Liver/Pancreas/Gallbladder Flashcards

1
Q

What is the role of the pancreas?

A

Production of enzymes that digest carbohydrates, proteins and fats

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2
Q

Name some exocrine and endocrine pancreatic secretions

A

Exocrine - trypsin, amylase

Endocrine - insulin (from beta islet cells)

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3
Q

What are the symptoms of acute pancreatitis?

A

Gradual or sudden severe epigastric or central abdominal pain

Radiates to the back, relieved sitting forward

Vomiting

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4
Q

What are the signs of acute pancreatitis?

A

Tachycardia, fever, jaundice, shock, ileus

Cullens and Grey Turners signs (periumbilical and flank bruising - from blood vessel autodigestion)

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5
Q

What causes acute pancreatitis? (GET SMASHED)

A

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpion venom
Hyper-lipidemia/calcemia
ERCP/emboli
Drugs

ALSO pregnancy and neoplasm

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6
Q

What are the key markers that are raised in acute pancreatitis?

A

Serum amylase (not raised in chronic), CRP, calcium (low),

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7
Q

How is acute pancreatitis managed?

A

IV fluids and analgesia (pethidine, morphine)

Treat gallstones with ERCP

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8
Q

What causes chronic pancreatitis? (GAAS)

A

Genetic (PRSS1 and SPINK-1)
Alcohol
Autoimmune
Smoking

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9
Q

How is chronic pancreatitis diagnosed?

A

Pancreatic calcifications on USS and CT

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10
Q

What treatment is given to those with chronic pancreatitis?

A

Artificial pancreatic enzymes (creon)

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11
Q

What is the pathology behind pancreatic cancer?

A

Mostly ductal adenocarcinoma (metastasise early, present late) - 60% in the head

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12
Q

What are the complications of acute and chronic pancreatitis?

A

Acute - SIRS, organ dysfunction, pancreatic necrosis, pseudocyst, haemorrhage, abscess
Chronic - chronic pain, DM, malabsorption, biliary obstruction, pancreatic cancer

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13
Q

What are the symptoms of pancreatic cancer?

A

Head - painless obstructive jaundice (2WW)

Body and tail - epigastric pain, radiating to back (late symptom)

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14
Q

What tumour marker is raised in pancreatic cancer?

A

Ca19-9

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15
Q

What would imaging show of pancreatic cancer?

A

USS/CT - pancreatic mass, dilated biliary tree and hepatic metastases
EUS - staging
ERCP - biliary tree anatomy and site of obstruction

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16
Q

What is the treatment for pancreatic cancer?

A

Surgery - Whipples pancreatoduodenectomy (if no mets), or laparoscopic excision
Chemotherapy - not curative
Palliative

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17
Q

What is the prognosis of pancreatic cancer?

A

Mean survival <6 months, 5 year survival: 3%

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18
Q

What genetic mutation is found in 95% of patients with pancreatic cancer?

A

KRAS2 gene mutation

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19
Q

What is the role of the gallbladder?

A

Storage of bile

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20
Q

What is the role of the biliary tree?

A

Hepatic duct transports bile to the gallbladder and common bile duct.
Common bile duct transports bile to the duodenum

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21
Q

What is the role of bile?

A

Bile is an alkaline substance containing cholesterol, bile pigments and phospholipids, that helps digestion of fats

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22
Q

What are the different types of gallstones?

A

Pigment stones - small, friable and irregular, from haemolysis

Cholesterol stones - large, from age and obesity

Mixed stones - faceted

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23
Q

What is biliary colic?

A

Right upper quadrant pain that comes and goes (with the stones obstructing the cystic duct or CBD)

NB - gallstones are only symptomatic if they block a duct

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24
Q

How is biliary colic managed?

A

Analgesia

Elective laparoscopic cholecystectomy

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25
Q

What are the complications of gallstones in:

a) the gallbladder?
b) the bile ducts?
c) the gut?

A

a) biliary colic, cholecystitis, mirizzis syndrome (impacted at gallbladder neck)
b) cholangitis, pancreatitis, obstructive jaundice
c) gallstone ileus

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26
Q

What is acute cholecystitis and how is it managed?

A

Inflammation and fever, usually in response to cholesterol stone impaction in the neck of the gallbladder

Treat with cefuroxime or perform laparoscopic cholecystectomy

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27
Q

What sign is positive in cholecystitis?

A

Murphys - pain caused why you lay 2 fingers over the RUQ and ask patient to breathe in

28
Q

What is chronic cholecystitis?

A

Chronic inflammation and colic, causing flatulent dyspepsia

Treat with MRCP/ERCP/cholecystectomy

29
Q

How would cholecystitis appear on USS?

A

Thickened, shrunken gallbladder
Presence of stones
Dilated CBD (>6mm)

30
Q

What is cholangitis?

A

Infection of the biliary tree, causing RUQ pain, jaundice and fever (charcot’s triad)
It is usually caused by bacteria ascending from the junction with the duodenum

31
Q

How is cholangitis treated?

A

Cefurozime and metronidazole

32
Q

What are the perpiheral signs of chronic liver disease?

A
  • Jaundice, scratch marks, bruising, spider naevi (>5), palmar erythema, leukonychia, clubbing, duptyruns
  • Ascites, splenomegaly
  • Encephalopathy and confusion
  • Caput medusa (distended epigastric veins)
  • Gynaecomastia (from oestrogen excess)
  • Oedema and hair loss on legs
  • Hepatic flap
33
Q

What is the role of hepatocytes?

A

Fat, protein and carbohydrate metabolism

34
Q

What is the role of Kupffer cells?

A

Inflammation

35
Q

What is the role of stellate cells?

A

Fibrosis

36
Q

How does cirrhosis form from chronic hepatitis?

A
  • Fibrotic tissue disrupts hepatic architecture, causing portal hypertension
  • This HTN and disorganised, nodular regeneration causes deregulated hepatocyte function
  • This leads to:
    1. Reduced clearance of waste products
    2. Reduced synthetic capacity
    3. Portal hypertension
    4. Risk of hepatoma
    5. Hypovolaemia due to poor salt and water handling
    6. Failure of sex hormone metabolism
37
Q

What causes cirrhosis?

A
  • Alcoholic liver disease
  • Non alcoholic fatty liver disease
  • Viral hepatitis (B,C)
  • Genetic causes
  • Autoimmune
  • Drugs
  • Idiopathic
38
Q

What are the genetics causes of cirrhosis?

A

Haemochromatosis (iron overload C282Y, H63D treat with venesection)
Wilson’s disease (copper poisoning)
Alpha a1 trypsin deficiency (serpinopathy/deficiency of inflammatory markers - common in children, comorbid respiratory)

39
Q

What are the autoimmune causes of cirrhosis, and how are these managed?

A

Primary sclerosing cholangitis
Primary biliary cirrhosis
Autoimmune hepatitis

Manage with immunosuppresants

40
Q

What happens in primary biliary cirrhosis?

A

Chronic autoimmune granulomatous inflammation damages the bile ducts, causing cholestasis, fibrosis and cirrhosis

Causes jaundice, lethargy, pruritus and hepatosplenomegaly

41
Q

What happens in primary sclerosing cholangitis?

A

Progressive cholestasis with bile duct inflammation and strictures

Causes pruritus, fatigue, and ascending colangitis

42
Q

What happens in autoimmune hepatitis?

A

Autoantibodies form against hepatocyte surface antigens

Causes fever, malaise, urticaria, polyarthritis and cirrhosis in young women

43
Q

What drugs causes cirrhosis?

A

Methotrexate, amoidarone, methyldopa

44
Q

Which LFTs are raised in cirrhosis?

A

Bilirubin, GGT, ALT and AST

45
Q

What would cirrhosis look like on imaging?

A

USS - could be either small or big hepatomegaly, splenomegaly, focal liver lesions

MRI - large caudate lobe with small islands of regenerating nodules

46
Q

What can cause liver decompensation and what are the features?

A

Spontaneous bacterial peritonitis, variceal bleeding, metabolic causes, malignancy or drugs can cause an acute deterioration in liver function.

It will present as:

  • Jaundice
  • Ascites
  • Encephalopathy

NEED TO ACT FAST TO PREVENT LIVER FAILURE, HEPATORENAL SYNDROME AND DEATH

47
Q

What is the Childs-Pugh scoring system?

A

A method of grading variceal bleeding and cirrhosis
<6 - compensated
7-9 - significant compromise
>10 - decompensated

Takes into account encephalopathy, ascites, bilirubin, albumin and prothrombin time

48
Q

How are the following drugs used in cirrhosis:

a) colestyramine?
b) ursodeoxycholic acid?
c) penicillamine?
d) spironolactone?

A

a) pruritus (itching)
b) hepatitis induced cirrhosis
c) Wilsons disease
d) ascites

49
Q

What is alcoholic liver disease, and what would LFTs show?

A

A term encompassing fatty liver (reversible), alcoholic hepatitis, and cirrhosis related to alcohol.

LFTs would show abnormally high AST, typically gives obstructive picture

50
Q

What is non alcoholic liver disease, and what would LFTs show?

A

A term encompassing:

  • Non alcoholic fatty liver disease
  • Non alcoholic steatohepatitis

These are usually caused by a metabolic syndrome and NAFLD may progress to NASH
LFTs would show mild raises in AST/ALT/GGT

51
Q

How are these with chronic liver disease followed up?

A

6 monthly USS and AFP(tumour marker) to check for carcinoma

Gastroscopy every 2 years to check for varices

52
Q

What is unconjugated hyperbilirubinaemia, and what causes it?

AKA hemolytic/prehepatic jaundice

A

Build up of water insoluble bilirubin due to:

  • Increased delivery of Hb (haemolysis, ineffective erythropoiesis, haematoma, trauma)
  • Failure to conjugate bilirubin (Gilberts syndrome)
53
Q

What is Gilbert’s syndrome?

A

A harmless genetic condition in which there is a deficiency in the enzyme used to conjugate bilirubin

54
Q

What is conjugated hyperbilirubinaemia, and what causes it?

A

Build up of water soluble bilirubin due to:

  • Hepatocellular dysfunction (AKA hepatic jaundice)
  • Biliary obstruction (AKA obstructive/post-hepatic jaundice))
55
Q

Why is it important to test for PT in liver disease?

A
  • Vitamin K deficiency (due to bile obstruction)
  • Hepatic encephalopathy
  • Inherited clotting deficiencies
56
Q

Why is it important to test for albumin in liver disease?

A

If low it indicates decompensated liver or a severe infection

57
Q

Why is it important to test for platelets in liver disease?

A

Low platelets could be due to splenomegaly (as spleen is eating up all the platelets)

58
Q

Name some drugs which damage the liver

A
Nitrofurnatoin
Antiepileptics 
Co-amoxiclav
Flucloxacillin
Statins
59
Q

How should liver cancer be managed?

A
  • Liver transplant
  • Cryotherapy
  • Alcohol injection
60
Q

What is alpha fetoprotein?

A

A tumor marker that is raised in hepatic carcinoma

61
Q

How does alpha-1 antitrypsin commonly present?

A

Early onset COPD

Liver disease progressing to cirrhosis

62
Q

What test should be done for Wilson’s disease?

A

Serum caeruloplasmin - LOW

63
Q

How does Wilson’s disease commonly present?

A

Fulminant hepatic failure/cirrhosis

Neurological symptoms

64
Q

What is the mechanism behind spider naevi?

A

Liver failure means that oestrogen is not metabolised. High oestrogen levels affect arteriole muscle, causing haemorrhages.

65
Q

What investigation should be done in a patient with suspected oesophageal varies and why?

A

Endoscopy - allows confirmation of the diagnosis, and treatment of the bleed with ligation