Mood Disorders: Depression and Bipolar Flashcards
(46 cards)
Reactive sadness
Transient emotional reaction to a minor event
Grief
Normal response to a major interpresonal loss, can be prolonged
Clinical Depression
Persistent sadness that interferes with normal functioning
* loss of interest
* Low-self esteem
What are the signs and symptoms of depression?
- Persistent sad, anxious, or “empty” feelings
- Feelings of hopelessness or pessimism
- Feelings of guilt, worthlessness, or helplessness
- Irritability, restlessness
- Loss of interest in activities or hobbies once pleasurable
- Fatigue and decreased energy
- Difficulty concentrating, remembering details, and making decision
- Insomnia, early-morning wakefulness, or excessive sleeping
- Overeating, or appetite loss
- Thoughts of suicide, suicide attempts
- Aches or pains, headaches, cramps, or digestive problems that do not ease even with treatment
What are the risk factors for depression?
- Female (particularly in adolescence, post-partum, and in older age)
- Prior depressive episodes
- Medical comorbidity
- Substance use disorder
- Lack of social support
- Stress
What are the DSM-V criteria for depression?
- Must have 5 or more symptoms in same 2 week period
- Must include depressed mood and/or anhedonia
- Must represent change from previous functioning
- Cause social or occupational impairment
- Not be due to an organic disorder or other cause
What is a manic episode?
Consists of a persistent elevated or irritable mood that is extreme, which lasts for at least one week
* And at least three (four if only irritable mood) other features are also involved:
- Inflated self-esteem for sleep
- Decreased need for sleep
- More talkative than usual or compelled to keep talking
- Experiencing racing thoughts or ideas
- Easily distracted
- Increase in goal-oriented activity or excessive movements
- Excessive involvement in potentially risky pleasurable behavior
Monoamine hypothesis
Decreased synaptic concentrations of monoamines results in sustained depression
Dysregulation hypothesis
Dysregulation of neurotransmission release results in changes in pre- and post- synaptic receptors, which ultimately result in sustained depression
Neuroendocrine hypothesis
Dysregulation of thyroid and HPA axis result in sustained depression
What were the findings of depressed patients that support the monoamine deficiency hypothesis?
- Relapse of depression with tyrosine hydroxylase inhibitors or depletion of dietary tryptophan
- Increase mutation in the brain specific form of tryptophan hydroxylase (TPH-2)
- Increase MOA ligand binding
- Subsensitive 5-HT1A receptors
- Malfunction in 5-HT1B receptors
- Polymorphisms of the serotonin-reuptake transporter
- Inadequate response of G proteins to monoaminergic signals
- Decrease levels of cAMP, inositol and CREB in postmortem brains
What are the findings in depressed patients that support the endocrine hypothesis?
- Cortisol level are sometimes increased in severe depression; non-suppression of cortisol by dexamethasone (dexamethasone suppression test. DST), reversed by antidepressants
- Size of anterior pituitary, adrenal cortex is increased
- CRH levels in CSF and CRH expression in the limbic brain regions are increased
- Hippocampal size and numbers of neurons and glia decrease (due to decrease BDNF?)
What are the general mechanism of increasing neurotransmission including increasing the “synpatic residence time”?
- Blocking the reuptake of NE, 5-HT, and DA into nerve terminals (reuptake inhibitors)
- Blocking the metabolism of NE and 5-HT in nerve terminals (monoamine oxidase inhibitors)
What is the onset of therapeutic?
- Week 1 – sleep, appetite, energy, anxiety
- Weeks 1-3 – activity, drive, concentration, memory
- Weeks 4-6 – mood, hopelessness
What is an adequate trial of antidepressant?
Approximately 6-8 weeks
Name the class of antidepressants
- TCAs
- MAOIs
- SSRIs
- SNRI
- NDRI
- 5-HT and/or NE modulators
What are the disvantages of tricyclic antidepressants?
- Toxic in overdose
- Side effects
What are the side effects of tricyclic depressants?
- Orthostatic hypotension
- Tachycardia
- EEG changes
- Anticholinergic effects
- Seizure threshold lowered
- Weight gain
T/F: Tricyclic are not stimulants
T
What are the mechanism of action of tricylic depressants?
- Block reuptake of monoamines (both NE and 5-HT) to varying degrees
- Neurotransmitter levels in the synaptic cleft increase, but clinical effect are delayed around 2-3 weeks
- Also bind to histamine (H1 & H2), alpha 1 & 2, GABA-A, and muscurinic receptors, which accounts for many side effects
What are the pharmacokinetics of tricylic depressants?
- Well absorbed orally and have long half-lives. Highly protein-bound
- Cause sedation–dose at. bedtime
- Drug inactivation by hepatic metabolism
T/F: Tricyclic depressants used to be the first most common cause of overdose fatalities in developed countries
F; second
Why aren’t tricyclic depressant not first line?
Anticholinergic and cardiac side effects
What is the mechanism of MAOIs?
- Increase neurotransmission by increasing NE, 5-HT, and DA levels in nerve terminal
- Inhibition of MAOIs is irreversible
