Geriatric Medicine Flashcards
main diff between dementia and delirium
other factors to suggest delirium
impairment of conscious level
other factors to suggest delirium:
- short hx
- Fluctuation of syms (worse at night, then periods of normality)
- Abnormal perception (illusions, hallucinations)
- Agitation, fear
Delusions
pressure ulcers
- what scale?
- grading
- mx
· Waterlow scale screens for those at risk
NOTES predispose to dev: - malnourishment - incontinence - lack of mobility - pain (leads to a reduction in mobility)
Grade Findings
1 Non-blanchable erythema of intact skin.
Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin
2 Partial thickness skin loss involving epidermis or dermis, or both.
The ulcer is superficial and presents clinically as an abrasion or blister
3 Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
4 Extensive destruction, tissue necrosis, or damage to muscle, bone or
supporting structures with or without full thickness skin loss
Management
- a moist wound envt encourages ulcer healing. Hydrocolloid dressings and hydrogels may help facilitate this. The use of soap should be discouraged to avoid drying the wound - wound swabs should not be done routinely as the vast majority of pressure ulcers are colonised with bacteria. The decision to use systemic antibiotics should be taken on a clinical basis (e.g. Evidence of surrounding cellulitis) - consider referral to the tissue viability nurse - surgical debridement may be beneficial for selected wounds
what drugs worsen symptoms in LB dementia
neuroleptics (can dev irreversible parkinsonism) - antipsychotics
LB dementia
- pathology- dx
- mx
Pathological ft: alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
Diagnosis
• usually clinical
• single-photon emission computed tomography (SPECT): increasingly used (a DaTscan)
○ Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope.
○ sensitivity 90% with a specificity of 100%
Management acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer's.
pick’s disease
- Characterised: personality change and impaired social conduct.
- Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours.
Focal gyral atrophy with a knife-blade appearance
Macroscopic changes: Atrophy of the frontal and temporal lobes
Microscopic changes include:- • Pick bodies - spherical aggregations of tau protein (silver-staining) • Gliosis • Neurofibrillary tangles Senile plaques
chronic progressive aphasia
- a type of ?
- fts
- non fluent speech. They make short utterances that are agrammatic. Comprehension is relatively preserved.
frontotemporal lobar degeneration
semantia dementia
- a type of
- fts
frontotemporal lobar degeneration
- fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. - Unlike in Alzheimer's memory is better for recent rather than remote events.
· Pt w LB dementia: carbidopa-levodopa dose increased 2mos ago to target resting tremor + bradykinesia
Now having visual hallucinations, paranoid delusions, aggressive:
mx?
decrease dose
vascular dementia
mx
tight control of vascular RF (to slow disease progression)
alzheimer’s mx
Pharm
1. Mild-mod: acetylcholinesterase inh (donepezil, rivastigmine, galantamine) 2. Memantine (NMDA rec antagonist)
Memantine uses
- moderate AD who are intolerant/CI to acetylcholinesterase inhibitors - Mod-severe: as an add-on drug to acetylcholinesterase inhibitors - monotherapy in severe Alzheimer's
donepezil. what is it, SE, CI
Donepezil
acetylcholinesterase inh
• is relatively contraindicated in patients with bradycardia
• adverse effects include insomnia
acetylcholinesterase inh (3)
donepezil, rivastigmine, galantamine)
memantine what is it
NMDA rec antagonist
pathology of AD
Pathological changes
• macroscopic: widespread cerebral atrophy, esp involving the cortex and hippocampus
• microscopic:
○ cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
○ hyperphosphorylation of the tau protein has been linked to AD
• biochemical
○ deficit of acetylcholine from damage to an ascending forebrain projection
Neurofibrillary tangles
• paired helical filaments are partly made from a protein called tau
• tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
• in AD are tau proteins are excessively phosphorylated, impairing its function
RF of AD
RF • increasing age • FHx of Alzheimer's disease • 5% inherited as an AD trait ○ mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form • apoprotein E allele E4 - encodes a cholesterol transport protein • Caucasian ethnicity Down's syndrome