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Pharmacology- Test 4 > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

Point prevalence of depression

A

At any point in time, 5-6% of the population is depressed

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2
Q

Lifetime prevalence of depression

A

10% of people may become depressed during their lives

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3
Q

How much of the population suffers from a specific form of effective disorder called Bipolar Disorder (Manic- Depressive Illness)?

A

1.2%

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4
Q

T/F Prevalence for depression in men is twice that of women, equal for bipolar disorder.

A

FALSE; women is TWICE that of men, equal for bipolar disorder

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5
Q

How many people do not get treatment for their depressive disease?

A

up to 2/3

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6
Q

How many patients typically respond to available treatments?

A

85% (70% to drugs, another 15% to ECT)

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7
Q

If left untreated, how many depressed adult patients commit suicide?

A

15-20%

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8
Q

What are other patterns of morbidity seen in depressed patients?

A

(1) Unemployment
(2) Divorce
(3) Alcoholism
(4) Financial ruin
etc. ..

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9
Q

Risk of depression increases if: (4)

A

(1) Family history of depression
(2) During postpartum period
(3) When patient is on certain drugs
(4) Undergoing anticipated stress

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10
Q

What is the criteria for Major Depressive Episode? (3)

A
  • Dysphoric mood, loss of interest or pleasure in all or most usual activities and pastimes that used to be pleasurable to them.
  • Symptoms cause significant distress or impairment in social, occupational, or other areas
  • Not due to general medical condition/substance use/not due to bereavement if loss of loved one occurred less than 2 months ago
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11
Q

(Major Depressive Episode) At least 5 of the following symptoms occurring nearly every day for at least 2 weeks: (8)

A

(1) Poor appetite or significant weight loss (change of more than 5% body weight in a month)
(2) Insomnia or hypersomnia
(3) Psychomotor agitation or retardation
(4) Decrease in sexual drive
(5) Fatigue or loss of energy
(6) Feelings of worthlessness, self reproach, or inappropriate guilt
(7) Diminished ability to think or concentrate
(8) Recurrent thoughts of death, or suicide, or suicide attempt

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12
Q

Tricyclic Antidepressants: Drugs

A

(1) Imipramine

(2) Amitryptiline

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13
Q

Why are there so many different types of drugs?

A

They are all equally effective and variously ineffective because they are dependent upon the person (all are the equally efficacious)

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14
Q

What are the 4 classes of Antidepressant drugs?

A

(1) Tricyclic Antidepressants
(2) Heterocyclic Antidepressants
(3) SSRIs
(4) Monoamine Oxidase Inhibitors (MAO)

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15
Q

Heteroyclic Antidepressants: Drugs

A

(1) Mirtazapine
(2) Venlafaxine
(3) Bupropion

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16
Q

Selective Serotonin Reuptake Inhibitors (SSRI): Drugs

A

(1) Fluoxetine
(2) Paroxetine
(3) Sertraline

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17
Q

Monoamine Oxidase (MAO) Inhibitors: Drugs

A

(1) Phenelzine

18
Q

Therapeutic Mechanism of Antidepressants

A

Antidepressants either block NE and/or serotonin (5HT) uptake by presynaptic nerve endings (tricyclics, heterocyclics, and SSRIs) or slow down the breakdown or such monoamines. Therefore, it has been hypothesized that increasing the synaptic concentrations of the biogenic amines NE and especially 5HT may be implicated in their mechanism of action.

However, while the pharmacological effects of antidepressants (i.e. inhibition of reuptake or breakdown) occur rapidly, there is a 2-3 week delay in therapeutic relief of depression.

19
Q

What is the biogenic amine hypothesis?

A

An examination of the several elements in the 5HT signaling pathways, has suggested the following sequence of events:

  • The 5HT1A receptors on presynaptic neurons act to inhibit the firing of serotogergic neurons. Additionally, both presynaptic alpha2 adenoreceptors and presynaptic 5-HT receptors act to inhibit the release of serotonin
  • Antidepressant drugs prolong the exposure of synaptic receptors to transmitter. However, initially the effects the transmitters on the receptors of the presynaptic cells provide negative feedback which opposes the increase in serotoneric tone.
  • After extended treatment, the inhibitory elements desensitize allowing the antidepressant drugs to have increased postsynaptic effects
20
Q

What have animal studies suggested as a model for depression? How?

A

Chronic stress; it produces long term elevation in corticosteroids which in turn has been shown to produce diminished synaptic plasticity and decreased hippocampal volume

21
Q

What do tricyclic antidepressants do?

A

block NE and 5-HT uptake

22
Q

What receptors do tricyclic antidepressants block? What do blocking these receptors cause?

A

(1) Muscarinic-cholinergic
(2) Histaminergic
(3) Alpha-1 adrenergic
- results in significant side effects including atropine-like symptoms of dry mouth, blurring vision, and constipation, hypotension, fatigue

23
Q

What happens if you give a tricyclic antidepressant to a patient with bipolar disorder?

A

Has been associated with switching into mania.

24
Q

What is the difference between Venlafaxine, Mirtazapine, and Bupropion? (what do they inhibit, side effects, receptor blocking)

A

(1) Venlafaxine inhibits NE and 5HT without blockade of the receptors seen in tricyclics. Side effects like SSRIs
(2) Mirtazapine enhances NT at serotonin receptors by blocking alpha-1 receptors and presynaptic serotonin receptors. Side efects like SSRIs but not nausea. May have anxiolytic properties
(3) Bupropoin is a monoamine uptake blocker (NE, 5HT, and DA). Special indication for smoking cessation

25
Q

What are SSRIs becoming increasingly utilized?

A

Because they inhibit reuptake of biogenic amines at the transporter in presynaptic membrane but they are SPECIFIC in blocking reuptake of 5HT.

26
Q

SSRIs: side effects

A

(1) Nausea
(2) Vomiting
(3) Headache
(4) sexual dysfunction

27
Q

T/F SSRIs inhibit cytochrome P-450 enzymes in liver

A

TRUE

28
Q

Which SSRI has the longest half life?

A

Floxetine

29
Q

What are MAO inhibitors used for? What do these enzymes do?

A
  • Reverse psychomotor retardation of depressed patients and also may increase the psychomotor activity to a hypomanic or manic state.
  • oxidatively deaminate monoamines including catecholamines, serotonin, and others like tyramine
30
Q

What are 5 negative things related to MAO inhibitors?

A

(1) Combining MAO with SSRI results in excess serotonin or “central serotonin syndrome” which can lead to hyperpyrexia, confusion, and death
(2) chronic toxicity includes hepatotoxicity, tremors, insomnia, and hyperhidrosis, convulsions
(3) interferes with metabolic degradation of variety of drugs
(4) potentiate CV effects which produces hypertensive crisis
(5) tyramine foods (cheeses, beer, wine, yeast, coffee, etc)

31
Q

Which two drugs are relatively free of the sexual dysfunction side effect?

A

(1) mirtazapie- works on pre-synpatic receptors
(2) bupropion- direct reinforcing effects
(common for many especially SSRIs)

32
Q

What is bipolar disorder? Name the elevated states.

A
  • Distinct period of persistently elevated or irritable mood for at least one week (following depressive episode)
  • gradiosity, decreased sleep, more talkative, racing thoughts, increased distractability, increased motor activity, excessive involvement in high risk activities
33
Q

What are the 3 mood stabilizers that are used in biploar disorder? Which two are anticonvulsants (starred)?

A

(1) Lithium
(2) Divalproex- for acute mania
(3) Carbamazapine

34
Q

Is schizophrenia classified as part of bipolar disorder?

A

NO

35
Q

T/F Administration of lithium results in dose dependent disruption of distal tubular secretion in the kidney manifesting in oligouria.

A

FALSE; disruption of distal tubular reabsorption manifesting in polyuria

36
Q

What is the pharmacology of lithium?

A
  1. Lithium is therapeutically effective in a relatively high concentration range of ≈1 mM. In this concentration range many brain systems may be affected.
  2. Some of the potentially most important effects of lithium have been noted on second messengers such as cAMP and intracellular calcium signaling through the phosphoinositide pathway and protein kinase C. These pathways regulate long-term changes in synaptic function (e.g. LTP or LTD).
  3. The permeability of lithium through sodium channels and synaptic ion channels (especially glutamate receptors) to may allow lithium to especially accumulate in active neurons.
37
Q

What is the therapeutic uses for lithium?

A

(1) lithium salts for recurrent episodes of mania/depression
(2) chronic use as prophylaxis
(3) acute treatment of manic phase and adjunct medication with antidepressants for depressive stage

38
Q

T/F Lithium has a low therapeutic index. Stating this, you need an adequate sodium intake to avoid lithium intoxication.

A

TRUE; low sodium diet and lithium is contraindicated

39
Q

What are other side effects and toxicity for anti-depressants?

A
  1. Orthostatic hypotension (all but SSRIs).
  2. Anticholinergic properties (Tricyclics and most hetrocyclics): dry mouth, blurred near vision, constipation, urinary hesitancy or retention; potentially confusion, agitation, delirium, and tachycardia in severe cases.
  3. Sedation due to H1 antagonism The tertiary amines are typically more sedating and anticholinergic than the secondary amines. Nortriptyline has the least of these side effects for the tricyclics.
  4. Cardiac toxicity: quinidine-like effect slowing intracardiac conduction (tricyclics).
  5. Risk of death with overdose.
  6. Generally need to monitor blood levels for therapeutic range.
40
Q

What additional potential applications for antidepressants are there? (13)

A
  1. Depression with psychotic features (combined with antipsychotic)
  2. During the depressed phase of Bipolar disorder (usually combined with mood stabilizer)
  3. Atypical depression (SSRIs or monoamine oxidase inhibitors)
  4. Panic disorder
  5. Bulimia
  6. Neuropathic pain (tricyclic drugs)
  7. Enuresis (Imipramine best studied)
  8. Obsessive-compulsive disorder (SSRIs and Clomipramine)
  9. Attention-deficit/hyperactivity disorder
  10. Cataplexy due to narcolepsy
  11. Dysthymia (chronic low grade depression)
  12. Organic mood disorders (caused by brain injury)
  13. Smoking cessation (Bupropion)

Pharmacology- Test 4 (11 decks)

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