Demographics-young old-65-74 middle old-75-84



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Questions to ask when differentiating b/t delerium and dementia—


-how long has this been going on?

-days/weeksdelerium

-months/yearsdementia

-how abruptly did it start?

-acute—delerium

-insidiousdementia

-is the situation progressing, and if so, how fast?

-deleriumhours to days

-dementiamonths to years
Dementia

Two sub-types—


-dementia of the alzheimer’s type (DAT)—60%

-vascular dimentia—15%

DAT—


-multiple cognitive deficits, including memory impairment and at least on of the following: aphasia, apraxia, agnosia, disturbed executive functioning (planning, organizing, abstracting)

-cognitive deficits severe enough to impair occupational or social functioning

-cognitive deficits representing a decline from previously higher function

-these deficits not occurring exclusively during the course of the delerium (more chronic onset)



-Dx of DAT—

1. Hx—learning new things?

-IADLs / ADLs?

-reasoning ability

2. clinical exam—

-abnl findings

-MMSE, neuro exam—still hard to Dx

-Proposed causes of DAT—

-role of beta-amyloid deposition in the brain

-role of apolipoprotein E4 produced by the gene of the same name (if have3x risk of getting, but not present in q DAT pt

-genetics—don’t know



-Vascular Dementia—2 subtypes—

-multi-infarct dementia—on neuro PE—see focal assymetrical abnls (assymetrically decreased DTRs)

-MRI—see multiple infarcts

-subcortical vascular dementia—gait problems—see nl MRI

-in either vascular dementia—RFs of CVD

-Dx criteria for vascular dementia—

-multiple cognitive deficits the same as DAT

-focal neuro signs and sx (exaggerated DTRs, gait abnls, or lab evidence indicative of CerebroVD (multiple infarcts in cortex of white matter)

-sx not occurring exclusively during the course of delerium. ie. they keep the signs and sx



-Proposed causes of vascular dementia—

-inadequate O2 and cell death due to—

-vascular blockage

-vascular rupture


-Presentation of Dementia—

-generally, pts do not present themselves (family, etc)

-insight is often preserved until late in the illness

-preservation of social skills—

-can converse and seem OK

-keep long term memory

-cant remember ball, tree, cat

-Possible etiologies and aggravators of dementia—

-first r/o delerium

-D rugs

-E motional illness (including depression)



-M etabolic / endocrine (thyroid, uremia, normal pressure hydrocephalus, B12, folate)

-E ye / ear / environment

-N utritional / neuro

-T umors / trauma

-I nfection

-A lcoholism / anemia / atherosclerosis

-Drugs—

-any OTC could cause dementia type illness



-more specifically—

-sedatives

-centrally acting antiihypertensives—clonidine, methyldopa, aldomet

-some b-blockers

-Emotional illness—

-depression

-schizophrenia

-Metabolic / endocrine—

-dehydration

-hypoglycemia / hyperglycemia

-hypercalcemia

-hypoxia


-hypercapnia

-hyper/hyponatremia

*think delerium b/c they are short lasting

-Eyes and ears

-visual problems

-hearing loss

-environment—all not common

-Nutrition / neuro—

-folate / B12

-NPH / Parkinsons

-Tumors / trauma—

-frontal lobe tumor can present as dementia

-trauma

-Infxs—


-atypical presentations of dz can present with dementia sx

-Alcoholism / anemia / atherosclerosis

-etoh—known cause

-anemia—not common



DEPRESSION—


-Differences from dementia—

-abrupt onset

-short duration (maybe, maybe not!)

-often previous psych hx (including undiagnosed depressive episodes)

-highlights disabilities (c/o memory loss)

-don’t know answers

-diurnal variation in mood, but generally more consistent than demented pt)

-fluctuating cognitive loss

-often does not try so hard but is more distressed by losses

-depressed—don’t care / don’t know; 15 different complaints

-demented—wants to please you; no complaints—someone made them come in

-equal memory loss from recent and remote events (demented remember remote NOT recent)

-depressed mood (if present) occurs firt

-associated with depressed or anxious mood, sleep disturbance, appetite disturbance, and/or suicidal thoughts

-anhedonia and depressed mood*

-crying spells, sleepy, ADL and IADL changes’

-Depression—

-used to be called pseudodementia (b/c presentation is similar)

-should be suspected in anyone with less than 1 year abrupt onset of dementia sx

-should be considered in the dementia pt who’s sx worsen

-HISTORY—*delerium / dementia—abrupt; depression—chronic

-are the cognitive changes of recent onset or have they been developed over a period of months?

-has the pt had a change in functional activities?

-what chronic medical problems exist?

-what is the pts level of alertness?

-PE—

-notice gait, balance, and mobility before they get undressed

-formal MMSE

-neuro exam

-observe for signs of Parkinson’s

-check for contributory factors



-LABS—delerium, dementia, depression—

-CBC


-chem 7

-TSH


-B12 and folate

-RPR


-Ca++

-glucose


-Brain imaging—

-C-T or MRIbest—it differentiates infarcts / hemorrhages / etc

-SPECT scan—single photon emission something something—help Dx Alzheimer’s

-PET scan—positive emission tomography—good in addition for Alzheimer’s



-Tx—

-if deleriumtx the cause

-if depressed, tx with appropriate meds

-if demented, may tx with meds



-Tx of confusion—

-Aricept, Cognex, ERT, NSAIDS

-see the handout!

-Alzheimer’s Tx—

-Cognex—1st choice—cholinesterase inhibitor

-Aricept—2nd choice—same

-does not cure

-may delay sx by 6mo or so

-Alzheimer’s—fewer neurons—therefore less AcHless transmission of impulses thru synapses

6/8/00
Tx of Dementia—

-regular office visits

-Rx Tx—

-Aricept


-Cognex

-ERT—decreases risk of Alzheimer’s

-the longer you take it, the less risk of getting Alz

-NSAIDS—e.g. ibuprofen—associated with a decreased risk of Alz

-GI bleeds

-Vitamin E—slows progression of Alz

-Eldepryl—same (also for parkinsons)

-gingko biloba—antioxidant, and increase circulation

Tx of Depression—

-Drugs—


-SSRIs—work just as well as TCAs, etc—but much less SEs

-e.g. drowsiness

-Paxil, Zoloft, Zyprexa

-TCAs—the only benefit in the elderly is chronic pain

-MAOIs—refer first

-St. Johns Wort—

-gingko biloba

-psychotherapy


Dysmobility and Immobility—

-dysmobility states—

-a community-wide study in Boston showed that 15.5% of the 65+ population reported difficulty walking

-Causes—


-musculoskeletal

-neurological

-CVD

-sensory deficits



-foot d/o’s

-environmental conditions—steps, etc

-medication use—polypharmacy

-OA—


-a chronic progressive d/o

-pain


-deformity—heberdon’s (distal) and bouchard’s nodes (proximal)

-limitation of joint ROM

-usually monoarticular

*joint stiffness can occur but generally lasts less than 30min

-generally, no systemic sx such as fatigue, wt loss, and/or fever

*generally, aggravated with activity and alleviated with rest (but as gets worse—pain at rest)

-often described as deep aching discomfort

-except for the hip, it usu localizes to the joint

-hip—upper thigh, inguinal region

-PE—


-the “get up and go” test

-may have decreased ROM

-joint deformity

-bony hypertrophy

-an occassional effusion

-crepitus

-pain on ROM

-may have mild tenderness to palpation

-Labs—

-no specific lab tests for it



-ESR and CBC are nl

-may be able to help with dx with lab analysis of a joint effusion

-Xray—

-this in addition to your H&P is how you make the dx



-xray changes such as joint space narrowing, osteophytes, etc

-more expensive imaging (CT, MRI) has almost no role

-Management Goals—

-maximize pain relief

-try to prevent further joint damage

-maximize functional abilities

-Non-Pharmacologic Mgt—

-weight loss

-rest (during acute sx)

-avoidance of activities that exacerbate it

-heat (or cold)

-aids to improve mobility (ADLs)

-keep as active as possible

-ROM exercises

-endurance (Aerobic) activities

-strengthening

-Pharmacologic Mgt—

-APAP—safest, no GI, no drowsy

-NSAIDS—better analgesia than APAP, more GI

-nonacetylated salicylates—salcylate

-salicylates—ASA—better in RA—great antiinfl

-intraarticular steroids—may cause separation from one—overall good though

-cox-2 inhibitors—celebrex / vioxx—less GI, more $$

-Synvisc—artificial lubricant

-moderate analgesia

-local effect

-Surgical Mgt—

-joint replacement is last resort—b/c of the risks

-Other sources to get involved—

-arthritis foundation

-PT

-check home environment—home health aid



RA—

-symmetric, polyarticular, infl arthritis

-etiology unknown

-can first present in old age but is less common

-Clinical Characteristics—

-gradual onset of:

-symmetric

-polyarticular

-prolonged morning stiffness—30min

-systemic signs of dz—fatigue, wt loss, fever

-swelling—more than OA

-joint tenderness

-joints affected—

-PIPs


-metacarpals—common

-wrists—common

-elbows

-knees


-ankles

-metatarsals

-Labs—

-increased ESR



-normocytic anemia

-positive RF

Gout—

-crystal induced



-usual onset in middle age (but can present in older age)

-increased production or decreased excretion (usually) of uric acid

-Presentation—

-acute distal monoarthritis

-erythematous swollen painful joint

-podhera—when it affects the big toe

-more men

-precipitates—binge etoh, diuretics

-Dx of gout—

-Hx and PE

-analysis of synovial fluid—usually not done

-UA level—can be nl (30% of pts)still have gout

-negative birefringent crystals

-Tx—


-NSAIDS—indocin—rough on GI

-lower serum UA to WNL by using such drugs as allopurinol

Pseudogout—

-rarely seen under age 50 and increases with age

-presentation (and Hx) is much like gout

-10-15% of 65-75yo

-1/3 of 85yo

-usu asymptomatic

-CPPD increased

-Ca2+ crystals

-Dx—

-by Hx and PE



-Xray findings—knee—sunrise view—see crystal deposits

-positive birefringent crystals

-Tx—

-sometimes corticos in joint



-no allopurinol

-NSAIDS / APAP

Paget’s Dz—

-idiopathic—virus?

-increased metabolic activity of bone surfaces

-accelerated action of osteoblasts / osteoclasts / mineralization

-resultenlargedand weakened bones

-occurs rarely under 30

-almost exclusively in the elderly

-characterized by increased bone resorption and formation

*most are asymptomatic but, if a sx does ocur it is usu PAIN

Tx—


-NSAIDS—indocin

-bisphosphates—Phosamax, etc

-Ca2+

-vit D


-Xray—

-see cotton wool appearance

-osteolytic activity (osteoclasts)

-bony prominences

Osteoporosis—

-reduction of bone mass to the joint that fx occur even with minimal trauma

6/13/00
DIZZINESS—

-very common in elderly

-not common in younger

-each year, 20% of pts over 60yo are seen for dizziness



-FOUR TYPES OF DIZZINESS—

-vertigo—spinning

-presyncopal lightheadedness—feel as if pass out

-dysequilibrium—balance off—sensation in feet

-other

-Vertigo—a sensation of movement-spinning, merry go round, rocking, etc

-Central or Peripheral—

-central—

-facial numbness

-dyplopia

-slurred speech

-facial numbness

-dysphagia

-if none of theseperipheral

-Peripheral—see flow sheet

-Retrocochlear Causes—NEED TO CONSIDER

-acoustic neuroma—inner ear tumor

-presentation—vertigo, tinnitus, pressure in ear, hearing loss

-a progressive, chronic decline

PE—neuro changes—CNV, VI, X (b/c of site of tumor)

-Cochlear Causes

-Benign Positional Vertigo—common finding

*sx occur only during or after position changes—rolling over in bed, standing up

-intense vertigo that lasts <1min

-sx last days to <6mo (so can be recurrent)

-should only be dx when others are ruled out

*usually no hearing loss, tinnitus or neuro changes on exam

-hallpike maneuver positive—

-lay down and extend neck off of table

-turn head to R and sit updizzy/nystagmus

-same with left

-stimulating semicircular canals

-Meniere’s Dz

-tinnitus

-pressure in the ear

-hearing loss

-vertigo


-paroxysmal episodes with above sx

-lasts minutes to hours

-decrease in frequency after multiple attacks which may recur in months or years

-Acute Labrynthitis

-may get hx of occurring after an OM

-secondary to viral infx of inner ear

-patient gives hx of URI (followed by)

-vertigo


-tinnitus

-hearing loss

-sx resolve entirely in 3-6wks without residual deficits

-Vestibular Neuronitis

-same as acute labrynthitis except:

-no hearing loss

-less severe

-solely vertigo

-no hx of OM

-viral process-no antibiotics

-Ototoxins

-ask if hx of streptomycin or gentomycin


-Central Vertigo—etiologies

-TIAs and CVAs

-should look in the hx for brainstem sx such as dyplopia, facial numbness, slurred speech, etc

-Multiple Sclerosis

-Migraine HAs


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