introduction of pathophysiology

8/10/2019 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

introduction of pathophysiology

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