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Spring Pharm > Anti-Depressants, Mood Stabilizers & Anxiolytics > Flashcards

Anti-Depressants, Mood Stabilizers & Anxiolytics Flashcards

1
Q

Depression definition

A

Biogenic amine hypothesis –> depression is caused by a deficiency of monoamines, particularly NE & 5HT
Receptor sensitivity hypothesis –> post-synaptic neuron tries to compensate for a lack of stimulation & deficiency of NE & 5HT & takes up all the NTs leading none for other neurons

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2
Q

Depression Treatment Focus

A
  • Block action of MAO
  • Block re-uptake of monoamines so they’re more readily available for other neurons & down regulation of the
  • Desensitization of super-sensitized/upregulated neurons
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3
Q

Lag period

A

Time between starting the medication & obtaining full symptom relief; believed to occur as a result of down regulation

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4
Q

Down regulation

A

Reducing stimulation at the post-receptor (post-synaptic) site; cell is less sensitive to the neurotransmitter

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5
Q

Guidelines for Antidepressant use

A
  • start low & go slow –> too fast & they’re more likely to have adverse effects
  • Many have “lag period”
  • Most SE’s occur in 1-2 weeks or upon dose changes
  • Suicide risk increases with energy level –> black box warning; it takes a while to increase up to the desired baseline so during the process they are still in a depressed state with potential suicidal thoughts while the meds give them increased energy which could increase the likelihood to act on those thoughts
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6
Q

Antidepressant medication selection

A
  • target symptoms
  • side effect profile (ie. giving a med with lethargy side effects to someone who has sleeping problems may be beneficial)
  • Medical illness/other medications
  • Relative’s response/genetics (ie. if patient’s mom did well on med, patient might too)
  • Suicide risk (ie. how fatal the med is if overdose occurs)
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7
Q

Tricyclics Antidepressants (TCAs)

A

MOA –> inhibits reuptake of NE & 5HT, and intermediary neurochemical events and/or changes occur over time
-have varying affinity for cholinergic, adrenergic, histamine & DA receptors
Monitoring –> need to titrate/taper down the medication when stopping the med, need a baseline ECG & follow-ups, draw plasma levels

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8
Q

TCAs Adverse Effects

A
  • Hypotension
  • Anticholinergic effects
  • Sedation (possibly a good thing if patient needs help sleeping)
  • Diaphoresis
  • Cardiotoxicity –> arrhythmias
  • Seizures –> med decreases seizure threshold
  • Hypomania –> less severe form of mania (affects patients with bipolar)
  • Yawngasm
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9
Q

TCAs Interactions & Toxicity

A

Interactions: CNS depressants, anticholinergics, sympathomimetics, MAOIs
Toxicity: cadiotoxic (direct & indirect effects), anticholinergic symptoms (agitation, confusion, seizures, coma)

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10
Q

TCAs Patient Education

A

Measures to minimize adverse effects of orthostatic hypotension (stand up slowly), anticholinergic effects (drink water), hazards of sedation & other (report suicidality & chest pain)
Measures to minimize adverse interactions: avoid anticholinergic drugs, CNS depressants

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11
Q

Monoamine Oxidase

A

Enzyme present in monoamine-containing neurons that converts monoamine transmitters into active products (ie. MAO-A & MAO-B) which work to breakdown NTs; inactivates NE & 5HT after reuptake

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12
Q

Monoamine Oxidase Inhibitors (MAOI)

A

MOA –> prevent the inactivation of NE & 5HT, allowing for increased amounts of transmitters to be released
-result in irreversible inhibition (10-14 days) meaning recovery requires new synthesis of the enzyme

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13
Q

MAOI Drug Interactions

A

Decreasing MAO in the liver results in a decrease in metabolism of other drugs (can lead to toxic levels of other meds)

  • Anesthetics
  • Narcotics
  • Antidepressants
  • Sympathomimetics
  • Cocaine
  • Anti-hypertensives
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14
Q

MAOI Food Interactions

A

Interacts with TYRAMINE (occurs naturally in food & is degraded by MAO) and causes a Hypertensive Crisis

  • foods that have aged & have to be ripened before being eaten
  • Examples: avocado, bananas, liver, caffeine, cheese, papaya, pickled herring, raisins, soy sauce, sour cream, yogurt
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15
Q

Hypertensive Crisis

A

Sudden severe increase in BP

  • puts patient at risk for intracranial hemorrhage
  • Warning signs: throbbing occipital headache, rtetroorbital pain, stiff neck, apprehension, nausea, chils/fever, pallor, sweating, flushing of skin, palpitations, chest pain
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16
Q

MAOI Patient Education

A

Measures to minimize adverse effects: HTN crisis, orthostatic hypotension, food education
Measures to minimize adverse interactions: MANY drug-drug interactions; use only one pharmacy to ensure no interactions occur

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17
Q

SSRI Pharmacokinetics

A
  • highly bound to plasma proteins
  • extensive hepatic metabolism with resulting active metabolites
  • prolonged half-life –> steady state plasma levels in about 4 weeks
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18
Q

Fluoxetine

A

Selective Serotonin Reuptake Inhibitors
MOA –> inhibition of 5HT reuptake which results in increased availability & intensified transmission t post-synaptic site (active changes occur in response to prolonged uptake blockade)

19
Q

SSRI Side Effects

A

-Suicidality
-Nervousness, insomnia, anxiety –> occurs when the dose is increased too quickly
-Headache
-Nausea
-Potential weight gain of weight loss (Fluoxetine)
-Sexual dysfunction
-Activation of mania/hypomania (esp. in people with bipolar)
-Skin rashes –> possible SJS
-Bruxism –> teeth grinding
-Risk for platelet dysfunction –> increased risk of bleeding, hemorrhage
-Risk of hyponatremia
Interactions: antidepressants & protein-binding meds

20
Q

SSRI Withdrawal (Discontinuation)

A
  • occurs abruptly & can persist for a few hours to a few weeks
  • severity depends on duration of med use, dosage & half-life
  • GI –> GI upset, flu-like symptoms
  • Neuro –> headache
  • Somatic –> “I feel off,” generalized pain
  • Psychological –> anxiety & irritability
21
Q

Serotonin Syndrome

A

-may begin within minutes to hours after initiation of any medication that increases serotonin levels (or taking too many serotonergic meds-ie. St Johns Wart)
Mild –> restlessness, diaphoresis & increased HR, myoclonus (spasm)
Moderate –> agitation & decreased LOC, HTN, shivering, hyperthermia, rigidity
Severe –> coma, shock, tonic-clonic seizures

22
Q

SSRI Patient Education

A

Measures to minimize adverse effects: sexual dysfunction, caloric intake, hazards of dizziness/fatigue, signs of bruxism
Measures to minimize adverse interactions: avoid other serotonergic meds, NSAIDS & anticoagulants

23
Q

Venlafaxine

A

SNRI (serotonin-norepinephrine reuptake inhibitor)

-does not block cholinergic, histaminergic or alpha1-adrenergic receptors

24
Q

Venlafaxine Side Effects

A

Common Side effects –> headache, anorexia, insomnia, discontinuation/withdrawal
Less common side effects –> serotonin syndrome, NMS, HTN, bleeding, increase in serum lipids, activation of mania

25
Q

Buproprion

A

NDRI (NE & DA reuptake inhibitor)

  • contraindicated ind anyone with purging or restricting eating disorder (decreases the seizure threshold)
  • adverse effect: seizures
26
Q

Trazadone

A

SSRI & 5HT2 antagonist

  • usually used for sleep treatment
  • sedating side effects are usually too severe to reach therapeutic levels for depression treatment
  • adverse effect: Priapism
27
Q

Mitrazepine

A

NaSSA (noradrenergic & specific serotoniergic antidepressant)
-adverse effects: very sedating, increases appetite

28
Q

Problems with Antidepressant Treatment

A
  • Inadequate dosing –> dose too low to reach therapeutic level
  • discontinuation of drug prior to full recovery –> take drug for an additional year after symptoms have stopped & then re-evaluate
  • lack of tapering when discontinued
  • treatment resistance requiring antidepressant combo. therapies and/or augmentation with additional meds
29
Q

Adjunct Depression Meds

A

Benzodiazepines –> decrease anxiety, agitation & irritability (used short term)
Mood Stabilizers –> control of labile, erratic mood
Antipsychotics –> used as adjunct for depression symptoms & in severe cases of depression depression with psychotic symptoms

30
Q

Mood Stabilizers

A
  • relieve symptoms during manic & depressive episodes of BPAD
  • prevent recurrence of manic & depressive episodes of BPAD
  • relieve & prevent recurrence of labile mood in non-BPAD disorders
31
Q

Lithium

A

Mood Stabilizer
MOA –> alters distribution of neuron important ions (Na), modulation of synaptic transmissions (stabilizes electrical activity of neurons), influences second messenger systems that are excitatory (decreases neuronal activity)
Pharm –> rapidly metabolized & excreted by the kidneys
-Na depletion causes accumulation of lithium in the kidneys, which crystalizes
-dehydration causes retention

32
Q

Therapeutic Plasma Levels of Lithium

A

Therapeutic levels: 0.6-1.2 mEq/L (possibly up to 1.5 for acute manic phases)
Intoxication: 1.5-1.9 (marked tremor, nausea & diarrhea, blurred vision)
Life threatening toxicity: 2.0 or > (neurotoxicity, delirium & encephalopathy)

33
Q

Lithium Adverse Effects

A

Early –> transient; headache, GI, muscle weakness, fatigue, confusion
General –> mild/fine tremor, goiter/hypothyroidism, weight gain, ECG changes (K+ or sinus dysrhythmias), renal toxicity, fetal effects (cardiac defect affecting tricuspid valve & RV of heart)
Persistent –> polyuria, polydipsia, leukocytosis

34
Q

Lithium Side Effects Acronym

A 
Leukocytes
Increased
Tremors
Hypothyroid
Increased
Urine
Mom's to be
35
Q

Assessment prior to Starting Lithium

A
  • Health status
  • Renal function
  • Thyroid function
  • CBC (leukocyte levels)
  • Electrolytes (Na & K levels)
  • Baseline ECG (cardiac status)
36
Q

Lithium Toxicity

A

Early indications –> thirst & polyuria, lethargy, slurred speech, muscle twitching, fine tremor
Most common indications –> N/V, diarrhea
Progressive S/S –> anuria/oliguria, confusion, impaired LOC, poor coordination, frank twitching, seizures, blurred vision, tinnitus, coma & death

37
Q

Lithium toxicity treatment

A 
Mild-moderate toxicity (1.5-2): hold medication, check levels & re-evaluate the damage
Severe toxicity (>2): top medication, increase excretion (method depends on time elapsed since ingestion) via emetic, lavage, meds (kayexelate, golytely, renal dialysis)
38
Q

Lithium Monitoring & Dosing

A

Monitoring –> check lithium levels 5 days after initiation or dose change, then every 6 months; after 6 months also check CBC, electrolytes, renal & thyroid functions
Dosing –> individualized to plans levels; 300mg TID/QID (max = 1200mg - most people titrate up to 900mg, check a level & adjust as needed)

39
Q

Lithium Interactions

A
  • Diuretics: thiazide & loop (increase Li+ levels), osmotic & K+ sparing (decrease Li+ levels)
  • Anticholinergic meds
  • NSAIDS (can increase Li+ levels)
  • Theophylline
  • Muscle relaxants used during anesthesia
  • SSRIs
40
Q

Valproic Acid

A

Mood stabilizing med - anticonvulsant
MOA –> suppresses Na+ channels, suppresses Ca2+ influx, increases GABA effects, may inhibit glutamante/NMDA receptor-mediated neuronal excitation
Adverse reactions –> hepatotoxicity, pancreatitis, PCOS, possbile SJS, stomach upset (need to take with food), increase liver enzymes

41
Q

Alprazolam

A

Benzodiazepine
MOA –> bind to specific receptor sites in GABA receptor-channel complex & enhance/amplify actions of GABA (increase the GABA receptor’s affinity for GABA)
Distribution –> high lipid solubility
Metabolism –> extensive alteration
Advantages –> rapid onset, well-tolerated, few drug-drug interaction, little effect of cardiovascular system, generics available at lower cost

42
Q

Benzodiazepine adverse effects

A
  • CNS depression (increased lethargy)
  • respiratory depression
  • anterograde amnesia
  • tolerance, dependence, toxicity & abuse
  • readily cross the placenta & enter breast milk
43
Q

Buspirone

A

Anti-anxiety agent
MOA –> not sure; binds with high affinity to 5HT receptors and lower affinity to DA receptors
-better absorbed when taken with food
-lag time to peak effectiveness: 3-6 weeks
Adverse effects –> dizziness, nausea, headache, nervousness, excitement

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