1- cell and tissue injury. ppt
TRANSCRIPT
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By: Dr Tarek Atia
Introduction
ofPathology
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Pathology is "Scientific study of disease Study of
structural and functional changes in disease.
You need to have a basic knowledge of normal
Anatomy (structure) and Physiology (function) tounderstand Pathology.
"Pathology deals with knowledge of what causes
disease, how disease starts, progresses & it explains
the reason for signs and symptoms of patient"
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Diseases is an expression of "discomfort" due
to structural or functional abnormality.
This abnormality can be caused by various
agents Eg. Bacteria, virus, heat, radiation etc.
collectively called 'etiology'.
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Factors causing disease are mainly two types.
Environmental (or external) factors and Genetic (or
Internal) factors.
Diseases which present since birth are calledCongenital diseases and all other diseases are
known as Acquired diseases.
Diseases which occur in families are known as
Familial diseases.
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Pathology of a disease is formally studied under four
subdivisions.
- Etiology - Study of cause / causative agent of disease
- Pathogenesis- Study of disease progression or
evolution.
- Morphology - Study of structural changes in disease
(Gross & microscopic)- Clinical Significance - Study of how clinical features
are related to changes.
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Major groups of diseases are Inflammatory, Degenerative
& Neoplastic.
Inflammatory disorders are due to damage to tissues by
various injuries (physical, chemical, infections etc.)
Degenerative disorders are due to lack of growth or
ageing.
Neoplastic disorders are due to excess cell division
forming tumours.
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Cell & Tissue Injury
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Human disease occurs because of injury to cells /
tissue.
Most human disease results from injury to epithelium.
Injury to one tissue usually affects the adjacent or
underlying tissue as well.
Cell injury produces morphologic changes.
Principles
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Visual changes in the cell
or tissue morphology is
seen under microscopy
when cells are stained.
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Cell Injury
Damage or alteration of one or more cellular components
1. Many types of injury are tissue-specific because of
anatomic relationships and tissue response to
chemical and infectious agents.
2. Cell injury disrupt cell physiology; so the cell does
not function at full capacity.
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Stages in the cellular response to stress and
injurious stimuli
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Consequences of Injury
1. (Reversible): No long term effects- the cell
damage is repaired, the effects of the injury are
reversible.
2. The cell adapts to the damaging stimulus.
3. (Irreversible): The cell dies, undergoing necrosis.
The damage is irreversible.
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Adaptation to injury
1. Atrophy: decrease in the size and functional capacity
of the cell. after normal growth has been attained.
( O2, blood, nerve supply)
2. Hypertrophy: an increase in the size of the cell
secondary to an increase in cell function. Increase in
the number of mitochondria and ER, etc.
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3. Hyperplasia: an increase in the number of cells of a
tissue in response to a stimulus or injury.
4. Metaplasia: replacement of one type of tissue with
another in response to an injury.
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5. Hypoplasia: underdevelopment or incomplete
development of an organ / tissue (less severe in degree
than aplasia).
6. Aplasia: lack of development of an organ or tissue
(may have a rudimentary organ). can also refer to lack
of production of cells from an organ or tissue (eg
aplastic anemia).
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Uterine hypertrophy
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Muscular hypertrophy
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Diagram of columnar to squamous metaplasia.
Metaplasia
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Cell Atrophy
Causes
1. Loss of blood supply or innervations
2. Loss of endocrine factors (eg. TSH)
3. Decrease in the workload
4. Aging, chronic illness
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Outcomes from cell injury depend upon:
1. Type of injury
2. Severity of the injury
3. Duration of the injury
4. Type of cell being injured- Some cell types sustain injury
better than others; some tissues (e.g. liver) have a capacity to
regenerate.
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Reversible Cell Injury
1. Cell swellingusually accompanies all types of injury.
Results from an increase in water permeability.
Reverses once membrane function is restored
2. Increase in extracellular metabolite- Because of a
biochemical derangement. i.e.: Increase in extracellular
glycogen in diabetes.
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3. Fatty change in liver. Vacuoles of fat accumulate
within the liver cell following many types of injury:
alcohol intoxication, chronic illness, diabetes
mellitus, etc.
This may be due to:
An increase in entry of free fatty acids.
An increase in synthesis of free fatty acids.
A decrease in fatty acid oxidation.
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Vulnerable Sites of the Cell
1. Cell membranes
2. Mitochondria
3. Endoplasmic reticulum
4. Nucleus
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Causes of Cell and Tissue Injury
1. Physical agents
2. Chemicals and drugs
3. Infectious pathogens
4. Immunologic reactions
5. Genetic mutations
6. Nutritional imbalances
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7. Hypoxia and Ischemia: cell injury resulting
from inadequate levels of oxygen.
Causes:
A. Inadequate blood supply
B. Lung disease
C. Heart failure
D. Shock
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Susceptibility of specific cells to ischemic
injury
Neurons: 3 to 5 min.
Cardiac myocytes, hepatocytes, renal epithelium: 30
min. to 2 hr.
Cells of soft tissue, skin, skeletal muscle: many hours
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Cell Death
Apoptosis
Necrosis
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Apoptosis
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Morphology of Necrosis
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Pyknosis
Shrunken nucleus with dark staining
Seen in a necrotic (dead) cell
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Karyorrhexis
Fragmentation of pyknotic nucleus
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Karyolysis
Extensive hydrolysis of pyknotic nucleus with
loss of staining
Represents breakdown of the denatured
chromatin
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Karyolysis
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Types of Necrosis
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1- Coagulative Necrosis
Dead cells remain as ghost-like remnants of
their former self
Classically seen in an MI
C di l fib
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Cardiac muscle fibers
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Kidney (necrotic renal tubules)
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2- Liquefactive Necrosis
The dead cell undergoes extensive autolysis, caused by
the release of lysosomal hydrolases (proteinases,
DNases, RNases, lipases, etc.)
Seen classically in the spleen and brain following
infarction.
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Liquefactive
Necrosis
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(A) Coagulative vs. (B) Liquefactive Necrosis
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3- Caseous Necrosis (caseum -cheesy)
Resembles cottage cheese
Soft, friable, whitish-grey
Present within infected tissues
Seen in Tuberculosis (Mycobacterium tuberculosis)
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Caseous Necrosis
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Caseous Necrosis
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4- Fat Necrosis
Leakage of lipases from dead cells attack triglycerides
in surrounding fat tissue and generate free fatty acids and
calcium soaps
These soaps have a chalky-white appearance
Seen in the pancreas following acute inflammation
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