C&C GIT Workshop - Week 5 & 6 Flashcards
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)
- 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)
Explain how brown gallstones are often formed?
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.
Risk factors for gall stone formation
- Females
- Oral contraception (particularly methods contain oestrogen)
- Obesity
- Rapid weight loss
Microscopic appearance of H. pylori
Gram +ve (purple) rod.
Virulence factors of H. pylori
- Urease
- Flagella
- LPS – enables adherence
- Exotoxin release (e.g., VGCA – causes apoptosis, CAGA – disrupts cell integrity & structure -> inflammation).
Pathophysiology of H. pylori
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.
Diagnosis tools for H. pylori ulcer
- 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.
ALT, AST elevation indicates
Hepatocyte injury (e.g., hepatitis).
Remember ‘AT’ in hepATocytes.
ALP, GGT elevation indicates
Biliary tract injury - enzymes released by epithelial cells lining canaliculi (e.g., obstruction).
Causes of pancreatitis include:
Gallstones, ethanol/alcohol, trauma, steroids, mumps, autoimmune, scorpion bite, hyperlipidaemia, ERCP, drugs
where ERCP = endoscopic retrograde cholangiopancreatography.
Remember pneumonic GET SMASHED.
Why would serum lipase be elevated in obstructive cholecystitis?
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).
Why is pain associated w acute cholecystitis characterised by a 1hr post prandial onset?
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.
What must be ruled out in patients presenting with painless jaundice?
Pancreatic cancer.
What may multiple vomiting episodes followed by haematemesis indicate?
Mallory-Weiss tear.
Exudative causes of diarrhoea.
Bacteria, parasites, viruses, inflammation (e.g., UC).
Osmotic causes of diarrhoea
Ingested substances (e.g., sorbitol, magnesium, lactulose) & malabsorption (e.g., lactose intolerance, Coeliac’s disease, pancreatic insufficiency).
Secretory causes of diarrhoea
Pro-secretory enterotoxin, bile acid malabsorption, hormones, inflamation.
Motility-related causes of diarrhoea
Increased motility due to thyrotoxicosis, opiod withdrawal.
Investigations for pts presenting w diarrhoea
- Hydration status assessment
- Stool culture
- FBC
- Endoscopy/gastroscopy
- CT
How does diarrhoea lead to death?
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.
First line treatment of diarrhoea
Treatment: ions, glucose , water (isotonic solution).
Why is glucose an important ion to include in rehydration therapy for pts suffering from diarrhoea?
Req. for sodium reuptake into endothelial cells & provides pts w energy.
What electrolyte disturbance is commonly seen in pts suffering from severe vomiting?
Due to high amount of Cl- present in stomach due to HCl forming gastric acid, prolonged, severe vomiting -> hypochloraemia.
What may a +ve tranglutaminase antibody indicate? Why?
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.
Microcytic anaemia w low Fe & low ferritin & high TIBC may indicate
Iron deficiency anaemia.
Microcytic anaemia w low Fe & low ferritin & low TIBC may indicate
Anaemia of chronic disease.
Macrocytic anaemia w megoblasty may indicate
B12 and/or folate deficiency (may be drug-induced).
Macrocytic anaemia w non-megaloblasty may indicate
Alcohol abuse, myelodysplastic syndrome, liver disease, congenital bone marrow failure syndromes.
Macrocytic anaemia w non-megaloblasty may indicate
Alcohol abuse, myelodysplastic syndrome, liver disease, congenital bone marrow failure syndromes.
Faecal impaction vs bowel obstruction
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).
