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TCD > Case 3: liver, biliary and pancreatic disease > Flashcards

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
Q

most common cancer in the biliary region

A

Carcinoma of the head of pancreas

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26
Q

When would you image for a carcinoma in the head of pancreas?

A

> 40

painless obstructive jaundice

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27
Q

what is serum alpha-fetoprotein a marker of?

A

is raised in 70% of patients with liver cancer

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28
Q

What is the max alcohol recommendation per week?

A

14 units

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29
Q

Alcohol advice

A

No more than 14 units per week
Best to spread drinking evenly over 3+ days
Do not drink at all if pregnant

30
Q

What is delirium tremens

A

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
Q

Pharmacotherapy to treat symptoms of acute alcohol withdrawal

A

Benzodiazepine or carbamazepine

OR clomethiazole

32
Q

Pharmacotherapy for delirium tremens

A

1st line: oral lorazepam

2nd line if Sx persist or oral medication declined: parenteral lorazepam or haloperidol

33
Q

Pharmacotherapy for alcohol withdrawal seizures

A

quick acting benzodiazepine e.g. lorazepam

do not offer phenytoin

34
Q

Signs of liver disease on examination

A

Spider naevi

palmar erythema

35
Q

Signs of portal hypertension (caused by cirrhosis of liver)

A 
GI bleeding - black/tarry stools, vomiting blood
Ascites
Varices (swollen veins)
Encephalopathy
Reduced platelets, blood cells, WBCs
36
Q

Pathophysiology of why you get pale stools in obstructive jaundice

A

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
Q

Pathophysiology of why you get dark urine in obstructive jaundice

A

Blocked conjugated bilirubin is water soluble so can still get into the bloodstream and pass into the kidneys/urine

38
Q

What is the breakdown product of haemoglobin

A

Bilirubin

39
Q

Where is bilirubin conjugated

A

Liver

40
Q

What happens when bilirubin is conjugated?

A

It becomes water soluble

41
Q

Where is bilirubin excreted?

A

Bowel

42
Q

3 causes of jaundice

A

Prehepatic - haemolysis –> high levels of unconjugated bilirubin
Hepatic (with signs of liver failure)
Obstructive (signs of pale stools, dark urine, itching)

43
Q

How long til hepatitis becomes chronic

A

> 6months

44
Q

After acute hepatitis, what 3 things can be the outcome

A

Recovery
Chronic hepatitis
Fulminant hepatitis (poor prognosis - death or need transplant)

45
Q

Why do you get coagulopathy (bruising) with liver failure

A

Cannot produce clotting factors

46
Q

What are the effects of liver failure

A 
Jaundice
Coagulopathy
Decreased drug metabolism
Decreased hormone production (increased oestrogen particularly in men)
Increased sepsis
47
Q

As a result of portal hypertension, can get varices.. where?

A

Oesophageal (if bleed, 25% mortality rate)
Rectal (piles)
Round umbilicus

48
Q

Signs of portal hypertension

A 
Varices
Piles
Ascites
Encephalopathy
Renal failure
49
Q

Tx of portal hypertension

A

Portal system shunts

Beta blockers

50
Q

Causes of liver cirrhosis

A 
Excess alcohol
Chronic hepatitis B/C
Autoimmune liver disease
Haemochromatosis
Wilsons disease
Chronic obstruction
51
Q

Signs of liver cirrhosis

A

palmar erythema
leukonykia (pale nails due to decreased albumin)
spider nivae
caput medusa

52
Q

What is steatosis

A

Retention of fat within an organ

53
Q

Signs of alcohol hepatitis

A 
Jaundice
Large tender liver
Vomiting
unable to eat
Stops drinking alcohol because feel so ill
Alcohol withdrawal
Liver failure and risk of death
54
Q

At what point can you refer to be assessed for liver transplantation

A

THey still have decompensated liver failure disease after best management
3 months abstinence from alcohol
are otherwise suitable candidates for liver transplantation

55
Q

When can you offer corticosteroid Tx for alcohol liver disease?

A

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
Q

what are the classic features of obstructive jaundice?

A

Pale stools, dark urine

57
Q

Most common primary liver tumour

A

hepatocellular carcinoma

58
Q

What is the best advice to give a pt with NAFLD?

A

Weight loss

59
Q

Clinical picture: pt with skin yellowing, no dark urine, no pale stools.
Is this prehepatic, hepatocellular, or obstructive jaundice?

A

Prehepatic

60
Q

Clinical picture: pt with skin yellowing, dark urine, pale stools.
Is this prehepatic, hepatocellular, or obstructive jaundice?

A

Obstructive

61
Q

Hepatitis A: acute or chronic

Mode of transmission?

A

Acute (12 weeks)

Faeco-oral

62
Q

Hepatitis A: what does IgG positive, but IgM negative mean?

A

Previous infection with HepA

63
Q

Hepatitis A: what does IgM positive, and IgG positive/negative mean?

A

Acute infection with HepA

64
Q

Causes of hepatitis

A

Hereditary - Wilsons, haemachromatosis
Drug induced: medication, paracetmol, alcohol
Infection
Autoimmune

65
Q

Describe the flow of bile

A

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
Q

Causes of acute pancreatitis

A 
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion stings
Hyperlipidaemia/hypercalcaemia
ERCP
Drugs
67
Q

Symptoms of acute pancreatitis

A

Sudden and intense epigastrum pain
Pain radiates to the back
Nausea, vomiting, fever

68
Q

What blood reveal acute pancreatitis

A

Raised amylase and lipase (pancreatic enzymes)

not useful in chronic pancreatitis

69
Q

What scan confirms acute pancreatitis

A

CT - shows swollen pancreas or fluid around it

70
Q

Symptoms of chronic pancreatitis

A

Intermittent or chronic epigastric pain
Radiates to back
Worse when eating fatty foods

71
Q

Signs of liver cirrhosis

A 
Spider naevi
Palmar erythema
Hepatomegaly
Splenomegaly or ascites
Abnormal collateral veins in abdomen

TCD (7 decks)

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