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IHL Exam 2 > Hypersensitivity (Bowden) > Flashcards

Hypersensitivity (Bowden) Flashcards

1
Q

What is the Type I hypsersensitivity

A

Immediate (IgE)

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2
Q

3 properties of IgE control in Type I immediate Hypersensitivity

A

changes half life of IgE (binding IgE to cell R)
control of IgG and IgE production by T cells
Cross linking of IgE on surface of mast and basophils

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3
Q

Describe how Type I hypersensitivity is T cell dependent

A

Supressive Th1
Promotes Th2
class switch IL-4

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4
Q

What causes type I reactions

A

Allergens. usually protein

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5
Q

How are allergens classified

A

source, route and nature of protein

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6
Q

What are the classical allergens

A

low doses: inhaled about 1mg/yr

high doses: food (egg milk, nuts, fish)

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7
Q

What happens during repeated exposure to allergen

A

Mast cells release mediators

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8
Q

Types of mediators and when they are released

A 
Preformed(under 5min) Histamine, heparin, and tryptase
Newly Generated(5-30 min) Leukotrience D4, Arachidonic Acid, Prostaglandin D2
Cytokines take hours. IL-4 and TNFa
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9
Q

What are the symptoms/signs of mediators effects

A

Vascular leak, broncho-constriciton, intestinal hypermotility, inflammation, tissue damage, killing of parasites and host cells

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10
Q

How do we test allergies

A

Wheal and Flare reaction.
The wheal is the extravasation of sera
The flare is the axon reflex

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11
Q

What is a Late Phase Reaction

A

4-6 hours after initial Type I reaction. lasts 1-2 days

Infiltration of PMNs, eosinophils, macrophages, lymphocytes and basophils

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12
Q

what causes the late phase reaction

A

MAst cells produce TNFa and IL-1 leading to expression of adhesion molecules. Mast cells produce chemotactic IL8 and there is onsite release of IL-3 IL-5 IL-8 and GM-CSF (hematopoietic)

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13
Q

What is the Type II hypersensitivity

A

Antibody Mediated

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14
Q

What are the necessary components in Type II hs

A

IgG IgM FcR on effector cells and C’ and the surfaces that have the Ab

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15
Q

What are the IgM and IgG Abs binding to in Type II hs

A

“fixed Ag”

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16
Q

What are more pathogenic: Ab against cell surface Ag or internal Ag

A

Ab against cell surface Ags are usually pathogenic

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17
Q

What components from activated C’ system cause chemotaxis of PMNs, basophils and eosinophils

A

C3a and C5a

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18
Q

How does the Fc R communicate with the bound Ab in type II hs

A

either binds the Fc or binds bound C’ components

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19
Q

What do the effectors do in type II hs

A

Cytokine and chemokine by activated Eos, Neutrohils, NKs, Macrophages which release TNFa and IL1

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20
Q

Describe frustrated phagocyte

A

unable to take in the Ag so releases all its contents to kill it

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21
Q

what hemolytic disease occurs by type II hs

A

Hemolytic disease of newborn (Rh factor) also happens for blood types- more rare

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22
Q

Describe transfusion reaction

A

Fever, hypotension, nausea/vomiting, back&chest pain. donated blood- not whole blood unless emergency
Abs (IgM) will cause agglutination, C’a ctivation and intravascular hemolysis

23
Q

Describe warm/cold Abs and what they assoc with

A

Autoimmune hemolytic anemias, type II hs.

warm: different epitopes then when transfused.
cold: high titer IgM- usually old people in winter.

24
Q

How can drugs cause autoimmune hemolytic anemias

A

drugs bind RBCs and Ab to drug. Drug-Ab- immune complex gets absorbed by RBCs and is activated by C’ to be lysed.

25
Q

What disease has Ab to the acetylcholine R

A

Myasthenia Graves- extreme mm weakness.
IgG and C’
partial block of ACh, increases R turnover rate

26
Q

What is type III hs

A

Immune complexes

27
Q

What are the components of type III hs

A

IgG IgM FcR of effector cell, C’ and soluble Ag!!

Ab mediated

28
Q

What makes up the immune complex

A

Ab/Ag/C’

29
Q

What usually removes immune complexes from circulation

A

monophagocyte system. Normall IC binds C’ and removed by liver and spleen after binding CR1 on RBCs

30
Q

Where are immune complexes in tissue

A

determined by localization of Ag in tissue, and size matters

31
Q

3 groups of Immune complex hs

A

Persistent infection
autoimmune
inhalation of Ag

32
Q

What is the function of immune complexes

A

when inflammed, they act on basophils and platelets to produce vasoactive amine release.

33
Q

What amines are released by IC activation

A

histamine and tryptamine to cause endothelial cell retraction and increase vascular permeability

34
Q

What is the net result of increased vascular permeability

A

leaky endothelium– complex deposition in some areas

35
Q

What happens when IC are deposited in leaky endothlium

A

incudes platelet aggregation and C’ activation- Microthrombi form. Neutrophils are attracted by C’ products– leading to more damage
Increase BP and vascular turbulence in the area leading to increasing the complex deposition

36
Q

Atrhrus Reaction

A

type III hs. Presensitization. Ag reaction with marked edema and hemorrhage 4-10 hours after exposure.
chronic allergy shots and allergic alveolitis (farmers lung)

37
Q

What is serum sickeness

A

large injections of foreign antigen- causes deposition of IC in blood vessels. Leads to arthritis and glomerulunephritis

38
Q

How are type II and III hs alike and different?

A

inflammatory pathways are identical.
Ags type II are fixed surfaces
Ags type III are soluble

39
Q

Innapropriate activation of Ag in type II and III can lead to

A

Tissue damage, increase inflammation, and perpetuation of the disease.

40
Q

Type IV hypersensitivity

A

delayed-type hypersensitivity- Ag specific T cells

41
Q

Describe DTH

A

effector T cells activate macrophages

takes 24-72 hours post exposure

42
Q

If Ag persists in DTH what can happen

A

granuloma formation

can lead to autoreactive T cells

43
Q

Types of DTH

A

Contact- point of contact with allergen
Tuberculin- soluble Ag
Granulomatous- clinically most important

44
Q

2 stages of contact sensitivity

A

Sensitization and Elicitation

45
Q

Describe sensitization phase of contact allergen

A

10-14 days: epidermis
this is hapten driven- so like poison oak or ivy
protein/hapten taken up by langerhans
Class II HLA

46
Q

Describe elicitation phase of contact allergen

A

recruitment of CD4+ T cells to contact site. monocytes, macrophages
mainly CD4, small CD8

47
Q

What is the PPd test looking for

A

recall response to previous encounter with Ag

48
Q

What happens during a + PPD test

A

infiltrate of neutrophils, monocytes, T cells

49
Q

What does tuberculin tests measure generally

A

cell-mediated immunity

50
Q

When do you usually see granulomatous DTH

A

chronic infections assoc with TH1-like responses

absence of infection. non-immune- foreign body

51
Q

What characteristics of IC allow them to deposit easily

A

small, positively charged

52
Q

Persistence of Ag in type Iv hs causes macrophages to change how?

A

differentiate into epithelioid cells. fusion to form giant cells

53
Q

What cytokine is granuloma formation dependent on

A

TNF a because dependent on T cell activation of macrophages

IHL Exam 2 (11 decks)

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