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Lecture 22 Flashcards

1
Q

How does blood return to the heart?

A

Via the hepatic vein into the IVC.

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2
Q

What does the hepatic artery do?

A

Bring fresh blood from the heart.

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3
Q

What does the portal vein do?

A

Bring blood form the intestines.

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4
Q

What does the bile duct do?

A

Drains bile to the intestines.

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5
Q

Where does blood go in the hepatic lobule?

A

From outside, through the mass of liver cells ( filtration) to the central vein.

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6
Q

Where doe bile go in the hepatic lobule?

A

From the inside to the bile duct.

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7
Q

Describe the ways to measure liver function?

A

AST and ALT are enzymes involved amino acid processing and gluconeogenesis. Measuring them in the blood stream, and are released in the circulation as part of cell breakdown.
GGT and ALP are enzymes found in the portal tract.
Can also measure bilirubin.
Can measure albumin, prothrombin ration and glucose.

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8
Q

What happens when you have an inflammatory process of the central part of the lobule?

A

Increase release of AST and ALT into the bloodstream.

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9
Q

What are the processes that cause inflammation of the liver in the central part?

A

Viral hepatitis.
Liver toxins/drugs.
[Hepatocellular].

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10
Q

What happens when you have an inflammatory process of the outside part of the lobule?

A

Increased release of GGT and ALP into the bloodstream. And if you have some problem with the processing of bilirubin, bilirubin blood level will go up as well.

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11
Q

What are the processes that cause inflammation of the liver on the outside

A

Gallstones and some drugs.

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12
Q

Describe the process of bilirubin metabolism?

A
  1. Bilirubin comes from haem in meat.
  2. It has to be shield from water, (it is insoluble) so it is attached to albumin. Where the unconjugated (unprocessed) bilirubin is >85%.
  3. Liver then uptakes bilirubin where it is conjugated. It adds a sugar to make the bilirubin soluble; usually glucuronide -> Bilirubin-glucuronide. Can get out through urine.
  4. Bilirubin-glucuronide goes out through the portal duct, where it is converted by bacteria to urobilinogen. This can then be excreted out as faeces and can be reabsorbed.
  5. Urobilinogen can get back into the bloodstream and be excreted as urine.
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13
Q

What happens if you have a blockage in the processing of bilirubin?

A

Increased amount of bilirubin-glucuronide. The conjugated bilirubin concentration will go up, as it does not get a speedy way to get into the gut. Thus the blood level will go up, in both absolute terms and portion of bilirubin. And then will end up in urine.

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14
Q

What happens if you have an increase in haem release - haemolysis?

A

You get an increase of unconjugated bilirubin, thus an increase of work of the liver. You will then get an increase amount of Bilirubin-glucuronide made. If it has a nice easy flow to the gut then you’ll get increase of urobilinogen. This will be reabsorbed and will go out into the urine as increased amounts.

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15
Q

What happens if you have a process that affects the flow of the bile system e.g. mass?

A

There won’t be bilirubin into the gut, thus the amount of urobilinogen formed will be low. Thus hardly any in the urine. The blood level of conjugated bilirubin goes up. So you can measure it as an increase in the conjugated fraction = direct bilirubin.

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16
Q

What happens if there is a problem on the conjugation step? (gilbert’s syndrome)

A

Stick on a sugar molecule with enzyme. Genetic variability in this step, which can result in the portion of the population to have slower conjugation and slightly higher bilirubin. Especially in times when the person is stressed.

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17
Q

What happens if there is a problem within the liver itself?

A

There is a problem of getting the bilirubin into the bile canaliculi. This can lead to cholestasis. Drugs, pregnancy and thyroid disease can cause this.

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18
Q

What happens if there is an obstruction in the liver?

A

The obstruction of the flow of bilirubin down the portal tracks. Could be hepatitis (inflammation - where it affects ALT and AST), the pressure inside the liver goes up. This means less room for things to pass through the liver structure. Can have cirrhosis, across the liver or across the portal tract - binary cirrhosis.
Can have many liver masses, metastatic liver disease.

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19
Q

What happens if there is an obstruction outside the liver?

A

Gallstones - sits there, and obstruct a valve.
Cancer (pancreas) - end of bile system flows through system and cancer blocks this.
Pancreatitis - raise bilirubin by an obstructive process.

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20
Q

What does Alkaline Phosphatase (ALP) do?

A

It transfers/hydrolyses phosphate groups amongst molecules.

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21
Q

What is the main reason for wide age-related variation of ALP?

A

The two most important sources of Alp is the liver and the bone. While levels in the blood don’t change, however bone levels do. During puberty where bone grows rapidly, increased bone turnover, and ALP involved in osteoblasts will be released in blood stream at greater amounts. This happens in puberty and menopause.

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22
Q

Why does ALP change during late pregnancy?

A

The placenta makes ALP.

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23
Q

What are other reasons of ALP increases?

A

Tumours, cancers and inflammation.

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24
Q

What happens if there is high levels of ALP?

A

It can mean a lot of things i.e. metastases, gallstones, primary biliary cirrhosis. However many of other things can be the cause of high ALP levels i.e. hepatitis.

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25
Q

What is the origin of Gamma-Glutamyl Transferase (GGT)?

A

Biliary origin.

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26
Q

What does GGT do?

A

Transfers two carbon units around.

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27
Q

What is the main source of GGT?

A

main source is the liver, however the heart, pancreas and lungs can source GGT.

28
Q

What is the cause of elevation of GGT?

A

1) Inflammation/obstruction of biliary system.
2) If you are exposing patient to certain drugs (phenytoin, rifampicin) or alcohol can get increase in GGT. As GGT is involved in the processing of the substances.

29
Q

What can cause a mild increase in GGT?

A

Alcohol and fatty liver. Fatty liver is someone in the NZ general population, due to problems with obesity.

30
Q

What is the stats of GGT levels for heavy drinkers?

A

Around 2/3 of heavy drinkers will have a high GGT (1-3x). The sensitivity is not that great. The likelihood of alcohol being the explanation is less than 1/3.

31
Q

What are the stats of GGT levels for weekend drinkers (5 drinks x2-3 nights)?

A

Mean rise of 25% (1/2 had > 50% rise of GGT).
Peaks 2-3 days and falls over 5-6 days.
ALT rises only about 10-15%. Time sensitive.

32
Q

How long does it take for GGT levels to go back to normal?

A

If a patient has been drinking, and has abstained from drinking it will take 6 plus weeks to return to normal levels.

33
Q

What is the problem with GGT elevation levels?

A

GGT does not correlate with liver biopsy. If there has been prolonged exposure to a drug (such as alcohol) there can still be cirrhosis and nodules formed on the liver. This will mean that the normal levels of GGT shown will no longer apply, there will be chronic obstruction of the biliary system.

34
Q

What does ALT do?

A

Amino acid processing and gluconeogenesis, and converting alanine to pyruvate. Important in the processing pathway.

35
Q

What are the sources of ALT?

A

1) Liver - hepatocytes. Very specific test to he liver. Restricted to cytoplasm in the cell.
2) (minor) muscle, heart and red cells. However there needs to be major damage to these structures for ALT levels to increase.

36
Q

What does AST do?

A

Converts aspartate to oxaloacetate.

37
Q

What are the sources of AST?

A

1) Mainly the liver. Located in the cytosol and mitochondria. Will get release of both cytosolic and mitochondrial AST components if there is damage to the liver. Thus AST will go up higher than ALT.
2) Muscle, heart and red cells.

38
Q

What is the half life of AST and ALT?

A 
AST = 8 hours (S = short).
ALT = 48 hours (L = long).
39
Q

What does high levels (in the 1000s) of ALT and AST reflect in the liver?

A

Diffused damage right across the liver lobule. This is resulting in the enzyme being released. This is shown in people with Early hepatitis.

40
Q

What is the source of Albumin?

A

The liver in adults.

41
Q

What is the cause of fallen albumin levels?

A

1) Decreased synthesis (cirrhosis). Major functional problem of the liver.
2) Increased loss (e.g. kidney). Patients who have nephrotic levels of pro-urea. Can also happen with the gut.
3) Illness (non-specific). Not to a great degree (2-3g) due to the cytokines that are released, which tell liver to switch off album synthesis. Common to see in hospitalised patients.
4) Redistribution. Albumin normally restricted to inter-vascular blood stream, but can get out due to increased permeability of interstitial fluid.

42
Q

What do globulins reflect?

A

Reflect common inflammation. They are involved with the immune system, and chronic immune stimulus. Can go up to high levels in patients with serious chronic liver disease.

43
Q

What does the Prothrombin Ratio (PR)(INR) reflect?

A

Do this test when patients are on blood thinners e.g. warfarin. Reflects the liver synthesis of clotting factors 2,7,9,10. If liver can’t make these factors you will get a rise in INR (also happen if patient deficient in Vit K).

44
Q

What does glucose reflect?

A

The liver is the main organ that maintains blood sugar between meals. If you can’t maintain your blood sugar. So it is an ominous sign.

45
Q

What are the signs of liver scarring and declining function?

A

1) Persistent GGT, ALP elevation. Markers of the biliary tree, as become increasingly scar they go up.
2) Increased AST/ALT ratio (>1).
3) Increased globulins, due to chronic inflammation.
4) Decreased albumin.
5) Increased Bilirubin.
6) Increased prothrombin ratio (low Vit K).
7) Decreased glucose and increased NH3.

46
Q

Describe Case 1?

A
  • 23yo Man.
  • Strong family history of bowel cancer.
  • Rectal bleeding.
  • Right upper quadrant abdominal discomfort.
  • Examination is normal.
47
Q

Describe Case 1 results?

A

1) AST is normal. AST is 28.
2) ALP/GGP are significantly raised.
3) Marginal decrease in albumin.
4) Normal bilirubin.
5) CEA (carcinoembryonic antigen) is quite high.

48
Q

Describe Case 1 discussion?

A

1) History - Not been well, family history of bowel cancer and loosing blood.
2) Albumin - Mild fall in the albumin, could be unwell.
3) Increased GGT/ALP and normal Bilirubin- Primarily increased the two enzymes. Could be a blockage in the way bile is processed. Could be a mass in the liver, or several. And could result in increase in GGT/ALP in part of the tree distal to the blockage, but the rest of the tree is still patent. Liver is still able to produce bilirubin, and keep it at normal range. Isolated in elevation of GGT and normal bilirubin is concerning.
Normal AST - Minimal liver cell inflammation.
CEA - High level so quite worrying.
Final diagnosis: Metastatic cancer.

49
Q

What is CEA?

A

Carinoembryonic Antigen. Can mark cancer in the colon, breast, lung, pancreas and thyroid. Also can mark hepatitis, cirrhosis, ulcerative colitis, renal failure and smoking.

50
Q

What are the levels of CEA?

A

1) 3-5ng/ml - 99% non-smokers and 95% smokers.
2) 5-10ng/ml - Smokers and most with benign disease.
3) 10-20ng/ml - 20ng/ml - almost always malignant.

51
Q

Describe Case 2?

A
  • 20yo male medical student.
  • Intermittent jaundice (yellow sclerae, worse when tired, sick or after school).
  • No change in colour or urine/faeces.
  • Otherwise well.
  • Examination normal.
52
Q

Describe Case 2 results?

A

1) Albumin - normal.
2) Bilirubin - twice the upper limit of normal. At 55 umol/L.
3) GGT/ALP - normal.
4) AST/ALT - normal.

53
Q

Describe Case 2 discussion?

A

There is a mild bilirubin rise, so it’s probably unconjugated as the urine is not dark. All the enzymes are normal.
Typical of gilbert’s syndrome. Diagnosis is based on clinical picture.

54
Q

What are the features of Gilbert’s syndrome?

A

1) Common in the population - 3-5% of the population.
2) Causes variance in bilirubin conjugation.
3) Other liver function tests normal.
4) Bilirubin in conjugated (indirect);

55
Q

How to diagnose Gilbert’s syndrome?

A

1) well patient/persisitent mild jaundice (2x.

4) Genetic - usually unhelpful.

56
Q

Describe Case 3?

A
  • 35yo woman.
  • History of excessive alcohol intake.
  • Symptoms: nausea, vomiting and weakness.
  • Intake high over last few weeks.
57
Q

Describe Case 3 results?

A

1) Alubmin - low at 25g/L.
2) Bilirubin - high at 82umol/L.
3) GGT and ALP - high.
4) AST and ALT - high.
5) Prothrombin ratio (INR) - high.

58
Q

Describe Case 3 discussion?

A

1) History - possible alcoholic liver disease.
2) Tests - Increased AST/ALT indicated recent liver cell damage. Mild increase in ALP/GGT/Bilirubin indicated secondary liver damage. And Decreased albumin and increased PR indicated reduced liver function.
3) Exclude viral hepatitis.
4) Final diagnosis = hepatitis (alcoholic) and long standing liver disease.

59
Q

What are the common causes of viral hepatitis?

A

1) Infectious mono - 50% - use VCA-IgM test.
2) Hepatitis A - 25% - use HAV-IgM test.
3) Hepatitis B - 15% - use Hep B Ag and Hep B IgM test.
4) Hepatitis C - 5% - use Hep C Ab test.
5) Cytomegalovirus - 2% - use CMV-IgM test.

60
Q

Describe Case 4?

A
  • 52yo man.
  • Long history of excess alcohol.
  • Symptoms: vomited blood (portal hypertension).
  • Gastroscopy - oesophageal varices.
61
Q

Describe Case 4 results?

A

1) Albumin - low.
2) Bilirubin - High at 263umol/L.
3) GGT/ALP - high.
4) AST/ALT - high.
5) Prothrombin ration (INR) - mildly high.

62
Q

Describe Case 4 discussion?

A

1) History - alcoholic cirrhosis (liver scarring) and secondary portal hypertension.
2) Main LFT changes - Increased bilirubin, Alp and GGT can indicate scarring. Increased ALT/AST can indicate ongoing inflammation. Decreased albumin and increased PR can indicate impaired function.
3) Scan - shrunken scarred liver and no bile duct dilation.
4) Final diagnosis - alcoholic liver disease and cirrhosis and portal hypertension.

63
Q

Describe Case 5?

A
  • 43yo man presents acutely.
  • Large overdose of paracetamol (30gm).
  • O/E: alert and tender enlarged liver.
  • 3 days later - unconscious.
  • 5 days later - dies.
64
Q

Describe Case 5 results?

A

1) Albumin - normal.
2) Bilirubin - Really high at 160umol/L.
3) GGT/ALP - high.
4) AST/ALT - extremely high (10,000).
5) Glucose - Low at 2.4mmol/L.
6) Prothrombin ratio - high at 8.5.

65
Q

Describe Case 5 discussion?

A

1) Severe liver cell injury - due to very increased ALT/AST.
2) Liver failure - synthesis is low, as shown by decreased glucose (hypoglycaemia) and clotting factors thus you get an increase PR. Metabolism - increased bilirubin.
3) Unconscious - due to increased ammonia.
4) Final diagnosis - paracetamol poisoning, liver failure.

66
Q

What are the causes of LFT abnormalities?

A
  • Fatty liver - 45%.
  • Viral hepatitis - 27%.
  • Alcohol - 8%.
  • Haemochromatosis - 3%.
  • Other - 16% - drugs, autoimmune, porphyria, wilson’s dis, granulomatous, malignancy, coeliac disease, heart failure, antitrypsin deficiency and rare metabolic.

DS (32 decks)

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