Pathology is the medical discipline that provides diagnostic information to patients and clinicians. It impacts nearly all aspects of patient care, from diagnosing cancer to managing chronic diseases through accurate laboratory testing.
CONTENTS Coagulation 244
Inflammation 227 Sepsis 251
Cellular adaptation 231 Shock 252
Cell injury 232 Disorders o f the genital tra ct 255
W ound healing 237 Disorders in pregnancy 265
Neoplasia 239 Pathology - specific blood tests 268
In fla m m a tio n
1. T he in fla m m a to ry response consists o f 2 m ain co m p o n e n ts
• Vascular response
• C ellular response
2. Vascular response
• C h ron o lo g y o f vascular response (Fig. 7.1)
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w tm m
Figure 7.1 C hronology o f vascular response
® Vasodilation
i. Is the earliest manifestation o f acute inflam m ation
ii. Involves arterioles firs t
iii. Is induced by th e action o f
s Histamine
e NO
iv. Results in increased b lo o d flo w
V. R e s u lts in in c r e a s e d h y d r o s ta tic n r e s s u r e
, 228 Chapter 7 Pathology _______________ ' -■ j
• Exudation results in
i. Reduced intravascular osm otic pressure
ii. Increased interstitial osm otic pressure
iii. Oedem a
• Exudate is an inflam m atory extravascular flu id th a t has a high p ro te in concentration and a
specific gravity > 1.02
• Increased vascular perm eability occurs in distinct phases
i. Phase 1 - im m ediate transient response
* Is m ediated by histamine, leukotrienes, neuropeptide substance P, and bradykinin in
venules
* Is sh o rt lived (less than 30 minutes)
® Is reversible
ii. Phase 2 - delayed response
* Is mediated by kinin and com plem ent products
■ Is long lived
■ Involves venules and capillaries
■ O n se t is delayed fo r 2 -1 2 h
iii. Phase 3 - prolonged response a fte r d ire c t endothelial injury, which affects all levels o f
m icrocirculation
3. C e llu la r response
• Involves 2 events
i. Leucocyte extravasation
ii. Phagocytosis
• Extravasation is th e sequence o f events in th e m ovem ent o f leucocytes fro m th e vessel
lum en t o the inte rstitia l tissue (Fig. 7.2)
Figure 7.2 Extravasation sequence
• Leucocyte adhesion to th e endothelium is regulated via endothelial binding receptors that
belong to 4 main groups
i. Selectins
ii. Im m unoglobulin super-family
iii. Integrins
iv. M ucin-like glycoproteins
• Diapedesis
i. Is th e process o f transm igration across th e endothelium
ii. O ccurs predom inantly in the venules
• C hem otaxis is elicited by
i. Exogenous agents (e.g. bacterial products)
ii. Endogenous agents
■ C om ponents o f th e com plem ent system
■ Leukotriene
■ Cytokines
• M icrobicidal substances
i. A re released in to the extracellular space and phagolysosomes during phagocytosis by
leucocytes
ii. Include
■ Lysosomal enzymes
■ Reactive oxygen interm ediates (e.g. H 20 2)
■ Products o f arachidonic acid m etabolism (e.g. leukotrienes and prostaglandins)
iii. A re capable o f causing endothelial and tissue damage (leucocyte-induced injury)
including
■ A cu te respiratory distress syndrom e
■ A cu te transplant rejection
■ Asthm a
■ Reperfusion injury
4. C h e m ical m e d ia to rs o f in fla m m a tio n include
• Hageman fa c to r activation
i. Source = live r and plasma
ii. A lso know n as fa c to r 12
iii. Functions
■ Activates kinin system
* Activates clo ttin g system
® Activates fib rin o ly tic system
* Activates com plem ent system
• C o m plem e n t system
i. Source = live r and plasma
• Cytokines and N O
i. Source = endothelium and macrophage
» Platelet-activating fa cto r
i. Source = endothelium and leucocytes
• Serotonin
i. Source = platelets and mast cells
ii. Increases vascular perm eability
• Histam ine
i. Source = platelets and mast cells
ii. Associated w ith IgE
• Bradykinin
i. T he kinin system is triggered by th e activation o f th e Hageman fa cto r
ii. Functions
■ Increased vascular perm eability
■ Vasodilation
■ Sm ooth muscle co n tra ctio n
* C hem otaxis
* Activates Hageman fa cto r
iii. Is fo rm e d by th e action o f kallikrein (converts kininogen —» bradykinin)
iv. Is inactivated in th e lungs by ACE
v. ACE in h ib ito r (ACEi) prevents inactivation o f kinin in th e lungs
• Prostaglandins
• Leukotrienes
• Platelet-activating fa c to r
• Lysosomal enzymes
5- Signs o f in fla m m a tio n
• Raised ESR (due to RBC clum ping)
• Leucocytosis —increased num ber o f im m ature neutrophils
® 4 cardinal signs
, § 230 Chapter 7 Pathology
i. R ubor (redness)
ii. T u m o u r (swelling)
iii. C a lo r (heat)
iv. D o lo r (pain)
• V irc h o w sign (loss o f function)
6. Systemic acute phase response is predom inantly induced by
• ln te rle u kin -1
• TNF
7. T h ere are 2 patterns o f inflammation
• A cute
• C h ron ic
A cu te in fla m m a tio n
1. Characteristics
• Rapid onset
• Short duration
2. Vascular and cellular changes
• A lte ra tio n in vascular calibre
i. Initial vasoconstriction fo llo w e d by vasodilation
ii. Slowing o f circulation (stasis)
iii. Margination o f leucocytes
iv. C entral sludging o f RBCs
• Increased vascular perm eability
• Exudation o f flu id
■ Serous
■ Fibrinous
■ Purulent
• Emigration o f leucocytes (predom inantly neutrophils)
3. O utcom es
• C o m plete resolution
• Fibrosis
• Abscess fo rm a tio n
• C h ron ic inflam m ation
4. Morphological patterns o f acute inflamm ation
• Serous inflam m ation
• Fibrinous inflam m ation
• Suppurative inflam m ation
• Ulcers
C hronic in fla m m a tio n
1. Chronic inflammation is caused by
• Persistent infection (e.g. Mycobacterium)
• Prolonged exposure to foreign agents (e.g. silica)
• Im m une reaction to o w n tissue (e.g. autoim m une disease)
2. Can start de novo w ith ou t acute inflamm ation
3. Features
• Long duration
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