PATHOLOGY

SGD (First Shifting)

PATHOLOGY
SGD #1: Cell Adaptation, Cell Injury, and
Necroses

Case 1: Hypertensive px à hypertrophic heart

1. Identify the form of adaptation seen in the px:
Hypertrophy
• Increase in PVR (Peripheral Vascular Resistance)
à increase in afterload (pressure that the heart
must overcome) à increase force of contraction to
overcome the increase in afterload à Hypertrophic
− - Remember: not all atrophic changes has fibrotic
heart
tissue/ fibrosis
• Patient’s heart weighs 600g ; left ventricle is the
• Necrosis/ inflammation à always fibrotic
biggest chamber of the heart and contributed so
• Pathophysiologic mechanism of poliomyelitis à
much on this weight
denervation or lack of stimulus
• Other causes:
− Aging (loss of hormones/ decrease in
hormones)
− Malnutrition
− Disuse
• Atherosclerosis à atrophy due to decrease in
blood supply (eg. Brain)
• Example of a localized atrophy à cast
• Kwashiorkor à decrease protein/ protein
malnutrition ; edematous ; atrophy of muscles
• Nucleus (check the photo above)
CASE 3
- hypertrophic and hyperchromatic. The edge is

squarish instead of blunt
- wider diameter and increase in size
- heart cells are arrested in S phase, it can’t undergo
mitotic division because they lack centriole.
• Ultrastructural changes that can be seen:
− Organelles , nucleus
Case 2: Poliomyelitis
• Poliomyelitis à loss of motor function and innervation;
Micrograph of an endometrium in
proliferative phase
hypofunctioning due to decrease # of cells
• x/s gastrocnemius: atrophy à decrease in # of cells

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Why is there bleeding?
• As the endometrial lining becomes
thicker, the blood supply cannot
cope → the upper portion will be
ischemic → necrose → lead to
bleeding

CASE 4

Micrograph of the curettage from a 50 y/o
female complaining of irregular vaginal
bleeding

Proliferative phase
• Due to ↑ estrogen levels
• Physiologic hyperplasia
• Some women can have longer
proliferative phases
• Pseudostratified columnar
epithelium (?)

Secretory Phase
• Due to ↑ progesterone
• No more proliferative activity
• Always 14 days
• Simple columnar epithelium
Biopsy of the endocervix.
Abnormal Hyperplasia
• Varying size of glands Identify the 2 types of epithelium seen.
• Irregular distribution of glands • Stratified squamous epithelium
• Still pseudostratified and simple tall columnar
• Some glands are cystically dilated epithelium
• ↑ levels of estrogen
o Normally, estrogen levels What is the normal epithelium of the
should go down before endocervix?
ovulation • Simple tall columnar epithelium
o If estrogen levels stay ↑ with mucus-secreting cells,
without counteraction from basally-oriented nuclei
progesterone, cells continue • Presence of crypts (Not glands)
to proliferate
o Can lead to the formation of What is the form of cellular adaptation
an adenocarcinoma seen?
• More mitosis than normal • Metaplasia
o Some portions are tall
columnar while the other

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portions are stratified • Reversible injury – cellular
squamous swelling
• Causes: hypoxia/ischemia,
What is the usual stimulus that may presence of toxic chemicals
lead to this type of cellular adaptation?
• Inflammation Enumerate the ultrastructural
changes.
Metaplasia in the endocervix happens • Mitochondria – will have anaerobic
in 2 ways: respiration as the main source of
• In-growth of ectocervival lining energy
into the endocervix – o ↓ ATP levels in the cell
epithelilization o ↓ Activity of active pumps
• Reserve cell hyperplasia such as the Na/K ATPase →
o Normally, basal cells will increased Na and other ions
differentiate into columnar within the cell → osmosis or
cells movement of water into the
o In chronic inflammation, cell → swelling/water
basal cells will develop into retention
stratifies squamous cells • ER – also swollen
o Some of the ribosomes fall
In the respiratory tract, give 2 possible off from the ER
stimuli that may lead to this form of • Cytoskeletal filaments –
adaptation. conglomerate in one side
• Chronic smoking o Other areas will have less
• Chronic exposure to toxic gases cytoskeleton → produce
• These stimuli cause metaplasia – blebs
pseudostratified columnar ciliated • Lysosomes – will fuse with
epithelium into stratified “exhausted” mitochondria and
squamous epithelium other organelles → autophagy →
lead to formation of lipofuscin
CASE 5 pigment (wear and tear pigment)

CASE 6

Micrograph of the renal tubules of a 54
y/o female who had a sudden drop of BP
that lasted for about an hour

Identify the reversible pattern of cell
injury seen under the light microscope. Identify the type of necrosis seen.
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• Coagulative necrosis • The area with necrosis is replaced
by inflammatory cells, neutrophils
Describe the microscopic features. (violet), and necrotic debris
• Outline/architecture of cells still
seen but no more nucleus Give the possible causes and organs
• If the cell is striated, at first the where they occur.
striations are still visible but later • Stimulus: hypoxia for the brain,
on the striations will no longer be Pathologic stimulus for other
visible organs: pyogenic organism (Beta
helomytic Streptococcus sp.,
Give the possible causes and organs Staphylococcus sp.) for other
where they occur. organs
• Stimulus: hypoxia
• All organs except for the brain Explain the etiopathogenesis.
• Di ko gets ito
Explain the etiopathogenesis. • Occurs when autolysis or
• Not sure. Wala akong notes ditto. heterolysis predominates over
• Protein denaturation with the protein denaturation
preservation of the cell and tissue • Digestion of dead cells resulting in
framework transformation of the tissue into a
• The necrotic tissue undergoes liquid viscous mass
either heterolysis (degradation by
lysosomal enzymes of invading CASE 8
leukocytes) or autolysis (digestion
by its own lysosomal enzymes)

CASE 7

Identify the type of necrosis seen.
• Caseous necrosis

Liquefactive necrosis, brain tissue Describe the microscopic features.
• Amorphous eosinophilic material
Identify the type of necrosis seen. with cell debris
• Liquefactive necrosis • Necrotic area appears as a
structureless collection of
Describe the microscopic features. fragmented or lysed cells and
• Architecture of cells no longer amorphous granular debris
visible enclosed with a distinctive

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inflammatory border, which is lipases can release the fatty
known as a granuloma acids from triglycerides and
the FA will complex with
Give the possible causes and organs calcium to create soaps
where they occur. Explain the etiopathogenesis.
• Most often in tuberculosis
infections
• TB – lungs, etc.

Explain the etiopathogenesis.
•
CASE 9

Identify the type of necrosis seen.
• Enzymatic fat necrosis
Describe the microscopic features
• Vague cell outlines with calcium
depositions
Give the possible causes and organs
where they can occur
• Acute hemorrhagic pancreatitis
o Alcohol + Fatty food
o Pancreatic enzymes are
normally inactive in the
acini and become active
only in the duodenum
o Chronic pancreatitis –
alcohol → spasm of the
pancreatic duct (? O
pancreas ba ito) →
stimulate enzymes and
activate them while in the
parenchyma of the
pancreas → proteases can
degrade the blood vessel
wall causing hemorrhage,

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