PSYCH ROTATION Flashcards

1
Q

ADHD

A

has to affect them in different areas of their life, in multiple settings: school/work, home, etc.

Manifests in childhood with symptoms of hyperactivity, impulsivity and/or inattention

CAUSE = GENETIC + ENVIRONMENTAL FACTORS
⦁ Increased chance of sibling having ADHD
⦁ Even higher chance of twin having ADHD (not guaranteed to have ADHD though)

Symptoms affect cognitive, academic, behavioral, emotional and social functioning

these patients experience their emotion in a more intense fashion; may seem to be an “inappropriate reaction” to a stress

Now realizing that ADHD can manifest in adults who didn’t show symptoms as a child; instead of school functioning issues, impulsivity/inability to follow through with tasks at work, multiple job changes, unhappiness at work/failure at work; mostly productivity

ADHD = one of the most common disorders of childhood

Having oppositional defiant disorder / conduct disorder = more likely to also have ADHD. Same with kids who have anxiety disorder and learning disabilities

More prevalent in males

ADHD = frequently associated with other psychiatric disorders

NEUROPATHOGENESIS OF ADHD
- brain imaging reveals decreased activation in areas of basal ganglia + anterior frontal lobe

  • major NEUROTRANSMITTERS involved in ADHD = ****Dopamine + NE*****
  • Most of dopamine sensitive neurons = located in the frontal lobe
  • Dopamine system = associated with reward, attention, STM tasks, planning, motivation, taking risks or being impulsive
  • Dopamine limits and selects sensory information arriving from the thalamus to the forebrain

The sensory information gets unorganized and unfiltered; it’s difficult for people with ADHD to filter info and store it properly –> so move around a lot, or are doing other things while listening or looking elsewhere but still able to process what’s going on

Too little dopamine (like Parkinson’s) - so need medication that will increase dopamine

FRONTAL LOBE = ability to project future consequences resulting from current actions, and being able to choose between good and bad decisions (or even between better and best choices).
- Frontal lobe also allows for the override + suppression of socially unacceptable responses, and the determination of similarities + differences between things/events

Attention deficit hyperactivity disorder (ADHD) is a developmental disorder characterized by limited attention span and poor impulse control. It is associated with a decrease in frontal lobe volume* or metabolism, but does not result in a lower intelligence level*

  • the impulsivity will decrease with behavioral interventions and as the person ages

DIFFERENCE IN BRAIN FUNCTION OF THOSE WITH ADHD

  • decreased activation in areas of basal ganglion and anterior frontal lobe
  • there is an increase in dopamine transporter activity –> clears dopamine from the synapse too quickly
  • Hypoactivity of dopamine, norepinephrine, and epinephrine in the prefrontal cortex

THE BASIS OF TREATMENT OF ADHD WITH METHYLPHENIDATE***
⦁ increases extracellular dopamine + NE in the brain
⦁ changes the areas of function in the frontal lobe
⦁ in patients without ADHD, methylphenidate does NOT have the same effect on the frontal lobe function

CRITERIA FOR DIAGNOSIS
- NEED 6+ SYMPTOMS OF INATTENTION OR 6+ SYMPTOMS OF HYPERACTIVITY/IMPULSIVITY***

  • Symptoms must be present of at least 6 MONTHS
  • The majority of the time, children have symptoms of BOTH subtypes
  • Need 5+ for age 17 or older
  • Symptoms should be inappropriate for the given age**
  • symptoms negatively impact social + academic or occupational activities
  • symptoms developed PRIOR to age 12** = have to have started between ages 6 - 12
  • symptoms present in 2+ settings***
  • symptoms present for at least 6 months**
  • symptoms not better explained by other psych disorders

Patients with ADHD have normal intelligence

Tourette syndrome is a childhood tic disorder often associated with ADHD

ADHD = Classified as

1) Inattentive
2) Hyperactive (overly active + impulsive)
3) Both = MOST COMMON**

ADHD INATTENTIVE SYMPTOMS (9)
⦁ Easily distracted; miss details, frequently switch from one activity to another, forget things. Easily distracted when multiple things are happening simultaneously
⦁ Difficulty maintaining focus on one task or learning something new
⦁ Failure to give close attention to detail; misses details, may make careless mistakes

⦁ Failure to listen** when spoken to directly, Failure to follow instructions
⦁ Difficulty organizing tasks and activities; difficulty completing assignments
⦁ Reluctance to engage in tasks that require sustained mental effort
⦁ Forget things or lose things needed to complete activities and tasks (pencil); (did my hw, but I lost it - very common with ADHD).
⦁ Forgetfulness in daily activities
⦁ Becomes bored with a task after a few minutes, unless doing something enjoyable

ADHD IMPULSIVE-HYPERACTIVITY SYMPTOMS (9)
⦁ Fidgetiness with hands and feet or squirms in seat
⦁ Constantly in motion; may often leave their seat - difficulty remaining seated in class
⦁ Has trouble sitting for long periods (ex: doing homework, dinner, school)
⦁ Difficulty doing quiet tasks or engaging in quiet activities
⦁ Often talks excessively or non-stop = Excessive talking and blurting out answers before questions have been completed
⦁ Excessive running or climbing in inappropriate situations; Dashes around, touching or playing with everything in sight = Restlessness
⦁ Blurts out appropriate or inappropriate comments; shows unrestrained emotions
⦁ Is often “on-the-go” or acts as if “driven by a motor”
⦁ Difficulty awaiting turns (while waiting in line); Impatient
⦁ Interrupting and intruding on others; Interrupts the conversation or activities of others

MEDICAL EVALUATION FOR ADHD
- Parents + Teacher need to fill out form - such as the Vanderbilt form
- Refer for vision + hearing tests* - r/o that kid isn’t just having difficulty seeing or hearing at school
- Complete hx, ROS, and PE to rule out other causes / psych illnesses
- If history suggests, may consider the following
⦁ blood lead level
⦁ TSH
⦁ sleep study
⦁ neurology consult if concern for seizures or other neurologic disorder

Poor sleep quality can lead to ADHD-like symptoms or learning disabilities; so ask about snoring, look in mouth (tonsils), large neck, obesity, etc.

DIAGNOSIS + TREATMENT OF ADHD IN ADULTS

  • diagnosis should be made by a mental health professional
  • symptoms often continue into adulthood, and can have significant effects on social + occupational functioning
  • same meds used for adults + kids with ADHD

often kids with ADHD are able to come off the med as an adult due to decrease in symptoms; unsure if changes in brain development or whether due to adaptation to ADHD over time

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2
Q

ADHD TREATMENT

A

1) BEHAVIOR MODIFICATION

Cognitive behavioral therapy is the FIRST LINE PSYCHOTHERAPY for patients with attention deficit hyperactivity disorder

⦁ CBT = often targeted at children. Focuses on teaching kids things like better time management and organizational skills (creating structured routines)

  • Behavioral Therapy Treatment = has NOT been shown to reduce symptoms in the absence of a concurrent stimulant Rx for a patient that truly has a diagnosis of ADHD
  • other alternative treatments, such as cognitive treatment, dietary modification and multivitamins have NOT been shown to be effective in controlled studies
    2) SYMPATHOMIMETIC MEDICATIONS (STIMULANTS) = pharmacologic treatment of choice**
⦁	Methylphenidate (Ritalin / Concerta)
⦁	Amphetamine / Dextroamphetamine (Adderall)
⦁	Dexmethylphenidate (Focalin)
⦁	Dextroamphetamine (Dexedrine)
⦁	Lisdexamfetamine (Vyvanse)

Stimulant MOA = blocks dopamine + norepinephrine reuptake ==> increases release of dopamine + norepinephrine in extra-neuronal space

Stimulant Indications = ADHD, Narcolepsy, Excessive Daytime Sleepiness

Stimulant SE
⦁ Anxiety
⦁ Hypertension
⦁ Tachycardia
⦁ Weight loss (decreased appetite)
⦁ Growth delays
⦁ Addiction

Methylphenidate, dexmethylphenidate and amphetamines are equally effective
Have similar side effect profiles

  • The fast release of dopamine causes euphoria and can be addictive (methamphetamine), which is why it is imperative to have a slow release of dopamine (ADHD meds)-> helps with focus and attention = what the ADHD stimulant meds do

Dose Titration: know that the initial dose is not necessarily the effective dose, so need to titrate up, and education patient/parents that drug won’t be effective until reach effective dose, but important to start on lower dose initially

  • children < 6 = need short acting stimulant
  • short acting stimulant can also be used to determine optimal dosing before switching to long acting agent
  • long acting stimulant can be used in patients > 6; start at lowest dose, titrate up
    3) NONSTIMULANTS

⦁ Atomoxetine (Strattera)

Nonstimulant MOA = SNeRI - selective norepinephrine reuptake inhibitor

  • similar efficacy and side effect profile as stimulants, however, side effects occur less often and have a less addictive ability
  • for children > 6
  • may take 1-2 weeks before see effects*** (unlike stimulants - will know pretty quickly)
  • also can’t take “pill holiday” with strattera the way you can with stimulants
  • Similar efficacy and SE profile as stimulants, however, SE occur less often with Strattera, and there are less addictive properties

4) Adjunctive Medications
- Bupropion (Wellbutrin)
- Venlafaxine (Effexor)
- Guanfacine (Intuniv)
- Clonidine (Catapres)

Clonidine and guanfacine are α2 agonist medications that are used in combination with central nervous system stimulants for patients with ADHD

CRITERIA FOR INITIATION OF THERAPY
⦁ Complete diagnostic assessment that confirms ADHD
⦁ ≥ 6 years old
⦁ Parental consent
⦁ School is cooperative (if dosing during school hours)
⦁ No previous sensitivity to the chosen medication
⦁ Normal heart rate and BP
⦁ No history of seizure disorder (if so refer to neurology to treat ADHD too)
⦁ Does not have Tourette syndrome, Autism spectrum disorder, anxiety disorder, or substance abuse among household members

if there is a hx of substance abuse in household members, can prescribe a non-stimulant therapy

PRETREATMENT WORK UP
o need a comprehensive medical evaluation (above info) + EKG to r/o arrhythmia
o document pretreatment height / weight / BP / HR
o document the presence of any of the following symptoms PRIOR to treatment
⦁ general appetite
⦁ sleep pattern
⦁ headaches
⦁ abdominal pain

o assess for substance use or abuse
⦁ need treatment for this before starting ADHD meds

EVALUATION AT EACH FOLLOW-UP
⦁	Decreased appetite***
⦁	Poor growth*** (take summer drug holidays)
⦁	Dizziness (monitor BP)
⦁	Insomnia/Nightmares
⦁	Mood lability (can occur when drug is wearing off - consider switching to longer acting or increasing to BID or TID)
⦁	Rebound
⦁	Tics
⦁	Psychosis
⦁	Diversion and misuse

REASONS FOR TREATMENT FAILURE

  • not sticking to medication regimen
  • possibility of medication diversion (giving it to another person - selling it)
  • are treatment goals / expectations realistic?
  • is there a comorbid psychiatric diagnosis?

o Can try another stimulant medication
o if pt fails multiple stimulants or experiences intolerable side effects = try Atomoxetine (Strattera) or a centrally-acting alpha-2 adrenergic (Clonodine - Cataprex) (Guanfacine - Tenex)

DRUG HOLIDAYS

  • discontinuation of stimulant medication on weekends or during the summer
  • decide on a case by case basis
  • not an option for atomoxetine (strattera) or alpha-2 adrenergic agonists because of the extended half life**

MAINTENANCE OF THERAPY

  • once on a stable dose - follow up in office every 3-6 months
  • continue to monitor weight / BP / HR (SE of decreased appetite, hypertension, tachycardia)

TERMINATION OF THERAPY

  • May abruptly discontinue stimulants or atomoxetine (Strattera)***
  • for alpha-2 adrenergic agonists + TCAs = should taper off over several weeks*

both Ritalin + Adderall can cause anxiety, weight loss, psychosis and heart problems in at risk pts. High potential for addiction and abuse

DEXTROAMPHETAMINE (DEXEDRINE)

  • previously used for OTC diet pill
  • among the most effective treatments for ADHD***
  • sudden death in ppl that have heart problems or cardiac defects (like ritalin + adderall)

LISDEXAMFETAMINE (VYVANSE)

  • is converted to dextroamphetamine after oral ingestion
  • is less addictive*** but is still a schedule II drug like rest
  • amphetamines cause release of catecholamines (primarily dopamine + NE) from their storage sites in presynaptic nerve terminals

ATOMOXETINE (STRATTERA)

  • non-stimulant - was initially the only approved non-stimulant treatment until Intuniv
  • non-stimulant - so DOESN’T WORK ON DOPAMINE, only works on NE*** - but therefore also why its less effective than a stimulant
  • was initially tested for depression, but didn’t do much

**BBW - INCREASED RISK OF SUICIDAL BEHAVIOR IN PTS < 25 **

  • may not be as effective as stimulant meds
  • is expensive

Strattera - SE
⦁ dry mouth, insomnia, nausea, decreased appetite, constipation, decreased libido/ED, urinary hesitancy, dizziness, sweating

  • RISK OF SUICIDAL IDEATION IN CHILDREN AND ADOLESCENTS*
  • so need to weight risk vs benefits, and should be monitored closely for suicidal thinking and behavior
  • families/caregivers should be advised of the need for close observation + communication with the provider

GUANFACINE (INTUNIV)

  • alpha-2 adrenergic agonist - antihypertensive
  • but also approved for treatment of ADHD

***So if patient has ADHD + Hypertension = give Guanfacine (Intuniv)

SE of Guanfacine = can become HYPOTENSIVE**
**Caution with KIDNEY OR LIVER DISEASE **

BUPROPION (WELLBUTRIN)

  • alternative treatment for ADHD (as well an antidepressant and to quit smoking) = miscellaneous antidepressant
  • SE = anxiety + insomnia
  • DON’T give in bulimics - can lower the seizure threshold
  • can be used as add on therapy with SSRI to prevent sexual SE
  • increases dopamine
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3
Q

ANOREXIA NERVOSA

A

⦁ Very low weight (< 85% of normal body weight)
⦁ fear of gaining weight
⦁ distorted view of body

  • Refusal to maintain a minimally normally body weight - fueling a relentless desire for thinness
  • Morbid fear of fatness or gaining weight, even though the patient is underweight
  • Depression is the most common psychological disease that coexists with anorexia nervosa.

2 types = Restrictive and Binge / Purge

MC age of onset = mid teens

90% of patients = Women
60% = 15-24y/o

Frequently seen in athletes, dancers, or other conditions requiring thinness

60% incidence of depression

CLINICAL MANIFESTATIONS

  • Exhibits behaviors targeted at maintaining a low weight or certain body image
  • Excess water intake, food-related obsessions (hoarding, collecting)

RESTRICTIVE TYPE = reduced calorie intake, dieting, fasting, excessive exercise, diet pills

BINGE/PURGE TYPE = primarily engages in self-induced vomiting, diuretic / laxative / enema use

binge/purge anorexia vs bulimia = For those with binge-purge anorexia, what they are doing results in a net intake lower than their output for long enough to become, or maintain, a too-low weight (underweight). For those with bulimia, the net input is enough to maintain or gain weight (normal weight or overweight)

  • so people can start out with bulimia and end up with anorexia over time…or vice versa
SIGNS/SYMPTOMS
⦁	dry skin							
⦁	cold intolerance / hypothermia (hypothyroidism)
⦁	blue hands / feet
⦁	constipation
⦁	bloating
⦁	delayed puberty
⦁	primary or secondary amenorrhea
⦁	fainting
⦁	orthostatic hypotension
⦁	lanugo hair
⦁	scalp hair loss
⦁	early satiety
⦁	weakness / fatigue
⦁	short stature
⦁	osteopenia / osteoporosis
⦁	breast atrophy
⦁	atrophic vaginitis
⦁	pitting edema
⦁	cardiac murmurs / sinus bradycardia

Decreased bone density due to decreased estrogen levels and

DIAGNOSIS
- BMI = 17.5 kg or weight < 85% of ideal weight

mild anorexia = BMI > 17
moderate anorexia = BMI between 16-17
severe anorexia = BMI between 15-16
extreme anorexia = BMI < 15

PHYSICAL EXAM

  • emaciation (abnormally thin / weak)
  • hypotension
  • bradycardia
  • skin / hair changes (ex: lanugo - fine hairs), dry skin, brittle hair
  • salivary gland hypertrophy
  • amenorrhea (no periods)
  • arrhythmias
  • osteoporosis

Metatarsal stress fractures are the most common type of fracture seen in patients with severe anorexia nervosa.

o Vital signs - include Orthostatic vitals
o Skin + Extremity evaluation =dryness, bruising, lanugo
o Cardiac Exam = Bradycardia, Arrhythmia, MVP** (heart muscle shrinks but the valves don’t)
o Abdominal Exam
o Neuro Exam - evaluate for other causes of weight loss or vomiting (brain tumor)

LABS

  • leukopenia (decreased WBC count)
  • anemia
  • hypokalemia***
  • hyponatremia
  • hypochloridemia
  • HYPERCAROTENEMIA**
  • HYPERCHOLESTEROLEMIA**
  • increased BUN (dehydration), decreased GFR
  • hypothyroidism
  • low levels of FSH, LH, TSH, and prolactin
  • metabolic alkalosis –> ketonuria***

due to impaired liver functions, there could be hypercholesterolemia and hypercarotenemia.

Individuals suffering from anorexia nervosa tend to bleed and bruise more easily due to lower levels of platelets.

low creatinine level is seen in individuals suffering from anorexia nervosa due to loss of muscle mass.

TREATMENT
o medical stabilization: hospitalization if < 75% of ideal body weight, or if patients have medical complications; electrolyte imbalances may lead to cardiac abnormalities, dehydration, arrested growth/development, etc

Psychotherapy and nutritional rehabilitation are the first line treatments for anorexia nervosa.

o Psychotherapy = CBT, supervised meals, weight monitoring

o Pharmacotherapy: if depressed = SSRIs, or atypical antipsychotics - Olanzapine (Zyprexa) - (may also help with weight gain)

o Nutrition
- Goal = to regain 90-92% of ideal body weight
- Inpatient treatment varies by facility
+ oral liquid nutrition
+ nasogastric tube feedings
+ gradual caloric increase with “regular” food - but take it easy during first 2 weeks - so don’t get heart failure + pitting edema

ANOREXIA OUTCOME
o 50% = good outcome - return of menses + weight gain
o 25% = intermediate outcome - some weight regained
o 25% = poor outcome
⦁ associated with later age of onset
⦁ longer duration of illness
⦁ lower minimal weight
⦁ Overall mortality rate = 6.6%. 1/5 anorexia deaths are due to suicide

SUMMARY
Anorexia nervosa is an eating disorder characterized by a low weight, fear of gaining weight, a strong desire to be thin, and food restriction. Many people with anorexia see themselves as overweight even though they are underweight. If asked they usually deny they have a problem with low weight. Often they weigh themselves frequently, eat only small amounts, and only eat certain foods. Some will exercise excessively, force themselves to vomit, or use laxatives to produce weight loss. Complications may include osteoporosis, infertility and heart damage, among others. Women will often stop having menstrual periods.

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4
Q

BULIMIA NERVOSA

A

Bulimia patients (vs anorexia) = patients with bulimia have NORMAL WEIGHT or are OVERWEIGHT

  • more common in females
  • average onset = late teens
  • concerned about body image
  • 2 types: Purging and Non-Purging

ASSOCIATED WITH
⦁ OCD
⦁ Depression
⦁ Anxiety

EPIDEMIOLOGY

  • occurs in 1-5% of high school girls
  • occurs in as high as 10% of college women

Typically occurs in young girls with low self-esteem and who have a strong desire for control
- Are often fixated on food (amount and calorie count)

DSM IV CRITERIA FOR BULIMIA / clinical manifestations

1) Recurrent BINGE EATING: an episode of binge eating is characterized by BOTH of the following
⦁ Recurrent episodes of eating a large amount of food in a small amount of time (2hrs) = (larger amount of food than what most individuals would eat in a similar period of time)
⦁ A sense of a lack of control over eating during the episode
- **Occurs at least weekly x 3 months

2) Recurrent inappropriate COMPENSATORY BEHAVIORS to prevent weight gain

o Purging Type
⦁ self-induced vomiting
⦁ misuse of laxatives, diuretics, enemas, other meds

o Non-Purging Type
⦁	reduced calorie intake
⦁	dieting
⦁	fasting
⦁	excessive exercise
⦁	diet pills / stimulants

3) The binge eating + inappropriate compensatory behaviors both occur, on average, at least 1x per week x 3 months
4) Self evaluation is influenced by body shape and weight
5) the disturbance does not occur exclusively during periods of anorexia nervosa

Usually starts out with them making an unrealistic goal (ex: score 100% on exam) - then goal is not met –> binge eat –> compensatory mechanism to fix / control the binge phase

SIGNS/SYMPTOMS OF BULIMIA NERVOSA
⦁ mouth sores
⦁ pharyngeal trauma
⦁ dental caries / teeth pitting / enamel erosion*
⦁ halitosis
⦁ Russell’s Sign = Calluses on back of knuckles/fingers from sticking hand in mouth to gag
⦁ Heartburn / chest pain
⦁ Transmural esophageal rupture (boerhaave’s) or Mallory Weiss Syndrome from forceful / repetitive vomiting –> hematemesis
⦁ Impulsivity: stealing / alcohol abuse / drugs / tobacco
⦁ Muscle cramps
⦁ weakness
⦁ bloody diarrhea
⦁ bleeding or easy bruising
⦁ irregular periods - menstrual irregularities; may develop amenorrhea
⦁ fainting
⦁ swollen parotid glands** - Bilateral Parotid Sialadenosis - parotid gland hypertrophy
⦁ Hypotension (from dehydration)
⦁ Tachycardia

parotid gland hypertrophy - attempt to increase saliva release in order to buffer acidity from vomiting

-metabolic alkalosis from vomiting

HISTORY
⦁ maximum height + weight
⦁ exercise habits: intensity + hours/week
⦁ stress levels
⦁ habits + behaviors: smoking / alcohol / drugs / sexual activity
⦁ eating attitudes + behaviors
⦁ ROS (review of systems)

PHYSICAL EXAM - BULIMIA
All previous elements +
⦁ Parotid Gland Hypertrophy (if purging type)
⦁ Erosion of teeth enamel (caries) (if purging type)

LABS

  • metabolic alkalosis from vomiting*****
  • may have hypokalemia (from vomiting)
  • may have hypomagnesemia (from vomiting)
  • electrolyte imbalance may lead to cardiac arrhythmias

Low levels of Na, K, Mg, Ca, Phosphate

***Biggest concern = HYPOKALEMIA –> can lead to muscle weakness and cardiac arrhythmias –> death

*****AT RISK FOR DEVELOPING DIABETES - purging / food restriction –> starvation state of the body’s cells. unable to process glucose –> further cell starvation

TREATMENT FOR BULIMIA
o CBT** is effective! (not very effective with anorexia, but IS effective for bulimia)

o Pharmacotherapy = high success rate (unlike anorexia)
⦁ SSRIs** = 1st line tx - Fluoxetine (Prozac) - up to 67% reduction in binge eating, and 56% reduction in vomiting - has been shown to reduce binge-purge cycle, but may have CV SE if electrolyte abnormalities are present
⦁ TCAs
⦁ Topiramate (Topamax) - reduced binge eating by 94% and average weight loss of 6.2 kg (seizure med that is also used to treat migraines, and now bulimia)
⦁ Ondansetron (Zofran) - 24mg/day (often food is associated with vomiting - helps prevent nausea/urge to throw up after - Sublingual available - Dwight prefers this)

**do NOT give Wellbutrin (Bupropion) = (miscellaneous antidepressant) - can lower seizure threshold in bulimics

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5
Q

CONVERSION DISORDER

FUNCTIONAL NEUROLOGICAL SYMPTOM DISORDER

A

Neurological dysfunction that is suggestive of a physical disorder, BUT CANNOT CLINICALLY BE EXPLAINED
- cannot be explained by neurological pathophysiology

  • physical symptoms that suggest neurological problems**
  • sensory impairment: any modality
    ⦁ paresthesias
    ⦁ blindness
    ⦁ paralysis
  • SUDDEN onset
  • SUDDEN termination
  • SUDDEN reappearance

Conversion Disorder

  • 2-10x more common in women
  • age of onset = late childhood to early adulthood (rarely before 10, rarely after 35)
  • onset is acute or sudden; symptoms remit after about 2 weeks, but recur about 25% of the time
  • mostly affects women, but also affects men in combat
  • often misdiagnosed

**Conversion disorder is more common in:
⦁ rural areas
⦁ lower SES
⦁ lower educational levels

“LA BELLE INDIFFERENCE” = a condition in which the person is UNCONCERNED with symptoms caused by a conversion disorder

EXAMPLE OF LA BELLE INDIFFERENCE = A middle-aged woman was referred to the psychiatric emergency room when a rather thorough medical examination could not explain the sudden onset of a complete paralysis below the waist. Additionally, the resident was concerned because her “affect” was rather strange. It seems that, despite what one might normally consider a rather devastatingly traumatic event–the loss of one’s ability to walk or to experience any sensation below the waist–the patient was laughing and joking with the medical resident.

6 CRITERIA FOR CONVERSION DISORDER
1) one or more symptoms or deficits affecting voluntary motor or sensory function that suggests a Neurological or other General Medical Condition

2) Psychological factors are judged to be associated with the symptom or deficit because the initiation or exacerbation of the symptom or deficit is preceded by conflicts or other stressors
3) the symptom or deficit is not intentionally feigned (not factitious or malingering disorder)
4) the symptom or deficit cannot be fully explained by a general medical condition or by the direct effects of a substance
5) the symptom/deficit causes clinically significant distress or impairment in functioning
6) the symptom or deficit is not limited to pain or sexual dysfunction; does not occur exclusively during course of Somatization Disorder, and is not better accounted for by another mental disorder

CONVERSION DISORDER = severe physical dysfunctioning (paralysis, blindness, etc) without corresponding physical pathology

  • affected people are genuinely unaware that they can function normally
  • may coincide with other problems, especially somatization disorder
  • most prevalent in low SES groups, women, and men under extreme stress (soldiers)

Conversion disorder is a condition where a person loses bodily functions due to excess stress, falls under the scope of somatic symptom disorder.

CAUSES = life stresses or psychological conflict –> incapactiating symptoms

Symptoms may be exaggerated and irrational for us, but they are REAL for the patient

  • symptoms cause significant distress or impairment

SYMPTOMS ARE NOT INTENTIONALLY PRODUCED OR FEIGNED
**(NOT due to malingering)**

Patients often have depression, anxiety, schizophrenia or personality disorders

CLINICAL MANIFESTATIONS
- symptoms tend to be episodic and may recur during times of stress

MC in females
Onset = usually in adolescence or young adulthood

o MOTOR DYSFUNCTION
⦁	Paralysis*****
⦁	Aphonia
⦁	Mutism*****
⦁	Seizures
⦁	Gait abnormalities
⦁	Involuntary movements
⦁	Tics
⦁	Weakness
⦁	Swallowing
o SENSORY DYSFUNCTION
⦁	Blindness*****
⦁	Anesthesia
⦁	Paresthesias
⦁	Visual changes
⦁	Deafness

o Patients often have depression, anxiety, schizophrenia or personality disorders**

TREATMENT
⦁ Psychotherapy
- Behavioral therapy = TREATMENT OF CHOICE***

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6
Q

CLUSTER A PERSONALITY DISORDERS

“WEIRD”

A

⦁ PARANOID - “accusatory”
⦁ SCHIZOID - “aloof”
⦁ SCHIZOTYPAL - “awkward”

  • SOCIAL DETACHMENT with unusual behaviors
  • WEIRD, ODD, ECCENTRIC BEHAVIOR
"weird" = cluster A
"wild" = cluster B
"worried" = cluster C

All Cluster A personality disorders are linked to higher rates of Schizophrenia

People with relatives of Schizophrenia are at higher risk for developing a Cluster A personality disorder (suggests a genetic link)

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7
Q

SCHIZOID PERSONALITY DISORDER (cluster A)

A

“ALOOF” = avoid social interaction because they simply aren’t interested in getting to know others

  • Long pattern of VOLUNTARY SOCIAL WITHDRAWAL
  • ANHEDONIC INTROVERSION (constricted affect)

Usually early childhood onset

  • Loner
  • “hermit like behavior” (reclusive)
  • MC in Males

The diagnostic criteria for schizoid personality disorders include four of more of the following:

1) Does not desire or enjoys close relationships
2) Always chooses solitary activities
3) Little interest in sexual experiences
4) Takes pleasure in few, if any, activities
5) Lacks close friends
6) Appears indifferent to praise or criticism
7) Shows flattened affect, detachment, or emotional coldness

CLINICAL MANIFESTATIONS
⦁ Inability to form relationships
⦁ Lifelong pattern of social withdrawal
⦁ Anhedonic = appears indifferent to others; lack response to praise or criticism or feelings expressed by others
⦁ Prefers to be alone
⦁ Little enjoyment in close relationships or sex
⦁ Appears eccentric, isolated, or lonely
⦁ “cold” flattened affect, quiet, usually not sociable

MANAGEMENT
⦁ Psychotherapy = 1st line (individual or group)
⦁ Pharmacologic = antipsychotics** antidepressants or psychostimulants

Group therapy is a type of psychotherapy that is the first line treatment for schizoid personality disorder.

Schizoid - “aloof” - avoid social interaction because they aren’t interested in getting to know others. Results in isolation, like Paranoid, but because they want to be isolated, and not because other people isolate them due to their behavior. Schizoid = find less pleasure in physical contact - like sex or holding hands.
= far less likely to seek out relationships than the average person
- may also have a flat affect or emotional blunting- don’t show positive or negative emotions

Schizoid personality disorder is a personality disorder characterized by a lack of interest in social relationships, a tendency towards a solitary lifestyle, secretiveness, emotional coldness, and apathy. Affected individuals may simultaneously demonstrate a rich, elaborate and exclusively internal fantasy world.

  • hardly ever diagnosed
  • least commonly diagnosed personality disorder*

Schizoid personality disorder is the mildest form of the “schizo” disorders, in terms of how it affects their daily life.
Schizoid

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8
Q

PARANOID PERSONALITY DISORDER (cluster A)

A
  • “ACCUSATORY”
  • MC in males
  • begins in early adulthood
  • PERVASIVE PATTERN OF DISTRUST + SUSPICIOUSNESS OF OTHERS***

CLINICAL MANIFESTATIONS
⦁ Distrust + suspiciousness
⦁ Misinterprets the actions of others as Malevolent
⦁ Sees hidden messages
⦁ easily insulted
⦁ appears cold + serious
⦁ lack of interest in social relationships
⦁ bears grudges
⦁ doesn’t forgive
⦁ blames their problems on others
⦁ preoccupation with doubt regarding the loyalty of others*****

PROJECTION = Projection is the major defense mechanism seen in this PARANOID personality disorder, in which patients take an unacceptable internal impulse, wish, or desire and attributes it to an external source. For example, a man may think about cheating on his wife so he blames his wife for having an affair. Another example would be a boy who talks about his stuffed animal as having certain feelings, which are really what the boy feels. Projection is an immature defense mechanism and paranoia tends to result from the use of projection

  • generally distrustful + suspicious of people
  • Assumes others will disappoint them, manipulate them, and talk about them behind their back…
  • Think excessively about whether or not they have the loyalty of their friends + family; these beliefs are so strong that they end up having a huge impact on the person’s behaviors
  • They then react severely if they feel they have been lied to or slighted in any way
  • Can result in them holding grudges for a long time - Can almost lead to a self-fulfilling prophecy. The strong reactions may lead to others actually talking about them behind their back
  • Tend to have superficial relationships and be in a state of isolation since they’re so suspicious of others

Paranoid personality disorder is a mental disorder characterized by paranoia and a pervasive, long-standing suspiciousness and generalized mistrust of others. Individuals with this personality disorder may be hypersensitive, easily feel slighted, and habitually relate to the world by vigilant scanning of the environment for clues or suggestions that may validate their fears or biases. Paranoid individuals are eager observers. They think they are in danger and look for signs and threats of that danger, potentially not appreciating other evidence.

There is a genetic association between paranoid personality disorder and schizophrenia.

People with paranoid personality disorder are typically difficult to treat because of the lack of trust that defines the disorder.

TREATMENT FOR PPD =
⦁ Psychotherapy - CBT, individual or group therapy = therapy of choice*****
⦁ Pharmacological treatment = low dose of antipsychotics if severe (Haldol) or Benzos (for anxiety / agitation) if necessary, SSRIs

Paranoid Personality Disorder vs Schizophrenia

  • Schizophrenia = more paranoia than PPD, and delusions***
  • NO PSYCHOSIS in paranoid personality disorder
  • Also have the positive symptoms of hallucinations and racing thoughts
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9
Q

SCHIZOTYPAL PERSONALITY DISORDER (cluster A)

A

“AWKWARD”

“awkward” - engage in excessive magical thinking - think that 2 random events are linked - like waking up on left side of the bed means its going to rain, because that happened last time.

  • Ideas of Reference - belief that everything, including innocuous events or coincidences in the world, directly relate to ones own destiny

Speak in overconfidence and self-centered way of speaking that leads to socially inappropriate actions that turn people off

  • Poor at gauging other people’s perception of them;
  • Also have few social relationships, like Schizoid, but unlike schizoid (don’t want to be social), schizotypals want to be social - have a strong desire for relationships, but have a hard time maintaining them

schizotypal want social interaction, but are too “weird”

Patients with schizotypal personality disorder usually want to have interpersonal relationships.

Unlike the other cluster A disorders, patients with schizotypal personality disorder experience perceptual and cognitive dysfunction

Patients with schizotypal personality disorder that have behaviors similar to schizophrenia are often treated with haloperidol, an antipsychotic medication

Patients with schizotypal personality disorder that have behaviors similar to obsessive-compulsive disorder are often treated with SSRIs

TREATMENT

1) Psychotherapy: CBT, individual or group therapy = treatment of choice**
2) Pharm therapy: low dose antipsychotics, antidepressants or benzos

SchizoiD = Distant
SchizoTypal = magical Thinking

These patients often have BIZARRE ATTIRE, SPEECH AND BEHAVIOR. They may wear MISMATCHING CLOTHING and say UNUSUAL / MADE-UP WORDS. They often have IDEAS OF REFERENCE in which they interpret events that are completely unrelated as having specific meaning toward themselves. The treatment of choice, as with all personality disorders, is psychotherapy.

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10
Q

CLUSTER B PERSONALITY DISORDERS

“WILD”

A

⦁ ANTISOCIAL
⦁ BORDERLINE
⦁ HISTRIONIC
⦁ NARCISSISTIC

= Dramatic, WILD, Erratic, Impulsive, Emotional

Genetic relationship to mood disorders such as depression and bipolar disorder

These are the substance abuse disorders

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11
Q

ANTISOCIAL PERSONALITY DISORDER (cluster B)

A

Behaviors **Deviating sharply from the norms, values and laws of society
- Harmful or hostile to society

  • May commit criminal acts with disregard to violation of laws
  • May begin in childhood as conduct disorders, but MUST BE >/= 18 to diagnose
  • 3x MC in Males
  • have a total disregard for moral values and societal norms
  • lack empathy and impulse control
  • will hurt others to get ahead, show aggressive behaviors, or will break the law
  • at times, earn the label sociopath or psychopath
  • are often in prison and are drug users
  • do not show remorse or guilt
  • do not accept responsibility for the harm they have caused others
  • can be superficially charming - often use this to manipulate others for their personal gain

FOR DIAGNOSIS
must be > 18 y/o
must have hx of conduct disorder

CLINICAL MANIFESTATIONS
⦁ Inability to conform to social norms - with disregard and violation of the rights of others
⦁ lack of empathy
⦁ pattern of criminal behavior
⦁ shows little anxiety
⦁ extremely manipulative, deceitful, impulsive, promiscuous, spouse/child abuse, lacks remorse, lies frequently, endangers others (ex: drunk-driving common)

Can be really CHARMING, and often use that to MANIPULATE others for their personal gain

Have a DISREGARD FOR MORAL VALUES + SOCIETAL NORMS

LITTLE EMPATHY and POOR IMPULSE CONTROL, making them more willing to hurt others if it helps them, making them prone to aggressive or unlawful behavior, making them a “sociopath” or “psychopath”

Over-represented in prison populations and have higher rates of substance abuse

Are charming - manipulate others for their personal gain, have no remorse or guilt

Antisocial personality disorder is characterized by disregard for and violation of the rights of others, criminality, and impulsivity.

AGGRESSIVE + UNLAWFUL BEHAVIOR

Don’t accept responsibility for any harm that they cause

Individuals MUST BE OVER 18 and may have a history of conduct disorder in order to meet diagnosis

Antisocial personality disorder is characterized by a pervasive pattern of disregard for, or violation of, the rights of others. An impoverished moral sense or conscience is often apparent, as well as a history of crime, legal problems, and/or impulsive and aggressive behavior

***After age 18, many of conduct disorder patients will meet criteria for diagnosis of antisocial personality disorder.

Patients have to be at least 18 years old to be diagnosed with antisocial personality disorder.

TREATMENT
⦁ Psychotherapy - establishing limits
- Pharmacologic treatment = NOT helpful

A history of preceding conduct disorder before the age of 18 is necessary to diagnose a patient with antisocial personality disorder.

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12
Q

BORDERLINE PERSONALITY DISORDER (cluster B)

A

Unstable, Unpredictable Mood + Affect
Unstable self image
Unstable relationships - will have intense + passionate relationships that quickly turn dramatic and sour over time

MC in Women

CLINICAL MANIFESTATIONS
⦁ Extreme pattern of instability in relationships, but cannot tolerate being alone
⦁ “Mood Swings”
⦁ Marked sensitivity to criticism + rejection (fear of abandonment)
⦁ “Black + White” thinking - think in extremes - all good or all bad, no middle ground
⦁ Impulsivity in self-damaging behaviors = suicide threats, self-mutilation, substance abuse, reckless driving, binge-eating, spending

Unstable moods - intense joy one minute to rage the next minute

Leads to intense relationships that become dramatic

“Stable Instability” because the only consistent thing is instability

TERRIFIED OF ABANDONMENT - will sometimes threaten suicide to prevent someone from leaving

SPLITTING is an ego defense mechanism seen commonly in patients with borderline personality disorder.

Borderline personality disorder is a personality disorder. The essential features include a pattern of impulsivity and unstable behaviors, unstable sense of self, and unstable emotions.. There may be uncontrollable anger and depression. There is often an extreme fear of abandonment, frequent dangerous behavior, a feeling of emptiness, and self-harm. Substance abuse, depression, and eating disorders are commonly associated with Borderline PD.

Patients with borderline personality disorder often have unstable moods and relationships, impulsivity, a sense of emptiness, self-mutilation, and suicidality.

TREATMENT
⦁ Psychotherapy: Dialectical, CBT, group therapy = treatment of choice***
⦁ Pharmacologic tx: short term low doses of antipsychotics, antidepressants or benzos

Dialectical behavior therapy = FIRST LINE** psychotherapy used in the management of patients with borderline personality disorder.

DIALECTICAL BEHAVIORAL THERAPY = targets specific thoughts / behaviors

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13
Q

HISTRIONIC PERSONALITY DISORDER (cluster B)

A

attention seeking + excessive emotions

  • starts by early adulthood

MC seen in women

Someone with histrionic personality disorder is often described as very emotional, attention seeking, and sexually provocative.

  • OVERLY EMOTIONAL, DRAMATIC, SEDUCTIVE
  • ” Attention-seeking”
  • Manipulate others to draw attention - like being overly flirtations and telling over-dramatic stories

CLINICAL MANIFESTATIONS
⦁ Self-absorbed
⦁ “temper tantrums”
⦁ efforts to draw attention to themselves with the need to be the center of attention
⦁ often inappropriate, sexually provocative, seductive with shallow or exaggerated emotions
⦁ seek reassurance + praise often
**may believe their relationships are more intimate than they actually are**
⦁ can be suggestible = easily influenced by others or circumstances

May act inappropriately flirtatious or tell overly dramatic stories to remain center of attention. Result in superficial relationships with lots of people, but few solid friends, because people tend to view them as shallow and egocentric

  • Superficial relationships: lots of acquaintances and few deep relationships
  • viewed as shallow, flighty, and egocentric

Patients with histrionic personality disorder often show a tendency towards instant gratification, and are highly suggestible.

Histrionic personality disorder is characterized by excessive attention-seeking behavior.

TREATMENT
⦁ Psychotherapy - CBT, individual or group therapy = treatment of choice***

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14
Q

NARCISSISTIC PERSONALITY DISORDER (cluster B)

A

Grandiose, often excessive sense of self-importance - but needs praise and admiration

MC in Males

CLINICAL MANIFESTATIONS
⦁ Inflated self-image - considers themselves special, entitled, requires extra special attention, BUT they have a fragile self-esteem
⦁ Occupied with fantasies, jealousy of others, believes others are envious of them, has difficulty with the aging process
⦁ Reacts to rejection / criticism with rage
⦁ Often becomes depressed
⦁ Lacks empathy for others

grandiose self image - think they’re more attractive/intelligent/talented than they are

Believe they are so special, so believe they deserve the best of everything

Think their ideas are the best, and other people should always believe so

Fragile self-esteem, however, that is vulnerable to the slightest criticism but lash out if they feel slighted

Pretentious, self-centered, entitled

Often lack empathy and are oblivious to other’s feelings.

A person who has narcissistic personality disorder can be described as being very competitive, and reacts poorly to criticism.

A patient with narcissistic personality disorder is characterized by grandiose ideation, a sense of entitlement, lack of empathy for others, and requirement for excessive admiration.

Narcissistic personality disorder is a personality disorder in which a person is excessively preoccupied with personal adequacy, power, prestige and vanity, mentally unable to see the destructive damage they are causing to themselves and often others

Narcissistic personality disorder is included in cluster B, and is characterized by lack of empathy for others but excessive requirement for admiration.

TREATMENT
⦁ Psychotherapy - individual or group therapy = treatment of choice***

A patient with a personality change after head trauma or substance abuse cannot be said to have narcissistic personality disorder.

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15
Q

CLUSTER C PERSONALITY DISORDERS

A

“WORRIED”

⦁ AVOIDANT - “cowardly”
⦁ DEPENDENT - “clingy”
⦁ OBSESSIVE-COMPULSIVE PERSONALITY DISORDER - “compulsive”

anxious or fearful

“worried”

  • all have a genetic association with anxiety disorders

Anxiety disorders have a genetic relationship with avoidant, obsessive-compulsive, and dependent personality disorders (cluster C).

The non-medical treatments often used in patients with cluster C personality disorders are social skill training, anxiety management, and group therapy.

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16
Q

AVOIDANT PERSONALITY DISORDER (cluster C)

A
  • Desires relationships but avoids them due to “inferiority complex”
  • Intense feelings of inadequacy, sensitive to criticism, fears rejection / humiliation
  • Timid, shy, lacks confidence

“cowardly” - shy / timid / socially inhibited

  • extremely low self esteem. See themselves as inadequate, incapable, undesirable
  • Want close relationships, but avoid social situations - rarely take social risks => makes it hard for them to meet new people
  • Hypersensitive to negative feedback and rejection –> become even more withdrawn when that happens

don’t date, don’t get out much - afraid of being seen as inadequate, fear of social situations, social phobia** - stay in house and don’t leave

Unlike schizoid personality disorder, patients with avoidant personality disorder (do/do not) do desire relationships with others.

Avoidant personality disorder is characterized by social inhibition, feelings of inadequacy, and hypersensitivity to negative evaluation.

Some overlap with avoidant personality and social phobias, however, social phobias = anxiety in specific situations such as public speaking or dancing in public

While avoidant personality = anxiety in more general situations

A person who avoids social interaction due to fear of being humiliated or rejected likely has avoidant personality disorder.

A child who has grown up with anxiety disorders can develop avoidant personality disorder, withdrawing from social situations in their future.

Avoidant personality disorder is a cluster C personality disorder recognized in the DSM handbook as afflicting persons when they display a pervasive pattern of social inhibition, feelings of inadequacy and inferiority, extreme sensitivity to negative evaluation, and avoidance of social interaction despite a strong desire to be close to others. Individuals afflicted with the disorder tend to describe themselves as uneasy, anxious, lonely, unwanted and isolated from others

MANAGEMENT
⦁ Psychotherapy = social training, CBT or group therapy
⦁ Pharmacotherapy = may try beta blockers for anxiety or SSRIs for depression

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17
Q

DEPENDENT PERSONALITY DISORDER (cluster C)

A
  • Dependent, Submissive behavior
  • “needy + clingy”
  • Constantly needs to be reassured
  • Relies on others to make decisions / emotional support
  • Will not initiate things
  • Intense discomfort when alone
  • May volunteer for unpleasant tasks

“clingy” - intense fear of separation and rejection.

Overly depend or “cling” to relationship.
Lack self-confidence, and can’t adequately care for themselves. Difficult to make simple decisions, and become desperate and hold on to people who can completely take care of them.

Often get trapped in abusive relationships

difficulty making everyday decisions with an excessive amount of advice and reassurance from others, have a hard time being assertive, will do things they don’t want to do to avoid criticism, always in relationships

Dependent personality disorder is a personality disorder that is characterized by a pervasive psychological dependence on other people. This personality disorder is a long-term (chronic) condition in which people depend on others to meet their emotional and physical needs, with only a minority achieving normal levels of independence.

Patients with dependent personality disorder are characterized as submissive and clingy with low self-confidence, and often get stuck in abusive relationships.

MANAGEMENT
⦁ Psychotherapy - behavioral + group therapy
⦁ Pharmacotherapy - may try anxiolytics or antidepressants may be used in some cases for symptomatic control

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18
Q

OBSESSIVE-COMPULSIVE PERSONALITY DISORDER (cluster C)

A

PERFECTIONISTS who require a great deal of Order + Control

  • rigid adherence to routine = rules, lists, details
  • inflexible, stubborn, lacks spontaneity
  • any change in their routine may lead to extreme anxiety
  • often makes moral judgment on others

This condition is more common in first born males (i.e., oldest brother), who had a harsh discipline upbringing (i.e., his father working in the army).

  • Preoccupied with minute details - may find it difficult to finish projects, hesitates to delegate work to others, devotes themselves to their work
  • May avoid intimacy

“compulsive” - obsessed with orderliness, perfectionism, having complete control: rules / details / schedules

  • Often inflexible and are easily stressed
  • Often inefficient because they spend so much time planning and worrying that they don’t get the task itself done.
  • Very rigid moral beliefs and values.
  • Stubborn

Overlap in symptoms with OCD (actions & thoughts).

OCD = anxiety disorder that revolves around repetition of ritualistic actions (checking door over and over again to make sure that it is locked)

Defense mechanism of UNDOING = This mechanism consists of performing the reverse of unacceptable behavior in an attempt to counteract it, such as repeated hand washing after shaking people’s hands or opening doors

Key difference = with OCD = person is Ego-Dystonic - meaning they wish they could stop, don’t like this about themselves. are aware that they have a problem.
With OCPD = Ego-Syntonic - happy with how they are and don’t want to change their behavior. Don’t think they have a problem.

Unlike in obsessive-compulsive disorder, the behavior of a person with obsessive-compulsive personality disorder IS consistent with their beliefs and attitudes.

Behaviors of people with obsessive-compulsive personality disorder are ego-SYNTONIC, in that the behaviors to deal with their obsessions are known and wanted by the person.

Obsessive-compulsive personality disorder (OCPD), also called anankastic personality disorder, is a personality disorder characterized by a general pattern of concern with orderliness, perfectionism, excessive attention to details, mental and interpersonal control, and a need for control over one’s environment, at the expense of flexibility, openness, and efficiency. Workaholism and miserliness are also seen often in those with this personality disorder. In contrast to OCD, the symptoms seen in OCPD, though they are repetitive, are not linked with repulsive thoughts, images, or urges. OCPD characteristics and behaviors are known as ego-syntonic, as persons with the disorder view them as suitable and correct.

MANAGEMENT
⦁ Psychotherapy
⦁ Pharmacotherapy = may try beta blockers for anxiety or SSRIs for depression

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19
Q

OBSESSIVE COMPULSIVE DISORDER (OCD)

A

Obsessive–compulsive disorder (OCD) is a mental disorder where people feel the need to check things repeatedly, perform certain routines repeatedly (called “rituals”), or have certain thoughts repeatedly.

  • average onset = 19 y/o
  • equally common in men + women
  • Perfectionists who require a great deal of ORDER + CONTROL - rigid adherence to routine (rules, lists, details, inflexible, stubborn, lacks spontaneity
  • Any change in their routine may lead to extreme anxiety; often makes moral judgement on others
  • Preoccupied with minute details - may find it difficult to finish projects, hesitates to delegate work to others, devotes themselves to work
  • May avoid intimacy

People are unable to control either the thoughts or the activities. Common activities include hand washing, counting of things, and checking to see if a door is locked. Some may have difficulty throwing things out. These activities occur to such a degree that the person’s daily life is negatively affected. Often they take up more than an hour a day.

To diagnose obsessive-compulsive disorder, both obsessions and compulsions DO NOT have to be present.

Most adults realize that the behaviors do not make sense. The condition is associated with tics, anxiety disorder, and an increased risk of suicide.

In order to diagnose an individual with obsessive-compulsive disorder, the repetitive activities done in response to obsessions must be time-consuming.

Tourette syndrome is the most common comorbid psychiatric condition associated with OCD

Ego-dystonic behavior is seen in patients with obsessive-compulsive disorder.

Obsessive-compulsive disorder is characterized by recurring and intrusive thoughts, feelings, or sensations that cause distress and are partly relieved by performing certain repetitive actions.

Exposure and response prevention is a type of cognitive behavioral therapy that is first-line psychotherapy for patients with obsessive-compulsive disorder

  • Characterized by intrusive thoughts that produce uneasiness, apprehension, fear or worry (obsessions), repetitive behaviors aimed at reducing the associated anxiety (compulsions), or a combination of such obsessions and compulsions

o OBSESSIONS
- recurrent + persistent thoughts, impulses, or images that cause distressing emotions, such as anxiety or disgust

o COMPULSIONS
- repetitive behaviors or mental acts that the person feels driven to perform in response to an obsession
⦁	cleaning
⦁	repeating
⦁	checking
⦁	ordering + arranging

TREATMENT
o Psychotherapy
⦁ 1st line = CBT - exposure + response prevention

o Medication
⦁ 1st line = SSRI (FLUVOXAMINE - LUVOX, fluoxetine, sertraline, paroxetine)
⦁ TCA = 2nd line (clomipramine - anafranil)
⦁ SNRI = 3rd line (venlafaxine)

First line treatment of choice is an SSRI such as fluvoxamine or fluoxetine.

SSRIs are used in conjunction with cognitive behavioral therapy as first-line treatment for the management of obsessive-compulsive disorder.

CLOMIPRAMINE (Anafranil) is the first-line TCA used for the management of obsessive-compulsive disorder.

  • can use beta blockers for anxiety or SSRIs for depression
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20
Q

CYCLOTHYMIC DISORDER

A

Cyclothymia = milder form of bipolar II = have milder episodes of hypomania, and also have milder forms of depression - frequently switch between the two

a milder form of bipolar disorder where for AT LEAST 2 YEARS there are fluctuating periods of mild hypomanic and depressive symptoms.

Duration = AT LEAST 2 YEARS

  • Does not meet DSM criteria for major depression, but still have hypomania (mild)
  • Is considered to be one of the bipolar disorders, and is treated with same kinds of meds
  • Defined by the presence of numerous periods of hypomania and depression, **Persisting for AT LEAST 2 YEARS

⦁ this is different from bipolar I and bipolar II - where there is a predominance of depressive symptoms

so in Cyclothymia = normal to hypomanic to normal to depressed (not high enough to be classified as manic, not low enough to be classified as major depression)

Similar to bipolar disorder II, but LESS SEVERE

Prolonged period of MILDER ELEVATIONS AND DEPRESSIONS IN MOOD

about 15% may eventually develop bipolar disorder

CLINICAL MANIFESTATIONS
- recurrent episodes of HYPOMANIC symptoms that don’t meet criteria for “hypomania” that cycles with RELATIVELY MILD DEPRESSIVE EPISODES for AT LEAST A 2 YEAR PERIOD in adults, and 1 YEAR in children

  • these patients may have symptom free periods, however, those symptom-free periods don’t last longer than 2 months at any time

***manic or mixed episodes DO NOT OCCUR

TREATMENT
- similar to bipolar I = mood stabilizers and neuroleptics

MOOD STABILIZERS
⦁ Lithium
⦁ Anti-convulsants - Valproic Acid, Carbamazepine

NEUROLEPTICS = anti-psychotics

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21
Q

TRICHOTILLOMANIA

A

Trichotillomania, also known as trichotillosis or hair pulling disorder, is an obsessive compulsive disorder characterized by the compulsive urge to pull out one’s hair, leading to hair loss and balding, distress, and social or functional impairment.

Trichotillomania patients often eat their own hair, and may thus present with trichobezoars (hairballs) in their intestines.

The body area most affected by trichotillomania is the scalp, but hair loss is significant over all other areas of the body as well.

Habit reversal therapy is a type of psychotherapy that trains people to identify and react to the impulses that lead to their repetitive behaviors.

Women suffer more from trichotillomania, an impulse control disorder that may be difficult to treat.

OTHER REPETITIVE BEHAVIORS
Dermatophagia, which involve picking or biting the inside of the mouth, the cheeks, and the lips, often appears alongside onychophagia, and onychotillomania.

People with excoriation disorder feels an irresistible urge to pick at their skin which can lead to skin lesions, infection, and scarring

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22
Q

OPPOSITIONAL DEFIANT DISORDER

A

WILLFUL DEFIANCE
- present > 6 months

  • Persistent pattern of negative, hostile, + DEFIANT BEHAVIOR TOWARDS ADULTS

ODD = defiant behavior that is both persistent and willful

At least 6 months of the following 3 components

1) angry / irritable mood (often blames others for their misbehaviors, has negative attitudes, has anger / resentment) = emotional
2) argumentative / defiant behavior = behavioral
3) vindictiveness = cognitive

No association with psychosis

***May progress to conduct disorder (which can then progress to antisocial personality disorder)

ODD –> conduct disorder –> antisocial personality

Emotional / Behavioral / Cognitive disruption must persist >/= 6 months, and must disrupt social interactions (family / school / etc)

⦁ emotional dysregulation –> irritable and resentful towards others
⦁ behavioral dysregulation –> frequent arguments, angry outbursts, and dislikes authority (teachers)
⦁ cognitive dysregulation –> vindictive and spiteful - believe that others are to blame for their own behavior

  • may deliberatively annoy their family or friends
  • purposely defy anyone that tries to control their behavior

Oppositional defiant disorder is characterized by a pattern of angry/irritable mood, argumentative/defiant behavior or vindictiveness lasting at least 6 months. Cannot be due to substance abuse or a psychotic disorder

Presentation includes recurrent loss of temper, arguing, refusing to comply with rules, deliberately annoying others, blaming others for behavior, and resentfulness

ODD is often co-morbid with ADHD, and can sometimes lead to the development of conduct disorder. ADHD must first be ruled out in children with ODD, and treatment consists of therapy for the patient and parent management training

MANAGEMENT
⦁ Psychotherapy - behavioral therapy

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23
Q

CONDUCT DISORDER

A

WILLFUL AGGRESSION
- present > 12 months

Behaviors used to classify conduct disorder would fall into the 4 main categories of

(1) aggression toward people and animals
(2) destruction of property without aggression toward people or animals
(3) deceitfulness, lying, and theft
(4) serious violations of rules

Conduct disorder has a lot of overlap with ODD, but also has one key feature = aggressive behavior towards people and animals

  • Such people may
    ⦁ violently destroy property
    ⦁ steal things
    ⦁ hurt pets
  • considered antisocial behaviors because they completely break the boundaries of social norms
  • 2 types
    ⦁ childhood onset: < 10 y/o
    ⦁ adolescent onset = 10-18
  • the earlier the onset of symptoms = the more severe the behavioral problems

NOT all patients with ODD will go on to develop conduct disorder, and not all patients with conduct disorder will go on to develop antisocial personality disorder

Individuals with a conduct disorder have numerous antisocial activities such as lying, stealing, running away, physical violence, sexually coercive behaviors, and destruction of property. Children and adolescence with conduct disorder will have defiant behavior toward everyone. In oppositional defiant disorder the poor behavior is directed toward authority figures.

Conduct disorder is characterized by physical aggression and kleptomania in a child. These behaviors are often referred to as “antisocial behaviors.” It is often seen as the precursor to antisocial personality disorder, which is not diagnosed until the individual is 18 years old

A 16 year old boy who started behaving very aggressively towards his parents after suffering head trauma CANNOT be said to have conduct disorder.

Patients have to be YOUNGER than the age of 18 for a diagnosis of conduct disorder to be made.

Conduct disorder < 18 > antisocial personality disorder

Patients under the age of 18 years with conduct disorder exhibit repetitive and pervasive behavior violating the basic rights of others or societal norms.

Conduct disorder is a psychological disorder diagnosed in childhood or adolescence that presents itself through a repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate norms are violated. These behaviors are often referred to as “antisocial behaviors.” It is often seen as the precursor to antisocial personality disorder, which is not diagnosed until the individual is 18 years old

Physical aggression and Kleptomania are characteristic of conduct disorder. Have little regard for others’ bodies or property. Any other diagnosis would require additional symptoms and would be in addition to a diagnosis of conduct disorder.

MANAGEMENT
⦁ Cognitive behavioral therapy is the first line psychotherapy used in managing conduct disorder.

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24
Q

TOURETTE’S SYNDROME

A

ONSET

  • usually in childhood (2-5 y/o)
  • MC in boys

*** Associated with OCD + ADHD

CLINICAL MANIFESTATIONS = TICS

TIC = quick, non-rhythmic movements or vocalizations that happen over and over again. Are not caused by another disorder such as Huntington’s or substance abuse

1) MOTOR TICS*** of the face, head and neck
⦁ blinking
⦁ shrugging
⦁ head thrusting
⦁ sniffling
⦁ obscene gestures (copropraxia)
⦁ repeating motions of others (echopraxia)

2) VERBAL or PHONETIC TICS***
⦁    grunts
⦁    throat clearing
⦁    obscene words (coprolalia)
⦁    repetitive phrases
⦁    repeating the words/phrases of others (echolalia)

3) SELF-MUTILATING TICS
⦁ hair pulling
⦁ nail biting
⦁ lip biting

  • Abnormal because they occur in inappropriate situations
  • May engage in repetitive behaviors such as clapping, grimacing or grunting, or even hidden behaviors such as moving the tongue

⦁ Simple Tics = usually shorter (milliseconds) such as blinking / clearing throat
⦁ Complex Tics = a bit longer (seconds / minute) and are a combination of tics such as shaking head + shrugging shoulders

DIAGNOSIS
- Need a Tic + additional criteria
⦁    A) number of tics
⦁    B) duration of tics
⦁    C) age on onset
  • For diagnosis of Tourette’s
    ⦁ A) need 2+ motor tics AND 1+ vocal tic (don’t have to happen at same time)
    ⦁ B) tics must persist for 1+ year
    ⦁ C) onset must be before 18

If < 1 year = diagnosed with Provisional Tic Disorder

TREATMENT
⦁ Habit reversal therapy / CBT = 1st line tx
- 50% have symptom resolution by 18 y/o

  • Medications = usually only if severe
    ⦁ dopamine blocking agents (antipsychotics) = haloperidol, risperidone, fluphenazine, pimozide
    Pimozide = only FDA approved drug for Tourette’s

⦁ alpha-adrenergics = clonidine, guanfacine (usually if in addition to ADHD) or strattera
In a patient with Tourette syndrome, it is important to avoid CNS stimulants that can further increase dopaminergic signaling

⦁ benzos = clonazepam (klonopin)
⦁ can also use botox

Tics tend to lessen when person is calm, so treating anxiety / depression can also help

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25
Q

PYROMANIA

A
  • people who purposefully and repeatedly start fires
  • unlike arsonists = are not motivated by destruction of property or political power
  • simply driven by compulsion - feel a strong impulse to set fires
  • often gives them relief and happiness when they set fires
  • fixated by anything with fire = hang around fire stations, watch videos of fires, want to be firefighter
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26
Q

KLEPTOMANIA

A
  • strong impulse to steal things
  • don’t steal out of need, but theft is for pleasure and for relief of tension they get once they steal something
  • often steal items that are of little value to them, or items that they could easily afford
  • often associated with conduct disorder
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27
Q

GENERALIZED ANXIETY DISORDER

A

GAD = EXCESSIVE ANXIETY OR WORRY FOR
6+ MONTHS ABOUT VARIOUS ASPECTS OF LIFE

Excessive, persistent, and unreasonable anxiety about everyday things

Can range from mild (able to function socially and hold down a job) to severe (completely debilitated)
- feelings of anxiety may worsen or improve over time

GAD is not episodic (like panic disorder)
GAD is not situational (like phobias)
GAD is not focal

Associated with >/= 3 of the following symptoms
⦁  fatigue
⦁  restlessness
⦁  difficulty concentrating
⦁  muscle tension
⦁  sleep disturbance** (common - can have significant impact on physical well-being)
⦁  irritability
⦁  shakiness
⦁  headaches

= NOT due to medical illness

GAD = more common in FEMALES
onset of symptoms = usually in early 20’s

SIGNS/SYMPTOMS
⦁	can't relax
⦁	startle easily
⦁	have difficulty concentrating
⦁	trembling
⦁	irritability
⦁	sweating
  • may have stomach pain from eating too much or not eating enough (due to anxiety)

Generalized anxiety disorder (GAD) involves persistent and excessive worry pertaining to multiple events or domains that continues for > 6 months

Anxiety is not related to a specific focus, but rather is generalized to most issues

GAD is the most common psychiatric illness seen by primary care providers.**

DSM-5 DIAGNOSTIC CRITERIA FOR GAD
o Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 months, about a number of events or activities (such as work or school performance).

o The individual finds it difficult to control the worry.

o The anxiety and worry are associated with three (or more) of the following six symptoms (with at least some symptoms having been present for more days than not for the past 6 months): Note: Only one item is required in children.

  • present for 90+ days out of 180 days
  • adults = 3+ symptoms
  • children = 1+ symptom

⦁ Restlessness or feeling keyed up or on edge.
⦁ Being easily fatigued.
⦁ Difficulty concentrating or mind going blank.
⦁ Irritability.
⦁ Muscle tension
⦁ Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep).

The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of

The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism).

EVERYDAY ANXIETY VS ANXIETY DISORDER
- Everyday Anxiety
⦁ worry about paying bills, landing a job, a romantic breakup, other important life events
⦁ embarrassment or self-consciousness in an uncomfortable or awkward social situation
⦁ nerves/sweating before a big test, business presentation, stage performance, etc.
⦁ realistic fear of a dangerous object, place or situation
⦁ anxiety, sadness or difficulty sleeping immediately after a traumatic event

  • Anxiety Disorder
    ⦁ constant worry that causes significant distress + interferes with daily life
    ⦁ avoiding social situations for fear of being judged / embarrassed / humiliated
    ⦁ out of the blue panic attacks, preoccupation with the fear of having another panic attack
    ⦁ irrational fear or avoidance of an object / place / situation that poses little or not threat of danger
    ⦁ recurring nightmares / flashbacks / emotional numbing related to a traumatic event that occurred several months or years before

Anxiety is not related to a specific person, situation, or event in generalized anxiety disorder.

At least 80% of patients with GAD have had at least one other anxiety disorder in their lifetime.

Patients with GAD are at increased risk of developing other conditions such as depression and bipolar disorder.

CAUSE = uncertain, but thought to be a combination of genetic + environmental factors

GABA and serotonin levels are DECREASED in patients with generalized anxiety disorder.
⦁ MOST IMPORTANT = decreased GABA levels*****
do have decreased serotonin as well

Norepinephrine levels are INCREASED in patients with generalized anxiety disorder

GAD-7 scale = out of 21 points = 0 / 1 / 2 / 3 on 7 questions regarding feelings of anxiety in past 2 weeks

TREATMENT FOR GAD
- 1st line = Combo or Monotherapy of
⦁ Psychotherapy (CBT) - alone or with SSRI
⦁ SSRI: Paroxetine (Paxil), Sertraline (Zoloft), Escitalopram (Lexapro)

*****SSRI of choice = Paxil; sertraline is more activating - has more stimulation, which is not good for GAD…unless patient also has significant depression

⦁ SNRI = alternative to 1st line - Effexor (venlafaxine) or Duloxetine (Cymbalta)

SNRI of choice = Effexor

  • 2nd line =
    ⦁ Buspirone (Buspar) - can be used solo or with SSRI
    = stimulates serotonin receptors, and blocks dopamine receptors. May take several weeks to see clinical improvement
  • ** Buspirone does NOT cause sedation**
  • SE = nausea, RLS, EPS, dizziness

⦁ Benzo’s (low dose)

- short half life = alprazolam (Xanax) (11.2 hrs) or lorazepam (Ativan) (12 hrs)
- longer half life = diazepam (valium) (45-100 hrs) or flurazepam (dalmane) (74-90hrs)

Benzos = short term use only) - used in interim until SSRI takes effect or for acute exacerbations / anxiety attacks / panic attacks (not used long-term due to abuse potential)

⦁ TCAs
⦁ Beta-Blockers
⦁ Pregabalin (Lyrica)

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28
Q

SELECTIVE MUTISM

A

Selective mutism (SM), formerly called elective mutism, is best understood as a childhood anxiety disorder characterized by a child or adolescent’s inability to speak in one or more social settings (e.g., at school, in public places, with adults) despite being able to speak comfortably in other settings (e.g., at home with family).

Affected individuals understand language use and, although they have the physical and cognitive ability to speak, they demonstrate a persistent inability to speak in particular settings over a particular period of time due to anxiety

Selective mutism is a disorder in which an individual is not able to speak aloud in specific situations when there is an expectation of conversational speech.

Communicative language is generally intact in such individuals, although selective mutism can coexist with language and communication disorders.

Selective mutism can be accompanied by other anxiety disorders such as separation anxiety disorder, social anxiety disorder (formerly called social phobia), agoraphobia, and panic disorder, as well as by shyness and anxiety; however, it can also exist without other anxiety-related disorders.

Selective mutism is an anxiety disorder in which a person who is normally capable of speech does not speak in specific situations or to specific people.

Selective mutism usually co-exists with shyness or social anxiety.

People with selective mutism stay silent even when the consequences of their silence include shame, social ostracism or even punishment.

Most patients with selective mutism suffer from social anxiety and do not speak even when significant social or occupational dysfunction occurs as a result.

Selective mutism is an anxiety disorder in which a person who is normally capable of speech does not speak in specific situations or to specific people

TREATMENT

⦁ Fluoxetine / Prozac (SSRI) is the pharmacologic treatment that has shown efficacy to treat this type of anxiety disorder.

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29
Q

MALINGERING

A

INTENTIONAL FALSIFICATION OR EXAGGERATION OF SIGNS / SYMPTOMS OF MEDICAL OR PSYCHIATRIC ILLNESS

NOT a mental illness

The primary motivation of their actions is SECONDARY GAIN (financial gain - insurance money / lawsuits), food, shelter, avoidance of prison / school / work / military services / to obtain drugs (narcotics)

Both factitious disorder (munchausen’s) and malingering are associated with intentionally faking signs and symptoms. Difference = in malingering, they feign illness for secondary gain, whereas in factitious disorder, the primary motive is to “assume the sick role” and get sympathy

Malingering is fabricating or exaggerating the symptoms of mental or physical disorders for a variety of “secondary gain” motives, which may include financial compensation (often tied to fraud); avoiding school, work or military service; obtaining drugs; getting lighter criminal sentences; or simply to attract attention or sympathy.

Failure to detect actual cases of malingering imposes a substantial economic burden on the health care system

False attribution of malingering imposes a substantial burden of suffering on a significant proportion of the patient population.

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30
Q

DYSTHYMIA

PERSISTENT DEPRESSIVE DISORDER

A

Dysthymia is a more chronic and milder form of depression that lasts at least two years.

Dysthymia, also called persistent depressive disorder, is a mood disorder consisting of the same cognitive and physical problems as in depression, but persisting for at least two years. Dysthymia is less acute and severe than major depressive disorder.

CHRONIC DEPRESSED MOOD > 2 YEARS IN ADULTS (> 1 year in children / adolescents)
*usually milder than major depression, but can include symptoms of chronic major depression

  • no symptoms of hypomania, mania or psychotic features
  • patients are usually able to function**
  • may experience mild decreased productivity

MC IN WOMEN
- onset = begins MC in late teens / early adulthood

May progress over time to develop into MDD or bipolar disorder

CLINICAL MANIFESTATIONS
⦁ Generalized loss of interest, social withdrawal, PESSIMISM, decreased productivity

⦁ Chronic depressed mood > 2 years in adults (> 1 year in children / adolescents) for most of the day, more days than not. In that 2 year period, the patient is not symptom free for > 2 months at a time
- may say things like “I’ve always been this way”

At least 2 of the following conditions must be present:

1) Insomnia / hypersomnia
2) fatigue
3) low self-esteem
4) decreased appetite / overeating
5) hopelessness
6) poor concentration
7) indecisiveness

TREATMENT
⦁ SSRIs = 1st line tx
- similar to depression - psychotherapy = principal tx
⦁ SNRIs, Bupropion, TCAs, and in some cases, MAOIs = 2nd line tx

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31
Q

BODY DYSMORPHIC DISORDER

A

Type of Obsessive-Compulsive Disorder

  • Excessive PREOCCUPATION THAT >/= 1 BODY PART IS DEFORMED, OR AN OVEREXAGGERATION OF A MINOR FLAW

Body dysmorphic disorder is a type of obsessive-compulsive disorder characterized by preoccupation with a minor or imagined defect in appearance, leading to significant emotional distress.

Someone experiencing body dysmorphic disorder ruminates over the perceived bodily defect for multiple hours everyday.

  • this often causes a person to be ashamed or to feel self-conscious - causes functional impairment

Body dysmorphic disorder presents as a compulsion to normalize appearance of an otherwise unnoticeable flaw.

The perceived bodily defect in body dysmorphic disorder is typically on the nose, thighs, stomach, or skin.

o used to be a somatoform disorder in DSM III, but now categorized within Obsessive Compulsive spectrum

  • Excessive concern with real or imagined defects in appearance, especially facial marks or features
  • Person may commit repetitive acts in response to this preoccupation of physical flaw / defect
    ⦁ mirror checking / mirror fixation or mirror avoidance
    ⦁ skin picking
    ⦁ seeking reassurance
  • or mental acts
    ⦁ comparison to others

Suicidal ideation and suicidal behavior are common

  • frequent visits to plastic surgeons
  • culturally influenced, but not culture bound
  • may be a symptom of a more pervasive disorder (Obsessive-compulsive or delusional disorder)

CHARACTERISTICS OF BODY DYSMORPHIC DISORDER
⦁ Preoccupation with an imagined defect in appearance. If a slight physical anomaly is present, the person’s concern is markedly excessive.
⦁ The preoccupation causes clinically significant distress or impairment in functioning
⦁ The preoccupation is not better accounted for by another mental disorder

ASSOCIATIONS
⦁	 Excessive checking/grooming
⦁	 removal of mirrors
⦁	 social isolation
⦁	 surgical procedures
⦁	 suicide
  • likely greatly underdiagnosed

MC IN FEMALES

  • often begins in teenage years
  • patients may also have anxiety disorder or depression

Body dysmorphic disorder is often associated with social anxiety disorder in an individual who avoids the public in an attempt to hide flaws.

Body dysmorphic disorder can be mistaken for major depressive disorder or social phobia.

Body dysmorphic disorder is a mental disorder characterized by an obsessive preoccupation that some aspect of one’s own appearance is severely flawed and warrants exceptional measures to hide or fix it.
⦁ In BDD’s delusional variant, the flaw is imagined
⦁ If the flaw is actual, its importance is severely exaggerated
- Either way, one’s thoughts about it are pervasive and intrusive, occupying up to several hours a day. The DSM-5 categorizes BDD in the obsessive–compulsive spectrum, and distinguishes it from anorexia nervosa.

TREATMENT
⦁ Antidepressants = SSRIs (Prozac), TCAs (Clomipramine) - like 2nd line OCD tx
⦁ Psychotherapy

CBT = 1st line psychotherapy used for patients with body dysmorphic disorder.

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32
Q

EXCORIATION DISORDER

A

Excoriation disorder is repetitive picking, scratching, rubbing, digging, or squeezing of skin, resulting in visible damage and impairment in social functioning.

Excoriation disorder (skin picking disorder) is defined in the DSM-V as repetitive picking, scratching, rubbing, digging, or squeezing of skin, resulting in visible damage and impairment in social functioning. It is grouped with trichotillomania and body dysmorphic disorder.

Patients with excoriation disorder have polymorphic lesions of varying size and severity due to their own scratching by fingers, teeth, or sharp instruments.

Acute lesions may have a serosanguinous crust, and older, scarred and pigmented lesions are also present.

The excoriations can be made until they are deep below the skin and are at risk of infections and ulcerations. They are scattered symmetrically within reach of the hands, especially on the face. Patients may scratch normal skin or already existing minor skin lesions, such as this patient with her IV site, or insect bites, acne, or a mole. Psychiatric referral is strongly encouraged due to the high rate of comorbidities.

Excoriation disorder (also known as dermatillomania, skin-picking disorder, neurotic excoriation, acne excoriee, pathologic skin picking (PSP), compulsive skin picking (CSP) or psychogenic excoriation) is a mental disorder characterized by the repeated urge to pick at one’s own skin, often to the extent that damage is caused.

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33
Q

OBSESSIVE COMPULSIVE RELATED DISORDERS

A
⦁  OCD
⦁  Body Dysmorphic Disorder
⦁  Trichotillomania
⦁  Hoarding Disorder
⦁  Excoriation Disorder
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34
Q

SOMATOFORM DISORDERS

A

⦁ SOMATIC SYMPTOM DISORDER
⦁ Illness Anxiety Disorder (Hypochondriasis)
⦁ Conversion Disorder (Functional Neurological Symptom Disorder)
⦁ Factitious Disorder
⦁ Malingering

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35
Q

FACTITIOUS DISORDER

MUNCHAUSENS

A

INTENTIONAL FALSIFICATION OR EXAGGERATION OF SIGNS + SYMPTOMS OF MEDICAL / PSYCHIATRIC ILLNESS FOR PRIMARY GAIN = motivation = assuming the sick role to get sympathy

Patients with factitious disorder have an inner need to be seen as ill or injured, but NOT for concrete personal gain, like with malingering, but to get attention and sympathy

Factitious disorder imposed on self = presents themselves as injured, impaired or ill

Factitious disorder imposed on another (by proxy) = present another as injured, impaired or ill - such as child, elder or mentally disabled family member
= considered a form of premeditated child or elder abuse

consciously cause symptoms to be evident in another person.
- They know what they are doing, but not why they are doing it.

CLINICAL MANIFESTATIONS
⦁ Creation or exaggeration of symptoms of illness
ex: may hurt themselves to create symptoms, alter diagnostic tests, lie or mimic symptoms. May inject substances to make them sick
- Medical hx = usually dramatic + inconsistent

⦁ May be willing or eager*** to undergo surgery repeatedly, or undergo painful tests in order to obtain sympathy

  • “hospital jump” - have multiple prior hospital visits
  • use aliases
  • go to different cities to access care
  • often have extensive knowledge about medical terminology, hospitals, or great detail about their “illness”
  • May even work in healthcare

TREATMENT
⦁ nonspecific treatment
- no known treatment, but family therapy is helpful

  • for Induced Factitious = separate the person being harmed, treat them for induced illness/injury and emotional trauma

Although there is no formal treatment for Munchausen syndrome, family therapy often helps all parties involved understand the illness.

Although there is no known treatment for Munchausen syndrome by proxy, separation of the two individuals involved is a start to therapy.

36
Q

SOMATIC SYMPTOM DISORDER

Somatization Disorder) or (Somatoform Disorder

A

Type of Somatoform Disorder

  • Chronic condition in which the patient has PHYSICAL SYMPTOMS INVOLVING >/= 1 PART OF THE BODY, BUT NO PHYSICAL CAUSE CAN BE FOUND

MC in Women
Onset = usually before 30y/o

Many patients previously diagnosed with hypochondriasis are now classified as having somatic symptom disorder

  • Having PHYSICAL SYMPTOMS that are not explained by any physical or mental disorder
  • symptoms are NOT FAKED
  • symptoms are real, and are often made worse by the fact that they cannot be scientifically explained

DIAGNOSIS
⦁ must experience 1+ somatic (physical) symptoms that are distressing / result in significant disruption of daily life for > 6 months
⦁ These symptoms cannot be explained by a physical or medical cause
⦁ 2+ symptoms = high likelihood of somatization disorder

SYMPTOMS
- Incredibly varied
- Mnemonic = Symptoms Described as Body Laments + Ailments Void a Physical cause
⦁ SOB
⦁ Dysmenorrhea
⦁ Burning in sexual organ
⦁ Lump in throat (dysphagia)
⦁ Amnesia
⦁ Vomiting
⦁ Painful extremities

The location, kind, and severity of symptoms changes over time, however, the one symptom that is pretty persistent is PAIN = hard to treat, as there is no particular underlying cause

somatic symptoms may not be continuously present, but the symptoms are persistent: usually > 6 months

SPECIFIERS: WITH PREDOMINANT PAIN***** - the one symptom that does tend to persist over time

COGNITIVE SYMPTOMS
⦁ Excessive thoughts, feelings or behaviors related to the somatic symptoms
⦁ disproportionate + persistent thoughts about the seriousness of symptoms
⦁ persistently high level of anxiety / worry about symptoms or health
⦁ excessive time + energy devoted to the symptoms and health concerns
⦁ catastrophic thoughts about death

Often it is the cognitive symptoms in response to the physical symptoms (more than the physical symptoms themselves) that are the basis for the diagnosis (and why it is often mistaken for hypochondriasis)

Physicians rate the severity of Somatic Symptom Disorder based on the cognitive symptoms, and not the physical symptoms
⦁ mild = 1 cognitive thought (ex: ruminating)
⦁ mod = 2+ cognitive thoughts ( ruminating + anxiety)
⦁ severe = 2+ cognitive thoughts + multiple physical symptoms or 1 severe physical symptom (severe pain)

CAUSE
- used to be thought that people were developing these symptoms due to high levels of stress / anxiety

  • now thought that people with SSD are hypersensitive to bodily symptoms, so common experiences, such as indigestion, may be amplified in these individuals

In order to diagnose a person with somatic symptom disorder, the patient must have unexplained symptoms and appear excessively worried about their symptoms.

A person with somatic symptom disorder is not deliberately appearing with unexplained symptoms repeatedly, unlike in factitious disorders.

TREATMENT
⦁ regularly scheduled visits to healthcare provider: as patients are usually reticent to seek mental health counseling
⦁ Treatment is aimed at reducing cognitive symptoms = CBT - 1st line tx

A physician can help a patient with somatic symptom disorder by scheduling regular office visits with them.

37
Q

ILLNESS ANXIETY DISORDER (HYPOCHONDRIASIS)

A
  • PREOCCUPATION WITH THE FEAR OR BELIEF ONE HAS OR WILL CONTRACT A SERIOUS, UNDIAGNOSED DISEAS
  • despite reassurance + medical workups showing no disease

Symptoms last 6+ months

SOMATIC SYMPTOMS USUALLY NOT PRESENT***

  • if they are present = they are mild in intensity
  • usually not severe pain (common with somatic disorder) but rather a typical body occurrence that the person escalates into being a disease

Age 20-30

  • Frequently get tested
  • “doctor shop”

KEY POINTS
⦁ Patients are worried about having or developing a serious illness
⦁ This preoccupation is present for at least 6 months
⦁ Is not better explained by another mental disorder (e.g., obsessive-compulsive disorder and somatic symptom disorder)

DSM-5 CRITERIA
⦁ Preoccupation with having or acquiring a serious illness.

⦁ Somatic symptoms are not present or, if present, are only mild in intensity. If another medical condition is present or there is a high risk for developing a medical condition (e.g., strong family history is present), the preoccupation is clearly excessive or disproportionate.

⦁ There is a high level of anxiety about health, and the individual is easily alarmed about personal health status.

⦁ The individual performs excessive health-related behaviors (e.g., repeatedly checks his or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doctor appointments and hospitals).

⦁ Illness preoccupation has been present for at least 6 months, but the specific illness that is feared may change over that period of time.

⦁ The illness-related preoccupation is not better explained by another mental disorder, such as somatic symptom disorder, panic disorder, generalized anxiety disorder, body dysmorphic disorder, obsessive-compulsive disorder, or delusional disorder, somatic type.

Care-seeking type: Medical care, including physician visits or undergoing tests and procedures, is frequently used.

Care-avoidant type: Medical care is rarely used.

TREATMENT
⦁ Regularly scheduled appointments with medical provider for continued reassurance

The goal is to improve coping skills while never dismissing their fears -caregivers should closely follow their patients and develop a therapeutic alliance

Group/insight-oriented therapy

Regular appts with provider for reassurance

Medications: (SSRIs) if concurrent/underlying anxiety or major depressive disorder

EXAMPLE
a 25-year-old male graduate engineering student who is at your office for the fourth time in 1 week to be sure he does not have chlamydia. He reports that he has only had sex once but learned that chlamydia is hard to culture. He reports he may have dysuria intermittently but is not sure. He has been evaluated at each visit, and physical and laboratory examination has been completely normal each time.

38
Q

HOARDING DISORDER

A

Hoarding is defined as the persistent difficulty discarding or parting with possessions regardless of their actual value. The difficulty is due to a perceived need to save the items and to distress associated with discarding them. Hoarding disorder or pathological hoarding occurs when possessions are accumulated to such an extent that they congest active living areas so much so that their use is substantially compromised

DSM 5 CRITERIA
⦁ Persistent difficulty discarding or parting with possessions, regardless of their actual value

⦁ This difficulty is due to a perceived need to save the items and to distress associated with discarding them

⦁ Difficulty discarding leads to an accumulation of possessions that congest and clutter living areas and substantially compromises their intended use

⦁ The hoarding causes clinically significant distress or impairment in social, occupational, or other important areas of functioning

⦁ The hoarding is not attributable to another medical condition

⦁ The hoarding is not better explained by the symptoms of another mental disorder

39
Q

MAJOR DEPRESSIVE DISORDER

CLINICAL DEPRESSION

UNIPOLAR DEPRESSION

A

MDD = classified as a mood disorder

RISK FACTORS

  • family history
  • female (female: male = 2:1)
  • highest incidence = 20-40s

MDD = depressed mood or anhedonia (loss of pleasure) or loss of interest in activities with 5+ /9 associated symptoms - occur almost every day, for most days, for at least 2 weeks

Lifetime incidence of up to 20% in women
Lifetime incidence of up to 12% in men

One of the most common reasons people seek out mental health services

Interferes with one’s daily life - affects working, studying, eating, sleeping, etc, essentially leading to this overall feeling that life isn’t enjoyable

The diathesis-stress model of major depressive disorder specifies that a preexisting vulnerability can be activated by stressful life events.

  • depression has been linked to damage of the CEREBELLUM

CAUSE
⦁ genetic - ppl who have family members with depression are 3x more likely to have it themselves
⦁ biological
⦁ environmental
⦁ psychological
- genetic, biological, environmental and psychological factors

Most medications focus on neurotransmitters (signaling molecules in the brain)

PATHOPHYSIOLOGY

  • alteration in neurotransmitters = serotonin, epinephrine, norepinephrine, dopamine, acetylcholine and histamine.
  • Neuroendocrine dysregulation
  • PHQ-2 form = initial screen for MDD
  • if positive = use PHQ - 9

3 main neurotransmitters to focus on with depression
⦁ SEROTONIN
⦁ NOREPINEPHRINE
⦁ DOPAMINE

Monoamine Deficiency Theory = the basis of depression is low levels of serotonin, NE, or dopamine, which are all monoamines (have 1 amine group)

Certain levels of these NTs may cause certain symptoms more
⦁ Low serotonin = obsessions + compulsions
⦁ Low NE = attention + anxiety
⦁ Low dopamine = attention + motivation + pleasure

Serotonin = thought to be the main player, and even wonder whether serotonin has some function in regulation of the other 2 NTs (NE + Dopamine)

Tryptophan = the amino acid used to make Serotonin. So low levels of tryptophan = body can’t make as much serotonin

Unknown why these NT/s are low in patients with depression - research is ongoing.

DIAGNOSIS - DSM 5 CRITERIA FOR DEPRESSION
⦁ must be at least 2 weeks
⦁ must be affected by 5/9 of symptoms - most of the day, nearly every day
- depressed mood
- diminished pleasure or interest in activities
- significant weight loss or gain
- inability to sleep or oversleeping
- psychomotor agitation or impairment (reduction in physical movement)
- fatigue
- feelings of worthlessness or guilt
- decreased ability to think or concentrate
- recurrent thoughts of death or suicidality = include suicidal thoughts with or without a plan, and suicide attempts

must have depressed mood or anhedonia + SIGECAPS
Sleep disturbance (insomnia or hypersomnia)
Interest = loss of interest
Guilt or feelings of worthlessness
Energy loss or fatigue (almost all day)
Concentration difficulty
Appetite / weight changes (significant gain or loss)
Psychomotor retardation / agitation
Suicidal ideations or recurrent thoughts of death

  • ***Can have Somatic Symptoms = constipation, headache, skin changes, chest or abdominal pain, cough, dyspnea

Patients with major depressive disorder have MORE episodes of REM sleep per sleep cycle.

⦁ these symptoms must cause significant impairment in a person’s life

⦁ not related to substance use or medical condition

⦁ cannot be better further explained by another mental disorder, such as schizoaffective disorder

⦁ no manic or hypomanic episodes at any point (would be bipolar I or II)

Depression severe enough to impair functioning, and lasting more than two weeks after the death of a loved one CAN be classified as major depression if it meets the other criteria

SUBTYPES
o post-partum depression (start 3-4 weeks after delivery)

  • Postpartum depression is a condition presenting after childbirth with depressed affect, anxiety, and poor concentration

o depressive disorder with peri-partum onset = starts during pregnancy

  • hormonal changes likely play a role
  • can also be due to an abrupt change in lifestyle - as men can also suffer from these

o atypical depression = improved mood when exposed to pleasurable or positive events = “mood reactivity”
⦁ hyperphagia
⦁ hypersomnia
⦁ leaden paralysis (heavy limbs)

o melancholic depression = no improved mood, even during what used to be positive/pleasurable events

  • Mood reactivity is the main distinguishing feature of atypical depression that separates it from melancholic depression.

o dysthymia = persistent depressive disorder = milder symptoms of depression that persist for longer periods of time

  • Chronic depressed mood > 2 years in adults (> 1 year in children / adolescents) for most of the day, more days than not. In that 2 year period, the patient is not symptom free for > 2 months at a time
  • may say things like “I’ve always been this way”

At least 2 of the following conditions must be present:

1) Insomnia / hypersomnia
2) fatigue
3) low self-esteem
4) decreased appetite / overeating
5) hopelessness
6) poor concentration
7) indecisiveness

TREATMENT

1st line TX for depression = CBT + SSRIs

1) Nonpharmacologic approaches
⦁ physical activity = increased endocannabinoids, neurotransmitters and endorphins, relaxed muscles, increased body temp
⦁ diet
⦁ psychotherapy (talk therapy) = preferred for young patients and patients with milder symptoms
- CBT or interpersonal therapy
2) Pharmacologic approaches - single or combination
⦁ SSRIs (MC)****
⦁ SNRIs
⦁ Bupropion + Mirtazapine = 2nd line
⦁ MAOIs + TCAs = 3rd line
- last line = ECT - for patients to fail to respond to medical therapy, have had a previous positive response to ECT, or for rapid response in patients with severe symptoms. ECT = safe in pregnancy & elderly

antidepressants should be continued for a minimum of 3-6 weeks to determine efficacy**

40
Q

SEASONAL AFFECTIVE DISORDER (SAD)

A
  • the presence of depressive symptoms at the same time each year
  • MC in the winter - “winter blues” - due to reduction of sunlight + cold weather

TREATMENT
⦁ SSRIs
⦁ light therapy
⦁ bupropion

41
Q

ATYPICAL DEPRESSION

A
  • shares many of the typical symptoms of MDD, but patients experience MOOD REACTIVITY

MOOD REACTIVITY = improved mood in response to positive events
⦁ significant weight gain
⦁ appetite increase
⦁ hypersomnia
⦁ heavy / leaden feelings in arms or legs
⦁ oversensitivity to interpersonal rejection

TREATMENT

  • CBT + SSRIs
  • MAOIs
42
Q

MELANCHOLIA

A
  • characterized by anhedonia - unlike atypical depression = inability to find pleasure in things, even in things that they enjoyed previously
  • lack of mood reactivity
  • depression
  • severe weight loss / loss of appetite
  • excessive guilt
  • psychomotor agitation / retardation
  • sleep disturbance = increased REM time + reduced sleep

sleep disturbances may lead to early morning awakening or mood that is worse in the morning

43
Q

CATATONIC DEPRESSION

A
  • motor immobility
  • stupor
  • extreme withdrawal
44
Q

PANIC ATTACKS

A
  • a feature of many different anxiety disorders
  • panic attack = not a disorder in + of itself
  • there is some imminent threat or danger present
  • accompanied by physiological sympathetic symptoms such as palpitations, dizziness, SOB, etc.

PANIC ATTACK = episode of intense fear or discomfort that something bad is going to happen

  • develops abruptly
  • usually peaks within 10 minutes (or 10-20 min)
  • usually lasts < 60 minutes (some can last hours)

patients may even feel as if they are having a heart attack or some other life-altering illness

  • are unpredictable - can even happen in familiar places where patient is comfortable and there are no real threats —> this increases anxiety about when the next panic attack may happen (have panic attack about having another panic attack)
- need 4+ of the following symptoms of sympathetic overdrive
⦁  dizziness**
⦁  trembling
⦁  choking feeling
⦁  paresthesias
⦁  sweating
⦁  SOB**
⦁  chest pain / discomfort
⦁  chills or hot flashes
⦁  fear of losing control
⦁  fear of dying
⦁  palpitations, increased HR**
⦁  nausea or abdominal distress
⦁  depersonalization (being detached from oneself) or derealization (feelings of unreality)

some symptoms are physical whereas others are thoughts / personal ideas

TREATMENT FOR AN ACUTE ATTACK
⦁ 1st line = BENZOS (Lorazepam or Alprazolam)
- watch for dependence or abuse

45
Q

PANIC DISORDER

A
  • Recurrent + unexpected panic attacks (at least 2 panic attacks) that may or may not be related to a trigger
  • usually sudden in onset
  • peaks within 10 minutes
  • usually lasts < 60 minutes

at least 1 of the following must occur for at least 1 month
⦁ panic attacks are often followed by the concern about future attacks
⦁ persistent worry about the implication of the attacks (ex: losing control)
⦁ significant change in behavior related to the attacks

*****To diagnose panic disorder, symptoms must be present for MORE THAN 1 MONTH after an attack.

Panic disorder is characterized by recurrent spontaneous panic attacks without an obvious cause with at least one month of persistent fear of experiencing another attack or significant behavioral changes related to the attack.

MUST HAVE AT LEAST 4/13 of the typical symptoms of panic attacks (above)

2-3x MC in women
symptom onset = usually before 30 y/o

Symptoms NOT due to substance use, medical condition or other mental disorder

  • characterized by episodic, unexpected attacks that occur without a clear trigger

“PANIC ATTACKS” - are characterized by a fear of disaster, or a fear of losing control even when there is no real danger
- ppl become discouraged and feel ashamed, because they cannot carry out simple tasks

2x as common in women; affects 6 million adults
- begins in late adolescence or early adulthood

ANTICIPATORY ANXIETY = patients can actually have panic attacks about having another panic attack
- can lead to development of Agoraphobia = patient does not want to leave house / be in social situations due to fear of having panic attack in public

SIGNS/SYMPTOMS OF A PANIC ATTACK
- sudden + unexpected repeated attacks of fear
- feeling of being out of control during a panic attack
- During panic attack
⦁ pounding or racing heart
⦁ sweating
⦁ weakness or dizziness

DIAGNOSIS OF PANIC DISORDER
- attacks can occur at any time
- peaks in 10 minutes; usually lasts about an hour
- attack is followed by one month of:
⦁ persistent worry about additional attacks
⦁ significant of maladaptive change in behavior

Important to treat patients with panic disorder before they develop AVOIDANCE- avoid places where panic attacks occurred or avoid activities that they think may trigger an attack

TREATMENT
⦁ 1st line = SSRIs (paroxetine, sertraline, fluoxetine)
- or SNRIs (Venlafaxine - Effexor)

SSRIs and venlafaxine (Effexor) are the first-line agents for the management of panic disorder.

2nd line = TCAs or Benzos

⦁ CBT treatment = focuses on thinking + behavior - relaxation, desensitization, examining behavior consequences, etc.

ACUTE ATTACK MANAGEMENT
⦁ BENZOS = alprazolam (Xanax), clonazepam (Klonopin)
- watch for dependence or abuse

Benzodiazepines are a class of sedative drugs often used in the acute management of panic disorder.

46
Q

AGORAPHOBIA

A
- Anxiety about being in places or situations from which escape may be difficult x AT LEAST 6 MONTHS
⦁   open spaces
⦁   enclosed spaces
⦁   crowds
⦁   public transportation
⦁  outside of the home - alone

To diagnose agoraphobia, anxiety must occur nearly every time an unfamiliar environment is encountered for at least six months.

Agoraphobia is a condition that involves an exaggerated fear of being in open spaces, using public transportation, being in lines or crowds, or leaving home alone

Agoraphobia is often associated with the progression of PANIC DISORDER

Most people develop agoraphobia AFTER the onset of panic disorder

Agoraphobia = now seen as a separate entity from panic disorders, and can occur with other psychiatric disorders

  • fear or anxiety about situations where help may not be available or where it may be difficult to leave a situation in the event of developing panic-like symptoms or other incapacitating or embarrassing symptoms - avoidance of situations
  • Fear of an actual anticipated situation; could be anything (more like an unfamiliar place or setting, any situation in which they are uncomfortable and can’t get out of)
    ⦁ fear of using public transportation
    ⦁ fear of open or enclosed spaces
    ⦁ fear of standing in line or being in a crowd

Agoraphobia - usually starts before age 35
- MC in women

RISK FACTORS FOR AGORAPHOBIA
⦁ tendency to be nervous or anxious
⦁ experiencing stressful life events
⦁ having a blood relative with agoraphobia

SIGNS/SYMPTOMS OF AGORAPHOBIA
⦁	Fear of leaving the house
⦁	Dependence on others
⦁	Fear of being alone
⦁	Fear of being in places that would be difficult to escape
⦁	symptoms of a panic attack

Agoraphobia is an anxiety disorder characterized by anxiety in situations where the sufferer perceives the environment to be dangerous, uncomfortable, or unsafe

These situations can include wide-open spaces, uncontrollable social situations, unfamiliar places, shopping malls, airports, and bridges.

Agoraphobia is a subset of panic disorder in DSM-IV, involving the fear of incurring a panic attack in those environments. In the DSM-5, however, agoraphobia is classified as being separate from panic disorder. The sufferers may go to great lengths to avoid those situations, in severe cases becoming unable to leave their homes or safe havens.

Patients with agoraphobia can experience panic attacks when in unfamiliar situations, which are characterized by a rapid increase in epinephrine.

TREATMENT
o CBT
⦁	exposure therapy
⦁	service dogs or other animals
o Medication
⦁	same as with panic disorder - SSRIs = 1st line, 2nd = SNRI, 3rd = TCA / Benzos
  • can give benzos initially to help calm the patient down, but give SSRIs for long term treatment
47
Q

PTSD

POST-TRAUMATIC STRESS DISORDER

A

MC in young adults

  • trauma for men includes combat experience + urban violence
  • trauma for women includes rape or assault
  • common in adult survivors of sexual abuse

CRITERIA
⦁ Exposure to actual or threatened death, serious injury or sexual violence via
- direct experience of traumatic event
- witnessing the event in person
- learning the event happened to someone close (family member or friend)
- experiencing extreme or repeated exposure to aversive details of the traumatic event (ex: first responders collecting human remains during 9/11)

  • trauma + stress-related symptoms persist for > 1 month

⦁ Presence of 1+ of the following intrusion symptoms after the event that may lead to significant distress or impairment in function (occupation, social, etc)

1) RE-EXPERIENCING = > 1 month of repetitive recollections (distressing dreams) + dissociative reactions (flashbacks - feels / acts as if the event is recurring) –> leads to physiologic distress / physiologic reactions
2) AVOIDANCE of stimuli associated with the traumatic event (reminders of the event)

3) NEGATIVE ALTERATIONS IN COGNITION + MOOD = inability to remember an important aspect of the event
= persistent exaggerated beliefs (“the world is unsafe”)
- horror, guilt, anger, shame
- may include disinterest in activities

4) HYPERAROUSAL = angry outbursts, irritable behavior, reckless or self-destructive behaviors, hypervigilance, sleep disturbances, concentration issues, exaggerated startle responses
- a debilitating condition that can occur in people who have experienced or witnessed a natural disaster, a serious accident, a terrorist incident, a sudden death of a loved one, war, violent personal assault such as rape, or other life-threatening events

  • have trouble with relationships with family & friends
  • PTSD can occur at any age
SIGNS/SYMPTOMS
o RE-EXPERIENCING SYMPTOMS
⦁	flashbacks
⦁	bad dreams
⦁	frightening thoughts
o HYPERAROUSAL SYMPTOMS
⦁	being easily startled
⦁	feeling tense
⦁	difficulty sleeping
⦁	having an angry outburst

Post-traumatic stress disorder can cause hyperarousal, a distressing state with exaggerated startled response.

o AVOIDANCE SYMPTOMS
⦁ staying away from events / places / objects

o NEGATIVE CHANGES IN COGNITION + MOOD
⦁ feeling emotionally numb
⦁ not remembering certain aspects of the event
⦁ feeling strong guilt, depression, worry
⦁ persistent exaggerated beliefs

o CHILDREN
⦁	bedwetting
⦁	forgetting how or being able to talk
⦁	acting out event during playtime
⦁	being unusually clingy
  • young children are less likely to exhibit symptoms of PTSD

people who go through extreme trauma as a child are more likely to develop PTSD in response to traumas as an adult

  • lots of people with PTSD self-medicate with alcohol / drugs = can worsen symptoms of PTSD, as well as their overall health

DISSOCIATIVE IDENTITY DISORDER (split-personality) is a dissociative disorder often seen in patients with PTSD

Symptoms must last longer than 1 MONTH for a diagnosis of PTSD

TREATMENT
⦁ 1st line = SSRIs (paroxetine, sertraline, fluoxetine); only paroxetine + sertraline = FDA approved for PTSD
⦁ TCAs / MAOIs
⦁ Trazodone = helpful for insomnia***
⦁ Prazosin = helpful for nightmares
***
⦁ sleep aids - since lack of sleep / restlessness is so prevalent in PTSD

  • CBT - individual and/or group counseling
  • Exposure therapy - expose patients to situations that cue recall of the trauma
  • Group therapy - provides survivors with a safe place + supportive environment
48
Q

ACUTE STRESS DISORDER

A

Acute stress disorder is a milder form of post-traumatic stress disorder that lasts between 3 days to 1 month.

Unlike with PTSD, pharmacotherapy is NOT recommended with acute stress disorder

Similar to PTSD, but symptoms last < 1 month + symptom onset occurs within 1 month of the event

TREATMENT

  • counseling / psychotherapy
  • pharmacotherapy NOT recommended with acute stress disorder
  • if persistent = treat as PTSD
49
Q

SOCIAL ANXIETY DISORDER

SOCIAL PHOBIA

A

Social anxiety disorder is defined as excessive fear, anxiety or avoidance of social situations.

  • persistent ( > 6 months) intense fear of social or performance situations, in which the person is exposed to the scrutiny of others for fear of embarrassment
  • intense fear, anxiety, and avoidance of social situations where there is the potential of being scrutinized or negatively judged by others

Social Phobia affects 5-12% of the US population

  • affects women and men equally
  • usually begins in childhood or early adolescence

the fear of being judged / scrutinized by others is so severe that it affects them in their everyday lives

CAUSE

  • unclear
  • thought to be a combination of genetic (close relative with social anxiety disorder) + environmental factors (hx of abuse and neglect)

SIGNS/SYMPTOMS
⦁ Anxious about being with other people - have a hard time talking with others
⦁ self-conscious and feel embarrassed
⦁ afraid other people will judge them

ex:
⦁ public speaking (MC)
⦁ meeting new people
⦁ eating / drinking in front of people

Physical symptoms of social anxiety disorder include 
⦁ excessive blushing
⦁ sweating
⦁ palpitations
⦁ trembling

Exposure to social situations almost always provokes anxiety and causes EXPECTED panic attacks

  • patient may realize that these feelings are excessive and unreasonable, but can’t help it
  • patient will avoid social situations
  • has to be present for > 6 MONTHS*****
  • experience distress in specific social situations = some patients have anxiety about small talk, some may be meeting new people, and some may be speaking in public…or could be combinations

The most common social anxiety disorder involves the fear of public speaking.

  • Ego-dystonic (just like with OCD) = patients are aware that they have a problem, know that their anxiety is unwarranted / extreme –> leads to more anxiety

TREATMENT
⦁ Psychotherapy - CBT / insight-oriented therapy
- CBT = 1st line

⦁ SSRIs - Paroxetine, Fluoxetine, Escitalopram
⦁ SNRIs - Venlafaxine
⦁ Beta-blockers = can be used for performance anxiety - Propranolol, Atenolol
⦁ Benzodiazepines - if tx needed infrequently

1st line pharmacotherapy = SSRIs or Venlafaxine

For occasional anxiety-inducing events in social anxiety disorder, benzodiazepines or beta-blockers are prescribed.

50
Q

SPECIFIC PHOBIAS

A
  • Persistent ( > 6 months) intense fear / anxiety of a SPECIFIC SITUATION (ex: heights, flying) or SPECIFIC OBJECT (pigeons, snakes, blood) or SPECIFIC PLACE (hospitals)

The fear is out of proportion to any real danger

The phobic object / situation / place is actively avoided or endured with intense fear or anxiety

A specific phobia is defined as fear, anxiety or avoidance of a circumscribed object or situation. The reaction is often out of proportion.

EVERYDAY ACTIVITIES MUST BE IMPAIRED BY DISTRESS OR AVOIDANCE OF THE SITUATION OR OBJECT

5 MAJOR SPECIFIERS
⦁	animals (snakes)
⦁	natural environment
⦁	blood - injection - injury (needles)
⦁	situational (heights)
⦁	other
  • specific phobias affect females more than males
  • 1/10 people
  • runs in the family
  • usually first appears in adolescence or adulthood

SYMPTOMS
⦁ persistent fear that is excessive or unreasonable
⦁ exposure to the phobia provokes immediate anxiety response
⦁ fear or anxiety is out of proportion to the actual danger posed

Individuals with a specific phobia have persistent severe anxiety or fear for ≥ 6 months due to anticipation or presence of a specific situation or object.

TREATMENT
⦁ Exposure / Desensitization therapy = tx of choice**
- childhood phobias may disappear or lessen with age

Treatment of specific phobias is with systematic desensitization to the stimulus.

⦁ Short-term benzos or beta-blockers can be used in some patients

TREATMENT
o Specific Phobia
⦁	1st line = CBT - most effective treatment
⦁	2nd line = Benzos
⦁	3rd line = SSRIs
51
Q

BRIEF PSYCHOTIC DISORDER

A

1+ psychotic symptoms with onset + remission < 1 month***

  • Presence of one or more of the following symptoms
    ⦁ Delusions
    ⦁ Hallucinations
    ⦁ Disorganized speech
    ⦁ Grossly disorganized or catatonic behavior

at least one of them must be 1, 2 or 3 (delusions, hallucinations, or disorganized speech)

Brief psychotic disorder is a rare psychiatric disorder that is characterized by psychotic symptoms similar to schizophrenia that persist for less than one month. They are COMMONLY RELATED TO STRESS, and these patients usually recover completely, particularly when the stressor is removed.

Brief psychotic disorder is a period of psychosis whose duration is generally shorter, non-recurring, and not caused by another condition.

Brief Psychotic Disorder is a psychotic disorder defined as a transient (< 1 month), acute psychotic syndrome with no attention problems and a clear sensorium.

** PSYCHOSIS > 1 DAY BUT < 1 MONTH ** OF PSYCHOTIC SYMPTOMS

ex: police officer has been having delusions of persecution for the last 2 weeks. Has had a “short fuse” lately, keeps blinds closed. Has increased suspicion for less than 1 month. Bizarre actions, loose/disorganized answers to questions. Labs & imaging normal
- The diagnosis of Brief Psychotic Disorder is made when symptoms of psychosis persist for > 1 day but < 1 month

**Important to differentiate from schizophrenia because 50-80% of patients diagnosed with a Brief Psychotic Disorder NEVER have another psychotic episode; however, brief psychotic disorder is associated with an increased risk of suicide

TREATMENT

. The first-line treatment is with ANTIPSYCHOTICS such as risperidone or quetiapine.

  • The pharmacotherapy of brief psychotic disorder has not been well-studied, but antipsychotic medications such as risperidone can be prescribed.

Anticholinergics can be used to manage side effects of antipsychotics.

Benzodiazepines can be prescribed to manage agitation.

The diagnosis of brief psychotic disorder is often made retrospectively after symptoms have resolved.

52
Q

SCHIZOPHRENIFORM DISORDER

A

SCHIZOPHRENIA THAT LASTS 1 MONTH + BUT
< 6 MONTHS

schizophrenia-like symptoms for 1 month +, but < 6 months (so longer than a Brief Psychotic Episode, but shorter than Schizophrenia)

NEED 2+ OF THE FOLLOWING SYMPTOMS
⦁ Delusions
⦁ Hallucinations
⦁ Disorganized speech
⦁ Grossly disorganized or catatonic behavior
⦁ Negative symptoms (diminished emotional expression or avolition)

Most people diagnosed with schizophreniform disorder are between the ages of 18 and 24.

ex: woman had a 4 month period of psychotic episodes. Has now been in remission for 3 weeks. She heard voices, and thought her mind was being controlled. At her 3 week remission follow up - no longer hears voices, and work performance has improved significantly. PE/Labs/Imaging normal

**Important to differentiate from Schizophrenia because 1/3 of patients recover within 6 months, however, the remaining 2/3 (66%) progress to be diagnosed with Schizophrenia. So if patient was at 4 month mark, but was still having ongoing symptoms = suspicious that no longer Schizophreniform and patient will develop full-blown Schizophrenia

Approximately 66% of patients with schizophreniform disorder progress to schizophrenia.

Schizophreniform disorder with good prognostic features usually has all of the common symptoms of schizophrenia without social or occupational impairment.

53
Q

SCHIZOPHRENIA

A

6+ MONTHS duration of illness, with 1 MONTH OF ACUTE SYMPTOMS + FUNCTIONAL DECLINE

Schizophrenia = syndrome - lots of different symptoms associated with it, different patients may experience different symptoms

CRITERIA

  • need 2+ symptoms (positive or negative)
  • at least 1 symptom must be hallucination, delusion or disorganized speech

o POSITIVE SYMPTOMS = hallucinations, delusions, disorganized speech / thinking, abnormal behavior
- Thought to be caused by EXCESS DOPAMINE RECEPTORS in mesolimbic pathway

⦁ Hallucinations

  • Auditory (MC) - hear sounds or voices
  • Visual - simple (flashing lights) or complex (see faces)
  • Olfactory - stench or foul smells common
  • Tactile - insects on skin or being touched
  • Somatic - sensation arising from within the body
  • Gustatory - can be a part of persecutory delusions (tasting poison in food)

⦁ Delusions

  • Persecutory - person or force is interfering with them, observing them, or wishes harm to them
  • Reference - random events have personal significance - are messages directed at them
  • Control - Some agency is taking control of patient’s thoughts, feelings + behaviors
  • Grandiose - unrealistic beliefs in one’s powers / abilities
  • Nihilism - exaggerated belief in the futility of everything + catastrophic events
  • Erotomanic - believes another is in love with them
  • Jealousy - somebody is suspected of being unfaithful
  • Doubles - believe a family member or close person has been replaced by an identical double
o NEGATIVE SYMPTOMS - thought to be caused by a DOPAMINE DYSFUNCTION in mesocortical pathway
⦁  Flat emotional affect******
⦁  Social withdrawal
⦁  Lack of emotional expression
⦁  Avolition (lack of self-motivation)*****
⦁  Lack of communication + reactivity
⦁  silent patients / poor eye contact
⦁  Alogia (poverty of speech)******

o COGNITIVE SYMPTOMS
⦁ decline in memory / learning / understanding

EPIDEMIOLOGY
lifetime prevalence = 1%
- Male > female  (1.4 : 1) = MC in Males
- Peak age of onset = 
early 20's (men), late 20s (women)
symptoms more severe in men than women
⦁	Males = 18-25
⦁	Females = 25-35, 2nd peak at menopause ( so thought to have some association with hormone levels - estrogen levels, and estrogen regulation of dopamine?)

Schizophrenia presents LATER in women than in men, with symptoms starting in the late 20s / early 30s.

Prognosis of Schizophrenia is WORSE in Men

Even with treatment, prognosis of schizophrenia is still poor

Schizophrenia is a major problem; several factors of schizophrenia make it a very difficult issue to deal with
⦁ highly disabling for most patients
⦁ generally persists throughout a patient’s life
⦁ Social Ostracism + poor care for both patient and their families
⦁ Only about 1/2 of all Schizophrenia patients obtain treatment, despite severity of the disorder

Patients have a hard time with insight into their illness = part of not getting treatment; will then end up on the streets after losing touch with reality/self care/no support system

Schizophrenics have associations with heart disease
- often smoke (self medicating)

GENETICS**
- biggest risk factor = FAMILY HISTORY
**
- 10% incidence in patients with a schizophrenic 1st degree relative
Highest genetic prevalence of schizophrenia = with Monozygotic Twins
⦁ General population prevalence = 1%
⦁ Non-twin sibling prevalence = 8%
⦁ Child with one afflicted parent prevalence = 12%
⦁ Dizygotic twin prevalence = 12%
⦁ Child with two afflicted parents prevalence* = 40%
⦁ Monozygotic twin prevalence* = 47%

Siblings of patients with schizophrenia have increased risk for developing the disease.

  • Patients with schizophrenia have:
    ⦁ decreased CNS gray matter
    ⦁ increased ventricle size
    ⦁ increased CNS dopamine receptors

Schizophrenia symptoms have to last more than SIX MONTHS before a diagnosis can be made.

Frequent recreational use of the drug cannabis is associated with triggering schizophrenia in teens.

DIAGNOSIS
- Diagnosis of Schizophrenia according to the DSM-5 = Need TWO of the following for a significant portion of time during a 1 month period (or less if successfully treated)

  • Schizophrenia needs to be going on for at least 6 MONTHS (prodromal phase = withdrawn / spend most of their time alone, active phase or residual phase = cognitive symptoms or becoming withdrawn again) and AT LEAST 1 MONTH has to be in the active phase

THESE ARE ACTIVE PHASE SYMPTOMS
⦁ Delusions
⦁ Hallucinations
⦁ Disorganized speech (frequent derailment or incoherence)
⦁ Grossly disorganized or catatonic (shutdown/not moving/speaking/eating) behavior
⦁ Negative symptoms (affective flattening or poverty of speech)

⦁ social or occupational dysfunction
⦁ continuous signs of the disturbance persisting for at least 6 months and within this, at least 1 month of “active-phase” symptoms (above)

POSITIVE SYMPTOMS OF SCHIZOPHRENIA (new / additional)
⦁ delusions
⦁ hallucinations
⦁ disorganized speech (word salad)
⦁ disorganized behavior (ex: wearing winter coats in summer)
⦁ catatonic behavior (resistant to moving or in unresponsive stupor)

Auditory hallucinations are the most common type of hallucination seen in patients with schizophrenia.

NEGATIVE SYMPTOMS OF SCHIZOPHRENIA (removal or reduction of processes)
⦁ affective flattening - inappropriate response**
⦁ poverty of speech (alogia)
** = lack of content in their speech
⦁ blocking (losing train of thought)
⦁ poor grooming
⦁ lack of motivation (avolition**)
⦁ anhedonia (don’t find pleasure in anything anymore)
⦁ social withdrawal

Negative symptoms of schizophrenia include anhedonia and affective flattening.

  • decrease in emotions (flat affect)**
  • loss of interest (anhedonia)
  • alogia = poverty of speech: ex: Do you have kids? - response = yes. Instead of yeah, I have 3; 2 boys and 1 girl.
  • avolition = decrease in motivation to complete goals

Positive symptoms (delusions / hallucinations) are easier to treat/respond better to treatment than negative symptoms. Schizophrenics that predominantly have positive symptoms have relatively good responses to treatment. Schizophrenics that predominantly have negative symptoms have poor responses to treatment

Need 2+ symptoms to diagnose schizophrenia (hallucinations, delusions, disorganized speech, disorganized thought process / catatonic behavior, negative symptoms) and AT LEAST 1 OF THE SYMPTOMS has to be delusions, hallucinations or disorganized speech*****

The Schneiderian First-Rank Symptoms of schizophrenia include:

o Auditory hallucinations
⦁ Third person
⦁ Running commentary
⦁ Hearing thoughts spoken aloud

o Delusional perception

o Passivity phenomena
⦁ Somatic passivity
⦁ Actions influenced by external agents 
⦁ Thought withdrawal
⦁ Thought insertion
⦁ Thought broadcast

Many standard antipsychotics used to treat schizophrenia target dopaminergic pathways such as the mesolimbic, mesocortical, and tuberoinfundibular pathways.

o The tuberoinfundibular pathway regulates hormone secretion in the pituitary gland; as a result, many antipsychotics can cause and an unintentional increase in prolactin secretion.

o The mesocortical pathway, which functions in modulating the prefrontal cortex, is associated with negative symptoms including decreased pleasure, emotion, relationships, and motivation.

o Positive symptoms are believed to originate in the mesolimbic pathway.

SUBTYPES OF SCHIZOPHRENIA

o PARANOID TYPE
⦁ preoccupation with one or more delusions or frequent auditory hallucinations
⦁ no disorganized speech, no disorganized or catatonic behavior, no flat or inappropriate affect - just delusions or hallucinations (positive symptoms)

o DISORGANIZED TYPE
⦁ disorganized speech, disorganized behavior, flat or inappropriate affect (negative symptoms)

o CATATONIC TYPE
⦁ motor immobility
⦁ excessive purposeless motor activity
⦁ extreme negativism or mutism
⦁ peculiarities in voluntary movement (bizarre posturing, stereotyped movements)
⦁ echolalia (repeating words that you said) & echopraxia (repeating movements that you do)

o SENSORIUM & COGNITION
⦁ Usually oriented to person, time, and place - lack of orientation should prompt clinicians to investigate the possibility of medical/neurological brain disorder
⦁ Memory usually intact (may be difficult, however, to get patient to attend closely enough in order to perform memory tests for adequate assessment
⦁ Classically described as having poor insight into nature/severity of disorder

o IMPULSIVENESS

  • may be agitated and have little impulse control when ill
  • may also have decreased social sensitivity (ex: grabs another person’s cigarettes without asking, changes tv channels abruptly, throws food on floor) - this is often a response to an auditory hallucination command

ENVIRONMENTAL RISK

OB complications - higher risk of baby having schizophrenia
⦁	hemorrhage
⦁	fetal hypoxia
⦁	blood group incompatibilities
⦁	pre-term labor
⦁	maternal infection

(babies born in spring more likely to have schizophrenia because mothers more likely to get viral infection then –> inflammation)
- link to early / prenatal infection

Inflammation

  • increased levels of circulating cytokines can alter the BBB or be produced in the brain by activated microglia
  • autoimmune disorders such as thyrotoxicosis, acquired hemolytic anemia, and celiac disease** have higher rates of psychosis
  • Rheumatoid arthritis patients have a LOWER RATE of schizophrenia

Cluster A personality disorders often have a genetic association with schizophrenia.

PROGNOSIS OF SCHIZOPHRENIA
- only about 10-20% of patients can be described as having had a good outcome
- more than 50% of patients can be described as having a poor outcome
⦁ repeated hospitalizations
⦁ exacerbations of symptoms
⦁ episodes of major mood disorders
⦁ suicide attempts

Schizophrenia doesn’t always run a deteriorating course; it is estimated that 20-30% of all schizophrenic patients are able to lead somewhat normal lives

  • Violent Behavior: (excluding homicide)
  • violent behavior is common among untreated schizophrenics
    ⦁ emergency treatment may include restraints & seclusion
    ⦁ acute sedation with lorazepam (ativan) 1-2mg IV - may be repeated every hour as needed to prevent the patient from doing harm to others
  • **Approximately 50% of all schizophrenic patients attempt suicide (often due to misdiagnosing flat affect as depression or a medication SE)
  • providers often think flat affect or depression of bipolar = just depression

A common cause of death in patients with schizophrenia is suicide.

At least one POSITIVE symptom, including delusions, hallucinations, or disorganized speech is necessary for a diagnosis of schizophrenia, in addition to one more positive or negative symptom.

TREATMENT
- Schizophrenia = caused by dopamine abnormalities in mesolimbic and prefrontal brain regions

The mesolimbic pathway in the brain is a dopaminergic pathway in the brain that is the target of antipsychotics for schizophrenia.

The main support for the theory that too much dopamine causes schizophrenia is the fact that antipsychotic medications, which are used to treat schizophrenia, block dopamine receptors. The medications are designed to bind to dopamine receptors in the brain

  • due to the fact that antipsychotics are treatment for schizophrenia = means that schizophrenia probably has to do with INCREASED LEVELS OF DOPAMINE
  • the antipsychotics block dopamine receptors (D2 receptors) - which decreases levels of dopamine in neurons

Two prominent theories of the underlying mechanisms of schizophrenia are the dopamine and glutamate hypotheses.
⦁ The dopamine hypothesis proposes excessive D2 receptor activation is a possible cause of schizophrenic symptoms.
⦁ For the glutamate hypothesis, NMDA receptor hypofunctioning is believed to be an underlying pathophysiological change present in the disorder. Research suggests those diagnosed with schizophrenia have fewer N-methyl D-aspartate (NMMA) glutamate receptors in their brains. Ketamine and phencyclidine (PCP) are NMDA receptor antagonists that can produce symptoms very similar to those of schizophrenia.

Deletion of the COMT gene is associated with an increase in dopamine levels in the brain, and thus a higher likelihood of developing schizophrenia.

  • Antipsychotics are not always effective, and work really well for some / not for others ==> conclusion that probably much more than just dopamine levels that are causing schizophrenia

Antipsychotics decrease the POSITIVE symptoms of schizophrenia by influencing mesolimbic dopaminergic pathways.

  • ex: Clozapine (MARTA antipsychotic) = weak D2 antagonist - meaning probably other NTs involved, such as NE, serotonin, GABA, etc.
  • Hospitalization for acute psychotic episodes

Tobacco abuse is the most common form of substance abuse in people with schizophrenia. 75-90% of people with schizophrenia are addicted to nicotine, three times greater compared to the general population.

Substance abuse is the most common comorbidity with schizophrenia and is associated with worsening patient prognosis. Drug abuse increases the risk for many other illnesses including infections and heart disease. In addition, many commonly abused substances interact with the mechanisms of schizophrenia or the drugs used to treat it, exacerbating symptoms and making the disorder more difficult to treat. Many researchers suggest substance abuse is often an attempt of patients to self-medicate, with nicotine being the first-choice followed by alcohol and marijuana.

Nicotine is the most common drug abused by patients with schizophrenia. Some research suggests nicotine helps in alleviating some of the cognitive deficits associated with schizophrenia. However, the health risks (cardiovascular disease, mortality, decreased effectiveness of prescribed drugs) greatly outweigh the potential benefits. 25-30% of the general population is addicted to nicotine; this rate triples to 75-90% in patients with schizophrenia. Buproprion is helpful in assisting smoking cessation in people with schizophrenia.

⦁ ANTIPSYCHOTICS = dopamine receptor antagonists
- 1st line tx = 2nd generation antipsychotics - risperidone, olanzapine, quetiapine
MOA = dopamine + serotonin antagonists
- Clozapine = may be used in refractory cases (no significant improvement after 2-6 weeks of antipsychotics)

  • beware of antipsychotic SE - such as tolerance, dependence + withdrawal

Atypical antipsychotics are the first line drugs for schizophrenia

  • 2nd line tx = 1st generation antipsychotics = Haloperidol (Haldol) and Chlorpromazine (Thorazine) = better at treating positive symptoms, but are associated with increased extrapyramidal symptoms
54
Q

SCHIZOAFFECTIVE DISORDER

A

psychosis + mood disorder (depressive or manic episodes), however, psychosis also has to occur in the ABSENCE of mood symptoms

PSYCHOSIS must occur for at least 2 WEEKS without a major mood episode

different from schizophrenia in that psychosis is experienced AS WELL AS a mood disorder (either major depressive or manic episode) AND the patient must also have experienced delusions or hallucinations IN THE ABSENCE OF mood symptoms

Having periods of delusions, hallucinations, disorganized thought WITHOUT a mood episode, and periods of concurrent hallucinations or delusions WITH a mood episode are symptoms of schizoaffective disorder.

Will have times where mood disorder + psychosis occur at the same time, but also have to occur separately in order to diagnose schizoaffective

(ex: pt gets depressive episodes 2x/year. depressive episode resolved 6 weeks ago, but pt has been experiencing psychosis)

**Important to differentiate schizophrenia from schizoaffective disorder because the prognosis for schizoaffective disorder is BETTER than the prognosis for schizophrenia

**Major difference between schizoaffective disorder + either Major Depressive Disorder with Psychotic Features and Bipolar Disorder with Psychotic Features = schizoaffective disorder has psychosis occurring at different time as mood symptoms. Major Depressive Disorder with Psychotic Features and Bipolar Disorder with Psychotic Features is mood symptoms and psychosis occurring at the same time

In order to diagnose schizoaffective disorder, psychosis must occur for longer than two weeks without a major mood episode, and not be associated with other mental illnesses, drug use, toxins, or poisons.

DIAGNOSIS
The diagnosis is made when the patient has features of both schizophrenia and a mood disorder—either bipolar disorder or depression—but does not strictly meet diagnostic criteria for either alone.

2 TYPES
⦁ Bipolar type
⦁ Depressive type

The bipolar type is distinguished by symptoms of mania, hypomania, or mixed episode

The depressive type by symptoms of depression only.

Common symptoms of the disorder include hallucinations, paranoid delusions, and disorganized speech and thinking. The onset of symptoms usually begins in young adulthood, currently with an uncertain lifetime prevalence

In order to diagnose schizoaffective disorder, psychosis must occur for longer than two weeks without a major mood episode, and not be associated with other mental illnesses, drug use, toxins, or poisons.

Use of cannabis excessively in early adolescence is linked to developing psychotic illnesses, such as schizoaffective disorder and schizophrenia, as an adult

TREATMENT
⦁ Antipsychotics = Risperdal (Risperidone), Seroquel (Quetiapine), Zyprexa (Olanzapine), Invega (Paliperidone)
⦁ if refractory to antipsychotics (no improvement after 2-6 weeks) = Clozapine (Clozaril)

An antipsychotic medication that can be given to a patient with schizoaffective disorder that is not responding to first-line atypical antipsychotics, such as risperidone, is clozapine (MARTA = multi - acting receptor targeted antipsychotic)

A non-medicated treatment for schizoaffective disorder that is commonly encouraged is cognitive therapy.

55
Q

BIPOLAR I

A
  • History of at least 1 MANIC EPISODE, with or without a past major depressive episode
Manic Episode
⦁ energetic
⦁ overly happy / optimistic
⦁ euphoric
⦁ high self-esteem
  • while these seem like positive symptoms, these can reach a dangerous extreme during Mania
  • may behave recklessly (spend all their money, have affairs, risky activities)
  • may have pressured speech (talk constantly at rapid-fire pace)
  • may have racing thoughts and feel wired - as if they don’t need sleep
  • may have delusions of grandeur (believe they are on a mission from God, or they have supernatural powers)
  • may make poor decisions without any regard for later consequences

MANIA = abnormal + persistently elevated, expansive or irritable mood AT LEAST 1 WEEK (or less if hospitalization is required) with MARKED SOCIAL / OCCUPATIONAL FUNCTION IMPAIRMENT
- Must have 3+ of the following symptoms

o MOOD
⦁ euphoria
⦁ irritable
⦁ labile
⦁ dysphoric
o THINKING
⦁ racing thoughts
⦁ flight of ideas
⦁ disorganized
⦁ easily distracted
⦁ expansive or grandiose thoughts (highly inflated self-esteem)
⦁ judgment is impaired (spending sprees)
o BEHAVIOR
⦁ physical hyperactivity
⦁ pressured speech
⦁ decreased need for sleep (may go days w/o sleep)
⦁ increased impulsivity
⦁ excessive involvement in pleasurable activities (risk-taking and hypersexuality)
⦁ disinhibition
⦁ increased goal directed activity
  • Psychotic symptoms (paranoia, delusions, hallucinations) may be seen in these patients**

GREATEST RISK FACTOR FOR BIPOLAR DISORDER = FAMILY HISTORY (1st degree relatives)
= 10x more likely to have bipolar disorder if family member has it

  • Average age of onset = 20s-30s
  • new onset = rare after 50
  • the earlier the onset, the greater the likelihood of psychotic features, and the poorer the prognosis
  • depression is not required for the diagnosis of bipolar I disorder, however, depression is present more commonly than mania for most patients
  • depression should last at least 2 weeks (MDD), then at least 1 week of Mania (less of hospitalization occurs)
    , but don’t need depression to diagnose Bipolar I.
  • In order to diagnose Bipolar I - it is NECESSARY to meet criteria for a MANIC EPISODE

So…with Bipolar I = need a manic episode…that’s it! (with or without a depressive episode)

  • need ONE MANIC episode with or without depressive episode

“Mixed” symptoms = simultaneous occurrence of 3+ manic symptoms + depression

“Rapid Cycling” = 4+ episodes of depression or mania within 1 year

  • an untreated manic episode can last as long as 3-6 months
  • marked by relapses + remissions
  • often alternating pattern between manic & depressive episodes
  • 90% of ppl who have one manic episode have another in 5 years
  • 90% of ppl with bipolar disorder have at least one psychiatric hospitalization and the majority of 2 or more

**DEPRESSIVE SYMPTOMS MORE FREQUENT THAN MANIC IN BIPOLAR I (3:1) - which is interesting, because this disorder is characterized by a manic episode, not depressive episode

“Lows” = same as MDD (unipolar depression)

In patients with bipolar disorder, mood and functioning DO return to normal in between episodes.

TREATMENT
⦁ 1ST LINE = LITHIUM**
⦁ Valproic Acid (Depakote)
⦁ Carbamazepine (Tegretol)
⦁ 2nd generation antipsychotics (ex: Olanzapine)
⦁ 1st generation antipsychotics (ex: Haloperidol)
⦁ Benzodiazepines

Lithium = mood stabilizer; treats both the mania and depression of bipolar disorder, however, it treats mania better than depression, so patients are often on additional meds
- however, certain ADs such as SSRIs can trigger manic episodes

Mood stabilizers and atypical antipsychotics are the drugs of choice for the treatment of bipolar disorder***

First line treatment in a manic episode is lithium or valproate, a mood stabilizer, in combination with an antipsychotic

Mood Stabilizers = Lithium, anticonvulsants (Depakote, tegretol)
Neuroleptics = antipsychotics
Benzodiazepines if psychosis or agitation develops

End-stage renal disease (ESRD) is a strict contraindication for the use of lithium. Lithium can be used in both the acute manic and depressive stages of bipolar disorder but has a narrow therapeutic range and should not be used in patients with impaired renal function.

Lamotrigine = 2nd-line agent for the treatment of depressive symptoms of bipolar II disorder and is the only agent listed aside from lithium which is used in the depressive stage. Also, Lamotrigine is now the drug of choice in all 3 trimesters of pregnant patients with bipolar disorder, although, one must take special care during the first trimester.

Other Options
⦁ ECT
⦁ SSRIs / MAOIs / TCAs
- talk therapy and CBT = not very effective in treating bipolar disorder, however, can still be very helpful, such as right after manic episode, or helps patients develop better skills to handle stressful situations, which can therefore prevent manic episodes

however, antidepressant medications may precipitate mania**

Therapy - cognitive / behavioral / interpersonal
good sleep hygiene recommended

**CERTAIN DRUGS/MEDICATIONS CAN TRIGGER MANIC EPISODES***
⦁ ANTIDEPRESSANTS (SSRIs)
- don’t give SSRIs to patients with depression unless sure they don’t have bipolar disorder

56
Q

BIPOLAR II

A
  • History of AT LEAST ONE EPISODE OF MAJOR DEPRESSION and AT LEAST ONE HYPOMANIC EPISODE

1+ HYPOMANIC EPISODE and 1+ MAJOR DEPRESSIVE EPISODE

  • “Mixed” symptoms = simultaneous occurrence of 3+ hypomanic symptoms + depression

HYPOMANIA = symptoms are similar to manic symptoms = period of elevated, expansive or irritable mood for AT LEAST 4 DAYS - that is clearly different from usual non-depressed mood, but DOES NOT CAUSE MARKED IMPAIRMENT, NO PSYCHOTIC FEATURES (unlike possibility in Bipolar I), and DOES NOT USUALLY REQUIRE HOSPITALIZATION
- does not include racing thoughts or excessive psychomotor agitation

  • HYPOMANIA MUST LAST FOR AT LEAST 4 DAYS
  • can last longer - generally last for a few weeks to a few months
  • less severe manic episodes than what is seen in Bipolar I. Both are needed to diagnose Bipolar II
  • Similar to Bipolar I, depressive symptoms are much more frequent than hypomania (or mania in bipolar I)
  • NO HISTORY of a manic episode

Need a hypomanic episode and a depressive episode, but NO MANIC episode

  • less well studied of a course, and therefore, less well understood
  • but we do know that depressive symptoms are much more frequent than hypomanic episodes (suggested to be 38:1)

“Lows” = same as MDD (unipolar depression)

GREATEST RISK FACTOR FOR BIPOLAR DISORDER = FAMILY HISTORY (1st degree relatives)
= 10x more likely to have bipolar disorder if family member has it

In patients with bipolar disorder, mood and functioning DO return to normal in between episodes.

TREATMENT

Mood stabilizers and atypical antipsychotics are the drugs of choice for the treatment of bipolar disorder***

  • similar to Bipolar I = mood stabilizers, antipsychotics, and benzodiazepines

⦁ Acute Mania =

  • Mood Stabilizers (LITHIUM or Depakote / Tegretol
  • Antipsychotics (2nd gen)

⦁ Depression =

  • LITHIUM or Depakote / Tegretol
  • Antipsychotics (2nd gen)

⦁ Mixed

  • Antipsychotics (2nd gen)
  • Valproate (Depakote)

End-stage renal disease (ESRD) is a strict contraindication for the use of lithium. Lithium can be used in both the acute manic and depressive stages of bipolar disorder but has a narrow therapeutic range and should not be used in patients with impaired renal function.

Lamotrigine = 2nd-line agent for the treatment of depressive symptoms of bipolar II disorder and is the only agent listed aside from lithium which is used in the depressive stage. Also, Lamotrigine is now the drug of choice in all 3 trimesters of pregnant patients with bipolar disorder, although, one must take special care during the first trimester.

**CERTAIN DRUGS/MEDICATIONS CAN TRIGGER MANIC EPISODES***
⦁ SSRIs
- don’t give SSRIs alone to patients with depression unless sure they don’t have bipolar disorder

57
Q

PSYCHOSIS

A

Psychosis refers to an abnormal condition of the mind described as involving a “loss of contact with reality”

People experiencing psychosis may exhibit some personality changes and thought disorder. Depending on its severity, this may be accompanied by unusual or bizarre behavior, as well as difficulty with social interaction and impairment in carrying out daily life activities.

DEFINITION - PSYCHOSIS is broadly defined as a loss of contact with reality

Psychotic states are high risk periods:
⦁	Agitation
⦁	Aggression
⦁	Impulsivity (Suicide)
⦁	Other forms of behavioral dysfunction

CLINICAL MANIFESTATIONS

  • delusions
  • hallucinations
  • thought disorganization / speech disorganization

o DELUSIONS
- strongly held false beliefs that are not part of the patient’s cultural or religious backgrounds

  • may be bizarre or non-bizarre (unrealistic vs slightly realistic/could happen)

o HALLUCINATIONS

  • wakeful experiences of content that is not actually present
  • involves any of the 5 senses
  • auditory hallucinations = most common
  • followed by visual, tactile, olfactory and gustatory hallucinations

o THOUGHT DISORGANIZATION / SPEECH
⦁ Alogia/poverty of content - inability to speak or reduction in amount of speech - seen with dementia as well as with psychosis/schizophrenia
⦁ Thought blocking - suddenly loosing train of thought
⦁ Loosening of Association - sequences not well connected (ex: He went to the ballpark and bought Frank’s beer belly home in a bag of grass seed)
⦁ Tangentiality - answers to questions veer off topic (go off on tangent)
⦁ Clanging - rhyming
⦁ Word salad - real words that are linked incoherently - don’t make sense together (ex: Horse paper handbags skipping forests play together)
⦁ Perseveration - repeating words or ideas even after topic has changed

58
Q

DELUSIONS

A
  • strongly held false beliefs that are not part of the patient’s cultural or religious backgrounds
  • may be bizarre or non-bizarre (unrealistic vs slightly realistic/could happen)

Types of Delusions
⦁ Persecutory (police/gov’t is watching me, they have tapped my phone)

⦁ Grandiose (I am god’s vessel on earth, I have supernatural powers)

⦁ Erotomanic (Brad Pitt and I are in love and we’re going to get married)

⦁ Somatic (almost hypochondriac - belief that something is medically wrong)

⦁ Delusions of reference (think things are directed at them rather than the public)

⦁ Delusions of control (thoughts are being transmitted or implanted or stolen)

PERSECUTORY DELUSION
This is the most common form of delusional disorder. In this form, the affected person fears they are being stalked, spied upon, obstructed, poisoned, conspired against or harassed by other individuals or an organization

DELUSIONS OF GRANDEUR
In this form of delusion, the person believes they are much greater or more influential than they really are. Belief that one is a famous or important figure, such as Jesus Christ or Napolean. Alternately, delusions of grandeur may involve the belief that one has unusual powers that no one else has

EROMATIC DELUSIONS
In this form of delusion, the patient is often firmly convinced that a person he or she is fixated upon is in love with them. This obsession leads to stalking, unnatural jealousy and rage when the object of their affection is seen with their spouse or partners. Erotomanis often concern a famous person or someone who is in a superior status and usually there is no contact between the patient and the victim, who has never encouraged the patient.

SOMATIC DELUSIONS
In this disorder, a person is convinced something is wrong with them. This type of delusion may often lead to multiple consultations with physicians, surgical procedures, depression and even suicide

DELUSIONS OF REFERENCE
A neutral event is believed to have a special and personal meaning. For example, a person with schizophrenia might believe a billboard or a celebrity is sending a message meant specifically for them

DELUSIONS OF CONTROL
Belief that one’s thoughts or actions are being controlled by outside, alien forces. Common delusions of control include thought broadcasting (“My private thoughts are being transmitted to others”), thought insertion (“Someone is planting thoughts in my head”), and thought withdrawal (“The CIA is robbing me of my thoughts”)

Delusions of control is different that Auditory Hallucination = “hearing voices that are telling me what to do”

“I can’t believe that they’ve sabotaged my care. Last week they stole my mail. I know they’re following me every time I leave the house” = Delusion of Persecution

“God has chosen me to be the world representative of Mars” = Delusion of Grandeur

“Invaders from space have infiltrated my testicles so I wouldn’t be allowed to father any children” = Bizarre Delusion

“It doesn’t matter anyway; my thoughts are controlled by the government” = Delusion of Control

“The DJ is really giving me instructions on what to do. He just disguises it so no one will pick up on it” = Delusion of Reference

59
Q

DELUSIONAL DISORDER

A

1+ DELUSION lasting 1+ MONTH
WITHOUT OTHER PSYCHOTIC SYMPTOMS

Delusional disorder is characterized by the presence of one or more delusions for at least a month in an otherwise normally functioning individual.

delusion WITHOUT other signs/symptoms of psychosis

Delusions are non-bizarre (address situations that can occur in everyday life)

  • delusions are possible, but still highly unlikely
    ex: being poisoned
  • Apart from the delusion, behavior is not particularly odd or bizarre, and there is no significant impairment in function

Not explained by another disorder

ex: ex: 38yo man goes to police station complaining that the FBI has been following him unjustly for at least 1 month. Is successfully employed, no impaired functioning. Doesn’t feel particularly threatened, but requests that the police intervene for him. PE/labs/imaging normal

A patient with a fixed, false belief system lasting more than ONE MONTH can be said to have a delusional disorder.

Besides the false, fixed belief system a patient with delusional disorder has, functioning IS NOT otherwise impaired.

Delusional disorder is a disorder that can actually be shared by individuals in close relationships, also referred to as folie à deux. (a psychiatric syndrome in which symptoms of a delusional belief and sometimes hallucinations are transmitted from one individual to another. The same syndrome shared by more than two people may be called folie à trois, folie à quatre, folie en famille (“family madness”), or even folie à plusieurs (“madness of several”). )

TREATMENT

  • 1st line = CBT
  • usually ANTIPSYCHOTIC medication is recommended
60
Q

DEMENTIA

A

Progressive, chronic, intellectual deterioration of selective functions

MEMORY LOSS** AND loss of impulse control, motor and cognitive functions

Includes language dysfunction, disorientation, inability to perform complex motor activities, and inappropriate social interaction

NOT due to delirium, medications or psychiatric illness

RISK FACTORS

  • age (especially > 60)
  • vascular disease
61
Q

POST-PARTUM BLUES

A
  • occurs in 50-85% of new mothers*
  • Transcultural - PPD (Post partum depression) thought to be found more in developed countries

TIME COURSE

  • begins within 48 hours after delivery (starts within 2 days after delivery)
  • peaks at 3-5 days
  • lasts around 2 weeks**

ETIOLOGY
- Thought to be sudden hormone withdrawal that occurs after pregnancy; Estrogen, progesterone, and cortisol levels all plummet about 48 hours after giving birth

  • if lasts longer than 2 weeks = consider PPD

RISK FACTORS FOR PPB (POSTPARTUM BLUES)
⦁ history of depression
⦁ depressive symptoms during pregnancy
⦁ family history of depression
⦁ premenstrual or OCP associated mood changes
⦁ stress around child care
⦁ psychosocial impairment in the areas of work, relationships and leisure activities

SYMPTOMS OF PPB
⦁	mood lability
⦁	tearfulness
⦁	sadness or elation
⦁	anxiety
⦁	irritability
⦁	insomnia
⦁	decreased concentration

TREATMENT FOR PPB
o supportive + educational treatment - reassurance to the mother and her family
o allow the woman to have enough rest
o perhaps get someone to take care of the infant at night
o PPB generally resolves on its own
o careful monitoring of PPB for the development of PPD (postpartum depression)

62
Q

POSTPARTUM PSYCHOSIS

A
  • affects 1-2/1000 postpartum women
  • same rate for western + nonwestern countries

ONSET
- usually within 2 weeks of delivery**

women are more likely to experience psychosis following childbirth than at any other time in their lives

Women with PPP are more likely to commit suicide or infanticide = MEDICAL EMERGENCY!!!

PATHOGENESIS

  • the complete etiology is not known
  • research suggests hormonal & genetic factors
  • rapid hormonal changes following childbirth may play a role as a trigger

PPP is currently thought of as a manifestation of BIPOLAR DISORDER

RISK FACTORS FOR PPP
⦁ First pregnancy
⦁ history of bipolar disorder
⦁ history of puerperal psychosis (postpartum psychosis)
⦁ family history of puerperal psychosis (PPP)
⦁ recent discontinuation of lithium or other mood stabilizers

maternal age > 35 = 2x increased risk
hx of bipolar disorder & psychotic episode raises risk by 50%
interestingly found that women with diabetes had a lower risk of PPP

SYMPTOMS OF PPP
⦁	Delusions
⦁	Hallucinations (visual / auditory / olfactory)
⦁	Thought disorganization
⦁	Severe insomnia
⦁	Suicidal ideation
⦁	Homicidal ideation
⦁	Aggression
⦁	Agitation
⦁	Impulsivity
TREATMENT FOR PPP
o usually acute hospitalization
o Antipsychotics*****
o Therapy
o ECT if pharmacotherapy is unsuccessful

**CANNOT send this woman home alone with her baby/or if husband works all day and she has no other social support

THIS IS A TRUE MEDICAL EMERGENCY*

63
Q

POSTPARTUM DEPRESSION

A
  • 12-15% of women**
  • 10-26% of men**

2 weeks - 12 months

RISK FACTORS FOR PPD
⦁ Marital conflict
⦁ stressful life events, lack of social support for pregnancy
⦁ lack of emotional and financial support of partner
⦁ living without a partner
⦁ unplanned pregnancy
⦁ previous miscarriage
⦁ having contemplated terminating the pregnancy
⦁ a poor relationship with one’s own mother
⦁ high number of visits to prenatal clinic
⦁ congenitally malformed child
⦁ personal history of bipolar disorder

DSM IV = up to 4 months postpartum; many experts believe that women remain at an increased risk for depression for up to 1 year postpartum

Significantly lower levels of PPD in nonwestern cultures - due to greater extended social support structure for mothers in nonwestern cultures

PPD affects the bonding of mother with child

higher rate of PPD among adolescent mothers
highest rate of Male PPD = 3-6 months after birth - are affected by mother’s mood (as mother’s depression goes up, so does the fathers)

SYMPTOMS OF PPD
⦁ irritability and anger
⦁ significant anxiety often with panic attacks
⦁ feelings of inadequacy, and of being a failure as a mother
⦁ feelings of guilt
⦁ feelings of hopelessness or despair
⦁ feelings of being overwhelmed or unable to care for the baby
⦁ not bonding to the baby –> further exacerbates feelings of shame/guilt
⦁ typical = insomnia, weight changes, decreased libido, decreased energy levels**

Often leads to women suffering in silence

NEED TO RULE OUT A MEDICAL CAUSE
⦁	anemia
⦁	diabetes
⦁	thyroid disorders
	- 1-3 months = hyperactivity
	- 3-4 months = hypoactivity
	- 7-8 months = stabilization
	- postpartum thyroiditis

The pituitary gland swells during pregnancy; damage can occur, leading to problems in the feedback mechanism to the thyroid gland

Postpartum Thyroiditis = hair loss, debilitating fatigue, depression, anxiety, insomnia, and low milk supply

KATHERINE STONE

  • 6 stages of PPD = Denial, Anger, Bargaining, Depression, Acceptance (5 stages of grief)
  • she added a 6th stage: PTSD - where even after acceptance and treatment, she still isn’t 100%. Still worries that PPD will return; constantly looking over shoulder. Every time she feels bad, she’s convinced she’s gone back to PPD. Has lost confidence in herself as a mother. Worries she hurt her child long-term because of how she behaved when he was a baby

NORTHWESTERN UNIVERSITY STUDY 2015 - MEN’S PPD

  • why do men experience PPD?
  • perhaps due to testosterone levels during pregnancy of significant other

SYMPTOMS OF MEN’S PPD
⦁ increased anger/conflict with others
⦁ increased used of alcohol or other drugs
⦁ frustration or irritability
⦁ violent behavior
⦁ losing weight without trying
⦁ isolation from family and friends
⦁ being easily stressed
⦁ impulsiveness + taking risks - reckless driving + extramarital sex
⦁ feeling discouraged
⦁ increases in complaints about physical problems
⦁ ongoing physical symptoms, like headaches, digestion problems or pain
⦁ problems with concentration and motivation
⦁ loss of interest in work / hobbies / sex
⦁ working constantly
⦁ frustration or irritability
⦁ misuse of prescription meds
⦁ increased concerns about productivity & functioning at school or work
⦁ fatigue
⦁ experiencing conflict between how you think you should be as a man and how you actually are
⦁ thoughts of suicide

PPD TREATMENT
o Psychotherapy
⦁ Interpersonal - marital strain / role transitions
⦁ Cognitive - changing negative cognitive distortions / aid in developing coping behaviors
o Group therapy (support groups)

CONSIDERATIONS
- Breastfeeding - risk vs benefit of taking medication for PPD - drug transfer (depends on protein binding, lipid solubility, molecular weight of drug, and drug half-life) & evaluation of infant

very few drugs are contraindicated in breast feeding; recommended women breastfeed for at least 6 months, and longer if possible

High protein binding restricts drugs to maternal plasma & prevents transfer into breast milk
High Lipid solubility transfers more quickly / in greater amounts into breast milk
Low Molecular weight drugs pass more easily into breast milk
Longer Drug half life = greater the risk of accumulation in mother and infant

  • so prefer high protein binding, low lipid solubility, high molecular weight drug, and shorter half life

premature & newborns = at greater risk from maternal medications than older infants due to immature hepatic & renal systems. Infants with poor GI stability = also at greater risk from maternal medications

TREATMENT

  • SSRIs
  • SNRIs
  • TCAs (not preferred due to CV + anticholinergic SE with overdose
  • Benzos
  • Sedative hypnotics

PREFERRED TX = SSRIs = ZOLOFT + PAXIL

64
Q

DYSLEXIA

A

Dyslexia, also known as reading disorder, is characterized by trouble with reading despite normal intelligence. Different people are affected to varying degrees. Problems may include difficulties in spelling words, reading quickly, writing words, “sounding out” words in the head, pronouncing words when reading aloud and understanding what one reads. Often these difficulties are first noticed at school. When someone who previously could read loses their ability, it is known as alexia. The difficulties are involuntary and people with this disorder have a normal desire to learn.

  • 15% of public school children
  • more common in boys
  • tends to run in families
SIGNS/SYMPTOMS
- delayed language production
- speech articulation difficulties
- difficulties remembering the names of letters / numbers / colors
- reversals or visual confusion can occur
⦁	d becomes b
⦁	m becomes w
⦁	h becomes n
⦁	was becomes saw
⦁	on becomes no

INDIVIDUALS WITH DYSLEXIA COMMONLY HAVE PROBLEMS:
⦁ Processing and understanding what they hear
⦁ They may have difficulty comprehending rapid instructions
⦁ Following more than one command at a time
⦁ Remembering the sequence of things
⦁ Individuals with dyslexia may also try to read from right to left
⦁ May fail to see (and sometimes hear) similarities and differences in letters and words
⦁ May not recognize the spacing that organizes letters into separate words
⦁ May be unable to sound out the pronunciation of an unfamiliar word

SCREENING & DIAGNOSIS OF DYSLEXIA

  • *THERE IS NO SINGLE TEST FOR DYSLEXIA**
  • Diagnosis involves an evaluation of: medical / cognitive / sensory processing / educational / & psychological factors
  • Vision & hearing & neurologic examinations
  • Psychological assessment

TREATMENT FOR DYSLEXIA
There’s no known way to correct the underlying brain malfunction that causes dyslexia.
Treatment is by remedial education.
Psychological testing will help identify the areas pts. need to work on

May use techniques involving hearing, vision and touch to improve reading skills. Helping an individual to use several senses to learn — for example, by listening to a taped lesson and tracing with a finger the shape of the words spoken — can help them process the information.

The most important teaching approach may be frequent instruction by a reading specialist who uses these multisensory methods of teaching**

PROGNOSIS

  • tutoring may involve several individual or small-group sessions per week
  • progress may be slow, however, generally a good prognosis with dyslexia
  • milder forms = good prognosis, usually do well with tutoring
  • severe dyslexia = have a much harder time, really have to work hard
65
Q

DYSGRAPHIA

A
  • WRITING DISABILITY - a learning disability that results from the difficulty in expressing thoughts in writing
  • DSM -5 uses the phrase “an impairment in written expression learning disorder” rather than dysgraphia
  • dysgraphia is more than just bad handwriting

In Dysgraphia = Have Difficulties With:
⦁ handwriting
⦁ grammar + syntax
⦁ formulating, expressing, and organizing ideas in writing
⦁ spelling “encoding” = the ability to use sound-letter relationships effectively

66
Q

DYSCALCULIA

A
  • MATH DISABILITY - difficulty performing math calculations

SIGNS/SYMPTOMS

  • difficulty understanding number lines
  • difficulty carrying + borrowing numbers
  • difficulty with word problems

STRATEGIES

  • allow use of fingers and scratch paper
  • use diagrams and draw out math concepts
  • provide peer assistance
  • suggest use of graph paper
67
Q

ACUTE MANIA

A
Symptoms of an acute manic episode can be remembered with the mnemonic DIG FAST
 ⦁ distractibility
 ⦁ irresponsibility
 ⦁ grandiosity
 ⦁ flight of ideas
 ⦁ activity increase
 ⦁ sleep deficit
 ⦁ talkativeness

At least three of the symptoms within DIG FAST must be present and persist for at least a week, causing the inability for one to take care of oneself for diagnosis.

Acute mania is a component of bipolar disorder. It is a medical emergency and warrants prompt treatment with an antipsychotic and mood stabilizer, such as lithium or valproate. Signs of mania include elevated mood, reckless behavior and pressured thoughts and speech.

First line treatment for acute manic episodes = antipsychotics; but can also use lithium or other mood stabilizers

First line treatment in a manic episode is lithium or valproate, a mood stabilizer, in combination with an antipsychotic

68
Q

LITHIUM

A

Mood Stabilizer - primarily used to treat bipolar disorder - smooths out the highs and lows experienced

  • significantly decreases the frequency + severity of both manic and depressive episodes in about 70% of patients
  • can also be used for unipolar depression (MDD) that does NOT RESPOND to antidepressants

MOA
- may decrease NE + Dopamine turnover (which helps relieve mania) by increasing NE + Serotonin receptor sensitivity

  • blocks the development of dopamine receptor super-sensitivity
  • may augment the synthesis of acetylcholine by increasing cholamine uptake into nerve terminals

Use less first line with new atypical antipsychotics; may work better in the maintenance phase of therapy

WHY?
- lithium has a VERY NARROW therapeutic window
⦁ acute management phase = 0.8-1.2
⦁ maintenance therapy level = 0.6-0.7
- requires constant blood level monitoring

  • renal clearance of lithium is reduced by about 25% with diuretics (loops + thiazides will therefore increase lithium levels, as renal clearance of lithium is reduced with them)**
  • loop diuretics (Lasix) + thiazide diuretics (HCTZ) + NSAIDS (Ibuprofen + indomethacin) = increase lithium levels

COMMON SE = TREMOR - counter this with beta blocker

OTHER SE
⦁	decreased thyroid function (hypothyroidism)
⦁	polydipsia
⦁	polyuria
⦁	edema
⦁	weight gain

Lithium is taken orally and is rapidly absorbed. Is NOT metabolized by the liver. Is excreted almost exclusively by the kidneys

NARROW THERAPEUTIC WINDOW –> require close serum levels - monitor every 4-8 weeks**

Patients with ESRD or patients who are on medications such as loop diuretics, thiazides, NSAIDS and ACEI ===> prevents lithium from being properly eliminated –> easy to overdose on lithium

Causes kidney damage + thyroid dysfunction - so have to monitor kidneys + thyroid often
LABS
⦁	BUN, Creatinine
⦁	Thyroid function q6m
⦁	Lithium levels

levels should be drawn 12 hours after dosing
- lots of cardiac rhythm disturbances, and lots of drug interactions

end-stage renal disease (ESRD) which is a strict contraindication for the use of lithium. Lithium can be used in both the acute manic and depressive stages of bipolar disorder but has a narrow therapeutic range and should not be used in patients with impaired renal function.

Lamotrigine is a second-line agent for the treatment of depressive symptoms of bipolar II disorder and is the only agent listed aside from lithium which is used in the depressive stage. Also, Lamotrigine is now the drug of choice in all 3 trimesters of pregnant patients with bipolar disorder, although, one must take special care during the first trimester.

Common side effects of lithium include:
⦁ Weight gain********(hypothyroidism)
⦁ Impaired memory
⦁ Poor concentration
⦁ Confusion
⦁ Mental slowness (hypothyroidism)
⦁ Hand tremor or tremors******* (seizures, tremor, headache, sedation)
⦁ Sedation or lethargy*******
⦁ Impaired coordination (hypothyroidism)
⦁ Nausea, vomiting, or diarrhea*********
⦁ Hair loss (hypothyroidism)
⦁ Acne
⦁ Excessive thirst and dry mouth******* (polydipsia)
⦁ Excessive urination****** (polyuria)
⦁ Decreased thyroid function (which can be treated with thyroid hormone)******
⦁  Edema
⦁  Heart Block** - 1st degree and complete heart block, along with other arrhythmias
⦁  hyperparathyroidism (Hypercalcemia)

Lithium blocks ADH from binding to its receptor in the kidneys –> prevents you from reabsorbing water –> polyuria –> polydipsia / dry mouth
- water becomes very dilute, but plasma osmolality is very concentrated (dehydrated) which triggers thirst
= NEPHROGENIC DIABETES INSIPIDUS

Lithium also blocks TSH from binding to its receptor –> low levels of T3/T4 –> HYPOTHYROIDISM –>
⦁ weight gain
⦁ cold sensitivity
⦁ mental slowness
⦁ constipation
⦁ bradycardia
- can result in goiter (hypertrophy / hyperplasia in an effort to release more thyroid hormone)

**Lithium also causes LEUKOCYTOSIS (increased WBC count)

**NOT SAFE DURING PREGNANCY = increases risk for congenital heart defects = EBSTEIN’S ANOMALY - tricuspid valves are located lower than normal - into the right ventricle

If LITHIUM TOXICITY occurs = can result in acute kidney failure as well as severe neurological symptoms, such as : ataxia, confusion, dysarthria (disorganized speech), coma and death

Adverse effects of lithium include tremor, edema, heart block, hypothyroidism, teratogenesis, and nephrogenic diabetes insipidus. It is diagnosed by a lack of urine osmolality change with water deprivation. The normal response to dehydration is to concentrate urine, causing urine osmolality to increase and stabilize above 280 mOsm/kg. Patients with diabetes insipidus will have an increase in osmolality of less than 30 mOsm/kg per hour for at least 3 hours.

Teratogenesis*** (harmful to fetus!!!!)
Nephrogenic diabetes insipidus (polyuria / polydipsia / dry mouth - thirst)

In patients undergoing pharmacotherapy for bipolar disorder and later present with thirst and polydipsia, primary polydipsia and nephrogenic diabetes insipidus secondary to lithium may be the cause. If urine osmolality does not improve with water restriction, the most likely diagnosis is diabetes insipidus.

69
Q

AUTISM SPECTRUM DISORDER

A

Autism - meaning self = condition in which someone is removed from social interaction and communication, leaving them alone or isolated

  • 1/68 children
  • 4x more common in males

ETIOLOGY = unclear; both genetic & non-genetic factors present

  • no consistent psychopathologic pattern has been reported in parents of autistic children
  • 90% concordance in monozygotic twins**

AUTISM is widely recognized as a NEURODEVELOPMENTAL DISORDER that affects the functioning of the brain
⦁ not bad parenting!
⦁ not a behavioral / emotional / conduct disorder
⦁ no medical tests to diagnose autism

Spectrum of developmental disorders, probably linked to a combination of prenatal viral exposure, immune system abnormalities and/or genetic factors

CLINICAL MANIFESTATIONS

1) Primary Signs
⦁ Social interaction difficulties - significant emotional discomfort or detachment (avoid eye contact, no response to cuddling or affection)
- no social reciprocity (ex: prefers to be alone)
- no joint attention (ex: doesn’t show parents toy, doesn’t show interest or amusement in an object with parent)

  • hard time developing / maintaining friends

⦁ Impaired communication - either inability to communicate or has the ability to communicate but chooses not to in social settings. Difficulty understanding what is not explicitly stated (metaphors, humor, sarcasm, etc)

  • difficulty with nonverbal communication / cues - has difficulty using or interpreting nonverbal cues (ex: won’t put arms out when they want to be picked up, or can’t tell that parent is upset with them when they frown / cross their arms)

⦁ Restrictive / Repetitive Behaviors

  • lining up toys
  • flapping hands
  • imitating words or phrases
  • fixed on certain routines (route to school, time schedule)
  • restrictive thinking - get fixated on certain subjects and will know everything about that (ex: trains)

2) Other Signs
⦁ persistent failure to develop social relationships
⦁ failure to show preference to parents over other adults
⦁ unusual sensitivity to visual, auditory or olfactory stimuli
⦁ unusual attachments to ordinary objects
⦁ savantism (unusual talents - remembering birthdays)

Children with autism spectrum disorder are sometimes savants, children with extraordinary skills not exhibited by most persons.

Intellectual disability is MORE COMMON in autism than savantism.

  • each child will have a unique spectrum of symptoms

DSM-5 AUTISM

1) social interaction and communication deficits
2) restrictive or repetitive behaviors / interests / activities

Male : Female = 4:1
Boys are more likely to have autism spectrum disorder.

There is a/an INCREASED HEAD / BRAIN SIZE in children with autism spectrum disorders.

CLASSIC AUTISTIC DISORDER
⦁ Very limited emotional connection with anyone, and they are very into their own world.
⦁ They want everything to be the same all of the time
⦁ Can be deeply affected by noises, bright lights and smells.
⦁ Generally considered to be low functioning

KEY DIAGNOSTIC FACTORS OF AUTISM
⦁ Severe deficits in social responsiveness and interpersonal relationships
⦁ Abnormal speech and language development
⦁ Verbal and nonverbal communication impairment
⦁ Repetitive, rigid, or stereotyped interests or behaviors

onset = before age 3**

Severe deficits in reciprocal social interaction (huge emotional toll on parents)

(First year of life)
⦁ Delayed or absent social smile*
⦁ Failure to anticipate interaction with parents
⦁ Lack of attention to parent’s face

(Toddlers)
⦁ Deficiencies in imitative play
⦁ Lack of interest in interactions with others
⦁ Language development delay

COMMUNICATION

  • avoid eye contact
  • act as if deaf
  • develop language, then abruptly stop talking
  • fail to use spoken language without compensating by gesture

SOCIAL RELATIONSHIPS

  • act as if unaware of the coming + going of others
  • are inaccessible - as if in a shell
  • fail to seek comfort
  • fail to develop relationships with peers
  • have problems seeing things from another person’s perspective, leaving the child unable to predict or understand other people’s actions
  • may physically attack and injure others without provocation

EXPLORATION OF ENVIRONMENT

  • remain fixated on single item or activity
  • repetitive actions like rocking or hand-flapping
  • sniff or lick toys or put unusual objects in mouth - or need toys to chew on
  • well beyond age of teething
  • show no sensitivity to burns or bruises, and engage in self-mutilation
  • are intensely preoccupied with a single subject, activity or gesture
  • show distress over change
  • insist on routine or rituals with no purpose
  • lack fear

COMPLICATIONS OF AUTISM
⦁ 30% eventually develop seizure disorder*****
⦁ Those with higher cognitive abilities may become depressed as they become aware of their deficits
⦁ Some adults live in 24-hour care facilities or require immense community support

Children with autism spectrum disorder (ASD) are at an INCREASED RISK TO DEVELOP EPILEPSY with a comorbidity of about 20%**

DSM-5 AUTISM SPECTRUM DISORDER
- No longer has categories for Asperger’s or pervasive developmental disorder not otherwise specified

  • DSM-5 Autism Spectrum Disorder and specify if:
    ⦁ With or without accompanying intellectual impairment
    ⦁ With or without accompanying language impairment
    ⦁ Associated with a known medical or genetic condition
    ⦁ Associated with another neurodevelopmental, mental or behavioral disorder
    ⦁ With catatonia
  • then rank level of severity by how much support is needed in communication & behavior
    ⦁ LEVEL 1 = requiring support
    ⦁ LEVEL 2 = requiring substantial support
    ⦁ LEVEL 3 = requiring very substantial support

ASPERGER’S SYNDROME

  • have some characteristics of autism, such as difficulty with social interaction and non-verbal communication, however, don’t usually have delays in language or cognitive development, therefore, Asperger’s is sometimes referred to as a “high-functioning form of autism”
  • Pervasive Developmental Disorder (PDD) - along with childhood disintegrative disorder + autism

CHILDHOOD DISINTEGRATIVE DISORDER

  • used to describe LATE ONSET of developmental delays
  • these children developed normally for their age initially, but then seem to lose their social and communicative skills sometime between age 2 and 10
  • Pervasive Developmental Disorder (PDD) - along with asperger’s + autism

Autism disorder symptoms must present in early childhood for a diagnosis to be made.

  • Autism, Aspergers, and Childhood disintegrative disorder = all fall under PDD - Pervasive Developmental Disorders

TREATMENT FOR AUTISM SPECTRUM DISORDER
Autistic children require specialized therapy and special schooling or residential schooling although attempts of integrations are also started.

Special techniques for teaching autistic children and special psychotherapeutic approaches were developed.

Sometimes antipsychotic drugs and antidepressants are used to cope with aggressive behavior and depression or to treat co-morbid psychiatric diagnoses.

Risperidone and aripiprazole are the only medications FDA-approved for use on hyperactivity and irritability associated with autism.

TREATMENT = referral for neuropsychologic testing, behavioral modification strategies, medications

Risperdal + Abilify = only FDA approved meds for hyperactivity / irritability associated with autism

AS A PRIMARY CARE PROVIDER, YOUR JOB WITH AUTISM IS TO SCREEN + REFER

o MCHAT = checklist for Autism in Toddlers (18-24 months = 1.5 - 2 years old)

o STAT = screening tool for autism in toddlers & young children

o surveillance at every visit by asking 3 questions
⦁ Does your child look at you and point when he/she wants to show you something?
⦁ Does your child look when you point to something?
⦁ Does your child use imagination to pretend play?

70
Q

ASPERGER’S SYNDROME

A
  • have some characteristics of autism, such as difficulty with social interaction and non-verbal communication, however, don’t usually have delays in language or cognitive development, therefore, Asperger’s is sometimes referred to as a “high-functioning form of autism”

Asperger disorder is a pervasive developmental disorder that differs from autism in that the patients are more communicative, appear more socially aware, and do not have language impairments found in autism. They do have social impairments, repetitive behaviors, and sometimes obsessional interests. Early language development is not delayed in this condition. These children will grow up to have average or above average IQs.

As a milder autism spectrum disorder, Asperger syndrome differs from other autism spectrum disorders by relatively NORMAL language and intelligence.

  • considered under Pervasive Developmental Disorder (PDD) - along with childhood disintegrative disorder + autism

Asperger syndrome has been reclassified in the diagnostic and statistical manual of mental disorders-V and is no longer a separate disease, considered now a part of the autism spectrum disorder.

71
Q

CHILDHOOD DISINTEGRATIVE DISORDER

A

used to describe LATE ONSET of developmental delays

these children developed normally for their age initially, but then seem to lose their social and communicative skills sometime between age 2 and 10

  • considered a Pervasive Developmental Disorder (PDD) - along with asperger’s + autism
72
Q

PREMENSTRUAL DYSPHORIC DISORDER (PMDD)

A

PMDD is a more severe, debilitating form of premenstrual syndrome (PMS).

In the late luteal phase following ovulation, patients with PMDD display symptoms of depression (anxiety, anger, irritability, lack of interest in relationships and activities, decreased energy, sadness, hopelessness, difficulty with concentration and sleep).

Consequently, patients with PMDD are at an increased risk of substance abuse, eating disorders, and suicide.

Physical symptoms include headaches, muscle aches, abdominal bloating, and breast tenderness.

Diagnosis of premenstrual dysphoric disorder via the DSM-V requires documentation of AT LEAST 2 consecutive ovulation cycles. Symptoms must markedly interfere with daily activity and follow a pattern consistent with menstrual cycles.

A healthy lifestyle is the first step in managing premenstrual dysphoric disorder. The front line pharmacological treatment is an SSRI such as fluvoxamine. Adjunct cognitive behavioral therapy is shown to be an effective combination against mood symptoms associated with PMDD. Diuretics and NSAIDS are also sometimes given for symptomatic relief.

(PMDD) is a severe and disabling form of premenstrual syndrome (PMS) characterized by a “cluster of affective, behavioral and somatic symptoms” that recur monthly during the luteal phase of the menstrual cycle and result in impairment in function or clinically significant distress.

PMDD is a depressive disorder that often follows ovulation and remits within a few days of menses.

Symptoms associated with premenstrual dysphoric disorder typically begin in the LUTEAL PHASE of the menstrual cycle = 1-2 weeks before menses, is relieved within 2-3 days of menses onset

Mood symptoms are most dominant in premenstrual dysphoric disorder.

It is hypothesized that those who suffer from PMDD are more sensitive to normal levels of hormone fluctuations.

To be diagnosed with PMDD, at least 5 / 11 qualifying symptoms must be present during MOST menstrual cycles throughout the year.

The physical symptoms of PMDD include abdominal bloating, breast tenderness, and headache.

The emotional symptoms of PMDD are anxiety, irritability, mood lability, and perceived loss of control.

PMDD is a more severe, debilitating form of premenstrual syndrome (PMS). In the late luteal phase following ovulation, patients with PMDD display symptoms of depression (anxiety, anger, irritability, lack of interest in relationships and activities, decreased energy, sadness, hopelessness, difficulty with concentration and sleep).

Patients with PMDD are at an increased risk of substance abuse, eating disorders, and suicide.

Physical symptoms include head and muscle aches, abdominal bloating, and breast tenderness.

Diagnosis of premenstrual dysphoric disorder via the DSM-V requires documentation of at least two consecutive ovulation cycles. Symptoms must markedly interfere with daily activity and follow a pattern consistent with menstrual cycles.

A healthy lifestyle is the first step in managing premenstrual dysphoric disoder. The front line pharmacological treatment is a selective serotonin re-uptake inhibitor such as fluvoxamine. Adjunct cognitive behavioral therapy is shown to be an effective combination against mood symptoms associated with PMDD. Diuretics and nonsteroidal anti-inflammatory drugs are also sometimes given for symptomatic relief.

TREATMENT

**1st line TREATMENT = SSRIs***

SSRIs do not need to be taken everyday to be effective for women suffering from PMDD

  • Drosperinone-containing OCPs (induce anovulation) for PMDD = progestin analog = in Yasmin + Angeliq
  • can also use GnRH agonists

PMDD = severe PMS with functional impairment

73
Q

TYPICAL ANTIPSYCHOTICS

A

d

74
Q

ATYPICAL ANTIPSYCHOTICS

A

d

75
Q

TOBACCO USE/DEPENDENCE

A
  • tobacco = major cause of pulmonary, cardiac and cancer deaths (most modifiable risk factor)

one of the leading causes of preventable disease and death worldwide

cigarette smoke has over 4000 toxins - damages endothelial cells —> INFLAMMATION

Inflammation of the vasculature leads to increased risk of MI, Stroke, and PVD (peripheral vascular disease - causes pain in the legs)

Tobacco also causes pulmonary problems - as the toxins deposit in the lungs –> damages lung tissue => more likely to get infected

Associated with Cancers of the
⦁	mouth
⦁	throat
⦁	lungs
⦁	bladder
⦁	pancreas
⦁	uterus

Nicotine = fat soluble molecule that releases pleasurable effects. Nicotine = considered responsible for high rates of dependence and addiction

  • Some of Nicotine gets burned off with heat, other is inhaled through smoke; therefore, patients are able to self-titrate the amount of Nicotine they inhale by smoking more frequently, inhaling more deeply, or inhaling for longer amounts of time

Once in the bloodstream, Nicotine binds to Nicotinic Acetylcholine Receptor (found throughout brain and body). Once Nicotine binds to the receptor, NTs such as Dopamine, Acetylcholine and Glutamate are released
- this is why nicotine is considered an acetylcholine agonist

76
Q

TOBACCO WITHDRAWAL

A
⦁	restlessness
⦁	anxiety
⦁	irritability
⦁	sleep abnormalities
⦁	depression
⦁	nicotine craving
77
Q

ALCOHOL EFFECTS / ABUSE

A

Men are more likely to be diagnosed with alcoholism.

Behavioral / mood effects
⦁ disinhibition
⦁ depression: slurred speech, impaired judgment, somnolence, ataxia
⦁ labile mood: erratic behavior, aggression

Psychological effects
⦁ prolonged reaction time
⦁ muscular incoordination
⦁ facial flushing

Chronic Effects
⦁ WERNICKE’S ENCEPHALOPATHY = triad of ATAXIA, CONFUSION & OCULOMOTOR PALSY (due to thiamine/B1 deficiency

⦁ KORSAKOFF SYNDROME = Amnesia (both retrograde + antegrade)

⦁	Hepatomegaly
⦁	palmar erythema
⦁	cirrhosis
⦁	Dupuytren's contractures
⦁	Gynecomastia
⦁	Testicular atrophy
⦁	Increased MCV (mean corpuscular volume)

Serum γ-glutamyl transferase levels are a sensitive test for alcohol use

PATHOPHYSIOLOGY
Ethanol = GABA agonist (gaba = inhibitory NT)
Ethanol = Glutamate antagonist (blocks Glutamate = excitatory NT)
Ethanol also activates opioid receptors –> releases endorphins –> release of dopamine + serotonin

Ethanol also activates the nucleus accumbens and amygdala (pleasure centers of brain) —> ethanol produces pleasant or rewarding feelings, like euphoria

Ethanol also affects the Cerebral Cortex - thought processing center of the brain. Ethanol slows everything down - making it more difficult to think and speak

Ethanol slows behavioral inhibition centers : Prefrontal Cortex - makes people more relaxed and less self-conscious

Ethanol affects Cerebellum - responsible for movement / coordination / balance - lose coordination = hard to walk / drive, etc.

Ethanol affects Hypothalamus + Pituitary Gland - which regulates mood and hormones; Ethanol increases sexual arousal but decreases ability to engage in sex

Ethanol affects Medulla - automatic functions of breathing, consciousness and body temperature

DRINKING TOO MUCH
⦁ binge drinking for men = 5+ drinks consumed on one occasion (within 2-3 hrs)
⦁ binge drinking for women = 4+ drinks consumed on one occasion (within 2-3 hrs)
⦁ 15+ drinks/wk for men or 8+ drinks/wk for women
⦁ ANY alcohol use by a pregnant women, or ANY alcohol use of those under 21

2/3 of victims who suffered violence by an intimate partner reported that alcohol had been a factor. Among spouse victims, 3/4 incidence involved someone who had been drinking

CAGE QUESTIONNAIRE
- It is commonly used in the medical setting and has been validated as a sensitive and specific tool for detecting problem drinking (primarily in men)

2+ indicates a likely diagnosis of alcohol dependence

C = Have you ever felt the need to Cut down on your drinking?
A = Have you ever felt Annoyed by criticism of your drinking?
G = Have you ever had Guilty feelings about your drinking?
E = Do you ever take a morning Eye-opener? (a drink first thing in the morning to steady your nerves or get rid of a hangover)

ALCOHOL USE DISORDER = 2+ of the following:

1) consuming more alcohol than intended
2) inability to cut down on alcohol usage
3) alcohol use takes up a lot of time
4) cravings to use alcohol
5) alcohol affects responsibilities
6) using alcohol despite causing interpersonal problems
7) giving up important activities for alcohol
8) using alcohol in physically dangerous situations
9) using alcohol even if it worsens a problem
10) becoming tolerant to alcohol
11) feeling withdrawal symptoms from alcohol

  • having 2-3 = mild alcohol use disorder
  • having 4-5 = moderate alcohol use disorder
  • having 6+ of the above = severe alcohol use disorder

ALCOHOL ABUSE = associated 1+ of the following, occurring in a 12-month period:
⦁ Failure to fulfill work, school or social obligations
⦁ Recurrent substance use in physically hazardous situations
⦁ Recurrent legal problems related to substance use
⦁ Continued use despite alcohol-related social or interpersonal problems

ALCOHOL DEPENDENCE (“alcoholism”): a maladaptive patterns of use associated with 3+ of the following, occurring at any time in the same 12-month period:
⦁ Tolerance
⦁ Withdrawal
⦁ Substance taken in larger quantity than intended
⦁ Persistent desire to cut down or control use
⦁ Time is spent obtaining, using, or recovering from the substance
⦁ Social, occupational or recreational tasks are sacrificed
⦁ Use continues despite physical and psychosocial problems

MEDICAL MORBIDIDTY OF ALCOHOL ABUSE
Alcohol abuse associated with greater risk of:
⦁ HTN, cardiomyopathy
⦁ Hepatitis, cirrhosis (½ the cases in U.S. Secondary to alcohol), pancreatitis
⦁ TB, Pneumonia
⦁ Psych problems: anxiety, depression & eating disorders
⦁ Cancers of the stomach, mouth, larynx, breast and esophagus

2 main causes of pancreatitis = gallstones & alcohol

FOR ADOLESCENTS & COLLEGE STUDENTS = CRAFFT screening tool
o Car - have you ever ridden in a car driven by someone (or yourself) who was “high” or had been using alcohol or drugs

o Relax - do you ever use alcohol or drugs to relax / feel better about yourself / fit in

o Alone - do you ever use alcohol or drugs while you are alone

o Forget - do you ever forget things you did while using alcohol or drugs

o Friends/Family - do your family or friends ever tell you to cut down on drinking or drugs

o Trouble - have you ever gotten into trouble while using alcohol or drugs

2+ CRAFFT = indicate problem use, abuse, or dependence
CRAFFT performs better than CAGE for adolescent/college age group

Moderate drinking:
⦁ Men: 2 drinks or less a day
⦁ Women: 1 drink or less a day

Heavy drinking:
⦁ Men: > 14 drinks/week, or 4 drinks/occasion
⦁ Women: > 7 drinks/week or 3 drinks/occasion

Binge drinking:
⦁ Men: 5+ drinks in a row
⦁ Women: 4+ drinks in a row

1 drink = 1.5 oz of a shot, 5 oz of wine, 12 oz of beer

Ethyl Alcohol or Ethanol
Absorption: 10% consumed alcohol absorbed in the stomach, remainder from the small intestines

When concentration of alcohol in stomach becomes too high—mucus secretion and pyloric valve closure results in slowed absorption

Pylorospasm results in VOMITING

Metabolism:
90% metabolized in liver through oxidation
Metabolized by two enzymes:
Alcohol dehydrogenase (ADH) catalyzes conversion of alcohol into acetaldehyde, which is toxic
Aldehyde dehydrogenase(ALDH) catalyzes conversion of acetaldehyde into acetate

Alcohol (ADH) –> Acetaldehyde (ALDH) –> Acetate

EFFECTS OF ALCOHOL ON THE BRAIN
⦁ CNS depression much like benzodiazepines
⦁ Relatively mild levels: thought, judgment and restraint are loosened
⦁ Increasing levels: voluntary muscle dysfunction and entire motor area of the brain depressed
⦁ Yet increasing levels—confusion, stupor, coma and finally primitive centers that control breathing and heart rate are affected and can result in death either secondary to direct respiratory depression or aspiration of vomitus

EFFECTS OF ALCOHOL ON THE LIVER
Metabolism of alcohol leads to chemical attack on the liver (it is unknown if damage is caused by acetaldehyde or other metabolites)

Even after all alcohol intake has stopped and all alcohol has been metabolized, the processes that damage liver cells may continue for weeks to months

Three patterns of hepatocellular injury:
⦁ Fatty liver - reversible
⦁ Alcoholic hepatitis - reversible
⦁ Cirrhosis (rate is 10-15% of all alcoholics) - irreversible, and can lead to HCC

see Mallory Bodies
cirrhosis = scarred/shrunken liver

Cirrhosis –> Portal hypertension → abdominal varices (caput medusa) and esophageal varices & hemorrhoids

Alcohol use can cause dilated cardiomyopathy, arrhythmias, stroke, liver issues - steatosis / steatohepatitis / fibrosis / cirrhosis, pancreatitis
- also associated with certain cancers - mouth, esophagus, throat, liver, and breast

Alcoholism can cause (disease) pancreatitis, which presents with severe epigastric pain radiating through to the back, with raised serum amylase and lipase.

  • can also lead to vitamin deficiencies
  • ** Wernicke-Korsakoff Syndrome - due to thiamine deficiency —> leads to ataxia (loss of coordination in gait / voluntary muscle movements), vision problems (ocular abnormalities), and impaired memory (amnesia)

Vitamin B1 (thiamine) is the most common vitamin deficiency associated with alcoholism.

WERNICKE-KORSAKOFF SYNDROME
Occurs in persons who have been drinking heavily for many years—rare to see in persons younger then 35YO: Caused by thiamine deficiency due to poor nutrition/malabsorption

o WERNICKE’S ENCEPHALOPATHY = ACUTE SYMPTOMS which are completely reversible when treated with high dose thiamine
⦁ gait ataxia/vestibular dysfunction, confusion and ocular abnormalities

o KORSAKOFF’S SYNDROME = CHRONIC CONDITION - only 20% of patients recover - can be treated with po thiamine
⦁ impaired recent memory and anterograde amnesia (can’t make new memories)

GIVE THIAMINE BEFORE GIVING GLUCOSE**

Wernicke's = abnormal gait, balance, confusion, vision
Korsakoff = memory

TREATMENT FOR ALCOHOL DEPENDENCE
⦁ Naltrexone
⦁ Acomprosate (Campral)
⦁ Disulfiram (Antabuse)

NALTREXONE = mu-opioid receptor antagonist = blocks the euphoric effects of alcohol and blocks feelings of intoxication
- this can help patients reduce heavy drinking enough to where they stay motivated to continue treatment and avoid relapse

ACOMPROSATE = can be administered immediately following alcohol withdrawal - can help restore some GABA and glutamate pathways that are disrupted by alcohol

DISULFIRAM = inhibits the enzyme acetaldehyde dehydrogenase, which converts acetaldehyde to acetate. So by inhibiting acetaldehyde dehydrogenase, acetaldehyde builds up, causing a HANGOVER FEELING immediately after alcohol is consumed –> decreases likelihood that person with drink

Disulfiram is a drug that treats alcohol addiction by inhibiting acetaldehyde dehydrogenase.

78
Q

ALCOHOL WITHDRAWAL

A
MILD SYMPTOMS OF ALCOHOL WITHDRAWAL
⦁	Insomnia
⦁	Tremors
⦁	Mild anxiety
⦁	GI upset/anorexia - Nausea / vomiting
⦁	Headache
⦁	Diaphoresis
⦁	Palpitations
  • ***mostly tachycardia, hypertension + tremor
  • fever, agitation, diaphoresis*****

ALCOHOL WITHDRAWAL SYMPTOMS

  • anxiety
  • depression
  • irritability
  • fatigue
  • tremors
  • palpitations
  • clammy skin
  • dilated pupils
  • sweating
  • headaches
  • difficulty sleeping
  • vomiting
  • seizures
  • mild symptoms begin within 6 hrs of cessation of drinking, and resolve within 24-48 hrs

WITHDRAWAL SEIZURES

  • occur within 48 hrs after last drink
  • tonic-clonic seizures - 3% of chronic alcoholics
  • TREATMENT = BENZODIAZEPINES**
ALCOHOLIC HALLUCINOSIS
Develops within 12-24 hrs. of last drink
Resolves with 24-48 hrs. 
NOT delirium tremens
Usually visual; but can be auditory or tactile

⦁ 6-24 hours = Increased CNS activity - tremor, insomnia, nausea, vomiting, anxiety, tachycardia, hypertension, tachypnea

⦁ 6-48 hours = seizures, hyperreflexia

⦁ 2-5 days = DELIRIUM TREMENS = altered sensorium: visual or auditory hallucinations (fornication - “something crawling on me” - especially at night), altered mental status, seizures, coma death. Often occurs when hospitalized for a non-related illness and unable to drink

DELIRIUM TREMENS
5% of patients who withdraw from alcohol develop this
Begin 48-96 hrs. after last drink
Can last 1-5 days

Benzodiazepines are the 1st line agents for the treatment of delirium tremens in alcoholics.

⦁	Hallucinations (visual + maybe even tactile)
⦁	Disorientation
⦁	Tachycardia
⦁	Hypertension
⦁	Low grade fever / high fever
⦁	Agitation
⦁	Diaphoresis
Risk factors:
⦁	History of sustained drinking
⦁	History of previous DTs
⦁	Age > 30
⦁	Presence of concurrent illness

MORTALITY RATE OF 5%** occurs late in diagnosis

THE FOLLOWING AGENTS COMPLICATE ALCOHOL WITHDRAWAL
⦁	Ethanol
⦁	Antipsychotics
⦁	Anticonvulsants
⦁	Central acting alpha-2 agonists
⦁	Beta-blockers
⦁	Baclofen 

Place patient in quiet, protective environment
May need mechanical restraint
Most patients tend to be dehydrated w/ hypokalemia—replace with IV fluids and KCL

give Thiamine 100mg IV or IM BEFORE glucose

⦁ Minimal: (no disorientation or hallucinations) = Thiamine and supportive care

⦁ Mild: Thiamine + supportive care, Medications to reduce symptoms + monitoring

⦁ Moderate and Severe: Thiamin + Supportive care, Hourly monitoring, especially respiratory rate, Medication—benzodiazepines

1ST LINE TX FOR DELIRIUM TREMENS = BENZOS***

BENZODIAZEPINES
Diazepam (Valium), Chlordiazepoxide (Librium) and lorazepam (Ativan) are used
Can give orally or IV

Refractory DTs (Delirium Tremens)—Add phenobarbitol or Propofol

Antipsychotics lower seizure threshold—DO NOT USE WITH ALCOHOL OR DURING ALCOHOL WITHDRAWAL

Seizures:
If status epilepticus use phenobarbitol
DO NOT USE carbemazepine**

79
Q

BENZODIAZEPINE EFFECTS

A

Behavioral / mood effects
⦁ disinhibition
⦁ depression: slurred speech, impaired judgment, somnolence, ataxia
⦁ labile mood: erratic behavior, aggression

INTOXICATION TX = FLUMAZENIL (ROMAZICON)

80
Q

COCAINE

A

PSYCHOACTIVE STIMULANT

  • induces euphoria
  • reduces inhibitions

Studies show that WOMEN have much higher rates of cocaine addiction, especially if they inject the drug instead of snorting or smoking it.

A person who is using increased amounts of cocaine over a longer time period than intended likely has cocaine dependence.

A person with consistent cravings and urges to use cocaine, even in inappropriate settings, is said to have cocaine dependence.

MOA
Blocks presynaptic reuptake pumps for dopamine, norepinephrine and serotonin
Also blocks voltage-gated membrane sodium ion channels

Cocaine blocks reuptake receptors on presynaptic axon terminals for the neurotransmitters dopamine, norepinephrine, and serotonin.

Increased level of the neurotransmitter norepinephrine cause the physical “high” or feeling of hyper-stimulation.

***Cocaine causes a dopamine flood –> downregulates amount of dopamine receptors available in the brain because there’s too much dopamine –> decreased effect of cocaine –> so have to increase amount of cocaine used over time in order to feel same euphoric effects

Cocaine increases the release of neurotransmitters, as and also blocks reuptake receptor proteins, therefore the NTs: Dopamine / NE / Serotonin are kept in synapse longer –> increased effects

Elevated / euphoric mood
Restlessness
Pressured speech

PSYCHOSIS: mild = anxiety
can result in paranoia, aggression, agitation, hallucinations (tactile, auditory)

TREAT COCAINE INTOXICATION WITH BENZODIAZEPINES, Neuroleptics, and BP reduction

SYMPTOMS = Sympathetic Stimulation
⦁ sweating
⦁ tachycardia
⦁ hypertension
⦁ pupil dilation****
⦁ peripheral vasoconstriction
⦁ MI
- compulsive / stereotyped behavior: picking at skin
- rhabdomyolysis

Tactile hallucinations are often seen in cocaine abusers.

COCAINE INTOXICATION
Intended effects: increased energy, alertness, sociability; elation or euphoria; decreased fatigue, decreased need for sleep and appetite; “total body orgasm”

Adverse effects: anxiety, irritability, panic attacks, paranoia, grandiosity, impairment in judgment, psychotic symptoms

Physiological effects: tachycardia, pupil dilation, diaphoresis, nausea, HTN

CV: arterial vasoconstriction and enhanced thrombus formation, causes tachycardia and HTN

CNS: agitation, seizures, HA, coma, intracranial hemorrhage

Lungs:
When smoked can cause angioedema and pharyngeal burns
Passive cocaine exposure: those in close proximity to users of inhalational cocaine can present w/ toxicity

INITIAL LABS WITH COCAINE
fingerstick glucose
acetaminophen &amp; salicylate levels
EKG
pregnancy test in women of childbearing age
others as indicated

SLOWEST TO FASTEST
- ingestion –> insufflation (snorting) –> smoking –> injection (fastest!)

Injecting cocaine leads to much higher rates of dependence than other routes of administration.

TREATMENT
⦁ CBT
- has been shown to be the most effective long-term psychotherapy for cocaine addiction.

⦁ Treat cocaine intoxication with BENZODIAZEPINES, Neuroleptics, and BP reduction

81
Q

COCAINE WITHDRAWAL

A
  • craving
  • dysphoria
  • agitation
  • anxiety
  • diaphoresis
  • hypersomnia**
  • increased appetite**
  • nightmares
  • suicide ideation**
  • headache
  • irritability
  • extreme fatigue
  • muscle cramps

Fatigue, reduced concentration, suicidal ideation, and the sensation of insects crawling over the skin are symptoms of cocaine withdrawal.

82
Q

OPIOID USE / DEPENDENCE

A
  • includes heroin, oxycodone, morphine, meperidine, and codeine
CLINICAL MANIFESTATIONS - OPIOID INTOXICATION
⦁  Euphoria
⦁  Sedation
⦁  drowsiness
⦁  impaired social function
⦁  impaired memory
⦁  slow / slurred speech
⦁  may develop N/V / seizures / coma
PHYSICAL EXAM FINDINGS
⦁  pupillary constriction*****
⦁  respiratory depression*****
⦁  may develop Biot's Breathing (groups of quick, shallow inspirations, followed by regular or irregular periods of apnea)
⦁  bradycardia****
⦁  hypotension****
⦁  N/V
⦁  flushing
⦁  hypothermia

**Patients on long-term narcotics may develop constipation - opioid receptors in GI tract reduce GI motility

TREATMENT

  • acute intoxication = NALOXONE (NARCAN) - used in acute intoxication or overdose to reverse effects of opioids
  • onset of Narcan = about 2 minutes IV (5 minutes IM) - most commonly used in patients with respiratory depression

LONG-TERM MANAGEMENT OF DEPENDENCE / DETOXIFICATION
⦁ Methadone maintenance program
⦁ Suboxone therapy (Buprenorphine + Naloxone)

Buprenorphine CANNOT be given to pregnant women
Methadone CAN be given to pregnant women

83
Q

OPIOID WITHDRAWAL

A
⦁  Lacrimation / rhinorrhea****
⦁  hypertension
⦁  pruritus
⦁  tachycardia
⦁  N/V
⦁  abdominal cramps
⦁  diarrhea
⦁  sweating
⦁  yawning
⦁  piloerections**** (goosebumps)
⦁  pupil dilation****** (mydriasis)
⦁  flu-like symptoms: rhinorrhea, joint pain, myalgia

TREATMENT

  • symptomatic control = CLONIDINE - decreases sympathetic symptoms
  • Loperamide - for diarrhea
  • NSAIDS for joint / muscle pain/cramps
  • Suboxone = Buprenorphine + Naloxone
  • Methadone tapering
  • Benzos may help with some cases of mild withdrawal
84
Q

INSOMNIA

A
  • Difficulty initiating or maintaining sleep, or waking up early in the AM without being able to return to sleep

INSOMNIA = trouble falling asleep AT LEAST 3X/WEEK

  • Acute Insomnia = < 1 month
  • Chronic Insomnia = > 1 month

Insomnia affects both quantity and quality of sleep

MOA
- have higher levels of cortisol –> receptors are more sensitive to cortisol –> wake up easier

  • Insomnia also associated with reduced levels of estrogen + progesterone (menopause)

commonly ppl self-medicate with alcohol or benzodiazepines

Insomnia = common symptom of hyperthyroidism

SYMPTOMS
⦁	daytime sleepiness
⦁	fatigue/malaise
⦁	irritability
⦁	poor attention/concentration
⦁	anxiety / depression

can lead to professional / personal problems

DIAGNOSIS
A sleep study, recording activity while sleeping, is the most common way to evaluate a patient for sleeping disorders such as insomnia.

TREATMENT FOR INSOMNIA

NON-PHARM TREATMENT FOR INSOMNIA
⦁	Good sleep hygiene
⦁	Avoid any stimulants
⦁	Go to bed only when sleepy
⦁	Relaxation therapy
⦁	Cognitive therapy

Exercising regularly at least four to five hours prior to bedtime is an example of sleep hygiene, which can help treat insomnia.

BENZODIAZEPINES
⦁	Alprazolam (Xanax)
⦁	Estazolam (ProSom)
⦁	Flurazepam (Dalmane)
⦁	Lorazepam (Ativan)
⦁	Quazepam (Doral)
⦁	Temazepam (Restoril)
⦁	Triazolam (Halcion)

BZD MOA

  • Selectively acts on polysynaptic neuronal pathways throughout the CNS
  • Developed to improve the safety profile of barbiturate-type compounds
  • Enhance the effects of GABA (an inhibitory neurotransmitter) in the CNS (sleep hormone)
  • Treats Insomnia- Facilitate the effects of GABA in the ascending reticular activating system

BZD SHORT/INTERMEDIATE/LONG ACTING DRUGS
Short acting (need to TRY harder - Halcyon)
⦁ Triazolam (Halcion)

Intermediate acting (Test = you are intermediate at tests…not good, not bad)
⦁ Temazepam (Restoril)
⦁ Estazolam (ProSom)

Long acting (flu - feel queasy) (dalmation, doral)
⦁ Flurazepam (Dalmane)
⦁ Quazepam (Doral)

Adverse events
⦁ Drowsiness
⦁ Impaired motor function
⦁ Prolonged use –> Physical dependency

Benzos prolong stage 2, and decrease stage 3 –> drowsy, don’t wake up feeling as refreshed
- need to taper off BZDs, abrupt d/c –> rebound insomnia

NREM = 4 STAGES
⦁ 1st stage = wake/sleep - light sleep
⦁ 2nd stage = sleep spindles - longest stage; benzodiazepines help prolong stage 2
⦁ 3/4 = deep sleep - restorative - where sleepwalking occurs; decreases with age - slow waves; Benzos decrease stage 3 sleep

INTERACTIONS
⦁ alcohol (caution)
⦁ low-dose contraceptives

CONTRAINDICATIONS
⦁	Acute narrow-angle glaucoma
⦁	Preg X***
⦁	Lactation 
⦁	Abuse potential 

NON-BENZODIAZEPINE RECEPTOR AGONISTS (NBRAs)
short half life - 5 hrs
- also affect GABA like BZDs - but greater receptor specificity of GABA BZ complex
- smaller addiction profile than Benzo’s, but still has dependence potential

NON-BENZODIAZEPINE RECEPTOR AGONIST DRUGS
⦁ Eszopiclone (Lunesta)
⦁ Zolpidem (Ambien)
⦁ Zaleplon (Sonata)

ESZOPICLONE (LUNESTA)
- Good for sleep maintenance - pts who have no trouble falling asleep, but wake up in the middle of the night and can’t go back to bed

MOA = interacts with GABA receptors near BZD receptors
DOSAGE = start at 2mg immediately before bed, can start on 3mg or increase to 3mg to aid in sleep maintenance
ELDERLY = start with 1mg to help fall asleep, increase to 2mg for sleep maintenance

ADVERSE EFFECTS
⦁ headache
⦁ dry mouth
⦁ dizziness

CONTRAINDICATIONS
⦁ hypersensitivity

Pregnancy category C

ZOLPIDEM (AMBIEN)
- helps to initiate sleep

Sleep-onset insomnia, or difficulty falling asleep, is often treated with short-acting sedative-hypnotics, such as zolpidem, on an as-needed basis. They are first-line agents used in conjunction with non-pharmacological options.

MOA = modulates the GABA receptors to suppress neurons
DOSAGE = 5-10mg PO qhs, or ER 6.25-12.5 mg PO qhs
ADVERSE EFFECTS
⦁	morning drowsiness
⦁	hangover
⦁	HA
⦁	**DEPENDENCE** + can cause **PSYCHOTIC EPISODES/PSYCHOSIS** - sleep driving , sleep eating, sleep telephone calls, etc.

CONTRAINDICATIONS
⦁ hypersensitivity

PREG CATEGORY C (just like Lunesta)

ZALEPLON (SONATA)
- helps decrease sleep initiation time, but not good for increasing total sleep time & doesn’t help with maintaining sleep (if you wake up in the middle of the night, won’t help you get back to sleep)

MOA = Interacts with GABA-BZ omega 1 receptor
DOSAGE = Start: 10mg PO qhs; Range 5-20mg qhs

ADVERSE EFFECTS
⦁ back or chest pain
⦁ migraine
⦁ constipation

CONTRAINDICATIONS
⦁ hypersensitivity

PREG CATEGORY C (just like Lunesta + Ambien)

NBRAs & MOOD DISORDERS
- may be possible to combine antidepressant therapy with a sleeping medication

Combining Eszopiclone (Lunesta) and fluoxetine (Prozac) improved both mood and sleep

Another study found that treating insomnia with zolpidem (Ambien), after successful SSRI treatment, improved sleep and daytime functioning

Agents most often prescribed for insomnia in bipolar patients is this class of drugs, such as Eszopiclone (Lunesta), Zaleplon (Sonata), and zolpidem(Ambien).

o ANTI-HISTAMINES
- most commonly used OTC sleep-inducing agents
⦁ Diphenhydramine (Benadryl)

MOA of BENADRYL = unknown, but acts as a CNS depressant
ADVERSE EFFECTS
⦁ excessive daytime drowsiness
⦁ impaired psychomotor function

o ANTI-DEPRESSANTS
⦁ Imipramine (Tofranil) = tertiary TCA
⦁ Amitriptyline hydrochloride (Elavil) = tertiary TCA
⦁ Nortriptyline (Pamelor) = secondary TCA

NEWER AGENTS
⦁ Nefazodone hydrochloride (Serzone)
⦁ Venlafaxine (Effexor) = SNRI

o DOXEPIN (SILENOR)
**only FDA approved TCA for insomnia** (tertiary TCA) = more potent serotonin increase
MOA = increased serotonin &amp; NE
but due to increased NE = increased anticholinergic SE
ADVERSE EFFECTS
⦁	dizziness
⦁	drowsiness
⦁	blurred vision
⦁	constipation

CONTRAINDICATIONS
⦁ glaucoma
⦁ urinary retention

o TRAZODONE (DESYREL) = other antidepressant
MOA = increases serotonin
good for sleep, and little to no anticholinergic effects

Trazodone is an atypical antidepressant that is used more commonly for insomnia.

ADVERSE EFFECTS
⦁ dizziness
⦁ drowsiness

CONTRAINDICATIONS

  • use of MAOIs in last 2 weeks
  • Linezolid or IV Methylene blue

BBW - suicidal thoughts

o AMITRIPTYLINE (ELAVIL) = tertiary TCA
MOA = increases serotonin &amp; NE, more potent serotonin

ADVERSE EFFECTS
⦁ Sedation
⦁ Dizziness
⦁ HA

CONTRAINDICATIONS
⦁ History of MI***
⦁ MAOIs

PREGNANCY CATEGORY C
BBW = SUICIDAL THOUGHTS

o TCA ANTIDEPRESSANTS are frequently used as sleep-promoting agents in doses that are subtherapeutic for depression
- In patients with mood disorders and significant insomnia, these agents may be useful to manage both sleep & mood symptoms

SSRIs, SNRIs, and older MAOIs tend to cause insomnia
- their activating effects may be helpful in depressed patients with fatigue or hypersomnia, but their use in patients with depression & insomnia by worsen the sleep disturbance and lead to the need of hypnotics or sedating antidepressants specifically for sleep

o MELATONIN AGONISTS
⦁ Ramelteon (Rozerem)

MOA = Potent, selective agonist of melatonin receptors MT1 and MT2 within the suprachiasmic nucleus of the hypothalamus

Melatonin = produced in the pineal gland - helps set sleep/wake cycles
Melatonin agonists help stimulate melatonin receptors - helps you go to sleep

Dosage
⦁	8mg daily within 30 min of bedtime
Adverse Events
⦁	Somnolence
⦁	HA
⦁	Fatigue 

CONTRAINDICATIONS
⦁ Fluvoxamine (Luvox)****

OREXIN RECEPTOR ANTAGONISTS
⦁ Suvorexant (Belsomra)

MOA = blocks binding of wake-promoting neuropeptides (orexin A & B) to receptors - so keeps you from waking up

ADVERSE EFFECT
⦁ drowsiness
⦁ headache
⦁ abnormal dreams**

CONTRAINDICATIONS
⦁ narcolepsy**

Pregnancy Category C

85
Q

NARCOLEPSY

A

Narcolepsy = daytime sleepiness

Lose ability to regulate sleep-wake cycles

MOA
- lack of OREXIN - NT that helps with state of awakefulness

*Most common cause of disabling daytime sleepiness after OSA
⦁ sleep attacks/drop attacks

Symptoms of Narcolepsy
⦁ daytime sleepiness
⦁ cataplexy
⦁ hypnagogic (upon sleeping) or hypnopompic (upon waking) hallucinations
⦁ sleep paralysis
- not all actually experience 4 key symptoms of narcolepsy

  • generally don’t sleep more than normal people do in a 24hr period
  • FALL ASLEEP REALLY QUICKLY
  • go into REM sleep quickly –> very vivid dreams
  • SLEEP PARALYSIS

Narcolepsy is associated with significantly decreased REM latency. Patients with narcolepsy often enter REM sleep within a few minutes of falling asleep.

  • **CATAPLEXY*** = when a strong emotion, such as laughter or anger, triggers a transient muscle weakness
  • muscle weakness is often partial, affecting the face, neck or knees
  • but severe episodes can cause total body weakness or paralysis

usually takes 90 minutes to enter REM sleep; takes narcoleptics 10 minutes to enter REM cycle

NON-PHARM TREATMENT OF NARCOLEPSY
⦁ Good sleep hygiene
⦁ 2-3 naps per day
⦁ avoid problem drugs

PHARM TX FOR NARCOLEPSY
o 1st line = Modafinil (Provigil) or Armodafinil (Nuvigil)
MOA = not well understood, but may increase dopaminergic signaling

ADVERSE EFFECTS
⦁	headache
⦁	nausea
⦁	nervousness
⦁	dry mouth

Pregnancy category C

o 2nd line = Dextroamphetamine (DEXEDRINE)
MOA = not well understood, blocks reuptake and increases release of NE + dopamine

SIDE EFFECTS ARE COMMON
⦁ HTN
⦁ anorexia
⦁ addiction

Pregnancy category C
BLACK BOX WARNING *****
⦁ high abuse potential
⦁ cardiac events

86
Q

REM SLEEP BEHAVIOR DISORDER

A

o REM SLEEP BEHAVIOR DISORDER = dream-enactment behaviors during a loss of REM sleep atonia - “bruce lee” dreamers who become active/violent during REM (normally don’t move in REM sleep)

  • symptom onset is gradual and progressive
  • delay of several years between onset & diagnosis

NON-PHARM TREATMENT OF REM SLEEP BEHAVIOR DISORDER
o Establish a safe sleep environment
⦁ lock up firearms
⦁ remove sharp or breakable items

PHARM TREATMENT FOR REM SLEEP BEHAVIOR DISORDER
o 1st line = MELATONIN

MOA = prepares the body for sleep
SIDE EFFECTS
⦁	abnormal heartbeat (palpitations/PVCs with melatonin - not common)
⦁	dizziness
⦁	fatigue

o Clonazepam (Klonopin)

MOA = binds to benzo site of GABA receptors
- effective add-on or alternative drug

SIDE EFFECTS
⦁ morning sedation
⦁ dizziness
⦁ motor impairment

87
Q

RESTLESS LEG SYNDROME

MOVEMENT DISORDER

A

o MOVEMENT DISORDER = characterized by often unpleasant or uncomfortable urge to move legs - occurs during periods of inactivity, usually in the evening

Description of symptoms = “crawling” / “tingling & restless” / “cramping & painful” / “tension & itching”

NON- PHARM TREATMENT OF MOVEMENT DISORDERS
⦁ behavioral strategies (don’t wear itchy socks to bed)

PHARM TREATMENT FOR MOVEMENT DISORDERS
o 1st step = IRON REPLACEMENT (for serum ferritin levels < 75)
⦁ ferrous sulfate
⦁ people with restless legs have low iron levels in brain due to altered iron metabolism in the brain. May have normal ferritin levels. By restoring iron in substantia nigra, can restore dopamine, which helps restless legs. Iron stores in the substantia nigra are depleted, and this is where dopamine is made

o CARBIDOPA-LEVODOPA (Sinemet) = Dopaminergic Agents

SE
⦁ sleepiness
⦁ GI problems

o Pramipexole (Mirapex) = Dopamine Agonists
o Ropinirole (Requip)
o Rotigotine (Neupro) = patch

MOA = stimulate postsynaptic dopamine receptors in caudate putamen in the brain

ADVERSE EVENTS
⦁ nausea
⦁ lightheadedness

Pregnancy Category C

o GABAPENTIN (NEURONTIN) = Anticonvulsants

MOA = reduce presynaptic GABA release

ADVERSE EFFECTS
⦁ fatigue
⦁ dizziness
⦁ blurred vision

Pregnancy Category C