Case 3: liver, biliary and pancreatic disease Flashcards

1
Q

Cause of jaundice

A

High bilirubin

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2
Q

Unconjugated vs conjugated bilirubin

A

Unconjugated bilirubin has not come from the liver/biliary tree
Conjugated bilirubin has come from the liver/biliary tree - therefore levels are a sign of liver/biliary tree disease

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3
Q

Sign of conjugated hyperbilirubinemia

A

dark urine
pale stools
(most common in clinical practice)

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4
Q

What is obstructive jaundice?

A

blockage of bile flow through bile ducts or intra/extrahepatic ducts

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5
Q

causes of obstructive jaundice

A
Common bile duct stones (not gallstones)
carcinoma of head of pancreas
Chronic pancreatitis
sclerosing cholangitis
cholangiocarcinoma
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6
Q

What is hepatocellular jaundice?

A

hepatocyte damage

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7
Q

Causes of hepatocellular jaundice

A
alcohol hepatitis/cirrhosis
viral hepatitis
drug induced e.g. paracetamol overdose
non-alcoholic fatty liver disease
autoiimune liver disease
haemochromatosis
wilsons disease
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8
Q

Typical location of pain for biliary colic

A

RUQ

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9
Q

Typical location of pain for pancreatitis

A

epigastrium, radiates to back

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10
Q

What is cholangitis

A

inflammation of the bile duct

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11
Q

Common causes of pancreatitis

A

alcohol excess

gallstones blocking the common bile duct

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12
Q

what must we consider with painless jaundice

A

pancreatic cancer

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13
Q

what are the 2 liver transaminases

A

AST

ALT (liver specific)

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14
Q

What does a rise in ALT/AST more than a rise in ALP indicate?

A

hepatocellular damage

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15
Q

What does a rise in ALP more than a rise in ALT/AST indicate?

A

obstructive causes

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16
Q

2 primary reasons for ordering LFTs

A

To confirm clinical suspiscion on liver injury/disease

To distinguish between hepatocellular injury (hepatic jaundice) or cholestasis (obstructive or post-hepatic jaundice)

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17
Q

What do ALT, AST, ALP and GGT tell you

A

whether something is hepatocellular damage or obstructive

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18
Q

What are Bilirubin, albumin and PT levels used for?

A

To assess the liver’s synthetic function

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19
Q

Synthetic functions of the liver

A

Conjugation and elimination of bilirubin
Synthesis of albumin
Synthesis of clotting factors
Gluconeogenesis

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20
Q

What does ALT > AST indicate?

A

chronic liver disease

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21
Q

What does AST > ALT indicate?

A

cirrhosis and acute alcoholic hepatitis

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22
Q

What is the purpose of measuring GGT?

A

If ALP is raised and GGT is also raised –> very strong obstructive link for cause.
If ALP is raised but GGT is NOT raised –> there could be another cause for the rise in ALP rise e.g. bony mets, primary bone cancer, vitD deficiency, recent bone fracture, renal osteodystrophy

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23
Q

Common causes of acute hepatocellular injury

A

poisoning (paracetamol overdose)
infection (hep A/B)
liver ischaemia

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24
Q

Common + less common causes of chronic hepatocellular injury

A

Common: alcoholic fatty liver disease, NAFLD, chronic infection (hep B/C), primary biliary cirrhosis
Less common: alpha 1 antitrypsin deficiency, Wilsons, haemochromatosis

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25
most common cancer in the biliary region
Carcinoma of the head of pancreas
26
When would you image for a carcinoma in the head of pancreas?
>40 | painless obstructive jaundice
27
what is serum alpha-fetoprotein a marker of?
is raised in 70% of patients with liver cancer
28
What is the max alcohol recommendation per week?
14 units
29
Alcohol advice
No more than 14 units per week Best to spread drinking evenly over 3+ days Do not drink at all if pregnant
30
What is delirium tremens
An acute state confusion when someone who drinks alcohol excessively daily, suddenly stops drinking. Presentation: agitation, disorientation, hallucination, fever, diaphoresis, autonomic hyperactivity (tachycardia, HTN). If untreated, seizures --> death
31
Pharmacotherapy to treat symptoms of acute alcohol withdrawal
Benzodiazepine or carbamazepine | OR clomethiazole
32
Pharmacotherapy for delirium tremens
1st line: oral lorazepam | 2nd line if Sx persist or oral medication declined: parenteral lorazepam or haloperidol
33
Pharmacotherapy for alcohol withdrawal seizures
quick acting benzodiazepine e.g. lorazepam | do not offer phenytoin
34
Signs of liver disease on examination
Spider naevi | palmar erythema
35
Signs of portal hypertension (caused by cirrhosis of liver)
``` GI bleeding - black/tarry stools, vomiting blood Ascites Varices (swollen veins) Encephalopathy Reduced platelets, blood cells, WBCs ```
36
Pathophysiology of why you get pale stools in obstructive jaundice
Bilirubin cannot get into the bowel So there is reduced metabolism of bilirubin Therefore less production of stercobiligen And it is stercobiligen that normally makes your faeces brown
37
Pathophysiology of why you get dark urine in obstructive jaundice
Blocked conjugated bilirubin is water soluble so can still get into the bloodstream and pass into the kidneys/urine
38
What is the breakdown product of haemoglobin
Bilirubin
39
Where is bilirubin conjugated
Liver
40
What happens when bilirubin is conjugated?
It becomes water soluble
41
Where is bilirubin excreted?
Bowel
42
3 causes of jaundice
Prehepatic - haemolysis --> high levels of unconjugated bilirubin Hepatic (with signs of liver failure) Obstructive (signs of pale stools, dark urine, itching)
43
How long til hepatitis becomes chronic
>6months
44
After acute hepatitis, what 3 things can be the outcome
Recovery Chronic hepatitis Fulminant hepatitis (poor prognosis - death or need transplant)
45
Why do you get coagulopathy (bruising) with liver failure
Cannot produce clotting factors
46
What are the effects of liver failure
``` Jaundice Coagulopathy Decreased drug metabolism Decreased hormone production (increased oestrogen particularly in men) Increased sepsis ```
47
As a result of portal hypertension, can get varices.. where?
Oesophageal (if bleed, 25% mortality rate) Rectal (piles) Round umbilicus
48
Signs of portal hypertension
``` Varices Piles Ascites Encephalopathy Renal failure ```
49
Tx of portal hypertension
Portal system shunts | Beta blockers
50
Causes of liver cirrhosis
``` Excess alcohol Chronic hepatitis B/C Autoimmune liver disease Haemochromatosis Wilsons disease Chronic obstruction ```
51
Signs of liver cirrhosis
palmar erythema leukonykia (pale nails due to decreased albumin) spider nivae caput medusa
52
What is steatosis
Retention of fat within an organ
53
Signs of alcohol hepatitis
``` Jaundice Large tender liver Vomiting unable to eat Stops drinking alcohol because feel so ill Alcohol withdrawal Liver failure and risk of death ```
54
At what point can you refer to be assessed for liver transplantation
THey still have decompensated liver failure disease after best management 3 months abstinence from alcohol are otherwise suitable candidates for liver transplantation
55
When can you offer corticosteroid Tx for alcohol liver disease?
For pts with severe alcohol related hepatitis and a discriminant function of 32 or more. only after: - effectively treating any infection or GI bleed - controlling any renal impairment - discussing potential benefits and risks - explain that Tx improve short term improvement, but there is no evidence on improving long term improvement. Increased risk of severe infection in the first 3 months of Tx
56
what are the classic features of obstructive jaundice?
Pale stools, dark urine
57
Most common primary liver tumour
hepatocellular carcinoma
58
What is the best advice to give a pt with NAFLD?
Weight loss
59
Clinical picture: pt with skin yellowing, no dark urine, no pale stools. Is this prehepatic, hepatocellular, or obstructive jaundice?
Prehepatic
60
Clinical picture: pt with skin yellowing, dark urine, pale stools. Is this prehepatic, hepatocellular, or obstructive jaundice?
Obstructive
61
Hepatitis A: acute or chronic | Mode of transmission?
Acute (12 weeks) | Faeco-oral
62
Hepatitis A: what does IgG positive, but IgM negative mean?
Previous infection with HepA
63
Hepatitis A: what does IgM positive, and IgG positive/negative mean?
Acute infection with HepA
64
Causes of hepatitis
Hereditary - Wilsons, haemachromatosis Drug induced: medication, paracetmol, alcohol Infection Autoimmune
65
Describe the flow of bile
Made in the liver Leaves the liver through the common hepatic duct Through the cystic duct Stored in the gallbladder CCK hormone causes the gallbladder to contract Bile exits through the cystic duct Enters the common bile duct Enters the duodenum To the ileum - absorption of bile salts and fats
66
Causes of acute pancreatitis
``` Idiopathic Gallstones Ethanol Trauma Steroids Mumps Autoimmune Scorpion stings Hyperlipidaemia/hypercalcaemia ERCP Drugs ```
67
Symptoms of acute pancreatitis
Sudden and intense epigastrum pain Pain radiates to the back Nausea, vomiting, fever
68
What blood reveal acute pancreatitis
Raised amylase and lipase (pancreatic enzymes) | not useful in chronic pancreatitis
69
What scan confirms acute pancreatitis
CT - shows swollen pancreas or fluid around it
70
Symptoms of chronic pancreatitis
Intermittent or chronic epigastric pain Radiates to back Worse when eating fatty foods
71
Signs of liver cirrhosis
``` Spider naevi Palmar erythema Hepatomegaly Splenomegaly or ascites Abnormal collateral veins in abdomen ```