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(1)

Definitions

Pathology is a dicipline bridging clinical

practice & basic sience

To render diagnosis & guide therapy

Identity changes in :

Gross

(2)

The scientific focus of pathology is :

Etiology

• On the cause of disease

Pathogenesis

• Mechanisme of its development & the

pathways by which morphologic changes

occur

Normal Homeostasis

If cell adjusting structure & function

to accommodate changing demands &

(3)

Stages in the cellular response to stress & injurious

stimuli

Stresses/pathologic stimuli the cell:

Adaptation

• Atrophy

• Hypertrophy

• Hyperplasia

• Metaplasia

(4)

Perubahan sel & jaringan :

Agenesis

Aplasia

Hypoplasia

Atrophy

Hypertrophy

Hyperplasia

Metaplasia

Dysplasia

Anaplasia

Granuloma

Complete absent of an

organ

E.g. :

– Renal agenesis

– Ovarial agenesis

– Tubal agenesis, etc.

Agenesis

Aplasia

Anlarge is present but

never develops

E.g. :

(5)

!

Anlarge develoved incompletly but the tissue

histhologicaly normal

Ex. : microcephaly

Hypoplasia

Decrease in the:

Size

Function of a cell

But not dead

(6)

"

Causes of atrophy :

1. functional demand (immobilitation in fracture, prolonged

bed rest)

2. Inadequate supply O2 (ischemia)

3. Insufficient nutrients (starvation, inadequate nutrition, chronic disease)

4. Interrruption of trophic signals transmitted by chemical mediators (endocrine system/Neuromusculator transmission) e.g. : thyroid, adrenal cortex, ovarium, testis.

5. Persistent cell injury by chronic inflamation e.g. : chronic gastritis, prolonged pressure 6. Aging : brain, heart (Senile Atrophy)

(7)

4

The mechanism of atrophy :

synthesis

catabolism

Influenced by a number of hormones

e.g. :

Insulin

Tyroid stimulating hormon

Glucocorticoids

in the size of cell accompanied by augmented

functional capacity

Hypertrophy is a response to trophic signals

(8)

5

… hypertrophy

Physiological (hormonal) hypertrophy

• in puberty

production of sex hormon

• Hypertrophy breast tissue

• Abnormal hormon production in cancer

Functional demands

• Exercise

• Pathological conditions (myocardial cell) • Kidney hypertrophy on surgical removed

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(9)

:

Hyperplasia

the number of cells in an organ / tissue

1. Physiologic hyperplasia

Hormonal hyperplasia

Compensatory hyperplasia

2. Pathologic hyperplasia

Excessive hormonal / growth factor stimulation

e.g. : Endometrial hyperplasia

(10)

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Metaplasia

Reversible change in which 1 adult cell type is replace by another adult cell type (convertion of 1 differentiated cell type of

another)

Metaplasia is usually reversible if the stimulus is

removed

• Squamous metaplasia of the bronchial epithelium to tobacco

• Lower oesophagus by reflux acidic gastric

• Endocervical metaplasia

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(11)

Metaplasia of normal columnar (left) to squamous epithelium (right) in a bronchus, shown (A) schematically and (B)

histologically

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1. Variation in the size & shape of cells

2. Enlargment, irregularity & hyperchromatism of the

nuclei

3. Disorderly arrangement of the cells within the

epithelium

Dysplasia

(12)

Dysplasia included in the morphological classification of the stage if intraepithelial neoplasia

Dysplasia is a preneoplastic lession in the sense

that it is a necessary stage in the multistep cellular

evolution to cancer.

Normal cell

primitive cell

E.g. : Malignant cell

Carcinoma

Sarcoma

Adenocarcinoma

Lymphoma

Etc.

(13)

2 principal pattern of cell death :

• Commonly : coagulative necrosis • Cellular swelling

• Protein denaturation • Organellar breakdown • Cell rupture

NECROSIS

• Regulated event • Programmed death

(14)

Term

Definition

Necrosis

Antemortem pathologic cell death

Apoptosis

Antemortem programmed cell death

Autolysis

Postmortem cell death

CAUSES OF CELL INJURY

Hypoxia Physical Agent Chemical and drugs Microbiology Agents Immunologic Reaction

Genetic Defects Nutritional Inbalance

(15)

!

• Anemia

• Ischemia

• Intoxication CO2

• Aerobic oxidative respiration

• Mechanical trauma

• Extreme temprature : heat, cold

• Radiation: X-ray, sun light

• Electric shock

• Athmosphere pressure

Hypoxia Physical Agent

… CAUSES OF CELL INJURY

• Sufficiently concentrated :

– Glucose – Salt – O2

• Air pollutants

• Insecticides

• Asbestosis

• Ethanol

• Cellular metabolism (i.e. waste products)

• Tape worms

• Rickettsia

• Virus

• Bacteria

• Fungi

… CAUSES OF CELL INJURY

(16)

"

… CAUSES OF CELL INJURY

Anaphylactic reaction

Autoimmune diseases

Immunologic Reaction

Genetic Defects

• Congenital malformation • Sickle cell anemia

• G-6-PD

Nutritional Imbalance

• Protein calori insufficiency • Vitamins defficiency • Diabetes

(17)

4

Cellular response to injurious stimuli depends on :

• Injury type • Duration • Severity Current Status : • Nutritional • Hormonal • Adaptibility

of the cell

Intercellular systems : • Cell membrane

integrity • Aerobic

respiration • Protein synthesis • Integrity genetic

apparatus

O2& oxygen derived free radicals :

• Ischemic • Hypoxic

injury

Mechanism of Cell Injury

The ultrastructural features of these stages of cell injury. Normal cell & changes in reversible & irreversible cell injury

(18)

5

Reduced of :

– Oxidative

phosphorylation in mitochondria

– Activity Na Pump

Cellular swelling

Loss of microvilli

Glycogen depleted ↓ protein synthesis

Formation of cell surface blebs

Severe vacuolization of

the mitochondria

Damage of :

– Mitochondrial matrix

– Plasma membrane

Swelling of lysosomes

Accumulation of

amorphous calcium

Rich dentities in

mitochondrial matrix

(19)
(20)
[image:20.612.128.488.94.359.2]

;

Figure 1-6.

Cellular features of

necrosis (

left

) &

apoptosis (

right

)

1. Reversible acute cell injury

2. Necrosis (cell death after irreversible injury)

3. Apoptosis (cell death by suicide)

4. Subcellular alteration as a respond to chronic or persistent injury stimuli

5. Intracellular accumulations of a number of substance

(21)

Sublethal Damage

1. Recoverable (but

necrosis is not)

2. Ultrastructural damage mitochondria

3. Swelling of cellular organelles ( hydrophic deg.)

4. Fatty change is impairment of metabolism

Morphologic changes that follow cell death in living tissue

1. Intense eosinophilia of the dead cell is due to

loss of RNA & coagulation of protein

2. Nuclei undergo:

1. Pyknosis 2. Karyorhexis 3. Karyolysis

Leaving a shrunken cell devoid of nucleus

1. Protein may be liberated from the dead cell

(22)

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Autolysis

: is a cell death by hydrolitic

enzymes.

Heterolysis

: cell death by the lysosomes of

invading inflammatory cells.

Nuclear Changes: This nucleus is faded -- karyolysis.

(23)

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(24)

Types of Necrosis

Depends on :

(25)

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Coagulative Necrosis

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(26)

"

• Gumatous Necrosis

• Dead tissue, it is firm & rubbery like caseous necrosis in the spirochetal infection syphilis.

• Hemorrhagic Necrosis

• Dead tissue suffused with extravasated red cell, when cell death is due to blockage

• Fat Necrosis

• Not really necrosis.

• Focal areas of fat destruction tipically occuring following pancreatic injury /after trauma to fat for (ex. in the breast)

• Describes foci of hard yellow material seen in dead adipose tissue

Fibrinoid Necrosis

Fibrin deposited in damage necrotic vessel

walls in hypertension and vasculitis

Gangrene

(27)

4

APOPTOSIS

• Responsible for the programmed cell death in several important physiology processes

• Including :

– During embryogenesis (in implantation, organogenesis, & developmental involution)

– Hormon dependent physiologic involution (endometrium, lactating, prostate after castration)

– Cell deletion in proliferating population (intestinal crypt epithelium / cell dead in tumor)

– Deletion of autoreactive T cell in the thymus, cell death of cytokine starved lymphocytes

CLINICAL EFFECTS OF NECROSIS

Abnormal function

Kidney

: renal failure

Cortex in brain : muscle paralysis

Heart

: heart failure

Lung

: hemoptysis

(28)

5

Realease of contens of necrotic cells

Liver

: elevation SGOT

Heart : creatine kinase

Systemic effects

Fever

Inflamatoar Reaction

Local effects

Hemorrhage

Ulceration

Apoptosis of epidermal cells in an

immune-mediated reaction

A. Apoptotic cells are visible in the epidermis with eosinophilic cytoplasm and small, dense nuclei.

B. High power of apoptotic cell in liver in immune-mediated hepatic cell injury.

(29)

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Granuloma

Special type of chronic inflamation in tissue

reaction.

Cause :

infection :

TBC fungal syphilis,

etc

non-infection :

sarcoidosis
(30)

;

NECROBIOSIS

Gradual cell damage

Progressive

Singly or small group cells.

Reversible (+/-)

Example : hepar cell

deg.

cell death

healing

fibrosis.

Alterations in structure and function that may

lead to cell death, or at least diminished capacity

of the cell to respond an injury

Reduced cell in :

Pleomorphic vacuolated mitochondria

(31)

Morphologic alteration in :

• Pleomorphic vacuolated mitochondria

endoplasmic reticulum

• Disorted Golgi Apparatus

• Accumutaion of lipofuscin pigment

Cellular senescence is multifactorial :

1. The cumulative effects of extrinsic influences:

free radical damage

(32)

DEGENERATION

Cloudy

swelling

Fatty

change

Hydropic

Atropy

Hyaline

Mucoid

Amyloid

Calcifica-tion

(33)

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Figure 1-6.

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