Hypersensitivity

Question 1

Heightened state of immune
responsiveness

Answer 1

Hypersensitivity

Question 2

Cell bound antibody reacts with antigen to
release physiologically active substances

Answer 2

Hypersensitivity type 1

Question 3

Are those in which free antibody reacts with
antigen associated with cell surface

Answer 3

Hypersensitivity type II

Question 4

Antibody reacts with soluble antigen to form
complexes that precipitate in the tissues.

Answer 4

Hypersensitivity type III
• Antibody reacts with soluble antigen to form

Question 5

Complement plays a major role in producing
tissue damage.

Answer 5

Hypersensitivity type 3

Question 6

Sensitized T cells rather than antibody are
responsible for the symptoms that develop.

Answer 6

Hypersensitivity type 4

Question 7

Immune mediators of type 1 to 4

Answer 7

Type 1 = ige
Type 2 = igg
Type 3 = igg origm
Type 4 = t cells

Question 8

Which hypersensitivityhas complement involvement

Answer 8

Type 2 and 3

Question 9

Mechanism of type 1 hypersensitivity

Answer 9

RELEASE OF
MEDIATORS
FROM MAST
CELLS AND
BASOPHILS

Question 10

Hypersensitivity type 2 mechanism

Answer 10

CYTOLYSIS DUE
TO ANTIBODY
AND
COMPLEMENT

Question 11

Hypersentivity type 3 mechanism

Answer 11

DEPOSITS OF Ag-
Ab COMLEXES

Question 12

Hypersensitivity’s type 4 mechanism

Answer 12

RELEASE OF
CYTOKINES

Question 13

Example oftype 1 hypersensitivity

Answer 13

ANAPHYLAXIS,
HAY FEVER,
FOOD
ALLERGIES

Question 14

Example of type 2 hypersensitivity

Answer 14

TRANSFUSION
REACTIONS,
HDN

Question 15

Type 3 hypersensitivity

Answer 15

SERUM
SICKNESS, SLE

Question 16

Type 4 hypersensitivity

Answer 16

CONTACT
DERMATITIS,
TUBERCULIN
TEST

Question 17

Antigen contact, typically low dose via mucous
membrane (respiratory, GI) → IgE production

Answer 17

Sensitization

Question 18

Pre-formed IgE (allergens-specific) triggers
mast cell activation → mediator release

Answer 18

Elicitation

Question 19

 Can occur within seconds-minute of exposure
 Severity ranges from irritating to fatal

Answer 19

Reactions

Question 20

In type 1, Total IgE and specific antibodies are measured
by a

Answer 20

modification of enzymes immunoassay
(ELISA).

Question 21

Increased IgE levels are indicative of

Answer 21

atopic
condition.

Question 22

Type 1 teatment

Answer 22

Antihistamine, anchromolyn sodium

Leukotriene

Bronchodilators such as irsprotrenol derviatives

Thopylline

Hyposensitvity

Suppressor t cell

Igg blocing antibodies

Question 23

nhibits mast cells
degranulation, probably by inhibiting Ca++
influx.

Answer 23

Chromolyn sodium i

Question 24

elevates
cAMP-phosphodiesterase and inhibits
intracellular Ca++ release is also used to relieve
bronchopulmonary symptoms.

Answer 24

Thophylline

Question 25

• that specifically inhibits IgE antibodies may play a role.

Answer 25

Suppressor T cells

Question 26

also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues

Answer 26

Type 2 hypersensitivity

Question 27

The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to

Answer 27

type II hypersensitivity.

Question 28

Can lead to type 2 hypertension

Answer 28

• Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia

Question 29

Diagnostic test of type 2

Answer 29

detection of circulating antibody against tissues involved and the presence of antibody and complement in the lesion (biopsy) by immunofluorescence.

Question 30

It is also known as immune complex hypersensitivity.

Answer 30

Type 3 hypersensitivity

Question 31

The reaction may be general (serum sickness) or may involve individual organs including skin (systemic lupus erythematosus, arthus reaction), kidney (lupus nephritis), lung (aspergillosis), blood vessels (polyarteritis), joints (rheumatoid arthritis) or other organs.

Answer 31

Type 3

Question 32

Ho long is the reaction for type 3, what siit mediated by and what type of antigenis used

Answer 32

• The reaction may take 3-10 hours after exposure to the antigen. • It is mediated by soluble immune complexes. They are mostly of IgG class, although IgM may also be involved. • They antigen may be exogenous or endogenous in nature. The antigen is soluble and not attached to the organ involved.

Question 33

Diagnosis of type e

Answer 33

• Diagnosis involves examination of tissue biopsies for deposits of Ig and complement by immunofluorescence. • Polyethylene glycol mediated turbidity (nephelometry), binding of C1q and Raji cell test are utilized to detect immune complexes. • The immunoflurorescent staining in type III hypersensitivity is granular. Presence of immune complexes in serum and depletion in complement level are also diagnostic.

Question 34

Treatment of type 3

Answer 34

Anti inflammation

Question 35

It is also known as cell mediated or delayed type hypersensitivity.

Answer 35

Type 4 hypersensitivity

Question 36

The classical example of this hypersensitivity is tuberculin (montoux) reaction which peaks 48hours after the injection of antigen (PPD or old tuberculin). The lesion is characterized by induration and erythema.

Answer 36

Type 4 hypersensitivity

Question 37

is involved in the pathogenesis of many autoimmune and infectious diseases and granulomas due to infections and foreign antigens.

Answer 37

Type IV hypersensitivity

Question 38

Another delayed hypersensitivity is

Answer 38

contact dermatitis (poison ivy, chemicals, heavy metals) in which the lesions are more popular.

Question 39

Mechanism for type 4

Answer 39

include T lymphocytes and monocytes and/or macrophages. Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells and recruit and activate monocytes and macrophages, which cause the bulk of the damage.

Question 40

Major lymphokines involved in delayed hypersensitivity reaction include

Answer 40

monocyte chemotactic factor, interleukin-2, interferon, TNF.

Question 41

Diagnostic test in type 4 hypersensitivity

Answer 41

Diagnostic test in vivo include delayed cutaneous reaction (montoux test) and patch test (for contact dermatitis). • In vitro tests for delayed hypersensitivity include mitogenic response, lympho-cytotoxicity and IL-2 production.

Question 42

Treatment fortype 4 hypersensitivity

Answer 42

Corticosteroids and other immunosuppressive agents are used in treatment.

Question 43

Mechanism of type 4

Answer 43

Mechanism: • The mechanism includes T lymphocytes and monocytes and/or macrophages. • Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells, recruit and activate monocytes and macrophages, which cause the bulk of the damage • The delayed hypersensitivity lesions mainly contain monocytes and a few T cells.