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SMIT Pathology > Chapter 2: Immunity > Flashcards

Chapter 2: Immunity Flashcards

1
Q

Effect of stress on the body

A

Contribute directly to
- The development or exacerbation of disease
- Negative behaviors such as smoking and drug abuse

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2
Q

General Adaptation Syndrome

A

Cluster of systemic manifestations that represent an attempt to cope with a stressor.

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3
Q

Alarm Stage of General Adaptation Syndrome

A

Initial reaction

Sympathetic nervous system stimulation -> release of catecholamines and cortisol - the fight-or-flight response

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4
Q

Resistance Stage of General Adaptation Syndrome

A
  • Adaptation stage - Cortisol levels and the sympathetic nervous system return to normal
  • Limit the stressor
  • Stress management techniques(e.g.meditation and relaxation) can assist in the desensitization process.
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5
Q

Exhaustion Stage of General Adaptation Syndrome

A
  • Adaptation failing - the body becomes depleted and damage may appear as homeostasis can no longer be maintained
  • Disease develops
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6
Q

Local Adaptation Syndrome

A

Localized version of the general adaptation syndrome.Restricted to one location.

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7
Q

Describe the coping mechanism of local adaptation syndrome

A
  • Ability to deal with the stressor
  • Influenced bygenetics, age, gender, life experiences, dietary status, and social support
  • Including: adaptive coping strategies and maladaptive coping strategies
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8
Q

Adaptive Coping Strategies

A

physical activity, adequate sleep, optimal dietary status, relaxation, distraction, and biofeedback

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9
Q

Maladaptive coping strategies

A

smoking, consuming alcohol or drugs, and overeating

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10
Q

Physiological response to stress

A

Fight-or-flight response

Result from activation of the sympathetic and the endocrine systems

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11
Q

Key characteristics of the Immune system

A
  • Self - regulated
  • Self - limiting
  • Must be able to distinguish self from non-self
  • The ability to recognize and respond to a foreign agent, or antigen
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12
Q

Function of the immune system

A

responsible for protecting the body against an array of microorganisms (e.g., bacteria, viruses, fungi, protozoans, and prions) as well as removing damaged cells and destroying cancer cells.

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13
Q

First line of Defense

A
  • Includes physical and chemical barriers that indiscriminately protect against all invaders (nonspecific immunity).
  • Nonspecific - Does NOT distinguish between pathogens
  • But distinguishes self from non-self
  • Includes
    Skin and mucous membranes
    Chemicals eg., hydrochloric acid in the stomach
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14
Q

Second life of defenses

A
  • Responds to antigens that penetrate the first line
  • Inflammatory response
    1. Pyrogens
    2. Interferons
    3. Complement proteins
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15
Q

What is the inflammatory reaction

A
  • characterized by erythema (redness), edema (swelling), heat, and pain at the site of injury
  • Triggered by mast cells
  • Process: Vasoconstriction -> vasodilatation -> Leukocyte migration -> Phagocytosis of pathogens
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16
Q

Pyrogens

A
  • Fever producing molecules
  • Produced my macrophages that have been exposed by bacteria
  • Create an unpleasant environment for bacterial growth
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17
Q

Interferons

A
  • Proteins released from virus infected cells
  • Bind to nearby uninfected cellswhich release an enzyme that prevents viral replication
  • When the virus infects the cells they are unable to replicate
  • Interferons do not protect cells already infected by a virus, but rather stop the spread of the virus to new cells.
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18
Q

Complement Proteins

A
  • Plasma proteins that enhance the action of antibodies
  • Circulate in the blood in an inactive form but gets activated by foreign substances that invade the body.
  • Play a role in the immune and inflammatory response
  • They form a membrane attack complex which attacks and kill the bacteria.
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19
Q

Third line of defense

A
  • Specific
  • Develops over time
  • Uses memory system
  • Distinguishes self from non-self AND between pathogens
  • Includes
    T cells: cell mediated immunity
    B cells: humoral (antibody) mediated immunity
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20
Q

Acquired Immunity

A
  • The immunity that is not present at birth but acquired after that
  • Includes two types: active immunity vs. passive immunity
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21
Q

Active immunity

A
  • Sources include having the disease and vaccinations
  • Long lasting but takes a few days to become effective
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22
Q

Passive immunity

A
  • Sources include the maternal-fetal transfer of immunoglobulins and breastfeeding
  • Short lasting
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23
Q

What are alterations in immunity?

A
  • Hypersensitivity
  • Autoimmune
  • Immunodeficiency
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24
Q

Autoimmune

A

mistakes self as non-self
Eg., Systemic Lupus Erythematosus (SLE)

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25
Q

Immunodeficiency

A

inadequate immune reaction
Eg., Acquired Immunodeficiency Syndrome (AIDS)

26
Q

Hypersensitivity

A

inflated immune response to a foreign substance

27
Q

Type I hypersensitivity - IgE mediated

A
  • Produces an immediate response
  • Local or systemic
  • Allergen activate helper T cells that stimulates IgE production by the B- cells.
  • The IgE antibodies bind to mast cells.
  • At next exposure, the antigen binds with the surface IgE, releasing mediators and triggering the complement system

Examples:
hay fever, food allergies, and anaphylaxis

  • Treatment includes epinephrine, antihistamines, corticosteroids, and desensitizing injections
28
Q

Type II Hypersensitivity Reaction

A
  • Generally involves the destruction of a target cell by an antibody-directed, cell-surface antigen.
  • IgG or IgM type antibodies that react to foreign tissue of cells and activate the complement system.
  • Lysis of cells occurs because of the activation of the complement followed by phagocytosis.
  • Usually immediate responses

Eg: Blood transfusion reaction and erythroblastosis fetalis

  • Treatment includes ensuring blood compatibility and administering medication to prevent maternal antibody development
29
Q

Type III Hypersensitivity - Immune Complex mediated

A
  • Circulating antigen-antibody complexes accumulate and are deposited in the tissues like kidneys, joints, skin, and blood vessels.
  • Triggers the complement system and inflammation

Eg., Autoimmune conditions (e.g. systemic lupus erythematosus)

  • Treatment is disease specific
30
Q

Type IV Delayed Hypersensitivity Reaction

A
  • Cell-mediated rather than antibody-mediated
    Involves a delayed processing of the antigen by macrophages
  • Once processed, the antigen is presented to the T cells, resulting in the release of lymphokines, causing inflammation and antigen destruction.

Examples: tuberculin skin testing, transplant reactions, and contact dermatitis

  • Treatment: disease specific
31
Q

Types of transplants

A

Allogenic
Syngenic
Autologous
Xenogenic

32
Q

Allogernic

A

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

33
Q

Syngenic

A

donor and recipient are identical twins

34
Q

Autologous

A

donor & recipient are the same person; most successful

35
Q

Xenogenic

A

transplants use tissue from another species. e.g., pig heart valves to replace diseased valves.

36
Q

Hyperacute transplant reaction

A
  • Immediate or 3 days after transplant
  • Activation complement system -> tissue necrosis
37
Q

Acute transplant reaction

A
  • Most common - occurs between 4 days and 3 months after transplant
  • Cell mediated rejection - treatable
  • Manifestations: fever, erythema, edema, site tenderness, and impaired function of transplanted organ
38
Q

Chronic transplant reactions

A
  • Occurs 4 months to years after transplant
  • Likely antibody-mediated response
  • Antibodies and complements deposit in vessel walls of transplanted tissue, resulting in ischemia
39
Q

Host vs. Graft Disease

A
  • Host fights the graft
  • The recipient’s immune system attempts to eliminate the donor cell
40
Q

Graft vs. Host Disease

A
  • Graft fights the host
  • Frequent and potentially fatal complications of bone marrow transplants
  • Occurs when immunocompetent cells recognize host tissue as foreign and mount a cell-mediated immune response
  • Host is usually immunocompromised and unable to fight graft cells, and the host’s cells are destroyed
41
Q

Describe autoimmune disorders

A
  • 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
42
Q

Known characteristics of Autoimmune disorders

A
  • Genetics
  • More prevalent in females
  • Onset is frequently associated with an abnormal stressor, either physical or psychological
  • Are frequently progressive relapsing-remitting disorders characterized by periods of exacerbation and remission

E.g., SLE, Rheumatoid arthritis, etc

43
Q

Describe Systemic Lupus Erythematosus (SLE)

A
  • Chronic inflammatory, autoimmune condition affecting connective tissues.
  • Remission and exacerbations-stressors tend to trigger
  • Disease progression varies from mild to severe
  • 9x more often in women than in men
44
Q

Etiology of SLE

A
  • unclear
  • Proposed: B cells are activated to produce autoantibodies and autoantigens that combine to form immune complexes, which attack the body’s own tissues
45
Q

Diagnostic Criteria of SLE

A
  1. Butterfly rash over the cheeks of the face
  2. Skin rash of patchy redness with hyperpigmentation and hypopigmentation that can cause scarring
  3. Photosensitivity
  4. Mucous membrane ulcers
  5. Arthritis
  6. Pleuritis or pericarditis
  7. Renal abnormalities
  8. Brain irritation
  9. Blood abnormalities
  10. Immunologic disorder
  11. Antinuclear/Anti-DNA antibody
46
Q

Diagnosis of SLE

A

X-rays, elevated sedimentation rate, c-reactive protein, and blood testing for complications

*Prognosis improves with early diagnosis and treatment

47
Q

Treatment of SLE

A
  • No cure
  • Stress management and health promotion behaviors
  • Pharmacological
    NSAIDs, corticosteroids, and immunosuppressant
  • Plasmapheresis
48
Q

Describe immunodeficiency

A
  • Diminished or absent immune response
  • Opportunistic infections which can be difficult to treat successfully and can become life threatening.
  • May be acute or chronic
  • Classifications: primary vs. secondary
49
Q

Primary Immunodeficiency

A

Detect with the immune system

50
Q

Secondary immunodeficiency

A

Underlying disease suppressing the immune system

51
Q

Describe AIDS

A
  • Acquired immunodeficiency syndrome (AIDS) is a deadly, sexually transmitted disease caused by the human immunodeficiency virus (HIV), a retrovirus.
52
Q

What cell is infected in AIDS?

A

CD4+ T cells

53
Q

Differentiate HIV vs. AIDS

A
  • HIV isthe virus which attacks the T-cells in the immune system
  • AIDS isthe syndrome which appears in advanced stages of HIV infection.
54
Q

Differentiate HIV vs. AIDS

A
  • HIV isa virus that attacks the T-cells in the immune system
  • AIDS isa syndrome that appears in the advanced stages of HIV infection.
55
Q

Symptoms of AIDS

A

Chills, fever, sweats, swollen lymph glands, weakness, and weight loss

56
Q

Diagnosis of AIDS

A
  • CD4 cell count drops below 200 cells/mm3
  • Developing opportunistic illnesses:
    Infections (bacterial, viral, etc)
  • Secondary neoplasms
57
Q

AIDS Treatment

A
  • No cure
  • Combination therapy works best - Highly Active Antiretroviral Therapy (HAART)
  • 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
58
Q

HIV Transmission

A
  • Sexual contact by:
    1. direct inoculation into the bloodstream
    or
    2. Infection of host mucosal dendritic cells or CD4+ T cells
  • Parenteral inoculation: IV drug users
  • Vertical transmission:
    1.Transplacental in utero
    2. During delivery
    3. Ingestion of breast milk
59
Q

Stage 1: Acute HIV infection

A
  • Within2 to 4 weeksafter infection with HIV, a flu-like illness
  • This is the body’s natural response to infection
60
Q

Stage 2: Clinical latency (HIV inactivity or dormancy)

A
  • asymptomatic HIV infectionorchronic HIV infection
  • During this phase, HIV is still active but reproduces at very low levels
  • At the end of this phase, viral load starts to go up and the CD4 cell count begins to go down ->
    Progress to stage 3
61
Q

Stage 3: AIDS

A
  • The most severe phase of HIV infection
  • Prone to opportunistic illnesses
  • Without treatment -> survive about 3 years

SMIT Pathology (4 decks)

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