Session 7 - Liver, Biliary tree and pancreas 2

Question 1

What defences does the GI have against MOs?

Answer 1

1) saliva
2) Gastric acid
3) Colonic mucus
4) Enzymatic secretions
5) Anaerobic environment
6) Peristalsis - moves gut and prevents bacterial attachment

Question 2

Explain how the liver handles toxins

Answer 2

Absorption of toxins from the GI tract:

1) Toxins absorbed by villi in the GI tract
2) Taken via the hepatic portal system.
3) Kupffer cells in the liver can extract toxins form the blood and put it into the bile and secrete into the bile duct.

Question 3

What blood proteins does the liver syntehsis?

Answer 3

Albumin and clotting factors

Question 4

What components would be elevated in cholestasis? What is cholestasis?

Answer 4

Bilirubin and alkaline phosphatase

Bile cant flow from liver to duodenum

Question 5

How would you assess poor synthetic function of the liver?

Answer 5

Lack of serum album and high prothrombin time (due to clotting factors)

Question 6

How would you assess hepatic damage?

Answer 6

Aminotransferases ALT / AST.

Y-glutamyl transpeptidase, y-GT

Question 7

Name the 3 ways in which jaundice can be caused.

Answer 7

• Prehepatic (haemolytic)
• Hepatic (parenchymal)
• Post hepatic (cholestatic)

Question 8

Explain how excessive haemolysis can cause jaundice. What lab findings would there be? What would cause it?

Answer 8

Excessive haemolysis results in build up of bilirubin and liver cannot cope with the all the bilirubin.

Lab findings:

o Unconjugated hyperbilirubinemia

o Increase in LDH

o Decrease in haptoglobin – binds free Hb in blood and prevents its oxidative action Indicative of anaemia due to excessive haemolysis

Causes:

o Inherited – Red cell membrane defects, haemoglobin abnormalities, metabolic defects

o Congenital hyperbilirubinaemias – Gilbert’s syndrome, Crigler-Najjar syndrome, Dublin-Johnson syndrome

o Acquired – Immune, mechanical, acquired membrane defects, infections, drugs, burns.

Question 9

What causes hepatic jaundice? What lab findings would there be?

Answer 9

Deranged hepatocyte function

Lab findings:

o Mix of conjugated and unconjugated hyperbilirubinaemia

o Increase in liver enzymes ALT and AST (reflect liver damage)

o Increase or same alkaline phosphatase (ALP) due to cholestasis o Abnormal clotting

Cause:

o Congenital – Gilbert’s syndrome

o Hepatic – Hep A, EBV, Alcohol

o Drugs – paracetamol

o Cirrhosis – Alcohol

o Hepatic tumours – Metastases

Question 10

What is cholestatic jaundice? What causes cholestatic jaundice? What lab findings would there be?

Answer 10

Obstruction of biliary system – intrahepatic or extrahepatic

Results in passage of conjugated bilirubin being blocked

Lab findings:

o Bilirubin in urine (dark)

o No urobilinogen in urine (no bilirubin enters bowel)

o Same or increase in liver enzymes (mild hepatocyte damage due to build up of pressure)

Causes:

o Intrahepatic – hepatitis, drugs, cirrhosis

o Extrahepatic – Gallstones, carcinoma, pancreatitis

Question 11

Describe the key progressions of alcoholic liver disease pathology

Answer 11

• Fatty change
• Alcoholic hepatitis
• Cirrhosis – results in increased resistance to blood flow and deranged liver function. Leads to portal hypertension

Question 12

Explain the associated pathologies of portal hypertension

Answer 12

1) All blood from the gut goes through the portal vein and into the liver
2) However, in portal hypertension it cannot due to the high resistance. Therefore, the build up of the pressure results in blood from the portal system entering the systemic circulation, therefore toxins enter the blood.
3) Anastomoses also aren’t made for lots of blood to go through; e.g. oesophageal anastomoses bleed heavily, haemorrhoids from anastomoses in the rectum, opening of the ligamentum teres leading to caput medusa, opening of anastomoses in the liver bypassing it.

Question 13

What are the clinical manifestations of portal hypertension?

Answer 13

• Splenomegaly
• Ascites
• Caput medusae
• Oesophageal/rectal varices –> haemorrhage

Question 14

Describe hepatic encephalopathy and why it occurs

Answer 14

• This is a reversible neuropsychiatric deficit
• The liver is unable to remove ammonia from the blood due to liver damage
• Results in build up of ammonia in blood which manifests as:

o Flapping tremor

o Personality changes

o Intellectual deterioration

Question 15

Give 3 causes of gallstones

Answer 15

• Obstruction
• Infection
• Inflammation
• Neoplasia

Question 16

What are the possible consequences of gall stones on: a) the gall bladder b) the pancreas c) the liver

Answer 16

a) Biliary colic, cholecystitis, perforation
b) acute pancreatitis
c) obstructive jaundice

Question 17

Give 4 possible causes of acute pancreatitis.

Answer 17

G - gall stones

E - ethanol

T - trauma

S - steroids

M - mumps

A - autoimmune

S - scorpion bite

H - hyperlipidaemia

E - ERCP

D - Drugs

Question 18

What are the acute and chronic consequences of pancreatitis?

Answer 18

• Acute – oedema, haemorrhage, necrosis
• Chronic – fibrosis, calcification

Question 19

What would lab analysis find in pancreatitis?

Answer 19

• Increase in pancreatic amylase
• Decrease in calcium
• Increase in ALP
• Increase in glycaemia

Question 20

What clinical symptoms would occur in acute pancreatitis?

Answer 20

• Severe pain
• Vomiting
• Dehydration
• Shock

Question 21

What clinical symptoms would occur in chronic pancreatitis?

Answer 21

• Pain
• Malabsorption – steatorrhea, decrease in albumin, weight loss
• Jaundice

Question 22

What are the clinical features of pancreatic carcinoma?

Answer 22

• Symptomless for a long time
• Obstructive jaundice – palpable gallbladder
• Pain
• Vomiting
• Carcinomatosis
• Malabsorption
• Diabetes