Inflammation (JW) Flashcards
Acute Inflammation
acute inflammation = cell injury + vascular changes + neutrophil leukocytosis
VASCULAR CHANGES - dilatation, activation of coagulation cascade
NEUTROPHIL LEUKOCYTOSIS + ACCUMULATION
Results in acute inflammatory exudate (fluid, fibrin, neutrophils)
Local effects of acute inflammation
Warmth (calor) Redness (rubor) Swelling (tumour) Pain (dolor) Loss of function
Systemic effects of acute inflammation
fever
liver secretes CRP
hormon production eg ADH, cortisol, arenaline - malaise, weakness, appetite loss
CRP
acute phase protein produced by the liver
CRP is an OPSONIN
Facilitates phagocytosis of bacteria
Outcomes of acute inflammation
Regeneration/resolution (best)
Repair with scarring
Progression to chronic inflammation
Depends on the severity of the injury and the type of cell damaged
Regeneration
complete restoration of the normal structure and function. for example a split thickness skin graft
Repair
results in fibrous scar formation
2 steps:
- organisation (granulation tissue replacement)
- scar formation (fibrous tissue)
Scars are structurally strong but have a loss of function
What is an abscess?
a localised collection of pus within a newly formed cavity in a tissue
has clearly defined zones
(empyemas are different from abscesses as they form in pre-existing cavities rather than newly formed)
Chronic inflammation
persistent tissue injury and destruction
ongoing inflammatory response to limit the damage
attempts to organise and heal by fibrosis/scarring
Consequences of chronic inflammation
scarring = fibrosis tissue destruction development of cancer diversion of nutrients amyloidosis
Granulomatous inflammation
a specific type of chronic inflammation
a granuloma is an aggregate of activated macrophages
causes of granulomatous inflammation
infections eg mycobacteria
sarcoidosis
crohns disease
TB pathology
most common infection disease in the world, rising incidence
mycobacterium tuberculosis - small rod shaped bacillus
latent form for many years before being reactivated
activated macrophages form granulomas around the mycobacteria - protective –> GHON COMPLEX
People at risk of active TB
immunocompromised immigrants elderly alcoholics diabetes mellitus
active pulmonary TB symptoms
feeling unwell for weeks or months
persistent cough
constitutional symptoms - weight loss, fever, night wets, loss of appetite
Diagnosis of active pulmonary TB
- compatible history
- radiological findings (CXR, CT)
laboratory findings (3 respiratory samples, one early morning), Ziehl-Neelsen stain
CULTURE IS GOLD STANDARD
Atherosclerosis
A chronic inflammatory process affecting the intima of arteries. characterised by the formation of lipid-rich plaques in the vessel wall.
Modifiable risk factors for atherosclerosis
- smoking
- HTN
- DM
- dyslipidaemia
Why does atherosrerlosis develop
damage to the endothelium
cells become dysfunctional
increased permeability
produce adhesion molecules and cytokines which attract inflammatory cells and prothrombotic molecules
recruitment of inflammatory cells which differentiate into macrophages
What do macrophages to in athersclerosis
produce free radicals that drive LDL oxidation to form oxidised LDL
engulf oxidised LDL and cholesterol crystals, becoming foam cells
foam cells produce growth factors that stimulate migration of smooth muscle cells from the media to the intima
what is the fatty streak in athersclerosis
oxidised LDL accumulates within macrophages and smooth muscle cells just underneath the endothelial cells.
collections of lipid-laden macrophages sitting in the intimal later may be visible as yellow elevations called fatty streaks
the fatty streak has no clinical significant but it is important because it may progress to an atherosclerotic plaque
What is the atherosclerotic plaque
core of lipid debris forms as the foamy macrophages die and the lipid in their cytoplasm is released
the cap represents the boys attempt to repair by scarring
