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Pathophysiology with Price > Unit 4 > Flashcards

Unit 4 Flashcards

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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
What does an ESR test for?
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
26
What does a CRP test for?
Liver produces this quickly after inflammation
27
Define leukocytosis
Increase in circulating neutrophils
28
What is "shift-to-the-left"?
We are pumping out neutrophils so fast that we are sending immature neutrophils out into the blood due to mature neutrophil depletion
29
What are the events of acute inflammation?
Activation three plasma protein systems: Complement system, coagulation system, and kinin system
30
Describe the complement system
It consists of a group of plasma proteins (C1-C9) and participates at all levels of inflammation
31
List the three pathways of the complement system
Classical, Alternative, and Lectin
32
Explain the classical pathway
(C1) is activated by antigen-antibody complexes that bind to macrophages that enhance inflammation
33
What is opsonization?
Flagging the cell to be eaten
34
What does C1 activate?
Cascade of C2-C5a that enhances inflammation by opsonization (C3b) and inducing mast cell degranulation (C3a and C5a) which encourages neutrophil chemotaxis
35
C3a and C5a are responsible for what?
Inflammation
36
What C5b-C9 responsible for?
Forming membrane attack complex (MAC) that puts holes in the cell resulting in cell lysis
37
Explain the alternative pathway
(C3b) is activated by biological substances like bacteria, fungi, and toxins
38
Explain the lectin pathway
mannose binding
39
Describe the coagulation system
Stops bleeding, localized microorganisms, and provides a meshwork for healing
40
Describe the kinin system
Activated by the coagulation system (intrinsic pathway) augments inflammation through vascular permeability, vasodilation, and smooth muscle contraction; primary kinin is Bradykinin
41
What are the cellular components of inflammation?
Cytokines
42
What are cytokines?
Chemical signals form one cell that affects another (how cells talk) that can be pro- or anti- inflammatory
43
Give a few examples of cytokines
Interleukins, interferons, chemokines, etc
44
What are Interleukins?
Cytokines produced by macrophages and lymphocytes in response to microorganisms and products of inflammation
45
What are the functions of interleukins?
Encourage cell adhesion molecule expression, chemotaxis, proliferation and maturation of WBCs and pro- and anti- inflammatory
46
What are interferons?
Natural anti-virals; proteins (alpha, beta, and gamma) made by leukocytes produced to protect against viral infections and encourage the immune response
47
What is the function of interferons?
Defend against viral infections
48
Describe a mast cell
Large, granular cells in loose connective tissue, adjacent to blood vessels that are critical for the inflammatory response
49
Define degranulation
Quick release of preformed mediators (histamines and chemotactic factors) that cleave to basement membrane (tryptase) and increase endothelial cell permeability
50
Synthesized vs. Preformed mast cells
Synthesized cells maintain the response - prostaglandins, leukotrienes, PAF, and histamine Preformed cells are an instant response - histamine and tryptase
51
What are the effects of histamine?
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
What are leukotrienes?
Cells that produce histamine-like effects that provide a slower, more prolonged response; may be helpful in allergic rhinitis
53
Give some examples of leukotrienes
Montelukast (singulair), zafirlukast (accolate), and zileuton (zyflo)
54
What are prostaglandins?
Cells made by enzymes; cyclo-oxygenases (COX) that encourage vascular permeability, chemotaxis, and pain
55
Give an examples of COX inhibitors
Non-steroidal anti-inflammatory drugs like aspirin
56
List the 5 steps in phagocyte migration
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
Neutrophils vs. macrophages
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
What is the difference between acute and chronic inflammation?
Duration; chronic inflammation lasts longer than 2 weeks
59
When does chronic inflammation occur?
When the body fails to remove the cause of inflammation due to weak pathogens, large resistant or persistent pathogens, or weak immune response
60
What occurs due to chronic inflammation?
Granuloma
61
What is a granuloma?
Formed by macrophages that join together to encircle the infected site
62
What is the goal of healing in inflammation?
Regeneration
63
Define regeneration
Restoration of the structure and function
64
Define repair
Replacement of destroyed tissues with scar tissue which restores only strength
65
What is the first step in wound healing?
Clean up the wound by phagocytizing particulate matter; debridement
66
What occurs next after debridement?
Filling in the wound, covering/sealing the wound, and shrinking the wound
67
Define simple wound
minimal tissue loss; edges come back together (paper cut, incised wounds, sutured laceration)
68
How are simple wounds healed?
Primary intention
69
Define open wound
Requires more tissue replacement and healing (pressure sore, non-sutured laceration, burns)
70
How are open wounds healed?
Secondary intention; slower process
71
What are the phases of regeneration and repair?
1. Inflammation 2. Proliferation and new tissue formation 3. Remodeling and maturation
72
What is occurring during inflammation in regeneration and repair?
Coagulation and infiltration of cells to facilitate healing along with debridement and angiogenesis
73
What is occurring during proliferation and new tissue formation in regeneration and repair?
Fibroblast proliferation, collagen synthesis, and epithelialization; angiogenesis to decrease blood flow
74
What is occurring during remodeling and maturation in regeneration and repair?
Cellular differentiation, scar tissue remodeling, capillaries removed from scar tissue
75
Describe dysfunctional wound healing
Dysfunction during the inflammatory phase; hemorrhage, infection, or chronic inflammation (granuloma formation)
76
What affects dysfunctional wound healing?
Diabetes, hypoxia, nutritional deficiency, reactivation or inflammatory responses, and anti-inflammatory medication
77
Dysfunction during reconstructive phase
Impaired collagen synthesis effected by nutritional deficiency of vitamin C (scurvy), iron, calcium, and copper
78
Dysfunction due to excessive collagen synthesis
Adhesions, hypertropic, and keloid scars
79
Dysfunction due to wound disruption
Reopening (dehiscence) due to collagen disruption; primary intention is now healing by secondary intention
80
Dysfunction due to excessive wound contraction
Vasoconstriction

Pathophysiology with Price (5 decks)

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