Acute inflammation Flashcards
What is inflammation?
Rapid response to injury of vascularised living tissue.
Delivers defensive materials to a site of injury
What are the 6 common causes of acute inflammation?
Foreign bodies - splinters, dirt, suture
Immune reaction
Infections (bacteria, viral, parasitic) and microbial toxins
Tissue necrosis
Trauma (blunt and penetrating)
Physical and chemical agents
What are the 5 clinical signs of acute inflammation?
Rubor = redness
Calor = heat
Tumour = swelling
Dolor = pain
Loss of function - (this enforces rest)
Describe the changes in blood flow in inflammation?
Vasoconstricton (seconds)
Vasodilation (minutes) causing heat and redness
Permeability increases leading to oedema formation
Red cell stasis
How is vasodilation brought about?
By vasoactive mediators
Arterioles dilate - flow accerelates in to capillaries pressure rises
Increases delivery of fluid and leucocytes to area of injury
What happens to the wallls of the venules following vasodilation of the arterioles?
Become leaky and plasma can escape through tiny gaps between endothelial cells
What are prostaglandins?
What do they cause?
How can their production be blocked?
Substances which are produced in inflammation from cell membrane phospholipids
Cause vasodilation, and make the skin more sensitive to pain and cause fever
Blocked by asprin and NSAIDs so can reduce pain and swelling
Describe Starlings’ law of movement of fluid into tissue?
Fluid movement controlled by balance:
Hydrostatic pressure - pressure exerted on a vessel wall by fluid - this pushes fluid away
Oncotic pressure - pressure exerted by plasma proteins - draws fluid towards
In Acute inflamation describe what happens in:
Vasodilation
To the membrane permeability
What the final out come is?
– Vasodilatation = increased capillary hydrostatic pressure
– Increased vessel permeability = loss of plasma proteins into interstitium (increased interstitial oncotic pressure)
– Net flow of fluid OUT of vessel INTO interstitium
– OEDEMA (swelling – TUMOR)
Describe the formation of an exudate?
Occurs in inflammation – Increased vascular permeability – Protein rich (delivering proteins to area of injury)
Describe the formation of a transudate?
Fluid loss due to increased capillary hydrostatic pressure or reduced capillary oncotic pressure
No change of vascular permeability
Occurs in heart failure/hepatic failure/renal failure
What are the mechanisms that increase vascular permeability?
Endothelial contraction (gaps between endothelial cells)
Histamine, leukotrienes – Endothelial cytoskeleton reorganisation
Cytokines IL-1, TNF – Direct injury
Chemical, toxic burns – Leucocyte dependent injury
Enzymes and toxic oxygen species from leucocytes
Describe the four stages that are required for neutrophils to escape vessels?
- Stasis causes neutrophils to line up at the edge of blood vessels along the endothelium = MARGINATION
- Neutrophils then roll along endothelium, sticking to it intermittently = ROLLING
- Then stick more avidly = ADHESION
- Followed by EMIGRATION of neutrophils through blood vessel wal
How do neutrophils move through the interstition?
Through chemotaxis
Here they move along a chemical gradient of chemoattractants
Describe the phagocytotic roles of neutrophils?
What is opsonisation by neutrophils?
Describe what happens in appendicitis?
Blocked lumen (commonly faecolith) causes accumulation of bacteria, increased pressure, reduced blood flow
Describe what happens in Pneumonia
Many causative organisms – Streptococcus pneumoniae, Haemophilus influenzae
Signs and symptoms – Shortness of breath, fever, cough, sputum production, chest pain
Risk factors – Smoking, pre-existing lung condition (Chronic Obstructive Pulmonary Disease, asthma, malignancy)
