Acute Inflammation

Question 1

Acute inflammation

Answer 1

A series of protective changes occurring in living tissue as a response to injury. Non-specific response.

Question 2

Causes of acute inflammation

Answer 2

Micro-organisms; bacteria, fungi, viruses, parasites. Mechanical; trauma, injuries include sterile one (surgery).
Chemical; acid/alkali, bile and urine.
Physical; heat, cold, ionising radiation
Dead tissue; cell necrosis irritates adjacent tissue.
Hypersensitivity; allergy, asthma, anaphylaxis

Question 3

Benefits of acute inflammation

Answer 3

• It’s a rapid response to a non-specific insult.
• Cardinal signs and a loss of function provide transient protection of inflamed area.
• Neutrophils destroy organisms and denature antigen for macrophages.
• Plasma proteins localise the process.
• Resolution and normality is eventually restored.

Question 4

Sequence of microvascular changes

Answer 4

It is localised to affected tissue and occurs in the microcirculation. Triple response; flush, flare, wheal
1) Transient arteriolar constriction
2) Local arteriolar dilation/active hyperaemia.
3) Relaxation of vessel’s smooth muscle
A tiny change in the radius of a vessel leads to a big change in flow.

Question 5

Sequence of events in exudate formation

Answer 5

1) Increase in vascular permeability
2) Plasma proteins, leukocytes, and more fluid from the blood form an exudate and exude into the tissue space.
3) Oedema; the accumulation of fluid in the extravascular space and so explains swelling.
4) Swelling leads to pain and reduced function.

Question 6

Local effects of acute inflammation

Answer 6

Rubor/redness, calor/heat, tumor/swelling, dolor/pain, loss of function

Question 7

Systemic effects of acute inflammation

Answer 7

Pyrexia, malaise, anorexia, nausea, abdo pain, vomiting, neutrophilia, lymphadenopathy, weight loss, anaemia, shock (peripheral vasodilation, tachy, hypotension, haemorrhagic skin rash).

Question 8

Complications of acute inflammation

Answer 8

1. Suppuration - pus formation, pyogenic membrane surrounds pus. Abscess - collection of pus under pressure. Empyema - pus in a hollow viscus. Pyaemia - discharge to blood stream.
2. Organisation; healing and repair by granulation tissue leading to fibrosis and a scar.
3. Dissemination; septic shock (spread to bloodstream), bacteraemia (bacteria in blood), septicaemia (growth of bacteria in blood stream), toxaemia (toxic products in blood stream).
4. Chronic inflammation

Question 9

Granulation tissue

Answer 9

Repair kit/universal patch formed of new capillaries, fibroblasts, collagen and macrophages.

Question 10

Cell surface mediators

Answer 10

ICAM-1; adhesion molecules on endothelial cells that help neutrophils stick.
P-selectin; interacts with neutrophil surface.

Question 11

Mediators released from cells

Answer 11

• Histamine causes vasodilation and occurs in IgE mediated reactions.
• 5-Hydroxytryptamine is released when platelets degranulate in coagulation and increases vascular permeability.
• Prostaglandins cause vasodilation many of which promote histamine and inhibit inflammatory cells.
• Leukotrines increase vascular permeability.
• Omega-3 polyunsaturated FA decrease synthesis of above 2.
• Platelet activating factor decreases permeability by enhancing platelet degranulation.
• cytokines and chemokines (TNF) cause fever and attract inflammatory cells.
• NO causes vasodilation and relaxes smooth muscle, anti-platelet, regulates leukocyte recruitment.
• O2 free radicals amplify other mediator effects.

Question 12

Plasma mediators

Answer 12

Blood coagulation pathway
Fibrinolysis
Kinin system (bradykinin)
complement cascade

Question 13

How can the process of acute inflammation be altered to the detriment of the patient?

Answer 13

1. vasodialtion/constriction
2. altered permeability
3. neutrophil adhesion
4. chemotaxis
5. itch/pain
   Both positive and negative effects resulting in a dynamic balance which either favours or inhibits acute inflammation relative to need.