Hypersensitivity Reactions

Question 1

Name the acting antibody, Ag, effector mechanism, and reaction of Type I Hypersensitivity

Answer 1

Aby: IgE
Ag: soluble
Eff mech: mast cell activation –> H, L & P
Reaction: anaphylaxis, allergic rhinitis, asthma

Question 2

Name the acting antibody, Ag, effector mechanism, and reaction of Type 2 Hypersensitivity

(2 subcategories)

Answer 2

Aby: Both use IgG

Ag: cellular matrix assoc Ag
eff mech: complement –> phagocytosis & NK cells
reaction: drug allergy

Ag: cell surface R
Eff Mech: Aby alters signal
Reaction: chronic urticaria

Question 3

Name the acting antibody, Ag, effector mechanism, and reaction of Type 3 Hypersensitivity

Answer 3

Aby: IgG
Ag: soluble
Eff mech: complement & phagocytosis
Rxn: serum sickness, arthrus rxn

Question 4

Name the acting recognition cell, Ag, effector mechanism, and reaction of Type 4 Hypersensitivity

(3 subcategories)

Answer 4

Th1 cell mediated

• Ag: soluble
• mech: macrophage activation
• rxn: contact derm, tuberculin

Th2 mediated

• Ag: soluble Ag
• mech: eos activation
• rxn: chronic asthma

CTC mediated
Ag: cell assoc Ag
mech: cytotoxicity
Rxn: contact dermatitis

Question 5

Use the mnemonic/memory tool saying ABCD to remember the 4 types of HSR’s

Answer 5

4 types (ABCD):Anaphylactic and Atopic(typeI), antiBody-mediated (typeII), Immune Complex(typeIII), Delayed(cell-mediated, typeIV). TypesI,II,andIIIareallantibody-mediated.

Question 6

Lets go through HSR T1 mechanism. Talk me through it

Answer 6

allergen binds B cells –> leads to production/activation of igE –> igE binds mast cells and basophils –> bound IgE on a mast cell that encounters an Ag leads to prodxn of H, L, & P –> bronchoconstrxn, vasodilation, leaky vessels etc [i.e. anaphylaxis]

**will also have memory of this forever

Question 7

How is IgE produced?

Answer 7

IL-4 triggers CD4+ cells to switch from IgM to IgE (via somatic hypermutation)

Question 8

Please go review first aid HSR … i think a lot better then my random questions on this

Answer 8

….

Question 9

What does TNFa cause in HSR?

Answer 9

activate endothelium & increases cytokine prodxn

Question 10

What does IL4 do in HSRs?

Answer 10

stimulates and increases the Th2 response

Question 11

What do IL 3 & 5 and GM-CSF do in HSR?

Answer 11

promote eosinophil prodxn

(remember gmcsf, colony stimulating factors)

Question 12

How does epinephrine help in anaphylaxis?

Answer 12

closes vascular tight

Question 13

Whats the hygiene hypothesis?

Answer 13

basically we keep kids to clean nowadays and thus they aren’t being exposed to enough to cause Th differentiation

Question 14

Describe how Rh negative blood type can be involved in HSR

What type of HsR is this?

Answer 14

Rh⊝pregnant patient; Rh⊕fetus.

First pregnancy: patient exposed to fetal blood (often during delivery) –> formation of maternal anti-DIgG.

Subsequent pregnancies: anti-D IgG crosses placenta –> attacks fetal and newborn RBCs –> hemolysis.

***this is Type II HSR

Question 15

Describe an arthrus rxn? What type HSR is this?

Answer 15

Arthrus rxn = local rxn, usually at injection site, that causes small complexes to deposit in small blood vessels –> red & swollen, Ag & Ab & C precipitation –>can cause clots/occlude small vessels

Usually goes away within a day

Type III HSR!!

Question 16

What is serum sickness? What HSR type is this?

Answer 16

basically a generalized arthrus rxn –> causes system wide swelling/rash and deposition of Aby complexes

* most often affects the kidney?

7-10 days after dosing it appears? or it resolves in 7-10 days, not sure based on notes

Type III HSR

Question 17

Name 6 ways we can treat allergies/anaphylaxis and how these treatments work

(5 are immediate treatments, one is subsequent)

Answer 17

• epinephrine –> vasoconstrxn & bronchodilation –> increased HR to combat cardiovascular collapse/shock
• corticosteroids and leukotriene antagonists –> reduce inflam and relax bronchioles
• antihistamines —> block H Ag on blood vessels and SMC
• cromolyn –> inhibits mast cell degranulation
• anti-Ige –> neutralizes IgE
• Desensitization –> subsequent treatments to induce T cell tolerance or ihibit IgE and switch produxn to different Aby class?