Acute Inflammation Flashcards
What is inflammation
Response of living tissue to injury
Features of acute inflammation
Immediate Short duration Innate Stereotyped- same respomse regardless what the injury is Limits damage
What are the two phases of acute inflammation called and what happens
Vascular phase- all about changes in blood flow. Accumulation of exudate
Cellular phase - delivery of neutrophils
What is acute inflammation controlled by
Chemical mediators
What causes inflammation
1) trauma/foreign body
2) micro-organisms
3) hypersensitity
4) other illnesses (e.g necrosis)
What are the clinical signs
Rubor-redness
Tumor- swelling
Dolor- pain
Calor-heat
Describe the vascular phase of inflammation
1) vasoconstriction for a few seconds
2) vasodilation for minutes- more blood can flow to affected area causing heat and redness
3) increased permeability of vessels , they become leaky.fluids and cells can escape.
What is the starling’s law
Movement of fluid is controlled by the balance of hydrostatic pressure( pressure exerted on a vessel wall by fluid) and the oncotic pressure ( pressure exerted by proteins).
What happens to hydrostatic and oncotic pressure in acute inflammation
Vasodilation- more blood flowing through vessels so increased capillary hydrostatic pressure
Increased vessel permeability- plasma proteins move into interstitium and increases interstitial oncotic pressure.
What does the movement of fluid out of vessel cause
Increased viscosity of blood
Reduced flow through vessel- stasis
What are the two types of interstitial fluid? Compare them
Exudate- increased vascular permeability
Protein rich fluid ( delivers proteins to area of injury). Occurs in inflammation. May contain some white and red cells.
Transudate- vascular permeability unchanged. Fluid movement due to increased capillary hydrostatic pressure and reduced capillary oncotic pressure. This occurs in heart failure/ hepatic failure/ renal failure
how does a vessel wall become permeable
1) retraction of endothelial cells as they shrink. this is brought about by chemical mediators such as histamine, nitric oxide, leukotrienes
2) or by direct injury- by burns , toxins and direct trauma
3) leucocyte dependent injury- wbc activated in acute inflammation and release enzymes and free radicals
how is the vascular phase effective?
presence of interstitial fluid dilutes toxins reducing capability to cause damage
exudate delivers proteins e.g fibrin- mesh limits spread of toxin to other parts of the body. immunoglobulins from adaptive immune response that specifically target certain antigens, microbes or toxins
fluid carries the microbes to lymph nodes and presents them to APCs stimulating an adaptive immune response.
which white blood cell is involved in the cellular phase of acute inflammation and how can it be identified
neutrophils
trilobed nucleus
what is the end goal of cellular phase
getting neutrophils out into the tissue so they can go out and deal with the trauma/infection etc
how do neutrophils escape vessels
1) margination- movement of neutrophils from middle of blood vessels to the edge
2) rolling - brought about by weak intermittent bonds between neutrophils and endothelial cells. selections on activated endothelial cells are responsible for this
3) adhesion -brought together by tight strong bonds between neutrophils and endothelial cells. integrins on neutrophil surface are responsible for this. they have a conformational change changing them from low to high affinity state and tether in the high affinity state
4) emigration (diapedesis)- movement of neutrophils out into interstitial space.
how do the neutrophils move through the interstitium
chemotaxis
movement along an increasing chemical gradient of chemoattractants.
chemoattractant are released by either the area of injury or the pathogens.
examples are bacterial peptides, inflammatory mediators.
they rearrange the neutrophil cytoskeleton to propel it to an area of high chemoattractant conc.
what do neutrophils do ?
phagocytosis- neutrophil wraps around bacteria forming phagosome which then fuses with lysosomes. this produces secondary phagolysosomes .
they also release inflammatory mediators
how do neutrophils recognise what to phagocytose
opsonisation
toxin will be covered in C3b and Fc (opsonins)
receptors for these are on the neutrophil surface
how do neutrophils destroy pathogens
oxygen dependent- reactive oxygen intermediates (superoxide anion, hydroxyl radicals , hydrogen peroxide) or reactive nitrogen intermediates ( Nitric oxide, nitrogen dioxide)
oxygen independent - lysozyme, hydrolytic enzymes , defensins
how is the cellular phase effective
removal of pathogens and necrotic tissue
releases inflammatory mediators
what do inflammatory mediators do and where do they originate from
they are chemical messengers that control coordinate the inflammatory response. they originate from activated inflammatory cells, platelets, endothelial cells and toxins
which inflammatory mediators bring about vasodilation
histamine
serotonin
prostaglandin
nitric oxide
which inflammatory mediators increase vascular permeability
histamine
bradykinin
leukotrienes
C3a & C5a
which inflammatory mediators are involved in chemotaxis
C5a
TNF-a
IL-1
bacterial peptides
which inflammatory mediators bring about systemic response ( hot, sweating fever etc)
IL-1
IL-6
TNF-a
which inflammatory mediators bring about pain
bradykinin
Substance P
Prostaglandin
what are the local complications of acute inflammation
swelling - can lead to compression of tubes
exudate build up in pericardial space resulting in a pressure called cardiac tamponade
loss of fluid in burns as the exudate evaporates
pain -muscle atrophy, psychical consequences
what are the systemic complications of acute inflammation
fever -some inflammatory mediators(prostaglandins,IL-1,IL-6,TNF-a) are pyrogens and act on the hypothalamus to alter temp. NSAIDs are used reduce fever and pain symptoms as they block cyclo-oxygenase enzymes(involved in the production of prostaglandins)
leucocytosis- increased production of abc.
acute phase response- malaise(discomfort), reduced appetite , altered sleep, tachycardia. this all induces rest for healing
septic shock - huge release of chemical mediators , widespread vasodilation, hypotension ,tachycardia, multi-organ failure
what does a high CRP count suggest
inflammation
what happens after acute inflammation
1) complete resolution- mediators dilated, vessels back to normal, neutrophils undergo apoptosis and get phagocytose, exudate is drained via lymphatics
2) fibrosis-repair with connective tissue
3) progression to chronic inflammation
what is appendicitis, how does it present
inflamed appendix
blocked lumen between caecum and appendix
accumulation fo bacteria and exudate increasing pressure leading to perforation
vague abdominal pain, sharp ;localised pain a few days later
appendix is yellow/green this is the fibrin and exudate
examples of acute inflammation
appendicitis
pneumonia
bacterial meningitis
causes of pneumonia, signs and symptoms ,risk factors
streptococcus penumoniae, haemophilus influenzae
shortness of breath
cough
sputum
fever
risk factors ; smoking , pre existing lung condition
what is bacterial meningitis, what causes is and what are the signs and symptoms
inflammation of the meninges. this is a protective layer between brain and skull.
brain is compressed
caused by group b streptococcus, e.coli, neisseria meningitides
headache, neck stiffness photophobia , altered mental state
what is abscess
accumulation of dead or dying neutrophils
can cause compression of surrounding structures cause pain and blockage of ducts
how do serous cavities becomes inflamed
exudate pours into them
name some disorders of acute inflammation
hereditary angio-oedema
alpha-1 antitrypsin deficiency
chronic granulomatous disease
