Module 2 EB Flashcards

(213 cards)

1
Q

-In the geriatric population, how do diseases often present?
-Do all abnormalities require evaluation and treatment?

A

-present atypically or with nonspecific sx
-not all abnormalities require evaluation and treatment

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2
Q

-in addition to conventional assessment of symptoms AND diseases, the comprehensive assessment addresses 3 topics for the geriatric population. what are they?

A

-prognosis, values/preference, ability to function independently

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3
Q

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?

A

-as you would in young person
-made based on ability to improve patient’s prognosis and quality of life

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4
Q

What do most frail older adults prioritize maintaining (in comparison to)?

A

independence over prolonged survival

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5
Q

-25% of pt >65syo and 50% of >85yo need help with what?
-Thus, it is important to assess what?

A

-ADLs
-functional screening –> assessment of ADLs/IADLs

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6
Q

Dementia:
-def
-dementia is NOT ___________.

A

-progressive decline of intellectual function; loss of short-term memory + 1 other cognitive deficit; deficit severe enough to cause impairment of function
-delirium

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7
Q

-agnosia
-aphasia
-apraxia

A

-inability to recognize objects
-word-finding difficulty
-inability to perform motor tasks

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8
Q

General considerations for dementia

A

-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

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9
Q

Dementia:
-diagnosis

A

-significant decline in function that is severe enough to interfere with work, social life, performance of routine activities

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10
Q

How many of dementia patients have Alzheimer’s?

A

2/3 in US

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11
Q

What is the most common concomitant of early dementia?

A

Depression

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12
Q

-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?

A

-Susceptibility gene associated with late-onset Alzheimer’s disease (APOE-e4)
-NO
-genetic counseling

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13
Q

-Lab work for dementia patients
-Lab work not part of routine testing

A

CBC, CMP (serum electrolytes, calcium, Cr, glucose), TSH, vitB12
-not part of routine testing: liver panel, HIV, RPR, heavy metal screen

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13
Q

Tools for cognitive impairment
-Mini-cog
-Montreal cognitive assessment (MoCA)

A

-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

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14
Q

-How is imaging helpful in dementia patients?
-when is MRI warranted?

A

-rules out subdural hematoma, tumor, previous stroke, hydrocephalus
-younger patients + focal neuro deficits, seizures, gait abnormalities

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15
Q

How is delirium distinguished from dementia?

A

delirium is acute in onset, fluctuating coarse, deficits in attention

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16
Q

what are medications that cause delirium?

A

anticholinergic, hypnotics, neuroleptics, opioids, NSAIDs, antihistamines, corticosteroids

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17
Q

what kind of imaging is used for older patient with classic Alzheimer findings?

A

non-contrast CT

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18
Q

when do you refer a dementia patient?

A

refer to neuropsychological testing to distinguish dementia from depression
-dx dementia in those with poor education, aid dx when impairment is mild

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19
Q

Dementia: cognitive impairment
-drug class
-use
-drugs
-MOA

A

-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

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20
Q

Dementia: cognitive impairment
-drug used for advanced disease

A

memantine
-N-methyl-D-aspartate (NMDA) antagonist

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21
Q

Dementia: behavioral problems
-nonpharmacological approach

A

-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

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22
Q

Dementia: behavioral problems
-pharmacological approach
*who is this approach reserved for?
*drug class used?
*drug names

A

-patients who are a danger to others/themselves or symptoms are very distressing to patient
-atypical psychotropics
-risperidone, olanzapine, quetiapine, aripiprazole

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23
Q

Dementia: behavioral problems
-pharmacological approach
*medication used to improve symptoms of agitation?

A

citalopram

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24
Fragility -essentials of diagnosis
syndrome characterized by loss of physiologic reserve and dysregulation across multiple systems --> greater risk of poor health outcomes
25
Fragility -how to diagnose
3+ features must be present: *weakness, slow gait speed, dec physical activity, weight loss, exhaustion, low energy
26
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
27
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
28
Immobility -hazards of bedrest in older adults
hazards are multiple, serious, quick to develop, and slow to reverse
29
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)
30
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)
31
Falls & Gait Disorders: -what is the most common/significant reversible cause of falls?
polypharmacy
32
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
33
Depression: -among which geriatric population has the highest rates for suicide?
-older single men
34
Depression: what questions are highly sensitive for determining depression in geriatric population?
1. during the past 2 weeks, have you felt down, depressed, or hopeless? 2. during the past 2 weeks, have you felt little interest or pleasure in doing things?
35
Depression: what drug is first line?
-SSRI
36
Delirium: -essentials of diagnosis
-rapid onset -fluctuating course -primary deficit in attention rather than memory -may be hypoactive/hyperactive -dementia frequently coexists
37
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
38
Delirium: -delirium assessment tool (and what it requires)
-CAM *acute onset and fluctuating course *inattention and either: disorganized thinking or altered level of consciousness
39
Delirium: -medications known to cause delirium
-sedative/hypnotics, anticholinergics, opioids, benzos, H1/H2 antihistamines
40
Delirium: -lab work
CBC, BUN, cr, glucose, calcium, albumin, liver panel, UA, ECG (select cases CXR, UDS, lumbar puncture)
41
Delirium: -do any medications prevent or improve outcomes?
NO
42
Delirium: -tx
supportive, tx underlying causes, eliminate unnecessary meds, avoid indwelling catheters/restraints
43
Delirium: -prognosis -when to admit
-most episodes clear in matter of days after correction of precipitant -pt w/ delirium of unknown cause
44
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
45
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
46
Urinary incontinence: -what is one of the most common causes of urinary incontinence?
-pharmaceuticals *D/C any anticholinergic meds first!
47
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
48
Involuntary weight loss: -what can be used to help?
-oral nutritional supplements of 200-1000kcal/day -megestrol acetate (appetite stimulant)
49
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
50
Pressure injury: what is the primary risk factor?
immobility
51
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
52
Hearing impairment: -those with hearing loss >65yo -those with hearing loss >85yo
-1/3 -1/2
53
Hearing impairment: -what test helps determine if hearing impairment?
Whisper test
54
Contributing risk factors to pressure ulcers
-immobility -reduced sensory perception -moisture (urinary/fecal incontinence) -poor nutritional status -friction/shear forces
55
when is a pressure ulcer unstagable?
-base is covered in slough (yellow, tan, gray, green, brown) or eschar (tan, brown, black)
56
who should be consulted for a pressure injury?
Wound care
57
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
58
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
59
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
60
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
61
what type of seizure is most common in those with epilepsy?
-focal onset seizures (partial seizures)
62
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)
63
Generalized onset seizures: motor seizures -postictal phase
-HA -disorientation -confusion -drowsiness -nausea -soreness of muscles
64
Generalized onset seizures: Motor seizures -myoclonic
single/multiple jerks
65
Generalized onset seizures: motor seizures -atonic
very brief, <2sec loss of muscle tone = falls
66
Generalized onset seizures: motor seizures -epileptic spasms
sudden flexion or extension of truncal muscles (infancy)
67
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)
68
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
69
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
70
Epilepsy: what is the most common cause of lower concentration?
suboptimal patient adherence
71
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
72
ETOH Withdrawal seizures -def -tx
-1 or more generalized tonic-clonic seizures that occur within 48 hours of withdrawal -benzos
73
Tonic-clonic status epilepticus -medical emergency? -most common cause?
-YES, requires airway management -poor adherence to regimen
74
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.)
75
Epilepsy: diagnostic studies
MRI EEG
76
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
77
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)
78
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
79
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
80
Epilepsy: -what determines the extent and severity of autonomic dysfunction?
evaluation of the patient + presence of associated neurological s/s
81
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
82
Dysautonomia: syncope -is recovery rapid or slow?
recovery is rapid once patient is recumbent; headache, nausea, fatigue are COMMON
83
Dysautonomia: treatment -avoid? -supportive tx
-abrupt postural change, prolonged recumbency -wear waist-high elastic hosiery, salt supplementation, sleeping in semierect position
84
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)
85
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
86
Stroke: -risk factors -distinctive neuro signs reflect what?
-HTN, DM, tobacco use, a-fib, atherosclerosis -region of brain involved
87
what is the 5th leading cause of death? what is the leading cause of disability?
STROKE STROKE
88
TIA: -LOC? -confusion? -sx
-rarely -rarely -depends on arterial distribution affected
89
TIA: -imaging
-CT/MRI: indicated within 24 hours of sx onset -MRI w/ diffusion weighted sequences reveals acute or subacute infarction (wake-up strokes)
90
TIA: -treatment goal -tx
-prevent future attacks + stroke -supportive tx
91
Stroke: -essentials of dx
sudden onset of neurologic deficit of cerebrovascular origin
92
Stroke: -types of stroke?
ischemic heomrrhagic
93
Stroke: -types of ischemic stroke -types of hemorrhagic stroke
-lacunar infarct; carotid circulation obstruction -spontaneous intracerebral hemorrhage; subarachnoid hemorrhage
94
Stroke: -secondary tx for ischemic stroke
Antiplatelet
95
-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
96
-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
97
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)
98
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
99
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
100
Parkinson Disease: -essentials of dx
-any combination of tremor, rigidity, bradykinesia, progressive postural instability -cognitive impairment (sometimes prominent) -occurs in all ethnic groups
101
Parkinson Disease: -onset -progressive or static?
-45-65 years -progressive
102
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)
103
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
104
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
105
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
106
Parkinson Disease: -impact on muscle strength -impact on DTRs
-no muscle weakness or altered DTRs
107
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)
108
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
109
Huntington Disease: -characterized by? -imaging
-chorea and dementia -CT scan/MRI; PET
110
Huntington Disease: S/S -onset -timeline of disease (how many years) -genetic counseling?
-30-50 years -15-20 years -offer to offspring
111
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
112
RLS: -essentials of dx *common? *what can cause RLS?
-common -idiopathic OR r/t Parkinson's disease, pregnancy, IDA, peripheral neuropathy
113
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
114
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
115
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
116
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
117
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
118
Pathology: multifocal ischemic change -Alzheimer? Vascular dementia? Dementia with Lewy Bodies? Frontotemporal dementia (FTD)?
Vascular dementia
119
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
120
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)
121
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
122
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
123
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)
124
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
125
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
126
Dementia: -what medications to avoid in tx
-paroxetine/TCAs - anticholinergic -avoid OTC antihistamines/benzos - worsen cognition, cause delirium
127
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
128
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
129
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.
130
-MS: -do pts have residual deficits? -what is the most common form of the disease?
-yes -relapsing-remitting
131
MS: -tx
-corticosteroids -many drugs; choose initial agent based on tolerance, risks, pt preference, disease severity
132
MS: -glatiramer acetate/interferon -ocrelizumab
-initial med -only med effective in SLOWING DISABILITY PROGRESSION IN PRIMARY PROGRESSIVE MS
133
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)
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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
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Acute idiopathic polyneuropathy (GBS): -tx
-plasmapharesis -IVIG x5days
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Bells Palsy: -essentials of dx *sudden or progressive onset? *what other symptoms may occur?
-sudden -hyperacusis or impaired taste may occur
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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
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Bells Palsy: -imaging? -S/S
-none -facial paresis, facial pain, ipsilateral restriction of eye closure, disturbance of taste, hard to eat/drink
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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
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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
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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)
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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)
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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
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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
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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)
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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
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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
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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
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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
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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
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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)
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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
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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)
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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
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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
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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
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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)
158
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
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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
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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
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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
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what is the most common sx patients seek care for?
Cough
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what sx would indicate pneumonia?
acute cough + tachycardia, tachypnea, fever
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what does wheezing and rhonchi indicate?
bronchitis
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Differentials for persistent cough
chronic sinusitis, postnasal drip, asthma
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what would be indicated with sx of cough + dyspnea + JVD?
HF
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What dx would be indicated with airspace consolidation (rales, dec breath sounds, fremitus, egophony)
CAP
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Cough: -Acute -persistent -subacute -chronic
<3 weeks 3-8 weeks postinfectious cough 3-8 weeks >8 weeks
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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
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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
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Cough: -when to refer
failure to control cough; recurrent sx referred to otolaryngologist, pulmonologist, gastroenterologist
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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)
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Postnasal drip -step 1 (empiric therapy) -step 2 (definitive testing)
-therapy for allergy or chronic sinusitis -sinus CT scan; ENT referral
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Asthma -Step 1 (empiric therapy) -step 2 (definitive testing)
-beta-2-agonist -spirometry: consider methacholine challenge if normal
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GERD -step 1 (empiric therapy) -step 2 (definitive testing)
-lifestyle and diet modification with or without proton pump inhibitors -esophageal pH monitoring
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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
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Dyspnea -tx
immediately provide supplemental O2
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-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
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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
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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
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do NP's treat hypothermia?
NO, refer to ED.
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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
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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)
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Rule of 9's
Entire arm 9% Posterior surface of each leg 9% Entire head and neck 9% Posterior surface of upper trunk (9%)
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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
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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.
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Pieces of a neuro exam
-mental status -motor/sensory systems -reflexes -gait -cerebellar function -pronator drift
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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)
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Make sure to consider these differential diagnoses with acute headache:
-imminent or completed vascular events -infections -intracranial masses -preeclampsia -carbon monoxide poisoning
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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
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What medication can be used for chronic migraine treatment when unresponsive to other therapy?
Ketamine infusions
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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
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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)
194
Medication treatment of Migraine headaches -preventative therapy (2)
-Acupuncture -Botulinum toxin Type A
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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)
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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
197
what is the most common type of primary headache disorder?
Tension-type HA
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What type of HA can you not use Triptans to treat?
Tension-type headache
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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)
200
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
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Tx for post-traumatic HA
simple analgesics
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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
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treatment for primary cough headache
indomethacin PO daily
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How to diagnose intracranial mass (imaging)?
CT/MRI
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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)
206
Does trigeminal neuralgia occur on both side or one side of face?
Unilateral
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Trigeminal neuralgia -treatment *first line *if ineffective, then what? *tx of trigeminal neuralgia + MS
-oxcarbazepine or carbamazepine -phenytoin -gabapentin
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-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!
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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
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Spontaneous SAH -tx
nimodipine
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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