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Psychiatric Disorders Flashcards

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1
Q

Positive Symptoms of Schizophrenia

A

Delusions-thoughts not real

Hallucinations-sensory ex. Not real

Inappropriate affect-an emotional resp not approp

Incoherent speech or thoughts

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2
Q

Negative Symptoms of Schizophrenia

A

Affective flattening-flat emotions

Alogia – reduction or absence of speech

Avolition - reduction or absence of motivation

Anhedonia – inability to experience pleasure

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3
Q

These will increase likelihood of schizo

A

Birth complications, early infections, stress, autoimmune reactions, toxins, traumatic brain injury—when combined with the right genes may result in schiz

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4
Q

Chlorpromazine
&
Reserpine

A

Treats positive symptoms of Schizophrenia

All of these drugs decreased dopamine

side effects similiar to Parkinsons

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5
Q

Dopamine Theory of Schizophrenia

A

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

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6
Q

Reserpine was known to be a dopamine …

A

antagonist

it depleted the brain of dopamine by causing them to leak from their vesicles

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7
Q

Stimulants w/ regarding dopamine theory

A

agonist of dopamine (increase levels of dopamine)

trigger schizophrenic episodes in healthy subjects at high doses

ex:cocaine psychosis
amphetamine psychosis

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8
Q

Chlorpromazine’s job is….

A

it blocks dopamine receptors and dopamine levels are the same….just not receiving dopamine

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9
Q

Revised Dopamine theory

A

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

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10
Q

Evidence that Serotonin plays a role in schizophrenia

A

Clozapine - binds poorly to D2 receptors yet binds to serotonin receptors

suggest that serotonin receptors may be involved in schizophrenia

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11
Q

Why does it take several weeks for neuroleptics to work?

A

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

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12
Q

cortical abnormalities of schizophrenia are most prevalent in the …

A

small cerebral cortices and large ventricles

prefrontal (organization of thoughts)

cingulate (important for emotion)

temporal (auditory stimui) cortices

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13
Q

Is Schizophrenia a Neurodevelopmental disorder?

A

no

No obvious ongoing degeneration in the brain of schizophrenic patients

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14
Q

Why are neuroleptics effective against only some of the symptoms of schizophrenia

positive symptoms

A

Because positive symptoms are caused by excess D2 activity and are helped

Negative symptoms are due to permanent brain damage and cannot be helped

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15
Q

Probability of suffering from clinical depression during one’s lifetime

A

10%

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16
Q

Reactive Depression

A

stress from negative experience (someone passing away)

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17
Q

endogenous depression

A

no apparent external triggers (comes from within)likely depressed throughout life

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18
Q

SAD – Seasonal Affective Disorder

A

Triggered by reduction of sunlight

Winter or northern regions

Light therapy reduces symptoms

no drugs needed, fairly easy to treat

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19
Q

Postpartum Depression

A

Follow 10% of deliveries

Lasts at least 1 month; usu. No longer than 3 months

20
Q

Drugs that treat depression

A

Monamine Oxidase Inhibitors (MAOI) not perscribed anymore

Tricyclic Antidepressants

21
Q

Drugs that treat Bipolar

A

Lithium –metallic ion

Treats mania without increasing depression

stabilizes mood

22
Q

What do
Monamine Oxidase Inhibitors (MAOI)
do?

A

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

23
Q

Tricyclic Antidepressants

A

agonistic

block the reuptake of both 5-HT and NE

24
Q

Selective serotonin-reuptake inhibitors (SSRIs)

A

Prozac, Paxil, Xoloft, Luvox, Remeron

25
Q

Selective norepinephrine-reuptake inhibitors (SNRIs)

A

Reboxetine

26
Q

Lithium

A

Used to treat bipolar disorder

Treats mania without increasing depression

Mood stablizer

27
Q

Diathesis - Stress Theory of Depression

A

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

28
Q

Monoamine Theory of Depression

A

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

29
Q

Treatment of Depression with Brain Stimulation

A

Stimulation of anterior cingulate gyrus you will see decreased depression

used for patients that have tried everything

30
Q

Anxiety

A

chronic fear that persists in the absence of any direct threat

31
Q

Anxiety disorder

A

anxiety so severe it disrupts normal functioning

32
Q

Most prevalent of all psychiatric disorders

A

anxiety disorder

33
Q

Generalized anxiety disorders

A

occur in the absence of any obvious precipitating events

34
Q

Panic disorders

A

– rapid-onset anxiety attacks

35
Q

Obsessive-Compulsive Disorders (OCD)

A

– frequent, reoccurring, uncontrollable, anxiety-producing thoughts (obsessions) and impulses (compulsions)

36
Q

Posttraumatic Stress Disorder (PTSD)

A

after exposure to extreme stress

37
Q

Benzodiazepines - e.g. Libriuim and Valium

A

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

38
Q

Buspirone

A
  • 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

39
Q

Relationship between Anxiety and Depression

A

Comorbidity – tend to occur together in the same individual

Antidepressants often work with anxiety disorders

Anxiolytics often work with depression

40
Q

Anxiety disorders and the brain

A

deficits in GABAergic and 5-HT transmission

Low GABA (inhibit) and low serotonin

Over activity of amygdala and Anterior cingulate

41
Q

Tourette Syndrome

A

Tics – involuntary, repetitive, stereotyped movements or vocalizations

0.7 % of population

More males than females

42
Q

Tourette Syndrome has a high comorbity rate with which disorders

A

ADHD and OCD

43
Q

Barriers to studying Tourette syndrome

A

No strong animal model

No strong link to gene

No postmortums – pts. grow out of it

44
Q

the brain on tourette syndrome

A

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

45
Q

telling someone with tourette syndrome to stop results in…

A

increased tics

46
Q

Treatment for tourette syndrome

A

Neuroleptics – Dopamine receptor blockers (similiar to schizo)

Can reduce tics by 70%

bio psy (7 decks)

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