Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Chapter 2 > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are leukocytes?

A

White blood cell which is a major component of inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 3 granulocytes?

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Neutrophils

A

Phagocytosis of bacteria and these are the first to arrive with inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Eosinophils

A

Toxic to parasitic worms (eg. role of allergies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Basophils

A

Histamine release with allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the stages of acute inflammation?

A
  1. vascular stage

2. cellular stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are complement proteins?

A
  • Plasma proteins that enhance antibodies
  • Activated by antigens
  • Play a role in the immune and inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does cellular immunity begin?

A

t cells recognize antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where are t cells produced?

A

in the bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where do t cells mature?

A

in the thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the two types of t cells?

A

t helper & t suppressor (effector/killer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does humoral immunity begin?

A

b cells encounter an antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Where in b cells mature?

A

bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the 2 types of B cells

A

memory cells and immunoglobulin-secreting cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

When are antibodies produced?

A

72 hours after encounter with antigen

30
Q

What are the 2 types of acquired immunity?

A

Active and passive

31
Q

What is Active immunity?

A
  • Acquired by having the disease (i.e., prior antigen exposure) and by vaccinations
  • Long lasting but takes a few days to become effective
32
Q

What is passive immunity?

A
  • Receiving antibodies from external sources: maternal–fetal transfer of immunoglobumins and breastfeeding
  • Short lasting
33
Q

What are the 3 alterations in . immunity?

A
  1. Hypersensitivity
  2. Autoimmune
  3. Immunodeficiency
34
Q

What is hypersensitivity immunity?

A

Exaggerated immune response to a foreign substance

35
Q

What is autoimmune immunity?

A

mistakes self as nonself

36
Q

what is immunodeficiency immunity?

A

Inadequate immune reaction

37
Q

What is hypersensitivity?

A
  • Inflated response to antigen
  • Leads to inflammation, which destroys healthy tissue
  • Can be immediate or delayed
38
Q

Type 1 hypersensitivity

A

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
Q

type 2 hypersensitivity

A

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
Q

type 3 hypersensitivity

A

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
Q

type 4 hypersensitivity

A

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
Q

What are the four categories for transplants?

A
  1. Allogenic
  2. Syngenic
  3. Autologous
  4. Xenogenic
43
Q

What is Allogenic transplant?

A

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

44
Q

What is syngenic transplant?

A

donor and recipient are identical twins

45
Q

What is autologous transplant?

A

donor and recipient are the same person; most successful

46
Q

what is Xenogenic transplant?

A

use of tissue from another species

47
Q

What are the 3 patterns of transplant reactions?

A
  1. hyperacute tissue rejection
  2. acute tissue rejection
  3. chronic tissue rejection
48
Q

What is hyperacute tissue rejection?

A
  • Immediate or three days after transplant
  • Due to the complement system
  • Tissue becomes permanently necrotic
49
Q

What is acute tissue rejection?

A
  • 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
Q

what is chronic tissue rejection?

A
  • 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
Q

What is Host vs. graft disease?

A

Host fights the graft.

The recipient’s immune system attempts to eliminate the donor cells.

52
Q

What is graft vs. host disease?

A
  • 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
Q

What happens with autoimmune disorders?

A
  • 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
Q

What are known characteristics of autoimmune disorders?

A
  • 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
Q

What is Systemic Lupus Erythematosus?

A

-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
Q

How is systemic lupus diagnosed?

A

11 criteria, X-rays, elevated sedimentation rate,

C-reactive protein, urinalysis, echocardiogram, and blood test for complications

57
Q

What is the treatment for lupus?

A

-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
Q

What is immunodeficiency (Aids)?

A
  • 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
Q

How does aids progress?

A

-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
Q

What is HIV composed of?

A

2 strands of viral RNA

3 enzymes
reverse transcriptase
integrase
protease

61
Q

What are the 4 clinical manifestations of AIDs?

A
  1. HIV wasting syndrome (fever, diarrhea, & weight loss)
  2. Generalized lymphadenopathy
  3. Opportunistic infections
  4. malignancy
62
Q

What are examples of opportunistic infections that occur with AIDS?

A
  1. Pneumocystis carinii pneumonia (PCP)
  2. Candidiasis “Thrush”
  3. Cytomegalovirus (CMV)
  4. Tuberculosis
63
Q

What are examples of malignancies that occur with aids?

A
  1. Kaposi’s Sarcoma
  2. Non-Hodgkin’s Lymphoma
  3. Cervical carcinoma
64
Q

What is AIDS diagnostic testing used for?

A

used for diagnosis and for determining progression

65
Q

What are the tests for AIDS and what do they measure?

A
  • HIV antibody
    • Rapid test
    • Home test
    • Polymerase chain reaction
  • Measures amount of HIV DNA or viral load
  • Good for infants and infected mothers
66
Q

What are the 2 AIDS classification systems?

A

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

67
Q

What laboratory findings will you see with Aids?

A

Laboratory findings—CD4 cell count
Category 1: > 500 cells/μL
Category 2: 200–499
Category 3: < 200

68
Q

What clinical presentations will you see with AIDS?

A

Clinical presentation
Category A: asymptomatic
Category B: some less serious manifestations of immune deficiency
Category C: AIDS-defining illnesses present

69
Q

What are the treatments for AIDS?

A

-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
Q

Who are the people primarily at risk for immune dysfunction?

A
  • 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
Q

What are Immune-Building strategies?

A
  • 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

Pathophysiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions