Membranes, Lipids and Signalling Flashcards
Anaemia
Affects the RBC cytoskeleton
Mutations in genes encoding spectrin/ankyrin
Results in abnormally shaped erythrocytes
Degraded more rapidly by spleen
Alzheimer’s disease - cause and clinical feature
Caused by nerve cells in the brain dying and connections between nerve cells degenerating
Build up of amyloid-beta peptide plaques derived from amyloid precursor protein (APP)
Clinical features:
Amnesia- recent memory affected
Aphasia - language problems
Agnosia - difficulty recognising and naming objects
Apraxia - difficulty in complex tasks
Visuospatial difficulties, functional impairment, mood disorders, psychosis
Depression
Affective disorder (disorder of mood rather than disturbances of thought/cognition) Two types: unipolar depression or bipolar affective disorder Functional deficit of monoaminergic transmission (noradrenaline, dopamine and serotonin)
Cholera toxin
G-protein disease
Cholera toxin acts by normal Gs activation
Ligand binds to receptor
Gs gets switched on
Looses a phosphate
Gets switched off
Cholera toxin prevents GTPase activity of Gs, therefore GTP remains bound to Gs and it stays in the “ON” state. This leads to over-stimulation of adenylate cyclase and accumulation of cyclic AMP. In intestinal epithelial cells, elevated cAMP increases loss of Cl- ions through chloride channels. The resultant osmotic gradient leads to water being excreted into the intestinal lumen and hence diarrhoea and dehydration.
Symptoms of atherosclerosis
chest pains palpitations heart attack stroke cerebral haemorrhage pain ischaemia (restriction of blood supply to tissue) ulceration gangrene (tissue death due to lack of blood supply)
Treatment of hypercholesterolaemia
Statins - Prevent cholesterol synthesis in the liver
Cholesterol absorption inhibitors - prevent uptake from the intestine
Fibrates - reduce triglycerides and increase HDL, less effective LDL
