Alterations in the immune response

Question 1

Role of the immune response

Answer 1

1. Defense
2. Homeostasis
3. Surveillance

Question 2

Impact of alterations of the immune response

Answer 2

• Impacts ability to fight off stressors (disease, infection)
• Impacts healing
• Can result in overreaction in the immune system that
can damage the body (hypersensitivity reaction)
• Can result in the body attacking itself (autoimmune
disorders)

Question 3

Four types of hypersensitivity reactions

Answer 3

1. Anaphylactic Reactions
2. Cytotoxic/Cytolytic Reactions
3. Immune-Complex Reactions
4. Delayed Hypersensitivity Reactions

Question 4

Type I Anaphylactic Reactions only occur in who

Answer 4

Only occur in susceptible people or are sensitized to

specific antigens

Question 5

First exposure in a Type I Anaphylactic Reaction

Answer 5

IgE antibodies are produced in response to allergen

and bind to mast cells and basophils

Question 6

Subsequent exposures in a Type I Anaphylactic Reaction

Answer 6

Allergen links to Ig E antibodies on mast cells and
basophils and trigger degranulation releasing potent
chemical mediators (Table 16-8) that target organs and
cause symptoms

Question 7

Is Type I Anaphylactic Reaction genetic predisposition common or uncommon?

Answer 7

Common

Question 8

Local Type 1 Anaphylactic Reaction

Answer 8

§ i.e. – ‘wheal & flare’ reaction – cutaneous reaction -
pale wheal (pink, raised, edema, pruritus) surrounded
by flare (hyperemia); occurs in minutes – hours, not
dangerous – mosquito bite
§ Antihistamines (topical, oral)

Question 9

Systemic Type 1 Anaphylactic Reaction

Answer 9

§ i.e. – anaphylaxis - systemic release of chemical
mediators – occurs within minutes, life threatening d/t
bronchial constriction, airway obstruction, vascular
collapse (shock)
§ SC epinephrine to full circulatory support (IV fluids,
oxygen, vasopressor therapy)

Question 10

Neurological Clinical Manifestations of systemic anaphylactic reactions

Answer 10

Headache
Dizziness
Paresthesia
Feeling of impending doom

Question 11

Integumentary Clinical Manifestations of systemic anaphylactic reactions

Answer 11

Pruritus
Angioedema
Erythema
Urticaria

Question 12

Respiratory Clinical Manifestations of systemic anaphylactic reactions

Answer 12

Hoarseness
Coughing
Sensation of narrowed airway
Wheezing
Stridor
Dyspnea
Tachypnea
Respiratory arrest

Question 13

Cardiovascular Clinical Manifestations of systemic anaphylactic reactions

Answer 13

Hypotension
Dysrhythmias
Tachycardia
Cardiac arrest

Question 14

Gastrointestinal Clinical Manifestations of systemic anaphylactic reactions

Answer 14

Cramping
Abdominal Pain
Nausea
Vomiting
Diarrhea

Question 15

Atopic Reactions

Answer 15

Common – 20% of population are ‘atopic’ – inherited tendency to become sensitive to environmental allergens

Question 16

Allergic rhinitis aka ‘hay fever’

Answer 16

most common; seasonal or perennial - air born allergens – dust, dander mold, pollens etc.; targets URI – rhinorrhea, pruritus, sneezing, lacrimation, local tissue edema; antihistamines

Question 17

Asthma

Answer 17

characterized by bronchoconstriction and

inflammation – dyspnea, wheeze, tightness, sputum

Question 18

Types of atopic reactions

Answer 18

Atopic dermatitis (eczema)
Urticaria (hives)
Angioedema

Question 19

Atopic dermatitis (eczema)

Answer 19

pattern – exacerbation and remissions; generalized lesions; vasodilation, edema, vesicle formation; pruritus, r/f infection d/t skin breakdown; topical corticosteroids, bleach baths, hydration of skin

Question 20

Urticaria (hives)

Answer 20

‘wheals & flare’; vary in location/size/shape; develops rapidly after exposure; lasts minutes to hours; histamine – vasodilation – erythema; also cause pruritus; flaring – dilation of blood vessels

Question 21

Angioedema

Answer 21

localized cutaneous lesion similar to urticaria in the deep layers of the skin and submucosa; target eyelids, lips, tongue, larynx, hands, feet, GI tract, genitalia; starts in face then airways then elsewhere; histamine causes ++ edema; no welts; skin has reddish hue; burn/itch/sting; GI tract – and pain; rapid onset or over hours and last about 24 hours

Question 22

TYPE II CYTOTOXIC AND

CYTOLYTIC REACTIONS

Answer 22

§ Direct binding of antibodies (IgG and IgM) to an antigen in the cell surface
§ Antigen-antibody complexes activates the complement system

Question 23

Rapid tissue destruction in type 2 reactions by:

Answer 23

1. Cytolysis d/t complement cascade

2. Phagocytosis

Question 24

Target cells in Type 2 reactions

Answer 24

Erythrocytes, platelets, leukocytes

Question 25

Antigens involved in a type 2 reaction

Answer 25

ABO blood group, Rh factor, drugs

Question 26

Examples of Type II cytotoxic and cytolytic reactions

Answer 26

• Transfusion reactions (ABO incompatibility, Rh incompatibility) agglutination, blocking small vessels requiring overuse of existing clotting factors causing bleeding; agglutinated cells are phagocytized by neutrophils and and macrophages; complement attaches to the antigen – cytolysis – causes release of Hgb into urine and plasma – cytotoxic reaction – vascular spasms kidneys d/t blockage in renal tubules - ARF • Autoimmune and drug related hemolytic anemias • Leukopenia, thrombocytopenia, erythroblastosis fetalis (hemolytic disease of the new born) • Goodpasture’s Syndrome – targets basement membranes of lungs (alveolar – pulmonary hemorrhage) and kidneys (glomerular – glomerulonephritis)

Question 27

TYPE III IMMUNE-COMPLEX | REACTIONS

Answer 27

§ Damage is caused by antigen-antibody complexes formed from soluble antigens and IgG and IgM § Too small to be removed by phagocytes § Deposited in tissue or small blood vessels § Complement, release of chemotactic factors – inflammation and destruction of involved tissues § Local or systemic § Immediate or delayed § Manifestations vary based on location (most commonly – kidneys, skin, lungs, joints, blood vessels)

Question 28

Severe type III reactions are associated with...

Answer 28

autoimmune disorders such as SLE, RA, glomerulonephritis.

Question 29

Type IV Delayed hypersensitivity reactions

Answer 29

§ Cell mediated immune response § Sensitized T lymphocytes attack antigens or release cytokines to attract macrophages which destroy tissue § Takes 24-28 hours to occur

Question 30

Examples of Type IV Delayed hypersensitivity reactions

Answer 30

§ Contact dermatitis § Hypersensitivity reactions to bacterial, fungal and viral infections; § Transplant reactions § Some drug sensitivities

Question 31

Contact Dermatitis

Answer 31

llergic contact dermatitis § Skin is exposed to substance that combine with epidermal proteins and this substance becomes antigenic § Over 7-14 days memory cells for the antigen form § With subsequent exposure, the sensitized person develops eczema skin lesions in 24-28 hours § Metals (nickel, mercury); rubber compounds; catechols in poison ivy/oak/sumac; cosmetics; dyes

Question 32

Acute Contact Dermatitis

Answer 32

§ Lesions – erythematous and edematous with papules, vesicles and bullae § Very pruritic, may burn/sting

Question 33

Chronic Contact Dermatitis

Answer 33

§ Lesions resemble atopic dermatitis –thickened, scaly, lichenfication § Contact dermatitis is localize to area exposed vs. atopic dermatitis is typically widespread

Question 34

Example of Microbial Hypersensitivity Reactions

Answer 34

Tuberculosis (TB) (tubercle bacillus)

Question 35

Tuberculosis

Answer 35

§ Invasion of lung tissue by tubercle bacillus – organism is not damaging to lung tissue but antigenic material released from it reacts with T lymphocytes causing a cell mediated immune response § Causes caseous necrosis of the lung § After initial exposure –memory cells remain § Re-exposure to tubercle bacillus of purified protein can cause delayed hypersensitivity reaction § This is the basis for purified protein derivative (PPD) TB skin test which yields results in 48-72 hours after the subdermal injection