Psychiatric Disorders Flashcards
Positive Symptoms of Schizophrenia
Delusions-thoughts not real
Hallucinations-sensory ex. Not real
Inappropriate affect-an emotional resp not approp
Incoherent speech or thoughts
Negative Symptoms of Schizophrenia
Affective flattening-flat emotions
Alogia – reduction or absence of speech
Avolition - reduction or absence of motivation
Anhedonia – inability to experience pleasure
These will increase likelihood of schizo
Birth complications, early infections, stress, autoimmune reactions, toxins, traumatic brain injury—when combined with the right genes may result in schiz
Chlorpromazine
&
Reserpine
Treats positive symptoms of Schizophrenia
All of these drugs decreased dopamine
side effects similiar to Parkinsons
Dopamine Theory of Schizophrenia
chlorpromazine and reserpine reduced brain dopamine levels
schizophrenia is associated with excessive activity in the dopaminergic systems in the brain
reduction of dopamine was alleviating schizophrenia symptoms
Reserpine was known to be a dopamine …
antagonist
it depleted the brain of dopamine by causing them to leak from their vesicles
Stimulants w/ regarding dopamine theory
agonist of dopamine (increase levels of dopamine)
trigger schizophrenic episodes in healthy subjects at high doses
ex:cocaine psychosis
amphetamine psychosis
Chlorpromazine’s job is….
it blocks dopamine receptors and dopamine levels are the same….just not receiving dopamine
Revised Dopamine theory
schizophrenia caused by excess activity at D2 receptors
thus schizophrenia is alleviated by drugs that block activity at D2 receptors
drug haloperidol binds to D2 only; while chlorpromazine binds to both D1 and D2
Evidence that Serotonin plays a role in schizophrenia
Clozapine - binds poorly to D2 receptors yet binds to serotonin receptors
suggest that serotonin receptors may be involved in schizophrenia
Why does it take several weeks for neuroleptics to work?
The therapeutic effect of blockade is mediated by neural adaptation (slow compensatory changes) to the blockade of dopamine receptors, rather than by the blockade itself
cortical abnormalities of schizophrenia are most prevalent in the …
small cerebral cortices and large ventricles
prefrontal (organization of thoughts)
cingulate (important for emotion)
temporal (auditory stimui) cortices
Is Schizophrenia a Neurodevelopmental disorder?
no
No obvious ongoing degeneration in the brain of schizophrenic patients
Why are neuroleptics effective against only some of the symptoms of schizophrenia
positive symptoms
Because positive symptoms are caused by excess D2 activity and are helped
Negative symptoms are due to permanent brain damage and cannot be helped
Probability of suffering from clinical depression during one’s lifetime
10%
Reactive Depression
stress from negative experience (someone passing away)
endogenous depression
no apparent external triggers (comes from within)likely depressed throughout life
SAD – Seasonal Affective Disorder
Triggered by reduction of sunlight
Winter or northern regions
Light therapy reduces symptoms
no drugs needed, fairly easy to treat
Postpartum Depression
Follow 10% of deliveries
Lasts at least 1 month; usu. No longer than 3 months
Drugs that treat depression
Monamine Oxidase Inhibitors (MAOI) not perscribed anymore
Tricyclic Antidepressants
Drugs that treat Bipolar
Lithium –metallic ion
Treats mania without increasing depression
stabilizes mood
What do
Monamine Oxidase Inhibitors (MAOI)
do?
increase level of monoamines which are norepinephrine (NE) and serotonin (5-HT)
agonistic - stop activity of enzymes that break down monoamine NT in the presynaptic cell
Tricyclic Antidepressants
agonistic
block the reuptake of both 5-HT and NE
Selective serotonin-reuptake inhibitors (SSRIs)
Prozac, Paxil, Xoloft, Luvox, Remeron
Selective norepinephrine-reuptake inhibitors (SNRIs)
Reboxetine
Lithium
Used to treat bipolar disorder
Treats mania without increasing depression
Mood stablizer
Diathesis - Stress Theory of Depression
individual inherits a diathesis (genetic predisposition) for depression
if the individual is stressed early in life their systems become altered so that they are hypersensitive to stress the rest of their lives
60% concordance rate
Monoamine Theory of Depression
Depression may be due to underactivity at 5-HT and NE synapses (serotonin & norenephrine)
Since lack of monoamines, there are now more receptors in order to receive anything
Treatment of Depression with Brain Stimulation
Stimulation of anterior cingulate gyrus you will see decreased depression
used for patients that have tried everything
Anxiety
chronic fear that persists in the absence of any direct threat
Anxiety disorder
anxiety so severe it disrupts normal functioning
Most prevalent of all psychiatric disorders
anxiety disorder
Generalized anxiety disorders
occur in the absence of any obvious precipitating events
Panic disorders
– rapid-onset anxiety attacks
Obsessive-Compulsive Disorders (OCD)
– frequent, reoccurring, uncontrollable, anxiety-producing thoughts (obsessions) and impulses (compulsions)
Posttraumatic Stress Disorder (PTSD)
after exposure to extreme stress
Benzodiazepines - e.g. Libriuim and Valium
used to treat anxiety disorders
Thought to be mediated by agonistic action on GABAA receptors
Also used as hypnotics, anticonvulsants and muscle relaxants
Adverse side effects: sedation, ataxia, tremor, nausea,
Withdrawal lead to anxiety rebound
Buspirone
- effective
- A serotonin agonist
– agonists effect for 5-HT1A (serotonin) receptor
Antianxiety effects without ataxia, muscle relaxation, or sedation
Side effects – nausea, dizziness, headache, insomnia
Relationship between Anxiety and Depression
Comorbidity – tend to occur together in the same individual
Antidepressants often work with anxiety disorders
Anxiolytics often work with depression
Anxiety disorders and the brain
deficits in GABAergic and 5-HT transmission
Low GABA (inhibit) and low serotonin
Over activity of amygdala and Anterior cingulate
Tourette Syndrome
Tics – involuntary, repetitive, stereotyped movements or vocalizations
0.7 % of population
More males than females
Tourette Syndrome has a high comorbity rate with which disorders
ADHD and OCD
Barriers to studying Tourette syndrome
No strong animal model
No strong link to gene
No postmortums – pts. grow out of it
the brain on tourette syndrome
Smaller caudate nuclei (part of basal ganglia, imp for motor movement)
Suppression of tics - increased activity in prefrontal cortex (suppresses caudate nuclei)
thinning of sensorimotor cortex, esp. areas associated with face, mouth and larynx
telling someone with tourette syndrome to stop results in…
increased tics
Treatment for tourette syndrome
Neuroleptics – Dopamine receptor blockers (similiar to schizo)
Can reduce tics by 70%
