Case 10- imaging and microanatomy Flashcards

1
Q

Biliary colic

A

Pain- RUQ pain or epigastric pain. Pain is usually after eating and at night. It radiates to the back
Symptoms- Nausea and vomiting
Cause- Gallstones causing obstruction or passing through the cystic duct

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2
Q

Acute cholecystitis

A

Pain- RUQ pain or epigastric pain
Symptoms- nausea and vomiting. Increased white cell count. Local peritonism (inflammation of the peritoneum)
Cause- Impacted stone in the neck of the gallbladder or cystic duct causing inflammation and ischaemia. Inflammation of the gallbladder

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3
Q

Acute cholangitis

A

Pain- RUQ pain or epigastric pain
Symptoms- nausea and vomiting. Fever/rigors. Raised white blood cells, jaundice. Decreased blood pressure. Delirium
Cause- bacterial infection of the obstructed biliary tree

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4
Q

Pancreatitis

A

Pain- RUQ pain or epigastric pain, can radiate to the back
Symptoms- nausea and vomiting, fever, increased heart rate, increased serum amylase or lipase
Cause- Gallstones can obstruct the outflow of the pancreatic duct. Enzymes are released which digest the tissue

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5
Q

Diagnosing biliary colic

A

Ultrasound- look for calculi and assess size of the common bile duct

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6
Q

Diagnosing acute cholecystitis

A

Ultrasound- look for calculi, thickened gallbladder, surrounding fluid

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7
Q

Diagnosing acute cholangitis

A

Ultrasound- look for calculi in the CBD, biliary dilation and thickening. Used to assess secondary effects on the biliary tree
MRCP/ERCP- visualise the stone and remover it

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8
Q

Diagnosing pancreatitis

A

Blood tests- raised amylase and lipase
CT- can confirm diagnosis and show complications like pseudocysts or necrosis
Ultrasound- Calculi present

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9
Q

What test do you always perform when you are worried about the foregut

A

A liver function test

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10
Q

Pseudocyst

A

Occur after 4 weeks and are capsulated pancreatic fluid, they are not lined with epithelium so they are not a true cysts. The necrosis is due to inflammation, it forms walled of collections after a few weeks.

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11
Q

Magnetic resonance cholangiopancreatography (MRCP) Pro’s and cons

A

Pro’s- no ionising radiation, no contrast required, good soft tissue images
Con’s- contraindicated with metallic implants, claustrophobic

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12
Q

Endoscope retrograde cholangiopancreatography (ERCP)

A

You pass an endoscope into the duodenum, enter the ampulla of Vater. Inject contrast media into the CBD (common bile duct). You then take real time images of the biliary tree. You can also remove stones, stent the duct and take biopsies.
• Pro’s- diagnosis and intervention in one.
• Con’s- risk of pancreatitis, cholangitis, bleeding and perforation. Radiation risk. Contrast is needed.

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13
Q

Diagnosing Cirrhosis and risk factors

A

Risk factors- alcohol excess, viral hepatitis, autoimmune hepatitis, NASH (non-alcoholic fatty liver disease).
Imaging- ultrasound, elastography

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14
Q

Diagnosing Hepato cellular carcinoma (primary liver cancer)

A

Risk factors- chronic liver disease
Imaging- Ultrasound, blood tests to assess for AFP (Alpha fetoprotein). CT to assess for local and distant metastasis and spread of cancer

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15
Q

Diagnosing secondary liver cancer and cause

A

Risk factors- Cholorectal, gastric, pancreatic, breast, lung and eye cancer.
Imaging- Ultrasound, CT or MRI. Dependent on specific patient circumstances

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16
Q

Most common causes of secondary liver cancer

A

Colorectal, breast, lung and eye cancer

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17
Q

Elastography

A
A type of ultrasound that is used to assess for liver stiffness.
• <2.5-7 mild fibrosis
• 7-9.5 moderate fibrosis
• 9.5-12.5 severe fibrosis
• >12.5 cirrhosis
18
Q

How to divide the liver up

A

The Liver has 4 lobes, the lobes can be divided up into lobular structures. Within the lobules you have 4 different cell types

19
Q

Where is bile produced

A

Within the hepatocytes

20
Q

The capillaries within the liver

A

The Sinusoids

21
Q

How the portal triad travels through the liver

A

The portal triad divides into branches, but the three vessels stay together throughout the liver in bundles. These bundles will still be called portal triads.

22
Q

Roles of the hepatocytes

A
  • Protein synthesis
  • Protein storage
  • Transformation of carbohydrates
  • Synthesis of cholesterol, bile salts and phospholipids
  • Detoxification, modification, and excretion of exogenous and endogenous substances
  • Initiation of formation and secretion of bile
23
Q

What enters the hepatocytes

A
  • Hepatic artery- oxygen, nutrients and circulating drugs.

* Hepatic portal vein- food, drugs, toxins and recycled bile salt.

24
Q

What leaves the Hepatpcytes?

A
  • Hepatic vein- metabolites, glucose

* Bile- metabolites, bile salts

25
Q

Structure of the lobules

A

The lobules are separated with a border of connective tissue. At the different corners of the lobule you have the portal triad’s.

26
Q

How blood travels through the lobule

A

The blood from the portal vein and hepatic arteries travel in the sinusoids to enter the central vein. The sinusoids are between the hepatocytes. The central vein is in the centre of the lobule. They return the blood to circulation via the hepatic veins.

27
Q

Structures within the hepatic lobule

A

Portal triads, Sinusoids, Central vein, Hepatocytes (arranged as cords) and the Bile canaliculi.

28
Q

What is exchanged at the hepatocytes

A

They take the toxins and nutrients up and release metabolites and glucose

29
Q

How bile moves through the liver

A

Bile is produces from the hepatocytes drains into the bile canniculi and then into the bile ducts

30
Q

The 4 cell types in the lobule

A
  • Hepatocytes
  • Kupffer cells (Macrophages)
  • Stellate cells (Perisinusoidal/Ito)
  • Sinusoid endothelial cells.
31
Q

Hepatocyte structure

A

Linked by cell junctions in cell plates. They contain a cytoplasmic glycogen store which they can then break down and release as glucose. They have lots of endoplasmic reticulum for biosynthesis. The cell surface is in contact with bile canaliculi, so that the bile can drain directly into them.

32
Q

The space of Disse

A

The space between the Hepatocyte’s and endothelial cells

33
Q

Hepatic acinus

A

A different way to describe the structure of the liver. A more functional description

34
Q

Hepatic acinus structure

A

A combination of two hepatic lobules, there are two central veins which are surrounded by multiple portal triads. A line is drawn between the central veins. The acinus is the triangle between the 2 central veins and the closest portal triad

35
Q

Zones of the hepatic acinus

A

You draw rings around the central vein. The inner zone is closest to the central vein, then the middle zone and outer zone

36
Q

Hepatic acinus- the outer zone

A

High in oxygen from the hepatic artery. Contains the hepatocytes which perform Glycogen and protein synthesis. So, there will be high nutrients in the cell.

37
Q

Hepatic acinus- the middle zone

A

Transition between the function of the hepatocytes in the outer zone (metabolism) and inner zone (detoxification).

38
Q

Hepatic acinus- The inner zone

A

High levels of metabolic waste. Contains the hepatocytes which undergo oxygen detoxification. It is the most vulnerable to damage. Low levels of oxygen.

39
Q

Function of the space of disse

A

The gap between the sinusoid epithelium and hepatocytes. Allows movement of blood across it, it contains fibroblasts. There are gaps between the sinusoid epithelium (fenestrated epithelium) which allows the blood through into the space. Molecules can now be exchanged between the hepatocytes and the blood.

40
Q

Space of disse pathology

A

Fibroblast proliferation in disease can lead to portal hypertension as the sinusoid is narrowed.

41
Q

Liver fibrosis

A

When the hepatocytes are damaged the stellate cells are activated, there is also fibroblast proliferation. The stellate cells produce a scar matrix which further narrows the sinusoid.

42
Q

Cirrhosis- damage to the liver

A

You get liver fibrosis and the accumulation of lipids in the Liver. It is characterised by death and steatosis (lipid retention) of hepatocytes. Can be caused by alcohol, hepatitis and obstruction of the portal triad. Hepatocytes can regenerate but there is also destruction in the architecture of the connects of the hepatocytes. The is due to fibroblast proliferation and scar matrix formation. This will effect the sinusoids, blood vessels and bile ducts.