Anti-depressants Flashcards
What are the symptoms of MDD?
- Depressed mood most of the day, nearly every day, as indicated by either subjective report, or observation made by others.
- Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day.
- Significant weight loss when not dieting or weight gain, or decrease or increase in appetite nearly every day.
- Insomnia or hypersomnia nearly every day.
- Psychomotor agitation or retardation nearly every day (observable by others,
feelings of restlessness or being slowed down). - Fatigue or loss of energy nearly every day.
- Feelings of worthlessness or excessive or inappropriate guilt nearly every day
(not merely self-reproach or guilt about being sick). - Diminished ability to think or concentrate, or indecisiveness, nearly every day.
- Recurrent thoughts of death
How many symptoms, and for how long do they need to be present, in order for MDD to be diagnosed?
5 or more symptoms (1 - depressed mood- or 2- loss of interest- must be present) in a two-week period.
How many symptoms, and for how long do they need to be present, in order for dysthymia to be diagnosed?
Symptoms must be present for at least two years.
Why is it not adequate to explain that anti-depressants work by raising nt levels?
Medications rapidly increase neurotransmitter levels, but the antidepressant action has a slow-onset.
What is the focus of one current theory of how anti-depressants work?
Current theories focus on the long term effects of antidepressants on second messenger systems
What are the two functions of second messenger systems?
Neuron protection from damage due to injury or trauma. AND Promote and maintain the health and stability of newly formed neurons.
What are the current thoughts about why anti-depressants work the way they do? And what are its 4 main points?
Current thought centers on the neurogenic theory. 1. Existing neurons can repair and remodel 2. The brain can make new neurons 3. Depression is associated with the damage and loss of neurons 4. Depression is associated with the failure to make new neurons.
Where, in the brain, is neurogenesis critical in understanding depression? What do they do? Why are they critical?
The frontal cortex and the Hippocampus which influences attention, concentration and memory. It is sensitive to trauma including stress.
How are anti-depressants thought to work?
Antidepressants increase neurogenesis.
What evidence supports the neurogenesis theory of how anti-depressants work?
The timing of neurogenesis and net neuron gains in response to antidepressant drugs fits with the time frame of therapeutic response in patients (unlike neurotransmitter levels).
How could neurotransmitters play a role in depression?
Thought to exert affects on gene expression that alter neurogenesis and neuroprotection.
How does inadequate activity of serotonin and NE play a role in depression?
Inadequate neurotransmitter activity for serotonin and/ or NE is thought to lead to less CREB and BDNF activity in individual suffering depression.
What is BDNF thought to be involved in? Why is it thought to be the key?
- BDNF affects the normal development and health of the nervous system. 2. Chronic stress decreases the production of BDNF. 3. BDNF is decreased in blood levels in depressed patients (reversed with antidepressants).
What is the model for anti-depressant medications and stress?
Idea that depression is a consequence of stress. Antidepressants act at a cellular level to reverse stress-induced damage.
What are 2 other theories on the pathophysiology of depression?
- Depression is caused by deficits in monoamine neurotransmitters (serotonin, norepinephrine, dopamine). 2. Depression is caused by disruption of the hypothalamus-pituitary-endocrine hormone axis. 3. Combination of both.
What were the earliest anti-depressants?
(1960s) Tricyclic Antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs).
What does light therapy target? What light are they missing?
Within the photoreceptor cells is the photopigment: Melanopsin. They are missing blue light.
How do TCAs and MAOIs help depression?
By increasing the levels of norepinephrine and serotonin in the brain.
What kind of drug is Imipramine (Tofrenil)
It is a TCA.
What are 2 ways in which TCAs work? (what is their mechanism of action?)
- Inhibit presynaptic norepinephrine and serotonin reuptake transporters. 2. Inhibit postsynaptic histamine, acetylcholine and several other receptors
What kind of drug is Doxepin?
A TCA
What kind of side effect do TCAs have? (3 main effects).
Anticholinergic activity can lead to confusion, memory and cognitive impairment, dry mouth, blurred vision, increased heart rate, and urinary retention. Antihistaminic activity can cause drowsiness and sedation. Antiadrenergic effects can cause postural hypotension. Cardiac effects like arrythmias. Excitement and convulsions. Respiratory depression and coma.
What does Anticholinergic mean?
inhibiting the physiological action of acetylcholine, especially as a neurotransmitter.
What does Antihistaminic mean?
A drug or other compound that inhibits the physiological effects of histamine, used especially in the treatment of allergies.
What side effects can Anticholinergic activity lead to?
Anticholinergic activity can lead to 1. confusion, 2. memory and 3. cognitive impairment, 4. dry mouth, 5. blurred vision, 6. increased heart rate, and 7. urinary retention.
What side effects result from antihistamine activity?
Antihistaminic activity can cause drowsiness and sedation.
What kind of side effects do Antiadrenergic effects result in?
Antiadrenergic effects can cause 1. postural hypotension. 2. Cardiac effects like arrhythmias. 3. Excitement and convulsions. 4. Respiratory depression and 5. coma.
What are the mechanisms of action for MAOIs?
MAO-A metabolizes dopamine, is inhibited by MAOIs, causing build-ups of those nts. MAO-B metabolizes dopamine.
