTINUATION OR WITHIN CLASS SWITCH

83
Q

What are the two ways to switch antidepressants?

A

Can either overlap, taper first drug, and titrate second, or…

Discontinue first drug and start second drug

84
Q

SSRI- BLACK BOX WARNING

A

SUICIDE
There may be an increased risk of suicide with SSRIs in children and adolescents
Also an increase in geriatric patients

BUT…
Suicide rates in teens have decreased with increased use of SSRIs
In all clinical trials, no suicide was committed
“Negative” trial does not mean placebo was better
Is it the drug or the disease?
Be cautious and determine risk vs. benefit

85
Q

What is considered first line for depression for geriatric patients?

A

SSRIs are considered first-line (tolerability)
NEF, BUP, and VLFX XR also options
TCAs–Generally problematic due to SE profile, DESI and NORT recommended if required

86
Q

What anti-depressive drugs that should be used in pregnancy/lactation?

A

SSRIs or TCAs

FLX most studied of the SSRIs

Pharmacology III (19 decks)

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