acute inflammation 1 and2 Flashcards
understand
what is acute inflammation
series of protective changes occurring in living tissue as a response to injury
characteristics of acute inflammation
it is a dynamic homeostatic mechanism that occurs in higher beings with a living tissue.
what are the cardinal signs of inflammation
redness
heat
swelling
pain
loss of function
what are the causes of acute inflammation
1.microorganisms such as bacteria and fungi
2.mechanical such as trauma injury to tissue
all injury even sterile injuries such as surgery might cause injury.
3.chemical causes such as acid and alkali , bile and urine example in the peritoneum.
4.weather conditions which might cause stress on the body.These conditions include ; heat , cold, and ionising radiation.
5.hypersensitivity for example allergic reactions.
6.dead tissue which is caused by necrosis and irritates adjacent tissue.
what is microcirculation
this is capillary beds that are fed by arterioles and drained by venules.
extracellular compartment has fluid which is drained into the
lymphatic system
what is the dynamic balance of the microcirculation capillaries
hydrostatic( blood pressure ) and colloid osmotic pressure ( pressure exerted by the plasma proteins)
steps in acute inflammation
1.changes in vessel radius - flow
2.change in the permeability of the vessel wall – exudation of fluid
3.movement of neutrophils from the vessel to the extravascular space - emigration
results of increased diameter of the blood vessels
for increased flow of the blood ; there is always reduced resistance with the increased diameter.
triple response
flush , flare , wheal
flush - dilation of the local capillary that is affected.
flare - dilation of adjacent arterioles
wheal - accumulation of fluid that is oedema in the local vessels.
rapid local changes in the blood vessel in an acute inflammation
1.few moments after injury there is constriction as a protective measure .
2.there is dilation of the artery .
3.relaxation of the smooth muscle- this is the flush flare wheal.
benefits of endothelial permeability
1.movement of materials such as plasma into the extravascular space and this is known as exudation.
2. the rate of flow slows and there is a change in the flow of blood.
what is exude ?
this is fluid that is rich in protein and plasma
effects of exudation
oedema is formed and there is accumulation of fluid in the extravascular space.
describe the normal laminar flow
the erythrocytes on the periphery, the neutrophils on the innermost.
what changes are seen in the capillary blood flow during inflammation
there is neutrophil pavementation and adhesion on the endothelial lining .
the red cells aggregate in the centre.
phases of migration of the neutrophils
movement to the periphery of the vessel,
adhesion to the surface that is pavementation.
movement out of the vessel that is called emigration
examples of acute inflammation
pleural inflammation
appendicitis
acute pyelonephritis
bacterial endocarditis
what are the outcomes of acute inflammation
nciting agent isolated and destroyed
macrophages move in from blood and phagocytose debris;
then they leave
epithelial surfaces regenerate
inflammatory exudate filters away
vascular changes return to normal
inflammation resolves
what are the benefits of acute inflammation
apid response to non-specific insult
cardinal signs and loss of function
transient protection of inflamed area
neutrophils destroy organisms and denature antigen for macrophages to phagocytose
plasma proteins localise process
resolution and return to normal
what are the names of inflammation on different sites in the body
structure”-itis
peritoneal cavity -peritonitis meninges -meningitis appendix -appendicitis
lungs -pneumonia
pleural cavity -pleurisy
function of neutrophils
phagocytosis - they recognise the foreign antigen and they move to it through chemotaxis.
direct killing of the cells - there granules contain enzymes and oxidants such as sodium peroxide that cause degradation of the foreign materials.
what is pus
a collection of dead neutrophils ,bits of cells, organisms and endogenous proteins
what is the role of plasma proteins in inflammation
immune response
clotting factors that drive process of clotting
what are the effects of the mediators for acute response
vasodilation
increased permeability
adhesion of the neutrophils
chemotaxis
itch and pain
mediators in acute response
molecules on endothelial cell surface membrane
molecules released from cells
molecules in the plasma
molecules inside cells
molecules involved in the adhesion of neutrophils on the blood vessel
CAM-1 helps neutrophils to stick together with the endothelial cell.
P selectin helps to roll over the neutrophils
so that they can easily attach to the endothelial cells.
molecules that are released from the cells
histamine
serotonin
prostaglandins
cytokines
nitric oxide
oxygen free radicals
pattern associated molecular patterns
danger associated molecular patterns
intracellular inflammatory pathways
JAK -STAT
MAPK
NF-KB
role of histamine in inflammatory response
causes vasodilation and increased permeability
acts on H1 receptors on the endothelial cells
which cells release histamine
mast cells that are beside blood vessels , platelets and basophils .
results of IgE mediated reactions
release of histamine from mast cells
effect of serotonin
causes vasoconstriction
performed in platelets
released when platelets degranulate in coagulation
prostaglandins precursor
arachidonic acid
cells that produce prostaglandins
endothelial cells and leukocytes
thromboxane
thromboxane promotes aggregation and vasoconstriction and are anti-inflammatory
properties of thromboxane that makes it a good NSAID
thromboxane promotes vasoconstriction , aggregation of platelets and inhibits inflammatory response .
what are cytokines and chemokine s
small protein molecules that are produced by macrophages , lymphocytes and endothelium in response to inflammatory stimuli
function of cytokines
they stimulate intracellular pathways and signalling.
effect of nitric oxide
produced by many cells
cause smooth muscle relaxation , antiplatelets , regulate leukocyte recruitment to inflammatory focus.
oxygen free radicals
H2O2 , and OH-, O2 ;released by neutrophils during phagocytosis and they amplify other mediator effects.
pattern associated molecules
1-these could be microbial antigen which are genetically hard wired to recognise or innate and adaptive immunity .
NF -kB( nuclear factor kappa B)
intracellular inflammatory pathway that is stimulated by a ligand
signalling molecules for acute inflammation
pattern associated molecular patterns
danger associated molecular patterns
examples of intracellular inflammatory pathways
NF-kB ( nuclear factor kappa B)
MAPK( it is activated by surface receptors such as toll like receptors )
JAK-STAT pathway( signal transducer and activator to transcription pathway which causes direct translation of extracellular signal to molecular expression)
plasma role in inflammation
1.blood coagulation pathways are activated the clotting factors present in the plasma fluid.
2.fibrinolysis the degradation of fibrin during the formation of fibrin fibres.
3.kinin system for example bradykinin which causes pain.
4.complement cascade ties inflammation with immune system and active components which stimulate increased permeability , chemotaxis ,phagocytosis and cell breakdown.
what are the immediate systemic effects of inflammation
1-pyrexia which is raised temperature
feeling unwell also known as malaise ,
2-anorexia and nausea , together with abdominal pain and vomiting in children.
3-neutrophilia which is raised white cell count.; bone marrow count increases.
long term effects of acute inflammation
1.lymphadenopathy which is regional
2.lymph node enlarge as a result of immune response
3.weight loss
4.anaemia - from the loss of blood.
pus formation
dead tissue , dead micro - organisms , exudate , neutrophils , fibrin and red cells and debris.
pyogenic membrane
capillary sprouts ,neutrophils , fibroblasts which lay off the walls off the pus.
a collection of pus under pressure
abscess
suppuration
an abcess that is under pressure ; the pressure comes from the growing granulation tissue
what causes a multiloculated abscess
a pus that bursts through pyogenic membrane and forms new cavities.
pus in the pleural cavity
empyema
outcomes of acute inflammation
granulation tissue which leads to healing and repair and also leads to fibrosis and formation of a scar.
sepsis
spread to bloodstream - patient “septic”
bacteraemia - bacteria in blood
septicaemia - growth of bacteria in blood
toxaemia - toxic products in blood
life threatening organ dysfunction caused by a dysregulated host response to infection characterised by increased organ dysfunction
sepsis
septic shock
a subset of sepsis
profounds circulatory , cellular and metabolic abnormalities which are at a greater risk of mortality than with sepsis alone.
effects of systemic infection
shock which is caused by the inability of oxygen to perfuse tissues.
presentations of sepsis
peripheral vasodilation
tachycardia which is high heart rate to cater for the reduced vascular resistance.
low blood pressure
haemorrhagic skin rash
pathogenesis of septic shock
release of mediators from the cells into the plasma.
the mediators cause vasodilation leading to loss of systemic vascular resistance.
there is increased catecholamine release.
increased tachycardia to maintain the flow of the cardiac output.
what happens when compensation for septic shock is reduced
there is tissue hypoxia
loss of tissue and organ failure
Outcome of septic shock
rapidly fatal
tissue hypoxia - cell death
haemorrhage
requires urgent intervention and support
awareness and early recognition
ability of young people to compensate
admit to hospital and intensive care
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