immune disease 2 (W12) Flashcards

1
Q

association between autoimmune disease?

A

having one increases likeliness for having another

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2
Q

how can autoimmunity start

A

self antigens become modified
microbial antigens resemble self
hidden antigens can be exposed by damage
inflammation breaks anergy (stimulating bystander lymphocytes)

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3
Q

susceptibility genes for autoimmunity and example diseases?

A

MHC alleles (AS, type 1 diabetes, SLE, RA)

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4
Q

tissue targeted autoimmunity diseases?

A

type 1 diabetes
MS
graves’ disease
myasthenia gravis
primary biliary cholangitis

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5
Q

multisystem autoimmunity diseases?

A

SLE
RA

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6
Q

2 antibody mediated reactions (damaging)

A

binding of antibody to own cells
hypersensitivity reaction

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7
Q

hypersensitivity reaction example?

A

haemolytic anaemia: antibodies bind to red blood cells (due to molecular mimicry of recent viral infection) or antibody binds to specific drug-protein complex on red cell surface. antibodies tag these cells for removal even though they are healthy

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8
Q

disease examples where autoantibody binds to cell surface receptor? explain?

A

graves disease - stimulates TSH receptor leading to hyperthyroidism
Myasthenia gravis - blocks Ach receptor leading to neuromuscular weakness

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9
Q

what occurs if transfused blood is not the right type

A

anti-A or anti-B antibodies bind to foreign red cells, induce complement, causing red cell lysis, inflammation in the circulation, haemolysis and intravascular coagulation. System wide cytokine storm and shock.

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10
Q

which blood group can be given to anyone? why?

A

O - lacks A and B antigens

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11
Q

which blood group can receive any blood type? why?

A

AB - lacks A and B antibodies

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12
Q

rhesus reaction?

A

IgG response to protein. rhesus negative (RhD-) mother has RhD+ baby, risk of mother being exposed to RhD+ blood cells. problem for next pregnancy as now has anti-RhD antibodies that will react to future RhD+ babies.

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13
Q

damage from antibody binding extracellular targets

A

antigen-antibody complexes become saturated in the circulation, leads to deposition (small blood vessels in particularly joints, skin). Complement usually breaks these up but it can exceed their capacity.

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14
Q

unsensitised vs sensitised hypersensitivity?

A

unsensitised - haven’t been exposed to allergen protein
sensitised - has been expensed to allergen protein before

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15
Q

chronic antigen exposure - autoimmunity disease example?

A

SLE - nuclear autoantigens from dying cells

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16
Q

chronic antigen exposure - chronic infection example?

A

infectious endocarditis

17
Q

damage from cytotoxic T cell killing - autoimmunity example?

A

type 1 diabetes:
CTL kill pancreatic islet beta cells (target insulin-related peptides)

18
Q

damage from cytotoxic T cell killing - hypersensitivity examples?

A

coeliac disease
allergic contact dermatitis

19
Q

coeliac disease?

A

sentinel intraepithelial CD8 T cells kill intestinal epithelium stressed by cytokines from Th1 cells sensitised to modified dietary gliadin (idk what this means)

20
Q

allergic contact dermatitis?

A

manifests 2-4 days after re-exposure. red plaques, vesicles, acute oedema, evolving to dry scaly skin. effector memory T cell reaction to neoantigen. sensitised cytotoxic T cells kill keratinocytes that have bound to an allergen (eg nickel from bracelet, topical drugs etc).

21
Q

damage from Th cell activation of macrophages - example disease?

A

some sarcoid cases