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

25
pathology of acute cellular rejections
5-30 days cellular infiltration type IV hypersensitivity CD4 and CD8, T cells
26
treatment of acute cellular rejection
immunosuppression
27
advantages of inactivated vaccines
can be made quickly elicit good antibody responses easy to store usually safe
28
disadvantages of inactivated vaccines
not very potent - doesnt stimulate clonal expansion of B and T cells > requiring multiple injections
29
how are neutrophils attracted to site
by release of cytokines (TNFa)
30
complement system activation
antigen-antibody binding called C1 complex which in turn activate C3 convertase
31
alternative pathway
C3b production leads to more C3 convertase activation - C3b binds to pathogen surface and associates with other complement proteins, forming C5 convertase
32
what are C3b and C5b
proinflammatory mediators
33
what can happen with a complement deficiency
predisposes to bacterial infections (esp meningitis)
34
what are TLRs
toll like receptors - respond to PAMPS - expressed on phagocytes and dendrites as built-in burglar alarm for microbes
35
outcome of TLR activation
pro-inflammatory cytokines and type 1 interferon secretion
36
TLR dysfunction
can lead to immunodeficiency (too little) autoimmunity (too much)
36
TLR dysfunction
can lead to immunodeficiency (too little) autoimmunity (too much)
37
what is TNF alpha
immediate early fire alarm signal response to many stressors
38
how to vaccinations work
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)