HISTOPATHOLOGIC AND CYTOLOGIC TECHNIQUES - LECTURE

CELLULAR INJURY AND CELL DEATH

PRELIMS | A.Y. 2022-2023 | PROF. DOREN VENUS OTOD

OUTLINE ● Detachment of ribosomes from ER

I. Cellular Injury ○ The ribosomes wil now be detached on the
A. Causes endopasmic reticulum, specifically the
B. Morhological Alterations rough endoplasmic reticulum.
II. Cellular Death ● Clumping of nuclear chromatin
A. Difference between the Two Princial
Pathways of Cell Death
II. CELLULAR DEATH
III. Apoptosis
.
A. Reasons in Following Conditions
IV. Necrosis CELLULAR DEATH
A. Types According to Location or Extent ○ Right after cellular injury; can lead to cellular death
B. Types According to Morphology ○ There are two types of cellular death. I can be (1)
apoptosis or (2) necrosis
I. CELLULAR INJURY

CELLULAR INJURY
● Alteration in cell structure or function due to stress
or pathologic stimuli
● This is the most common response of the cells in
almost all types of diseases.

A. CAUSES

● Hypoxia
○ There is loss of oxygen level on that Figure 1. Two pathways of cellular death
specific organ or on that specific cell
● Physical Agents A. DIFFERENCES BETWEEN TWO PRINCIPAL
○ This can be due to accidents or any form PATHWAYS OF CELL DEATH
of physically-induced type of injury
● Chemical Agents and Drugs Apoptosis Necrosis
○ Chemical and drugs that can be harmful to Cell Size Reduced Enlarged
the body there is swelling
● Infectious Agents Plasma Intact Disrupted
○ Bacteria, parasites, and the viruses. Membrane
● Immunologic Reactions Cellular Intact Enzymatic digestion;
○ Allergies Contents -the composition/
substances inside the
● Genetic Abnormalities cell may leak out
○ Comes from parents; passed to you during Adjacent No (because Frequent (due to
pregnancy Inflammation phagocytes rapidly leakage of cellular
● Nutritional Imbalances devour the cells) contents)
○ There is no homeostasis on the tissues Nucleus Fragementation into Pyknosis (clumping)
that resulted to cellular injury nucleosome-size → Karyorrhexis
fragments
(fragmentation) →
B. MORPHOLOGICAL ALTERATIONS Karyolysis (dissolution)
.
● Generalizing swelling of cells and organelles
○ The first and foremost or the earliest
manifestation of cell injury
● Blebbing of plasma membranes Physiologic Physiologic Pathologic
○ This one is due to increase in the number or -death by destiny -death by disease
Pathologic? -ex. RBC lifespan is -sudden death of cell
of free radicals and the plasma membrane
120 days -brought about by
will now protrude. pathologic sources or
○ The protruded portion of the lasma origin
membrane is called the Blebs.

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 III. APOPTOSIS
.
APOPTOSIS
● Induced by a tightly regulated suicide program in
which cells destine to die activate enzymes that
degrade the cells’ own proteins and nuclear DNA
● Presence of cleaved, active caspases is a marker
for cells undergoing apoptosis
○ CASPASES: These are cysteine proteases
that can cleave the aspartic residue.
● Cells break up into apoptotic bodies, which are
tasty targets for phagocyte
● Always remember: triggered by a physiologic.
● The advantage of this type of cell death is it will
prevent further damage of other neighboring cells
and it will prevent as well the growth of unwanted
cells such as those cancerous cels.
● Once the appearances of caspases, automatically,
they will be phagocytized by the phagocytic cells
● The outcome usually of the cells that undergo
apoptotic death is shrunken, the cell membranes
and components are still intact, and there is no any
form of leakage.
● The cause of this one can be hypoxia, physical
agents, chemical agents, or biological products
A. REASONS IN FOLLOWING CONDITIONS
● PHYSIOLOGIC
○ Eliminates cells that are no longer needed
or those that have served their purposes
○ Its timespan is alread finished
● PATHOLOGIC
○ Eliminates cells that are injured beyond
repair without eliciting host reaction
IV. NECROSIS
NECROSIS
● Consequence of severe injury
● triggered by a pathologic origin or cause.
● The consequences of this cell is severe. There is
no benefit of having a necrotic death because the
neighboring cell.will be injured due to the leakage
of cellular components during cell bursting.
● The outcome of the cell that will undergo necrosis
is there is damage and inflammation on the tissue,
the cell will swell, and the contents will leak.
A. TYPES ACCORDING TO LOCATION OR EXTENT
. Figure 3. Pus formation in the Brain that undergoes
● FOCAL
○ The inflammation or the injury only
happened on the certain area of the body
● MASSIVE
○ The inflammation or the injury is
widespread.
A. TYPES ACCORDING TO MORPHOLOGY
COAGULATIVE
● Tissue is firm because architecture is preserved
● Eosinohilic due to denaturation and precipitation
of cellular proteins AND enzymes
○ The cytoplasm of the organ or the cell
undergoes rapid coagulation
● Occurs on affected tissue when vessel is
obstructed leading to ischemia (except brain)
○ Infarct - localized area of necrosis
● Main cause: ISCHEMIA
○ lack/low oxygen supply on organ/tissue
● This tye of necrosis appears to be firm. It looks like
it was cooked. The tissues will appear dull or dirty.
Figure 2. Yellowish part of the Kidney that undergoes
Coagulative type of Necrosis
LIQUEFACTIVE
● Tissue becomes liquid viscous mass due to
digestion of dead cells
● There is rapid total enzymatic dissolution of the cell
that can be usually seen in brain tissues with
bacterial infection.
● This can lead to pus formation. There is
liquefaction. There is a softening of an infected
part.
● Occurs during microbial infection
● It appears creamy yellow because of pus
● Affects CNS
Liquefactive type of Necrosis
GANGRENOUS
● This is considered as a “massive tissue death”
● Due to ischemia (loss of blood suppy); may be
superimosed with bacterial infection
● Combination of coagulation and liquefaction
necrosis
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 ● Two Types of Gangrenous Necrosis:
○ Dry Gangrene:
■ Considered as a sterile type of
gangrenous necrosis and the
reason for this one is arterial
occlusion and ischemic type of
necrosis.
■ There is a sharp demarcation line.
The demarcation line determines
up to what extent the gangrene is. Figure 5. A lung of a patient that undergoes a Caseous type
■ As to the odor, it is less foul of Necrosis
because there is less bacterial
action. FAT
■ The presence of discoloration is ● Fat destruction due to pancreatic lipase
due to the release of black/blood ○ Lipase splits the neutral fats into fatty
pigments. acids (FA) and glycerol without affecting
the cell membrane
○ Wet Gangrene: ○ Fatty Acids + Calcium = Chalky-white
■ This is a venous occlusion and the areasl soap-like appearance (fat
odor is more foul because there is saponification)
increased bacterial actions plus ● Seen in acute pancreatitis
ischemic injury. The appearance
looks like it is rottening.
■ There is nio sharp demarcation
lline. In the picture below, yu
cannot see up to what extent.
■ There is stagnation of venous
blood. That is why the odor is
more foul and more offensive.

Occlusion Odor Demarcation

line
Dry Arterial Less Foul Sharp Figure 6. A mesentery with a production of adipose tissue
Gangrene
Wet Venous More Foul None FIBRINOID
Gangrene
● Seen in immune reactions when antigen-antibody
complexes are deposited in walls of arteries
○ Usually, this is due to a genetic origin so it
involves your immune complex
● Immune complex + fibrin = fibrinoid (bright pink
and amorphous appearance in H&E staining.

Figure 4. (a) Dry Gangrene and (b) Wet Gangrene

CASEOUS
● Cheese-like
● Friable white appearance of necrotic area
● Seen in tuberculosis, granuloma
● This one is characterized by a collection of soft and
whitish gray debrees that resembles a cheese.
● The photo below is a lung of a patient with
tuberculosis. The cells of this type of necrosis will
Figure 7. An artery with an accumulation of fibrinoid
die and will form an amorphous, proteinatious in
which the resemblance is far to its normal
appearance.

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