Flashcards in Session 2 Deck (16):
What are the two key features of acute inflammation?
Innate and stereotyped
I.e active from birth and always the same
What are the major causes of acute inflammation
Acute phase hypersensitivity reactions
What are the characteristic clinical signs of acute inflammation?
Loss of functoin
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.
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.
What are prostaglandins?
They are produced in inflammation from arachadonic acid via COX 1/ COX 2 and cause vasodilation, pain and fever.
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
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
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
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
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
What are the systemic consequences of acute inflammation?
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.
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
What are the sequelae of acute inflammation?
Chronic inflammation and fibrous repair
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.