Gastroenterology Flashcards
GLP-1 and GIP
Semaglutide (GLP-1)
Tirzepatide (GLP-1 and GIP)
GLP-1 = glucagon like peptide 1
- Proglucagon cleavage product secreted by L cells in duodenum
- slows gastric emptying + increases insulin/ reduces glucagon
- metabolised by DPP4
- SE: pancreatitis, nausea, tachycardia
GIP = gastrin inhibitory peptide
- secreted by K cells in small intestine
- increases glucose dependent insulin secretion
Parietal cell function + therapies
HCl stimulated by gastrin, histamine (ranitidine), and ACh (vagotomy/ distal gastrectomy)
PPI inhibit H+/K+ pump directly
- risk associations: pneumonia, gastroenteritis, c. diff, osteoporosis/ falls, hypomagnesemia, gastric polyps, AKI, AIN, microscopic colitis
Causes of hypergastrinaemia (7)
- PPI/ histamine antagonist
- Atrophic gastritis - pernicious anaemia, h. pylori
- Vagotomy/ small bowel resection
- Gastrin secreting tumors (Zollinger-ellison)
- Renal failure (less excretion)
- Hypercalcemia
- artifactual = hyperlipidemia
Zollinger Ellison syndrome- where, investigations, associations
- Gastrinoma Triangle (distal stomach, prox duodenum)
- Fasting Gastrin > 10,000
- Gallium 68 DOTATATE CT-PET scan
- Secretin Provocation test
- 1/3 patients MEN1
- Auto Dominant, Chromosome 11q13
- Hyperparathyroidism – 100% age 40
- Pituitary & Pancreatic Cancer
Gastropancreatic neuroendocrine tumors - types and tests
- 60% non functioning - carcinoid, insulinoma, gastrinoma, VIPoma, glucagonoma
- 95% patients with carcinoid syndrome metastatic disease at diagnosis
- Urinary 5HIAA: sn 70% - false positive with pineapple, avocado; insulin/ c peptide; gastrin etc
- Ki-67 Index (determines aggressivness)
A 35 year old man is referred to a gastroenterologist because of epigastric pain not responding to omeprazole 20mg BD and a fasting gastrin level of 650pg/mL
The most likely reason for this finding is:
A. Hypercalcaemia
B. PPI intake
C. Gastrinoma
D. Patient not properly fasted
B. PPI intake - commonest cause
gastrinoma unlikely due to modest rise
Autonomic nervous system of the gut (4 types)
- Parasympathetic - vagal and sacral
- Sympathetic - splanchnic
- Enteric neurons - intrinsic to gut wall
- Interstitial cells of Cajal - pacemaker cells controlling peristalsis
Pancreatitis - mechanism + causes
Activation of trypsinogen by cathepsin
Causes
1. Gallstones
2. EtOH
3. ERCP
Others: Hypertryglceredemia, drugs, autoimmune, trauma, infection, genetic
Chronic pancreatitis diagnosis (5)
- 72-hr quantitative faecal fat >7g (gold-standard)
- Faecal elastase (high sens/spec)
- Abdominal XR - Calcification of pancreatic duct (vascular calcifications can be falsely interpreted)
- CT – pancreatic atrophy, duct dilatation, parenchymal and intraductal calcifications
- MRCP - progressive glandular atrophy, irregularity of the pancreatic duct contour with focal areas of narrowing and dilation, and ectasia of the side branches
Inherited/ autoimmune causes of pancreatitis (3)
Trypsin associated =
- PRSS1 - autosomal dominant, 7q35, 5yo, recurrent mild episodes, risk of cancer
- SPINK1 - adolescent, normal trypsinogen activity
Ductal associated = Cystic fibrosis, variant common chymotrypsin C
Autoimmune pancreatitis = IgG4
- mild recurrent attacks
- mass (other including salivary glans, retroperitoneal fibrosis)
- raised IgG4
- responds to steroids
Pancreatic fluid collections
Acute fluid/ necrotic collection (<4 weeks) = delay
Pseudocyst (>4weeks) = drain if obstructive
Walled-off necrosis (>4 weeks with solid debris) = deride
Endoscopic trans gastric better than surgical
ABCB4 disease
- Transmembrane floppase
- Transports phosphatidylcholine into bile duct
- Heterozygotes: intrahepatic cholestasis of
pregnancy, LPAC, Can Treat with ursodeoxycholic acid - Homozygotes: PFIC-3 – neonatal cholestasis, liver transplant
*Probably increase risk DILI
Incidental pancreatic cysts: prevalence, risk, premalignant types
50% patient with MR imaging for other reasons
0.01% risk for malignancy: size >3cm, solid component, main duct dilation (investigate with EBUS if 2 or more)
Premalignant
- mutinous cystic neoplasm (MCN) - tail
- intraductal papillary mucinous neoplasm (IPMN) - head
- neuroendocrine tumor
H.pylori natural history
100% who get acute infection go onto chronic infection
- 80% non-atrophic pangastritis (reduced acid output)
- 15% antral-predominant (20% duodenal ulcer)
- 5% corpus-predominant (10% gastric ulcer)
A 40-year-old man is seen for follow-up at the outpatients’ department. Eight weeks prior, he had presented with melaena and was found to have a duodenal ulcer and Helicobacter pylori gastritis. He was treated with a combination pack containing omeprazole, amoxycillin and metronidazole for two weeks and took all the prescribed tablets according to the instructions.
A urea breath test performed six weeks following the end of the eradication regimen was positive.
The most likely explanation for the failure of the eradication of Helicobacter pylori in this patient is:
A. metronidazole resistance.
B. amoxycillin resistance.
C. the short duration of therapy.
D. the low sensitivity and specificity of the urea breath test
following eradication therapy.
E. an insufficient period between the end of the eradication
therapy and the urea breath test.
A. metronidazole resistance
Now on PBS = 7 days amoxicillin, clarithromycin, pantoprazole
second-line 2-weeks of amoxicillin, tetracycline, bismuth, PPI (otherwise levofloxacin or moxifloxacin)
