Transcript Cel l and Tissue Injury

Introduction of
Pathology
By: Dr Tarek Atia
• Pathology is "Scientific study of disease“ Study of
structural and functional changes in disease.
• Diseases is an expression of "discomfort" due to
structural or functional abnormality.
• "Pathology deals with knowledge of what causes disease,
how disease starts, progresses & it explains the reason
for signs and symptoms of patient"
Branches of Pathology:
Histopathology / Anatomic Pathology : Pathologists
specialising in anatomical changes in disease. Usually using a
tissue biopsy.
Cytopathology: Pathologists specialising in study of body
fluids & Cells.
Haematology: Study of blood and blood forming organs.
Morbid Anatomy: Autopsy or Post mortem study for legal or
educational purpose.
• Factors causing disease could be :– Environmental or external factors \ and Genetic or
Internal factors.
• Diseases which present since birth are called
Congenital diseases and all other diseases are
known as Acquired diseases.
• Diseases which occur in families are known as
Familial diseases.
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.
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.
Cell & Tissue Injury
Principles
• 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.
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.
Stages in the cellular response to stress and
injurious stimuli
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.
Cell Injury Produces:
1. Signs: abnormal physical findings Objective
2. Symptoms : complaints experienced
by the patient - Subjective
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.
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.
Hypertrophy versus Necrosis
Uterine hypertrophy
Muscular hypertrophy
Metaplasia
Diagram of columnar to squamous metaplasia.
Cell Atrophy
Causes
1.
2.
3.
4.
Loss of blood supply or innervations
Loss of endocrine factors (eg. TSH)
Decrease in the workload
Aging, chronic illness
A: Atrophy of the brain in an 82-year-old male with atherosclerotic disease.
Note that loss of brain substance narrows the gyri and widens the sulci.
B: Normal brain of a 36-year-old male.
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.
Reversible Cell Injury
1. Cell swelling– usually accompanies all types of
injury. Results from an increase in water
permeability
degeneration.
leading
Reverses
function is restored.
to
hydropic
once
or
membrane
2. Fatty change in liver. Vacuoles of fat
accumulate within the liver cell following
many types of injury: alcohol intoxication,
chronic illness, diabetes mellitus, etc.
Vulnerable Sites of the Cell
1.
2.
3.
4.
Cell membranes
Mitochondria
Endoplasmic reticulum
Nucleus
Cell Death
• Apoptosis
• Necrosis
Apoptosis
Morphology of Necrosis
Pyknosis
• Shrunken nucleus with dark staining
• Seen in a necrotic (dead) cell
Karyorrhexis
• Fragmentation of pyknotic nucleus
Karyolysis
• Extensive hydrolysis of pyknotic nucleus
with loss of staining
• Represents breakdown of the denatured
chromatin
Karyolysis
Types of Necrosis
1- Coagulative Necrosis
• Dead cells remain as ghost-like remnants
of their former self
• Classically seen in an MI
Cardiac muscle fibers
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.
(A) Coagulative vs. (B) Liquefactive Necrosis
3- Caseous Necrosis
(caseum - cheesy)
• Resembles cottage cheese
• Soft, friable, whitish-grey
• Present within infected tissues
• Seen in Tuberculosis
(Mycobacterium tuberculosis)
Caseous Necrosis
Caseous Necrosis
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
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
7.
Hypoxia and Ischemia: cell injury resulting from
inadequate levels of oxygen.