Diagnoses IV Flashcards
3 subtypes of mental retardation based on etiology
Mental retardation
- Organic (idiopathic)
- Prenatal (genetic)- Fragile X, Downs, TORCHES (perinatal infection), Prader-Willi
- Perinatal or postnatal: fetal alcohol, lead or mercury exposure
Criteria for mental retardation
MR/ID: Subaverage IQ below 70 + developmental disability
Developmental disability = deficits in 2+
- self care, learning, mobility
- receptive/expressive language
- self-direction, independent living
- economic self sufficiency
Which 2 diseases overlap significantly w/ Tourette’s syndrome
High comorbidity/overlap btwn Tourette’s, OCD, and ADHD
Tourettes
(a) more common in which gender?
(b) neurochemical mechansim
(c) time criteria
Tourette’s
(a) 3:1 M:F
(b) Dopamine dysregulation in the caudate
(c) 12+ months of both motor and vocal tics
What makes it difficult to treat comorbid Tourettes and ADHD
Tourette’s and ADHD are often comorbid, but stimulants can make the tics worse => have to find a good balance
- pimozide or haloperidol for Tourette’s
- low stimulant for ADHD (low enough to not exacerbate tics)
- clonidine
Psychopharm to treat Tourette’s d/o
- typical antipsychotic: usually pimozide or haloperidol
- clonidine = alpha2 agonist
Enuresis
(a) time requirement
(b) age requirement
Enuresis = involuntary voiding of bladder
(a) 3+ months, twice a week
(b) after age 5
Distinguish chronic pain vs. chronic pain syndrome
Both are pain w/o apparent biological cause
Chronic Pain: 3+ months, NOT maladaptive
Chronic Pain Syndrome: 6+ months, MALADAPTIVE**
-factors: depression, inactivity
Intermittent Explosive D/o
(a) more common in which gender
(b) neurochemical etiology
(c) symptoms
(d) differentiate from ATPD
Intermittent explosive d/o
(a) almost always in females
(b) low 5HT
(c) impulses of assault or property destruction out of proportion to the trigger
(d) intermittent explosive d/o- pts usually feel remorseful afterwards (while ASPD don’t have remorse)
Treatment for Intermittent Explosive D/o
Intermittent explosive d/o treatment
- SSRI, anticonvulsant, lithium, propanolol
- group therapy
**psychotherapy not helpful
What is kleptomania?
Kleptomania = stealing not for personal or monetary gain
-pleasure is derived from the act of stealing
Kleptomania
(a) more common in which gender
(b) common comorbidity
(c) therapy
Kleptomania
(a) F > M
(b) 1/4 of bulimics are kleptomaniacs
(c) insight-oriented psychotherapy
Pyromania
(a) more common in which gender
(b) common morbidity
Pyromania
(a) F > M
(b) common in MR
Criteria for pyromania
Criteria: 1+ intentional fire setting
- tension before fire, relieved after
- fascination w/ fire
- not for monteary gain or expression of anger
Tx for pyromania
- behavior therapy
- SSRI
What is trichotillomania?
Trichotillomania = recurrent pulling out of hair resulting in visible hair loss
-can be eyebrows, public hair
- tension before, relieved by action
- causes marked distress or impairment
Trichotillomania
(a) more common in which gender
(b) common comorbidity
(c) common trigger
(d) treatment
Trichotillomania
(a) F > M
(b) comorbid w/ OCD/OCPD
(c) often after stressful event
(d) tx: SSRI, antipsychotic, hypnosis, behavioral therapy
Define delirium
Basically a change in mental status w/ evidence of underlying cause
- impaired consciousness
- change in cognition or perception
- acute onset, fluctuates
WHIMP acronym for delirium
Etiologies of delirium
W- Wernicke's encephalopathy (B12 deficiency) H- hypoxemia I- intracranial bleeding M- meningitis P- poisons
Delirium vs. dementia
Main difference
(a) onset
(b) duration
(c) alertness and attention
(d) sleep
(e) consistently of course
Delirium vs. dementia
Change in mental status vs. memory problems
Delirium
(a) acute onset
(b) transient, hours to days
(c) alertness and attention are impaired
(d) awake at night (same as dementia)
(e) fluctuates**
Dementia
(a) insidious, gradual onset
(b) much longer lasting: months to years
(c) alertness and attention are normal
(d) awake at night
(e) symptoms stable throughout the day
Treatment for delirium
(a) Use
(b) Don’t use
Delirium treatment
(a) Quetiapine or haloperidol
(b) Avoid benzos- can have paradoxically worsening effect in elderly
Hallmarks symptoms of delirium
Waxing and waning symptoms (may have lucid intervals)
- visual hallucinations
- short attention span
- impairment in recent memory
- disorientation: usually to time and place
Most common finding in delirium
Impairment in recent memory
What can cause delirium?
Almost any medical condition can cause delirium
Most common causes
- infection
- meds
- intoxication or withdrawal
- electrolyte imbalance
Delirium + hemiparesis
Delirium + focal neurological symptom (like hemiparesis)- think CVA (cerebral vascular accident- TIA/stroke) or mass lesion
=> get brain CT/MRI
Delirium + elevated BP + papilledema
Delirium + elevated BP + papilledema (optic disc swelling) = hypertensive encephalopathy
=> get brain CT/MRI
Delirium + dilated pupils + tachycardia
Delirium + dilated pupils + tachycardia = drug intoxication (ex: cocaine)
=> get UTOX
Delirium + fever + nuchal rigidity + photophobia
Delirium + fever + nuchal rigidity + photophobia = meningitis
=> get lumbar puncture
Delirium + tachycardia + tremor + thyromegaly
Delirium + tachycardia + tremor + thyromegaly = thyrotoxicosis
=> get T4 or TSH level
Delirium + cogwheel rigidity + resting tremor
Lewy body dementia vs. Parkinsons disease
Dementia + obesity + constipation + cold intolerance
Hypothyroidism
Dementia + diminished position and vibration sensation + megaloblasts on CBC
Vitamin B12 deficiency
Dementia + tremor + abnormal LFTs + Kayer-Fleischer rings
Wilson disease
Dementia + diminished position and virbation sensation + Argyll Robertson Pupils
Argyll Robertson Pupils = accommodation response present, response to light absent
= Neurosyphilis
Screening test for dementia
Mini mental status exam (MSSE)
- assesses orientation, attention/concentration, language, recall
- sensitive for dementia, particularly moderate to severe forms
- perfect score (30), dysfunction under 25
List the 3 most common types of dementia
Dementia
Most common type = Alzheimers: 60-70%
Second = Vascular dementia: 15-20%
Third = Lewy Body Dementia: 10-15%
Fourth = frontotemporal (Pick’s disease) 5%
Neurochemical mechanism of Alzheimer’s
Decrease in acetylcholine due to loss of noradrenergic neurons in the basal ceruleus and decreased choline acetyltransferase (required for ACh synthesis)
-due to amyloid cascade hypothesis: excess of A-beta peptides
ApoE4
Gene that increases susceptibility to Alzheimer’s
What kind of cognitive decline is associated w/ Down’s syndrome
Down’s syndrome pts have increased risk of Alzheimer’s
-neurofibrillary tangles and senile plaques are found in both
Pharma treatment for Alzheimer’s
(a) 2 drugs for mild to moderate disease
(b) 1 drug for moderate to severe disease
Alzheimer’s drugs
(a) Mild to moderate disease: use cholinesterase inhibitors
- Donepezil (Aricept)
- Rivastigmine (Exelon)
(b) Moderate to severe disease: NMDA antagonist
- Memantine (Namenda)
Risk factors for vascular dementia
- hypertension
- CAD
- Afib
CT findings of vascular dementia
Multiple small lacunar infarcts (small vessel disease)
-multiple cortex lesions => step-wise process as these accumulate
Pathological process of lewy body dementia
LBD = 3rd most common dementia
-lewy bodies (pathologic alpha-synuclein aggregates) in the brain, primarily in the basal ganglia
3 key features of lewy body dementia
- waxing and waning course
- visual hallucinations
- Parkinsonism
Treatment for lewy body dementia
- cholinesterase inhibitors (Donepazil, Rivastigmine) help improve VH
- L-dopa and dopamine agonists may improve cognition, psychomotor slowing
Key features of frontotemporal dementia
- faster progression to death (4-6 years, vs. 10 years for Alzheimer’s)
- profound personality changes w/ preservation of language and memory
Most common dementia caused by infectious disease
HIV-associated dementia
Percent of Parkinson’s pts that develop dementia
30-40%
-resemble Alzheimer’s type, but the dementia is not the initial symptom
Most common clinical feature of CJD
Creutzfeld-Jakob Disease
-90% of pts have myoclonus (sudden muscle spasms)
Name 2 types of potentially reversible dementia
- normal pressure hydrocephaglus
- hypothyroidism induced dementia
Clinical triad of NPH
Normal pressure hydrocephalus: 3 W’s
Wobbly: gait disturbance = apraxia (often appears first)
Wet = urinary incontinence
Wacky = Dementia (mild, insidious onset)
Differentiate presenting symptoms of Alzheimer’s and Vascular dementia
Vascular dementia- same symptoms of Alzheimer’s + focal neurological findings
-also Vascular dementia proceeds in step-wise fashion
Cardinal signs of Parkinson-type dementia
-bradykinesia, tremor, rigidity, postural rigidity
Treatment of normal pressure hydrocephalus
Shunting of cerebral aqueduct
-provide CSF drainage
What is transient global amnesia
Inability to learn new info + inability to recall recent info
-personal ID not lost
-almost always recover
Kofsakoff’s syndrome
Alcohol induced amnesia Comorbid Wernicke's encephalopathy = confusion, ataxia, opthalmoplegia (paralysis of muscles around the eye) -confabulation -apathy -passivity
Prognosis for Kosakoff’s syndrome
Thiamine => 25% recover totally
-25% never recover
What is amnestic disorder
Inability to learn new info OR inability to recall old info due to a medical condition (axis III)
-poor insight => confabulate
Define hazardous drinking for M and F
Hazardous drinking
Men: 5+ drinks/day
Women: 4+ drinks/day
How long can the following be detected in the urine
(a) EtOH
(b) Cocaine
(c) PCP
(d) Sedative hypnotics
(e) Amphetamines
(f) Opioids
UTOX
(a) EtOH- not in urine! use breathalyzer or BAC
(b) Cocaine- positive for 3 days
(c) PCP positive for about 1 week
(d) Benzos positive for about 1 week
(e) Amphetamines for about 3 days (same as cocaine)
(f) Opioids for 12-36 hrs
Treating alcohol withdrawal
(a) good vs. bad liver fxn
(b) supportive
(c) long term plan
Treating alcohol withdrawal
(a) Benzossss
- Lorazepam (or Oxazepam/Temazepam) if poor liver fxn
- longer acting if good liver fxn
(b) supportive = banana bag
(c) AA
Name the 3 components of a banana bag and their functions
Banana bag = IV fluids + thiamine + folic acid + MgSO4
(a) thiamine- B1 to prevent Wernicke-Korsakoff syndrome
(b) folic acid to replenish (quickly depleted w/ alcohol intake
(c) MgSO4 to prevent seizures
Which 2 drugs of abuse don’t have a withdrawal syndrome?
No withdrawal syndrome = PCP and hallucinogens
PCP: no withdrawal but flashbacks common
Alcohol withdrawal
(a) 6-24 hr
(b) within 72 hrs
Alcohol withdrawal
(a) 6-24 hrs: insomnia, anxiety, irritability, tachycardia, hyperreflexia, delirium, HTN, seizures, hallucinosis
- hallucinosis = hallucinations while alert and oriented
(b) w/in 72 hrs: DT
- delirium tremens, 20% mortality
- visual/tactile hallucinations
Pupillary reaction to
(a) cocaine/amphetamine intoxication
(b) PCP
(c) benzos
(d) opioid intoxication
(e) hallucinogen intoxication
(f) opioid withdrawal
Pupillary rxn
(a) Cocaine/amphetamine intoxication = dilated pupils (tons of sympathetic tone)
(b) PCP => rotary nystagmus
(c) Benzos => nystagmus
(d) Opioid intoxication: constricted pupils (miosis)
(e) hallucinogens => dilated pupils
(f) opioid withdrawal => dilated pupils (mydriasis)
Serotonin syndrome vs. NMS
(a) reflexes
(b) use of bromocriptine
(c) rigidity
(d) degree of dysautonomia
(e) CPK level
(f) reason for fever
SS vs. NMS
SS
- hyperreflexia
- bromocriptine could make it worse
- rigidity less severe, more cogwheel not lead pipe
- less severe dysautonomia
- mildly elevated CPK (like 400s)
- fever produced peripherally
NMS
- hyporeflexia
- bromocriptine (DA agonist) helpful
- severe rigidity
- severe dysautonomia
- extremely elevated CPK (like 60-80,000)
- fever produced by DA blockade at hypothalamus (centrally)
Explain the following in SS/NMS
(a) CPK levels
(b) renal risk
SS/NMS
(a) CPK levels are elevated b/c of muscle rigidity
(b) Renal risk b/c of the tons of protein breakdown products the kidney has to deal with
What are the effects of hallucinogens?
(a) duration of effect
Hallucinogens: psilocybin (shrooms) and LSD (lysogenic acid diethylamide) have stimulant-like effects
- dilated pupils
- perceptual distortions
(a) last 8-12 hrs
How to treat opioid
(a) overdose
(b) withdrawal
(b) dependence
Opioid
a) overdose => Naloxone (opioid receptor blocker
(b) withdrawal:
- clonidine (alpha agonist)
- buprenorphone
How to treat PCP intoxication
(a) Way to increase rate of clearance
(b) Treating symptoms
(c) For psychosis- why may not treat this?
PCP intoxication
(a) increase clearance by acidifying urine (give ammonium, NH4+)
(b) Treating symptoms
- tx muscle rigidity => benzos, DA agonist
(c) If psychosis- potentially give haloperidol
- however this worsens the hyperpyrexia
Lab values in PCP intoxication: two things that are elevated
PCP intoxication:
- elevated CPK
- elevated AST
Mechanism of PCP
PCP = NMDA antagonist
Symptoms of PCP intoxication
- aggression
- increased pain tolerance
- rotary nystagmus
- ataxia
- muscle rigidity
Mechanisms by which benzo withdrawal can be fatal
Seizures
How to treat overdose of
(a) cocaine/amphetamines
(b) barbiturates
(c) benzos
Treating overdose
(a) cocaine/amphetamine tx w/ benzos
(b) barbiturate OD- alkalinize urine
(c) Benzos- Flumazenil
Describe opioid withdrawal
Wet:
- lacrimation (tears)
- rhinorrhea (runny nose)
- N/V/D
- piloerection (goose bumps)
- generalized myalgias
- mydriasis (dilated pupils)
- yawning
*not life threatening, but treat (w/ clonidine/buprenorphone) b/c uncomfortable for pt
