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Rapid Review Pathology > Chapter 3 - Inflammation and Repair > Flashcards

Chapter 3 - Inflammation and Repair Flashcards

0
Q

What three responses are involved in acute inflammation?

A

AI: chemical, vascular, cellular responses

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1
Q

Define acute inflammation.

A

AI: transient and early response to injury

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2
Q

Rubor, calor, and dolor are mediated by what?

A

Rubor, calor, tumor: histamine-mediated

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3
Q

Dolor is mediated by what two compounds?

A

Dolor (pain): mediated by PGE2 and bradykinin

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4
Q

What mediates vasodilation of arterioles?

A

Vasodilation of arterioles: histamine, nitric oxide

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5
Q

In acute inflammation, what do mast cells release?

A

Mast cells: release preformed histamine

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6
Q

How does histamine affect venule endothelial cells resulting in what?

A

Histamine: contracts venule endothelial cells; ↑venular permeability

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7
Q

Describe edema fluid.

A

Edema fluid: transudate (low protein and cell levels)

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8
Q

What are the primary leukocytes in acute inflammation?

A

Neutrophils: primary leukocytes in AI

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9
Q

How does the circulating pool and marginating pool of neutrophils differ between Caucasians and African Americans?

A

Neutrophils: in white people, 50% circulating and 50% marginating; in black people, marginating pool > circulating pool

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10
Q

What alters the distribution of neutrophils?

A

Neutrophil distribution: altered by activating/inactivating adhesion molecules

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11
Q

What does margination of neutrophils mean?

A

Margination: neutrophils pushed to periphery

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12
Q

What are selectins?

A

Selectins: carbohydrate-binding adhesion molecules

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13
Q

Where are L-selectin ligands located?

A

L-selectin: selectin ligand on leukocytes

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14
Q

Where are E-selectin molecules located?

A

E-selectin: selectin molecule on endothelial cells

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15
Q

From where is P-selectin derived?

A

P-selectin: derived from Weibel-Palade bodies in endothelial cells

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16
Q

What two cytokines activate selectins?

A

Selectins activated by IL-1 and TNF

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17
Q

Describe the process of selectin adhesion.

A

Selectin adhesion: “rolling” (bind−detach) of neutrophils

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18
Q

What do β2-Integrins do and what are they activated by?

A

β2-Integrins: firm adhesion of neutrophils; activated by C5a/LTB4

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19
Q

How catecholamines and corticosteroids affect the firm adhesion of neutrophils?

A

Catecholamines and corticosteroids inactivate neutrophil β2-integrins: produces neutrophilic leukocytosis

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20
Q

How do endotoxins affect β2-integrins producing what?

A

Endotoxins activate neutrophil β2-integrins: produces neutropenia

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21
Q

What are ICAM/VCAM and what are they activated by?

A

ICAM/VCAM: endothelial cell integrin adhesion molecules (ligands); activated by IL-1/TNF

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22
Q

Name one clinical finding of leukocyte adhesion deficiency due to selectin or CD11a/CD18 deficiency.

A

Delayed separation of umbilical cord: LAD due to selectin or CD11a/CD18 deficiency

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23
Q

Describe transmigration (diapedesis).

A

Transmigration (diapedesis): movement of neutrophils from venules into interstitial space

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24
Q

What is an exudate?

A

Exudate: protein- and cell-rich fluid (pus)

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25
Q

Name two functions of exudate.

A

Exudate: dilutes bacterial toxins; provides opsonins

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26
Q

What is chemotaxis?

A

Chemotaxis: directed migration of neutrophils

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27
Q

Name four chemotaxis mediators.

A

Chemotaxis mediators: C5a, LTB4, bacterial products, IL-8

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28
Q

Name two opsonins. What do they do?

A

Opsonins: IgG and C3b; enhance neutrophil ability to ingest bacteria
Opsonins: IgG and C3b; enhance neutrophil recognition and attachment of bacteria

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29
Q

In Bruton agammaglobulinemia, there is a defect in what?

A

Bruton agammaglobulinemia: opsonization defect (lack of IgG)

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30
Q

Describe the process of neutrophil ingestion.

A

Neutrophil ingestion: phagosome → phagolysosome

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31
Q

What cannot form in Chédiak-Higashi syndrome?

A

Chédiak-Higashi syndrome: cannot form phagolysosomes

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32
Q

What is myeloperoxidase?

A

MPO: neutrophil/monocyte lysosomal enzyme

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33
Q

What is the most potent microbicidal system available to neutrophils and monocytes?

A

O2-dependent MPO system: most potent microbicidal system

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34
Q

What does the NADPH oxidase complex do?

A

NADPH oxidase enzyme complex: converts molecular O2 to superoxide FRs

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35
Q

What does superoxide dismutase do?

A

SOD converts superoxide free radicals to H2O2

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36
Q

What is the end product of the O2-dependent MPO system?

A

End-product O2-dependent MPO system: bleach

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37
Q

In G6PD deficiency, what is lacking? How does this affect the MPO system?

A

G6PD deficiency: lack of NADPH interferes with normal function of the O2-dependent MPO system

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38
Q

Give two examples of O2-independent microbial systems.

A

O2-independent systems: lactoferrin (neutrophils), MBP (eosinophils)

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39
Q

What is the most important chemical mediator of acute inflammation?

A

Histamine: most important chemical mediator of AI

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40
Q

What is the most common cause of skin abscess?

A

S. aureus: most common cause of a skin abscess

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41
Q

What is fibrinous inflammation?

A

Fibrinous inflammation: exudate covering serosal surfaces (heart, lungs, peritoneum)

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42
Q

What is serous inflammation? Give two examples of serous inflammation.

A

Serous inflammation: thin watery exudate; blister, viral pleuritis

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43
Q

What two microbes may cause pseudomembranous inflammation?

A

Pseudomembranous inflammation: diphtheria, Clostridium difficile

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44
Q

Describe the role of fever in acute inflammation.

A

Fever is beneficial: OBC right-shifted, ↓bacterial/viral reproduction

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45
Q

Describe the half-life of chemical mediators in acute inflammation.

A

Chemical mediators have a short half-life.

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46
Q

What is the role of lipotoxins in acute inflammation?

A

Lipoxins: inhibit transmigration/chemotaxis; enhance apoptosis

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47
Q

What is the role of resolvins in acute inflammation?

A

Resolvins: inhibit recruitment inflammatory cells

48
Q

How are neutrophils cleared in acute inflammation?

A

Neutrophils cleared from the inflammatory site by apoptosis

49
Q

List four consequences of acute inflammation.

A

Consequences: resolution, scar tissue, abscess, progression to chronic inflammation

50
Q

What is the most common cause of chronic inflammation?

A

Infection: most common cause of chronic inflammation

51
Q

What are the primary leukocytes in chronic inflammation?

A

Monocytes and/or macrophages: primary leukocytes in chronic inflammation

52
Q

What does granulation tissue consists of?

A

Granulation tissue: blood vessels, fibroblasts

53
Q

What is a precursor of scar tissue?

A

Granulation tissue: precursor of scar tissue

54
Q

What is fibronectin and what does it do?

A

Fibronectin: key adhesion glycoprotein in ECM; chemotactic factor for fibroblasts and endothelial cells

55
Q

What is granulomatous inflammation?

A

Granulomatous inflammation: specialized type of chronic inflammation

56
Q

Name two types of granulomatous infections.

A

Granulomatous infections: TB, systemic fungi (e.g., histoplasmosis)

57
Q

Name two examples of noninfectious granulomatous inflammation.

A

Noninfectious granulomatous inflammation: sarcoidosis, Crohn disease

58
Q

What are the cell types in a tuberculous granuloma?

A

Cell types in tuberculous granuloma: macrophages and CD4 helper T cells

59
Q

What are epithelioid cells?

A

Epithelioid cells: macrophages activated by interferon-γ from CD4 TH1 cells

60
Q

How are multinucleated giant cells formed?

A

Multinucleated giant cells: formed by fusion of epithelioid cells

61
Q

Name two factors involved in tissue repair.

A

Tissue repair: parenchymal cell regeneration, repair by connective tissue

62
Q

What two cell types can regenerate?

A

Cell regeneration: only labile and stable cell can regenerate

63
Q

What cell type cannot regenerate?

A

Cell regeneration: permanent cells cannot regenerate

64
Q

What is G0 phase of the cell cycle?

A

G0 phase: resting phase of stable cells

65
Q

What is the most variable phase of the cell cycle?

A

G1 phase: most variable phase in cell cycle

66
Q

What occurs during the G1 phase of the cell cycle?

A

G1 phase: synthesis of DNA, RNA, protein

67
Q

What occurs during the G2 phase of the cell cycle?

A

G2 phase: synthesis of tubulin for mitotic spindle

68
Q

What occurs during the a phase of the cell cycle?

A

M phase: two daughter cells are produced

69
Q

What is the most critical phase in the cell cycle?

A

G1 to S phase: most critical phase in cell cycle

70
Q

Name two control proteins involved in the regulation of the G1 checkpoint.

A

Control proteins: Cdk4, cyclin D

71
Q

Describe the role of RB1 in the cell cycle.

A

RB1 protein phosphorylation by Cdk4: causes the cell to enter S phase

72
Q

Name two genes that control the G1 checkpoint.

A

Genes controlling G1 to S phase: RB1 and p53 suppressor genes

73
Q

What does the p53 protein product do?

A

p53 protein product: inhibits Cdk4 (cell arrested in G1 phase)

74
Q

In the event that there is excessive DNA damage, the p53 suppressor gene produces protein products that do what?

A

Severe DNA damage, p53 protein products: inhibit translation of BCL-2 antiapoptosis genes (initiates apoptosis) and inhibits translation of growth promoting genes (initiates growth arrest)

75
Q

What is required for restoration to normal of a regenerating cell?

A

Restoration to normal: intact basement membrane; intact ECM

76
Q

What is laminin?

A

Laminin: key adhesion glycoprotein in basement membrane

77
Q

What is granulation tissue essential for?

A

Granulation tissue: essential for normal connective tissue repair

78
Q

What is type III collagen? Describe one of its properties.

A

Type III collagen: initial collagen in wound repair; poor tensile strength

79
Q

Name the cofactor in collagenase.

A

Zinc: cofactor in collagenase

80
Q

What is the tensile strength of a wound after remodeling?

A

Tensile strength of the wound ~80% of the original after remodeling

81
Q

Describe three features of scar tissue.

A

Scar tissue: acellular; lacks inflammatory cells/adnexal structures; surfaced by intact epidermis

82
Q

Describe healing by primary intention.

A

1° intention: clean wound approximated by suturing

83
Q

Describe healing by secondary intention.

A

2° intention: contaminated wound left open for reepithelialization

84
Q

Describe healing by tertiary intention.

A

3° intention: contaminated wound débrided and treated with antibiotics before surgically closing the wound

85
Q

What is the most common cause of impaired wound healing?

A

Infections: MCC of impaired wound healing

86
Q

What is the most common pathogen causing wound infection?

A

S. aureus: MC pathogen causing wound infection

87
Q

MRSA is resistant to what type of antibiotics?

A

MRSA: resistant to β-lactam antibiotics

88
Q

What are the greatest risk factors for wound infection?

A

Greatest risk factors for wound infection: disruption of skin and malnutrition

89
Q

What percentage of people carry MRSA in the anterior nares?

A

MRSA carriers: 20%–40% people carry MRSA in anterior nares

90
Q

The majority of CA-MRSA produce what? There may be possible progression to what?

A

MRSA: majority CA-MRSA produce Panton-Valentine leukocidin (accelerates apoptosis neutrophils); possible progression to necrotizing fasciitis

91
Q

Diabetes mellitus increases the susceptibility to infection by what?

A

Diabetes mellitus: ↓blood flow, ↑tissue glucose levels

92
Q

List three nutritional deficiencies that impair wound healing.

A

Nutritional deficiencies: malnutrition, insufficient vitamin C and copper/zinc

93
Q

How do glucocorticoids impair wound healing?

A

Glucocorticoids: prevent scar formation

94
Q

What are keloids?

A

Keloids: raised scars extending beyond borders of original wound

95
Q

What is a hypertrophic scar?

A

Hypertrophic scar: raised scar remaining in confines of original wound

96
Q

How are collagen bundles arrayed in a normal scar?

A

Normal scar: haphazard collagen bundles

97
Q

How are collagen bundles arrayed in a keloid or hypertrophic scar?

A

Keloid/hypertrophic scar: collagen bundles in same plane as epidermis

98
Q

If there is severe injury to the liver, what occurs and what is there danger of occurring?

A

Severe injury liver: regenerative nodules and fibrosis; danger of cirrhosis

99
Q

What is the repair cell in lung injury?

A

Lung injury: type II pneumocyte is repair cell

100
Q

What occurs in response to a brain injury?

A

Brain injury: proliferation of astrocytes (gliosis) and microglial cells

101
Q

What is Wallerian degeneration?

A

Wallerian degeneration: distal degeneration of the axon

102
Q

What is the key to reinnervation in peripheral nerve transection?

A

Peripheral nerve transection: Schwann cell is key in reinnervation

103
Q

What type of tissue is cardiac muscle? If damaged, how is it repaired?

A

Cardiac muscle damage: permanent tissue; repair by fibrosis

104
Q

Postexercise, how is skeletal muscle repaired?

A

Skeletal muscle postexercise: myofiber repair by satellite cells (muscle stem cells)

105
Q

What is neutrophil if leukocytosis?

A

Neutrophilic leukocytosis: cytokine release of postmitotic neutrophils from the bone marrow

106
Q

What is a left-shifted smear?

A

Left-shifted smear: ↑band neutrophils (>10%) in peripheral blood

107
Q

What is toxic granulation?

A

Toxic granulation: dark blue to purple primary granules in neutrophils

108
Q

Toxic granulation is a sign of what?

A

Toxic granulation: sign of severe inflammatory condition (infectious and noninfectious)

109
Q

What are Döhle bodies?

A

Döhle bodies: gray-blue inclusions in neutrophils; accompanies toxic granulation

110
Q

What is the predominant immunoglobulin in acute inflammation?

A

IgM: predominant immunoglobulin in AI

111
Q

List two findings in chronic inflammation.

A

CI: absolute monocytosis and increased serum IgG

112
Q

What is the effect of corticosteroids in the blood?

A

Corticosteroid effect in blood: ↑neutrophils; ↓B/T lymphocytes, monocytes, eosinophils by apoptosis

113
Q

Define ESR.

A

ESR: rate of settling of RBCs in vertical tube in mm/hour

114
Q

What is rouleaux formation? What causes it and how does it affect the ESR?

A

RBC rouleau (stack of coins appearance): ↑ESR; ↑fibrinogen/immunoglobulins

115
Q

What is CRP a marker of?

A

CRP: marker of necrosis and disease activity

116
Q

Describe the SPE in AI.

A

SPE in AI: ↓albumin; no alteration in γ-globulin peak

117
Q

Polyclonal gammopathy is a sign of what?

A

Polyclonal gammopathy: sign of CI

Rapid Review Pathology (14 decks)

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