MOD S3 Flashcards
What are some causes of acute inflammation?
Microbial infections Hypersensitivity reactions (aka allergies) Physical agents Chemical agents Tissue necrosis
What is acute inflammation?
The response of living tissue to injury, initiated to limit tissue damage
What are the macroscopic signs of inflammation?
Calor - heat
Rubor - redness
Tumor - swelling
Dolor - pain
+ loss of function
What are the microscopic features of acute inflammation?
Vasodilation Gaps form in endothelium Exudation Margination and emigration Macrophages and lymphocytes
Describe the changes in blood flow in acute inflammation
Transient vasoconstriction of arterioles (a few secs)
Vasodilation of arterioles and then capillaries
Increased blood vessel permeability
Stasis- increased concentration of RBCs in small vessels and blood viscosity
What are some chemical mediators of vasodilation?
HISTAMINE
Prostoglandins
C3a
C5a
Describe histamine
-Released ~30 mins into acute inflammation
-Many stimuli
-Released by mast cells, basophils and platelets
-Causes:
>Vasodilation
>Transient increase in vascular permeability
>Pain
What are some chemical mediators of increased vascular permeability?
HISTAMINE
Prostoglandins
Kinins
What determines fluid flow across blood vessel walls?
Starling’s Law
The balance of hydrostatic and colloid osmotic pressure
An increase in either will increase fluid movement out of blood vessel
What is a build up of tissue fluid called?
Oedema
What does oedema lead to?
Increased lymphatic drainage
What is a transudate?
Fluid loss from blood vessels due to hydrostatic pressure only
Has a low protein content
Caused by cardiac failure or venous outflow obstruction
What is exudate?
Fluid loss from blood vessels
Seen in inflammation
Has a high protein content
What are some chemical mediators of leukocyte emigration?
Leukotrienes
IL-8
C5a
What is another name for a neutrophil?
A polymorph
What do neutrophils do?
Move to the site of cell injury by chemotaxis
Phagocytose microorganisms by making contact, recognising and internalising them
Phagosomes then fuse with lysosomes to destroy contents
Activated neutrophils may release toxic metabolites and enzymes with damage host tissue
What is the difference between transudate and exudate?
Transudate has a low protein content
Exudate has a high protein content
What are some signs of the acute phase response of inflammation?
Decreased appetite
Tachycardia
Altered sleep patterns
Changes in plasma concentrations of acute phase proteins eg CRP, Fibrinogen and α1-anti trypsin
What causes fever?
Production of endogenous pyrogens eg IL-1 TNFα and prostoglandin
What is leukocytosis
The process by which white blood cell production is accelerated
By IL-1, TNFα
Colony simulating factors released by macrophages and t-lymphocytes
What are the possible end results of acute inflammation?
Complete resolution
Continued acute inflammation and chronic inflammation (eg abscess)
Chronic inflammation with fibrous repair
Death
How may the mediators of acute inflammation be inactivated?
Degradation
Dilution
Inhibition
(Most have short half lives so degrade normally anyway)
Name the stages of neutrophil invasion in acute inflammation
Margination
Rolling
Adhesion
Emigration
Describe margination (in acute inflammation)
First stage
Stasis causes neutrophils to line up along the edges of blood vessels
Describe rolling (in acute inflammation)
Second stage
Neutrophils roll along endothelium, intermittently sticking to it
Describe adhesion (in acute inflammation)
Third stage
The neutrophils stick more firmly to the endothelial walls of blood vessels
Describe emigration (in acute inflammation)
Final stage
Neutrophils move through blood vessel walls into tissues
When is complete resolution impossible?
When cell architecture of damaged cells is destroyed
How is complete resolution achieved?
All the changes of acute inflammation reverse Mediators are inactivated Neutrophils present die Exudate drains via lymphatics Fibrin is degraded by plasmin ect Vascular changes stop: >Neutrophils no longer marginate >Vessel calibre and permeability returns to normal
What are some possible complications of acute inflammation?
Blockage of tubes Compression Loss of fluid Pain Loss of function
Give a few clinical examples of acute inflammation
Skin blister
Abscess
Pericarditis
What happens in the case of sun blisters?
Caused by heat, sunlight or chemicals Pain and profuse exudate Collection of fluid strips off overlying epithelium Resolution or scarring Few inflammatory cells so clear exudate
What happens in the case of abscesses?
Occur in solid tissues
Inflammatory exudate forces tissues apart
Liquefactive necrosis at centre
May cause high pressure so pain
May cause tissue damage or compress adjacent tissues
What happens in pericarditis?
Inflammation of serous cavity
Pericardium becomes enflamed so increases pressure on heart
Give examples of some hereditary disorders of the acute inflammation process
α1 anti trypsin deficiency
Complement deficiencies
Defects in neutrophil function
Defects in neutrophil numbers
Describe α1-anti trypsin deficiency
α1 antitrypsin inhibits elastase
If deficient, elastase will break down elastin in lung and liver tissue
Can cause emphysema and liver sclerosis
