pt16 Flashcards
(50 cards)
What are the main treatment strategies for Alzheimer’s disease?
Symptom management (antidepressants, antipsychotics, orexin antagonists), slow progression (cognitive therapy), acetylcholinesterase inhibitors, and experimental monoclonal antibodies.
What is donanemab and how does it work?
A human IgG1 monoclonal antibody targeting N-terminally truncated, insoluble β-amyloid → promotes microglial phagocytosis of plaques.
What was the design of the TRAILBLAZER-ALZ 2 donanemab trial?
Phase 3, 76-week, randomized, double-blind, placebo-controlled; ∼1,736 early symptomatic AD patients (MMSE 20–28; amyloid & tau positive) received IV donanemab or placebo every 4 weeks.
What did the TRAILBLAZER-ALZ 2 trial demonstrate?
Donanemab slowed clinical progression across multiple cognitive and functional scales versus placebo over 76 weeks.
Which sleep factors increase Alzheimer’s risk?
Obstructive sleep apnoea; very short or very long habitual sleep duration.
What is “sundowning” in Alzheimer’s patients?
Evening agitation with wandering and disrupted sleep patterns.
What is the glymphatic system’s role in the brain?
Perivascular pathways that exchange CSF and interstitial fluid to clear metabolites and waste.
How is glymphatic clearance regulated?
Enhanced during sleep under circadian control; suppressed in neurodegeneration.
How does gut microbiota dysbiosis relate to Alzheimer’s?
Alters immune responses, increases pro-inflammatory mediators, and may promote brain amyloid aggregation; potential biomarker and intervention target.
What are key Alzheimer’s risk factors?
Age (risk doubles every 5 years after 65), Down’s syndrome, cardiovascular disease, head injury, APOE ε4 genotype, and sleep apnoea.
What defines frontotemporal dementia (Pick’s disease)?
Early-onset (<65 yrs) shrinkage of frontal and temporal lobes with intracellular tau deposits, neuronal loss, microvacuolation, and astrocytosis.
What are frontotemporal dementia symptoms?
Dramatic personality changes (disinhibition, loss of empathy), language disturbance, overeating; memory and spatial skills relatively preserved.
How is vascular dementia caused?
Reduced cerebral blood flow from single or multiple infarcts (stroke) or small-vessel disease leading to white-matter lesions.
What are vascular dementia symptoms?
Confusion, short-term memory loss, wandering, incontinence, and difficulty following instructions.
What causes Parkinson’s disease and what are its core signs?
Degeneration of dopamine-producing neurons in substantia nigra → tremor, rigidity, bradykinesia, and postural instability.
How is Parkinson’s disease treated?
Levodopa ± carbidopa (dopamine precursor) and deep brain stimulation to control motor symptoms.
What genetic defect underlies Huntington’s disease?
Autosomal dominant CAG-repeat expansion (36–120 repeats) in HTT gene → toxic polyglutamine fragments that aggregate in neurons.
What are Huntington’s disease symptoms?
Early clumsiness and mood swings; later chorea (jerking movements), slurred speech, personality changes, and dysphagia.
What is the difference between meningitis and encephalitis?
Meningitis—inflammation of brain/spinal meninges; Encephalitis—inflammation of brain parenchyma.
What are meningitis symptoms?
High fever, severe headache, stiff neck, photophobia, nausea/vomiting, rash non-blanching in infants.
What are encephalitis symptoms?
Fever, headache, photophobia, neck stiffness, confusion, drowsiness, seizures, and possible sudden dementia.
How are CNS infections treated?
Bacterial—antibiotics; Viral—antivirals; plus anticonvulsants, corticosteroids, sedatives, and supportive hospitalization.
What causes Creutzfeldt–Jakob disease (CJD)?
Misfolded prion proteins that accumulate, causing spongiform degeneration of brain tissue.
What are the main types of CJD?
Sporadic (spontaneous prion misfolding), variant (BSE-linked), and familial (PRNP gene mutations).
