MoD: Inflammation

Question 1

What is acute inflammation?

Answer 1

The initial tissue reaction to injury. INNATE IMMUNITY

Characteristic cell is the neutrophil polymorph

Question 2

Physical characteristics of acute inflammation?

Answer 2

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

Question 3

What are the 3 major components of acute inflammation?

Answer 3

1) Changes in vessel calibre
2) Increased vascular permeability and fluid exudate formation
3) Cellular exudate formation

Question 4

What is exudate?

Answer 4

Extravascular fluid with high protein concentration, containing cellular debris

Question 5

What are some of the changes in vessel calibre during acute inflammation?

Answer 5

Vasodilation
Increases blood flow
Heat and redness
Mediated by histamine and NO on vascular smooth muscle

Question 6

What are some effects of the fluid exudate?

Answer 6

Dilution of toxins
Entry of antibodies
Transport of drugs
Fibrin formation
Delivery of nutrients/ oxygen

Question 7

What are the 4 plasma derived mediators of Acute Inflammation?

Answer 7

1) Complement System
2) Kinin System
3) Coagulative System
4) Fibrinolytic System

Question 8

What are 5 cell derived mediators of Acute Inflammation?

Answer 8

1) Histamine (released by mast cells, increases vascular dilation and permeability)
2) Prostaglandins (long chain fatty acids from arachidonic acid)
3) Lysosomal components
4) Leukotrienes
5) Cytokines

Question 9

Synthetic pathways of mediators: how do glucocorticoids work?

Answer 9

Glucocorticoids (cortisol, cortisone, prednisolone, dexamethasone) bind to the glutocorticoid receptor (GR). The activated GR complex:

• –Upregulates the expression of anti-inflammatory proteins in the nucleus (transactivation)
• –Represses the expression of proinflammatory proteins in the cytosol (transrepression)

Question 10

Synthetic pathways of mediators: how do NSAIDS work?

Answer 10

NSAIDS (aspirin, ibuprofen, naproxen) inhibit the activity of COX-1 and COX-2 and therefore the synthesis of prostaglandins and thromboxanes.
Inhibiting COX-2 = anti-inflam, analgesic and antipyretic effects. (however inhibiting COX-1 may cause GI bleeding and ulcers)

Question 11

What is chronic inflammation?

Answer 11

Innate and Adaptive immunity.
Angiogenesis, fibrosis.
Involves macrophages, lymphocytes, plasma cells.

Question 12

How does chronic inflammation arise?

Answer 12

• Progression from acute eg) H. Pylori
• Recurrent episodes of acute eg) chronic cholecystitis
• Persistent infection from certain microorganisms eg)TB, leprosy
• Prolonged exposure to potentially toxic agents (endogenous eg- bone, exogenous eg- asbestos, sutures)
• Autoimmunity eg) rheumatoid arthritis
• Unknown eg) Crohn’s disease, ulcerative colitis

Question 13

What is a granuloma?

Answer 13

A collection of activated epithelioid macrophages (pink cytoplasm, indistinct cell membranes, oval nucleus)
Surrounded by mononuclear leucocytes
Caseating or non-caseating

Question 14

What does caseating mean?

Answer 14

Appears cheese-like. Contains necrosis. (typically a feature of granulomas of TB)