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EMS > T3 Immunopathology & hypersensitivity > Flashcards

T3 Immunopathology & hypersensitivity Flashcards

1
Q

main function of cytokines

A
  • chemical signals

- attract cells (chemokines)

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2
Q

main function of acute phase proteins

A

opsonise pathogens

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3
Q

functions of complement system

A
  • opsonisation
  • killing
  • activation
  • chemoattraction
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4
Q

what do pattern recognition receptors recognise?

A
  • Pathogen-associated Molecular Patterns (PAMPs)

- Danger Associated Molecular Patterns (DAMPs)

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5
Q

examples of pattern recognition receptors

A
  • Toll-like receptors (TLR)

- Inflammasomes (NLRP3)

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6
Q

what are the causative associations of autoimmunity?

A
  • sex:&raquo_space;women
  • age:&raquo_space;elderly
  • environment: infection; trauma-tissue damage; smoking
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7
Q

how do autoreactive B cells & autoantibodies contribute to autoimmunity?

A
  • directly cytotoxic

- activation of complement

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8
Q

how do autoreactive T cells contribute to autoimmunity?

A
  • directly cytotoxic

- inflammatory cytokines production

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9
Q

typical organ specific autoimmune disease

A

autoimmune thyroid

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10
Q

typical systemic autoimmune disease

A

connective tissue diseases

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11
Q

aetiology of Hashimotos thyroditis

A
  • destruction thyroid follicles

- autoimmune

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12
Q

autoantibodies in Hashimotos thyroditis

A
  • thyroglobulin

- thyroid peroxidase

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13
Q

what does Hasimotos thyroditis lead to

A

hypothyrodism

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14
Q

aetiology of Grave’s disease

A
  • inappropriate stimulation of thyroid gland by anti-TSH-autoantibody
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15
Q

what does Grave’s disease lead to

A

hyperthyroidism

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16
Q

systemic autoimmune diseases

A
  • systemic lupus erythematosus
  • scleroderma
  • polymyositis
  • sjorgen’s syndrome
  • vasculitis
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17
Q

what are the distinctions of an autoinflamamtory disease

A
  • defect in innate immune system
  • recurrent inflammation (long term)
  • lack of 1ry pathogenic role of adaptive system
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18
Q

what substance is inhibited to treat Muckle-Wells Syndrome

A

IL-1

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19
Q

what gene is heterozygously mutated in Familial Cold Urticaria, Muckle-Wells Syndrome & NOMID/CINCA (order of severity), on what chromosome

A
  • NLRP3

- Ch1q44

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20
Q

what is the inheritence pattern fo FMU & MWS

A

AD

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21
Q

symptoms of FCU

A
  • cold induced rash
  • arthralgia
  • conjuctivitis
22
Q

symptoms of MWS

A
  • urticarial rash
  • sensorineural deafness
  • AA Amyloidosis
23
Q

inheritance pattern of NOMID

A

sporadic

24
Q

symptoms of NOMID

A
  • chronic progressive
  • meningitis
  • destructive arthiritis
25
Q

table summing up autoimmune vs autoinflammation disease

A

see weekly summary notes

26
Q

1ry vs 2ry immunodeficiencies

A
  • 1ry: genetics

- 2ry: external factors

27
Q

causes of 3ry immunodeficiency

A
  • stress
  • surgery
  • burns
  • malnutrition
  • cancer - lymphoproliferative disease
  • drugs: affectign lymphocytes & neutrophils
  • irradiation
  • AIDS
  • infections
28
Q

aetiology of Severe Combined Immunodeficiency (SCID) syndromes

A
  • defect in B&T cells
29
Q

treatment of SCID

A
  • bone marrow transplantation

- gene therapy

30
Q

fungi & protozoa causes of defects in T cells

A
  • candida

- pneumocystis

31
Q

investigations of chemicals in SCID

A
  • normal IgG
  • reduced IgM
  • no IgA
  • reduced/absent T & NK cells
  • present B cells
32
Q

what antibody is involved in type I hypersensitivity reactions and which cells does it degranulate?

A
  • IgE

- mast cells; basophils

33
Q

what mediators are released in type I hypersensitivity reactions?

A
  • preformed

- de novo synthesized

34
Q

what are the clinical features of type I hypersensitivity reactions?

A
  • fast onset

- weal & flare

35
Q

which cells are involved in late phase response in type I hypersensitivity

A
  • eosinophils

- Th2 T cell

36
Q

what substances are released in 1ry response of type 1 hypersensitivity reactions

A
  • histamine
  • proteases
  • chemotactic factors
37
Q

what substances released by 2ry response of type 1 hypersensitivity reactions

A
  • prostoglandins

- leukotrienes

38
Q

mechanism of type II (cytotoxic) hypersensitivity reaction

A

IgG/IgM –> complement activation/phagocytosis

39
Q

clinical features of type II hypersensitivity reactions

A
  • mins - hrs

- lysis & necrosis

40
Q

common antigens in type ii cytotoxic cells

A

penicillin

41
Q

diseases that result in type 2 hypersensitivity reactions

A
  • Goodpasture’s nephritis

- blood transfusion reaction

42
Q

mode of action in blood transfusion reaction

A
  • complement –> cytotoxic action

- MCA attack complex

43
Q

mechanism of type 3

A
  • IgG/IgM Ab against soluble antigen - immune complex deposition
  • clonal B expansion
44
Q

clinical features of type 3

A
  • 3-8 hrs

- vasculitis

45
Q

type 3 associated disease

A

SLE

46
Q

mechanism of SLE

A
  • C1 from complement system binds to Ab
  • C1-9 +++ increased vessel permeability
  • C3&4 in large amount
47
Q

describe characteristics of vasculitis

A
  • kidneys: complexes in high conc due to filtering

- joint: plasma filtered to synovial fluid

48
Q

mechanism of type iv hypersensitvity (delayed)

A

antigen specific T-cell mediated

49
Q

clinical features of type 4

A
  • 48-72 hrs

- erythema

50
Q

antigens of type 4

A
  • metals (nickle)
  • tuberculin test
  • poison ivy
51
Q

associated disease with type iv

A

contact dermatitis

52
Q

summary of hypersensitivity reactions

A

check out weekly summary

EMS (10 decks)

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