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Unit 10 > Week 2: Liver function > Flashcards

Week 2: Liver function Flashcards

1
Q

Give an overview of the 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
6. Detoxification of harmful substances absorbed from the GIT

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2
Q

What vessels supply blood to the liver?

A

Recives oxygenated blood from the hepatic artery (branch of coeliac trunk)
Recives oxygen-depleted but nurient rich blood from the hepatic portal vein

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3
Q

Describe the dynamics of blood flow to the liver and why this important for its function.

A

Recieves 300mL per minute from the hepatic artery
Recives around 1litre of blood per minute from the portal vein.
This is around 27% of cardiac output
Pressure in the hepatic vein is ommHg, pressure in the hepatic portal vein is 9mmHg, this difference in pressure means the liver has low resistance to blood flow and a low blood pressure.

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4
Q

Describe the importance of the liver as blood store?
How can it act as a blood store?

A

Is an expandable organ so can store large amounts of blood - up to 450ml.

This is common in cardiac failure when high pressure in right atrium causes backpressure (peripheral congestion) hence expansion in the liver.

This allows the liver to act as a store and source of blood

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5
Q

What is the basic functional unit of the liver?
Describe its structure?

A

A liver lobule

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6
Q

What is the flow of blood out of the liver?

A

Central veins
Unite into the left, right and middle hepatic veins, into the IVC

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7
Q

What are the features of hepatic plates?

A

Generally two layers of hepatocytes thick
interspaced with bile canaliculi that empty into the bile ducts

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8
Q

What is the role of space of disse?

A

Contains stellate cells
Plasma content/proteins drain easily into the space due to sinusoidal capillaries in the sinusoids.
Drains excess fluid into lymphatic vessels in the interlobular septa

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9
Q

What is the role of kupfer cells?

A

Macrophages like cells in the liver
Phagocytose pathogens, ageing erythrocytes and particulate matter and foreign matter in the hepatic sinus blood - final part of gut barrier.
Line the sinusoids alongside endothelial cells.

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10
Q

How do capillaries found int he liver vary from capillaries found elsewhere in the body?

A

Are sinusoidal
Have a high filtration co-efficient
Has large intercellular gaps and fenestrations and an incomplete basement membrane
This allows for efficient transport between blood and hepatocytes via the Space of Disse

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11
Q

Describe how altered activity of Kupfer cells can result in pathology

A

Normally have a high level of tolerance - to prevent unwanted immune response against gut content
Loss of tolerance - inflammatory response - due to close proximity to parenchymal and stromal cells int he liver can cause hepatocellular injury. This is the case in non-alcoholic fatty liver disease
Absense of lowered activity increases risk of systemic infections

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12
Q

What is the function of hepatocytes?

A

Secretory epithelial cells - specialised for exchange between the space of disse and bile canaliculi.
Uptake metabolism and excrete bile salts, biluribin, drugs and toxins.

Method of bile:
1. Uptake blood from sinusoidal membrane
2. Transport within cell
3. Control chemical modification or degradation
4. Export bile across the canalicular membrane

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13
Q

What is the physiological function of hepatic stellate cells?

A

Found in space of disse
Responsible for storing vitamin A in large lipid droplets inside the cell cytoplas,

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14
Q

What cell type can stellate cells transition into?
What is the consequence of this?

A

Activated and transformed into myofibrilbasts
Differentiated cell type for wound healing and tissue remodelling
Often occurs due to liver injury.
Helps remodel ECM, produce cytokines and deposit collagen.
In pathological condition can cause cirrhosis

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15
Q

Describe the changes that occur in liver injury that lead to fibrosis

A

Activated kupffer cells (from acetyldehde in alcohol consumption) secrete cytokines, chemokines, ROS and RNS - this changes the activity of stellate cells and hepatocytes
Hepatocytes loose microvilli and are gradually destroyed. Bile ducts and endothelial cells are also destroyed.
Endothelial cells loose fenestrations making filtration between the blood and hepatocytes harder.
Stellate cells become myofibroblasts - leading to VitA depletion, fibrosis narrowing the space of dissee.

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16
Q

Describe the gross appearance of a healthy liver.

A

Smooth surface with a homogenous texture
Red in colour

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17
Q

Describe the histological appearance of a healthy liver.

A

Sinusoids are organised
Vascular strucutres are evenly distributed
No/very little fibrosis
Regulate hepatocyte lobules

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18
Q

Describe the gross appearance of a cirrhotic liver.

A

Orange- tawny colour
Irregular surface with a nodular texture

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19
Q

Describe the histological features of a cirrhotic liver

A

Architecture is disorganised
Nodules surrounded by heavy fibrosis
fibrous disrputs the hepatocyte plates within a lobule and marks the boundaries between previous lobules

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20
Q

What substances might the liver store?

A

Glucose
Vitamin B12
Vitamin D
Vitamin K
Copper
Iron

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21
Q

What substances does the liver degrade?

A

Insulin
Bilirubin
Ammonia
Drugs

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22
Q

What metabolic processes occur in the liver?

A

Carbohydrate - gluconeogenesis, glycogenesis, glycogenolysis
Lipid - cholesterol synthesis and lipogenesis

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23
Q

What substances are synthesised in the liver?

A

Serum albumin
Coagulation factors
CRP
Carrier proteins (haptoglobin etc)
Hormones (IGF-1, and thrombopoietin)
Pro-hormones (angiotensinogen
Apoplipoproteins
Complement proteins
Non-essential amino acids

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24
Q

Describe the process of cholesterol metabolism in the liver?

A

Acetyl CoA is derived from glucose, FA and AA
Acetyl-Coa is converted to HMG-CoA
Then mevalonate
Then cholesterol
Cholesterol is utilised by the liver.
Cholesterol is exported to the blood in the form of very low density lipoproteins VLDLs.

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25
Q

What factors influence the rate of cholesterole synthesis in the liver?

A

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

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26
Q

Describe the process of lipid transport from the GIT to the liver.

A

Lipids are absorbed from the GIT into plasma in the form of chylomicrons
Lipoprotein lipase enzyme (LPL) breaks triglycerides into FA and glycerol.
These enter nearby cells for storage or energy production
The chylomicron remnants are transported to the liver and broken down

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27
Q

What are lipoproteins?
What makes different types different?

A

Are transport vehicles for moving water-insoluble lipids around the body.
All made up of cholesterol, triglycerides, phospholipids and protein but in different concentration.

Vary in density with denser lipoprotein containing more protein and less triglyceride

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28
Q

Describe what happens to chylomicrons and lipids in the liver.

A

May be modified to produce cholesterol, TG, Phospholpipids and cholesterol esters
Incorporated into VLDL.
Released into the blood stream to travel to cells

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29
Q

Describe what happens to VLDL when it leaves the liver?

A

Travels in blood stream, LPL enzyme breaks triglycerides down into FA and glycerol
Loss of triglycerides results in the formation of less hence lipoprotein
INtermediate > Low density lipoprotein
LDL is needed to transport cholesterol to body cells.
HDL picks up excess cholesterol that returns to the liver is remodified to cholesterol and repackaged as VLDL

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30
Q

What is the consequence of too much LDL?

A

Increased risk of cardiovascular disease

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31
Q

What is the role of High Densirty Lipoprotein?

A

HDL
Made in the liver and GIT
Very dense as high protein content.
Pick up cholesterol from the body cells and return to the liver for disposal

32
Q

What does the Liver metabolise cholesterol into? for usage in liver system

A

Synthesise bile
This includes primary bile acids - cholic acid and chendeoxycholic acid
Cholesterol and cholesterol esters are also included in bile directly

33
Q

How are secondary bile acids produced?

A

Primary bile salts are hydroxylated by bacteria in terminal ileum and colon.

34
Q

What are the different secondary bile acids?

A

Deoxyhcholic Acid
Lithocholic Acid

35
Q

How are bile salts produced?

A

Primary/Secondary Bile acids are conjugated with glycine or taurine in the liver.

36
Q

What are the different components of bile?

A

Bile salts
Cholesterol
Phospholipids
Bile pigments
Ions
Water

37
Q

What is meant by enterhepatic circulation?

A

A loop consisting off:
Primary bile acids (and bile) secreted in liver
May be converted into secondary bile acids
Return to the liver in portal blood

38
Q

What drug might be offered to prevent a build up in cholesterol?

A

Statins
Inhibit HMG-CoA reductase
This prevents the conversion of HMG-CoA to mevalonate - a step in cholesterol metabolism in the liver
Results in inhibited cholesterol production

39
Q

What is the role of albumin?

A

Regulate blood volume - main osmolarity factor
Transporter of endogenous and exogenous molecules

40
Q

What happens in the liver during protein metabolism?

A

Amino acids are acted on by enzymes (such as ALT) to cause transamination and deamination.
Non-nitrogenous part is then converted to glucose (gluconeogenesis) or lipids.
Produce non-essential fatty acids.
Hepatocytes also synthesise new plasma proteins

41
Q

What are some of the plasma proteins produced in the liver?
Seperated by role

A

Metabolism - albumin and lipoporteins
Inflammation: CRP and C3
Endocrine: angiotensinogen, plasma binding protein
Blood coagulation: pro-thrombin, plasminogen, fibrinogen, Factor 7,9,10

42
Q

Give an overview of the role of the liver in maintaining normal blood glucose levels.

A

Regulates blood glucosee by glycogen syntehsise and breakdown.
Site of glycogenolysis, gluconeogenesis and glycogen storage.
These processes are infuelcned by insulin, glucagon, catecholamines and the sympathetic nervous system.

43
Q

What are the three main precursors to gluconeogenesis?

A

Lactate - from anaerboic glycolysis in exercising muscles and from rbcs via the Cori cycle.

Glycerol - released from the adipose tissue during the breakdown of triglycerides

Amino acids - mainly alanine from the break down of protein

44
Q

What process occurs during high blood glucose?

A

insulin is secreted from pancreatic β-cells.
This causes decreased gluconeogenesis and glycogenolysis, and increased glycogen storage.

45
Q

What process occurs during low blood glucose?

A

Glucagon and glucocorticoids work together to increase gluconeogenesis and glycogenolysis and reduced glycogen storage

46
Q

Does glucose promote anabolism or catabolism?

A

Anabolism

47
Q

What is the role of insulin in adipose tissue?

A

Increase glucose uptake - exocytotic insertion of GLUT4
Increased glycogen storage - transcription of hexokinase and glycogen synthases
Promotes triglyceride production - increases esterfication and inhibits hormone sensitive lipase

48
Q

What is the role of insulin in skeletal muscle?

A

Increase glucose uptake - eoxcytotic insertion of GLUT4
Increased glycogen storage - transcription of hexokinase and glycogen syntahse
Promotes protein production
Promotes glycolysis

49
Q

What is the role of insulin in the liver?

A

Increase glycogen storage - transcription of hexokinase and glycogen syntahse
Promotes protein production
Promotes glycolysis
inhibits gluconeogenesis
Promotes the synthesis and storage of fats

50
Q

What enzymes are involved in gluconoegnesis in the liver?

A

PEPCK - gluconeogenic enzyme, hepatocytes to produce glucose from pyruvate derived main acid metabolism - oxaloacetate to pyruvate precursor
Fructose 1,6 biphosphatase and glucose 6-phosphatase

51
Q

Is glucagon catabolic or anabolic

A

Catabolic

52
Q

What is the role of glucafon in the adipose tissue?

A

Accelerates lipolysis - increase FA available for use in gluconeogenesis in the liver

53
Q

What is the role fo glucagon in the liver?

A

INhibits glycolysis
Promotes glycogenolysis - activates glycogen phosphorylase
Activates gluconeogenesis (activate PEPCK< fructose 1,6 bisphosphate and glucose 6-phosphatase)
Promotes oxidation of fats and formation of ketone bodies (increasing activity of carnitine acetyltransferase)

54
Q

How will the activity og glucagon reflect on blood tests?

A

Increased blood glucose
Increased blood fatty acids
increased blood ketones

55
Q

How will the acticity of insulin relfect on blood tests?

A

Decreased blood glucose
Decreased blood fatty acids
Decreased blood ketones
Decreased blood amino acids
Decreased K+

56
Q

Describe how the liver coordinates the response to fasting.

A

First few hours of starvation - mainly relies of glycogenolysis. Glycogen stores are rapidly depleted.
Eventually over first 24 hours - switches from carbohydrate to fat metabolism.
Lipolysis and ketongensis are used initially peaking at 12 hours.
Gluconeogenesis from amino acids and glycerol will also increase to a lesser extent, reaching a peak at 48 hours.
Protein is often used to feed the CNS, whilst ketones and FA supply other tissue.
However, after 2 days cells change to rely on ketones, FA or the cori cycle - less demand for glucose for gluconeogenesis can decrease protein catabolism to preserve vital functional proteins.
As a consequence of this fatty acids are used elsewhere and ketones are prioritised for usage in the CNS.

57
Q

What is ketoacidosis?

A

ketone production in normally prevented by insulin.
Absence of insulin and maintained presence of glucagon causes the release of fatty acids and glycerol from adiposcytes
Fatty acids can be rapidly converted to acetyl-CoA then ketone bodies in the liver.
Ketones acidify the blood stream leading to vomiting.
Patients can become rapidly dehydrated and fall into a coma
If conincidied with hyperglycaemia (due to lack of insulin) urine output increases.
Diabetic ketoacidosis is a medial emergency

58
Q

What are the three different ketone bodies that can be produced?

A

Acetoactate - acidemia, anions of strong salt
Acetone - sweet smell detected on breath
Beta-hydroxybutyrate - academia, anions of strong salt

59
Q

What is the reticuloendothelial system?

A

System of fixed and circulating phagocytic cells

60
Q

What colour is billirubin?

A

Yellow

61
Q

Describe the initial process of red blood cell breakdown to produce unconjugated bilirubin.

A

Marcophages in teh reticuloendothelial system metabolise the haemoglobin in rbcs into haem and globin.
Globin is broken down into amino acids which can be recycled
Haem is broken down in iron and unconjugated bilirubin
The iron can be recyled

62
Q

What is the role of haem oxygenase?

A

Breaks haem down into iron and unconjugated bilirubin

63
Q

How does unconjugated bilirbuin reach the liver?

A

Is insoluble in water
Needs to be bound to albumin to travel in the bloodstream to the liver.

64
Q

What happens to unconjugated bilirubin in the liver?

A

Glucuronyl transferase adds glucuroninc acid to unconjugated bilirubin to form conjugated bilirubin (which is soluble)
Conjugated bilirubin can then be excreted into the duodenum by the gallbladder

65
Q

What happens to bilirubin in the small intestine?

A

Bacteria deconjugate bilirubin to form urobilinogen
Some of this can be further oxidised by bacteria to form sterocobilin which is excreted through faeces

66
Q

What happens to urobilinogen that is not excreted in faeces?

A

Reabsorbed into the blood stream as part of enterohepatic circulation
Some is recycled to produce bile in the liver
Some reaches the kidney and is oxidised into urobilin which is excreted in urine to give its characteristic coloue

67
Q

What are the potential causes of increased urobilin excretion in the urine?

A

Increased production of bilirubin
Increased reabsorption of urobilinogen from the colon
Decreased hepatic clearance of urobilinogen

68
Q

Describe what causes jaundice

A

Damaged hepatocytes can no longer conjugate bilirubin or release bilirubin, this causes conjugated or unconjugated bilirubin to leak back into the plasma.
Accumulates to high concentrations - giving a yellow colour in the collagen rich skin and sclera
Excess bilirubin may also be excreted in the urine turning it a darker colour than normal.

69
Q

Describe the important role the liver plays in iron homeostasis?

A

Hepatocytes contain large amount of apoferritin
During high conc iron, apoferritin binds reversibly to iron to form ferritin
In low conc iron ferritin released iron to increase supply
Therefore the liver acts as a blood iron buffer and an iron storage medium

70
Q

What is cirrhosis of the liver?

A

Scarring (fibrosis) of the liver caused by long term liver damage.
This scarring prevents liver function
Destroyed hepatocytes are replaced with fibrous tissue that eventually contracts around the blood vessels impeding portal blood flow - results in portal hypertension.
Often caused by chronic alcoholism or excess fat accumulation in the liver and subsequent inflammation

71
Q

Describe the effect of cirrhosis on the architecture of the liver.

A

Triggers stellate cells to adapt a myofibroblast-like phenotype and deposit collagen in the Space of Disse.
This leads to compression of the sinusoidal capillaries - increasing resistance to blood flow from the sinusoids into the hepatic vein
Collagen also blocks fenesterations in sinusoidal capillaries

72
Q

How does cirrhosis affect albumin levels?

A

Collagen depositis block fenestration in the sinusoidal capillaries
Reduces movement of albumin from hepatocytes into circulation - leading to hypoalbuminenia

73
Q

What are some clinical features of liver cirrhosis?

A

Tiredness and weakness
Nasuse and loss of appetite - weight loss
Spider naevia
Jaundice
Vomiting blood
Pale coloured faeces
Ascites
Dark urine
Bleeding or brusining easily
Oedema
Gynaecomastia

74
Q

Describe the mechanism underpinning ascites formation

A

1.Liver cirrhosis leads to increased resistance to blood flow causing portal hypertension.
2.Reduced plasma albumin content, combined with portal hypertension increases fluid filtration across hepatic and intestinal capillaries causing an increase in peritoneal fluid volume. Splanchnic blood pooling continues
3. Less blood drains back into the IVC, reduces IVC blood pressure and triggers reduced firing of cardiopulmonary baroreceptors, this is interpreted as a fall in blood volume and body attempts to increase blood vol.
4. Triggers sympathetic outflow to the kidneys to trigger RAAS and increase Na+ reabsoprtion
5. Increased Na+ blood content and increase blood volume - this helps cope with the loss of fluid and causes overt symptoms of ascites as exaggerates fluid movement into peritoneal cavity

75
Q

How does splanchnic circulation worsen portal hypertension in liver cirrhosis?

A

Pooling of blood in splanchnic arteries, causing NO release in arterioles increasing blood flow by splanchinc arteriolar vasodilation. This increases the blood stored within splanchnic veins and causes portal hypertension.

76
Q

What medication can be given to help prevent ascites?

A

Spironolactone (a potassium-sparing diuretic)
Blocks aldosterone receptor-mediated action
Reduced ability to support an expanded blood volume
Slows filtration into the peritoneal cavity and allows the lymph system to redistribute some fluid from the peritoneal fluid into the blood stream

Unit 10 (37 decks)

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