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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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| − | | |
| − | ===[[General Pathology - Degenerations and Infiltrations|Degenerations and Infiltrations]]===
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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
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| − | *** Dependant upon lipids as an energy source.
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| − | * 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.
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| − | ** 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).
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| − | ** 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.
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| − | ** 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).
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| − | *** 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
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| − | ***** 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.
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| − | # '''Lipotrope Derangement'''
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| − | #* 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.
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| − | #** E.g. choline, methionine.
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| − | #** Dietary deficiency of these leads to fatty change within the cells.
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| − | #* Some poisons also prevent stages of lipoprotein formation.
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| − | #** 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.
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| − | *** This leads to fatty change.
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| − | * Examples:
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| − | ** Diabetes mellitus in dogs
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| − | *** Deficiency of the hormone insulin required for cellular glucose utilisation.
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| − | ** 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
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| − | liver.
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| − | * Examples:
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| − | ** Anaemia
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| − | *** Reduced numbers of red blood cells circulating in the blood
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| − | *** 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).
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| − | ** Circulatory disorders
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| − | *** Ischaemia
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| − | **** Reduced blood supply to a tissue
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| − | *** Chronic venous congestion
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| − | **** Slowing of blood flow through the vasculature e.g. due to a failing heart.
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| − | | |
| − | =====Toxins=====
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| − | | |
| − | * Many toxins will cause fatty change in the liver.
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| − | ** In these cases fatty change may be considered to be a more severe form of [[General Pathology#Cellular Swelling|cellular swelling]].
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| − | * Examples:
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| − | ** Bacterial and fungal toxins
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| − | *** May be:
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| − | **** Produced in the bloodstream by circulating bacteria (septicaemia/bacteraemia)
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| − | **** Produced elsewhere and absorbed into the bloodstream.
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| − | ** Chemical toxins
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| − | *** For example, CCl4, phosphorus, arsenic and lead.
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| − | ** Plant toxins
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| − | *** Some plant toxins will cause fatty change in the very early stages of poisoning.
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| − | | |
| − | ====Distribution of Fatty Change in the Liver====
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| − | | |
| − | * Fatty change in the liver tends to be throughout the whole lobule.
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| − | * Occasionally there is a preferential localiasation - this may give some clue as to the inciting cause.
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| − | ** E.g. in chronic venous congestion
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| − | *** Due to a failing heart (a cause of anoxia).
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| − | *** Blood pools in the centrilobular area (due to ineffective blood flow back to the heart), as well as fatty change being induced.
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| − | **** Gives a striking gross appearance - areas of yellow interspersed with red.
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| − | ***** Described as a 'nutmeg liver'.
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| − | *** When found post-mortem examination, indicated the heart should be examined for the cause.
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| − | | |
| − | ====Significance of fatty change====
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| − | | |
| − | * Fatty change is '''reversible''', provided that the underlying cause is brought under control.
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| − | * '''Necrosis'''
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| − | ** 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.
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| − | *** In toxic effects, the fatty change can be considered as a more serious form of cellular swelling.
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| − | **** There may be evidence of necrosis.
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| − | *** If a metabolic defect is prolonged, cellular function may be impaired by the substantial amount of fat.
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| − | **** Necrosis may also result in this instance.
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| − | * '''Wallerian Degeneration'''
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| − | ** A special form of fatty change in the nervous system.
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| − | ** Damage to myelinated nerves results in the degeneration of the myelin that ensheaths them.
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| − | * '''Extracellular accumulation of lipids'''
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| − | ** Necrosis of cells containing lipid may release lipid into the extracellular space.
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| − | *** Haemorrhage or tissue damage may result in cholesterol being released from cells or pooled from lipoproteins in crystalline form (cholesterol clefts).
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| − | | |
| − | ===Mucoid Degeneration===
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| − | | |
| − | * Mucoid degeneration is also known as mucinous or myomatous degeneration.
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| − | * Mucoid degeneration involves chanages in epithelial tissue or the extracellular matrix/ ground substance.
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| − | * An extracellular phenomenon of some specific cells.
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| − | ** Tend to show a bluish tinge in H&E stained sections.
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| − | | |
| − | ====Epithelium====
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| − | | |
| − | * The specific cells involved in mucoid degeneration in the eptihelium are:
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| − | ** The goblet cells of wet mucous membranes.
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| − | ** The mucous glands themselves.
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| − | * This is not really a degeneration, but an increased production of mucin.
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| − | ** It is a beneficial reaction; the product
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| − | *** Is important as a lubricant.
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| − | *** Soothes inflamed surfaces.
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| − | *** Traps and dilutes harmful agents.
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| − | *** 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 features a material which is fibrin-like.
| |
| − | * 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 granular material.
| |
| − | *** Pinkish-red (i.e. eosin-staining).
| |
| − | *** Has some of the appearance and staining properties of fibrin.
| |
| − | *** Consists partly of degenerated muscle and elastic fibres, and partly of an increased amount of protein ground substance around the degenerated fibres.
| |
| − | *** Looks like a red smudge in the vessel wall when viewed histologically.
| |
| − | * The presence of the fibrin-like material may suggest
| |
| − | ** A local hypersensitivity reaction
| |
| − | ** Hypertension
| |
| − | | |
| − | ====Amyloidosis====
| |
| − | | |
| − | * Also known as amyloid infiltration
| |
| − | * Deposition of a proteinaceous hyaline substance in extracellular sites.
| |
| − | ** Sites of deposition vary with species.
| |
| − | * The kidney is a common site of deposition.
| |
| − | ** Amyloid is deposited under the capillary endothelium and progressively increases in volume.
| |
| − | * There are various categories of amyloid.
| |
| − | ** Is essentially an abnormal protein produced in the body
| |
| − | ** In most cases, it is produced in response to sustained antigenic stimulation caused by a chronic suppurative process.
| |
| − | *** E.g. a foot abscess, mastitis.
| |
| − | * Amyloid is a relatively inert substance.
| |
| − | ** When it accumulates, it is not easily removed.
| |
| − | | |
| − | ===Glycogen Infiltration===
| |
| − | | |
| − | * Glycogen is normally present in substantial amounts in the liver and muscle.
| |
| − | ** Is a readily utilisable source of energy.
| |
| − | * Moderate glycogen infiltration in the liver:
| |
| − | ** Grossly - doesn't have much effect.
| |
| − | ** Histologically - shows up as foamy cytoplasmic vacuoles, similar to that of fat.
| |
| − | * Some conditions may result in an increase in glycogen deposits.
| |
| − | ** '''Diabetes mellitus'''
| |
| − | *** Gives an increase in hepatic glycogen stores.
| |
| − | *** May be overshadowed by the increased fat in the hepatocytes, and therefore difficult to see.
| |
| − | **** Renal tubular deposits are more easily observed.
| |
| − | ** '''Excessive glucocorticoids'''
| |
| − | *** Could be due to:
| |
| − | **** Hyperadrenocortism
| |
| − | **** Animals being maintained on glucocorticoid therapy over a long period of time.
| |
| − | ***** Has more dramatic effect.
| |
| − | *** Huge amounts of glycogen infiltration.
| |
| − | **** Liver appears larger and paler.
| |
| − | **** Vacuoles may be so extensive that the rest of the cytoplasm appear as pink strands passing from the nucleus to the plasma membrane.
| |
| − | ***** A "feathery appearance" or "web-like effect".
| |
| − | ** '''Glycogen storage diseases'''
| |
| − | *** Due to an inherited deficiency of an enzyme required for the breakdown of glycogen to glucose.
| |
| − | **** Cells continuously accumulate glycogen.
| |
| − | *** Seen in all tissues of the body but exerts its major effect in the CNS.
| |
| − | * Selective staining must be employed to distinguish glycogen vacuoles from fatty vacuoles in the liver.
| |
| − | ** Alcohol fixation is preferred.
| |
| − | ** Best's Carmine is the commonly used stain.
| |
| − | *** Stains the intracellular glycogen red.
| |
| − | | |
| − | ===Cellular Inclusions===
| |
| − | | |
| − | ====Viruses====
| |
| − | | |
| − | * Either in the nucleus or cytoplasm.
| |
| − | | |
| − | ====Storage Products====
| |
| − | | |
| − | * Due to '''hereditary storage diseases''' in which there is a missing or defectivecellular enzyme. There are many types known in domestic animals.
| |
| − | ** Break down/ build up of intracellular substances is halted.
| |
| − | *** The intermediate substance accumulates in the lysosomes.
| |
| − | ** Affects all tissues
| |
| − | *** The central nervous system is particularly vulnerable.
| |
| − | * Due to '''age'''
| |
| − | ** Lysosomes will accumulate non-degradable products
| |
| − | *** E.g. lipofuscin - the 'ageing' or 'wear and tear pigment'.
| |
| − | **** Cmmonly seen in middle-aged cats in the hepatocytes nearest the centrilobular veins.
| |
| − | | |
| − | ====Intracellular Bacteria====
| |
| − | | |
| − | * For example, [[Mycobacteria spp.|''Mycobacterium tuberculosis'']] in macrophages.
| |
| − | | |
| − | ====Protein Accumulation====
| |
| − | | |
| − | * In the renal tubular epithelium.
| |
| − | * Occurs when there is leakage of protein out through a damaged glomerulus.
| |
| − | | |
| − | ==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=====
| |