Psychopharm Midterm—Spring MSII

I. Types of therapy

A. Cognitive behavioral therapy (CBT)

1.Identify, reality test, and correct cognitive distortions

2.Examine the evidence for and against distorted thoughts

3.Substitute more reality based thoughts for distorted ones

4.Pt keeps logs, homework, activity schedules

B. STEPPS: System Training for Emotional Predictability and Problem Solving

1.Shorter and less labor-intensive than CBT

2.Uses “systems” component that recognizes importance of family and friends

3.Identify and challenge distorted perceptions, help c behavioral changes

C. Emotion management skills

1.Goal setting to manage problem behaviors

2.Improve communication skills—describe and define feelings

3.Identify distorted thinking and develop new ways

4.Identify problems, then plan and carry out action steps

II. Personality Disorders

A. Code on Axis II

B. Age considerations for Dx

1.In children <18, Sx must be present for >1 year

2.Antisocial PD is NOT Dx prior to 18

3.New onset may suggest general medical condition

C. Cluster A: “Weird” (Accusatory, Aloof, Awkward) (all may have v brief psychosis)

1.Paranoid: Distrust and suspiciousness c/o justification.

a. not unrealistic but will missinterprete “chip on the shoulder” didnt get promotion b/c someone doesnt like them

2.Schizoid: voluntary social withdrawal, restricted affect, socially isolated, little interest in pleasure (schizoid = avoid)= detachment and restricted range of expression

a. May have brief psychosis (only minutes to hrs)

b. Can be premorbid to schizophrenia

3.Schizotypal: eccentric appearance, odd thinking/speech or magical thinking, interpersonal awkwardness, illusions

a. Tx: therapy to correct reality distortions

b. Antipsychotics and antidepressants

4.Tx:

a. Therapy: accept unsociability but ↓ isolation as tolerated

b. Individual NOT group therapy

c. Educate and correct distortions about the world

d. Go SLOW—need time to develop relatedness

D. Cluster B: “Wild” (Bad to the Bone)

1.Antisocial: disregard for and violation of the rights of others

a. M>F

b. Also called psychopath, sociopath

c. Must have some elements of conduct disorder before 15yo

d. Lack of remorse/indifference to their actions

e. Burnout—may remit in 40’s

f. Tx:

1) Inpatient self help peer group- no guilt/remorse/empathy (hard to tx)

2) Anticonvulsants, Li, and beta blockers help impulse control

3) Antidepressants- comorbid mood/anxiety

2.Borderline: instability of mood and relationships, impulsive, self-mutilate, sense of emptiness

a. F>M

b. Impulsivity in 2 areas: gambling, money, drugs, EtOH, driving, sex

c. IMPULSIVE: Impulsivity, Mad, Paranoid, Unstable relationships, Labile Suicide, Imagined abandonment, View of self, Emptiness

d. Brief stress-related paranoia and dissociation

e. Splitting—divide the world into all good and all bad

f. Suicide is a real risk

g. Tx: therapy is Tx of choice

1) Dialectical behavior therapy: teach skills to cope c sudden intense surges of emotion

a)Part 1: explore a problem in detail and go through alternative solutions

b)Part 2: group sessions to teach interpersonal skills, emotion regulation, reality acceptance

2) Rx: antidepressants, mood stabilizers, anxiolytics

3.Histrionic: Excessive emotionality & attention seeking

a. F>M

b. Center of attention, shallow, inappropriately sexually seductive, dramatic, ealisly influenced, considers relationships to be more intimate than in reality

c. Co-morbid: depression, conversion & somatization disorders

d. Tx:

1) Antidepressants- co-morbit mood/anxiety

2) Insight oriented Tx: based on Freudian psychoanalytic theory- Hard to dev therapeutic relationship

a)Develop understanding of psychological function and personality (feelings, responses, behaviors, current relationships)

b)Examine responses to therapist and important ppl in childhood

4.Narcissistic: Need for admiration, lack of empathy, grandiosity

a. M>F

b. Arrogant, entitled, exaggerated self-importance, lacks empathy

c. Envious/believes other are envious of him

d. Co-morbid: Depression

e. Tx: Antidepressants, Self-psychology

E. Cluster C: “Worried” (Cowardly, Compulsive, Clingy)

1.Avoidant: “shy, timid, lonely, isolated”

a. M=F

b. Inadequacy, Hypersensitive to criticism

c. Desire relationships c others (differs from schizoid)

d. Similar to social phobia, but more severe

e. Avoids ppl and activities that may result in rejection, criticism, or disapproval

f. May improve/remit c age

g. Tx: individual and group assertiveness training and systematic desensitization

1) Rx: beta blockers, SSRIs, anxiolytics

h. Systematic desensitization (behavior modification)

1) Learn relaxation skills

2) Create anxiety hierarchy

3) Pair relaxation c feared stimulus and progress

2.Dependent: excessive need to be cared for, fear inability to fxn as an adult

a. F>M

b. Need lots of help and reassurance for everyday decisions

c. Can’t start projects on their own

d. Submissive, clingy behavior

e. Frequent childhood hx of separation anxiety or illness

f. Tx: individual, group, family, and behavioral (assertiveness training)

1) Rx: antidepressants for mood

3.OCD: Preoccupation c orderliness, perfectionism & control, at expense of flexibility, openness, efficiency

a. M>F

b. Perfectionism that interferes c task completion, difficulties delegating

c. Inflexible about values

d. Miserly, stubborn and rigid

4.Tx Cluster C:

a. B blockers, SSRI/ antidepressants, Anxiolytics

b. CBT- Cognitive Behavioral Therapy:

1) Based on idea that an individual’s affect and behavior are largely determined by how they structure their world

2) Monitor negative, automatic thoughts

3) Recognize connection between cognition, affect & behavior

4) Examine evidence for & against distorted thoughts- substitute reality for distorted

5) Pt keeps logs, homework & activity schedules

c. Behavioral Therapy- Systematic Desensitization (classical therapy)

1) Behavior modification- phobias & fears

2) Relaxation skills, anxiety hierarchy

d. All tx: involve family, vocational training & social services

III. Somatoform disorders

A. Somatization disorder

1.Multiple physical complaints (involves at least 4 organ systems)

a. Not intentionally produced

b. Not explained by medical condition

c. Not the result of substance abuse

d. Results in seeking medical care

e. Causes impairment in fxn

2.Diagnosis

a. Pattern of Sx before 30yo

b. Algorithm: 4/2/1/1

1) 4 painful areas

2) 2 GI Sx other than pain: N/V/D, bloating, food intolerance

3) 1 sexual Sx other than pain, sexual indifference, ED, Irreg menses

4) 1 pseudoneruological Sx: balance, aphonia, blindness, deafness, weakness, seizures, lump in throat

c. r/o: MS, SLE, HIV, others; Comorbid: anxiety, mood disorders, schizophrenia

3.Tx

a. Biological treatment:

1) Comprehensive exam + family member interview

2) Minimize invasive/dx procedures, habit forming Rxs & prn Txs

3) Antidepressants/anxiolytics-mood & anxiety Sxs

b. Social Tx:

1) Minimize # Drs.

2) Regular, structured visits c treatment contracts

3) Set long/ short term goals

4) Recognize early Sxs & give pt/ fam feedback

c. Psych Tx:

1) Legitimize suffering, remove blame

2) Link stressful events c Sxs

3) Practice coping, relax/exercise, daily log

4) Promote pt control & autonomy

d. Diagnostic feedback (there are 3 types, not all are helpful)

1) Rejection—imaginary source or the reality of Sx is denied

2) Collusion—physician goes along c pt

3) Empowerment—work c pt via explanation of Sx

e. Legitimize pt suffering, remove blame

f. Link stress c Sx

g. Minimize # physicians, tests

h. Avoid prn Tx and habit forming Rx

i. Rx: antidepressants, SSRIs

j. CBT: promote healthy behavior, keep daily log, relaxation exercises

B. Conversion disorder: sudden loss of sensory or motor fxn, often following acute stress

1.Causes distress/ impairment

2.Sxs not limited to pain/ sexual dysfxn

3.Psychodynamic Model of Conversion Disorder: Behavior affected by unconscious/ past experiences

4.Tx: reassurance problem will resolve

a. Physiotherapy

b. Psychotherapy may be counterproductive

c. Anxiolytics and relaxation techniques

C. Hypochondriasis: preoccupied c fear of serious disease b/c misinterpret Sxs

1.>6mo

2.Not accounted b another mental disorder

D. Body Dysmorphic Disorder: Thinks something is wrong c his/her body

1.Not caused by another mental disorder

2.Ex: MSI who wouldnt go to school b/c didn’t want his pic taken

E. Factitious Disorder: Intentional production of physical/physio Sxs

1.Motivation is to assume the sick role, NO external motives (ie $)

F. Malingering- not an actual DSMIV disorder

1.Intentional production of fals/exaggerated Sxs b/c external incentives (ie $)

2.Tx Factitous/ Malingering:

a. No specific Tx, recognize early & avoid unnecessary Tx/procedures

IV. Psychopharmacology I

A. Components of a therapeutic trial

1.Dosing

2.Duration

3.Compliance

4.Rx interactions

5.Choice of Rx- fam hx/insurance/indication

6.Special considerations: young/old, Preg/nursing, Hep/renal inufficiency

B. Norepinephrine

1.Neurons in locus coeruleus and tegmental regions

2.Modulates attention, mood, energy, movement, HR, BP

3.↓in depression, ↑ in anxiety

4.Descending spinal pathway involved c pain

5.a2 presynaptic receptor-> blocks NE release

6.Postsynaptic: a1, a2, B1

C. Serotonin (5-HT)

1.Projects from raphe nucleus to limbic/cortex

2.Involved in : depression, anxiety, OCD & sleep

3.↓ in anxiety and depression (↓5HT & ↑Recptors)

4.5-HT1A receptor

a. Presynaptic—controls 5HT release

1) Down regulation → ↑ 5HT release → improves depression, anxiety

b. Postsynaptic

1) Stimulation improves: depression, anxiety, OCD, panic, bulimia

2) Disrupts temp regulation

5.5-HTD1 presynaptic autoreceptor: anti-migraine effects

6.5-HT2 postsynaptic receptor

a. Agitations, anxiety, psychosis, sexual dysfunction, sleep disorders, hot flashes

b. Improves OCD and bulimia

7.Other subtypes: 5-HT2A/2C/3/4

D. Dopamine (DA)

1.Precursor to NE (L-tyrosine → L-dopa → DA → NE)

2.From ventral tegmentum to substantia nigra, hypothalamus, nucleus accumbens, basal ganglia

3.Parkinson’s: under activity of DA in nigro-striatum

4.Over activity in nucleus accumbens → pleasure seeking

5.↑ in schizophrenia, ↓ in Parkinson’s and depression

6.Pathways

a. Mesolimbic: ↑ DA → positive Sx of psychosis

b. Mesocortical: ↓ DA/D2 blockade → negative Sx of psychosis

c. Nigrostriatal: acts on basal ganglia

d. Tuberoinfundibular: acts on hypothalamic-pituitary axis

7.Recptr Subtypes: D1-5

E. Acetylcholine (Ach)

1.Associated c memory, learning, attention, cognition

2.From nucleus basalis of Meynert and septum to cerebral cortex and hippocampus

3.Interacts c and balances DA in the striatum

4.↓ in Alzheimer’s, Huntington’s, REM sleep

F. GABA

1.Inhibitory NT

2.GABA receptor site of action for barbiturates, benzos, and EtOH

3.↑ GABA improves anxiety

G. Glutamate

1.Excitatory

2.3 types:

a. NMDA

b. AMPA

c. Kaniate

3.NMDA present on ALL neurons in CNS

a. Involves memory and learning

4.Excess activity involved in seizures

5.Antagonists (angel dust)-> delusions, combative, agitation

V. Psychopharmacology II

A. SSRIs

1.Block somatodendritic & axon 5-HT reuptake → ↑ 5-HT in dendritic regn →

2.5HT1A autoreceptors down regulate → ↑ 5-HT at the synapse

3.Post-synaptic receptors downregulate and return to a euthymic state

4.5-HT originates from raphe nucleus and is ↓ when acting on various areas:

a. Depression—frontal cortex

b. OCD—basal ganglia

c. Panic disorder—limbic-hippocampus

d. Bulimia—hypothalamus

5.Stimulation of 5HT1A improves:

a. Depression, OCD, panic, social anxiety, bulimia

6.Stimulation of 5HT1D improves: migraines

7.Stimulation of 5HT2A results in:

a. Improves: depression, OCD, bulimia

b. Worsens: anxiety, agitation, hallucinations, ↑ temp, panic attacks, insomnia, sexual dysfunction

8.Stimulation of 5HT3: nausea, GI distress, diarrhea, HA

9.Side effects:

a. Agitation: ↑ sensitivity from midbrain to limbic cortex and hippocampus

b. Nausea: 5HT3 in chemoreceptor trigger zone and gut (5HT3&4)

c. Sleep disturbance: 5HT2 in brainstem sleep centers, disrupt slow-wave sleep

d. Sexual: 5HT2 neurons in descending pathways ↓ libido and completion

B. DA Sx of mental illness

1.Positive Sx (have a better Px):

a. Delusions

b. Hallucinations

c. Agitation

d. Disorganized behavior

e. Disorganized speech

2.Negative Sx

a. Dull affect

b. Emotional/social withdrawal

c. Passivity

d. Anhedonia

e. Attention impairment

f. Amotivation

3.Pathways

a. Mesolimbic: ↑ DA → positive Sx of psychosis

b. Mesocortical: ↓ DA/D2 blockade → negative Sx of psychosis

c. Nigrostriatal: acts on basal ganglia

d. Tuberoinfundibular: acts on hypothalamic-pituitary axis

C. Antipsychotics

1.Typical agents

a. Haloperidol

b. Pimozide

c. Fluphenazine

d. Loxapine

e. Thioridazine

f. Mesoridazine

2.Mechanism of action (D2 HAM)

a. Block D2 receptors- improve positive Sxs

b. Block M1 (anticholinergic)

c. Block α1 (antiadrenergic)

d. Block H1 (antihistamine)

3.EPS: dystonia, akathesia, Parkinson’s Sx, tardive dyskinesia

a. Due to blockade in basal ganglia in Nigrostrial pthway

4.Tuberoinfundibular block

a. Hyperprolactinemia, galactorrhea, sexual dysfunction

b. Thirst, hunger, temp control

5.Typical antipsychotics

a. Main action is D2 block in mesolimbic-mesocortical pathway

b. Helps more c positive Sx (may exacerbate negative Sx)

c. More risk of EPS

d. NOT 1st line in children/adolescents

6.Low potency: thioridazine

a. More antihistamine → sedating

b. Antiadrenergic → hypotension

c. Anticholinergic → cardiac side effects

d. Lower EPS risk

e. More anticholinergic effects

7.High potency

a. More selective for DA receptor > anticholinergic activity

b. More EPS risk

c. Better for older pt on a lot of meds (less interaction, less hypotension)

8.Atypical antipsychotics: 5HT2A/D2 antagonists

a. Effect positive AND negative Sx

b. Few EPS

c. Minimal endocrine effects, can cause agranulocytosis

d. 5HT neuron stimulation normally inhibits DA release, block of 5HT will ↑ DA:

1) In nigrostriatal → reduces EPS & TD

2) In tuberoinfundibular → reduces hyperprolactinemia

3) In mesocortical → improves negative Sx

e. D2 block in mesolimbic ↓ positive Sx

D. Anxiolytics: benzos, barbiturates, EtOH

1.Bind and stimulate GABAa receptors

a. In reticular formation, thalamus, cerebral cortex → sleep and ↓ anxiety

b. Opens Cl channels and hyperpolarizes membrane ↓ synaptic transmission

E. Mood stabilizers

1.Li

2.Anticonvulsants

3.Atypical antipsychotics

F. Tx guide:

1.Rx to treat mental illness, not just control inappropriate behavior

2.Minimize use of multiple rxs

VI. Childhood disorders

A. ADHD

1.DSM IV criteria

a. Short attention span

b. Impulsive, hyperactive

c. Onset before 7yo (girls by 10yo)

d. Impairments must be seen in 2 settings (school, home, friends)

e. Subtypes:

1) Predominately inattentive

a)Disorganized, distractible, forgetful, poor frustration tolerance

2) Predominantly impulsive/hyperactive

a)Restless, motor-driven, interrupts

3) ADHD- Combined

2.Workup

a. ADHD rating from teachers and parents

b. Psychological testing not necessary unless:

1) Need to r/o: LD, MR, developmental delays

2) Need to Dx comorbidity

c. Hx

3.Pathways

a. DA and NE responsible for arousal, attention, planning

1) 5HT- Obsessive Compulsive/ Anxiety (NOT for ADHD)

b. Locus ceruleus → prefrontal cortex

1) Affects executive fxns: activation, focus, effort, emotion, memory

4.Tx

a. Rx

1) Stimulants

a)Methylphenidate (Ritalin)

b)Methamphetamine salts (Adderall)

c)Lisdexamfetamine dimesylate (Vyvanse)

i. 1st prodrug

ii. Indicated for ages 6-12 and adults

iii. L-lysine must be cleaved to be active (low abuse potential)

d)Side effects: tics, anxiety, mood change, psychosis, appetite/sleep changes, HA, DEATH-CV

2) Central α2 agonists

a)Clonidine (sedating)

b)Guanfacine (non-sedating)

c)Side effects: hypotension, dizziness, bradycardia, AV block, syncope, somnolence, fatigue

3) SNRIs (atomoxetine)

a)↑ DA and NE in prefrontal cortex

b)Best in maintenance of ADHD

c)Little DA involvement in nucleus accumbens or striatum

i. Doesn’t stimulate reward paths

d)May take 4-6wks for full effect

4) Atypical antidepressants

a)Bupropion—inhibits DA reuptake

b)Side effects: ↑ suicidal thoughts, GI effects, agitation

5) TCAs

a)Desipramine

b)Imipramine

b. Psychotherapy

1) Behavior mod, anger management

a)Create a schedule, set up reward system

2) Family therapy, individual therapy

3) Social skills training

4) School involvement: special learning plans

c. Diet has not been shown to affect ADHD

B. Tics- rapid involuntary movements/ sounds

1.From ADHD tx c DA impacting Striatum- Should clear after DC

C. Tourette’s= ADHD + OCD + TICS

1.Starts c motor tics then progress to vocal

2.Rostrocaudal progression

3.Can suppress

4.Starts around 8-10yo and may burn out in adolescence

5.Tx

a. Typical antipsychotics

1) Haloperidol

2) Pimozide

b. Atypical antipsychotics

1) Risperidone

2) Olanzapine

3) Quetiapine

4) Aripiprazole

c. Alpha2 agonists

d. Preferred Rx: clonidine > risperidone > haloperidol

D. OCD

1.Criteria

a. Obsessions: intrusive, recurrent thoughts or images that exceed real life worries

b. Compulsions: repetitive behaviors the pt is driven to perform

2.Tx

a. SSRIs (may require higher doses than those used for depression)

1) Fluoxetine

2) Sertraline

3) Paroxetine

4) Fluvoxamine

5) Citalopram

6) Escitalopram

b. TCAs

1) Clomipramine—specific TCA for OCD

c. Atypical antipsychotics

d. Behavioral interventions

1) CBT- Exposure Response Prevention

2) Relaxation techniques- breathing, mm relaxation, imagery

3) Thought stopping

4) Desensitization—stepwise ↑ in stimulation

5) Flooding—max amount of stimulus all at once

E. Tx challenges

1.ADHD meds may focus pt into OCD

2.OCD Tx (SSRIs) may activate ADHD

F. Suicide M=F

1.Adolescent: M>F

2.Risk factors:

a. Hoplessness

b. Psychopath- mood d/o, substance abuse, disruptive behavior

c. Family- Hx..

d. Stressful life events, abuse, school probs, exposure, sexual minority

3.Assessment: talk openly, calm, non-judgmental, inquire, SUDDEN CHANGES

4.Intervention= Prevention- school, community & health care

5.Tx:

G. Pervasive developmental disorders (PDD)

1.Autism

a. Impaired: reciprocal social interaction & verbal/non-verbal communication

b. Limited activities and interests

2.Asperger’s syndrome

a. Normal IQ and language

b. Limited range of interests

c. Social impairment

3.Rett’s Synd

a. F>M

4.Childhood Disintegrative Disorder

a. M>F Onset >3yo

5.Tx

a. Physician required to refer family to early intervention service

b. Early intervention: ABA—applied behavioral analysis

1) Goal: learn language, social, play skills thru behavior interventions

2) After age 4—no benefit- get free public edu

c. High structure

d. Specialized education and behavior mod program

e. Communication therapy (language fxn by age 5 is strong predictor of outcome)

f. Social skill development

g. Sensory integration- for sterotypies, OCD Sx, Aggression/temper

h. Rx

1) Sx control: impulses, OC, self-injurious behavior, attention span, mood/anxiety, neg sxs

2) Tx of positive and negative Sx of schizophrenia

3) Atypical antipsychotics

a)Risperidone

i. Improved aggression, irritability, hyperactivity, stereotypic behaviors

ii. No impact on social/language

b)Olanzapine

c)Ziprasidone

d)Quetiapine

e)Aripiprazole

f)Invega

g)Saphris

VII. Disorders of cognition

A. Cognition: memory, language, attention, orientation, problem solving, judgment

B. Delirium

1.S/Sx

a. Develops very quickly (over hrs or days)

b. Disturbance of consciousness

1) Impaired alertness, focus

2) Reduced concentration, awareness

c. Change in cognition- developes over short time in resp to a cause

1) Disorientation

2) Disorganized thought and speech

3) Impaired memory

4) Visual hallucinations

5) Agitation and lability

d. Sympathetic arousal: tachycardia, wide PP, dilated pupils, tremor

e. Waxes and wanes

1) Impaired sleep-wake cycle

2) Sundowners—Sx ↑ as sun goes down

f. Usually seen in severely ill person

g. At Risk: Elderly, Medically fragile, Medical/surg stressed

2.Tx- Find and fix underlying medical cause

a. Provide medical, physical, sensory, and environmental support

1) Prevent accidents

2) Don’t sensory deprive nor overstimulate

3) Surround c familiar decorations and objects

4) Have family, friends, or a sitter

5) Provide a clock/calendar

3.Px

a. Serious, often leads to mortality & morbidity in short term

b. Rapid full recovery if cause is fixed

C. Dementia

1.S/Sx

a. Multiple cognitive deficits including memory:

1) Amnesia (Short before long-term)

2) Aphasia- language

3) Apraxia—can’t carry out motor activities, but motor fxn intact

4) Agnosia—failure to recognize objects

5) Impaired executive fxn

b. 1st Sx: mile memory loss /personality change

c. Most are progressive and not reversible

d. Differs from delirium

1) No impaired alertness

2) Does not wax and wane

3) No autonomic arousal- stable ANS

4) Not acute or reversible

5) Insidious onset

6) Often includes behavioral component

2.Alzheimer’s dementia (most common type)

a. Gradual onset, Fatal

b. Risk factors:

1) Hx of head injury

2) 1st degree relative

3) Female

4) Down syndrome (begins younger)

5) Age

6) Confounding depression

3.Vascular dementia (2nd most common) aka Multi-Infarct Dementia

a. Due to multiple brain infarcts- may superimpose on Alzheimers

b. Abrupt onset c variable course (may progress stepwise)

c. Often have neurologic deficits d/t stroke

d. Risk: vascular disease

4.Lewy bodies dementia: similar to Alzheimer’s c

a. May have visual hallucinations and Parkinsonism

b. More aggressive progression than Alz

5.Pick’s dementia

a. Frontotemporal: disinhibition, language impairment

b. Slower progression than Alz

6.Huntington’s

a. AD inheritance chromo 4

b. Striatal atrophy

c. Onset in middle age, progressive

d. Choreoathetosis

7.Other causes: HIV, Parkinson’s, CJD, head trauma, substance induced

D. Tx

1.Correct reversible and slow irreversible factors

2.Discontinue polypharmacy, esp anticholinergic meds

3.Cholinesterase inhibitors (Achi) –GI Side effects

a. Tacrine

1) 1st Rx for dementia

2) Hepatotoxicity—not often used anymore

b. Donepezil

1) Selective reversible acetylcholinesterase inhibitor

c. Rivastigmine

1) Inhibits acetylcholinesterase and butylcholinesterase

d. Galantamine

1) Inhibits AchE and stimulates nicotinic receptors

4.NMDA antagonist

a. Memantine

1) Non-competitive, antagonist

a)Excess glutamate-> cell death

2) Well tolerated; side effects: HA, constipation, confusion, dizziness

3) Neuroprotective effect

5.General

a. Antidepressants- depression and irritability

b. Benzos- anxiety, restlessness

c. Antipsychotics- hallucinations, delusions, aggression, agitation, hostility

d. Meds may only turn back dz 6-12 months

e. Psychosocial intervention is key

E. Amnestic disorders

1.Inability to learn new info or recall previously learned info

2.Many causes, most common is EtOH related

3.Wernicke-Korsakoff

a. Caused by thiamine (B1) deficiency d/t chronic alcoholism

b. Wernicke’s encephalopathy is acute phase:

1) Confusion

2) Ataxia

3) Ophthalmoplegia

4) Tx: Thiamine!

c. Korsakoff’s is chronic phase

1) Loss of short-term memory

2) Confabulation

3) Poor Px

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