Depression Flashcards
(56 cards)
Mood disorder that has high worldwide prevalence.
Wide range of severity of symptoms (mild -> disabling)
Depression
DSM-IV diagnosis
presence of 2 or more symptoms affecting energy level, sleep, appetite, self-esteem, concentration, and decision making
Major Depression Symptoms
low mood
loss of interest, motivation, libido
feeling of helplessness/hopelessness
sleep disturbance
suicidal thoughts
eating disturbance
pessimism
depression and suicide
8th leading cause of death in adults
2nd in 15-29
3rd in children 5-14
increased risk of other diseases
Reduced CV health (MI)
Ostreoporosis, PUD, DM
Increased Cortisol levels
Chronicity of disease
depression persists without appropriate treatment
Common features of all depressive disorder classifications
Sadness, emptiness, or irritable mood accompanied by somatic and cognitive changes that significantly affect the individual’s capacity to function
2 major categories of depression
Major Depressive Disorder
Dysthymic
Symptoms for 2 or more weeks (sadness, emptiness, irritable)
Mild chronic depression
Presence of more depressive moments than not for at least 2 YEARS and persistence of the depression for longer than 2 MONTHS
Dysthymic Disorder
diagnosis can be challenging since there are no
biologic markers
Multifactorial including _____, ______, ______, and _____ factors
genetic, social, lifestyle, environmental
Etiology: Factors leading to higher rates of depression
- First-degree relatives
- many diseases and disorders
- life events and hassles
- environmental factors (violence, abuse, neglect, poverty)
- traumatic events
Pathophysiology of depression
exact pathogenesis not completely understood
- monoamine hypothesis
- receptor downregulation, sensitivity changes
- neuroplasticity hypothesis
deficiency or imbalance of monoamines (serotonin, NE, dopamine)
Limiting reuptake of NTs appears to reduce depression symptoms
- TCS, SSRI’s, SNRI’s reduce reuptake
- MAOI’s inhibit monoamine breakdown
monoamine hypothesis
secondary adaptive changes
may explain why it takes weeks for drugs to show clinical changes in pts
receptor downregulation, sensitivity changes
neurohistological changes lead to a disorder of the hardwiring of the brain
antidepressants reverse structural and functional consequences of stress in hippocampus and prefrontal cortex
neuroplasticity hypothesis
D: Pharmacological Treatment
Antidepressant meds (SSRI + TCA)
- effective for mod-severs but are not 1st line of treatment for mild cases
- shouldn’t be used for children
D: non-pharmacological/ psychosocial therapy
- effective in mild w/o med
- uses with med in mod-severe
includes:
- cognitive behavior therapy (CBT)
- problem solving therapy (PST)
- exercise
- socialization
Antidepressant MOA
Block reuptake of serotonin or NE
- excess NT accumulates in synaptic cleft
- downregulation of receptors (relief)
Desensitization of autoreceptors
- autoreceptors act as “shut-off” switch when there is excess NT
- drug desensitization of these receptors blocks their action = continued NT release
Enhancement of NE release
- increases serotonergic cell firing
- elevated NT concentration leads to downregulation of receptors
Accumulation of high levels of serotonin, usually via therapeutic use of serotonergic drugs
variable symptoms from mild to life threatening
Serotonin Syndrome
Mild SS symptoms
HTN
Tachycardia
Mydriasis
Diaphoresis
Shivering
Tremor
Myoclonus
Hyperreflexia; usually afebrile
Mod SS symptoms
all mild plus hyperthermia-104, hypereactive bowels, mild agitation