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Y2 > 11 Hepatic > Flashcards

11 Hepatic Flashcards

1
Q

What are the two part of a simple emulsifier molecule?

A

Hydrophilic head and hydrophobic tail

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2
Q

An emulsifier molecule is a ________

A

Amphiphile

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3
Q

What is an amphiphile?

A

Has a lipophilic portion and a hydrophilic portion

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4
Q

What is bile?

A

A dark green-to-orange fluid produced by the liver which helps the digestion of lipids in the SMALL INTESTINES

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5
Q

Where is bile stored and discharged?

A

Stored in the gallbladder and is discharges in the duodenum

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6
Q

What are the main functions of the liver?

A

Metabolic & synthesis

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7
Q

What are the lobes of the liver and what separates them?

A

Left and right
Joined by a ligament (Falciform and round)

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8
Q

How many segments are there in the liver?

A

8

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9
Q

Describe how blood enters the liver

A
  1. Hepatic artery 25% - oxygenated from circulation
  2. Hepatic portal vein 75% - deoxygenated from the small intestines (ascending & descending colon)
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10
Q

Describe how blood leaves the liver

A

Hepatic vein into the IVC back towards the heart.

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11
Q

How does bile leave the liver?

A

Leaves via hepatic ducts to the gallbladder

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12
Q

What are sinusoids?

A

Low pressure vascular channels receiving blood from terminal branches of the hepatic artery and vein

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13
Q

What are sinusoids lined with?

A

Endothelial cells and flanked with plates of hepatocytes

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14
Q

Where do hepatocytes receive plasma from?

A

Small intestine

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15
Q

Where does nutrient rich plasma collect from the small intestines?

A

In the space of Disse and flows back towards portal tracks collecting in lymphatic vessels

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16
Q

What are Kupffer cells?

A

A type of macrophages that ingest foreign particles and other cells

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17
Q

What are the fat-soluble vitamins?

A

A, D, E, K, B12 and folic acid

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18
Q

Beside metabolic and synthetic, what other functions does the liver have?

A
  • Immunological
  • Storage of fate soluble vitamins
  • homeostasis of glucose
  • production of bile
  • clearance of medication, toxins and bilirubin
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19
Q

Describe carbohydrate metabolism in the liver

A

It is one of the most important functions of the liver and with the pancreas, tightly controls blood glucose levels.
After a meal, your blood glucose levels increase and a large amount is stored as glycogen, other sugars are also converted and lots of intermediate products are formed form carbohydrates.

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20
Q

What is the process that converts starch into glucose?

A

Gluconeogenisis

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21
Q

How is glucose levels sensed in the liver?

A
  1. Glycogen phosphorylase - in the presence of glucose is able to be activated
  2. This then releases the hormone PP1
  3. PP1 converts glycogen synthase B into the active form
  4. Glycogen synthase B is then able to covert glucose into glycogen to be stored
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22
Q

Describe some of the functions of the liver when it comes to protein synthesis

A
  • deamination of amino acids
  • interconversions of the various amino acids and synthesis of other compounds from amino acids
  • removal of ammonia from the liver, can become toxic in the body. High levels can lead to hepatic encephalopathy
  • formation of urea
  • produce plasma proteins
  • able to interconvert other amino acids
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23
Q

Why would we want to remove ammonia?

A

Produces by the bacteria in the gut
Toxic in high levels
Think about patients who cannot remove ammonia –> hepatic encephalopathy (brain dysfunction due to liver damage)

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24
Q

What would the liver not working mean for clotting factors?

A

The liver synthesises vitamin-K-dependant clotting factors
If not able to carry out function, the liver won’t produce as much of these clotting factors
This would result in the patient having increased risk of bleeding

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25
Q

What would happen if patient is unable to produce bile salts in regard to vitamin K?

A

Vitamin K is fat soluble
If patient is unable to produce bile salts, fat cannot be emulsified well
Thus much reduced absorption of vitamin K

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26
Q

Where is albumin produced?

A

Liver

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27
Q

What is albumin?

A

Major plasma protein and is involved in drug transportation and other protein bound components such as bilirubin

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28
Q

What would happen if a patient was low in albumin?

A

Water leaves out of the vascular space –> oedema or ascites

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29
Q

What is oncotic pressure?

A

Oncotic pressure is the pressure exerted by large molecules in the blood, such as proteins, that pulls fluid back into capillaries.

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30
Q

What is bile made up of?

A

Bile salts, cholesterol, phospholipids, bile pigments, electrolytes and water

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31
Q

What are bile pigments?

A

Excretory products of the liver

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32
Q

What is bilirubin?

A

Breakdown product of haemoglobin and is conjugated by the liver

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33
Q

Where is bilirubin excreted?

A

Normally excreted in the faeces and gives the appearance of brown

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34
Q

What would problems in the liver or bilirubin system result in?

A

A building up of bilirubin in the blood —> jaundice and lightening of the stools - less pigments

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35
Q

What makes up most of bile?

A

H2O (97%)

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36
Q

What is the responsibility of reticuloendothelial cells (macrophages)?

A

Responsible for the maintenance of blood

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37
Q

How do reticuloendothelial cells maintain blood?

A
  • take up red blood cells and break down haemoglobin into HAEM and GLOBIN
  • globin is further broken down into amino acids
  • haem is broken down into iron and biliverdin
  • biliverdin is reduced to produce bilirubin
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38
Q

What catalyses haem —> iron & biliverdin?

A

Haemoxygenase

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39
Q

What reduces biliverdin to bilirubin?

A

Biliverdin reductase

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40
Q

Bilirubin + albumin?
Where does this occur?

A

Bilirubin-albumin
Vasculature

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41
Q

Unconjugated bilirubin binds to what?

A

Albumin in the bloodstream

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42
Q

Glucuronic acid is added to ______ to form _______

A
  1. UDPGT
  2. UDPGT1A1
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43
Q

What is the main form of conjugated bilirubin?

A

Bilirubin digluconide

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44
Q

Where is conjugated bilirubin excreted?

A

Into the duodenum in the bile into the stools

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45
Q

What does colonic bacteria do?

A

Removes the glucuronic acid resulting in urobilinogen

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46
Q

How much of urobilinogen is reabsorbed as part of hepatic circulation?

A

Roughly 20%

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47
Q

What happens to urobilinogen?

A

It is further oxidised to produce stercobilin and excreted in faeces giving colour

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48
Q

What happens to reabsorbed urobilinogen?

A

Carried to the liver and either recycled for bile production or reaches the kidneys

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49
Q

What is Gilbert’s syndrome?

A

Slower metabolism of bilirubin due to reduced levels of glucuronyl transferase leading to elevated unconjugated bilirubin levels

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50
Q

What are bile caniculi?

A

Small duct network between hepatocytes that collect bile and eventually merge into bile ducts, forming the common hepatic duct.

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51
Q

Describe the pathway between bile caniculi to the gall bladder

A

Bile caniculi —> bile ducts —> common hepatic duct —> cystic duct —> gall bladder

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52
Q

What two ducts lead to the common bile duct?

A

Cystic duct and common hepatic duct

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53
Q

What are the constituents of bile?

A

Bile acid-dependent and bile acid-independent

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54
Q

What makes bile acid-independent constituents of bile?

A

Made by ductal cells lining the bile ducts

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55
Q

What do hepatocytes secrete?

A

Bile acids, bile pigments and cholesterol

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56
Q

Where do both dependent and independent components of bile enter?

A

They enter intrahepatic bile ducts which drain into the biliary tree

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57
Q

What is the biliary tree?

A

A series of ducts that transport bile from the liver to the gallbladder and duodenum

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58
Q

How does the gall bladder concentrate bile?

A

By removing the water and ions

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59
Q

What processes occur in phase I metabolism?

A

Oxidation, reduction and hydrolysis

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60
Q

What processes occur in phase II metabolism?

A

Glucuronidation, gluthione conjugation, acetylation and sulphation

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61
Q

What processes occur in phase III metabolism?

A

Active elimination

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62
Q

Give examples of hormones does the liver catabolises

A
  • insulin
  • glucagon
  • oestrogens
  • glucocorticoids
  • growth hormones
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63
Q

Why is the liver being an important site for drug and alcohol metabolism significant?

A

Fat soluble drugs are converted to water-soluble to facilitate excretion into bile or urine

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64
Q

At a steady rate, define the rate of elimination of a substance/drug?

A

The rate of presentation of the drug to the liver (I.e. blood flow) and the rate of exit of the drug from the liver

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65
Q

What is the equation for clearance of the liver?

A

Cl = Q x E
Q - blood flow
E - rate of exit of the drug from the liver

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66
Q

What are high extraction ratio drugs?

A

Drugs that are highly first-pass metabolism
(You lose most of the drug before it even reaches circulation)

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67
Q

Why is high extraction drugs an issue with people with reduced blood flow?

A

Less drug is metabolised there for more active drug will enter circulation
Hepatic blood flow reduced = bioavailability increased

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68
Q

Give examples of high extraction ratio drugs

A

Propranolol, morphine and sertraline

69
Q

What does hepatic clearance depend on?

A

Blood flow

70
Q

What would you need to alter when giving high extraction ratio drugs to patients with reduced hepatic blood flow?

A

Alter the dose and dose interval to avoid an accumulation of the drug

71
Q

Describe the enterohepatic recirculation of bile

A

Bile is continuously produced but is only needed during and after meals. The gallbladder concentrates bile by removing water and ions.

72
Q

Describe the metabolism of bilirubin.

A
  • Unconjugated bilirubin is transported to the liver bound to albumin.
  • Glucuronic acid is added to unconjugated bilirubin by UDPGT, forming conjugated bilirubin, primarily bilirubin diglucuronide.
  • Conjugated bilirubin is excreted in bile.
  • Colonic bacteria deconjugate bilirubin, producing urobilinogen.
  • Urobilinogen is oxidised to stercobilin (giving faeces their colour) and partially reabsorbed.
  • Reabsorbed urobilinogen is either recycled or reaches the kidneys, where it’s oxidised to urobilin and excreted in urine.
73
Q

Summarize the phases of liver metabolism (including Phase III).

A

Phase I: Oxidation, reduction, hydrolysis.
Phase II: Glucuronidation, glutathione conjugation, acetylation, sulphation.
Phase III: Active elimination

74
Q

Describe the breakdown of haemoglobin and the formation of bilirubin.

A

Reticuloendothelial cells (macrophages) break down red blood cells, separating haemoglobin into haem and globin. Globin is broken down into amino acids, while haem is converted to iron and biliverdin by haemoxygenase. Biliverdin is then reduced to bilirubin by biliverdin reductase.

75
Q

What factors can reduce hepatic blood flow?

A

Cirrhosis.
Portal vein thrombosis.
Cardiac failure.
Shock (very low BP).
Portal systemic shunting.

76
Q

What does it mean for a drug to be ‘free’ in the bloodstream, and how does this relate to albumin?

A

A non-bound drug is considered ‘free’ and able to elicit an effect. Drugs that are highly protein-bound bind to albumin for transportation, so only the unbound portion is free to act.

77
Q

What might happen if two drugs with high protein binding are taken together?

A

This could lead to competitive binding for the binding sites on albumin.
The drug with a higher affinity for albumin would displace the other, increasing the amount of the displaced drug that is ‘free’ in the bloodstream. This can lead to an increased effect and potentially higher risk of side effects from the displaced drug.

78
Q

What are low extraction ratio drugs?

A

Low extraction ratio drugs are drugs that are not highly metabolised on their first pass through the liver.

79
Q

What is the impact of reduced hepatic blood flow on the bioavailability of low extraction ratio drugs?

A

If hepatic blood flow is reduced, the bioavailability of low extraction ratio drugs is not affected, except for drugs that are highly protein bound.

80
Q

What is the main factor that determines the metabolism of low extraction ratio drugs?

A

The metabolism of low extraction ratio drugs is dependent on the functional capacity of the liver.

81
Q

What happens to the elimination and half-life of low extraction ratio drugs when the functional capacity of the liver is reduced?

A

If the functional capacity of the liver is reduced, the elimination of low extraction ratio drugs from the systemic circulation is delayed, and their half-life is prolonged.

82
Q

What adjustments might be necessary to the dose interval of low extraction ratio drugs in patients with reduced liver function?

A

In patients with reduced liver function, it may be necessary to adjust the dose interval of low extraction ratio drugs

83
Q

Give two examples of low extraction ratio drugs.

A

Citalopram and theophylline.

84
Q

What are the two main patterns of liver damage?

A

Cholestatic and hepatocellular

85
Q

What is cholestatic liver damage?

A

Disruption of the flow of bile from the liver. Bile builds up in the biliary tree and the liver.

86
Q

What are the two classifications of cholestatic liver damage?

A

Intrahepatic and extrahepatic

87
Q

Give some examples of intrahepatic cholestatic liver damage.

A
  • Primary biliary cholangitis
  • Certain drugs
  • Inflammation of the bile ducts
88
Q

Give some examples of extrahepatic cholestatic liver damage.

A
  • Inflammation of the bile ducts
  • Gallstones
  • Strictures
89
Q

What is hepatocellular liver damage?

A

Injury to the hepatocytes

90
Q

What are some causes of hepatocellular liver damage?

A
  • Toxins, such as alcohol or medicines
  • Viruses
  • Other infections
91
Q

What is steatosis?

A

An accumulation of fat within the hepatocytes. Can be seen on a microvascular and a macrovascular scale

92
Q

What is hepatitis?

A

Inflammation within the liver. Can be acute or chronic

93
Q

Define acute hepatitis

A

History of onset of symptoms should be less than 6 months

94
Q

List the categories of acute hepatitis.

A
  • Hyperacute (within 7 days)
  • Acute (within 8-28 days)
  • Subacute (within 28-72 days)
95
Q

Define chronic hepatitis.

A

Symptoms that persist for longer than 6 months.
Generally associated with cirrhosis which can be defined as compensated and decompensated.

96
Q

Describe the progression of damage to the liver.

A

From a healthy liver (F0) to a cirrhotic liver (F4)

97
Q

What causes damage to the liver?

A
  • Viral causes
  • Alcohol
  • Drug use
98
Q

What is fibrosis?

A

Persistent, and extensive hepatic damage leads to active deposition of collagen and formation of scar tissue.

99
Q

What is cirrhosis?

A

Consistent damage further collagen deposition and scar formation leading to irreversible damage.

100
Q

What are the results of cirrhosis?

A
  • Disruption to the blood flow into the liver
  • Erratic regeneration of the liver leading to nodules and irregular surface of the liver
101
Q

How are patients with cirrhosis defined?

A

Compensated or decompensated. Decompensated cirrhosis will present with features of complications.

102
Q

What is the most common method pharmaceutical companies use to classify the degree of impairment of the liver?

A

The Child’s Pugh scoring system.

103
Q

What is the disadvantage of the Child’s Pugh scoring system?

A

It is difficult to pinpoint a really clear set of instructions. Two people with the same Child’s Pugh score could have very different presentations of their liver disease.

104
Q

Give examples of how two people with the same Child’s Pugh score could present differently.

A
  • One person might have ascites which could affect drug distribution.
  • Another person could be encephalopathic which results in higher blood brain barrier permeability and increased central effect.
105
Q

List some investigations that might be used to assess liver damage

A
  • Liver Ultrasound
  • Computerised tomography (CT scan)
  • Endoscopic Retrograde Cholangio-pancreatography (ERCP)
  • Magnetic Resonance Cholangiopancreatography (MRCP)
  • Magnetic Resonance Imaging (MRI)
  • Ultrasound elastography (Fibroscan)
  • Liver Biopsy
  • Calculate MELD or UKELD Model for End-Stage Liver Disease or UK Model for End-Stage Liver Disease
106
Q

List some signs and symptoms of decompensated liver disease.

A
  • Jaundice
  • Ascites
  • Unexplained bruising and bleeding
  • Varices
  • Encephalopathy
  • Abdominal pain
  • Pale stools and dark urine
  • Gynaecomastia
  • Fatty stools
  • Spider naevi
  • Finger clubbing and pruritus
107
Q

Define jaundice.

A

A term used to describe the yellowing of the skin and the whites of the eyes caused by a build-up of bilirubin in the blood and tissues of the body.

108
Q

What is clinical jaundice defined as?

A

Serum bilirubin above 50micromol/L

109
Q

What are some common signs of jaundice?

A
  • Yellowing of the skin, eyes and mucus membrane
  • Pale-coloured stools (faeces)
  • Dark-coloured urine
110
Q

List the three main types of jaundice.

A

Pre-hepatic, intra-hepatic and post-hepatic.

111
Q

What is pre-hepatic jaundice?

A

Disruption before the bilirubin has been transported from the blood to the liver caused by conditions such as sickle cell anaemia or other haemolytic conditions.

112
Q

What is intra-hepatic jaundice?

A

Disruption inside the liver. Can be caused by cirrhosis with reduced hepatocyte function to conjugate bilirubin, or Gilbert’s Syndrome where there is a slower metabolism of bilirubin due to reduced levels of glucuronyl transferase.

113
Q

What is post-hepatic jaundice?

A

Disruption that prevents the bile from draining out of the gallbladder and into the digestive system caused by conditions such as gallstones or tumours.

114
Q

What is ascites?

A

An accumulation of fluid within the peritoneum that can be very painful and uncomfortable for the patient.

115
Q

What are some causes of ascites?

A
  • Albumin levels
  • Fluid retention
116
Q

What is the first-line treatment for ascites?

A

Fluid restriction, usually 1.5L daily, but sometimes much more aggressive restriction, and sodium restriction.

117
Q

What is the second-line treatment for ascites?

A

Adding in diuretics, such as spironolactone and furosemide.

118
Q

What is a potential problem with using diuretics to treat ascites?

A

Patients sometimes struggle with the diuretic burden

119
Q

What are some cautions associated with the use of diuretics to treat ascites?

A
  • Lowers blood pressure.
  • Lowers sodium and can increase/lower potassium levels.
  • Side effects of dizziness and increased urination.
120
Q

What is the third-line treatment for ascites?

A
  • Paracentesis
  • TIPS procedure
121
Q

When would a patient be considered for a third-line treatment for ascites?

A

If they are not tolerating diuretics, they would be classed as diuretic resistant.

122
Q

What is the mortality rate for diuretic resistant ascites?

A

25-50% mortality rate within 12 months

123
Q

What is a paracentesis?

A

A needle is inserted into the abdomen to drain fluid.

124
Q

What must be done when performing a paracentesis?

A

Maintain adequate circulating volume with colloids, albumin and potentially terlipressin.

125
Q

What should be given for every 2L of fluid drained during a paracentesis?

A

100mL albumin. Normal saline should be avoided as this will just accumulate back in the abdomen.

126
Q

What are the risks associated with a paracentesis?

A
  • Infection
  • Increased risk of varices or other bleeding
127
Q

What is the main purpose of a paracentesis?

A

To relieve pressure. It is not a long-term fix.

128
Q

What does TIPS stand for?

A

Transjugular intrahepatic portosystemic shunt

129
Q

Describe how portal hypertension affects blood flow before a TIPS procedure.

A

Portal hypertension causes blood flow to be forced backward, causing veins to enlarge and varices to develop across the oesophagus and stomach from the pressure in the portal vein. The pressure backup also causes the spleen to enlarge.

130
Q

Describe how blood flow is affected after a TIPS procedure.

A

The shunt allows the blood to flow normally through the liver to the hepatic vein. This reduces portal hypertension and allows the veins to shrink to a normal size, helping to stop variceal bleeding.

131
Q

What must be monitored in patients with ascites?

A
  • Daily U&Es – especially sodium, potassium, and creatinine
  • Daily weight – aim for 0.5-1kg/day loss
  • Fluid chart – note fluid restriction, urine output
132
Q

What should be avoided in patients with ascites?

A

High sodium preparations (e.g. soluble preparations)

133
Q

What are some complications associated with ascites?

A
  • Dilutional hyponatraemia
  • Hepatic Encephalopathy (HE)
  • Hepatorenal Syndrome (HRS)
  • Gynaecomastia
  • Hyperkalaemia
  • Muscle cramps
  • Spontaneous Bacterial Peritonitis (SBP)
134
Q

What is Spontaneous Bacterial Peritonitis (SBP)?

A

Infection of the ascitic fluid without an intra-abdominal source of sepsis

135
Q

Where does SBP usually originate?

A

75% from gut, 25% from skin

136
Q

What is the neutrophil count in SBP?

A

> 250 cells per mm3

137
Q

What is the mortality rate associated with SBP?

A

~40%

138
Q

What medications can be used to treat SBP?

A
  • 3rd gen cephalosporins
  • Co-amoxiclav
  • Tazocin
139
Q

What medications can be used as prophylaxis for SBP?

A

Norfloxacin / ciprofloxacin

140
Q

What is hepatic encephalopathy (HE)?

A

Brain dysfunction. Can occur in acute or chronic liver disease. Classified into 4 main clinical grades.

141
Q

What are the main theories for the cause of HE?

A

Accumulation of toxins
Increased BBB permeability
Increased levels of neurotransmitters

142
Q

What are some potential precipitating factors of HE?

A

Increased protein load
Reduced ammonia secretion
Electrolyte imbalance / disturbance
Infections
Dehydration
Drugs

143
Q

What are some conditions with similar symptoms to HE?

A

Hypoglycaemia
Alcohol intoxication
Alcohol withdrawal

144
Q

How is ammonia produced?

A

From dietary amino acids and by catabolism of amino acids, amines, nucleic acids, glutamine and glutamate (nitrogenous wastes) in peripheral tissues (especially skeletal muscle).

145
Q

How do gastrointestinal micro-organisms contribute to ammonia production?

A

They convert dietary amino acids and urea into ammonia in the gastrointestinal system.

146
Q

What happens to ammonia after it is absorbed into the portal circulation?

A

It is taken up by the liver and converted, via the urea cycle, into urea.

147
Q

What happens to urea after it is produced in the liver?

A

It is excreted into the gastrointestinal system and into the urine.

148
Q

What proportion of ammonia is shunted into the urea cycle?

A

80-90%

149
Q

What happens to the ammonia that is not shunted into the urea cycle?

A

The remaining 10-20% is metabolised by peripheral tissues, including the kidney, heart, and brain.

150
Q

What is asterixis?

A

Also known as liver flap, it is a tremor of the hand when the wrist is extended, sometimes said to resemble a bird flapping its wings.

151
Q

What are the treatment options for HE?

A

Lactulose
Rifaximin
Metronidazole
Neomycin
Sodium benzoate

152
Q

What is the aim of lactulose treatment?

A

2-3 loose stools per day

153
Q

How does lactulose work?

A

Promotes growth of beneficial micro-organisms
Reduces gut protein load
Lowers colonic pH which discourages ammonia producing bacteria

154
Q

When are enemas used in HE treatment?

A

When the patient is constipated

155
Q

What is the standard dose of rifaximin for HE?

A

550mg twice daily

156
Q

Describe the properties of rifaximin.

A

Semi-synthetic rifamycin derivative that is poorly absorbed resulting in reduced systemic side effects.
It is broad-spectrum with activity against aerobic and anaerobic, gram positive and negative organisms.

157
Q

How does rifaximin work?

A

Binds to the β-subunit of bacterial DNA-dependent RNA polymerase resulting in inhibition of bacterial RNA synthesis
Reduces gut bacteria that would produce ammonia, reduces absorption of ammonia from intestinal lumen

158
Q

When should rifaximin not be used?

A

In acute infection
When patient on broad-spectrum antibiotics

159
Q

What is portal hypertension caused by?

A

Increased resistance to flow due to:
1. Disruption of hepatic architecture
2. Compression of hepatic venules by regenerating nodules

160
Q

What is the effect of collateral vessels forming?

A

They enable blood to bypass the liver.

161
Q

What is a serious complication of portal hypertension?

A

Variceal bleed.

162
Q

What is the mortality rate associated with variceal bleeds?

A

50% index bleed
30% for subsequent bleeds

163
Q

What is the mechanism of action of terlipressin in treating variceal bleeds?

A

Increases the tone of vascular and extravascular smooth muscle cells. The increase in arterial vascular resistance leads to decrease of splanchnic hypervolemia. The decrease of the arterial blood supply leads to reduction of pressure in the portal circulation.

164
Q

Describe the properties of terlipressin.

A

Synthetic analogue of vasopressin which acts on 3 vasopressin receptors
Greater selectivity for V1 and longer half-life

165
Q

What is the effect of V1a receptor activation?

A

Very potent splanchnic vasoconstriction (also liver gluconeogenesis, platelet aggregation and release of factor VIII)

166
Q

Describe the biphasic action of terlipressin.

A

Immediate vasoconstriction effect
Prolonged effect with transformation of terlipressin in-vivo to lysine vasopressin

167
Q

What is the standard dose of terlipressin?

A

1-2mg every 4-6 hours, continued until haemostasis achieved

168
Q
A

Y2 (6 decks)

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