ICS - Pathology Flashcards
5 cardinal signs of inflammation/ macroscopic appearances of acute inflammation
- Rubor - REDNESS
- Calor - HEAT
- Tumor - SWELLING
- Dolor - PAIN
- LOSS OF FUNCTION
What is acute inflammation?
The initial and often transient series of tissue reactions to injury - may last few hrs to few days
define inflammation
local physiological response to tissue injury
name 2 benefits of inflammation
- destruction of invading microorganisms
- the walling off of an abscess cavity - thereby preventing the spread of infection.
name 2 limitations of inflammation
- disease - e.g. abscess in brain acts as a space occupying lesion compressing vital surrounding structures.
- fibrosis - from chronic inflammation may distort tissues and permanently alter function
6 causes of acute inflammation
- microbial infections eg : pyogenic (pus causing) bacteria, viruses
- hypersensitivity reactions eg parasites, tubercle bacili
- physical agents eg: trauma, ionising radiation, heat, cold (frostbite)
- chemicals eg : corrosives, acids, alkalis, reducing agents
- bacterial toxins
- tissue necrosis eg ischaemic infarction
What is the acute inflammatory response process?
- changes in vessel calibre (gets wider) - consequently increased vessel flow.
- increased vascular permeability and formation of the fluid exudate.
- formation of the cellular exudate - emigration of the neutrophil polymorphs into the extravascular space.
vascular component: DILATION OF VESSELS
exudative component: VASCULAR LEAKAGE OF PROTEIN-RICH FLUID
(oedema fluid, fibrin and neutrophil polymorphs accumulate in extracellular spaces of damaged tissue)
explain the outcomes of acute inflammation
- RESOLUTION - goes away
- SUPPARATION - pus formation e.g.: abscess
- ORGANISATION: healing by fibrosis (scar formation) when there is substantial damage to the connective tissue framework and/or tissue lacks the ability to regenerate specialised cells. when this happens, dead tissues and acute inflammatory exudate are 1st removed from damaged areas by macrophages. the defect becomes filled by ingrowth of specialised vascular connective tissue (GRANULATION TISSUE) = organisation. the granulation tissue then produces collagen to form a fibrous (collagenous) scar.
- PROGRESSION - to chronic inflammation.
Explain the vascular changes in acute inflammation
- capillaries have no smooth muscle in walls to control calibre, so narrow RBC must pass through in a single file.
- smooth muscle of arteriolar walls form precapillary sphincters which regulate blood flow through the capillary bed
- in acute inflammation, sphincters relax, increase blood flow through capillaries = REDNESS AND HEAT
- in normal conditions the high osmotic pressure inside the vessel due to plasma proteins, favours fluid return to the vascular compartment
- under normal circumstances, the high hydrostatic pressure at the arteriolar end of capillaries forces fluid out into the extravascular space, but this fluid returns into the capillaries at the venous end, where hydrostatic pressure is low.
- in acute inflammation, capillary hydrostatic pressure increased, escape of plasma proteins into extravascular space (due to increased pressure) = increased osmotic pressure = more fluid leaving the vessels than is returned to them = increased vascular permeability.
3 causes of increased vascular permeability
- IMMEDIATE TRANSIENT - chemical mediators eg: histamine, bradykinin
- IMMEDIATE SUSTAINED - severe direct vascular injury eg trauma
- DELAYED PROLONGED - endothelial cell injury eg x-rays and bacterial toxins
stages in neutrophil polymorph emigration
- MARGINATION - in normal circulation, cells are confined to axial stream (central), don’t flow in the peripheral (plasmatic) zone near to endothelium. loss of intravascular fluid and increase in plasma viscosity with slowing of flow at site of acute inflammation allows neutrophils to flow in this plasmatic zone.
- ADHESION - adhesion of neutrophils to vascular endothelium at site of inflammation = PAVEMENTING. neutrophils randomly come into contact with endothelium in normal tissues but don’t adhere. pavementing occurs early in acute - only in VENULES. increased leukocyte (wbc) adhesion from interaction between paired adhesion molecules on leukocyte and endothelial surfaces.
- NEUTROPHIL EMIGRATION - leukocytes migrate through the walls of venules and small veins but don’t commonly exit from capillaries. neutrophils, eosinophil polymorphs and macrophages all insert pseudopodia between endothelial cells, migrate through the gap so created between the endothelial cells, and then on through the basal lamina into the vessel wall.
- DIAPEDESIS - rbc may also escape from vessels, but this is passive and depends on hydrostatic pressure forcing rbc out. loads of rbc in extracellular space = severe vascular injury = tear in vessel wall.
- CHEMOTAXIS - attraction of neutrophil polymorphs towards certain chemicals eg at site of inflammation
neutrophil polymorph histology
under h and e stain - nucleus stains blue. cytoplasm pink/purple
what is chronic inflammation?
subsequent and often prolonged tissue reactions to injury following the initial response. - lymphocytes, plasma cells and macrophages predominate.
causes of chronic inflammation
- primary chronic inflammation = no initial phase of acute inflammation
- transplant rejection
- progression from acute inflammation (usually suppurative)
example of acute inflammation
APPENDICITIS
explanation:
-Unknown precipitating factor
-Neutrophils appear
-Blood vessels dilate
-Inflammation of serosal surface occurs
-Pain felt
-Appendix either surgically removed or inflammation resolves or appendix bursts with generalised peritonitis and possible death
