behavior and psych Flashcards
what criterion is the APGAR based off of
a score below what requires evaluation? what does the APGAR score relate about future childhood development
APGAR= NOT prognostic for future childhood developmental milestones
what are the infant reflexes and when do they disappear
moro reflex = extension of limbs when startled
palmar reflex= grasping of objects in palm
babinski reflex
rooting reflex= nipple seeking when cheek is brushed
disappear within first year
what is the finnegan scale
what are the criterion
assess neonates for the common signs and symptoms of neonatal drug withdrawal syndrome
CNS, respiratory, metabolic, and GI disturbances
-scare determines the severity of drug withdrawal sx and assesses the rsolution of sx after trx has begun
how to neonates with intrauterine opioid intoxication present
- at birth
- day 2-3
treatment at birth vs long term trx
- at birth
- respiratory depression, CNS depression, pinpoint pupuls
- low birth weight, premature birth, intrauterine growth retardation syndrome
- trx= naloxone
- day 2-3
- opiate withdrawal= neonatal abstinence syndrome
- tachycardia, dilated pupils, diaphoresis, sympa hyperactivity, diarrhea and vomiting, excessive crying and agitation
- long term trx= methadone to relieve the sx of withdrawal, eventually taper down to weane pt off
- what are the four classic signs+sx of narcolepsy
- what type of hallucinations are associated with narcolepsy
- what kind of sleep does the patient immediately enter after a narcoleptic episode
- how can narcolepsy be treated
- cataplexy (sudden, transiety loss of M tone), sleep paralysis (inability to talk/move upon waking or falling asleep), hypnagogic hallucinations, excessive daytime sleepiness
- associated with hypnagogic hallucinations = occur before falling asleep (‘gogic =’go to sleep’)
- vs hypnopompic hallucinations= occur during waking, can also be associated with narcolepsy
- REM sleep within 10 min of falling asleep
- trx=
- CNS stimulants (methylphenidate amphetamine) for excessive daytime sleepiness
- TCAs (clomipramine and imipramine) for cataplexy (sudden loss of M tone)
- +lifestyle changes (reducing stress, increasing exercise, and taking frequent daytime naps)
what EEG findings are associated with major depressive disorder
decreased REM latency and decreased stage 4, slow-wave sleep
-effective trx with antidepressants can reverse these findings
what are the 5 stages of falling asleep, with the associated EEF waveforms
what drugs affect stage 4 sleep
what physiological changes occur in REM
- awake w eyes closed
- alpha waves
- stage 1
- light sleep = 5%
- theta waves
- stage 2
- deeper sleep (45%)
- sleep spindles and K complexes
- stage 3-4
- deepest, non-REM sleep (25%)
- delta waves= lowest frequency, highest amplitude, slow wave sleep
- stage 4: shortened by imipramine (TCA) and benzos –> trx enuresis and night terrors, respectively
- REM (25%)
- dreaming, loss of motor tone
- beta waves
- inc in pulse rate and variability + REMs + inc BP with inc variability : penile/clitorial swelling/ vascular engorgement
- at what stage of sleep does nocturnal enuresis occur
- by what age is nocturnal enuresis a problem
- what pharamcologic agent can treat the condition in older children
- stage 4 sleep, the deepest form of sleep that’s not REM
- girls can stop by 6 yo, and boys by 7 yo
- imipramine= a TCA –> trx for primary nocturnal enuresis
- decreases the duration of stage 4 sleep
what NT
- initiates sleep,
- promotes REM,
- reduces REM
- initiates sleep,
- seretonin
- promotes REM,
- Ach
- reduces REM
- NE
what are night terrors and what drugs are used to treat them
night terrors = abdrupt awakenings from sleep, often with gasping/screaming. afterwords, the pt goes back to sleep and has no memory of the event
benzos are used to treat night terrors, bc they shorten stage 4 sleep
which antidepressant drugs …
- x the metabolism of NE and 5-HT
- x alpha-1 receptors on presynaptic noradrenergic receptors
- x NE reuptake
- x 5-HT reuptake
- work on Dopamine
- blocks H1 receptors
- is a 5-HT(1A) partial agonist
- is a nAchR partial agonist
- is a 5HT(1A) agonist and 5HT(2) antagonist
- x the metabolism of NE and 5-HT
- MAO-inhibitors (MAO is in the pre-synaptic N and will breakdown the NE+5HT into metabolites
- x alpha-1 receptors on presynaptic noradrenergic receptors
- mirtazapine
- x NE reuptake
- TCAs, SNRIs, bupropion
- x 5-HT reuptake
- TCA, SSRI, SNRI, trazodone
- work on Dopamine
- MAO inhibitors and bupropion
- block H1 receptor
- trazodone (also 5HT2, alpha adrenergic)
- is a 5-HT(1A) partial agonist
- Vilazodone (+5HT reuptake inhib)
- is a nAchR partial agonist
- varenicline
- is a 5HT(1A) agonist and 5HT(2) antagonist
- vortioxetine
the ____pathway connects the hypothalamus to the pituitary gland is responsible for the tonic inhibition of prolactin secretion
tuberoinfundibular
differentiate between somatic symptom disorder, conversion disorder, factitious disorder
what drugs are used to end the craving for alcohol
- what is the MOA
what drug ends the dopamine release from nicotine stimulation (end the reason for addiction)
naltrexone = mu opioid receptor antagonist
- inhibits rewarding and reinforcing effect
acamprosate= modulating glutamate
- modulate neurotransmission at the NMDA receptor
varenicline
- ends the dopamine release from nicotine stimulation (end the reason for addiction)
what is the treatment with
- serotonin syndrome
- neuroleptic malignant syndrome
- drug-induced antiparkinsonianism
- akathisia
*
- serotonin syndrome
- Cyproheptadine: 5HT2 blocker
- neuroleptic malignant syndrome
- Dantrolene: direct acting skeletal M relaxant
- drug-induced antiparkinsonianism
- (caused be D2 block in nigrostiatal pathway via antipsychotics/antiemetics)
- benztropine: anticholinergic agent
- DONT USE levodopa– can exacerbate/precipitate psychosis
- akathisia
- (subjective restlessn and inability to sit still rather than rigidity and tremor)
- diazepam: benzodiazepine + propranolol: beta blocker
define the defense mechanism ‘reaction formation’
TCA’s cardiotoxic effects are due to action at which receptor
what is the treatment for narcolepsy first line
narcolepsy = modafinil (nonamphetamine stimulant, probably at D-receptor)
amphetamines are second line
what is the difference between brief psychotic disorder, schizophreniform disorder, schizophrenia
differentiate between oppositional defiant disorder and disruptive mood dysregulation disorder
- what stage of sleep do nightmares happen (describe the EEG findings of this stage)
- differentiate from night terrors
nightmares= REM
night terrors= stage 4 sleep
who are the low potency and high potency first generation generation antipsychotics
MOA
and what are their adverse effects and trx of them
MOA= block D2 receptors in mesolimbic and striatofrontal systems
all 1st gen=
- highly lipophilic =slow to be removed from body
- prolactinemia (via adverse effect of blocking D in tubuloinfundibular pathway)
- metabolic syndrome = dyslipidemia, weight gain, hyperglycemia
- inc risk SEIZURES
- QT prolongation = torsades de pointes, sudden cardiac death
- neuroleptoc malignant syndrome (all drugs, but inc risk with high potency)
- Chlorpromazine= Corneal deposits: Thioridazine= reTinal deposits
- (M-block in low potency)anti-muscruinc : dry mouth, constipation >> others
- (H1 block in low potency) sedation
- (alpha-1 block in low potency) orthostatic hypotension and tachycardia
1st gen, high potency = characterized by EPS
“ADAPT” = order of EPS sx AD-A-P-T
- hrs: Acute Dystonia = M spasms and stiffness, oculogyric forced, sustained elevation of eyes
- trx= benztropine, diphenhydramine
- days-wks: Akathisia= restlessness + inability to sit still + Parkinsonism
- trx akathisia- beta-block, benztropine, benzopiazepine ::::: trx parkinsonian= benztropine, amantadine
- months-yrs: Tardaive Dyskinisia (chorea, esp orofacial= lip smacking, tongue protrusions, grimacing)
- trx=atypical antipsychotics clozapine, valbenazine, deutetrabenazine
what are the big three symptom types seen in Huntington vs Freidrich Ataxia
HD:
- chorea
- psychiatric sx
- subsequent dementia
Freidrich Ataxia:
- neurologic dysfunction
- cardiomyopathy
- diabeted mellitus
what are the 4 mood stabilizers used in the treatment of bipolar ds and what are the AEs of each
-which of the above drugs can also be used as anticonvulsants
Valproate, carbamezapine, and lamotrigine are also anticonvulsants
clozapine and olanzapine are both drugs in which class??
what AE are they both at high risk of causing, and how should patients on these meds be monitored
which toxicities are the following antidotes used for:
- physostigmine
- flumazenil
- naloxone
- cycloheptadine
- fomepizole
fomepizole= alcohol toxicity
drugs and MOA used to treat opioid addiction
what is the initial approach to parents who refuse to treatment for their family member (child, elderly parent..)
describe the 3 types of neuropsych AEs that can be seen with chronic antupsychotic use
what are the 4 dopaminergic pathways in the brain
which ones are affected by antipsychotics, and to what effect
what are the 4 most characteristic physiologic signs seen with marijuana use
which antiepileptic drugs work by
- blocking voltage gated Na channels
- blocking SV2A
- blocking voltage gated Ca channels
- agonizing GABA(A)
- antagonizing NT re-uptake
- inhibiting the formation of siccininc semi-aldehyde (SSA)
- blocking voltage gated Na channels
- –> block release of glutamate
- carbamezapine, (fos)phenytoin, lamotrigine, topiramate, valproic acid
- blocking SV2A
- block glutamate vesicle activation towards the membrane for glutatmate release
- levetiracetam
- blocking voltage gated Ca channels
- block Ca influx–> glutamate vesicle activation towards the membrane for glutatmate release
- ethosuximide, gabapentin
- agonizing GABA(A)-R
- GABA(A)-R activation –> Cl- influx –> inhibit AMPA and NMDA receptor-influenced depolarization
- benzos, phenobarbital, topiramate, propofol
- antagonizing NT re-uptake
- inhibit GABA reuptake receptor
- tiagabine
- inhibiting the formation of siccininc semi-aldehyde (SSA)
- inhibit GABA transaminase = x(GABA–>SSA)
- valproic acid, vigabatrin
co-administration with what drugs can lead to lithium toxicity
signs and sx of acute + chronic lithium toxicity
any drug that dec GFR : lithium build up
in patients with pre-disposed risk of having bipolar disease, what medication can precipitate a manic episode?
antidepressants
what PE findings are associated with anorexia nervosa..
differentiate between the fears and behaviors associated with anorexia vs bulimia
anorexia : low weight, amenorrhea, small hairs inc on arm, parotid gland swelling (if associated with vomiting)
differentiate between borderline personality disorder, dependent personality disorder, and histrionic personality disorder
define classical vs operant conditioning
what ways should you conduct a motivational interview with patients at the following stages of change
- precontemplation
- contemplation
- preperation
- action
- maintenence
- identification
distribution of what drug can precipitate opioid withdrawal in a patient with opioid dependence
what assessments can be done in the ED to assess for
- orientation
- comprehension
- concentration
- short term memory
- long term memory
- langiage
- visual spatial
- executive function
