Module 2 EB Flashcards
-In the geriatric population, how do diseases often present?
-Do all abnormalities require evaluation and treatment?
-present atypically or with nonspecific sx
-not all abnormalities require evaluation and treatment
-in addition to conventional assessment of symptoms AND diseases, the comprehensive assessment addresses 3 topics for the geriatric population. what are they?
-prognosis, values/preference, ability to function independently
Assessment of prognosis:
-life expectancy >10y, how should PCP consider tests/treatments for geriatric patient?
-life expectancy <10y, how should PCP consider tests/treatments for geriatric patient?
-as you would in young person
-made based on ability to improve patient’s prognosis and quality of life
What do most frail older adults prioritize maintaining (in comparison to)?
independence over prolonged survival
-25% of pt >65syo and 50% of >85yo need help with what?
-Thus, it is important to assess what?
-ADLs
-functional screening –> assessment of ADLs/IADLs
Dementia:
-def
-dementia is NOT ___________.
-progressive decline of intellectual function; loss of short-term memory + 1 other cognitive deficit; deficit severe enough to cause impairment of function
-delirium
-agnosia
-aphasia
-apraxia
-inability to recognize objects
-word-finding difficulty
-inability to perform motor tasks
General considerations for dementia
-acquired, persistent, progressive impairment in intellectual function
-compromise of memory + one other cognitive domain:
1. aphasia (words)
2. apraxia (motor tasks)
3. agnosia (recognize)
4. impaired executive function
Dementia:
-diagnosis
-significant decline in function that is severe enough to interfere with work, social life, performance of routine activities
How many of dementia patients have Alzheimer’s?
2/3 in US
What is the most common concomitant of early dementia?
Depression
-What is the susceptibility gene associated with dementia?
-is it recommended to be tested?
-if so, what kind of counseling should coincide with this test?
-Susceptibility gene associated with late-onset Alzheimer’s disease (APOE-e4)
-NO
-genetic counseling
-Lab work for dementia patients
-Lab work not part of routine testing
CBC, CMP (serum electrolytes, calcium, Cr, glucose), TSH, vitB12
-not part of routine testing: liver panel, HIV, RPR, heavy metal screen
Tools for cognitive impairment
-Mini-cog
-Montreal cognitive assessment (MoCA)
-combo of 3-item word recall with a clock drawing task, completed within 3 min; if patient fails, requires further cognitive function evaluation with standardized measurement
-30pt test, takes 10 min, examines several areas of cognitive function. Score <26 = cognitive impairment
-How is imaging helpful in dementia patients?
-when is MRI warranted?
-rules out subdural hematoma, tumor, previous stroke, hydrocephalus
-younger patients + focal neuro deficits, seizures, gait abnormalities
How is delirium distinguished from dementia?
delirium is acute in onset, fluctuating coarse, deficits in attention
what are medications that cause delirium?
anticholinergic, hypnotics, neuroleptics, opioids, NSAIDs, antihistamines, corticosteroids
what kind of imaging is used for older patient with classic Alzheimer findings?
non-contrast CT
when do you refer a dementia patient?
refer to neuropsychological testing to distinguish dementia from depression
-dx dementia in those with poor education, aid dx when impairment is mild
Dementia: cognitive impairment
-drug class
-use
-drugs
-MOA
-acetylcholinesterase inhibitors
-mild-mod Alzheimer disease
-donepezil, galantamine, rivastigmine
-produce modest improvement in cognitive fx that is not likely to be detected in routine clinical encounters
*DOES NOT DELAY FUNCTIONAL DECLINE OR HOSPITALIZATION
Dementia: cognitive impairment
-drug used for advanced disease
memantine
-N-methyl-D-aspartate (NMDA) antagonist
Dementia: behavioral problems
-nonpharmacological approach
-rule out delirium, pain, urinary obstruction, fecal impaction FIRST
-determine if caregiver/institutional staff can tolerate behavior
-Keep log describing behavior + antecedents’ events
-use simple language, break down activities into simple component tasks
Dementia: behavioral problems
-pharmacological approach
*who is this approach reserved for?
*drug class used?
*drug names
-patients who are a danger to others/themselves or symptoms are very distressing to patient
-atypical psychotropics
-risperidone, olanzapine, quetiapine, aripiprazole
Dementia: behavioral problems
-pharmacological approach
*medication used to improve symptoms of agitation?
citalopram
Fragility
-essentials of diagnosis
syndrome characterized by loss of physiologic reserve and dysregulation across multiple systems –> greater risk of poor health outcomes
Fragility
-how to diagnose
3+ features must be present:
*weakness, slow gait speed, dec physical activity, weight loss, exhaustion, low energy
Fragility
-at risk for?
-treatment
-falls, hospitalizations, functional decline, death, worse outcomes after surgery
-supportive, multifactorial, individualized based on pt goals, life expectancy, co-morbidities, may need palliative care
**Exercise (strength/resistance training) is intervention with the strongest evidence for benefit
Immobility
-associated with increased rates of?
-prevention
-most common etiology
-morbidity, hospitalization, disability, mortality
-structured physical activity programs (reduce mobility-related disability)
-hospital-associated bed rest
Immobility
-hazards of bedrest in older adults
hazards are multiple, serious, quick to develop, and slow to reverse
Falls & Gait Disorders:
-how often do falls occur in >65yo?
-percent of falls that cause serious injury?
-complication from falls
-1/3
-10%
-leading cause of death from injury in person >65yrs (hip fracture common precursor to functional impairment, nursing home placement, death)
Falls & Gait Disorders:
-what test helps determine a thorough gait evaluation?
-up and go test
*ask pt to stand up from sitting position without use of hands, walk 10ft, turn around, walk back, sit down: should take <10sec; abnormal if takes >13.5 sec (INCREASED RISK OF FALLS)
Falls & Gait Disorders:
-what is the most common/significant reversible cause of falls?
polypharmacy
Falls & Gait Disorders:
-what must be considered in any elderly patient presenting with new neuro sx/signs?
*what sx may be absent?
-chronic subdural hematoma
*HA and trauma
Depression:
-among which geriatric population has the highest rates for suicide?
-older single men
Depression: what questions are highly sensitive for determining depression in geriatric population?
- during the past 2 weeks, have you felt down, depressed, or hopeless?
- during the past 2 weeks, have you felt little interest or pleasure in doing things?
Depression: what drug is first line?
-SSRI
Delirium:
-essentials of diagnosis
-rapid onset
-fluctuating course
-primary deficit in attention rather than memory
-may be hypoactive/hyperactive
-dementia frequently coexists
Delirium:
-general considerations
-cause
-risk factors
-acute, fluctuating disturbance of consciousness - change in cognition or development or perceptual disturbances
-pathologic consequence of underlying general condition (infection, coronary ischemia, hypoxemia, metabolic disturbance)
-cognitive impairment; severe illness, polypharmacy, use of psychoactive meds, sensory impairment, depression, alcoholism
Delirium:
-delirium assessment tool (and what it requires)
-CAM
*acute onset and fluctuating course
*inattention and either: disorganized thinking or altered level of consciousness
Delirium:
-medications known to cause delirium
-sedative/hypnotics, anticholinergics, opioids, benzos, H1/H2 antihistamines
Delirium:
-lab work
CBC, BUN, cr, glucose, calcium, albumin, liver panel, UA, ECG (select cases CXR, UDS, lumbar puncture)
Delirium:
-do any medications prevent or improve outcomes?
NO
Delirium:
-tx
supportive, tx underlying causes, eliminate unnecessary meds, avoid indwelling catheters/restraints
Delirium:
-prognosis
-when to admit
-most episodes clear in matter of days after correction of precipitant
-pt w/ delirium of unknown cause
Urinary incontinence:
-stress
-urge
-overflow
-leakage of urine upon coughing, sneezing, standing
-urgency and inability to delay urination
-variable presentation; leak or dribble urine because bladder is too full
Urinary incontinence:
DIAPPERS
-D: delirium
-I: infection
-A: atrophic urethritis/vaginitis
-P: pharmaceuticals
-P: Psychological factors (depression)
-E: excess urinary output
-R: restricted mobility
-S: stool impaction
Urinary incontinence:
-what is one of the most common causes of urinary incontinence?
-pharmaceuticals
*D/C any anticholinergic meds first!
Involuntary weight loss:
-what happens to appetite as we age?
-what are the main causes?
-what should be considered if not cause identified?
-reduces
-medical, psychiatric, unknown
-Frailty syndrome should be evaluated
Involuntary weight loss:
-what can be used to help?
-oral nutritional supplements of 200-1000kcal/day
-megestrol acetate (appetite stimulant)
Pressure injury:
-stage 1
-stage 2
-stage 3
-stage 4
-Unstageable
-Deep tissue
-stage 1: non-blanchable erythema or intact skin
-stage 2: partial-thickness skin loss with exposed dermis
-stage 3: full-thickness loss
-stage 4: full-thickness and tissue loss
-unstageable: obscured full-thickness and tissue loss
-persistent non-blanchable deep red, maroon, purple discoloration
Pressure injury:
what is the primary risk factor?
immobility
Vision impairment:
-how often should geriatric patients receive eye exams?
complete eye exam by optho annually or biannually!!!
-age-related refractive error “presbyopia”, macular degeneration, cataracts, glaucoma, diabetic retinopathy, physical/mental health comorbidities, falls, mobility, impairment, reduced quality of life
Hearing impairment:
-those with hearing loss >65yo
-those with hearing loss >85yo
-1/3
-1/2
Hearing impairment:
-what test helps determine if hearing impairment?
Whisper test
Contributing risk factors to pressure ulcers
-immobility
-reduced sensory perception
-moisture (urinary/fecal incontinence)
-poor nutritional status
-friction/shear forces
when is a pressure ulcer unstagable?
-base is covered in slough (yellow, tan, gray, green, brown) or eschar (tan, brown, black)
who should be consulted for a pressure injury?
Wound care
Elder Mistreatment & Self-Neglect:
-def
-what is the most common form of elder mistreatment?
-actions that cause harm or create a serious risk of harm to an older adult by caregiver or other person who stands in a trust relationship to the older adult, failure by caregiver to satisfy the elder’s basic needs or to protect the elder from harm
-self-neglect
Epilepsy:
-def
-seizure is a transient disturbance of cerebral function due to an abnormal paroxysmal neuronal discharge in the brain
-if the patient has a readily reversible cause (withdrawal from ETOH/drugs, hypoglycemia, hyperglycemia, uremia) - DO NOT HAVE EPILEPSY
-recurrent unprovoked seizures; characteristic EEG changes + seizures; mental status abnormalities or focal neuro sx persisting for hours postictally
Epilepsy: focal onset seizures (also known as partial seizures)
-EEG
-focal motor
-nonmotor
-only a restricted part of 1 cerebral hemisphere has been activated; ictal manifestations depend on area of brain involved
-clonic jerking
-paresthesia, tingling, gustatory, olfactory, visual/auditory sensations
Epilepsy: complex partial seizure (also known as focal seizure)
-awareness vs impaired awareness
-knowledge of self or environment, and events occurring during seizure
-impaired awareness may be preceded, accompanied, or followed by various motor/non-motor sx
what type of seizure is most common in those with epilepsy?
-focal onset seizures (partial seizures)
General Onset Seizures: Motor seizures
-tonic-clonic phase
-sudden LOC
-rigid, falls to ground
-respiration arrested
-tonic phase <1min
-clonic phase (jerking 2-3 min)
-flaccid coma/drift into sleep/further convulsion without recovery (status epilepticus)
Generalized onset seizures: motor seizures
-postictal phase
-HA
-disorientation
-confusion
-drowsiness
-nausea
-soreness of muscles
Generalized onset seizures: Motor seizures
-myoclonic
single/multiple jerks
Generalized onset seizures: motor seizures
-atonic
very brief, <2sec loss of muscle tone = falls
Generalized onset seizures: motor seizures
-epileptic spasms
sudden flexion or extension of truncal muscles (infancy)
Epilepsy: treatment
-what does the choice of medication depend on?
depends on seizure type
-gradually increase dose until seizures are controlled or SE prevent further increases
-if seizures persist despite max dose, add 2nd medication w/ dose increased until tolerated (gradually withdraw 1st medication)
Epilepsy: are medications safe in pregnant women?
NO! Teratogenic!!!
????????????
during pregnancy, if break-through seizure occurs, dose change, another interacting med is added to regiment
Epilepsy: how to titrate treatment medications
dose of antiepileptic is increased depending on clinical response regardless of serum drug level
-when dose is achieved (either controls or is max tolerated) - steady state trough drug level may be obtained
Epilepsy: what is the most common cause of lower concentration?
suboptimal patient adherence
Epilepsy: when can you discontinue seizure medications?
when adult has been seizure free for 2 years
-gradually reduce dose (weeks-months)
-if seizure recurs, reinstitute tx
ETOH Withdrawal seizures
-def
-tx
-1 or more generalized tonic-clonic seizures that occur within 48 hours of withdrawal
-benzos
Tonic-clonic status epilepticus
-medical emergency?
-most common cause?
-YES, requires airway management
-poor adherence to regimen
Epilepsy: etiology
-perinatal injuries (pediatric)
-trauma (any age)
-vascular dx (stroke) = most common cause w/ onset age >=60yo
-genetics
-metabolic (pyridoxine deficiency, -mitochondrial disease) - childhood presentation
-immune (SLE, limbic encephalitis)
-Tumor
-degenerative (Alzheimer’s)
-infectious (meningitis, herpes encephalitis, etc.)
Epilepsy: diagnostic studies
MRI
EEG
Epilepsy:
-when is lumbar puncture necessary?
-S/S
-with any sign of infection present or in evaluation of new-onset seizures in acute setting
-HA, mood alterations, lethargy, myoclonic jerking; aura
Dysautonomia
-essentials of dx
-etiology
-postural hypotension or abnormal heart rate regulation; abnormalities of sweating, intestinal motility, sexual function, sphincter control; syncope may occur; symptoms occur in isolation or any combo
-pathological processes in central/peripheral nervous system - manifested by variety of sx (abnormal bp, thermoregulatory sweating, GI function, sphincter/sexual function, respiration, ocular function)
Dysautonomia
-CNS causes
-Postural hypotension: spinal cord transection; myelopathies (tumor) above the t6 level, brainstem lesions (syringobulbia/posterior fossa tumors); sphincter/sexual disturbances
**primary degenerative disorders: parkinsonism, pyramidal sx, cerebellar deficits
Epilepsy:
-causes in PNS
*pure autonomic neuropathy
*GBS
*Metabolic disturbance
-Pure autonomic neuropathy: viral infection; paraneoplastic disorder r/t small cell lung cs
-marked hypo/hypertension, cardiac arrhythmias
-diabetic, uremic, amyloidotic; leprosy, changas disease
Epilepsy:
-what determines the extent and severity of autonomic dysfunction?
evaluation of the patient
+ presence of associated neurological s/s
Dysautonomia:
-S/S
-syncope
-postural hypotension
-paroxysmal HTN
-persistent tachycardia without other cause
-facial flushing
-hypohidrosis/hyperhidrosis
-vomiting
-constipation
-diarrhea
-dysphagia
-abd distention
-disturbances of micturition/defecation
-erectile dysfunction
-apneic episodes
-declining night vision
Dysautonomia: syncope
-is recovery rapid or slow?
recovery is rapid once patient is recumbent; headache, nausea, fatigue are COMMON
Dysautonomia: treatment
-avoid?
-supportive tx
-abrupt postural change, prolonged recumbency
-wear waist-high elastic hosiery, salt supplementation, sleeping in semierect position
TIA:
-acute or chronic onset?
-does clinical deficit resolve completely? if so, how long?
-risk factors
-acute
-resolves completely within 24 hrs
-vascular disease (present)
TIA:
-characterized by?
-30% of patients have a ________ within 90d
-when is the risk of stroke high following TIA?
-focal ischemic cerebral neuro deficits, lasting for <24 hours (usually 1-2 hours)
-stroke
-3 months; >60yo, DM, TIA lasting >10m with residual focal neuro deficits
Stroke:
-risk factors
-distinctive neuro signs reflect what?
-HTN, DM, tobacco use, a-fib, atherosclerosis
-region of brain involved
what is the 5th leading cause of death?
what is the leading cause of disability?
STROKE
STROKE
TIA:
-LOC?
-confusion?
-sx
-rarely
-rarely
-depends on arterial distribution affected
TIA:
-imaging
-CT/MRI: indicated within 24 hours of sx onset
-MRI w/ diffusion weighted sequences reveals acute or subacute infarction (wake-up strokes)
TIA:
-treatment goal
-tx
-prevent future attacks + stroke
-supportive tx
Stroke:
-essentials of dx
sudden onset of neurologic deficit of cerebrovascular origin
Stroke:
-types of stroke?
ischemic
heomrrhagic
Stroke:
-types of ischemic stroke
-types of hemorrhagic stroke
-lacunar infarct; carotid circulation obstruction
-spontaneous intracerebral hemorrhage; subarachnoid hemorrhage
Stroke:
-secondary tx for ischemic stroke
Antiplatelet
-what imaging type is used to dx lacunar infarct?
-what imaging type is used to dx carotid circulation obstruction?
-MRI w/ diffusion-weighted sequences (CT is insensitive acutely)
-Noncontrast CT (exclude hemorrhage); diffusion-weighted MRI is gold standard
-what imaging type is used in dx of spontaneous intracerebral hemorrhage?
-what type of imaging is used to dx subarachnoid hemorrhage?
-Noncontrast CT (superior to MRI for detecting bleeds of <48 hours duration); do not perform LP!!
-CT: confirm dx; if CT negative and suspicion high, perform LP. Angiography: used to determine source of bleed in candidates for tx
Essential Familial Tremor
-family hx?
-how does ETOH effect it?
-any other abnormal findings?
-cause
-yes, common
-improves temporarily
-no abnormal findings
-uncertain; sometimes inherited (autosomal dominant manner)
Essential Familial Tremor
-tx
-when to refer
-often unnecessary; propranolol 60-240mg PO daily; primidone if propranolol is ineffective; botox
-1st line tx with propranolol or primidone refractory; additional neuro signs present
Essential Familial Tremor
-S/S
*onset
*tremor presentation
*physical exam
*prognosis
-any age; enhanced by emotional stress
-involves one or both hands, head, or hands + head (legs are spared); TREMOR WITH ACTION, NOT PRESENT AT REST!!!
-no other abnormalities noted
-little disability
Parkinson Disease:
-essentials of dx
-any combination of tremor, rigidity, bradykinesia, progressive postural instability
-cognitive impairment (sometimes prominent)
-occurs in all ethnic groups
Parkinson Disease:
-onset
-progressive or static?
-45-65 years
-progressive
Parkinson Disease:
-etiology
-dopamine depletion due to degeneration of dopaminergic nigrostriatal system leads to imbalance of dopamine and acetylcholine (NTs normally present in corpus striatum)
Parkinson Disease:
-tx of motor disturbance
-what is associated with decreased risk of developing Parkinson disease?
-risk factors
-blocking effect of acetylcholine with anticholinergic med or administration of levodopa (precursor of dopamine)
-ibuprofen
-age, family hx, male sex, ongoing herbicide/pesticide exposure, significant prior head trauma
Parkinson Disease:
-cardinal motor features
-non-motor features
-tremor, rigidity, bradykinesia, postural instability
-depression, anxiety, apathy, cognitive changes, fatigue, sleep disorders, anosmia, autonomic disturbances, sensory complaints or pain, seborrheic dermatitis
**TREMOR AT REST IS ENHANCED BY EMOTIONAL STRESS AND LESS SEVERE WITH VOLUNTARY ACTIVITY
Parkinson Disease:
-tremor characteristics
-what is dx based on?
-confined to 1 limb or limbs on 1 side for months - years before becoming generalized
-clinical exam: relatively immobile face with widening palpebral fissures, infrequent blinking, fixity of facial expression
Parkinson Disease:
-impact on muscle strength
-impact on DTRs
-no muscle weakness or altered DTRs
Parkinson Disease:
-treatment
-amantadine
-levadopa
-sinemet
-anticholinergic meds (aid in alleviating tremor/rigidity - poorly tolerated in older adult)
-antipsychotics (can be d/t dopa therapy or underlying illness; clozapine and quetiapine)
-rivastigmine (cognitive impairment/psychiatric sx)
Huntington Disease:
-essentials of dx
*gradual or acute onset?
*what sx progress?
*family hx?
*responsible gene ID’s on chromosome _____?
-gradual onset
-progression of chorea and dementia or behavioral change
-family hx
-4
Huntington Disease:
-characterized by?
-imaging
-chorea and dementia
-CT scan/MRI; PET
Huntington Disease: S/S
-onset
-timeline of disease (how many years)
-genetic counseling?
-30-50 years
-15-20 years
-offer to offspring
Huntington Disease:
-treatment
*can progression be halted?
*is there a cure?
*meds to tx
-no
-no cure
-Tetrabenazine; deutetrabenazine, amantadine, deep brain stimulation, phenothiazines haloperidol, quetiapine, clozapine
RLS:
-essentials of dx
*common?
*what can cause RLS?
-common
-idiopathic OR r/t Parkinson’s disease, pregnancy, IDA, peripheral neuropathy
RLS:
-def
-onset
-complications
-restlessness and curious sensory disturbances lead to an irresistible urge to move the limbs (esp during periods of relaxation); movement of limbs provides relief
-occurs exclusively in the evening and at night; worse at night (flexion at ankle, knee and hip)
-disturbed nocturnal sleep + excessive daytime somnolence
RLS:
-what labs should always be measured?
-tx
-ferritin level
-low iron = PO oral iron sulfate
-physical sx: pramipexole, ropinirole or rotigotine
-improve sx: gabapentin, pregabalin
-unresponsive to normal meds: levodopa
Dementia:
-acute or progressive?
-is this related to delirium?
-is this related to psychiatric disease?
-main risk factor
-more common in women or men?
-onset?
-progressive
-no
-no
-AGE (2nd), family hx (3rd)
-women
->60yr
Dementia:
-progressive decline in intellectual function impacts what?
-how to promote cognitive reserve?
-social and occupational functioning
-increased physical activity, education, ongoing intellectual stimulation, social engagement
pathology: plaques containing beta-amyloid peptide, and neurofibrillary tangles containing tau protein, occur throughout the neocortex
-Alzheimer? Vascular dementia? Dementia with Lewy Bodies? Frontotemporal dementia (FTD)?
Alzheimer’s disease
Pathology: multifocal ischemic change
-Alzheimer? Vascular dementia? Dementia with Lewy Bodies? Frontotemporal dementia (FTD)?
Vascular dementia
Pathology: histologically indistinguishable from Parkinson disease: alpha-synuclein-containing Lewy bodies occur in the brainstem, midbrain, olfactory bulb, and neocortex.
*what disease pathology may coexist?
-Alzheimer? Vascular dementia? Dementia with Lewy Bodies? Frontotemporal dementia (FTD)?
Dementia with Lewy bodies
-Alzheimer’s disease
Pathology: neuropathology is variable and defined by the protein found in intraneuronal aggregates. Tau protein, TAR DNA-binding protein 43 (TDP-43), or fused-in-sarcoma (FUS) protein account for most cases
-Alzheimer? Vascular dementia? Dementia with Lewy Bodies? Frontotemporal dementia (FTD)?
Frontotemporal dementia (FTD)
Dementia:
-types of neuropsych assessments?
-Folstein mini mental state exam (MMSE)
-Montreal cognitive assessment (MoCA)
-Mini-Cog: insensitive to mild cognitive impairment or do not correlate with functional capacity
Dementia:
-imaging
-MRI/CT without contrast
*goal to exclude cerebrovascular disease, tumor, other identifiable structural abnormality
-PET: sensitive to amyloid pathology - positive evidence for Alzheimer disease in pt w/ cognitive decline
Dementia:
-tx
*non-pharmacologic
-no cure
*aerobic exercise 45m/day
*frequent mental stimulation
*maintain an active role in family/community
*vitamin E (does not affect cognition or prevent development of Alzheimer’s disease in pt with mild cognitive impairment)
Dementia:
-tx
*how to treat cognitive sx
-cholinesterase inhibitors - first line therapy for Alzheimer’s disease + dementia with Lewy bodies
*does not prevent progression
*Donepezil, rivastigmine, galantamine
*memantine: tx of mod-severe Alzheimer’s disease
Dementia:
-labs
-mood/behavioral disturbances
-vitB12/free T4/TSH; RPR/HIV; CBC, electrolytes, glucose, lipid)
-SSRIs, citalopram (agitation) - can cause prolonged QTc
-trazadone: treats insomnia
Dementia:
-what medications to avoid in tx
-paroxetine/TCAs - anticholinergic
-avoid OTC antihistamines/benzos - worsen cognition, cause delirium
MS:
-essentials of dx
*can a single pathologic lesion explain clinical findings?
*how to diagnose?
-no, single pathologic lesion cannot explain clinical findings
-MRI - multiple foci
MS:
-greatest incidence among what population?
-patho
-young patient of western Europeans who live in temperate zones
-focal, perivenular areas of demyelination with reactive gliosis scattered in white matter of brain/spinal cord/optic nerves + axonal damage
MS:
-imaging
-labs
-dx
-MRI brain/cervical cord
-used to exclude infections, connective tissue diseases (SLE, Sjogrens), sarcoidosis, metabolic disorders (vitB12 def), lymphoma
-McDonald criteria: only dx if 2 + different regions of central white matter have been affected at different times.
-MS:
-do pts have residual deficits?
-what is the most common form of the disease?
-yes
-relapsing-remitting
MS:
-tx
-corticosteroids
-many drugs; choose initial agent based on tolerance, risks, pt preference, disease severity
MS:
-glatiramer acetate/interferon
-ocrelizumab
-initial med
-only med effective in SLOWING DISABILITY PROGRESSION IN PRIMARY PROGRESSIVE MS
Acute idiopathic polyneuropathy (GBS)
-essentials of dx
*acute or subacute?
*is weakness or sensory impairment more severe?
*triggers
-subacute or acute
-weakness
-infective illness, inoculations, surgical procedures (campylobacter jejuni enteritis; immunologic basis)
Acute idiopathic polyneuropathy (GBS):
-labs
-main complaint
-where do S/S begin in the body?
-CSF fluid (LP): high protein concentration + normal cell count; WBC > 50cells = consider alternative dx
-weakness that varies widely in severity; proximal emphasis + symmetric distribution
-begins in legs, spreads and frequently involves arms/both sides of face
Acute idiopathic polyneuropathy (GBS):
-tx
-plasmapharesis
-IVIG x5days
Bells Palsy:
-essentials of dx
*sudden or progressive onset?
*what other symptoms may occur?
-sudden
-hyperacusis or impaired taste may occur
Bells Palsy:
-cause?
-triggers
-more common in what population?
-idiopathic; inflammatory rx involving facial nerve
-herpes simplex; varicella zoster virus infection
-pregnant women and DM pts
Bells Palsy:
-imaging?
-S/S
-none
-facial paresis, facial pain, ipsilateral restriction of eye closure, disturbance of taste, hard to eat/drink
Bells Palsy:
-TX
60% recover completely w/o treatment
-Corticosteroids (prednisone 60mg PO daily x5days) = increases change of complete recovery at 9-12 MO
-Acyclovir/valacyclovir: only indicated when there is evidence of herpetic vesicles in external ear canal
Myasthenia Gravis:
-essentials of dx
*do patients feel weak or strong?
*what kind of muscles are impacted?
*what sx are produced?
*does activity help with sx or worsen them?
-weak
-voluntary muscles
-diplopia, ptosis, difficulty swallowing
-activity increases weakness of affected muscles
Myasthenia Gravis:
-what medications transiently improve weakness?
-what ages impacted?
-what population is most impacted?
-onset is progressive or acute?
-short-acting anticholinesterases
-all ages
-young women w/ HLA-DR3
-progressive (insidious)
Myasthenia Gravis:
-when do exacerbations occur?
-patho
-menstrual period, during/shortly after pregnancy
-variable degree of block of neuromuscular transmission caused by autoantibodies binding to acetylcholine receptors (reducing # of functioning acetylcholine receptors)
Myasthenia Gravis:
-labs (what lab is used to dx)
-S/S
-acetylcholine receptor antibodies assay –> elevated, use to dx MG
-ptosis, diplopia, difficulty chewing/swallowing, resp difficulties, limb weakness
Myasthenia Gravis:
-characteristics of weakness experienced by these patients
-findings from clinical exam for dx
-remain localized to few muscle groups or become generalized
-ocular palsies and ptosis (asymmetric), normal pupillary response, sustained activity of affected muscles increases the weakness, improves after brief rest; sensation is normal, no reflex changes
Myasthenia Gravis:
-tx
-what kind of surgery can help?
-anticholinesterase meds (neostigmine, pyridostigmine)
-corticosteroid prednisone 20mg PO daily, inc by 10mg increments
-IVIG/plasmapheresis (hosp pts.)
-thymectomy (perform when thymoma is present; consider in ALL patients)
Palliative care
-goal of care?
-what does palliative care manage?
-def
-addresses and treats sx, supports patients’ families, helps ensure that care aligns wit patients’ preferences, values, goals
-physical sx (pain, dyspnea, N/V, constipation, delirium, agitation), emotional distress, existential distress (spiritual crisis)
-interdisciplinary team of experts
Palliation of Common Nonpain Sx:
-dyspnea
*def
*characterized by?
*Tx
-subjective experience of difficulty breathing
-tightness in chest, SOB, breathlessness, feeling of suffocation
-directed at cause (opioids - single best class of meds for dyspnea)
IR morphine (PO or IV)
SR Morphine: ongoing dyspnea
Supplemental O2
Benzos
Palliation of Common Nonpain Sx:
-N/V
*what is the best modality to manage with medication?
*helpful treatments
*optimize sx control by regular dosing and multiple meds
*Nasogastric suction
-metoclopramide (partial gastric outlet obstruction)
-transdermal scopolamine (reduce peristalsis, cramping pain)
-Ranitidine (reduce gastric secretions)
*vomiting due to disturbance of vestibular apparatus: anticholinergic/antihistaminic agents (Benadryl, scopolamine)
-benzos: effective in preventing anticipatory nausea associated w/ chemo
Palliation of Common Nonpain Sx:
-delirium and agitation
*sx
*tx
*neuroepileptic agents
-waxing/waning LOC + change in cognition that develops over short time; terminal restlessness
-reversible causes: urinary retention, constipation, anticholinergic meds, pain
-haloperidol, risperidone
Palliation of Common Nonpain Sx:
-constipation
*triggers
*ask about…?
*prevention
*prophylactic bowel regimen
-frequent use of opioids, poor dietary intake, physical inactivity, lack of privacy
-difficulty with hard or infrequent stools
-increase activity, intake of fluids, provide privacy, undisturbed toilet time, bedside commode (rather than bedpan)
-stimulant laxative (senna or bisacodyl) should be started when opioid treatment is begun
*Naloxegol/libiprostone: FDA approved to treat opioid-induced constipation in patients w/ chronic non-cancer pain
Palliation of Common Nonpain Sx:
-fatigue
*what is the most common complaint of cancer patient?
*contributing factors to fatigue
*coexisting factors
*psychostimulants
-fatigue
-anemia, hypothyroidism, hypogonadism, cognitive/functional impairment, malnutrition
-pain and depression
-methylphenidate (AM, afternoon), modafinil (cancer-related fatigue)
Pain Management:
-acute pain
*when does it resolve?
*management
*what tool is used to guide #-needed-to-treat-for-specific doses of various meds?
-within the expected period of healing (self-limited)
-depends on type (somatic, visceral, neuropathic); acute pain that is NOT ADEQUATLEY treated develops into chronic pain
-Oxford League Table of Analgesics
Pain Management:
-acute pain
*what meds are used most helpful for acute pain?
*what are the SE of these meds?
*other medication options to manage acute pain?
-NSAIDs or COX inhibitors; PO, IM, IV, intranasal, rectal
-gastritis, kidney dysfunction, bleeding, HTN, MI/stroke
*ketorolac
-acetaminophen - most widely used and best tolerated; opioids (morphine/fentanyl)
Pain Management:
-chronic pain
*def
*what kind of management does this type of pain require?
*Does best practice support use of prolonged opioid therapy for chronic low back pain?
-persists beyond expected period of healing; itself is a disease state (>3-6MO)
-Interdisciplinary management
-NO
Pain Management:
-Cancer pain
*is cancer pain more acute or chronic?
*what is a complication (related to pain) from chemotherapy?
*what is a complication (related to pain) from radiation?
*what is a complication (related to pain) from surgery?
*WHO Analgesic Ladder (1986)
-Acute AND chronic pain
-peripheral neuropathies
-Neuritis or skin allodynia
-persistent postsurgical pain syndromes (post-mastectomy or post-thoracotomy pain syndromes)
-start tx with nonopioid analgesics, then weak opioid agonist, followed by strong opioid agonist
Pain Management:
-Pain at end of life
*pain management may take priority over promoting ________ _________.
*tx for ongoing cancer pain
*according to CDC, FDA, and US supreme court, what is the responsibility of the clinician in regard to seriously or terminally ill patients?
*restorative function
*long-acting opioid analgesic can be given around the clock + short-acting opioid medication PRN “breakthrough” pain
*appropriate treatment of pain
Pharmacologic pain management strategies:
-Non-opioid
-acetaminophen (no risk of GI bleed)
*500-1000mg q6hr
-aspirin
*325-650mg/4hr
*do not use in children/teens due to risk of bleeding, allergy, association with reye syndrome
-NSAIDs (can use PPI for GI bleeding prevention)
-Celecoxib (use in caution with: fluid retention, kidney injury, HF exacerbations)
Pharmacologic pain management strategies:
-Opioids
*Full opioid agonists
*Short-acting formulations
*IR fentanyl patch
*Buprenorphine
-hydrocodone and codeine (typically combined with Tylenol or NSAID)
-oral morphine sulfate, hydromorphone or oxycodone
-cancer pain tx that breaks through long-acting meds or administered before activity known to cause more pain
-short-acting analgesic reserved for pain management specialists
Pharmacologic pain management strategies:
-opioids
*methadone
*Buprenorphine
*common SE of opioids
-long-acting opioid, inexpensive; higher methadone doses = risk of prolonged QT (need baseline ECG)
-moderate to severe chronic pain
-tolerance, dependance, addiction
Pharmacologic pain management strategies:
-neuropathic pian “burning, shooting, pins/needles, electricity”
*gabapentin/pregabalin
*SSRIs
*Tricyclics
*1st line treatment; can cause dizziness, ataxia, GI upset
*duloxetine (Cymbalta), venlafaxine; take on full stomach
*nortriptyline, desipramine
Common emergencies:
-cough
*when to get chest Xray
*patho
*what does an effective cough depend on?
-unexplained cough >3-6 weeks
-stimulation of mechanical/chemical afferent nerve receptors in bronchial trees
-depends on intact afferent-efferent reflex arc, adequate expiratory/chest wall muscle strength, normal mucocilliary production and clearance
what is the most common sx patients seek care for?
Cough
what sx would indicate pneumonia?
acute cough + tachycardia, tachypnea, fever
what does wheezing and rhonchi indicate?
bronchitis
Differentials for persistent cough
chronic sinusitis, postnasal drip, asthma
what would be indicated with sx of cough + dyspnea + JVD?
HF
What dx would be indicated with airspace consolidation (rales, dec breath sounds, fremitus, egophony)
CAP
Cough:
-Acute
-persistent
-subacute
-chronic
<3 weeks
3-8 weeks
postinfectious cough 3-8 weeks
>8 weeks
Cough: acute
-what confirms diagnosis?
-adults with acute cough, abnormal VS, abnormal CXR suggests what?
*what could C-reactive protein be?
-tx
-fever, nasal congestion, sore through
-pneumonia
*>30 (improves dx accuracy)
-target underlying etiology of illness, cough reflex, exacerbating factors of cough
Cough: acute
-influenza tx
-Chlamydophila/mycoplasma tx
-bronchitis + wheezing tx
-acute cough + accompanying postnasal drip tx
-PO oseltamivir/zanamivir (initiate w/i 30-48 hours of illness onset)
-erythromycin/doxy
-inhaled beta 2 agonist
-antihistamines, decongestants, nasal corticosteroids
Cough:
-when to refer
failure to control cough; recurrent sx referred to otolaryngologist, pulmonologist, gastroenterologist
Cough: persistent/chronic cough
-when should a cough resolve?
-what should be considered when cough lasts more than 3 weeks (in adults/teens)?
-what are most cases of persistent/chronic cough due to?
-what imaging should be used if ACE-I related and postinfectious cough are excluded?
-how to treat pertussis
-by 3 weeks
-pertussis
-postnasal drip, asthma, GERD
-macrolide antibiotic (early ID, revaccinate with Tdap, tx pts who work or live with high risk persons (pregnant, infant <1 year, immunosuppressed)
Postnasal drip
-step 1 (empiric therapy)
-step 2 (definitive testing)
-therapy for allergy or chronic sinusitis
-sinus CT scan; ENT referral
Asthma
-Step 1 (empiric therapy)
-step 2 (definitive testing)
-beta-2-agonist
-spirometry: consider methacholine challenge if normal
GERD
-step 1 (empiric therapy)
-step 2 (definitive testing)
-lifestyle and diet modification with or without proton pump inhibitors
-esophageal pH monitoring
Dyspnea
-def
-diagnostic studies of pneumonia
-diagnostic studies of HF
-diagnostic studies of PE
-subjective experience or perception of uncomfortable breathing
-CXR + elevated procalcitonin/CRP
-low procalcitonin, CXR (new onset CHF), proBNP
-tachycardia + hypoxemia + normal CXR/ECG = obtain spiral CT scan
Dyspnea
-tx
immediately provide supplemental O2
-Heat stroke hallmark sx
-what type of thermometer can you use?
-is core body temp elevated in heat cramps or heat exhaustion?
-are oral salt tabs recommended tx for heat cramps?
-do antipyretics have effect on environmentally induced hyperthermia?
-cerebral dysfunction with core body temp over 40C
-internal rectal, foley, esophageal
-heat exhaustion
-NO, need electrolytes
-NO
Accidental Systemic Hypothermia:
-what is core body temp below?
-at what temp does core body need to be at to terminate resuscitation efforts?
-what should hypothermic patient be evaluated for?
-below 35C
-above 32C
-hypoglycemia, trauma, infection, overdose, peripheral cold injury
Accidental Systemic Hypothermia:
-Stage I
-Stage II
-Stage III
-Stage IV
-core body temp between 32-35C; shivering, normal LOC, hemodynamically stable
-core body temp between 28-32C; shivering stops, bradycardia, confusion, J wave or Osborn wave on ECG
*will cardiac arrest if core body temp <28C
-Core body temp between 24-28C; loss of consciousness but present VS
-Core body temp <24C; loss of VS; coma, loss of reflexes, asystole, or v-fib
*can reverse even at this stage
do NP’s treat hypothermia?
NO, refer to ED.
Frostbite
-when to refer?
-what to avoid
-method of rewarming
-ALWAYS
-secondary exposure to cold; hypovolemia and to improve perfusion (provide PO and IV hydration)
-warm bath immersion (immersed for several min in moving water bath heated to 40-42C until the distal tip of the part being thawed flushes
Thermal Burns:
-palm of hand constitutes what percent of body surface area in adults (TBSA)?
-1st degree burn Superficial burns
-2nd degree burn Superficial partial-thickness.
-Deep partial-thickness
-3rd degree burn (full-thickness)
-1%
-superficial burn: red, gray, excellent cap refill; not blistered initially
-superficial partial-thickness burn: blistered, appears pink and wet
-appears white and wet, bleed if poked; maintains cutaneous sensation
-loss of adnexal structures; appear white/yellow in color; may have black charred appearance that’s still, dry skin dose NOT bleed when poked (lost cutaneous sensation)
Rule of 9’s
Entire arm 9%
Posterior surface of each leg 9%
Entire head and neck 9%
Posterior surface of upper trunk (9%)
Neurological Disorders: Acute headache
-imaging used for acute headache
-follow-up initial imaging with what? what is the purpose?
-CT without contrast: excludes intracranial hemorrhage, intracranial mass
-LP; excludes infectious causes of HA
Neurological Disorders: Acute headache
-sx of meningeal inflammation?
-if patient is older than 60YO with severe headache, what should you examine?
-in the physical exam, what are crucial assessment pieces?
-which type of exam should be completed?
-fever + acute HA: meningeal inflammation (Kernig/Brudzinski signs; absence of jolt accentuation of HA cannot accurately rule out meningitis - need LP)
-scalp or temporal artery tenderness
-careful assessment of visual acuity, ocular gaze, visual fields, pupillary defects, optic disks < and retinal vein pulsations
-complete neuro exam; if any abnormality, need emergency neuroimaging.
Pieces of a neuro exam
-mental status
-motor/sensory systems
-reflexes
-gait
-cerebellar function
-pronator drift
OTTAWA SAH Clinical Decision Rule
-100% sensitivity in predicting SAH
-use on pt seeking care in ED c/o acute nontraumatic HA
-need to have one or more of the following (6):
-40 years or older
-neck pain/stiffness
-Witnessed LOC
-Onset during exertion
-Thunderclap headache (instantly peaking pain)
-Limited neck flexion (on exam)
Make sure to consider these differential diagnoses with acute headache:
-imminent or completed vascular events
-infections
-intracranial masses
-preeclampsia
-carbon monoxide poisoning
Treatment for migraine headaches
*and what should you avoid as first line therapy?
-NSAIDs
-metoclopramide
-dihydroergotamine
-triptans (PO, nasal, subQ)
*morphine/hydromorphone as first line therapy
What medication can be used for chronic migraine treatment when unresponsive to other therapy?
Ketamine infusions
Migraines
-how long do they usually last?
-what is a main characteristic of migraine headaches?
-is pain generalized or unilateral?
-what aggravates migraines?
-sx
-does an aura precede migraine HA?
-4-72hr
-pulsatile
-unilateral
-routine physical activity
-nausea, vomiting, photophobia, phonophobia.
-Commonly visual, may precede migraine but not always
Medication treatment of Migraine headaches
-symptomatic therapy (acute attack)
*ergotamines
*triptans
*other agents
*Neuromodulation
-Cafergot (ergotamine tartrate + caffeine); do not take when pregnant, CV disease or RF, pts taking potent CYP3A4 inhibitors
-Sumatriptan - helps abort attacks; eletriptan (immediate therapy); frovatriptan (long-half-life)
*greater benefit when combined with Naproxen
-chlorpromazine, butalbital-containing combo meds, opioid analgesics (can cause rebound HA)
Medication treatment of Migraine headaches
-preventative therapy (2)
-Acupuncture
-Botulinum toxin Type A
Medication treatment of Migraine headaches
-prophylactic treatment of migraine
-antiepileptic
-cardiovascular (guanfacine, propranolol, verapamil))
-antidepressant (Amitriptyline, venlafaxine)
-other: acupuncture, botulinum toxin A, riboflavin (changes urine color)
Tension-Type Headache
-sx
-location
-exacerbated
-tx
-precranial tenderness, poor concentration, other non-specific sx + constant daily HA that are described as “vist-like or tight” in quality; not pulsatile or associated with focal neuro sx
-most intense at neck or back of head; can be generalized
-stress, fatigue, noise or glare
-NO triptans; address comorbid anxiety or depression; similar to migraine tx
what is the most common type of primary headache disorder?
Tension-type HA
What type of HA can you not use Triptans to treat?
Tension-type headache
Cluster HA
-most prevalent in what population?
-family hx of headaches or migraines?
-sx
-middle-aged men
-no family hx
-episodic, severe unilateral periorbital pain; occurs daily for several weeks
*accompanied by 1 or more of the following: ipsilateral nasal congestion, rhinorrhea, lacrimation, redness of the eye, and Horner syndrome (ptosis, pupillary meiosis, facial anhidrosis or hypohidrosis)
Cluster HA
-at what time of day do these HA typically occur?
-do these HA cause patient to wake up?
-tx
-night
-awakens patients from sleep
-1st line: sumatriptan; prophylactic meds: lithium, verapamil, topiramate
Tx for post-traumatic HA
simple analgesics
Analgesic rebound HA
-cause?
-R/F
-what meds can cause this? and for how long after taking these meds consistently can this type of HA occur?
-medication overuse
-chronic daily HA
-ergotamines, triptans, meds containing butalbital, opioids –> when taken for more than 10 days; Tylenol, acetylsalicylic acid, NSAIDs –> when taken more than 15 days per month
treatment for primary cough headache
indomethacin PO daily
How to diagnose intracranial mass (imaging)?
CT/MRI
Facial Pain
-Trigeminal neuralgia
*sx
*exacerbated by?
*most common in what demographic? at what age?
*is neuro exam abnormal?
-stabbing facial pain, commonly arises near one side of mouth and shoots toward ear, eye, or nostril on that side
-exacerbated by touch, movement, drafts, eating
-middle and later life; affects women > men.
-no abnormality except if sx of underlying lesion (ie MS)
Does trigeminal neuralgia occur on both side or one side of face?
Unilateral
Trigeminal neuralgia
-treatment
*first line
*if ineffective, then what?
*tx of trigeminal neuralgia + MS
-oxcarbazepine or carbamazepine
-phenytoin
-gabapentin
-R/F associated with postherpetic neuralgia
-tx
*do systemic corticosteroids help?
-elderly, immunocompromised, hx of shingles
-acyclovir (5x/day) or valacyclovir (3x/day) when given w/i 72 hours of rash onset - reduces postherpetic neuralgia by 50%
*NO!
Spontaneous SAH
-s/s
-LOC
-diagnostic imaging
-any focal neuro deficits?
-sudden “thunderclap” HA of a severity never experienced previously by the patient –> N/V
-confused and irritable
-CT scan (angiography preferred); should be performed immediately
-absent
Spontaneous SAH
-tx
nimodipine
Pseudotumor Cerebri - “Idiopathic Intracranial Hypertension””
-sx
-what kind of palsy is common?
-cause?
-is CSF normal or abnormal?
-tx
-HA - worse on straining, visual obscurations or diplopia (due to papilledema and abducens nerve dysfunction)
-idiopathic (most often)
-normal
-acetazolamide 3x/day
