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*4a. Gastrointestinal > Gall bladder disease - pathology > Flashcards

Gall bladder disease - pathology Flashcards

1
Q

Anatomy:
- Label the parts of the gall bladder

A
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2
Q

Anatomy:
- Label the ducts

A
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3
Q

Anatomy:
- Label the openings into the duodenum

A
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4
Q

Physiology
- What is bile made out of?

A

Micelles
- Bile acids/salts
- Phospholipids (lecithin)
- Cholesterol

Bile pigments
- Bilirubin
- Biliverdin

Water, electrolytes (Ca2+), bicarbonate (HCO3-)

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5
Q

Physiology: bile acids/salts
- Where are they made?
- What are they made from?
- Difference between bile acid/salt?

A

Made in the liver, from cholesterol.
Acid has H+, salt doesn’t.

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6
Q

Physiology: micelles in bile
- How do they form?

A

Amphipathic bile salts (or acids) and phospholipids surround cholesterol (non polar)

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7
Q

Physiology: fat metabolism
- Describe the role of cholecystokinin and secretin

A
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8
Q

Physiology: fat metabolism
- Describe how bile aids in fat digestion

A
  • Bile salts and pancreatic lipase are released via the Ampulla of Vater/ Sphincter of Oddi into the duodenum
  • Bile salts emulsify fat (triglycerides) into smaller particles (micelles)
  • This assists pancreatic lipase to hydrolyse the triglycerides into glycerol + fa’s
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9
Q

Physiology: fat metabolism
- Where are bile salts reabsorbed?

A

In the terminal ileum

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10
Q

Gall stones
- 3 types?

A
  • Cholesterol stones
  • Black pigment stones
  • Brown pigment stones
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11
Q

Gall stones: cholesterol stones
- Composition?
- Mechanisms of formation

A

Precipitated cholesterol, may be bound to calcium carbonate

Cholesterol is precipitated due to
- Too much cholesterol
- Not enough bile salts/acids + phospholipids
- Gall bladder stasis (can lead to cholesterol falling out)

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12
Q

Gall stones: cholesterol stones
- Risk factors?

A
  • Female: high oestrogen levels
  • Fertile: high estrogen levels in pregnancy, OCP
  • Fat: obesity associated with increased cholesteorl
  • Fair: white people
  • Forty
  • Rapid weight loss (eg. following bariatric surgery) increases cholesterol levels in bile
  • Drugs: octreotide, ceftriaxone
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13
Q

Gall stones: black pigment stones
- Composition?
- Mechanism of formation?

A

Calcium bilirubinate (bilirubin is unconjugated)

At bile pH, unconjugated bilirubin is an anion. It can either bind to bile salts, or Ca2+

When there is too much unconjugated bilirubin levels, or not enough bile salts, this favours bilirubin binding with Ca2+ –> calcium bilirubinate

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14
Q

Gallstones: black pigment stones
- Risk factors?

A

Excess bilirubin
- Prehepatic: chronic haemolysis
- Intrahepatic: liver cirrhosis, Gilbert’s syndrome

Bile salt malabsorption
- Terminal ileal diseases eg. Crohn’s disease
-Terminal ileum resection

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15
Q

Gallstones: brown pigment stones
- Composition?
- Mechanism of formation?
- Where does it often form?
- Risk factor?

A

Calcium bilirubinate (also unconjugated bilirubin)

Occurs due to infection
Bacteria have hydrolytic enzymes which hydrolyse conjugated bilirubin (deconjugating it) and phospholipids; both combine with Ca2+ –> precipitate as the stone.

In the bile ducts, unlike the gall bladder (more common for the latter two)

Asian populations - some agents of gallbladder infections (eg. Ascaris lumbricoides) are endemic to Asian countries

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16
Q

Gall stones: pathophysiology
- Why does pain occur?
- What happens if the stone falls into the common bile duct

A

Contracting onto a gallstone.
Bile backs up into bloodstream –> jaundice

17
Q

Gall stones: complications?

A
18
Q

Cholecystitis: what are the two types?

A

Calculous cholecystitis (with gallstones); ~90% of cases
Acalculous cholecystitis (without gallstones)

19
Q

Calculous cholecystitis
- Aetiology?
- Pathophysiology?

A
20
Q

Calculous cholecystitis?
- Complications?

A
21
Q

Acalculous cholecystitis
- 3 mechanisms?

A
22
Q

Cholangitis
- Definition?
- Causes?

A

Infection of` the biliary tree

23
Q

Cholangitis
- Pathophysiology

A
24
Q

Cholangitis
- Complications?

A
  • Hepatic infection
  • Sepsis
  • LIFE THREATENING
25
Q

Prevention of cholesterol stones from forming?

A

Reduce fat: diet, exercise
Ursodeoxycholic acid: lowers cholesterol saturation in the bile

26
Q

Explain the normal function of the hepatobiliary tree in fat digestion

A
  • Your liver makes bile, which is a substance that helps with breaking down fat.
  • Bile is stored and concentrated in the gall bladder.
  • When you eat a fatty meal, your small intestine tells your gall bladder to contract to secrete bile into the small intestine. Once in the small intestine, it helps to break down fats.
27
Q

Explain gallstones

A
  • Bile can get too thick and form gall stones
  • Most common type of gall stone is cholesterol gall stones, which form when there is too much cholesterol in the bile. Risk factors are female, fertile, fat, forty, fair.
  • During a fatty meal, the gall bladder contracts onto these stones, causing pain
28
Q

Explain cholecystitis

A
  • Inflammation of the gall bladder
  • Usually occurs when a gallstone gets stuck in the opening of the gall bladder, or the ducts.
  • Bile gets stuck in the gall bladder, irritating it, causing an immune response.
29
Q

Explain cholangitis

A
  • Infection of the duct system
  • Normally bile flows down the duct system, flushing out bacteria and making them difficult for it to grow.
  • Stone –> bile gets stagnant and can’t wash out bacteria –> bacterial infection
30
Q

Explain jaundice

A

There is a pigment in your bile called bilirubin. Like the rest of bile, it is usually released into the small intestine and into your faeces, giving it a brown pigment.

When the ducts are blocked below a certain point, bile can’t get down into the small intestine. It backs up into the bloodstream. Instead makes your skin and eyes turn yellow. Pigment isn’t getting to poop so it looks paler than usual. It can irritate your skin, causing an itch.

*4a. Gastrointestinal (7 decks)

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