Liver and Biliary System 3 Flashcards
(73 cards)
1
Q
Inflammation of the liver is termed?
A
Hepatitis
2
Q
Describe the features of acute hepatitis
A
- Degeneration / necrosis of hepatocytes
- Leukocyte infiltration in: periportal connective tissue and/or within sinusoids [bacterial infections: neutrophils; viral infections: lymphocytes…]
- Increased numbers of leukocytes in sinusoids
- Activation of Kupffer cells
3
Q
Cholestasis implies?
A
Impediment of bile flow
4
Q
How does acute inflammation look histologically?
A
- Inflammatory cells are smaller that hepatocytes, get more nuclei clustered together so it looks more basophilic
- Pigments (bile associated with cholestasis)
5
Q
Describe chronic hepatitis
A
- Predominantly periportal infiltration by lymphocytes and plasma cells
- Progressive periportal fibrosis -> bridging fibrosis
- Hepatocyte apoptosis/necrosis and some evidence of regeneration
- Necrosis leads to loss of architecture
6
Q
How does repair of the liver occur in chronic inflammation?
A
Fibrosis
7
Q
Chronic active hepatitis is important in which spp/breed?
A
Dogs - Doberman (e.g. Doberman hepatitis)
8
Q
Describe chronic active hepatitis, including its causes
A
- Activity: determined by quantity of inflammation and extent of hepatocellular death
- Cause: unknown (idiopathic) in most canine cases, but some cases seen in association with leptospirosis, infectious canine hepatitis, aflatoxicosis, copper
9
Q
What is the progression/end stage of chronic active hepatitis?
A
Cirrhosis
10
Q
Define hydropic degeneration
A
Entry of fluid into hepatocytes
11
Q
Define cholangitis / cholangiohepatitis
A
= inflammation originating from the biliary tree
12
Q
Progressive chronic changes of cholangitis / cholangiohepatitis lead to?
A
Biliary cirrhosis
13
Q
Feline cholangitis / cholangiohepatitis is often associated with which conditions?
A
Inflammatory bowel disease
Chronic pancreatitis
14
Q
What are the clinical findings of Feline cholangitis / cholangiohepatitis?
A
Ascites
Jaundice
Polyphagia (excessive eating/appetite)
Weight loss
15
Q
Describe the three characteristic histological lesions/stages of Feline cholangitis / cholangiohepatitis
A
- Suppurative cholangitis / cholangiohepatitis
- Lymphocytic and plasmacytic periportal infiltration, bile duct hyperplasia and periportal fibrosis
- Biliary cirrhosis (severe porto-portal fibrosis, bile duct hyperplasia, nodular hepatic hyperplasia)
16
Q
Name 6 example causes of viral hepatitis
A
1) Infectious canine hepatitis [CAV-1]
2) Equine herpesvirus infection [EHV-1]
3) Canine herpesvirus infection [CaHV-1]
4) Rabbit haemorrhagic disease [calicivirus]
5) Feline calicivirus (FCV)
6) Feline infectious peritonitis [coronavirus]
17
Q
What is the viral agent of infectious canine hepatitis?
A
Canine adenovirus type I
18
Q
Describe the pathogenesis of infectious canine hepatitis throughout the body
A
Oronasal infection -> tonsils, regional lymph nodes, lymphatics, thoracic duct -> blood (viraemia) -> liver (hepatocytes, Kupffer cells), eye (corneal epithelium), kidney (glomerular endothelium), blood vessels (endothelium)
19
Q
Compare high vs low titre infections of infectious canine hepatitis in how they affect the liver
A
- High titre: acute (necrotising) hepatitis
* Low titre: chronic hepatitis, fibrosis, persistent infection
20
Q
Describe the histology of a liver with infectious canine hepatitis
A
- Sharply delineated hepatic necrosis (mainly peri-acinar), i.n. inclusion bodies
- Centrilobular necrosis
- Necrotic hepatocytes
21
Q
Describe the gross and pathological features of canine infectious hepatitis
A
- Liver: fibrin deposition, multifocal to coalescing haemorrhage due to damage to endothelium
- Activation of clotting cascade
- Exhaustion of clotting factors
- Also seen in kidney cortex, lung and brain
- Oedema of the gall bladder
22
Q
Describe the pathogenesis of Equine herpes virus 1
A
Transplacental infection
• Uterus (endothelial cells), (peri)vasculitis, thrombi -> placental detachment -> late abortion (> 7th month)
23
Q
Describe the lesions caused by equine herpes virus 1
A
Fetus: multifocal necrosis in:
• Liver, lungs, thymus, spleen (follicles), brain, adrenal glands
24
Q
Describe the histology of a liver with equine herpes virus infection
A
Disseminated multifocal necrosis, inflammation and intranuclear inclusion bodies
25
Describe the pathogenesis and features of canine herpes virus infection
- Intra-uterine infection/infection during birth/ingestion or inhalation as neonate
- Death common in fetal infection or neonates infected by 1 week of age
- Multifocal necrosis (i.n. inclusion bodies) with haemorrhage, DIC
26
Rabbit haemorrhagic disease is caused by which agent?
Calicivirus
27
Describe the pathogenesis of rabbit haemorrhagic disease
- Faecal-oral infection (highly contagious; transmitted on fomites)
• (per)acute disease with:
- Massive necrosis of hepatocytes (the virus infects hepatocytes)
- DIC (microthrombi e.g. in lung capillaries and renal glomeruli)
28
How does rabbit haemorrhagic disease present clinically?
Haemorrhage
Multi-organ failure
Death
29
What is the viral agent of feline infectious peritonitis?
Feline coronavirus
30
Describe the pathogenesis of feline infectious peritonitis
* Oral infection -> infection of enterocytes -> monocyte-associated viraemia
* Granulomatous (peri)phlebitis / serositis / hepatitis etc.
* Viral hepatitis occurs in the course of systemic infection (i.e. viraemia)
31
What are the two main affects of bacterial hepatitis on the liver?
Liver abscesses and granulomas
32
Where are the route of entry to the liver for bacterial access
- The portal vein
- Umbilical veins in neonates
- Hepatic artery (generalised bacteraemia)
- Ascending infection via the bile duct / system
- Parasitic migration
- Direct extension of infection from an adjacent tissue
33
Which agent causes necrobacillosis?
Fusobacterium necrophorum
34
Necrobacillosis affects which spp?
Ruminants: rumenitis-liver abscess syndrome
35
Hoe does rumenitis-liver abscess syndrome (necrobacillosis) occur?
- Carbohydrate-rich diet
- > ruminal acidosis
- > defects in ruminal mucosa
- > access of bacteria to blood vessels
- > portal vein
- > liver: multifocal necrosis, abscess formation
36
Describe the features of rumenitis-liver abscess syndrome (necrobacillosis)
- Coagulative necrosis > liquefies > abscess formation
- Capsular surface: raised white/creamy nodules
- Maybe incidental finding at abattoir (cattle), but will cause weight loss and decreased milk yield
37
Multifocal nodules of a similar size indicate?
Haematogenous spread (via the blood)
38
Which agent causes Tularaemia?
Francisella tularensis (ZOONOSIS)
39
What acts as the reservoir/vector of Tularaemia?
Ticks
40
Describe the pathogenesis of Tularaemia
- Inoculation site (skin lesions, tick bite, prey animals: intestine)
• localised infection and regional lymphadenitis -> bacteraemia, dissemination
41
Describe the pathological and gross appearance of Tularaemia
- Ulceration of lymph nodes (or Peyer`s patches with enteric infection)
- Necrotising lymphadenitis
- Hepatitis
- Splenitis
- Multifocal hepatic and splenic necrosis
42
What is the agent of Pseudotuberculosis?
Yersinia pseudotuberculosis (zoonosis)
43
Describe the pathogenesis of pseudotuberculosis
- Hares, rodents, ruminants, cats
- Primarily enteric infection -> invasion of mucosa and Peyer’s patches -> microabscesses in intestinal wall and mesenteric lymph nodes
- In immunosuppressed individuals: dissemination (liver, spleen kidneys)
- Invasion of intestinal mucosa via M cells (overlying GALT) > bacteraemia (often in immunosuppressed animals)
44
Describe the overall pathogenesis of Leptospirosis
- Penetration of mucous membranes / abraded skin -> replication in blood -> kidneys, liver, spleen, brain, eyes, genital tract
• Serum antibodies clear spirochaetes from organs, but: persistence in renal tubular epithelium can occur
45
Describe the pathogenesis of Leptospirosis in dogs
* Liver: dysfunction due to cell damage by leptospiral toxins (hepatocellular necrosis); development of chronic active hepatitis
* Kidneys: tubular necrosis (esp. L. grippotyphosa, L. canicola)
* Also: DIC, uveitis, abortion
46
Describe the gross effects of Leptospirosis in the kidneys, liver and lungs of a dog
- Kidneys: interstitial nephritis and tubular necrosis
- Liver: mottled appearance due to haemorrhage and necrosis
- Lung: multifocal haemorrhage (DIC)
47
What are the consequences of periportal inflammation and necrosis due to Leptospirosis?
- Intracanalicular bile plugs > jaundice
| - Intravascular haemolysis > jaundice > centrolobular necrosis (hypoxia)
48
How does leptospirosis cause jaundice?
* Due to intravascular haemolysis (some serovars) AND/OR bile stasis (bile plugs)
* Haemolysis leads to anaemia; centrolobular necrosis in liver secondary to ischaemia / hypoxia
49
Describe the histological liver lesions in a dog with Leptospirosis
```
• Loss of tight junctions between hepatocytes [loss of pressure between cells = hepatocyte dissociation]
- Signals regeneration of the liver
- Induction of mitosis
• Rounded cells
• Eosinophilic granular cytoplasm
• Dark shrunken basophilic nuclei
• Loss of cords/plates (dissociation)
• Multifocal haemorrhage, hepatocellular dissociation, mitoses and binucleated cells
```
50
Name the agent that causes Tyzzer's disease
Clostridium piliforme (zoonosis)
51
Which species are affected by Tyzzer's disease?
- Laboratory rodents, guinea pigs, foals, dogs, cats
| - Young or immunocompromised animals
52
Describe the pathogenesis of Tyzzer's disease
Contact with rodent (prey) faeces -> proliferation in intestinal epithelial cells (ulcerative, necrotising colitis and typhlitis) -> with immunosuppression (?): spread to liver -> necrosis
53
How are different organs grossly affected by Tyzzer's disease?
Colon - diffuse fibrino-necrotising colitis
| Liver - disseminated multifocal necrosis
54
Name 3 protozoal infections that cause parasitic hepatitis
- Toxoplasmosis [Toxoplasma gondii]
- Coccidiosis [Eimeria stiedai]
- Leishmaniasis [Leishmania infantum]
55
Describe the features of Toxoplasmosis
- Zoonosis
- Seen in numerous species
- Hepatitis with generalised infection
- Sheep, goat, swine: with uterine infection
- Tachyzoites in hepatocytes -> multifocal necrosis
56
Where does Coccidiosis replicate?
Bile duct epithelium -> induction of proliferation of the bile duct epithelium
57
Describe the features of Leishmaniasis
- Infection via biting insects
- With generalised, chronic infection
- Infection of macrophages -> replication -> rupture of cells, release -> infection of new cells (and biting flies)
58
How does Leishmaniasis affect the liver?
- Granulomatous hepatitis
| - Swollen, rounded liver with texture abnormality
59
Which spp cause metazoan infections of the liver?
Trematodes [liver flukes: Fasciola hepatica, Dicrocoelium dendriticum]
60
Describe the process of acute fascioliasis
* Due to larval migration (1 mm long flukes)
* Migration pathways cause haemorrhage and necrosis with eosinophils and granulomatous inflammation
* Granulomatous inflammation occurs with larval death (encystment of flukes which fail to reach the bile duct)
61
What are the 3 outcomes of acute fascioliasis in the liver
1) Healing - granulation tissue followed by residual scarring resulting in a diffuse fibrosis
2) Black disease (Clostridium novyi) - Spores are latent in macrophages (liver), need anaerobic areas to proliferate!
3) Chronic fascioliasis
62
Describe the histological appearance of acute fascioliasis
blood-filled tunnels Containing cellular debris, inflammatory cells (eosinophils) and larvae; the surrounding parenchyma undergoes coagulation necrosis.
Histiocytes and multinucleated giant cells remove debris
63
Describe the gross clinical features in a liver with acute fascioliasis
Multifocal haemorrhage and granulomatous hepatitis
64
What is the cause of chronic fascioliasis?
Mature flukes in bile ducts
65
Describe the lesions of chronic fascioliasis
Chronic hyperplastic cholangitis, peribiliary fibrosis + calcification (mechanical irritation, bile stasis, excretions)
• Fibrosis +/- mineralisation
• Granulomatous inflammation
66
What are the consequences of chronic fascioliasis?
Anaemia, hypoproteinaemia, chronic debilitation, death (sheep)
67
Describe the histology of chronic fascioliasis
Chronic hyperplastic cholangitis and peribiliary fibrosis (result of traumatic activities of the adult flukes)
68
Describe the pathophysiology of chronic fascioliasis
- Haematophagic activities of the flukes plus the traumatic irritation of the spines cause a hyperplastic cholangitis resulting in haemorrhage leading to anaemia
- Albumin loss from "leaky" intercellular junctions (protein-losing enteropathy) -> hypoproteinaemia with ascites and wasting
69
Chronic cholangitis/fascioliasis has what appearance?
'Pipe stream'
70
Which 2 cestode spp affect the lungs?
Echinococcus
| Cysticercus
71
Describe the pathophysiology of cestodes
- Egg > oncosphere migrates thorough intestinal mucosa > Blood > predilection site >larval stage >lymph > lung
- Hydatid cyst = one of larval stages (metacestode)
- Hydatid cyst: numerous brood capsules which bud off inner epithelium > fluid “hydatid sand”
- Clinical signs are rare; often incidental finding at abattoir
72
Name 2 nematodes that affect the liver
Ascaris suum
| Toxocara canis
73
What affect do Ascaris suum have on the liver?
“milk spot liver” (pig)
• Egg hatches in intestine > migrates to the liver (L2) > L3 > blood
• Milk spot = cloudy whitish spot <1cm diameter
• Fibrous repair
