mental illness Flashcards
(31 cards)
what is the difference between neurological disorders and psychiatric disorders?
neurological
- nervous system disorders
psychiatric
- disorders affecting mind/phsyche
what is comorbidity?
if diagnosed with one illness, there is an increased risk of being diagnosed with another
what is are anxiety disorders?
- inappropriate expression of fear
- encompasses generalized anxiety disorders, OCD, phobias and more
- most common psychiatric disorder
what are symptoms of anxiety?
- increased vigilance
- sympatheic response
- HPA axis activation
how is anxiety treated?
- benzodiazepines
- SSRIs
- cognitive behavioral therapy
- tricyclic antidepressants
what do benzodiazepines do?
- have an immediate response
- activate GABA channels, but can be addictive
- ethanol also binds to these channels
what do SSRIs so?
- have a delayed response
- therapeutic effect may instead be bs nervous system adapts to chronically elevated brain serotonin
what does cognitive behavioral therapy do?
- delayed response
- experience dependent plasticity to rewire learned responses
what do tricyclic antidepressants do?
block serotonin and NE reuptake
- delayed response (weeks)
- experience-dependent plasticity
what is cortisol?
what does it do?
a glucocortorid
- increases blood concentration of glucose
what is HPA regulated by?
amygdala
what is the amygdala involved in?
emotional and stress response
amygdala controls our stress response in stressful and potentially dangerous situations
what does too much activity in the amygdala do?
cause anxiety
what does the hippocampus do?
inhibits HPA axis
what are the types of affective disorders?
- major depressive disorder and bipolar disorder
- mood disorders
- may have genetic component
- somewhat more common in women than men
what are symptoms of major depressive order?
No longer responds to surroundings but persists in a state of low mood or inability to feel joy (“anhedonia”)
■ Sleep (too much or too little)
■ Weight/appetite (might eat too much or not enough, lose or gain weight)
■ Self-esteem (sense of worthlessness, guilt)
○ Depressive episodes can come and go but major depression only diagnosed when symptoms have been present for 2 weeks
major depressive disorder treatments?
Antidepressants:
a. MAO inhibitors ⇒ blocks enzyme that breaks down NE & 5-HT b. Tricyclics ⇒ block reuptake of NE and 5-HT
c. SSRIs ⇒ block reuptake of 5-HT only (more precise)
2. CBT
3. Ketamine
4. Electroconvulsive Therapy (ECT)
- Very effective in altering mood
- Immediate effect, specific reservations
5. Stimulations:
a. Deep Brain Stimulation in ventral caudate nucleus
b. Vagus Nerve Stimulation: interaction of viscera-brain, can help with
symptoms, also for seizures
c. TMS: reversibly stimulate or depress cortical areas lying just below the
skull
what contributes to mood disorders?
- dysfunction of monoamine systems
- HPA axis
- anterior cingulate cortex
- gonadal hormones and stress
describe dysfunction of monoamine systems?
Dysfunction can happen at multiple possible levels: Synthesis, release, reuptake, breakdown, receptors, 2nd messenger systems
describe treatment for monoamine systems?
○ Treatment: drugs that potentiate monoamine systems (MAOIs, tricyclics, SSRIs)
■ MAO inhibitor: Inhibits monoamine oxidase (enzyme that breaks 5-HT and
NE)
■ Tricyclic antidepressants: Inhibit reuptake of 5-HT and NE from cleft
■ SSRIs (Fluoxetine/Prozac): more precise b/c affects reuptake of 5-HT
preferentially
○ BUT takes several weeks to have effects → mood disorder therapies probably
promote long-term adaptive changes in the brain
how might the HPA axis contribute to mood disorders
Depression increases cortisol release and adrenal gland size, and CRH can induce
depression-like symptoms
○ May explain comorbidity with anxiety b/c HPA axis affects both
○ Diathesis-stress hypothesis of affective disorders: genetic predisposition for an
illness (diathesis) compound with stressful events and conditions (stress)
■ Genes and early childhood experiences influence the number of HPPC
cortisol receptors
how is the anterior cingulate cortex contribute to mood disorders?
- increased resting-state metabolic activity in depressed patients
- connects frontal cortex, hippocampus, amygdala, hypothalamus, and brainstem
- may link our internally-generated emotional state and the HPA axis
how might gonadadal hormones and stress contribute to mood disorders?
puberty: estrogen levels are usually higher
- estrogen may modulate mood systems
menopause: estrogen levels drop
- associated with decreased severity and frequency of depressive events
describe bipolar disorder?
unusual shifts in mood, energy, activity levels, and ability to carry out day-to-day tasks
- people can cycle between feeling normal, deperession, hypomanic and manic
