Chapter 2Body Defenses

Stress

• Universal experience

• Result of both positive and negative experiences

• Important to understand

• Response to change

Stress Adaptation

• Hans SeyleoObserved bodily changes produced by

stress• General Adaptation Syndrome• Local Adaptation Syndrome• Influenced by several factorsonatural reserve, time, genetics, age,

gender, health status, nutrition, sleep–wake cycles, hardiness, and psychosocial factors.

Physiological Response to Stress

• Fight-or-flight response• Result from activation of the sympathetic and the

endocrine systems• Includes increased heart rate, increased

respirations, diaphoresis, increased blood flow to muscles, increased muscle strength, increased mental alertness, increased fat and protein and fat mobilization, increased glucose availability, and decreased inflammation

Stages of General Adaptation Syndrome

1. AlarmoInitial reactionoSympathetic

nervous system

2. ResistanceoAdaptationoLimit stressor

3. ExhaustionoAdaptation failingoDisease develops

Local Adaptation Syndrome

• Local version of the general adaptation syndrome

• Body’s attempt to minimize the damage of the stress to a small location

Coping

• Ability to deal with the stressor

• Influenced by – genetics, age, gender, life experiences, dietary

status, and social support

• Adaptive coping strategies include – physical activity, adequate sleep, optimal dietary

status, relaxation, distraction, and biofeedback

• Maladaptive coping strategies include – smoking, consuming alcohol or drugs, and

overeating

Immune System

• Self-regulated

• Self-limiting

• Must be able to distinguish self from non-self

• Antigens

First Line of Defense• Nonspecific

• Distinguishes self from non-self

• Does NOT distinguish between pathogens

• Includes• Skin and mucous membranes

• Chemicals

Second Line of Defense

• Responds to antigens that penetrate the first line

• Includeso Inflammatory responseoPyrogenso Interferons oComplement proteins

Inflammatory Response

• Vascular reaction

• Triggered by mast cells

• Manifestations include erythema, edema, and warmth

Pyrogens

• Fever producing molecules

• Produced my macrophages

• Create an unpleasant environment for bacterial growth

Interferons

• Proteins released from virus infected cells

• Bind to nearby uninfected cells

• The uninfected cells release an enzyme that prevents viral replication

• When the virus infects the cells the are unable to replicate

Complement Proteins

• Plasma proteins that enhance antibodies

• Activated by antigens

• Play a role in the immune and inflammatory response

Third Line of Defense• Specific• Develops over time• Uses memory system• Distinguishes self from non-self AND

between pathogens• IncludesoT cells-cell mediated immunityoB cells-humoral immunity

Acquired Immunity• Active ImmunityoSources include having the disease

and vaccinations oLong lasting but takes a few days to

become effective• Passive ImmunityoSources include maternal-fetal

transfer of immunoglobumins and breastfeeding

oShort lasting

Alterations in Immunity

• Hypersensitivityoinflated immune response to a

foreign substance

• Autoimmuneomistakes self as non-self

• Immunodeficiencyoinadequate immune reaction

Types of HypersensitivityType 1, IgE mediated

oProduces an immediate responseoLocal or systemicoAllergen activate IgE which bind to mast

cellsoAt next exposure, the antigen binds with the

surface IgE, releasing mediators and triggering the complement system

oExamples:ohay fever, food allergies, and anaphylaxis

oTreatment includes epinephrine, antihistamines, corticosteroids, and desensitizing injections

Types of HypersensitivityType II, cytotoxic hypersensitivity reaction

o IgG or IgM type antibodies that react to foreign tissue of cells

o Lysis of blood cells occurs because of the activation of the complement

oUsually immediate responseso Examples:

• Blood transfusion reaction and erythroblastosis fetalis

o Treatment includes ensuring blood compatibility and administering medication to prevent maternal antibody development

Types of Hypersensitivity

Type III, immune complex-mediated hypersensitivity reactionoCirculating antigen-antibody complexes

accumulate and are deposited in the tissueoTriggers the complement system and

inflammationoExample

• Autoimmune conditions (e.g. systemic lupus erythematosus)

oTreatment is disease specific

Types of Hypersensitivity

Type IV, delayed hypersensitivity reactionoCell-mediated rather than antibody-

mediated involving the T cellsoExamples

• tuberculin skin testing, transplant reactions, and contact dermatitis

oTreatment is disease specific

Transplants• Making the best match of tissue antigens is

the core for success• Donor sources may be living or a cadaver• 3 Categories

o Allogenic-donor and recipient are related or unrelated, but share similar tissue types

o Syngenic-donor and recipient are identical twins

o Autologous-donor & recipient are the same person; most successful

Patterns of Transplant Reactions• Hyperacute

o immediate or 3 days after transplanto due to the complement system

• Acuteo most commono treatableo occurs between 4 days and 3 months after transplanto Manifestations: fever, erythema, edema, site

tenderness, and impaired function of transplanted organ

• Chronico occurs 4 months to years after transplanto likely antibody-mediated responseo Antibodies and complements deposit in vessel

walls of transplanted tissue, resulting in ischemia

Transplant Reaction Classifications

• Host vs Graft DiseaseoHost fights the graftoThe recipient’s immune system

attempts to eliminate the donor cells

Transplant Reaction Classifications• Graft v/s Host Disease

o Graft fights the hosto Frequent and potentially fatal complication of

bone marrow transplantso Occurs when immuno-competent fatal cells

recognize host tissue as foreign and mount a cell-mediated immune response

o Host usually immuno-compromised and unable to fight graft cells, and the host’s cells are destroyed

Autoimmune Disorders• Immune system losses the ability to recognize self• Defenses are directed against host• Can affect any tissue• Mechanism that triggers this response is not clear• Known characteristics

o Genetics play a roleo More prevalent in femaleso Onset is frequently associated with an abnormal

stressor, either physical or psychologicalo Are frequently progressive relapsing-remitting

disorders characterized by periods of exacerbation and remission

Systemic Lupus Erythematosus

• Chronic inflammatory condition• Remission and exacerbations-stressors tend to trigger• May affect connective tissue of any body organ• Disease progression varies from mild to severe• More common in women • Cause is unclear, but thought that B cells are activated

to produce autoantibodies and autoantigens that combine to form immune complexes, which attack the body’s own tissues

Systemic Lupus Erythematosus

• Diagnostic criteria (four or more of the following)1. Butterfly rash over the cheeks of the face2. Skin rash of patchy redness with hyperpigmentation

and hypopigmentation that can cause scarring3. Photosensitivity4. Mucous membrane ulcers5. Arthritis6. Pleuritis or pericarditis7. Renal abnormalities8. Brain irritation9. Blood abnormalities10. Immunologic disorder11. Antinuclear antibody

Systemic Lupus Erythematosus• Prognosis improves with early diagnosis and

treatment

• Diagnosiso 11 criteria, X-rays, elevated sedimentation rate, c-

reactive protein, and blood testing for complications

• Treatmento no cureo Stress management and health promotion behaviors

o Pharmacological • NSAIDs, antimalarials, corticosteroids, and

immunosuppressives

o Plasmapheresis

Immunodeficiency

• Diminished or absent immune response• Renders the person susceptible to

disease normally preventedoOpportunistic infections

• May be acute or chronic• ClassificationsoPrimary oSecondary

AIDS

• HIV o parasitic retrovirus that infects CD4 &

macrophages upon entry• Two primary types

o Type I is the most common straino Type 2 is more common in West Africa;

progresses to disease more slowly• In the US, rates rising among women and

African Americans• Transmission

o Blood and bodily fluids

AIDS Progression

• Asymptomatic phaseovirus is reproducing, usually for several

years

• Infections begin as the viral number rise destroying the CD4

• Progression takes three formso ImmunodeficiencyoAutoimmunityoNeurological dysfunction

AIDS Progression

• Diagnostic test (used for diagnosis and determine progression)oHIV antibody

• Rapid test• Home test• Enzyme-linked immunosorbent assay• Followed up with confirmation w/ the Western Blot

assay• Polymerase chain reaction

oMeasures amount HIV DNA or viral loadoGood for infants and infected mothers

AIDS Classification System

• Two systems, one based on lab findings and the other based on clinical manifestations

• Laboratory findingso Category 1: >500 cells/microLo Category 2: 200-499o Category 3: <200

• Clinicalo Category A: asymptomatico Category B: some less serious manifestations of

immune deficiencyo Category C: AIDS defining illnesses present

AIDS Treatment

• No cure

• Combination therapy works bestoHighly Active Antiretroviral Therapy

• May have to change regimen d/t viral adaptation

• Other meds and vaccines will be used to prevent opportunistic infections as needed

• Vaccinations

• Transmission prevention

At Risk Individuals for Immune Dysfunction

• Very young and very old• Poor nutrition• Impaired skin integrity• Circulatory issues• Alterations in normal flora due to antibiotic therapy• Chronic diseases especially diabetes mellitus• Corticosteroid therapy• Chemotherapy• Smoking• Alcohol consumption• Immunodeficiency states

Immune Building Strategies

• Increasing fluid intake

• Eating a well-balanced diet

• Increasing antioxidants and protein intake

• Getting adequate sleep

• Avoiding caffeine and refined sugar

• Spending time outdoors

• Reducing stress