Flashcards in Acute Inflammation Deck (205):
What is acute inflammation?
The response of living tissue to injury
What is acute inflammation initiated to do?
Limit tissue damage
What is the purpose of acute inflammation?
It is a protective reposponse
What are the features of acute inflammation?
Immediate and early
What is meant by acute inflammation being innate?
You are both with it
What is meant by acute inflammation being stereotyped?
It is the same every time it happens, and doesn’t get better or worse
What is the duration of acute inflammation?
Minutes/hours/few days, depending on process
What type of reactions occur in acute inflammation?
What is the result of vascular and cellular reactions in acute inflammation?
Accumulation of fluid exudate
Neutrophils in tissues
What is acute inflammation controlled by?
A variety of chemical mediators
What are the chemical mediators that control acute inflammation derived from?
Why is control of acute inflammation very strict?
Don’t want it to get out of control
When is acute inflammation a good thing?
Nearly all the time
When is acute inflammation not a good thing?
It can lead to local complications and systemic effects
What causes acute inflammation?
What type of microbial infections particularly cause acute inflammation?
What are pyogenic organisms?
What are hypersensitivity reactions?
What part of hypersensitivity reactions causes acute inflammation?
What physical agents cause acute inflammation?
Other forms of energy
What are the clinical features of acute inflammation?
Loss of function
Why isn’t loss of function independent from the other clinical features?
Because it occurs partly because whatever is inflamed is sore, swollen, hot and red
What changes does acute inflammation cause in tissues?
Changes in blood flow
Exudation of fluid into tissues
Infiltration of inflammatory cells
What is required for each step of acute inflammation?
What happens in the vascular phase of acute inflammation?
Changes in blood flow
What are the stages of the vascular phase of acute inflammation?
- Transient vasoconstriction of arterioles
- Vasodilation of arterioles and then capillaries cause increase in blood flow to injured tissue
- Increased permeability of blood vessels
- Concentration of red blood cells in small vessels and the increased viscosity of blood leads to stasis
How long does transient vasoconstriction of arterioles take?
A few seconds
What is the result of increased blood flow to injured tissue?
Causes heat and redness
What does the increased permeability of blood vessels lead to?
Exudation of protein rich fluid from plasma into tissues
Slowing of circulation
Why does increased permeability of blood vessels slow the circulation?
If liquid leaves the blood, left with cells, so slows
What does slowing of circulation lead to?
What is the chemical mediator of the immediate early response of the vascular phase of acute inflammation?
What kind of molecule is histamine?
Where is histamine released from?
Mast cells, basophils, platelets
What is histamine released in response to?
Many stimuli, including-
Factors form neutrophils and platelets
What does histamine cause?
Transient increase in vascular permeability
What are the chemical mediators of the persistent response in the vascular phase of acute inflammation?
Many and varied chemical mediators, which are interlinked and of varying importance
What is the problem with studying the chemical mediators of the persistent response of the vascular phase of acute inflammation?
They are incompletely understood
Give two examples of chemical mediators of the persistent response of the vascular phase of acute inflammation?
What are leukotrienes derived from?
What is significant about leukotrienes?
They are the most important chemical mediator
What law does fluid loss from vessels follow?
What is Starling’s Law?
Fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure comparing plasma and interstital fluid
What is hydrostatic pressure?
The blood pressure- force with which the blood flows
What is colloid osmotic pressure?
The protein level between plasma and interstitial fluid
What does increased hydrostatic pressure lead to?
Increased fluid flow out of the vessel
Why is hydrostatic pressure increased in acute inflammation?
Because of the increased flow
What does increased colloid osmotic pressure of the interstitium cause?
An increase in fluid flow out of the vessel
Why does in increased colloid osmotic pressure cause an increase in fluid flow out of the vessel?
Because it sucks fluid out to balance the levels
What does exudation of fluid cause in inflammation?
Protein levels to increase
Why does exudation of fluid occur in acute inflammation?
Increased permeability of vessel walls
Why does arteriolar dilatation cause exudation of fluid?
Because it causes an increase in hydrostatic pressure
Why does increased permeability of vessel walls cause exudation of fluid?
Because it leads to loss of protein to the interstitium
What does net flow of fluid out of vessels lead to?
What is oedema?
Increase fluid in tissue spaces
What can fluid be?
Transudate or exudate
What does oedema lead to?
Increased lymphatic drainage
Why does oedema lead to increased lymphatic drainage?
Because if fluid gets into tissue space by leaking out of vessels, there has to be a means for it to get away again, and therefore it is drained out of the lymphatic system
What is exudate?
Fluid loss in inflammation
What is the protein content of exudate?
What is transudate?
Fluid loss due to hydrostatic pressure imbalance
What is the protein content of transudate?
Low- the same as plasma
When does transudate formation occur?
When there is cardiac failure or venous outflow obstruction
What are the mechanisms of vascular leakage?
Leukocyte dependent injury
Why does endothelial contraction cause vascular leakage?
Because it leads to the formation of gaps, which are leaky
What is endothelial contraction mediated by?
Why does cytoskeletal reorganisation lead to vascular leakage?
Leads to formation of gaps
What is cytoskeletal reorganisation mediated by?
What kinds of direct injury can cause vascular leakage?
What can cause leukocyte dependent injury?
Toxic oxygen species
Enzymes from leukocytes
What causes transcytosis?
Channels across endothelial cytoplasm, where fluid moves along normally for a lot of physiological systems
What mediates an increase in transcytosis in inflammation?
What is exudate rich in?
Where is fibrin an important component?
The acute inflammatory process
What is fibrin good at?
Making stuff sticky, and keeping it together
What is the purpose of fibrin?
To localise area of inflammation around injured tissue
Where is fibrins role in acute inflammation important?
If get inflammation in an organ that has a serosal surface
Give 3 examples of organs with serosal surfaces?
Why is fibrin important if you get inflammation in an organ that has a serosal surface?
Because where there is acute inflammatory infiltrate on a serosal surface, you run the risk that you’ll exudate all of the blood volume into the cavity. Fibrin is good at preventing this.
What is a neutrophil leucocyte?
A primary type of white blood cell involved in inflammation
What kind of cell is a leucocyte?
A type of granulocyte, also known as a polymorphonuclear leucocyte. This means that they are myeloid cells.
What are the characteristics of myeloid cells?
Granular cytoplasm with lots of cells in it
What is the predominant purpose of neutrophil leucocytes?
What are the stages of infiltration of neutrophils?
- Stasis causes neutrophils to line up at the edge of blood vessels
- Neutrophils roll along endothelium, becoming loosely adherent, sticking to it intermittently
- They then stick more avidly
- Followed my emigration of neutrophils along the blood vessel wall
Why does stasis occur?
Due to laminar flow
Why does laminar flow cause stasis?
Blood cells tend to flow down the middle of the vessel, not the edges, however, when the blood gets static, the blood cells go to the periphery
What is the process of neutrophils sticking intermittently to the endothelium called?
What is the process of more avid neutrophil sticking called?
What is responsible for each of the different stages of neutrophil infiltration?
White cells and endothelial ligands have different receptors
How do neutrophils escape from vessels?
Relaxation of inter-endothelial cell junctions
Digestion of vascular basement membrane
Movement of white cells
Why does the digestion of the vascular basement membrane allow neutrophils to escape from vessels?
It creates gaps, and the cells move into the gaps
What happens to the digested vascular basement membrane at the end of inflammation?
It is rebuilt
What is chemotaxis?
Movement along concentration gradients of chemoattractants
Why is chemotaxis important?
Because it’s how, once a polymorph gets out of a capillary, it knows where to go and what to do, as it needs to get to the bit of tissue thats most injured
What can chemotaxis occur due too?
Give 3 examples of chemotaxins
What is C5a?
An activated component of complement
Where is lTB4 from?
What are bacterial peptides?
Stuff from outside the body that are very potent chemotaxins
Where are the receptors for receptor-ligand binding?
On the surface of white cells
What happens in receptor-ligand binding?
Once the receptor has bound to the ligand on a neutrophil, it rearranges the cytoskeleton and produces a pseudopod
What are pseudopods important for?
They are how cells move
What is the main function of white cells?
What are the three stages of phagocytosis?
What happens once internalisation has happened?
It means all things that sit inside lysosomes and the cytoplasm can do their job
What is phagocytosis facilitated by?
Give two examples of opsonins?
What is Fc?
A fixed component of immunoglobulin
What is C3b?
A complement component
What changes does phagocytosis involve?
What is produced when phagosomes fuse with lysosomes?
What are the two classes of phagocytitic killing mechanisms?
What are the oxygen dependent killing mechanisms?
Production of superoxide and hydrogen peroxide
Hydrogen peroxide-myeloperoxidase-halide system
What is produced in the hydrogen peroxide-myeloperoxidase-halide system?
What are the oxygen independent killing mechanisms?
Lysosome and hydrolases
Bacterial Permeability Increasing Protein (BPI)
Cationic proteins (defensins)
What are the stages of neutrophil chemotaxis and phagocytosis?
What are the chemical mediators of acute inflammation?
Where are proteases produced?
Where are proteases found?
What is the function of proteases in acute inflammation?
What proteases are involved in the complement system?
Why are proteases important in the complement system?
In producing chemotaxins and opsonins
What are prostaglandins/leukotrienes?
Metabolites of arachidonic acid, produced by different enzymatic reactions
Where are cytokines/chemokines produced by?
White blood cells
Give two examples of cytokines/chemokines?
What do the chemical mediators of acute inflammation cause?
Increased blood flow
What chemical mediators cause increased blood flow?
What chemical mediators cause vascular permeability?
What chemical mediators cause neutrophil chemotaxis?
What chemical mediators cause phagocytosis?
Why are the immune system and the inflammatory response said to by symbiotic?
They work together, and both as defence mechanisms, but are different
What is the hallmark of acute inflammation?
Exudate of fluid
Infiltrate of inflammatory cells
What is the purpose of the exudation of fluid?
Delivers plasma proteins to area of injury
Increases lymphatic drainage
What plasma proteins need to be delivered to the site of injury?
What is the advantage of the increase in lymphatic drainage in acute inflammation?
Delivers microorganisms to phagocytes and antigens to the immune system
What is the purpose of infiltration of cells in acute inflammation?
Removes pathogenic organisms and necrotic debris
What is the purpose of vasodilation in acute inflammation?
What is the purpose of pain and loss of function in acute inflammation?
Reduces chance of further traumatic damage
What are the local complications of acute inflammation?
Loss of fluid
Pain and loss of function
What can swelling in acute inflammation lead to?
Blockage of tubes
When is swelling causing blockage of tubes likely to be problematic?
If you have acute inflammation in a small tube with a narrow lumen
What can a blocked bile duct cause?
What problems can exudate cause?
Give an example of when compression can be problematic
What happens in cardiac tamponade?
Fluid splints the heart, stopping it from beating
What is serositis?
Inflammation of a serosal surface
When my loss of fluid be a problem?
In burns, when plasma can be lost through the skin
When can pain and loss of function be particularly problematic?
What are the systemic complications of acute inflammation?
Acute phase response
Why does acute inflammation cause fever?
‘Endogenous pyrogens’ produced
Give two examples of endogenous pyrogens
How can aspirin reduce temperature
It inhibits the production of prostaglandins
What is leukocytosis?
An increased number of WBC in blood
What do IL-1 and TNF α produce?
Accelerated release from marrow
What do macrophages and T lymphocytes produce?
What do bacterial infections recruit?
What do viral infections recruit?
What happens when there is severe acute inflammation?
There is a big area of infarcted tissue
Give an example of where they will be severe acute inflammation?
What can severe acute inflammation lead to?
Systemic pathological symptoms
What systemic pathological systems will severe acute inflammation lead to?
Raised pulse rate
Altered sleep patterns
Change in plasma concentrations of acute phase proteins
What acute phase protein concentrations are changed when there is severe acute inflammation?
Serum amyloid A protein
How can Cr-reaction protein be useful?
Can help tell if a patient has had an infarction
What happens if inflammation doesn’t work?
It doesn’t rapidly localise and deal with infection, so can get spread of microrganisms and toxins
What is shock?
Clinical syndrome of circulatory failure
What kind of shock is inflammatory shock?
What can happen after development of acute inflammation?
Continued acute inflammation with chronic inflammation
Chronic inflammation and fibrous repair
What outcome of acute inflammation happens most of the time?
What happens in complete resolution of acute inflammation?
Changes gradually reverse
Vascular changes stop
Exudate drains to lymphatics
Fibrin is degraded by plasmin and other proteases
Neutrophils die, break up and are carried away, or are phagocytosed
What happens when vascular changes stop in complete resolution?
Neutrophils no longer marginate
Vessel permeability returns to normal
Vessel calibre returns to normal
Can damaged tissue regenerate in acute inflammation?
May be able too
When is complete resolution not possible?
If tissue architecture has been destroyed
What does continued acute inflammation with chronic inflammation lead to when there is a pus forming microorganism?
What are the mechanisms of resolution of acute inflammation?
All mediators of acute inflammation have short half lives
May be inactivated by degradation
Inhibitors may bind
May be unstable
May be diluted in exudate
Specific inhibitors of acute inflammatory changes
Give an example of a mediator of acute inflammation that is inactivated by degradation
Give an example of a mediator of acute inflammation that is stopped by a binding inhibitor
Give an example of a mediator of acute inflammation that is unstable
Some arachidonic acid derivatives
Give an example of a mediator of acute inflammation that is diluted in the exudate
Fibrin degradation produces
Give two examples of specific inhibits of acute inflammatory changes
What happens in bacterial meningitis?
Bacterial infection in the meninges causes acute inflammation in them
What are meninges?
Spaces surrounding the brain
What can acute inflammation in meninges cause?
Vascular thrombosis and reduced perfusion
What is the outcome of bacterial meningitis?
If recognised and treated quickly, fine.
If don’t, death
What causes death in bacterial meningitis?
Because the acute inflammatory exudate in meningeal space in the hard skull results in a raised intracranial pressure.
What can acute inflammation in meninges damage?
Things that cross in the meningeal space- blood vessels, cranial nerve
What happens in lobar pneumonia?
Inflammatory exudate and infiltrate into alveolar space
What can happen if lobar pneumonia is severe?
What causes lobar pneumonia?
What are the symptoms of lobar pneumonia?
What is the outcome of lobar pneumonia if treated?
Can resolve completely
What can skin blisters be due to?
What are the predominant features of skin blisters?
What causes the skin blister?
Collection of fluid strips off overlying epithelium
Why is the exudate clear in a skin blister?
Because inflammatory cells are relatively flew
Why is bacterial infection a problem in burns?
There is no skin, so no protection
What is the outcome of skin blisters?
Either resolves or scars
What are abscesses?
Solid tissues that occur when inflammatory exudate forces tissue apart, with liquefactive necrosis in the centre
When do abscesses occur?
When acute inflammation can’t get out
When there are pus forming organisms that the body can localise, but not deal with
What can abscesses cause?
Squash adjacent structures
Why do abscesses cause pain?
Because causes high pressure
What happens when you get acute inflammation in serous cavities?
Exudate pours into the cavity
What can acute inflammation in serous cavities cause?
Pleural or pericardial effusion
What can pleural or pericardial effusion cause?
Respiratory or cardiac impairment
How is acute inflammation in serous cavities dealt with?
Localised fibrin deposition, which helps localise the inflammation, favouring resolution rather than continuation of inflammation