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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
Q

What cell is responsible for the cytokine release that stimulates acute phase protein release?

A

Macrophages

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26
Q

What are the examples given in lecture for acute phase proteins?

A

Fibrinogen + Prothrombin + Plasminogen + FVII + C-reactive proteins + SAA + Alpha-1 Antitrypsin

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27
Q

What are the functions of acute phase proteins?

A

Hemostasis
Lysis of bacteria
Bacteriostasis
Mopping up free radicals

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28
Q

What inflammatory mediators are responsible for fever?

A

IL-1 + TNF + IL-6 + PGE2

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29
Q

What inflammatory mediators are responsible for Nausea?

A

IL-1 + TNF

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30
Q

What are the inflammatory mediators responsible for pain?

A

Bradykinin + PGE2

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31
Q

What inflammatory mediators lead to tissue damage in acute inflammation?

A

MMP + Super oxide + Hydroxyl radical + NO

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32
Q

What are the endogenous triggers for fever?

A

Phagocytosis + Tissue damage + Immune complexes

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33
Q

What are the exogenous pyrogens?

A

Bacterial endotoxins - LPS

34
Q

What does PGE2 do to the hypothalamus?

A

increased body temperature through vasoconstriction + shivering

35
Q

What needs to be reduced in order to reduce fever?

A

PGE2

36
Q

What are the two ways the hypothalamus cause an increase in body temperature?

A

Vasoconstriction + Shivering

37
Q

What are the clinical signs of acute inflammation?

A

Redness + Heat + Swelling + Pain + Loss of function

38
Q

What is erythema?

A

Redness of the skin due to hyperemia

39
Q

Is fever seen with allergic dermatitis?

A

No

40
Q

Is there pain with allergic dermatitis?

A

Possible - due to bradykinin and PGE2

41
Q

What is produced in regards to Ig with allergic dermatitis?

A

IgE

42
Q

With a secondary infection post trauma and fracture repair will there be a fever? If so, from what?

A

Yes - IL-1 + TNF + IL-6 + PGE2

43
Q

Describe effusion.

A

Fluid leaks into the body cavity rather then tissues

44
Q

What would effusion look like if it DID NOT come from acute inflammation?

A

No fibirin + blood + cells/pus/exudate
Appears clear
Surrounding tissues will seem normal

45
Q

What does serous effusion look like?

A

Clear, pale yellow appearance

46
Q

What is transudate?

A

Extravascular ultra-filtrate of plasma with little protein and few to no cells

47
Q

What is exudate?

A

Extravascular fluid that is rich in protein and/or cells

Fluids appears grossly cloudy

48
Q

What are three types of exudate that is seen?

A

Sanguinous + Fibrinous + Purulent

49
Q

What is sanguinous exudate?

A

Effusion with RBC’s

50
Q

What is fibrinous exudate?

A

Fibrin strands are present derived from a protein rich exudate

51
Q

What is purulent exudate?

A

Numerous neutrophils are present

52
Q

What is purulent exudate when located in the pleural space?

A

Empyema

53
Q

What does the presence of fibrin tell you in exudate?

A

Acute inflammation + Leaky blood vessels

54
Q

Why does fibrin occur with acute inflammation?

A

Fibrinogen is an acute phase protein released by the liver, and polymerizes once outside the vessels forming fibrin

55
Q

What causes chylous ascites?

A

Blockage in the lymphatic drainage

56
Q

What is type I hypersensitivity known as?

A

Immediate hypersensitivity

57
Q

What is type I hypersensitivity’s immunologic component?

A

IgE

58
Q

What is type I hypersensitivity’s antigen?

A

Allergen

59
Q

What is type I hypersensitivity mechanism?

A

IgE produced
Mast cell release of vasoactive amines
Recruitment of other inflammatory cells

60
Q

What occurs in type I hypersensitivity?

A

Vascular dilation edema
Smooth muscle contraction
Mucus production
Inflammation

61
Q

What is type 2 hypersensitivity known as?

A

Antibody mediated

62
Q

What is type II hypersensitivity’s immunologic component?

A

IgG + IgM

63
Q

What is type II hypersensitivity’s antigen?

A

Cell + Matrix + Surface receptor

64
Q

What is type II hypersensitivity’s immune mechanism?

A

IgG/IgM produced
Bind to Ag on target cell
Phagocytosis of cell via complement or Fc receptor
Leukocyte recruitment

65
Q

What occurs due to type II hypersensitivity?

A

Cell lysis + Inflammation

66
Q

What is type III hypersensitivity known as?

A

Immune complex method

67
Q

What is type III hypersensitivity’s antigen?

A

Soluble antigen (Bacterial or viral)

68
Q

What is type III hypersensitivity’s immunologic component?

A

IgG + IgM

69
Q

What is type III hypersensitivity’s mechanism?

A

Ag+Ab complex deposition
Complement activation
Leukocyte recruitment
Release of toxic enzymes + molecules

70
Q

What occurs due to type III hypersensitivity?

A 
Necrotizing vasculitis (aka Fibrinoid necrosis) 
Inflammation
71
Q

What is type IV hypersensitivity carried out by?

A

Cell mediated

72
Q

What is type IV hypersensitivity’s immunologic component?

A

T cell

73
Q

What is type IV hypersensitivity’s antigen?

A

Soluble antigen contact

Cell-associated

74
Q

What is type IV hypersensitivity’s mechanism?

A

Activated T cells
Cytokines + Macrophages
T cell mediated cytotoxicity

75
Q

What occurs with type IV hypersensitivity?

A

Perivascular cell infiltrates
Edema
Cell destruction
Granuloma formation

76
Q

What are examples of type I hypersensitivity?

A

Anaphylaxis

Atopyy

77
Q

What are examples given in lecture for type II hypersensitivity?

A 
Autoimmune 
Hemolytic anemia 
Neonatal isoerythrolysis 
Transfusion reactions 
Drug reactions 
Pemphigus
78
Q

What are examples given in type III hypersensitivty?

A

Systemic lupus

Forms glomerulonephritis

79
Q

What are examples given in lecture for type IV hypersensitivity?

A

Contact dermatitis
Transplant rejection
Tuberculosis
Chronic allergic diseases

80
Q

What is the cause of autoimmune disease?

A

Loss of immune tolerance to self; abnormal production or excessive activity of self-reactive Ab’s or T-cells

81
Q

What are the three basic ways that inflammation can act?

A

Primary mechanism
Secondary contributor
Precursor to chronic inflammation

Pathology I (19 decks)

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