Antidepressants Flashcards
(41 cards)
Major Depressive Disorder
Depression with Psychotic Features
Depression NOS
Depression with Seasonal Pattern
Dysthymia
Obsessive Compulsive Disorder
Panic Disorder
Social Anxiety Disorder/Social Phobia
Generalized Anxiety Disorder
Post-Traumatic Stress Disorder
Bulimia Nervosa
Smoking Cessation
Insomnia
Fibromyalgia
Pain Management
Migraine Headaches
Antidepressant Indications:
Also known as the Biogenic Amine Theory of Depression
Depression is thought to be caused be a deficiency of norepinephrine (NE) and/or serotonin (5HT)
Monoamine Neurotransmitter Dysfunction
Biogenic amines or mono amines -are Norepinephrine, dopamine and serotonin
Deficiencies in __ and ____ may be a result of:
1. Enzyme breakdown of NE and 5 HT - Monoamine oxidase breaks NE/5HT down to be recycled or restored within the neuron
2. Rapid fire of neurons - Rapid fire of the neurons may lead to NE/5HT depletion
3. Upregulation - The # or sensitivity of postsynaptic receptors may increase therefore depleting the NE/5HT levels. (also called upregulation)
NE; 5 HT
is the enzymes that catalyzes the breakdown of monoamines such as serotonin, dopamine, and norepinephrine
Monoamine oxidase
Tricyclic Antidepressants (TCA’s)
Monoamine Oxidase Inhibitors (MAOI’s)
FIRST GENERATION
Selective Serotonin Reuptake Inhibitors
Serotonin and Norepinephrine Reuptake Inhibitors
Atypical Antidepressants
SECOND GENERATION
TCA’s all reduce the reuptake of 5HT and NE into nerves
This leads to an accumulation of NE and 5HT in the presynaptic cleft
This also leads to increased stimulation of the postsynaptic receptors
TCAs also block dopamine, acetylcholine (cholinergic) and histamine receptors
Tricyclic Antidepressants (TCA’s)
Non-selective
TCA’s all reduce the uptake of 5HT and NE into nerves
This leads to an accumulation of NE and 5 HT in the presynaptic cleft
This also leads to increased stimulation of the postsynaptic receptors
TCAs also block dopamine, acetylcholine (cholinergic) and histamine receptors
Tricyclic Antidepressants (TCA)
Inhibit Monoamine oxidase (MAO)
Allows accumulation of NE, 5 HT and dopamine in the synaptic cleft and the neuronal storage vesicles of the presynaptic neuron
Monoamine Oxidase Inhibitors
Specifically block 5HT with little to no effect on NE
Increase the levels of 5HT in the synaptic cleft
Less adverse effects than TCAs and MAOIs
Prototype: fluoxetine (Prozac)
Selective Serotonin Reuptake Inhibitors
Prevent the reuptake of 5HT and NE
Also, weakly inhibit Dopamine reuptake
This leads to accumulation of 5HT, NE and Dopamine in the Synaptic Cleft
Selective Serotonin Norepinephrine
Reuptake Inhibitors (SSNRI/SNRI)
used as a sleep aid – ______
trazadone
ABSORPTION
GI Tract
DISTRIBUTION
Widely distributed through the body
METABOLISM
Liver
EXCRETION
Kidneys
Cross Placenta and enter breast milk
Antidepressants ADME
*MAOIs are not trialed until two other chemical classes have failed
*First drug is tapered off while second one is started in most cases
*MAOI and RIMA need a 2 week wash out period
Considerations in Dosing for Antidepressants
*Sexual side effects
SSRI
*Sexual side effects
*Hyponatremia (SIADH)
*Palpitations
*Increased blood pressure
SSNRI
*Drowsiness, dizziness, headache, sedation
*Constipation, dry mouth, sweating
*GI upset
*Serotonin Syndrome
*Antidepressant Discontinuation Syndrome (except fluoxetine)
ALL ANTI-DEPRESSANTS
If stopped suddenly, the following symptoms can occur:
Flu like symptoms
Emotional lability
Dysesthesia (electric shock sensations)
Vivid dreams/nightmares
Impaired concentration and confusion
Anxiety and agitation
Tremor
Dizziness
Risk of seizure
(not prozac - long half life)
Antidepressant Discontinuation Syndrome
Cause: excessive serotonin in the synaptic cleft, caused by:
combining medications that increase CNS serotonin levels
Severe cases:
Hyperthermia, seizures, rhabdomyolysis
Serotonin Syndrome
Risk Factors:
Recent start or increase of medication known to increase serotonin levels
Polypharmacy with more than one drug that increases serotonin (including herbal medication and illicit drugs)
Serotonin Syndrome
Prevention and Treatment:
1. Provide person-centred education
2. Assess all medications, supplements, foods and recreational drugs
3. Discontinue all substances that may be the causative factors
4. Treat the symptoms either inpatient or outpatient dependent on severity.
- Muscle relaxants and/or medications to control pulse and blood pressure
- Serotonin Blocking Agents (cyproheptadine)
- IV and O2
Serotonin Syndrome
Signs and Symptoms: Hyperreflexia, tremors, myoclonus, diaphoresis, confusion, agitation
Lab Findings: Non specific
Cause: Increased serotonin
Onset: Minutes to Hours
Fever: Moderate
Hyperreflexia: Moderate
Myoclonus: Moderate
Muscle Rigidity: Moderate
Serotonin Syndrome
Signs and Symptoms: Severe muscle rigidity, diaphoresis, delirium, fluctuating BP, tachycardia, EPS
Lab Findings: Elevated CPK and leukocytosis (high white blood cell)
Cause: Blockade of dopamine receptors OR abrupt withdrawal of a dopamine agonist
Onset: Days to Weeks
Fever: High
Hyperreflexia: Rare
Myoclonus: Rare
Muscle Rigidity: High
Neuroleptic Malignant Syndrome
Lethal doses of TCAs are close to accepted dose range
Overdose risk is high
Death may result from: hypotension, uncontrollable seizures and or cardiac arrhythmia
TCAs should NOT be prescribed for any clients at risk of suicide or a history of suicidal ideation
TCAs and Suicidal Ideation
