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Gastrointestinal > Physiology and Pharmacology of the Liver > Flashcards

Physiology and Pharmacology of the Liver Flashcards

1
Q

What processes of carbohydrate metabolism is the liver involved in?

A

Gluconeogenesis, glycolysis, glycogenesis, glycogenolysis.

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2
Q

What processes of fat metabolism is the liver involved in?

A

Processing of chylomicron remnants, synthesis of lipoproteins (for export) and cholesterol (for steroid hormone and bile acid synthesis), ketogenesis (in starvation).

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3
Q

What processes of protein metabolism is the liver involved in?

A

Synthesis of plasma proteins, transamination and deamination of amino acids, conversion of ammonia to urea.

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4
Q

What hormones are deactivated by the liver?

A

Insulin, glucagon, ADH (vasopressin), steroid hormones.

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5
Q

What hormones does the liver activate?

A

Conversion of thyroid hormone (also occurs elsewhere), conversion of vit D to 25-hydroxyvitamin D2 (calcifediol, further activation occurs in the kidney).

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6
Q

What does the liver store?

A

Fat soluble vitamins, water soluble vit B12 (hydroxycobalmin), iron, copper and glycogen.

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7
Q

What are the 2 destinations of the proteins produced by the liver?

A

Metabolic processes of the organ, for export.

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8
Q

What proteins are synthesised for export by the liver?

A

Coagulation factors (II, VII, IX and X), proteins C and S, albumin, complement proteins, apolipoproteins, carrier proteins.

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9
Q

What are other names of Kupffer cells?

A

Liver phagocytes, stellate cells.

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10
Q

What are the functions of Kupffer cells?

A

Digest/destroy particulate matter (e.g. bacteria) and senescent (old) erythrocytes.

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11
Q

What does the liver produce to protect the body from attack?

A

Produce the immune factors host defence proteins (acute phase proteins).

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12
Q

What endogenous substances does the liver detoxify?

A

Many e.g. bilirubin as a metabolite of haemoglobin breakdown.

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13
Q

What exogenous substances (xenobiotics) does the liver detoxify?

A

Drugs, ethanol (alcohol).

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14
Q

What happens to bile between meals?

A

Stored and concentrated in gall bladder (sphincter of Oddi closed).

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15
Q

What is the advantages of bile being slightly alkaline?

A

Assists micelle formation, neutralisation of chyme, pH adjustment for digestive enzyme action, protection of the mucosa.

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16
Q

In bile formation, what do the hepatocytes secrete and where into?

A

Primary juice into canaliculi which drain into biliary ductules and ducts.

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17
Q

What does the primary juice contain?

A

Primary bile acids, water and electrolytes, lipids and phospholipids, cholesterol, IgA, bilirubin, metabolic wastes and conjugated drug metabolites.

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18
Q

When may ursodeoxycholic acid be used in cholelithiasis?

A

In patients with unimpaired gall bladder function who have small/medium sized radiotranslucent stones which it dissolves.

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19
Q

What is an adverse effect of ursodeoxycholic acid?

A

Diarrhoea.

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20
Q

Why may morphine worsen biliary colic?

A

It may constrict sphincter of oddi and increase intrabiliary pressure.

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21
Q

What are alternative analgesics used for severe biliary colic?

A

Buprenorphine and pethidine.

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22
Q

What may relieve biliary spasm?

A

Atropine or GTN.

23
Q

What are the primary bile acids and when are they converted into secondary bile acids?

A

Mainly cholic and chenodeoxycholic acids, a fraction are dehydroxylated by bacteria in the gut (deoxycholic acid and lithocholic acid).

24
Q

What electrolytes are found in bile acid?

A

Sodium, potassium calcium, chloride and bicarbonate.

25
Q

What proportion of secondary bile acids are returned to the liver?

A

All of them.

26
Q

Name 3 bile acid sequestrants (resins).

A

Colveselam, colestipol, colestyramine.

27
Q

What is the mechanism of action of bile acid resins?

A

Bind to bile acids, preventing their reabsorption.

28
Q

What are the clinical uses of bile acid binding resins?

A

Hyperlipidaemia (limited effect), cholestatic jaundice (itch), bile acid diarrhoea.

29
Q

What are the limitations and adverse effects of bile acid resins?

A

Unpalatable and inconventient (large doses), frequently cause diarrhoea, reduce absorption of fat soluble vitamins and some drugs e.g. thiazide diuretics.

30
Q

How can the liver convert a drug so that it is not readily absorbed by the kidney, facilitating excretion?

A

By converting them to more polar metabolites.

31
Q

What is the usual effect of liver conversion on a parent drug?

A

Makes it less pharmacologically active.

32
Q

What is the conversion of enalapril to enalaprilat an example of?

A

An inactive prodrug being converted into an active compound.

33
Q

What is the conversion of diazepam to nordiazepam an example of?

A

Conversion where there is no change in activity?

34
Q

What is the conversion of codeine to morphine an example of?

A

When a drug gains activity after liver metabolism.

35
Q

Give an example where a metabolite of a parent drug in the liver possesses a different type of action.

A

Aspirin (anti-inflammatory and anti-platelet activity) becomes salicylic acid (anti-inflammatory, not anti-platelet).

36
Q

What other organs metabolise drugs?

A

The GI tract, lungs and plasma.

37
Q

What do the 2 phases of liver drug metabolism often involve?

A

Phase I - oxidation, reduction, hydrolysis.

Phase II - conjugation.

38
Q

Describe phase I of liver drug metabolism.

A

Makes drug more polar, adds a chemically reactive group (handle) permitting conjugation (functionalisation).

39
Q

Describe phase II of liver drug metabolism.

A

Adds an exogenous compound increasing polarity e.g. glucaronyl, sulphate, methyl, acetyl, glycyl or glutathione groups.

40
Q

Do drugs have to go through both phases of liver metabolism.

A

No. Some drugs just do phase I, some just do phase II and some drugs are excreted unchanged.

41
Q

Describe the metabolism of aspirin.

A

Aspirin -> (phase I) -> salicylic acid -> (phase II) -> glucuronide (conjugate).

42
Q

What are the cytochrome P450 (CYP) family of monooxygenases?

A

Haem proteins located in the ER of hepatocytes mediating oxidation reactions (phase I) of many lipid soluble drugs.

43
Q

How are cytochrome P450 proteins classified?

A

CYP followed by a defining set of numbers and letters (e.g. CYP3A4).

44
Q

What are the main gene families of CYP in the human liver?

A

CYP1, CYP2 and CYP3.

45
Q

After phase II reactions, are products usually active or inactive?

A

Inactive.

46
Q

Describe glucuronidation (common reaction in phase II).

A

Transfer of glucuronic acid to electron rich atoms of the substrate (N, O or S forming amide, ester or thiol bonds).

47
Q

Where does the glucuronic acid come from in glucuronidation?

A

UDP-alpha-glucuronide.

48
Q

What is the enzyme involved in glucuronidation?

A

UDP-glucuronlyl transferase.

49
Q

Give 2 examples of endogenous substances that are subject to glucuronidation.

A

Bilirubin, adrenal corticosteroids.

50
Q

What causes hepatic encephalopathy?

A

Increase in blood ammonia levels due to failure of liver to detoxify ammonia via the urea cycle.

51
Q

Describe the stages of hepatic encephalopathy.

A

Incoordination, drowsiness, coma and ultimately death due to cerebral oedema.

52
Q

What is the mechanism of action of lactulose in hepatic encephalopathy?

A

When broken down in the colon it acidifies the stool which converts ammonia into ammonium which is not absorbed.

53
Q

What antibiotics may be used in hepatic encephalopathy?

A

Neomycin, rifamixin (both poorly absorbed).

54
Q

Why do we use antibiotics in hepatic encephalopathy?

A

They suppress colonic flora and this inhibit ammonia generation.

Gastrointestinal (26 decks)

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