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Phase 2a - Introductory Clinical Sciences > Immunology > Flashcards

Flashcards in Immunology Deck (160)
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91

what are two methods by which tumours can "escape" the immune system?

1. immune responses change tumours so tumours are no longer "seen" by immune system - tumour escape
2. tumours change immune response by promoting immune suppressor cells - immune evasion

92

what type of immunoglobulin is typically involved in allergy?

IgE

93

what are the cells involved in allergy?

mast cells, eosinophils, lymphocytes, dendritic cells.
effectors of allergic response - smooth muscle, fibroblasts, epithelia

94

what cells express low-affinity IgE receptors?

B cells, T cells, monocytes, eosinophils, platelets, neutrophils

95

what cells express high-affinity IgE receptors?

MAST CELLS
basophils, eosinophils

96

describe the development of mast cells

derived from specific cell lineage. require c-kit protein to develop. immature mast cells circulate, mature in tissues

97

what activates mast cells?

indirect activators act via IgE - allergens, some bacterial/viral antigens.
phagocytosis.
direct activators - cold. aspirin, NO2, proteases, C3a, C5a

98

describe anaphylaxis

occurs within mins-hrs.
mast cell or basophil activation - IgE or direct activation.
histamine and tryptase are elevated.
vasodilation, vascular permeability, low BP, bronchoconstriction, rash, swelling, GI pain, vomiting etc.

99

what is a type I hypersensitivity reaction?

immediate hypersensitivity ('allergy') - due to activation of IgE antibody on mast cells or basophils.

100

what is a type II hypersensitivity reaction?

antibody to cell-bound antigen - triggered by antibodies reacting with antigenic determinants on cell membrane of target tissue. often involves drugs/their metabolites binding to RBC.

101

what is a type III hypersensitivity reaction?

immune complex hypersensitivity - results from deposition/formation of immune complexes in tissues

102

what is a type IV hypersensitivity reaction?

delayed-type hypersensitivity. mediated by T lymphocytes reacting with antigen - sensitisation. secondary challenge results in delayed-type reaction - local inflammation taking 2-3d to develop.

103

what causes primary immunodeficiency?

an intrinsic defect in the immune system

104

what causes secondary immunodeficiency?

an underlying condition - much more common than primary.
occurs when synthesis of key immune components is suppressed or their loss accelerated.

105

how would a patient with an antibody deficiency present?

recurrent bacterial infections of resp tract

106

how would a patient with defects in cellular immunity present?

invasive and disseminated viral, fungal and opportunistic bacterial infections involving any organ

107

what is panhypogammaglobulinaemia?

a silly word.
also, defects in antibody synthesis that involves different classes of Igs

108

what is selective antibody deficiency?

defects in antibody synthesis involving only one class/subclass of Ig

109

what are the presentations of primary antibody deficiencies?

recurrent infections of upper and lower resp tract.
congenital forms present between 4m-2yrs due to passive protection provided by maternal IgG.
skin sepsis
gut infection
meningitis
arthritis
splenomegaly
purpura

110

what are the most common infecting organisms in antibody deficiency?

pyogenic bacteria:
staph
H influenzae
strep pneumoniae

111

why aren't patients with primary antibody deficiency unduly susceptible to viral/fungal infections?

cell mediated (T cell) immunity is preserved

112

describe the features of X-linked agammaglobulinaemia (XLA) - bruton's disease

boys present w/ recurrent pyogenic infection between 4m-2yo.
infections similar to other antibody deficiency + enteroviruses.
no mature B cells circulating.
very low serum Ig.
gene found on long arm of x chromosome, produces Bruton's tyrosin kinase (Btk) - cytoplasmic enzyme - which is needed for B cell development. mutations = XLA.

113

describe the features of hyper-IgM syndrome

normal/high serum IgM in absence of other types.
X linked mutation in CD4+ T cell.

bacterial infections and Pneumocystis jirovecii neumonia.

replacement Ig therapy needed, bone marrow transplant is gold standard.

114

describe the features of selective IgA deficiency

normal IgG and IgM, no IgA.
IgA deficiency = asymptomatic. selective IgA deficiency predisposes to other disorders. prompt Abx therapy for infection, immunisation against respiratory pathogens.

115

describe the features of common variable immunodeficiency (CVID)

group of disorders presenting as antibody deficiency in late childhood/adults. recurrent bacterial infections, higher risk of autoimmune disease (purpura, pernicious anaemia etc). granulomas can cause end-organ damage.
replacement Ig therapy

116

name some primary antibody deficiencies

panhypogammalgobulinaemia.
transient hypogammaglobulinaemia of infancy.
XLA - bruton's disease.
hyper-IgM syndrome.
selective IgA deficiency.
common variable immunodeficiency.

117

describe the features of severe combined immunodeficiency (SCID)

seen in infants - major failure of T cell (and variable B/NK cell) function.
genetic variables.
first few weeks/months - failure to thrive, chronic diarrhoea, respiratory infections. lymphopenia.
avoid live vaccines and blood transfusions.
SCID patients die before reach 2yo without haemopoietic stem cell transplants.

118

describe the features of primary C1, C4 or C2 deficiency

malar rash (facial rash), arthralgia, glomerulonephritis, fever or chronic vasculitis - immune complex deposition in tissues

119

describe the features of C3 deficiency

occurs as primary, or secondary to factor H or factor I deficiency.
increased susceptibility to life-threatening bacterial infections (pneumonia, septicaemia, meningitis)

120

describe the features of C5, C6, C7 or C8 deficiencies

recurrent bacterial infection.