Acute inflammation Flashcards
what are the main causes (aetiologies) of acute inflammation?
micro-organisms injury/ trauma to tissue chemical extreme conditions dead tissue hypersensitivity
microorganisms and acute inflammation
e.g bacteria, fungi, viruses, parasites- Pathogenic organisms that cause infection
Recognise the benefits of acute inflammation
rapid response to injury site
cardinal signs (redness, swelling, pain and heat) and loss of function
neutrophils move from blood vessels to E.C space -destroy organisms and denature antigen for macrophages- can eradicate the infection
plasma proteins localise the process
resolution and return to normal
what are the cardinal signs of inflammation? ie simple sign of symptoms
Rubor (redness) Calor (heat) Tumor (swelling) dolor (pain) loss of function
Injury/trauma to tissue and acute inflammation
All injuries, even sterile (e.g surgery) cause acute inflammation
‘mechanical’= a blow, crush, cut, or penetrating wound
Chemical cause for acute inflammation
upset stable environment (e.g acid or alkali, bile (alkaline) and urine cause irritation when in inappropriate place)
Extreme conditions (physical) cause for acute inflammation
e.g sunburn from heat, frostbite from cold, ionising radiation
Hypersensitivity for acute inflammation
several classes of reaction
dead tissue cause of acute inflammation
in tissue that dies, cell necrosis irritates adjacent tissue
what microvascular changes occur because of acute inflammation?
- change in vessel radius/ flow
- change in vessel permeability as blood vessels dilate and more gaps arise for things to infiltrate it.
- movement of neutrophils from the vessel to the extra-cellular ‘space’ compartment
increased blood flow?
blood vessels dilate which increases the blood flow to the site of inflammation. RESULT= observed redness and heat
Increased permeability?
an increase in permeability of the capillaries allows fluid and plasma proteins to move into the interstitial spaces. This process is called EXUDATION. What is leakes is called exudate. Exudation causes the formation of an oedema (accumulation of fluid in the extra-vascular space).
This explains the swelling of tissue in acute inflammation. Swelling causes pain and reduces function.
Define exudation?
process by which there is an increase in permeability of the capillaries, allowing fluid and plasma proteins to move into the interstitial spaces
Exudate?
a mass of cells and fluid rich in protein that has seeped out of blood vessels. It contains immunoglobulin and fibrinogen.
Migration of neutrophils
- margination- the neutrophils (WBCs) move to endothelial aspect of lumen (lining)
- pavementing/adhesion- neutrophils adhere (stick) to endothelium
- emigration- neutrophils squeeze between endothelial cells to extravascular tissues- guided to site of infection
describe sequence of events in exudate formation
An increase in permeability of capillaries during acute inflammation allows exudate to leak into extravascular space. It explains the swelling of tissue in acute inflammation. Can lead to oedema, which is the accumulation of fluid in the extravascular space. This swelling causes pain, due to pain receptors being stretched, and loss of function.
What are the local effects of acute inflammation?
- Transient (lasting only a short time) arteriolar constriction. Lasts a few moments, probably protective
- local arteriolar dilation. Relaxation of smooth muscle of vessel.
List the systemic effects of acute inflammation
- pyrexia- raised temperature
- feel unwell (malaise) anorexia, nausea, abdominal pain and vomiting in children
- neutrophilia- raised white cell count, produced and released by bone marrow
- septic shock
Outcomes of acute inflammation
suppuration (pus formation) abscess organisation dissemination chronic inflammation
suppuration
sup backwards = pus
pus formation, made up of dead tissue, organisms, exudate, neutrophils, fibrin, red cell and debris. ‘membrane’ surrounds pus to keep it contained locally. May extend into other tissues (still contained) and progress inflammation further
many neutrophils die at the site of their action so form the pus that is found at infection site
abscess
a collection of pus (suppuration) under pressure. Can be a single locule, or multiloculated (when pus bursts through the pyogenic membrane and forms new cavities)
dissemination
spread to the bloodstream, and the patient becomes ‘septic’
bacteraemia= bacteria in the blood
septicaemia= growth of bacteria in blood
toxaemia= toxic products in blood
inflammation leads to the following stages
granulation tissue- occurs after a large amount of damage, or an ability to remove dirt from wound-
capillaries grow into the inflammatory mass. Means plasma proteins, macrophages and fibroclasts which lay down collagen to repair damage have access
-healing and repair
-scar formation
how can process of acute inflammation be detrimental to patient
- release of lysosomal enzymes by inflammatory cells may have harmful effects
- digestion of normal tissue
- swelling
- inappropriate inflammatory response
digestion of normal tissue effect on patient
enzymes such as collagenases and proteases may digest normal tissues, resulting in their destruction. This may result particularly in vascular damage e.g type III hypersensitivity
Swelling:- effect on patient
Swelling of acutely inflamed tissues may be harmful. Inflammatory swelling is especially serious when it occurs in an enclosed space such as the cranial cavity. Thus, acute meningitis or a cerebral abscess may raise intacranial pressure to the point where blood flow into the brain is impaired.
Inappropriate inflammatory response:- effect on patient
Sometimes acute inflammatory responses appear inappropriate, such as those which occur in type I hypersensitivity reactions (e.g hay fever) where the provoking environmental antigen (e.g pollen) otherwise poses no threat to the individual. Such allergic inflammatory responses may be life- threatening, for example extrinsic asthma.
mediators of vasodilation and vasoconstriction
histamine causes vasodilation while serotonin causes vasoconstriction. These two molecules contradict each other in terms of vasodilation and vasoconstriction and so balance each other out through homeostasis
mediators of altered permeability
prostaglandins and leukotrienes produce molecules that aid and prevent increased permeability, and so balance each other out
mediators of neutrophil adhesion
molecules can either aid or inhibit the process of neutrophil adhesion
what effect do mediators have?
mediators can have positive and negative effects, and result in a dynamic balance. They can favour or inhibit acute inflammation relative to need.
Is inflammation a quick response?
Yes
Oedema
accumulation of fluid in the extravascular space- swelling
What flow is there in a normal vessel?
laminar flow
velocity of the fluid through vessel is constant at any point in the fluid
Margination
movement of neutrophils from centre of vessel to the vessel wall
Diapedesis
movement of white blood cells out of through capillary walls
Inflammation terminology
(add -itis usually)
meninges- meningitis
appendix- appendicitis
others:- pneumonia
pleural cavity
effector mechanism of inflammation- cell?
neutrophil
neutrophils
- can recognise foreign antigens
they move towards the antigen by chemotaxis
When do neutrophils die?
when granule contents are released
they produce pus
although it’s contained, it might extend into other tissues- progressing inflammation
fibrinogen
helps blood to coagulate in vessels and clot exudate outwith vessels
performs like a plug
localises inflammatory process- stops spreading
chemotaxis
movement of neutrophils in response to inflammation
Move up a conc. gradient to where the messenger is coming from- requires energy
mediators of acute inflammation
vasodilation and vasoconstriction altered permeability neutrophil adhesion chemotaxis itch and pain
What can septicemia cause/lead to?
septic shock- tachycardia, peripheral vasodilation, hypotension (low bp)
shock is the inability to perfuse tissues
what effects can mediators have on acute inflammation
they can promote/ inhibit inflammatory response
Summary of outcomes of acute inflammation
resolution suppuration organisation dissemination chronic inflammation
Histamine
it’s a neurotransmitter. it’s in form of granules that are released from inside mast cells
IgE and antigen reaction changes mast cell membrane
the histamine binds to H1 receptors and causes vasodilation, increased permeability
Anti-histamines
work by blocking/inhibiting H1 receptors (histamine receptors)
pyrexia
raised temperature
Abscess
collection of pus under pressure
single locule, multiloculated
can release discharge
collapses- healing and repair
depending on size small may drain naturally, or simply shrink, dry up and disappear
Large- may need antibiotics to clear the infection + pus may need to be drained.
multiloculated abscess
pus bursts through pyogenic membrane and forms new cavities
Pyaemia
discharge to bloodstream
what is normal laminar flow like?
white blood cells in the middle surrounded by red blood cells
flow in inflammation
neutrophils found near endothelium so capillary walls (margination)
RBCs aggregate in centre of lumen (rouleaux)
what do neutrophils do in terms of granule release?
their granules possess oxidants eg H2O2 and enzymes eg proteases
they release the granule contents
phagocytose/destroy foreign antigens
when neutrophils release their contents they die and produce pus
