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Clinical Unit 10 > Liver Function > Flashcards

Liver Function Flashcards

1
Q

5 Functions of the liver

A
  1. Filtration and storage of blood
  2. Metabolism of carbohydrates, proteins, fats, hormones and foreign chemicals
  3. Formation of bile
  4. Storage of vitamins and iron
  5. Formation of coagulation factors
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2
Q

What is a Kupffer cell

A
  • Resident macrophages that line the sinusoids
  • Acts as final component of the gut barrier to pathogens taken up via the GI system
  • Help to remove ageing erythrocytes and particulate matter from the blood
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3
Q

What are hepatocytes

A

Secretory epithelial cells specialised fro exchanging solutes between the space of disse and the bile canaliculi

Are able to uptake, metabolise and excrete a wide range of solutes (bile salts, bilirubin, drugs and toxins)

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4
Q

What is the function of hepatocytes?

A
  1. Import the compounds from the blood across its sinusoidal membrane
  2. Transport the material within the cell
  3. Can chemically modify or degrade the compound
  4. Excrete the molecule or its product/s into the bile
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5
Q

What are organic anion transporters (OAT)?

A
  • Membrane proteins
  • Members of the SLCO family

They mediate the Na+ independent uptake of a wide range of compounds (bile acids, bilirubin, eicosanoids, steroid and thyroid hormones, prostaglandins, statin drugs, methotrexate)

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6
Q

What are hepatic Stellate cells?

A

At rest- responsible for storing vitamin A in large lipid droplets inside of the cell

Once activated- participate in fibrogenesis through remodelling of the ECM, production of cytokines and deposition of type I collagen (can lead to cirrhosis)

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7
Q

What are the liver’s functions of fat metabolism?

A
  1. Oxidation of fatty acids to supply energy for other body functions
  2. Synthesis of large quantities of cholesterol, phospholipids and most lipoproteins
  3. Synthesis of fat from proteins and carbohydrates
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8
Q

How does the liver obtain cholesterol?

A
  1. Intestine- dietary cholesterol as chylomicrons (chylomicrons transport dietary triglycerides, in adipocytes and muscle lipoprotein lipase enzyme hydrolysis triglycerides to fatty acids and glycerol, the resultant cholesterol-enriched remnant chylomicrons are delivered as cholesterol to the liver)
  2. The liver takes up cholesterol in low-density lipoproteins (LDLs)
  3. The liver synthesises cholesterol itself- fat is split into glycerol and fatty acids, fatty acids are split into acetyl coenzyme A (acetyl CoA)
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9
Q

Explain Cholesterol metabolism in the liver

A
  • Acetyl CoA -> 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) -> mevalonate -> cholesterol -> very-low-density lipoproteins (VLDLs) into the blood

Hepatic synthesis of cholesterol is:

  • Inhibited by dietary cholesterol and fasting
  • Increased with bile drainage and bile duct obstruction
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10
Q

Coagulation factors formed in the liver:

A
  • Fibrinogen
  • Prothrombin
  • Accelerator globulin
  • Factor VII (and other important factors)

Vitamin K is needed to form these substances (absence of VK causes levels to drop and can prevent blood coagulation)

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11
Q

Carbohydrate metabolism in the liver

A
  • Regulation of blood glucose by glycogen synthesis and breakdown
  • Gluconeogenesis
  • Conversion of carbohydrate and proteins into fatty acid and triglyceride
  • Controlled by insulin, glucagon, circulating catecholamines and the sympathetic nervous system
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12
Q

What is the effect of insulin on: Skeletal muscle

A
  • Increase glucose uptake
  • Increase glycogen storage
  • Promotes protein production
  • Promotes glycolysis
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13
Q

What is the effect of insulin on: Liver

A
  • Increase glycogen storage
  • Promotes glycolysis
  • Inhibits gluconeogenesis
  • Promotes the synthesis and storage of fats
  • Promotes protein production
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14
Q

What is the effect of insulin on: Adipose tissue

A
  • Increase glucose uptake
  • Increase glycogen storage
  • Promotes triglyceride production
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15
Q

Role of glucagon in: Skeletal muscle

A

Activates proteolysis

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16
Q

Role of glucagon in: Liver

A
  • Promotes glycogenolysis
  • Inhibits glycolysis
  • Activates gluconeogenesis
  • Promotes oxidation of fats and formation of ketone bodies
17
Q

Role of glucagon in: Adipose tissue

A

Accelerates lipolysis

18
Q

Explain the cori cycle

A

Blood: glucose - enters muscle
Muscle: glucose (glycolysis) -> 2 pyruvate (and 2 ATP) -> 2 lactate
Blood: 2 lactate - enters liver
Liver: 2 lactate -> 2 pyruvate (uses 6 ATP for gluconeogenesis) -> glucose

19
Q

How does ketoacidosis occur?

A
  • Absence of insulin and maintained presence of glucagon
  • Body releases free fatty acids from adipocytes
  • They are rapidly concerted to ketone bodies in liver
  • Acidify the bloodstream- leading to vomiting
  • Patients rapidly become dehydrated and can fall into a coma

Diabetic ketoacidosis is a medical emergency

20
Q

Describe bilirubin metabolism

A
  • Breakdown of ageing RBC by the reticuloendothelial system
  • Usually carried in the bloodstream bound to albumin
  • It is deconjugated (disruption of conjugated double bonds leading to loss of conjugation) by intestinal bacteria and converted to colourless urobilinogen
  • Further bilirubin metabolism is responsible for colouring urine and faeces

Excess bilirubin in ECF = jaundice

21
Q

Pathophysiology of liver cirrhosis:

A
  • Liver parenchymal cells are destroyed
  • Replaced with fibrous tissue that eventually contracts around the blood vessels impeding the flow of portal blood through the liver
  • Portal system is also occasionally blocked by a large clot developing in portal vein (or its major branches) = portal hypertension -> death

Cirrhosis is scarring of the liver caused by long term liver damage

22
Q

Pathophysiology of Ascites

A
  • Cirrhosis triggers stellate cell to assume myofibroblast-like phenotype
  • Causes them to deposit collagen in the space of disse
  • Contract leading to compression of sinusoidal capillaries- increasing resistance of blood flow through sinusoids into hepatic vein
  • Collagen deposits also block fenestrations in sinusoidal capillaries
  • Reduces movement of albumin from hepatocytes not the circulation -> hypoalbuminemia (low albumin in blood)
  • Increased resistance triggers sinusoidal capillary and portal hypertension
  • Portal hypertension is worsened as the build up of pressure in splanchnic circulation triggers greater NO production
  • Elicits vasodilation of the upstream arterioles of splanchnic arterioles- increasing blood flow to splanchnic circulation
  • Leads to a greater volume of blood stored in splanchnic veins
  • Reduction in plasma albumin content of blood, as well as sinusoidal and portal hypertension increases fluid filtration across hepatic and intestinal capillaries
  • Pooling of blood in splanchnic circulations and higher resistance of blood flor through sinusoids to hepatic vein leads to a reduction in blood reaching the inferior vena cava
  • Reduced volume of blood in vena cava = reduction of blood pressure there
  • Triggers reduced firing of the cardiopulmonary baroreceptors
  • Important in blood volume regulation
  • When firing falls, body interprets it as a fall in blood volume and acts to expand blood volume (in reality it hasn’t changed, its just abnormally distributed)
  • Triggers increased sympathetic outflow to kidneys
  • Triggers increased Na+ absorption and activation of renin-angiotensin II-aldosterone system
  • Angiotensin II and aldosterone increase blood volume by stimulating an increase in Na+ content of blood (occurs via dietary intake increase and reduced loss of Na+ in urine- also increase thirst)
  • Helps expand blood volume
  • Ensures the body can support large-scale loss of water from the blood into peritoneal cavity
23
Q

How does spironolactone reduce ascites

A

It reduces the ability of the body to support an expanded blood volume

This slows filtration of fluid into peritoneal cavity and allows lymph system to start to redistribute some of the peritoneal fluid back into the bloodstream

Clinical Unit 10 (3 decks)

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