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mechanism of disease > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Inflammation

A

Reaction of vascularized tissue to injury

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2
Q

3 main functions of inflammation

A

Bring exudate to help in tissue healing

Bring exudate to tissue to destroy causative agent

Bring exudate to tissue to mediate local defense

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3
Q

2 types of inflammation

A

Acute

Chronic

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4
Q

Reaction phases of inflammation

A

Vascular

Cellular

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5
Q

Causes of inflammation

A

Microbial infections

Hypersensitivity

Physical agents

Irritants and corrosives chemicals

Tissue necrosis

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6
Q

Cardinal sign of acute infection

A 
Redness (rubor) 
Heat ( calor)
Swelling (tumor)
Pain (dolor)
Loss of function
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7
Q

Typical lab findings of inflammation

A

High neutrophil
High ESR
High acute phase proteins

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8
Q

Constitutional symptoms of inflammation

A

Pyrexia
Malaise
Anorexia
Nausea

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9
Q

Hematological change of inflammation

A

Increased erythrocytes sedimentation rate

Leukocytosis

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10
Q

When do you have eosinophilia

A

Allergic disorders and parasitic infections

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11
Q

When do you have lymphocytosis

A

Chronic infection
Viral infection
Whooping cough

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12
Q

When do you have monocytosis

A

Infectious mononucleosis

Bacterial infections

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13
Q

Why would you have anemia in inflammation

A

Inflammatory exudate with blood loss

Haemolysis ( bacterial toxins)

Anemia of chronic disorders

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14
Q

Why is there amyloidosis in inflammation

A

Happens in chronic inflammation with elevated serum amyloid A protein deposited in all tissues

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15
Q

Acute inflammation

A

Rapid onset and short duration inflammation with exsudation of protein rich fluid with a lot of neutrophils

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16
Q

Steps of acute inflammation

A 
Transient vasoconstriction 
Vasodilation 
Increased blood flow to area with transient transsudation 
Increased fluid exudate 
Increased viscosity 
Stasis 
Margination
Pavementing of leucocytes 
Emigration of leucocytes 
Chemotaxis 
Phagocytosis
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17
Q

Where does vasodilation happens ?

A

Precapillary arterial level

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18
Q

What causes calor and rubor

A

Hyperemia due to increased blood flow

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19
Q

What molecules cause vasodilation in acute inflammation?

A

Histamine

Nitric oxide

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20
Q

How is plasma able to escape into tissue ?

A

Thanks to increased vascular permeability

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21
Q

Why does viscosity of blood increases ?

A

Fluid loss in tissue makes RBC concentration higher

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22
Q

Immediate transient response

A

When mild injury , increased permeability at venules and small veins

Fast , short lived

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23
Q

Mediators of immediate transient response

A

Bradykinin
Histamine
Leukotriene

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24
Q

Delayed prolonged response

A

In moderate injury
After 2-12h
Last for hours to days
Affects venules and capillaries

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25
Q

Immediate sustained response

A

After severe injury
Cause cell death and detachment
All levels of micro circulation affected
Fluid leaked immediate and last for days

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26
Q

Mechanism of increased permeability

A

(Immediate transient)Endothelial gaps in venules due to myosin contraction caused by histamine bradykinin leukotrienes substance p c5a and c3a

(Delayed response)Structural reorganization of cytoskeleton due to endothelial cell retraction by IL1 TNF INFgamma

( immediate sustained injury )Direct endothelial injury with necrosis and detachment

(Leucocyte mediated injury-immediate sustained )neutrophils adhering to endothelium causing injury

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27
Q

Main cell of acute inflammation

A

Neutrophils

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28
Q

During acute inflammation , how is the number of developing neutrophils increased

A

Growth factors derived from inflammation stimulate myeloid precursors division

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29
Q

Steps of neutrophils action in acute inflammation

A

Margination
Rolling
Adhesion To Endothelium
Migration to interstitium with chemotactic gradient

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30
Q

Margination in acute inflammation

A

Stasis causes movement of leucocytes to periphery of endothelium

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31
Q

Neutrophils pavementing in acute inflammation

A

Neutrophils adhere to endothelium through adhesion molecules (rolling)
Endothelium lined with neutrophils

32
Q

Emigration of neutrophils in acute inflammation

A

Motile leucocytes escape from blood

Occur mostly in venules except in lungs

33
Q

Neutrophils life span

A

13 days

34
Q

First leucocyte you move in viral and ricketsial infection

A

Lymphocytes

35
Q

Dominant leucocyte in type I hypersensitivity

A

Eosinophils

36
Q

Predominant leucocyte in typhoid fever

A

Macrophages

37
Q

Chemotaxis in acute inflammation

A

Leucocyte migrate towards site of injury by chemotactic agents ( C5a, arachidonic acid, IL8)

38
Q

Phagocytosis

A

A process in which a cell ingest solid particles

39
Q

Stages of phagocytosis

A

Recognition and attachment
Engulfment
Killing and degradation

40
Q

Opsonization

A

Particles are coated by serum proteins to enhance phagocytosis

41
Q

Major opsonins

A

IgG
Fibronectin
C3b

42
Q

2 types of bacterial killing mechanism

A

Oxygen dépendant mechanism

Oxygen independent mechanism

43
Q

Species involved in oxygen dépendant phagocytosis

A

Hydrogen peroxide

Toxic Hypohalite ions (halogen and oxidase action to kill constituents)

Peroxide anions

Hydroxyl radicals

Nitric oxide

44
Q

Oxygen independent phagocytosis

A 
Phospholipase 
Lactoferrin (iron binding protein)
Lysozyme muraminidase
Defensins
Low pH
45
Q

Chronic granulomatous disease

A

Deficient oxygen dependent phagocytosis due to defects in gene
Lead to recurrent bacterial infections

46
Q

Cell derived mediators of inflammation

A 
Vasoactive amines
Arachidonic acid 
Cytokines
Lysosomal cpds 
Nitric oxide
47
Q

Plasma derived mediators of inflammation

A

Plasma processes
clotting systems
Kinin systems

48
Q

Preformed mediators

A

Histamine
Serotonin
Lysosomal enzymes

49
Q

Histamine action (vasoactive amines)

A

Vascular dilatation

Immediate transient

IgE mediate hypersensitivity

Stored in mast cells basophils eosinophils platelets

Endothelial cell contraction

Increased membrane permeability

Makes endothelium sticky

50
Q

Histamine release is stimulated by

A

Complement c3a, c5a and lysosomal proteins

51
Q

Serotonin

A

Found in platelet

Acts like histamine

52
Q

Serotonin release mediated by

A 
Platelet aggregation 
Collagen 
Thrombin
ADP
antigen antibody complexes
53
Q

Platelet activating factor action

A

Platelet aggregation

Vasoconstriction

Bronchoconstriction

Vasodilation at low concentration

Leucocyte adhésion

Chemotaxis

Oxidative burst

54
Q

Arachidonic acid metabolism

A

Prostaglandins - vasodilators , pain , fever

Leucotrienes - neutrophils aggregation and chemotaxis ( LTB4) , increased vascular permeability ( SRS A) , endogenous negative regulators (lipoxins)

55
Q

What type of drugs inhibit COX

A

NSAIDs like aspirin

56
Q

What are the molecules inhibited by glucocorticoids to repress inflammation

A 
Cox 1
Cox 2 
Il1 
TNF
NO
AA
57
Q

Role of pro inflammatory cytokines

A 
Growth 
Differentiation 
Chemotaxis 
Activation 
Cytotoxicity 
Immune regulation
58
Q

Chemokines types

A

CXC a-chemokines (neutrophils)

CC b-chemokines (monocytes, eosinophils, basophils, lymph’s)

C y-chemokines (lymphocytes)

59
Q

Nitric oxide

A

Vasodilatation

Reduces platelet aggregation and adhesion

60
Q

Plasma protease types

A

Complement system - act on vessel wall, form MAC for lysis of microbes

Kinin system- produce bradykinin ( vascular permeability, vascular dilatation, smooth muscle contraction and pain )

Clotting system - fibrin in exudate, thrombin increase leucocyte adhésion, coagulation factor xii activate coagulation

61
Q

Effect of c3a and c5a

A

Anaphylatoxins
Vasodilation
Release histamine
Chemotaxis (c5a)

62
Q

C3b action

A

Opsonins

63
Q

What molecules participate in termination of acute inflammation

A

Anti inflammatory cytokines ( il4, th2, il10, tgfb,
Glucocorticoids
Protein c

64
Q

Morphologic patterns of acute inflammation

A

Serous inflammation

Fibrinous inflammation

Suppurative inflammation

Abcess

Empyema

Haemmorhagic inflammation

Catarrhal inflammation

Pseudomembranous inflammation

Membranous inflammation

Gangrenous inflammation

65
Q

Serous inflammation

A

Proteinaceous exudates with few cells

66
Q

Fibrinous inflammation

A

Fibrin rich exudate with shaggy strands

67
Q

Suppurative inflammation

A

Numerous polymorphes and cell debris

68
Q

Abcess

A

Localised collection of pus

69
Q

Empyema

A

Collection of pus in a natural body cavity

70
Q

Hemorrhagic inflammation

A

Vascular damage by highly virulent organisms and ischaemia

71
Q

Catarrhal inflammation

A

Watery fluid secretion from epithelial surface with acute inflammation seen in common cold

72
Q

Paeudomembranous inflammation

A

Superficial mucosal ulceration with formation of membrane like surface containing fibrin mucus and inflammatory cells but no epithelial cells

73
Q

Membranous inflammation

A

Epithelial surface coated by fibrin , desquamated epithelial cells

74
Q

Gangrenous inflammation

A

Vascular stasis leading to thrombus leading to necrosis. Inflammatory response against nécrose

75
Q

How are drugs transported to site of infection

A

Through exudate

mechanism of disease (22 decks)

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