9.1 Dementia & Delirium Flashcards
explain the pathophysiology of Alzheimer’s via amyloid plaques
amyloid precursor protein normally replaced by alpha and gamma secretases chopping it up to soluble parts
however beta secretes gets involved and now resulting parts are insoluble, the peptides accumulate outside of cells to beta amyloid plaques
plaques fill spaces between neurones, reaching signal transmission and maybe also saying inflammatory process which weakens blood vessels
explain the pathophysiology of Alzheimer’s via tau tangles
beta amyloid plaques induce hyperphosphorylation of tau proteins in cells, changing their shape so they can no linger stabilise microtubules in neural cytoskeleton = neurone death
aggregate to tangoes intracellularly
treatments of Alzheimers
-acetylcholinesterase inhibitors
-memantine for advanced cases: glutamate receptors antagonist so protects nerve cells from too much glutamate
what’s mutated in familial Alzheimers?
PSEN 1/2 genes gamma secretase = plaque aggreagtions
cause of death in alzheimers
linked to immobilisation so lack of food + water, weight loss
other disease processes which could cause ‘dementia’ symptoms
hypothyroidism
hypercalcaemia
b12 deficiency
delirium
pathophysiology of Lewy body dementia
misfiling of alpha synucelin, aggregates to levy body deposits
treatment of Lewy body dementia
symptom based
levodopa (dopamine analogue)
pathophysiology of HIV/AIDS dementia
HIV entry into macrophages in brain the n CD4 below threshold, viral prate s cause injury/inflammation which damages neurones
causes of delirium
drugs
epilepsy
liver failure
infection
retenion
low oxygen
uraemia
metabolism
diagnosis of delirium
not explained by previous neurological conditon
attributed to known risk factor e.g. UTI
treatment of delirium
-minimise precipitating factors
-encourage normal day/night cycle
-allow wandering if safe
-involve family
-distraction techniwues
-lastly meds
