D’YOUVILLE COLLEGE
BIOLOGY 307/607 - PATHOPHYSIOLOGY
Lecture 2 - INFLAMMATION
Chapter 2
1.
Tissue Fluid Exchange:
• anatomy of microcirculation (fig. 2 – 1 & ppt. 1)
- arterioles, metarterioles, venules
- capillaries, precapillary sphincters
- permeability of capillaries (fig. 2 – 2 & ppt. 2); tight & leaky endothelia
• pressures promoting fluid exchange (fig. 2 – 3 & ppt. 3)
- main filtration (outward) forces: blood hydrostatic P, tissue osmotic P
- main absorption (inward) forces: blood osmotic P, tissue hydrostatic P
- role of lymphatic drainage: compensate absorption shortfall (ppt. 4)
2.
Acute Inflammation:
• cardinal signs
- redness (rubor), warmth (calor), swelling (tumor), pain (dolor), altered
function (functio laesa)
• vascular changes
- vasodilation --> hyperemia—causes transudate (protein-free edema) (figs.
2 – 3, 2 – 4 & ppt. 5)
- increased permeability of post-capillary venules (fig. 2 – 5 & ppt. 6) -->
slowing or stasis of blood flow causes exudate (protein-rich edema)(fig. 2 – 6 & ppt.
7)
• cellular changes
- axial flow of formed elements (fig. 2 – 7 & ppt. 8)
- behavior of leukocytes: margination, pavementing, ameboid movement,
emigration, chemotaxis & phagocytosis (figs. 2 – 8, 2 – 9, 2 – 10, 2 – 11 & ppt. 9)
Bio 307/607 lec. 2
- p. 2 -
- types of defensive cells: tissue macrophages, mast cells, neutrophils
(=PMNs), monocytes, eosinophils, and lymphocytes
Bio 307/607 lec. 2
- p. 3 -
• phagocytosis:
- chemotaxis, opsonization & engulfment (fig. 2 – 12 & ppts. 10 & 11)
- bactericidal capabilities of phagocytic cells (fig. 2 – 13 & ppt. 12):
preformed agents block bacterial proliferation, destroy bacterial cell walls, produce
acid &/or toxic conditions that debilitate bacteria; metabolically-produced oxygen
free radicals & halogen derivatives have powerful toxic effects on bacteria
• exudates
- types of exudate: vary with severity of injury: serous, fibrinous (proteinrich), purulent or suppurative (contain white cells); may be diffuse (cellulitis) or
localized (abscesses)
- beneficial effects of exudates: toxin dilution, swelling  pain (behavior
protective of affected part), proteins including antibodies (opsonins), bactericidal,
antimicrobial agents & clotting factors (wall off inflammation site)
• chemical mediators of inflammation (tables 2 – 1 & 2 – 2)
- histamine (from mast cells & platelets) & serotonin (from platelets) 
increased permeability of PC venules; blocked by antihistamines
- eicosanoids (derivatives of arachidonic acid from plasma membrane of
leukocytes & mast cells); formed by cyclooxygenase (COX) pathways (e.g.,
prostaglandin E2) or lipoxygenase pathway (leukotrienes) (figs. 2 – 14, 2 – 15 & ppts.
13 & 14)
 prolong permeability increase; includes prostaglandins (also
vasodilators), and leukotrienes (also vasoconstrictors & chemotaxins); COX
pathways blocked by steroids, NSAIDs, acetaminophen, ASA, ibuprofen (figs. 2 – 14
& 2 – 15)
- nitric oxide (produced by macrophages during inflammation) 
modulates inflammatory response (vasodilator)
- platelet-activating factor (from platelets, leukocytes, & endothelium) 
activates platelets & leukocytes
- plasma-borne substances (originally formed in liver, Hageman factor,
activated by infection/tissue damage, further activates enzyme cascades in plasma)
(fig. 2 – 16 & ppts. 15 & 16):
- fibrin degradation products (from clots, found in plasma) 
chemotaxis, leukocyte activation
- kinins (from liver, e.g. bradykinin)  activate pain receptors
- complement system (from liver, circulates in plasma)  chemotaxis,
opsonization, membrane attack complex (MAC)
- summary of chemical mediators (ppt. 17)
Bio 307/607 lec. 2
- p. 4 -
• systemic effects (ppts. 18 - 20):
- fever, lassitude, weakness, possibility of spread along lymphatics
(lymphangitis) or to bloodstream (possible bacteremia)
- leukocytosis: neutrophilia (bacterial infections or tissue injury),
lymphocytosis (viral infections) or eosinophilia (allergies or parasitic infections)
• therapies
- necessary to oppose possible inappropriate effects (fig. 2 – 17)
- application of cold reduces swelling and resultant pain; heat application
potentiates phagocytic response
- elevation of or application of pressure to affected region alleviates
swelling by restricting blood flow to region and improving lymphatic drainage of
region
3.
Chronic Inflammation:
• unresolved injurious agent (table 2 -- 3) prolongs inflammation for months
or years
• inflammatory cells dominate site, replacing and/or damaging functional
tissue; macrophages stimulated by lymphokines from immune system cells
(migration inhibiting factor & macrophage activation factor) (fig. 2 – 18)
- tissue damage may accrue from ‘frustrated phagocytosis’ – inability of a
phagocytic cell to engulf a large injurious agent results in release of the phagocytic
products, which then attack healthy tissue & stimulate further macrophage activation
(ppt. 21)
- site may be diffuse, or localized, with characteristic lesion (granuloma
populated by abnormal macrophages and lymphocytes) (fig. 2 – 19 & ppts. 22 & 23);
or it may be diffuse without granuloma (fig. 2 – 20) (summary of inflammation -- ppt.
23)