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Pathology > Inflammation I > Flashcards

Inflammation I Flashcards

1
Q

What is inflammation?

A

Local reaction of vascularized tissue to injury

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2
Q

What is the timeline for acute inflammation?

A

0-2 days in duration

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3
Q

What is the timeline for subacute inflammation?

A

2-14 days in duration

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4
Q

What is the timeline for chronic inflammation?

A

> 14 days

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5
Q

What are the primary cells seen in acute inflammation?

A

PMNs

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6
Q

What are the primary cells seen in subacute inflammation?

A

PMNs, monocytes, lymphocytes, plasma cells, fibroblastic elements, angioblastic elements

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7
Q

What are the cells seen in chronic inflammation?

A

Monocytes/Macrophages
Lymphocytes
Plasma cells
Granuloma cells

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8
Q

What are monocytes? Macrophages?

A

Same cell, but monocytes in blood, macrophages in tissue

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9
Q

What are granuloma cells?

A

Epitheliod cells and giant cells

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10
Q

What are the histological characteristics of acute inflammation?

A

Large eosinophilic areas, with neutrophils (poly nuclear eosinophilic)

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11
Q

What are the histological characteristics of subacute inflammation?

A

Changed to monocytes/macrophages

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12
Q

What are eosinophils found in?

A

Predominant inflammatory cells in allergic reactions and parasitic infections

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13
Q

How do eosinophils appear histologically?

A

Cells with pink granules

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14
Q

What is the range of eosinophils? What are the two disease processes you should suspect if it is above this value?

A

0.5-5%

Allergies or parasitic infection

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15
Q

What are the plasma derived molecular systems?

A
  1. Immune system
  2. Kinin system
  3. Clotting system
  4. Fibrinolytic system
  5. Acute phase proteins
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16
Q

What are the tissue derived molecular system

A
  1. Vasoactive amines
  2. Acidic lipids
  3. Cytokines
  4. Others
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17
Q

What are the uses of inflammation? (2)

A
  1. To rid the body of initial cell injury (microbe)

2. To rid the body of tissue injury

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18
Q

How is inflammation harmful?

A
  1. Autoimmune
  2. hypersensitivity rxns
  3. Produce scarring
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19
Q

What are the six cardinal signs of inflammation?

A
  1. Heat
  2. Redness
  3. Swelling
  4. Pain
  5. Loss of function
  6. Systemic changes
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20
Q

What causes the heat and redness of inflammation? Cytokines?

A

Increased blood flow to site from–histamine, PGs, bradykinin

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21
Q

What causes the swelling of inflammation? Cytokines?

A

Increased postcapillary venule permeability–Histamine, C5a, C3a, Leukotrienes C4 D4 E4

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22
Q

What causes the pain of inflammation?

A

PGE2, Bradykinin sensitize neurons

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23
Q

What causes fever? How?

A

Il-1, TNFalpha increase PGE2 synthesis in the hypothalamus via COX pathway

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24
Q

What are the two major cytokines involved in inflammation?

A

IL-1, TNF-alpha

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25
Q

What is serous inflammation?

A

Outpouring of watery, relatively protein-poor fluid (effusion) derived from either serum or mesothelial cell secretions

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26
Q

What is fibrinous inflammation?

A

Seen in more severe injury; increased vascular permeability allows leakage of larger molecules (fibrinogen)

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27
Q

What happens if fibrin is not completely removed during fibrinous inflammation?

A

ingrowth of fibroblasts and blood vessels

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28
Q

What is suppurative inflammation?

A

(purulent inflammation) manifested by large amounts of pus

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29
Q

What is pus?

A

dead PMNs, necrotic tissue

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30
Q

What is an abscess?

A

Focal collections of pus; central necrotic region surrounded by layer of preserved PMNs

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31
Q

What happens to abscesses in chronic inflammation?

A

Walling of via fibroblasts

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32
Q

What is ulceration?

A

Local defect, excavation produced by sloughing of inflammatory necrotic tissue; can only occur on or near a surface

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33
Q

What are in the margins of the skin that sloughs off in ulceration?

A

PMNs, and vascular dilation

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34
Q

What are the four outcomes of acute inflammation?

A
  1. Resolution (complete restoration)
  2. Healing by scarring
  3. Abscess
  4. Chronic infx
35
Q

When does healing by scarring occur? (2)

A
  1. After substantial damage

2. In tissues that cannot regenerate

36
Q

What happens to blood flow in inflammation? How?

A

Increases, via alterations in vascular caliber

37
Q

What enables plasma proteins and leukocytes to leave the circulation?

A

Structural changes in the microvasculature

38
Q

What are the two possible hemodynamic changes in vasculature in inflammation? When does each occur?

A

Vasoconstriction (first)

Vasodilation (after)

39
Q

What allows capillaries to enlarge in inflammation?

A

Relaxation of precapillary sphincters

40
Q

What is transudation? Is there protein leakage?

A

Increased hydrostatic pressure, and lower colloid osmotic pressure in capillaries leading to fluid leakage. THERE IS NO PROTEIN LEAKING OUT

41
Q

What is exudation? Is there protein leakage? Why?

A

Vasodilation leading to fluid AND proteins d/t loss of junction b/t endothelial cells

42
Q

What is the difference between transudation vs exudation?

A

Exudation is the result of endothelial cells separating, whereas transudation is d/t changes in osmotic/oncotic pressure in capillaries

43
Q

What are the four mechanisms that lead to vascular leakage?

A
  1. Direct injury
  2. Leukocyte injury
  3. New blood vessel leakage
  4. endothelial cell contraction
44
Q

What are the hemodynamic changes in vasculature? (3)

A
  1. Leakage of fluid to interstitial space
  2. Stasis of circulation
  3. Decreased absorption of fluid from interstitial space
45
Q

What is margination?

A

leukocytes line up along EC surface

46
Q

What is adhesion?

A

Cells sticking to EC surface

47
Q

What is emigration?

A

Migration between EC and across BM to interstitial space

48
Q

What is chemotaxis?

A

Directed movement along chemical gradient towards injury

49
Q

What is the cellular structure that allows leukocytes to migrate?

A

Filopodium

50
Q

What is the mechanism of leukocyte exudation?

A

Rolling, adhesion, transmigration

51
Q

What are the two proteins that allow leukocytes to stick and integrate (respectively)

A
  1. Selectins allow for adhesion

2. Integrins allow for integration

52
Q

What are the three classes of cell adhesion molecules (CAM) that allow for leukocyte attachment and participation in the inflammation response?

A
  1. Selectins
  2. Immunoglobulin family
  3. Integrins
53
Q

What type of molecules are CAMs?

A

Glycoproteins

54
Q

What are selectins? What ion are they dependent on?

A

Ca-dependent lectins that allow for ROLLING

55
Q

Are selectins involved in firm adhesions?

A

No, just slow down circulating leukocytes

56
Q

What are the three family membranes of selectins?

A

P selectin
E selectin
L selectins

57
Q

What is ICAM-1? Where is it found? What does it bind to?

A

Intercellular adhesion molecule 1 in immunoglobin 1 family

expressed on the endothelium

binds to integrin LFA-1 and Mac-1

58
Q

What is VCAM-1? Where is it found? What does it bind to?

A

Immunoglobin family II

Binds to integrin VLA-4 that is on molecule on lymphocytes/monocytes

59
Q

What is PECAM-1? Where is it found? What does it bind to?

A

Immunoglobin family II (CD31)
Found on both endothelium and leukocytes.

Homophilic binding to CD-31

Plays an important role in diapedesis step of leukocytes emigration

60
Q

What are beta1 integrins? What are the two molecules of this group, where are they found, and what do they bind to?

A

Integrin family I

VLA4 expressed on leukocytes and binds to VCAM -1 on endothelium

61
Q

What is the integrin family I?

A

Group of adhesion molecules composed of heterodimers of alpha and beta subunits, which act in regulation of cell-matrix and cell-cell adhesion

62
Q

What are the integrin family II members? What are the three molecules of this group, where are they found, and what do they bind to?

A

Beta-2 integrins

LFA1, CR3/CR4, which bind to ICAM1 and assist in localization of phagocytes to injury sites and extravasation

63
Q

What are the five principle processes of acute inflammation?

A
  1. Increased blood flow/exudation
  2. Attraction of leukocytes
  3. Activation of chemical mediators
  4. Degradation of extracellular debris
  5. Restoration of tissue
64
Q

The suffix “-itis” means what?

A

Inflammation

65
Q

The suffix “-osis” means what?

A

Full of

66
Q

Can normal tissues be restored after fibrinous inflammation?

A

Yes

67
Q

Can there be inflammation if there is no vasculature to the area?

A

No

68
Q

What is suppurative/purulent inflammation? What are the contents of pus?

A

Inflammation with pus, (where pus = PMNs, necrotic cells, edema)

69
Q

What are ulcers?

A

Excavation produced by sloughing off of necrotic tissue

70
Q

True or false: ulcers can present anywhere on or in the human body

A

False-Necrotic tissue must be near a surface

71
Q

What are the two divisions of molecular systems?

A
  1. Plasma derived

2. Cell/tissue derived

72
Q

Increased permeability in acute inflammation occurs at which vessel level?

A

Capillaries and postcapillary venules

73
Q

What are the two changes in sterling’s law forces that allow for the acute inflammation?

A
  1. Increased capillary hydrostatic pressure

2. Increase extracellular osmotic pressue

74
Q

What is the sequence of events of leukocyte exudation? (4)

A
  1. Margination
  2. Adhesion
  3. Emigration
  4. Chemotaxis
75
Q

What are the major chemotactic agents?

A

C5a, Leukotriene B4

76
Q

Where are P selectins stored? What signals their release? What does it bind to?

A

Stored in Weibel-Palade bodies, released in response to TNF or IL-1

Binds to P-selectin glycoprotein ligand 1

77
Q

Where are E selectins stored? What signals their release? What does it bind to?

A

Synthesized de novo by endothelium

activated by TNF or IL-1

Binds to sialylated Lewis-X type oligosaccharides on surface proteins

78
Q

What is the function of L selectins? What does it bind to?

A

homing receptors of Leukocytes to bind to endothelium via CD34

79
Q

Which of the selectins recognize sialylated Lewis-X type oligosaccharides on surface proteins

A

P and E

80
Q

Which of the selectins recognized CD34?

A

L

81
Q

What is the endothelial receptor that binds to LFA-1/Mac-1 on leukocytes?

A

ICAM-1

82
Q

What is the cell receptor that binds to integrin VLA-4?

A

VCAM-1

83
Q

What is the cell adhesion molecule that binds to CD-31?

A

opposing PECAM-1

84
Q

What is the cell adhesion molecule that plays an important role in the diapedesis step of leukocyte emigration?

A

PECAM-1

Pathology (32 decks)

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