Alterations in the immune response Flashcards
Role of the immune response
- Defense
- Homeostasis
- Surveillance
Impact of alterations of the immune response
• 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)
Four types of hypersensitivity reactions
- Anaphylactic Reactions
- Cytotoxic/Cytolytic Reactions
- Immune-Complex Reactions
- Delayed Hypersensitivity Reactions
Type I Anaphylactic Reactions only occur in who
Only occur in susceptible people or are sensitized to
specific antigens
First exposure in a Type I Anaphylactic Reaction
IgE antibodies are produced in response to allergen
and bind to mast cells and basophils
Subsequent exposures in a Type I Anaphylactic Reaction
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
Is Type I Anaphylactic Reaction genetic predisposition common or uncommon?
Common
Local Type 1 Anaphylactic Reaction
§ 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)
Systemic Type 1 Anaphylactic Reaction
§ 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)
Neurological Clinical Manifestations of systemic anaphylactic reactions
Headache
Dizziness
Paresthesia
Feeling of impending doom
Integumentary Clinical Manifestations of systemic anaphylactic reactions
Pruritus
Angioedema
Erythema
Urticaria
Respiratory Clinical Manifestations of systemic anaphylactic reactions
Hoarseness Coughing Sensation of narrowed airway Wheezing Stridor Dyspnea Tachypnea Respiratory arrest
Cardiovascular Clinical Manifestations of systemic anaphylactic reactions
Hypotension
Dysrhythmias
Tachycardia
Cardiac arrest
Gastrointestinal Clinical Manifestations of systemic anaphylactic reactions
Cramping Abdominal Pain Nausea Vomiting Diarrhea
Atopic Reactions
Common – 20% of population are ‘atopic’ – inherited tendency to become sensitive to environmental allergens
Allergic rhinitis aka ‘hay fever’
most common; seasonal or perennial - air born allergens – dust, dander mold, pollens etc.; targets URI – rhinorrhea, pruritus, sneezing, lacrimation, local tissue edema; antihistamines
Asthma
characterized by bronchoconstriction and
inflammation – dyspnea, wheeze, tightness, sputum
Types of atopic reactions
Atopic dermatitis (eczema)
Urticaria (hives)
Angioedema
Atopic dermatitis (eczema)
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
Urticaria (hives)
‘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
Angioedema
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
TYPE II CYTOTOXIC AND
CYTOLYTIC REACTIONS
§ Direct binding of antibodies (IgG and IgM) to an antigen in the cell surface
§ Antigen-antibody complexes activates the complement system
Rapid tissue destruction in type 2 reactions by:
- Cytolysis d/t complement cascade
2. Phagocytosis
Target cells in Type 2 reactions
Erythrocytes, platelets, leukocytes
Antigens involved in a type 2 reaction
ABO blood group, Rh factor, drugs
Examples of Type II cytotoxic and cytolytic reactions
• 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)
TYPE III IMMUNE-COMPLEX
REACTIONS
§ 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)
Severe type III reactions are associated with…
autoimmune disorders such as SLE, RA, glomerulonephritis.
Type IV Delayed hypersensitivity reactions
§ Cell mediated immune response
§ Sensitized T lymphocytes attack antigens or release cytokines to attract macrophages which destroy tissue
§ Takes 24-28 hours to occur
Examples of Type IV Delayed hypersensitivity reactions
§ Contact dermatitis
§ Hypersensitivity reactions to bacterial, fungal and viral infections;
§ Transplant reactions
§ Some drug sensitivities
Contact Dermatitis
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
Acute Contact Dermatitis
§ Lesions – erythematous and edematous with papules, vesicles and bullae
§ Very pruritic, may burn/sting
Chronic Contact Dermatitis
§ Lesions resemble atopic dermatitis –thickened, scaly, lichenfication
§ Contact dermatitis is localize to area exposed vs. atopic dermatitis is typically widespread
Example of Microbial Hypersensitivity Reactions
Tuberculosis (TB) (tubercle bacillus)
Tuberculosis
§ 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
