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MRCS Part B > HPB > Flashcards

HPB Flashcards

1
Q

Describe the course and tributaries of the portal vein.

A

Formed by the confluence of the superior mesenteric and the splenic vein. It lies anterior to the IVC and posterior to the head of the pancreas and first part of duodenum.
Other tributaries include:
R&L gastric veins
Superior pancreaticoduodenal
Cystic vein
Peri-umbilical vein in the ligamentum teres

It ascends in the free edge of the lesser omentum posterior to the bile duct and hepatic artery
At the porta hepatis it divides into two and supplied the respective halves of the liver

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2
Q

Describe the ligaments of the liver.

A

The falciform ligament: attaches the anterior surface of the liver to the abdominal wall. It splits the anatomical lobes of the liver. The free border is the ligamentum teres (the remnant of the umbilical vein).

The R and L coronary ligaments attach the R and L lobes of the liver to the diaphragm. It starts from the falciform ligament and diverges at the superior aspect. It surrounds the bare area.

The R and L triangular ligaments are the edges of the coronary ligaments.

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3
Q

What is the relationship of the liver and the omentum?

A

The lesser omentum emerges from the porta hepatis to the lesser curve of the stomach. It consists of the hepatogastric ligament and the hepatoduodenal ligament.

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4
Q

Where are the hepatic recesses and what are their clinical signficance?

A

Subphrenic: between diaphragm and anterior liver.
Subhepatic: between inferior liver and the transverse colon
Morrisons pouch: potential space between visceral liver and R kidney. This is the deepest part of the peritoneal cavity when supine.

They are clinically significant as they are sites of fluid collection and therefore abscess sites in infection

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5
Q

How many lobes does the liver have?

A

8
Caudate (on posterior aspect between the IVC and the ligamentum venosum.
Quadate: anterior, latral to the falciform ligament.
2 and 3 are lateral,
5,6,7,8 are medial

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6
Q

What are the anatomical and functional lobes of the liver?

A

Anatomical: R and L divided by the falciform ligament.

Functional: R and L divided by an imaginary line between GB and IVC

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7
Q

What is the microscopic structure of the liver?

A

The hepatocytes are arranges into lobules which are hexagonal and are drained by a central vein. Peripherally they have portal triads with a sinusoid, portal vein and hepatic artery alongside lymphatics and branches of the vagus nerve.

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8
Q

What is the blood supply to the liver?

A

70% is via the portal vein (formed by the confluence of the SMV and splenic vein behind the neck of the pancreas)
30% is via the hepatic arteries (from the coeliac trunk).
30% of people have accessory hepatic arteries arising from the SMA and the L gastric.

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9
Q

Describe the venous drainage of the liver.

A

The L hepatic vein drains the functional left lobe (segments 2 and 3)
The middle hepatic vein drains segments 5 and 8 which drains into the R hepatic.
The R hepatic drains lobes 6 and 7.
The caudate drains directly into the IVC`
All hepatic veins drain into the IVC.

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10
Q

What is the porta hepatis?

A

This is a fissure extending across the posterior R lobe transmitting the common hepatic duct, common hepatic artery and the portal vein (+ lymphatics and nerves)

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11
Q

What is the nerve supply to the liver?

A

The hepatic plexus contains sympathetic nerves from the coeliac plexus and parasympathetic fibres from the Vagus nerve.
Both enter via the porta hepatis.
Glisson’s capsule is also innervated by the lower intercostal nerves.

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12
Q

Describe the lymphatic drainage of the liver.

A

Anterior: hepatic lymph nodes to coeliac nodes.
Posterior: phrenic and posterior mediastinal

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13
Q

What is the surface anatomy of the liver?

A

Draw a line between the 3 points:
Mid axillary line of the 10th costal cartilage on the Right, the 4th intercostal space in the midaxillary line on the right and the 5th intercostal space midclavicular line on the left

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14
Q

What are the functions of the liver?

A
  1. Protein and Ammonia metabolism (including albumin, globulin, fibrinogen, CRP, clotting factors, angiotensinogen)
  2. Vitamin metabolism (vitamin D)
  3. Carbohydrate metabolism (gluconeogenesis and glycogenolysis)
  4. Lipid metabolism
  5. Immune function.
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15
Q

How does liver failure affect clotting?

A

Almost all the clotting factors are synthesised by the liver.
Vitamin K is essential to the carboxylase enzyme that makes factors, 2,7,9,10 and protein C and S and therefore if no bile is produced vitamin K cannot be absorbed.

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16
Q

How does lipolysis occur in the liver?

A

Triglycerides form fatty acids and glycerol.
Fatty acids then bind to albumin to become soluble and transport to the liver. Glycerol enters the hepatocytes and undergoes the glycolysis pathway.
Fatty acids undergo beta-oxidation and enter the TCA cycle to form ATP.
Excess acetyl CoA from this process is converted into ketone bodies which can be used as energy.

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17
Q

What does liver failure cause?

A
  • Increased ammonia leading to Encephalopathy.
  • reduced clotting factors leading to bleeding
  • reduced CRP and acute phase proteins therefore immunosuppression
  • reduced lipid and carbohydrate metabolism leading to lactic acidosis and hypoglycaemia
  • reduced albumin leading to ascitis.
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18
Q

Describe the lifecycle of bilirubin.

A

Reticuloendothelial cells (macrophages responsible for the maintenance of blood) metabolise haem and globin. The iron from haem is recycled and the remaining substance is called bilividen.
Bilividen then becomes unconjugated bilirubin, this then conjugates with albumin and travels to the liver.
Once in the liver glucoronic acid is added via the enzyme gluconyl transferase to form conjugated bilirubin which is water soluble and therefore can be excreted in bile.
The bile is then excreted in bile and once in the colon bacteria deconjugate it to urobilinogen and stercobilin. Stercobilin is excreted in faeces and urobilinogen is reabsorbed into the enterohepatic circulation whilst some will be excreted as urobilin in urine

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19
Q

What is the purpose of the enterohepatic circulation?

A

This is where bile salts are reabsorbed in the terminal ileum and then pass via the portal system back to the liver where they can be reabsorbed.

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20
Q

What are the causes of jaundice?

A

Prehepatic:
Will have high unconjugated bilirubin, normal ALP, AST, PT and normal urine/stool.
Causes include:
- haemolytic anaemia (malaria and sickle cell crisis)
- Spherocytosis
- ABO incompatibility

Hepatic:
Will have high unconjugated or high conjugated bilirubin, high AST , high ALY, high PT (not correctable with VitK)
Caused by hepatocellular dysfunction including cirrhosis, hepatitis, toxins, TPN, haemochromatosis.

Post-hepatic:
Will have a high unconjugated bilirubin with normal ALT, high ALP, prolonged PT (correctable with VitK), often pale stools and dark urine.
Caused by bile duct obstruction.

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21
Q

What are the drug causes of Jaundice?

A

Hepatic Jaundice:
- paracetamol
- amiodarone
-diclofenac
-fluconazole
- heparin
- labetalol

Obstructive:
- co-amoxiclav
- flucloxacillin
- erythromycin
-cotrimoxazole

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22
Q

What are some causes of post-operative Jaundice?

A

Operative complications:
- retained CBD stone
-CBD injury

Anaesthetic complications:
- drug induced hepatitis
- hypotension causing liver ischaemia

Pre-existing conditions:
- decompensation of pre-existing liver failure

Other:
- haemolysis secondary to major transfusion
- TPN

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23
Q

What is the embryological structure that forms the portal vein, SMV and splenic vein?

A

The vitilline veins

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24
Q

Why do caput medussae form?

A

In adults a small lumen still persists in the ligamentum teres (remnant of the umbilical vein) therefore in portal HTN it can recannulate and forms a site of porto-systemic anastamosis and this causes the dilatation

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25
Q

What are the features of Chronic Liver Failure?

A

Clubbing
Leukonychia
Duputryens
Palmar erythema
Liver flap
Spider Naevi
Caput Medussa
Jaundice
Bruising
Splenomegaly
Ascitis
Gynaecomastia

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26
Q

Describe the Child-Pugh score.

A

This is a scoring system for liver failure.
It scores 5 items with 1-3 points, and the corresponding total score gives the stage.
A = score 5-6
B = score 7-9
C = score 10-15

Componants:
Bilirubin (<34, 34-50, >50)
INR (<1.7, 1.8-2.2, >2.2)
Albumin (<35, 28-35, <28)
Encephalopathy (none, drowsy or confused, major confusion or coma)
Ascitis (none, ascitis, resistant ascitis)

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27
Q

What would the below score on the Child Pugh Liver score:

Bilirubin 36
INR 2.0
Albumin 30
Mild confusion, mild ascitis

A

10

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28
Q

What would the below score on the Child Pugh Score:

Bilirubin 60
INR 2.1
Albumin 30
No confusion
Mild ascitis

A

10

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29
Q

What is the normal pressure of the portal vein?

A

3-5mmHg

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30
Q

What pressure do complications of Portal HTN start to occur?

A

> 10mmHg

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31
Q

What are some of the complications of portal hypertension?

A

splenomegaly
ascitis
hepatic failure
varices
hepatorenal syndrome

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32
Q

Where do varices occur?

A

They occur at areas of porto-systemic anastamosis:
- L gastric vein and azygous vein in distal oesophagus
- Superior with middle and inferior rectal veins
-umbilical vein and the epigastric vessels
- bare area of the liver and retroperitoneum

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33
Q

Explain the pathophysiology of hepatorenal syndrome.

A

High intrahepatic/ portal pressures lead to splanchnic vasodilation which leads to RAAS activation which leads to vasoconstriction of the kidneys.

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34
Q

What are some of the causes of Portal HTN?

A

Pre-sinusoidal:
- Thrombus
- schistomiosis
- sarcoid

Sinusoidal:
- cirrhosis

Post-sinusoidal:
- budd-chiari
- intrahepatic occlusion
- constrictive pericarditis

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35
Q

Give some examples of benign liver lesions.

A

Focal nodular hyperplasia
Adenoma
Haemangioma

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36
Q

What is a cyst?

A

A fluid filled epithelial lined sac

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37
Q

A patient presents with some mild abdominal pain reduced appetite. They have normal LFT and an USS liver which shows:
anechoic, well defined thin walled spherical lesion with strong posterior wall acoustic enhancement.
What is your top differential diagnosis?

A

Liver Cyst

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38
Q

How do you manage a simple liver cyst?

A

Conservative: if under 4cm then a follow up USS should be done to check growth for 2-3 years.

If symptomatic then USS guided drainage or surgical drainage

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39
Q

What are your differentials for liver cysts?

A
  • simple liver cyst
  • hyatid cyst
  • cystic adenoma
  • polycystic liver
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40
Q

What is a cystadenoma of the liver?

A

This is a pre-malignant lesion which develop as a result of abnormal biliary epithelial development.
Around 10% have malignant transformation.

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41
Q

How do you manage a suspected cystadenoma of the liver?

A

Due to the 10% chance of malignant transformation, they should be resected.
USS/CT are useful imaging modalities.
They should not be aspirated due to risk of tumour seeding and therefore lobe resection is the treatment of choice.

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42
Q

What causes a Hyatid Cyst?

A

Ecchinococcus Granulosa. Passed via the faeco-oral route

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43
Q

What are the features of a Hyatid cyst?

A

generally they are asymptomatic but may present with RUQ pain if there is an associated infection or rupture.

On imaging they will have calcified, spherical lesions with septations and may have daughter cysts.

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44
Q

How do you treat a hyatid cyst?

A

3 months of mebendazole
Surgery to deroof after at least 1 month of mebendazole

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45
Q

What are the common pathogens that cause liver infection?

A

E.coli
Klebsiella
Strep
Staph

In immunocompromised individuals then consider fungal infections.

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46
Q

What are the risk factors for developing a liver infection?

A

Diabetes, transplant, HPB disease, IBD and immunosuppression

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47
Q

What are the features of a liver infection?

A

Fevers, jaundice, TUQ pain, diarrhoea, raised ALP and raised WCC

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48
Q

How would you manage a liver infection?

A

Abx (Tazocin/ceftriaxone and metronidazole) for 6 weeks.
Percutaneous drainage
Surgical drainage

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49
Q

What causes an amoebic abscess?

A

Enteromoeba histolytica

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50
Q

What are the features of an amoebic abscess?

A

RUQ pain, fever, jaundice, weight loss, deranged LFT, USS with poorly defined lesion, recent travel history

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51
Q

How do you manage an amoebic abcess?

A

Metronidazole for 7-10 days and luminal agent to clear any bowel colonisation

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52
Q

What is focal nodular hyperplasia?

A

This is proliferation of the hepatocytes due to hyperperfusion.
It has no malignant potential.

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53
Q

What is an important differential to consider in focal nodular hyperplasia?

A

Fibrolamella HCC which may present similarly on imaging however it is very aggressive

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54
Q

What is hepatocellular adenoma?

A

This is monoclonal proliferation of the hepatocytes.

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55
Q

What is hepatocellular adenoma associated with?

A

More common in females, associated with the COCP, steroid use and obesity

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56
Q

What are factors that make hepatocellular adenoma at high risk of malignant transformation?

A

Being Male
>5cm
Beta-catenin mutation +ve

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57
Q

How do you manage hepatocellular adenoma?

A

Conservative: stop COCP, annual MRI and AFP measurements
If any concerns about malignancy then resect.

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58
Q

What is a liver haemangioma?

A

This is a benign lesion which grow very large and may present with obstructive symptoms

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59
Q

What is the classic MRI sign of a liver haemangioma?

A

The light bulb sign (arterial enhancement)

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60
Q

What are the risk factors for HCC?

A
  • Liver cirrhosis (normally HepB/C related)
  • Aflotoxin exposure (cottons and peanuts)
  • Hepatocellular adenoma
  • smoking
  • diabetes
  • haemochromatosis
  • alpha-1-antitrypsin deficiency
  • PBC
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61
Q

What is the histopathological findings in a HCC?

A

Microscopic: well vascularised lesion with wide trabeculae and prominant acinar pattern

Macroscopic: high cell density with trabeculae irregularity

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62
Q

What investigations would you perform if you were considering HCC?

A

AFP (typically will be over 400)
CT (hypodense lesion with arterial enhancement and washout in venous phase)
USS (heterogenous lesion however difficult to distinguish from cirrhosis)

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63
Q

Would you biopsy a HCC?

A

No due to risk of tumour seeding.

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64
Q

What is the Barcelona staging?

A

This is a staging score for Liver cancer:

0 = single tumour <2cm with normal LFT, child-pugh A and ECOG 0

1 = single tumour to 3 nodules <3cm. Child-pugh A/B, ECOG 0

2 = Multifocal (>3 lesions) or >3cm. Child-pugh A-C, ECOG 0

3 = Vascular invasion or lymph node positive or mets. Child-pugh A-C. ECOG 0

4 = end stage with Child Pugh C

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65
Q

What are the treatment options for HCC?

A

There are 3 curative options:
- Ablation
- Resection
- Transplant

Other options include: trans-arterial chemo-embolisation which may cause tumour necrosis but it is not possible if there is portal vein invasion or thrombosis. It has poor long term outcomes and therefore only using in a palliative setting.

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66
Q

What is the Milan Criteria?

A

This is a criteria that must be met to have a liver transplant:
- one lesion <5cm or up to 3 lesions <3cm
- No vascular infiltration
- No extrahepatic manifestations.

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67
Q

What is the prognosis after liver transplant for HCC?

A

60-75% 5 year survival.
10% post op mortality

68
Q

What are the most common primary cancers when liver mets are found?

A

Colorectal is the most common, followed by pancreas, breast and lung

69
Q

What are the poor prognostic factors when liver metastases are found?

A
  • bilobar disease
  • multiple mets
  • venous invasion
  • absence of pseudocapsule
  • extrahepatic disease
  • recurrance
70
Q

How do you manage liver metastases?

A

Systemic chemotherapy and resection
Ablation or transarterial chemo-embolisation should be considered.

71
Q

Describe the Grades of Liver trauma.

A

Grade 1 =
Subscapular haematoma <10%
Laceration/capsule tear <1cm in depth

Grade 2 =
Haematoma 10-50%
Laceration 1-3cm depth and <10cm length

Grade 3 =
Haematoma >50%
Laceration >3cm depth

Grade 4 =
Haematoma with parenchymal disruption involving 1-3 segments of >25% of a lobe

Grade 5 = parenchymal disruption of >3 segments of >75% of a lobe

72
Q

If a liver laceration is 5cm in depth, what grade is the liver injury?

A

Grade 3

73
Q

If in liver trauma there is a haematoma covering 60% what is the liver injury?

A

Grade 3

74
Q

If there is a laceration 0.4cm deep what grade is the liver injury?

A

Grade 1

75
Q

What are the parameters for a grade 2 liver injury?

A

Haematoma 10-50%
Laceration 1-3cm in depth or <10cm in length

76
Q

What are the parameters for a grade 1 liver injury?

A

Haematoma less than 10% and laceration less than 1cm in depth

77
Q

What are the key steps in surgical access to the liver?

A
  1. Mobilisation: divide the L and R triangular ligaments, coronary ligament and falciform ligament from the anterior abdo wall and diaphragm and mobilise off the IVC
  2. Inflow control: Pringles manouvre (should be released every 15 mins)
  3. Outflow control: reduce CVP and control hepatic veins
78
Q

What is pringles manouvre?

A

This is inserting a clamp through the foramen of Winslow to clamp the portal triad

79
Q

What is ascitis?

A

This is an accumulation of fluid in the peritoneal cavity

80
Q

How can you categorise ascitis?

A

Transudate vs Exudate

Transudate has a protein content of <30g/L or a Serum-ascitis-alumin-gradient or >1.1g/dL

Exudate has a protein content of >30g/L or a Serum-ascitis-albumin gradient or <1.1g/dL

81
Q

What are some causes of ascitis?

A

Transudates:
These are due to:
1. increased portal venous pressure:
- cirrhosis
- right sided CV failure
- constrictive pericarditis
- Budd chiari
- thoracic duct obstruction
2. decreased oncotic pressure i.e. low albumin
- liver failure
- protein losing enteropathy
- starvation
- renal failure

Exudate:
Generally due to inflammatory process leading to increased capillary permeability.
- peritonitis
- pancreatitis
- post-radiation
- peritoneal metastases

82
Q

What is starlings equation and why is it relevant to the liver?

A

Starlings equation illustrates the role of the hydrostatic and oncotic forces across the capillary membrane.
At the arterial end the hydrostatic pressure is greater than the oncotic pressure, so the fluid moves out but at the venous end the oncotic pressure is higher than the hydrostatic pressure and therefore the net movement is in.

If the hydrostatic pressure is increased or the oncotic pressure is reduced then there will be an imbalance and the net movement of fluid will be out.

83
Q

What is the function of the gallbladder?

A

The gallbladder is a store of bile.
It can store approximately 30-50l

84
Q

What is Hartman’s pouch in relation to the gallbladder?

A

This is a mucosal fold in the neck of the gallbladder which is a common location for gallstones to become lodged.W

85
Q

What is the arterial supply of the gallbladder?

A

The cystic artery (branch of the right hepatic)

86
Q

What is Calots triangle?

A

The borders are:
the inferior border of the liver, the cystic duct and the common hepatic duct.
It contains the cystic artery.

87
Q

What is the innervation to the gallbladder?

A

Receives parasympathtic innervation via the vagus nerve (stimulates contraction)
The main control however is hormonal via cholecystokinin

88
Q

Describe the anatomy of the biliary tree.

A

The right hepatic duct drains the lobes 5,6,7,8 and the left hepatic drains lobes 2,3,4.
These converge to form the common hepatic duct.
The cystic duct joins and it becomes the common bile duct. This has 3 parts: supra-duodenal, retro-duodenal and para-duodenal.
The pancreatic duct normally joins just before the CBD inserts into the 2nd part of the duodenum via the ampulla of Vater

89
Q

What is bile composed of?

A

Bilirubin (conjugated with glucoronic acid to become water soluble)
Cholesterol
Bile salts (cholic acid and choriodeoxychiolic acid which act to emulsify fats)
Inorganic salts (NaCl and bicarb) for neutralisation of gastric acid
Lethicin (increases the solubility of cholesterol)

90
Q

Explain the bile salt circulation.

A

Primary bile acids act to aid solubility of food and allow absorption in the jejunum.
Bacteria in the small bowel convert them to secondary bile salts.
80-90% are reabsorbed in the terminal ileum and the rest are excreted in faeces.

91
Q

What is the hormonal/neural control of the GB?

A

CCK - secreted in response to acid, calcium and fatty acids in the duodenum by I cells.
Causes GB contraction and relaxation of the Sphincter of Oddi.

Secretin - increases bile production and the bicarb/water content of bile.

Vagus nerve

Cephalic reflex: presence of food in the mouth causes relaxation of the sphincter of oddi.

92
Q

What is the pathogenesis of cholesterol gallstones?

A

Cholesterol is excreted in bile as the precursor for bile acids. It is not water soluble so it has to be aggregated with bile salts/ lethicin.
When concentrations are very high there is supersaturation and crystals form and due to hypersecretion of mucus these crystals aggregate together to form stones.

93
Q

What are the types of GS?

A

Cholesterol stones, pigmented stones, mixed stones.

94
Q

Which GS are radio-opaque?

A

Pigmented stones due to their calcium content.

95
Q

What are the risk factors for GS?

A

Fat, female, fertile, forty, family Hx, pregnancy, COCP, haemolytic anaemia, malabsorption

96
Q

What are the complications of gallstones?

A

Biliary colic
Cholecystitis
Cholangitis
Pancreatitis
Mirizzi syndrome
Empyema
Abscess
Gallstone ileus
Bouverets syndrome (GS in duodenum causing GO obstruction)

97
Q

What is charcots triad?

A

This is a triad of symptoms used to identify ascending cholangitis.
RUQ pain
Jaundice
Fever

98
Q

What is cholangitis?

A

Infection of the biliary tract due to a combination of biliary outflow obstruction and infection. During obstruction the stasis of fluid combined with the high luminal pressure leads to bacterial colonisation.
Common organisms are E.coli, Klebsiella and enterococci

99
Q

What are the indications for an ERCP?

A

Diagnostic
Theraputic: stone removal, stent insertion, sphincterotomy, stricture dilatation

100
Q

What are the complications of an ERCP?

A

Damage to teeth/gums
Pancreatitis/cholangitis
Perforation/peritonitis
Failure/ need for further procedure

101
Q

What is the typical histopathological subtype of cholangiocarcinoma?

A

Adenocarcinoma

102
Q

Where is the most common site of cholangiocarcinoma?

A

At the bifurcation of the R and L hepatic ducts. These are called Klatskin tumours. They may invade local structures including portal vein and hepatic arteries.

103
Q

What are the risk factors for cholangiocarcinoma?

A

Primary sclerosing cholangitis
Intraductal GS
Toxins
Cirrhosis
Congential (choledochal cysts)
Hepatitis/cholangitis

104
Q

What is primary sclerosing cholangitis and how would you manage it?

A

This is chronic fibrosis of the biliary tree affecting young adults.
It is associated with UC/HIV.
It has a 10-20% lifetime risk of Cancer
Management is steroids +/- liver transplant.

105
Q

What is courvosiers Law?

A

In the presence of jaundice and a palpable gallbladder, malignancy of the biliary tree/pancreatic head should be strongly suspected.

106
Q

How would you investigate and manage a cholangiocarcinoma?

A

MRCP is the gold standard imaging.
Staging CT TAP/ contrast MRI liver.

Management: resection and adjuvent chemo.
Palliative stenting and radiotherapy can be considered.

107
Q

What are the complications of a lap chole?

A
  • pain
  • bleeding
  • infection
  • scars
  • port site hernia
  • anaesthetic risks
  • DVT/PE
  • damage to bile duct /bile leak
  • damage to liver bed
  • damage to bowel
  • conversion to open
  • retained stone
108
Q

Why may patients complain of shoulder tip pain post lap chole?

A

This is due to retained CO2 irritating the diaphragm via the phrenic nerve which may cause referred pain.

109
Q

What are the anatomical relations to the pancreas?

A

The stomach
Duodenum
Transverse mesocolon
CBD (behind the 1st part)
Spleen (connected by the lineorenal ligament)
Aorta and IVC
SMA sits posterior to the neck, but anterior to the ucinate process.
SMV and splenic vein unite behind the neck to form the portal vein
The splenic artery sits on the superior border of the pancreas

110
Q

Describe the general structure of the pancreas and its relations.

A

Head: sits in the C shape of the duodenum

Neck: overlies the SMA and the SMV/Splenic confluence

Body: crosses the L renal vein, L crus, L psoas and the L adrenal and L renal hilum

Tail: This is the only intraperitoneal part, it sits within the lineorenal ligament.

Ucinate process: a projection away from the head extending medially, it lies posterior to the SMA.

111
Q

What is the duct of santorini?

A

This is a duct that drains the ucinate process directly into the duodenum via the minor duodenal papilla

112
Q

What is the function of the pancreas?

A

The exocrine pancreas acts as a serous gland producing digestive enzymes in the precursor form.

The endocrine produced insulin and glucagon.

113
Q

What is the arterial supply of the pancreas?

A

The Head/ucinate are supplied by the superior and inferior pancreaticoduodenal.
The superior is a branch of the gastroduodenal, which is a branch of the common hepatic, which is a branch of the coeliac trunk.
The inferior stems from the SMA.

The neck/body and tail are branches of the splenic artery.

114
Q

What is the venous drainage?

A

The venous drainage is via the SMV for the head, and the pancreatic veins into the splenic veins from the neck/body/tail

115
Q

Can you name an embyro-logical anatomical variant seen in the pancreas?

A

The annular pancreas. This occurs as during rotation of the two pancreatic buds in embryo it encircles the second part of the duodenum. It may present with obstructin.

116
Q

What stimulates the acinar cells in the pancreas to secrete the digestive enzymes?

A

CCK and Vagal stimulation

117
Q

Can you give some examples of the exocrine enzymes in the pancreatic secretions?

A

Trypsinogen, amylase, phospholipase, lethicin, NaCl, H20, chymotrypsinogen, K+ and bicarb

118
Q

What endocrine function does the pancreas have and what cells produce them?

A

The endocrine cells reside is the islets of Langerhan.

Beta cells - insulin
Alpha cells - glucagon
Delta cells - somatostatin
F cells - pancreatic polypeptide

119
Q

How does insulin act?

A

Insulin acts via tyrosine kinase to stimulate glucose uptake, inhibit lipolysis, ketogenesis and proteolysis

120
Q

What is the function of glucagon?

A

Stimulates gluconeogenesis and fatty acid oxidation

121
Q

What is the function of somatostatin?

A

Decreases digestion, decreases gastric motility, decreases gastric secretions and decreases the secretion of insulin and glucagon

122
Q

What is the pathophysiology of pancreatitis?

A

A rise in intracellular calcium causes the activation of protease/proteolytic enzymes. These then start autodigestion which damages the blood vessels and leads to ischaemia causing to further “leakage” of enzymes.

123
Q

Can you name some scoring systems for acute pancreatitis?

A

Glasgow Imrie
Apache II
Ranson

124
Q

What are the parameters for the Glasgow score in acute pancreatitis?

A

PO2 <8kpa
Albumin <32
Neutrophils >15
Calcium <2
Renal: Urea >16
Enzyme: LDH >600
Age >55
Sugar: glucose >10

A score of over 3 in the first 24 hours indicates a severe attack

125
Q

What are the causes of acute pancreatitis?

A

Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion
Hypercalcaemia, hypertriglyceridemia, hypothermia
ERCP
Drugs (NSAIDs, azathioprine, thiazide)

126
Q

What are some of the complications of acute pancreatitis?

A
  • Psuedocyst
  • Infected psuedocyst
  • Haemorrhagic pancreatitis
  • Infected Pancreatic Necrosis
  • Abscess
  • ARDS
  • Chronic pancreatitis
  • Multiorgan dysfunction
  • Ileus
127
Q

What is the definition of chronic pancreatitis?

A

This is inflammation and fibrosis causing irreversible damage affecting both the endo and exocrine tissue.
Often caused by alcohol, but may be secondary to cystic fibrosis, high calcium or autoimmune.

128
Q

What are the features of chronic pancreatitis?

A

Malnutrition
Pain
Diabetes
Erythema ab-igne

129
Q

How would you manage chronic pancreatitis?

A

Conservative: alcohol advice
Medical: analgesia, enzyme supplementation, antioxidants
Surgical: transplant

130
Q

What are the features of pancreatic cancer?

A

Weight loss, malaise, painless jaundice, steatorrhea, trosseaus sign (migratory thrombophlebitis)

131
Q

How would you manage pancreatic Ca?

A

Head of pancreas tumour= Whipples/PPPD with adjuvant chemo

Body/Tail = normally poor prognosis but could consider distal pancreatectomy

Palliative stenting or bypass, coeliac block or chemo/radiotherapy for symptom control

132
Q

Where does pancreatic Ca typically spread?

A

Lymphatics: coeliac axis to the paraduodenal/ lesser curve nodes

Direct: duodenum, stomach, retroperitoneum

Haematogenous: lungs and liver

133
Q

What are some of the neuroendocrine tumours of the pancreas?

A

Gastrinoma
Insulinoma
Somatostatinoma

134
Q

What are the signs of Gastrinoma?

A

These often present with peptic ulceration. They are typically found at the junction of the neck/body of the pancreas, or at the junction of the CBD and cystic duct.

135
Q

How would you diagnose a gastrinoma?

A

Fasting serum glucose and a triple phase CT

136
Q

What are gastrinoma associated with?

A

MEN 1 - zollinger ellison syndrome

137
Q

How would an insulinoma present?

A

These are normally solitary benign lesions. They present with hypoglycaemia and low glucose on fasting.

138
Q

How do somatostatinoma present?

A

Slow growing, malignant tumour.
Present with diabetes, gallstones, weight loss and steatorhoea

139
Q

What is ARDS?

A

This is an acute respiratory failure/lung injury with an onset within 1 week of apparent clinical insult with progression of respiratory symptoms. It is characterised by non-cardiogenic pulmonary oedema with infiltrates and alveolar collapse.

140
Q

What is the pathophysiology of ARDS?

A

High trypsin and phospholipase A2 leads to a loss of surfactant, atalectasis and irritation in the lungs.
The subsequent inflammatory response leads to increased endothelial permeability and therefore oedema.
The decreased surfactant causes alveolar collapse.
These lead to reduced O2 and respiratory failure.

141
Q

How would you manage ARDS?

A

Supportive therapy via ITU
Prone ventilation
Chest physio
PEEP

142
Q

What is the epiploic foramen?

A

This is the opening between the lesser and greater sac.

143
Q

What are the boundaries of the Epiploic foramen?

A

Anterior: portal triad in the free edge of the lesser omentum
Posterior: IVC
Inferior: 1st part of duodenum
Superior: caudate lobe

144
Q

What is the clinical significance of the epiploic foramen?

A

Pringles manoeuvre to control bleeding in liver trauma or cystic artery damage.

145
Q

Describe the main sites of portosystemic anastomoses in the body.

A

Lower oesophagus: L gastric (P) and azygous (S)
Rectum: Superior rectal (P) and middle/lower rectal (S)
Bare area of the liver: Liver (P) and veins of the diaphragm (S)
Umbilicus: Re-canalisation of the ligamentum teres (P) Inferior/superior epigastric (S)
Retroperitoneal: portal tributaries in the mesentery (P) and retroperitoneal veins (S).

146
Q

What is Grey-Turners sign an indication of?

A

This is bruising of the flanks. It may suggest a retroperitoneal bleed. It takes 24-48 hours to develop. Associated with pancreatitis (with haemorrhagic necrosis).

147
Q

What is the porta hepatis?

A

This is the deep fissure extending transversely across the under surface of the left portion of the right lobe of the liver. It transmits the following (anterior to posterior):
The common hepatic duct, hepatic artery, portal vein.

148
Q

Why does the appendix become gangrenous following inflammation, but the gallbladder does not?

A

The appendix is supplied by an end-artery. The gallbladder has the cystic artery but also has some supply from the liver bed which is adheres to.

149
Q

What is the most common area for gallstones in the biliary system and what effects do they cause?

A

Hartman’s pouch (in the gallbladder neck). They can cause, biliary colic, cholecystitis, gallstone ileus, obstructive jaundice, ascending cholangitis.

150
Q

What are some causes of ARDS?

A

– Infection (local or sepsis)
- aspiration
- Smoke inhalation
- Fat embolism
- Surgery
- Pancreatitis
- transfusion related lung injury
- Trauma
- Intubation
- DIC
- Bypass

151
Q

How can you tell if pulmonary oedema is cardiogenic or non-cardiogenic

A

pulmonary artery catheter should be inserted. A pulmonary wedge pressure of <16mmHg is a non-cardiogenic cause as the left atrial pressure is not elevated.

152
Q

What is the prognosis for patients with ARDS?

A

Poor with 50-60% mortality. ARDS secondary to sepsis has a mortality of up to 90%.

153
Q

Why does Grey-Turners sign occur?

A

It is secondary to the blood vessel damage from the digestive enzymes.

154
Q

Why might amylase be normal in acute pancreatitis?

A

Levels start to fall in the first 24-48 hours so the peak window may be missed in some cases

155
Q

Is there another enzyme that may be useful to test for in acute pancreatitis, other than amylase?

A

Lipase (more sensitive and specific)

156
Q

Are there any concerns you may have about giving morphine to a patient with acute pancreatitis.

A

Traditionally it has been thought that morphine may increase contraction of the sphincter of Oddi. However, morphine is currently widely used clinically

157
Q

What is the role of antibiotics in acute pancreatitis?

A

Routine use of antibiotics is not recommended in acute pancreatitis. They may be used if
evidence of superimposed infection or adverse features such as necrosis

158
Q

Why do you get hypocalcaemia in pancreatitis?

A

The digestion of fats leads to saponification of the calcium.

159
Q

What is the tumour marker for pancreatic cancer?

A

Ca 19:9

160
Q

What are the findings of acute pancreatitis on a CT?

A

Oedema, fat stranding, unidentifiable borders, abscess formation, cyst

161
Q

What is the difference between a true pancreatic cyst and a pseudocyst?

A

A pseudocyst does not have a defined epithelial membrane.

162
Q

How would you treat pancreatic pseudocysts?

A

Conservative: monitor, follow up scans (40% will resolve themselves)
Medical: analgesia, abx if infected
Surgical: if complications or >6cm, Cystogastrostomy/cystojejunostomy

163
Q

What are the complications of a pancreatic pseudocyst?

A

Infection
Abscess
Rupture: Peritonitis/ GI bleed/ fistula
Pressure affects: BO and obstructive jaundice
Pain

164
Q

What is hepatitis C?

A

This is a single stranded RNA virus.
It presents with acute or chronic liver failure.

165
Q

What is cirrhosis?

A

This is end stage liver damage due to dirsuption of the normal parenchyma of the liver by bands of fibrosis and regenerative nodules of hepatocytes.

166
Q

What are the clinical features of cirrhosis?

A

It causes liver failure:
Jaundice
Signs of portal HTN (caput medussae, , raised JVP, varices, ascitis, hepatorenal syndrome, splenomegaly)
Malnutrition
Duputryens
Hyperoestrogen - spider naevi, gynacomastia
Encephalopathy
Coagulopathy
HCC

MRCS Part B (14 decks)

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