Week 1 Flashcards
(52 cards)
what are DALY’s?
disability associated life years - the sum of years lost to premature mortality and years lost to disability in a given population
what are the 2 approaches to prevention?
individual strategies - high risk
population strategies - public health
describe individual strategies in prevention.
clinical approach to disease prevention
individually focused - high risk ind
screen opportunistically
not all symptomatic people get the disease and vice versa
undertake interventions appropriate for that ind
problems with costs of screening; but cost effective for that specific ind
temporary effect - doesn’t address the underlying cause of disease
describe population strategies in prevention.
primary prevention and screening
screen asymptomatic people
may be changes in environmental or behavioural norms
attempt to reduce underlying cause of disease
small changes become very significant in a population when its done by the whole population
limited benefit to the ind, poor motivation
what are the screening guidelines?
- the condition: must be well known and significant health problem; should have a clear latent/ early symptomatic stage
- the test: should be simple, acceptable, cost effective, non-invasive
- treatment: should be effective treatment for patients identified with evidence that early detection leads to better prognosis; there should be an agreed policy on who should be treated and how
- outcome: there should be evidence of improved mortality and morbidity as a result of screening and that the benefits of screening outweigh the harms; the cost of case finding should be economically balanced in relation to possible expenditure on medicare
- consumer: should be well informed about evidence so that they can be a decision in participation?
what are the 4 strategies for the ottawa charter health promotion?
- build healthy public policy
- create supportive environments
- strengthen community action
- reorient health services
- develop personal skills
what are the changes in that occur with cell injury, in order?
biochemical changes
structural changes
light microscope changes
gross changes
some features of coagulative necrosis?
GA: firm texture, pale segment contrasting surrounding well vascularized tissue
H: stain pink, no nuclei, ghost cells (hard to identify a new start from dead cells)
some features of liquefactive necrosis?
lysosomes released upon bacterial infection leading to pus and fluid from necrotic tissue (liquefaction)
some features of caseous necrosis?
GA: cheesy chalky white granular appearance
H: appearance of granulomas, pink staining, walled off
some features of fat necrosis?
due to pancreas damage leading to the release of pancreatic enzymes - split TAGs contained within fat cells and released FA combine with calcium to form chalky white nodules
some features of grangrenous necrosis?
usually due to loss of blood supply in entire limb
H: initially coagulative necrosis from blood loss (dry gangrene) then liquefactive necrosis if blood loss superimposed with bacterial infection (wet gangrene)
what do macrophages secrete?
C3, fibronectin, factor 9, alpha-1 antitrypsin
functions of Ab?
opsonization
neutralize toxin/ virus
enhance complement mediated killing
prevent pathogen attachment
factors that influence immunogenity?
foreignness
molecular size
chemical components
individual, route, dose
what are PAMP and PRR stand for? where are they found?
pathogen associated molecular patterns - found on pathogen
pathogen recognition receptor - found on sensor cells
what specialized receptors do macrophages have?
specialized toll like receptor called TLR4 - which binds LPS ligand which sends signal to sensor cells and genes within sensor cells are transcribed - produce inflammatory cytokines
how do sensor cells induce and inflammatory response?
produce chemokine and cytokines
what are the components of innate immunity?
genetic susceptibility
cells: phagocytic (neutrophils, macrophages) and NKC
physical/ chemical barriers
protein molecules: cytokine/ complement
3 key functions of complement?
promote inflammation
bind onto microorganisms - more efficient uptake
punch holes in the membrane and form a tunnel allowing plasma/ water and microbes to flow in
activation of lectin complement pathway?
triggered by binding go MBL - mannose binding lectin to sugars, microbial cell walls/ capsule
activation of classical complement pathway?
triggered by Ab binding to pathogen surface
activation of alternative classical pathway?
hydrolysis of C3 into CS(H20) to deposit C3 convertase on microbial surfaces
what is the outcome of all 3 complement pathways?
cleavage of C3 via C3 convertase into C3b which is bound to microbial wall and the release of C3a
