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Pathophysiology and Pharmacology > Alterations in the immune response > Flashcards

Alterations in the immune response Flashcards

1
Q

Role of the immune response

A
  1. Defense
  2. Homeostasis
  3. Surveillance
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2
Q

Impact of alterations of the immune response

A

• 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)

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3
Q

Four types of hypersensitivity reactions

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

Type I Anaphylactic Reactions only occur in who

A

Only occur in susceptible people or are sensitized to

specific antigens

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5
Q

First exposure in a Type I Anaphylactic Reaction

A

IgE antibodies are produced in response to allergen

and bind to mast cells and basophils

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6
Q

Subsequent exposures in a Type I Anaphylactic Reaction

A

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

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7
Q

Is Type I Anaphylactic Reaction genetic predisposition common or uncommon?

A

Common

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8
Q

Local Type 1 Anaphylactic Reaction

A

§ 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)

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9
Q

Systemic Type 1 Anaphylactic Reaction

A

§ 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)

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10
Q

Neurological Clinical Manifestations of systemic anaphylactic reactions

A

Headache
Dizziness
Paresthesia
Feeling of impending doom

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11
Q

Integumentary Clinical Manifestations of systemic anaphylactic reactions

A

Pruritus
Angioedema
Erythema
Urticaria

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12
Q

Respiratory Clinical Manifestations of systemic anaphylactic reactions

A 
Hoarseness
Coughing
Sensation of narrowed airway
Wheezing
Stridor
Dyspnea
Tachypnea
Respiratory arrest
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13
Q

Cardiovascular Clinical Manifestations of systemic anaphylactic reactions

A

Hypotension
Dysrhythmias
Tachycardia
Cardiac arrest

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14
Q

Gastrointestinal Clinical Manifestations of systemic anaphylactic reactions

A 
Cramping
Abdominal Pain
Nausea
Vomiting
Diarrhea
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15
Q

Atopic Reactions

A

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

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16
Q

Allergic rhinitis aka ‘hay fever’

A

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

17
Q

Asthma

A

characterized by bronchoconstriction and

inflammation – dyspnea, wheeze, tightness, sputum

18
Q

Types of atopic reactions

A

Atopic dermatitis (eczema)
Urticaria (hives)
Angioedema

19
Q

Atopic dermatitis (eczema)

A

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

20
Q

Urticaria (hives)

A

‘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

21
Q

Angioedema

A

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

22
Q

TYPE II CYTOTOXIC AND

CYTOLYTIC REACTIONS

A

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

23
Q

Rapid tissue destruction in type 2 reactions by:

A
  1. Cytolysis d/t complement cascade

2. Phagocytosis

24
Q

Target cells in Type 2 reactions

A

Erythrocytes, platelets, leukocytes

25
Q

Antigens involved in a type 2 reaction

A

ABO blood group, Rh factor, drugs

26
Q

Examples of Type II cytotoxic and cytolytic reactions

A

• 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)

27
Q

TYPE III IMMUNE-COMPLEX

REACTIONS

A

§ 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)

28
Q

Severe type III reactions are associated with…

A

autoimmune disorders such as SLE, RA, glomerulonephritis.

29
Q

Type IV Delayed hypersensitivity reactions

A

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

30
Q

Examples of Type IV Delayed hypersensitivity reactions

A

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

31
Q

Contact Dermatitis

A

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

32
Q

Acute Contact Dermatitis

A

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

33
Q

Chronic Contact Dermatitis

A

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

34
Q

Example of Microbial Hypersensitivity Reactions

A

Tuberculosis (TB) (tubercle bacillus)

35
Q

Tuberculosis

A

§ 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

Pathophysiology and Pharmacology (17 decks)

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