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Pain in acute inflammation occurs due to
A Prostaglandins
B Bradykinin
C Pressure by tissue fluid
D Leukotrienes
E Vasodilatation
Features of acute inflammation are increased
A ESR
B Leukocyte count
C C reactive protein
D Monocyte count
E IgG
The outcome of acute inflammation are
A Chronic inflammation
B Resolution
C Fibrosis
D Tumour
E Autoimmune disease
Events that occur early in acute inflammation are
A Emigration of neutrophils
B Dilatation of blood vessels
C Synthesis of C reactive protein
D Production of antibody by plasma cells
E Proliferation of blood vessels
Features associated with acute inflammation are
A Increased ESR
B Toxic granules in neutrophil
C Increased C-reactive protein
D Increased monocyte count
E Increased IgG
Acute inflammation is characterized by
A Alteration in vascular caliber that lead to an increased Blood Flow
B Structural changes in microvasculature that permit plasma protein & leukocyte to leave circulation
C Leukocyte emigration from microcirculation
D Tissue destruction and attempts of healing
E Mononuclear cell infiltration
The following mediators increase capillary permeability in acute inflammation
A Histamine
B Bradykinin
C Prostacyclin
D Platelet Derived Growth Factor (PDG
E Angiotensin
In acute inflammation, the chemical mediators have the following role
A Histamin causes vasodilatation
B C3a is a chemotactic agent
C TNF causes direct tissue damage
D Pain is produced by PAF
E Leukotriene have no effect on blood vessels
The following chemical mediators are responsible for vasodilatation in acute inflammation
A Bradykinin
B Histamin
C Nitric oxide
D Prostaglandins
E Leukotriene
Role of complement component in acute inflammation
A C3a increases vascular permeability
B Neutrophils are attracted by C5a
C C3b helps in phagocytosis
D C4a produces endothelial damage
E C5 activates kinin system

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