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Pathology I > Session 3 - Acute Inflammation > Flashcards

Session 3 - Acute Inflammation Flashcards

1
Q

What three cellular changes can occur with chronic inflammation?

A

Metaplasia
Dysplasia
Neoplasia

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2
Q

What are the four key components to acute inflammation?

A

Dilated + Permeable blood vessels
Neutrophils
Plasma proteins
Cell mediators

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3
Q

What are the plasma proteins involved in acute inflammation?

A

Fibrinogen + Fibrin

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4
Q

Describe suppurative.

A

Neutrophilic inflammation with high plasma protein content

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5
Q

Describe an abscess.

A

Encapsulated accumulation of neutrophils

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6
Q

What are the four bacteria commonly associated with pus and abscesses?

A

Staphylococcus
Streptococcus
E. Coli
Listeria monocytogenes

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7
Q

What are three key characteristics of acute inflammation?

A

Vasodilation
Vascular leakage
Emigration of neutrophils

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8
Q

What other sides, besides neutrophils, are seen in acute inflammation?

A

Mast cells and Platelets

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9
Q

What occurs with vasodilation during acute inflammation?

A

Leads to greater blood flow to area of inflammation leading to redness + heat

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10
Q

What causes vascular leakage?

A

Endothelial gaps in venules

Leakage of protein-rich fluid into EC spaces

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11
Q

What is edema called in body cavities?

A

Effusion

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12
Q

What are the six steps in emigration of neutrophils in the inflammatory response?

A

Rolling + Firm adhesion + Diapedesis + Chemotaxis + Phagocytosis + Killing bacteria

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13
Q

What plays a part in the rolling part of emigration?

A

Selectins

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14
Q

Where are selectins located?

A

Leukocytes + Endothelium

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15
Q

What two things play a roll in firm adhesion of emigration?

A

Integrins + ICAM-1

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16
Q

Where is ICAM-1 located?

A

Endothelium

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17
Q

What cell are integrins located on?

A

Neutorphils

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18
Q

What component is responsible for diapedesis?

A

CD31

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19
Q

What is CD31?

A

Cell to cell adhesion molecule

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20
Q

What two components are responsible for chemotaxis in emigration?

A

C5a + LTB4

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21
Q

What two components play a role in phagocytosis in emigration?

A

C3b + IgG

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22
Q

What is responsible for killing bacteria in emigration?

A

Superoxides + Lysozymes from neutrophil granules

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23
Q

Where do acute phase proteins come from?

A

Liver

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24
Q

What cytokines stimulate the liver to release acute phase proteins?

A

IL-1 + IL-6 + TNF

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25
What cell is responsible for the cytokine release that stimulates acute phase protein release?
Macrophages
26
What are the examples given in lecture for acute phase proteins?
Fibrinogen + Prothrombin + Plasminogen + FVII + C-reactive proteins + SAA + Alpha-1 Antitrypsin
27
What are the functions of acute phase proteins?
Hemostasis Lysis of bacteria Bacteriostasis Mopping up free radicals
28
What inflammatory mediators are responsible for fever?
IL-1 + TNF + IL-6 + PGE2
29
What inflammatory mediators are responsible for Nausea?
IL-1 + TNF
30
What are the inflammatory mediators responsible for pain?
Bradykinin + PGE2
31
What inflammatory mediators lead to tissue damage in acute inflammation?
MMP + Super oxide + Hydroxyl radical + NO
32
What are the endogenous triggers for fever?
Phagocytosis + Tissue damage + Immune complexes
33
What are the exogenous pyrogens?
Bacterial endotoxins - LPS
34
What does PGE2 do to the hypothalamus?
increased body temperature through vasoconstriction + shivering
35
What needs to be reduced in order to reduce fever?
PGE2
36
What are the two ways the hypothalamus cause an increase in body temperature?
Vasoconstriction + Shivering
37
What are the clinical signs of acute inflammation?
Redness + Heat + Swelling + Pain + Loss of function
38
What is erythema?
Redness of the skin due to hyperemia
39
Is fever seen with allergic dermatitis?
No
40
Is there pain with allergic dermatitis?
Possible - due to bradykinin and PGE2
41
What is produced in regards to Ig with allergic dermatitis?
IgE
42
With a secondary infection post trauma and fracture repair will there be a fever? If so, from what?
Yes - IL-1 + TNF + IL-6 + PGE2
43
Describe effusion.
Fluid leaks into the body cavity rather then tissues
44
What would effusion look like if it DID NOT come from acute inflammation?
No fibirin + blood + cells/pus/exudate Appears clear Surrounding tissues will seem normal
45
What does serous effusion look like?
Clear, pale yellow appearance
46
What is transudate?
Extravascular ultra-filtrate of plasma with little protein and few to no cells
47
What is exudate?
Extravascular fluid that is rich in protein and/or cells | Fluids appears grossly cloudy
48
What are three types of exudate that is seen?
Sanguinous + Fibrinous + Purulent
49
What is sanguinous exudate?
Effusion with RBC's
50
What is fibrinous exudate?
Fibrin strands are present derived from a protein rich exudate
51
What is purulent exudate?
Numerous neutrophils are present
52
What is purulent exudate when located in the pleural space?
Empyema
53
What does the presence of fibrin tell you in exudate?
Acute inflammation + Leaky blood vessels
54
Why does fibrin occur with acute inflammation?
Fibrinogen is an acute phase protein released by the liver, and polymerizes once outside the vessels forming fibrin
55
What causes chylous ascites?
Blockage in the lymphatic drainage
56
What is type I hypersensitivity known as?
Immediate hypersensitivity
57
What is type I hypersensitivity's immunologic component?
IgE
58
What is type I hypersensitivity's antigen?
Allergen
59
What is type I hypersensitivity mechanism?
IgE produced Mast cell release of vasoactive amines Recruitment of other inflammatory cells
60
What occurs in type I hypersensitivity?
Vascular dilation edema Smooth muscle contraction Mucus production Inflammation
61
What is type 2 hypersensitivity known as?
Antibody mediated
62
What is type II hypersensitivity's immunologic component?
IgG + IgM
63
What is type II hypersensitivity's antigen?
Cell + Matrix + Surface receptor
64
What is type II hypersensitivity's immune mechanism?
IgG/IgM produced Bind to Ag on target cell Phagocytosis of cell via complement or Fc receptor Leukocyte recruitment
65
What occurs due to type II hypersensitivity?
Cell lysis + Inflammation
66
What is type III hypersensitivity known as?
Immune complex method
67
What is type III hypersensitivity's antigen?
Soluble antigen (Bacterial or viral)
68
What is type III hypersensitivity's immunologic component?
IgG + IgM
69
What is type III hypersensitivity's mechanism?
Ag+Ab complex deposition Complement activation Leukocyte recruitment Release of toxic enzymes + molecules
70
What occurs due to type III hypersensitivity?
``` Necrotizing vasculitis (aka Fibrinoid necrosis) Inflammation ```
71
What is type IV hypersensitivity carried out by?
Cell mediated
72
What is type IV hypersensitivity's immunologic component?
T cell
73
What is type IV hypersensitivity's antigen?
Soluble antigen contact | Cell-associated
74
What is type IV hypersensitivity's mechanism?
Activated T cells Cytokines + Macrophages T cell mediated cytotoxicity
75
What occurs with type IV hypersensitivity?
Perivascular cell infiltrates Edema Cell destruction Granuloma formation
76
What are examples of type I hypersensitivity?
Anaphylaxis | Atopyy
77
What are examples given in lecture for type II hypersensitivity?
``` Autoimmune Hemolytic anemia Neonatal isoerythrolysis Transfusion reactions Drug reactions Pemphigus ```
78
What are examples given in type III hypersensitivty?
Systemic lupus | Forms glomerulonephritis
79
What are examples given in lecture for type IV hypersensitivity?
Contact dermatitis Transplant rejection Tuberculosis Chronic allergic diseases
80
What is the cause of autoimmune disease?
Loss of immune tolerance to self; abnormal production or excessive activity of self-reactive Ab's or T-cells
81
What are the three basic ways that inflammation can act?
Primary mechanism Secondary contributor Precursor to chronic inflammation

Pathology I (19 decks)

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