First Aid CH8 NCDs Flashcards

1
Q

three main categories of NCDs

A

delirium, mild NCDs, major NCDs

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2
Q

define delirium

A

acute brain failure, disorder of orientation (attention, awareness) and language/vision, medical emergency that’s generally reversible but potentially deadly

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3
Q

onset time of delirium

A

hours to days, sxs worse at night (usually)

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4
Q

risk factors for delirium

A

polypharm, advanced age, immobility, pre-existing cog impairment, ETOH use, severe/terminal illness, malnutirtion

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5
Q

medications that can cause delirium

A

TCAs, Benzos
Anti-cholinergics, H2 blockers
Corticosteroids, Meperidine (opioid)

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6
Q

five categories of delirium

A

substance intoxication/withdrawal
medication-induced
delirium d/t medical condition/multiple etiologies

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7
Q

three types of delirium based on psychomotor activity (one of the five categories then gets sub-classed with one of these)

A

mixed: most common, normal psychomotor or fluctuating
hypoactive: most likely to go undetected, presents as drowsiness or lethargy
hyperactive: agitation, uncooperative, disruptive, MC in drug withdrawal/toxicity

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8
Q

CAM test

A

evaluation for suspected delirium

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9
Q

sxs of delirium

A

short attention span, disorientation, fluctuations in lvl of consciousness, visual hallucinations, poor short-term memory

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10
Q

MC precipitants of delirium in kids

A

febrile illness, meds

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11
Q

delirium does what on EEG?

A

background slowing of activity

- exception is delirium tremens (fast activity)

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12
Q

delirium tx

A

treat underlying cause, keep family member at bedside for redirection and reorientation
- Haloperidol for agitation

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13
Q

when are benzos appropriate in delirium tx?

A

if the pt is delirious d/t benzo or ETOH withdrawal

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14
Q

can folks with mild NCDs maintain independence? major NCDs?

A

yes (can perform activities of daily living)

no

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15
Q

what tests are typically included in initial eval of any psych illness?

A

thyroid function tests

- look for sx pattern (hypo vs hyper)

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16
Q

efficacy of mini mental state exam (MMSE)

A

sensitive for major NCDs
- dysfunction < 25
unreliable sensitivity for mild NCDs and early major NCDs

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17
Q

define Mini-Cog

A

3-item recall + drawing clock

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18
Q

define Alzheimer’s Dx

A

MC underlying etiology of major NCDs, d/t accumulation of beta-amyloid plaques and tau proteins, seen as gradual progressive decline in cog function that affects memory, learning, and language

  • personality changes
  • mood swings
  • paranoia
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19
Q

what other dx state are the beta-amyloid plaques and tau proteins found?

A
down syndrome (T21), inc risk of early-onset Alzheimer's in these pts
- can be seen with NORMAL aging
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20
Q

what’s the definitive diagnostic test for Alzheimer’s?

A

postmortem path studies of brain

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21
Q

genetics that inc risk for Alzheimer’s

A

autosomal dominant mutation

  • presenilin 1 or 2
  • episilon-4 variant of apolipoprotein gene
22
Q

typical diagnostic age of Alzheimer’s

A

65 yo

23
Q

tx for Alzheimer’s dx

A

no cure

  • cholinesterase inh (donepezil/aricept, rivastigmine, galantamine) slows clinical deterioration by 6-12 months in 50% of pts with mild-mod dx
  • NMDA R ant (memantine/Namenda)
  • low-dose antipsychotics (inc mortality in pts w/ dementia)
  • environmental interventions (puzzles, music, etc)
24
Q

define vascular cognitive impairment (vascular dx)

A

2nd MC cause of major NCD (20% of cases), cog decline occurs in step-wise fashion d/t cortical strokes and microvascular dx in white matter

25
Q

risk factor for vascular cog impairment

A

HTN, diabetes, smoking, obesity, hyperlipidemia, a-fib, old age

26
Q

what can occur with a vascular lesion to the frontal lobe?

A

personality changes, disinhibition, inappropriate behavior, aggression, apathy (lack of interest/concern), paranoia

27
Q

can vascular cognitive impairment be confirmed by testing?

A

yes, neuroimaging

28
Q

tx for VCI

A

no cure

  • manage risk factors
  • environmental interventions (puzzles, music, etc)
29
Q

define Lewy body dx

A

(core fxs) progressive NCD revolving around path features of Lewy bodies (aggregations of alpha-synuclein) in brain (basal ganglia), visual hallucinations and extrapyramidal signs (Parkinsonism) common

suggestive fxs

  • pt may have violent movements during sleep
  • pt sensitive to antipsychotics
30
Q

does Lewy body dx have a definitive diagnostic test?

A

yes.. but during autopsy

31
Q

Lewy body dx tx

A

cholinesterase inh (donepezil/Aricept, rivastigmine, galantamine)

  • quetiapine or clozapine (mine EPS and NMS)
  • levo-carbidopa
32
Q

define Frontotemporal degeneration (FTD)

A

diverse clinical and path disorders that present age 45-65, cog deficits in: attention, abstraction, planning, problem solving, speech and comprehension, disinhibited behavior (verbal, physical, sexual), apathy/inertia

33
Q

pathological presentation of Frontotemporal degen, is this definitive?

A

atrophy of frontal and temporal lobes

- not definitive unless studied in autopsy

34
Q

tx for Frontotemporal degen

A

tx sxs, SSRIs or Trazodone may reduce impulsive behaviors

35
Q

what’s the most common infectious agent known to cause cognitive impairment?

A

HIV (causes mild NCD)

36
Q

tx for HIV-related NCD

A

HAART antiviral tx for HIV

37
Q

define Huntington’s Dx

A

genetic disorder causing motor (chorea = jerky dance-like movements, bradykinesia), cognitive (executive functioning), and psychiatric (depression, apathy, impulsivity, obsessions) sxs
- avg diagnostic age = 40

38
Q

genetics of Huntington’s Dx

A

CAG trinucleotide repeat in..
HTT gene that encodes huntingtin protein all on..
Chromosome 4
autosomal dominant inheritance pattern

39
Q

tx for HD

A

treat sxs

  • Tetrabenazine (movement disorder tx, MOA unknown)
  • atypical antipsychotics
40
Q

define Parkinson’s Dx

A

idiopathic progressive neurodegenerative dx d/t depletion of dopamine in the basal ganglia, causes cogwheel rigidity, resting pill-rolling tremor, bradykinesia, and postural instability (Joan needed to hold things while walking)

  • 75% of PD pts have major NCD
  • perceptual disturbances may occur
41
Q

PD tx

A

carbidopa-levodopa (or other dopamine agonists)

- quetiapine or clozapine used for psychotic sxs (careful w/ dosing d/e risk of exacerbating PD sxs)

42
Q

what are the only two antipsychotics recommended in PD?

A

quetiapine

clozapine

43
Q

define Prion dx

A

rapidly progressing form of encephalopathy d/t proteins that act like infectious particles, bind to molecules in the body and change their function

  • MC example = Creutzfeldt-Jakob dx
  • 90% of pts experience myoclonus (jerky contractions of muscle groups)
  • other sxs: ataxia, nystagmus, hypokinesia
44
Q

diagnosis based on

A

brain tissue biopsy

45
Q

supportive diagnostics

A

periodic sharp-wave complexes on EEG
CSF positive for 14-3-3 proteins
lesions in putamen or caudate nucleus on MRI

46
Q

Prion dx tx

A

none, prognosis poor w/ death in 1 year

47
Q

restlessness and a feeling of wanting to jump out of ones self

A

akathesia

- caused by antipsychotics

48
Q

define Normal Pressure Hydrocephalus (NPH)

A

potentially reversible cause of cog dysfunction, d/t enlarged ventricles with inc CSF pressure BUT normal opening pressures on lumbar puncture, stems from infection or hemorrhage preventing appropriate CSF reabsorption

49
Q

how does NPH present?

A

3 W’s:

  • wobbly (gait disturbance, feet stuck on floor, postural instability)
  • wet (urinary urgency)
  • wacky (cog impairment, dec attention, apathy)
50
Q

tx of NPH

A

ventriculoperitoneal shunt, CSF removal via lumbar puncture