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P2 - Gastrointestinal system > Liver, LFTs, cirrhosis > Flashcards

Liver, LFTs, cirrhosis Flashcards

1
Q

List the normal functions of the liver:

A

Removing waste

Breakdown of drugs

Vitamin and mineral storage (A, D, K and B12, copper and iron)

Glycogen storage

Acute phase proteins

Amino acid, carbohydrate and lipid metabolism

Plasma protein and enzyme synthesis

Production of bile

Detoxification and immune functions

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2
Q

What is portal hepatus?

A

Point in which vessels enters the liver - hepatic artery, portal vein, common hepatic duct

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3
Q

What are the cells that make up the liver?

A

Basic structure made by hepatocytes

Kupffer cells

Sinusoidal epithelial cells

Stellate cells

Endothelial cells

Perisinusoidal cells

Liver-associated lymphocytes

Cholangiocytes

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4
Q

What are the recesses associated with liver?

A

Subphrenic recess - separates the diaphragm from the liver, divided into left and right by falciform ligament

Hepatorenal recess - between the liver, the right kidney and the right suprarenal gland

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5
Q

Describe the important ligaments of the liver

A

Falciform ligament - attaches it to the anterior abdominal wall

Hepatogastric ligament, hepatoduodenal ligament - to duodenum and stomach;

Anterior and posterior coronal ligaments, right and left triangular ligaments - to the diaphragm

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6
Q

What is the bare area of the liver?

A

Under the diaphragm, no visceral peritoneum

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7
Q

What are the connective tissues of the liver?

A

Capsula, portal tract (fibrous tissue, collagen I and III), parenchymal reticulin

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8
Q

Discuss the biliary system of the liver

A

Bile canaliculi - active transport, run in opposite way then blood, hectagonal arrangement, in space between 2 opposing hepatocytes and drains bile from the liver into the biliary ductules;

Bile ductules - lined by classic columnar epithelial cells - cholangiocytes and drain into the bile ducts;

Bile ducts - forms the right and left hepatic duct, connected to the gallbladder via the cystic duct and to intestine via the common bile duct

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9
Q

Discuss the hepatic lobule of the liver

A

Plate of hepatocytes and parenchyma divided up by sinusoids, surrounding central vein, branches of the portal vein and hepatic artery are located on the peripheral triad, during inactive periods many sinusoids are collapsed, blood drains into the central branches of the hepatic vein

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10
Q

What is the portal triad?

A

Branches of portal vein, hep artery and bile ducts run in parallel; according to the distance from the hepatic triad or vein the zones are distinguished

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11
Q

What is the space of Disse?

A

Separates the hepatocyte from the sinusoidal endothelium

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12
Q

Describe the 3 zones of the liver

A

Zone 1/periportal - closest to the afferent arteriole,

Zone 2 - ill-defined intermediate area,

Zone 3/perivenular - closer to the terminal hepatic veins

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13
Q

What functions are performed in the zone 1 of a liver?

A

Respiratory chain, citric acid cycle, fatty acid oxidation, gluconeogenesis, urea synthesis, production and bile excretion

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14
Q

What functions are performed in the zone 3 of a liver?

A

Glycolysis, glutamine synthesis, xenobiotic metabolism

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15
Q

Describe hepatocytes

A

Most abundant of liver cells lie in plates and cords, exchange material with blood at sinusoidal surfaces, arranged with microvilli and the fenestration for good slow exchange of blood and nutrients

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16
Q

What are sinusoidal epithelial cells and what are their features?

A

Line the liver cells, more leaky than capillary; their epithelium is fenestrated and lacks complete basement membrane

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17
Q

What are the features of stellate cells?

A

Storage site for retinoids, growth factors for hepatocytes, synthesise collagen in abnormal situations

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18
Q

How much and what type of blood supplies the hepatic artery?

A

30-40% blood supply, oxygenated blood

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19
Q

How much and what type of blood supplies the portal vein?

A

60-70% blood supply, this blood has already been through one capillary bed from small, large intestine, stomach, spleen and has low pressure, thinned walled with wide diameteer, superior and inferior mesenteric veins plus splenic vein join to form the portal vein

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20
Q

What drains blood away from the liver?

A

Connecting sinusoids that drain into the hepatic vein

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21
Q

What are the components of bile?

A

Water, electrolytes, phospholipids, bile salts or acids, bile pigments, cholesterol, haem waste products, and other substances from blood

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22
Q

How is bile produced?

A

Formed by the hepatocyte and modified down stream by absorptive and secretory properties of the bile duct epithelium

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23
Q

How is bile secreted?

A

Begins at the bile canaliculi, enters the hepatic ducts and then the bile duct

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24
Q

What are the functions of bile?

A

Bile acids are needed for fat absorption, mechanism to remove cholesterol and waste

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25
Q

List the liver function tests

A

Alkaline phosphatase and biliribun (increased in cholestasis), gamma glutamyl-transpeptidase (increased in cholestasis or enzyme induction), aspartate aminotransferase - AST and alanine aminotransferase - ALT (inc in hepatocyte damage), Albumin (decreased in long-term impaired synthesis), Prothrombin time (increased in short-term impaired synthesis)

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26
Q

Outline the pattern of abnormal LFTs in pre-hepatic jaundice

A

Total bilirubin increased, conjugated bil normal, unconj. Bil increased, urobilinogen normal or increased, ALP+ALT+AST are normal, normal colour of stool and urine

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27
Q

Outline the pattern of abnormal LFTs in hepatic jaundice

A

All bilirubin forms increased, increased urobilinogen and thus dark colour of urine but normal colour of stool, increased ALP, and even more increased ALT and ASP

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28
Q

Outline the pattern of abnormal LFTs in post-hepatic jaundice

A

Total bil and conj. Bil are extra increased, unconj. Bil is normal, urobilinogen decreased, urine is dark because of increased conj. Bil, stool pale as lacks bil based substances, ALP extra increased, Alt and AST increased

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29
Q

Define cirrhosis

A

End-stage liver disease, a result of chronic inflammation and scarring of the liver, development: normal - inflammed - fibrosed - cirrhosis

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30
Q

Describe the possible causes of cirrhosis

A

Alcohol, viruses (hepatitis A, B, C, D, E and G), biliary disease, toxins and drugs (paracetamol, antibiotics, anabolic steroids), inherited conditions (hemochromatosis - iron overload)

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31
Q

Describe the pathogenesis of cirrhosis

A

Hepatocyte injury leads to progressive liver cells loss which leads to 1. chronic inflammation and fibrosis, 2. hepatocyte regeneration and hyperplasticity with formation of nodules; both lead to architectural abnormality and ischaemia which causes further injury to cells,

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32
Q

What is the role of hepatic stellate cells and tissue macrophages in cirrhosis?

A

These cells phagocytose and secrete pro-inflammatory mediators like transforming growth factor-beta and platelet-derived growth factor (leads to transdifferantion of stellate cells to myofibroblasts and their proliferation); macrophages scar matrix by matrix metalloproteinases, inhibited by concurrent myofibroblasts and macrophage production of tissue inhibitors of metalloproteinases; results in progressive matrix deposition and scar accumulation

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33
Q

Is fibrosis or cirrhosis reversible?

A

Fibrosis can be eliminated if the cause is eliminated, cirrhosis can only regress

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34
Q

What are the types of cirrhosis?

A

Micronodular and macronodular cirrhosis

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35
Q

Define micronodular cirrhosis

A

Regenerating nodules up to 3 mm in size, uniform involvement of the liver, often caused by alcohol or biliary tract disease

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36
Q

Define macronodular cirrhosis

A

Nodules are of variable size and normal acini may be seen within larger nodules, caused by chronic viral hepatitis

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37
Q

What are the consequences of liver failure?

A

Impaired production of secretory proteins (albumin, coagulation proteins, complements..) –> jaundice, coagulation disorder, altered intermediary metabolism (urea and glycogen), altered xenobiotic metabolism, immune, circulatory and endocrine disturbances

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38
Q

What are the signs and symptoms of cirrhosis?

A

Encephalopathy, sparse body hair, spider angioma, muscle wasting, fibrotic liver, dilated vessels, ascites, red palms, jaundice

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39
Q

List the possible complications of cirrhosis

A

Portal hypertension - portal-systemic shunts and varices, ascites, splenomegaly; liver failure, hepatocellular cancer, renal failure, spontaneous bacterial peritonitis

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40
Q

How does portal hypertension arise?

A

Cirrhosis increases resistance to blood flow through liver and thus increases pressure in portal circulation

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41
Q

Which veins join to make the portal vein?

A

The superior mesenteric and splenic veins

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42
Q

What is the normal pressure within the portal vein?

A

5 - 8 mmHg

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43
Q

What pressure is considered portal hypertension

A

Hepatic venous pressure gradient of 10 mmHg or more

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44
Q

What is the classification of portal hypertension?

A

Pre-hepatic (portal vein blocked), intrahepatic, post-hepatic

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45
Q

What happens in prolonged portal hypertension?

A

Compliant venous system dilates, collateral formation, microvasculature of the gut becomes congested giving rise to portal hypertensive gastropathy and colonopathy - punctuate erythema and erosions, a risk of bleeding

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46
Q

What are the main sites of collaterals in portal hypertension

A

Gastro-oesophageal junction, rectum, left renal vein, diaphragm, retroperitoneum and umbilical vein

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47
Q

Describe the risk of gastro-oesophageal junction collaterals in portal hypertension

A

Varices are superficial and tend to rupture

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48
Q

What is the treatment of portal hypertension?

A

Treat underlying cause or liver transplant

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49
Q

What are the pharmacological treatments for portal hypertension?

A

Beta-blockers, nitrates, vasoactive drugs

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50
Q

Describe the use of beta-blockers in portal hypertension

A

Non-selective beta-blockers: reduce rates of bleeding in patients with oesophageal varices, may also protect against spontaneous bacterial peritonitis; carvedilol

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51
Q

Describe the use of nitrates in portal hypertension

A

With B-blockers, contribute to reducing pressure, may reduce rates of variceal re-bleeding

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52
Q

Give an example of vasoactive drug and its function

A

Terlipressin and octreotide; control of acute variceal bleeding

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53
Q

What are the endoscopic procedures used to manage portal hypertension

A

Endoscopic vein ligation, to prevent bleeding of oesophageal varices, or gastric varices by variceal obturation with tissues adhesives; can be also used to detect and monitor

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54
Q

What is the transjugular portosystemic shunt

A

Radiological procedure connecting the portal and hepatic veins using a stent, to decompress the portal venous system, prevent re-bleeding from varices and/or to reduce the formation of ascites

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55
Q

What are the surgical procedures?

A

Surgical portosystemic shunt and devascularisation procedure

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56
Q

What are ascites?

A

Complication of cirrhosis among other, fluid within the peritoneal cavity

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57
Q

What are the lifestyle recommendations for managing portal hypertension

A

Reduce salt intake, avoid alcohol, aspirin and NSAIDs

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58
Q

Describe the effects of liver failure

A

Jaundice, coagulation disorders, altered intermediary metabolism e.g. impaired synthesis of urea and glycogen, altered xenobiotic metabolism; immune, circulatory and endocrine disturbances

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59
Q

Describe the role of the liver in carbohydrate metabolism

A

Storage and release of glycogen, gluconeogenesis, conversion of fructose and galactose to glucose phosphates, glucose as energy for glycolysis, citric acid cycle, synthesis of FA and TG

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60
Q

What is gluconeogenesis?

A

Synthesis of glucose from other sources, e.g. lactate, pyruvate, glycerol and alanine

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61
Q

Describe the role of lipid metabolism

A

Mitochondrial beta-oxidation of short chain fatty acids, synthesis of FA, TG, CHOL , phospholipids and lipoproteins

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62
Q

Describe the role of the liver in protein metabolism

A

Synthesis of non-essential aa and plasma proteins (except immunoglobulins), glycation of proteins, disposal of ammonia by converting it to urea, interconverting and deaminating aa, s

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63
Q

What is the first-pass metabolism of the liver?

A

Portal vein brings in blood from the gut and toxic chemicals are picked up by hepatocytes, these then can be converted within the liver

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64
Q

What is the role of Kuppfer cells and what level of liver detoxification are they?

A

Remove bacteria and other materials from blood as they are phagocytic, physical level

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65
Q

Describe the biochemical level of detoxification of the liver

A

Hepatocytes contain numerous enzymes which modify endogenous and exogenous toxins, the products end up more soluble and less susceptible to reuptake by intestine; these reactions are divided into phase I and II reactions

66
Q

What are the phase I reactions of the detox liver system?

A

Oxidation, hydroxylation, other reactions catalysed by cytochrome P450

67
Q

What are the phase II reactions of the detox liver system?

A

Conjugation to promote excretion, either excreted to bile or blood stream

68
Q

What is the role of the liver in excretion?

A

Secretion of large water-soluble catabolites that cannot be excreted through kidneys, excretion of plasma protein bound molecules, excretion in bile, important because with accumulation these become harmful

69
Q

Give examples of molecules that are bound to plasma protein and excreted by the liver

A

Give examples of molecules that are bound to plasma protein and excreted by the liver

70
Q

What is the mechanism of excretion by the liver?

A

Substances are taken up by hepatocytes by membrane transporters, substances are metabolized at the level of microsomes and in the cytosol membrane, bile stabilizes even lipophilic substances and all is excreted in faeces

71
Q

What is the role of the liver in the coagulation pathway?

A

Synthesis of factors II, VII, IX, X and protein C, storage of protein and gamma-carboxylation of these factors, vitamin K is co-factor

72
Q

Signs and symptoms of liver disease

A

Severe vomiting and failure to thrive, recurrent episodes of vomiting and encelopathy with acidosis, progressive retardation or seizures with hepatomegaly, jaundice

73
Q

What is bile made out of?

A

Cholesterol - converted to make bile acid; water, electrolytes, phospholipids, bile pigment, heme waste products

74
Q

What is bile function?

A

Fat absorption, mechanism to remove cholesterol and waste

75
Q

Describe the role of liver in metabolism of amino-acids and disposal of urea

A

Nitrogen conversion into urea in the liver and excreted by the kidneys, ammonia production and clearance

76
Q

Describe the biotransformation and excretion of proteins by the liver

A

For detoxification but can generate toxic or carcinogenic metabolites, phase 1 reactions is the smooth endoplasmic reticulum mediated by cytochrome P450 to produce hydroxylated or carboxylated compounds, phase 2 reactions: subsequent conjugation with glucuronic acid, acetyl or methyl radical or glycine, taurine or sulphate

77
Q

What are bile pigments?

A

Generated from breakdown of haem group from haemoglobin in macrophages of the reticuloendothelial system in the spleen/bone marrow/liver

78
Q

What is one haemoglobin molecule composed of?

A

4 haem groups in haemoglobin plus 4 globin monomers

79
Q

What happens to the globin monomers?

A

Broken down to constituent amino acids and recycled

80
Q

What happens to the haem group?

A

Fe2+ is recycled, porphyrin ring is converted to bilirubin for transport to the liver for modification and excretion

81
Q

Which enzyme catalyses the breakdown of Haem and what are the products?

A

Haem oxygenase, O2->CO, Biliverdin, Fe2+

82
Q

What catalyses the reaction of biliverdin to bilirubin and what else is needed?

A

Biliverdin reductase, NADPH –> NADP+

83
Q

What are the properties of unconjugated bilirubin?

A

Hydrophobic/water-insoluble, cannot be excreted or transported in blood unless bound to albumin, straightened Haem without Fe2+, orange-yellow pigment

84
Q

How does the unconjugated bilirubin enter hepatocyte?

A

Travels in blood bound to albumin, transported by Sinusoidal Bilirubin Transporter

85
Q

How does unconjugated bilirubin become conjugated?

A

Reaction catalysed by UDP Glucuronyl Transferase, using 2x UDP-Glucuronic acid; results in formation of conjugated bilirubin and 2x UDP

86
Q

What are the properties of conjugated bilirubin?

A

Hydrophilic, Bilirubin-monoglucuronide and diglucuronide formed, can be transported out of hepatocytes into bile canaliculi for accumulation in bile

87
Q

What happens after conjugation of Bilirubin?

A

Bilirubin is stored in gallbladder, released into small intestine where it undergoes the enteric bilirubin metabolism

88
Q

Describe the enteric bilirubin metabolism

A

C-bilirubin converted by Beta-glucuronidase to U-bilirubin in the small intestine, this is then converted by intestinal microflora to Mesobilinogen, Stercobilinogen and urobilinogen

89
Q

What happens to mesobilinogen in the large intestine?

A

Converted to Stercobilinogen, and some converted to Mesobilin (brown pigment) by intestinal microflora

90
Q

What happens to stercobilinogen in the large intestine?

A

Converted to Stercobilin by intestinal microflora, excreted in faeces brown pigment; some can be reabsorbed back to portal circulation

91
Q

What happens to Urobilinogen?

A

Converted to stercobilinogen, and some converted to urobilin by intestinal microflora, yellow pigment; or urobilinogen reabsorbed into the portal vein, goes through the liver either to be stored as bile or continues to kidneys to be secreted and urine oxidizes it to Urobilin

92
Q

What are bile salts?

A

Biological emulsifiers made from cholesterol combined with either glycine or taurine to give Glycolic acid or Taurocholic acid

93
Q

What are the properties of bile salts that make them good emulsifiers?

A

They are water and lipid-soluble: Hydrophilic face and hydrophobic face

94
Q

What is emulsification?

A

Breakdown of large lipid droplet into small uniformly distributed droplets, hydrophobic protein binds to and disperse large triglyceride lipid droplets, hydrophilic portion prevents large droplets reforming

95
Q

What is the aim of emulsification of lipid droplets?

A

Increase of surface area on which triglyceride lipase can act

96
Q

What is the role of triglyceride lipase?

A

breakdown of triglyceride molecules in monoglyceride and 2 FA, then into glycerol and 3 fatty acids

97
Q

How big are micelles and what they are?

A

4-7 nm, lipid aggregates with hydrophilic head groups on outside and hydrophilic tails pointing in

98
Q

What are micelles made out of?

A

Bile salts, fatty acids, monoglycerides, phospholipids, cholesterol and fat-soluble vitamins (A, D, E, K)

99
Q

How are the contents of micelles absorbed?

A

Micelles continuously breakdown and reform, each time contents are released and some is able to diffuse across the intestinal lining, TAGs reform in epithelial cells and are packaged into chylomicrons which enter the blood via the lymph (lacteals) by secretory vesicles

100
Q

What is sphincter of Oddi?

A

Muscular valve that controls flow of bile and pancreatic fluid into the duodenum

101
Q

How is bile secretion controlled?

A

Pressure increases in the common bile duct and bile flows into the gallbladder, epithelial cells reabsorbs water and electrolytes, thus concentrating the bile

102
Q

What stimulates bile secretion?

A

Fatty acids and amino acids enter the duodenum stimulate endocrine cells to release cholecystokinin (CCK), CCK stimulates contraction of gallbladder smooth muscle and relaxes the sphincter of Oddi

103
Q

What is the effect of acidic chyme on bile in duodenum?

A

Stimulates other endocrine cells to release secretin, secretin stimulates duct cells in the liver to release bicarbonate into the bile and also stimulates bile production

104
Q

What is the effect of vagal nerve stimulation on gallbladder?

A

Weak contraction

105
Q

Describe the recycling of bile salts

A

By the enterohepatic circulation, bile salts are moved by transporters to the intestinal capillaries, then transported to the liver via the hepatic portal vein, hepatocytes take up bile salts from the blood and increase bile salts secretion into bile canaliculi, only 5% is lost in faeces

106
Q

What are the 3 classifications of jaundice?

A

Pre-hepatic, hepatic and post-hepatic

107
Q

What is jaundice?

A

Defined by elevated levels of bilirubin –> hyperbilirubinaemia, obvious clinical feature present in a variety of conditions

108
Q

What are the reference values of jaundice?

A

Total bilirubin (adult) < 21 micromol/L

Conjugated bilirubin (adult) < 7 micromol/L

109
Q

What is the value of total bilirubin when jaundice becomes visible in the sclera and in the skin?

A

Sclera: total bilirubin > 30 micromol/L

Skin: total bilirubin > 100 micromol/L

110
Q

Discuss pre-hepatic jaundice

A

Elevated haemolysis and liver cannot cope with increased levels of unconjugated bilirubin so there is build up of unconjugated bilirubin

111
Q

Causes of pre-hepatic jaundice

A

Tropical disease: yellow fever, malaria; side-effect of quinine-based anti-malarial drugs, genetic disorders - sickle cell anaemia

112
Q

Describe physical jaundice of the newborn

A

Common and usually harmless, caused by replacement of foetal haemoglobin with adult haemoglobin and undeveloped liver lacks glucuronyltransferase and thus cannot cope with elevated haemolysis

113
Q

What is the course and treatment of physical jaundice of the newborn

A

Lasts up to 14 days and peaks at days 3-5, treated with phototherapy - blue light changes unconjugated bilirubin to water-soluble form

114
Q

Describe haemolytic disease of the newborn

A

Rh incompatibility between mother and fetus results in haemolysis, can cause very high bilirubin concentration; risk of kernicterus - bilirubin crosses the immature blood-brain barrier, deposition of bilirubin in basal ganglia and brainstem nuclei resulting in brain damage if untreated

115
Q

What is the treatment for haemolytic disease of the newborn?

A

High dose of phototherapy and blood transfusion

116
Q

Discuss hepatic jaundice

A

Liver damage at any point: impaired uptake of unconjugated bilirubin, impaired conjugated bilirubin (Gilberts - reduced glucuronyl transferase activity), impaired transport of conjugated bilirubin into bile canaliculi

117
Q

Name examples of impaired transport f conjugated bilirubin into bile canaliculi

A

Primary biliary cholangitis (autoimmune destruction of small bile ducts), present in conditions that result in liver damage causing cholestasis due to swelling and oedema resulting from inflammation

118
Q

Discuss post-hepatic jaundice

A

Blockage of bile ducts, present in conditions associated with obstruction of hepatic, cystic or common bile duct, bile is blocked from release into the small intestine

119
Q

Discuss the causes of post-hepatic jaundice

A

Gallstones - cholesterol pebbles, block ducts, arise if the capacity of bile salts and phospholipids to solubilise cholesterol is exceeded; pancreatitis - acute or chronic inflammation of the pancreas following infection of damage, can block bile flow; pancreatic tumours

120
Q

Describe what happens when gallstones arise

A

Can be asymptomatic but become increasingly problematic when gallbladder contractions cause stones to move further along the bile ducts

121
Q

What happens if gallstones block the cystic bile duct?

A

Painful contraction, this one joins gallbladder to common bile duct

122
Q

What happens if the common bile duct is blocked by gallstones?

A

No bile secretion into gut, steatorrhea (fatty faeces due to lack of bile salts), grey faeces (no bile pigments), pos-hepatic jaundice (reduced excretion of bilirubin)

123
Q

What happens when the duodenal papilla is blocked by gallstones?

A

No bile or pancreatic secretion into gut, causes malnutrition, acute pancreatis

124
Q

What are the implications of post-hepatic jaundice for surgery?

A

Vit K is not digested and as it is required for efficient coagulation as a co-factor for liver gamma-glutamyl carboxylase, which activates coagulation factors II, VII, IX and X, course of vit K is administered parenterally

125
Q

What does liver function test include?

A

Bilirubin, albumin, alkanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma glutamyl transferase, total protien

126
Q

Describe unconjugated hyperbilirubineamia and give example

A

>85% of unco B out of total B, occurs with increased bilirubin production or defects in hepatic uptake or conjugate (Gilbert’s disease)

127
Q

Describe conjugated hyperbilirubinaemia

A

In inherited or acquired defects in hepatic excretion, conj bilirubin >50% of total B

128
Q

What can bilirubin elevation indicate?

A

Excess production following haemolysis of trauma, reduced level of conjugation, hepatocyte failure, biliary obstruction

129
Q

What does elevation of aminotransferases indicate?

A

Hepato-cellular injury

130
Q

What is the role of aminotransferases?

A

Participate in gluconeogenesis by catalysing the transfer of amino groups from aspartic acid or alanine to ketoglutaric acid to produce oxaloacetic acid and pyruvic acid respectively

131
Q

What are the strengths and weaknesses looking at aspartate aminotransferase?

A

Signals breakdown of cells, present in liver, cardiac and skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes and erythrocytes - less sensitive and specific for the liver, plasma half-life 48 hours

132
Q

What are the strengths and weaknesses looking at alanine aminotransferase?

A

Higher distribution in liver and thus more specific, increase of ALT is more specific to the liver and has plasma half-life 18 hours

133
Q

Explain the testing of gamma-glutamyl transferase

A

Indicates alcohol intake, microsomal enzyme which transport gamma-glutamyl peptides onto other peptides or aa, present in other organs too but plasma activity correlates with liver, has poor specificity but helps to determine the cause of raised ALP of liver origin or chronic alcohol consumption

134
Q

Explain excess alcohol consumption in relation to GGT

A

People with chronic liver disease will have raised GGT, this may be due to alcohol-related damage or chronic disease damage, only half of alcoholic patients will have raised GGT and it will return to normal after 8 weeks of abstinence, but there is no relationship between GGT and duration of alcohol consumption

135
Q

Explain the use of alkaline phosphatase as a liver function marker

A

Group of enzymes that hydrolyse phosphate esters in alkaline solutions, found on the exterior surface of the bile canalicular membrane and enters the bloodstream paracellularly, ALP rises in bile duct obstruction and is associated with bone disorders

136
Q

Explain the use of plasma proteins as a liver function markers

A

Site of synthesis of all plasma protein apart from immunoglobulins, prothrombin time measures the rate of conversion prothrombin to thrombin and thus the synthetic function of the liver

137
Q

What is the normal level of Bilirubin?

A

6 - 22 umol/L

138
Q

What is the normal level of alkaline phosphatase?

A

80 - 280 U/L

139
Q

What is the normal level of AST?

A

<40 U/L

140
Q

What is the normal level of ALT?

A

<50 U/L

141
Q

What is the normal level of GGT?

A

<70 U/L

142
Q

What is the normal level of albumin?

A

36 - 53 g/L

143
Q

What is the normal level of C-reactive protein?

A

<10 mg/L

144
Q

What is the normal erythrocyte sedimentation rate?

A

1 - 20 mm/hr

145
Q

What is C-reactive protein?

A

Produced by liver in response to inflammation due to different causes like infection or cancer

146
Q

What is the initial interpretation of elevated transaminases?

A

Hepatocellular injury

147
Q

What is the initial interpretation of elevated ALP and GGT?

A

Cholestasis - bile is not going to duodenum

148
Q

What pattern suggests hepatocellular disease?

A

AST increased more than 3 time the URL, while ALP less than 2x URL

149
Q

How can the acute vs chronic hepatitis be distinguished further using LFTs?

A

If normal albumin then acute hepatitis, if decreased albumin then it is likely to be chronic hepatitis

150
Q

What is the pattern of cholestatic disease in terms of LFTs?

A

AST less than 3x URL, ALP increased more then 2x URL

151
Q

How do you distinguish between acute and chronic cholestasis?

A

Acute cholestasis - normal albumin, chronic cholestasis - decreased albumin

152
Q

What determines whether cholestasis is intrahepatic or extrahepatic?

A

Ultrasound or percutaneous cholangiography (X-ray with contrast)

153
Q

What signifies increased ALP, but normal GGT?

A

Bone disease

154
Q

What signifies increased ALP, GGT in terms of dilated and undilated ducts?

A

If dilated ducts then stones, strictures or space occupying lesions; if nondilated ducts then biliary cirrhosis or possible sclerosing cholangitis, stones

155
Q

Describe the hepatocellular pattern

A

ALT or AST > 150 U/L, ALP <200 U/L, determine with serology and possibly also liver biopsy

156
Q

Describe the cholestatic pattern

A

ALP 180 U/L, ALT < 150 U/L, GGT >100 U/L, Bilirubin < 50 umol/L, consider ultrasound, MRCP (Magnetic resonance cholangiopancreatography), ERCP (Endoscopic-retrograde Cholangio-pancreatohgraphy)

157
Q

What are the levels of ALT like in hepatitis B?

A

Raised in initial acute infection when clinical symptoms appear and in chronic infection

158
Q

What is Gilbert’s syndrome?

A

Benign autosomal dominant condition caused by deficiency of enzymes that conjugate bilirubin (bilirubin uridine disphosphate glucoronate glycoronyl transferase), jaundive tends to be increased in tiredness, fasting, or with other illness e.g. influenza

159
Q

What is the ration of AST/ALT in alcoholic liver disease?

A

>2

160
Q

What is the ration of GGT/ALP in chronic alcoholic

A

>5

161
Q

Describe the features of non-alcoholic steatohepatitis.

A

Increased GGT, ALT and AST; no alcohol, diabetes or medication; moderate hepatomegaly, on biopsy large droplets steatosis, mild fibrosis, portal and lobular inflammation

162
Q

Define non-alcoholic steatohepatitis

A

Chronic liver disorder characterised by macrovesicular fatty degeneration and parenchymal inflammation in a patient without alcohol or little alcohol consumption and no serological evidence of hepatitis

P2 - Gastrointestinal system (5 decks)

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