Immuno 2

Question 1

Prevention and Treatment for Tetanus

Answer 1

> Prevention: Tetanus toxoid (inactivated toxin) – humoral immunity.
Treatment: Tetanus immune globulin – acute tx, prevention after wound injury.

Question 2

Hypersensitivity reactions

[Humoral and cellular components, examples]

Answer 2

> Type I: immediate (Ige; Mast cells, basophils) – anaphylaxis, allergies.
Type II: cytotoxic (IgM, IgG, complement; neutrophils, macrophages, complement) – Autoimmune hemolytic anemia, Goodpasture syndrome.
Type III: immune complex (IC deposition, complement; neutrophils) – serum sickness, PSGN, Lupus nephritis.
Type IV: delayed (no humoral involved; T cells, macrophages) – contact dermatitis, Tuberculin skin test.

Question 3

Transplant rejection (hyperacute, acute, chronic)

Answer 3

> Hyperacute (mins-hrs): preformed antibodies vs graft antigens – cyanosis, gross mottling; thrombosis.
Acute (less than 6 mos): humoral/cellular activation of naive immune cells – vasculitis, lymphocyte infiltrate in vessel wall.
Chronic: low-grade immune response refractory to immunosuppressants – wall thickening, interstitial fibrosis, parenchyma atrophy (arteriosclerosis, obliterative vascular fibrosis)

Question 4

What type of hypersensitivity is involved in Acute hemolytic transfusion reaction?

Answer 4

Type II HSR
>Pre-existing anti-ABO antibodies bind antigens on transfused donor RBCs – complement activation – lysis (by MAC), vasodilation, sx of shock.
>Fever, hypotension, chest and back pain, hemoglobinuria.

Question 5

How does inactivated influenza vaccine work?

Answer 5

Induces neutralizing antibodies against hemagglutinin – prevents viral entry

Question 6

Chronic granulomatosis disease

[Px, organs, dx]

Answer 6

Mutation inactivating NADPH oxidase – no respiratory burst – Recurrent infections w/ catalase (+) organisms.
>Commonly involves lungs, skin, lymph nodes, liver – diffuse granuloma formation.
>Dx: Nitroblue tetrazolium (NBT) testing [dark blue precipitate], Dihydrorhodamine (DHR) flow cytometry [fluorescent green]

Question 7

Intrinsic pathway of apoptosis

Answer 7

Stress or cessation of survival signals trigger replacement of anti-apoptotic proteins (Bcl-2) w/ pro-apoptotic proteins (BAK, BAX) in mitochondrial membrane – inc. mitochondrial permeability into cytoplasm – release of cytochrome c – activates caspases in cytosol

Question 8

How does Rh(D) alloimmunization happen?

Answer 8

Rh(-) mom has Rh(+) fetus – fetal RBCs enter maternal circulation – maternal IgG and memory B cells form against Rh – Hemolytic dse of newborn.
>Subsequent pregnancies w/ Rh(+) fetus will be affected.

Question 9

Prevention of Rh alloimmunization

Answer 9

Give anti-Rh(D) immune globulin (anti-D IgG) – 28 wks AOG, immediate postpartum.
Maternal immune system won’t react, and the administered Igs won’t cause significant transplacental fetal hemolysis.

Question 10

Serum sickness

[HSR type, px]

Answer 10

Type III HSR to nonhuman proteins.
Tissue deposition of IC – vasculitis.
>Fever, pruritic skin rash, arthralgias
>Dec. serum C3 – deposition of IgG/IgM (complement fixing) means complement consumption