Chapter 2 Flashcards
1
Q
What are the stages of General Adaptation Syndrome?
A
1. Alarm Initial reaction Sympathetic nervous system 2. Resistance Adaptation Limit stressor 3. Exhaustion Adaptation failing Disease develops
2
Q
What is local adaptation syndrome?
A
- Local version of the general adaptation syndrome
- Body’s attempt to minimize the damage of the stress to a small location
3
Q
Facts about the immune system
A
- Self-regulated
- Self-limiting
- Must be able to distinguish self from nonself
- Two major actions: defending and attacking
4
Q
What are innate defense barriers?
A
-Nonspecific
-Immediate response
-Distinguish self from nonself
-Do not distinguish between
pathogens
-Include
-Skin and mucous
membranes
-Chemicals (tears,
stomach acid)
5
Q
What is inflammation?
A
-Inflammation is an automatic non-specific response to cell injury that:
-Neutralizes harmful
agents
-Dilutes and destroys
damaged cells
-Removes dead tissue &
microbes
6
Q
What is the inflammatory response?
A
- Vascular reaction.
- Triggered by mast cells.
- Manifestations include erythema (redness), edema (swelling), warmth, heat, and pain.
- due to infection
7
Q
What cells are involved with inflammation?
A
Epithelial Cells
- Line the blood vessels
- Release inflammatory mediators
- Regulate immune cell proliferation
- Promote healing through angiogenesis
Platelets
- When activated release over 300 chemicals
- Many of these chemicals promote inflammation
8
Q
What are leukocytes?
A
White blood cell which is a major component of inflammatory response
9
Q
What are the 3 granulocytes?
A
- Neutrophils
- Eosinophils
- Basophils
10
Q
Neutrophils
A
Phagocytosis of bacteria and these are the first to arrive with inflammation
11
Q
Eosinophils
A
Toxic to parasitic worms (eg. role of allergies)
12
Q
Basophils
A
Histamine release with allergic reactions
13
Q
What are the stages of acute inflammation?
A
- vascular stage
2. cellular stage
14
Q
Vascular stage of inflammation
A
Changes that occur in the blood vessels immediately after injury
-Prostaglandins and leukotrienes affect blood vessels.
-Arterioles capillaries and venules dilate.
-Increasing blood flow to
injured area
-Redness and warmth
result
-Capillaries become more permeable.
-Allowing exudate to
escape into the tissues
-Swelling, warmth and
pain result
15
Q
Cellular stage of inflammation
A
White blood cells enter the injured tissue:
- Destroying infective organisms
- Removing damaged cells
- Releasing more inflammatory mediators to control further inflammation and healing
- clotting can occur
16
Q
What is the acute-phase response to inflammation?
A
Leukocytes release interleukins and tumor necrosis factor
-Affect thermoregulatory
center --> fever
-Affect central nervous
system -- >lethargy
-Skeletal muscle
breakdown
-flu like symptoms
-Liver makes fibrinogen and C-reactive protein
-Facilitate clotting
-Bind to pathogens
-Moderate inflammatory
responses
- a lab can be drawn
17
Q
What is the WBC to inflammation?
A
- Inflammatory mediators cause WBC production
- WBC count rises
- Immature neutrophils (bands) released into blood
- the demand is exceeding the supply which is a systemic infection because immature cells are being sent out to fight and the ability to fight it is decreased
18
Q
What is chronic inflammation?
A
- Self perpetuating lasting weeks, months or years.
- Macrophages accumulate in the damaged area and keep releasing inflammatory mediators.
19
Q
What are pyrogens?
A
- a type of protein
- Fever-producing molecules
- Produced by macrophages
- Create an unpleasant environment for bacterial growth
- Severe fever—life-threatening
20
Q
What are complement proteins?
A
- Plasma proteins that enhance antibodies
- Activated by antigens
- Play a role in the immune and inflammatory response
21
Q
What are adaptive defenses?
A
-Specific
-Develop over time
-Use memory system
-Distinguish self from nonself and between pathogens
-Include
-T cells: cell-mediated
immunity
-B cells: humoral
immunity
22
Q
How does cellular immunity begin?
A
t cells recognize antigen
23
Q
Where are t cells produced?
A
in the bone marrow
24
Q
Where do t cells mature?
A
in the thymus
25
What are the two types of t cells?
t helper & t suppressor (effector/killer)
26
How does humoral immunity begin?
b cells encounter an antigen
27
Where in b cells mature?
bone marrow
28
What are the 2 types of B cells
memory cells and immunoglobulin-secreting cells
29
When are antibodies produced?
72 hours after encounter with antigen
30
What are the 2 types of acquired immunity?
Active and passive
31
What is Active immunity?
- Acquired by having the disease (i.e., prior antigen exposure) and by vaccinations
- Long lasting but takes a few days to become effective
32
What is passive immunity?
- Receiving antibodies from external sources: maternal–fetal transfer of immunoglobumins and breastfeeding
- Short lasting
33
What are the 3 alterations in . immunity?
1. Hypersensitivity
2. Autoimmune
3. Immunodeficiency
34
What is hypersensitivity immunity?
Exaggerated immune response to a foreign substance
35
What is autoimmune immunity?
mistakes self as nonself
36
what is immunodeficiency immunity?
Inadequate immune reaction
37
What is hypersensitivity?
- Inflated response to antigen
- Leads to inflammation, which destroys healthy tissue
- Can be immediate or delayed
38
Type 1 hypersensitivity
Type I, IgE mediated
-Produces an immediate response.
-Local or systemic.
-Allergen activates T-helper cells that stimulate B cells to produce IgE.
-IgE coats mast cells and basophils, sensitizing them to the allergen.
-At next exposure, the antigen binds with the surface IgE, releasing mediators and triggering the complement system.
-Repeated exposure to large doses of allergen is necessary to cause this response.
-Examples:
-Hay fever, food allergies,
and anaphylaxis
-Treatment includes epinephrine, antihistamines, corticosteroids, and desensitizing injections.
39
type 2 hypersensitivity
Type II, cytotoxic hypersensitivity reaction
-IgG or IgM type antibodies bind to antigen on individual’s own cells.
-Antigen may be intrinsic or extrinsic.
-Recognition of these cells by macrophages triggers antibody production.
-Lysis of cells occurs because of the activation of the complement and by phagocytosis.
-Usually immediate responses.
Examples:
-Blood transfusion
reaction and
erythroblastosis fetalis
-Treatment includes ensuring blood compatibility (transfusion) and administering medication to prevent maternal antibody development (Rho[D]).
40
type 3 hypersensitivity
Type III, immune complex–mediated hypersensitivity reaction
-Circulating antigen–antibody complexes accumulate and are deposited in the tissue.
-Triggers the complement system, causing inflammation.
-Example:
-Autoimmune conditions
(e.g., systemic lupus
erythematosus)
-Treatment is disease specific.
41
type 4 hypersensitivity
Type IV, delayed hypersensitivity reaction
-Cell-mediated rather than antibody-mediated involving the T cells.
-Antigen presentation results in cytokine release, leading to inflammation.
-Causes severe tissue
injury and fibrosis
-Examples:
-Tuberculin skin testing,
transplant reactions, and
contact dermatitis
-Treatment is disease specific.
42
What are the four categories for transplants?
1. Allogenic
2. Syngenic
3. Autologous
4. Xenogenic
43
What is Allogenic transplant?
donor and recipient are related or unrelated, but share similar tissue types
44
What is syngenic transplant?
donor and recipient are identical twins
45
What is autologous transplant?
donor and recipient are the same person; most successful
46
what is Xenogenic transplant?
use of tissue from another species
47
What are the 3 patterns of transplant reactions?
1. hyperacute tissue rejection
2. acute tissue rejection
3. chronic tissue rejection
48
What is hyperacute tissue rejection?
- Immediate or three days after transplant
- Due to the complement system
- Tissue becomes permanently necrotic
49
What is acute tissue rejection?
- Most common
- Treatable
- Occurs between four days and three months after transplant
- Manifestations: fever, erythema, edema, site tenderness, and impaired function of transplanted organ
50
what is chronic tissue rejection?
- Occurs four months to years after transplant.
- Likely antibody-mediated response.
- Antibodies and complements deposit in vessel walls of transplanted tissue, resulting in ischemia.
51
What is Host vs. graft disease?
Host fights the graft.
| The recipient’s immune system attempts to eliminate the donor cells.
52
What is graft vs. host disease?
- Graft fights the host.
- Frequent and potentially fatal complication of bone marrow transplants.
- Occurs when immunocompetent fatal cells recognize host tissue as foreign and mount a cell-mediated immune response.
- The host is usually immunocompromised and unable to fight graft cells; the host’s cells are destroyed
- Treatment: Immunosuppressive therapy
53
What happens with autoimmune disorders?
- Immune system loses the ability to recognize self.
- Defenses are directed against host.
- Can affect any tissue.
- The mechanism that triggers this response is not clear.
54
What are known characteristics of autoimmune disorders?
- Genetics plays a role.
- More prevalent in females.
- Onset is frequently associated with an abnormal stressor, physical or psychological.
- Are frequently progressive relapsing-remitting disorders characterized by periods of exacerbation and remission.
55
What is Systemic Lupus Erythematosus?
-Chronic inflammatory autoimmune condition.
-May affect connective tissue of any body organ.
-Remission and exacerbations
—stressors tend to trigger.
-Disease progression varies from mild to severe.
56
How is systemic lupus diagnosed?
11 criteria, X-rays, elevated sedimentation rate,
| C-reactive protein, urinalysis, echocardiogram, and blood test for complications
57
What is the treatment for lupus?
-No cure—only symptom management
-Stress management and health promotion behaviors
-Pharmacological
-NSAIDs, antimalarials,
corticosteroids,
immunosuppressants
-Plasmapheresis
-Prognosis improves with early diagnosis and treatment.
58
What is immunodeficiency (Aids)?
- Diminished or absent immune response
- Renders the person susceptible to disease normally prevented
- Opportunistic infections
- May be acute or chronic
- Classifications
- Primary (born)
- Secondary (infection)
59
How does aids progress?
-Asymptomatic phase.
-Virus is reproducing,
usually for several years.
-Infections begin as the viral number rises, destroying the CD4.
-Progression takes three forms.
-Immunodeficiency
-Autoimmunity
-Neurological dysfunction
60
What is HIV composed of?
2 strands of viral RNA
3 enzymes
reverse transcriptase
integrase
protease
61
What are the 4 clinical manifestations of AIDs?
1. HIV wasting syndrome (fever, diarrhea, & weight loss)
2. Generalized lymphadenopathy
3. Opportunistic infections
4. malignancy
62
What are examples of opportunistic infections that occur with AIDS?
1. Pneumocystis carinii pneumonia (PCP)
2. Candidiasis “Thrush”
3. Cytomegalovirus (CMV)
4. Tuberculosis
63
What are examples of malignancies that occur with aids?
1. Kaposi’s Sarcoma
2. Non-Hodgkin’s Lymphoma
3. Cervical carcinoma
64
What is AIDS diagnostic testing used for?
used for diagnosis and for determining progression
65
What are the tests for AIDS and what do they measure?
* HIV antibody
- Rapid test
- Home test
- Polymerase chain reaction
* Measures amount of HIV DNA or viral load
* Good for infants and infected mothers
66
What are the 2 AIDS classification systems?
Two systems, one based on lab findings and the other based on clinical manifestations
67
What laboratory findings will you see with Aids?
Laboratory findings—CD4 cell count
Category 1: > 500 cells/μL
Category 2: 200–499
Category 3: < 200
68
What clinical presentations will you see with AIDS?
Clinical presentation
Category A: asymptomatic
Category B: some less serious manifestations of immune deficiency
Category C: AIDS-defining illnesses present
69
What are the treatments for AIDS?
-No cure.
-Combination therapy works best.
*Highly active antiretroviral
therapy
-May have to change regimen due to viral adaptation.
-Other medicines and vaccines will be used to prevent opportunistic infections as needed.
-Vaccinations.
- Transmission prevention.
70
Who are the people primarily at risk 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
71
What are 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
