Professional Documents
Culture Documents
Definitons
Pathology is a dicipline bridging clinical practice
and basic sience
To render diagnosis and guide therapy
- Identity changes in gross
- Morphology ( microscopy ) appearan
of cell tissues
The scientific focus of pathology is :
Etiology : on the cause of disease
Pathogenesis : mechanisme of its developmen
and the pathways by which morphologic chan
occur
air pollutants
insecticides
asbestosis
ethanol
4. Microbilogy Agents
- tape worms
- rickettsia
- virus
- bacteria
- fungi
5. Immunologic Reaction
- anaphylactic reaction
- autoimmune diseases
6. Genetic Defects
- congenital Malformation
- sicle cell anemia
7. Nutritional Inbalance
- protein calori insufficiency
- vitamins defficiency
- diabetes
8. Aging
Intercellular systems
>
>
>
>
Reversible Injury
Irreversible Injury
Severe vacuolization of the mitochondria
Demage of the mitochondrial matrix
Demage of plasma membrane
Swelling of lysosomes
Accumulation of amorphous calcium
Rich dentities in mitochondrial matrix
Sublethal Damage
1. Recoverable necrosis is not
2. Ultrastructural damage to mitochondria
NECROSIS
Refers to a sequence of morphologic changes
that follow cell death in living tissue
Morphologic Evidence of
Necrosis
A Early Change
1 3 hour before changes of necrosis are
recognizable on electron microscopy
6 8 hour on light microscopy organelle
degeneration
B. Nuclear Change
Pyknosis : The chromatine clumps into
coare strands
The nucleus becomes a shrunken
dense, basophilic mass
ribonucleases
C. Cytoplasmic Change
About 6 hour after cell necrosis
Cytoplasma becomes homogenous and
deeply
`
acidophilic. Enzymatic digestion
Tipes of Necrosis
Depends on :
1. Cells compotitions
2. Speed of necrosis
3. Type of injuries
> Coagulative Necrosis
Implies preservation of basic structural outline of
the coagulated
cell or tissue
for a span of days.
The structural protein and the enzymatic protein
thus blocking
cellular
proteolysis
Coagulation necrosis is cahareteristic of hypoxic
death of cells in
all tissue except
the brain
eq. Myocardial Infarction
APOPTOSIS
including :
The programmed destruction of cells during em
genesis as in implantation, organogenesis, and
developmental involution
CELL DEATH
APOPTOSIS
What
vs. NECROSIS
DEATH is IRREVERSIBLE
REVERSIBLE CHANGES
REDUCED
oxidative
phosphorylation
ATP
depletion
Cellular
SWELLING
IRREVERSIBLE
CHANGES
MITOCHONDRIAL
IRREVERSIBILITY
IRREVERSIBLE
MEMBRANE DEFECTS
LYSOSOMAL DIGESTION
REVERSIBLE = INJURY
IRREVERSIBLE = DEATH
SOME INJURIES CAN LEAD
TO DEATH IF PROLONGED
and/or SEVERE enough
THE
USUAL
SUSPECTS
But
WHO are
the
THREE
PHYSICAL Agents
CHEMICAL Agents
INFECTIOUS Agents
Immunologic
Genetic
Nutritional
What is Death?
What is Life?
DEATH is
IRREVERSIBLE MITOCHONDRIAL
DYSFUNCTION
PROFOUND MEMBRANE DISTURBANCES
LIFE
is..???
REVERSIBLE
IRREVERSIBLE
DEATH
EM
LIGHT MICROSCOPY
GROSS APPEARANCES
DEATH:
ELECTRON MICROSCOPY
DEATH:
LIGHT MICROSCOPY
NECROSIS BROTHERS:
Liquefactive (Brain)
WET
DRY
Ischemic (non-specific)
LIQUEFACTIVE NECROSIS,
BRAIN
CASEOUS NECROSIS, TB
FIBRINOID NECROSIS
WET GANGRENE
DRY GANGRENE
EXAMPLES of Cell
INJURY/NECROSIS
Ischemic (Hypoxic)
Ischemia/Reperfusion
Chemical
ISCHEMIC INJURY
REVERSIBLE
IRREVERSIBLE
DEATH
(INFARCT)
ISCHEMIA/REPERFUSION INJURY
NEW Damage
Theory
CHEMICAL INJURY
Toxic Chemicals,
e.g CCl4
Relationship
APOPTOSIS
NORMAL
(preprogrammed)
PATHOLOGIC
(associated with
Necrosis)
NORMAL APOPTOSIS
Embryogenesis
Hormonal
Cell
Involution
Post
Inflammatory Clean-up
Elimination
Cytotoxic
of HARMFUL cells
T-Cells cleaning up
PATHOLOGIC APOPTOSIS
Toxic
Duct
obstruction
Tumor
cells
Apoptosis/Necrosis
spectrum
APOPTOSIS MORPHOLOGY
DE-crease
IN-crease
in chromatin
concentration, i.e., hyperchromasia,
pyknosis karyorhexis karyolysis
IN-crease
in membrane blebs
Phagocytosis
SHRINKAGE/HYPERCHROMASIA
PHAGOCYTOSIS
APOPTOSIS BIOCHEMISTRY
Protein
DNA
Digestion (Caspases)
breakdown
Phagocytic
Recognition
Auto-Digestion
Smooth Endoplasmic Reticulum
(SER) activation
Mitochondrial
Cytoskeleton
Thin
SWELLING
Breakdown
INTRAcellular
ACCUMULATIONS
Lipids
Neutral
Fat
Cholesterol
Hyaline
= any proteinaceous
pink glassy substance
Glycogen
Pigments (EX-ogenous, ENDogenous)
Calcium
LIPID LAW
ALL
Lipids are
YELLOW grossly and
WASHED out
(CLEAR)
microscopically
FATTY LIVER
FATTY LIVER
PIGMENTS
EX-ogenous--- (tattoo,
Anthracosis)
END-ogenous--- they all look the
same, (e.g., hemosiderin,
melanin, lipofucsin, bile), in
that hey are all golden
yellowish brown on routine
Hematoxylin & Eosin (H&E)
stains
Hemosiderin/Melanin/etc.
Abnormal function
Kidney
Cortex in brain
Heart
Lung
Bacterial infection
:
:
:
:
renal failure
muscle paralysis
heart failure
hemoptysis
: gangrene
Systemic effects
Fever
Inflamatoir Reaction
Local effects
Hemorrhage
Ulceration
The
plasia brothers
HYPERHYPO- (A-)
NORMOMETA-
Agenesis
Aplasia
HYPO-PLASIA
DE-CREASE IN NUMBER OF CELLS
Hypoplasia
The
trophy brothers
HYPERHYPO- (A-)
DYS-
A-TROPHY
DE-CREASE IN SIZE OF CELLS? YES
SHRINKAGE
ATROPHY
DECREASED
WORKLOAD
DENERVATION
DECREASED BLOOD FLOW
DECREASED NUTRITION
AGING (involution)
PRESSURE
A t r o p h y
Causes of atrophy :
-Endocrin system
-Neuromucculator transmission
eq. Thyroid
Adrenal cortex
Ovarium
Testis
5. Persistant cell injury
Caused by chrinic inflamation
eq. - chronic gastritis
- prolonged pressure
6. Aging
Particularly in non replacating cells such bra
heart.
> Senile Atrophy
HYPER-TROPHY
IN-CREASE IN SIZE OF CELLS
I.
HYPER-PLASIA
IN-CREASE IN NUMBER OF CELLS
HYPERPLASIA
is an increase in the number of cells in an
or tissue
Hyperplasia can be :
I . Physiologic hyperplasia
- hormonal hyperplasia
- compensatory hyperplasia
1. Hormonal stimulation
- estrogen increased endometrium ( hyperp
- gynecomastia
2. Increased functional demand
- secondary polycytemia
- lymphocyte hyperplasia
METAPLASIA
A
WHY?
METAPLASIA
is a reversible change in which one adult ce
type is replace by another adult cell type
( Metaplasia is the convertion of one differen
ted cell type of another )
It is almost invariably a response to persistent inj
and can be thought of as an adaptive mechanism
Most common is the replacment of a glandular ep
um by a squamous cell.
- Squamous metaplasia of the bronchial epit
to tobacco
- lower oesophagus by reflux acidic gastric
- endocervical metaplasia
Metaplasia is usually reversible if the stimulus is
removed
DYSPLASIA
cellular dysplasia refers to an alteration in the
size, shape and organization of the cellular com
ponent of a tissue
The cells an epithelium exhibit uniformity of size,
And nucleus.
Anaplasia
normal cell
primitive cell
Exc : malignan cell (carcinoma,
sarcoma, adenocarcinoma,
lymphoma, etc)
Granuloma
C E L L U L A R
A G I N G
Alterations in structure and fuction that may
to cell death, or at least diminished capacity
the cell to respond an injury
Reduced cell in :
- pleomorphic vacuolated mitochondria
- repair of chromosomal damage
Morphologic alteration in :
pleomorphic vacuolated mitochondria
decreased endoplasmic reticulum
disorted Golgi Apparatus
accumutaion of lipofuscin pigment