quiz 1 Flashcards

1
Q

what is delirium

A

-Acute, transient, usually REVERSIBLE confusional state
-alteration of consciousness with reduced ability to focus, sustain, or shift attention
-Results in cognitive or perceptual disturbances that is not better explained by a pre-existing, established, or evolving dementia
-Develops over a short period of time (hours to days)
-underlying pathology present with not well understood pathophysiology
-can be the only sign of acute illness in elderly
-Very common in acute hospitals

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2
Q

delirium risk factors + precipitating factors

A

Risk
-Advanced age
-Recent surgery
-Pre-existing brain disease (e.g. dementia, stroke, Parkinson’s)
-30% of elderly patients experience delirium during hospitalization -> Higher rates in ICUs

Precipitating factors:
-Polypharmacy
-Infection
-Dehydration
-Malnutrition

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3
Q

DSM criteria for delirium

A
  1. Disturbance in attention and awareness (1st)
    - distractability = hallmark
  2. Develops over short period of hours
    - days; most severe night/evenings
  3. Cognitive disturbance including perceptual
    - ex: memory deficit, disorientation, language, visuospatial ability, perception
    4.Not explained by another neurocognitive disorder or coma
  4. Evidence (h&p,labs) that disturbance is caused by medication, condition or substance
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4
Q

course of delirium: what phases

A
  1. Prodromal phase (often not caught)- fatigue, sleep disturbance, depression/anxiety, restlessness, irritability, hypersensitivity to light or sound
  2. perceptual disturbance and cognitive impairment
  3. quiet/hypoactive - not interacting with environment (mc) OR agitated and confused
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5
Q

signs of delirium

A

-Change in level of consciousness
-Inability to direct, focus, sustain or shift attention
-Memory loss, disorientation, difficulty with language or speech -> Speech may be tangential, disorganized, incoherent
-Advanced: drowsy, lethargic, semi-comatose

It is important to get a good HISTORY on these patients, look for:
-Recent febrile illness
-hx of organ failure
-medication list and changes
-alcoholism or drug abuse
-recent depression

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6
Q

It is important to get a good HISTORY on delirium patients, look for what signs + what test to perform

A

look for:
-Recent febrile illness
-hx of organ failure
-medication list and changes
-alcoholism or drug abuse
-recent depression

tests:
- MMSE
- test attention: serial 7s or spell “world” backward
-Focused exam on hydration status, skin, vitals and sources of infection

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7
Q

MC etiologies of delirium

A

-Post operative states (very common in elderly)
-Drug toxicity (30% off all cases)
-Fluid / Electrolyte disturbance - NATREMIA, dehydration
-Infections- UTI, skin and soft tissue, pneumonia
-ETOH or other substance intoxication
-Barbiturates, benzodiazepines, ETOH withdrawal
-Metabolic disorders - shock
-Low perfusion states

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8
Q

drug culprits of delirium

A

-NSAIDs *
- Opioids*
-Benzodiazepines*
- anticholinergics: diphenhydramine**
-Acyclovir
-Antimalarials, Interferon, Amphotericin B, Cycloserine
-Cephalosporins, Fluoroquinolones, Macrolides, Metronidazole, Penicillins, Sulfonamides, Aminoglycosides, Linezolid
-Isoniazid, Rifampin
-Corticosteroids
-Hypoglycemics!
-CV: antiarrhythmics, BB, Clonidine, Digoxin, Diuretics, Methyldopa
-CNS-active agents: Lithium, IL-2, Phenothiazines, Donepezil
-Anticholinergics: atropine, benztropine, scopolamine, trihexyphenidyl, diphenhydramine!!!!!
-Dopamine Agonists: Amantadine, Bromocriptine, Levodopa, Pramipexole, Ropinirole
-Anticonvulsants: carbamazepine, levetiracetam, phenytoin, valproate, vigabatrin
-GI: antiemetics, antispasmodics, H2 Blockers, Loperamide
-Muscle Relaxers: Baclofen, Cyclobenzaprine
-Herbals: St. John’s Wort, Valerian

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9
Q

tx and prevention of delirium

A

-treat underlying cause
-treat their distress
-antipsychotic rarely needed (<10%)
-optimize conditions for brain recovery
-orientation protocols and psychological support
-monitor for recovery
-resolves in less than a week usually
-antipsychotics: Haloperidol, Risperidone, Olanzapine, Quetipaine, Aripiprazolex

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10
Q
A
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11
Q

major neurocognitive disorder (DEMENTIA)

A

-Progressive and gradual deterioration! of selective functions
-Must represent decline from previous baseline and severe enough to interfere with daily function! and independence
-Cognitive decline involving 2+ domains:
-learning
-memory (new information)
-language
-executive function (complex tasks, poor judgement)
-complex attention
-perceptual-motor
-social cognition
-Risk factors: age (>60 y/o), vascular disease (HTN, DM)
-MC cause: Alzheimer Disease (60-80%)
-Less common causes: alcohol-related, CTE, normal pressure hydrocephalus, chronic subdural hematoma, CNS illness (Creutzfeldt-Jakob disease, HIV), copper/B12/Folate deficiency
-AAN and USPSTF recommends routine screening for dementia in asymptomatic adults

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12
Q

clinical manifestation of dementia

A

-1. memory loss- 1st manifestation- presents as forgetfulness (trouble remembering recent events)
-2. Deficits in other cognitive domains (with or after memory loss)
-(a) Executive dysfunction (less organized/a, difficulty multitasking) - early
-(b) Impaired visuospatial skills (getting lost in familiar places) - early
-(c) Language dysfunction (word finding) – late
-(d) Behavioral symptoms (apathy, social disengagement, irritability; agitation, aggression, wandering, psychosis) – middle/late
-3. Non-cognitive neurologic deficits – late
-Pyramidal/Extrapyramidal motor signs, myoclonus (uncontrollable twitching), seizures
-(4) Life expectancy after diagnosis: 8-10 years (range: 3-20)

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13
Q

dementia exam: assessment

A

-MMSE or MoCA
-Complete physical exam
-Labs:
-Routine labs such as CBC, CMP, Calcium, UA
-B12 deficiency and hypothyroidism screening (AAN recommendation)
-Any other indicated labs based on their history / physical (ex: heavy metal, ETOH/Drug screening, syphilis)
-Imaging: MRI brain without contrast (AAN recommendation, over CTH)
-Consider:
-LP: rule out infectious, inflammatory, neoplastic causes
-EEG: Atypical syndrome with concern for Creutzfeldt Jakob disease (less than 60 years old, rapidly progressive symptoms)
-PET: distinguish a vascular cause from Alzheimer’s
-Brain biopsy: definitive but rarely done

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14
Q

alzheimers dementia (AD)

A

-Most common cause of dementia (60-70%)
-Pathophysiology:
-Accumulation of !amyloid beta (Aβ) deposition in the brain that forms neuritic (senile) plaques and neurofibrillary tangles (NFTs) composed of tau protein filaments! with eventual loss of neurons (PANCE question)
-Often a cholinergic deficiency causing memory, language, and visuospatial changes early on
-Major genetic risk factor: ε4 allele of the apolipoprotein E (ApoE) gene
-RF: !Age > 65!, female, family history, CVD, APOE-e4 allele

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15
Q

AD dx and management

A

-dx -> excluding 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
-Side effects: 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 can cause cell death
-Vitamin E

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16
Q

brain death

A

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

17
Q

establish brain death

A

-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 the 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: imaging that shows no brain flow, or absent electrical brain activity
-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

18
Q

brain death exam

A

-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

19
Q

oculovestibular reflex

A
  • CN 6
    -cold caloric reflex
    -cold water in ear
    -WNL- slow movement of eyes towards ear with water and then snap back to center
20
Q

oculocephalic reflex (doll eye)

A

-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

21
Q

declaring brain death

A

-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

22
Q

Mild TBI (mTBI) vs concussion

A

Mild: 13-15 ± brief LOC (<30min)
-Trauma induced alteration in mental status : GCS 13-15 ± brief LOC (<30min)
-mTBI may lead to significant, debilitating short- and long-term sequelae.
-concussion: the S&S that occur after a mTBI; Trauma-induced brain dysfunction w/o structural injury

-“Mild” is a misnomer -> -Often used interchangeably with “concussion” WRONG
-Moderate TBI: GCS 9-12
-Severe TBI: GCS ≤8

23
Q

Concussion: MOA

A

Definition: Sequelae of S/S after a mild TBI = Jolting of the head

MOA: Functional not structural injury*
- Shear forces disrupt neural membranes -> K+ efflux out of neuron to the ECF
- increase of Ca 2+ and excitatory amino acids
- followed by further potassium efflux and subsequent SUPPRESSION of neuron activity

24
Q

concussion MCC and risk factors

A

-MC in elderly = Falls
-MC in young = Motor vehicle accident

Risk factors:
-Previous concussions
-Younger age
-High risk sports (football, ice hockey, lacrosse, rugby, womens soccer)
-Female > male

25
Q

concussion: early vs late symptoms

A

S/S (Early): within hours
- Confusion and Amnesia = hallmarks!!!!*
-Retrograde amnesia: loss of recall for events immediately before
-Anterograde amnesia: loss of recall for events immediately after
- Headache
- Dizziness
- Nausea/vomitting
- Mental fogging/slowing
- Concentration difficulties
- others: fatigue, lack of awareness of surroundings, unsteadiness

S/S (Late): within hours/days
- Mood or cognitive disturbances
- Sensitivity to light/noise
-Sleep disturbances

26
Q

Concussion: signs

A

-Incoordination
-No focal neuro deficits

Neuropsychiatric impairments:
-Emotionality out of proportion**
-Memory deficit *
-Vacant stare
-Delayed verbal expression
-Inability to focus
-Disorientation
-Slurred or incoherent speech

27
Q

Concussion testing and dx:

A

Testing:
-Neuro exam
-Mental status exam
-Standardized assessment of concussion (SAC) or Sport concussion assessment tool (SCAT5)
-Consider CT head NON-contrast based on Canadian CT head or PECARN criteria

Diagnosis:
-Hx of head injury ± brief LOC
-Neurologic symptoms: Confusion/memory loss
-GCS

28
Q

concussion/MTIBI tx

A

Step 1: initial rest
-Observation for 24 hours
-Physical and cognitive rest 24-48 hours-> Gradual return to activity
-Analgesics for pain
-avoid medications that alter cognition (opioids, tramadol, muscle relaxers, benzos, ETOH, ilicit drugs, aspirin, sleeping pills)
- limit screen time
- don’t drive until cleared by profession
- return to play/sport once cleared by healthcare professional

consider:
-Referral to concussion specialist: Physiatrist, sports medicine, neurologist
-if prolonged symptoms >21 days
-Hx of multiple concussions
-Uncertain diagnosis

29
Q

concussion: return to play protocol

A

any LOC episode -> ER for evaluation
-Suspected Cervical -spine injury -> immobilize, ER
-High impact, high risk -> ER
-Skull fracture findings -> ER
-Seizure post trauma -> ER
-Focal neuro signs (weakness, confusion, or imbalance) -> ER
Suspected concussion should be removed from play immediately -> When in doubt, sit them out!”
-Re-evaluation in 1-2 days with specialist
-Clearance by licensed health professional usually requires symptom resolution off meds

30
Q

Migraines
Acute Tx:

A

Simple analgesics +/- antiemetics (metoclopramide, prochlorperazine, promethazine)

Add Triptans if mod/severe:
PO: take 1 tab and can repeat in 2 hrs, 2 tabs/24hrs and no more than 8 days/month -> too much causes sensitization
ADRS: nausea, dizziness, dry mouth, fatigue, flushing chest pain, less common: chest tightness, arm discomfort/tingling, throat discomfort, cramps
CI because it constricts blood vessels: Prinzmetal angina, Ischemic CVD/CVA, pregnancy (might be safe), uncontrolled HTN

Gepants
ditans

Avoid: estrogen in BC -> can increase stroke risk in women with aura migraines

31
Q

Migraines Prevent/prophylax:

A

Indicated in pts with 4+ HA/month, 2+ debilitating attacks/month, CI to acute tx, use abortive tx > 2x/wk
- Start low and go slow: takes 6-8 wks for improvement and 6 months for full effect
- Goal: ~40% reduction in # of HAs, decreased duration of headache, or improvement in response to acute therapy
- Change tx if no response after 2 months

Beta-Blockers: Propranolol 160 mg QD (first line)*
- Avoid: asthma/COPD, Bradycardia, AV conduction disorders

Anticonvulsants: Topiramate or Divalproex
- Avoid: pregnancy and liver ds
- ADRS: paresthesia (MC); kidney stones, hepatotoxicity, needs laboratory monitoring

Amitriptyline:
- Highest risk of ADRs: sedation, anticholinergic (anti- SLUDGE), orthostatic hypotension
- Avoid: elderly, BPH, glaucoma, seizure ds, mania
Good for: depression, insomnia

32
Q

Cluster Headaches: tx symptomatic and prevent/prophylax

A

Symptomatic Tx:
- O2: first line: 6-10L of 100% by mask
- SQ Triptans: first line pharmacology
- Ergot alkaloids
- Anesthetics

Prevent/prophylax:
- Verapamil CCB: MOST effective**
Steroids
- Mood stabilizers: lithium
- Anticonvulsants: Topiramate

33
Q

Tension Headaches: tx

A

Acute Tx: NSAIDS

Prevent/prophylax: Amitriptyline*
- Massage
- CBT
- HA clinic

34
Q

meningitis csf findings

A
35
Q
A