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Mechanisms of Disease > Immunopathology I Mechanisms- Friedlander > Flashcards

Immunopathology I Mechanisms- Friedlander Flashcards

1
Q

what is the one thing that seems to help older folks’ immune responses?

A

physical exercise

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2
Q

what are haptens?

A

atoms or little molecules that bind to some body protein

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3
Q

what cells are the basis of adaptive immunity?

A

B and T lymphocytes, specific and diverse receptors to deal with a particular antigen we may encounter

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4
Q

what kind of stain identifies NK cells?

A

CD 57

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5
Q

what is the architecture of a lymph node?

A

cortex: B cells
medulla: T cells

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6
Q

Where do B cells mature?

A

germinal follicles of lymph nodes

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7
Q

what does it mean when a lymph node is swollen in our necks?

A

B cells are proliferating

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8
Q

where are plasma cells most often found?

A

mostly in tissues rather than blood

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9
Q

what is the appearance of plasma cells?

A

soccer ball nucleus

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10
Q

what does the term hypersensitivity mean?

A

disease caused by the immune system itself harming the body

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11
Q

type 1 hypersensitivity is an inappropriate function of what system?

A

Th2/IgE/mast cell/eosinophil system

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12
Q

what chemical(s) play a role in type 1 IMMEDIATE immune injury? fxn?

A

*histamine: vasodilation and leakage (this is what Kenna talked about)
leukotrienes: contract smooth m. and leakage
PGD2: bronchospasm and mucus production

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13
Q

what is the most important eosinophil attractant/activator?

A

IL-5

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14
Q

what is Urticaria and what is often due to?

A

hives due to IgE/type 1 immune injury

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15
Q

what chemical causes DELAYED Type 1 HS?

A

Leukotrienes

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16
Q

what is allergic rhinitis?

A

“hay fever” sneezing, itchy, due to airborne antigens (pollen, dust, mites, animal dander)

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17
Q

what is allergic asthma?

A

bronchoconstriction from inhaled allergen; IgE, lots of Eosinophils, plugs airways and remodels them

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18
Q

what is anaphylaxis?

A

life threatening emergency (massive IgE response)

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19
Q

What is anaphylactic shock? tx?

A

entire vascular bed opens and leaks, BP drops catastrophically; Tx= Epi

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20
Q

what should you think with eosinophilic gastroenteritis?

A

food allergy

21
Q

what is atopic dermatitis? looks like (where)? due to? tx?

A

Eczema, cracks and red spots in creases of elbows, knees; d/t: food allergies, Fc linkage on dendritic macrophages; tx= corticosteroids

22
Q

what are the 3 kinds of urticaria?

A
  1. cold: decrease temp causes degranulation
  2. chronic: autoimmunity, food, unknown
  3. cholinergic: heat-induced post shower or exercise
23
Q

what type of rxn is Type 2 HS?

A

antibody mediated IgG or IgM bind to Ag on cells/within tissue and cause cell destruction

24
Q

what are the 3 mechanisms that destroy anti-body coated cell?

A
  1. opsonization: IgG coated cells phagocytosed
  2. complement mediated lysis
  3. Ab dependent cell mediated cytotoxicity (Thelper cells)
25
Q

how do you test for a type 2 rxn?

A

Direct Coomb’s test; pt’s blood with anti-IgG Coomb’s reagent, will agglutinate for positive Abs

26
Q

what is goodpasture’s dz caused by?

A

Abs against basement membrane of lung and kidney

27
Q

what is Issac’s dz?

A

Abs keep nerves firing m. all the time

28
Q

what is type 3 HS rxn?

A

deposition of circulating Ab-Ag complexes into tissue

29
Q

what are the conditions needed for complexes to occur?

A

Ag must equal Ab

30
Q

where do complexes most often deposit? pathophysiology that follows?

A

intima of blood vessels; activates complement, attracts neutrophils, release lysosomal enzymes

31
Q

what does type 3 HS produce?

A

vasculitis, artritis, and/or glomerulonephritis

32
Q

what is an Arthus rxn? example?

A

local formation of Ab-Ag complexes after intradermal injection of Ag; vaccine booster

33
Q

what is serum sickness?

A

rxn to proteins in antiserum derived from animal source; immune complexes form in which Ab to foreign proteins are produced

34
Q

what causes most serum sickness now?

A

drugs (not serum)

35
Q

SXS of Serum sickness?

A

5-10 days after exposure: fever, urticaria, arthralgias, proteinuria, lymphadenopathy

36
Q

what is the worst type of Type 3 HS rxn? looks like?

A

hyperacute transplant rejection: pt already has Ab against donor HLA, complexes plug blood supply to organ, turns white before surgeon’s eyes

37
Q

what is a type 4 HS rxn?

A

t-helper mediated “delayed”; Th cells recognize “altered self” Ag, release cytokines, activate macrophages; cell-mediated, no Ab involved

38
Q

What is a true Type 4?

A

TB skin test

39
Q

what is the anergy test?

A

lots of little needs on a white thing, failure of skin to mount response, Th cells don’t work

40
Q

what is an example of type 4 HS rxn?

A

contact dermatitis: happens change body protein, immune system reacts to change= allergy

41
Q

what are some of the autoimmune disorders caused by type 4 rxns?

A

MS, G-B Syndrome, Hashimoto’s, vitiligo, halo nevus

42
Q

acute transplant reject occurs when? mediated how?

A

weeks to months; mediated cellularly (t cell) or humorally (b cells)

43
Q

chronic transplant reject occurs when?

A

in every transplant eventually but slowly, months to years,

44
Q

what happens in chronic rejection?

A

vessels narrow, initima is thickened, fibrosis

45
Q

when does graft v host dz most often occur (what kind of transplant)?

A

BMT OR immunosuppressed and has blood transfusion OR liver transplant

46
Q

what are the early signs of GVHD?

A

loss of epidermis, generalized rash, starts on palms, GI ulcers

47
Q

what are the later stages of GVHD? SXS?

A

after 100+ days, more fibrosis and less obvious necrosis

SXS: organ dysfxn, maculopaular rash, hemolysis/jaundice, HSM, diarrhea, N/V/abd. pain

48
Q

when someone has a viral infection what kind of HS rxn are they having?

A

Type 3; think flu

49
Q

what should we think of with anergy?

A

sarcoidosis, lymphoma, CA, HIV, measles, really bad disseminated infetions

Mechanisms of Disease (8 decks)

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