Hypersensitivity reactions

Question 1

Hypersensitivity reactions

Answer 1

exaggerated, inappropriate immunologic reaction that is harmful to the host
4 types

Question 2

sensitization

Answer 2

first exposure to antigen with immune response (antibody)

subsequent exposures cause hypersensitivity reactions

Question 3

type I Hypersensitivity reactions

Answer 3

allergy or anaphylaxis

Question 4

type I mechanism

Answer 4

First exposure to antigen causes IgE formation
IgE binds to mast cells
Subsequent exposure – antigen binds to IgE bound-mast cell
Degranulation of mast cells
Release of mediators

Question 5

antigens in type I

Answer 5

are substance that most people do not react to pollen animal dander foods drugs

Question 6

type I timing and result

Answer 6

minutes

result increases vascular permeability edema smooth muscle contraction (throat closing)

Question 7

type I clinical manisfestionas

Answer 7

edema, erythema, itching, urticaria, eczema, rhinitis, conjunctivitis, asthma
more severely: systemic anaphylaxis

Question 8

systemic anaphylaxis

Answer 8

severe bronchoconstriction and hypotension

Question 9

urticaria

Answer 9

hives

Question 10

allergic response

Answer 10

During sensitization, APC picks up the allergen (antigen) and presents part of it to a T helper 2 cell, which helps a B cell become a effector cell

effector cells produce allergen-specific antibodies called IgE, which binds to mast cells.

When allergen returns, mast cells release histamine and other chemicals

In addition, Th2 cells release many different chemicals that attract inflammatory cells such as eosinophils

This results in allergy symptoms such as sneezing, mucus production, swelling, itching, runny nose, coughing, and wheezing

Question 11

Slow-reacting substance of anaphylaxis (SRS-A)

Answer 11

consist of leukotrienes

increases vascular permeability and smooth muscle contraction

Question 12

Eosinophil chemotactic factor of anaphylaxis (ECF-A)

Answer 12

release histamine and arylsulfatsae

Question 13

arylsulfatase

Answer 13

release by ECF A degrades histamine and SRS-A

Question 14

serotonin

Answer 14

capillary dilation increase vas perm and smooth muscle contraction

Question 15

Prostaglandins and thromboxanes

Answer 15

Dilation and increased permeability of capillaries and bronchoconstriction
Aggregate platelets

Question 16

Aggregate platelets

Answer 16

Prostaglandins and thromboxanes

help with clotting

Question 17

Platelet-activating factor (PAF)

Answer 17

bronchoconstriction, hypertension and vascular permeability

Question 18

cross linking

Answer 18

the allergen cross-links the bound IgE on those cells. This causes degranulation and release of mediators

Question 19

medications of Anaphylactic allergic reaction

Answer 19

epinephrine, corticosteroids, fluids for hydration, diphenhydramine (antihistamine) promethazine (antiemetic)

Question 20

promethazine (Phenergan

Answer 20

antiemetic anti nausea medication

nauseous due to dump of adrenaline

Question 21

diphenhydramine (Benadryl)

Answer 21

antihistamine

Question 22

Systemic histamine release in anaphylaxis causes what symptoms

Answer 22

Hypotension
Nausea
Hives
Swollen hands/feet

Question 23

type II

Answer 23

Cytotoxic Hypersensitivity
Antibody mediated cytotoxic reaction
antigens on a cell surface combine with IgG antibody this leads to complement mediated lysis of the cells

Question 24

type II timing

Answer 24

hours to days

Question 25

clinical manifestations of type II

Answer 25

hemolytic anemia, Rh incompatibility, rheumatic fever

Question 26

hemolytic anemia

Answer 26

type II
antibody IgG attaches to antien on RBC
Complement mediated lysis via MAC
Complement also attracts phagocytes

Question 27

Type III

Answer 27

IgG
Immune Complex Hypersensitivity
antibody immune complexes are deposited in tissues, complement is activated, and polymorphonuclear cells are attracted to the site. They release lysosomal enzymes, causing tissue damage

Question 28

Type III timing

Answer 28

2 to 3 weeks

Question 29

type III clinical manifestations

Answer 29

Systemic lupus erythematosus, rheumatoid arthritis, poststreptococcal glomerulonephritis

Question 30

type III steps

Answer 30

Antigen–antibody immune complexes form and deposit in tissue

Inflammatory response induced in tissue wall of blood vessel
C3a and C5a are released

Complement activated, and PMNs attract to the site neutrophils by c5a
Lysosomal enzymes released destroy endothelium and red cells escape
results in Tissue damage

Question 31

Systemic lupus erythematosus (SLE

Answer 31

type III
antibodies are formed to DNA and cell nuclei ANA
goes through type III steps
causes pleural effusions, heart problems, butterfly rashes, arthritis, raynaud’s phenomenon

Question 32

Rheumatoid Arthritis

Answer 32

type III
Serum and synovial fluid have “rheumatoid factor” (i.e., IgM and IgG antibodies that bind to the Fc fragment of normal human IgG)
Deposits of immune complexes on synovial membranes and in blood vessels
Activate complement and attract polymorphonuclear cells, causing inflammation.

Question 33

Rheumatoid Arthritis titers

Answer 33

Patients have high titers of rheumatoid factor and low titers of complement in serum especially during periods when their disease is most active

Question 34

Type IV Delayed (Cell-Mediated) Hypersensitivity timing

Answer 34

2 to 3 days

Question 35

Type IV Delayed (Cell-Mediated) Hypersensitivity examples

Answer 35

Contact dermatitis, poison oak/ivy, tuberculin skin test reaction, drug rash, Stevens-Johnson syndrome,

Question 36

type IV mechanism

Answer 36

the macrophage ingest antigen process and preens on it surface as MHC class II 
T helper I cell is activated and produced gamma interferon and actives macrophage

Question 37

berculosis, coccidioidomycosis

Answer 37

CD4 (helper) T cells and macrophages

Question 38

CD8 (cytotoxic) T cells

Answer 38

Contact dermatitis