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Year 3 Sem 1 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

what are DALY’s?

A

disability associated life years - the sum of years lost to premature mortality and years lost to disability in a given population

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2
Q

what are the 2 approaches to prevention?

A

individual strategies - high risk

population strategies - public health

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3
Q

describe individual strategies in prevention.

A

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

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4
Q

describe population strategies in prevention.

A

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

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5
Q

what are the screening guidelines?

A
  1. the condition: must be well known and significant health problem; should have a clear latent/ early symptomatic stage
  2. the test: should be simple, acceptable, cost effective, non-invasive
  3. 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
  4. 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
  5. consumer: should be well informed about evidence so that they can be a decision in participation?
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6
Q

what are the 4 strategies for the ottawa charter health promotion?

A
  1. build healthy public policy
  2. create supportive environments
  3. strengthen community action
  4. reorient health services
  5. develop personal skills
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7
Q

what are the changes in that occur with cell injury, in order?

A

biochemical changes
structural changes
light microscope changes
gross changes

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8
Q

some features of coagulative necrosis?

A

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)

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9
Q

some features of liquefactive necrosis?

A

lysosomes released upon bacterial infection leading to pus and fluid from necrotic tissue (liquefaction)

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10
Q

some features of caseous necrosis?

A

GA: cheesy chalky white granular appearance
H: appearance of granulomas, pink staining, walled off

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11
Q

some features of fat necrosis?

A

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

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12
Q

some features of grangrenous necrosis?

A

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)

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13
Q

what do macrophages secrete?

A

C3, fibronectin, factor 9, alpha-1 antitrypsin

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14
Q

functions of Ab?

A

opsonization
neutralize toxin/ virus
enhance complement mediated killing
prevent pathogen attachment

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15
Q

factors that influence immunogenity?

A

foreignness
molecular size
chemical components
individual, route, dose

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16
Q

what are PAMP and PRR stand for? where are they found?

A

pathogen associated molecular patterns - found on pathogen

pathogen recognition receptor - found on sensor cells

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17
Q

what specialized receptors do macrophages have?

A

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

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18
Q

how do sensor cells induce and inflammatory response?

A

produce chemokine and cytokines

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19
Q

what are the components of innate immunity?

A

genetic susceptibility
cells: phagocytic (neutrophils, macrophages) and NKC
physical/ chemical barriers
protein molecules: cytokine/ complement

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20
Q

3 key functions of complement?

A

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

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21
Q

activation of lectin complement pathway?

A

triggered by binding go MBL - mannose binding lectin to sugars, microbial cell walls/ capsule

22
Q

activation of classical complement pathway?

A

triggered by Ab binding to pathogen surface

23
Q

activation of alternative classical pathway?

A

hydrolysis of C3 into CS(H20) to deposit C3 convertase on microbial surfaces

24
Q

what is the outcome of all 3 complement pathways?

A

cleavage of C3 via C3 convertase into C3b which is bound to microbial wall and the release of C3a

25
Q

what do all 3 complement pathways generate?

A

C3 convertase

26
Q

what are the 3 outcomes after C3 has been cleaved via complement pathway

A

C3a and C5a recruit phagocytic cells to the site of infection and promote inflammation
phagocytes with receptors for C3b engulf and destroy pathogens
completion of complement cascade leads to formation of membrane attack complex which disrupts cell membrane and causes cell lysis

27
Q

what is the first Ab produced in humoural response?

A

IgM

28
Q

what happens if there is lectin pathway deficient?

A

bacterial infections, mainly in child hood

29
Q

what happens if there is a classical pathway deficiency?

A

immune complex disease

30
Q

what happens if there is a deficiency in the alternative pathway?

A

infection with pyogenic bacteria but no immune complex disease

31
Q

what are polymorphonuclear cells? mononuclear cells?

A

neutrophils
eosinophils
basophils

monocytes
lymphocytes

32
Q

function of IL1-beta?

A

activates vascular endothelium, activates lymphocytes, local tissue destruction, increased access of effector cells

= fever, IL6 production

33
Q

TNF- alpha function?

A

activates vascular endothelium, increases vascular permeability, increased IgG entry/ complement and increased fluid draining to lymph

= fever, shock, mobilization of metabolites

34
Q

IL6 function?

A

lymphocyte activation and increased Ab production

= fever, induces acute phase protein production

35
Q

CXCL 8 function?

A

chemotactic function that recruits neutrophils, basophils and T cells to site of infection

36
Q

IL12 function?

A

activates NKC, induces differentiation of CD4 T cells into Th1 cells

37
Q

function of perforin and granzymes?

A

perforin: forms pores in plasma membrane
granzymes: enter cell, break down proteins, lysing the cell

38
Q

how often do you screen for overweight?

A

every 2 years
12 months for ABTSI, T2DM, CVD, stroke, gout
6 months for obese people

39
Q

how often do you screen nutrition?

A

every 2 years

6months if obese/ overweight, CVD, T2DM

40
Q

3 broad blocks for prevention?

A

community prevention
addiction medicine
applied prevention

41
Q

what is screening?

A

asking questions of or conducting tests on patients to identify those who are more likely to be helped and harmed by further tests or tx to reduce the risk of disease or its complications

42
Q

what are the physiological changes in cellular adaption?

A

hypertrophy
hyperplasia
atrophy
metaplasia

43
Q

when does apoptosis occur?

A

when the cell is deprived of GF or DNA/ proteins are damaged beyond repair

44
Q

what type of granules is 5HT found in?

A

platelet granules

released during platelet aggregation to induce vasoconstriction

45
Q

function of pathogen recognition receptors?

A

switch on genes needs for inflammation

46
Q

what are the components of innate immunity?

A

genetic susceptibility
cells = phagocytic (neutrophils &macs)& NKC
physical/ chemical barriers
protein molecules: cytokines and complement

47
Q

different functions of macrophages?

A 
phagocytosis
Ag presentation
activation of bactericidal mechanisms (ROS)
tumour cell destruction
tissue re-organization and wound healing
secretion of pro-inflammatory mediators
48
Q

function of red pulp in spleen?

A

deposition of senescent red blood cells

49
Q

how is the white pulp in the spleen formed?

A

lymphocytes surround the arterioles running int the spleen to form the white pulp

50
Q

what happen sot cell size in necrosis and apoptosis?

A 
necrosis = swelling 
apoptosis = shrinking
51
Q

what is TORCH infection?

A 
toxoplasmosis
other (syphillis, varicella-zoster)
rubella
cytomegalovirus (CMV)
herpes

increases risk of miscarriage and birth defects

52
Q

screening questions for falls?

A

have you had 2+ falls in the past 12 months
are you presenting here today due to a fall?
are you having difficulty walking along or balance?

Year 3 Sem 1 (12 decks)

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