Liver 1, 2 and 3 Flashcards

Question

What are regenerative nodules and how do they appear? What else is characteristic other than the three main? What can cause it? What are the sequelae?

Answer 1

Regen nodules- composed of hepatocytes, lack of lobular organisation, often hydropic degeneration, surrounded by fibrous connective tissues Further characteristics- parenchymal injury and fibrosis, balance between regeneration and constrictive scarring, reorganisation of vascular structure Causes Majority- idiopathic Dogs- persistent CAV-1 or leptospira Rare- parasitic, post-necrotic, pigment, biliary, toxic Sequalae- Jaundice- icterus- due to impairedred function Ascites- portal hypertension Heptatoencephalic syndrome- failure to remove ammonia

Answer 2

High billirubin in the blood causing yellow tinge of all tissues- sclera, omentum, mesentery, fat, aorta Seen only grossly and diffusely

Answer 3

Due to excessive haemolysis of erythrocytes in peripheral blood- unconjugated bilirubin in blood Causes- Infections- lepto, EIA, haemolytic strep, anthrax, snake venom Massive internal haemorrhage- bilirubin from disintegrating erythrocytes Icterus neonatorum

Answer 4

Due to severe heptic injury by: toxic substances, infectious agents Damaged hepatocytes do not uptake bilirubin or perform conjugation or Severe hepatocyte swelling blocks outflow of bile from canaliculi- reabsorbed into the blood

Answer 5

Due to obstruction of normal bile-flow- reabsorbed into blood- obstructive Causes- hepatic jaundice, obstruction (flukes), fibrous tissue (cirrhosis), cholangitis, pressure, closure of excretory duct Haemoglobin breakdown- Haem-\> biliverdin- \>bilirubin-\> (in macrophages) bind to albumin, uptake by hepatocytes, conjugation with glucoronic acid-\> bilirubin glucuronides then exreted into gall bladder Bile- water, cholesterol, bile salts, bile pigments from Hb

Answer 6

Jaundice Hypoalbuminaemia- reduced synthesis and secretion of albumin Coagulopathy- reduced synthesis of clotting factors Hyperammoniameia- reduced detoxification by conversion to urea Portal hypertension- cities

Answer 7

Seen with hepatic failure it is due to exogenous metabolites in circulation which pass the blood-brain barrier Hyperammonemia- inhibit the generation of excitatory and inhibitory post-synaptic signals, ammonia alters the transit of amino acids, water, electrolytes across the neuronal membrane Lesions- Cerebral oedema Neuronal necrosis and swelling Degeneration of astrocytes

Answer 8

Nodular hyperplasia- Not a neoplasm- common in older dogs, single or multiple Compression of normal adjacent tissue, containing portal areas (not regenerative) Regenerative nodules- not a neoplasm, common in older dogs, multiple or numerous, adjacent tissue usually fibrotic, loss of lobular architecture

Answer 9

Usually single Sharply delineated No portal areas/lobular structure Compression of adjacent tissue Benign- size main issue

Answer 10

Compression and invasion of adjacent tissue Metastasis Growth pattern- Trabelular Acinar Solid Viral aetiology- hepatitis B in humans

Answer 11

Bile duct adenoma- often cystic, usually single sharply delineated, compression may be problematic with size Bile duct carcinoma- Commonly spreads along the biliary tract, metastasis- hepatic serosa, LNs to lungs Often induce desmoplasia

Answer 12

Liver as the primary site or metastasis Secondary neoplasms common- portal vein, contact- often lymphomas

Answer 13

Degeneration/necrosis of hepatocytes Leukocyte infiltration in periportal connective tissue and/or within sinusoids Septicaemia- increased numbers of leukocytes in sinusoids activation of kupffer cells

Answer 14

Chronic hepatitis- predominantly periportal infiltration by lymphocytes and plasma cells progressive periportal fibrosis- bridging fibrosis hepatocyte apoptosis/necrosis and some evidence of regeneratoin Chronic active hepatitis- Dogs- dobermans Activity- determined by the quantity of inflammation and extent of hepatocellular death Cause- unknown- lepto? End stage- cirrhosis

Answer 15

Cholangitis- inflammation originating from the biliary tree Feline cholangitis- often associate with inflammatory bowel disease and chronic pancreatitis clinical findings- ascites, jaundice, polyphagia, weight loss Three characteristic lesions suppurative cholangitis Lymphocytic and plasmacytic periportal infiltration, bile duct hyperplasia and periportal fibrosis Biliary cirrhosis

Answer 16

Infectious canine hepatitis- CAV-1 Equine herpesvirus infeciton- EHV-1 Canine herpesvirus infection- CaHV-1 Rabbit haemorrhagic disease- calicivirus Feline systemic calicivirus infection Feline infectious peritonitis- FCov Viral hepatitis occurs in the course of systemic infection- viraemia

Answer 17

Agent- canine adenovirus type 1 Pathogenesis- Oronasal infection- tonsils, regional lymph nodes, lymphatics, thoracic duct to the blood- viraemia To the liver (hepatocytes and kupffer cells), eye (corneal epithelium), kidney (glomerular epithelium) and blood vessels High titre- acute necrotising hepatitis Low titre- chronic hepatitis, fibrosis, persistent infection In animals which survive the acute phase of the disease- full liver regeneration can occur Dog- necrotic hepatocytes, intranuclear bodies

Answer 18

Equine herpesvirus 1- rarely 4 Pathogenesis- Transplacental infection- to the uterus Uterus endothelial cells, perivasculitis, thrombi to placental detachment leading to late abortion \>7mo Foetus- multifocal necrosis in liver, lung, thymus, spleen, brain, adrenal glands Gross- disseminated, multifocal necrosis Histology- inflammation and intranucelar bodys

Answer 19

Adult- venereal, respiratory Localised infection and replication Persistence in respiratory and genital tracts- latency Stress, immunosuppression, and pregnancy leads to latent infection and replication Neonate- Ingestion, inhalation \> 2 weeks leads to same as adult \<1 week- epithelial cell replication, mucosal invasion Can lead to latent infection or leukocyte associated anaemia Foetus- in utero Leukocyte associated viaemia Lymphoid hyperplasia Generalised infection- diffuse necrotising vasculitis, multifocal haemorrhagic necrosis of many organs Recovery- residual CNS signs Neonatal- illness, death Pre-natal- abortion, still birth

Answer 20

Rabit haemorrhagic disease- calicivirus Pathogenesis- faeco-oral transmission acute disease with massive necrosis of hepatocytes, DIC FIP- feline coronavirus Pathogenesis Oral infectoin- infection of enterocyres to monocyte-associated viraemia granulomatous (peri)phlebitis/serositis/heptatitis

Answer 21

Portal vein Umbilical arteries Hepatic arteries Ascending infection via the bile duct systeem Parasitic migration Direct extension of infection from adjacent tissue

Answer 22

Enteric bacteria Francisella tularensis Nocardia asteroides Actinobacillus spp Mycobacterium Fusobacterium necrophorum

Answer 23

Fusobacterium necrophorum- filamentous, gram-negative, anaerobe, commensal in GI Ruminants- rumenitis-liver abscess syndrome Carbohydrate-rich diet- ruminal acidosis: defects in ruminal mucosa, access of bacteria to blood vessels, portal vein multifocal necrosis, abscess formation

Answer 24

Agent- Francisella tularensis- zoonosis Pleomorphic- gram-negative, non-spore-forming bacillus Ticks are reservoirs and vectors Pathogenesis- inoculation site- skin lesions, tick bite, prey animals (intestine) localised infection and regional lymphadenitis- bacteraemia, dissemination Gross pathology- ulceration of lymph nodes or Peyer's patches with enteric infection necrotising lymphadenitis, hepatitis, splenitis

Answer 25

Motile, filamentous, spiral-shaped Dogs, cats, horses, ruminants- zoonosis Pathogenesis- penetration of mucous membranes, abraded skin- replication in blood to the kidneys, liver, spleen, brain, eyes, genital tract Dogs- dysfunction due to cell damage by toxins, development of chronic active hepatitis, mottled from haemorrhage and necrosis- mottled haemorrhage Kidneys- tubular necrosis DIC, uveitis, abortion Jaundice- due to intravascular haemolysis and/or bile stasis haemolysis leads to anaemia, centrilobular necrosis in the liver secondary to ischaemia Liver lesions- loss of tight junctions between hepatocytes, induction of mitosis Silver impregnation- warthin-starry stain shows leptospira

Answer 26

Agent- clostridium piliforme- motile, spore-forming, gram-negative, obligate intracellular, commensal in GI Young or immunocompromised animals Pathogenesis- Contact with rodent faeces- proliferation in intestinal epithelial cells Immunosuppression- spread to the liver- necrosis

Answer 27

Protoxoan- toxoplasmosis, coccidiosis, leishmanias Metazoan infections- trematodes, cestodes, nematodes

Answer 28

Toxoplasmosis tachyzoites in hepatocytes Coccidiosis- eimeria stiedai- proliferation of bile duct epithelium Leishmaniasis- infection via biting insects, generalised chronic infection infection of macrophages- rupture of cells

Answer 29

Acute fascioliasis- due to larval migration- haemorrhage and necrosis with eosinophils and granulomatous inflammation Consequences- hepatic dysfunction, anaemia- healing, black disease or chronic Chronic fascioliasis- Mature fluked in bile ducts Lesions- chronic hyperplastic cholangitis, peribilliary fibrosis +/- calcification Possible consequences- anaemia, hypoproteinaemia, chronic debilitation, death

Answer 30

Hepatophilic- cystic echinococcosis- echinococcus granulosus Alveolar echinococcosis- E. multilocularis Cysticerus cellulosae- C. bovis Serophillic- C. tenuicollis, C. pisiformis

Answer 31

Traumatic lesions due to migrating larvae Ascaris sum- milk spot liver

Liver 1, 2 and 3 Flashcards

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