Acute Inflammation

Question 1

Clinical features of acute inflammation (Latin)

Answer 1

Rubor - redness
Tumor - swelling
Calor - heat
Dolor - pain
And loss of function

Question 2

Where is histamine released from and in response to what?

Answer 2

Mast cells, basophils, platelets.

Physical damage, immunologic reactions, C3a, C5a, IL-1, factors from neutrophils and platelets

Question 3

What does histamine cause?

Answer 3

Vascular dilation
Transient increase in vascular permeability
Pain

Question 4

What is fluid loss from vessels a result of?

Answer 4

Increased hydrostatic(blood) and oncotic(interstitium) pressure.

Question 5

Protein content in transudate and exudate

Answer 5

Exudate - high protein

Transudate - low protein

Question 6

Mechanisms of vascular leakage

Answer 6

Endothelial contraction
Cytoskeletal reorganisation
Direct injury
Leukocyte dependent injury
Increased transcytosis - channels across endothelial cytoplasm

Question 7

Infiltration of neutrophils

Answer 7

Margination - stasis causes neutrophils to line up at the edge of
blood vessels along the endothelium

Rolling - roll along endothelium

Adhesion - stick more avidly

Emigration - through blood vessel wall

Question 8

How do neutrophils escape from vessels?

Answer 8

Relaxation of inter-endothelial cell junctions.

Digestion of vascular basement membrane.

Question 9

O2 dependent killing mechanism

Answer 9

Produces superoxide and hydrogen peroxide.

H2O2-Myeloperoxidase-halide system - produces HOCl.

Question 10

O2 independent killing mechanism

Answer 10

Lysozyme & hydrolases

Bactericidal Permeability Increasing Protein (BPI)

Cationic proteins (‘Defensins’)

Question 11

Function of neutrophils

Answer 11

Phagocytise microorganisms

Results in purple to necrosis

Question 12

Chemical mediators

Answer 12

Protease - kinins, complement system, coagulation/fibrinolytic system

Prostaglandins/Leukotrienes

Cytokines/Chemokines - interleukins, TNF

Question 13

Increased blood flow chemical mediators

Answer 13

Histamine and prostaglandins

Question 14

Vascular permeability chemical mediators

Answer 14

Histamine and leukotrienes

Question 15

Neutrophils chemotaxis chemical mediators

Answer 15

C5a, LTB4, bacterial peptides

Question 16

Phagocytosis chemical mediators

Answer 16

C3b

Question 17

How does exudation of fluid combat injury?

Answer 17

Delivers plasma proteins to area of injury - immunoglobulins, inflammatory mediators, fibrinogen
Dilutes toxins
Increases lymphatic drainage - delivers microorganisms to phagocytes and antigens to immune system

Question 18

What are the mechanisms that help combat injury?

Answer 18

Exudation of fluid
Infiltration of cells - removes pathogenic bacteria and necrotic debris
Vasodilation - increases delivery and temperature
Pain and loss of function - enforces rest, reduces chance of further traumatic damage

Question 19

Local complications of acute inflammation

Answer 19

Swelling - blockage of tubes
Exudate - compression e.g. cardiac temponade
Loss of fluid
Pain and loss of function

Question 20

Systemic effects of acute inflammation

Answer 20

Fever - IL-1 and TNFalpha
Leukocytosis - increase in wbc
Acute phase response - decreased appetite, raised pulse rate, altered sleep pattern
Acute phase proteins - CRP, alpha1 antitrypsin, heptoglobin, fibrinogen, serum amyloid A protein

Question 21

Lobar pneumonia: causative organism, clinical course

Answer 21

Streptococcus pneumoniae.
Worsening fever, prostration, hypoxaemia, dry cough and breathlessness.
If treated can resolve completely.

Question 22

Skin blister: causes, predominant features

Answer 22

Heat, sunlight, chemical.
Pain and profuse exudate, few inflammatory cells therefore exudate clear unless bacterial infection develops, resolution or scarring.

Question 23

Abscess

Answer 23

Solid tissue. Inflammatory exudate forces tissue apart. Liquefactive necrosis in centre. High pressure therefore pain. Tissue damage and squash adjacent structures.

Question 24

Acute inflammation in serous cavity

Answer 24

Ascites, pleural or pericardial effusion. Localised fibrin deposition.