MBB3 Flashcards

(266 cards)

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children who are withdrawn and unresponsive exhibit what disorder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
when can babies lift their head?
1-3 months
26
Premenstrual Dysphoric Disorder - incidence - what is it - how is diagnosis confirmed - treatment
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
27
How is Premenstrual Exacerbation of Depression distinguished from PMS/PMDD? How might you address it?
symptoms persist during follicular phase - can increase antidepressant premenstrually or add hormonal contraceptive
28
List some risk factors for depression in pregnancy. What is the BIGGEST risk factor?
-History of depression = biggest risk factor also: - younger age - poor social support - more children - marital conflict - ambivalent about pregnancy
29
consequences of untreated depression in pregnancy?
- poor self care - substance use - suicide - OB complications (preterm, LBW, SGA) - possible effects on infant development
30
treatments for depression in pregnancy
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
31
what are medical causes of postpartum depression that must be ruled out?
- transient hypothyroidism - anemia - infection
32
definition of menopause
cessation of menses for 1 year or longer
33
what is perimenopause
5-10 year transition from regular menses to menopause signific fluctuations in estrogen and progesterone
34
risk factors for depression in perimenopause
- adverse life events - vasomotor symptoms (eg hot flahses) - previous repro-related mood disturbances
35
Are menopause-related mood symptoms associated with changes in reproductive hormonal levels or low levels
CHANGES
36
Treatment of depression in peri- and post-menopausal women?
first line: antidepressants psychotherapy is very important estrogen helps vasomotor symptoms and mood in PERI menopausal only. NOT considered firstline for depression tho
37
helpful questions to assess for IPV
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
38
definition of infertility
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)
39
where does grief from miscarriage come from?
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
40
predominant reaction to abortion?
relief! new episodes of psychiatric illness are rare **aborting wanted pregnancy due to fetal defect is similarly emotional to miscarriage
41
three cases where women may have denial of pregnancy?
- schizophrenia - older women who thought her amenorrhea was due to menopause - young women without much knowledge of reproduction
42
what is pseudocyesis
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
43
T or F: all antidepressants are excreted into breast milk
True
44
List the major classes of abused drugs
Sympathomimetic stimulants Opiates/Opioids Depressants Dissociative anesthetics Cannabis Hallucinogens Inhalants Caffeine SOD is CHIC
45
what is drug tolerance
reduced drug effect with repeated use; need higher doses to get the same effect (dose-response curve shifts right)
46
what is drug dependence
physiological and/or behavioral changes when you stop the drug, which are reversible by resuming drug
47
compare timing and severity of withdrawal symptoms for - long acting drug - short acting drug - short acting drug w/ antagonist
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
48
what is the difference between spontaneous and precipitated withdrawal?
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)
49
What is psychological dependence what is physical dependence
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
50
name and describe two pharm strategies for treating drug abuse
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
51
how do heroin and morphine differ
effects similar but heroin is 3x more potent
52
reinforcing and most other effects of abused opiates mediated by what receptors
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)
53
what is addiction
continued compulsive use of a substance despite negative consequences
54
what has lower abuse liability: partial or full opioid agonists?
partial
55
4 initial effects of opioid agonists?
Rush (with IV - intense euphoria) Relaxation Miosis (constricted pupils) Respiratory Depression
56
what are 6 signs of opioid overdose
``` unconsciousness resp depression pinpoint pupils bradycardia hypotension pulmonary edema ```
57
what is Salvinorin A and what receptor does it act on?
Kappa receptor opioid agonist | produces dissociative-like effect; no approved medical use
58
what is a good measure of pain severity (esp for pts with substance use)
function
59
to avoid overdose death, avoid increasing dosage to?
>= 90 morphine equivalent/day
60
symptoms of opioid withdrawal
``` 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
61
opioid overdose treatments
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)
62
signs of Benzodiazepene overdose
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
63
what is the treatment for benzodiazepene overdose, and MOA?
activated charcoal Flumazenil - benzo antagonist, give IV every min up to 9 doses *may cause seizures (bc precipitates withdrawal)
64
signs of stimulant overdose?
physical - HTN, tachy, diaphoresis - dilated pupils - tremor - arrythmia - seizure psych: - anxiety - paranoia - psychosis (delusions, hallucinations)
65
treatment for stimulant overdose (4 )
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
66
symptoms in early and later ETOH withdrawal?
early (first 48h) - incr vital signs - hand tremors - diaphoresis - seizures later: -anxiety, agitation, delirium, disorientation (DTs)
67
list 5 predictors of alcohol withdrawal severity
* Prior h/o significant alc withdrawal - older age - severity of drinking/tolerance - major med/surg problems - sedative/hypnotic use
68
what are three labs that can be helpful in determining severity of alcohol use and withdrawal potential
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
69
what is CIWA and how is it used
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
70
when does Delirium Tremens happen and what are some symptoms
after 48 hours - diaphoresis, N/V - rapid severe fluctuations in vitals - visual hallucinations LIFE THREATENING!!
71
treatment for alcohol withdrawal
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
72
what is included in supportive care for alcohol withdrawal?
thiamine (MUST give thiamine AT LEAST 2H before starting dextrose fluids!!) folic acid multivitamins
73
how does buprenorphine's unique pharmacology make it great for treating opioid dependence?
- 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!!
74
4 meds for alcohol dependence and MOA
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
75
3 pharmacotherapies for smoking cessation
Nicotine replacement Antidepressant (Bupropion) -blocks dopamine and NE reuptake Nicotine Partial Agonist (Varenicline)
76
Neural basis of tobacco use
nicotonic receptor activation facilitates DOPAMINERGIC activation of brain reward pathways
77
are light cigarettes safer
not really | they're just engineered to deliver less nicotine/tar....but smokers get around it by covering vent holes, puffing longer
78
what are two measures of recent smoking
Cotinine (a nicotine metabolite) | and Expired CO
79
list 4 abused CNS depressants
alcohol barbiturates benzos non-barb/non-benzo sedatives
80
what is rate-limiting step of alcohol metabolism? what causes asian flush
alcohol dehydrogenase lack of acetaldehyde dehydrogenase causes acetaldehyde buildup which makes u sick
81
cellular mechanisms of action of ethanol (3)
- enhanced GABA-A chloride flux - inhibit glutamate calcium flux thru NMDA - fluidization of membrane (at high doses)
82
what BAC is usually lethal in a non-tolerant individual
0.40%
83
lethality of depressant drug overdose mainly due to?
respiratory depression
84
initial effects of stimulants (4)
euphoria feelings of well-being incr energy feelings of competency
85
Neural basis of stimulant Abuse
inhibits dopamine transporter -> more in presynaptic terminal affinity: DAT = NET > SERT
86
phases of stimulant use episodes
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
87
what are two classical hallucinogens
substituted phenethylamines (mescaline, MDA, MDMA aka molly, ecstasy; designer drugs) indolamines (structurally resemble serotonin) (LSD, psilocybin, DMT)
88
what receptors do most hallucinogens act on
5-HT2A partial agonist (post-synaptic) tho MDMA acts on 5-HT
89
acute effects of hallucinogens
Sympathomimetic activation!! mood lability, altered thought process, altered perception, impaired judgment; experience insights
90
main dangers of hallucinogen abuse
panic attacks (sympathomimetic activation plus subjective effect of hallucinogens) irrational behavior (taking dumb risks) psych illness especially MDMA flashbacks adulteration and misrepresentations
91
what drug class are sometimes used as "hallucinogens"?
muscarinic antagonists (eg atropine, scopolamine) hence in suspected hallucinogen OD, check for anti-muscarinic effects and tx w/ cholinesterase inhibitors if needed
92
what are the 4 major dopaminergic pathways in the brain
mesolimbic mesocortical tuberoinfundibular nigrostriatial
93
four aspects of DSM-5 definition of substance use disorder
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
94
what is the Allostasis/ Reward-deficiency hypothesis of addiction
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
95
describe what's happening in the brain in the three stages of addiction
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
96
how do dopamine receptors change in addiction
lose Dopamine receptors
97
incentive salience model of addiction
Sighs and sounds associated with drug effects acquire incentive salience and start controlling behavior by themselves
98
what is the impulsivity hypothesis of addiction
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)
99
action of stimulants (e.g. cocaine)
bind DAT and NET (little SERT) thus preventing reuptake of dopamine and norepi
100
acute CNS effects of caffeine (4)
- incr alertness - decr fatigue - greater capacity for sustained activity - sleep disruption
101
acute CNS effects of HIGH doses of caffeine ("caffeinism") | over 150mg
Nervousness restlessness tremors insomnia CONVULSIONS at very high doses or ppl with seizure susceptibility
102
6 systemic effects of caffeine
- 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
103
6 conditions where caffeine may be contraindicated
``` HTN heart rhythm disorders gastritis, peptic ulcer, GERD insomnia anxiety and panic disorders pregnancy (avoid excess) ```
104
caffeine withdrawal - onset - peak - duration
onset 12-24h peak at 20-48h duration up to 1 week
105
symptoms of caffeine withdrawal
``` HEADACHE irritability lethargy/fatigue unable to concentrate or work effectively anxiety (mild) ```
106
primary MOA of caffeine
antagonize adenosine receptors (esp A2A) | there are lots of adenosine receptors in indirect pathway
107
in what way do the behavioral effects of methylxanthines and psychomotor stimulants differ the most?
reward/reinforcement
108
two meds to treat narcolepsy
Modafinil (provigil) - amphetamine used to treat narcolepsy Gamma hydroxybutyrate (xyrem)- depressant that normalizes sleep
109
three clinical uses of psychomotor stimulates
narcolepsy weight control (suppresses appetite) ADHD
110
list 3 problems for use of psychomotor stimulants for weight control
- rapid tolerance (must incr dose which can bring closer to toxicity) - hangover, crash when drug wears off - CI in HTN, CHG, seizure disorder
111
list three major monoamine neurotransmitters
dopamine norepi serotonin
112
what is the monoamine theory of depression? - evidence supporting this theory? - evidence against?
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
TCAs have lots of side effects, as they also have affinity for what receptors
block H1 and muscarinic receptors
114
side effects of TCAs | -what are they due to
due to lack of selectivtiy - sedation - orthostatic hypotenstion - decreased sexual ability/desire - dry mouth - urinary retention - tachycardia - weight gain - cardiotoxicity
115
in TCAs, how do parent drugs differ from their N-demythlated metabolites
parent drugs are more selective for serotonin and more sedating (metabolites are more NE selective) Ex Imipramine --> Desipramine Amitryptyline--> nortriptyline
116
what is bupropion - use - MOA and unique features
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
how do antidepressants change receptor regulation
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
5HT1A receptors are coupled to what signaling pathway
Gi
119
what is BDNF
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
how should you initiate antidepressants
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
what side effects are particularly a problem with SSRIs
anorgasmia, reduced libido
122
what significant side effect should you look out for in all antidepressants
SUICIDE
123
mechanism of MAOI
inhibit monoamine oxidase (enzyme that inactivates catecholamines and serotonin)
124
MAOI side effects
- orthostatic hypotension | - weakness, dizziness
125
list three drug or diet interactions with MAOI
- other antidepressants - sympathomimetic stimulants (amphetamines, OTC cold remedies) - tyramine containing foods (--> HTN, tachy, diaphoresis)
126
list some tyramine-containing foods
interact with MAOI - aged cheese - pickled herring, smoked fish - certain wines and beers - cured meats - liver many more
127
what is serotonin syndrome - when does it occur - when is risk greatest - symptoms
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
when might you use ketamine as an off-label antidepressant? - MOA - advantages - disadvantages
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
what can Li be used for when is it not effective
- unipolar manic disorder - bipolar affective disorder - prophylaxisis unipolar depression - in combination w/ antidepressants NOT effective for acute manic episode
130
it is important to do what for Li
monitor blood levels
131
signs of Li toxicity (low and high)
low: - tremor - thirst, edema, nausea - fatigue high: - diarrhea, vomiting - muscular weakness, tremors, ataxia - blurred vision - coma or seizures
132
list three anticonvulsants that can be used in mania/bipolar
- 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
SSRI and SNRIs lack many of the major side effects of older TCAs bc they lack affinity for which binding site of TCAs
muscarinic H1 alpha1
134
cause of Prader-Willi syndrome symptoms
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
cause of Angelman syndrome symptoms
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
what is Global Developmental Delay
significant delay in at least 2 developmental domains term for children <5-6yo
137
Fragile X inheritance symptoms
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
Rett syndrome inheritance symptoms
X-linked (mostly affects females bc prob lethal in males) MECP2 gene rapid regression with loss of acquire skills late motor deterioration seizures
139
Sotos syndrome inheritance symptoms
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
PTEN hamartoma syndrome inheritance symptoms
AD macrocephaly characteristic skin findings- trichilemmomas, papillomatous papules incr risk for breast, thyroid, endometrial, and renal cancer
141
PTEN hamartoma syndrome includes what 4 conditions
- Cowden syndrome (also have autism/ID) - Bannayan-Riley-Ruvalcaba syndrome - PTEN-related Proteus syndrome - Proteus-like syndrome
142
PKU due to
deficiency of phenylalanine hydroxylase (converts Phe to Tyr)
143
if no other etiology of intellectual disability can be found, it is called?
multifactorial (or non-syndromic ID)
144
list some prenatal causes of ID
infections (eg rubella, CMV, syphilis, HIV) exposures (eg alcohol, teratogenic meds such as anticonvulsants)
145
list some perinatal causes of ID
- prematurity - infection - hypoxia - intracranial hemorrhage - trauma
146
list some postnatal (environmental) causes of ID
- trauma - CNS hemorrhage - hypoxia - env toxins (lead, mercury) - psychosocial deprivation - malnutrition - intracranial infections - CNS malignancy
147
blueberry muffin lesions seen in
congenital rubella
148
risk of congenital CMV highest in
1st trimester if primary infection during pregnancy
149
steps in evaluating pts with GDD or ID
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
Phencyclidine (PCP) mechanism of action
(related to ketamine) | NMDA (glutamate) allosteric antagonist
151
street names for PCP
oral = "T" | smoked or injected = "angel dust"
152
effects of PCP intoxication
- altered perception - reduced pain sensitivity - mood elevation - higher doses= inebriation, amnesia, mood swings, anxiety, aggression
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frequent PCP abuse can result in
PCP psychosis similar to schizophrenia symptoms
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3 approved medical uses of cannabinoids in US
- glaucoma - chemo induced nausea - wasting syndrome in AIDS
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CB1 receptors found in
nervous system immune system testis
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CB2 receptors found in
mostly immune system
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acute effects of cannabis
- incr HR - conjunctival injection - moderation sedation - mood alteration - altered perception, altered time estimation, impaired judgment - impaired short term memory
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rapid tolerance develops to what effect of cannabis
impaired short term memory
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list 3 abused inhalants
- nitrous oxide - volatile solvents and fuels - aliphatic nitrites
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where can abused N2O be found
whipped cream propellant (don't shake, just inhale) balloons
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examples of ppl who abuse N2O
concertgoers affluent health professionals late teens, college students
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dangers of N2O
hypoxia | accidents, falling
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what are some volatile solvents, fuels, anesthetics
``` 1,1,1-tricholoethane ether toluene butane gasoline ```
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what type of ppl abuse solvents, fuels, anesthetics
young disadvantaged international
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abuse of inhaled solvents produce effects that are most like what drug class?
CNS depressants
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pharmacological actions of abused volatile nitrites
- vasodilation - venous pooling in periphery --> dizziness, enhanced erections - smooth muscle relatxation
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what can cause Neuroleptic Malignant syndrome
``` all neuroleptics (Incl atypicals) and other D2 blockers ``` or abrupt withdrawal of dopamine agonists in parkinsons
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risk factors for NMS
- dehydration, malnutrition - prior NMS episode - rapid rate of neuroleptic loading - severe EPS, catatonia, prolonged restraints - Fe deficiency - Lithium?
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exam findings of NMS
same as malignant hypertension - elevated temp - muscle rigidity and other neuro symptoms - altered consciousness - autonomic dysfunction (labile bp, tachy, diaphoresis, urinary incontinence)
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lab findings of NMS
increased CPK (800 to >100,000) elevated WBC (10,000-40,000)
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what meds should you stop/not stop in NMS
STOP - neuroleptic - other D2 blockers - lithium - anticholinergics KEEP -dopamine agonists
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the most effective tx for severe NMS
ECT
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clinical features of serotonin syndrome
- delirium, restlessness, agitation - myoclonus, ataxia, seizures, rigidity, hyperreflecia - GI - autonomic fluct BP, incr pulse, respirations, sweating - hyperthermia
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treatment of serotonin syndrome
- stop all serotonergic drugs - supportive care Cyprohepatadine
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goals of community reinforcement approach
eliminate positive reinforcement for drinking/drugs enhance positive reinforcement for sobriety/abstinence
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what is the goal of motivational interviewing
create and amplify discrepancy between present behavior and pt's broader goals
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what is SBIRT
``` 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
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topographic model divides brain into what parts structural model divides brain into what parts
unconscious, preconscious, conscious id, ego, superego
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what is Takotsubo cardiomyopathy
acute HF in a stressful situation
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relationship between depression and CAD
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
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relationship between asthma and anxiety
anxiety aggravates asthma SOB causes anxiety many asthma drugs cause anxiety
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what are 5 major types of anxiety disorders
- GAD - OCD - panic disorder - PTSD - social phobia/social anxiety disorder
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moa Buspirone advantages / disadvantages
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
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hydroxyzine
H1 antagonist (antihistamine) Is an anxiolytic at doses that cause sedation (thus not widely used)
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what drug blocks sympathetic nervous system signs of fear and anxiety? under what circumstances can it be used for
propranolol (beta-adrenergic antagnoist) situation-specific anxiety and acute panic symptoms
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Kubler Ross stages of grief
``` Denial Anger Bargaining Depression Acceptance ```
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what are some differences between grief and depression
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
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what is the strongest predictor of future suicide attempt
previous suicide attempt
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list 4 treatment options for suicide risk
- containment (hospitalize) - decrease/modify risk factors - increase protective factors - restrict means
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components of a patient Safety Plan
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
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methods of making the environment safe (means restriction)
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)
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list 5 trauma/stressor related disorders
- Reactive Attachment Disorder (RAD) - Disinhibited social engagement disorder (DSED) - Acute stress disorder (ASD) - PTSD - Adjustment disorder
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list three types of extremely insufficienct care that can lead to Reactive Attachment Disorder or Disinhibited Social Engagement Disorder
- 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)
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Disinhibited Social Engagement Disorder describe their behavior
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
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Reactive Attachment Disorder describe their behavior
- 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
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treatment for RAD and DSED
safe healthy home env therapy to work on bond btwn child and new caretaker treat comorbid conditions meds aren't indicated
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categories of symptoms for ASD or PTSD
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)
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ASD vs PTSD
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
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what is PTSD with delayed expression
onset at least 6 months after the event
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PTSD treatment
NO BENZOS trauma focused therapy CBT SSRI, SNRI
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What is adjustment disorder -first line treatment?
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
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name and describe the three clusters of personality disorders, and the PDs in each cluster
Cluster A: odd-eccentric (paranoid, schizoid, schizotypal) Cluster B: dramatic-emotional (histrionic, narcissistic, antisocial, borderline) Cluster C: anxious-fearful (avoidant, obsessive compulsive, dependent)
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paranoid PD
(cluster A) pervasive distrust and suspiciousness of others
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schizoid PD
(cluster A) does not desire or enjoy close relationships restricted emotions, lacks empathy ex: lighthouse keeper
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schizotypal PD
magical thinking ideas of reference odd thinking and speech
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antisocial PD
(cluster B) no concern for others assoc w/ conduct disorder in childhood
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borderline PD
(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
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histrionic PD
(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
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narcissistic PD
(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
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avoidant PD
(cluster C) - pervasive social inhibition - feeling inadequate - fears being criticized, embarrassed, rejected - sees self as socially inept, unappealing, inferior to others
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dependent PD
(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
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obsessive-compulsive PD
(culster C) - preoccupied with perfectionism and the expense of flexibility, efficiency - rigid and stubborn
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selective mutism
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
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social anxiety disorder definition | -treatment?
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
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criteria for panic disoder | -treatment
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
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agoraphobia definition | -situations (5)
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
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GAD criteria list 6 symptoms that are associated with the anxiety/worry of GAD
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
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negative symptoms of schizophrenia
- affective flattening - avolition/apathy - asociality
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positive symptoms in schizophrenia
delusions hallucinations thought disorders motor disturbances
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what is Dopamine Hypothesis
schizophrenia / psychosis in general is result of excess Dopamine
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most imp feature in diagnosing autism spectrum disorder
impairment in social interactions - impaired reciprocal social interaction - self-absorption - lack affective contact - avoid eye contact - disinterest in others
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behaviors in autism spectrum d/o
- must maintain routines - speech- makes sounds, repeats words or phrases, idiosyncratic use of language - hand-flapping, toe walking, posturing - self abusive - idiot savant
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screening PCP office can identify children with Autism Spectrum D/o as young as
18 months (using M-CHAT)
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biologic etiology of ASD
fail to achieve normal pruning occasionally specific medical etiology (PKU, rubella, Fragile X)
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most common reason for evaluation for ASD
speech delay
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what must be ruled out before diagnosing ASD
hearing impairment
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most effective treatment for core symptoms in children w/ ASD
Applied Behavioral Analysis (ABA) no meds indicated for CORE symptoms Early intervention is critical!!
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meds for ASD and... - aggression/behavior prob - concurrent ADHD - self-stim behavior and sterotypies
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
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treatment for ASD with self-injurious behaviors
naltrexone | beta blockers
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according to DSM-V, ADHD is diagnosed before age
12
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neuromedical causes of ADHD (7)
- prenatal (alcohol, smoking) - lead - CNS infection - thyroid disorders - drug-induced - constipation (discomfort->fidgeting) - hunger
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psychosocial causes of ADHD (3)
- abuse (physical or sexual) - neglect - boredom
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name 3 nonmedication interventions for ADHD
- preferential seating - chunking tasks - behavior counseling
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course of ADHD in infancy
infant: - difficult temperament - minor congenital anomalies - poor mother-infant fit
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course of ADHD in toddler age
"restless dynamo" - accident prone - poorly coordinated - enthusiasitically intrusive - emotionally labile - hard to discipline - peer problems - low frustration tolerance
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course of ADHD in school age
- most referrals in this time b/c first experience w/ structure, rules - distractible, fidgety - poor self-concept
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describe the vicious cycle in ADHD
poor performance --> disapproval --> frustration --> low self-esteem --> worse performance
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course of ADHD in adolescence
- delinquency | - antisocial behavior
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psychostimulants to treat ADHD? - advantages - side effects
- methylphenidate - dextroamphetamine short acting, can take as needed not a/w later abuse SE: sleepiness, agitation GI upset, decreased appetite tics
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what other drugs can treat ADHD
TCAs (comorbid anxiety, depression) Clonidine, Guanfacine- a2 agonists (if aggression, irritability) SSRIs, bupropion buspirone if stmiulant not available atomoxetine Li, antipsychotics, anticonvulsants
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definiton body dysmorphic disorder
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
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definition hoarding disorder | -gold standard tx?
persistent diff discarding possessions CBT sessions in and out of home teach decision making and categorization exposure and habituation to discarding
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trichotillomania
recurrent pulling out one's hair repeated attempts to decrease or stop hair pulling
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excoriation disorder
(skin picking disorder) recurrent skin picking reuslting in lesions repeated attempts to decrease or stop picking
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name and describe two types of anorexia
both have low BMI restricting - no binging and purging; mostyl just diets, fasts, excess exercise binge-eating/purging type
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physical signs of anorexia
- 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
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treatment of anorexia in kids/teens? adults?
kids/teens- family based treatment. no meds adults- CBT or IPT
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common comorbid conditions with bulimia? (2)
substance abuse | borderline PD
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what is Russell's sign
calluses on knuckles | when bulimia forces self to purge, teeth can bite down on kunckles
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bulimia treatments
CBT | SSRI (firstline Fluoxetine)
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most common eating disorder
binge-eating disorder
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somatic symptoms disorder
physical symptom(s) that cause distress/impairment way out of proportion to objective disease signs
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etiologies of somatic symptoms disorder
- 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
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consequences of somatic symptom disorder
iatrogenic: incidentalomas, polypharmacy, polysurgery, radiation exposure, drug dependence frustrating MD-patient relationship --> doctor shopping invalidism and disability high medical costs missed actual medical illness!
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managing somatic symptom disorder
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
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illness anxiety disorder
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
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name two variations of illness anxiety disorder
care seeking care avoidant
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what is counterproductive in illness anxiety disorder?
getting too many tests (won't convince pt)
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what should you be alert for in illness anxiety disorder
complications of self-treatment (eg laxative abuse, hypervitaminosis A)
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what is conversion disorder - how diagnosed - when does it happen
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
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Hoover's sign
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)
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list 4 other tests tha could indicate conversion disorder
- 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)
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management conversion disorder
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)
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malingerirng
conscious faking to get a specific gain
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malingering mainly occurs in what groups
opioid addicts prisoners soldiers in wartime
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``` factitious disorder (aka Munchausen's syndrome) -what groups is it more common in ```
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