Download Pathologic hyperplasia

By: Dr. Raham Bacha
MD KMU
MSc Sonology Gold Medalist
(UOL)
The university of
Lahore
Introduction to Basic
Pathology
Dr. Raham Bacha
What is
Pathology?
??
Pathology is originated, from
Greek words
Pathos: “suffering,” “disease,”
“feeling,”
and
logos: saying, speech,
discourse, thought,
Study.
Simply; it is the Study of
disease.
More precisely
It is the “Scientific study of
disease"
Pathology serves as a
"bridge"
between
the
preclinical
sciences
(anatomy, physiology, etc.)
and the courses in clinical
medicine.
The scientific study of
the nature of disease
and its;
causes,
processes,
development
and
consequences.
Classification:
• It is divided in to:
• General pathology:
• The basic response of cells and
tissue to abnormal stimuli. It
describe the basic principles of
the development of the disease.
• For example basic principles of
inflammation
• Special pathology:
• It is the specific response of
tissue and organs to one or
more definite stimuli. It deals
with the diseases of special
organs or systems.
• For example inflammation of
the respiratory system or
urinary system.
What is
Disease??
?
What is the Disease?
• It is taken from “Dis” mean with
out and “ease” easiness.
• It is the “State in which an
individual exhibits an anatomical,
physiological, or biochemical
deviation from the normal”
• Disease may be defined as:
• An abnormal alteration of
structure or function in any part of
the body.
Classification of disease
• Inflammatory diseases
• Hepatitis
• Appendicitis
• UTI and so on
• Degenerative diseases
• Osteoarthritis etc.
• Neoplastic diseases
• Lung cancer, breast cancer etc.
• Traumatic diseases.
• Fractures etc.
Pathology focuses on 4
aspects of disease:
Knowledge of etiology
remains the backbone of:
• Disease diagnosis
• Understanding the nature
of diseases
• Treatment of diseases.
Etiology
“Study of the cause of a
disease"
• An etiologic agent :
is the factor (bacterium, virus,
etc.) responsible for lesions or
a disease state.
• Predisposing
Causes
of
Disease:
Factors which make an
individual more susceptible to
a disease (damp weather, poor
ventilation, cigarette smoking,
etc.)
• Exciting Causes of Disease:
Factors which are directly
responsible for a disease
(hypoxia, chemical agents….
etc.).
Etiology
Etiology:
What is the cause?
Acquired or Environmental
agents:
• Physical
• Chemical
• Nutritional
• Infections
• Immunological
• Psychological
Genetic Factors:
• Abnormality in chromosome
and
• Genes
pathogenesis
The
sequence
events
during the response of the
cells or tissues to the
etiologic agent, from the
initial stimulus to the
ultimate expression of the
disease,”from the time it is
initiated to its final
conclusion in recovery or
death”
Clinical Significance:
Symptoms & Signs
• Clinical signs are seen only in
the living individual.
• “Functional
evidence
of
disease
which
can
be
determined objectively or by
the
observer"
(fever,
tenderness,
increased
respiratory rate, etc.)”
prognosis
• Expected outcome of the
disease, It is the clinician's
estimate of the severity and
possible result of a disease.
Summary.
• Etiology: Why a disease
arise?
• Pathogenesis: How a
disease develop?
• Morphological changes:
How a disease present?
• Clinical manifestation:
What type of Signs and
symptoms are present?
• Prognosis: what will be
likely out-comes?
cytology
• The study of cell is called
cytology.
• Mainly there are two type of
cells
• 1- prokaryotic cells:
without nucleus and
membrane bounded bodies
i.e. bacteria and RBCs
• 2- Eukaryotic cells:
having distinct nucleus
membrane bounded bodies
i.e. all cells of the body
other than RBCs
Structure of cell
• Cell has three main
parts.
• Cell membrane
• Nucleus
• Cytoplasm
• Cytoplasmic
organelles.
Cell membrane
• It is selective
permeable membrane,
permits some
substances to pass
through it while other
are not. it protects the
cell and maintain cell
structure.
• It maintain fluid and
electrolytes balance.
Nucleus
•It is the control
center of the cell.
It contain DNA
and is bounded
nuclear
membrane.
Mitochondria
•It is the power
house of the cell. It
extract energy from
nutrients in the form
of ATPs (adenosine
triphosphate) energy
packet.
• RIBOSOMES:
• They synthesize protein
in the cell
• LYSOSOMES:
• Thy Provides
intracellular digestive
system. Which allow the
cell to digest and
eliminate the unwanted
substance i.e. bacteria
and other pathogens.
Endoplasmic
reticulum.
•They detoxify the
damaging
substances to the
cell.
Tissue.
• Aggregate of cells with
similar structure and
function is called tissue.
• Mainly there are four
types of tissues.
• Epithelial,
• Connective,
• Nervous,
• Muscle.
Epithelial
Tissue.
• Epithelial tissue protects
your body from moisture
loss, bacteria, and internal
injury. There are two kinds
of epithelial tissues:
Covering and lining
epithelium
• Covering epithelium cover
the external body surface
i.e. outer layer of the skin
and other organs.
• lining epithelium line the
internal body surfaces i.e.
lumen of the vessels and
digestive tract and urinary
tract etc.
Terms that help us understand what
kinds of tissues we are identifying:
• Terms referring to the
layers
• Simple = one layer
•
Stratified = more
than one layer
• Pseudo-stratified = false
layered (appears to be
more than one layer, but
only one);
Terms referring to the
cell shapes
• ciliated = with cilia
• Squamous = flat
• Cuboidal = cube
• Columnar = rectangular
(column)
• Transitional = ability to
change shape
Simple columnar
• One layer rectangular cells
present in GIT (Gastrointestinal Tract, Cervix, And
Gall bladder.
Ciliated Pseudo-Stratified
• These are false layered cells with cilia,
lining the respiratory tract.
Stratified Squamous
• Having multiple layers of
squamous cells, it is present in
skin epidermis, Lips and oral
cavity, tongue, pharynx and
esophagus.
Transitional Stratified
epithelium.
• It is epithelium of multiple
layers and the cells having
the ability to change in
shape.
Chapter 2
CELL
INJURY
AN D
ADAPTA
TION.
Normal Cell
• Under normal
circumstances cells are in
steady state (regular)
(homeostasis).
Homeostasis mean to
remain stable and regular.
• The cell that constantly
adjusting their structure
and function to
accommodate changing
demands and extracellular
stresses, is said to be
normal cell.
Adaptation
• As cells encounter
physiologic stresses or
pathologic stimuli, they
can undergo adaptation,
achieving a new steady
state and preserving
viability and function.
The principal adaptive
responses are hypertrophy,
hyperplasia, atrophy, and
metaplasia.
Injury
• If the adaptive capability is
exceeded or if the external
stress is inherently harmful,
cell injury develops.
• It may either be reversible or
irreversible ;
• Reversible; Within certain
limits, injury is reversible, and
cells return to a stable
baseline;
• Irreversible; if the stress is
severe, persistent and rapid in
onset, it results in irreversible
injury and death of the
affected cells.
Cell death
• Cell death is one of the
most crucial events in the
evolution of disease in any
tissue or organ. It results
from diverse causes,
including ischemia (lack
of blood flow), infections,
toxins, and immune
reactions. Cell death also
is a normal and essential
process in embryogenesis,
the development of
organs, and the
maintenance of
homeostasis.
The relationship among normal,
adapted, reversibly injured, and dead
myocardial cells
Cellular Response to Stress
And Injurious Stimuli.
• Whether a specific form
of stress induces
adaptation or causes
reversible or
irreversible injury
depends not only on the
nature and severity of
the stress but also on the
vulnerability of the cell.
several other variables,
including basal cellular
metabolism and blood
and nutrient supply,
determine cell
vulnerability.
CELLULAR
ADAPTATIONS TO
STRESS
• Adaptations are reversible
changes in the number, size,
phenotype, metabolic
activity, or functions of cells
in response to changes in their
environment. Physiologic
adaptations usually represent
responses of cells to normal
stimulation by hormones or
endogenous chemical
mediators (e.g., the hormoneinduced enlargement of the
breast and uterus during
pregnancy). Pathologic
adaptations are responses to
stress that allow cells to
modulate their structure and
function and thus escape
injury. Such adaptations can
take several distinct forms i.e.
Hypertrophy
• Hypertrophy is an
increase in the size of
cells resulting in
increase in the size of
the organ. Hypertrophy
can be physiologic or
pathologic and is caused
either by increased
functional demand or by
growth factor or
hormonal stimulation.
Physiologic Hypertrophy
The massive physiologic
enlargement of the uterus
during pregnancy occurs as a
consequence of estrogen
stimulated smooth muscle
hypertrophy and smooth
muscle hyperplasia.
In contrast, in response to
increased demand the striated
muscle cells in both the
skeletal muscle and the heart
can undergo only
hypertrophy because adult
muscle cells have a limited
capacity to divide.
Therefore, the chiseled
physique of the avid
weightlifter stems solely
from the hypertrophy of
individual skeletal muscles
pathologic Hypertrophy
• An example of pathologic
cellular hypertrophy is the
cardiac enlargement that
occurs with hypertension or
aortic valve disease.
Two types of mediators are
commencing hypertrophy.
• Mechanical trigger, i.e. stress.
• Tropic trigger. Soluble
mediators stimulate
intracellular protein synthesis.
An adaptation to stress can
progress to functionally
significant cell injury if the
stress is not relieved.
Hyperplasia
• An increase in cell number because
of proliferation of differentiated
cells and replacement by tissue
stem cells (undifferentiated
biological cells).
• It may occur concurrently with
hypertrophy and often in response
to the same stimuli.
Hyperplasia can be
• PHYSIOLOGIC
or
• PATHOLOGIC
In both situations, cellular
proliferation is stimulated by growth
factors that are produced by a
variety of cell types.
physiologic hyperplasia
• There are two type of
Physiologic hyperplasia
• HORMONAL
HYPERPLASIA
• Exemplified by the
proliferation of the
glandular epithelium of
the female breast at
puberty and during
pregnancy
• COMPENSATORY
HYPERPLASIA
• In which residual tissue
grows after removal or loss
of part of an organ. For
example, when part of a
liver is resected, mitotic
activity in the remaining
cells begins as early as 12
hours later, eventually
restoring the liver to its
normal weight.
Pathologic hyperplasia
• pathologic hyperplasia are
caused by excessive hormonal
or growth factor stimulation.
For example, after a normal
menstrual period there is a
burst of uterine epithelial
proliferation that is normally
tightly regulated by
stimulation through pituitary
hormones and ovarian
estrogen and by inhibition
through progesterone.
However, a disturbed balance
between estrogen and
progesterone causes
endometrial hyperplasia,
which is a common cause
of abnormal menstrual
bleeding.
• Important point is that in
all of these situations, the
hyperplastic process
remains controlled; if the
signals that initiate it reduce
in strength, the hyperplasia
disappears. It is this
responsiveness to normal
regulatory control
mechanisms that
distinguishes pathologic
hyperplasia from cancer, in
which the growth control
mechanisms become
deregulated or ineffective.
Nevertheless, in many
cases, pathologic
hyperplasia constitutes a
fertile soil in which cancers
may eventually arise. For
example, patients with
hyperplasia of the
endometrium are at
increased risk of developing
endometrial cancer
Atrophy : without
nourishment.
• Shrinkage in the size of the
cell by the loss of cell
substance is known as
atrophy. When a
sufficient number of cells
are involved, the entire
tissue or organ
diminishes in size,
becoming atrophic.
Although atrophic cells
may have diminished
function, they are not dead.
Causes of atrophy include
a decreased workload, loss
of innervation, diminished
blood supply, inadequate
nutrition, loss of endocrine
stimulation, and aging
Metaplasia
• Meta mean "after" or "beyond“
or “changing”
• Plasia mean formation.
• Metaplasia is a reversible
change in which one adult
cell type is replaced by another
adult cell type. In this type of
cellular adaptation, a cell type
sensitive to a particular stress is
replaced by another cell type
better able to withstand the
adverse environment.
• Epithelial metaplasia is
exemplified by the squamous
change that occurs in the
respiratory epithelium of
habitual cigarette smokers (Fig.
1–5). The normal ciliated
columnar epithelial cells of
the trachea and bronchi are
focally or widely replaced by
stratified squamous epithelial
cells.
• Although the metaplastic
squamous epithelium has
survival advantages, important
protective mechanisms are
lost, such as mucus secretion
and ciliary clearance of
particulate matter. Moreover,
the influences that induce
metaplastic change, if
persistent, may predispose to
malignant transformation of
the epithelium.
Summary of adaptation
• Hypertrophy: increased cell and organ
size, often in response to increased
workload; induced by growth factors
produced in response to mechanical
stress or other stimuli; occurs in tissues
incapable of cell division
• Hyperplasia: increased cell numbers in
response to hormones and other growth
factors; occurs in tissues whose cells are
able to divide or contain abundant tissue
stem cells
• Atrophy: decreased cell and organ
size, as a result of decreased nutrient
supply or disuse; associated with
decreased synthesis of cellular
building blocks and increased
breakdown of cellular organelles
• Metaplasia: change in phenotype of
differentiated cells, often in response to
chronic irritation, that makes cells better
able to withstand the stress; usually
induced by altered differentiation
pathway of tissue stem cells; may
result in reduced functions or
increased propensity for malignant
transformation
Cell injury.
• cell injury results when
cells are stressed so
severely that they are no
longer able to adapt or
when cells are exposed to
inherently damaging
agents or suffer from
intrinsic abnormalities
(e.g., in DNA or proteins)
• Different injurious stimuli
affect many metabolic
pathways and cellular
organelles. Injury may
progress through a
reversible stage and
culminate in cell death.
Reversible cell injury
• In early stages or mild
forms of injury the
functional and
morphologic changes
are reversible if the
damaging stimulus is
removed. At this stage,
although there may be
significant structural and
functional
abnormalities, the
injury has typically
not progressed to
severe membrane
damage and nuclear
dissolution
Cell death/ irreversible cell
injury
• With continuing damage,
the injury becomes
irreversible, at which
time the cell cannot
recover and it dies. There
are two types of cell
death.
• necrosis and apoptosis
which differ in their
mechanisms, morphology,
and roles in disease and
physiology. When damage
to membranes is severe,
enzymes leak out of
lysosomes, enter the
cytoplasm, and digest the
Basic Language of
Pathology
etiology
•The origin of a
disease including
the underlying
causes and
modifying
factors.
•PATHOGENESIS
• The steps in the
development of a
disease.
•HOMEOSTASIS
• The maintenance of a
steady state of
physiologic
parameters
•ADAPTATION
S
•Achieving a new
steady state to
preserve viability
and function. These
are REVERSIBLE
changes of cells in
response to a
change in their
environment.
•HYPERPLASIA
•(Greek - Huper-,
“Above or more" +
plasis, "formation”)
•An increase in cell
number, which can
also lead to a
hypertrophic organ.
• DYSPLASIA
• (Greek - dys-, "difficulty" +
plasis, "formation”)
• An abnormality of
development where cell
maturation and differentiation
are delayed.
• HORMONAL
HYPERPLASIA
• One of the two forms of
physiologic hyperplasia. It
results in an increase in
cell/organ size as a result of
hormonal stimulation (i.e.,
uterus during pregnancy).
• COMPENSATORY
HYPERPLASIA
• One of the two forms of
physiologic hyperplasia. This
is residual tissue growth after
removal or loss of part of an
organ.
•
PATHOLOGICAL
HYPERPLASIA
• Excessive cell replication
typically caused by excessive
hormonal or growth factor
stimulation. This is reversible
which is the main
characteristic that
distinguishes it from cancer.
•HYPERTROPH
Y
• Hypertrophy (from Greek
"excess" + "nourishment") is
the increase in the volume of
an organ or tissue due to the
enlargement of its component
cells. It should be
distinguished from
hyperplasia, in which the cells
remain approximately the
same size but increase in
number. Although hypertrophy
and hyperplasia are two
distinct processes, they
frequently occur together, such
as in the case of the
hormonally-induced
proliferation and enlargement
of the cells of the uterus
during pregnancy.
•HYPERTROPHY
• An increase in the SIZE of
individual cells resulting in
an increase in organ size.
•ATROPHY
• Without nourishment;
Shrinkage in the size of a
cell by the loss of cell
substance; the retreat of the
cell to a smaller size where
survival is still possible.
• DISUSE ATROPHY
• Atrophy as a result of a
decrease in workload.
• PRESSURE ATROPHY
• The tissue destruction and
reduction in size as a
consequence of prolonged or
continued pressure on a local
area or group of cells.
• METAPLASIA
• A reversible change where one
adult cell type is changed to
another adult cell type.
•TROPHIC
TRIGGERS
•Soluble mediators
that stimulate cell
growth.
•ISCHEMIA
•Hypoxia due to
reduced/lack of
blood flow.
•PATHOLOGIC
ADAPTATIONS
• Cellular responses to
stress that allows cells
to modulate their
structure and function
in order to escape
injury.
•HYPOXIA
•Oxygen
deficiency from
any cause (is
not necessarily
caused by a
reduction in
blood flow, i.e.,
in anemia).
• INFARCTION
• Irreversible injury
resulting in cell death.
• Infarction is tissue death
(necrosis) caused by a
local lack of oxygen,
due to an obstruction of
the tissue's blood supply
• PHYSIOLOGICAL
ADAPTATIONS
• Responses of cells to
normal stimulation.
•NECROSIS
•The premature,
pathological death
of cells caused by
factors external to
the cell or tissue;
it elicits an
inflammatory
response.
• APOPTOSIS
• The cells of a multicellular
organism are members of a
highly organized
community. The number of
cells in this community is
tightly regulated—not
simply by controlling the
rate of cell division, but
also by controlling the rate
of cell death. If cells are no
longer needed, they
commit suicide by
activating an intracellular
death program. This
process is therefore called
programmed cell death,
although it is more
commonly called apoptosis
(from a Greek word
meaning “falling off,” as
leaves from a tree).
•APOPTOSIS
• An often physiologic
form of cell death
(aka, "Programmed
cell death") that
serves as a means of
eliminating unwanted
cells. May also be a
pathological death
after some forms of
cell injury, especially
DNA and protein
damage. It does NOT
elicit an inflammatory
response.
•RE-
PERFUSION
INJURY
• When restoration of
blood flow to an
ischemic area results
in cell death. Usually
as a result of:
• Reperfusion injury
is the tissue damage
caused when blood
supply returns to the
tissue after a period of
ischemia or lack of
oxygen.
• The absence of
oxygen and nutrients
from blood during the
ischemic period
creates a condition in
which the restoration
of circulation results
in inflammation and
oxidative damage
through the induction
of oxidative stress
rather than restoration
of normal function
•REVERSIBLE
CELL INJURY
•Injury in a cell
that can be
corrected,
allowing the cell
to return to
normalcy
Learning Pathology:
• General Pathology
• Common changes in all tissues. e.g..
Inflammation, cancer, ageing, edema,
hemorrhage ….etc.
• Systemic Pathology
• Discussing the pathologic
mechanisms in relation to various
organ systems e.g. CVS, CNS,
GIT…..etc.
What should we Know
About A Disease
• Definition.
• Epidemiology – Where &
When.
• Etiology – What is the
cause?
• Pathogenesis - Evolution
of dis.
• Morphology - Structural
Changes
• Functional consequences
• Management
• Prognosis
• Prevention
Cell injury and
adaptation
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
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
• 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
• 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
• 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