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Systematic pathology
• The descriptions of specific diseases as they affect
given organs or organ systems
3) Cellular adaptation
Stimuli result in new but altered state that maintains
the viability of the cell
Intracellular mechanisms particularly
vulnerable to cellular injury
• Maintenance of membrane integrity - critical for ionic
and osmotic homeostasis of the cell
• Hypoxic/ischemic injury
Common causes
1. Upper airway obstruction (eg., sudden swelling of
laryngeal mucosa, foreign body aspiration)
Pathomechanism
• A decrease of blood pressure for hours
• Hypoxia of tubular epithelial cells ATP depletion
malfunction of Na+/K+ ATPase influx of sodium
and water into tubular cells
Morphologic features
• Light microscopy (LM)....
• Electron microscopy (EM)....
LM: the tubular epithelial cells are vacuolated, and
the brush border of proximal tubules is lost.
Hydropic change on EM: accumulation of water in the
cytoplasm, in the invaginations of the surface plasma
membrane (hydropic vacuoles), in the cisterns of the RER,
and in the mitochondria; loss of microvilli of proximal tubules
Clinical consequence
• Acute renal failure: decreased urinary
output; hemodialysis is necessary
• If systemic hypotension can be corrected,
the renal function normalizes within days
Irreversible ischemic injury and cell death
• The transition from reversible to irreversible
state is gradual and occurs when adaptive
mechanisms have been exhausted
• Depletion of ATP, influx of Ca 2+, activation of
multiple cellular enzymes, such as
1. Coagulative necrosis
2. Liquefactive necrosis
Grossly 3. Caseation
visible 4. Fat necrosis
5. Gangrene
1. Fibrinoid necrosis
Coagulative necrosis
Types:
anemic infarct
hemorrhagic infarct
Anemic infarct
Gross:
circumscribed yellowish lesion, the margins are
hyperemic
Circumscribed yellowish lesion, the margins are hyperemic
Anemic infarct
Gross:
yellowish lesion, the margins are hyperemic
LM:
dead cells become eosinophilic with loss of
nuclear staining, the border of necrotic tissue is
hyperemic and infiltrated by neutrophils
LM of myocardial infarction: eosinophilia of necrotic fibers,
disappearance of nuclear staining. Neutrophils in the interstitium
Hemorrhagic infarct
In the lungs, due to occlusion of a segmental
pulmonary artery; sec. hemorrhage via
bronchial arteries
Hemorrhagic infarct of lung: wedge shaped, raised, dark-red
area
Hemorrhagic infarct
In the small bowels, due to occlusion of the
mesenteric superior artery;
sec. hemorrhage via anastomosing arcades
Hemorrhagic infarct of small bowels
36
Liquefactive necrosis
The necrotic tissue undergoes softening due to
action of hydrolytic enzymes
Examples
1. Brain infarct
2. Abscess
1. Brain infarct
Occlusion of cerebral artery leads to anemic
infarct; then enzymes released from dead cells
liquefy the necrotized area
Brain infarct: the necrotic area is softened and pale
Infarcted area
Caudate nucleus
Internal capsule
Brain infarct. Macrophages scavenge necrotic, lipid-rich debris.
Liquefactive necrosis
2. Abscess - localized purulent inflammation.
Mitochondrion Execution
caspases
Bcl-2 , Bax
• Atrophy
• Hypertrophy
• Hyperplasia
• Metaplasia
• Dysplasia (to be lectured later)
• Intracellular accumulation of various
substances
Atrophy
• Physiologic:
- hypertrophy of uterus in pregnancy,
- compensatory hypertrophy of the remnant kidney
after unilateral nephrectomy,
- exercise
Increased exercise leads
to hypertrophy of muscles
Hypertrophy
• An increased cell mass leading to an increased
size of organs
• Physiologic: ...
• Physiologic:
- proliferation of the glandular epithelium of the
breast during lactation
Pathologic hyperplasias
Endogeneous
• Jaundice (icterus): systemic bilirubin retention;
yellow skin and sclera discoloration
Dystrophic
• In nonviable or dying tissues; the serum Ca++ level is
normal.
• Precipitation of a crystalline Ca-phosphate starts with
nucleation (initiation) on membrane fragments, followed
by propagation of crystal formation.
• Very common, with serious clinical consequences
Examples
• Arteries in atherosclerosis
• Damaged heart valves
• Areas of various necrosis
Dystrophic calcification of aortic valves
(calcifying aortic stenosis)
Metastatic calcification
Results from hypercalcemia
Radial art.
Ulnar art.