Basic Pathology

Pathology

The term pathology itself may be used

broadly to refer to the study of disease in
general, incorporating a wide range
of bioscience research fields and medical
practices
Pathos: suffering

The Cell Hyperplasia

Increase in NUMBER of cells

Increase in size of organ/tissue

Similar end result as hypertrophy

May occur with hypertrophy

Aplasia

Failure of cell production

How do cells react to environmental stress? Agenesis or absence of an organ:fetus

Hypertrophy Loss of precursor cells:adults

Hyperplasia
Hypoplasia
Aplasia
Hypoplasia Decrease in cell production
Atrophy
Metaplasia

Hypertrophy

Increase in protein synthesis/ organelles

Increase in size of cells

Increase in organ/tissue size

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 Atrophy

Decrease in mass of preexisting cells What are the causes of injury/stress?

Hypoxic cell injury

Free radical injury
Smaller tissue/organ Chemical cell injury
Most common causes:
Hypoxic cell injury
disuse Complete lack of oxygen/ decreased oxygen
poor nutrition Anoxia or hypoxia
lack of oxygen
lack of endocrine stimulation Causes:
aging
injury of the nerves ischemia
anemia
carbon monoxide poisoning
decrease tissue perfusion
poorly-oxygenated blood

Early stage Hypoxic cell injury

Decrease in production of ATP

Changes in cell membrane
Cellular swelling
o endoplasmic reticulum
o mitochondria
Metaplasia
Ribosomes disaggregate
Replacement of one tissue by another tissue Failure of protein synthesis
Clumping of chromatin
Several forms:
Free radicals: superoxide and hydroxyl radicals
Squamous metaplasia
Cartilaginous metaplasia Seen in:
osseous metaplasia
normal metabolism
myeloid metaplasia
oxygen toxicity
ionizing radiation
UV light
drugs/chemicals
ischemia

Squamous to columnar change in cells

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 Morphologic patterns of cell death:
NECROSIS AND APOPTOSIS

Necrosis

sum of all the reactions seen in an injured

tissue, leads to cell death
What will neutralize free radicals?
autolysis cells enzymes

Heterolysis extrinsic factors

Types of necrosis

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Gangrenous necrosis
Fibrinoid necrosis
Fat necrosis

Mechanisms to detoxify free radicals Coagulative necrosis

Glutathione Interruption of the blood supply

Catalase Poor collateral circulation
Superoxide dismutase o heart
Vitamin A, C, E o kidney
Cysteine, selenium, ceruloplasmin
Characteristic nuclear changes
Spontaneous decay

Chemical Injury

Carbon tetrachloride and liver damage

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 Liquefactive necrosis 2. Dry type: complicated by coagulative
necrosis
Interruption of blood supply
Enzymes liquefy the tissue Gangrenous necrosis types
o Brain
Suppurative infections
o Bacteria

Fibrinoid necrosis

Immune-mediated vascular damage

Protein like material in the blood vessel
Caseous necrosis walls
Coagulative + liquefactive
cheese - like
Part of granulomatous inflammation
Classic picture:
o Tuberculosis

Fat necrosis

a form of necrosis characterized by the

action upon fat by digestive enzymes
Fat necrosis can occur anywhere in the
breast, salivary glands and is usually
associated with trauma of
the pancreas or acute pancreatitis

APOPTOSIS
Gangrenous necrosis falling away from
Another cell death pattern
Interuption of the blood supply to the lower
Programmed cell death
extremities or bowels
Removal of cells
2 types: Prevents neoplastic transformation

1. Wet type: complicated by liquefactive

necrosis
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 Necrosis versus apoptosis Accumulation of intracellular parenchymal
triglycerides
Gross irreversible Physiologic
o increased transport
cell injury programmed
Passive form of cell removal o decrease mobilization
cell death Active form of o decreased use
Does not require cell death o overproduction
genes, protein Requires genes,
synthesis proteins, energy Hyaline change
Marked No
inflammatory Accumulation of hyaline
inflammatory
reaction HYPERTENSION; DIABETES
reaction
MELLITUS
Morphological features in apoptosis glassy appearance

Involves small clusters of cells only

No inflammatory cells
Cell membrane blebs
Cytoplasmic shrinkage
Chromatin condensation
Phagocytosis of apoptotic bodies

Exogenous pigments

Lungs
o carbon
o silica
o iron dust

Reversible Cellular changes

Fatty change
Hyaline change
Accumulation of exogenous pigments
Accumulation of endogenous pigments
Pathologic calcifications

Fatty change

Liver, heart, kidney

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 Endogenous pigments

Bilirubin Hemosiderin

Pathologic calcification

is a common process in a wide variety of

disease states
it implies the abnormal deposition of
calcium salts with smaller amounts of iron,
magnesium, and other minerals.

Types of Pathologic calcification

Dystrophic calcification:

When the deposition occurs in dead or dying

tissues
it occurs with normal serum levels of
calcium
Dystrophic calcification is encountered in
areas of necrosis of any type or injuries
It is certain in the atheromas of advanced
atherosclerosis, associated with intimal
injury in the aorta and large arteries
may also be a cause of organ dysfunction

Metastatic calcification:

The deposition of calcium salts in normal

tissues caused by hypercalcemia (usually a
consequence of parathyroid hormone
excess)
It almost always reflects some derangement
in calcium metabolism (hypercalcemia)