Liver 1, 2 and 3 Flashcards

1
Q

What are the three common congenital defects of the liver?

A

Absence/supernumerary lobes

Intrahepatic congenital cysts-
cats, polycystic kidney syndrome- Persian cats

Congenital portosystemic vascular shunts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is an intrahepatic shunt and what causes it and what species?

What is an extrahepatic shunt and what species?

What doe they cause and how does the liver appear grossly?

What does it show histologically?

Why can it lead to cranial displacement of the stomach?

A

Intrahepatic shunt is caused by the persistence of the foetal ductus venosus which is the foetal connection between the left umbilical vein and caudal vena cava
-large breed dogs

Extrahepatic shunt- due to direct connections between the portal vein and vena cava
-Small breed dogs and cats

Large amount of blood bypasses the liver- causing a small liver

Histology- small hepatocytes, small/absent portal veins in triads, replications of arterioeles

Microheptatica- liver is small and therefore results in cranial displacement of the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can a liver be dislocated?

What can cause liver rupture?

What predisposes to liver rupture?

What does liver rupture lead to?

A

Diaphragmatic hernia
Torsion

Rupture-
RTA/ physical abuse- direct blunt truama
Usually when softer- alterations in parenchyma- (amyloid accumulation, neoplasms)

Ruptured liver- haemoperitoneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What circulatory disorders can affect the liver?

A

Passive hyperaemia- acute/chronic congestion

Acquired portosystemic shunts

Teleangiestasis

Peliosis hepatis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes acute congestion of the liver?

What causes chronic congestion of the liver?

What condition does chronic lead to?
How does it appear grossly and histologically?

Describe the pathogenesis of chronic liver congestion

A

Acute congestion- heart failure as the animal died

Chronic- congestive heart failure

Leads to nutmeg liver
Grossly- slightly nodularr and rough, ascites, fibrin
Histological- centrolobular necrosis, fibrosis around central vein

Pathogenesis- congestion > decreased oxygen supply > hypoxia/anoxia > necrosis > fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes acquired portosystemic shunts?

A

Due to chronic liver disease- extrahepatic shunts form

Hepatic fibrosis and/or cirrhosis-
development of portal hypertension
dilation of non-functional veins between portal vein and vena cava

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is telengiectasis?
What species are more affected?

What is peliosis hepatis?
What causes it and what species mainly affected?

A

Telangiectasias-
dilation of functional blood vessels
Liver- intense dilation of small groups of sinusoids- pathogenesis unclear
Mainly in cattle and cats

Peliosis hepatis-
Irregular blood-filled cystic spaces in the liver parenchyma
Due to focal necrosis
mainly in cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why do hepatocytes easily degenerate?

How do they appear with degeneration?

A

High metabolic rate- prone to alterations in oxygenation of blood

‘Cloudy swelling’ or hydrophobic degeneration
non-specific change, the influx of Na and water into the cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is atrophy a specific type of?

What is it?

What causes hepatocyte atrophy?

A

Atrophy is a specfic type of degeneration

Reduction is the size of cells

Due to:
pressure from internal organs
reduced blood supply- shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is hepatic lipidosis?

Describe the different pathogenesis?

What normally happens to fat in the liver?

A

Steatosis/lipidosis- abnormal accumulation of triglycerides with hepatocytes

Pathogenesis-

  • Nutritional
  • Excessive release of free fatty acids from adipose tissue
  • Hypoxic lipidosis
  • Toxic lipidosis

Normal-
free fatty acids from digestion to the liver into hepatocytes, free fatty acids esterified to triglycerides and form lipoproteins in circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What clinical scenarios predispose to lipidosis in a horse?

A
  • Enterocolitis
  • Feed restriction for treatment of colic
  • Obesity
  • Pregnancy
  • Lactation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What 5 specific conditions can cause hepatic lipidosis?

A

Hyperlipidaemia-
diabetes Mellitus, pancreatitis, hypothyroidism, hyperadrenocorticism
with high dietary fat intake
Equine hyperlipidaemia, feline idiopathic

Ketosis- with starvation, diabetes mellitus, pregnancy/lactation
increased demand for gluconeogenesis or impaired utilisation of glucose- breakdown of adipose

Hypoglycaemia and fatty liver syndrome in small dog breeds

Hyperadrenocorticism-
glucocorticoids
decrease in lipogenesis
increase in lipolysis of adipose tissue, catabolism of skeletal muscle proteun, gluconeogenesis in liver

Tension related- cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is glycogen?

What can cause an abnormal accumulation in the liver generally?
What specifically?

What stain can be used for diagnosis?

A

Glycogen- rapidly available energy store in cytoplasm or hepatocytes

Accumulation with abnormal glucose or glycogen metabolism

Specific-
Diabetes mellitus
Glycogen storage disease
Steroid induced hepatopathy- dogs (exogenous/iatrogenic, cushings)

PAS- periodic acid- Shiff- shows polysaccharides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is amyloid?

What causes amyloidosis?

What can cause secondary amyloidosis?

A

Amyloid is a pathological proteinaceous substance normally in between cells-
space of dissé and sinusoids

Usually AA- amyloid associates-
synthesised in hepatocytes derived from serum amyloid A (SAA) precursor
usually systemic- several organs

Secondary- reactive
Immunoglobulin complication of chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What different pigments can be stored abnormally in the liver?

A
  • Bile- jaundice
  • Lipofuscin ceroid- older animals
  • Melanin- sheep, cattle
  • Iron porphyrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is haemochromatosis of the liver?

What are the pathological findings?

What stain can be used for diagnosis?

A

Hepatic haemosiderin accumulation due to increased iron uptake
common in some birds

Pathological findings-
Hepatomegaly
Haemosiderin accumulation in hepatocytes, Kuppffer cells, lymph nodes, pancreas, spleen
Periportal bridging fibrosis and nodulat regeneratoin

Perls prussion blue stain shows iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the two causes of photosensitisation?

What can cause the two types?

A

Due to defective pigment synthesis-
endogenous pigment accumulation with defect in porphyrin metabolism
photodynamic agents- uroporphyrin, coprophyrin, protoporphryin
Bovine congenital erythropoietin porphyria- reddish-brown pigment deposition in dentin and bone and liver, skin leions develop because uropotphyrins absorb UV-A- reactive O2 speceis

Due to intoxications-
St John wort
Buckwheat
Spring parsely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What type of necrosis usually affects the liver?

How is hepatic necrosis classified?

How do they appear and what can cause them?

A

Usually coagulative necrosis- not liquefactive

Classified according to the location:

  • Focal- aggregates of necrotic hepatocytes ‘random’-
    disseminated infections
  • Zonal necrosis- a particular part of lobule/acinus- in the whole liver
  • Massive necrosis- necrosis of the entire lobe
    with extensive zonal or circulation, pigs with vit E/selenium, torsion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the three types of zonal necrosis?

Which is the most common

A

Centrolobar/periacinar necrosis-
Most frequent
hepatocytes most at risk of hypoxia, metabolically active (C-P450)

Mid-zonal
rare

Periportal necrosis
unusual, biliary inflammation, portal circulation
peri-portal necrosis- ascending inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the name for the disease caused by Vitamin E/Selenium deficiency in pigs?

What does it cause?

A

Hepatosis dietetica

Associated with
Massive necrosis
Oedema of the gall bladder
Mulberry heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the potential outcomes of liver necrosis?

A

Removal of dead hepatocytes

Resolution by

  • Regeneration of hepatocytes
  • Replacement of parenchyma by fibrous scar- due to destruction of reticular framework
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does fibrosis pattern depend on?- give examples

A

Depends on the distribution of injury

Periportal- biliary fibrosis

Centrilobular- periacinar fibrosis

Diffuse- bridging fibrosis

Post-necrotic scarring- massive necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

With diffuse necrosis and then bridging fibrosis of the liver, what are the different types?

A

Central- central- connects central veins with chronic congestion

Porto-portal- follows inflammation which extends to portal venules

Porto-central- after centrolobular necrosis

24
Q

What is liver cirrhosis?

What are the characteristic features?

A

Cirrhosis- end-stage liver disease

Characteristic
Degeneration- disruption of entire liver architecture
Regeneration- regenerative nodules of heptocytes
Repair- bridging fibrosis

25
Q

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?

A

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

26
Q

What is jaundice?

A

High billirubin in the blood causing yellow tinge of all tissues-
sclera, omentum, mesentery, fat, aorta

Seen only grossly and diffusely

27
Q

What is pre-hepatic jaundice?

What causes pre-hepatic jaundice?

A

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

28
Q

What causes hepatic jaundice?

A

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

29
Q

What is post-hepatic jaundice?

What causes it?

Describe haemoglobin breakdown?

What are the components of bile?

A

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

30
Q

What is associated with disturbances of liver function?

A

Jaundice

Hypoalbuminaemia- reduced synthesis and secretion of albumin

Coagulopathy- reduced synthesis of clotting factors

Hyperammoniameia- reduced detoxification by conversion to urea

Portal hypertension- cities

31
Q

What is hepatic encephalopathy?

What causes it?

What lesions does it lead to?

A

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

32
Q

What is nodular hyperplasia?

What are regenerative nodules?

A

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

33
Q

Describe the characteristics of hepatocellular adenoma?

A

Usually single

Sharply delineated

No portal areas/lobular structure

Compression of adjacent tissue

Benign- size main issue

34
Q

Describe the characteristics of hepatocellular carcinoma

What can cause it?

A

Compression and invasion of adjacent tissue

Metastasis

Growth pattern-
Trabelular
Acinar
Solid

Viral aetiology- hepatitis B in humans

35
Q

What neoplasms can affect the bile ducts?

How do they function?

A

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

36
Q

What can cause liver haemangiosarcomas?

A

Liver as the primary site

or metastasis

Secondary neoplasms common- portal vein, contact- often lymphomas

37
Q

What does acute hepatitis cause?

What happens in acute hepatitis due to septicaemia?

A

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

38
Q

What happens with chronic hepatitis?

What species and breed is affected by chronic active hepatitis?
What does it cause and what is the end stage?

A

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

39
Q

What is cholangitis/cholangiohepatitis?

What is feline cholangitis associated with?
What are the clinical findings?
What are the three characteristic lesions?

A

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

40
Q

What 6 viruses cause viral hepatitis?

A

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

41
Q
A
42
Q

What causes infectious canine hepatitis?

Describe the pathogenesis?

What happens to the liver with high titre and low titre?

How does it appear histologically?

A

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

43
Q

What herpes virus can cause viral hepatitis?

Describe the pathogenesis?

How does it grossly appear?

How does it histologically appear?

A

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

44
Q

How does the canine herpes virus transmit and affect adults, neonates and foetuses?

A

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

45
Q

What agent causes rabbit haemorrhagic disease?

What causes feline infectious peritonitis?

What is the pathogenesis?

A

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

46
Q

What are the routes of entry for liver abscesses or granulomas?

A

Portal vein

Umbilical arteries

Hepatic arteries

Ascending infection via the bile duct systeem

Parasitic migration

Direct extension of infection from adjacent tissue

47
Q

Name the 6 bacteria that can cause liver abscessed and granulomas?

A

Enteric bacteria

Francisella tularensis

Nocardia asteroides

Actinobacillus spp

Mycobacterium

Fusobacterium necrophorum

48
Q

What agent causes necrobacillosis?

What conditions does it cause in ruminants’ livers and why?

A

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

49
Q

What agent causes tularemia?

What are the reservoirs for the agent?

What is the pathogenesis?

What does it cause grossly?

A

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

50
Q

What kind of bacteria is leptospirosis?

What species can it infect?

Describe the pathogenesis and gross lesions on the liver

A

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

51
Q

What agent causes Tyzzer’s disease?

What animals are more commonly affected?

What is the pathogenesis?

A

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

52
Q

What can cause parasitic hepatitis?

A

Protoxoan- toxoplasmosis, coccidiosis, leishmanias

Metazoan infections- trematodes, cestodes, nematodes

53
Q

Where are toxoplasmosis tachyzoites found?

Where does Eimeria stiedia (coccidiosis) replicate in hare/rabbit?

How do animals get infected with leishmaniasis?
What does it cause and infect?

A

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

54
Q

What is acute fascioliasis?
What are the potential outcomes?

What is chronic fascioliasis?
What lesions occur?
What are the possible consequences?

A

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

55
Q

What metazoan/cestodes cause parasitic hepatitis?

A

Hepatophilic-
cystic echinococcosis- echinococcus granulosus
Alveolar echinococcosis- E. multilocularis
Cysticerus cellulosae- C. bovis

Serophillic-
C. tenuicollis, C. pisiformis

56
Q

Why do nematodes cause parasitic hepatitis?

What causes milk spot liver in pigs?

How does it appear histologically?

A

Traumatic lesions due to migrating larvae

Ascaris sum- milk spot liver