C&C GIT Workshop - Week 5 & 6

Question 1

3 main types of gallstones, what they are composed of and common causes (& state whether or not they can be seen on XRT and why)

Answer 1

• Cholesterol stones – composed of precipitated cholesterol (75-90%)
  1. Supersaturation of bile salt w cholesterol due to high concentration of cholesterol
  2. Not enough salts/acid/phospholipids in bile salt
  3. Gallbladder statis
  NB: Usually can’t be seen on XRT, but if they contain CaCO3 they may be.
• Bilirubin stones/pigmented stones – composed of unconjugated bilirubin & calcium
  NB: Usually observed on XRT
• Brown stones – composed of unconjugated bilirubin & calcium & hydrolysed phospholipids
  1. E. coli
  2. Ascaris lmbricoides (roundworn)
  3. Cionorcnis sinesis (liver fluke)

Question 2

Explain how brown gallstones are often formed?

Answer 2

Formed via hydrolytic enzymes of pathogen (e.g., E. coli) present in the gall bladder during a gall bladder infection -> break down conjugated bilirubin -> increased unconjugated Br -> pairing w calcium -> gallstones.

Question 3

Risk factors for gall stone formation

Answer 3

• Females
• Oral contraception (particularly methods contain oestrogen)
• Obesity
• Rapid weight loss

Question 4

Microscopic appearance of H. pylori

Answer 4

Gram +ve (purple) rod.

Question 5

Virulence factors of H. pylori

Answer 5

• Urease
• Flagella
• LPS – enables adherence
• Exotoxin release (e.g., VGCA – causes apoptosis, CAGA – disrupts cell integrity & structure -> inflammation).

Question 6

Pathophysiology of H. pylori

Answer 6

Uses urease to make ammonia -> neutralises acidity of stomach -> swims w flagella down towards simple columnar epithelium of stomach cells -> secretes exotoxins -> disrupts tight junctions of stomach cells -> inflammation (exaggerated by IL-8 release) -> cell apoptosis -> ulcer formation.

Question 7

Diagnosis tools for H. pylori ulcer

Answer 7

• Urea breath test
  1. C of urea is chemically tagged
  2. Urea sample enters stomach
  3. H. pylori converts tagged urea -> CO2 & H2O
  4. CO2 travels via bloodstream to heart and then lungs
  5. Chemically tagged CO2 will be detected on exhalation
• Faecal sample.

Question 8

ALT, AST elevation indicates

Answer 8

Hepatocyte injury (e.g., hepatitis).
Remember ‘AT’ in hepATocytes.

Question 9

ALP, GGT elevation indicates

Answer 9

Biliary tract injury - enzymes released by epithelial cells lining canaliculi (e.g., obstruction).

Question 10

Causes of pancreatitis include:

Answer 10

Gallstones, ethanol/alcohol, trauma, steroids, mumps, autoimmune, scorpion bite, hyperlipidaemia, ERCP, drugs
where ERCP = endoscopic retrograde cholangiopancreatography.
Remember pneumonic GET SMASHED.

Question 11

Why would serum lipase be elevated in obstructive cholecystitis?

Answer 11

Elevated serum lipase indicate blockage of pancreatic duct -> blockage of pancreatic enzyme secretion into the common bile on its way to the duodenum -> accumulation of pancreatic enzymes in the pancreatic ducts & pancreas -> auto-digestion of the pancreas -> entry into the bloodstream via blood vessels in the pancreas -> increased serum lipase levels (potentially also serum amylase levels).

Question 12

Why is pain associated w acute cholecystitis characterised by a 1hr post prandial onset?

Answer 12

Pain onset is approximately 1 hr after eating a fatty meal, because it takes approximately 1 hr for food to be digested by the stomach and pass into the duodenum. Once in the duodenum, CCK release @ SI is triggered -> bile released from GB -> triggered pain due to blocked biliary ducts.

Question 13

What must be ruled out in patients presenting with painless jaundice?

Answer 13

Pancreatic cancer.

Question 14

What may multiple vomiting episodes followed by haematemesis indicate?

Answer 14

Mallory-Weiss tear.

Question 15

Exudative causes of diarrhoea.

Answer 15

Bacteria, parasites, viruses, inflammation (e.g., UC).

Question 16

Osmotic causes of diarrhoea

Answer 16

Ingested substances (e.g., sorbitol, magnesium, lactulose) & malabsorption (e.g., lactose intolerance, Coeliac’s disease, pancreatic insufficiency).

Question 17

Secretory causes of diarrhoea

Answer 17

Pro-secretory enterotoxin, bile acid malabsorption, hormones, inflamation.

Question 18

Motility-related causes of diarrhoea

Answer 18

Increased motility due to thyrotoxicosis, opiod withdrawal.

Question 19

Investigations for pts presenting w diarrhoea

Answer 19

• Hydration status assessment
• Stool culture
• FBC
• Endoscopy/gastroscopy
• CT

Question 20

How does diarrhoea lead to death?

Answer 20

Cl- pumped out on the luminal side of epithelial cells -> drawing out Na+ -> consequently, drawing out H2O from the cells -> electrolyte disturbance (hypokalaemia).
Complications include cardiac arrhythmias, CVS collapse & acute kidney injury.

Question 21

First line treatment of diarrhoea

Answer 21

Treatment: ions, glucose , water (isotonic solution).

Question 22

Why is glucose an important ion to include in rehydration therapy for pts suffering from diarrhoea?

Answer 22

Req. for sodium reuptake into endothelial cells & provides pts w energy.

Question 23

What electrolyte disturbance is commonly seen in pts suffering from severe vomiting?

Answer 23

Due to high amount of Cl- present in stomach due to HCl forming gastric acid, prolonged, severe vomiting -> hypochloraemia.

Question 24

What may a +ve tranglutaminase antibody indicate? Why?

Answer 24

Transglutaminase is an enzyme involved in digesting gluten. In Coeliac disease, antibodies are produced by the body’s immune system which surround and paralyse function of transglutaminase -> body cannot digest gluten -> inflammation of immune response -> Crypt hyperplasia & villous atrophy in the SI -> reduced ion absorption -> water drawn out of endothelial cells -> diarrhoea/loose stools.
Prolonged inflammation can also lead to other more systematic symptoms incl. itchy rash over the abdominal region.
Should follow this result up with a gastroscopy & biopsy of SI on glutenous diet/gluten challenge to check for structural changes or abnormalities present in SI endothelial cells.

Question 25

Microcytic anaemia w low Fe & low ferritin & high TIBC may indicate

Answer 25

Iron deficiency anaemia.

Question 26

Microcytic anaemia w low Fe & low ferritin & low TIBC may indicate

Answer 26

Anaemia of chronic disease.

Question 27

Macrocytic anaemia w megoblasty may indicate

Answer 27

B12 and/or folate deficiency (may be drug-induced).

Question 28

Macrocytic anaemia w non-megaloblasty may indicate

Answer 28

Alcohol abuse, myelodysplastic syndrome, liver disease, congenital bone marrow failure syndromes.

Question 29

Macrocytic anaemia w non-megaloblasty may indicate

Answer 29

Alcohol abuse, myelodysplastic syndrome, liver disease, congenital bone marrow failure syndromes.

Question 30

Faecal impaction vs bowel obstruction

Answer 30

NB: Faecal impaction occurs when the small or large bowel lumen is blocked by hard faeces = severe constipation. A bowel obstruction occurs when the small or large bowel lumen is blocked by something other than faeces (i.e., inflammation, hernia, blood vessel, abnormal growth).