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| | {{frontpage | | {{frontpage |
| | |pagetitle =Liver - General Pathology | | |pagetitle =Liver - General Pathology |
| − | |pagebody = *The lobed [[Liver - Anatomy & Physiology|liver]] is the largest gland in the body | + | |pagebody = <div style="text-align: left; direction: ltr; margin-left: 1em;"> |
| | + | *The lobed [[Liver - Anatomy & Physiology|liver]] is the largest gland in the body |
| | *A healthy [[Liver - Anatomy & Physiology|liver]] is dark reddish-brown in colour with a smooth rubbery texture | | *A healthy [[Liver - Anatomy & Physiology|liver]] is dark reddish-brown in colour with a smooth rubbery texture |
| | *[[Liver - Anatomy & Physiology|Liver]] lesions are common because: | | *[[Liver - Anatomy & Physiology|Liver]] lesions are common because: |
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| | *Although [[Liver - Anatomy & Physiology|liver]] lesions are common, they seldom produce liver failure | | *Although [[Liver - Anatomy & Physiology|liver]] lesions are common, they seldom produce liver failure |
| | *Diagnostic value because often indicates the presence and causes of disease in other organs and systems of the body | | *Diagnostic value because often indicates the presence and causes of disease in other organs and systems of the body |
| | + | </div> |
| | |contenttitle =Content | | |contenttitle =Content |
| | |contentbody =<big><b> | | |contentbody =<big><b> |
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| | </b></big> | | </b></big> |
| − | |logo = | + | |logo =path-logo.png |
| | }} | | }} |
| | | | |
| | + | {{Learning |
| | + | |flashcards = [[Liver_Flashcards_-_Pathology|Liver Pathology Flashcards]] |
| | + | }} |
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| − |
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| − |
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| − | ==[[Liver Failure]]==
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| − |
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| − | [[Icterus]]
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| − | ===Syndromes in liver failure===
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| − |
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| − |
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| − | ====Photosensitisation====
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| − |
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| − | *'sunburn-like' lesions
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| − | *cattle and sheep
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| − | *sharply confined to the unpigmented areas of the skin
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| − | *occurs as a result of the effect of strong sunlight
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| − | **due to the effect of UV light on a photodynamic agent (PDA) present in the skin, such as is '''phylloerythrin''' derived from chlorophyll
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| − | **therefore, the disease occurs mostly in those animals consuming large quantities of grass
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| − | **the UV light is changed to a longer wavelength which produces the necrosis of the skin
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| − | *many unknown/poorly understood causes
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| − | **feeding rape, kale, lucerne, alfalfa
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| − | **mouldy hay
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| − | **lush pasture
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| − | **corticosteroid induced
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| − |
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| − | =====Primary photosensitisation=====
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| − |
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| − | ======Causes======
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| − | *normal ingestion of growing lush green plants containing PDA
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| − | **plants containing such fluorescent pigments
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| − | ***''Hypericum perforatum'' (St John's Wort) - active principle is hypercin
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| − | ***''Lolium perenne'' (Perennial Rye Grass) - active principle is perloline
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| − | *drugs
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| − | **phenothiazine
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| − | **thiazides
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| − | **tetracyclines
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| − | **sulphonamides
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| − | *inherited porphyria
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| − |
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| − | =====Secondary photosensitisation=====
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| − | *photosensitisation secondary to liver damage
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| − | ======Cause======
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| − | *hepatogenous photosensitisation
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| − | **chlorophyll is metabolised to '''phylloerythrin'''
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| − | **when the liver or bile ducts are malfunctioning (eg hepatitis or bile duct obstruction) due to severe toxic damage, '''phylloerythrin''' escapes into the circulation and settles in the tissues including the skin
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| − | **the pigment accumulates causing photosensitisation
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| − | *hepatotoxic plants
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| − | **''Senecio jacobea'' (Ragwort)
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| − | **''Lantana camara'' (Lantana)
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| − | **''Lupinus angustifolius'' (Lupins)
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| − | **Blue-green algae
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| − |
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| − | =====Clinical Signs=====
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| − |
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| − | *localised to lightly pigmented skin areas
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| − | *clear cut demarcation of affected area
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| − | *teats, muzzle, ears
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| − | *skin only
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| − | *skin and liver signs
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| − |
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| − | =====Microscopically=====
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| − | *subepidermal vesicles
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| − | **ulcerate
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| − | **become secondarily infected
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| − |
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| − | =====Treatment=====
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| − | *remove from sunlight
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| − |
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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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| − |
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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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| − |
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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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| − |
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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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| − |
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| − | ======Periportal (centroacinar)======
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| − | *rare
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| − | *eg phosphorous poisoning
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| − |
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| − |
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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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| − |
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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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| − |
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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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| − |
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| − | 2. cellular necrosis occurs at some stage in the disease
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| − |
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| − | 3. there is nodular regeneration of liver cells
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| − |
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| − | 4. fibrosis occurs and is diffuse
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| − |
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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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| − |
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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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| − |
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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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| − |
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| − | 2. via the gastric veins through the oesophageal veins also to the azygous
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| − |
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| − | 3. various venous plexuses, draining back into the renal vein
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| − |
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| − | 4. several prominent subcutaneous veins are also seen, running radially from the umbilicus over the abdomen
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| − |
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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]] |
