Y - Pysch Part Ii

Front 1

five types of anxiety disorders

*what is their underlying fear??

Back 1

1. GAD
- most symptoms, most of time

2. PANIC DISORDER
- random panic attacks

3. OCD
- compulsions reduce anxiety

4. PHOBIAS
- specific stimulus

5. PTSD & Acute stress disorder
- following/related to specific TRAUMA

Front 2

Symptoms of anxiety

Back 2

1. MOOD: fear, dread, panic, easily fatigued, etc

2. "ALERT": worry, on edge, scanning, irritable, etc

3. MOTOR: trembly, shaky, muscle ache, dizzy, nausea

4. ANS: dyspnea, palpitations ,sweaty, clammy, insomnia, decreased concentration

*motor & ANS symptoms can lead pt to believe he has a medical problem

Front 3

CAUSES OF ANXIETY IN ANXIETY DISORDERSS

Back 3

PSYCHOLOGICAL:
- Unconscious factors: old fears/earlier events
- Learning factors: associating danger/pain with certain stimuli
- Existential factors: you're not important

BIO:
- dominant role in anxiety disorders

Front 4

GENERALIZED ANXIETY DISORDER

(GAD)

Back 4

EXCESSIVE, UNREALISTIC WORRY

>6MO
- Pervasive: multiple life circumstances
- hard to control
- 3+ symptoms (sleep problem, irritable, muscle tension, can't focus, etc)

Front 5

GAD COURSE: onset, comorbid, progression, risk factors

Back 5

ONSET: 20-30s

Increased risk: many negative circumstances

*MILD IMPAIRMENT but long-standing*
- Pts self medicate w/ alcohol or other depresssants --> ADDICTION

25% --> panic disorder
MANY --> MDD

Front 6

PANIC ATTACK

- diag criteria
- panic disorder vs. other anxiety disorder

Back 6

EPISODE of intense fear

*SYMPTOMS: 4+
- dizzy, dyspnea, tachy, trembly, sweaty, fear of dying, losing control,

*SUDDEN: exp symptoms w/in first 10 minutes

ask: what's triggering it?
- nothing? unexpected = panic disorder
- Specific stimuli = phobias, OCD, PTSD

Front 7

PANIC DISORDER

- essential features
- course (onset)
- progression
- comorbid

Back 7

1. Attacks are RECURRENT & UNEXPECTED
2. DETRIMENTAL
(1+mo. of worrying & causing significant change in behavior)

ONSET: 20s-40s
- 1st attack: 78% no clear trigger
(or with stress or street drugs)

Progression:
- Fear/avoid previous attack sites
- Fear/avoidance spreads to any open space where escape is difficult
= AGORAPHOBIA --> depression

COMORBID:
- AGORAPHOBIA
- DEPRESSION: 40-80%
- Substance abuse: 20-40%

women are more common

Front 8

PANIC DISORDER & PRESENTATION IN ER

Back 8

Focus on the autonomic symptoms (instead of anxiety) = rush to ER for fear of MI

*symptoms of dyspnea can be similar to mitral valve prolapse

Front 9

OCD

- FEATURES
- MAJOR PATTERNS

Back 9

obsessions & compulsions that cause:

1. marked distress
2. Inordinate time consumption
3. Significant interference with person's routine, functioning, etc.

*ordinary thoughts don't cause this much distress or interference

MAJOR PATTERNS:
1. Contamination fear = washing
2. Doubt = checking
3. Obsessions only = rare
4. Obsessional slowness: need for symmetry or precision

Front 10

OCD

- PREVALENCE
- ONSET
- COURSE
- COMORBID

Back 10

Prev: 2-3%; but only 44% get tx
- can wait 5-10 yrs to get tx


Onset: 18-24yo (can start as kid)
- 50-70% is after stressful event

50% have chronic, unremitting course if untreated
- worse with stress/fatigue

COMORBIDITY:
50%: DYSTHYMIA, MDD
46%: phobias (related to obsessions)
24%: alcohol abuse
6%: OC personality disorder

Front 11

OCD DIFF DX

- ordinary thoughts/habits
- tic disorders
- partial complex seizures
- depression w/ obsessive brooding
- schizophrenia
- addictions

Back 11

1. Ordinary thoughts/ habits: don't interfere as much
2. Tic disorders: involuntary
3. Partial complex seizures: automatisms are NOT intentional or purposeful
4. Depression w/ obsessive brooding: thoughts are meaningful (NOT senseless)
5. Schizophrenia: FIXED delusions
6. Addictions: behavior is stil pleasurable

Front 12

OCD ETIOLOGY

Back 12

BEHAVIOR THEORIES (LEARNING):
- Obsessions are CONDITIONED stimuli
- Compulsions are developed to REDUCE anxiety --> REINFORCEMENT

Front 13

OCD
- OBSESSIONS?
- COMPULSIONS?

Back 13

OBSESSIONS: passive occurrences
- UNWANTED, intrusive mental events
- NOT a delusion of thought insertion
(pt knows that ideas are from their mind)

COMPULSIONS: Actions
- repetitive, INTENTIONAL, purposeful axns
- in RESPONSE to an obsession or certain rules
* done to neutralize discomfort or prevent dreaded event
- pt. knows it's illogical/excessive
- pt. WANTS to stop, but it brings relief
- compulsion is NOT fun (unlike addictive behavior)

Front 14

OCD & BIOLOGICAL FACTORS

Back 14

even more than OTHER anxiety disorders, bio/neural factors play a HUGE HUGE HUGE ROLE in OCD

Front 15

PHOBIAS

- gen
- essential
- categories

Back 15

MOST COMMON psych disturbance

- Persistent, Excessive fear
- SPECIFIC stimulus
--> immediate anxiety response
- Avoidance (or endured with great distress)
* INTERFERES WITH YO LIFE*

CATEGORIES:
- Agoraphobia
- social phobia
- specific phobias

Front 16

AGORAPHOBIA

Back 16

FEARS NO ESCAPE
- situations where escape is difficult or embarrassing if panic attacks occur

Complications: ^ restriction of activities
- commonly associated w/ panic disorder (but not always)

* can become housebound if extreme *

Front 17

SOCIAL PHOBIA

-specific vs. gen
- complications

Back 17

Fear of 1+ social situations & marked anxiety symptoms while IN the situation

fears:
- scrutiny, judgment
- doing something humiliating or embarrassing

Specific Social Phobia vs. General Social Phobia

Complications:
- AVOIDANCE
- WORK RESTRICTIONS
- SOCIAL ISOLATION =(

Front 18

OCD & Causes

Back 18

50-70% onset after stressful event:

- sexual or marital conflict
- pregnancy or delivery
- illness of death of relative

Front 19

SPECIFIC PHOBIAS

Back 19

ALL OTHER PHOBIAS (NOT AGORAPHOBIA OR SOCIAL)

DISORDER IF:
- DISRUPTIVE
- EXCESSIVE/UNREASONABLE

Front 20

PERSONALITY STYLE/TRAIT VS DISORDER

Back 20

disorder = INFLEXIBLE & MALADAPTIVE
- impairs relationships, causes distress, impairs functions

Long-lasting (insidious onset)
Bothers others more
GLOBAL problem

*ABRUPT personality change is NOT a personality disorder

Front 21

DSM-IV categories of personaility disorders

- CLUSTERS

*timeline & age are KEY*

Back 21

Cluster A = THE WEIRD
*More Men*
- paranoid: ideas of reference
- schizoid: don't care
- schizotypal: weird uncle

CLUSTER B = THE WILD
- antisocial: grifters
- histrionic
- borderline: unstable sense of self
- narcisstic

CLUSTER C = THE WORRIED
- Avoidant: fear of rejection
- dependent
- obsessive-compulsive: anthony hopkins

Front 22

PARANOID PERSONALITY DISORDER

CLUSTER A

ess, defense mechanism

Back 22

ESS: Pervasive distrust & suspiciousness of others
- expects disolyalty & deception
- reluctant to confide
- Collects injustices/grudges
*ideas of reference*

ASSC'D features:
- Accepts no blame (always victim)
- Needs an enemy
- Fears intimacy

Defense Mechanism:
PROJECTION of hostile impulses onto others

*freq conflits w/ authority in jobs
*cold, hostile, distant
* vulnerable to brief psychotic disorder

Front 23

PARANOID PERSONALITY DISORDER

- distinguish from other paranoid disorders
- May be in the schizophrenia spectrum

Back 23

Paranoid personality: SUSPECTS it
- still organized thoughts, not as fixed

Delusional: BELIEVES it
- very fixed

SCHIZOPHRENIA:
Believes it AND has super reduced functioning
*disorganized, fixed thoughts

3X MORE COMMON IN FIRST-DEGREE RELATIVES W/ SCHIZOPHRENIA

Front 24

DEALING WITH PARANOID PERSONALITY DISORDER PATIENTS

Back 24

Neither reinforce nor dispute their suspicions (just accept as a given)

- focus on underlying distress, anxiety, fear
- be non-defensive
- give them as much control as possible

*focus on underlying distress, anxiety and fear of losing control

Front 25

SCHIZOTYPAL PERSONALITY DISORDER

"SCHIZO LYTE"

- ESS
- Manifestations

Back 25

ESS: PECULIARITY in perceptions, ideation, speech, look, behavior
- CHRONIC interpersonal deficits

MANIFESTATIONS:
- SPACEY: magical thinking, ideas of reference, illusions/unusual perceptions
- Digressive, vague, abstract speech
- WEIRD CLOTHES & axns

- Few/no friends (but it's ok)
- Super uncomfortable in social interactions (more suspicious than shy)

Front 26

SCHIZOTYPAL

- Relation to schizophrenia
- course
- dealing with them

Back 26

MILD version of schizophrenia
- increased incidence in family hx w/ schizo
- constricted affect, poor functioning (but without obvious drop off)


LIFELONG COURSE
- a little better than schizo
- does NOT turn into schizo
- In stress, can turn into brief psychotic disorder

APPROACH:
- respect their inner world/beliefs
- encourage social skills/reduce siolation

Front 27

SCHIZOID PERSONALITY DISORDER

CLUSTER A

ESS
MANIFESTATIONS

Back 27

INDIFFERENT toward others

Essential:
- Detached from social relationships
- Restricted range of emotional experience & expression
"robotic"?

Manifestations:
- Doesn't desire close friends
- Like solitary pursuits
- little desire for sexual experiences
- Indifferent to others' opinions
- No strong emotions
- Constricted affect = aloof, cold, detached

Front 28

SCHIZOID

- Relation to schizophrenia
- course
- shyness

Back 28

Mild Schizophrenia; maybe on the schizo spectrume

*NO FAMILY HX INCREASES W/ SCHIZOID & SCHIZO*

COURSE:
- do well in intellectual pursuits (like math)
- may be involved in committees in that topic
- no close friends
- Very active FANTASY life

*most schizoid adults were shy kids; not all shy kids --> schizoid*

Front 29

CLUSTER B PERSONALITY DISORDERS

- GENERAL

Back 29

1. Focused on SELF
- always the victim

2. Entitlement
- they "deserve" special treatment

3. Rejection sensitivity
- overreact to PERCEIVED slights
- reflects underlying insecurity & fear of abandonment

4. Anger: in multiple forms

5. Demanding: wants everyone to meet their needs

6. Maniuplative

*HIGH COMORBIDITY OF SUBSTANCE ABUSE*

Front 30

CLUSTER B PERSONALITY DISORDERS

- MANAGING THESE PTS

Back 30

1. set ground rules
- strong emotional reactions need to be talked out, NOT acted on
- pt is accountable for axns
- set clear, realistic goals & expectations regarding tx

2. Examine & deal w/ your own rxns
- look hard for something to genuinely admire/like about that pt

3. Deal with inappropriate demands/axns
- Re-direct their entitlement rather than challenge it.
- AVOID: reflexively denying & agonizing over every request

*BUT give each rquest a fiar hearing
- NOT based on how it was asked*

- BE CONSISTENT
- focus on pt's ability to CHOOse his axns, rather than negative consequences
- keep ball in their court

Front 31

NARCISSISTIC PERSONALITY DISORDER

Back 31

ESS:
- Grandiosity
- Need for admiration (can't give it to themselves)
- Lack of empathy for others
*hypersensitive to others' opinions of them

MANIFESTATIONS:
- Preoccupied with fantasies of success, power, etc
- Entitlement: feels superior, special, expects automatic compliance
- Envious of others or thinks everyone's jealous of them
- Reacts to criticism w/ rage/shame/humiliation
- Exploitative

Illness:
- blow to self-esteem
- may separate pt from tasks by which he receives admiration
*May ignore/deny illness or comply poorly

MANAGING:
- Be generous w/ compliments and admiration
- Frame goals of tx in terms of optimizing his ability to continue his important tasks

Front 32

ANTISOCIAL PERSONALITY DISORDER

- ess
- common manifestations <15 yo vs adult

*THESE PTS HAVE A VENEER OF CHARM/SEDUCTION/SINCERITY

Back 32

ESSENTIAL:
- Pervasive pattern of disregard for, & violation of, the rights of others
- ONLY personality disorder diagnosed in childhood (begins before age 15)
*conduct disorder is like a childhood P.D.*

Commons Prior age 15:
- Truancy
- fights
- running away
- physically cruel to people/animals
- fire setting,property destruction
- lying/stealing
- bedwetter

ADULTHOOD:
- Irresponsible: leaves job/school w/o realistic plans
- fails to honor financial obligations
- impulsively seeks adventure
- fails to care for his kids
- Reckless

Front 33

ANTISOCIAL PERSONALITY DISORDER

- antisocial behavior
- genetics vs. enviroment
- things that don't play a role

*THESE PTS HAVE A VENEER OF CHARM/SEDUCTION/SINCERITY

Back 33

ANTISOCIAL:
- Repeatedly breaks law
- Aggressive, fights, irritable, wife beater
- Lying, conning, use of aliases
- Serial, brief exploitative romantic relationships

LACK OF REMORSE
- indifferent to other's pain he inflicts
- Rationalizes away the effect of his axns

GENETICS: YES
- Dad w/ alcoholism/antisocial PD (even if not raised by him)
- 15% prevalence in 1st degre male lrelatives (vs. 3% prev in males)

Environment: YES
- good, strict discipline
- Consistent emotional ties w any significant adult

DON'T PLAY A ROLE:
- Membership in a deviant subgroup
- bad associates
- living in high crime neighborhood

Front 34

ANTISOCIAL P.D.

- course
- managements

Back 34

- Some grow out of it
>21 yo, 2% per year cease antisocial activities

Comorbidities:
- Depression
- Alcoholism: 25-30%
- Somatoform disorders (multiple physical complaints)

MANAGEMENT:
- avoid acting on a natural tendency to be punitive toward them
- Keep rules clear; avoid special exceptions
- Frame arguments for tx about how it's in the patient's OWN best interest
- Don't get manipulated (Rx)
- Don't leave wallet/keys lying around

Front 35

HISTRIONIC PD

(Scarlett O'hara)

- ESS
- COMMON MANIFESTATIONS
- ASSC'D FEATURES
- MANIFESTATIONS OF ATTN SEEKING

Back 35

Excessive Emotionality (fickle)
- Dramatic
- Emotions shift rapidly; shallow
- Expressionistic, global speech (no details)
- Strong convictions quickly adopted & dropped
- Thinks relationships are more intimate than they actually are

Attention Seeking
- Needs to be center of attn
- Seeks/demands reassurance, approval, praise
- Overly concerned w/ physical appearance

COMMONS:
- Bored easily; immediate gratification
- Creative, imaginative
- Impressionalbe (overly trusting)

Front 36

Histrionic PD

- MANAGEMENT IN A MEDICAL SETTING

Back 36

- Pts very threatened by potential loss of attractiveness
- Compliment behavior/appearance
- Acknowledge their neediness while handling demands
- Be more authroitarian (they like it)

Front 37

BORDERLINE PERSONALITY DISORDER

*glenn close in fatal attraction*

"Bordeline" b/w neurosis & psychosis

- ess
- commons & assc'd features

Back 37

INSTABILITY of:

1. Relationships:
- unstable & intense: fluctuate b/w extremes of idealizing / devaluing
- Inappropriate, intense anger
- Frantically avoids real or imagined abandonment
- MANIPULATIVE acts/threats (suicidal self-mutilation)

2. Mood:
- Reacts to stuff w/ frequent shifts to depression, irritable, anxiety
- Shifts usu last couple hours; many in a day possible
- Events causing shifts are usually considered as slights/rejection

3. Self-image:
- No clear, constant sense of who they are/should be
- Uncertain sexual orientation, goals, career, friend type

4. Impulse Control:
- Substance abuse, spending, reckless driving, promiscuity

Assc'd
- feels bored/empty
- cuts on self to "feel something" or relieve anxiety/tension
- Recurrent suicidal gestures, threats
- Transient STRESS-related psychotic or dissociative symptoms

Front 38

BORDERLINE PD

- Causes
- Suicide

Back 38

1. History of early abuse: 80% women
- Impairs trust & developing sense of self & others
= DEEP SEATED RAGE

2. Splitting: categorizes world as black and white: all good or all bad

3. Lack of object constancy: Can't emotionally access or carry w/ them a constant sense of others
- Once gone, always gone (fear of abandonment)
- Once bad, always bad (can't remember past goodness)
- Nothing is dependable: people can change so fast

4. Dramatic Triangle: Victim, persecutor & rescuer
- pt can influence people to act out these roles

5. Conflict bw desperate dependency & fear of closeness
- severe oscillations in relationships

MANIPULATIVE SUICIDAL GESTURES BC:
- Meets dependency needs (people come 2 support)
- Punishes those who don't care enough
- punishes self in response to intense feelings of worthlessness, self hate.

Front 39

borderlin pd

medicalsetting implications

Back 39

1. Don't believe pt too quickly about experiences w/ past doctors
- you may quickly fall into category of crappy doctors
- first idealizing you as a rescuer

2. Simultaneously demands and refuses care
- dependency + hostility
- give pt the choice

3. Staff can be split against each other
- pt is very manipulative
- hear other person's story (don't reinforce the pt's complaint about someone else)
- Keep communication clear, open, frequent amont staff

*everyone needsto go in to see pt together*

Front 40

DEPENDENT PERSONALITY DISORDER

Back 40

ESSENTIAL:
PERVASIVE pattern of EXCESSIVE
- dependent behavior
- submissive behavior (2' fears of seperation)

Inappropriate dependency:
- can't make basic everyday decisions
- needs constant advice, reassurance
- needs other to assume major responsibility
- goes ot great lenghts to obtain nuturance from others (even if hurting himself)
- has exaggerated fears of being unable to care for self

Excessive submission/fear
- puts up w/ abuse so dependency needs are met
- agrees, even if she thinks she's right
- Urgently seeks another relationship after breakup

*often pairs up w/ domineering, infantalizing person
*problem w/ appropriate assertiveness

AS A PATIENT:
- looks to doctor to make all decisions
- have to work w/ spouse/bf
- gets frustrated when recovery is slow, bc she idealized the doctor

Front 41

AVOIDANT PERSONALITY DISORDER

"i'm not good enough"

Back 41

ESSENTIAL:
- FEAR OF REJECTION/negative eval
- Social Inhibition (feelings of inadequacy

Fear of REJECTION:
- Avoids occupational activites with lotsa interpsonal contact
- Shows restraint w/in intimate relationships
- Preoccupied w/ being criticized/rejected in social situation
- Reluctant to take personal risks/do new things <--- embarrassing

Manifestations:
- unwilling to get involved unless being like is SURE
- Inhibitied in new situations
- Views self as socially inept

ILLNESS:
- Pt forced into something he hates: meeting different new people
- Initially feaful of, then overly reliant on doctor
- Develop trust & security
- Avoid criticism
- minimize new staff interations
- Avoid being a parent; encourage active role in decisions/tx

Front 42

OBSESSIVE COMPULSIVE PERSONALITY DISORDER

-ess
- compare w/ OCD

ex// anthony hopkins

Back 42

Preoccupied with: orderliness, perfectionism, mental&interpersonal control

At the expense of: flexibility, openness, efficiency

"type A" personality"

Front 43

OC Personality Disorder

- spectrum from traits --> disorders
- common dynamie

Back 43

traits can be VALUABLE/HELPFUL (not so in other disorders)

- but MALADAPTIVE in the extreme
- can obsess about decisions

Common dynamic = issue of CONTROL
- need to control outcome, emotions, and environment

Front 44

OC PERSONALITY DISORDER

- IN A MEDICAL SETTING

Back 44

- Productivity/achievement threatened/interrupted; fights hard to get back to work

- Yielding control to doctors is difficult; give them some control

- Involve pt as a full-fledged partner in the team

- Explain the pathophy& tx in detail
*if he knows the pertinent variables & possibilities, there is less uncertainty

- Frame recuperation/lifestyle changes as a responsibility
*help form routines/schedules incorporating new habits

Front 45

Influence of genetics in GAD AND PANIC DISORDER AND OCD

Back 45

PANIC PREVALENCE:
- Gen: 1-1.5%
- 1st degree relatives: 20%
*monozygotic concordance rate > dizygotic rate*


GAD:
- Gen: 2%
- 1st degree: 25%

OCD:
- 1st degree relatives: 35%

Front 46

Brain NTs of Anxiety
- NE
- 5HT
- GABA

*EVIDENCE*

Back 46

NE: fear system
- LC stimulation causes fear response
- LC ablation = no generation of fear response
- Manipulating NE receptors/NT release can module anxiety symtpoms

5HT: Meds
- ONLY effective meds in OCD are potent SSRIs
- Serotonergic drugs also help GAD & panic disorder

3. GABA: Meds (benzodiazepenes)
- GABA-a receptors bind benzos
- BZ binding causes enchancement of GABA binding
*MORE Cl- flows when BZ is there
- Barbiturates & Ethanol also enhance GABA effects @ the receptor

Front 47

BENZODIAZEPENE RECEPTOR LIGANDS THAT ARE ANXIOGENIC

(WHAT'S THE ENDOGENOUS LIGAND?)


**BZ receptors are in LIMBIC system & Neocortex**
(GABA-a R)

Back 47

*don't know*
similar to BETA CARBOLINES

- Act as inverse agonists
*cause anxiety & seizures*

- Beta-CCE has been found in human urine

**May be possible that TOO much stimluation of BZ receptor by the endogenous anxiogenic ligand can cause ANXIETY**

Front 48

NE / 5HT / GABA INTERPLAY IN ANXIETY

Back 48

SENSORY INPUT (pain/danger) --> activate limbic sites (amygdala) & LC --> many places --> ANXIETY!!

*MODIFICATIONS*:
- Limbic & cortical areas talk
- BZ Receptors at cortical & limbic sites
- 5HT input: INHIBITS LC

Front 49

COMMON MEDICAL CAUSES OF ANXIETY SYMPTOMS

Back 49

1. Hypoxia
2. Cardiac arrythmias
3. Endocrine disturbances
4. Hypoglycemia
5. Premenstrual syndrome
6. Caffeine & caff withdrawal
7. Alcohol & other CNS depressant WITHDRAWAL

Front 50

BIOLOGIC CONTRIBUTORS TO PANIC DISORDER

- central hypersensitivity

Back 50

1. CENTRAL HYPERSENSITIVITY:
- anxiety response systems (LC/NE) are HYPERSENSITIVE
--> trigger a cascade --> panic attack

DATA:
1. CNS leads the way
- it's not a generalized hypersensitive peripheral ANS rxn

2. Peripheral ANS response to NON-anxiety stimuli is NORMAL
- but it DOES follow, once CNS factors get the panic rolling


2. ^ NE or Suffocation alarm systems

3. Effective meds that reduce panic attack frequency = REDUCED rates of LC firing (dec NE)

Front 51

SUBSTANCES THAT PRECIPITATE PANIC ATTACKS

- relation to panic disorder pathophysiology

Back 51

Stuff assc'd with HYPOXIA & Detection of suffocation:
- Lactate
- CO2

* lower levels of this stuff is needed to produce panic symptoms in pts w/ panic disorder
= hypersensitive!
(esp suffocation alarm systems or areas that communicate w/ them)

ALSO: Stuff w/ ^ NE release
- Caffeine
- Yohimbine (antag of NE a2-autoR)
--> causing ^ release of NE

^ NE release = ^ flight/fight response (SNS)

Front 52

OCD AND BIOLOGICAL FACTORS

Back 52

- GENETICS: 35% 1st degree reatives

- PET/SPECT studies ipmlicate ORBITO-FRONTAL CORTEX & CAUDATE VIA THE THALAMUS
& the anterior cingulate:

1. OFC, Caudate, and Ant. cingulate are abnormally elevated at rest & with OCD symptom provocation maneuvers
2. This elevation is diminished w/ successful tx
3. Starting point for dysfxn = Inefficient CAUDATE
*cognitive tasks that increase caudate activity in normals fail to do so in pts w/ OCD*

SEROTONIN:
- SSRIs reduce OCD symptoms
- Primary abnormalities of 5HT functioning in OCD
- OCD is still MORE than just a 5HT system defect

Front 53

OCD PATHOPHYSIOLOGY

- WHAT CAUSES OBSESSIONS/COMPULSIONS
- PATHWAYS

Back 53

NORMAL CORTICO-STRIATAL-THALAMIC CIRCUIT:
(Loop):
OFC --> Caudate --> GP --> Thalamus --> OFC

*OFC has intrusive thoughts,
but healthy caudate gives appropraite input to thalamus,
- Thalamic GATING neutralizes the intrusive thoughts

OCD:
- Caudate dysfxn = no thalamic gating
- OFC is overactivated (strengthening thoughts)
- Ant. cingulate is overactivated by thalamus = ^ global anxiety

--> Dev of repetitive behaviors to drive the inefficient caudate
--> enough stimulation causes correct thalamic gating = reduced anxiety & diminished thoughts

Front 54

OCD PATHOPHYSIOLOGY

- WHAT CAUSES OBSESSIONS/COMPULSIONS
- PATHWAYS

Back 54

NORMAL CORTICO-STRIATAL-THALAMIC CIRCUIT:
(Loop):
OFC --> Caudate --> GP --> Thalamus --> OFC

*OFC has intrusive thoughts,
but healthy caudate gives appropraite input to thalamus,
- Thalamic GATING neutralizes the intrusive thoughts

OCD:
- Caudate dysfxn = no thalamic gating
- OFC is overactivated (strengthening thoughts)
- Ant. cingulate is overactivated by thalamus = ^ global anxiety

--> Dev of repetitive behaviors to drive the inefficient caudate
--> enough stimulation causes correct thalamic gating = reduced anxiety & diminished thoughts

Front 55

SYSTEMATIC DESENSITIZATION

Back 55

exposing the pt to the feared object/circumstance
- either in reality or mentally (or virtual reality)
- combined with relaxation/thinking techniques

= Desensitize the pt so that the fear focus no longer generates a disabling fear response

*Exposure is done in STEPWISE, GRADED fashion
- LEAST feared object/circumstance used first
- gradually work up to most feared

Front 56

COGNITIVE BEHAVIOR THERAPY

- for anxiety disorders

Back 56

- examines / identifies / attacks underlying automatic assumptions & mental habits which enhance/maintain state of fear/anxiety

Front 57

Exposure & Response Prevention

- what?
- for whom?

Back 57

for OCD pts
= COMBO of desensitization & cognitive therapy is used

1. Exposure techniques: hw assignements which involve increasing degress of exposure to simuli that cause discomfort
- goal = habituation will decrease discomfort

2. RESPONSE prevention:
- Learn/practice techniques that will reduce/delay/fully resist the compulsions that arise in presence of certain stimuli

Front 58

MEDS USED IN ANXIETY DISORDERS

Back 58

ANTIDEPRESSANTS
(ssri's)

&

BENZODIAZEPINES:
- GABA-a Receptor agonist: ^ Cl- influx = ^ inhibition

Front 59

indications for benzodiazepine use

Back 59

- acute situational anxiety
- chronic anxiety disorders
- insomnia
- reduce agitation
- anticonvulsant effects
- muscle relaxants
- tx of CNS sedative withdrawal (alcohol)
- brief sedation for med procedures

Front 60

LONG DURATION BENZODIAZEPINE

- DOWNSIDES

Back 60

1. Excessive daytime somnolence
2. Impaired motor skills & reflexes
3. Impaired anterograde memory
4. Increased Falls in the elderly

Front 61

BENZODIAZEPINES:

- Risk of withdrawal
- behavioral dependence

Back 61

WITHDRAWAL:
- ALL benzos show major rebound symptoms & withdrawal symptoms when you D/C the drug
**SHORTER duration of axn = MORE problems**
SOLUTION: taper the dose by 10% per week if pt's been on it >2-3 mo

BEHAVIORAL DEP/ADDICATION
- Most pts can use the same dose for months/years without getting addicted or becoming tolerant
- Pts at risk:
*Hx of dependence with other substances
*Benzos with rapid onset & short durations of axn

Front 62

PHARMACOLOGY OF BENZOS

- onset
- duration

Back 62

ONSET of axn: LIPID SOLUBILITY
- high lipophilicity crosses BBB faster

DURATION:
1. Receptor binding affinity (potency)
- tighter binding= longer effect

2. Lipid solubility:
- fast onset, but shorter duration (leave quickly to fat)

3. Elimination half-life:
- long half-lives can be countered by high lipid solubility

4. Presence of ACTIVE METABOLITE
- oxidative metabolism = active metabolites
*slowed by aging & P450 inhibitors
- Glucuronidation: NO active metabs
- not really affected by other drugs/aging
- Only THREE benzos use this pathway

Front 63

CHOOSING A BENZODIAZEPINE

- ANXIETY DISORDER

Back 63

IDEAL for treating anxiety disorders = safe medium-longterm use

1. High receptor affinity/potency
2. Lower Lipophilicity
3. Medium elimination half-life/Duration of axn
4. Metabolized via Glucuronide pathway or have no active metabolites after oxidative metab

CLOSEST TO IDEAL:
- Lorazepam
- clonazepam
- oxazepam

Front 64

PANIC DISORDER

- MEDS

Back 64

1. SSRIs = first line
- may take 2-4 weeks to work
2. Benzos: fast & effective
- more side effects & abuse liability
- no need for dose escalation or addiction potential
- Use w/ SSRI for first few weeks; taper off
3. TCAs & MAOIs are effective
but used as 2nd/3rd line choices

Front 65

GAD

- MEDS

Back 65

1. Antidepressants: first line
- Venlafaxine & SSRIs
- take few weeks to work
2. Benzos:
- used in pts w/o risk factors for abuse
3. Buspirone:
- non-benzo anxiolytic that can be helpful
- but NOT as effective as others

Front 66

OCD

- MED

**group therapy & CBT can also be helpful, esp in preventing relapse*

Back 66

1. Only antidepressants w/ HIGHLY serotonergic axns
- SRIs
- Clomipramine (TCA)
2. Higher doses than needed for depression
- Longer time to see benefits (12 weeks)
3. Response rates are lwoer than for depression
- many other meds are added to initial medication to try to further reduce symptoms

*Standard TCAs & MAOIs dont' work*

Front 67

GENERALIZED SOCIAL PHOBIA

- MEDS

Back 67

1. SSRIs = first line
2. Benzos also often used
3. TCAs & MAOIs are used 2nd/3rd line choices 2' side effects

*similar drug tx plan as Panic Disorder*

Front 68

SPECIFIC SOCIAL PHOBIA

(PERFORMANCE ANXIETY)

- MEDS

Back 68

Benzo or Beta blocker (propranolol) given right before performance

Front 69

ANXIOLYTICS

- BENZOS
- NON-BENZOS

(best for anxiety disorders = Lorazepam, clonazepam, oxazepam)

Back 69

BENZOS
- Alprazolam - Xanax
- Lorazepam - Ativan
- Clonazepam - Klonopin
- Diazepam - Valium

NON-BENZOS
- Zolpidem – very common hypnotic agent (Ambien)
- Eszopiclone Lunesta
- Buspirone – a partial agonist of serotonin. Buspar

Front 70

Disorders in which Psychotic symptoms are present

Back 70

PSYCHOTIC SYMPTOMS = Evidence of loss of touch with reality

- psychotic disorders (schizophrenia = prototypic)
- Mania
- Depression w/ psychotic features
- dissociative identity disorder (auditory hallucinations)
- delirium
- dementia

Front 71

How is schizophrenia "hidden" & devastating?

Back 71

HIDDEN:
1% of population has it; 25% of them are homeless
- most pts are out of the social mainstream

DEVASTATING:
- Permanent impairment in ability to relation & fxn socially & occupationally
- since early adulthood

Front 72

THREE KEY ELEMENTS TO SCHIZOPHRENIA DX

Back 72

1. At least two:
- Delusions
- Hallucinations
- disorganized speech
- grossly disorganized / catatonic behavior
- "NEGATIVE" symptoms
(only 1 if delusions are bizarre or hallucinations are a continuous voice/ voices talk to each other)

2. Clear cut decrement in social & occupational functioning

3. At least a six-month duration

Front 73

Delusions

- bizarre vs non-bizarre
- paranoid, grandiose, somatic
- thought control/broadcasting/withdrawal/insertion
- ideas of reference

Back 73

False beliefs SO FIXED that nothing can change their beliefs

Bizarre: could never happen
Non-bizarre: could happen (FBI are after me)
Paranoid/Grandiose: usu go together
Thought Control - outside force
Broacasting: project his thoughts into others minds
Withdrawal/insertion: outside force

Reference: events refer to one's own self/situation

*Direct, immediate, & TOTAL certainty w/ which the pt holds these beliefs.
- also consistently more bizarre

Front 74

HALLUCINATIONS

- WHAT
- MOST COMMON
- ASSOCIDATED WITH??

Back 74

False sensory perceptions not associated with real external stimuli
- vs. illusions (misperceptions BASED on REAL external stimuli)

in SCHIZOPHRENIA:
AUDITORY = most common (75%)
- usually voices

Visual = next most common; 1/3 pts

Other senses: much more commonly associated with PSYCHOSIS DUE TO A SUBSTANCE OR GENERAL MEDICAL CONDITION
(ex// olfactory, gustatory, somatosensory hallucinations)

Front 75

DISORGANIZED SPEECH

- loosening of associations
- blocking
- neologisms

Back 75

LOOSE ASSC
- u have to guess a connection or "fill in the gap"
- can get severe --> sentence frags, word salad

BLOCKING
- abrupt cessation of a flow of thought

NEOLOGISMS: made up words

Front 76

NEGATIVE SYMPTOMS

(VS. POSITIVE SYMPTOMS

Back 76

negative: things absent that should be present
(positive symptoms is opposite)

COMMONS:
- Blunted/flat affect
- Loss of motivation = apathy
- Diminished use of speech
- Impaired goal-directedness

Front 77

CATATONIA

- what
- symptoms

Back 77

Motor syndrome
- relatively rare
- seen more often w/ mood disorders than with schizophrenia

1. Motoric Immobility: stupor/remains in one position for loooong time

2. Excessive motor activity: purposeless; can alternate with immobility

3. Negativism (won'ts)
- won't obey, be moved, or talk

4. Unusual posturing or movementssuspiciousness

Front 78

SCHIZOS & DECREASED SOCIAL & OCCUPATIONAL FUNCTIONING

Back 78

Remains evern after full-blown psychotic symptoms have diminished w/ meds

- Impaired cognitive & intellectual functioning
- Loss of motivation & ability to plan & be goal-oriented
- Chronic presence of some hallucinations and/or delusions or

Front 79

SCHIZOPHRENIA SUB-TYPES

Back 79

- PARANOID: later onset, better prognosis
- DISORGANIZED
- CATATONIC: diff tx response
- RESIDUAL: most partial remissions fall into this type
- UNDIFFERENTIATED

Front 80

Life risk of schizo in general pop

- vs. first degree relatives

Back 80

About 1% (point prevalence 2-10/1000)
- Similar lifetime risk in males and females
- Females have later onset


1. Increased prevalence with increased genetic load:
a. First-degree relative - 10%-15%
b. Two schizophrenic parents - 40%
c. Monozygotic twin of patient with schizophrenia – 40-50%

2. Not just due to growing up with crazy parents:
a. Schizo parents; raised by someone else - 10%
b. non-schizophrenic parents but raised by parents, one of whom has schizophrenia - about 1%.

Front 81

FACTORS INCREASING RISK OF DEVELOPING SCHIZO

Back 81

1. Being a migrant
2. Older father
3. Cannabis use
4. Obstetrical complications
5. Urban rearing
6. Winter/spring birth

Front 82

VARIABLE PENETRANCE OF SCHIZO (?)

twin studies of ill vs non-ill twin & rates of passing on dz in respective offspring

Back 82

Variable penetrance - In monozygotic twins discordant for schizophrenia, the offspring of the non-ill twin are as likely to develop schizophrenia as the offspring of the ill twin.

Front 83

CLINICAL COURSE OF SCHIZOPHRENIA

- ONSET
- BEFORE ONSET
- Prognosis once illness is fully started

Back 83

A. Onset - Average age of first severe symptoms:
- Males - 15-25 years old
- Females - 25-35 years old

B. Were they totally normal before?
1. 25%-50% obviously were "different kids" (schizoid or schizotypal characteristics)
2. Subtle cognitive/intellectual impairments are present prior to the onset of psychosis


Course is chronic and relapsing with generally incomplete remissions

Front 84

SCHIZOPHRENIA

- COURSE
- poorer prognosis
- common causes of relapse

Back 84

Chronic & relapsing
- incomplete remissions
- relapse rate = 75%/year if no meds
- ON meds = 25% relapse/yr
- Impairment in a variety of cognitive fxns is present after 1st psychotic episode


Most common causes of relapse
- Stopped meds
- street drugs (esp stimulants0
- stress (much more vulnerable)


Overall prognosis:
- Highly variable; w/ tx

*POORER PROGNOSIS*
- Early age of onset of 1st psychotic symptoms
- prolonged period of untx'd illness
- worse severity of cognitive impairment and/or negative symptoms

Front 85

SUICIDE & SCHIZOS


who is at highest risk?

Back 85

1. Approximately one-third attempt suicide, and ~5% die by suicide
2. Highest risk are patients who have greatest sense of loss from the illness:
a. Better premorbid functioning (and potential)
b. Intact insight
3. Early in course of illness
4. Highest risk is during a period of post-psychotic depression

Front 86

SCHIZOS & VIOLENCE


- who is more likely to be violent?

Back 86

Most are NOT violent
- more likely to be VICTIMS of violence

increased rate of violence in:
- ^ severity of positive symptoms
- substance abuse
- impulsivity

Front 87

SUBSTANCE ABUSE

- which is assc'd w/ increased risk

Back 87

HIGH PREVALENCE OF SUBSTANCE ABUSE in pts w/ schizo
- nicotine dependence is 5x as prevalent

CANNABIS use is assc'd w/ increased risk of developing dz & earlier age of onset

Front 88

QUALITY OF LIFE & MORTALITY IN SCHIZOS

Back 88

INCREASED rates of homelessness & unemployment (<20% fully employed0

2/3 never marry & most have reduced outside contact

INCREASED MORTALITY
- DIE 15-20 yr sooner
- 25% of excess is due to suicide
(10% is due to accidents)
- rest of increased rates are due to increased medical conditions (esp CV dzs)

Front 89

DIFFERENTIAL DX OF PSYCHOSIS

Back 89

1. 2' general medication condition or substance
ex// CNS stimulants; hallucinogens, HIV, CNS lesions, basal ganglia disorders, endocrinopathies, medical drugs (DA agonists & steroids)

2. Presence of marked MOOD symptoms & different TIME course
- bipolar vs schizoaffective vs depression w/ psychotic features

3.Shorter duration
- brief psychotic disorder
- schizophreniform disorder

4. Milder symptom
- delusional disorder
- cluster A personality disorders

Front 90

SCHIZOAFFECTIVE DISORDER

- genetics
- tx
- prognosis


- psychotic symptoms can occur even during stable periods
(not the case in bipolar disorder or depression w/ psychosis)

Back 90

MOOD DISORDER + SCHIZOPHRENIA

1+ Positive symptoms
Mood episodes must be present often
- can be manic or depression
- Some hallucinations or delusions sTILL remain b/w mood episodes

*does NOT breed "true" in families
- not really a "unique" disorder

TX: Mood-stabilizer

Prognosis: in b/w mood disorders & schizos
- intermediate prognosis

Front 91

PSYCHOSIS OF BRIEF DURATION

<6 MO

- DIFF

Back 91

1. Brief psychotic disorder
one month or less

2. Schizophreniform disorder
1-6 months

3. More than six months = SCHIZOPHRENIA
(need clear social/occupational decline)

Front 92

BRIEF PSYCHOTIC DISORDER


- Essential features
- role of stress
- who is more vulnerable to get this

Back 92

DURATION: LESS THAN ONE MONTH
- usually abrupt onset

Follow clear & significant STRESSOR
- symptoms resolve in days w/ tx
(stressor not always present)

*Need to rule out medical illness as a cause**

More Vulnerable to Stressor:
- personality disorders (Clusters A & B)
- Adolescents, yount adults
- Lower SES, recent cultural change

Front 93

SCHIZOPHRENIFORM

- Diff from schizo
- indicators of poor prognosis

Back 93

IDENTICAL to schizo EXCEPT
- symptoms ALL resolve
- Pt returns to functioning in six months

a "waiting/ sorting out" period
- if >6 mo ---> schizo

Indicators of worse prog (-> schizo)
- Less abrupt; more insidious onset
- Poor premorbid functioning
- Blunted affect
- do NOT have confusion, disorientation, perplexity
(not usually seen in schizo)


*heterogenous group of pts*
- can be like schizo or mood disorder etc

Front 94

DELUSIONAL DISORDER




*no other weird things going on*
- mainly just behaviors/ideas revolving around one systematized, non-bizarre illusion

Back 94

MILDER than schizo & not as disabling

Non-bizarre: "COULD" happen
- often systematic; intricate
- RARE
- Distinct disorder: family members have increased rates of this specific disorder

*very rarely progress to schizo or mood disorder*

Diff from schio
- NO MAJOR DECLINE IN FXNING
(other than direct results of delusions)
- usu no hallucinations
- no loose assc
- no bizarre behavior (other than acting out on delusion)
- no blunted affect
- no bizarre delusions

**SEVEN types of delusion disorder**
- SOMATIC TYPE = will see medical elp

Front 95

DELUSIONAL DISORDER

- PROGNOSIS
- handling them

Back 95

Marital and social functioning often impaired

At long-term follow-up (years):
1) 50% - no delusion
2) 30% - no change
3) 20% - less delusional

Be sure to rule out medical causes of psychotic symptoms.

What do you say to these people?
- Don't agree with or argue about the delusion.
- Try to side with the patient by focusing on REAL areas of stress or distress in his/her life.

Front 96

HOW MIGHT PSYCHOSOCIAL EVENT RESULT IN CHANGES IN DISEASE?

Back 96

a. Changes in endocrine function
b. Changes in sympathetic nervous system function
c. Changes in immune function

Front 97

HOW DOES STRESS ALTER IMMUNE FXN?

- evidence

*depressed pts also have suppressed immunity
- esp in depressed hospitalized pts & older depressed
- it resolves as depression resolves

Back 97

1. Beta blockers prevent reduced immunity in people with acute stress

2. Humoral immune response changes day to day; depending on pt's outlook on the day

3. Higher incidence of mood disorders in immune-mediated illnesses
- greater incidence of depression pts receiving immunomodulating therapy (Hep C & CA)

4. Reduced immunity/NK cell activity in:
- medical students
- nuclear accident survivors
- alz's pts caretakers

Front 98

STRESS RESPONSE

- effects of stress on hormones/NTs

Back 98

1. NT: activates locus ceruleus
- increases catecholamines
- increased serotonin turnover (less 5HT); stress in depression

2. ENDOCRINE:
- High levels of CRF, ACTH, Glucocorticoids
---> fight/flight

3. IMMUNE
- High glucocorticoids inhibit immunity
- Also increases NE --> humoral activation (IL-1, IL-6, IFNy)
---> high levels of pro-inflamm cytokines in depression

Front 99

Interpersonal interactions and immune function

Back 99

- "Negative" mood or social interactions can decrease immune fxning
- even within the same day

2. Old pts w/ a confiding relationship had greater immune functioning

**Aspects of immune fxning are sensitive to changes in mood/psychosocial situations
- but are they clinically significant in disease onset/progression?

= they do have a big impact, but immunity might not be the bridging factor as to why people get better

Front 100

The cardiac consequences of acute stress

Back 100

Emotional stress is a trigger for 20-30% of acute coronary events.
- stress = increase BP, Pulse & SNS
- Depressed pts = ^ risk of arrhythmias
- During stress, 1/3 - 1/2 of CAD pts have cardiac ischemia
(^ risk of death)
- Elevated cortisol
--> amplifies cardiotoxic effects of catechoalmines
---> INCREASES RATE OF ARTERIOSCLEROSIS

Front 101

The evidence for stress contributing to hypertension

Back 101

Weaker than stress --> CAD

Rats
- stress - chronic elevated BP

HTN pts
- respond to stressful stiations w/ greater increases in BP than non-HTN pts

Front 102

The components of Type A behavior

Back 102

- easily aroused anger, impatience
- hostility, aggression
- competitive striving, intense achievement drive
- time urgency
- desire for recognition & achievement

Front 103

Previous and recent findings regarding Type A behavior and coronary artery disease risk

Back 103

PREVIOUS:
- 2X ^^ risk of MI & fatal coronary events
- counseling to reduce Type A behavior = significant reduction in recurrent MI

RECENT STUDIES = inconclusive/negative
- hard to tell bc of more effective cardiac drugs (beta blockers)
*assuming ^ SNS is mediating factor bw Type a PTS & <3 risk*

- Anger & Hostility are much less clearly linked
- Hostility = ^^ levels of catecholamines & lipids
---> increased risk of <3 disease

Front 104

The impact of (untreated) depression on the incidence and course of coronary artery disease

Back 104

Current OR past depression = ^ risk of CAD

UNTREATED DEPRESSION
- increased mortality after <3 sx
- 4x Higher mortality rate
- Unstable angina: Odds ratio of 6.73 for increased serious <3 events
- decreased quality of life after dx of <3 dz

**MDD in ~20% of pts following MI**
- anxiety disorders are present in 10-15% of <3 pts

Front 105

ANTIDEPRESSANTS IN CAD PTS

-Mechanism by which SSRIs may have a protective effect in CHD

Back 105

AVOID
- TCAs = type IA antiarrhythmics
(alters conduction at SA & ventricular pacemaking nodes)

USE:
- SSRIs: also reduce platelet activation & aggregation (less coronary occlusion)

PROTECTIVE effects of SSRIs
- BLOCK 5HT transporter protein on platelets
- Release of 5HT by platelets = critical for platelet aggreg & thrombus formation

*studies with sertraline (zoloft = SSRI)*

Front 106

Pathways by which depression may contribute to increased risk of cardiac disease

Back 106

1. Impaired adherence to tx plans/health modifications

2. Increased SNS activation, suppressed vagal tone
--> increased risk of <3 arrhythmias

3. Increased levels of Inflamm cytokines (NE --> iL-6)
---> atherogensis & coronary events

Front 107

The impact of social support on the course of coronary artery disease

Back 107

Low levels of social support = INCREASED RISK of bad outcome in CAD pts

Front 108

The risk of coronary artery disease in panic disorder patients with cardiac symptoms

Back 108

although panic attack can look/feel like an MI,

panic disorder pts w/ cardiac symptoms during their panic attacks are NOT MORE LIKELY to have actual <3 problems than panic disorder pts w/o cardiac symptoms

Front 109

CARDIOVASCULAR DISEASE / CAD

- Psychosocial factors that make it worse / worse prognosis

Back 109

2' sympathetic / neuroendocrine functioning caused by these emotional states

1. depression
2. Type A personality
3. Stress
4. Crappy social support

(NOT panic disorder w/ cardiac symptoms)

Front 110

The category of psychiatric disorders most commonly seen in pulmonary diseases

Back 110

PULMONARY DISEASES = Anxiety

--> Anxiety disorders & anxiety symptoms

- 30% of asthma pts = panic disorders
- 10% = depression & anxiety disorder

Main medical conditions = COPD & asthma

Front 111

The common psychiatric side affects of pulmonary medications

Back 111

meds = theophylline, inhalers w/ beta agonists

- jitteriness
- palpitations
- insomnia
- restlessness
- irritability
- steroids --> mood problems & mood lability

Front 112

The interrelationship between shortness of breath and anxiety

Back 112

1. Dyspnea & anxiety both contribute to the other
- symptoms can overlap
2. Overuse of inhalers possible
- mistake anxiety --> dyspnea
- worse jitters & anxiety
3. Depression
- increased subjective complaints of SOB
**Pulmonary pts w/ excessive SOB complaints
--> investigate for depression & anxiety disorders**

Front 113

Reasons behind the development of avoidance behaviors in pulmonary patients

Back 113

Emotional stimuli changes airway tone
- esp in larger upper airways (cholinergic innerv)
- emotional effects are greater in the presence of other triggers of bronchoconstrictors

*Pts w/ chronic resp disease may increasing avoid potentially emotional situations
- isolation; constriction of activities
- intense fear
- emotional lability
- sensitivity to rejection
- lack of persistence in difficult situations

Front 114

The effects of hypoxia on cognition

as many as 40% of COPD have sig DEPRESSION
(impaired efforts at rehab & smoking cessation)

Back 114

*Chronic lung dz = Chronic hypoxia*

Sudden O2 drop = marked confusion & delirium

SLOW O2 decline = decreased
- concentration
-memory
- abstract reasoning
- complex perceptual motor integration
- language function

*Steroid meds can also affect info processing
--> exacerbate hypoxemia effecs

**use an oxygen tank (but pts are often embarrassed to use it)

Front 115

Anxiety disorders commonly found in asthma patients

Back 115

DOUBLE CHECK THE DX
- inquire about what triggers SOB

HIGH COMORBIDITY
- GAD
- PANIC disorder
- social phobia
- specific phobia

again:
30% asthma pts = panic disorder
10% asthma pts = both Depression & anxiety disorders

*Family members have higher prevalence of mood disorders, PTSD, substance use, Antisocial PD
- genetic & social components invlved

Front 116

The impact of emotional stimuli on airway reactivity and asthma symptoms

Back 116

Emotional situations can trigger asthma attcks
--> significant bronchoconstriction w/ acute stress

MECHANISMS:
- Vagus n. mediates emotion --> airway reactivity
- Stress/emotion = increased Resp Resistance
- assc'd with Impaired medication adherence & increased use of emergency services

Front 117

The relationship of anxiety to coping with asthma

Back 117

You need to be "medium" anxious about your illness
- enough anxiety that you don't ignore symptoms; take your meds; stay at the hospital long enough

Increased anxiety
- increased hospitalizations
(regardless of illness severity)
- increased use & dose of meds
- just as bad as not caring about ur illness at all

(inverted U-shaped curve)

Front 118

the role of stress in peptic ulcer disease

Back 118

Many people w/ h. Pylori get no ulcers
- H. Pylori & NSAID = primary risk factors of peptic ulcer

STRESS is an indpt risk factor
- can decrease immune response
- vulnerable to H. pylori infxn

Front 119

The definition of irritable bowel syndrome (IBS)

- requirements & symptoms

Back 119

12+ weeks w/in the past year (not nec. consecutive weeks)
- abd discomfort/pain

3 of 5 features:
- relieved w/ defecation
- onset assc'd w/ change in frequency of stool
- onset assc'd with change in form of stool

Symptoms:
- >3BMs / day or less than 3 / week
(too much / too little)
- Abnormal stool form or passage
- Passage of mucus
- Bloating or feeling abd distention

Front 120

Symptoms which point to GI diseases other than IBS

Back 120

a. Nocturnal diarrhea
b. Rectal bleeding
c. Malabsorption
d. Weight loss
e. Pain that is progressive in nature, prevents sleep, leads to anorexia or inability to eat, or is associated with systemic findings such as weight loss.

Front 121

The contribution of IBS to work absenteeism

Back 121

Second only 2 common cold as cause of skipping work

- Most common GI disorder = 40% visits
- 23% of primary care visits
- 8-20% of general population will get it at one point
- Only a SMALL percentage of people w/ IBS seek tx

*Those who seek tx for IBS are different psychiatrically*

Front 122

Characteristics of patients seeking treatment for IBS

Back 122

High prevalence of psych disorders
- esp mood & anxiety disorders (50-60%)

1) Robust correlation between the severity of IBS symptoms and the severity of anxiety and/or depression
2) High rates of sexual dysfunction
3) High rates of other symptoms suggestive of anxiety and autonomic arousal


Higher reported rates of:
a) Childhood parental loss
b) Childhood sexual or physical abuse
c) Childhood history of frequent doctor’s visits
d) Pain syndromes
e) Losses or separations
f) Childhood family patterns in which somatic complaints were reinforced with parental rewards of attention, gifts, etc.

Front 123

Psychotherapies shown to be helpful in IBS

Back 123

1. CBT (improves physical symptoms --> improved quality of life)
2. Psychodynamic psychotherapy
3. Interpersonal psychotherapy
4. Group psychotherapy

Front 124

The effect of stress in IBS

Back 124

Typically precedes onset of IBS symptoms
- mostly SOCIAL stress (relationships)
-
*Social stress is SINGLE MOST IMPORTANT PREDICTOR of outcome in pts w/ IBS who attend a GI clinic*

Front 125

Basic principles of treatment of IBS

Back 125

Untx'd Pysch symptoms = poor IBS outcome

TREATMENT:
- low doses of TCAs: rapid; less good for pts w/ constipation
- SSRIs: slower onset; less good for pts w/ diarrhea
- Psychotherapy
- treat comorbid psych disorders = reduced GI symptoms

Internist is best for pts who insist on medical care
- deal sw/ somatization
- refer to psych when u develop trust
- educate pt: chronic, recurrent dz; triggers
- address alternative dx's fears
- schedule return appts (pt is needy)

Front 126

Which antidepressants are helpful in treating IBS

- also role of 5HT

Back 126

Most bioavailable 5HT in the GUT
- released from EC cells
- alterations of 5HT signaling in IBS
- Drugs that alter 5HT help with IBS symptoms
- unclear if 5HT alters mucosa or other way around

*low-dose TCAs & SSRIs*

Front 127

Psychiatric concomitants of globus

Back 127

Globus = "lump in the throat"
- related to swallowing
- no actual difficulty in swallowing / esophageal dysfxn

Related to: GRIEF, ANXIETY, DEPRESSION
- abates on its own
- responds to supportive psychotherapy
- carefully eval for axis I disorders

Front 128

NORMAL PATHOLOGY, ABNORMAL PHYSIOLOGY of IBS

(other GI symptoms = globus & esophageal dysfxn)

Back 128

histologically normal colons
- physiology of intestinal motility is weird

1. Lower pain threshold to bowel distention
2. Abnormal motility pattern (over-responsive to normal stim)
3. More frequent pre/post-prandial high amplitude prolonged colonic contractions
4. Greater amt of "slow" contractions in distal colon
5. Decreased lower esophageal sphincter pressure
- other weird esophagus motiility issues
6. Increased baseline colonic pressure
*maybe inflamm cytokines too*

Front 129

Effects of different treatments on complaints with patients with esophageal dysmotility

Back 129

Increased incidence of psych disorders assc'd with esophageal dysmotility
- MDD
- GAD
- Somatization
- substance dependence
- panic disorder & social phobia

Treatment to reduce PSYCH symptoms
- reduces frequency of esophageal complaints
(no real change in dysmotility)

Tx to reduce DYSMOTILITY
(via effects on smooth mm)
- NO reduction in esophageal complaints

Front 130

The characteristics of psychiatric disturbances related to B12 DEFICIENCY

Back 130

Most common = pernicious anemia

Psych problems can happen before or independently of other hematologic or neuro problems assc'd w/ B12 def

- B12 Def is asscd with EVERY SINGLE TYPE of psych symptoms
* even when B12 serum level is in very LOW NORMAL range*

Front 131

The characteristics of psychiatric disturbances related to PANCREATIC CA

Back 131

unusually HIGH rate of MDD
- even when compared to other CAs just as lethal & advanced

*unknown mechanism*

Front 132

Psychiatric symptoms commonly seen in HCV infection

- Psychiatric side effects of Interferon, and their treatment

Back 132

Higher risk of depression (than Hep B)
- IVDU mostly = higher risk of psych disorders

IFN TX:
• Fatigue in almost all cases
• High rates of depression
• Cognitive complaints
• Anger and hostility
- significant increases of depressive & anxiety disorders from baseline

**roughly 60% of pts receiving IFN-a tx = anxiety or depressive disorder
- severity of depression correlates w/ fatigue (not w/ hepatic dz severity)
- SSRIs used to tx

Front 133

INFLAMM BOWEL DISEASE & PSYCH DISORDERS

(CROHN'S & ULCERATIVE COLITIS)

Back 133

BIG life impact of illnes

higher rates of pre-existing panic disorder in Crohn's dz

Ulcerative colitis = prone to obsessive compulsive traits

Front 134

a. Difficult aspects of life on dialysis

(ESRD = End stage renal disease)

Back 134

fucks up your WHOOOLE life
- work, sexuality, life expectancy, family, meals, finances, painful, waiting, strict diet.
- preoccupation w/ thirst = stress
- dietary non-compliance = #1 immediate cause of death from CHF in ESRD
- Time consuming 24 hrs / week)
hemodialysis/ cont. / nocturnal

Front 135

Mortality rates in dialysis and transplant patients

- quality of life too

Back 135

Renal transplant = improved quality of life
- improved quality in pts w/ nocturnal hemodialysis

HIGH MORTALITY IN ESRD
- 23%
- Dialysis pts = 1/4 or 1/5 that of normals
- Transplant pts = live 70-80% as long as normals

Front 136

The impact of ESRD on cognition and sexuality

Back 136

Subtle, but real decrements in:
- concentration
- memory
- problem-solving

*Performance IQ declines 2' motor slowing*

SEXUALITY:
- decreased libido & decreased frequency
- erectile difficulties
- intact kidney fxn is necessary for fully normal sexual functioning

Front 137

The impact of depression on the course of ESRD

Back 137

ESRD = DEPRESSION
- most common psych problem
- decreased survival times
- diminished adherence (poor self-care)
- antidepressants can be helpful

**depression impairs judgment & impairs decision making**
--> affects decisions to stop dialysis

Front 138

Issues involved in assessing requests for dialysis discontinuation

Back 138

Type of suicide?
- not necessarily; elective procedure
- only 1-2% end dialysis to commit suicide

Rational TX withdrawal:
- 20-25% ESRD deaths
- 2 things: diabetes & increasing age (>60 yo)

Don't assume all pts are justified or that all are requesting suicide by withdrawing dialysis

*depression can affect decision making*

Front 139

The psychiatric risk factors contributing to LATE graft failure in renal transplants


-The best predictor for noncompliance with post-renal transplant treatment

Back 139

a. Age less than 30 years old
b. Substance dependence
c. Untreated major depressive disorder

3rd major cause of allograft rejection
= Non-compliance (diet, meds, appts)

Best predictor for non-compliance of POST-transplant tx is non-compliance of PRE-tranpslant tx (ex// dialysis)

Front 140

The diagnoses which may be part of the picture of the postpartum psychosis

recurrent rate = 20-30%
- rate of developing another psych episode (out of context of pregnancy) also INCREASED

Back 140

1) Major depression with psychotic features
2) Mania
3) Brief psychotic disorder
4) Or the symptoms may not fit neatly into any particular category.

The MAJORITY of psychotic symptoms occurring in the postpartum period develop in the context of a MDE

Front 141

The chemical component of oral contraceptives most associated with depression

Back 141

TWO RISK FACTORS:
- amt. of PROGESTIN
- Hx of previous depressive episodes, PMS, post-partum depression

Front 142

postpartum blues vs. postpartum depression



-Risk factors for the development of postpartum depression

Back 142

BLUES = COMMON, MILD
- tearful, sad
- 2' rapid withdrawal of hormones post-delivery or poor response 2 oxytocin (enhances bonding)
- begins w/in 48 hrs; peaks 3-5 days
- usu. resolve on own; no meds
- SUPPORT & REASSURE
- 50-85% of new moms
- about 20% --> depression

DEPRESSION:
- 4-16% MDE w/in 4 wk of delivery
- most begin w/ baby blues
- Directly inquire (moms may not report)

Risk factors for depression:
- depressive symptoms during pregnancy
- hx of previous MDE
- hx of premenstrual dysphoria

Front 143

Adverse consequences of postpartum depression and postpartum psychosis


- risk factors of psychosis (post partum)

*psychosis more common among women having 1st child*
- baby blues = no relation to parity

Back 143

Affects the INFANT
- poorer mom/baby interactions
- do poorly on behavioral tests
- moms contemplate harming their baby
(highest risk = first 6 months)
**ESP. if mom has psychotic symptoms*
- risk of recurrence is high (psychosis)

Post-partum psychosis risk factors:
- hx of psych illness
- family hx

Front 144

The definition of menopause and climacteric

Back 144

MENOPAUSE
- permanent cessation of menstruation 2' loss of ovarial activity

CLIMACTERIC (perimenopause)
- transition period from reproductive --> nonreproductive status
- time period: a little before menopause --> at least 1 yr afterward

Front 145

The findings regarding psychiatric disturbances associated with menopause

Back 145

Climacteric = increased psych distrubances
"involutional melancholia"
- maybe false

*Rates of physical symptoms are increased
- mood symptoms are NOT increased
- 52% of women do experience MDE (1st episode)
- pts w/ hysterectomy = more psych disturbance

Front 146

Nature and treatment of vasomotor symptoms in menopause

Back 146

80% experience:
- Hot flashes (+ palpitations & anxiety)
- Warm flushes
- Night sweats

TX:
- Mild: vit E & relaxation techniques
- Moderate --> Severe: HRT
* risks for MI, stroke, breast CA, & coagulopathies*
(use for brief periods)
- SSRIs & dual mech antidepressants (venlafaxine)

Front 147

Changes in sexual functioning occurring after menopause

Back 147

1. Dyspareunia (2' vaginal atrophy)
2. Atrophic vaginitis & decreased vaginal lubrication
(treat above w/ estrogen tx)

3. Decline in libido
- 2' testosterone reduction

*Non-bio factors also play a role
- poor marital health
- unsupportive husband

Front 148

CHRONIC PELVIC PAIN

- definition
- lap findings

Back 148

Pain in 1+ soft tissues of the paracervical area, vaginal area, abd wall, or over sacrum
- chronic (>6 mo)
- occurs during coitus, menses, bladder distention, etc.

Lap findings are very variable
- 17% - 90% have normal pelvic organs

(WE DON'T KNOW WHAT'S CAUSING THEIR PAIN)

Front 149

CHRONIC PELVIC PAIN

- PSYCH characteristics
- management

Back 149

41% w/ CPP have NO Pelvic Dz
These pts have Higher rates of:
- anxiety
- depression
- hostility
- non-pelvic somatic symptoms

General Majority (56%) rated within normal range on psych/emo factors
- rates of stress/early difficulties did not differ
- BUT STILL: SUBGROUP of CPP pts = sexual/physical ause

SINCE WE DON'T KNOW what's cuasing the pain
- address factors known to worsen pain
- help pt address psych factors that may be responsible for pain (CBT, relaxation, acupuncture, sex counseling etc)
- antidepressants &
recipitants of pain increase

Front 150

STROKE & DEPRESSION

- brain region
- marker of depression
- incidence (in ischemic strokes)

Back 150

STROKES = DEPRESSION
- 25-40% with ischemic strokes
- Left Anterior regions of brain
- Good marker for depression post-stroke = LACK OF MOTIVATION
(can be hard to dx bc of speech problems)

Front 151

Psychiatric symptoms seen with brain tumors

Back 151

almost any area can result in psych symptoms

- FRONT LOBE: mixed psych & behavioral syndromes assc'd w/ frontal lobe fxns

others: mood disturbance, emotional discontrol, occ psychotic symptoms

Front 152

Consequences of untreated depression in post-stroke patients

- effects of successful tx of depression in post-stroke pts

Back 152

1. Sig Delay in attainment of ADL (activity of daily living)
- depression = strongest predictor of poor ADL attainment
2. 3-4x increase in ten year mortality

*Treatment makes HUGE difference*
- reduced depressive symptoms
- rapid re-attainment of ADLs
- significantly lower mortality rates over 9 yr followup

**depressive symptoms = increased stroke risk AND increased stroke mortality**

Front 153

Definition of partial seizures and complex partial seizures

- usual foci in complex partial seizures & psych manifestations

Back 153

MOST seizures do NOT involve convulsions/loss of consciousness
- degree of spread is variable
ex// frontal & temporal lobe --> mostly non-motor manifestations

Partial seizures = localized
- Simple: don't alter pt's awareness of surroundings
- Complex: alter pt's consciousness

COMPLEX PARTIAL SEIZURES:
- Frontal or temporal lobes
- Pysch:
1) Depersonalization
2) Deja vu
3) Auras of fear, pleasure, or sadness
4) Illusions or hallucinations – occasionally “Lilliputian”
5) Amnesia

Front 154

Common emotional or psychiatric consequences to significant head trauma

Back 154

Significant = loss of consciousness for several hours or more

1. Irritability or increased aggrestion (70% pts)

2. Frontal lobe damage - type symptoms
- lability, shallow, socially inappropriate, bad at math, cognitive deficits, can't concentrate / abstract / analyze

3. Pre-existing mood disorders/syndromes can be WORSENED

Front 155

Common cognitive and emotion complaints of patients experiencing a concussion

Back 155

MILD head trauma; brief loss of consciousness

1) Memory dysfunction
2) Decreased concentration
3) Dysthymia
4) Anxiety
5) Irritability
6) Personality changes

c. Other symptoms commonly found in post-concussion patients are:
1) Decreased energy
2) Dizziness
3) Headaches
4) Depression

*not correlated w/ severity of injury or degree of loss of consciousness*

Front 156

Psychiatric disturbances that occur at a higher rate in patients with seizures

Back 156

Increased rates of psych distrubances in general

- HIGH rates of DEPRESSION
(esp in left hemisphere; L. Ant)
- 7% of seizure pts = schizophrenia-like symptoms

Front 157

Relationship of pseudoseizures to real seizures

Back 157

Convulsive-type
- don't fit typical seizure patterns
- NOT assc'd with weird EEG activity

= conversion or somatization

*High percentage of pseudo-seizure patients ALSO have TRUE seizures

Front 158

Psychiatric disorders occurring at a high rate in Parkinson’s disease

-Psychiatric side effects of Parkinsonian medications

Back 158

1. DEPRESSION
- 40-50% have MDE
- often have major anxiety symptoms
2. DEMENTIA
- 65% have it by 85 yo

MEDS / SIDE EFFECTS:
1. DA Agonists = psychotic symptoms
2. Anticholinergic meds: produce confusion & memory impairment

Front 159

Common psychiatric manifestations of Huntington’s disease

Back 159

Genetic caudate atrophy --> movement disorder, dementia, mood/behavior disturbance

Pysch symptoms = 1st manifestions of dz

1) Personality change
2) Mood disorder (in more than 50%)
3) Schizophrenia-like symptoms
4) Antisocial actions
5) Suicide (in almost 6%)
6. Dementia

Front 160

Common psychiatric manifestations of multiple sclerosis

Back 160

a. Some degree of intellectual decline
b. Personality changes
c. Depression (at times present before any neurologic symptoms)
d. Euphoria or hypomania

Front 161

Common psychiatric manifestations of neurosyphilis

Back 161

Dementia &

1. ) Headache
2) Lethargy
3) Decreased memory
4) Decreased concentration
5) Decreased judgment

Front 162

Means by which HIV causes brain dysfunction

Back 162

HIV = DIRECT BRAIN DAMAGE

1. Infected monocytes carry virus to brain
2. Macrophages are activated = release cytokines
3. Neuronal damage

*Hippocampus has high CD4 density = more vulnerable*

Front 163

Three contributors to psychiatric symptomatology in HIV

Back 163

a) Pre-existing Axis I or Axis II problems
b) The emotional impact of the illness and its consequences
c) Biological effects
- Direct CNS actions of the virus
- CNS disorders arising due to immunosuppression
- Psychiatric side effects of medications

*early stages of infxn: a & b predominate
- biological factors become more important as illness progresses

Front 164

Approach to the HIV-positive patient with a new onset of psychiatric symptoms

- two most important symptoms

Back 164

Assume it to be BIOLOGICAL in origin, unless proven otherwise

HIV in brain assc'd w/ every type of psych symptom

tWO MOST IMPORTANT
- DEPRESSION
- DEMENTIA

Front 165

Impact of depression on the course of HIV


- effect of tx

*responsive to TCAs, SSRIs & psychotherapeutic approach

Back 165

Incidence = 20%
- already common in populations at risk for HIV (ex// IVDU)
- rate of MDE is 2x as high

IMPACT:
- Decreased adherence --> decreased quality of life
- Increased time to start tx
- Higher rates of mortality

(treatment can reverse all that, as well as decrease involvement of high-risk behavior)

*Pyschoneuroimmunologic things at play in non-depressed people having better mortality rates*
- depression affects immunity

*FATIGUE is a big problem & closely assc'd with depression*
- responsive to CNS stimulants (methylphenidate & dextroamphetamine)

Front 166

Cognitive, motor, mood, and personality symptoms seen in HIV-associated dementia

Back 166

1. Minor cognitive disorders
- can be disabling
- bad short-term memory, word finding issues, difficult sequencing

2. HIV associated dementia (HAD)
- impairment in multiple cognitive domains
- if HAART is being used & virla load is low, HAD is unlikely to develop

Front 167

General principles for the treatment of psychiatric symptoms in HIV-positive patients

Back 167

1. HAART - decrease viral load
2. ANTIDEPRESSANTS
3. Psychostimulants
- improves severe fatigue
- abuse potential
4. Antipsychotics
- reduce severe agitation
5. Psychosocial interventions
- psychotx
- educate/counsel family
- support groups

Front 168

The most common psychiatric disturbance in patients with diabetes

- effect of depression on course of DM
- Emotional effects of hypo/hyper glycemia
- tx of depression

Back 168

DEPRESSION #1
- also anxiety disorders & phobias

Depression is assc'd with WORSE glycemic control & increased risk of diabetic complications
- bidirectional causality
- tx w/ meds/CBT improves adherence & glucose control
- Fluctuations in serum glucose cause significant emotional changes

Hypoglycemia: anxiety
Hyperglycemia: depression or anxiety; increased hostility

tX:
SSRIs are best
- decrease insulin needs
- weight loss
- improved adherence to dietary requirements
*TCAs = carb cravings and weight gain = BAD*

Front 169

The types of psychiatric symptoms commonly seen at lower steroid doses and how this changes with increasing dose

Back 169

MOOD AND ANXIETY symptoms present at lower doses of chronic steroids

INCREASED = risk of psychotic symptoms increases

Front 170

Emotional symptoms commonly seen in hypocorticalism

(Addison's dz)

Back 170

Depression symptoms
- apathy, anhedonia, fatigue, negativism, poverty of thought, etc.

- Rarely, psychotic sypmtoms

*Symptoms may NOT FULLY REMIT w/ replacement tx
- tx does not mimic the diurnal and other variations in natural cortisol secretion

Front 171

Emotional symptoms commonly seen in hyperthyroidism and their relationship to the severity of the thyroid excess

- meds to avoid

Back 171

ANXIETY IN 40% OF PTS
- Nervous, hyperactive, tremore, irritable, mood lability

*Severity of symptoms correlates w/ severity of the hyperthyroidism*
- mild psychotic symptoms & major cognitive impairment occurs in sever cases (as part of delirium)

MEDS TO AVOID:
- TCAs (more cognitive problems)
- LITHIUM (worsen exopthalmos)

Front 172

The percentage of hypercortisolemic patients with mental or emotional changes

(cushing's)

Back 172

85% of pts w/ high cortisol levels = mental/emo changes
- symptoms of depression or anxiety
- mild cognitive changes also seen
- psych symptoms can present BEFORE other signs of dz

Front 173

Emotional symptoms commonly seen in hypothyroidism
- Medications to avoid in hypothyroidism, and why

Back 173

- Slowed mentation; cognitive complaints; memory/concentration problems = 66-90%
- 40% are depressed mood

MORE RARE
- Delirium
- Dementia
- psychotic symptoms
*myxedema madness = auditory hallucinations & paranoia
- careful w/ antipsychotic meds, as metabolism is slower in hypoTH


**Symptoms usually resolve w/ thyroid replacement**
- may take up to 6mos
- if hypoTH was longstanding, some changes may be IRREVERSIBLE

*thyroid axis & mood disorders have a relationship*
- subclinical hypoTH pts = 50% Depression rates
- Low doses of T3 can boost the antidepressant response in pts who aren't responding.

Front 174

Which domains of symptoms contribute most to functional disability in schizophrenia

Back 174

The severity of NEGATIVE SYMPTOMS & COGNITIVE IMPAIRMENT are much more closely related with the severity of functional & social impairment

- not so much with positive symptoms (hallucinations & delusions) and amt. of social impairment

Front 175

What abnormalities of very early information processing are found in schizophrenia

Back 175

PREFRONTAL CORTEX
- small reduction in gray matter
- less blood flow/metabolic activity
- Reduced dendritic spine density of the large pyramidal neurons in the 3rd cortical layer of the dorsolateral prefrontal cortex

**PFC abnormalities --> NEGATIVE symptoms

- Also see ventricular enlargement

Front 176

What findings link limbic dysfunction to positive symptoms


**emotional processing of complex stimuli & language production **

--> hallucinations & thought disorders

Back 176

a. Small but consistent reduction of gray matter volume in the hippocampus, amygdala, and superior temporal gyrus
b. Diminished metabolic activation of medial temporal areas on tasks which challenge these areas

Reduced volume of superior temporal gyrus correlated w/ severity of auditory hallucinations or thought disorder

Actively hallucinating = active
- ant. cingulate gyrus
- bilateral temporal cortex
- Hippocampus
- Parahippocampal gyrus

Front 177

Definition of working memory

-What role deficient working memory is believed to play in schizophrenia

Back 177

Things from long-term memory that are pulled up and held "in mind"
- used to assess current situations & stimuli
- allows responses to be guided by PAST learning (not just instinct)

Schizo
- pattern of poor performance
- impaired PFC activation
- bad working memory =(

*DORSOLATERAL PFC BLOOD FLOW*
- assc'd with working memory
- decreased in schizo pts
- more severe in pts w/ worse negative symptoms

Front 178

Circuits that have been found to behave abnormally in schizophrenia

*Abnormalities in one part of the circuit leads to dysfxn in another*

Back 178

1. Cortical-Striatal Circuit
- PFC is underactive during working memory task
--> Basal ganglia is overactive
(no inhibition of subcortical areas by frontal input)

2. Limbic Circuit
- Overactive during hallucinations
- Underactive montoring areas
(misinterpretation of imagined voice as a real voice)

Front 179

The evidence that genetics play a role in schizophrenia

Back 179

Regardless of who raises the pt, increased genetic risk
- BUT, even an identical twin of schizo pt has only a 50% risk of getting it
**Genetic vulnerability triggered by environmental factors**

Front 180

About evidence that schizophrenia is a neurodevelopmental disorder:

- birth complications
- deficits noticed in infancy/childhood

Back 180

NEURODEV HYPOTHESIS:
- Pts have a higher rate of perinatal complications (high-risk)
- 2nd Trimester viral infxn (influenze epidemic)
- Abnormal infants (milestones, perception, eye contact, motor coord, etc)

*Congenital brain lesions have different manifestations at different stages of development*
(reason why birth defect can result in adult onset illness)

Front 181

About evidence that schizophrenia is a neurodevelopmental disorder:

- lack of gliosis
- histopathologic evidence of disturbed brain development

(??)

Back 181

- Heteromodal assc areas finish myelination in adolescence
*brain reorganizes to take advntage of these areas*

- Cortical, hippocampal, and other lesions of schizophrenia manifest more subtly before adolescence than they do afterward
--> heteromodal assc areas may be relied on more heavily after adolescence

*didn't really answer the front qeustions*
(gliosis = sign of past inflamm)

- Some, but not all, longitudinal studies have found persons with schizophrenia to have increased rates of ventricular enlargement and gray matter loss over time relative to controls
(schizo = neurodegen dz?)

Front 182

What the simple original DA hypothesis of schizophrenia was, and why it was proposed

- EVIDENCE
- PROBLEMS

Back 182

All effective antipsychotics affect DA systems
vs.
DA Agonists can cause psychotic symptoms

"Schizophrenia is due to dopamine overactivity: too much dopamine or too many dopamine receptors."

Direct evidence for this is sparse
- Increased DA2-R in the striatum
- Increased presynaptic striatal DA stores & synthesis capacityin acute psychosis

PROBLEMS:
- lacks enough direct evidence
- lacks explanatory power

Front 183

How a more complex current theory of DA dysfunction in schizophrenia relates to different symptom domains

Back 183

1. Hypoactive mesocortical DA system (PFC)
2. Cognitive dysfxn & negative symptoms
& Impaired regulation of subcortical areas
--> 3. HYPERACTIVE mesolimbic DA system
---> 4. Positive symptoms

New ideas:
- DA dysreg is only related to psychosis (+ symptoms)
- DA dysreg alters appraisal of salience (relevance of stimuli --> dev. of delusions & hallucinations
**Based on DA's involvement in brain reward, reinforcement, & motivational systems**

Front 184

Drug actions linking glutamate to schizophrenia

Back 184

Glu Antagonists = psychotic states like schizo
(PCP, ketamine)
- NDMA antags mainly produce psychosis in adolescents & adults (NOT pre-adolescents)
*same age the PCP works is same age of usual schizo onset

*Glutamate-System abnormality could be "silent" until adolescence
--> change in brain organization

- Some studies show reduced expression of Glu-R in PFC & hippo

Front 185

Drug actions linking GABA to schizophrenia



(5-HT: clozapine to improve schizophrenic symptoms more effectively and with fewer side effects than typical neuroleptics could be attributed to its ability to block 5-HT2A receptors)

Back 185

A repeated replicated finding in post-mortem studies in schizophrenia is reduced PFC levels of the main enzyme involved in GABA synthesis

Thus, a role for GABA involvement in PFC dysfunction is proposed, but remains speculative.

Front 186

Which psychotherapies are useful in the treatment of schizophrenia

Back 186

USED IN COMBO W/ ANTIPSYCHOTIC DRUGS

1. Family therapy
- esp useful in familias con "expressed emotion"
- teach appropriate expectations & assist in developing healthy interaction

2. Social Skills Training

3. Cognitive Therapy

Front 187

How to respond to a patient’s delusions

Back 187

1.Trust is the foundation upon which all else depends.
2.Neither argue with nor encourage delusions.
3.Focus on practical points of common concern.

Front 188

ANTIPSYCHOTICS
- first & 2nd gen


2nd gen APDs for

Back 188

(neuroleptics) 1st gen drugs
- low potency: Chlorpromazine
- Mid: Loxapine
- High: Haloperidol (haldol) & Fluphenazine

2nd generation drugs ( Atypical APDs)
1. Clozapine
2. Olanzapine
3. Risperidone
4. Quetiapine
5. Aripiprazole
6. Ziprasidone

Front 189

What symptoms are most responsive to APDs

Back 189

1. Hallucinations, delusions and thought disorganization (the “positive symptoms” of schizophrenia) are the most responsive


2. The “negative symptoms” of schizophrenia (blunted affect, amotivation, impaired concentration, impaired socialization) improve somewhat less

Front 190

The time course of response to APDs

Back 190

1. Agitation and combativeness may diminish in the first few hours

2.Onset of reduction in hallucinations, delusions and thought disorganization is seen in the first few DAYS, with full benefit not being present for WKs to MOs.

3. No antipsychotic consistently works faster than any other

Front 191

19. The likely neurochemical mechanism contributing most to the reduction of positive symptoms

Back 191

FIRST GENERATION
1. Block DA2-R
- also main path of side effects
* blocking DA2-R in mesolimbic pathway = reduce + symptoms

2. Block in OTHER pathways = SEs
- Nigrostriatal: motor
- Mesocortical: worse negative symptoms
- Pituitary DA: increased prolactin release & endocrine

SECOND GENERATION:
- Block DA2 & 5HT
- Other actions reduce SEs

*Aripiprazole = exception
- DA partial agonist

Front 192

Which drug is the most effective APD, and why it is not used first

*APDs are all kinda the same; just the SEs that differentiate them*

Back 192

CLOZAPINE
- also most dangerous

*Olanzapine is #2 in efficacy - also #2 worst side effects

Efficacy differences bw the rest of the 2nd and 1st gen drugs are small

Front 193

The side effects most associated with first generation APDs and those most associated with second generation APDs

Back 193

FIRST GEN:
- Neurologic/Motor: two categories (Acute vs late/idiosyncratic)
- Endocrine
(some: anticholinergic & antihistamine and a1 blockade)

SECOND GEN:
- METABOLIC

Front 194

About Acute onset motor side effects (EPS):
• The three types
• The symptoms of each type
• The brain pathway involved in EPS
• The treatment of each type

- LEAST EPS: chlorporamzine
- Middle: Loxapine
- Worse: EPS

Back 194

Neuro/motor side effects
- mainly associated with 1st gen drugs

ACUTE ONSET: (Extrapyramidal SEs)
1. Parkinsonism
- (resting) TRAP
2. Dystonia: sustained mm contraction
3. Akathisia: Marked subjective & objective motor restlessness

*EPS most likely due to DA blockade at nigro-striatal*

TX:
1. Parkinsonism & dystonia Anticholinergic or diphenhydramine
- Amantadine (mild DA agonist)

2. Propranolol: Akathisia

Front 195

About Tardive Dyskinesia (TD):
• Its symptoms
• Its prevalence in general and in geriatric patients
• Risk factors for its development

*Late / idiosyncratic neurologic/motor side effects*

Back 195

"Late, Bad movements"
- Involuntary, non-rhythmic muscle movements
- usu face / hands
- Worse w/ concentration / stress; less with enough sleep
- Dyskinesia doesn't start until THREE MO+ of DA blockage
- Severity varies

*May resolve or can become permanent*

OCCURENCE:
- 5% per year on 1st generation antipsychotics,
- about 0.5% per year on second generation antipsychotics.

RISK FACTORS:
i. Increased Age
ii. Mood Disorder
iii. Brain Damage
iv. EPS early in treatment
v. Female Gender

Front 196

TARDIVE DYSKINESIA

- COURSE
- TX

Back 196

Course
i. Develops gradually over weeks to months
ii. Generally plateaus in four years

Treatment
- If possible, stop the antipsychotic or lower the dose
- Switching the patient to Clozapine (which may not cause Tardive Dyskinesia) can decrease the symptoms

Front 197

The symptoms of Neuroleptic Malignant Syndrome (NMS) and its presumed pathophysiology

*rare; more common in 1st gen APDs
- Any patient on an antipsychotic who develops an unexplained fever, stiffness, or confusion must be closely evaluated for NMS

Back 197

CAN BE FAST & DEADLY
= SEVERE EXCESSIVE DA BLOCKADE OF MOST DA SYSTEMS

1. Nigro-striatal pathway = Marked muscular rigidity

2. Hypothalamic DA systems = High fever (impaired thermoreg)

3. Hypothalamic spinal DA efferents = Labile BP (SNS disrupted)

4. Mesocortical DA = Confusion, delirium, coma

Front 198

The treatment of NMS

Back 198

i. STOP THE ANTIPSYCHOTIC DRUG
ii. Intensive monitoring and supportive measures to reduce fever, dehydration and hypotension (usually in an ICU)
- Antidotes have been attempted, but it is not clear if they provide added benefit.

Front 199

The nature of the metabolic side effects seen with APDs

Which APDs have the greatest risk of metabolic side effects?
- what about insulin resistance?

*Asenapine: may have less metabolic SEs)

Back 199

WEIGHT / DIABETES / LIPIDS
- super serious

WORSE: clozapine, olanzapine
- usu 15-20lbs (can be 50-100 lbs)

Insulin resistance, elevated serum glucose and elevated serum lipids
i. commonly occurs with olanzapine and clozapine
ii. less so with the “--peridones” and quetiapine, and minimal with aripirazole and ziprasidone.

Middle: Risperidone, Quetiapine
Minimal: Aripiprazole, ziprasidone

Front 200

The major problems with Clozapine

*most effective; most difficult to use*

Back 200

1st second gen APD in US
- most effective in tx-refractory pts
- Reduces TD symptoms
- Separate anti-aggressive effect
- mood-stabilizer

DANGERS:
- Agranulocytosis (decreased WBCs) in 1/75 pts (1.5%)
- several fatalities
- check weekly WBCs
- Dose dept-lowering of seizure threshold
(definite increase of seizures >550 mg/day)

= Highest incidence & highest weight, glucose, & lipid changes

also:
- drooling (decreased swallowing)
- sedation

Front 201

The effect of APD’s on prolactin, the brain site of this effect, and its clinical manifestation

Back 201

INCREASED PROLACTIN
- DA blockade in hypothalamic tubero-infundibular tract

i. Galactorrhea
ii. Breast enlargement
iii. Impotence
iv. Amenorrhea
v. Osteoporosis

Occurrence
i. All 1st generation APDs cause this
ii. One 2nd generation APD causes this– Risperidone

Front 202

WHICH ANTIPSYCHOTIC TO USE FIRST?

- Balance bw benefit & side effcts

Back 202

1. Try ziprasidone or aripirazole (maybe asenapine)?
- lowest risk of either neuro or metab SEs

2. Choose next one based on SEs

3. If pt already has metabolic risk factors, consider 1st gen drug

4. If pt is likely to react poorly to EPS (paranoid pts), consider a 2nd gen drug other than clozapine

5. After 2-3 failed trials = Clozapine