BAB 2a Flashcards
What is the most important classification distinction for a mood disorder?
unipolar vs. bipolar
Are reactive or endogenous depressions more severe?
Endogenous
Epidemiology of depression.
Lifetime prevalence: 6% (more in women)
Age of Onset: 20-50 (peak in mid-20s)
Is Major Depressive Disorder heritable?
No linkage studies have been adequately accepted, but family, twin and adoption studies suggest mood disorders have a genetic basis.
What is the diurnal variation of depression?
worse in the morning, better as the day progresses.
What are the cognitive changes in depression?
- slowed thoughts, preoccupation, poor attention, can be confused for “dementia” in the elderly
- negativistic thoughts, helplessnes, hopelessness
- suicidality
What are: a. Cognitive Theory of Depression, and b. Learned Helplessness Paradigm
a. Cognitive Theory: all or none… “I failed the test, now I won’t be a doctor and won’t have kids.”
b. Learned Helplessness: the dogs that didn’t jump over the hurdle
What are some physical signs of depression?
a. obvious ones… poor eye contact, somatic complaints, decreased sex drive, fatigue, anorgasmia
b. agitation, retardation and crying spells
c. anorexia
d. insomnia
What are the effects on sleeping?
a. decreased sleep efficiency, frequent wakings
b. shorter REM latency
c. increased REM
d. reduced slow wave delta sleep
e. partial sleep deprivation can temporariy induce remission
How does depression commonly start? As depression resolves, what improves first?
Start: “wet” phase
Resolve: sleep, appetite grooming and activity improve first. Mood resolves last.
What is a “response” when treating depression?
a 50% improvement in symptoms.
What are some morbidities associated with depression?
Up: CVD, MI, risk of illness
Down: immune system, bone density
What is dysthymia?
A non-episodic, chronic depression that is less severe and begins insidiously, often in adolescence, and persists for at least 2 years.
What are the likely sites for the following:
a. negative thinking
b. mood reactivity
c. psychomotor activity
d. sleep disturbances
e. circadian rhythms
a. negative thinking: prefrontal, hippocampus, limbic
b. mood reactivity: hypothalamus, nucleus accumbens, thalamus amygdala
c. psychomotor activity: connection of prefrontal, thalamus and basal ganglia
d. sleep disturbances: thalamic dyreg, pons and medulla
e. circadian rhythms: suprachiasmatic nucleus of ant. hypothalamus
How long does it take antidepressants to work? What is the response rate?
a. 3-6 weeks
b. 60% initial, 90% after readjusting meds
What are the 4 vessels of the brain? Which one is protected and why?
a. ant. cerebral
b. post. cerebral
c. int. carotid
d. vertebral
Vertebral is protect bc it supplies the brainstem which is important for breathing, BP, HR, etc.
What percent of CO does the brain get? How is distribution managed?
15%
Distribution is managed by each organ demanding it’s supply, -eg exercise = muscles get more blood.
What happens when BP goes down in the brain? What is the MAP buffering zone?
When BP goes down, cerebral arteries dilate.
MAP buffering zone: ~60mmHg - ~14-mmHg
What are the early effects of glutatmate receptor activation? Aka- early effects of cerebral cell death?
a. Ca++ enters the cell
b. DNA is damaged
c. mitos are killed
d. structural breakdown
Why is glutamate released?
cell death from a stroke
What are delayed effects of cerebral cell death?
a. new genes are transcribed
b. heat shock proteins are released
c. cytokines are released
d. neuts come… then macs and astrogliosis (BBB is damaged)
What the difference between apoptosis and necrosis?
apopotosis: active process, low intensity insults, less damage to surrounding areas (penumbra).
necrosis: passive process, high intensity insults, lots of inflammatory response and damage to surrounding areas (core of stroke).
What is the order of events in an ischemic brain injury? (Means of protection)
mins: energy failure, core (thrombolysis)
hours: Glu/Ca++ released, second messenger mediation (Glu/Ca++ antagonists)
more hours: reactive O2 species (free radical scavengers)
days: inflammation and apoptosis, mediated by gene expression (anti-inflammatory and anti-apoptotic agents, growth factors and promoters of plasticity)
What does tPA do?
Busts clots.
What is a generalized seizure?
affects both cerebral hemispheres from the beginning of the seizure.
What is a myoclonic seizure?
Subtype of generalized, bilateral jerk of the body, ver short, consciousness is not impaired.
What is a tonic-clonic?
Subtype of generalized, lasts >2mins, loss of consciousness and post-seizure confusion.
- tonic: stiffening and fall, ictal cry (air forced thru vocal cords)
- clonic: rhythmic, bilateral extremity jerking
What type of seizure can you see in JME?
myoclonic
tonic-clonic