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Pathophysiology with Price > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

What is innate immunity?

A

Natural; you are with it

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2
Q

Describe characteristics of innate immunity

A

Chemical and physical barriers, non-specific mechanisms, and non-adaptive mechanisms

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3
Q

What is adaptive immunity?

A

Both specific and adaptive

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4
Q

What is involved with the first line of defense?

A

Physical and biochemical barriers

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5
Q

What are the physical barriers involved with first line defense?

A

Skin, mucous membranes, vomiting, coughing, urination, defecation

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6
Q

What are the biochemical barriers involved with first line defense?

A

Mucus, perspiration, saliva, tears, cerumen, chemicals derived from normal flora, and sebum

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7
Q

Is first line defense specific or non-specific?

A

Non-specific

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8
Q

What is involved with the second line of defense?

A

Inflammation and phagocytosis

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9
Q

Is second line defense specific or non-specific?

A

Non-specific

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10
Q

What is involved with the third line of defense?

A

Adaptive specific immunity; cell-mediated, antibody-mediated (humoral)

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11
Q

Define inflammation

A

A universal response to injury occurring in vascular tissues of the body

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12
Q

List the characteristics of inflammation in response to injury

A

Non-specific, non-adaptive, immediate, mediated by chemicals in circulation, increases plasma and blood cells in tissues of injury, defends against infections, promotes repair and healing, and can be painful and risky

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13
Q

Define non-adaptive

A

In case of a secondary exposure to a stimulus the same response will be demonstrated as in the initial incident

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14
Q

List the local symptoms of inflammation

A

Changes in the microcirculation; vasodilation, increased capillary permeability, white cell migration from the capillaries, and inflammatory chemicals stimulate nociceptores (pain)

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15
Q

What are the observable characteristics of inflammation?

A

Heat, redness, swelling, and pain

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16
Q

Why is vasodilation important in inflammation?

A

Because it increases blood flow and decreases blood flow velocity; getting more blood at a slower rate which allows for the infection to move out easier

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17
Q

Do endothelial cells retract and become “leaky” when stimulated by inflammation?

A

Yes

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18
Q

Define exudation

A

Process of excluding

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19
Q

What are the purposes and benefits of inflammation?

A

Destroy injurious agents, confine agents to limit their effects on the host, stimulate components of the adaptive immune system, and promote regeneration and repair of tissues

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20
Q

What are the systemic manifestations of inflammation?

A

Fever, increases in pro-inflammatory and anti-inflammatory plasma proteins, and leukocytosis

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21
Q

What is occurring with a fever?

A

There is a systemic increase in temperature which increases immune response; chemical mediators act to reset the hypothalamic thermostat

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22
Q

What organ produces pro-inflammatory and anti-inflammatory plasma proteins?

A

The liver

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23
Q

Define acute phase reactants

A

IDK

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24
Q

What tests are used to evaluate acute phase reactants?

A

Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)

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25
Q

What does an ESR test for?

A

Rate at which RBC’s fall through plasma and reflects the levels of fibrinogen and adhesion of RBC’s; They increases as acute-phase reactants increase

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26
Q

What does a CRP test for?

A

Liver produces this quickly after inflammation

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27
Q

Define leukocytosis

A

Increase in circulating neutrophils

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28
Q

What is “shift-to-the-left”?

A

We are pumping out neutrophils so fast that we are sending immature neutrophils out into the blood due to mature neutrophil depletion

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29
Q

What are the events of acute inflammation?

A

Activation three plasma protein systems: Complement system, coagulation system, and kinin system

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30
Q

Describe the complement system

A

It consists of a group of plasma proteins (C1-C9) and participates at all levels of inflammation

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31
Q

List the three pathways of the complement system

A

Classical, Alternative, and Lectin

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32
Q

Explain the classical pathway

A

(C1) is activated by antigen-antibody complexes that bind to macrophages that enhance inflammation

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33
Q

What is opsonization?

A

Flagging the cell to be eaten

34
Q

What does C1 activate?

A

Cascade of C2-C5a that enhances inflammation by opsonization (C3b) and inducing mast cell degranulation (C3a and C5a) which encourages neutrophil chemotaxis

35
Q

C3a and C5a are responsible for what?

A

Inflammation

36
Q

What C5b-C9 responsible for?

A

Forming membrane attack complex (MAC) that puts holes in the cell resulting in cell lysis

37
Q

Explain the alternative pathway

A

(C3b) is activated by biological substances like bacteria, fungi, and toxins

38
Q

Explain the lectin pathway

A

mannose binding

39
Q

Describe the coagulation system

A

Stops bleeding, localized microorganisms, and provides a meshwork for healing

40
Q

Describe the kinin system

A

Activated by the coagulation system (intrinsic pathway) augments inflammation through vascular permeability, vasodilation, and smooth muscle contraction; primary kinin is Bradykinin

41
Q

What are the cellular components of inflammation?

A

Cytokines

42
Q

What are cytokines?

A

Chemical signals form one cell that affects another (how cells talk) that can be pro- or anti- inflammatory

43
Q

Give a few examples of cytokines

A

Interleukins, interferons, chemokines, etc

44
Q

What are Interleukins?

A

Cytokines produced by macrophages and lymphocytes in response to microorganisms and products of inflammation

45
Q

What are the functions of interleukins?

A

Encourage cell adhesion molecule expression, chemotaxis, proliferation and maturation of WBCs and pro- and anti- inflammatory

46
Q

What are interferons?

A

Natural anti-virals; proteins (alpha, beta, and gamma) made by leukocytes produced to protect against viral infections and encourage the immune response

47
Q

What is the function of interferons?

A

Defend against viral infections

48
Q

Describe a mast cell

A

Large, granular cells in loose connective tissue, adjacent to blood vessels that are critical for the inflammatory response

49
Q

Define degranulation

A

Quick release of preformed mediators (histamines and chemotactic factors) that cleave to basement membrane (tryptase) and increase endothelial cell permeability

50
Q

Synthesized vs. Preformed mast cells

A

Synthesized cells maintain the response - prostaglandins, leukotrienes, PAF, and histamine
Preformed cells are an instant response - histamine and tryptase

51
Q

What are the effects of histamine?

A

Inflammation; vasodilation and increased permeability, contracts smooth muscle; bronchi, GI tract, and uterus, increases secretions, dilates cerebral blood vessels (headaches), stimulate gastric juice secretions, and stimulates nerve endings resulting in pain and itching

52
Q

What are leukotrienes?

A

Cells that produce histamine-like effects that provide a slower, more prolonged response; may be helpful in allergic rhinitis

53
Q

Give some examples of leukotrienes

A

Montelukast (singulair), zafirlukast (accolate), and zileuton (zyflo)

54
Q

What are prostaglandins?

A

Cells made by enzymes; cyclo-oxygenases (COX) that encourage vascular permeability, chemotaxis, and pain

55
Q

Give an examples of COX inhibitors

A

Non-steroidal anti-inflammatory drugs like aspirin

56
Q

List the 5 steps in phagocyte migration

A
  1. Rolling - cells slow down due to endothelium
  2. Margination - stickiness is increased due to adhesion proteins
  3. Diapedesis - emigration through retracted endothelium
  4. Exudation - exiting into the cell
  5. Phagocytosis
57
Q

Neutrophils vs. macrophages

A

Neutrophils are first on the scene, live about 5 days due to invading cells and killing themselves (apoptosis)
Macrophages come in after neutrophils after 24 hours and are professional antigen-presenting cells

58
Q

What is the difference between acute and chronic inflammation?

A

Duration; chronic inflammation lasts longer than 2 weeks

59
Q

When does chronic inflammation occur?

A

When the body fails to remove the cause of inflammation due to weak pathogens, large resistant or persistent pathogens, or weak immune response

60
Q

What occurs due to chronic inflammation?

A

Granuloma

61
Q

What is a granuloma?

A

Formed by macrophages that join together to encircle the infected site

62
Q

What is the goal of healing in inflammation?

A

Regeneration

63
Q

Define regeneration

A

Restoration of the structure and function

64
Q

Define repair

A

Replacement of destroyed tissues with scar tissue which restores only strength

65
Q

What is the first step in wound healing?

A

Clean up the wound by phagocytizing particulate matter; debridement

66
Q

What occurs next after debridement?

A

Filling in the wound, covering/sealing the wound, and shrinking the wound

67
Q

Define simple wound

A

minimal tissue loss; edges come back together (paper cut, incised wounds, sutured laceration)

68
Q

How are simple wounds healed?

A

Primary intention

69
Q

Define open wound

A

Requires more tissue replacement and healing (pressure sore, non-sutured laceration, burns)

70
Q

How are open wounds healed?

A

Secondary intention; slower process

71
Q

What are the phases of regeneration and repair?

A
  1. Inflammation
  2. Proliferation and new tissue formation
  3. Remodeling and maturation
72
Q

What is occurring during inflammation in regeneration and repair?

A

Coagulation and infiltration of cells to facilitate healing along with debridement and angiogenesis

73
Q

What is occurring during proliferation and new tissue formation in regeneration and repair?

A

Fibroblast proliferation, collagen synthesis, and epithelialization; angiogenesis to decrease blood flow

74
Q

What is occurring during remodeling and maturation in regeneration and repair?

A

Cellular differentiation, scar tissue remodeling, capillaries removed from scar tissue

75
Q

Describe dysfunctional wound healing

A

Dysfunction during the inflammatory phase; hemorrhage, infection, or chronic inflammation (granuloma formation)

76
Q

What affects dysfunctional wound healing?

A

Diabetes, hypoxia, nutritional deficiency, reactivation or inflammatory responses, and anti-inflammatory medication

77
Q

Dysfunction during reconstructive phase

A

Impaired collagen synthesis effected by nutritional deficiency of vitamin C (scurvy), iron, calcium, and copper

78
Q

Dysfunction due to excessive collagen synthesis

A

Adhesions, hypertropic, and keloid scars

79
Q

Dysfunction due to wound disruption

A

Reopening (dehiscence) due to collagen disruption; primary intention is now healing by secondary intention

80
Q

Dysfunction due to excessive wound contraction

A

Vasoconstriction

Pathophysiology with Price (5 decks)

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