brain death Flashcards

Question

alzheimers dementia symptoms

Answer 1

-Memory impairment (MC)- Especially anterograde episodic amnesia > Retrograde -Impaired executive function- Early on will be aware of these deficits and With time will have reduced insight (anosognosia) -Behavioral and psychologic symptoms- Especially apraxia, sleep disturbance -Gait dysfunction (late) -No motor or sensory deficits at presentation

Answer 2

-Mild: -Wandering, getting lost, repeating questions -Moderate: -Problems recognizing friends and family -Impulsive, loss of judgement and reasoning is inevitable -Disinhibition and uncharacteristic belligerence may occur- Alternate with passivity and withdrawal -End stages: -rigid, mute, incontinent, and bedridden -Need help w/ eating, dressing, and toileting -Hyperactive tendon reflexes and myoclonic jerks (sudden brief contractions of various muscles or whole body) -> occur spontaneously or in response to physical or auditory stimulation -Death: -2ndary to malnutrition, 2ndary infections, pulmonary emboli, heart disease -MC- aspiration -Changes in environment (hospitalization, travel, NH) tend to destabilize pt -8–10 years usually, but ranges from 1–25 years

Answer 3

-dx -> exclude other etiologies of dementia -CT/MRI brain: -Brain atrophy- Medial temporal lobe (reduced hippocampal volume)! -Mild ventricle dilation -Management: -Acetylcholinesterase inhibitors: DONEPEZIL!! 10mg QD (1st line), rivastigmine -Reverses cholinergic deficiency -SE: GI upset (nausea/diarrhea/cramps), altered sleep w/ vivid dreams, bradycardia, muscle cramps -NMDA antagonists: Memantine -> Blocks NMDA receptor, which means it blocks the excitatory glutamate, which causes cell death -Vitamin E

Answer 4

-2nd MCC of dementia -Brain disease due to chronic ischemia! and multiple small infarctions! (lacunar infarcts) -Highly assoc with older age and CVD (IHTN, DM, HLD, PAD, obesity, smoking, afib) -2 types: -Post stroke dementia -Vascular dementia without recent stroke -DSM 5 criteria -cognitive deficits manifested by both: -Impaired memory -Aphasia, apraxia, agnosia, disturbed executive function -Significantly impaired social, occupational function -Focal neurologic sx and signs of cerebrovascular disease -STEPWISE deterioration after each event

Answer 5

-pure vascular dementia is less common than multiple-etiology ("mixed") dementia. -Alzheimers is MC co-occurring pathology with vascular dementia

Answer 6

-Cortical and subcortical infarctions -Lacunar infarcts -Microbleeds

Answer 7

-Vascular risk modification -Antithrombotic therapy- Usually ASA -Cholinesterase inhibitor therapy: Donepezil or galantamine -Prognosis: -Bc its a heterogeneous disorder -> prognosis is not predictable

Answer 8

-Rare! -Focal degeneration! of frontal and/or temporal lobes! with distinctive round silver staining inclusions (called pick bodies) -Symptoms: -1. Marked personality and behavioral changes- disinhibition, apathy, altered food preferences, compulsive -2. Aphasia- Non-fluent, expressive aphasia common: Words remain but are presented in nonsensical format -3. No amnesia or visuospatial symptoms -> Lack CN, sensory, cerebellar changes at least initially -Changes occur early and progress quickly -Epidemiology: -Younger (mean age 58 yo) -Male predominance -MRI: !Frontal and/or temporal atrophy! -Tx: -symptomatic -Non-pharm interventions for safety: driving, exercise, speech therapy, behavioral modification -SSRI- Citalopram! Trazodone

Answer 9

-Pathophysiology: -Eosinophilic intracytoplasmic inclusions (Lewy Bodies) in brain -Dementia associated with: -Psychotic features: Visual hallucinations and delusions! -Motor parkinsonism!- bradykinesia, slow, rigid, shuffling -Cognitive fluctuations! -REM behavior disorder!- act out whats happening in sleep -Dysautonomia!- BP drops, neurocardiovascular instability, syncope -Visuospatial dysfunction

Answer 10

-CT/MRI: -Generalized atrophy and white matter lesions are nonspecific findings in dementia -No test can definitively dx DLB -go based on DSM criteria

Answer 11

-Cholinesterase inhibitor trial (1st line, for dementia + visual hallucinations) -Levodopa (for parkinsonism) -Melatonin or clonazepam (for REM behavioral disorder) -SSRI (for depression) -should NOT be given older, antipsychotic agents -> haloperidol (Haldol), fluphenazine (Prolixin), and chlorpromazine (Thorazine) -ADR- sedation, rigidity, postural instability, falls, increased confusion, and neuroleptic malignant syndrome, w/ assoc 2-3fold increase in mortality

Answer 12

-Dementia that occurs in later stages of Parkinson’s disease -Occurs 5-8 years after onset of motor symptoms of PD -(unlike DLB -> dementia starts first, followed by motor parkinsonism within a year of onset) -Parkinsonian features: -Tremor, rigidity, bradykinesia -Cognitive impairments -Gait dysfunction -Urinary incontinence -TX: -Levadopa 1st line -Cholinesterase inhibitors

Answer 13

-Organic and possibly reversible cause of dementia -CSF buildup in ventricle -> leads to increased ICP w/ edema of periventricular white matter -Oddly, do not have symptoms of ↑ ICP (HA, N/V, Visual loss) -Classic triad (not all 3 are required)- WET WHACKY WOBBLY -1. Urinary incontinence -Urgency, but unable to get to bathroom in time -Late: lack of concern due to ?frontal lobe impairment -2. Cognitive disturbance -Dementia, memory loss -Develops over months – years -Impaired executive function (early), apathy (depressed), psychomotor slowing, decrease attention and concentration -3. Gait disturbance -Difficulty with ambulation -"Glue-footed" gait: move slowly, take small steps, often wide base, with difficulty turning -tx- shunt- relief of pressure

Answer 14

-Rapid onset!* dementia -due to prion (misfolded protein) disease -Sporadic type: Normal brain protein misfolds -Variant type: Consuming misfolded proteins - MAD COW disease eat from cow with spongiform encephalopathy -Familial CJD: rare genetic form- misfold in adulthood -Iatrogenic CJD: obtain through blood transfusion or corneal transplant -Clinical features: -Neuropsychiatric symptoms! are uniformly seen and may manifest as dementia, behavioral abnormalities, and deficits involving higher cortical function including aphasia, apraxia, and frontal lobe syndromes -Myoclonus!, especially provoked by startle -Cerebellar manifestations!: nystagmus and ataxia -Signs of corticospinal tract involvement!: hyperreflexia, Babinski sign, spasticity. -Extrapyramidal! signs: hypokinesia, bradykinesia, dystonia, rigidity -DMS 5 criteria (dont need to know), normal EEG, Positive 14-3-3 CSF protein on LP suggest CJD (not always +) -Definitive dx post mortem with neuropathology -No known tx, fatal disease within 1 year of onset

Answer 15

-causes Wernicke's encephalopathy -Malnourished pt (alcoholism, AIDs, anorexia, ESRD, hematologic malignancies due to hypermetabolic state) -Triad: -1. Encephalopathy (disorientation, indifference, inattentiveness, memory loss) -2. Ataxia (gait problems) -3. Ocular motor dysfunction (diplopia, nystagmus) -Thiamine 100mg IV x 3 days followed by daily PO may reverse disease if given in first few days of onset (thiamine THEN glucose) -KORSAKOFFF SYNDROME- prolonged, untreated Wernicke’s encephalopathy -IRREVERSIBLE -Unable to recall old AND new information -Confabulations = unconsciously makes up stories to fill gaps in memory

Answer 16

-deficiency causes megaloblastic anemia -Produces spinal cord myelopathy!! that affects the: -Posterior columns -> loss of vibration and proprioception -Corticospinal tract -> hyperactive tendon reflex w/ babinski -Peripheral nerves -> neuropathy with sensory loss and depressed tendon reflex -Damage to myelinated axons may cause dementia

Answer 17

-(1) Cholinesterase Inhibitor: Donepezil!!!! (Aricept), Rivastigmine, Galantamine (Razadyne) -MOA: Reverses cholinergic activity deficiency, may not always slow down progression but helps symptomatic treatment -Indications: newly diagnosed AD, DLB, VaD, PD Dementia -ADR: GI upset (N/V, anorexia, diarrhea), bradycardia, rhabdo, NMS (rare) -CI: Known bradycardia, caution if using BB/CCB (2) Vitamin E 2000 IU/day!!!! -Indications: mild-moderate AD (only) interested in non-pharmacologic tx (3) NMDA Antagonist: Memantine!!! (Namenda)10 mg BID -MOA: blocks @ NMDA receptor, slows calcium influx and nerve damage -> Neuroprotective -Glutamate causes excitotoxicity of NMDA receptor, causing cell death -Indications: monotherapy or adjunct for moderate-severe Alzheimers dementia -Off-label use: Vascular dementia, Mild Alzheimer’s dementia, chronic pain, psychiatric disorders, mild cognitive impairment -ADR: Dizziness (MC), confusion, hallucinations, agitation, delusions

Answer 18

-Young onset dementia (<65yo) -Strong family HX -Non-Alzheimer dementia is suspected -Early age, rapid progression, severe behavioral changes, language problems, hallucinations, Parkinsonisms -Uncertainty about dx- Is it their age, depression, encephalopathy?

Answer 19

-AD -vascular -parkinsons -B12 deficiency- posterior involvement? -creutzfelt jakob -frontal temporal lobe dementia

Answer 20

-AMS is a symptom, not a disease! -Ascending reticular activating system (ARAS) = gives us consciousness -in the brain stem and its central connections to the thalamus and cerebral hemispheres.

Answer 21

-alert -awake but disoriented or aphasic -drowsy - lethargic but arousable to voice, light touch -obtunded- lethargic, but arousable to vigorous mechanical stimulation -stuporous- localizing to deep pain -comatose - meaningful responses are absent! -> no reflexes, abnormal posture, none or non-localizing responses

Answer 22

-objectively describe extent of impaired consciousness in all types of acute medical and trauma pts. -Individual elements as well as the sum are important -Scores are expressed as “GCS 9 – E2 V4 M3” -GCS ≤ 8 = Severe -GCS 9-12 = Moderate -GCS ≥ 13 = Minor -GCS 15 = Max, normal -GCS < 8 -> Intubate

Answer 23

-sternal rub -eyelid/brow -roll a pencil on nail bed -press on TMJs

Answer 24

-ABCs COME FIRST- Check for quick reversible causes, do they need naloxone? Glucose? Thiamine (for alcohol)? -always get a stat glucose -Get a good hx- What might be causing this AMS? -Do neuro exam- AMS from a structural brain lesion? -location of lesion? -Appropriate labs and imaging tests

Answer 25

-WHEN? -SUDDEN: SAH, basilar stroke, poisoning -GRADUAL: encephalitis, meningitis, sepsis, organ failure -FLUCTUATING: recurrent seizures, delirium -WHAT PRECEDED IT? -Fevers -> Meningitis, encephalitis, sepsis, certain drugs -Headaches -> SAH, ICH, meningitis -Focal deficits (motor, speech, vision) -> Strokes, ICH, other acute bleeds -Confusion -> Sepsis, drugs, medications -RECENT TRAUMA, SUBSTANCE ABUSE, suicidal Ideation, recent surgery, HOSPITALIZATIONS -UNDERLYING MEDICAL CONDITIONS ± MED CHANGES -WHAT IS THEIR BASELINE?

Answer 26

-barely went over -Underlying etiologies: Drugs / Ingestions -Structural brain lesions (CVA, tumor, anoxia) -Organ dysfunction (endo, lytes, resp, cardiac) -Sepsis/Infections -Seizures (think PRES)

Answer 27

-barely went over -Rapid glucose -Serum electrolytes (Na+, Ca+) -Serum bicarbonate -> acidosis, may clue to a broad differential diagnosis (CAT-MUDPILES). -BUN/Creatinine (uremia, upper GI bleed) -ABG or VBG (with co-oximetry for carboxy- or met-hemoglobinemia) -TFTs -Ammonia - cortisol -Toxic or medication causes

Answer 28

-barely went over -Head CT/ cervical spine CT -POCUS -Chest and Pelvis X-ray -Other imaging modalities as indicated

Answer 29

-barely went over -Blood cultures -CBC with differential -Serum lactic acid if meets SIRS (marker for severe sepsis or septic shock) -UA and culture -Chest X-ray -LP (with opening pressure); always obtain CT prior if you suspect ICP

Answer 30

-barely went over -EKG (certain medications such as TCA can prolong QTc and others like lithium cause other arrhythmias) -Drug screen (benzodiazepines, opioids, barbiturates, etc.) -Ethanol level -Serum osmolality (toxic alcohols)

Answer 31

-barely went over -Head CT (start w/o contrast for trauma or CVA) -MRI (if brainstem/posterior fossa pathology suspected) -Carotid/vertebral artery US -EEG (if non-convulsive status epilepticus suspected) -Hemodynamic instability causes -POCUS including bedside echocardiography -ECG -Cardiac enzymes (silent MI)

Answer 32

-State of unarousable unresponsiveness -Almost always traced back to either: -B/L hemispheric damage -Reduced ARAS activity -Pts may have brainstem responses, spontaneous breathing, purposeful motor movements -3 outcomes: -Recovery -Persistent coma (vegetative state) -Brain death

Answer 33

A = anoxia/apoplexy E = epileptic coma I = injury/infection O = opiates U = uremia

Answer 34

dont know all types -uncal hernation! -CN3 palsy -> pupils dilate unilateral -temporal lobe herniation -contralateral hemiparesis -if you see a dilated pupil -> stat CT

Answer 35

-severe neurologic condition -near total body paralysis with preserved consciousness -Cant move face or body, swallow, speak, look laterally -Vertical eye movements and controlled blinking are possible -Often mistaken for unconscious -Retained alertness and cognitive abilities -Stroke of brainstem or pontine hemorrhage -Specifically midbrain! or pons!!! where the ARAS!!! originates -Ex: basilar artery occlusion (MC)! -Prognosis: -High mortality rates (60%) in first 4 months -Better prognosis if potentially reversible cause: small stroke, TIA, GBS -Worse prognosis if irreversible or progressive: tumors -Supportive care is the mainstay of tx -Prevent systemic problems from immobilization: pressure ulcers, pneumonia, UTI, DVT/PE, limb contractures, malnutrition

Answer 36

-Complete and irreversible loss of function of cerebrum and brain stem -Common causes: brain injury from trauma, bleeding, stroke, loss of blood flow after cardiac arrest

Answer 37

-pre-requisite: establish an irreversible cause of coma -> anoxic brain injury, basilar artery thrombosis, high-grade SAH on neuroimaging can qualify -pre-requisite: exclude confounding factors -> cannot have: CNS depressants, paralytics, hypothermia, hypotension, or major metabolic derangements -ur not dead until ur warm and dead -exam: shows brainstem damage evidenced by neurologic exam: -Pupils fixed and non reactive to light -NO oculocephalic, oculovestibular reflexes -NO corneal, cough, and gag reflexes! -No meaningful motor responses (reflexes allowed) -Completely ventilator dependent -apnea testing: -testing respiratory drive in medulla -Show there is no spontaneous respiratory drive -Pre-oxygenate then disconnect from ventilator for 8-10 minutes, allow PaCO2 to rise, observe for respirations -CO2 must rise ≥60 AND 20 above starting -> and still not breathing on own -> fail -If unable to perform because of instability or hypoxia, perform ancillary tests -ancillary testing: confirm no blood flow in the brain -Only required if any previous step is doubtful -Includes: Cerebral angiogram, cerebral scintigraphy, transcranial dopplers, EEG

Answer 38

-Good overall physical exam -Specific exams for comatose patients: -Light reflex: -Remember: CN 2 in , brief stop in midbrain, CN 3 out -!!Blown (big) pupil = ipsilateral midbrain affected -Vestibulo-ocular reflex: -“Dolls eye” maneuver or “Cold calorics” -Vestibular nuclei in the medulla are stimulated by cold liquid, which activate pons CN6 nucleus in a contralateral fashion -Normal person= Eye looks toward cold water in ear then quickly corrects -Comatose = no response to cold water, or, no corrective saccade -Corneal reflex: -CN 5 is corneal reflex, CN 7 blinks, both nuclei are in the pons -Cough, gag reflex: -CN9 and CN10 in the medulla

Answer 39

-cold caloric reflex -cold water in ear -WNL- slow movement of eyes towards ear with water and then snap back to center

Answer 40

-Rapidly turn the head 90 degrees in both directions -NORMAL: Eye deviates to opposite way you turned the head "Doll eye" -you are always looking forward -ABNORMAL: No eye turning, eyes are not locking onto something

Answer 41

-Brain death: COMA + ABSENT BRAINSTEM REFLEXES + APNEA -Declaring brain death requires ALL of the following -> Prerequisites, examination, apnea testing, ancillary testing -Once dx, they are declared dead -In children, 2 separate brain death examinations is considered the minimum standard -Declare and document time of death -Organ donation or live fetus: May continue mechanical ventilation and medications to maintain blood pressure after death