Liver And Bliary System Pathology Flashcards

1
Q

What is cirrhosis

A

Cirrhosis develops in response to any chronic liver injury
◦ Ongoing inflammation causes fibrosis (lay down scar tissue)
◦ Associated with hepatocyte necrosis
◦ Resulting architectural changes (nodules - Hard fibrotic tissue - normal tissue poking out between rigid fibrotic bands)
These changes occur over the course of years
Non-reversible The end result is:
◦ Impairment of liver function
◦ Distortion of architecture leads to vascular changes (portal hypertension)

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2
Q

What can cause chrhossis

A

See slide

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3
Q

Describe teh changes in alacholoic liver disease

A

This can occur after exposure to alcohol
Three main mechanisms alcohol can affect the liver:
◦ Fatty change (weeks) – initially reversible
◦ Alcoholic Hepatitis (years) – initially reversible.- some inflammatory cells bc chronic insult
◦ Cirrhosis (years) – end stage; irreversible damage Thought to be partly due to build up of acetaldehyde?

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4
Q

Describe the Histology in alchcoolic liver diseases

A

SSS

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5
Q

What are the symptoms of alcoholic liver disease

A

Identified by the history
May be asymptomatic, or have general symptoms of liver disease
Fatty liver:
◦ Hepatomegaly
Alcoholic hepatitis:
◦ Rapid onset jaundice, tender hepatomegaly (RUQ pain)
◦ Symptoms of more severe disease e.g. nausea, oedema and ascites, splenomegaly
Aim to reduce alcohol intake

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6
Q

Give an overview of viral hepatitis

A

Chronic Hepatitis B or C Blood borne viruses Potential for chronic infection Also poses risk for hepatocellular carcinoma Remember: • Hep B has a vaccine but no cure
• May have symptoms during acute infection • Hep C has a cure but no vaccine
• Majority are asymptomatic during acute infection

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7
Q

What s Nafld

A

‘Non-!lcoholic Fatty Liver Disease’ (N!FLD)
Similar pathogenesis to Alcoholic Liver Disease
◦ (But without the alcohol!!) Accumulation of triglycerides and other lipids in hepatocytes Becoming more prevalent
◦ Obesity
◦ Diabetes
◦ Metabolic syndrome (dyslipidaemia) Reduce risk factors/lifestyle modification
Can be toxic and damaging to cell - abnormal metabolism to libidos

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8
Q

What is hereditary haemochromatosis

A

Hereditary haemochromatosis Abnormal iron metabolism
◦ Increased absorption of iron from the small intestine -> excess deposition
◦ Can affect liver and other organs
◦ Elevated serum iron and ferritin levels
◦ Abnormal LFTs
Damage bc too much - out of balance
Autosomal recessive
Management – venesection (Take of blood - larger amounts - patients come back repeatedly - this reduces amount of iron. Atm no other way around it. ), risk of developing hepatocellular carcinoma

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9
Q

What is Wilson’s disease

A

Wilson’s disease Abnormal copper metabolism
◦ Reduced secretion of copper from biliary system -> accumulation in tissues
◦ Can affect the liver and other organs
◦ Reduced serum copper and caeruloplasmin (which carries copper)
◦ Copper deposits on biopsy
- Kayser-fleischer ring is a sign. If not seen, then do a biopsy
Rare; autosomal recessive Management – chelating agents - get rid of copper , zinc, liver transplant
Copper accumulates in tissue

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10
Q

What are 2 types of autoimmune causes of cirrhosis

A

Autoimmune hepatitsi - attacking hepatocytes.

PBC and PsC.- attacking ducts

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11
Q

What is PSC

A

PRIMARY SCLEROSING CHOLANGITIS Fibrosis of intra- and extrahepatic bile ducts
Typically affects men Can be asymptomatic or present with pruritus, jaundice or cholangitis
Association with hepatobiliary malignancy and UC
Deranged LFTs (obstructive picture) and presence of antibodies (ANCA)

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12
Q

What is PBC

A

PRIMARY BILIARY CIRRHOSIS Destruction of intrahepatic bile ducts Typically affects women Can be asymptomatic or present with pruritus +/- jaundice
◦ May have other conditions e.g. RA Hepatomegaly in advanced disease Deranged LFTs (obstructive picture) and presence of antibodies (AMAs)

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13
Q

What are ther causes of liver disease

A

— A1 antitripsin deficiency (can be linked to emphysema)
— Glycogen storage
— budd chiari (problem of blood vessel of hepatic vein)

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14
Q

What are different deranged functions of the liver and the symptoms

A

Ss

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15
Q

Descrbe the portal system

A

Ss

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16
Q

Decsribe portal hypertension

A

Build up of blood in the portal venous system
◦ Fibrotic liver is not very expandable
◦ Compresses veins entering the liver from the portal venous system
Veins are no longer as distensible - a rom of obstruction - blood cant pass through easily - backlogs occur
◦ This causes increased hydrostatic pressure in the portal venous system; ascites - Increased amounts of fluid in the peritoneal cavity
When this happens:
◦ Blood can ‘shunt’ from the portal system to the systemic venous circulation
◦ This leads to distension of the veins at the site of anastomoses; varices
In normal liver - blood can g to either portal circ or systemic - no build up of reassure. In liver disease - build up of pressure more goes to sites. Anastamoses

17
Q

What are 3 important sites fo varices

A
  1. Oesophageal
    ◦ The distal portion of the oesophagus
    ◦ Can lead to mucosal varices
    ◦ If these rupture it can cause significant haematemesis - they are not designed to contain a lot of blood - just connections- can rupture - life threatening vomiting blood.
  2. Umbilical
    ◦ Ligamentum teres links the liver to th
    umbilicus
    ◦ Normally no blood flow - but can fill with blood in this
    ◦ Caput medusa
  3. Anorectal
    ◦ Between superior and middle & inferior rectal veins - enlargement
    ◦ Haemorrhoids
    ◦ Typically painless
18
Q

What is hepatorenal syndrome

A

This is the development of Acute Kidney Injury (AKI) in the presence of cirrhosis - liver disease comes first - causes AKI - reduced kidney function
Portal hypertension
Arterial vasodilation (splanchnic)
RAAS activated
Renal artery vasoconstriction (reduced blood flow to kidney)
Dilatation of splanchnic arteries - - pools in area - thinks there is reduced effective circulating system - raas activated - recused blood to kidney - reduced gfr

19
Q

What are gallstones

A

Gall bladder concentrated bile contents… can be pure cholesterol or a mix . Aggregate in gall bladder
Formed from bile contents:
◦ Cholesterol
◦ Bile pigments
◦ Phospholipids
Most are radiolucent (Most dont show up on X ray so US is used. Renal stones have high calcium content so they do show up )
◦ Comparison to renal calculi

20
Q

What are complications o f gallstones

A

Biliary colic, acute cholecystokinin, acute ascending cholangitis, ascending pancreatitis

21
Q

Wha is biliary colic pain

A

Biliary colic
Lasts for hours but it is a temporary obstruction . Fa content - release cck - contraction of GB - if stone is blocking exit - causes pain - temporary bc it can move away. Temporary blockage and releas e
◦ RUQ pain
◦ Temporary obstruction of a gallstone in the cystic duct or common bile duct (CBD)
◦ Seen on US
◦ Might have abnormal LFTs
◦ No features of inflammation
Management = analgesia, elective cholecystectomy (if it is cause a lot o pai etc)

22
Q

What is acute cholecystitis

A

◦ Initial presentation very similar to biliary colic
◦ Impaction of a stone in the cystic duct - stuck
◦ Inflammatory features
◦ Murphy’s sign - put had under where you think liver is. Ask to breathe in. Diaphragm pushes down which pushes liver down. If gall bladder touches tip of finger - patient will feel pain - will not be able to breathe in fully
◦ Seen on US – thick wall gallbladder
Management = initially conservative, then cholecystectomy

23
Q

What is acute ascending cholangitis

A

Acute (ascending) cholangitis
◦ Infection of the biliary tree
Gallstone stuck - infection behind stone bc of stairs and prevention of things moving
◦ Present with pain, features of inflammation, and jaundice
— ‘Charcot’s triad’
◦ Typically due to a CBD stone or other obstructive causes
Management = IV antibiotics, fluids, relieve obstruction

24
Q

Describe acute pancreatitis

A
◦ Acinar cell injury and necrosis 
◦ Evokes an inflammatory response
Presentation: Epigastric pain
◦ Radiates to back 
◦ Often associated with vomiting 
◦ Cullen’s & Grey Turner’s sign - Bruising in different areas. Cullen’s - umbilicus. Grey turner - flanks

◦ Release of pancreatic enzymes: amylase
◦ Rule out other causes - CT/MRI to identify any necrosis
◦ Management depends on severity
- Fluids
- Manage gallstones
- Organ support-