Session 2

Question 1

What is the aim of inflammation?

Answer 1

Protect the body against infection, clear damaged tissue and initiate tissue repair.

Question 2

What are the causes of acute inflammation?

Answer 2

Foreign bodies
Immune reactions
Infections and microbial toxins
Tissue necrosis
Chemical and physical agents

Question 3

What are the characteristic clinical signs of acute inflammation?

Answer 3

Color - heat
Rubor - redness
Tumor- swelling 
Dollar - pain
Loss of function

Question 4

Describe the steps of acute inflammation

Answer 4

Vasodilation of arterioles brought about by vasoactive mediators
Endothelial cells swell and retract to form gaps
Vessels become leaky and exudate leaks through
Circulating neutrophils adhere to swollen endothelial cells (margination) and then migrate through the basement membrane (emigration).
Macrophages and lymphocytes migrate in a similar way to neutrophils

Question 5

List some important chemical mediators of acute inflammation

Answer 5

Histamine - released from mast cells, basophils and platlets. Produces pain, arteriolar dilation, venous leakage and contraction of endothelial cells.
Bradykinin - causes pain and increased vascular permeability
Prostaglandin - causes pain, vasodilation and fever
Complement system - form a membrane attack complex to kill bacteria
Clotting and fibrinolytic cascades create inflammatory mediators
Exogenous mediators such as endotoxin

Question 6

What are the main types of defensive proteins in exudate?

Answer 6

Opsonins - coat foreign material making them easier to phagocytose
Complement - assemble to produce a bacteria perforating surface
Antibodies - bind to the surface of microorganisms and also act as an opsonin

Question 7

What is a transudate?

Answer 7

A protein poor fluid formed in normal vessels. Seen as oedema.

Question 8

Outline the steps in how a neutrophil kills a bacterium

Answer 8

Chemotaxis - be summoned to the place of injury by chemotoxins
Activation - switch to a higher metabolic level
Margination - stick to the endothelial surface
Diapedesis-crawl through the endothelium
Recognition/attachment of the bacterium
Phagocytosis

Question 9

Lost some examples of chemotoxins

Answer 9

Bacterial products (eg endotoxins), injured tissues, substances produced by leukocytes, spelled blood and complement components.

Question 10

How does a neutrophil become activated?

Answer 10

Binds to chemotaxin. Na+ and Ca2+ rush into the cell. Cell becomes stickier.

Question 11

How do neutrophils become trapped to vessel walls and crawl through epithelium?

Answer 11

Become trapped by adhesion molecules called selectins and integrins. Margination -> rolling -> adhesion. They dig themselves out of venules by producing collagenase that digests the basement membrane (diapedesis).

Question 12

How are phagocytosed organisms killed?

Answer 12

Oxygen dependent - using O2 derived free radicals for a respiratory burst
Oxygen independent - using enzymes

Question 13

How are mediators of inflammation limited?

Answer 13

They have a short life span and inhibitor molecules

Question 14

Describe some local complications of acute inflammation in tissues

Answer 14

Damage to normal tissue secondary to substances produced by neutrophils
Obstruction of tubes (eg bile duct) and compression of vital structures (eg cardiac tamponade) secondary to swelling
Loss of fluid (eg burns)
Pain and loss of function

Question 15

Describe some systemic complications of acute inflammation

Answer 15

Fever - due to mediators acting on the hypothalamus. Can be useful because it can kill some bacteria and inflammation is more effective at higher temperatures.
Leukocytosis - increase in the number of circulating leukocytes
Acute phase response - sleepiness and reduced appetite due to changes in plasma levels of certain proteins brought about by the liver.
Shock - dramatic drop in BP due to widespread vasodilation and increase in vascular permeability.

Question 16

What may happen after the development of acute inflammation?

Answer 16

Complete resolution
Continued acute inflammation with chronic inflammation (abscesses) and fibrous repair
Death

Question 17

Describe the process of resolution of acute inflammation

Answer 17

All mediators have short half lives and are inactivated by depredation, dilution or inhibition.
Vascular changes stop - neutrophils no longer marginate and vascular permeability returns to normal.
Exudate is reabsorbed by venules or drained by lymphatics. Fibrin is degraded and neutrophils undergo apoptosis.

Question 18

What are clinical examples of acute inflammation?

Answer 18

Lobar pneumonia - Infection by streptococcus pneumoniae.
Acute appendicitis
Bacterial meningitis - group B streptococci in newborns and Neisseria meningitis in children
Liver abscesses and ascending colangitis

Question 19

What is hereditary Anglo-oedema?

Answer 19

Rare autosomal dominant deficiency of C1 esterase inhibitor - a component of the complement system.
Patient experiences rapid attacks of non-itchy cutaneous Angio-oedema and abdominal pain due to intestinal oedema.

Question 20

What is chronic granulomatous disease?

Answer 20

Phagocytes are unable to produce superoxide molecules, so they cannot kill bacteria. Chronic infections occur along with granulomas and abscesses in the skin, liver and lymph nodes.