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Pathophysiology:
Introduction to Basic
Pathology
Lecture 1
Dr. Karen Ronquillo
Premed 2
Basic Pathophysiology
Basic Pathology
 Basic Microbiology
Bacteriology
Virology
Mycology
Immunology
 Basic Pharmacology

What is Pathology?
Pathology
Branch of Medicine
 “suffering’
 Studies the underlying causes of diseases
“etiology”
 Mechanisms that result in the signs and
symptoms of the patient
“pathogenesis”

Pathology
Bridge between basic science and clinical
practice
 Divisions:
General Pathology
Systemic Pathology

The Cell
How do cells react to
environmental stress?
Hypertrophy
 Hyperplasia
 Aplasia
 Hypoplasia
 Atrophy
 Metaplasia

Hypertrophy

Increase in protein synthesis/ organelles

Increase in size of cells

Increase in organ/tissue size
Hypertrophy
Hyperplasia

Increase in NUMBER of cells

Increase in size of organ/tissue
Similar end result as hypertrophy
 May occur with hypertrophy

Hyperplasia
Aplasia

Failure of cell production
Agenesis or absence of an organ:fetus
 Loss of precursor cells:adults

Technetium: scintigraphy
Aplasia
Hypoplasia

Decrease in cell production
Atrophy

Decrease in mass of preexisting cells


Smaller tissue/organ
Most common causes:
disuse
poor nutrition
lack of oxygen
lack of endocrine stimulation
aging
injury of the nerves
Atrophy
Metaplasia
Replacement of one tissue by another
tissue
 Several forms:
Squamous metaplasia
Cartilaginous metaplasia
osseous metaplasia
myeloid metaplasia

Metaplasia
Squamous to columnar change in cells
Barrett’s esophagus
What are the causes of
injury/stress?
Hypoxic cell injury
 Free radical injury
 Chemical cell injury

Hypoxic cell injury
Complete lack of oxygen/ decreased oxygen
 Anoxia or hypoxia
 Causes:
ischemia
anemia
carbon monoxide poisoning
decrease tissue perfusion
poorly-oxygenated blood

Hypoxic cell injury
Early stage Hypoxic cell injury

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
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Decrease in production of ATP
Changes in cell membrane
Cellular swelling
endoplasmic reticulum
mitochondria
Ribosomes disaggregate
Failure of protein synthesis
Clumping of chromatin
Late stage

Cell membrane damage
myelin blebs
cell blebs
Cell Death

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Irreversible damage to the cell membranes
Calcium influx
Mitochondria calcifies
Release of cellular enzymes
lab exams for AST, ALT, CKMB, LDH
Most vulnerable cells:
neurons
Cardiac enzymes
CKMB kit
Free radicals: superoxide and
hydroxyl radicals

Seen in:
normal metabolism
oxygen toxicity
ionizing radiation
UV light
drugs/chemicals
ischemia
What will neutralize free
radicals?
Mechanisms to detoxify free
radicals
Glutathione
 Catalase
 Superoxide dismutase
 Vitamin A, C, E
 Cysteine, selenium, ceruloplasmin
 Spontaneous decay

Chemical Injury

Carbon tetrachloride and liver damage
Morphologic patterns of cell death:
NECROSIS AND APOPTOSIS
Necrosis
sum of all the reactions seen in an
injured tissue, leads to cell death
 autolysis – cell’s enzymes
 Heterolysis – extrinsic factors

Types of necrosis
Coagulative necrosis
 Liquefactive necrosis
 Caseous necrosis
 Gangrenous necrosis
 Fibrinoid necrosis
 Fat necrosis

Coagulative necrosis

Interruption of the blood supply

Poor collateral circulation
heart
kidney
Characteristic nuclear changes
Coagulative necrosis
Coagulative Necrosis
Liquefactive necrosis
Interruption of blood supply
 Enzymes liquefy the tissue
Brain
 Suppurative infections
Bacteria

Liquefactive necrosis
Caseous necrosis
Coagulative + liquefactive
 “cheese - like”
 Part of granulomatous inflammation
 Classic picture:
Tuberculosis

Caseous necrosis
Gangrenous necrosis
Interuption of the blood supply to the
lower extremities or bowels
 2 types:
1. Wet type: complicated by liquefactive
necrosis
2. Dry type: complicated by coagulative
necrosis

Gangrenous necrosis types
Fibrinoid necrosis
Immune-mediated vascular damage
 Protein – like material in the blood vessel
walls

Fat necrosis

Traumatic fat necrosis: after injury
Breast
ENZYMATIC FAT NECROSIS:
PANCREAS
APOPTOSIS
“falling away from”
 Another cell death pattern
 “Programmed cell death”
 Removal of cells
 Prevents neoplastic transformation

Necrosis versus apoptosis
Gross irreversible cell
injury
 Passive form of cell
death
 Does not require
genes, protein
synthesis
 Marked inflammatory
reaction

Physiologic
programmed cell
removal
 Active form of cell
death
 Requires genes,
proteins, energy
 No inflammatory
reaction

Genes affecting apoptosis

Inhibits:
bcl-2

Facilitates:
bax
p53
Morphological features in apoptosis
Involves small clusters of cells only
 No inflammatory cells
 Cell membrane blebs
 Cytoplasmic shrinkage
 Chromatin condensation
 Phagocytosis of apoptotic bodies

Reversible Cellular changes
Fatty change
 Hyaline change
 Accumulation of exogenous pigments
 Accumulation of endogenous pigments
 Pathologic calcifications

Fatty change
Liver, heart, kidney
 Accumulation of intracellular parenchymal
triglycerides
-increased transport
-decrease mobilization
-decreased use
-overproduction

Fatty change: LIVER
Hyaline change
Accumulation of hyaline
 HYPERTENSION; DIABETES MELLITUS
 “glassy” appearance

Exogenous pigments
Lungs
carbon
silica
iron dust
 Lead – Plumbism
 Silver - Argyria

Endogenous pigments
Bilirubin
Hemosiderin
Lipofuscin
 “wear and tear”
pigment
 Elderly patients
 Liver, heart


Brown atrophy
Pathologic calcifications

Previously damages tissues
“dystrophic calcification”
scarred heart valves
Pathologic calcifications

Hypercalcemia
“metastatic calcification”
Question:
A young woman was admitted due to a bacterial
infection. CT scan showed an abscess in her
brain. What type of necrosis would you expect
to see?
 A.coagulative
 B.Caseous
 C.Liquefactive

Question:
A 15 year old girl was brought into your
clinic due to painful menses. She also said
that her menstrual blood flow was heavy
and had clumps of blood clots and
tissues.Menstruation is classified as:
 A. Apoptosis
 B. Coagulative Necrosis
 C. Liquifactive Necrosis
