Pathology- Inflammation Flashcards
What mediates vasodilation/ vasoconstriction?
Histamine and nitric oxide
Cellular change involves which 5 processes?
Stasis White cell margination Rolling Adhesions Migration
what chemicals increase selectin expression?
histamine and thrombin
What cells increase V+ICAM expression?
TNF and IL-1
Where is selectin expressed?
on endothelial cells and white cells
Where do integrins bind to?
vessel walls, cell matrix, ICAM, VCAM
Rolling
integrin-selectin interaction with their ligands is low affinity therefore binding on and off is fast
Role of chemokines in response to injury
they bind to proteoglycans on endothelial cell surface, which increase the affinity of V+ICAMs for interns
How is swelling caused?
increased vascular permeability-> loss of proteins-> change in osmotic pressure-> water follows protein-> swelling
3 phases of phagocytosis
- Recognition and attachment
- Engulfment
- Killing and degradation
Dolor
Pain
mediated by prostaglandins and bradykinin
Function laesa
loss of function
Main inflammatory cell in acute inflammation
neutrophil
- many lobes, granulocytic and has phagocytic and cytotoxic abilities
- mops up dead cells
Types of changes in acute inflammation
Vascular and cellular changes
Resolution
complete restoration of tissue to normal after inflammatory components are removed
minimal cell death
Why must there be a good vascular supply for resolution to occur
delivery of WBC and rapid removal of injurious agent
Suppuration
Production and accumulation of purulent exudate (pus)
What is pus comprised of?
living, dying and dead cells
neutrophils, bacteria, fibrin
empyema
walled off space filled with pus
Organisation
mucosa where damage goes beyond basement membrane
occurs if injury produces lots of necrosis, fibrin (that cant be cleared) and has a poor blood supply
Granulation tissue formation
Defect slowly infiltrated by capillaries then myofibroblast-> collagen and smooth muscle cells accumulate-> redness
Result of fibrosis
loss of function
cirrhosis
scarring and fibrosis in liver
cell which is characteristic of chronic inflammation
lymphocyte
small, round, blue cell
Chronic inflammation
not related to time
occurs in cases of persistent injury/ infection
This type of cell is granulated and an aggregate of epithelial histiocyte. It is involved in chronic inflammation.
Macrophage (type of monocyte)
Examples of endogenous foreign bodies which cause granulomatous inflammation
keratin, bone, crystal
Examples of exogenous foreign bodies which cause granulomatous inflammation
talc, asbestos, suture material, oil
Examples of infections which cause granulomatous inflammation
parasites, worms, mycobacterium (eg TB), eggs, syphylis
Changes within first 20 mins of MI
No macro/microscopic changes; there are changes on ECG
First signs of cell death
pyknosis, erythema, nucleus shrinks and darkens, marginal contraction bands appear
Changes within first 24hrs of MI
cell contents leak, complement cascade is initiated and acute inflammation occurs
wall of heart at its weakest, risk of cardiac rupture
Changes within first 48hrs of MI
neutrophils are replaced by macrophages, changes seen at autopsy-> macrophages create yellow appearance
Restitution
A gradual process in which progressive scarring occurs.
macrophages are replaced by fibroblasts over 6 weeks
Role of fibroblasts
gradually lay down collagen from wks 2-6.
this is why after the 6 week mark, an MI cannot be dated
