Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PATH FINAL > Histo: Liver > Flashcards

Histo: Liver Flashcards

1
Q

Describe the blood supply to the liver.

A

Dual blood supply: hepatic artery and hepatic portal vein

NOTE: this means that the liver does not tend to get affected by ischaemia

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

List the main cell types of the liver.

A
  • Hepatocytes
  • Bile ducts (cholangiocytes)
  • Endothelial cells
  • Kupffer cells
  • Stellate cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is the arrangement of endothelial cells in the liver different from other parts of the body?

A

The endothelial cells do not sit on a basement membrane and the endothelium is discontinuous (there are no tight junctions) - this arrangement is cruical for liver function.

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

What is the role of stellate cells and what could happen to them when activated?

A
  • Storage of vitamin A
  • When activated, they become myofibroblasts that lay down collagen (this is responsible for scarring in liver disease)

They are located in the space of disse (between endothelial cell (sinusoids) and hepatocytes.

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

outline the arrangement of structures within a normal liver.

A
  • There will be portal tracts (portal triad) consisting of a branch of the hepatic artery, a branch of the portal vein and a bile duct
  • Blood will flow from the portal tract to the central vein
  • Bile flows in opposite direction - through canaliculi into bile duct in portal triad.
  • There is a ring of collagen around the portal tract called the limiting plate
  • There are three zones of hepatocytes in between the portal tract and the central vein
  • Zone 1 (closest to portal triad) - periportal hepatocytes recieve more oxygen but affected first in viral heptatitis
  • Zone 3 is closest to the central vein (perivenular hepatocytes) and contains the most metabolically active enzymes hence more sensitive to toxins and ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the arrangement of hepatocytes, endothelial cells, stellate cells and Kupffer cells in a normal liver.

A
  • There are spaces in between endothelial cells and there is a gap in between the endothelial cells and the hepatocytes (space of Disse)
  • Stellate cells sit within the space of Disse
  • Kupffer cells are found within the sinusoids
  • Blood can easily get through the spaces in the endothelial cells in the space of Disse where they are exposed to hepatocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe how cells arrangements change in liver disease.

A
  • Kupffer cells become activated (inflammatory response)
  • Endothelial cells stick together so blood finds it more difficult to get into the space of Disse
  • Stellate cells become activated and secrete basement membrane-type collagens into the space of Disse
  • Hepatocytes lose their microvilli
  • All these changes make it difficult for blood to be exposed to hepatocytes and reduce the ‘filtering function of the liver’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the key features of cirrhosis?

A
  • The whole liver is involved
  • There is extensive fibrosis
  • nodules of regenerating hepatocytes (even in end stage liver disease liver is trying to regenerate)
  • Shunting occurs (disturbance of vascular architecture)

Definition = diffuse abnormality of liver architecture that inferferes with blood flow and liver function.

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

Explain why shunting occurs in Cirrhosis and Describe the two types of shunting that occur

A

Disruption of liver architecture (mostly due to fibrosis) increases resistance of blood flow through the liver. This results in portal hypertension. Blood from the portal vein must return to the systemic circulation - due to the increased resistance in the normal tracts it creates new abnormal connections.
These can be:

  • Extra-hepatic: blood never reaches the liver because it backlogs into sites of porto-systemic anastamosis causing them to swell up (e.g. oesophageal or anorectal varices)
  • Intra-hepatic: blood goes through the liver but it does not come into contact with hepatocytes (so the blood is unfiltered). This occurs when there is a fibrotic bridge between portal tract and central vein (extensive fibrosis connecting the two - blood moves through the fibrosis and does not even contact hepatocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can cirrhosis be described?

A
  • According to nodule size (old system):
    * micronodular (<3mm, uniform liver involvement)
    * macronodular (>3mm, variable nodule size)
  • According to aetiology: alcohol/insulin resistance or viral hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do these two classications of cirrhosis overlap?

A

Alcoholic tends to be micronodular

Viral tends to be macronodular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List some complications of cirrhosis.

A
  • Portal hypertension
  • Hepatic encephalopathy
  • Hepatocellular carcinoma

NOTE: cirrhosis may be reversible

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

What causes acute hepatitis?

A
  • Hepatitis virus (A and E)
  • Drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a common histological feature of all acute hepatitis?

A

Spotty necrosis (small foci of inflammation and infiltrates)

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

What are some causes of chronic hepatitis?

A
  • Viral hepatitis (B/D, C)
  • Drugs
  • Autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Differentiate between “stage” and “grade” in chronic hepatitis histology?

A
  • Severty of inflammation = grade (how bad does it look)
  • Severity of fibrosis = stage (how close is it to becoming cirrhosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the histology in chronic hepatitis

A

Inflammatory changes occuring in 3 places:
* Portal inflammation (lymphocytes in portal tract)
* Interface hepatitis (piecemeal hepatitis) - inflammation crosses limiting plate making it difficult to distinguish where protal tract ends and hepatocytes begin
* Lobular inflammation (widespread)

If inflammation is so severe that a bridge is formed from portal vein to central vein - it causes a intra-hepatic shunt and chronic hepatitis evolves into cirrhosis

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

What are the three histological stages of alcohol related liver disease?

A
  • Hepatic steatosis (Fatty liver)
  • Alcohol related hepatitis
  • Cirrhosis

NOTE: these may be sequential but may co-exist as they progress (they are not distinc entities)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Macroscopic & Microscopic characteristics of Hepatic Steatosis

A

Marcoscopic
* Large, pale, yellow greasy liver

Microscopic
* Accumulation of fat droplets in hepatocytes
* large white circles (fat) in histology - more in Zone 1
* Fully reversible if alcohol avoided

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

Macroscopic & Microscopic characteristics of Alcohol Related Hepatitis

A

Macroscopic
* Large, fibrotic liver

Microscopic
* Hepatocyte ballooning - cells swell and necrose due to accumulation of fat, water, protein
* Mallory Denk Bodies (clumped cytoskeleton)
* Pericellular fibrosis
* Predominant in Zone 3 - as these changes are caused by the metabolite of ethanol = acetylaldehyde (toxic metabolite) - metabolised by alcohol dehydrogenase

21
Q

Macroscopic & Microscopic characteristics of Alcohol Related Cirrhosis

A

Macroscopic
- yellow-tan fatty enlarged liver
- May then transform into shurnken non-fatty brown organ

Microscopic
- Micronodular cirrhosis - small nodules surrounded by bands of fibrosis

22
Q

Define Metabolic Associated Fatty Liver Disease and how to differentiate it from alcohol-related liver disaese

A

Hepatic steatosis in non-alcoholics - histologically looking very smiliar to alcohol-related hepatitis. It is commonly caused by insulin resistance. It includes Metabolic assocaited steatohepatitis (which can progress into cirrhosis)

Can be differentiated:
* Based on the history
* AST:ALT ratio <2 in MAFLD
* Risk factors: obesity, Diabetes mellitus, hyperlipidaemia

23
Q

List biliary causes of Cirrhosis

A

Primary Biliary Cholangitis
Primary Sclerosing Cholangitis

24
Q

What is primary biliary cholangitis?

A

Autoimmune conditions characterised by bile duct loss associated with chronic inflammation (with granulomas)

25
Q

What is the diagnostic test for PBC?

A
  • Anti-mitochondrial antibodies (AMA)

ALP, Cholesterol, IgM are raised

26
Q

What is the histological appearance of PBC?

A

Bile ducts surrounded by epithelioid macrophages, suggestive of chronic granulomatous destruction of bile ducts

27
Q

What is primary sclerosing cholangitis?

A
  • Autoimmune condition characterised by periductal bile duct fibrosis leading to loss of bile ducts

NOTE: in PBC, bile duct loss is caused by inflammation, whereas in PSC it is caused by fibrosis

NOTE: PSC is associated with ulcerative colitis and is associated with an increased risk of cholangiocarcinoma

28
Q

What is the diagnostic test for PSC?

A
  • Bile duct imaging - USS shows bile duct dilatation and ERCP showing fibrous stricutres (“bile duct beading”)
  • Raised p-ANCA

serum ALP raised

29
Q

What is the histological appearance of PSC?

A

Onion skinning fibrosis (concentric fibrosis - meaning fibroiss around the duct which looks like layers - hence onion skin)

30
Q

What is haemochromatosis?

A
  • Increased gut iron absorption resulting in excess iron - depositing in liver, heart, pancreas, joints causing parenchymal damage and fibrosis.
  • Autosomal recessive
  • mutation in HFe gene on chromosome 6

NOTE: women tend to present later because they have naturally lower iron levels

31
Q

Histological staining and findings in Haemochromatosis

A

Fe deposits in liver
Seen with Prussian blue stain (blue dots inside hepatocytes)

32
Q

Symptoms and Investigations in Haemochromatosis

A

Symptoms
Skin bronzing
Diabetes
Hepatomegaly with micronodular cirrhosis
Chronic pancreatitis
Myocarditis

Investigations
Increased Fe, Ferritin
Low TIBC

33
Q

What is haemosiderosis?

A

Type of iron overload characterised by the accumulation of iron in macrophages

Usually occurs as a result of receiving blood transfusions

Less severe than haemochromatosis as macrophages are better at handling iron.

34
Q

What is Wilson’s disease?

A

Characterised by an accumulation of copper due to the failure of excretion of copper by hepatocytes into the bile

Responsible gene (ATP7B) is found on Chr13
Autosomal recessive

35
Q

How does Wilson’s disease lead to movement disorders?

A

Accumulation of copper in the lentiform nucleus of the basal ganglie leads to movement disorders

36
Q

Symptoms of Wilson’s Disease

A

Liver disease: acute hepatitis, cirrhosis
Neuro disease: parkinsonism, psychosis, dementia

Kayser Felischer rings: copper deposits in cornea

37
Q

Histological staining and findings in Wilson’s Disease

A

Mallory bodies and fibrosis on microsocpy

Copper stains red with Rhodanine Stain

38
Q

Describe the levels of alpha-1 antitrypsin in the blood and liver in a patient with alpha-1 antitrypsin deficiency.

A
  • The mutation (autosomal recessive) means that the protein cannot fold properly and cannot exit hepatocytes
  • This leads to the alpha-1 antitrypsin forming globules within hepatocytes which causes damage leading to chronic hepatitis
  • An inability to exit the liver leads to a deficiency of alpha-1 antitrypsin elsewhere in the body which leads to an increased risk of emphysema
39
Q

Histological staining and findings in A1AT deficiency

A

Intracytoplasmic globules of A1AT which stain with Periodic acid Shiff (pink clumps)

40
Q

How is the severity of disease in autoimmune hepatitis different from viral hepatitis?

A
  • Autoimmune hepatitis is very active with lots of plasma cells
  • The degree of inflammation is usually worse than in viral hepatitis
41
Q

How is autoimmune hepatitis diagnosed?

A

Type 1
* Anti-smooth muscle antibodies (ASMA)
* Anti-nuclear Ig (ANA)

Type 2
* Anti-liver-kidney-microsomal Ig (Anti-LKM)
* seen mostly in children - less common in adults

42
Q

How is autoimmune hepatitis treated?

A

Steroids (responds very well)

43
Q

Why is the liver so susceptible to drug-related injury?

A

It is the main site of drug transformation

It is also where toxic drug metabolites are formed. Hence most damage in zone 3.

Drug-related liver injury = can be both acute or chronic hepatitis

May be dose dependent and

44
Q

List some causes of hepatic granulomas.

A
  • Specific: PBC, drugs
  • General: TB, sarcoidosis
45
Q

List the main types of benign liver tumour. State which is most common.

A
  • Liver cell (hepatic) adenoma
  • Bile duct adenoma
  • Haemangioma (MOST COMMON)
46
Q

What is the most common type of malignant liver tumour?

A

Secondary tumours
Liver is. large site for metastasis due to dual blood supply and especially portal circulation

47
Q

List some types of primary liver tumour.

A
  • Hepatocellular carcinoma (poor prognosis)
  • Hepatoblastoma (usually in infants/children as derives from primitive hepatic stem cells)
  • Cholangiocarcinoma (adenocarcinomas from bile ducts - can be intrahepatic or extrahepatic (gall bladder and biliary tree))
  • Haemangiosarcoma
48
Q

Tumour marker for HCC

A

Alpha-fetoprotein

49
Q

What are some risk factors for cholangiocarcinoma?

A
  • PSC
  • Worm infections
  • Cirrhosis

PATH FINAL (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions