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s2 case 2 - diarrhoea > Biliary Disease + Treatment > Flashcards

Biliary Disease + Treatment Flashcards

1
Q

What does 70% of hepatocyte SA face?

A

Sinusoid
= maximise blood exchange

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2
Q

What does 15% of hepatocyte SA face?

A

Bile canaliculi

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3
Q

What are gallstones (cholelithiasis) a result of?

A

Supersaturation of bile with cholesterol

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4
Q

What is choledocholithiasis?

A

Presence of gallstones within bile duct

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5
Q

What is acute cholecystitis?

A

Inflammation of gallbladder
Related to presence of gallstones

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6
Q

What is cholangitis?

A

Inflammation of bile ducts caused by polymicrobial bacterial infection

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7
Q

Describe the symptoms of cholelithiasis

A

Episodic pain in RUQ or epigastric pain associated with vomiting
= gallstone obstruction at neck of gallbladder

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8
Q

What are gallstones?

A

Crystalline concentration formed within gallbladder by accretion of bile components

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9
Q

When does cholesterol gallstones develop?

A

Bile contains high cholesterol + not enough bile salts

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10
Q

What are the causes of gallstones?

A

High calorie diet
Poor gallbladder contraction
Presence of proteins in liver promoting cholesterol crystallisation
Increased level of oestrogen

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11
Q

How does cholecystectomy work?

A

Keyhole surgery to remove stones

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12
Q

How does oral dissolution therapy work?

A

Oral administration of natural bile acid UDCA
Treatment up to 2 years

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13
Q

When are cholesterol agents used?

A

When gallstones are caused by cholesterol hypersecretion

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14
Q

What are the therapeutic options for cholesterol lowering agents?

A

Hepatic cholesterol biosynthesis
Intestinal cholesterol absorption

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15
Q

How do statins work?

A

Competitive inhibitors of 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase
= limit rate for cholesterol biosynthesis

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16
Q

Describe what ezetimibe do

A

Blocks NPC1L1 = blocks cholesterol absorption

17
Q

Why is it good to combine statin with ezetimibe?

A

Good clinical efficacy in reducing cholesterol load
= lower dose statin can be used
= reduce adverse effects

18
Q

What do bile acid sequestrants do?

A

Bind to bile acids to form insoluble complex that prevents reabsorption
= faecal excretion

19
Q

Why does depletion of bile salts beneficial?

A

Promotes increase bile acid synthesis
= reduces pool of intracellular cholesterol

20
Q

What are the pharmacokinetics of bile acid sequestrants?

A

Not absorbed in GI tract
Remain in intestine = where can combine with bile acids for 5hrs before excretion

21
Q

What are the adverse reactions of bile acid sequestrants?

A

Short-term, very mild
Possible from long term use = vomiting, diarrhoea, haemorrhoids

22
Q

What are the drug interactions for bile acid sequestrants?

A

Acidic drugs in GI tract = decrease absorption + effectiveness
eg. aspirin

23
Q

What do lipid lowering drugs (fibrates) do?

A

Stimulate beta-oxidative degradation of fatty acids
Liberate free fatty acids for storage in fat
Increase activity of lipoprotein lipase

24
Q

Describe cholecystitis

A

Inflammation of gallbladder
Cyst duct obstruction
Association with stones

25
Q

How do you treat cholecystitis?

A

Initial = control with fluids, antiemetics + analgesics
Broad-spectrum antibiotics

26
Q

How do you treat cholecystitis if presence of sepsis?

A

Aggressive fluid resuscitation + blood pressure support

27
Q

Describe cholangitis

A

Acute/chronic cholestatic disease
Due to non-specific inflammatory fibrosis of intra/extrahepatic bile ducts

28
Q

How do you treat cholangitis?

A

Antibiotics
Surgery

29
Q

Describe primary biliary cirrhosis

A

Chronic cholestatic disease
= destructive cholangitis of intrahepatic bile ducts

30
Q

Which drugs increase bile flow?

A

Phenobarbital, glucagon, insulin + theophylline

31
Q

Which drugs decrease bile flow?

A

Amiloride, oestrogens + chlorpromazine

32
Q

What does clofibrate do to bile?

A

Increases biliary cholesterol secretion + reduces bile acid concentration

s2 case 2 - diarrhoea (12 decks)

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