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MBB3 Flashcards

1
Q

What defines

  • premature birth?
  • very premature birth?
A

37 weeks - premature

32 weeks - very premature

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2
Q

what are the components of Apgar score?

what is the purpose

A 
Appearance (color)
Pulse (heartbeat- absent, slow, rapid)
Grimace (reflex irritability)
Activity (muscle tone)
Respiration (breathing regularity)

quantifies physical functioning in newborns, can be used to predict likelihood of immediate survival

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3
Q

what Apgar score indicates imminent survival threat

A

<4

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4
Q

Baby blues

  • incidence
  • time of onset
  • duration of symptoms
  • characteristics
A
  • 33-50%
  • within few days after delivery
  • lasts up to 2 weeks after delivery

exaggerated emotionality and tearfulness
interacts well with fam/friends
good grooming

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5
Q

Postpartum Depression

  • incidence
  • time of onset
  • duration of symptoms
  • characteristics
A

5-10%

  • during pregnancy or within 4 weeks after delivery
  • lasts up to 1 year without treatment (3-6 weeks with)
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6
Q

Postpartum psychosis

  • incidence
  • time of onset
  • duration of symptoms
  • characteristics
A
  1. 1-0.2%
    - within 4 weeks after delivery
    - lasts up to 1 month
    - symptoms include erratic behavior, confusion, delusions, risk of harming self or baby
    - psych EMERGENCY! usu need hospitalization
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7
Q

children who are withdrawn and unresponsive exhibit what disorder

A

Reactive Attachment Disorder

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8
Q

children who approach and attach indiscriminately to strangers exhibit what disorder

A

Disinhibited social engagement disorder

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9
Q

Freud’s stages of psychosexual development

A 
Oral
Anal
Oedipal
Latency
Genital
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10
Q

What are Id, Superego, Ego

A

Id - basic impulses, aggression, sex (motivate on a primitive level)

Superego - what society and culture imposes to keep people in line

Ego - meshing of id and superego

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11
Q

What is anaclitic depression

A

similar to reactive attachment disorder, often seen in orphanages - children do not relate well b/c do not have human contact like in families

encyclopedia:
a syndrome occurring in infants, usually after sudden separation from the mothering person. Symptoms include apprehension, withdrawal, detachment, incessant crying, refusal to eat, sleep disturbances, and, eventually, stupor leading to severe impairment of the infant’s physical, social, and intellectual development. If the mothering figure or a substitute is made available within 1 to 3 months, the infant recovers quickly with no long-term effects

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12
Q

List 6 infant reflexes (that disappear by age 1)

A 
Moro
Rooting
Stepping
Grasping
Crawling 
Babinski
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13
Q

babies hear what frequencies better

A

high

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14
Q

when do babies prefer patterned figures and begin to see schematic face rather than jumbled up face?

A

3 months

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15
Q

how much should a baby weigh by end of first year, compared to birth weight?

A

triple

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16
Q

when does social smile develop

A

6 weeks

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17
Q

when does stranger anxiety begin?

A

7 months

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18
Q

when does bowel/bladder control develop?

A

15 months - 3 years

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19
Q

much of adult neuronal structure present by when?

A

2 years

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20
Q

when do children first have sense of Core Gender Identity?

A

18 months

aware of sex differences and want to see and compare

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21
Q

3 endogenous temperaments

A

easy
difficult
slow to warm up

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22
Q

what is rapprochement? when does this happen?

A

vacillating between clinging to parent and fleeing

age 1.5 years

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23
Q

when can you usually toilet train

A

2.5-3 years

gain motor control over bowel/bladder by 3 years

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24
Q

when can babies turn over and sit unassisted?

A

5 months

6 months

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25
Q

when can babies lift their head?

A

1-3 months

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26
Q

Premenstrual Dysphoric Disorder

  • incidence
  • what is it
  • how is diagnosis confirmed
  • treatment
A

5% of menstruating women

  • mood disturbance (depressed, irritability, mood swings) that only occurs during premenstrual/luteal phase
  • confirm by charting symptoms over at least two cycles & see significant symptoms in premenstrual phase but none in follicular cycle
  • treatment
    • antidepressants (either thru cycle or only in luteal phase)
    • suppress ovulation with hormones
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27
Q

How is Premenstrual Exacerbation of Depression distinguished from PMS/PMDD?

How might you address it?

A

symptoms persist during follicular phase

  • can increase antidepressant premenstrually or add hormonal contraceptive
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28
Q

List some risk factors for depression in pregnancy. What is the BIGGEST risk factor?

A

-History of depression = biggest risk factor

also:

  • younger age
  • poor social support
  • more children
  • marital conflict
  • ambivalent about pregnancy
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29
Q

consequences of untreated depression in pregnancy?

A
  • poor self care
  • substance use
  • suicide
  • OB complications (preterm, LBW, SGA)
  • possible effects on infant development
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30
Q

treatments for depression in pregnancy

A

Psychotherapy (CBT, interpersonal therapy)

Antidepressants (SSRIs have lots of safety data. DON’T abruptly stop antidepressant during pregnancy!! depression itself is bad for pregnancy)

ECT

Transcranial magnetic stimulation

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31
Q

what are medical causes of postpartum depression that must be ruled out?

A
  • transient hypothyroidism
  • anemia
  • infection
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32
Q

definition of menopause

A

cessation of menses for 1 year or longer

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33
Q

what is perimenopause

A

5-10 year transition from regular menses to menopause

signific fluctuations in estrogen and progesterone

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34
Q

risk factors for depression in perimenopause

A
  • adverse life events
  • vasomotor symptoms (eg hot flahses)
  • previous repro-related mood disturbances
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35
Q

Are menopause-related mood symptoms associated with changes in reproductive hormonal levels or low levels

A

CHANGES

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36
Q

Treatment of depression in peri- and post-menopausal women?

A

first line: antidepressants

psychotherapy is very important

estrogen helps vasomotor symptoms and mood in PERI menopausal only. NOT considered firstline for depression tho

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37
Q

helpful questions to assess for IPV

A

do you feel safe at home?

how are disputes with your partner usually resolved?

  • must occur in safe, private, confidential setting w/o the partner
  • imp to ask them if it is safe to return home & help arrange support services (eg YWCA) including a safety plan
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38
Q

definition of infertility

A

inability to conceive after 12 months
(6 months if >35yo)

*women may get more depressed with every failed cycle

*fertility-enhancing drugs can cause mood symptoms (progesterone-depression
clomiphene- anxiety)

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39
Q

where does grief from miscarriage come from?

A

about anticipated outcomes

feelings of loss and failure can lead to pathological grief, postpartum depression, post-traumatic stress

friends and fam often fail to acknowledge loss and offer support

more intense grief with increasing gestational age

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40
Q

predominant reaction to abortion?

A

relief!

new episodes of psychiatric illness are rare

**aborting wanted pregnancy due to fetal defect is similarly emotional to miscarriage

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41
Q

three cases where women may have denial of pregnancy?

A
  • schizophrenia
  • older women who thought her amenorrhea was due to menopause
  • young women without much knowledge of reproduction
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42
Q

what is pseudocyesis

A

patient convinced she’s pregnant when she’s not

most are psychotic but not all

may be preceded by pregnancy loss, infertility

usually NOT receptive to psychiatric care

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43
Q

T or F: all antidepressants are excreted into breast milk

A

True

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44
Q

List the major classes of abused drugs

A

Sympathomimetic stimulants
Opiates/Opioids
Depressants
Dissociative anesthetics

Cannabis
Hallucinogens
Inhalants
Caffeine

SOD is CHIC

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45
Q

what is drug tolerance

A

reduced drug effect with repeated use; need higher doses to get the same effect (dose-response curve shifts right)

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46
Q

what is drug dependence

A

physiological and/or behavioral changes when you stop the drug, which are reversible by resuming drug

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47
Q

compare timing and severity of withdrawal symptoms for

  • long acting drug
  • short acting drug
  • short acting drug w/ antagonist
A

long acting - delayed onset withdrawal and over time, mild severity

short-acting (aka metabolized/eliminated faster) - severity is more intense but shorter duration

with antagonist - withdrawal even more intense and shorter duration

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48
Q

what is the difference between spontaneous and precipitated withdrawal?

A

spontaneous- happens when you stop taking the drug

precipitated - happens when given a drug antagonist
eg opiate-dependent ppl given antagonist naloxone experience and immediate intense withdrawal / flumazenil antagonist of benzos
(duration of precipitate withdrawal depends on duration of action of antagonist)

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49
Q

What is psychological dependence

what is physical dependence

A

intense craving and compulsive drug-seeking behavior
*is the key factor in addiction (rather than avoidance of withdrawal or reinforcement)

physical dependence = stereotyped withdrawal syndrome that is reversed by resumption of use

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50
Q

name and describe two pharm strategies for treating drug abuse

A

maintenance therapy:
- use drug like methadone to maintain opioid dependence / psych, social, vocational therapy to support during abstinence

detoxification:
-gradual or abruptly reducing drug dosage

pts on maintenance therapy may or may not be transitioned to detox

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51
Q

how do heroin and morphine differ

A

effects similar but heroin is 3x more potent

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52
Q

reinforcing and most other effects of abused opiates mediated by what receptors

A

mu opiate receptors (are GPCRs that couple to Gi/Go)

(mu KO mice don’t respond to rewarding effects and don’t go into withdrawal when given morphine repeatedly followed by antagonist)

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53
Q

what is addiction

A

continued compulsive use of a substance despite negative consequences

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54
Q

what has lower abuse liability: partial or full opioid agonists?

A

partial

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55
Q

4 initial effects of opioid agonists?

A

Rush (with IV - intense euphoria)
Relaxation
Miosis (constricted pupils)
Respiratory Depression

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56
Q

what are 6 signs of opioid overdose

A 
unconsciousness
resp depression
pinpoint pupils
bradycardia
hypotension
pulmonary edema
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57
Q

what is Salvinorin A and what receptor does it act on?

A

Kappa receptor opioid agonist

produces dissociative-like effect; no approved medical use

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58
Q

what is a good measure of pain severity (esp for pts with substance use)

A

function

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59
Q

to avoid overdose death, avoid increasing dosage to?

A

> = 90 morphine equivalent/day

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60
Q

symptoms of opioid withdrawal

A 
N/V
sweating, chills, hot flashes
diarrhea
craving
twitching/jerks
lacrimation, rhinorrhea, yawning

may also see:
dilated pupils, anxiety, insomnia, tachycardia, cramps

flu-like symptoms, generally NOT life threatening

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61
Q

opioid overdose treatments

A

OPIOID + SYMPTOMATIC TX

naloxone- short acting mu receptor antagonist
morphine- short acting

buprenorphine (preferred) - long acting partial mu agonist

methadone - long acting full opioid agonist

taper opioid over several days

+ symptomatic treatment of withdrawal (clonidine, sedatives, muscle relaxant, ibuprofen, antiemetic, antidiarrheal)

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62
Q

signs of Benzodiazepene overdose

A

symptoms essentially identical to alchol

physical:

  • slurred speech
  • impaired attention or memory
  • stupor or coma
  • incoordination, ataxia
  • nystagmus
  • decreased reflexes

psych:

  • mood lability
  • impaired judgment, inappropriate behavior
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63
Q

what is the treatment for benzodiazepene overdose, and MOA?

A

activated charcoal

Flumazenil - benzo antagonist, give IV every min up to 9 doses
*may cause seizures (bc precipitates withdrawal)

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64
Q

signs of stimulant overdose?

A

physical

  • HTN, tachy, diaphoresis
  • dilated pupils
  • tremor
  • arrythmia
  • seizure

psych:

  • anxiety
  • paranoia
  • psychosis (delusions, hallucinations)
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65
Q

treatment for stimulant overdose (4 )

A

monitor and control BP, HR

-vasodilator (nitroprusside, NTG, hydralazine)

  • alpha blocker (phentolamine) or nonselective adrenergic blocker (labetalol)
  • ***AVOID PURE BBLOCKERS (unopposed alpha effect)
  • sedative for anxiety (benzos)
  • antipsychotic for paranoia, psychosis (haloperidol) makes them easier to deal with clinically
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66
Q

symptoms in early and later ETOH withdrawal?

A

early (first 48h)

  • incr vital signs
  • hand tremors
  • diaphoresis
  • seizures

later:
-anxiety, agitation, delirium, disorientation (DTs)

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67
Q

list 5 predictors of alcohol withdrawal severity

A
  • Prior h/o significant alc withdrawal
  • older age
  • severity of drinking/tolerance
  • major med/surg problems
  • sedative/hypnotic use
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68
Q

what are three labs that can be helpful in determining severity of alcohol use and withdrawal potential

A

block alcohol level (but note you can get AW with negative BAL if haven’t drank in a few days)

elevated liver enzymes (GGTP more sensitive)

elevated erythrocyte MCV

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69
Q

what is CIWA and how is it used

A

Clinical Institute Withdrawal Assessment
-standardized assessment of AW symptoms, score >15 means impending delirium tremens

assessed every 4-8h until score is <8-10 for 24h

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70
Q

when does Delirium Tremens happen and what are some symptoms

A

after 48 hours

  • diaphoresis, N/V
  • rapid severe fluctuations in vitals
  • visual hallucinations

LIFE THREATENING!!

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71
Q

treatment for alcohol withdrawal

A

BENZODIAZEPENES!!
-targets the same receptor as ETOH (GABA-A)

  • VCU uses lorazepam b/c can be given IV and less liver metabolism
  • or chlordiazepoxide if no liver disease and can take oral meds
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72
Q

what is included in supportive care for alcohol withdrawal?

A

thiamine (MUST give thiamine AT LEAST 2H before starting dextrose fluids!!)
folic acid
multivitamins

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73
Q

how does buprenorphine’s unique pharmacology make it great for treating opioid dependence?

A
  • partial mu receptor agonist
  • high affinity for mu receptors = can displace full agonists and resist being displaced itself
  • low intrinsic activity = there is a ceiling for its mu agonist effects incl respiratory depression (hard to overdose on it)
  • dissociates slowly from receptor = prolonged suppression of opioid withdrawal symptoms

**Buprenorphine’s partial agonist effects can act as an antagonist in ppl dependent on full-agonist opioids, can PRECIPITATE withdrawal syndrome!!

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74
Q

4 meds for alcohol dependence and MOA

A

disulfiram (antabuse) - blocks acetaldeyhyde dehydrogenase

  • can cause hepatoxicity
  • best in monitored setting (parole, probation)

acamprosate - inhibits glutamatergic system
-reduces relapse in abstinent patients

naltrexone - blocks opioid receptors

  • reduced craving
  • reduce alcohol use (can give to ts who aren’t abstinent)
  • tablets or monthly IM injection

gabapentin - not FDA approved for alcohol dependence but similar efficacy as acamprosate
-better for pts whose drinking is driven by anxiety

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75
Q

3 pharmacotherapies for smoking cessation

A

Nicotine replacement

Antidepressant (Bupropion)
-blocks dopamine and NE reuptake

Nicotine Partial Agonist (Varenicline)

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76
Q

Neural basis of tobacco use

A

nicotonic receptor activation facilitates DOPAMINERGIC activation of brain reward pathways

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77
Q

are light cigarettes safer

A

not really

they’re just engineered to deliver less nicotine/tar….but smokers get around it by covering vent holes, puffing longer

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78
Q

what are two measures of recent smoking

A

Cotinine (a nicotine metabolite)

and Expired CO

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79
Q

list 4 abused CNS depressants

A

alcohol
barbiturates
benzos
non-barb/non-benzo sedatives

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80
Q

what is rate-limiting step of alcohol metabolism?

what causes asian flush

A

alcohol dehydrogenase

lack of acetaldehyde dehydrogenase causes acetaldehyde buildup which makes u sick

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81
Q

cellular mechanisms of action of ethanol (3)

A
  • enhanced GABA-A chloride flux
  • inhibit glutamate calcium flux thru NMDA
  • fluidization of membrane (at high doses)
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82
Q

what BAC is usually lethal in a non-tolerant individual

A

0.40%

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83
Q

lethality of depressant drug overdose mainly due to?

A

respiratory depression

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84
Q

initial effects of stimulants (4)

A

euphoria
feelings of well-being
incr energy
feelings of competency

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85
Q

Neural basis of stimulant Abuse

A

inhibits dopamine transporter -> more in presynaptic terminal

affinity: DAT = NET > SERT

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86
Q

phases of stimulant use episodes

A

stim often abused in cyclical fashion until run out of money or have to return to work

Run/binge
Crash
Mood and behavioral changes w/ craving and relapse

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87
Q

what are two classical hallucinogens

A

substituted phenethylamines (mescaline, MDA, MDMA aka molly, ecstasy; designer drugs)

indolamines (structurally resemble serotonin) (LSD, psilocybin, DMT)

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88
Q

what receptors do most hallucinogens act on

A

5-HT2A partial agonist (post-synaptic)

tho MDMA acts on 5-HT

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89
Q

acute effects of hallucinogens

A

Sympathomimetic activation!!

mood lability, altered thought process, altered perception, impaired judgment; experience insights

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90
Q

main dangers of hallucinogen abuse

A

panic attacks (sympathomimetic activation plus subjective effect of hallucinogens)

irrational behavior (taking dumb risks)

psych illness

especially MDMA

flashbacks

adulteration and misrepresentations

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91
Q

what drug class are sometimes used as “hallucinogens”?

A

muscarinic antagonists (eg atropine, scopolamine)

hence in suspected hallucinogen OD, check for anti-muscarinic effects and tx w/ cholinesterase inhibitors if needed

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92
Q

what are the 4 major dopaminergic pathways in the brain

A

mesolimbic
mesocortical
tuberoinfundibular
nigrostriatial

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93
Q

four aspects of DSM-5 definition of substance use disorder

A

Impaired control

  • using more or for longer than intended
  • persistent desire or unsuccessful efforts to cut/control use
  • lots of time spent in activities need to obtain substance
  • craving

Social consequences

  • fail to fulfill work/school oblig bc of time spent high
  • continued use despite negative social feedback or interpersonal prob

Risky use

  • recurrent use in physically hazardous situations
  • recurrent use despite psychological disturbance or medical problem

Pharmacological - tolerance, withdrawal

severity is mild, mod, severe based on number of symptoms

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94
Q

what is the Allostasis/ Reward-deficiency hypothesis of addiction

A

nothing motivates you but your drug of choice

repeated drug intoxication affects motivational neurocircuitrity so that you have a progressively decreasing set point of mood - neurobiologically incapable of strong motivation toward non drug rewards

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95
Q

describe what’s happening in the brain in the three stages of addiction

A

Intoxication- activation of brain’s reward regions enhanced by conditioned cues in areas of increased sensitization

Withdrawal- activation of brain regions involved in emotions results in negative mood and enhanced sensitivity to stress (bc incr corticotropin-releasing factor)

Preoccupation- decreased function of prefrontal cortex leads to inability to balance strong desire for drug with with will to abstain –> relapse and reinitiates cycle of addiction

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96
Q

how do dopamine receptors change in addiction

A

lose Dopamine receptors

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97
Q

incentive salience model of addiction

A

Sighs and sounds associated with drug effects acquire incentive salience and start controlling behavior by themselves

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98
Q

what is the impulsivity hypothesis of addiction

A

imbalance between impulsive and executive systems

strongly discount rewards with delayed receipt
poor future orientation

drug abuse can also cause impulsivity by frontocortical damage (which is the part of brain needed to stop abusing)

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99
Q

action of stimulants (e.g. cocaine)

A

bind DAT and NET (little SERT) thus preventing reuptake of dopamine and norepi

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100
Q

acute CNS effects of caffeine (4)

A
  • incr alertness
  • decr fatigue
  • greater capacity for sustained activity
  • sleep disruption
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101
Q

acute CNS effects of HIGH doses of caffeine (“caffeinism”)

over 150mg

A

Nervousness
restlessness
tremors
insomnia

CONVULSIONS at very high doses or ppl with seizure susceptibility

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102
Q

6 systemic effects of caffeine

A
  • HEART- stim myocardium, tachycardia, arrythmia
  • smooth muscle relaxation (eg bronchodilation)
  • constrict cerebrovasculature
  • central hypoglycemia (due to incr glucose use + decr blood to brain)
  • diuresis
  • increased gastric secretion
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103
Q

6 conditions where caffeine may be contraindicated

A 
HTN
heart rhythm disorders
gastritis, peptic ulcer, GERD
insomnia
anxiety and panic disorders
pregnancy (avoid excess)
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104
Q

caffeine withdrawal

  • onset
  • peak
  • duration
A

onset 12-24h
peak at 20-48h
duration up to 1 week

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105
Q

symptoms of caffeine withdrawal

A 
HEADACHE
irritability
lethargy/fatigue
unable to concentrate or work effectively
anxiety (mild)
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106
Q

primary MOA of caffeine

A

antagonize adenosine receptors (esp A2A)

there are lots of adenosine receptors in indirect pathway

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107
Q

in what way do the behavioral effects of methylxanthines and psychomotor stimulants differ the most?

A

reward/reinforcement

108
Q

two meds to treat narcolepsy

A

Modafinil (provigil) - amphetamine used to treat narcolepsy

Gamma hydroxybutyrate (xyrem)- depressant that normalizes sleep

109
Q

three clinical uses of psychomotor stimulates

A

narcolepsy
weight control (suppresses appetite)
ADHD

110
Q

list 3 problems for use of psychomotor stimulants for weight control

A
  • rapid tolerance (must incr dose which can bring closer to toxicity)
  • hangover, crash when drug wears off
  • CI in HTN, CHG, seizure disorder
111
Q

list three major monoamine neurotransmitters

A

dopamine
norepi
serotonin

112
Q

what is the monoamine theory of depression?

  • evidence supporting this theory?
  • evidence against?
A

depression could be related to deficiency of monoamine NT (usually NE or serotonin) at functionally important receptors in the CNS

(*mania results from excess neurotransmitter)

SUPPORT:

  • reserpine (blocks VMAT and depletes NT stores) can mimic depression
  • ampehtamine-like stimulants (which facilitate NT neurotransmission) enhance mood
  • decr urine, blood, or CSF levels of NE metabolites in depression
  • both MAOI and TCAs enhance monamine transmission (Tho different mechanisms)

AGAINST:

  • time course of antidepressant enhancement of monamines and clinical response differ
  • some drugs that also enhance monoamines aren’t useful as antidepressants (eg amphetamines)
  • newer antidepressants are quite selecective for blockade of either NE or serotonin uptake yet are all effective
113
Q

TCAs have lots of side effects, as they also have affinity for what receptors

A

block H1 and muscarinic receptors

114
Q

side effects of TCAs

-what are they due to

A

due to lack of selectivtiy

  • sedation
  • orthostatic hypotenstion
  • decreased sexual ability/desire
  • dry mouth
  • urinary retention
  • tachycardia
  • weight gain
  • cardiotoxicity
115
Q

in TCAs, how do parent drugs differ from their N-demythlated metabolites

A

parent drugs are more selective for serotonin and more sedating
(metabolites are more NE selective)

Ex
Imipramine –> Desipramine
Amitryptyline–> nortriptyline

116
Q

what is bupropion

  • use
  • MOA and unique features
A

second gen antidepressant (wellbutrin)
also marketed in lower dose for smoking cessation (zyban)

DA and NE reuptake blocker

lacks sedative and anticholinergic effects
no sexual dysfunction
but may be more epileptogenic

117
Q

how do antidepressants change receptor regulation

A

decr number of post-synaptic beta-aderenergic receptors
decr number of pre-synaptic 5HT1A receptors (less inhibition of 5HT release)

and/or

decrease the functional coupling of these receptors to their effector systems

118
Q

5HT1A receptors are coupled to what signaling pathway

119
Q

what is BDNF

A

Brain Derived Neurotrophic factor
stimulates adult neurogenesis and dendritic spine formation

BDNF levels and neuronal survival/proliferation are inhibited by stress
Many antidepressants reverse this in part by upregulating BDNF

120
Q

how should you initiate antidepressants

A

start w/ small divided doses and increase over 1-3 week period (want to give lowest dose possible)

therapeutic effects require 3-4 weeks for max response

121
Q

what side effects are particularly a problem with SSRIs

A

anorgasmia, reduced libido

122
Q

what significant side effect should you look out for in all antidepressants

123
Q

mechanism of MAOI

A

inhibit monoamine oxidase (enzyme that inactivates catecholamines and serotonin)

124
Q

MAOI side effects

A
  • orthostatic hypotension

- weakness, dizziness

125
Q

list three drug or diet interactions with MAOI

A
  • other antidepressants
  • sympathomimetic stimulants (amphetamines, OTC cold remedies)
  • tyramine containing foods (–> HTN, tachy, diaphoresis)
126
Q

list some tyramine-containing foods

A

interact with MAOI

  • aged cheese
  • pickled herring, smoked fish
  • certain wines and beers
  • cured meats
  • liver

many more

127
Q

what is serotonin syndrome

  • when does it occur
  • when is risk greatest
  • symptoms
A

any drugs that increase synaptic serotonin levels (incl TCAs, SSRI, SNRI, MAOI, MDMA)

  • risk greatest when:
    • starting tx
    • combing drugs
    • increasing dosage
    • switching to a different drug

mild symptoms

  • restlessness, agitation
  • confusion
  • pupil dilation
  • muscle rigidity or twitching, incr reflexes
  • sweating, diarrhea
  • headache
  • shivering, goosebumps

SEVERE life threatening”

  • hyperthermia, fever
  • seizures
  • cardiac arrythmia
  • unconsciousness
128
Q

when might you use ketamine as an off-label antidepressant?

  • MOA
  • advantages
  • disadvantages
A

non-comp NMDA antagonist

treatment-refractory depression

very rapid onset (hours)- could be useful in crisis/immediate suicide risk

but, abuse liabiliity, side effects (eg anxiety, confusion)
many not be effective for long term use

129
Q

what can Li be used for

when is it not effective

A
  • unipolar manic disorder
  • bipolar affective disorder
  • prophylaxisis unipolar depression
  • in combination w/ antidepressants

NOT effective for acute manic episode

130
Q

it is important to do what for Li

A

monitor blood levels

131
Q

signs of Li toxicity (low and high)

A

low:

  • tremor
  • thirst, edema, nausea
  • fatigue

high:

  • diarrhea, vomiting
  • muscular weakness, tremors, ataxia
  • blurred vision
  • coma or seizures
132
Q

list three anticonvulsants that can be used in mania/bipolar

A
  • valproate
  • lamotrigine
  • carbamazepine

cyclic nature of illness may involve neural mechanism of kindling, which is also thought to be involved in convuslive disorders

often effective in pts unresponsive to Li
becoming firstline bc hard to regulate blood Li levels

133
Q

SSRI and SNRIs lack many of the major side effects of older TCAs bc they lack affinity for which binding site of TCAs

A

muscarinic
H1
alpha1

134
Q

cause of Prader-Willi syndrome

symptoms

A

deletion on paternal chromosome 15
(or maternal uniparental disomy)

mild intellectual disability
hypotonia in infancy
feeding difficulty
voracious appetite, obesity
small hands, feet, gonads
short
135
Q

cause of Angelman syndrome

symptoms

A

deletion on maternal chromosome 15
(or paternal UPD)

severe-profound intellectual disability, very limited speech
short stature
spasticity/ataxia
happy, smiling ("happy puppet")
seizures
136
Q

what is Global Developmental Delay

A

significant delay in at least 2 developmental domains

term for children <5-6yo

137
Q

Fragile X inheritance

symptoms

A

XLD
CGG trinucleotide repeat in FMR-1 gene

Chin
Giant
Gonads

moderate intellectual disability
speech delay
protruding ears
large head, long face prominent forehead and chin

138
Q

Rett syndrome inheritance

symptoms

A

X-linked (mostly affects females bc prob lethal in males)

MECP2 gene

rapid regression with loss of acquire skills

late motor deterioration

seizures

139
Q

Sotos syndrome inheritance

symptoms

A

AD mutation in NSD1 gene

intellectual disability of variable level

overgrowth syndrome! rapid early growth, advance bone age

characteristic facial features:

  • macrocephaly
  • long thin face
  • down slanting palpebral fissures
140
Q

PTEN hamartoma syndrome inheritance

symptoms

A

AD

macrocephaly
characteristic skin findings- trichilemmomas, papillomatous papules

incr risk for breast, thyroid, endometrial, and renal cancer

141
Q

PTEN hamartoma syndrome includes what 4 conditions

A
  • Cowden syndrome (also have autism/ID)
  • Bannayan-Riley-Ruvalcaba syndrome
  • PTEN-related Proteus syndrome
  • Proteus-like syndrome
142
Q

PKU due to

A

deficiency of phenylalanine hydroxylase (converts Phe to Tyr)

143
Q

if no other etiology of intellectual disability can be found, it is called?

A

multifactorial (or non-syndromic ID)

144
Q

list some prenatal causes of ID

A

infections (eg rubella, CMV, syphilis, HIV)

exposures (eg alcohol, teratogenic meds such as anticonvulsants)

145
Q

list some perinatal causes of ID

A
  • prematurity
  • infection
  • hypoxia
  • intracranial hemorrhage
  • trauma
146
Q

list some postnatal (environmental) causes of ID

A
  • trauma
  • CNS hemorrhage
  • hypoxia
  • env toxins (lead, mercury)
  • psychosocial deprivation
  • malnutrition
  • intracranial infections
  • CNS malignancy
147
Q

blueberry muffin lesions seen in

A

congenital rubella

148
Q

risk of congenital CMV highest in

A

1st trimester

if primary infection during pregnancy

149
Q

steps in evaluating pts with GDD or ID

A

history, exam

specific testing for suspect syndromes

if no suspected syndrome, first tier:

  • chromosomal microarray analysis
  • testing for Fragile X syndrome

second tier:

  • single gene or gene panels
  • whole exome sequencing
150
Q

Phencyclidine (PCP) mechanism of action

A

(related to ketamine)

NMDA (glutamate) allosteric antagonist

151
Q

street names for PCP

A

oral = “T”

smoked or injected = “angel dust”

152
Q

effects of PCP intoxication

A
  • altered perception
  • reduced pain sensitivity
  • mood elevation
  • higher doses= inebriation, amnesia, mood swings, anxiety, aggression
153
Q

frequent PCP abuse can result in

A

PCP psychosis

similar to schizophrenia symptoms

154
Q

3 approved medical uses of cannabinoids in US

A
  • glaucoma
  • chemo induced nausea
  • wasting syndrome in AIDS
155
Q

CB1 receptors found in

A

nervous system
immune system
testis

156
Q

CB2 receptors found in

A

mostly immune system

157
Q

acute effects of cannabis

A
  • incr HR
  • conjunctival injection
  • moderation sedation
  • mood alteration
  • altered perception, altered time estimation, impaired judgment
  • impaired short term memory
158
Q

rapid tolerance develops to what effect of cannabis

A

impaired short term memory

159
Q

list 3 abused inhalants

A
  • nitrous oxide
  • volatile solvents and fuels
  • aliphatic nitrites
160
Q

where can abused N2O be found

A

whipped cream propellant (don’t shake, just inhale)

balloons

161
Q

examples of ppl who abuse N2O

A

concertgoers
affluent health professionals
late teens, college students

162
Q

dangers of N2O

A

hypoxia

accidents, falling

163
Q

what are some volatile solvents, fuels, anesthetics

A 
1,1,1-tricholoethane
ether
toluene
butane
gasoline
164
Q

what type of ppl abuse solvents, fuels, anesthetics

A

young
disadvantaged
international

165
Q

abuse of inhaled solvents produce effects that are most like what drug class?

A

CNS depressants

166
Q

pharmacological actions of abused volatile nitrites

A
  • vasodilation
  • venous pooling in periphery –> dizziness, enhanced erections
  • smooth muscle relatxation
167
Q

what can cause Neuroleptic Malignant syndrome

A 
all neuroleptics (Incl atypicals)
and other D2 blockers

or abrupt withdrawal of dopamine agonists in parkinsons

168
Q

risk factors for NMS

A
  • dehydration, malnutrition
  • prior NMS episode
  • rapid rate of neuroleptic loading
  • severe EPS, catatonia, prolonged restraints
  • Fe deficiency
  • Lithium?
169
Q

exam findings of NMS

A

same as malignant hypertension

  • elevated temp
  • muscle rigidity and other neuro symptoms
  • altered consciousness
  • autonomic dysfunction (labile bp, tachy, diaphoresis, urinary incontinence)
170
Q

lab findings of NMS

A

increased CPK (800 to >100,000)

elevated WBC (10,000-40,000)

171
Q

what meds should you stop/not stop in NMS

A

STOP

  • neuroleptic
  • other D2 blockers
  • lithium
  • anticholinergics

KEEP
-dopamine agonists

172
Q

the most effective tx for severe NMS

173
Q

clinical features of serotonin syndrome

A
  • delirium, restlessness, agitation
  • myoclonus, ataxia, seizures, rigidity, hyperreflecia
  • GI
  • autonomic fluct BP, incr pulse, respirations, sweating
  • hyperthermia
174
Q

treatment of serotonin syndrome

A
  • stop all serotonergic drugs
  • supportive care

Cyprohepatadine

175
Q

goals of community reinforcement approach

A

eliminate positive reinforcement for drinking/drugs

enhance positive reinforcement for sobriety/abstinence

176
Q

what is the goal of motivational interviewing

A

create and amplify discrepancy between present behavior and pt’s broader goals

177
Q

what is SBIRT

A 
Screening
Brief
Intervention
Referral for 
Treatment

a screening tool to identify people at risk of substance use disorder, or have SUD but not being treated

178
Q

topographic model divides brain into what parts

structural model divides brain into what parts

A

unconscious, preconscious, conscious

id, ego, superego

179
Q

what is Takotsubo cardiomyopathy

A

acute HF in a stressful situation

180
Q

relationship between depression and CAD

A

CAD is risk factor for depression

depression is risk factor for CAD

depression can lead to worse outcomes in CAD -mental stress causes silent ischemia in CAD & effects on platelet function, inflammation, reduced heart rate variability, autonomic imbalance
-depression causes delay in seeking care, noncompliance, physical inactivity, less likely to get major interventions

181
Q

relationship between asthma and anxiety

A

anxiety aggravates asthma

SOB causes anxiety
many asthma drugs cause anxiety

182
Q

what are 5 major types of anxiety disorders

A
  • GAD
  • OCD
  • panic disorder
  • PTSD
  • social phobia/social anxiety disorder
183
Q

moa Buspirone

advantages / disadvantages

A

5HT 1A partial agonist (treats anxiety)

advantages= not a benzodiazepine or hypnotic, no sedation, no abuse, tolerance or withdrawal

disadvantages

  • takes 1-2 weeks to become effective
  • poor transition from benzos to buspirone
184
Q

hydroxyzine

A

H1 antagonist (antihistamine)

Is an anxiolytic at doses that cause sedation (thus not widely used)

185
Q

what drug blocks sympathetic nervous system signs of fear and anxiety?

under what circumstances can it be used for

A

propranolol (beta-adrenergic antagnoist)

situation-specific anxiety and acute panic symptoms

186
Q

Kubler Ross stages of grief

A 
Denial
Anger
Bargaining
Depression
Acceptance
187
Q

what are some differences between grief and depression

A

GRIEF:

  • connected to others
  • knows sadness will end
  • consolable
  • has both positive and negative feelings
  • self esteem not affected
  • rarely suicidal

DEPRESSION

  • separated
  • sadness will never end
  • not consolable
  • only negative feelings
  • feel personally diminished, decr self esteem
  • often suicidal
188
Q

what is the strongest predictor of future suicide attempt

A

previous suicide attempt

189
Q

list 4 treatment options for suicide risk

A
  • containment (hospitalize)
  • decrease/modify risk factors
  • increase protective factors
  • restrict means
190
Q

components of a patient Safety Plan

A

1- warning signs that crisis may be developing

2- internal coping strategies

3- people and social settings that provide distraction

4- people to ask for help

5- professionals or agencies to call

6-making environment safe

191
Q

methods of making the environment safe (means restriction)

A

getting guns far away- sell, keep locked at someone else’s house, etc

removing other weapons

remove old/expired meds

safe prescribing (e.g. only prescribe 2 weeks at a time)

192
Q

list 5 trauma/stressor related disorders

A
  • Reactive Attachment Disorder (RAD)
  • Disinhibited social engagement disorder (DSED)
  • Acute stress disorder (ASD)
  • PTSD
  • Adjustment disorder
193
Q

list three types of extremely insufficienct care that can lead to Reactive Attachment Disorder or Disinhibited Social Engagement Disorder

A
  • social neglect or deprivation (persistent lack of having basic emotional needs met for comfort, stimulation, and affection)
  • repeated changes of primary caregivers = never able to form stable attachements
  • rearing in settings that severely limit chances to form selective attachments (e.g. institutions with high cihld:caregiver ratios)
194
Q

Disinhibited Social Engagement Disorder

describe their behavior

A

actively approaches and interacts w/ unfamiliar adults

overly familiar verbal or physical behavior

doesn’t check back with adult caregiver after venturing away (even in unfamiliar place)

willing to go off with an unfamiliar adult without hesitation

195
Q

Reactive Attachment Disorder

describe their behavior

A
  • little social and emotional responsiveness to others
  • don’t seek comfort / don’t response to being comforted when distressed
  • limited positive affect
  • episodes of unexplained irritability, sadness, fearfulness
  • don’t meet criteria for autism
  • disturbance evident before age 5, child has developmental age at least 9 months
196
Q

treatment for RAD and DSED

A

safe healthy home env

therapy to work on bond btwn child and new caretaker

treat comorbid conditions

meds aren’t indicated

197
Q

categories of symptoms for ASD or PTSD

A

Dissociative (depersonalization/derealization, can’t remember imp aspects of event)

Intrusion (recurrent intrusive distressing memories of event, recurrent distressing dreams of event, dissociative reactions e.g. flashbacks where they feel or act as if event were recurring, intesnse or prolonged psych distress or marked phsyiologic reaction to internal or external cues that symbolize or resemble aspects of event)

Avoidance

Negative mood

Arousal (sleep disturbance, irritable behavior/anger, hypervigilance, problems concentrating, exaggerated startle response)

198
Q

ASD vs PTSD

A

ASD lasts 3d - 1 month
symptoms start after event
need at least 9 symptoms from each category

PTSD lasts > 1 month
symptoms from each of five categories

199
Q

what is PTSD with delayed expression

A

onset at least 6 months after the event

200
Q

PTSD treatment

A

NO BENZOS

trauma focused therapy
CBT
SSRI, SNRI

201
Q

What is adjustment disorder

-first line treatment?

A

emotional/behavioral symptoms in response to a stressor (within 3 months)

  • distress out of proportion to severity of stress
  • signific impairment in social, occupational, other imp areas of functioning

Therapy is firstline

202
Q

name and describe the three clusters of personality disorders, and the PDs in each cluster

A

Cluster A: odd-eccentric
(paranoid, schizoid, schizotypal)

Cluster B: dramatic-emotional
(histrionic, narcissistic, antisocial, borderline)

Cluster C: anxious-fearful
(avoidant, obsessive compulsive, dependent)

203
Q

paranoid PD

A

(cluster A)

pervasive distrust and suspiciousness of others

204
Q

schizoid PD

A

(cluster A)

does not desire or enjoy close relationships

restricted emotions, lacks empathy

ex: lighthouse keeper

205
Q

schizotypal PD

A

magical thinking
ideas of reference
odd thinking and speech

206
Q

antisocial PD

A

(cluster B)
no concern for others

assoc w/ conduct disorder in childhood

207
Q

borderline PD

A

(cluster B)
-unstable interpersonal relationships, sense of self (kaleidoscope identity)

  • impulsivity in at least two areas that are self-damage (e.g. spending, sex, substance abuse, reckless driving, binge eating)
  • chronic feeling empty
208
Q

histrionic PD

A

(cluster B)

always wants to be center of attention

theatrical, shallow expression of emotions

speech lacks detail

thinks relationships are closer than they actually are

209
Q

narcissistic PD

A

(cluster B)

grandiosity

lack of empathy

thinks they are special and unique and can only be understood by/should only associated with other special or high status people

interpersonally exploitative

210
Q

avoidant PD

A

(cluster C)

  • pervasive social inhibition
  • feeling inadequate
  • fears being criticized, embarrassed, rejected
  • sees self as socially inept, unappealing, inferior to others
211
Q

dependent PD

A

(cluster C)

  • can’t make everyday decisions without tons of adivce and reassurance
  • trouble expressing disagreement
  • can’t do things on their on
  • go to lengths to obtain support from others, to the point of volunteering to do unpleasant things
  • preoccupied with fears of being left alone to care for self

assoc w/ chronic childhood illness and sep anxiety

212
Q

obsessive-compulsive PD

A

(culster C)

  • preoccupied with perfectionism and the expense of flexibility, efficiency
  • rigid and stubborn
213
Q

selective mutism

A

consistent failure to speak in specific social situations when expected to (e.g. school) DESPITE speaking in other situations

at least 1 month

not due to lack of knowledge or comfort with spoken language

214
Q

social anxiety disorder definition

-treatment?

A

fear/anxiety about one or more social situations where there’s possibility of scrutiny, being observed, or performing in front of others

various CBT incl desensitization/exposure
-SSRI/SNRI, benzo or propanolol as adjunct

215
Q

criteria for panic disoder

-treatment

A

recurrent and unexpected panic attacks

at least one attack is followed by at least one month of worry about future panic attacks AND maladaptive behavior change

CBT
SSRIs, benzos

216
Q

agoraphobia definition

-situations (5)

A

must have fear or anxiety in at least 2

  • using public transport
  • being in open spaces
  • being in enclosed places
  • standing in line or being in a crowd
  • being outside of home alone

fear is b/c escape may be hard or help may not be available if get panic like symptoms or embarrassing symptoms (e.g. elderly fear of fall, incontinence)

lasts 6 months or more

the fear, anxiety, or avoidance causes signific distress or impairment in social, occupational, other imp areas of functioning

217
Q

GAD criteria

list 6 symptoms that are associated with the anxiety/worry of GAD

A

Excessive anxiety and worry occurrining more days than not for at least 6 MONTHS

  • restlessness/on edge
  • easily fatigued
  • difficulty concentrating/mind going blank
  • irritable
  • muscle tension
  • sleep disturbance
218
Q

negative symptoms of schizophrenia

A
  • affective flattening
  • avolition/apathy
  • asociality
219
Q

positive symptoms in schizophrenia

A

delusions
hallucinations
thought disorders
motor disturbances

220
Q

what is Dopamine Hypothesis

A

schizophrenia / psychosis in general is result of excess Dopamine

221
Q

most imp feature in diagnosing autism spectrum disorder

A

impairment in social interactions

  • impaired reciprocal social interaction
  • self-absorption
  • lack affective contact
  • avoid eye contact
  • disinterest in others
222
Q

behaviors in autism spectrum d/o

A
  • must maintain routines
  • speech- makes sounds, repeats words or phrases, idiosyncratic use of language
  • hand-flapping, toe walking, posturing
  • self abusive
  • idiot savant
223
Q

screening PCP office can identify children with Autism Spectrum D/o as young as

A

18 months (using M-CHAT)

224
Q

biologic etiology of ASD

A

fail to achieve normal pruning

occasionally specific medical etiology (PKU, rubella, Fragile X)

225
Q

most common reason for evaluation for ASD

A

speech delay

226
Q

what must be ruled out before diagnosing ASD

A

hearing impairment

227
Q

most effective treatment for core symptoms in children w/ ASD

A

Applied Behavioral Analysis (ABA)

no meds indicated for CORE symptoms

Early intervention is critical!!

228
Q

meds for ASD and…

  • aggression/behavior prob
  • concurrent ADHD
  • self-stim behavior and sterotypies
A

antipsychotics, mood stabilizers, clonidine

-stimlants, TCAs, clonidine

fenfluramine-major side effects
SSRIs (similarity to OCD symptoms)
SGAs may help w/ extrem stereotypical behaviors, aggression and self-injurious behavior

229
Q

treatment for ASD with self-injurious behaviors

A

naltrexone

beta blockers

230
Q

according to DSM-V, ADHD is diagnosed before age

231
Q

neuromedical causes of ADHD (7)

A
  • prenatal (alcohol, smoking)
  • lead
  • CNS infection
  • thyroid disorders
  • drug-induced
  • constipation (discomfort->fidgeting)
  • hunger
232
Q

psychosocial causes of ADHD (3)

A
  • abuse (physical or sexual)
  • neglect
  • boredom
233
Q

name 3 nonmedication interventions for ADHD

A
  • preferential seating
  • chunking tasks
  • behavior counseling
234
Q

course of ADHD in infancy

A

infant:

  • difficult temperament
  • minor congenital anomalies
  • poor mother-infant fit
235
Q

course of ADHD in toddler age

A

“restless dynamo”

  • accident prone
  • poorly coordinated
  • enthusiasitically intrusive
  • emotionally labile
  • hard to discipline
  • peer problems
  • low frustration tolerance
236
Q

course of ADHD in school age

A
  • most referrals in this time b/c first experience w/ structure, rules
  • distractible, fidgety
  • poor self-concept
237
Q

describe the vicious cycle in ADHD

A

poor performance –> disapproval –> frustration –> low self-esteem –> worse performance

238
Q

course of ADHD in adolescence

A
  • delinquency

- antisocial behavior

239
Q

psychostimulants to treat ADHD?

  • advantages
  • side effects
A
  • methylphenidate
  • dextroamphetamine

short acting, can take as needed
not a/w later abuse

SE: sleepiness, agitation
GI upset, decreased appetite
tics

240
Q

what other drugs can treat ADHD

A

TCAs (comorbid anxiety, depression)

Clonidine, Guanfacine- a2 agonists (if aggression, irritability)

SSRIs, bupropion

buspirone if stmiulant not available

atomoxetine

Li, antipsychotics, anticonvulsants

241
Q

definiton body dysmorphic disorder

A

preoccupation with preceived defect or flaw in physical appearance

+ at some point has performed repetitive behaviors (eg mirror checking, excess grooming, skin picking, reassurance seeking) or mental acts in response

242
Q

definition hoarding disorder

-gold standard tx?

A

persistent diff discarding possessions

CBT sessions in and out of home
teach decision making and categorization
exposure and habituation to discarding

243
Q

trichotillomania

A

recurrent pulling out one’s hair

repeated attempts to decrease or stop hair pulling

244
Q

excoriation disorder

A

(skin picking disorder)

recurrent skin picking reuslting in lesions
repeated attempts to decrease or stop picking

245
Q

name and describe two types of anorexia

A

both have low BMI

restricting - no binging and purging; mostyl just diets, fasts, excess exercise

binge-eating/purging type

246
Q

physical signs of anorexia

A
  • lanugo
  • hair gets birttle and falls out
  • brittle nails
  • dry scaly skin w/ yellow or gray cast
  • decr body temp
  • hands and feet feel cold
  • thyroid function slows
  • RR and HR drop, BP drops
  • bone mass loss
247
Q

treatment of anorexia in kids/teens? adults?

A

kids/teens- family based treatment. no meds

adults- CBT or IPT

248
Q

common comorbid conditions with bulimia? (2)

A

substance abuse

borderline PD

249
Q

what is Russell’s sign

A

calluses on knuckles

when bulimia forces self to purge, teeth can bite down on kunckles

250
Q

bulimia treatments

A

CBT

SSRI (firstline Fluoxetine)

251
Q

most common eating disorder

A

binge-eating disorder

252
Q

somatic symptoms disorder

A

physical symptom(s) that cause distress/impairment way out of proportion to objective disease signs

253
Q

etiologies of somatic symptoms disorder

A
  • childhood abuse
  • childhood early sick role experiences
  • aelxithymia (can’t put feelings into words)
  • somatic hypersens
  • insexure attachment, addicted to sick role
  • social reinforcement of sick role
  • genetics
254
Q

consequences of somatic symptom disorder

A

iatrogenic: incidentalomas, polypharmacy, polysurgery, radiation exposure, drug dependence

frustrating MD-patient relationship –> doctor shopping

invalidism and disability

high medical costs

missed actual medical illness!

255
Q

managing somatic symptom disorder

A

acknolege symptoms and suffering
explain diagnosis
don’t promise cure, don’t schold pt

*regular schedule brief outpatient visits w/ partial exam based on symptoms

intervention basedon signs

treat cmorbid depression or anxiety

256
Q

illness anxiety disorder

A

excessive worry about getting a serious disease
NO major physical symptoms, just worry

excessive health-related behaviors (eg repeatedly taking pulse)
or maladaptive avoidance (eg avoiding doctors appt)

at least 6 months

257
Q

name two variations of illness anxiety disorder

A

care seeking

care avoidant

258
Q

what is counterproductive in illness anxiety disorder?

A

getting too many tests (won’t convince pt)

259
Q

what should you be alert for in illness anxiety disorder

A

complications of self-treatment (eg laxative abuse, hypervitaminosis A)

260
Q

what is conversion disorder

  • how diagnosed
  • when does it happen
A

neurologic symptoms that can’t be expalined by neuropathophysiology or internally inconsistent

dx by exam

often from emotional conflict or acute traumatic stressors (current or past sexual/physical abuse common)

some may be simple malfunction of nervous system

261
Q

Hoover’s sign

A

to test for Conversion disorder

ask to push down on your hand w/ right heel (don’t do anything)
hold right heel, then ask pt to lift other leg against resistance. the right hip will extend (and heel will push down into hand)

262
Q

list 4 other tests tha could indicate conversion disorder

A
  • seizure videotaped with simultaneous normal EEG
  • give-way weakness (initial resistance, then suddenly gives away)
  • tunnel vision
  • sensory loss that that doesn’t fit recognized distributions (dermatomes or stocking glove)
263
Q

management conversion disorder

A

PT (graceful way out, may be needed in chronic disuse)

don’t confront or tell them there’s nothing wrong/it’s all in their head

reassure

psychotherapy, behavior therapy (for those who have insight)

264
Q

malingerirng

A

conscious faking to get a specific gain

265
Q

malingering mainly occurs in what groups

A

opioid addicts
prisoners
soldiers in wartime

266
Q 
factitious disorder (aka Munchausen's syndrome)
-what groups is it more common in
A

feign or INDUCE illness for sake of it (pleasure of imposture, tricking doctors)

more common in healthcare workers and their adult children

borderline personlity in half

MBB (2 decks)

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