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==An Introduction to General Pathology==
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#REDIRECT[[:Category:General Pathology]]
 
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* 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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* In vacuolar degeneration, excess water is transferred to the endoplasmic reticulum (ER).
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* The ER  swells and eventually fragments.
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** A fluid vacuole remains in the cytoplasm.
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* Commonly occurs in cells that are very metabolically active and have well developed pumping mechanisms.
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** E.g. as the hepatocyte, renal tubular epithelium and pancreatic acinar cell.
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  −
===Cellular Fatty Change===
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* DOES NOT REFER TO THE THE FAT STORES OF THE BODY!
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** Fatty substances accumulate or increase within the cytoplams of specific cells.
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** In some instances, the fat stores may be involved in the transfer of fat to these specific cells.
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* Cellular fatty change is an important intracellular abnormality.
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** Principally concerns the intracellular fat in hepatocytes.
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* Fatty change is commonly seen in three organs of the body.
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** Prinicpally in the '''liver'''.
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** Also in the '''kidney''' and the '''heart'''.
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** This is  because these organs are either:
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*** Involved in the metabolism of fat, or
  −
*** Dependant upon lipids as an energy source.
  −
* Fatty change can be readily recognised at post-mortem.
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  −
==== Gross Appearance of Fatty Change====
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* '''Liver'''
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** This is the main organ involved in fatty change.
  −
** May be greatly increased in size.
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** Is tan to yellowish in colour.
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*** Is normally reddish brown.
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** Very prone to rupture with slight pressure (friable).
  −
** Parenchyma bulges outwards on being freed from the constraint of the capsule when cut.
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** Parenchyma is dull, yellowish and greasy.
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* '''Kidney'''
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** The cortex appears paler.
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***N.B. This is normal in e.g. the cat!
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*** Diffuse paleness is not the prominent feature, unlike in the liver.
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* '''Heart'''
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** Anoxia, as a result of anaemia, causes fatty change.
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** The heart is flabby.
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** Fatty change may occur as streaks in the papillary muscles.
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*** I.e. those muscles furthest away from the blood supply.
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** Contractile ability is reduced, and blood is therefore not umped efficiently.
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  −
====Histological Appearance of Fatty Change====
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  −
* The fat either appears as globules or is contained in varying sizes of vacuoles in the cytoplasm.
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** In the heart, fat appears as groups of tiny vacuoles dispersed along the myofibrils.
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** In the liver and kidney, vacuoles tend to coalesce to form larger ones.
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*** One or more large globules may fill the cytoplasm.
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**** The nucleus is displaced to the periphery of the cell.
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* The nucleus remains normal.
  −
** Nuclear changes are only seen if the degree of fatty change becomes incompatible with the continued existence of the cell.
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* In hepatocytes, it is necessary to stain for fat in order to ellucidate if a vacuole in the cytoplasm is fat-containing.
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** Two further conditions may produce vacuoles in hepatocytes.
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*** [[General Pathology#Vacuolar Degeneration|Vacuolar hydropic degeneration]]
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*** Glycogen accumulation
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** Stains commonly used include Sudan 111, Sudan 1V, and Oil Red O.
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*** Stain fat varying shades of orange to red.
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** Sections must be prepared differently to the routine paraffin embedding (used e.g. in H&E staining).
  −
*** The strong solvents used in paraffin embedding dissolve the fat out of the cell.
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*** When staining for fat,  the tissue to be examined is frozen and sectioned in a cryostat before being stained.
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**** These sections are more than twice as thick as those attained by sectioning paraffin blocks
  −
***** There may be some overlap of cells on the section.
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***** Individual cells are less clear.
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====Causes of Fatty Change====
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=====Dietary and Metabolic=====
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  −
# '''Starvation'''
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#*  A reduction in dietary intake neccessitates the increased mobilisation of fat from body fat stores to meet energy needs.
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#* Fat from stores is transported in the blood as fatty acids.
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#** The liver cannot cope with them all properly.
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#*** The fatty acids are stored in the liver as neutral fats.
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# '''Overeating'''
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#* When the dietary intake is greater than the energy expenditure, the fat is temporarily stored prior to movement to the body fat stores.
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#** Also occurs in fat-rich diets.
  −
# '''Lipotrope Derangement'''
  −
#* Lipotropes are substances which hasten the removal of fat from the liver cells.
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#* Lipotropes include the amino acids that allow conjugation of fat with proteins to form the lipoprotein that is excreted from cells.
  −
#** E.g. choline, methionine.
  −
#** Dietary deficiency of these leads to fatty change within the cells.
  −
#* Some poisons also prevent stages of lipoprotein formation.
  −
#** E.g. CCl4, phosphorus and alcohol
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  −
=====Metabolic diseases=====
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  −
* Certain metabolic diseases may result in deranged carbohydrate metabolism.
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* Glucose is not made available for uptake into the tissues.
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** The celles still require energy, and so alternative pathways are resorted to.
  −
*** This leads to fatty change.
  −
* Examples:
  −
** Diabetes mellitus in dogs
  −
*** Deficiency of the hormone insulin required for cellular glucose utilisation.
  −
** Ketosis in ruminants
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*** The body is exhorted to find another source of energy following drainage of the glucose reserves.
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**** Fat reserves are mobilised and transported to the liver.
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*** E.g.
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**** Twin lambs in sheep
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***** The condition is known as Pregnancy Toxaemia
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**** Milk producion in high-yielding dairy cattle shortly afer parturiton.
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***** Acetonemia
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=====Anoxia=====
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  −
* Any condition that reduces the oxygen supply to the tissues will cause fatty change in the
  −
liver.
  −
* Examples:
  −
** Anaemia
  −
*** Reduced numbers of red blood cells circulating in the blood
  −
*** Caused by sustained loss of erythrocytes from the vessels by
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**** Chronic haemorrhage
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**** Excessive destruction of erythrocytes (haemolysis).
  −
** Circulatory disorders
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*** Ischaemia
  −
**** Reduced blood supply to a tissue
  −
*** Chronic venous congestion
  −
**** Slowing of blood flow through the vasculature e.g. due to a failing heart.
  −
 
  −
=====Toxins=====
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  −
* Many toxins will cause fatty change in the liver.
  −
** In these cases fatty change may be considered to be a more severe form of [[General Pathology#Cellular Swelling|cellular swelling]].
  −
* Examples:
  −
** Bacterial and fungal toxins
  −
*** May be:
  −
**** Produced in the bloodstream by circulating bacteria (septicaemia/bacteraemia)
  −
**** Produced elsewhere and absorbed into the bloodstream.
  −
** Chemical toxins
  −
*** For example, CCl4, phosphorus, arsenic and lead.
  −
** Plant toxins
  −
*** Some plant toxins will cause fatty change in the very early stages of poisoning.
  −
 
  −
====Distribution of Fatty Change in the Liver====
  −
 
  −
* Fatty change in the liver tends to be throughout the whole lobule.
  −
* Occasionally there is a preferential localiasation -  this may give some clue as to the inciting cause.
  −
** E.g. in chronic venous congestion
  −
*** Due to a failing heart (a cause of anoxia).
  −
*** Blood pools in the centrilobular area (due to ineffective blood flow back to the heart), as well as fatty change being induced.
  −
**** Gives a striking gross appearance - areas of yellow interspersed with red.
  −
***** Described as a 'nutmeg liver'.
  −
*** When found post-mortem examination, indicated the heart should be examined for the cause.
  −
 
  −
====Significance of fatty change====
  −
 
  −
* Fatty change is '''reversible''', provided that the underlying cause is brought under control.
  −
* '''Necrosis'''
  −
** From the distribution of fat in a cell, it may be difficult to decide whether the fatty change is due to a toxic or metabolic defect.
  −
*** In toxic effects, the fatty change can be considered as a more serious form of cellular swelling.
  −
**** There may be evidence of necrosis.
  −
*** If a metabolic defect is prolonged, cellular function may be impaired by the substantial amount of fat.
  −
**** Necrosis may also result in this instance.
  −
* '''Wallerian Degeneration'''
  −
** A special form of fatty change in the nervous system.
  −
** Damage to myelinated nerves results in the degeneration of the myelin that ensheaths them.
  −
* '''Extracellular accumulation of lipids'''
  −
** Necrosis of cells containing lipid may release lipid into the extracellular space. 
  −
*** Haemorrhage or tissue damage may result in cholesterol being released from cells or pooled from lipoproteins in crystalline form (cholesterol clefts).
  −
 
  −
===Mucoid Degeneration===
  −
 
  −
* Mucoid degeneration is also known as mucinous or myomatous degeneration.
  −
* Mucoid degeneration involves chanages in epithelial tissue or the extracellular matrix/ ground substance.
  −
* An extracellular phenomenon of some specific cells.
  −
** Tend to show a bluish tinge in H&E stained sections.
  −
 
  −
====Epithelium====
  −
 
  −
* The specific cells involved in mucoid degeneration in the eptihelium are:
  −
** The goblet cells of wet mucous membranes.
  −
** The mucous glands themselves.
  −
* This is not really a degeneration, but an increased production of mucin.
  −
** It is a beneficial reaction; the product
  −
*** Is important as a lubricant.
  −
*** Soothes inflamed surfaces.
  −
*** Traps and dilutes harmful agents.
  −
*** Carried specific antibodues against infectious agents.
  −
*** Provides a means for removal of infectious agents.
  −
 
  −
====Connective tissue====
  −
 
  −
* Here, the mucin forms part of the ground substance between the fibroblasts that produce it.
  −
* A disturbance in the metabolism of the fibroblasts under some circumstances,means the ground substance takes on a bluish hue in H&E sections.
  −
* Mucoid degenration in the heart valves of middle-aged and older dogs is a common example.
  −
** Causes '''endocardiosis'''.
  −
*** A condition specific to the dog.
  −
 
  −
====Endocardiosis====
  −
 
  −
* Tends to affects middle-aged and older dogs.
  −
* Primarily occurs in the mitral valve.
  −
* Results in slowly developing heart failure
  −
* The valves become swollen and misshapen
  −
** The heart cannot pump blood effectively to the circulation from the left ventricle.
  −
*** Blood passes back into the left atrium, compromising the filling from the pulmonary vein.
  −
**** Leads to back pressure on the pulmonary capillaries.
  −
***** Oedema forms in the lungs, and can be heard as moist sounds on ausculatation.
  −
***** Reduces the oxygenation of blood leading to exercise intolerance.
  −
*** Failure of the left side eventually compromises the function of the right side.
  −
**** There is pooling of blood in the venous system i.e. in the liver.
  −
 
  −
===Hyaline Degeneration===
  −
 
  −
* The term "hyaline degeneration" is applied to several types of degeneration or infiltration.
  −
** "Hyaline" is a descriptive term meaning "glassy".
  −
*** Used in pathology when structureless material appears in section, and stains red with eosin
  −
**** Describes a variety of conditions in which structureless materials are present.
  −
* Is applied to both extra-  and intra-cellular degenrations/ infiltrations.
  −
** '''Extracellular'''
  −
*** Protein hyaline casts in the renal tubules.
  −
**** From excessive protein passing through glomerulus.
  −
**** When fresh urine is examined under the microscope, casts may be seen as elongated glassy tubes.
  −
***  Hyaline membranes
  −
**** Proteinaceous effusions into pulmonary alveoli
  −
**** Prevent gaseous exchange.
  −
** '''Intracellular'''
  −
*** Hyaline degeneration of skeletal muscle.
  −
**** In vitamin E/ selenium deficiency.
  −
* There are two forms of hyaline degeneration that deserve their own mention.
  −
** Fibrinoid degeneration.
  −
** Amyloid infiltration.
  −
 
  −
====Fibrinoid Degeneration====
  −
 
  −
Fibrinoid degeneration
  −
This implies that there is a
  −
material which is fibrin-like,
  −
and is essentially a focal death
  −
of cells in the walls of small
  −
blood vessels, usually
  −
arterioles. Parts of the vessel
  −
wall become replaced by a
  −
homogenous or granular
  −
eosin-staining material, which
  −
has some of the appearance
  −
and staining properties of
  −
fibrin. This pinkish-red
  −
material consists partly of
  −
degenerated muscle and elastic
  −
fibres, and partly of an
  −
increased amount of protein ground substance around the degenerated fibres. Its main
  −
importance is that it may suggest either a local hypersensitivity reaction or hypertension in
  −
the blood vessels. When viewed histologically, the fibrinoid degeneration is like a red
  −
smudge in part of the vessel wall.
  −
 
  −
====Amyloidosis====
  −
Amyloid infiltration - Amyloidosis
  −
It is the deposition of a proteinaceous
  −
hyaline substance extracellularly in
  −
specific tissues. The sites of
  −
deposition vary with the species. The
  −
kidney is a common site. Here the
  −
amyloid is deposited under the
  −
capillary endothelium and
  −
progressively increases in volume.
  −
Various categories of amyloid exist.
  −
It is essentially an abnormal protein
  −
produced in the body. In most natural
  −
cases in domestic animals, it is
  −
produced in response to sustained
  −
antigenic stimulation in the body caused by a chronic suppurative process such as a foot
  −
abscess, mastitis, etc.
  −
It is a relatively inert substance and when it accumulates, it is not easily removed.
  −
 
  −
===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=====
 
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