immunology Flashcards

1
Q

physiological conditions causing a secondary immune deficiency

A

extremes of life
- ageing
- prematurity

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2
Q

infections causing a secondary immune deficiency

A

HIV
measles

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3
Q

treatment interventions causing a secondary immune deficiency

A

immunosuppressive therapy
anti-cancer agents
corticosteroids

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4
Q

malignancy causing a secondary immune deficiency

A

cancer of the immune system- lymphoma, leukaemia, myeloma
metastatic tumours

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5
Q

biochemical and nutritional disorders

A

malnutrition
renal insufficiency/dialysis
type 1 and type 2 diabetes
specific mineral deficiencies eg iron, zinc

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6
Q

what is a granuloma

A

an organised collection of activated macrophages and lymphocytes

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7
Q

what can trigger the formation of a granuloma

A

non-specific inflammatory response triggered by diverse antigenic agents or by inert foreigh materials

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8
Q

how is a granuloma formed

A

the triggered response results in activation of T lymphocytes and macrophages
failure of removal of the stimulus results in persistent production of activated cytokines
end result is organised collection of persistently activated cells

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9
Q

differential diagnosis of lung granuloma

A

sarcoidosis
mycobacterial disease (TB, leprosy)
berylliosis, silicosis and other dust diseases
chronic stage of hypersensitivity pneumonitis
foreign bodies

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10
Q

presentation of antibody deficiencies

A

recurrent bacterial infection (recurrent respiratory tract infections, GI infections)
antibody mediated autoimmune diseases
- idiopathic thrombocytopaenia
- autoimmune haemolytic anaemia

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11
Q

common primary antibody deficiences

A

Common variable immune deficiency
selective IgA deficiency

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12
Q

what is common variable immune deficiency

A

low IgG, IgA and IgM
recurrent bacterial infections esp respiratory
often associated with autoimmune disease

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13
Q

what is selective IgA deficiency

A

very common
2/3rd individuals are asymptomatic
1/3rd have recurrent respiratory tract infections
genetic component

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14
Q

Hypogammaglobulinaemia

A

reduced serum immunoglobulin levels

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15
Q

primary causes of recurrent bacterial infections and hypogammaglobulinaemia

A

antibody deficiency
- common variable immune deficiency
- specific antibody deficiency
other conditions, rare in adults (bruton’s agammaglobunaemia)

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16
Q

secondary differential diagnoses of recurrent bacterial infections and hypogammaglobulinaemia

A

protein loss
- protein losing enteropathy
- nephrotic syndrome
failure of protein synthesis
- lymphoproliferative disease (chronic lymphocytic leukaemia, myeloma, NHL)

17
Q

function of natural killer cells

A

kill cells that lack MHC (molecules on surface)
- no need for antigen specifity
no long term memory
part of innate immunity

18
Q

moa of biologic drugs

A

most are artificial antibodies that block the body’s own proteins
so they act just like passive immunisation and have to be injected every couple of weeks

19
Q

what is adalimub

A

targets anti-TNF
is an antiinflammatory
used in rheumatic and inflammatory diseases

20
Q

what is pembrolizumab

A

acts of anti-PD1
activates T cells
used against cancer

21
Q

what is secukinumab

A

acts on anti-interleukin 17
main action: blocks one inflammation pathway
used in psoriaisis, arthritis, MS

22
Q

types of transplant rejection

A

hyperacute rejection
acute cellular rejection
acute vascular rejection
chronic allograft failure

23
Q

pathology of hyperacute rejection

A

takes minutes to hours to show
thrombosis and necrosis
type II hypersensitivity

24
Q

management of hyperacute rejection

A

none

25
Q

pathology of acute cellular rejections

A

5-30 days
cellular infiltration
type IV hypersensitivity
CD4 and CD8, T cells

26
Q

treatment of acute cellular rejection

A

immunosuppression

27
Q

advantages of inactivated vaccines

A

can be made quickly
elicit good antibody responses
easy to store
usually safe

28
Q

disadvantages of inactivated vaccines

A

not very potent
- doesnt stimulate clonal expansion of B and T cells > requiring multiple injections

29
Q

how are neutrophils attracted to site

A

by release of cytokines (TNFa)

30
Q

complement system activation

A

antigen-antibody binding called C1 complex which in turn activate C3 convertase

31
Q

alternative pathway

A

C3b production leads to more C3 convertase activation
- C3b binds to pathogen surface and associates with other complement proteins, forming C5 convertase

32
Q

what are C3b and C5b

A

proinflammatory mediators

33
Q

what can happen with a complement deficiency

A

predisposes to bacterial infections (esp meningitis)

34
Q

what are TLRs

A

toll like receptors
- respond to PAMPS
- expressed on phagocytes and dendrites as built-in burglar alarm for microbes

35
Q

outcome of TLR activation

A

pro-inflammatory cytokines and type 1 interferon secretion

36
Q

TLR dysfunction

A

can lead to immunodeficiency (too little)
autoimmunity (too much)

36
Q

TLR dysfunction

A

can lead to immunodeficiency (too little)
autoimmunity (too much)

37
Q

what is TNF alpha

A

immediate early fire alarm signal response to many stressors

38
Q

how to vaccinations work

A

produce memory in B cells and T cells
long lived memory B cells are generated during primary immune responses that can survive for many years even after the antigen has been eliminated
memory B cells rapidly re-activate in response to second encounter with that specific antigen
(clonal expansion, differentiated into plasma cells, antibody production)