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| − | ==An Introduction to General Pathology==
| + | #REDIRECT[[:Category:General Pathology]] |
| − | | |
| − | * The term '''pathology''' is derived from:
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| − | ** '''Pathos''', or suffering
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| − | ** '''Logos''', or reasoning/logic.
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| − | * Pathology is defined as the study of disease including:
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| − | ** '''Aetiology''' - causal factor(s)
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| − | ** '''Pathogenesis''' - the development of the disease within the body.
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| − | ** '''Lesions''' - the observable structural changes in the tissues and fluids of the body.
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| − | ** '''Pathophysiology''' - the functional changes in diseased tissues.
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| − | ** '''Sequel''' - the consequences of the disease in the body.
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| − | ** '''Remote effects''' - the effect of disease in one tissue on other tissues in the body.
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| − | | |
| − | ===Lesions===
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| − | | |
| − | * Lesions are the abnormalities or changes seen in living tissues due to disease.
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| − | * Observed in
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| − | ** The live animal
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| − | ** Tissues surgically removed from the live animal
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| − | *** Biopsy/ excision
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| − | ** Animals soon after death
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| − | *** Necropsy, post-mortem examination.
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| − | | |
| − | ====Decription of Lesions====
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| − | | |
| − | * Descriptions of lesions is very important
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| − | * Whole organs, tissues or individual lesions are described under headings such as
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| − | *# Size
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| − | *# Shape
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| − | *# Colour
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| − | *# Weight
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| − | *#* Generally in relation to body weight
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| − | *# Texture and Consistency
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| − | *# Appearance of the cut surface
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| − | *# Contents of hollow organs
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| − | *# Position, relationships and effects on adjacent tissues
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| − | | |
| − | ===Disease===
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| − | | |
| − | ====Definition and Type====
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| − | | |
| − | * '''Disease''' is a definite morbid (illness producing) process, having a characteristic train of symptoms or signs.
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| − | ** May affect the whole body or any of its parts.
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| − | ** The disease's aetiology, pathology and prognosis may be known or unknown.
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| − | * There are two main categories of disease.
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| − | *# '''Acute'''
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| − | *#* Characterised by sudden onset and short duration.
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| − | *#* The outcome of acute disease may be:
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| − | *#** Death
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| − | *#** Resolution due to host defence response or clinical therapy
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| − | *#** Progression to chronic disease
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| − | *# '''Chronic'''
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| − | *#* Characterised by insidious onset and protracted course.
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| − | *#* The outcome of chronic disease may be:
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| − | *#** Progressive destruction of tissue
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| − | *#*** Compromises funtion and endangers life,
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| − | *#** The halting of the course of disease, with tissue repair by scarring.
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| − | | |
| − | ====Factors Involved in the Development of Disease====
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| − | | |
| − | * There are three factors which conspire with each other to produce disease.
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| − | *# '''The individual animal'''.
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| − | *#* In particular, the animal's nutritional and immune status
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| − | *#** This is modified by:
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| − | *#*** Recent or concurrent disease
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| − | *#*** Previous exposure to the agent(s) responsible
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| − | *# '''The disease-causing agent(s)'''.
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| − | *#* Most do not cause a uniform pattern of disease
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| − | *#** Host defences are important in determining the presentation of the disease.
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| − | *#* An agent's capacity to produce disease depends upon:
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| − | *#** The dose
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| − | *#** The virulence of the agent
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| − | *#* Several agents may be involved.
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| − | *#** Usually one agent debilitates, allowing others to exert a greater effect within the body
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| − | *#* The presence of an agent does not necessarily mean it is the cause of the disease!
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| − | *#* A pathogenic agent may be absent from the tissues, due to:
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| − | *#** Clinical therapy
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| − | *#** Host defence systems
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| − | *# '''Environment''', for example:
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| − | *#* Overcrowding of animals
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| − | *#* Mixing animals from differing origins
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| − | *#** Carriers are allowed to infect susceptible animals.
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| − | *#*** Carriers are animals which harbour the pathogenic agent but do not show signs of disease.
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| − | *#* Changes in management routine
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| − | | |
| − | ====Types of Agents Causing Disease====
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| − | | |
| − | # '''Infectious organisms'''
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| − | #* [[Viruses|Viruses]]
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| − | #* [[Bacteria|Bacteria]]
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| − | #* [[Fungi|Fungi]]
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| − | #* [[Parasites|Parasites]]
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| − | # '''Physical'''
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| − | #* Trauma
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| − | #* Pressure
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| − | #* Heat
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| − | #* Cold
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| − | #* Radiation
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| − | # '''Chemical'''
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| − | #* Toxic organic and inorganic substances
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| − | #* Toxins produced by infectious organisms
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| − | # '''Nutritional'''
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| − | #* Deficiencies of vitamins and trace elements
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| − | #* Excess vitamins and trace elements
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| − | # '''Genetic defects'''
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| − | #* There is a very wide range of potential defects.
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| − | #** Some are incompatible with life
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| − | #** Others affect specific systems within the body
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| − | | |
| − | ====Aspects of Disease====
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| − | | |
| − | * There are many aspects of a disease that must be considered in order to understand it in full.
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| − | *# '''Incidence'''
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| − | *#* How much of the disease is present?
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| − | *#* Where is the disease found?
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| − | *#* In what species is the disease seen?
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| − | *# '''Aetiology'''
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| − | *#* Causal agent(s)
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| − | *#* Predisposing factors
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| − | *# '''Transmission'''
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| − | *#* How is the disease spread between individuals?
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| − | *#* Is the disease zoonotic?
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| − | *# '''Pathogenesis'''
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| − | *#* How the causal agent(s) exert their effect within the body.
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| − | *# '''Diagnosis'''
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| − | *#* History
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| − | *#* Clinical findings
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| − | *#** Clinical examination
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| − | *#** Clinical pathology
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| − | *#* Biopsy or post-mortem examination
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| − | *# '''Prognosis and Treatment'''
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| − | *# '''Control and Prevention'''
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| − | *#* The ideal situation
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| − | | |
| − | ====Post-Mortem Examination====
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| − | | |
| − | * Post-mortem examination (PME) investigates the observable structural changes in the animal.
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| − | * Information relating to the disease withing the body or specific tissue is gained from PME.
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| − | ** This includes information on the disease's
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| − | *** Aetiology (cause).
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| − | *** Pathogenesis (development).
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| − | * Several types of changes are encountered at post-mortem examination.
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| − | *# Those due to the '''disease'''
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| − | *#* Lesions
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| − | *# Those occuring '''immediately prior to death'''
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| − | *#* Agonal
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| − | *# Those occuring '''after death'''
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| − | *#* Post-mortem
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| − | | |
| − | ====Techniques Involved in Pathological Examination====
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| − | | |
| − | * '''Fluid examination'''
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| − | ** E.g. blood, urine, discharges from orifices and so on.
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| − | * '''Cytology'''
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| − | ** Examination of cells in smears, aspirates and fluids.
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| − | * '''Necropsy'''
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| − | ** Visual examination of the gross changes in the dead body.
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| − | * '''Histopathology'''
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| − | ** Microscopic examination of:
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| − | *** Tissues selected from the dead body after necropsy.
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| − | *** Biopsy/excision materials from lesions in the living animal.
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| − | * '''Histochemistry'''
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| − | ** Microscopic visualisation of enzymatic activity in tissues.
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| − | * '''Immunological methods'''
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| − | ** Specific antibody activity can be detected in tissues and fluids.
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| − | *** Examination of serum can show prior exposure to a particular infectious agent (i.e. specifice antibodies).
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| − | ** Specific antigens can be detected in tissues.
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| − | *** When linked to a marking agent (e.g. a fluorescent dye), an antibody can localise its antigen in the tissue.
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| − | * '''Electronmicroscopy'''
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| − | ** Electronmicrosopcy shows fine detail of the surfaces or internal structures of cells.
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| − | * '''Bacteriology/ Virology/ Parasitology'''
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| − | ** These techniques allow the isolation and identification of pathogenic bacteria, viruses and parasites.
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| − | * '''Toxicology'''
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| − | ** Analysis of tissues for particular poisons and toxins.
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| − | | |
| − | ==General Pathology - Contents==
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| − | | |
| − | ==Degenerations and Infiltrations==
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| − | | |
| − | * Degenerations and infiltrations are the morphological manifestation of an altered metabolism within the cell.
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| − | ** A particular kind of change within a cell or tissue may suggest that a specific type of alteration has occurred.
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| − | * Degenerations and infiltrations are types of structural changes.
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| − | ** These are best considered at a cellular level.
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| − | ** These structural changes are deviations from the cell's normal structure and function.
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| − | *** Parameters are outside the normal physiological range for the cell.
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| − | * '''Degeneration'''
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| − | ** The tissue cell shows some change in itself.
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| − | * '''Infiltration'''
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| − | ** Something accumulates in the cell or tissue.
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| − | | |
| − | ===Cellular Swelling===
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| − | | |
| − | * Cellular swelling is
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| − | ** The earliest detectable degenerative change.
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| − | ** The mildest from of cellular degeneration.
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| − | ** The first stage in injury to a cell.
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| − | ** Caused by a variety of insults, e.g.
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| − | *** Lack of oxygen (anoxia) to a tissue.
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| − | *** Toxic influences.
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| − | * Is due to the impairment of the integrity of the cell membrane.
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| − | * Cellular swelling is characterised by a moderate swelling of the individual cells.
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| − | ** Due to an influx of water into the cell.
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| − | | |
| − | ====Gross Appearance====
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| − | | |
| − | * Organs diffusely affected with cloudy swelling grossly appear pale.
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| − | ** This may be partly due to the swollen cells impeding the tissue's blood supply.
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| − | * Without cutting into an organ, it may be difficult to appreciate a gross enlargement of it.
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| − | ** Each individual cell is increased in size, meaning the entire volume of the organ is also increased.
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| − | ** E.g. on cutting the liver or kidney capsule, the underlying swollen parenchyma bulges outwards, making the cut ends of the capsule retract.
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| − | * The degree of gross swelling is not great.
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| − | ** Could be easily confused with early post-mortem changes in the organ.
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| − | | |
| − | ====Histological Appearance====
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| − | | |
| − | * Individual cells appear somewhat swollen.
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| − | * The cytoplasm appears more red in colour in hematoxylin and eosin (H&E) stained sections.
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| − | * The nucleus of the cell remains normal.
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| − | * Cellular swelling is best histologically appreciated in the liver and kidney in damage caused by circulating toxins that are not powerful enough to actually kill the cells.
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| − | | |
| − | ====Significance of Cellular Swelling====
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| − | | |
| − | * Cellular swelling is an important stage in degeneration.
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| − | ** Not commonly observed on its own without more serious changes
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| − | *** Not easy to identify at post-mortem unless the examination os perfomred very soon after the animal's death.
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| − | **** Early post-mortem (autolytic) change in dead tissue looks rather similar.
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| − | *** Cellular swelling is also reversible.
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| − | **** When the toxin is no longer exerting its effect, the tissue returns to normal.
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| − | *** Cellular swelling may be a transient stage in the more serious forms of degenerations which follow.
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| − | | |
| − | ===Hydropic Degeneration===
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| − | | |
| − | * Hydropic degeneration often indicates severe cellular damage due to viruses.
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| − | ** Is a more severe or advanced form of cellular swelling.
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| − | * There are two types of hydropic degeneration, in which:
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| − | *# The cells may swell up like a balloon prior to their destruction.
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| − | *#* '''Balloning Degeneration'''
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| − | *# There is a discrete bleb (vacuole) of fluid within the cytoplasm.
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| − | *#* '''Vacuolar Degeneration'''
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| − | | |
| − | ====Ballooning Degeneration====
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| − | | |
| − | * May occur in a variety of conditions.
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| − | ** Is particularly seen in viral conditions of epithelial tissue.
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| − | * [[Oral Cavity - Cavity & Gingiva#Foot and Mouth disease|Foot and Mouth Disease]] is the best example.
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| − | ** Foot and Mouth virus attacks the stratum spinosum of the epithelium of the tongue and feet.
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| − | ** Affected cells balloon up with water containing the replicating virus, swelling until they burst.
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| − | *** The fluid contained in the cells then forms microvesicles (blisters) in the stratum spinosum.
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| − | **** Blisters may later burst, shedding vast quantities of the virus.
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| − | ** On bursting, the edges of the erosions look ragged.
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| − | *** Within weeks, the germinal epithelium at the base of the erosion regenerates the epithelium, leaving no trace of a scar.
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| − | | |
| − | ====Vacuolar Degeneration====
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| − | | |
| − | the second type, the excess water is transferred to the
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| − | endoplasmic reticulum (ER) which swells and eventually fragments, leaving a fluid vacuole
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| − | in the cytoplasm. It commonly occurs in cells such as the hepatocyte, renal tubular
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| − | epithelium and pancreatic acinar cell which are very metabolically active and have welldeveloped
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| − | pumping mechanisms.
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| − | | |
| − | ===Cellular Fatty Change===
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| − | Cellular fatty change - an important intracellular abnormality, and concerns
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| − | principally intracellular fat in liver cells.
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| − | This is the accumulation or increase of fatty substances within the cytoplasm of specific
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| − | cells and does not refer to the fat stores of the body, although in some cases they may be
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| − | involved in the transfer of fat to these specific cells.
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| − | Fatty change is commonly seen in three organs of the body, i.e. principally in the liver but
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| − | also the kidney and heart; mainly because these organs are either involved in the metabolism
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| − | of fat or dependant upon lipids as an energy source.
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| − | It is an important condition, because it is something that can readily be recognised at postmortem
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| − | examination.
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| − | Appearance of fatty change
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| − | Liver: this is the predominant organ
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| − | involved in fatty change.
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| − | Grossly, the liver may be greatly
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| − | increased in size;
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| − | it is tan to yellowish in colour in
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| − | contrast to the normal reddish brown;
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| − | it is very prone to rupture with slight
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| − | pressure (friable);
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| − | on cutting through the surface the underlying
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| − | parenchyma bulges outwards having been freed
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| − | from the constraint of the capsule;
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| − | and this parenchyma is dull in appearance,
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| − | yellowish and greasy.
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| − | 16
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| − | Kidney: where not normal as in the cat, the cortex appears somewhat paler, but diffuse
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| − | paleness is not the prominent feature as it is in the liver.
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| − | Heart: fatty change is found in anaemia in animals and is the result of anoxia ;
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| − | the heart is flabby and the fatty change may occur as streaks in the papillary
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| − | muscles (those furthest away from the blood supply).
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| − | Overall it has reduced contractile ability, and does not pump blood efficiently.
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| − | Microscopically, the fat
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| − | appears as globules or
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| − | vacuoles of varying size
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| − | in the cytoplasm of the
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| − | cells. In the heart, it
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| − | appears as tiny groups of
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| − | vacuoles dispersed along
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| − | the myofibrils
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| − | throughout the whole
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| − | cell. In the liver and
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| − | kidney, these vacuoles
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| − | tend to, but not always,
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| − | coalesce (come together;
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| − | fuse with one another )
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| − | to form larger ones, and
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| − | you may see one or
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| − | more large globules
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| − | filling the cytoplasm
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| − | with displacement of the nucleus to the periphery of the cell. The nucleus remains normal
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| − | unless the degree of fatty change becomes incompatible with the continued existence of the
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| − | cell.
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| − | To decide whether or not a vacuole in the cytoplasm of a hepatocyte is fat ( because there are
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| − | two further conditions which may produce vacuoles in hepatocytes, namely the vacuolar
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| − | hydropic degeneration mentioned before and also the accumulation of glycogen ), it is
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| − | necessary to stain for the fat present. There are a variety of stains and common ones are
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| − | Sudan 111, Sudan 1V, and Oil Red O which stain fat varying shades of orange to red.
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| − | It is necessary to prepare the sections differently to the routine paraffin embedding as per
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| − | H&E. This is because in paraffin embedding, the fat is dissolved out of the cell by the strong
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| − | solvents employed. To get over this problem, the block of tissue to be examined is frozen
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| − | and sectioned in a cryostat (a cabinet containing a microtome and kept at - 20 0 C), before
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| − | being stained.
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| − | These sections are over twice as thick as those attained by sectioning paraffin blocks, and so
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| − | there may be some overlap of cells on the section, and less clarity of the individual cells.
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| − | 17
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| − | Causes of 'fatty change'
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| − | 1. Dietary and Metabolic
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| − | a. Starvation - this is an increased mobilisation of fat from the body fat stores in response to
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| − | energy needs occasioned by a reduction in dietary intake. These are transported in the blood
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| − | as fatty acids, the liver is unable to cope with them all properly, and so they are stored here as
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| − | neutral fats.
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| − | b. Overeating - obesity where the dietary intake is greater than the energy expenditure and
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| − | the fat is temporarily stored prior to movement to the body fat stores. It also occurs on a diet
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| − | rich in fat.
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| − | c. Lipotrope derangement - lipotropes are substances which hasten the removal of fat from
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| − | the liver cells. Some are the amino acids that facilitate conjugation of the fat with proteins to
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| − | form the lipoprotein that is excreted from the cell, and deficiency of these e.g. choline and
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| − | methionine in the diet, lead to fatty change within the cells.
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| − | Some poisons e.g. CCl4, phosphorus and alcohol also prevent stages leading to the
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| − | formations of lipoproteins.
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| − | 2. Metabolic diseases - those accompanying a deranged carbohydrate metabolism in which
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| − | glucose is not made available for uptake into the tissues. Alternative pathways are resorted to
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| − | for the production of energy needed by the cells, and this leads to fatty change.
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| − | Examples are Diabetes mellitus in dogs where there is a deficiency of the hormone insulin
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| − | which is required for cellular glucose utilisation, and Ketosis in ruminants where the drain on
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| − | glucose reserves in sheep caused by twin lambs ( condition is called Pregnancy Toxaemia) or
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| − | in the milk of high-yielding dairy cows shortly after parturition (Acetonemia), exhorts the
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| − | body to find another source of energy, with consequent mobilisation of fat reserves and their
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| − | transportation to the liver.
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| − | 3. Anoxia - an inadequate supply of oxygen to the tissues
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| − | Any condition that reduces the oxygen supply to the tissues will cause fatty change in the
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| − | liver. Anaemia ( a reduced numbers of red blood cells circulating in the blood ) caused by
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| − | sustained loss of erythrocytes from the vessels as in chronic haemorrhage or the excessive
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| − | destruction of erythrocytes within the vessels ( haemolysis ) are examples as are the various
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| − | circulatory disorders such as ischaemia ( reduced blood supply to a tissue ) and chronic
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| − | venous congestion ( slowing of blood flow through the vasculature ) due to a failing heart.
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| − | 4. Toxins. A large number of toxins will cause fatty change in the liver. In these cases,
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| − | consider the fatty change to be a more severe form of cellular swelling. Among these are;
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| − | a. bacterial and fungal toxins- either produced in the bloodstream from circulating bacteria
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| − | (septicaemia/bacteraemia) or produced elsewhere and absorbed into the bloodstream.
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| − | b. chemical toxins such as CCl4, phosphorus, arsenic and lead.
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| − | c. some plant and fungal toxins, will cause fatty change in the very early stages of
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| − | poisoning.
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| − | 18
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| − | Distribution of fatty change in the liver.
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| − | The distribution of fatty change in the liver lobule tends to be throughout the whole lobule
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| − | but occasionally there is a preferential localisation which may give some clue to inciting
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| − | cause.
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| − | Chronic venous congestion in the liver due to a failing heart ( a cause of anoxia ) will also
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| − | produce fatty change. In conjunction with the fatty change the pooling of the blood in the
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| − | centrilobular area due to ineffective flow back to the heart, gives a striking gross appearance
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| − | of areas of yellow interspersed with red, and this has been described as a 'nutmeg liver'.
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| − | The practical implication of this when found at post-mortem examination, is to examine the
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| − | heart for the cause.
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| − | Significance of fatty change
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| − | It is important to remember that fatty change is reversible, provided that the underlying cause
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| − | is brought under control. It may be difficult to decide whether the fatty change is due to a
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| − | toxic effect or metabolic defect, from the distribution of the fat within the cell.
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| − | In the former, fatty change can be considered as a more serious form of cellular swelling and
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| − | you may see evidence of a further change in the cells, which is death of the cell (necrosis).
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| − | But if the metabolic defect is prolonged for any period, the impairment of cellular function
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| − | occasioned by the substantial amount of cytoplasmic fat, may also result in death of the cell.
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| − | Wallerian Degeneration. This is a special form of fatty change in the nervous system, where
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| − | damage to myelinated nerves results in the degeneration of the myelin that ensheaths them. It
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| − | can be selectively stained and will be discussed further in the CNS lectures in Systematic
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| − | Pathology.
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| − | Extracellular accumulation of lipids
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| − | Lipid may be present outside the cell in some conditions. Necrosis of cells containing lipid
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| − | may release lipid into the extracellular space where they are visible. Cholesterol is released
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| − | from cells or pooled from lipoproteins in crystalline form( cholesterol clefts )as a result of
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| − | haemorrhage or tissue damage.
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| − | 4. Mucoid ( mucinous, myxomatous ) degeneration - changes in epithelial tissue
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| − | or ground substance (matrix) produced by fibroblasts in connective tissue..
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| − | This is an extracellular phenomenon of some specific cells. They tend to show a bluish tinge
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| − | in H&E stained sections.
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| − | a. Epithelium - specifically the goblet cells of wet mucous membranes and the mucous
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| − | glands themselves. It is a beneficial reaction and is not really degeneration, but an increased
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| − | production of mucin. Their secretions are important as lubricants and protective substances
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| − | 19
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| − | soothing inflamed surfaces, entrapping and diluting harmful agents, carrying specific
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| − | antibodies against infectious agents, and providing a means for their removal.
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| − | b. Connective tissue - the mucin here forms part of the ground substance between the cells
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| − | ( fibroblasts ) producing it. In some circumstances, there appears to be a disturbance in the
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| − | metabolism of the fibroblasts which produce the mucin and the ground substance takes on a
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| − | bluish hue in H&E sections.
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| − | The common example is the
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| − | mucoid ( myxomatous, myxoid )
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| − | degeneration that occurs in the
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| − | heart valves of middle-aged and
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| − | older dogs. It occurs primarily in the
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| − | mitral valve and is responsible for a
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| − | condition specific for this species
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| − | called endocardiosis.
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| − | It is important and results in slowly
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| − | developing heart failure due to the
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| − | inability of a heart with swollen
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| − | misshapen valves to effectively pump
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| − | blood from the left ventricle out into
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| − | the systemic circulation. A substantial
| |
| − | portion of the blood passes back into
| |
| − | the left
| |
| − | atrium and compromises the filling of the atrium from the pulmonary vein. This leads to
| |
| − | back pressure on the pulmonary capillaries with oedema formation in the lungs. This
| |
| − | 20
| |
| − | reduces the oxygenation of blood leading to exercise intolerance and may be heard as moist
| |
| − | sounds on auscultation of the lungs. Eventually, this failure of the left side compromises the
| |
| − | function of the right side and there is also pooling of blood in the venous system i.e. in the liver.
| |
| − | | |
| − | ===Mucoid Degeneration===
| |
| − | ===Hyaline Degeneration===
| |
| − | ====Fibrinoid Degeneration====
| |
| − | ====Amyloidosis====
| |
| − | ===Glycogen Infiltration===
| |
| − | ===Cellular Inclusions===
| |
| − | | |
| − | ==Necrosis==
| |
| − | ===Causes of Necrosis===
| |
| − | ===Gross and Histological Features of Necrotic Lesions===
| |
| − | ====Coagulation Necrosis====
| |
| − | ====Liquefactive Necrosis====
| |
| − | ====Caseation Necrosis====
| |
| − | ===Sequel to Necrosis===
| |
| − | ====Fat Necrosis====
| |
| − | ====Gangrene====
| |
| − | | |
| − | ==Post Mortem Change==
| |
| − | ===Types of Post Mortem Change===
| |
| − | ====Rigor Mortis====
| |
| − | | |
| − | ====Post Mortem Clotting of Blood====
| |
| − | ====Hypostatic Congestion====
| |
| − | ====Post Mortem Imbibition of Blood====
| |
| − | ====Inbibition of Bile Pigment====
| |
| − | ====Gaseous Distenstion of the Alimentary Tract====
| |
| − | ====Autolysis====
| |
| − | ====Putrefaction====
| |
| − | | |
| − | ==Pigmentation and Calcification==
| |
| − | | |
| − | ===Exogenous Pigmentation===
| |
| − | ====Carbon (Anthracosis)====
| |
| − | ====Pneumoconiosis====
| |
| − | ====Carotenoids====
| |
| − | | |
| − | ===Endogenous Pigmentation===
| |
| − | ====Melanin====
| |
| − | ====Blood Pigments====
| |
| − | =====Haemoglobin=====
| |
| − | =====Haemosiderin=====
| |
| − | =====Haematin=====
| |
| − | =====Jaundice=====
| |
| − | =====Haematoidin=====
| |
| − | =====Porphyria=====
| |
| − | ====Lipofuscin====
| |
| − | | |
| − | | |
| − | ===Mineralisation===
| |
| − | | |
| − | ====Calcification====
| |
| − | =====Dystrophic=====
| |
| − | =====Metastatic (Hypercalcaemia)=====
| |
| − | | |
| − | ==Circulatory Disorders==
| |
| − | | |
| − | ===Introduction====
| |
| − | | |
| − | ====Venous Congestion and Hyperaemia====
| |
| − | | |
| − | ====Oedema====
| |
| − | | |
| − | | |
| − | ====Dehydration====
| |
| − | | |
| − | ====Shock====
| |
| − | | |
| − | ====Haemorrhage====
| |
| − | =====Rhexis=====
| |
| − | =====Diapedesis=====
| |
| − | | |
| − | ====Haemostasis====
| |
| − | | |
| − | ====Thrombus====
| |
| − | =====Causes=====
| |
| − | =====Evolution=====
| |
| − | =====Embolism=====
| |
| − | =====Post Mortem Clots=====
| |
| − | | |
| − | ====Disseminated Intravascular Coagulation====
| |
| − | | |
| − | ==Inflammation==
| |
| − | | |
| − | ===Cardinal Signs===
| |
| − | | |
| − | ===Causes===
| |
| − | | |
| − | ===Acute===
| |
| − | ====Introduction====
| |
| − | ====Sequence of Events====
| |
| − | ====Fluids====
| |
| − | =====Serous=====
| |
| − | =====Catarrhal=====
| |
| − | =====Fibrinous=====
| |
| − | =====Diptheritic=====
| |
| − | =====Haemorrhagic=====
| |
| − | =====Purulent=====
| |
| − | =====Functions of Exudate=====
| |
| − | =====Sequel to Exudation=====
| |
| − | ====Cells====
| |
| − | =====Neutrophils=====
| |
| − | =====Eosinophils=====
| |
| − | =====Mast Cells=====
| |
| − | =====Basophils=====
| |
| − | | |
| − | ===Chronic===
| |
| − | ====Introduction====
| |
| − | ====Cells====
| |
| − | =====Macrophages=====
| |
| − | =====Lymphocytes=====
| |
| − | ====Types====
| |
| − | =====Granulomatous Inflammation=====
| |
| − | =====Granulation Tissue=====
| |
| − | =====Lymphocytic Inflammation=====
| |
| − | | |
| − | ===Changes in Inflammatory Cells Circulating in Blood===
| |
| − | ====Neutrophilia====
| |
| − | ====Neutopenia====
| |
| − | ====Eosinophilia====
| |
| − | ====Eosinopenia====
| |
| − | ====Lymphocytosis====
| |
| − | ====Lymphopenia====
| |
| − | ====Plasma Cells====
| |
| − | ====Monocytosis====
| |
| − | | |
| − | ===Role of The Lymph Node in Inflammation===
| |
| − | | |
| − | ===Healing and Repair===
| |
| − | ====Introduction====
| |
| − | ====Repair====
| |
| − | =====Regeneration=====
| |
| − | =====Replacement=====
| |
| − | ====In Particular Tissues====
| |
| − | =====Skin=====
| |
| − | ======First Intention======
| |
| − | ======Second Intention======
| |
| − | =====Bones=====
| |
| − | =====Respiratory Tract=====
| |
| − | =====Alimentary Tract=====
| |
| − | =====Urinary Tract=====
| |
| − | =====Genital Tract=====
| |
| − | =====Central Nervous System=====
| |
| − | | |
| − | ==Growth Disorders==
| |
| − | | |
| − | ===Congenital===
| |
| − | ====Causes====
| |
| − | ====Malformations====
| |
| − | =====Cyclops=====
| |
| − | =====Bulldog Calf=====
| |
| − | =====Cleft Palate=====
| |
| − | =====Cystic Kidney=====
| |
| − | =====Spina Bifida=====
| |
| − | =====Hydrocephalus=====
| |
| − | =====Cerebellar Hypoplasia=====
| |
| − | =====Skeletal Malformations=====
| |
| − | =====Skin Defects=====
| |
| − | =====Muscular Defects=====
| |
| − | =====Cardiac Defects=====
| |
| − | =====Sexual Organ Malformation=====
| |
| − | =====Metabolic Diseases=====
| |
| − | | |
| − | ===Growth Disorders During Life===
| |
| − | ====Atrophy====
| |
| − | ====Hypertrophy====
| |
| − | ====Hypoplasia====
| |
| − | ====Hyperplasia====
| |
| − | ====Metaplasia====
| |
| − | ====Dysplasia====
| |
| − | ====Anaplasia====
| |
| − | ====Neoplasia====
| |
| − | =====Benign Tumours=====
| |
| − | =====Malignant Tumours=====
| |
| − | =====Aetiology of Tumours=====
| |
| − | =====Phases of Tumour Growth=====
| |
| − | =====Tumour Classification and Nomenclature=====
| |