Module 2 EB Flashcards

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
Q

Fragility
-essentials of diagnosis

A

syndrome characterized by loss of physiologic reserve and dysregulation across multiple systems –> greater risk of poor health outcomes

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25
Q

Fragility
-how to diagnose

A

3+ features must be present:
*weakness, slow gait speed, dec physical activity, weight loss, exhaustion, low energy

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26
Q

Fragility
-at risk for?
-treatment

A

-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

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27
Q

Immobility
-associated with increased rates of?
-prevention
-most common etiology

A

-morbidity, hospitalization, disability, mortality
-structured physical activity programs (reduce mobility-related disability)
-hospital-associated bed rest

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28
Q

Immobility
-hazards of bedrest in older adults

A

hazards are multiple, serious, quick to develop, and slow to reverse

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29
Q

Falls & Gait Disorders:
-how often do falls occur in >65yo?
-percent of falls that cause serious injury?
-complication from falls

A

-1/3
-10%
-leading cause of death from injury in person >65yrs (hip fracture common precursor to functional impairment, nursing home placement, death)

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30
Q

Falls & Gait Disorders:
-what test helps determine a thorough gait evaluation?

A

-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)

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31
Q

Falls & Gait Disorders:
-what is the most common/significant reversible cause of falls?

A

polypharmacy

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32
Q

Falls & Gait Disorders:
-what must be considered in any elderly patient presenting with new neuro sx/signs?
*what sx may be absent?

A

-chronic subdural hematoma
*HA and trauma

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33
Q

Depression:
-among which geriatric population has the highest rates for suicide?

A

-older single men

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34
Q

Depression: what questions are highly sensitive for determining depression in geriatric population?

A
  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?
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35
Q

Depression: what drug is first line?

A

-SSRI

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36
Q

Delirium:
-essentials of diagnosis

A

-rapid onset
-fluctuating course
-primary deficit in attention rather than memory
-may be hypoactive/hyperactive
-dementia frequently coexists

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37
Q

Delirium:
-general considerations
-cause
-risk factors

A

-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

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38
Q

Delirium:
-delirium assessment tool (and what it requires)

A

-CAM
*acute onset and fluctuating course
*inattention and either: disorganized thinking or altered level of consciousness

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39
Q

Delirium:
-medications known to cause delirium

A

-sedative/hypnotics, anticholinergics, opioids, benzos, H1/H2 antihistamines

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40
Q

Delirium:
-lab work

A

CBC, BUN, cr, glucose, calcium, albumin, liver panel, UA, ECG (select cases CXR, UDS, lumbar puncture)

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41
Q

Delirium:
-do any medications prevent or improve outcomes?

A

NO

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42
Q

Delirium:
-tx

A

supportive, tx underlying causes, eliminate unnecessary meds, avoid indwelling catheters/restraints

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43
Q

Delirium:
-prognosis
-when to admit

A

-most episodes clear in matter of days after correction of precipitant
-pt w/ delirium of unknown cause

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44
Q

Urinary incontinence:
-stress
-urge
-overflow

A

-leakage of urine upon coughing, sneezing, standing
-urgency and inability to delay urination
-variable presentation; leak or dribble urine because bladder is too full

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45
Q

Urinary incontinence:
DIAPPERS

A

-D: delirium
-I: infection
-A: atrophic urethritis/vaginitis
-P: pharmaceuticals
-P: Psychological factors (depression)
-E: excess urinary output
-R: restricted mobility
-S: stool impaction

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46
Q

Urinary incontinence:
-what is one of the most common causes of urinary incontinence?

A

-pharmaceuticals
*D/C any anticholinergic meds first!

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47
Q

Involuntary weight loss:
-what happens to appetite as we age?
-what are the main causes?
-what should be considered if not cause identified?

A

-reduces
-medical, psychiatric, unknown
-Frailty syndrome should be evaluated

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48
Q

Involuntary weight loss:
-what can be used to help?

A

-oral nutritional supplements of 200-1000kcal/day
-megestrol acetate (appetite stimulant)

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49
Q

Pressure injury:
-stage 1
-stage 2
-stage 3
-stage 4
-Unstageable
-Deep tissue

A

-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

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50
Q

Pressure injury:
what is the primary risk factor?

A

immobility

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51
Q

Vision impairment:
-how often should geriatric patients receive eye exams?

A

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

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52
Q

Hearing impairment:
-those with hearing loss >65yo
-those with hearing loss >85yo

A

-1/3
-1/2

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53
Q

Hearing impairment:
-what test helps determine if hearing impairment?

A

Whisper test

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54
Q

Contributing risk factors to pressure ulcers

A

-immobility
-reduced sensory perception
-moisture (urinary/fecal incontinence)
-poor nutritional status
-friction/shear forces

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55
Q

when is a pressure ulcer unstagable?

A

-base is covered in slough (yellow, tan, gray, green, brown) or eschar (tan, brown, black)

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56
Q

who should be consulted for a pressure injury?

A

Wound care

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57
Q

Elder Mistreatment & Self-Neglect:
-def
-what is the most common form of elder mistreatment?

A

-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

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58
Q

Epilepsy:
-def

A

-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

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59
Q

Epilepsy: focal onset seizures (also known as partial seizures)
-EEG
-focal motor
-nonmotor

A

-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

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60
Q

Epilepsy: complex partial seizure (also known as focal seizure)
-awareness vs impaired awareness

A

-knowledge of self or environment, and events occurring during seizure
-impaired awareness may be preceded, accompanied, or followed by various motor/non-motor sx

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61
Q

what type of seizure is most common in those with epilepsy?

A

-focal onset seizures (partial seizures)

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62
Q

General Onset Seizures: Motor seizures
-tonic-clonic phase

A

-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)

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63
Q

Generalized onset seizures: motor seizures
-postictal phase

A

-HA
-disorientation
-confusion
-drowsiness
-nausea
-soreness of muscles

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64
Q

Generalized onset seizures: Motor seizures
-myoclonic

A

single/multiple jerks

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65
Q

Generalized onset seizures: motor seizures
-atonic

A

very brief, <2sec loss of muscle tone = falls

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66
Q

Generalized onset seizures: motor seizures
-epileptic spasms

A

sudden flexion or extension of truncal muscles (infancy)

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67
Q

Epilepsy: treatment
-what does the choice of medication depend on?

A

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)

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68
Q

Epilepsy: are medications safe in pregnant women?

A

NO! Teratogenic!!!
????????????
during pregnancy, if break-through seizure occurs, dose change, another interacting med is added to regiment

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69
Q

Epilepsy: how to titrate treatment medications

A

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

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70
Q

Epilepsy: what is the most common cause of lower concentration?

A

suboptimal patient adherence

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71
Q

Epilepsy: when can you discontinue seizure medications?

A

when adult has been seizure free for 2 years
-gradually reduce dose (weeks-months)
-if seizure recurs, reinstitute tx

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72
Q

ETOH Withdrawal seizures
-def
-tx

A

-1 or more generalized tonic-clonic seizures that occur within 48 hours of withdrawal
-benzos

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73
Q

Tonic-clonic status epilepticus
-medical emergency?
-most common cause?

A

-YES, requires airway management
-poor adherence to regimen

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74
Q

Epilepsy: etiology

A

-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.)

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75
Q

Epilepsy: diagnostic studies

A

MRI
EEG

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76
Q

Epilepsy:
-when is lumbar puncture necessary?
-S/S

A

-with any sign of infection present or in evaluation of new-onset seizures in acute setting
-HA, mood alterations, lethargy, myoclonic jerking; aura

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77
Q

Dysautonomia
-essentials of dx
-etiology

A

-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)

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78
Q

Dysautonomia
-CNS causes

A

-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

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79
Q

Epilepsy:
-causes in PNS
*pure autonomic neuropathy
*GBS
*Metabolic disturbance

A

-Pure autonomic neuropathy: viral infection; paraneoplastic disorder r/t small cell lung cs
-marked hypo/hypertension, cardiac arrhythmias
-diabetic, uremic, amyloidotic; leprosy, changas disease

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80
Q

Epilepsy:
-what determines the extent and severity of autonomic dysfunction?

A

evaluation of the patient
+ presence of associated neurological s/s

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81
Q

Dysautonomia:
-S/S

A

-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

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82
Q

Dysautonomia: syncope
-is recovery rapid or slow?

A

recovery is rapid once patient is recumbent; headache, nausea, fatigue are COMMON

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83
Q

Dysautonomia: treatment
-avoid?
-supportive tx

A

-abrupt postural change, prolonged recumbency
-wear waist-high elastic hosiery, salt supplementation, sleeping in semierect position

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84
Q

TIA:
-acute or chronic onset?
-does clinical deficit resolve completely? if so, how long?
-risk factors

A

-acute
-resolves completely within 24 hrs
-vascular disease (present)

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85
Q

TIA:
-characterized by?
-30% of patients have a ________ within 90d
-when is the risk of stroke high following TIA?

A

-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
Q

Stroke:
-risk factors
-distinctive neuro signs reflect what?

A

-HTN, DM, tobacco use, a-fib, atherosclerosis
-region of brain involved

87
Q

what is the 5th leading cause of death?
what is the leading cause of disability?

A

STROKE
STROKE

88
Q

TIA:
-LOC?
-confusion?
-sx

A

-rarely
-rarely
-depends on arterial distribution affected

89
Q

TIA:
-imaging

A

-CT/MRI: indicated within 24 hours of sx onset
-MRI w/ diffusion weighted sequences reveals acute or subacute infarction (wake-up strokes)

90
Q

TIA:
-treatment goal
-tx

A

-prevent future attacks + stroke
-supportive tx

91
Q

Stroke:
-essentials of dx

A

sudden onset of neurologic deficit of cerebrovascular origin

92
Q

Stroke:
-types of stroke?

A

ischemic
heomrrhagic

93
Q

Stroke:
-types of ischemic stroke
-types of hemorrhagic stroke

A

-lacunar infarct; carotid circulation obstruction
-spontaneous intracerebral hemorrhage; subarachnoid hemorrhage

94
Q

Stroke:
-secondary tx for ischemic stroke

A

Antiplatelet

95
Q

-what imaging type is used to dx lacunar infarct?
-what imaging type is used to dx carotid circulation obstruction?

A

-MRI w/ diffusion-weighted sequences (CT is insensitive acutely)
-Noncontrast CT (exclude hemorrhage); diffusion-weighted MRI is gold standard

96
Q

-what imaging type is used in dx of spontaneous intracerebral hemorrhage?
-what type of imaging is used to dx subarachnoid hemorrhage?

A

-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
Q

Essential Familial Tremor
-family hx?
-how does ETOH effect it?
-any other abnormal findings?
-cause

A

-yes, common
-improves temporarily
-no abnormal findings
-uncertain; sometimes inherited (autosomal dominant manner)

98
Q

Essential Familial Tremor
-tx
-when to refer

A

-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
Q

Essential Familial Tremor
-S/S
*onset
*tremor presentation
*physical exam
*prognosis

A

-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
Q

Parkinson Disease:
-essentials of dx

A

-any combination of tremor, rigidity, bradykinesia, progressive postural instability
-cognitive impairment (sometimes prominent)
-occurs in all ethnic groups

101
Q

Parkinson Disease:
-onset
-progressive or static?

A

-45-65 years
-progressive

102
Q

Parkinson Disease:
-etiology

A

-dopamine depletion due to degeneration of dopaminergic nigrostriatal system leads to imbalance of dopamine and acetylcholine (NTs normally present in corpus striatum)

103
Q

Parkinson Disease:
-tx of motor disturbance
-what is associated with decreased risk of developing Parkinson disease?
-risk factors

A

-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
Q

Parkinson Disease:
-cardinal motor features
-non-motor features

A

-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
Q

Parkinson Disease:
-tremor characteristics
-what is dx based on?

A

-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
Q

Parkinson Disease:
-impact on muscle strength
-impact on DTRs

A

-no muscle weakness or altered DTRs

107
Q

Parkinson Disease:
-treatment

A

-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
Q

Huntington Disease:
-essentials of dx
*gradual or acute onset?
*what sx progress?
*family hx?
*responsible gene ID’s on chromosome _____?

A

-gradual onset
-progression of chorea and dementia or behavioral change
-family hx
-4

109
Q

Huntington Disease:
-characterized by?
-imaging

A

-chorea and dementia
-CT scan/MRI; PET

110
Q

Huntington Disease: S/S
-onset
-timeline of disease (how many years)
-genetic counseling?

A

-30-50 years
-15-20 years
-offer to offspring

111
Q

Huntington Disease:
-treatment
*can progression be halted?
*is there a cure?
*meds to tx

A

-no
-no cure
-Tetrabenazine; deutetrabenazine, amantadine, deep brain stimulation, phenothiazines haloperidol, quetiapine, clozapine

112
Q

RLS:
-essentials of dx
*common?
*what can cause RLS?

A

-common
-idiopathic OR r/t Parkinson’s disease, pregnancy, IDA, peripheral neuropathy

113
Q

RLS:
-def
-onset
-complications

A

-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
Q

RLS:
-what labs should always be measured?
-tx

A

-ferritin level
-low iron = PO oral iron sulfate
-physical sx: pramipexole, ropinirole or rotigotine
-improve sx: gabapentin, pregabalin
-unresponsive to normal meds: levodopa

115
Q

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?

A

-progressive
-no
-no
-AGE (2nd), family hx (3rd)
-women
->60yr

116
Q

Dementia:
-progressive decline in intellectual function impacts what?
-how to promote cognitive reserve?

A

-social and occupational functioning
-increased physical activity, education, ongoing intellectual stimulation, social engagement

117
Q

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)?

A

Alzheimer’s disease

118
Q

Pathology: multifocal ischemic change
-Alzheimer? Vascular dementia? Dementia with Lewy Bodies? Frontotemporal dementia (FTD)?

A

Vascular dementia

119
Q

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)?

A

Dementia with Lewy bodies
-Alzheimer’s disease

120
Q

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)?

A

Frontotemporal dementia (FTD)

121
Q

Dementia:
-types of neuropsych assessments?

A

-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
Q

Dementia:
-imaging

A

-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
Q

Dementia:
-tx
*non-pharmacologic

A

-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
Q

Dementia:
-tx
*how to treat cognitive sx

A

-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
Q

Dementia:
-labs
-mood/behavioral disturbances

A

-vitB12/free T4/TSH; RPR/HIV; CBC, electrolytes, glucose, lipid)
-SSRIs, citalopram (agitation) - can cause prolonged QTc
-trazadone: treats insomnia

126
Q

Dementia:
-what medications to avoid in tx

A

-paroxetine/TCAs - anticholinergic
-avoid OTC antihistamines/benzos - worsen cognition, cause delirium

127
Q

MS:
-essentials of dx
*can a single pathologic lesion explain clinical findings?
*how to diagnose?

A

-no, single pathologic lesion cannot explain clinical findings
-MRI - multiple foci

128
Q

MS:
-greatest incidence among what population?
-patho

A

-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
Q

MS:
-imaging
-labs
-dx

A

-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
Q

-MS:
-do pts have residual deficits?
-what is the most common form of the disease?

A

-yes
-relapsing-remitting

131
Q

MS:
-tx

A

-corticosteroids
-many drugs; choose initial agent based on tolerance, risks, pt preference, disease severity

132
Q

MS:
-glatiramer acetate/interferon
-ocrelizumab

A

-initial med
-only med effective in SLOWING DISABILITY PROGRESSION IN PRIMARY PROGRESSIVE MS

133
Q

Acute idiopathic polyneuropathy (GBS)
-essentials of dx
*acute or subacute?
*is weakness or sensory impairment more severe?
*triggers

A

-subacute or acute
-weakness
-infective illness, inoculations, surgical procedures (campylobacter jejuni enteritis; immunologic basis)

134
Q

Acute idiopathic polyneuropathy (GBS):
-labs
-main complaint
-where do S/S begin in the body?

A

-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

135
Q

Acute idiopathic polyneuropathy (GBS):
-tx

A

-plasmapharesis
-IVIG x5days

136
Q

Bells Palsy:
-essentials of dx
*sudden or progressive onset?
*what other symptoms may occur?

A

-sudden
-hyperacusis or impaired taste may occur

137
Q

Bells Palsy:
-cause?
-triggers
-more common in what population?

A

-idiopathic; inflammatory rx involving facial nerve
-herpes simplex; varicella zoster virus infection
-pregnant women and DM pts

138
Q

Bells Palsy:
-imaging?
-S/S

A

-none
-facial paresis, facial pain, ipsilateral restriction of eye closure, disturbance of taste, hard to eat/drink

139
Q

Bells Palsy:
-TX

A

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

140
Q

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?

A

-weak
-voluntary muscles
-diplopia, ptosis, difficulty swallowing
-activity increases weakness of affected muscles

141
Q

Myasthenia Gravis:
-what medications transiently improve weakness?
-what ages impacted?
-what population is most impacted?
-onset is progressive or acute?

A

-short-acting anticholinesterases
-all ages
-young women w/ HLA-DR3
-progressive (insidious)

142
Q

Myasthenia Gravis:
-when do exacerbations occur?
-patho

A

-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)

143
Q

Myasthenia Gravis:
-labs (what lab is used to dx)
-S/S

A

-acetylcholine receptor antibodies assay –> elevated, use to dx MG
-ptosis, diplopia, difficulty chewing/swallowing, resp difficulties, limb weakness

144
Q

Myasthenia Gravis:
-characteristics of weakness experienced by these patients
-findings from clinical exam for dx

A

-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

145
Q

Myasthenia Gravis:
-tx
-what kind of surgery can help?

A

-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)

146
Q

Palliative care
-goal of care?
-what does palliative care manage?
-def

A

-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

147
Q

Palliation of Common Nonpain Sx:
-dyspnea
*def
*characterized by?
*Tx

A

-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

148
Q

Palliation of Common Nonpain Sx:
-N/V
*what is the best modality to manage with medication?
*helpful treatments

A

*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

149
Q

Palliation of Common Nonpain Sx:
-delirium and agitation
*sx
*tx
*neuroepileptic agents

A

-waxing/waning LOC + change in cognition that develops over short time; terminal restlessness
-reversible causes: urinary retention, constipation, anticholinergic meds, pain
-haloperidol, risperidone

150
Q

Palliation of Common Nonpain Sx:
-constipation
*triggers
*ask about…?
*prevention
*prophylactic bowel regimen

A

-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

151
Q

Palliation of Common Nonpain Sx:
-fatigue
*what is the most common complaint of cancer patient?
*contributing factors to fatigue
*coexisting factors
*psychostimulants

A

-fatigue
-anemia, hypothyroidism, hypogonadism, cognitive/functional impairment, malnutrition
-pain and depression
-methylphenidate (AM, afternoon), modafinil (cancer-related fatigue)

152
Q

Pain Management:
-acute pain
*when does it resolve?
*management
*what tool is used to guide #-needed-to-treat-for-specific doses of various meds?

A

-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

153
Q

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?

A

-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)

154
Q

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?

A

-persists beyond expected period of healing; itself is a disease state (>3-6MO)
-Interdisciplinary management
-NO

155
Q

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)

A

-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

156
Q

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?

A

*restorative function
*long-acting opioid analgesic can be given around the clock + short-acting opioid medication PRN “breakthrough” pain
*appropriate treatment of pain

157
Q

Pharmacologic pain management strategies:
-Non-opioid

A

-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
Q

Pharmacologic pain management strategies:
-Opioids
*Full opioid agonists
*Short-acting formulations
*IR fentanyl patch
*Buprenorphine

A

-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

159
Q

Pharmacologic pain management strategies:
-opioids
*methadone
*Buprenorphine
*common SE of opioids

A

-long-acting opioid, inexpensive; higher methadone doses = risk of prolonged QT (need baseline ECG)
-moderate to severe chronic pain
-tolerance, dependance, addiction

160
Q

Pharmacologic pain management strategies:
-neuropathic pian “burning, shooting, pins/needles, electricity”
*gabapentin/pregabalin
*SSRIs
*Tricyclics

A

*1st line treatment; can cause dizziness, ataxia, GI upset
*duloxetine (Cymbalta), venlafaxine; take on full stomach
*nortriptyline, desipramine

161
Q

Common emergencies:
-cough
*when to get chest Xray
*patho
*what does an effective cough depend on?

A

-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

162
Q

what is the most common sx patients seek care for?

A

Cough

163
Q

what sx would indicate pneumonia?

A

acute cough + tachycardia, tachypnea, fever

164
Q

what does wheezing and rhonchi indicate?

A

bronchitis

165
Q

Differentials for persistent cough

A

chronic sinusitis, postnasal drip, asthma

166
Q

what would be indicated with sx of cough + dyspnea + JVD?

A

HF

167
Q

What dx would be indicated with airspace consolidation (rales, dec breath sounds, fremitus, egophony)

A

CAP

168
Q

Cough:
-Acute
-persistent
-subacute
-chronic

A

<3 weeks
3-8 weeks
postinfectious cough 3-8 weeks
>8 weeks

169
Q

Cough: acute
-what confirms diagnosis?
-adults with acute cough, abnormal VS, abnormal CXR suggests what?
*what could C-reactive protein be?
-tx

A

-fever, nasal congestion, sore through
-pneumonia
*>30 (improves dx accuracy)
-target underlying etiology of illness, cough reflex, exacerbating factors of cough

170
Q

Cough: acute
-influenza tx
-Chlamydophila/mycoplasma tx
-bronchitis + wheezing tx
-acute cough + accompanying postnasal drip tx

A

-PO oseltamivir/zanamivir (initiate w/i 30-48 hours of illness onset)
-erythromycin/doxy
-inhaled beta 2 agonist
-antihistamines, decongestants, nasal corticosteroids

171
Q

Cough:
-when to refer

A

failure to control cough; recurrent sx referred to otolaryngologist, pulmonologist, gastroenterologist

172
Q

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

A

-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)

173
Q

Postnasal drip
-step 1 (empiric therapy)
-step 2 (definitive testing)

A

-therapy for allergy or chronic sinusitis
-sinus CT scan; ENT referral

174
Q

Asthma
-Step 1 (empiric therapy)
-step 2 (definitive testing)

A

-beta-2-agonist
-spirometry: consider methacholine challenge if normal

175
Q

GERD
-step 1 (empiric therapy)
-step 2 (definitive testing)

A

-lifestyle and diet modification with or without proton pump inhibitors
-esophageal pH monitoring

176
Q

Dyspnea
-def
-diagnostic studies of pneumonia
-diagnostic studies of HF
-diagnostic studies of PE

A

-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

177
Q

Dyspnea
-tx

A

immediately provide supplemental O2

178
Q

-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?

A

-cerebral dysfunction with core body temp over 40C
-internal rectal, foley, esophageal
-heat exhaustion
-NO, need electrolytes
-NO

179
Q

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?

A

-below 35C
-above 32C
-hypoglycemia, trauma, infection, overdose, peripheral cold injury

180
Q

Accidental Systemic Hypothermia:
-Stage I
-Stage II
-Stage III
-Stage IV

A

-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

181
Q

do NP’s treat hypothermia?

A

NO, refer to ED.

182
Q

Frostbite
-when to refer?
-what to avoid
-method of rewarming

A

-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

183
Q

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)

A

-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)

184
Q

Rule of 9’s

A

Entire arm 9%
Posterior surface of each leg 9%
Entire head and neck 9%
Posterior surface of upper trunk (9%)

185
Q

Neurological Disorders: Acute headache
-imaging used for acute headache
-follow-up initial imaging with what? what is the purpose?

A

-CT without contrast: excludes intracranial hemorrhage, intracranial mass
-LP; excludes infectious causes of HA

186
Q

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?

A

-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.

187
Q

Pieces of a neuro exam

A

-mental status
-motor/sensory systems
-reflexes
-gait
-cerebellar function
-pronator drift

188
Q

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):

A

-40 years or older
-neck pain/stiffness
-Witnessed LOC
-Onset during exertion
-Thunderclap headache (instantly peaking pain)
-Limited neck flexion (on exam)

189
Q

Make sure to consider these differential diagnoses with acute headache:

A

-imminent or completed vascular events
-infections
-intracranial masses
-preeclampsia
-carbon monoxide poisoning

190
Q

Treatment for migraine headaches
*and what should you avoid as first line therapy?

A

-NSAIDs
-metoclopramide
-dihydroergotamine
-triptans (PO, nasal, subQ)
*morphine/hydromorphone as first line therapy

191
Q

What medication can be used for chronic migraine treatment when unresponsive to other therapy?

A

Ketamine infusions

192
Q

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?

A

-4-72hr
-pulsatile
-unilateral
-routine physical activity
-nausea, vomiting, photophobia, phonophobia.
-Commonly visual, may precede migraine but not always

193
Q

Medication treatment of Migraine headaches
-symptomatic therapy (acute attack)
*ergotamines
*triptans
*other agents
*Neuromodulation

A

-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
Q

Medication treatment of Migraine headaches
-preventative therapy (2)

A

-Acupuncture
-Botulinum toxin Type A

195
Q

Medication treatment of Migraine headaches
-prophylactic treatment of migraine

A

-antiepileptic
-cardiovascular (guanfacine, propranolol, verapamil))
-antidepressant (Amitriptyline, venlafaxine)
-other: acupuncture, botulinum toxin A, riboflavin (changes urine color)

196
Q

Tension-Type Headache
-sx
-location
-exacerbated
-tx

A

-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
Q

what is the most common type of primary headache disorder?

A

Tension-type HA

198
Q

What type of HA can you not use Triptans to treat?

A

Tension-type headache

199
Q

Cluster HA
-most prevalent in what population?
-family hx of headaches or migraines?
-sx

A

-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
Q

Cluster HA
-at what time of day do these HA typically occur?
-do these HA cause patient to wake up?
-tx

A

-night
-awakens patients from sleep
-1st line: sumatriptan; prophylactic meds: lithium, verapamil, topiramate

201
Q

Tx for post-traumatic HA

A

simple analgesics

202
Q

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?

A

-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

203
Q

treatment for primary cough headache

A

indomethacin PO daily

204
Q

How to diagnose intracranial mass (imaging)?

A

CT/MRI

205
Q

Facial Pain
-Trigeminal neuralgia
*sx
*exacerbated by?
*most common in what demographic? at what age?
*is neuro exam abnormal?

A

-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
Q

Does trigeminal neuralgia occur on both side or one side of face?

A

Unilateral

207
Q
A
208
Q

Trigeminal neuralgia
-treatment
*first line
*if ineffective, then what?
*tx of trigeminal neuralgia + MS

A

-oxcarbazepine or carbamazepine
-phenytoin
-gabapentin

209
Q

-R/F associated with postherpetic neuralgia
-tx
*do systemic corticosteroids help?

A

-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!

210
Q

Spontaneous SAH
-s/s
-LOC
-diagnostic imaging
-any focal neuro deficits?

A

-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

211
Q

Spontaneous SAH
-tx

A

nimodipine

212
Q

Pseudotumor Cerebri - “Idiopathic Intracranial Hypertension””
-sx
-what kind of palsy is common?
-cause?
-is CSF normal or abnormal?
-tx

A

-HA - worse on straining, visual obscurations or diplopia (due to papilledema and abducens nerve dysfunction)
-idiopathic (most often)
-normal
-acetazolamide 3x/day