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Flashcards in Session 2 Deck (16):
1

What are the two key features of acute inflammation?

Innate and stereotyped
I.e active from birth and always the same

2

What are the major causes of acute inflammation

Microbial infections
Acute phase hypersensitivity reactions
Physical agents
Chemicals
Tissue necrosis

3

What are the characteristic clinical signs of acute inflammation?

Rubor
Tumor
Calor
Dolor
Loss of functoin

4

What are the tissue changes in acute inflammation and how are they brought about?

Vascular flow —> vasodilation of arterioles due to histamine. This causes flow to accelerate and capillary pressure rises. This increases delivery of fluid and leucocytes to area of injury.

5

What is histamine?

A vasoactive amine that is released from granules of mast cells, basophils and platelets and is released in response to physical damage, immune reactions and complement components.

6

What are prostaglandins?

They are produced in inflammation from arachadonic acid via COX 1/ COX 2 and cause vasodilation, pain and fever.

7

How is the exudate formed in acute inflammation

Walls of venules become leaky and proteins can escape through tiny gaps between endothelial cells

Increased pressure within vessels causes exudation of fluid into tissue spaces

8

How do neutrophils emmigrate to the site of injury?

Chemotaxis-movement along chemical gradient of chemoattractants towards site of injury

Activation- switch to higher metabolic level
Margination- rolling along endothelial surface
Diapedesis- crawl through endothelium
Recognition attachment- recognise bacterium and attach to it
Phagocytosis- engulf the bacterium
Oxygen dependent or independent killing

9

How do the clinical signs of acute inflammation relate to the tissue changes?

Rubor/calor- caused by increased blood flow to area

Dolor- prostaglandins and other chemical messengers cause pain to tell brain to protect that body part

Tumour- swelling caused by fluid exudate

10

How do the changes in acute inflammation help?

Increased delivery of nutrients, oxygen, cells, plasma proteins to site of injury

Dilution of toxins

Maintenance of temperature

Stimulation of immune response

Destruction and removal of dead or foreign material

Pain or loss of function enforcing rest

11

What are the local complications of acute inflammation?

Damage to normal tissue
Obstruction of tubes, compression of vital structures
Loss of fluid
Pain and loss of function

12

What are the systemic consequences of acute inflammation?

Fever
Leucocytosis

Acute phase response- change in levels of plasma proteins as liver changes its pattern of protein synthesis. Eg albumin, fibrinogen, C3, alpha 1 antitrypsin, CRP. APR is stimulated by cytokine release from immune cells. This causes sleepiness and a lack of appetite.

Shock

13

How is acute inflammation resolved?

Short half lives of inflammatory mediators
Trigger is removed
Normal vascular permeability returns
Cessation of emigration of neutrophils
Exudate reabsorbed into venules or drained by lymphatics
Fibrin is degraded
Neutrophils undergo apoptosis

If regeneration cannot occur, a fibrous scar will form

14

What are the sequelae of acute inflammation?

Abcess
Chronic inflammation and fibrous repair
Death

15

What is hereditary angioedema?

Rare autosomal dominant condition- patients have a C1 esterase inhibitor deficiency. Patients have attacks of non itchy cutaneous angio-oedema. They also have recurrent abdo pain due to intestinal oedema.

16

What is chronic granulomatous disease?

Phagocytes are unable to produce superoxide so cant kill pathogens. This results in granuloma formaiton. This also causes many chronic infections and abcesses.