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mechanism of disease > Inflammation > Flashcards

Inflammation Flashcards

(75 cards)

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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
Immediate sustained response
After severe injury Cause cell death and detachment All levels of micro circulation affected Fluid leaked immediate and last for days
26
Mechanism of increased permeability
(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
27
Main cell of acute inflammation
Neutrophils
28
During acute inflammation , how is the number of developing neutrophils increased
Growth factors derived from inflammation stimulate myeloid precursors division
29
Steps of neutrophils action in acute inflammation
Margination Rolling Adhesion To Endothelium Migration to interstitium with chemotactic gradient
30
Margination in acute inflammation
Stasis causes movement of leucocytes to periphery of endothelium
31
Neutrophils pavementing in acute inflammation
Neutrophils adhere to endothelium through adhesion molecules (rolling) Endothelium lined with neutrophils
32
Emigration of neutrophils in acute inflammation
Motile leucocytes escape from blood | Occur mostly in venules except in lungs
33
Neutrophils life span
13 days
34
First leucocyte you move in viral and ricketsial infection
Lymphocytes
35
Dominant leucocyte in type I hypersensitivity
Eosinophils
36
Predominant leucocyte in typhoid fever
Macrophages
37
Chemotaxis in acute inflammation
Leucocyte migrate towards site of injury by chemotactic agents ( C5a, arachidonic acid, IL8)
38
Phagocytosis
A process in which a cell ingest solid particles
39
Stages of phagocytosis
Recognition and attachment Engulfment Killing and degradation
40
Opsonization
Particles are coated by serum proteins to enhance phagocytosis
41
Major opsonins
IgG Fibronectin C3b
42
2 types of bacterial killing mechanism
Oxygen dépendant mechanism | Oxygen independent mechanism
43
Species involved in oxygen dépendant phagocytosis
Hydrogen peroxide Toxic Hypohalite ions (halogen and oxidase action to kill constituents) Peroxide anions Hydroxyl radicals Nitric oxide
44
Oxygen independent phagocytosis
``` Phospholipase Lactoferrin (iron binding protein) Lysozyme muraminidase Defensins Low pH ```
45
Chronic granulomatous disease
Deficient oxygen dependent phagocytosis due to defects in gene Lead to recurrent bacterial infections
46
Cell derived mediators of inflammation
``` Vasoactive amines Arachidonic acid Cytokines Lysosomal cpds Nitric oxide ```
47
Plasma derived mediators of inflammation
Plasma processes clotting systems Kinin systems
48
Preformed mediators
Histamine Serotonin Lysosomal enzymes
49
Histamine action (vasoactive amines)
Vascular dilatation Immediate transient IgE mediate hypersensitivity Stored in mast cells basophils eosinophils platelets Endothelial cell contraction Increased membrane permeability Makes endothelium sticky
50
Histamine release is stimulated by
Complement c3a, c5a and lysosomal proteins
51
Serotonin
Found in platelet Acts like histamine
52
Serotonin release mediated by
``` Platelet aggregation Collagen Thrombin ADP antigen antibody complexes ```
53
Platelet activating factor action
Platelet aggregation Vasoconstriction Bronchoconstriction Vasodilation at low concentration Leucocyte adhésion Chemotaxis Oxidative burst
54
Arachidonic acid metabolism
Prostaglandins - vasodilators , pain , fever Leucotrienes - neutrophils aggregation and chemotaxis ( LTB4) , increased vascular permeability ( SRS A) , endogenous negative regulators (lipoxins)
55
What type of drugs inhibit COX
NSAIDs like aspirin
56
What are the molecules inhibited by glucocorticoids to repress inflammation
``` Cox 1 Cox 2 Il1 TNF NO AA ```
57
Role of pro inflammatory cytokines
``` Growth Differentiation Chemotaxis Activation Cytotoxicity Immune regulation ```
58
Chemokines types
CXC a-chemokines (neutrophils) CC b-chemokines (monocytes, eosinophils, basophils, lymph’s) C y-chemokines (lymphocytes)
59
Nitric oxide
Vasodilatation Reduces platelet aggregation and adhesion
60
Plasma protease types
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
Effect of c3a and c5a
Anaphylatoxins Vasodilation Release histamine Chemotaxis (c5a)
62
C3b action
Opsonins
63
What molecules participate in termination of acute inflammation
Anti inflammatory cytokines ( il4, th2, il10, tgfb, Glucocorticoids Protein c
64
Morphologic patterns of acute inflammation
Serous inflammation Fibrinous inflammation Suppurative inflammation Abcess Empyema Haemmorhagic inflammation Catarrhal inflammation Pseudomembranous inflammation Membranous inflammation Gangrenous inflammation
65
Serous inflammation
Proteinaceous exudates with few cells
66
Fibrinous inflammation
Fibrin rich exudate with shaggy strands
67
Suppurative inflammation
Numerous polymorphes and cell debris
68
Abcess
Localised collection of pus
69
Empyema
Collection of pus in a natural body cavity
70
Hemorrhagic inflammation
Vascular damage by highly virulent organisms and ischaemia
71
Catarrhal inflammation
Watery fluid secretion from epithelial surface with acute inflammation seen in common cold
72
Paeudomembranous inflammation
Superficial mucosal ulceration with formation of membrane like surface containing fibrin mucus and inflammatory cells but no epithelial cells
73
Membranous inflammation
Epithelial surface coated by fibrin , desquamated epithelial cells
74
Gangrenous inflammation
Vascular stasis leading to thrombus leading to necrosis. Inflammatory response against nécrose
75
How are drugs transported to site of infection
Through exudate

mechanism of disease (22 decks)

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