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