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Block 6 Week 2 Colt > Types III and IV Hypersensitivity - Hunter > Flashcards

Types III and IV Hypersensitivity - Hunter Flashcards

1
Q

What type of immune reactant is used in type 3?

A

IgG

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2
Q

What type of antigen is used in type 3?

A

soluble Ag

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3
Q

What is the effector mechanism of type 3?

A

Complement, phagocytes

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4
Q

What are two notable type 3 reactions?

A

serum sickness and arthus reaction

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5
Q

What is the most sensitive organ to immune complexes?

A

kidney

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6
Q

High dose intravenous ag will result in what three reactions?

A

Vasculitis, nephritis,k and arthritis. Immune complexes deposited in blood vessel walls, glomeruli, and joint spaces

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7
Q

Subcutaneous ag delivery will result in what reaction?

A

Arthus reaction, immune complex deposited in perivascular area

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8
Q

Inhaled ag delivery will result in what reaction?

A

Farmer’s lung; deposition in alveolar-capillary interface

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9
Q

What is the visible finding of small scale vascular damage? Large scale?

A

Petechia is small, purpura is large

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10
Q

Do you get immune complex disorders with Ab or Ag excess?

A

Ag excess

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11
Q

when in the course of an infection do you have Ag excess?

A

early on in the infection

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12
Q

why do the Ag complexes not fix C early in the infection?

A

they are numerous, but too small to fix C

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13
Q

Immune Complexes Bind to RBCs and are Cleared by (blank)

A

Mononuclear Phagocytes

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14
Q

C3b/C4b bound to immune complexes binds CR1 on (blank)

A

RBCs

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15
Q

Splenic macrophages and liver Kupffer cells have (blank) receptors that engage immune complexes on RBCs

A

Fc

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16
Q

T/F: The immune complexes are stripped and destroyed from RBCs in the spleen, then the intact RBCs return to the circulation

A

true

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17
Q

What event do you need to be able to deposit immune complexes in arterial walls?

A

turbulent flow

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18
Q

where do immune complexes like to deposit

A

renal glomeruli and small vasculature of skin and joints–hence purpura and vasculitis

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19
Q

Immune complexes deposit (between/on top of) endothelial cells

A

between

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20
Q

Complement is activated by immune complexes on vasculature by releasing (blank)

A

anaphylatoxins C3a andC5a

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21
Q

What cells are recruited to immune complex plaques?

A

neutrophils

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22
Q

What do the attracted neutrophils do that actually causes the vasculitis in immune complex deposition?

A

frustrated phagocytosis leading to granule exocytosis, causing inflammation and tissue destruction

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23
Q

Describe what happens when an immune complex binds to endothelium?

A
  1. Activate complement allowing C3b to opsonize the immune complex
  2. Release of anaphylatoxins C3a andC5a which chemoattract neutrophils
  3. Frustrated phagocytosis results in granule release
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24
Q

What clinical findings do we see when we have immune complex deposition in the glomerulus? Why?

A

Hematuria and proteinuria; frustrated phagocytosis broke down the glomerular integrity allowing protein and blood into the urine

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25
Q

What is the most common post-infecious acute proliferative nephritis?

A

Post-strep glomerulonephritis

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26
Q

Does Post-strep glomerulonephritis have a good or bad prognosis?

A

good

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27
Q

How do patients present with post-strep glom.?

A

hematuria and proteinuria, elevated specific gravity

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28
Q

Why does the glomerulus become hypercelluar in post-strep glom?

A

neutrophil infiltration and proliferation of intrinsic glomerular cells

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29
Q

Immunofluorescence of post-strep glom. shows what characteristic?

A

it is lumpy-bumpy

30
Q

How do you confirm the Dx of post-strep glom?

A

evidence of invasive Streptococcus pyogenes infection such as a elevated anti-DNAase B titer

31
Q

Can viral infections result in immune complex deposition in the kidney?

A

yes, Hep B!`

32
Q

The Arthus reaction is limited to what area of tissue?

A

subcutaneous only

33
Q

What do you need to already have around to have an Ag injection cause an Arthus reaction? Why would you have this?

A

High levels of IgG to the Ag; let’s say someone just had an active infection of the Ag and is receiving a booster vaccine

34
Q

Describe the process of the Arthus reaction?

A
  1. Ag injection
  2. Local immune complex formation
  3. Activation of FcgRIII on mast cells; degranulation
  4. inflammation, edema, blood vessel occlusion
35
Q

What receptor do mast cells use to bind immune complexesin the Arthus reaction?

A

FcgRIII; interacts with IgG

36
Q

What vaccinations are the most common cause of Arthus reaction?

A

Tetanus and diphtheria

37
Q

T/F: Arthus reaction causes local vasculitis

38
Q

what are the clinical manifestations of Arthus rxn?

A

severe pain, swelling, induration, edema, hemorrhage, and occasionally necrosis

39
Q

Can a person have an arthus reaction if they have never been exposed to that Ag before?

A

NO; MUST BE PREVIOUSLY SENSITIZED

40
Q

What Ig forms complexes with the penicilloyl moiety?

41
Q

why do you get hives with serum sickness?

A

Complement activation releases C3a which causes histamine release from mast cells

42
Q

What are the three -itis things you get with serum sicknes?

A

vasculitis, nephritis, and arthritis

43
Q

What happens to pt’s with serum sickness when the Ag is removed?

A

they get better!

44
Q

What are the two other names for Farmer’s lung?

A

Extrinsic Allergic Alveolitis (Hypersensitivity Pneumonitis)
bird fancier’s disease

45
Q

what type of pathogen causes farmer’s lung?

46
Q

what type of Ig do you develop to inhaled molds?

47
Q

Why do you get lung inflammation in farmer’s lung?

A

immune complexes fix complement, releasing anaphylatoxins and causing inflammation

48
Q

T/F: serum Abs to the allergens can be measured via immunoassay

49
Q

what pathology can result to extended exposure to lung allergens?

A

lung fibrosis

50
Q

What can you use to treat acute farmer’s lung?

A

corticosteroids

51
Q

How do people with farmer’s lung present clinically?

A

headache, fever, shortness of breath, a non-productive cough and myalgia, PFT shows restrictive defects.

52
Q

What are two organisims that cause farmer’s lung?

A

Micropolyspora faeni and Aspergillus fumigatus

53
Q

DTH is mediated by what t cell?

54
Q

DTh is what type of hypersensitivity?

55
Q

In DTH, macrophages produce what?

56
Q

What does IL12 from macrophages do to TH1?

A

release of IFNg, increases macrophage activity, release of TNF-a, acts of vascular endothelium

57
Q

what do the macrophages produce that stimulate th17 in DTH?

A

TGF-b and IL23

58
Q

What do the Th17 cells release that attracts neutrophils in DTH?

A

Il17 and IL22

59
Q

What do CTLs happen to make in DTH?

60
Q

What causes allergic contact dermatitis?

A

activation of CD4 or CD8 cells

61
Q

allergic contact dermatitis Ags normally form what complex with self proteins?

A

hapten:protein complexes

62
Q

(blank) take up and process antigen, migrate to lymph nodes, and activate T cells; memory T cells migrate to the dermis in allergic contact

A

Langerhan’s dendritic cells

63
Q

A subsequent exposure to the sensitizing chemical in allergic contact activates the memory T cells which release mediators like (blank)

64
Q

In allergic contact, IFN-g stimulates (blank) to release a variety of cytokines and chemokines that enhance the inflammatory response by recruiting and activating monocytes

A

keratinocytes

65
Q

Hapten-modified peptides are presented in MHC Class (blank) molecules to CD4 T cells (genetic susceptibility and HLA)

66
Q

T/F: first time exposure to poison ivy only causes mild symptoms

67
Q

second exposure to poison ivy elicits a memory (blank) cell response

68
Q

Contact dermatitis presents clinically with (blank) and histologically with (blank)

A

epidermal blisters; mononuclear infiltrates

69
Q

How can you treat contact dermatitis?

A

SYSTEMIC corticosterioids

70
Q

How do metal allergies work?

A

metal ions bind to host proteins and activate T cells

71
Q

Once T cells are activated in metal allergies, what happens?

A

T cell releases IFNg, which activates keratinocytes to release mediators that cause mononuclear infiltration

72
Q

What is the only treatment of metal allergies?

A

avoidance of the metal

Block 6 Week 2 Colt (3 decks)

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