introduction of pathophysiology
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By: Dr Tarek Atia
1- Introduction of
Pathophysiology
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Pathology of disease is studied under four subdivisions:
Etiology: Study of causes or causative agents of
disease
Pathogenesis: Study progression or development of a
disease .
Morphology: Study of structural changes in diseased
tissue or organ (macroscopic & microscopic)
Clinical Significance: Study of how clinical features
are related to changes.
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Major groups of diseases are
Inflammatory, Degenerative & Neoplastic
Inflammatorydisorders 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 tumors.
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Cell Injury
Damage or alteration of one or more cellular components
Many types of injury are tissue-specific because of
anatomic relationships and tissue response to chemical
and infectious agents.
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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Cell Injury Produces
Symptoms: complaints
experienced by the
patient.
Signs: abnormal physical
findings.
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Outcomes from cell injury depend upon:
Type of injury
Severity of the injury
Duration of the injury
Type of cell being injured: Some types sustain
injury better than others; some tissues (e.g.
liver) have a capacity to regenerate.
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Consequences of Injury
(Reversible): No long term effects- the celldamage is repaired, the effects of the injuryare reversible.
The cell adapts to the mild damagingstimulus.
(Irreversible): The cell dies, undergoingnecrosis. 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 cellsecondary to an increase in cell function.
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Causes of Cell Atrophy
1. Loss of blood supply or innervations
2. Loss of endocrine factors (hormone)
3. Decrease in the workload
4. Aging, chronic illness
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3. Hyperplasia: an increase in the number of cells of
tissue in response to a stimulus or injury.
4. Metaplasia: replacement of one type of tissue with
another type in response to an injury.
4. Hypoplasia: incomplete development of an organ /
tissue.
6. Aplasia: lack of development of an organ or tissue.
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Muscular hypertrophy
Metaplasia
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Apoptosis: Programmed cell death:
It plays an important role in many physiological and
diseased conditions.
Death of aged cells.
Embryonic remodeling.
Cell DeathApoptosis Necrosis
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The apoptotic cells undergo series of changes including
membrane blebbing, and fragmentation of DNA
creatinga vacuolar nucleus.
Apoptotic cells shrink in size, break into smaller pieces
called apoptotic bodies that are recognized by
phagocytes.
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Membrane blebbing
Cell shrink
Cell
fragmentation
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1- Pyknosis
Shrunken nucleus
with dark staining
Seen in a necrotic
(dead) cell
Morphology of Necrotic nucleus
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KaryorrhexisFragmentation 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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1- Coagulative Necrosis
Dead cells remain as
ghost-like remnants of
their former self
Classically seen in an
Myocardial Infarction
Types of tissue necrosis Cardiac muscle fibers
Kidney (necrotic renal tubules)
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2- Liquefactive Necrosis
The dead cells undergo
extensive autolysis, caused by
the release of lysosomal
enzymes (proteinases, DNases,
RNases, lipases, etc.)
Seen classically in the spleen
and brain following infarction.
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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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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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Acuteinflammation
Chronic inflammation
RepairResolution
Injury
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Time course
Acute inflammation: Less than 48 hours
Chronic inflammation: Greater than 48 hours
(weeks, months, years)
Cell type
Acute inflammation: Polymorph-nuclear leukocyte
or neutrophils
Chronic inflammation: Mononuclear cells
(Macrophages, Lymphocytes, Plasma cells).
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Pathogenesis: Three main processes occur at the site
of inflammation, due to the release of chemical
mediators:
Increased blood flow (redness and warmth).
Increased vascular permeability (swelling,
pain & loss of function).
Leukocytic Infiltration.
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Mechanism of Inflammation
1. Vaso dilatation
2. Exudation - Edema
3. Emigration of cells
4. Chemotaxis
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Chronic Inflammation:
An immune reaction to some mild but persistent
antigen producing proliferation of lymphocytes
and/or plasma cells.
There are usually no pain, redness, swelling, or
warmth.
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Cells of Chronic Inflammation
Histologically, chronic inflammation includes:
Macrophages, Lymphocytes,andPlasma cells.
Proliferation of fibroblastsand small blood vessels
(revascularization).
Increased connective tissue (fibrosis)
Tissue destruction.
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Multinucleate giant cells: huge cells with many
nuclei formed by fusion of macrophages. They are
associated with foreign materials or accompany reactions
to certain organisms as TB.
Fibroblasts and collagen: Collagen production is a
common feature of chronic inflammation. Chemical
mediators stimulate collagen secreting cells and fibrosis.
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A: Chronic inflammation in the lung, showing all three characteristic histologic features: (1)
collection of chronic inflammatory cells, (2) destruction of parenchyma (alveoli are replaced
by spaces lined by cuboidal epithelium, arrowheads), and (3) replacement by connectivetissue (fibrosis, arrows).
B: By contrast, in acute inflammation of the lung (acute bronchopneumonia), neutrophils fill
the alveolar spaces and blood vessels are congested.
Chronic inflammation Acute inflammation
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