Final Exam: Chapter 22 Mental Health Flashcards

1
Q

Serotonin-selective reuptake inhibitors (SSRIs)

A
  • prolong actions of released serotonin at their receptors by inhibiting reuptake
  • not immediate effects
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2
Q

Major depression predisposing factors

A
  • recent stress
  • family history (genetic)
  • –heritability accounts for 30-40% variance in risk
  • childhood neglect/abuse
  • –chronic/persistent depression
  • —epigenetic mechanisms
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3
Q

Major Depression type 1 (most common)

A
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)
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4
Q

Major Depression type 2

A

ATYPICAL

  • fatigue
  • variable hedonic responses
  • –mood reactivity
  • –variable motivation
  • Hypersomnia
  • Hyperphagia
  • –weight gain
  • HPA axis dysfunction (lowered central drive)
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5
Q

Diathesis-Stress Hypothesis

A
  • 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
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6
Q

Antidepressant drugs

A

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

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7
Q

Schizophrenia

A
  • selective cell death
  • less myelin
  • decreased synaptogenesis
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8
Q

Positive symptoms of schizophrenia

A

presence of abnormal thoughts and behavior

  • delusions
  • hallucinations
  • disorganized speech
  • grossly disorganized or catatonic behavior
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9
Q

Negative symptoms

A

Reflect absence of responses

  • reduced expression of emotion
  • poverty of speech
  • difficulty in initiating goal directed behavior
  • memory impairment
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10
Q

Neuroleptic drugs

A
  • block dopamine receptors (specifically D2)

- decrease positive symptoms

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11
Q

Dopamine Hypothesis of of Schizophrenia

A

-psychotic episodes in schizophrenia triggered by activation of dopamine receptors

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12
Q

Glutamate hypothesis

A
  • 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
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13
Q

Why is the brain so vulnerable to disease?

A
  • 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
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14
Q

Concussion pathophysiology

A
  • 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
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15
Q

Stroke

A

-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

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16
Q

Stroke type: Occlusive strokes

A

Blockage

  • embolism (artery partially or totally blocked by clot)
  • thrombus (accumulation of stuff on walls of veins)
17
Q

Stroke type: Hemorrhagic strokes

A

bleed

  • aneurysm (blood balloon bursts)
  • AVM (vessels crossed over)
  • Cerebral hemorrhage (hole in vessel)
18
Q

Types of strokes

A

Occlusive and Hemorrhagic

19
Q

Ischemia

A

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

20
Q

chromatolytic

A

sick neuron

21
Q

Subdural hemmhorage aka hematoma

A

venous bleeding between dura and arachnoid meninges covering the brain

22
Q

Brain tumors

A
  • astrocytoma (not malignant, most common)

- Glioblastoma (GMB): most aggressive brain tumor because glial cells are hard to kill

23
Q

Alzheimer’s bio

A

B-amyloid cascaid hypoth, see diagram

24
Q

Possible ways to recover function after brain injury

A
  • chromatolytic neurons recover
  • adjustment in synaptic strength of neighboring axons (compensating for injury)
  • learned adjustments of behavior
25
Q

Spinal cord/long distance growth and connectivity

A
  • 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
26
Q

Components of regeneration

A
  • possible in PNS
  • never in CNS
    1. sprouting
    2. axonal elongation
    3. synapse formation
27
Q

Why brain “grows”

A
  • 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