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Inflammation I Flashcards

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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
What is serous inflammation?
Outpouring of watery, relatively protein-poor fluid (effusion) derived from either serum or mesothelial cell secretions
26
What is fibrinous inflammation?
Seen in more severe injury; increased vascular permeability allows leakage of larger molecules (fibrinogen)
27
What happens if fibrin is not completely removed during fibrinous inflammation?
ingrowth of fibroblasts and blood vessels
28
What is suppurative inflammation?
(purulent inflammation) manifested by large amounts of pus
29
What is pus?
dead PMNs, necrotic tissue
30
What is an abscess?
Focal collections of pus; central necrotic region surrounded by layer of preserved PMNs
31
What happens to abscesses in chronic inflammation?
Walling of via fibroblasts
32
What is ulceration?
Local defect, excavation produced by sloughing of inflammatory necrotic tissue; can only occur on or near a surface
33
What are in the margins of the skin that sloughs off in ulceration?
PMNs, and vascular dilation
34
What are the four outcomes of acute inflammation?
1. Resolution (complete restoration) 2. Healing by scarring 3. Abscess 4. Chronic infx
35
When does healing by scarring occur? (2)
1. After substantial damage | 2. In tissues that cannot regenerate
36
What happens to blood flow in inflammation? How?
Increases, via alterations in vascular caliber
37
What enables plasma proteins and leukocytes to leave the circulation?
Structural changes in the microvasculature
38
What are the two possible hemodynamic changes in vasculature in inflammation? When does each occur?
Vasoconstriction (first) | Vasodilation (after)
39
What allows capillaries to enlarge in inflammation?
Relaxation of precapillary sphincters
40
What is transudation? Is there protein leakage?
Increased hydrostatic pressure, and lower colloid osmotic pressure in capillaries leading to fluid leakage. THERE IS NO PROTEIN LEAKING OUT
41
What is exudation? Is there protein leakage? Why?
Vasodilation leading to fluid AND proteins d/t loss of junction b/t endothelial cells
42
What is the difference between transudation vs exudation?
Exudation is the result of endothelial cells separating, whereas transudation is d/t changes in osmotic/oncotic pressure in capillaries
43
What are the four mechanisms that lead to vascular leakage?
1. Direct injury 2. Leukocyte injury 3. New blood vessel leakage 4. endothelial cell contraction
44
What are the hemodynamic changes in vasculature? (3)
1. Leakage of fluid to interstitial space 2. Stasis of circulation 3. Decreased absorption of fluid from interstitial space
45
What is margination?
leukocytes line up along EC surface
46
What is adhesion?
Cells sticking to EC surface
47
What is emigration?
Migration between EC and across BM to interstitial space
48
What is chemotaxis?
Directed movement along chemical gradient towards injury
49
What is the cellular structure that allows leukocytes to migrate?
Filopodium
50
What is the mechanism of leukocyte exudation?
Rolling, adhesion, transmigration
51
What are the two proteins that allow leukocytes to stick and integrate (respectively)
1. Selectins allow for adhesion | 2. Integrins allow for integration
52
What are the three classes of cell adhesion molecules (CAM) that allow for leukocyte attachment and participation in the inflammation response?
1. Selectins 2. Immunoglobulin family 3. Integrins
53
What type of molecules are CAMs?
Glycoproteins
54
What are selectins? What ion are they dependent on?
Ca-dependent lectins that allow for ROLLING
55
Are selectins involved in firm adhesions?
No, just slow down circulating leukocytes
56
What are the three family membranes of selectins?
P selectin E selectin L selectins
57
What is ICAM-1? Where is it found? What does it bind to?
Intercellular adhesion molecule 1 in immunoglobin 1 family expressed on the endothelium binds to integrin LFA-1 and Mac-1
58
What is VCAM-1? Where is it found? What does it bind to?
Immunoglobin family II Binds to integrin VLA-4 that is on molecule on lymphocytes/monocytes
59
What is PECAM-1? Where is it found? What does it bind to?
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
What are beta1 integrins? What are the two molecules of this group, where are they found, and what do they bind to?
Integrin family I VLA4 expressed on leukocytes and binds to VCAM -1 on endothelium
61
What is the integrin family I?
Group of adhesion molecules composed of heterodimers of alpha and beta subunits, which act in regulation of cell-matrix and cell-cell adhesion
62
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?
Beta-2 integrins LFA1, CR3/CR4, which bind to ICAM1 and assist in localization of phagocytes to injury sites and extravasation
63
What are the five principle processes of acute inflammation?
1. Increased blood flow/exudation 2. Attraction of leukocytes 3. Activation of chemical mediators 4. Degradation of extracellular debris 5. Restoration of tissue
64
The suffix "-itis" means what?
Inflammation
65
The suffix "-osis" means what?
Full of
66
Can normal tissues be restored after fibrinous inflammation?
Yes
67
Can there be inflammation if there is no vasculature to the area?
No
68
What is suppurative/purulent inflammation? What are the contents of pus?
Inflammation with pus, (where pus = PMNs, necrotic cells, edema)
69
What are ulcers?
Excavation produced by sloughing off of necrotic tissue
70
True or false: ulcers can present anywhere on or in the human body
False-Necrotic tissue must be near a surface
71
What are the two divisions of molecular systems?
1. Plasma derived | 2. Cell/tissue derived
72
Increased permeability in acute inflammation occurs at which vessel level?
Capillaries and postcapillary venules
73
What are the two changes in sterling's law forces that allow for the acute inflammation?
1. Increased capillary hydrostatic pressure | 2. Increase extracellular osmotic pressue
74
What is the sequence of events of leukocyte exudation? (4)
1. Margination 2. Adhesion 3. Emigration 4. Chemotaxis
75
What are the major chemotactic agents?
C5a, Leukotriene B4
76
Where are P selectins stored? What signals their release? What does it bind to?
Stored in Weibel-Palade bodies, released in response to TNF or IL-1 Binds to P-selectin glycoprotein ligand 1
77
Where are E selectins stored? What signals their release? What does it bind to?
Synthesized de novo by endothelium activated by TNF or IL-1 Binds to sialylated Lewis-X type oligosaccharides on surface proteins
78
What is the function of L selectins? What does it bind to?
homing receptors of Leukocytes to bind to endothelium via CD34
79
Which of the selectins recognize sialylated Lewis-X type oligosaccharides on surface proteins
P and E
80
Which of the selectins recognized CD34?
L
81
What is the endothelial receptor that binds to LFA-1/Mac-1 on leukocytes?
ICAM-1
82
What is the cell receptor that binds to integrin VLA-4?
VCAM-1
83
What is the cell adhesion molecule that binds to CD-31?
opposing PECAM-1
84
What is the cell adhesion molecule that plays an important role in the diapedesis step of leukocyte emigration?
PECAM-1

Pathology (32 decks)

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