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RACP > Upper GI > Flashcards

Upper GI Flashcards

1
Q

What factors are involved in gastric emptying?

A 
Particle size (retained until <2mm)
Fat content (high = slower emptying)
Calorie content
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2
Q

Where are the parietal cells located? Function?

A

Upper 2/3 gastric mucosa. Produce HCl

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3
Q

Where are the chief cells located? Function?

A

Upper 2/3 gastric mucosa.

Secrete pepsinogen which initiates proteolysis

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4
Q

Which cells involved in digestion are located in the antrum of the stomach and what do they secrete? And function.

A
  1. D cells = somatostatin. Suppresses acid production by inhibiting gastrin and histamine release
  2. Mucous secreting cells
  3. HCO3-
  4. G cells = gastrin.
    Stimulates acid production directly and indirectly via histamine.
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5
Q

What are the 3 phases of acid secretion?

A
  1. Cephalic phase: sight/smell/thought of food stimulates the vagus to produce ACh
  2. Gastric phase:
    Distension stimulates secretory cells and gastrin release.
  3. Intestinal phase:
    Passage of food into the intestine stimulates GI hormone release
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6
Q

How is HCL produced?

A

By the parietal cells.
K+ and Cl- diffuse into the canaliculi within the cell. The H+/K+ ATPase pump, pumps K+ back into the main cell in exchange for H+ which enters the canaliculi. The pump is stimulated by a rise in cAMP and Ca2+
On the basal cell surface:
1. Gastrin stimulates CCKBB receptors (increases Ca2+) and histamine release
2. Histamine from ECL cells stimulates H2 receptors
3. ACh from the vagus stimulates M3 receptors. ACh also stimulates histamine release

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7
Q

What are the causes of high gastrin?

A
  • prolonged acid suppression by PPI/H2 blockers
  • H.pylori
  • atrophic gastritis from pernicious anaemia
  • SB resection
  • Zollinger- Ellison syndrome
  • Vagotomy
  • Hypercalcaemia
  • Hyperlipidaemia (artefact)
  • renal failure
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8
Q

What do the intestinal I cells secrete? Effects?

A

CCK

  • reduces gastric emptying
  • increases enzyme fluid secretion from pancreas
  • contraction of gallbladder/sphincter of oddi relaxation
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9
Q

What do the intestinal S cells secrete? Effects?

A

Secretin:

- Increases secretion of HCO3- from the pancreas

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10
Q

Where is VIP secreted from and what does it do?

A

Small intestine and pancreas.

Inhibits acid secretion

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11
Q

What do the D cells secrete?

A

Somatostatin: decreases acid and pepsin secretion by inhibiting gastrin and histamine release

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12
Q

What do the L cells secrete? Where are they? what is the effect?

A

Ileal L cells: GLP: regulates insulin release, inhibits gastric emptying, promotes satiety, slows intestinal transit.

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13
Q

What do the K cells secrete?

A

GIP (gastric inhibitory peptide): inhibits H+ and regulates insulin release.

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14
Q

What is the mechanism of action of PPIs?

A

Inhibit the H+/K+/ATPase pump

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15
Q

What are the indications for long term use of PPIs?

A

Barrett’s oesophagus
Erosive oesophagitis with strictures
Zollinger-Ellison syndrome
Scleroderma oesophagus
High risk patients on NSAIDs: Over 60, hx of PUD.
Or aspirin + concomitant use of NSAIDS, anticoagulant, SSRI, steroids

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16
Q

What are the potential risks/SEs of PPIs and what was an important recent study?

A
  • HypoMg, Ca, low B12
  • Infection: pneumonia, C.diff, gastroenteritis
  • Cancer
  • osteoporosis
  • dementia
  • interstitial nephritis
    Important study: 2019 COMPASS trial: large RCT looking at LT safety of PPI: found only a slightly increased risk of GI infection
17
Q

What is zollinger ellison syndrome, where is it found, how do you dx it and what should you consider?

A

Gastrin secreting tumour - 90% found in the gastrinoma triangle. Gastrin levels > 10000, a Gallium 68 DOTATATE CT-PET is very sensitive. Gold standard is a secretin provocation test.
1/3 of patients have MEN1 (AD, chromosome 11, PPP)

18
Q

What effect does smoking have on chronic pancreatitis?

A

Smoking cessation reduces the risk of pancreatic cancer in chronic pancreatitis

19
Q

What types of inherited pancreatitis are there?

A
  1. Hereditary pancreatitis
  2. SPINK1 mutation inherited pancreatitis
  3. CFTR mutation inherited pancreatitis
20
Q

Hereditary pancreatitis:

  1. What is the mode of inheritance,
  2. what is the mutation?
  3. What are diagnostic features?
A
  1. AD, 80% penetrance
  2. Trypsinogen PRSS1 mutation (ch 7)
  3. INcreased risk of cancer, small pancreas on CT, normal amylase/lipase as not much pancreas left.
21
Q

What is autoimmune pancreatitis and how is it classified?

A

Type 1 disease in which the pancreas is involved as part of an IgG4 systemic disease
Type 2 disease: idiopathic duct centric disease without systemic involvement

22
Q

How may autoimmune pancreatitis present, how is it diagnosed and what is the treatment?

A

Acute, recurrent pancreatitis. May have a pancreatic mass. Pancreatic and biliary duct strictures. May be associated with retroperitoneal fibrosis.
Diagnosed on biopsy, elevated IgG4 is supportive.
Treatment: steroids. Rituximab is 2nd line.

23
Q

What the different types of fluid collections associated with pancreatitis? How are they classified and how should they be managed?

A

< 4 weeks: acute fluid collection or acute necrotic collection
> 4 weeks: pseudocyst (no debris but does have an encapsulated wall. Or walled off necrosis.
Evidence to suggest conservative management associated with fewer complications than early surgical intervention.
If acute: wait
If pseudocyst: drain
If walled off necrosis: debride
Evidence shows that endoscopic trans gastric drainage using a metal stent has lower mortality/complications than necrosectomy.

24
Q

What is ABCB4 disease?

A

Newly recognised cause of recurrent pancreatitis, intraheptic cholestasis of pregnancy, progressive familial intraheptic cholestasis, low phospholipid associated cholelithiasis.
Codes for multi drug resistance protein 3 (MDR3)

25
Q

Which pancreatic cysts are benign and which can be premalignant?

A

Benign: pseudocysts and serous cystadenoma
Premalignant: MCN (mucinous cystic neoplasm), IPMN (intraductal papillary mucinous neoplasm), neuroendocrine tumour.
IPMN branches off the pancreatic duct.
MCN has ovarian like stroma histology

26
Q

What are the RFs for pancreatic Ca?

A

Smoking
Chronic pancreatitis, CF
Genetic: BRCA1, 2, Lynch syndrome, FAMMM (Familial atypical multiple mole melanoma), hereditary pancreatitis, Peutz-Jeghers syndrome,
FHx

27
Q

What are the RFs for Barrett’s oesophagus?

A

Male, older, smoking, reflux symptoms > 5 years, central obesity, caucasian.

28
Q

What is the estimated cancer risk for Barrett’s, low grade dysplasia and high grade dysplasia?

A

Barrett’s: 0.2%/year
low grade dysplasia: 0.7%/year
High grade dysplasia: 7%/year

29
Q

How is Barrett’s oesophagus managed?

A

Start on lifelong PPI (poor evidence)
If no dysplasia, endoscopy every 3-5 years
If low grade dysplasia, endoscopy + biopsy every 6 months
If high grade dysplasia, endoscopy + biopsy every 3 months +/- endoscopic ablative therapies/resection

30
Q

What is the main pathophysiological mechanism of reflux?

A

transient relaxations of the lower oesophageal sphincter

31
Q

What are the causes of low resting LES?

A

gastric distension, alcohol, caffeine, fat, CCK, smoking

32
Q

What is the relationship between symptoms of reflux and severity of endoscopic appearance?

A

there is no correlation

33
Q

Summarise the pathogenesis of coeliac disease

A
  • Gluten specific CD4+ T cell pro-inflammatory response.
  • CD8+ intraepithelial lymphocytes target and destroy ‘stressed’ epithelium
  • CD4+ T cells help B cells produce abs to gliadin, gluten peptides and transglutaminase
34
Q

What are the RFs associated with coeliac disease?

A
  • Infection with rotavirus/pseudomonas
  • female
  • first degree relative
  • type 1 DM
  • geography
  • seasonality
  • high gluten intake
  • HLADQ2
35
Q

What are the extra intestinal manifestations of coeliac disease?

A
  • weak tooth enamel
  • osteoporosis
  • AI: type 1 DM, pernicious anaemia, Addison’s, thyroid disease, alopecia
  • Haematological: neutropenia, anaemia, hyposplenism, thrombocytopenia, lymphoproliferative disorders
  • Neurological: peripheral neuropathy, migraines, depression
  • Infertility
  • GI: mouth ulcers, NAFLD, LFT abnormalities, autoimmune hepatitis, pancreatic insufficiency
36
Q

How do you diagnose coeliac disease?

A
  • Serology: either tTG-IgA abs + total IgA level
    or tTG-IgA + DGP-IgG
  • Duodenal Biopsy (should still be on gluten): villous atrophy, crypt hyperplasia, raised intraepithelial lymphocytes
  • HLADQ2/8 testing has very good negative predictive value
37
Q

What possible causes are there for villous atrophy?

A
  • coeliac
  • tropical sprue/small bowel overgrowth, giardia, H.pylori
  • Drugs: olmesartan, mycophenolate, NSAIDS
  • CVID, Crohn’s disease, cow’s milk protein intolerance, autoimmune enteropathy
38
Q

What are RFs for GORD?

A

+ve: age, hiatus hernia, obesity, pregnancy, asthma, scleroderma, smoking,
-ve: H.pylori

RACP (3 decks)

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