Difference between revisions of "General Pathology"

From WikiVet English
Jump to navigation Jump to search
(Redirected page to Category:General Pathology)
 
(115 intermediate revisions by 5 users not shown)
Line 1: Line 1:
==An Introduction to General Pathology==
+
#REDIRECT[[:Category:General Pathology]]
 
 
* The term '''pathology''' is derived from:
 
** '''Pathos''', or suffering
 
** '''Logos''', or reasoning/logic.
 
* Pathology is defined as the study of disease including:
 
** '''Aetiology''' - causal factor(s)
 
** '''Pathogenesis''' - the development of the disease within the body.
 
** '''Lesions''' - the observable structural changes in the tissues and fluids of the body.
 
** '''Pathophysiology''' - the functional changes in diseased tissues.
 
** '''Sequel''' - the consequences of the disease in the body.
 
** '''Remote effects''' - the effect of disease in one tissue on other tissues in the body.
 
 
 
===Lesions===
 
 
 
* Lesions are the abnormalities or changes seen in living tissues due to disease.
 
* Observed in
 
** The live animal
 
** Tissues surgically removed from the live animal
 
*** Biopsy/ excision
 
** Animals soon after death
 
*** Necropsy, post-mortem examination.
 
 
 
====Decription of Lesions====
 
 
 
* Descriptions of lesions is very important
 
* Whole organs, tissues or individual lesions are described under headings such as
 
*# Size
 
*# Shape
 
*# Colour
 
*# Weight
 
*#* Generally in relation to body weight
 
*# Texture and Consistency
 
*# Appearance of the cut surface
 
*# Contents of hollow organs
 
*# Position, relationships and effects on adjacent tissues
 
 
 
===Disease===
 
 
 
====Definition and Type====
 
 
 
* '''Disease''' is  a definite morbid (illness producing) process, having a characteristic train of symptoms or signs.
 
** May affect the whole body or any of its parts.
 
** The disease's aetiology, pathology and prognosis may be known or unknown.
 
* There are two main categories of disease.
 
*# '''Acute'''
 
*#* Characterised by sudden onset and short duration.
 
*#* The outcome of acute disease may be:
 
*#** Death
 
*#** Resolution due to host defence response or clinical therapy
 
*#** Progression to chronic disease
 
*# '''Chronic'''
 
*#* Characterised by insidious onset and protracted course.
 
*#* The outcome of chronic disease may be:
 
*#** Progressive destruction of tissue
 
*#*** Compromises funtion and  endangers life,
 
*#** The halting of the course of disease, with tissue repair by scarring.
 
 
 
====Factors Involved in the Development of Disease====
 
 
 
* There are three factors which conspire with each other to produce disease.
 
*# '''The individual animal'''.
 
*#* In particular, the animal's nutritional and immune status
 
*#** This is modified by:
 
*#*** Recent or concurrent disease
 
*#*** Previous exposure to the agent(s) responsible
 
*# '''The disease-causing agent(s)'''.
 
*#* Most do not cause a uniform pattern of disease
 
*#** Host defences are important in determining the presentation of the disease.
 
*#* An agent's capacity to produce disease depends upon:
 
*#** The dose
 
*#** The virulence of the agent
 
*#* Several agents may be involved.
 
*#** Usually one agent debilitates, allowing others to exert a greater effect within the body
 
*#* The presence of an agent does not necessarily mean it is the cause of the disease!
 
*#* A pathogenic agent may be absent from the tissues, due to:
 
*#** Clinical therapy
 
*#** Host defence systems
 
*# '''Environment''', for example:
 
*#* Overcrowding of animals
 
*#* Mixing animals from differing origins
 
*#** Carriers are allowed to infect susceptible animals.
 
*#*** Carriers are animals which harbour the pathogenic agent but do not show signs of disease.
 
*#* Changes in management routine
 
 
 
====Types of Agents Causing Disease====
 
 
 
# '''Infectious organisms'''
 
#* [[Viruses|Viruses]]
 
#* [[Bacteria|Bacteria]]
 
#* [[Fungi|Fungi]]
 
#* [[Parasites|Parasites]]
 
# '''Physical'''
 
#* Trauma
 
#* Pressure
 
#* Heat
 
#* Cold
 
#* Radiation
 
# '''Chemical'''
 
#* Toxic organic and inorganic substances
 
#* Toxins produced by infectious organisms
 
# '''Nutritional'''
 
#* Deficiencies of vitamins and trace elements
 
#* Excess vitamins and trace elements
 
# '''Genetic defects'''
 
#* There is a very wide range of potential defects.
 
#** Some are incompatible with life
 
#** Others affect specific systems within the body
 
 
 
====Aspects of Disease====
 
 
 
* There are many aspects of a disease that must be considered in order to understand it in full.
 
*# '''Incidence'''
 
*#* How much of the disease is present?
 
*#* Where is the disease found?
 
*#* In what species is the disease seen?
 
*# '''Aetiology'''
 
*#* Causal agent(s)
 
*#* Predisposing factors
 
*# '''Transmission'''
 
*#* How is the disease spread between individuals?
 
*#* Is the disease zoonotic?
 
*# '''Pathogenesis'''
 
*#* How the causal agent(s) exert their effect within the body.
 
*# '''Diagnosis'''
 
*#* History
 
*#* Clinical findings
 
*#** Clinical examination
 
*#** Clinical pathology
 
*#* Biopsy or post-mortem examination
 
*# '''Prognosis and Treatment'''
 
*# '''Control and Prevention'''
 
*#* The ideal situation
 
 
 
====Post-Mortem Examination====
 
 
 
* Post-mortem examination (PME) investigates the observable structural changes in the animal.
 
* Information relating to the disease withing the body or specific tissue is gained from PME.
 
** This includes information on the disease's
 
*** Aetiology (cause).
 
*** Pathogenesis (development).
 
* Several types of changes are encountered at post-mortem examination.
 
*# Those due to the '''disease'''
 
*#* Lesions
 
*# Those occuring '''immediately prior to death'''
 
*#* Agonal
 
*# Those occuring '''after death'''
 
*#* Post-mortem
 
 
 
====Techniques Involved in Pathological Examination====
 
 
 
* '''Fluid examination'''
 
** E.g. blood, urine, discharges from orifices and so on.
 
* '''Cytology'''
 
** Examination of cells in smears, aspirates and fluids.
 
* '''Necropsy'''
 
** Visual examination of the gross changes in the dead body.
 
* '''Histopathology'''
 
** Microscopic examination of:
 
*** Tissues selected from the dead body after necropsy.
 
*** Biopsy/excision materials from lesions in the living animal.
 
* '''Histochemistry'''
 
** Microscopic visualisation of enzymatic activity in tissues.
 
* '''Immunological methods'''
 
** Specific antibody activity can be detected in tissues and fluids.
 
*** Examination of serum can show prior exposure to a particular infectious agent (i.e. specifice antibodies).
 
** Specific antigens can be detected in tissues.
 
*** When linked to a marking agent (e.g. a fluorescent dye), an antibody can localise its antigen in the tissue.
 
* '''Electronmicroscopy'''
 
** Electronmicrosopcy shows fine detail of the surfaces or internal structures of cells.
 
* '''Bacteriology/ Virology/ Parasitology'''
 
** These techniques allow the isolation and identification of pathogenic bacteria, viruses and parasites.
 
* '''Toxicology'''
 
** Analysis of tissues for particular poisons and toxins.
 
 
 
==General Pathology - Contents==
 
 
 
==Degenerations and Infiltrations==
 
 
 
*  Degenerations and infiltrations are the morphological manifestation of an altered metabolism within the cell.
 
** A particular kind of change within a cell or tissue may suggest that a specific type of alteration has occurred.
 
* Degenerations and infiltrations are types of structural changes.
 
** These are best considered at a cellular level.
 
** These structural changes are deviations from the cell's normal structure and function.
 
*** Parameters are outside the normal physiological range for the cell.
 
* '''Degeneration'''
 
** The tissue cell shows some change in itself.
 
* '''Infiltration'''
 
** Something accumulates in the cell or tissue.
 
 
 
===Cellular Swelling===
 
 
 
* Cellular swelling is
 
** The earliest detectable degenerative change.
 
** The mildest from of cellular degeneration.
 
** The first stage in injury to a cell.
 
** Caused by a variety of insults, e.g.
 
*** Lack of oxygen (anoxia) to a tissue.
 
*** Toxic influences.
 
* Is due to the impairment of the integrity of the cell membrane.
 
* Cellular swelling is characterised by a moderate swelling of the individual cells.
 
** Due to an influx of water into the cell.
 
 
 
====Gross Appearance====
 
 
 
* Organs diffusely affected with cloudy swelling grossly appear pale.
 
** This may be partly due to the swollen cells impeding the tissue's blood supply.
 
* Without cutting into an organ, it may be difficult to appreciate a gross enlargement of it.
 
** Each individual cell is increased in size, meaning the entire volume of the organ is also increased.
 
** E.g. on cutting the liver or kidney capsule, the underlying swollen parenchyma bulges outwards, making the cut ends of the capsule retract.
 
* The degree of gross swelling is not great.
 
** Could be easily confused with early post-mortem changes in the organ.
 
 
 
====Histological Appearance====
 
 
 
* Individual cells appear somewhat swollen.
 
* The cytoplasm appears more red in colour in hematoxylin and eosin (H&E) stained sections.
 
* The nucleus of the cell remains normal.
 
* 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.
 
 
 
====Significance of Cellular Swelling====
 
 
 
* Cellular swelling is an important stage in degeneration.
 
** Not commonly observed on its own without more serious changes
 
*** Not easy to identify at post-mortem unless the examination os perfomred very soon after the animal's death.
 
**** Early post-mortem (autolytic) change in dead tissue looks rather similar.
 
*** Cellular swelling is also reversible.
 
**** When the toxin is no longer exerting its effect, the tissue returns to normal.
 
*** Cellular swelling may be a transient stage in the more serious forms of degenerations which follow.
 
 
 
===Hydropic Degeneration===
 
 
 
Hydropic degeneration - often indicates severe cellular damage due to viruses and is
 
a more severe or advanced form of cellular swelling in
 
which
 
a. the cells may swell up like a balloon prior to their destruction, or
 
b. there is a discrete bleb (vacuole) of fluid within the cytoplasm.
 
a. the former is sometimes called 'ballooning degeneration' and may occur in a variety of
 
conditions, but particularly viral conditions of epithelial tissue.
 
The best example is 'Foot and Mouth Disease' where
 
the virus attacks the stratum spinosum of the epithelium of
 
the tongue and feet. The affected cells are ballooned up
 
with water containing the replicating virus. The cells swell
 
until they burst and the fluid they contain forms
 
microvesicles (blisters) in this layer of the epithelium
 
which may later burst, shedding vast quantities of the
 
virus. When it bursts, the edges of the erosion look
 
ragged, but within weeks the germinal epithelium at the
 
base of the erosion regenerates the epithelium, leaving no
 
trace of a scar.
 
 
 
b. in vacuolar degeneration, the second type, the excess water is transferred to the
 
endoplasmic reticulum (ER) which swells and eventually fragments, leaving a fluid vacuole
 
in the cytoplasm. It commonly occurs in cells such as the hepatocyte, renal tubular
 
epithelium and pancreatic acinar cell which are very metabolically active and have welldeveloped
 
pumping mechanisms.
 
 
 
===Cellular Fatty Change===
 
Cellular fatty change - an important intracellular abnormality, and concerns
 
principally intracellular fat in liver cells.
 
This is the accumulation or increase of fatty substances within the cytoplasm of specific
 
cells and does not refer to the fat stores of the body, although in some cases they may be
 
involved in the transfer of fat to these specific cells.
 
Fatty change is commonly seen in three organs of the body, i.e. principally in the liver but
 
also the kidney and heart; mainly because these organs are either involved in the metabolism
 
of fat or dependant upon lipids as an energy source.
 
It is an important condition, because it is something that can readily be recognised at postmortem
 
examination.
 
Appearance of fatty change
 
Liver: this is the predominant organ
 
involved in fatty change.
 
Grossly, the liver may be greatly
 
increased in size;
 
it is tan to yellowish in colour in
 
contrast to the normal reddish brown;
 
it is very prone to rupture with slight
 
pressure (friable);
 
on cutting through the surface the underlying
 
parenchyma bulges outwards having been freed
 
from the constraint of the capsule;
 
and this parenchyma is dull in appearance,
 
yellowish and greasy.
 
16
 
Kidney: where not normal as in the cat, the cortex appears somewhat paler, but diffuse
 
paleness is not the prominent feature as it is in the liver.
 
Heart: fatty change is found in anaemia in animals and is the result of anoxia ;
 
the heart is flabby and the fatty change may occur as streaks in the papillary
 
muscles (those furthest away from the blood supply).
 
Overall it has reduced contractile ability, and does not pump blood efficiently.
 
Microscopically, the fat
 
appears as globules or
 
vacuoles of varying size
 
in the cytoplasm of the
 
cells. In the heart, it
 
appears as tiny groups of
 
vacuoles dispersed along
 
the myofibrils
 
throughout the whole
 
cell. In the liver and
 
kidney, these vacuoles
 
tend to, but not always,
 
coalesce (come together;
 
fuse with one another )
 
to form larger ones, and
 
you may see one or
 
more large globules
 
filling the cytoplasm
 
with displacement of the nucleus to the periphery of the cell. The nucleus remains normal
 
unless the degree of fatty change becomes incompatible with the continued existence of the
 
cell.
 
To decide whether or not a vacuole in the cytoplasm of a hepatocyte is fat ( because there are
 
two further conditions which may produce vacuoles in hepatocytes, namely the vacuolar
 
hydropic degeneration mentioned before and also the accumulation of glycogen ), it is
 
necessary to stain for the fat present. There are a variety of stains and common ones are
 
Sudan 111, Sudan 1V, and Oil Red O which stain fat varying shades of orange to red.
 
It is necessary to prepare the sections differently to the routine paraffin embedding as per
 
H&E. This is because in paraffin embedding, the fat is dissolved out of the cell by the strong
 
solvents employed. To get over this problem, the block of tissue to be examined is frozen
 
and sectioned in a cryostat (a cabinet containing a microtome and kept at - 20 0 C), before
 
being stained.
 
These sections are over twice as thick as those attained by sectioning paraffin blocks, and so
 
there may be some overlap of cells on the section, and less clarity of the individual cells.
 
17
 
Causes of 'fatty change'
 
1. Dietary and Metabolic
 
a. Starvation - this is an increased mobilisation of fat from the body fat stores in response to
 
energy needs occasioned by a reduction in dietary intake. These are transported in the blood
 
as fatty acids, the liver is unable to cope with them all properly, and so they are stored here as
 
neutral fats.
 
b. Overeating - obesity where the dietary intake is greater than the energy expenditure and
 
the fat is temporarily stored prior to movement to the body fat stores. It also occurs on a diet
 
rich in fat.
 
c. Lipotrope derangement - lipotropes are substances which hasten the removal of fat from
 
the liver cells. Some are the amino acids that facilitate conjugation of the fat with proteins to
 
form the lipoprotein that is excreted from the cell, and deficiency of these e.g. choline and
 
methionine in the diet, lead to fatty change within the cells.
 
Some poisons e.g. CCl4, phosphorus and alcohol also prevent stages leading to the
 
formations of lipoproteins.
 
2. Metabolic diseases - those accompanying a deranged carbohydrate metabolism in which
 
glucose is not made available for uptake into the tissues. Alternative pathways are resorted to
 
for the production of energy needed by the cells, and this leads to fatty change.
 
Examples are Diabetes mellitus in dogs where there is a deficiency of the hormone insulin
 
which is required for cellular glucose utilisation, and Ketosis in ruminants where the drain on
 
glucose reserves in sheep caused by twin lambs ( condition is called Pregnancy Toxaemia) or
 
in the milk of high-yielding dairy cows shortly after parturition (Acetonemia), exhorts the
 
body to find another source of energy, with consequent mobilisation of fat reserves and their
 
transportation to the liver.
 
3. Anoxia - an inadequate supply of oxygen to the tissues
 
Any condition that reduces the oxygen supply to the tissues will cause fatty change in the
 
liver. Anaemia ( a reduced numbers of red blood cells circulating in the blood ) caused by
 
sustained loss of erythrocytes from the vessels as in chronic haemorrhage or the excessive
 
destruction of erythrocytes within the vessels ( haemolysis ) are examples as are the various
 
circulatory disorders such as ischaemia ( reduced blood supply to a tissue ) and chronic
 
venous congestion ( slowing of blood flow through the vasculature ) due to a failing heart.
 
4. Toxins. A large number of toxins will cause fatty change in the liver. In these cases,
 
consider the fatty change to be a more severe form of cellular swelling. Among these are;
 
a. bacterial and fungal toxins- either produced in the bloodstream from circulating bacteria
 
(septicaemia/bacteraemia) or produced elsewhere and absorbed into the bloodstream.
 
b. chemical toxins such as CCl4, phosphorus, arsenic and lead.
 
c. some plant and fungal toxins, will cause fatty change in the very early stages of
 
poisoning.
 
18
 
Distribution of fatty change in the liver.
 
The distribution of fatty change in the liver lobule tends to be throughout the whole lobule
 
but occasionally there is a preferential localisation which may give some clue to inciting
 
cause.
 
Chronic venous congestion in the liver due to a failing heart ( a cause of anoxia ) will also
 
produce fatty change. In conjunction with the fatty change the pooling of the blood in the
 
centrilobular area due to ineffective flow back to the heart, gives a striking gross appearance
 
of areas of yellow interspersed with red, and this has been described as a 'nutmeg liver'.
 
The practical implication of this when found at post-mortem examination, is to examine the
 
heart for the cause.
 
Significance of fatty change
 
It is important to remember that fatty change is reversible, provided that the underlying cause
 
is brought under control. It may be difficult to decide whether the fatty change is due to a
 
toxic effect or metabolic defect, from the distribution of the fat within the cell.
 
In the former, fatty change can be considered as a more serious form of cellular swelling and
 
you may see evidence of a further change in the cells, which is death of the cell (necrosis).
 
But if the metabolic defect is prolonged for any period, the impairment of cellular function
 
occasioned by the substantial amount of cytoplasmic fat, may also result in death of the cell.
 
Wallerian Degeneration. This is a special form of fatty change in the nervous system, where
 
damage to myelinated nerves results in the degeneration of the myelin that ensheaths them. It
 
can be selectively stained and will be discussed further in the CNS lectures in Systematic
 
Pathology.
 
Extracellular accumulation of lipids
 
Lipid may be present outside the cell in some conditions. Necrosis of cells containing lipid
 
may release lipid into the extracellular space where they are visible. Cholesterol is released
 
from cells or pooled from lipoproteins in crystalline form( cholesterol clefts )as a result of
 
haemorrhage or tissue damage.
 
4. Mucoid ( mucinous, myxomatous ) degeneration - changes in epithelial tissue
 
or ground substance (matrix) produced by fibroblasts in connective tissue..
 
This is an extracellular phenomenon of some specific cells. They tend to show a bluish tinge
 
in H&E stained sections.
 
a. Epithelium - specifically the goblet cells of wet mucous membranes and the mucous
 
glands themselves. It is a beneficial reaction and is not really degeneration, but an increased
 
production of mucin. Their secretions are important as lubricants and protective substances
 
19
 
soothing inflamed surfaces, entrapping and diluting harmful agents, carrying specific
 
antibodies against infectious agents, and providing a means for their removal.
 
b. Connective tissue - the mucin here forms part of the ground substance between the cells
 
( fibroblasts ) producing it. In some circumstances, there appears to be a disturbance in the
 
metabolism of the fibroblasts which produce the mucin and the ground substance takes on a
 
bluish hue in H&E sections.
 
The common example is the
 
mucoid ( myxomatous, myxoid )
 
degeneration that occurs in the
 
heart valves of middle-aged and
 
older dogs. It occurs primarily in the
 
mitral valve and is responsible for a
 
condition specific for this species
 
called endocardiosis.
 
It is important and results in slowly
 
developing heart failure due to the
 
inability of a heart with swollen
 
misshapen valves to effectively pump
 
blood from the left ventricle out into
 
the systemic circulation. A substantial
 
portion of the blood passes back into
 
the left
 
atrium and compromises the filling of the atrium from the pulmonary vein. This leads to
 
back pressure on the pulmonary capillaries with oedema formation in the lungs. This
 
20
 
reduces the oxygenation of blood leading to exercise intolerance and may be heard as moist
 
sounds on auscultation of the lungs. Eventually, this failure of the left side compromises the
 
function of the right side and there is also pooling of blood in the venous system i.e. in the liver.
 
 
 
===Mucoid Degeneration===
 
===Hyaline Degeneration===
 
====Fibrinoid Degeneration====
 
====Amyloidosis====
 
===Glycogen Infiltration===
 
===Cellular Inclusions===
 
 
 
==Necrosis==
 
===Causes of Necrosis===
 
===Gross and Histological Features of Necrotic Lesions===
 
====Coagulation Necrosis====
 
====Liquefactive Necrosis====
 
====Caseation Necrosis====
 
===Sequel to Necrosis===
 
====Fat Necrosis====
 
====Gangrene====
 
 
 
==Post Mortem Change==
 
===Types of Post Mortem Change===
 
====Rigor Mortis====
 
 
 
====Post Mortem Clotting of Blood====
 
====Hypostatic Congestion====
 
====Post Mortem Imbibition of Blood====
 
====Inbibition of Bile Pigment====
 
====Gaseous Distenstion of the Alimentary Tract====
 
====Autolysis====
 
====Putrefaction====
 
 
 
==Pigmentation and Calcification==
 
 
 
===Exogenous Pigmentation===
 
====Carbon (Anthracosis)====
 
====Pneumoconiosis====
 
====Carotenoids====
 
 
 
===Endogenous Pigmentation===
 
====Melanin====
 
====Blood Pigments====
 
=====Haemoglobin=====
 
=====Haemosiderin=====
 
=====Haematin=====
 
=====Jaundice=====
 
=====Haematoidin=====
 
=====Porphyria=====
 
====Lipofuscin====
 
 
 
 
 
===Mineralisation===
 
 
 
====Calcification====
 
=====Dystrophic=====
 
=====Metastatic (Hypercalcaemia)=====
 
 
 
==Circulatory Disorders==
 
 
 
===Introduction====
 
 
 
====Venous Congestion and Hyperaemia====
 
 
 
====Oedema====
 
 
 
 
 
====Dehydration====
 
 
 
====Shock====
 
 
 
====Haemorrhage====
 
=====Rhexis=====
 
=====Diapedesis=====
 
 
 
====Haemostasis====
 
 
 
====Thrombus====
 
=====Causes=====
 
=====Evolution=====
 
=====Embolism=====
 
=====Post Mortem Clots=====
 
 
 
====Disseminated Intravascular Coagulation====
 
 
 
==Inflammation==
 
 
 
===Cardinal Signs===
 
 
 
===Causes===
 
 
 
===Acute===
 
====Introduction====
 
====Sequence of Events====
 
====Fluids====
 
=====Serous=====
 
=====Catarrhal=====
 
=====Fibrinous=====
 
=====Diptheritic=====
 
=====Haemorrhagic=====
 
=====Purulent=====
 
=====Functions of Exudate=====
 
=====Sequel to Exudation=====
 
====Cells====
 
=====Neutrophils=====
 
=====Eosinophils=====
 
=====Mast Cells=====
 
=====Basophils=====
 
 
 
===Chronic===
 
====Introduction====
 
====Cells====
 
=====Macrophages=====
 
=====Lymphocytes=====
 
====Types====
 
=====Granulomatous Inflammation=====
 
=====Granulation Tissue=====
 
=====Lymphocytic Inflammation=====
 
 
 
===Changes in Inflammatory Cells Circulating in Blood===
 
====Neutrophilia====
 
====Neutopenia====
 
====Eosinophilia====
 
====Eosinopenia====
 
====Lymphocytosis====
 
====Lymphopenia====
 
====Plasma Cells====
 
====Monocytosis====
 
 
 
===Role of The Lymph Node in Inflammation===
 
 
 
===Healing and Repair===
 
====Introduction====
 
====Repair====
 
=====Regeneration=====
 
=====Replacement=====
 
====In Particular Tissues====
 
=====Skin=====
 
======First Intention======
 
======Second Intention======
 
=====Bones=====
 
=====Respiratory Tract=====
 
=====Alimentary Tract=====
 
=====Urinary Tract=====
 
=====Genital Tract=====
 
=====Central Nervous System=====
 
 
 
==Growth Disorders==
 
 
 
===Congenital===
 
====Causes====
 
====Malformations====
 
=====Cyclops=====
 
=====Bulldog Calf=====
 
=====Cleft Palate=====
 
=====Cystic Kidney=====
 
=====Spina Bifida=====
 
=====Hydrocephalus=====
 
=====Cerebellar Hypoplasia=====
 
=====Skeletal Malformations=====
 
=====Skin Defects=====
 
=====Muscular Defects=====
 
=====Cardiac Defects=====
 
=====Sexual Organ Malformation=====
 
=====Metabolic Diseases=====
 
 
 
===Growth Disorders During Life===
 
====Atrophy====
 
====Hypertrophy====
 
====Hypoplasia====
 
====Hyperplasia====
 
====Metaplasia====
 
====Dysplasia====
 
====Anaplasia====
 
====Neoplasia====
 
=====Benign Tumours=====
 
=====Malignant Tumours=====
 
=====Aetiology of Tumours=====
 
=====Phases of Tumour Growth=====
 
=====Tumour Classification and Nomenclature=====
 

Latest revision as of 12:42, 15 February 2011