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Year 3 TCD > 3. Jaundice > Flashcards

3. Jaundice Flashcards

1
Q

What is jaundice and what is it caused by?

A

Jaundice is the yellow pigmentation of skin or sclerae (eyes) caused by high levels of bilirubin in the body.

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2
Q

Which type of bilirubin causes jaundice?

A

An excess of either unconjugated or conjugated bilirubin can cause jaundice.

However, conjugated hyperbilirubinemia is more common in clinical practice

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3
Q

When does jaundice become clinically apparent?

A

Jaundice is clinically apparent when bilirubin levels exceed 50 micromoles per litre in caucasian individuals.

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4
Q

Without performing any tests, how can you tell whether the jaundice is caused by conjugated or unconjugated bilirubin?

A

High levels of conjugated bilirubin causes dark urine and pale stools.

Whereas, high levels of unconjugated bilirubin does not cause these signs

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5
Q

What is bilirubin and why do we have it?

A

Bilirubin is the breakdown product of haemoglobin, specifically the haem part of it. This process occurs in order to recycle the iron in the haem.

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6
Q

What is the first breakdown product of haem called?

A

Biliverdin

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7
Q

Why is bilirubin conjugated?.

A

Unconjugated bilirubin is non-water soluble, so it is conjugated in order to become water soluble.

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8
Q

Where is conjugated bile normally excreted?

A

Conjugated Bilirubin is then normally excreted in bile from the gallbladder after a meal

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9
Q

What happens to the conjugated bile once its in the intestines?

A

it gets metabolised in the gut by bacteria, converting it to urobilinogen, which then undergoes spontaneous oxidation into urobilin, and then converted to stercobilinogen which is brown and is excreted in feces

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10
Q

What happens to the urobilin?

A

80% is lost via excretion in feces

20% is reabsorped into the blood, where 90% of it goes back to the liver, and 10% goes to the kidneys. In the kidneys, this urobilin is responsible for the yellow staining of urine.

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11
Q

How much bile is produced in a day?

A

Produced at rate of 500-1000 ml per day

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12
Q

When is bile normally excreted?

A

Released in response to hormonal (CCK-PZ) and vagal response to food

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13
Q

What is the composition and pH of bile?

A

98% water, bile salts (from cholesterol), bile pigments, and also contains HCO3 and thus an alkaline pH (8 – 8.6).

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14
Q

What are the 3 general causes of jaundice?

A
  • Haemolytic Jaundice / Prehepatic Jaundice
  • Hepatocellular Jaundice
  • Obstructive Jaundice
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15
Q

What is haemolytic jaundice?

A

This is where there is an abnormality, resulting in increased breakdown of red blood cells in the body. Therefore, there is increased amounts of haem that needs to be broken down and converted to conjugated bilirubin.

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16
Q

What are some of the conditions that cause haemolytic jaundice?

A
  • Hypersplenism (overactive spleen is breaking down too many RBCs)
  • Ineffective hematopoesis, such as sickle cell (RBCs are poor in quality, so they are constantly getting broken down)
  • Incompatible blood transfusion (wrong blood means your immune system will destroy it all)
  • drug reaction
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17
Q

What is the enzyme called that converts unconjugated bilirubin to conjugated bilirubin?

A

Glucuronyl Transferase (UGT)

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18
Q

What happens to Glucuronyl Transferase (UGT) in haemolytic jaundice?

A

It is fully saturated, meaning it is working at its maximum rate

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19
Q

What happens to unconjugated and conjugated bilirubin levels in haemolytic jaundice?

A

Massive increase in unconjugated levels, beyond the levels that glucuronyl transferase (UGT) can handle. This means there is excess unconjugated bilirubin in the blood.

A large amount of conjugated bilirubin as well (as UGT is fully saturated), but the body can just handle this.

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20
Q

What is at increased risk of happening in haemolytic jaundice, and why?

A

There is an increased risk for pigmented gallstones, because of the large amounts of conjugated bilirubin being synthesised, it results in the gallbladder becoming very large.

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21
Q

What is hepatocellular jaundice?

A

This is where the hepatocytes themselves struggle to perform their function of synthesising conjugated bilirubin from unconjugated bilirubin.

22
Q

What are the two types of causes of hepatocellular jaundice, and give examples of both.

A

CONGENITAL CAUSES

  • Neonatal jaundice
  • Gilberts syndrome
  • Crigler Najjar Syndrome

ACQUIRED CAUSES

  • Infection (viral hepatitis)
  • Cirrhosis caused by excessive alcohol intake
  • Cirrhosis caused by steatohepatitis
  • Damage by toxins or drugs (paracetamol overdose)
  • Non-alcoholic fatty liver disease
23
Q

What is neonatal jaundice? (cause, complications, prevalence and treatment)

A

It is an example of a congenital cause of hepatocellular jaundice.

Neonates naturally have low levels of UGT, meaning there are high levels of unconjugated bilirubin. This is normal unless the levels get really high, at which point it can collect in the basal ganglia, called Kernicterus, and causes brain damage and death.

It occurs in 60% of term infants and 80% of preterm infants in the first week of life.

It can be treated with phototherapy or with exchange transfusion. Fluid and caloric intake will prevent it worsening

24
Q

What is Gilberts Syndrome?

A

It is an example of a congenital cause of hepatocellular jaundice.

This is similar to neonatal jaundice, but lasts for life. There is a low amount of UGT, meaning any slight increase in unconjugated bilirubin can overwhelm the hepatocytes.

25
Q

What is Crigler Najjar Syndrome?

A

It is an example of a congenital cause of hepatocellular jaundice.

This is similar to neonatal jaundice, but lasts for life. This is where there is no UGT enzyme at all, so no way to get rid of unconjugated bilirubin naturally.

26
Q

What is steatohepatitis?

A

It is an example of an acquired cause of hepatocellular jaundice.

This is where liver fat cells release inflammatory mediators, resulting in creation of fibrous tissue. It is normally the result of excessive drinking.

27
Q

What is obstructive jaundice? Why is it an issue?

A

This is where there is something blocking the flow of bile.

Because there is still the production of bile, this builds up the pressure in the bile duct proximal to the obstruction. Once the pressure exceeds a certain level, the bile backtracks and seeps back out of the bile duct, into the tight junctions between hepatocytes and ultimately into the bloodstream.

28
Q

Why is bile backtracking into the bloodstream in obstructive jaundice an issue?

Hint: 3 main reasons

A
  • All the conjugated bilirubin produced now ends up directly in the blood. As this is water soluble, this gets its way into urine, giving it a dark colour
  • Bile salts, acids and cholesterol getting into the blood stream. If these deposit into the skin, it can lead to itchy skin (known as pruritus), and it can also cause hypercholesterolemia and xanthomas.
  • As there is no bile being secreted into the gut, you lose the brown stain of stools, making them now pale. In addition, as bile is important in the digestion and absorption of fats, it means you cannot digest fats as well. This results in increased fat excretion (called steatorrhea) as well as a decrease in absorption of the fat-soluble vitamins.
29
Q

What is pruritus?

A

an unpleasant sensation of the skin that provokes the urge to scratch

30
Q

What is a xanthelasma?

A

Fatty lumps on the eyelids

31
Q

What is a xanthomata?

A

Fatty lumps in the hands and fingers

32
Q

What are the common causes of obstructive jaundice?

A
  • Gallstones: if this is there for a while, then it can lead to cholecystitis (inflammation of the cystic duct) and if persistent then it can lead to cholangitis (infection of the cystic duct)
  • Carcinoma of the head of the pancreas
33
Q

What are some of the uncommon causes of obstructive jaundice?

A
  • Chronic pancreatitis
  • Sclerosing cholangitis (this is where you get scarring of the small bile ducts which causes an obstruction)
  • Cholangiocarcinoma (this is a cancer of the bile duct wall)
34
Q

If you suspect obstructive jaundice, what key piece of information would make you think it’s a carcinoma of the head of pancreas?

A

If the patient presents with painless jaundice

35
Q

What is urine and stool colour in haemolytic jaundice?

A

Normal urine and normal stools

36
Q

What is urine and stool colour in hepatocellular jaundice?

A

Variable

37
Q

What is urine and stool colour in obstructive jaundice?

A

Dark urine and pale stools

38
Q

What are the risk factors for jaundice?

A
  • Alcohol intake
  • Drug use including non-prescription drugs
  • Travel
  • Blood transfusions
  • Tattoos
  • Unprotected sexual activity
39
Q

What questions are important to ask someone with jaundice?

A 
NORMAL HISTORY 
- Do they have pain or no pain?
- How long has the jaundice lasted for?
- Are they itchy? 
- What is the colour of urine and stools?
SOCIAL HISTORY
- Drug, alcohol and cigarette history.
- Have they been on any foreign travel?
- Have they had unprotected sex? (hepatitis B)
40
Q

What else should you do during the history of someone with jaundice?

A

BE ON THE LOOKOUT FOR CANCER

  • Do they have risk factors predisposing them to cancer?
  • Does your patient look cachectic on examination, have hard lymphadenopathy, do they have a hard “craggy” liver edge?
  • Ask about unintentional weight loss- worry if there is no clear explanation
41
Q

If you can palpate the gallblader on examination of a jaundiced patient, what should you be thinking?

A

Cholangiocarcinoma (bile duct cancer)

42
Q

What do you need to check in cirrhotic patients and why?

A

Primary hepatocellular cancer is more common in liver cirrhosis patients, so their serum alpha-fetoprotein levels should be regularly checked as this goes up in cancer.

43
Q

What are the key things you should look for in an examination of a jaundiced patient?

A
  • Sclera and skin for yellow discolouration (Get them to look left and right without moving their head, as you’ll see the sclera better)
  • Scratches from pruritus
  • Evidence of weight loss (thenar wasting) - indicative of cancer and poor absorption of fats
  • Troisiers sign / virchows node (left supraclavicular node enlargement) - indicative of gastric cancer
44
Q

If there is right upper quadrant (RUQ) pain associated with fever and jaundice, what does it suggest? Why is this serious?

What are these symptoms otherwise known as?

A

It indicates cholangitis, which is an infection of the biliary duct.

This is serious as it can easily lead to sepsis.

RUQ pain, jaundice and fever all make up Charcots Triad, which indicates cholangitis.

45
Q

How would pancreatitis present itself on examination?

A

Severe epigastric pain that radiates to the back

46
Q

In someone with obstructive jaundice with an absense of abdominal pain, what are you thinking of?

A

Liver or pancreatic cancer

47
Q

Would higher or lower levels of albumin indicate poor liver functioning?

A

Lower levels

48
Q

Would a higher or lower prothrombin time / INR indicate poor liver functioning?

A

Higher

49
Q

When looking at liver enzymes, how can you detect hepatocellular jaundice?

A

There is a greater rise in ALT and AST compared to ALP.

This is because AST and ALT are found in normal hepatic cells, so they get raised when there is damage directly to the liver.

50
Q

When looking at liver enzymes, how can you detect obstructive jaundice?

A

There is a greater rise in ALP compared to ALT and AST.

This is all because ALP is found in hepatic bile duct cells, so damage involving the biliary tract will cause ALP containing cells to get damaged, hence, ALP gets raised.

51
Q

What should be one of the first examinations on someone with jaundice? What are you looking for?

A

Ultrasound of the liver looking for dilated ducts.

  • If there is duct dilation found, then perform a CT of the same area
  • If the ducts appear to be normal, then check for prehepatic or hepatocellular causes
52
Q

What is kernicterus?

A

it is when there is excessive levels of bilirubin in the blood in infancy, and it accumulates in the basal ganglia, causing brain damage and ultimately death

Year 3 TCD (36 decks)

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