FOBS Exam 2 LGT

Last LGT EVER!!!

Sumedh Mankar OMS III

Adapted from Kellen Choi, OMS IV
My 1 LGT Your Last LGT
st

Clinical Content
Pharmacological Content
Questions
 Personality Disorders- FUN
STUFF!!
DSM IV - Diagnostic and Statistical
Manual of Mental Disorders
First printed in 1952
Next revision likely to be released in
2011 (DSM-V)
 Personality Disorders
DSM says that a personality disorder is an enduring
pattern of inner experience/behavior that deviates
markedly from expectations of culture.
This pattern is manifested in 2 or more areas:
Cognition
Affectivity (ability to experience feelings, pos or neg)
Interpersonal functioning
Impulse control
Pattern is inflexible and pervasive
Leads to clinically significant distress or impairment in
social, occupational, or other areas of functioning
Is stable and of long duration, begin tracked back at
least to early adulthood
It cannot be better accounted for by another condition
Not due to direct physiological effects of a substance
or medical condition
 PD Clusters: ABCs (HY for exam,
boards, shelf)
A: Odd and Eccentric (Mad)
Paranoid Schizotypal Schizoid
Scary Street People
B: Dramatic, Emotional, Erratic (Bad)
Borderline Narcissistic
Histrionic Antisocial
Have Been A Nuance
C: Anxious and Fearful (Sad)
Avoidant Dependent
Obsessive-compulsive
 Cluster A
Personality Prevalence Etiology Defenses Treatment
**tq**
Paranoid: 0.5-1.5% Shame- Splitting/ Supp.
pervasive (~1%) inducing exp. projection Psychotx; low
distrust & dose
suspiciousness antipsychotics

Schizoid: 0.5-1% Supportive

detachment from (~1%) psychotherap
social
relationships
y

Schizotypal: 3% (higher in Partial Denial, Supp. Reality-

odd, eccentric, families with expression of distortion, based tx and
magical thinking schizophrenia schizophrenia projection, lowdose
**tq**) antipsychotics
fantasy
 Schizotypal vs Schizoid PD
Schizotypal goes to work wearing a
pickle = weird

Schizoid goes home to avoid

=dont like people
 Cluster B
Personality Prevalence Etiology Defenses Treatment

Borderline: 2% History of Splitting Guidelines,

instability in self abuse and **tq**, communication,
image, boundaries,
relationships, affect abandonmen projective
psychotx/Rx
and impulsiveness; t ID, acting
IMPULSIVE
out
Histrionic: 2%, more Sexualization Long term
extreme commonly dx of parent of psychotherapy
emotionality and
attention seeking
in females opp. sex
but thought to
be =
Narcissistic: less Poor Psychoanalytic,
love of self common parenting supp
from 6mo - psychotherapy
2yrs
Antisocial: 2-3%, males Common with Combo
exploiting others, substance individual/grp
disregard for
rights of others
abuse therapy
 More on Cluster B
Borderline: frequent cutting of limbs
(higher rate of death from suicide
attempts, although didnt mean to really
kill themselves; wants attention)
Defense mechanism is splitting for them: black
or white (either a person is good or bad) **tq*
E.g. Pt acts totally different when you (student)
interview VS attending Dr interviews the pt.
E.g. Pt could LOVE you for being nice once, and when
you disappoint him/her once, you are the WORST Dr
ever.
 Cluster C
Personality Prevalence Etiology Defenses Treatment
Avoidant: feeling 0.5-1% Inborn, Splitting/ Long-term
of inadequacy, fear psychotherapy,
suboptimal projection anxiolytic/anti-
of social settings
parental dep meds
response

Dependent: Reassurance
need to be taken , clarification,
care of; clingy,
submissive
clear
expectations

Obs.- 1% Fixation in Psychotherapy/a

nalysis; provide
Compulsive anal phase as much control
PERSONALITY (age 3), as possible
Disorder: preoccup. unconscious
with details
shame/guilt
 OCD vs OCPD **tq**
OCD: Knows their condition and
wants to change (unhappy that OCD
is interfering with their life)-
egodystonic
OCPD: Happy the way they are and
does not want to change; Pt sees
nothing wrong with their behavior-
egosyntonic (applies to ALL other PD)
Somatoform d/o, Factitious d/o,
Malingering
 Somatization
Definition
A process by which an individual
consciously or unconsciously uses
the
body or bodily symptoms for
psychological purposes or personal
gain.
Diagnosis: multiple somatic
complaints of
several years consisting of:
- four pain symptoms
- two gastrointestinal symptoms
- one sexual symptom
- one pseudoneurological
 Psych Disorders & Pain **HY slide**
Depression & pain closely linked.
Conversion disorder: one symptom that cannot be
explained medically and the patient is NOT intentionally
producing it (doesnt have to be pain)
CoNversion (N for Neurologic sx)
Somatoform disorder: pain is focus which causes distress,
and again its not intentionally produced
So Many form (many sxs)
Pain d/o pain causes distress, primary focus, psychological
factors, unconscious
Factitious disorders (Munchausens): patient IS intentionally
producing symptom; however the motivation is
unconscious
Malingering: intentional production motivated by conscious
external incentives; a legal tem, not a diagnosis
Hypocondraisis preoccupation with fear of having serious
disease, despite reassurance, unconscious
More on Factitious (Munchausens)
d/o
Munchausens - Triad of simulation of
disease, lying, wandering
Munchausens by proxy: Care-giver
(usually the mom) fakes a childs
sickness; psychologic condition as the
care-giver wants sympathy/attention
from the medical personnel
A type of child abuse must report to
CPS
 Malingering
Intentional product of illness

Motivated by external goal:

- Financial
- Avoiding military
- Avoiding criminal prosecution
- Obtaining drugs
- Shelter
Legal rather than medical/psychiatric
issue
Eating D/O

Food.?
 Differences in Anorexia and
Bulimia
Anorexia
Refusal to maintain recommended minimal
weight
Afflicts younger age group
Loss of menstrual period
Distorted body image is common
Existence of food-related problem is denied
More self-control
Vomiting less pervasive
Eating rituals
4-25% mortality rate
Bulimia
Normal or near normal weight (may be
overweight)
Afflicts older age group
Menstrual periods may or may not be lost;
irregularities common
Usually dont have a distorted body image
Eating is recognized as being abnormal
More impulsivity; some substance abuse
Greater incidence of vomiting and other
purging behavior
Tend to appear to eat more normally when not
binging and eating in public
Mortality rate is undetermined
 Youve recognized an eating
d/o now what?
Treatment Interventions for Eating
Disorders NOT a quick fix
Main difference between treating
Bulimia and Anorexia
Critical to have family involvement and
support when treating Anorexia.
CBT tends to be more successful with
Bulimia.
Individuals with Bulimia tend to have higher
comorbidity with personality disorders.
 Psychological therapy for
Obesity
There are a set of traditional tx. know why
they fail.
Meds - sibutramine, orlistat, fluoxetine,
phentermine, diethylpropion, bupropion,
zonisamide, topiramate, and sertraline
Surgery Gastric bypass, gastric banding,
Vertical banded gastroplasty, Roux-en-Y
bypass
CBT Phase 1 goal weight loss
Phase 2 weight maintenance
 Stages of Change Model
Stages include:
Precontemplation Stage May be pressured by
others but patient does not think behavior is
problematic.
Contemplation Stage Has awareness of problem but
not ready for action (ambivalent).
Preparation Stage Plans to take action soon and is
taking small steps. Learning how to change.
Action Stage Puts plan into action, making changes.
Maintenance - Works to prevent relapse; has been
successful for 6 months.
D/o of childhood and
adolescence
 Mental Retardation
Know IQ ranges *TQ*
M:F 2:1
Etiology: multifactorial and polygenetic
FAS = most FREQUENT cause and most
PREVENTABLE.
Down Syndrome MC Chromosmal cause
Fragile X synd MC HERITABLE cause
Seizures are more common in persons
with MR
 Autism
Communication problem
Social impairments
Restricted or repetitive behavior
Features:
Do not bond well with parents
Lack warmth, sensitivity and awareness
Maintain routine
MR
 ADHD
Hyperactive
Inattentive
Impulsive
3 types
Sx present b4 age 7
Tx with stimulants decrease risk for
substance abuse
Methylphendate
 The Rest
Conduct D/O pattern of behavior that
biolates the rights of other, adults =
antisocial personality d/o
Oppositional Defiant D/o defiant towards
authority (not as bad as conduct d/o)
Tourettes D/o MOTOR AND VOCAL tics
Separation Anxiety D/o refuse to go to
school , fake sx to come home (TX- send
em to school, and work to resolve social
issues [bullies etc])
Delerium, HIV and
Emergency Psyc.
 Delirium
Definition : reversible organic mental
disorder (however some cases may
progress to irreversible brain failure)
Disturbance of Consciousness, change
in cognition, develop acutely, evidence
it is caused by a medical cond.,
hallucinations, poor insitght,
 Dementia
Gradual decrease in cognition with
NO CHANGE in level of consciousness
Memory deficits, aphasia, apraxia,
agnosia, loss of abstract thought,
patient is alert .
Caused by Alzheimers dz, vacular
thrombosis/hemorrhage, HIV, CJD
 Differential Diagnosis of Delirium
I WATCH DEATH

Encephalitis, meningitis, syphilis

Infectious

ETOH, barbiturates, sedatives

Withdrawal

Acidosis, alkalosis, renal/hepatic

Acute metabolic failure

Trauma Heat stroke, severe burn, post-op

CNS pathology Abscess, hemorrhage, seizure, stroke,

tumor, normal pressure hydrocephalus

Adapted from: Harvard Board Review

 Differential Diagnosis of Delirium
I WATCH DEATH (cont)

Hypoxia Anemia, CO poisoning, hypotension,

pulmonary/cardiac failure
Deficiencies
Vitamin B12, niacin, thiamine

Endocrinopathies Hyper/Hypoadrenocortisolism,
Hyper/Hypoglycemia
Acute Vascular
Hypertensive encephalopathy, shock
Toxins or Drugs
Medications
Heavy metals
Lead, manganese, mercury

Adapted from: Harvard Board Review

 Agitation and Aggression
When to tx: What to tx with:
Psychomotor Oral benzo
activation Atypical
Affective lability antipsychiotcs
Verbal abuse Tablet, liquid
Catotonic concentrate, rapid
dissolving
excitement formulations
Aggression to
property
Potential to harm
self or others
 Trauma and Violence
Neurobiology of trauma:
Current evidence suggests the physiology involves
dysregulation of multiple neurochemical systems
noradrenaline, hypothalamic-pituitary-adrenocortical (HPA)
axis, thyroid and endogenous opioids
Trauma is associated with the release of stress-responsive
hormones: cortisol, adrenaline, noradrenaline, vasopressin,
oxytocin and endogenous opioids.
Downregulated adrenergic receptors in response to
increased circulating noradrenaline concentrations.
Serotonergic systems play a role in modulating noradrenergic
responsiveness to arousal
Reduced hippocampal volume
 Definitions
Child abuse: a child has suffered or there is a substantial risk
that a child will imminently suffer physical harm, inflicted
non- accidentally by parents or caregivers which causes a
substantial risk of causing disfigurement, impairment of
bodily functioning or other physical injury. (Fed. Juvenile
Justice Standard)
Domestic Violence: intentionally violent or controlling
behavior of a currently or previously intimate partner of a
victim. The goal is to coerce, assert power and maintain
control.
Child neglect- failure to fullfill obligation
Physical neglect- refusal/delay in health care, abandonment,
inadequate supervision
Educational neglect- permitted chronic truancy, failure to
enroll, inattention to special education needs
Emotional neglect- inadequate affective nurturance,
exposure to abuse, refusal of psychological care, permission
to abuse alcohol or drugs
 Child abuse
1 million children abused per year!!!
Characteristics
Premature, difficult temperament, fussy, colicky,
preceived as slow or different,.
Abuser
Closest member of the family, poverty, mental illness,
hx. Of victimization
Clinical ceatures
Impulsivity, hyperactive, depressed, substance abuse,
conduct d/o, learning impariment, poop hygine, bruises,
belt marks, rope marks, different stages of fracture,
burns or scalds (atypically located) retinal detachment,
Signs
STD, genital / anal trauma, recurrent UTI, promiscuity
 Elder Abuse
1 million cases reported per year!!!
Abuser closest member of family
People make excuses instead of reporting
(fell etc.)
Clinical feature similar to child abuse.
Unaccounted for financial expenses
Know to report any suspected abuse to
APS
 PTSD
A - Exposure to traumatic event experienced,
wittnessed, or response was intense fear,
helplessness and horror.
B event is persistently experienced
C - Persistent avoidance of stimuli associated
with the trauma and numbing of general
responsiveness
D - Persistent symptoms of increased arousal
PTSD B,C,D more than 1 mth acute vs.
chronic = 3 mths!
TX CBT, group, psycodynamic, social rehab,
hypnosis
SSRI antidepressants preferred rx for PTSD
Human Sexuality
 Paraphilias
Exhibitionism, or exposure of the genitals flashing (indecent
exposure is illegal)
Fetishism, or the use of nonliving objects (ie. Underwear)
(Partialism being sexually aroused by a body part feet,
breast, buttocks)
Frotteurism, or touching and rubbing against a
nonconsenting person (illegal)
Pedophilia, or the focus on prepubescent children (illegal)
(MUST REPORT)
Sexual masochism, or the receiving of humiliation or
suffering
Sexual sadism, or the inflicting of humiliation or suffering
(can involve rape, torture, even murder)
Transvestic fetishism, or cross-dressing
Voyeurism, or watching others engage in undressing or
sexual activity peeping tom
 Sleep
zzzzz
 Sleep d/o
Dyssomnias: problem with amount/quality
of sleep
Primary Insomnia
Narcolepsy
sleep attacks throughout the day, despite good sleep
Classic tetrad:
sleep attacks
cataplexy
hypnogogic (when you go into sleep), hypnopompic
hallucinations (when you wake up from sleep)
sleep onset/offset paralysis
Sleep apnea (Breathing-related Sleep Disorder)
Circadian Rhythm Sleep Disorder
Primary Hypersomnia

**Always r/o poor sleep hygiene!

 More on Sleep d/o
Parasomnias: Doing weird stuff on their sleep
Sleepwalking
during stage 4
Sleep Terror Disorder
dont recall next AM; during stage 4
Nightmare Disorder
recall next AM; during REM
Sleep D/O 20 to other mental d/o (insomnia
vs. hypersomnia)
Sleep D/O 20 to General Medical Condition
Substance Induced Sleep D/O
 Non-REM vs. REM SLEEP
Physiological Process NREM REM
brain activity decreases from wakefulness
increases in
motor and
sensory areas,
other areas
are similar to
NREM
heart rate slows from wakefulness increases
and varies

compared with NREM

blood pressure decreases from wakefulness increases
(up to 30 percent)
varies from
NREM
 Non-REM vs. REM SLEEP
Physiological Process NREM REM
blood flow to brain no change increases by 50 to 200 percent
from NREM depending on region

respiration decreases increases and varies from NREM may

show brief stoppages (apnea); coughing suppressed
airway resistance increases increases and varies from
wakefulness
 Non-REM vs. REM SLEEP
Physiological Process NREM REM
body temperature lower set point not regulated
shivering initiated no shivering
at lower no sweating
temperature than temperature
drifts
wakefulness toward that of the
local
environment

sexual arousal occurs infrequently increases

from NREM
Suicide
 Diagnosing Suicide Risk
SCOREREPORT:
SAD PERSONS 02Outpatientfollowup
Sex: male 34Supervisedoutptf/u
Age: <19 or >45 56Considerhospitalization
Depressed: yes or no 710Hospitalization
*Ifadepressed/psychpatientsays,Im
Prior Attempt goingtokillmyselfwiththeguninmy
EtOH use closet,thenyouhospitalizethem.There
isnoneedtogetmoreinformation.
Rational thought loss =
psychosis
Support lacking (no
family/friends)
Organized plan
No spouse
Sickness
Nicotine
 Nicotine
61 million in the U.S. smoke (remember 30%,
or even easier - 1/3 of Americans)
20% of youths 12-17 yr old
Responsible for 400,000 deaths/yr in US (1/4)
60% of health care costs treat smokers
1 Billion Smokers smoke 6 trillion
cigarettes/year; 3 million deaths worldwide
Smokers more likely to use other drugs &
alcohol
More educated smoke less
1/2 of all psych patients smoke, 3/4 of all
 Nicotine
Neuropharm
Agonist at the nicotinic subtype of the
acetylcholine receptors
1/4 of the nicotine from smoke enters the
bloodstream and within 15 seconds to the brain
half-life 2 hours
Activates the dopamine reward system and
releases glutamate
Binds to the cell bodies in the VTA (ventral
tegmental area) as well as the dopaminergic
terminal of the nucleus accumbens (Brain stem
to Cortex)
 Nicotineis good!
Reduced risk of developing Parkinson's disease,
Alzheimer's disease, and ulcerative colitis.
Increases the strength of synaptic connections
in the hippocampus (the brain region that
supports short-term memory). Several nicotine-
like compounds that stimulate acetylcholine
release are under study as cognitive enhancers
for treatment of Alzheimer's disease.
Improved attention, learning, reaction time,
and problem-solving ability
Lifts their mood, decreases tension, and
lessens depressive feelings
 Nicotine: Acute Toxicity
60mg fatal dose, 0.5mg in a cigarette (metabolized by
liver)
At least one of the following symptoms
insomnia
bizarre dreams
labile mood
derealization
interference with personal functioning
At least one of the following signs:
nausea or vomiting
sweating
tachycardia
cardiac arrhythmias

Nicotine
Treatment for addiction
Patch, gum, etc. (patch has better compliance)
Varenicline (Chantix): stimulates dopamine and
blocks nicotine receptors; Rxed for 12 wk
period may inc suicide ideation psychiatric hx
needed!)
Behavioral Therapy

Moms need to stop within first 3-4 months

of pregnancy to reduce their risk of low-
birth-wt
Addiction
 Addiction
An activity which initially provides
pleasure, and is relatively, and
usually harmless
Mesolimbic & Mesocortical
Pathways (as well as nigrostriatal)
 So What!
Remember the mesolimbic pathway is
currently thought to be involved in
pleasure/reward states. In other words,
when someone does crack, for example,
these are the neurons firing in response
and saying, this feels good, do it again.
Remember Dopamine is the major
neurotransmitter involved in this pathway,
and the more pleasurable the activity (or
the stronger the drug), the more dopamine
released from the VTA to the NA.
 Addiction & CREB
CREB (cAMP response element-binding
protein)
Increased dopamine directly increases cAMP
and Ca2+ ion concentrations
Regulates gene expression that is involved in
the production of dynorphin
Basically its negative feedback. The
dynorphin from the NA inhibits release of
dopamine from the VTA. So, the same amount
of drug doesnt feel as good.
Main point:Dynorphin & CREB contributes to
dependence **tq** (D for Dependence!)
 Non-Pharm Tx for Addiction
Therapeutic Communities (TC)
1 to 2 year program, dropout rate is high
Stepped program with hierarchial based
responsibility ladder which helps structure the life of
the addict
Primary social group and secondary self-help
Drug Abuse Treatment Outcome Study: said
the TCs work
Short-Term residential programs
CD units Minnesota Model
3-6 weeks inpatient followed by outpatient tx
Methadone maintenance programs for opiate
dependence and are MORE SUCCESSFUL than
outpatient psychotherapy/counseling
 Tolerance **know the diff!**
Pharmacokinetic
Change in distribution or metabolism that
decreases the concentration of a drug
Drugs to remember: alcohol, barbs, and
benzos due to induction of hepatic
metabolism
Pharmacodynamic
Change in target tissue response such as
reduced receptor density, uncoupling of
signal transduction pathways, or up-
regulation of negative feedback systems
Drug to remember: opioids
 Learned Tolerance
Behavioral: learn to walk a straight line or drive
while intoxicated
Conditioned: situation-specific, Pavlovian type
learning
Acute Tolerance
Occurs during repeated use of drug during a
single occasion (ex: cocaine binge) **tq**
Cross-Tolerance: self-explanatory (assoc.
opioids)
Reverse of tolerance is Sensitization
(associate cocaine & methamphetamine)
 Dependence
Physical dependence: Defined by the
occurrence of a withdrawal syndrome
upon cessation of drug use or
treatment with antagonist drug
Psychological Dependence (aka
Addiction): compulsive or obsessive
activity/thoughts associated with use
or obtaining drug
 Withdrawal
The only drugs that one can die
when withdrawing from them are the
GABA agonists: Ethanol, barbituates,
and benzos **tq**
However, overdosing on cocaine or
methamphetamines is more common
in practice
Pharmacology
 Obesity Pharm Treatment
Non-sympathomimetic treatment
Fluoxetine (Prozac)
SSRI not approved for wt control (off-label)
Tolerance develops within days or weeks
Sibutramine (meridia)
SNRI
Taken without regard to meals
Must monitor BP for HTN
Orlistat (Xenical)
Tetrahydrolipstatin, derivative of lipstatin from
Strepomyces toxytricini
Covalently bonds/inhibits gastric & pancreatic
lipases
SE: flatulence and loose stools, steatorrhea
 Amphetamine-related
anorexiants
MOA
Decrease in appetite
Less interest in food
Less pleasure from eating
Increased satiety with eating
Decrease in total energy intake
Limited by tolerance
Precaution:
Unusual reactivity to sympathomimetics, dental
problems (dec. salivary flow)
SE:
Insomnia, inc. BP, Anxiety, Tremor, abuse potential
OD:
Arrythemia, confusion, diarrhea, fever, assultive
behavior, hallucinations,
 Non-sympathomimetic
anorexants
Fluxetine (offlable)
SSRI
Apetite reduction (a SE of this rx, usually used
for Mood D/o)
Tolerance develops
Sibutramine
Inh. 5-HT and NE reuptake
Early Satiety
SE dry mouth, ha, constipation and insomnia
Orlistat
Tetrahydrolipstatin
SE : flatulance and loose stools,
Tx of ADHD
 ADHD Rx
Methylphenidate (Ritalin)
facilitation of release of central DA and NE
Toxicities
Insomnia, anorexia, weight loss and growth retardation
CI
HTN, glaucoma, anxiety, seizure
Amphetamine (Adderall)
Reverse re-uptake transporter at catecolamine
synapse (NE and DA levels are elevated)
SE:
Insomnia, weight loss, emotional lability
HIGH abuse potential
Pemoline (Cylert)
Similar to methylphenidate (used less due to
hepatotoxiity); NE selective re-uptake inhibitor; LOW
abuse potential; once a day
 Narcolepsy
Modafinil
DOC for narcolepsy
SE :
Amphetamine like but less intense
Insomnia, appetite suppression
Hypnotics
 Sedative/Hypnotic Abuse &
Dep.
Affect GABA transmission
EtOH (also affects glutamine), Barbiturates,
Benzodiazepines
BZD bind at jxn of alpha and beta subunits
All drugs capable of producing sleep
(hypnotics)
Sedative causes diminished awareness,
drowsiness, diminished motor activity
Hypnotic: an agent that promotes
sleep & inhibits wakefulness
Sedative/Hypnotic Abuse &
Dep.
BZD Overdose alone - not a problem
BZD + another sedative/hypnotic like
EtOH leads to potential for resp.
depression and death **tq**
BZD increase FREQUENCY of Cl-
Channel opening
(Ben-frequent ; Barbie-longer )
 Diazepam (Valium)
Long half-life (50+ hrs)
Second line drug for Status due to
shaky IV use (forms precipitate) and
because tolerance to anti-sz activity
develops
 Alprazolam (Xanax)
Intermediate-acting (12 hour half-life)
Less sedating
Tol/dep if overused
Used for anxiolytic and hypnotic
effect
Drug of Choice for anxious, type A
personality house wives and trial
lawyers/investment bankers
 Lorazepam (Ativan)
DOC for Status Epilepticus because its
more water soluble and therefore
better IV
Not for long-term tx of status (2-3 days
of treatment before tolerance develops
What is the DOC for long-term tx of
Status?
Clonazepam (Klonopin)
 Midazolam (Versed)
Not on drug list for exam, butmuy
importante
For procedural anesthesia
Short half-life
Sedative, makes patient sleepy
Also causes anterograde amnesia (Good for
procedures like a colonoscopy. Who wants to
remember that?!) **tq**
Used in combo with Fentanyl for analgesia
(Youll hear docs or nurses say 1 and 25 or
1 and 50 for 1 mg of Versed and 25/50 mcg
of Fentanyl )
 Barbiturates
Secobarbital, pentobarbital, phenobarbital
Increase DURATION of Cl- channel opening
Profound CNS Depression possible including
anesthesia, coma, resp dep
abuse potential high
High doses directly increase Cl- flux while no
dose of BZD's ever directly modulates Cl- flux,
only augments GABA's effects
Phenobarbital
seizure control
for inpatient insomnia
Poor therapeutic index
 Withdrawal signs and
Signs symptoms
tremors
seizures
Symptoms
ANXIETY
insomnia
nausea
Malaise
Symptoms of withdrawal occur before
signs of withdrawal, and anxiety/insomnia
are the first withdrawal symptoms
 Barbiturate Toxicity
Physical examination should focus on vital signs and
cardiorespiratory and neurologic function
Vital signs
Decreased respiratory rate & oxygen saturation
level
Hypotension
Central nervous system
General: Hallucination, Slurred speech, Ataxia,
Altered mental status, Coma, Impairment of
cognition
Examination
Nystagmus, Hypotonia, Weakness, Respiratory
depression, Hypotension
 Sedatives/Hypnotics
Relationship between Half-life and
the severity of withdrawal

Shorter the half-

life, greater the
severity.
 Benzos Half-life
Long acting: Chlordiazepoxide (Librium),
Diazepam (Valium), Flurazepam (Dalmane)
Intermediate: Alprazolam (Xanax),
Clonazepam (Klonopin), Lorazepam (Ativan)
Short Acting: Oxazepam (Serax), Triazolam
(Halcion)

Treat overdose with Flumazenil (Romazicon)

**tq**
 Dependence Syndrome
3+ of following for >1 mo. or <1 mo.
repeatedly within a years time
Strong desire/sense of compulsion to take drug
Unable to control taking it too much, too often
Physiological withdrawal state when
substance is stopped
Tolerance as evidenced by increased need for
increased dosage to achieve intoxication
Preoccupation with use interferes with daily
living
Persistent use despite understanding evidence
of negative consequences
Alcohol
 Alcohol
Zero Order Kinetics via liver
metabolism
~1 drink per hour (although lecture
does say 0.7)
One drink = 14 g of EtOH
Primary Route for
Metabolism
 Question
Which drug inhibits Alcohol Dehydrogenase?
A. Disulfiram
B. Acetazolamide
C. Varenicline
D. Fomepizole

What is a possible adverse reaction of this drug?

Seizures
Where does this reaction take place?
Cytosol
Why is this drug important?
Treatment of Methanol and Ethylene Glycol poisoning
 Secondary Metabolism
MEOS = Microsomal Ethanol Oxidizing
System
Where does this reaction take place?
SER **tq**
When is it important?
When the human has been ingesting large
amounts of alcohol and NAD levels are
inadequate to drive primary metabolism
NADPH is used instead
MEOS activity increases with chronic EtOH
use (SER enlargement in alcoholics)
 Acetaldehyde Metabolism
Via aldehyde dehydrogenase
Which drug inhibits this enzyme?
Disulfiram **tq** (must know!!! Trade
name is Antabuse)
What is acetaldehyde finally converted
into?
Acetate and then Acetyl CoA, which enters
citric acid cycle and used for energy
Excess acetate is converted to
acetoacetate leading to ketosis
 Acute EtOH
Liver: increased O2 need, decreased
gluconeogenesis, increased lactate, increased
fat accumulation
CV: vasodilation, dep of myocardial contractility
Endo: diuresis via inhibition of what? ADH
Neuro **tq**
BEC level Effect
50-100 sedation, subjective high
100-200 impaired motor fxn, slurred speech
200-300 emesis and stupor
300-400 coma
>500 resp depression and death (last yrs
answer)

Tx of
GIVE THIAMINE
EtOH Intoxication
Before you give any other treatments, give thiamine + folic
acid
Why?
to prevent Wernickes encephalopathy and permanent
opthalmoplegia; its a cofactor in many pathways dealing
with energy production and its absence can lead to cell
death and acidosis. Giving sugar before giving thiamine
will deplete any remaining reserves of this B vitamin.
**tq**
Then treat hypoglycemia, lactate acidosis, electrolyte
imbalances
Treatment is supportive, such as intubation for respiratory
depression and diazepam or chlordiazepoxide (Librium) for
symptomatic treatment of withdrawal delirium
 Alcohol & Parenchymal Dz
Liver: Steatosis (90%; reversible) -->
hepatitis/fibrosis (40%) --> cirrhosis/failure
(15-30%)
Pancreatitis (3x risk and 10% of all cases)
Whats two MCC of pancreatitis?
GS & EtOH

Gastritis, enteritis
Cancer risk increased 10x
CV
HTN: almost 1/4 of HTN in males 2/2 drinking
alcoholic dilated cardiomyopathy (cellular path?)

Alcohol Tolerance
There are 4 types of alcohol Tolerance:
Pharmacodynamic, Pharmacokinectic, Behavioral, &
Cross-Tolerance (more on these later)
Dependence is broken into physical and
psychological
Withdrawal syndrome ssx: hyperexcitability,
convulsions, psychosis, and
the DTs: delirium (duh), tremor (its in the name),
agitation & increased BP, pulse, and respirations
***basically when using alcohol, benzo and
barbituates, GABA increases and the brain is
SUPPRESED. When withdrawal happens, brain is no
longer suppressed and is prone to be overly excited
Seizure!
 Alcohol Neurotoxicity-COAT
RACK
Wernickes triad (COAT-T
for thiamine deficiency)
Acute confusion
Ataxia
Ophthalmoplegia
Korsakoffs: Wernickes +
confabulation due to
anterograde and retrograde
amnesia (RACK)
 Alcoholism Epidemiology
Monozygotic concordance higher than
dizygotic
4x increase even if adopted to alcoholic
parents
Prevalence = 10% in gen. pop.
CAGE: have you ever (>=2 is positive
test)
tried Cutting down on drinking?
been Annoyed if asked about drinking?
felt Guilty feelings about drinking?
drank an Eye-opener in the morning?
 Tx of Alcohol Dependence
Naltrexone
Opioid antagonist
Reduces the reward associated with drinking **tq**
Acamprosate
structural analogue of the amino acid homotaurine and the
inhibitory neurotransmitter gamma-aminobutyric acid
(GABA)
For patients who are currently not drinking
Thought to restore NT balance
Disulfiram-only for highly motivated individuals!
Inhibits aldehyde dehydrogenase
Creates an aldehyde syndrome if patient drinks
Aldehyde syndrome symptoms: facial flushing, tachycardia,
hypotension, N/V, HA, muscle weakness, insomnia,
EtOH Aversion
 Lab Findings in an Alcoholic
The following can be elevated
TG
MCV
Gamma-glutamyl transferase (GGT)
Serum uric acid
Carbohydrate-deficient transferrin (CDT)
What type of anemia would your patient
have if their H&H was low and had
evidence of alcoholism on their CBC?
NON-megaloblastic macrocytic anemia
Drugs of Abuse and Opoids
 Cocaine
Main Mechanism: Dopamine reuptake
inhibitor (via blockage of the DA transporter)
Also binds NE and 5-HT transporters; has
local anesthetic action - **tq** these actions
are what makes cocaine potentially fatal in
an overdose - (arrhythmias, szs, coma, CV
collapse, tactile hallucinations)
Cocaine + EtOH yields cocaethylene which
has a longer half life and the same
mechanism
 Amphetamines
Increases the release of DA into
synapse
No local anesthetic effect, and minimal
(if any) NE effects; so less CV toxicity
and sz potential less than cocaine
Uses: wt control, anti-fatigue,
enhanced concentration and ADHD,
narcolepsy
 Hallucinogens
Other Drugs
Indoleamine-like: LSD, DMT, shrooms (psilocbin)
Phenethylamine-like: DOM, Ecstasy (shown to destroy
serotonin-containing cells), Mescaline
PCP & Ketamine: non-competitive NMDA receptor
blocker; in overdose, patient will have vertical
nystagmus **tq**
Marijuana: binds to specific cannabinoid receptors;
medical uses limited to Anorexia in AIDS/CA; lipid
sol. - detectable up to 30 days after use
GHB: Gamma hydroxybutyric acid; mech unknown
Flunitrazepam (Rohypnol or roofie): sedative-
hypnotic
 Opioid Receptors
Mu Receptors (endorphins) ^_^
morphine selective and most importance subtype for
abuse/dependence
Responsible for most of well-known effects including:
analgesia, euphoria, miosis, sedation, resp dep,
dependence
Kappa (dynorphins) -__-
Responsible for dysphoria, disorientation, sedation,
vasodilation
Important for non-selective and mixed agonist/antagonists
Delta (enkephalins)
Analgesia at spinal and supraspinal sites
Antinocioception for thermal stimuli at spinal sites
Modulation of hormone and NT release
 Opioid Receptors
Distribution: All located in dorsal horn,
rostral ventral medulla, locus ceruleus,
and midbrain periaqueductal gray area
Selective Distribution as follows:
Mu: GABAergic neurons in VTA leading to
inhibition of GABA activity in VTA, which
does what?
increase dopamine release into the nucleus
accumbens **tq**
Kappa: dopaminergic neurons in VTA leading
to inhibition of dopamine release, which may
be why they are responsible for dysphoria
 Opioid Availability
Oral route limited by first pass
metabolism: specifically PHASE 2
Glucuronidation

Distributed to all body components

including fetus
 Opioids
Drug Potency/Eq Oral Abuse Formulation
uI.V. Dose Bioavailability Potential s

Morphine 10mg Low High Oral &

supp., I.V.

Heroin 4mg Very Low Very High Pro-drug,

I.V.

Methadone 10mg High High Oral &

Injection

Buprenorphine ?? ?? ?? ??

Oxycodone 4.5mg Medium Very High Oral, I.V.,

(non- Intranas.
equivalent)
 Opioid Antagonists
Naloxone
Managing acute overdose **tq**
Short-acting injectable (Near zero oral
bioavailability)
Partial agonist (acts like an antagonist)
Naltrexone
For chronic opioid abusers
Long-acting oral form
Why is naloxone included in the preparation of
buprenorphine (partial mu agonist), which is used
for outpatient maintenance-replacement therapy?
To prevent abuse/overdose
 Management of Opioid
Withdrawal
3 Approaches
Do nothing: patient will medically be
fine
Detox with methadone or buprenorphine
to lessen withdrawal syndrome
Treat with clonidine (alpha-2 agonist) to
decrease the sympathetic overactivity
**tq**
 Opioid Withdrawal vs.
Overdose
Withdrawal Overdose
Rhinorrhea Lethargy/coma
Lacrimation Depressed resp.
Chills Miosis (mydriasis
before death)

Mydriasis Hypotension/therm.
N/V/D Pulm. edema
Anxiety Covulsions
Hypervent/thermia Hypoxia
 Know COWS **tq**
(matching drug to OD/Withdrawal based on the pupil size )
Cocaine, Opiod Withdrawal, Stimulants
(amphetamine) = Mydriasis (pupil dilation)
Questions
 Question 1a
25 yo male with a psychotic disorder is started on
a neuroleptic medication. Two days after the
beginning of the treatment, he cannot stop pacing
and is unable to sit still. He reports he feels jittery
and complains that his legs are moving on their
own. Which of the following statements is true
with regard to these symptoms?
A. They are a rare neuroleptic side effect
B. They are an indication that the med is not working
and needs to be increased
C. They most often occur shortly after the
initiation of neuroleptics
D. They are well tolerated by most patients
E. They are associated with an increased risk of
neuroleptic malignant syndrome
 Akathisia
Subjective feeling of restlessness and
inability to stay still
Manifests as pacing, shifting position,
constant leg movements
Very common SE of neuroleptic
treatment
Occurs during FIRST FEW DAYS of
tx
 Question 1b
Which drug would be most helpful in
treating the side effect symptoms?
A. Propanolol
B. Phenytoin
C. Amantadine
D. Benztropine
 Question 2
12 yo boy is distraught because every time he
thinks or hears the word God or passes in front
of a church, swear words pop into his mind
against his will. He also feels compelled to repeat
the end of every sentence twice and to count to
20 before answering any questions. If he is
interrupted while counting, he has to start from
the beginning. Which of the following meds has
been proven effective with this disorder?
A. Alprazolam
B. Clomipramine (TCA): tx oCd
C. Propranolol
D. Phenobarbital
E. Lithium
 Question 3
7 yo boy is brought to a D.O. with a 1 year
history of making careless mistakes and
not listening in class. He is easily distracted
and forgetful and loses his schoolbooks
often. He is noted to be fidgety, talking
excessively, and interrupting others. Which
of the following meds is most likely to be
helpful with this boys symptoms?
A. Haloperidol
B. Alprazolam
C. Lithium
D. Methylphenidate
E. Paroxetine
 Question 4
19 yo male is diagnosed with paranoid
schizophrenia. He has command auditory
hallucinations and persecutory delusions, but
is also apathetic and withdrawn with a flat
affect. Which of the following medications is
most likely to treat both the positive and
negative symptoms of this patient?
A. Chlorpromazine
B. Fluphenazine
C. Olanzapine
D. Quetiapine
E. Trifluoperazine
 Atypicals
Olanzapine and Clozapine are the only
two antipsychotics that have been
proven to treat both positive and
negative symptoms
Olanzapine has a more favor side
effect profile: Oh so round and big!-
wt gain
What is the noteworthy adverse effect
of clozapine?
 Clozapine
Agranulocytosis **tq**
Screen with weekly CBCs
Other SE is seizures
If seizures continue, stop clozapine and
start phenobarbitol
Clozapine can be then be restarted at
50% of previous dosage and gradually
increased
 Question 5
42 yo man is diagnosed with a psychotic depression
and is started on imipramine and perphenazine.
When he develops a dystonia, he is begun on
bentropine 2mg/d. One week later, his wife reports
that he has become forgetful and seems
disoriented. On PE, he appears flushed, his skin and
palms are dry, and he is tachycardic. He is oriented
to name and place only. He showed none of these
symptoms during his last appointment. Which of
the following diagnoses is most likely?
A. Anticholinergic syndrome
B. Neuroleptic malignant syndrome
C. Extrapyramidal side effect
D. Akathisia
E. Dementia
 Anticholinergic Syndrome
Benztropine is an anticholinergic and
antihistaminergic
Used for the treatment of dystonias
caused by neuroleptics
Symptoms described in the question
(including the disorientation and
confusion) are classic when there is a
blockade of cholinergic receptors,
leading to a predominance of
sympathetic innervation
 Question 6a
A mentally retarded male adolescent who has
been increasingly aggressive and agitated
receives several consecutive IM doses of
haloperidol, totaling 30mg in 24 hours, as a
chemical restraint. The next day, he is rigid,
confused, and unresponsive. His BP is 150/96, P
110/min, Temp 102. His WBC is 25,000 and CPK
is 1,200. What is the most likely diagnosis?
A. Acute dystonic reaction
B. Neuroleptic-induced Parkinsons disease
C. Malignant hyperthermia
D. Neuroleptic malignant syndrome
E. Catatonia
 Question 6b
What med can be effective in
treating this condition?
A. Bromocriptine
B. Carbamazepine
C. Chlorpromazine
D. Lithium
E. Propanolol
 Neuroleptic Malig.
Syndrome
Rare but potentially fatal complication of
neuroleptic treatment
Hyperthermia, severe muscular rigidity, autonomic
instability, and changes in mental status
Assoc findings are increased CPK, liver enzymes,
leukocytes
More common in young males when high dose,
potent, neuroleptics are used in escalating dosages
First step is to discontinue neuroleptic (as well as
any anticholinergics) and administer bromocriptine
(Dopamine agonist) and antipyretics
Mortality can be as high as 30%
 Tardive Dyskinesia
Occurs after long-term treatment with
neuroleptics: Tardy
Mechanism: long term blockade of DA
causes up regulation of receptors;
increasing the dose of the neuroleptic will
help the TD at first because of the
increased blockade of the new receptors;
but symptoms will return, and the only
treatment is as follows:
Treatment is to decrease the dose of the
neuroleptic and give dantrolene if needed
for muscle rigidity
Initially, symptoms will worsen, known as
withdrawal dyskinesia
 Serotonin Syndrome

Treatment is with benzos, such as

diazepam
If patient requires more treatment,
dantrolene can be added for muscle
rigidity and hyperthermia
 Question 7a
19 you male is brough to ER by his parents who are
worried about his vomiting and diarrhea. On arrival,
his pupils are dilated, BP is 175/105, and his muscles
are twitching. His parents report that these
symptoms started 2 hours earlier. For the past few
days he has been homebound due to a sprained
ankle, and during this time, he has been increasingly
anxious and restless. He has been yawning
incessantly and has had a runny nose. Which of the
following drugs is this man likely to be withdrawing
from?
A. Heroin
B. Alcohol
C. PCP
D. Diazepam
E. Cocaine
 Question 7b
How long after cessation of use of
this substance does its withdrawal
syndrome usually peak?
A. 6 hours
B. 15 hours
C. 48 hours
D. 3 days
E. 1 week
 Heroin
Symptoms of withdrawal include
Anxiety & restlessness
Dysphoria
Yawning: d/t dopamine effects?
Lactimation
Mydriasis
Rhinorrhea
Twitching muscles & kicking movements of the lower
extremities (kicking the habit)
Fever
N/V/D
Increased BP, Pulse, and Temp
Symptoms usually begin within 8-12 hours after
cessation of drug use and peaks at 48 hours
after the last dose
 Question 8a
50 yo male is brought to ER by ambulance.
His respirations are shallow and
infrequent. His pupils are constricted, and
his is stuporous. He was noted to have
suffered a grand mal seizure in the
ambulance. Which of the following drugs
is this man likely to have overdosed on?
A. Cocaine
B. LSD
C. Meperidine
D. PCP
E. MDMA
 Question 8b
After ensuring adequate ventilation
for this patient, which of the following
interventions should be next?
IV naloxone
IV phenobarbitol
IV diazepam
Forced diuresis
IM haloperidol
 Opioid Overdose
Review slide on withdrawal vs.
overdose: ***Read on stem of the ques
if asking for w/d vs o/d
Treatment
Naloxone reverses effects of opiates and
is first line treatment in overdose once the
airway is secure
Distracters
Diazepam is for alcohol withdrawal symptoms
Forced diuresis can be used for
salicylate/Tylenol OD
Haloperidol is an antipsychotic and would have
no benefit in this case
 Question 9
35 yo man stumbles into the ER. His pulse is 100,
BP 170/95, and he is diaphoretic. He is tremulous
and has difficulty relating a history. He does
admit to insomnia the past two nights and sees
spiders walking on the walls. He has been a
drinker since 19 yo, but has not had a drink in 3
days. Which of the following is the most likely
diagnosis?
A. Alcohol-induced psychotic disorder
B. Wernickes psychosis
C. Alcohol withdrawal delirium (aka Delirium
Tremens)
D. Alcohol intoxication
E. Alcohol idiosyncratic intoxication
 Question 10
25 yo woman is dropped of on the
doorstep of the ER by two men who
immediately leave by car. She is agitated
and anxious, and she keeps brushing her
arms and legs to get rid of the bugs.
She clutches at her chest, moaning in
pain. Her pupils are wide, and her BP is
elevated. Which of the following
substances is she most likely using?
A. Alcohol
B. Heroin
C. Alprazolam
D. LSD
E. Cocaine
 Question 11
24 yo woman is hospitalized after a suicide gesture in which
she superficially slashed both her wrists. At the team meeting
3 days later, the male resident argues that the patient has
been doing quite well, seems to be responding to therapy, and
should be allowed to go on a pass. The nursing staff angrily
argues that the resident is showing favoritism to the patient,
and, because of her poor compliance with the unit rules, she
should not be allowed out. The resident insists the nurses are
being punitive. The defense mechanism being used by the
patient in this scenario is a feature of which of the following
personality disorders?
A. Narcissistic
B. Histrionic
C. Borderline (the defense mechanism described here is
splitting)
D. Antisocial
E. Dependent
 Question 12
43 yo woman comes to the ER with a temp of 101 and a
suppurating ulcer on her left shoulder. This is the third
such episode for the patient. Her PE is otherwise normal,
other than the presence of multiple scars on her
abdomen. The woman is admitted to the hospital and is
observed to be holding her thermometer next tot he light
bulb to heat it up. When confronted, she angrily denies
any such behavior and signs out AMA. The patient most
likely has which of the following diagnoses?
A. Malingering
B. Somatoform Disorder
C. Borderline Personality Disorder
D. Factitious Disorder (faking signs/symptoms
to assume a sick role for the primary gain of
being taken care of)
E. Body dysmorphic disorder