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16 Cards in this Set

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differential diagnosis for coma? 6 answers
1. brain death
2. persistent vegitative state (wakefulness, no awareness)
3. locked in syndrome (ventral pons lesion)
4. frontal lobe dz (bilateral, prefrontal)
5. idiopathic stupor --> transient loss of consciousness in the elderly
6. nonconvulsive status epilipticus
coma - how to approach localization in CNS?
+/- focal/lateralizing signs signs, +/- meningeal irritation/CSF analysis, CT/MRI findings:
1. no focal signs/lateralizing signs (symmetric abnormalities) ---> toxin-induced, metabolic, infectious, shock, hypertensive encephalopathy
2. focal signs --> brain stem / cerebral infarction/hemorrhage, tumor, abcess
3. meningeal irritation: need to workup for bacterial meningitis, viral enceph, subaracnhoid hemorrhage
coma - give 5-6 categories of signs to look for to determine etiology / localize
1. lateralizing signs: focal neuro injury
2. pupillary abnormalities / other cranial nerve lesions: brainstem injury
3. oculocephalic reflexes (+/-): resistant to metabolic dysfunction
4. meningeal irritation: if present, thing meningitis, encephalitis, subarachnoid hemorrhage
5. breathing pattern: if normal, usually brainstem spared
Evaluation of coma:
1. 5 imp pieces of hx
2. 3 VS (and why)?
3. 4 imp general physical exam (and why)
4. neuro exam (6 imp pieces)
5. Lab / initial workup (5-6)
6. Imaging / other tests depending upon initial workup
1. witnesses, how EMS found, PMH, hx of recent illness / fever, drug use
2.
-BP (HTN/hypotensive event),
-Temp (infxn, anticholinergic versus hypothermic)
-RR/O2 sat: brainstem lesion, determine if patient needs to be intubated
3. skin (bruising, color, jaundice), breath (uremia), abdomen (DKA), OP (bitten tongue in seizure)
4. GCS, meningeal signs, pupillary response, corneal reflex, oculocephalic reflexes, motor exam (for tone, reflexes)
5. 1)CBC, 2)Chem10 (lytes disturbance, glucose level), 3)tox screen 4)UA 5)CXR 6)ECG-arrhythmia/MI
6.
1)ABG (resp status) (acidosis, renal/liver failure)
2)CT/MRI (suspected infarct, hemorrhage, abcess, structural lesion)
3)LP (r/o menigitis)
4)EEG (?seizure disorder)
Treatment for 38 yo transiently unconscious man who lapses into deep coma, stiff neck, hepatomegaly, needle track marks, withdraws to painful stimulation (R>>>L), muscle tone / reflexes inc on left
In this patient, coma is likely due to secondary cause. Heroin OD should be suspected due to high suspicion of recent drug use. Hepatic encephalopathy also possible with hepatomegaly on exam. Meningitis, hepB, encephalitis, other infectious processes on differential due to high fever, meningeal signs, and suspected drug use.
address the
1. ABCs (protect airway, need for intubation?, BP - need for IVF, central line, pressors)
2. Naloxone (if opioid OD suspected, ?pinpoint pubils, low RR)
3. Broad spectrum antibiotics (IV ceftriaxone needed if high suspicion for bacterial meningitis or SBP)
definition of dementia?
memory impairment +/- cognitive decline in other domain (aphasia, apraxia, agnosia, exec fnxn)
differential diagnosis of dementia? 7 types and examples of each (specifically first)
1-Degenerative:
1)Alzheimers,
2)Parkinsons
3)Lewy body dementia,
4)frontotemporal
5)progressive supranuclear palsy (PSP)
2-Vascular (multiple infarcts, single stroke, vasculitis, infectious)
3-Psych (depression, drug/ETOH abuse)
4-Toxic/Metabolic (B12 def, hypothyroid, drug/metals
5-Trauma (subdural, anoxic injury)
6-Tumor-primary, metastatic
7-hydrocephalus
68 yo military vet 3 yr hx of prog memory difficulty. pmh sig for rep closed head injuries, 20 yr hx of HTN, family hx of mother with death after prog cognitive decline; complains of sadness/low energy, 30lb wt loss, bilat carotid bruits, disoriented to year, 0/3 recall, viswual-spatial difficulties, paraphrasic errors, stiff gait (small, shuffling steps), left babinski
most likely possibilities?
1. Alzheimers (progressive decline, language and visuospatial decline, weight loss)
2. Vascular dementia (multi-infarct, unctrolled HTN, left babinski, gait abnormalities)
3. Parkinsons (less likely, but shuffling gait supports)
4. aldomet-induced parkinsoniasm (w/ shuffling gait, cognitive decline)
5. Depression (weight loss)
68 yo military vet 3 yr hx of prog memory difficulty. pmh sig for rep closed head injuries, 20 yr hx of HTN, family hx of mother with death after prog cognitive decline; complains of sadness/low energy, 30lb wt loss, bilat carotid bruits, disoriented to year, 0/3 recall, viswual-spatial difficulties, paraphrasic errors, stiff gait (small, shuffling steps), left babinski - evaluation of this patient?
HX, Physical, Labs (5), others?
1. hx- of cog decline (timing, ADLs, iADLs change, safety issues, ROS (tremors, weakness, aphasia, difficulty swallowing, incontinence, vascular risk factors, PMH etc.)
2. physical: VS, BP, Mini-mental exam, full neuro (thorough mental status exam), weakness, gait analysis
3. Labs (CBC, Chem10, thyroid, B12, VDRL, neuroimaging (vascular, trauma)
4. Others (dep on situation): EEG, LP, infectious workup, tox screen / heavy metal screen, alcohol level
Treatment for Alzheimers:
1) self care
2) Cognitive/behavior improvement meds
3) Behavior modifiers
4) Disease modifying
1) Self-care @ home: home safety eval, indep living versus assisted living, checks by relatives/friends, VNAs (meds)
2)Nondrug treatments - therapy (CBT), cholinesterase inhibitors (improve/stabilize cognitive fnxn, +effects on behavior/ADLs)

MEDS:
1.Cholinesterase inhibitors (e.g. Aricept) -stabilize cognitive functions, improve memory, helps ADLs
c)Behavioral modifiers: antidepressants (SSRIs), atypical antipsychotics, mood stabilizers (for extreme behavioral issues)
d)VitE, hormone replacement, anti-inflammatories
differential diagnosis for seizure? confused with seizure?
Seizure
1. idiopathic epilepsy
2. theophylline withdrawal induced seizure
3. simple partial or complex partial with secondary generalization
4. drug toxicity (specifically cocaine in this case, also amphetamine, liodaine)
5. secondary metabolic (e.g. electrolyte abnormalities - hypoNa+,hypoCa+,hypoMg+, hyperglycemia)
6. Acute neurologic insult (e.g. stroke, infection)
7. Structural lesions- tumor, trauma, infection (abcess, meningitis, encephalitis)
8. Familial: primary generalized epilepsies
9 Genetic (unlikely in this patient): NF, TS, PKU
Confused with seizure: syncope, psychogenic siezures, CBA, migraine, narcolepsy, movement disorders, ETOH withdrawal
evaluation of first seizure?
1. Hx questions
2. Physical (3-4)
3. Labs
4. Other tests (depending upon suspicion of diagnosis/etiology)
1. Hx: witnesses of seziure to classify it, loss of consciousness, post-ictal state, prior seizures, meds, previous treatment for seizures, neuro deficits, ROS, family hx (e.g. tuberous sclerosis, NF)
2. Phys: VS, limb assymetries, neuro deficits, MS exam (post-ictal, change from baseline?)
3. CBC, BMP, tox screen, theophylline level, ESR, VDRL, tox screen, HIV status, ESR (?vasculitis)
4. EEG (characterize seizure), LP with CSF analysis (if indicated - suspect infectious, inflammatory etiology), neuroimaging (if structural/ischemia), EKG/holter (if syncope suspected), sleep study (narcolepsy)
3. ?CT scan (if suspect head trauma with seizure)
Describe difference between seizures and epilepsy.
Seizure: sudden change of behavior due to brain dysfunction.

Epilepsy (syndrome): presence of more than one (recurrent) seizure that is due to intrinsic CNS dysfunction and not attributed to secondary systemic process.

Non-epileptic seizures: non-recurrent, toxic-metabolic, other secondary cause- not assoc with neurophysiologic change of true epilepsy
24 yo man with single generalized tonic-clonic seizure. hx of febrile seizures, remote history of head injury with loss of consciousness (post-MVA) on theophylline, +sleep deprivation, +family hx for epilepsy in 1st degree relatives.

Would you treat this patient with anticonvulsants? Justify your answer.
4. Initiating treatment in this patient would likely be premature. This patient may have underlying epilepsy, however, given his cocaine use, sleep deprivation, and theophylline medication (all which can directly cause seizure or lower siezure threshold potential), this patient may never have another seizure if these secondary factors were not in play.I would therefore follow the patient, correct underlying factors that may be secondary cause of initial seizure, and for seizure activity, and monitor for future seizure activity, and if it does, then consider a diagnosis of epilepsy and initiation of anticonvulsant treatment.
Differential diagnosis for parkinsons disease (5 categories)?
1. Degenerative: Parkinsons disease, Huntington's
2. secondary parkinsoniasm (drug-induced - reglan, antopsychotics, toxins, head trauma, infection small vessel dz)
3. Other tremor states (e.g. ET, familial tremor)
4. Psych: depression, catatonia
5. Metabolic: hypothyroid, hypoglycemia
pathophys and anatomic structure involved in parkinsons?
Pathophys:
Parkinsons disease is thought to be the result of a pathophysiologic process involving depletion of the dopaminergic neurons in the substantia nigra (specifically the pars compacta region). Resulting loss in dopamine neurotransmission results in disruption of the nigrostriatal pathway, leading to dysfunction of basal ganglia output to the cortex via the thalamus, resulting in motor symptoms.