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Category:Liver - General Pathology (view source)
Revision as of 21:44, 25 July 2011
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==[[Liver Failure]]==
−===Syndromes in liver failure===
−[[Icterus]]
−[[Photosensitisation]]
−[[Hepatic Encephalopathy]]
−====Bleeding Tendencies====
−*in acute [[Liver - Anatomy & Physiology|liver]] damage
−*there is substantial necrosis of the [[Liver - Anatomy & Physiology|liver]] tissue even though it may not be pronounced on gross inspection
−*there is contact of blood with the damaged [[Liver - Anatomy & Physiology|liver]] parenchyma which triggers the clotting cascade, consuming the circulating clotting factors - have a short half life
−*since the [[Liver - Anatomy & Physiology|liver]] is also responsible for the production of these clotting factors, there is an acute shortage and an animal dying from such acute [[Liver - Anatomy & Physiology|liver]] damage may show petechial and ecchymotic haemorrhages in many organs of the body
−*see Canine Viral Hepatitis (ICH)
−**gross and microscopic appearances - haemorrhages will be seen in many tissues in this disease, particularly on the intestinal serosa
−====Hypoalbuminaemia====
−*in chronic [[Liver - Anatomy & Physiology|liver]] damage
−*[[Liver - Anatomy & Physiology|Liver]] will be unable to synthesise plasma proteins
−**especially albumin
−**this leads to oedema in body tissues and cavities due to lowering of the colloid osmotic pressure in the circulation
−*most common in dogs and cats
−==Liver response to injury==
−*Again, the [[Liver - Anatomy & Physiology|liver]] is liable to injury from many causes and this is especially the case for a number of reasons
−**''position''
−***the [[Liver - Anatomy & Physiology|liver]] acts as a second barrier between the non-sterile intestinal contents and the systemic circulation
−***is exposed to viruses, bacterial toxins, and poisons absorbed from the portal blood
−**''energy requirements''
−***relatively enormous amounts of energy are utilised by [[Liver - Anatomy & Physiology|liver]] cells and this renders them more vulnerable to anoxia and toxaemia
−**''detoxification''
−***the [[Liver - Anatomy & Physiology|liver]] acts as a detoxifying organ and may suffer in consequence
−===Necrosis===
−====Causes====
−*severe metabolic disturbances [as seen in degenerative pathology link?]
−*toxic substances [link?]
−*nutritional deficiencies
−*action of micro-organisms
−====Histological patterns====
−*[[Liver - Anatomy & Physiology|Liver]] cell necrosis has been classified on an anatomic basis with reference to the distribution of the lesion
−=====Random foci (focal)=====
−*microscopic foci of necrosis not related to any particular part of the [[Liver - Anatomy & Physiology|liver]] lobule
−*can be due to a variety of insults
−**systemic viral, bacterial,and parasitic infections
−**result of bacteria being absorbed from the gut
−*examples
−**Equine herpes virus infection
−***in aborted foetuses
−**Salmonellosis
−***in calves
−**Toxoplasmosis (miliary)
−***in dogs and cats
−=====Zonal necrosis=====
−*necrosis occurring mainly in a part of the lobule and further subdivided according to whether the lesions are situated centrally, peripherally, or in the mid-zone of the lobule
−*due to anoxia
−======Periacinar (centrilobular)======
−*most common
−*main reason is because the hepatocytes in this zone are furthest away from the incoming blood supply
−**therefore less oxygenated and relatively anoxic
−*reported to contain the greatest number of enzymes responsible for metabolising sunstances to more toxic metabolites capable of killing the hepatocytes
−*hypoxic states and toxic substances predominate in this type of necrosis
−*some viral conditions cause this necrosis
−**eg Infectious Canine Hepatitis
−*poisons
−**eg carbon tetrachloride
−======Midzonal======
−*rare
−*in pigs with alfatoxicosis
−*'Yellow Fever' in man
−======Periportal (centroacinar)======
−*rare
−*eg phosphorous poisoning
−=====Massive necrosis=====
−*necrosis of large areas of [[Liver - Anatomy & Physiology|liver]] cells comprising many lobules (complete acinus or several acini) and sometimes involving almost the whole organ
−*some cases of ICH infection or carbon tetrachloride poisoning, the severity of the injury replacing the zonal pattern
−======Subacute cytolytic necrosis======
−*a condition in the dog
−*aetiology is entirely unknown
−*Clinical
−**acute abdominal pain
−**collapse
−**invariably jaundice
−*Gross
−**[[Liver - Anatomy & Physiology|Liver]] is normal or reduced in size
−*Microscopically
−**severe necrosis
−======''Hepatosis dietica''======
−*similar condition to subacute cytolytic necrosis
−*occurs in rapidly growing pigs
−*related to diet
−**fed on large quantities of grain concentrates
−**poor quality or low quantity protein supplements
−*Cause
−**nutritional deficiencies of selenium and Vitamin E, and probably amino acids
−**triggering mechanism is environmental stress
−===Regeneration===
−*occurs quite readily when damaged
−*approximately 70% of the [[Liver - Anatomy & Physiology|liver]] can be removed surgically without danger to life
−**can reconstitute itself to its former mass in a few weeks
−**may not be its original shape
−NB: larger areas of necrosis or continual bouts of necrosis are accompanied by fibrosis and biliary hyperplasia
−[link to the last two terms]
−===Fibrosis - Repair===
−*any hepatic injury of consequence is going to cause a degree of fibrosis when the lesion has resolved
−*the fibrosis comes from the proliferation of the supportive connective tissue in the [[Liver - Anatomy & Physiology|liver]]
−*fibrosis isolates the [[Liver - Anatomy & Physiology|liver]] cells by effectively changing the sinusoids into capillaries
−*when a certain amount of fibrosis occurs, it can be self-perpetuating
−**the end result is a small scarred [[Liver - Anatomy & Physiology|liver]] with functional failure
−====Histological patterns====
−=====Periacinar fibrosis=====
−*the fibrosis surrounds the hepatic venule (centrilobular vein)
−*can be seen when there is chronic passive congestion with atrophy of the surrounding periacinar hepatocytes and condensation of the remaining connective tissue
−=====Biliary fibrosis=====
−*accompanying inflammation centered on the portal triads
−=====Post necrotic scarring=====
−*following massive necrosis where the necrotic cells are removed and the defect is reapired by fibrosis
−*seen as bands of fibrous tissue
−=====Diffuse fibrosis=====
−*resulting from repeated damage to one or more zones
−*the fibrosis generated proliferates throughout to involve all the tissue
−===Biliary hyperplasia===
−*bile duct proliferation
−*usually in association with portal fibrosis
−*reason is unknown
−[image - the picture shows fibroplasias invading between hepatocytes - some of the cells are likely to be distorted bile duct profiles]
−==Cirrhosis==
−*a term often used for fibrotic lesions, especially widespread fibrosis
−*it is an end stage liver with poor functional ability
−*much debate on the definition and classification of cirrhosis
−*in any case the following conditions prevail:
−1. the whole [[Liver - Anatomy & Physiology|liver]] is involved
−2. cellular necrosis occurs at some stage in the disease
−3. there is nodular regeneration of liver cells
−4. fibrosis occurs and is diffuse
−5. there is disorganisation of the lobular architecture, with fibrous tracts joining portal triads and central veins
−6. clinically it is a chronic disease
−7. [[Liver - Anatomy & Physiology|liver]] cell failure always supervenes and portal hypertension is often a feature
−===Aetiology===
−*precise aetiology is unknown
−*as in man, may be due to viral hepatitis in Rubarth's disease (ICH)
−===Gross===
−*smaller than normal
−*firm to cut
−**firmness is due to the presence of fibrous tissue
−*pale, sometimes yellow in colour
−*regenerating nodule
−**can be small and even in size with the [[Liver - Anatomy & Physiology|liver]] having a finely granular appearance
−**or much larger, uneven in size, and the [[Liver - Anatomy & Physiology|liver]] surface is deeply fissured and irregular
−===Microscopically===
−*exhibits all 3 responses to injury
−**nodular regeneration of the parenchyma
−***haphazard regeneration of liver cells forming islands of new cells surrounded by condensed portal areas
−**fibrosis
−***early cases show areas of fibrosis connecting two or more portal triads
−***later cases have prominent laying down of cartilage
−**biliary hyperplasia
−===Effects of cirrhosis===
−due to
−*[[Liver - Anatomy & Physiology|liver]] cell failure
−*development of portal hypertension
−**displacement and compression of efferent veins
−***fibrous connective tissue bands enclose veins and constrict them by contraction
−***regenerating nodules of [[Liver - Anatomy & Physiology|liver]] cells contribute as well
−**abnormal communications open up between arterial and venous branches
−**this transmits high arterial pressure directly to the low pressure venous system
−====Sequelae====
−the rise in the venous pressure leads to the development of an accessory portal circulation and contributes to the development of ascites
−*prominent collateral pathways form in an attempt to circumvent the portal obstruction
−1. via the intercostal veins to the azygous
−2. via the gastric veins through the oesophageal veins also to the azygous
−3. various venous plexuses, draining back into the renal vein
−4. several prominent subcutaneous veins are also seen, running radially from the umbilicus over the abdomen
−NB: oesophageal and gastric collaterals in the dog run '''subserosal''', not '''submucosal''' like man, therefore they are not as subject to traumatic rupture
−*ascites
−**common finding
−**other factors are involved: lowered plasma albumin, causing lowered colloid osmotic pressure
−[[Molecular pathogenesis of cholestasis]]
−[[Hepatic Stellate Cells]]
</b></big>
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−|logo =
+|logo =path-logo.png
}}
}}
+{{Learning
+|flashcards = [[Liver_Flashcards_-_Pathology|Liver Pathology Flashcards]]
+}}
−[[Category:Liver - Pathology]]
[[Category:Liver - Pathology]]
+[[Category:General Pathology]]