Final Exam: Chapter 22 Mental Health Flashcards
Serotonin-selective reuptake inhibitors (SSRIs)
- prolong actions of released serotonin at their receptors by inhibiting reuptake
- not immediate effects
Major depression predisposing factors
- recent stress
- family history (genetic)
- –heritability accounts for 30-40% variance in risk
- childhood neglect/abuse
- –chronic/persistent depression
- —epigenetic mechanisms
Major Depression type 1 (most common)
MELANCHOLIA -Anergia -Stable anhedonia: ---stable down mood ---very low motivation -Insomnia -Anorexia ---weight loss -HPA axis dysfunction (central drive inc, CRH ACTH and cortisol inc, no feedback inhibition GR)
Major Depression type 2
ATYPICAL
- fatigue
- variable hedonic responses
- –mood reactivity
- –variable motivation
- Hypersomnia
- Hyperphagia
- –weight gain
- HPA axis dysfunction (lowered central drive)
Diathesis-Stress Hypothesis
- diathesis=predisposition
- HPA axis is where genetic and environmental influences converge to cause mood disorders
- Normally, activation of hippocampal glucocorticoid receptors leads to feedback inhibition of HPA axis
- But in depressed patients,
- -> increase in adrenal glucocorticoid release
- –>decreases BDNF levels
- ->feedback disrupted, HPA function is hyperactive
- Antidepressants increase serotonin and norepinephrine,
- ->decrease glucocorticoid levels
- –>increase BDNF
Antidepressant drugs
Elevate levels of monoamine neurotransmitters in brain
1. Tricyclic compounds (ie imipramine)
-block reuptake of both norepinephrine and serotonin by transporters
2. SSRIs (ie fluoxetine)
-same as Tricyclic but act only on serotonin terminals
3. NE and 5-HT-selective reuptake inhibitors
(ie venlafaxine)
4. MAO inhibitors (ie phenelzine)
-reduce enzymatic degradation of serotonin and monoamine neurotransmitters
Schizophrenia
- selective cell death
- less myelin
- decreased synaptogenesis
Positive symptoms of schizophrenia
presence of abnormal thoughts and behavior
- delusions
- hallucinations
- disorganized speech
- grossly disorganized or catatonic behavior
Negative symptoms
Reflect absence of responses
- reduced expression of emotion
- poverty of speech
- difficulty in initiating goal directed behavior
- memory impairment
Neuroleptic drugs
- block dopamine receptors (specifically D2)
- decrease positive symptoms
Dopamine Hypothesis of of Schizophrenia
-psychotic episodes in schizophrenia triggered by activation of dopamine receptors
Glutamate hypothesis
- schiz reflects diminished activation of NMDA receptors in brain
- PCP blocks NMDA receptors, producing positive and negative symptoms
- Atypical neuroleptics/antipsychotics (like clozapine) enhance transmission through channel
- agents enhancing Glu activity improves symptoms of SZ
- agents that reduce Glu activity (PCP/Ketamine) worsen symptoms
Why is the brain so vulnerable to disease?
- post-mitotic: no new cell division of neurons
- non homogeneous organ; articulate organ: no silent region (4 arteries are thin walled, one smooth muscle cell layer)
- unique blood supply
- physical location
Concussion pathophysiology
- stretch+shearing of axonal membranes
- ion K+ flows out
- Increase in extracellular K+
- As Ek approaches 0, consciousness lost
- Blood supply reduced 50%
- ->less blood/oxygen, less ATP for pumps and depolarization
- ->Glu released from depolarized/dying neuron
Stroke
-lack of blood flow to the brain caused by a clot or rupture of blood vessel
-80% strokes are preventable
-FAST: face, arm, speech, time
Factors:
-hypertension (high blood pressure)
-smoking
-estrogen contraceptives
-age
-high cholesterol
-obesity
-sleep apnea
-head trauma
-high salt
-migrane
Stroke type: Occlusive strokes
Blockage
- embolism (artery partially or totally blocked by clot)
- thrombus (accumulation of stuff on walls of veins)
Stroke type: Hemorrhagic strokes
bleed
- aneurysm (blood balloon bursts)
- AVM (vessels crossed over)
- Cerebral hemorrhage (hole in vessel)
Types of strokes
Occlusive and Hemorrhagic
Ischemia
When embolism occurs and brain tissue irrigated by that artery is deprived of oxygen
-Infarct = dead neurons
-ischemia/penumbra=surrounding damaged neurons
Secondary effect: edema (swelling) explains why partial return of function eventually because neurons go back online when swelling goes down
Treatment: NMDA blockers to prevent spread of exotoxicity
chromatolytic
sick neuron
Subdural hemmhorage aka hematoma
venous bleeding between dura and arachnoid meninges covering the brain
Brain tumors
- astrocytoma (not malignant, most common)
- Glioblastoma (GMB): most aggressive brain tumor because glial cells are hard to kill
Alzheimer’s bio
B-amyloid cascaid hypoth, see diagram
Possible ways to recover function after brain injury
- chromatolytic neurons recover
- adjustment in synaptic strength of neighboring axons (compensating for injury)
- learned adjustments of behavior
Spinal cord/long distance growth and connectivity
- neural stem cells after severe spinal cord injury
- neurotrophic growth factors cause neuron to grow and be heathy or die
- injecting substances to block “nogo” receptors (equivalet of “slit” but released by oligos, causes axon to try to get away from receptor) promotes axonal growth after injury
Components of regeneration
- possible in PNS
- never in CNS
1. sprouting
2. axonal elongation
3. synapse formation
Why brain “grows”
- division and growth of glial cells
- myelination
- elongation of axons
- dev of dendritic arborizations
- dramatic increase in number of spines on dendrites (shaped by sensory experience)
- explosive increase in number of synapses
