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P1: GI > Liver and its Functions > Flashcards

Liver and its Functions Flashcards

1
Q

What divides the liver into 2 lobes?

A

→ Falciform ligament

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2
Q

What is the biliary tree?

A

system of ducts to transport bile out of the liver into small intestine

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3
Q

Where is the blood supply of the liver from?

A

→ Portal vein - Blood returning from the GI tract
- 75%
→ 25% - hepatic artery

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4
Q

Where do the central veins of the liver lobules drain?

A

→ Into the hepatic vein

→ Back into the vena cava

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5
Q

What do hepatocytes do?

A

→ 60% perform most metabolic functions

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6
Q

What do Kupffer cells do?

A

→ 30% types of tissue macrophages

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7
Q

What cells other than hepatocytes and kupffer cells does the liver have?

A

→ Stellate

→ Endothelial

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8
Q

What is the functional unit of the liver?

A

→ Hepatic lobule

→hexagonal plates of hepatocytes around central hepatic vein.

→at each of 6 corners is triad of branches of portal vein, hepatic artery and bile duct

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9
Q

What is around the central hepatic vein?

A

→ Hexagonal plates of hepatocytes

→ At each of the 6 corners is a triad of branches of the portal vein, hepatic artery and bile duct

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10
Q

Where does blood enter the lobules from and flow to?

A

→ Branches of the portal vein and hepatic artery
→Flows through small channels called sinusoids that are lined with hepatocytes
→ Hepatocytes remove toxic substances from the blood
→ Blood exits the lobule through the central vein
→ Blood flows in opposite direction to the bile

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11
Q

What is the oxygenation like at the hepatic artery?

A

→ Oxygen rich

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12
Q

Why does blood leaving the lobule have low levels of O2?

A

→ Hepatocytes near the sinusoids have used up the O2

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13
Q

Describe the flow of bile

A 
→ Bile is secreted by hepatocytes
→ Series of channels between cells (canaliculi)
→Small ducts
→ Large ducts
→ Anastomose onto common bile duct
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14
Q

How does the livers microstructure support its role?

A

→ Large SA - exchange of molecules
→ Sophisticated separation of blood from bile
→ Specific positioning of pumps to achieve localization of materials

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15
Q

How is portal blood filtered?

A

→ Through the sinusoid - removal of gut bacteria

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16
Q

What is bile?

A

→ Complex fluid : Water, electrolytes + mix of organic molecules
→ Organic molecules : bile acids, cholesterol, bilirubin + phospholipids

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17
Q

What are the functions of bile?

A

→ Essential for fat digestion + absorption via emulsification
→ Bile and pancreatic juice neutralize gastric acid as it enters the small intestine
→ Elimination of waste products from blood - bilirubin + cholesterol
→ 500mg of cholesterol converted to bile acids per day

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18
Q

Describe how bile gets to the gall bladder

A

→ Bile from hepatic ducts
→ Common bile duct
→ Duodenum or diverted via cystic duct
→ Gall bladder
→ Concentrated and stored (30-50ml)
→Released by cholecystokinin in response to presence of fat in duodenum
Causes contraction of gall bladder and relaxation of the sphincter

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19
Q

How is entry of bile into the duodenum controlled?

A

→ Opening of the sphincter of Oddi

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20
Q

What is bilirubin?

A

→ Yellow pigment formed from the breakdown of Hb

→ Useless and toxic but made in large quantities so must be eliminated

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21
Q

How are aged RBCs destroyed?

A

→ Dead/ damaged RBCs are digested by macrophages throughout the body
→ Fe is recycled
→ Globin chains are catabolized
→ Hb cannot be recycled so it is eliminated into bilirubin

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22
Q

How is bilirubin formed?

A

→ Heme is converted into free bilirubin in a series of steps
→ Released into the plasma and it is carried around bound to albumin
→ Free bilirubin is absorbed by hepatocytes and conjugated with glucuronic acid
→ Conjugated bilirubin is secreted into bile and metabolized by bacteria in the intestinal lumen
→ Eliminated in feces + urine
→Unconjugated bilirubin is conjugated to glucuronic acid

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23
Q

What is the major metabolite in feces?

A

→ Stercobilin

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24
Q

What is the major metabolite in urine?

A

→ Urobilin and urobilinogen

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25
Q

How is jaundice caused?

A

→ Excessive quantities of free or conjugated bilirubin accumulate in ECF

26
Q

What are the symptoms of jaundice?

A

→ Yellow discolouration of the skin, sclera and mucous membranes

27
Q

What is green jaundice caused by?

A

→ mutation of biliverdin reductase

facilitates the conversion of biliverdin to bilirubin

28
Q

What is pre hepatic jaundice?

A

→ excessive RBC breakdown
→ Excess unconjugated bilirubin is not excreted & remains in circulation
→Can be treated with phototherapy- causing isomerisation of bilirubin
→RBC are broken down after birth to have adult haemoglobin

29
Q

What is hepatic jaundice?

A

→ Hepatocyte damage

→Excess conjugated &/ unconjugated bilirubin

30
Q

What is post hepatic jaundice?

A

→ excess conjugated bilirubin
→ Obstruction into passage of duodenum
→ Enters circulation & into urine
→ pruritus(itch)

31
Q

What is used for neonatal jaundice in low resource countries?

A

→ Sunlight canopies
→Filters out most of the or sunburn. ray (UVA, UVB, UVC, IR etc) but allows therapeutic blue light to pass through » decreases risk of over-heating

32
Q

What toxic substances does the liver metabolize?

A

→ bilirubin
→ ammonia
→ hormones
→ Drugs & exogenous toxins

33
Q

How are steroid hormones inactivated?

A

→ By conjugation & excretion

34
Q

Why is accidental overdose common with paracetamol?

A

→ Narrow therapeutic index

35
Q

How can accumulation of fats in the liver be alleviated?

A

→ By secreting lipids into the blood

36
Q

What can be an effect of impaired detoxification?

A

→ Gynecomastia

→Enlargement of breast in men due to oestrogen accumulation

37
Q

What blood clotting factors are made in the liver?

A

→ Fibrinogen
→ Prothrombin
→ V, VI, IX, X, XII

38
Q

What is needed to make all the clotting factors?

A

→ Vitamin K
→Vitamin K is essential for formation of pro-thrombin and factors II,VII, IX & X

Converted within liver
The reduced Vit K is oxidised by carboxylase

Warfarin will block conversion of oxidised Vit K to reduced form

39
Q

What do stellate cells act as?

A

→ Important deports for storage of fat soluble vitamins (A,D,E,K)

40
Q

What does liver dysfunction lead to?

A

→ Fat malabsorption

→ Vitamin deficiency

41
Q

What vitamin does the liver store?

A

→ Vitamin B12

→ Folate

42
Q

What happens with a vitamin B12 deficiency?

A

→ Pernicious anaemia

43
Q

How is iron stored in the liver?

A

→ As ferritin

44
Q

How is bile secreted?

A

By hepatocytes:
synthesize bile salts, cholesterol & other organic constituents)

By epithelial cells lining bile ducts:
produce large quantity of watery solution of Na+ & HCO3-stimulated by hormone Secretin in response to acid in duodenum.

45
Q

Formation of bile acids…

A

→Cholesterol is converted into bile acids cholic & chenodeoxycholic acids.

→primary BAs are conjugated with amino acids glycine and to a lesser degree taurine in humans.

→This increases solubility, minimises passive absorption, and makes the BAs resistant to cleavage by pancreatic carboxypeptidase
→Exist as Na+ salts in intestine bile salts
→Bacterial metabolism in intestines- Secondary Bile Acids

46
Q

What is spider angioma?

A

→ an enlarged blood vessel in the skin (resembling the body of a spider), from which smaller blood vessels extend resembling the spider’s legs.
→more than five is indicative of liver damage.

47
Q

How do gallstones arise?

A

Imbalance in the chemical make-up of bile inside the gallbladder leads to gallstones.
→Gallstones can form anywhere along the biliary tract

48
Q

What are the two types of gallstones?

A

Cholesterol (80%) & Pigment (20%)

49
Q

Describe cholesterol gallstones

A

Risk factors cholesterol stones:
High fat diet
increased synthesis of cholesterol

Inflammation of GB epithelium changes absorptive characteristic of mucosa.
excessive absorption of H20 & bile salts  cholesterol concentrates.

50
Q

What are the risk factors of pigment gallstones?

A

Risk factors = obesity, excess oestrogen (e.g. during pregnancy), HRT

51
Q

What is the enterohepatic circulation of bile acids?

A

traverse the hepatocyte and are actively secreted into canalicular bile,

52
Q

What forms the protective barrier?

A

→Kupffer cells-found in sinusoids
Represent approx 80% of all fixed tissue macrophages

→function as mononuclear phagocyte system (MPS)

→exposed to blood from gut that contain pathogenic substances.

→clear gut-derived endotoxin from portal blood

53
Q

What happens after partial hepatectomy?

A

(removal of 70% of liver) or in response to toxic injury, they rapidly re-enter cell cycle and proliferate
→regeneration is rapid and proliferation stops once the original mass of the liver is established

54
Q

What types of cells are involved in liver regeneration?

A

Does NOT involve liver stem cells or progenitor cells, but replication of mature functioning liver cells

55
Q

What are the two pathways of liver regeneration?

A

Growth-factor mediated pathway → most important HGF (hepatocyte growth factor) and TGFα (transforming growth factor alpha)

Cytokine signalling pathway using IL-6 via TNFα binding to its receptor on Kuppfer cells

56
Q

What is the role of lipopolysaccharides in liver regeneration?

A

→upregulated after liver injury or hepatectomy and reach the liver through the portal blood supply
→They activate hepatic non-parenchymal cells
→increase the production of tumour necrosis factor (TNF) and interleukin (IL)-6.

57
Q

Describe the mechanism of liver regeneration

A

→increase in the production of tumour necrosis factor (TNF) and interleukin (IL)-6 by LPS.

→insulin, epidermal growth factor; EGF norepinepherine, hepatocyte growth factor; HGF. →Cooperative signals from these factors allow the hepatocytes to overcome cell-cycle checkpoint controls and move from G0, through G1, to the S phase of the cell cycle.
→leads to DNA synthesis and hepatocyte proliferation.

→TNF-alpha is blocked until synthesis is completed

58
Q

What is the purpose of liver function tests?

A

→Screen for liver infections, such as hepatitis
→Monitor the progression of a disease, such as viral or alcoholic hepatitis, and determine how well a treatment is working
→Measure the severity of a disease, particularly scarring of the liver (cirrhosis)
→Monitor possible side effects of medications

59
Q

What are the most common sections of the LFT?

A

Alanine aminotransferase (ALT)
Aspartarte aminotransferase (AST)
Alkaline phosphatase (ALP) - enzyme found in bile duct, indicates obstruction in bile flow
Gamma glutamyl transferase (GGT or ‘Gamma GT’) – also indicates obstruction
Bilirubin - jaundice
Albumin - decreased in chronic liver disease/malnutrition
Clotting studies, i.e. prothrombin time (PT) or international normalised ratio (INR) - if low levels of clotting factors are present, the prothrombin time is longer.

60
Q

What is the cystic duct?

A

allows bile to flow in and out of the gallbladder for storage and release.

61
Q

What is the role of sphincter of Odii?

A

controls entry into the duodenum

62
Q

What are the pathways of liver regeneration?

A

Gut-derived factors, such as lipopolysaccharide (LPS), are upregulated and reach the liver through the portal blood supply.
→They activate hepatic non-parenchymal cells (including Kupffer cells and stellate cells) and increase the production of tumour necrosis factor (TNF) and interleukin (IL)-6. ​
→Other factors are released from the pancreas (insulin), duodenum or salivary gland (epidermal growth factor; EGF), adrenal gland (norepinepherine), thyroid gland (triodothronine; T3) and stellate cells (hepatocyte growth factor; HGF).
→allow the hepatocytes to overcome cell-cycle checkpoint controls and move from G0, through G1, to the S phase of the cell cycle.
→Stellate cells produce hepatocyte growth factor allowing it to move to S-phase​
→TNF-alpha is blocked until synthesis is completed

P1: GI (15 decks)

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