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Transition SB > Immunology > Flashcards

Immunology Flashcards

1
Q

what are features suggestive of immunodeficiency

A

SPUR

Serious infections
Persistent infections
Unusual infections
Recurrent infections

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2
Q

what are other features suggestive of a primary immune deficiency

A 
Weight loss or failure to thrive
Severe skin rash (eczema)
Chronic diarrhoea
Mouth ulceration
Unusual autoimmune disease
Family history
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3
Q

what are conditions associated with secondary immune deficiency

A 
extremes of life - ageing, premature
HIV
Measles 
Immunosuppressive Tx
Anti-cancer Tx
Cancer of immune system - lymphoma, leukaemia, myeloma
Mets
Malnutrition
DM
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4
Q

what is the commonest form of severe combined immunodeficiency

A

X-linked SCID

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5
Q

what causes SCID

A

mutation of IL2 receptor

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6
Q

what does the mutation in SCID results in

A

In inability to respond to cytokines

  • failure of T cell and NK cell development
  • production of immature B cells
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7
Q

what is the number of T/B cells seen in X-linked SCID

A

Very low or absent T cells

Normal or increased B cells

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8
Q

presentation of severe combined immunodeficiency

A 
Unwell by 3 months of age
Persistent diarrhoea
Failure to thrive
Infections of all types
Unusual skin disease 
FX of early infant death
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9
Q

what is the IL12-gIFN network pathway

A
  1. macrophage infection with bacteria
  2. produces IL12
  3. IL12 induces T cells to secrete gIFN
  4. gIFN feeds back to macrophages and neutrophils
  5. stimulates production of TNF
  6. activates NADPH oxidase
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10
Q

what happens is there is no TNF

A

no functional granuloma

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11
Q

what is a granuloma

A

organised collection of activated macrophages and lymphocytes

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12
Q

what causes a granuloma to be formed

A
  1. inflammatory response triggered
  2. activation of T lymphocytes and macrophages
  3. failure of removal of stimulus
  4. persistent production of activated cytokines
  5. granuloma formed
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13
Q

what are examples of conditions where granulomas are formed

A 
Sarcoidosis
TB
Leprosy 
Silicosis 
Foreign bodies
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14
Q

what are antibody mediated autoimmune diseases

A

Idiopathic thrombocytopaenia

Autoimmune haemolytic anaemia

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15
Q

what are common variable immune deficiencies

A

Low IgG, IgA and IgM

Recurrent bacterial infections, esp. respiratory

Often associated with autoimmune disease

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16
Q

what is a relatively common antibody deficiency

A

Selective IgA deficiency

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17
Q

what are Sx of selective IgA deficiency

A

1/3rd have recurrent resp tract infections

2/3rd are asymptomatic

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18
Q

Ddx of recurrent bacterial infections AND hypogammaglobulinaemia

A

Antibody deficiency

Protein loss i.e. nephrotic syndrome

Failure of protein syntheses e.g. myeloma, lymphoma, CLL

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19
Q

what are the classifications of hypersensitivity reactions

A

Type I: Immediate hypersensitivity (IgE-mediated allergy)
Type II: Direct cell killing: antibody mediated
Type III: Immune complex mediated (example: SLE)
Type IV: Delayed type hypersensitivity

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20
Q

what organ secretes complement proteins

A

the liver

21
Q

what is lysis

A

direct killing of bugs by punching holes in it

22
Q

what is the function of natural killer [NK] cells

A

kill cells that lack MHC – molecules on surface

23
Q

what is meant by the term ‘natural’ in NK cells

A

no need for antigen specificity

24
Q

why couldn’t we just have NK cells

A

they have no long term memory

25
Q

what immune system are NK cells part of

A

innate immunity

26
Q

what receptors are seen on the cells that are part of the innate immunity

A

toll-like receptors [TLR]

27
Q

why are TLR important

A

expressed on phagocytes and dendrites as built-in burgler alarm for microbes

activation causes pro-inflammatory cytokines and type 1 Interferon secretion

28
Q

what can TLR dysfunction cause

A

immunodeficiency (too little) or autoimmunity (too much)

29
Q

what treatment activates TLR to boost immunity and through which number receptor

A

imiquimod,

activating TLR7/8

30
Q

what blocks pro-inflammatory cytokines

A

TNF inhibitors

31
Q

what is the job of TNF-alpha

A

secreted as an immediate-early ‘fire alarm’ signal in response to many stressors

32
Q

what are the 4 types of transplant rejection

A

hyperacute rejection
acute cellular rejection
acute vascular rejection
chronic allograft failure

33
Q

hyperacute rejection = time, pathology, mechanism, Tx

A

T - mins to hours

P - thombosis & necrosis, Type II hypersensitivity

M - preformed antibody and complement fixation

Tx - none

34
Q

acute cellular rejection = time, pathology, mechanism, Tx

A

T - 5 to 30 days

P - cellular infiltration, Type IV hypersensitivity

M - CD4 and CD8 T cells

Tx - immunosuppresion

35
Q

acute vascular rejection = time, pathology, mechanism, Tx

A

T - 5 to 30 days

P - vasculitis, Type II hypersensitivity

M - De novo antibody and complement fixation

Tx - immunosuppresion

36
Q

chronic allograft failure = time, pathology, mechanism, Tx

A

T - > 30 days

P - fibrosis, scarring

M - Immune and non-immune mechanisms

Tx - minimise drug toxicity, hypertension, hyperlipidaemia

37
Q

how do vaccinations work

A

produce memory in B cells and T cells

38
Q

how does vaccinations work on T cells

A

simulates rare naive T cells

induces a strong T-cell response in 14–21 days

some become effector T cells which =

  • mostly die by apoptosis in absence of antigen
  • Smaller no. become memory T cells maintained at low frequency
39
Q

what antibody quickly rises first in primary infection

A

IgM

- gone by 14 dyas

40
Q

what antibody rises steadily and decreases slowly in primary infection

A

IgG

- takes years to decrease

41
Q

what antibody is there more of in secondary infection

A

IgG

however, get the same rapid rise and fall in IgM

42
Q

what are key features of inactivated vaccines

A

Cannot replicate

Generally not as effective as live vaccines

Immune response primarily antibody based (not T cells)

Antibody titer may diminish with time

Require multiple doses to stimulate immune response

43
Q

advantages of inactivated vaccines

A

Can be made quickly (prevent epidemics)

Elicit good antibody responses

Easy to store; No refrigeration required

Usually safe

44
Q

disadvantages of inactivated vaccines

A

Doesn’t stimulate clonal expansion of B and T cells

Require multiple and booster injections

Require adjuvants to improve immunogenicity

45
Q

what are examples of inactivated vaccines

A

whole cell vaccines
- polio, hep A, cholera, rabies

fractional vaccines
- influenza, hep B, diptheria, tetanus

46
Q

adv of live attenuated vaccine

A

All relevant effector mechanisms elicited (antibody, activated T cells)

Localised, strong response

Usually only one single dose required

47
Q

disadv of live attenuated vaccines

A

safety - may cause infection in immunocompromised

fragile - must be stored carefully

48
Q

examples of live attenuated vaccine

A 
measles
mumps
rubella
yellow fever
MMR jab
BCG

Transition SB (5 decks)

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