PATHOLOGY 1!

The Department of Clinical

Patomorphology!
 ⼀一、History of Pathology
Autopsy → Organ pathology (1761)

LM → Cellular pathology (1854)

Ultrastructural pathology with the application

of EM (20 century 60s)

Immunopathology, Molecular pathology,

Genetic pathology, Quantitative pathology

2. Classification:
(1) Human pathology Autopsy
Biopsy
Cytology
(2) Experimental pathology

3. Position:
It’s a bridging discipline involving both

basic science and clinical practice

4. Text of Pathology:
(1) General pathology:

concerned with the basic reaction of

cells and tissues to abnormal stimuli

that underlie all diseases.

(2) Systemic pathology :

dedcribe the specific responses of specialized

organs and tissues to defined stimuli.

三、Techniques of
Pathology
1. Human pathology

(1) Autopsy

(2) Biopsy: surgical or diagnostic pathology

(3) Cytology: smear, fine needle aspiration

2. Experimental pathology

(1) Animal experiment: animal model

(2) Tissue and cell culture

 四、Observation and New
Technique of Morphology
（一）Gross appearance:
size, shape

weight

color

consistency

surface

edge, section
（⼆二）Histologic and cytologic
observation:
most common and basic formalin fixed

→ HE (hematoxylin and eosin) stained

Hemangioma of ventrical wall

（三）Histochemistry and cytochemistry

PAS→BM
Immunohistochemistry
1. Ag-Ab specific reaction

2. Applications

(1) Location analysis

cytokeratin→cell membrane

(2) Clinical diagnosis and distinguishing

diagnosis of tumor histogenesis

Leiomyosarcoma! Actin (+)
Ultrastructural observation
TEM (transmitting electron microscope)

Filtering membrane
SEM (scanning electron microscope)

Podocyte
Flow cytometry (FCM)
1. One kind of cells→quantitative

2. DNA ploidy analysis

3. Protein nucleus acid→quantitative

analysis

4. Selection of collection of cells

（七）Image analysis (IA)

Nuclei: diameter; circumference; area;

volume; morphology

（八）Laser scanning confocal

microscope (LSCM)

aliving cell→observation in situ or

development or quantitative
（九）Molecular biology technique
1. Polymerase chain reaction (PCR)

2. DNA sequencing

3. Biochip technique

(1) Gene chip (DNA chip)

(2) Protein chip (protein microarray)

(3) Tissue chip (tissue microarray)

Polymerase
chain
reaction
(PCR)
 Prospect Theory!
Daniel Kahneman !
!
(born. 5 marcg 1934 in Tel Aviv)!
!
Nobel Memorial Prize in
Economics laureate Daniel
Kahneman. It was the 2012
winner of the National
Academies Communication
Award for best creative work
that helps the public
understanding of topics in
behavioral science, engineering
and medicine. (together with
Amos Tverski).!
Prize motivation: "for having
integrated insights from
psychological research into
economic science, especially
concerning human judgment and
decision-making under uncertainty"!
 Example !
1. Read the word below carefully:!

FEEL!

2. And now fill in the missing letter:!

S_IN!
 Example !
1. Read the word below carefully:!

FEEL!

2. And now fill in the missing letter:!

S_IN!
 Who is Steve?!
As you consider the next question, please assume
that Steve was selected at random from a
representative sample. An individual has been
described by a neighbor as follows: “Steve is very
shy and withdrawn, invariably helpful but with little
interest in people or in the world of reality. A meek
and tidy soul, he has a need for order and structure,
and a passion for detail.” Is Steve more likely to be
a librarian or a farmer?!

Who is Steve: librarian or farmer?!

 Who is Steve?!
As you consider the next question, please assume
that Steve was selected at random from a
representative sample. An individual has been
described by a neighbor as follows: “Steve is very
shy and withdrawn, invariably helpful but with little
interest in people or in the world of reality. A meek
and tidy soul, he has a need for order and structure,
and a passion for detail.” Is Steve more likely to be
a librarian or a farmer?!

Who is Steve: librarian or farmer?!

 Hueuristic in problem
solving!
! "good enough?"

Heuristic !
A heuristic technique, often called simply a heuristic,
is any approach to problem solving, learning not
guaranteed to be optimal or perfect, but sufficient for
the immediate goals. The tendencies to think in
certain ways can lead to systematic deviations from a
standard of rationality or good judgment…. cognitive
biases.!
Cognitive bias is the general term for irrational perception of
reality!
 EXAMPLES!
• https://www.youtube.com/watch?
v=xNSgmm9FX2s!

• https://www.youtube.com/watch?
v=IGQmdoK_ZfY!
CELLULAR ADAPTATIONS
CELL INJURY
CELL DEATH!

Dariusz Grzanka, PhD!

Pathology!

Rudolph Virchow
1821-1902
The Father of
Modern Pathology!
 Core of Pathology

1.Etiology
2.Pathogenesis
3.Morphologic Changes
4.Functional Consequences!
 Pathogenesis!
Recovery!
pathomechanism!

Etiology!
Sympt Def.!
Scar!
oms! Disease!

Sympt Death!
oms!

Compila
tion !
Etiology

• is the study of disease causation

• Greek “aitologia”- giving a reason

Pathogenesis

• the sequence of events that give rise

to the manifestations of disease

• step by step development of a disease

and the chain of events leading to that
disease
Morphologic Changes

• structural alterations induced in the

cells and tissues by the disease
Functional Consequences

• clinical manifestation of the disease

 Pathogenesis!
Recovery!
pathomechanism!

Etiology!
Sympt Def.!
Scar!
oms! Disease!

Sympt Death!
oms!

Compila
tion !
whiteheads, blackheads, and inflamed red growths
(papules, pustules, and cysts)!
Acne vulgaris!
 Acne vulgaris!

Complications of acne!

Scars!
Homeostasis

• is a state of balance in the body,

organ, tissue, cell

• physiologic, metabolic capability to

adopt to some changes in their internal
and external environments

• normal cell is in steady state able to

handle physiologic demand according
to its adaptive capacity !
Homeostasis

• cells can alter their functional state in

response to modest stress and maintain
their homoeostasis
Cellular Adaptation

• occurs when excessive physiologic

stresses or pathologic stimuli result in a
new but altered state that preserves the
viability of the cell.!
Adapt - to conform to changes in
environment – internal and external !

To accommodate, to adjust, to fit,

to accept – concession or yielding !
Survival strategy – in response to
physiological or pathological demands !
Most cells have the inherent
plasticity - ! Survival of
the fittest or
the adaptable!
Homeostasis

• excessisve stress or adverse

pathologic stimuli

•Adaptation
•Reversible injury
•Irreversible injury --> Cell death
 Homeostatic imbalance!
Inability to adapt
Cellular Response
( exceeded limits of
Cellular adaptations
adaptive response, point
(reversible changes) of no return” - cell injury):
• hypertrophy
Cell death
• hyperplasia
• atrophy • Necrosis
• metaplasia • Coagulative
• Liquefative
• dysplasia
• Intracellular accumulations (in various • Apoptosis
organelles), degeneration– water • Others ( np. Autophagy, mitotic
(hydropic degeneration), proteins (hyaline catastrophe)!
!
deg.), fat (steatosis), calcifications etc.
Cellular Adaptations!
 REVERSIBLE = INJURY
IRREVERSIBLE = DEATH

SOME INJURIES CAN LEAD

TO DEATH IF PROLONGED
and/or SEVERE enough!
Necrosis !
 REVERSIBLE
CHANGES!
• REDUCED oxidative
phosphorylation
• ATP depletion
• Cellular “SWELLING”!
 IRREVERSIBLE
CHANGES!
• MITOCHONDRIAL
IRREVERSIBILITY
• IRREVERSIBLE
MEMBRANE DEFECTS
• LYSOSOMAL DIGESTION!
INJURY CAUSES (REVERSIBLE)!

THE
USUAL
SUSPECTS!

But…WHO
are the
THREE
WORST?!
INJURY CAUSES (REVERSIBLE)!
Hypoxia, (decreased O2)
PHYSICAL Agents
CHEMICAL Agents
INFECTIOUS Agents
Immunologic
Genetic
Nutritional!
CAUSES OF CELL INJURY!
 INJURY MECHANISMS (REVERSIBLE)!

DECREASED ATP - MITOCHONDRIAL

DAMAGE

INCREASED INTRACELLULAR CALCIUM

INCREASED FREE RADICALS

INCREASED CELL MEMBRANE

PERMEABILITY!
 CONTINUUM!
• REVERSIBLE à
• IRREVERSIBLEà T!
• DEATHà i
m
• EMà e!

• LIGHT MICROSCOPYà
• GROSS APPEARANCES!
Ischemic injury!

See also Ch. 1, p. 14,

Fig. 1-17!
 Calcium homeostasis!

Calcium in cell injury!

 Cellular swelling (slide 134)!
is the first manifestation of almost all forms of injury to cells.
It is a difficult morphologic change to appreciate with the
light microscope; !
!
it may be more apparent at the level of the whole organ.!
 Hydropic degenerate !

Mitochondria Swelling
 What is Death?
What is Life?!

• DEATH is
– IRREVERSIBLE MITOCHONDRIAL
DYSFUNCTION
– PROFOUND MEMBRANE
DISTURBANCES

• LIFE is……..???!
Apoptosis or Type I cell-death.!
!
!
!
Autophagic or Type II cell-death. (Cytoplasmic: characterized
by the formation of large vacuoles which eat away organelles
in a specific sequence prior to the nucleus being destroyed.)!
!
!
Necrotic cell death or Type-III!
Apoptosis!
APOPTOSIS

Physiologic (or programmed) cellular death

occurs when a cell within an organism dies
through activation of an internal suicide
program!
Events in apoptosis!
APOPTOZA!
Autophagy!
NECROSIS!
NECROSIS

Necrosis is the sum of the morphologic

changes that follow cellular death in living
tissue or organs.
NECROSIS

Two Processes in Basic Morphologic

Changes in Necrosis

1.Denaturation of Proteins
2.Enzymatic Digestion of organelles and
other cytosolic components
NECROSIS

Events that will Lead to NECROSIS

1.Mitochondrial vacuolization
2.Extensive damage to plasma membrane
3.Lysosomal swelling
4.Enzymatic leakage in cytoplasm
5.Enzymatic activation
NECROSIS

Fate of NECROSIS

1.Autolysis
• Digestion by lysosomal enzymes of the dead
cells themselves
2.Heterolysis
• Digestion by lysosomal enzymes of
immigrant leukocytes
NECROSIS

Types of Necrosis

1.Coagulation Necrosis
2.Liquefaction Necrosis
3.Caseous Necrosis
4.Fat Necrosis
5.Gangrenous
NECROSIS

Types of Necrosis

1.Coagulation Necrosis

• The most common pattern of

necrosis
• Characterized by denaturation of
cytoplasmic proteins with
preservation of the framework of the
coagulated cell
• Heart, Kidneys, Liver, other solid
organs!
NECROSIS

Types of Necrosis

3.Caseous Necrosis

• Characteristic of tuberculous lesions

and appears grossly as soft, friable,
“cheesy” material!
NECROSIS

Types of Necrosis

4.Fat Necrosis

• Necrosis in adipose tissues induced

by the action of lipases.
• Generate chalky white areas (fat
saponification)!
1. Liquefaction Necrosis - brain stroke!
 !
1. Liquefaction Necrosis - brain stroke
 NORMAL CORTEX

MARTWICA
(ROZPŁYWNA?)!

"red neurons"

MARTWICA
(ROZPŁYWNA?)!
Brain encephalomalacia!
Liquefaction Necrosis - late phase of brain stroke, lots
of macrophages !
Abscess

!
 !
Liver abscess: Liquifactive necrosis
N. Ghatak MD !
 !
Myocardial Infarction- Necrosis
 !
Splenic Infarction - Coagulative necrosis
 !
Renal Infarction - Coagulative
 !
Renal Infarction - Coagulative necrosis
Caseous necrosis
Tuberculosis
!
hilar lymphnode
Extensive
Caseous necrosis
!
Tuberculosis
 !
LANGHANS GIANT CELL

Caseous NECROSIS !
 !
Caseous necrosis - Tuberculosis
 Fat necrosis -- gross!

FAT NECROSIS - ENZYMATIC, BALSER'S TYPE !

 !
Fat Necrosis - Peritoneum.
 GANGRENE!
• GANGRENE ("gangrenous necrosis") is not a
separate kind of necrosis at all, but a term for
necrosis that is advanced and visible grossly.
If there's mostly coagulation necrosis, (i.e.,
the typical blackening, desiccating foot that
dried up before the bacteria could overgrow),
we call it DRY GANGRENE. If there's mostly
liquefactive necrosis (i.e., the typical foul-
smelling, oozing foot infected with several
different kinds of bacteria), or if it's in a wet
body cavity, we call it WET GANGRENE.!
 !
Gangrene - Diabetic foot
 !
Gangrene - Amputated Diabetic foot
 !
Gangrene Intestine - Thrombosis.
ADAPTATION!
 Steam cells!
Tissue renewal and
adaptation!
• Continuous steady state!
Differentiated cells; with capacity to divide when needed !
Stem Cell Conditionally
Continuously Dividing
Dividing Hepatocyte
Skin Pancreatic Acinar
Intestinal Mucosa Renal Tubular Cells
Respiratory Epithelium
Bone Marrow (HSC)
Uterine epithelium
CELL TYPES

Non Dividing
Skeletal and cardiac Muscle
Neuron!
“Other people come and we
fade away” Tennyson
“ We fade away and the
other people come” V. S. Naipaul
 Cell Signals!
• Cells give and receive signals –
• Cells respond to multiple intracellular
and extracellular signals
• They respond by increasing or
decreasing the cell number and /or cell
size
• The signals can be: Mitogens,
Morphogens or Motogens. !
 Cell Signals!
Hormone +
Receptor ! Transcription!

ENDOCRINE! PARACRINE! AUTOCRINE!

 Cell Signals!
• Endocrine: hormones, peptides produced by
endocrine cells, released into circulation.
Act on distant target organ/cells
• Paracrine: peptides produced and released
by one group of cells act on adjacent groups
of cells
• Autocrine: peptides released by the cell act
on the same cell
• Intracrine/Metacrine: molecules /
transcription factors/metabolites produced
within the cell act on the same cell
intracellularly !
GROWTH FACTORS: CONCEPTS !
CELLS MAY CONTAIN CELL SURFACE
AND CYTOSOLIC/NUCLER RECEPTORS!
CELL SURFACE WITH MORE THAN ONE
RECEPTOR: THUS, CELL IS THE TARGET FOR
MULTIPLE SIGNALS!
GROWTH FACTORS CAN BE MULTI-
FUNCTIONAL: ELICIT MORE THAN ONE
RESPONSE!
GROWTH FACTORS CAN BE
ONCOGENIC!
GROWTH FACTORS !

Hepatocyte Growth Factor (HGF) and its receptor c-

Met: HGF is mitogenic, motogenic and morphogenic !
Epidermal Growth Factor (EGF) and its
receptor c-erb B1: mitogenic and
differentiating!
Fibroblast Growth Factor (FGF)- acidic and
basic !
Vascular Endothelial Growth Factor (VEGF)!
Transforming Growth Factor β (TGFβ)!
 Cellular Adaptations!
• Hyperplasia: increase in the number of cells.
• Hypertrophy: increase in the size of cells.
• Atrophy: reduction in the size of cells.
• Metaplasia: change in differentiation from one cell
type to another.
• Dysplasia: abnormal hyperplasia.
• Cancer: cellular autonomy and uncontrolled growth.
Slide – Adaptation diagram!
Slide – Adaptation diagram!
Cellular Adaptation

• Hyperplasia
• increase in the number of cells in an
organ or tissue.
• occurs in cells capable of dividing!
Cellular Adaptation

• Hyperplasia
•Physiologic
•Hormonal
•Compensatory

•Pathologic!
 MORE CELLS PHYSIOLOGICAL!
(PROLIFERATION)! BREAST: (PUBERTY,
STEM CELL PREGNANCY,
COMPARTMENT LACTATION) UTERUS:
CONDITIONALLY-
PREGNANCY!
DIVIDING
NON-DIVIDING CELLS:
NO! HYPERPLASIA!

COMPENSATORY!
PATHOLOGICAL!
KIDNEY
(NEPHRECTOMY) PSORIASIS
LIVER (PARTIAL GOITER !
HEPATECTOMY)!
 HYPERPLASIA!
CONDITIONALLY DIVIDING: MORE OF
THE SAME!

RENEWING TISSUES: !
 !
BPH - Benign Prostatic Hyperplasia.
Endometrial Hyperplasia!
 GOITER!

LOW IODINE TSH FOLLICULAR

ENDEMIC AREAS CELL PROLIFERATION /
HYPERTROPHY!
 SCAR, KELOID!

TGFβ Overexpression, polyclonality of fibroblasts !

 Keloid –
most extreme example of scar!

Mr. Gordon- former slave

from Louisiana – 1800s’!
Hyperplasia. A. Normal adult bone marrow. B. Hyperplasia of the bone marrow.
Cellularity is i ncreased, fat is decreased. C. Normal epidermis. D. Epidermal

!
hyperplasia in psoriasis, shown at the same magnification as in C. The epidermis is
thickened, owing to an increase in the number of s quamous cells
 HYPERTROPHY!
• No change in cell number
• Reversible increase in cell size
• Hypertrophy is the rule in non-dividing
cells – since they can not divide
• Myocardium, skeletal muscle, neurons
• Increase amount of DNA, RNA,
protein
• Increased synthesis, reduced loss
Hypertrophy!
Do you want muscles? Or do
you want to look muscular?!
 plastic models illustrating the different densities and
consequent volume differences of fat and muscle tissue!
 When you have achieved a "normal" degree of leanness,
building a beautiful body has little to do with losing weight, it's
all about modulating the ratio of lean to fat mass!
• "building a bigger metabolic engine" and not
starving the latter away on a low-calorie diet,
is the cornerstone of maintainable reductions
in body fat levels!
• Sketch of a mammalian skeletal muscle fiber -
myonucleus (turqouis), mitochondria (blue),
sarcoplasmic rectilium (buff), tubules
(orange), myofibrils (pinkish)!
 If you picture a muscle fiber as a number of balloons which
are held together by an elastic net, then the myonuclei would
be within the individual balloons!
 Pathway A - hypertrophy via satellite cell recruitment and increases in the number
of myonuclei per muscle fiber,!
Pathway B - hypertrophy via increases in myonuclear domain size within an existing
muscle fiber, and!
Pathway C - hyperplasia, which would be the increase in muscle size by cell
division and thusly an increase in the number of muscle fibers!
sarcoplasmic
hypertrophy -
which focuses more
on increased
muscle glycogen
storage!
!
myofibrillar
hypertrophy - which
focuses more on
increased myofibril
size!
 Fiber composition of bodybuilders, recreational lifters,
endurance rowers and sedentary control; determined via
myosin heavy chain (MHC) isoform content of the triceps
brachii muscle !
 TESTOSTERONE?!
plastic models illustrating the different densities and
consequent volume differences of fat and muscle tissue!
Relative free testosterone and free estradiol levels in men
from the NHANES study; data expressed relative to
serum levels of "lean" men with <84.9cm ~ 33.4" waist
circumference!
 Mistake!

HPA axis!
The hypothalamic–
pituitary–adrenal axis is a
complex set of direct
influences and feedback
interactions among three
components: the
hypothalamus, the pituitary
gland and the adrenal
glands!
Przerost włókien mięśnia sercowego!
Slide – Adaptation diagram!
 Atrophy!

Cell! Organ!
•Reduction in cell •Reduction in
size size: cell size
•Reduced organelles and or
number*
•Reduced synthesis
of macromolecules •Hypoplasia – !
•Increased protein
*Reduced Proliferation
degradation!
* Increased loss!
Normal brain!
Atrophy - Alzheimer !
Atrophia testis!
Eccentric atrophy.!
Inanity !
Emphysema !
Zanik tłuszczowy miąższu nerki.!
Degenerations!
See Ch. 1, p. 23,
Fig. 1-24!
!
Intracellular accumulations
Lipids -- Ch. 1, pp. 23-24 !
• Steatosis (a/k/a fatty change)
• Accumulation of lipids within hepatocytes
• Causes include EtOH, drugs, toxins
• Accumulation can occur at any step in the pathway
– from entrance of fatty acids into cell to packaging
and transport of triglycerides out of cell
• Cholesterol (usu. seen as needle-like clefts in
tissue; washes out with processing so looks
cleared out) – E.g.,
• Atherosclerotic plaque in arteries
• Accumulation within macrophages (called “foamy”
macrophages) – seen in xanthomas, areas of fat
necrosis, cholesterolosis in gall bladder!
See Ch. 1, p. 24,

Steatosis!
Fig. 1-25!
Slide – Fatty liver!
Proteins -- Ch. 1, pp. 24-25!
• Accumulation may be due to inability of cells
to maintain proper rate of metabolism
• Increased reabsorption of protein in renal tubules à
eosinophilic, glassy droplets in cytoplasm
• Defective protein folding
• E.g., alpha-1-AT deficiency à intracellular
accumulation of partially folded intermediates
• May cause toxicity – e.g., some neurodegenerative
diseases!
Alpha-1-antitrypsin accumulation --
micro!
Gaucher’s disease -- micro!
Liver in EtOH -- micro!
Mallory hyaline -- micro!
Glycogen -- Ch. 1, p. 25!

• Intracellular accumulation of glycogen can

be normal (e.g., hepatocytes) or pathologic
(e.g., glycogen storage diseases)
• Best seen with PAS stain – deep pink to
magenta color!
Slide – Liver – normal glycogen!
Liver – Glycogen storage disease!
Pigments -- Ch. 1, pp. 25-26!

• Exogenous pigments
• Anthracotic (carbon) pigment in the lungs
• Tattoos!
Anthracotic pigment in lungs --
gross!
Slide – Anthracotic lymph node!
Anthracotic pigment in macrophages --
micro!
Pigments!

• Endogenous pigments
• Lipofuscin (“wear-and-tear” pigment)
• Melanin
• Hemosiderin!
Lipofuscin!

• Results from free radical peroxidation of

membrane lipids
• Finely granular yellow-brown pigment
• Often seen in myocardial cells and
hepatocytes!
Lipofuscin -- micro!
Lipofuscin!
Melanin -- Ch. 1, p. 26!

• The only endogenous brown-black pigment

• Often (but not always) seen in melanomas!
Slide -- Melanoma!
Hemosiderin -- Ch. 1, p. 26!

• Derived from hemoglobin – represents

aggregates of ferritin micelles
• Granular or crystalline yellow-brown pigment
• Often seen in macrophages in bone marrow,
spleen and liver (lots of red cells and RBC
breakdown); also in macrophages in areas of
recent hemorrhage
• Best seen with iron stains (e.g., Prussian blue),
which makes the granular pigment more
visible!
Hemosiderin -- micro!
Hemosiderin!
Hemosiderin in renal tubular cells --
micro!
Prussian Blue – hemosiderin in hepatocytes and
!
Kupffer cells -- micro
Dystrophic Calcification -- Ch. 1, pp. 26-27!

• Occurs in areas of nonviable or dying tissue

in the setting of normal serum calcium;
also occurs in aging or damaged heart
valves and in atherosclerotic plaques
• Gross: Hard, gritty, tan-white, lumpy
• Micro: Deeply basophilic on H&E stain;
glassy, amorphous appearance; may be
either crystalline or noncrystalline!
Calcification!
Slide – Ganglioneuroblastoma
with calcification!
Dystrophic calcification in wall of stomach --
micro!
Metastatic Calcification -- Ch. 1, p. 27!

• May occur in normal, viable tissues in the

setting of hypercalcemia due to any of a
number of causes
• Calcification most often seen in kidney, cardiac
muscle and soft tissue!
Metastatic calcification of lung in pt with
hypercalcemia -- micro !
Metaplasia!

•Metaplasia is a “reversible” change in which one

adult cell type is replaced by another adult cell type
•Metaplasia is a cellular adaptation in which
indigenous cells are replaced by cells that are better
suited to tolerate a specific abnormal environment
•Because of metaplasia, normal protective
mechanisms may be lost
•Persistence of signals that result in metaplasia often
lead to neoplasia
• Mataplazja
 !
Lung- Metaplasia in smoker
 !
Oesophagitis - Gastric metaplasia.
Metaplasia: Implications!
Complications due to functioning metaplastic epithelium:
gastric mucosa in Meckel diverticulum producing acid and
peptic ulceration !

Loss of normal function: loss of ciliary motile function in

trachea and bronchi due to squamous metaplasia !

Infections, calculi (stone) formation: gall bladder,

kidney !

Pre-neoplastic, neoplastic conversion: explains the

histogenetic origin of squamous carcinomas in lung:
adenocarcinomas in lower end of esophagus.!
Hyperplasia!
Metaplasia!

Neoplasia!

Dysplasia!
Dysplasia!

• E.g. Cervical dysplasia

• Dysplasia is a step toward cancer.
• Dysplasias may progress to malignant
neoplasms

“Cells having disordered arrangement”!

Cervical dysplasia!
Zawał krwotoczny płuca!