stomach Flashcards by Megan Scobie

what kind of bacteria is H pylori

gram negative helicobacter, microaerophilic which produces adhesins so it can stick to the stomach and mucinase

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what do parietal cells produce

HCL

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what do chief cells produce

pepsinogen (which is converted to pepsin under the acidic conditions of the stomach)

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what is the lining of the stomach made of

gastric pit which leads to the gastric gland (in which you find parietal cells, chief cells an enteroendocrine cells)

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RF of gastric cancer

H pylori, male, smoking, pernicious anaemia, eating a diet high in salt

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how does h pylori cause its problems

it produces a urease enzyme which breaks down urea into CO2 and ammonia. This neutralises the stomach acid and allows bacteria to invade.

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O/E of gastric cancer

may be able to feel a mass, chronic anaemia (occult blood loss), troisier sign (presence of a left supraclavicular node), acanthosis migrans and a periumbilical nodule

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gold standard Ix for upper GI cancer

OGD with biopsy

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staging for GI cancer

staging CT CAP and a staging laparoscopy

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surgical option for a proximal gastric cancer

total gastrectomy

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surgical option for a distal gastric cancer

subtotal gastrectomy

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surgical option for a T1 gastric tumour

endoscopic mucosal resection

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reconstruction surgery after a gastrectomy

roux en Y

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Complications of gastrectomy

1) vit B 12 deficiency
2) dumping syndrome (food moves too quickly through and get fluid shift and rebound hypoglycaemia)
3) increased reflux
4) early satiety

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what are the 2WW criteria for upper GI

ANYONE with dysphagia
-anyone over 55 with weight loss and new upper abdo pain OR reflux OR dyspepsia

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anyone who presents with dyspepsia should have what and what are the options for this

Firstly need to exclude alarm features then can have

1) 4 week PPI

H pylori test
-do a urea breath test
-stool antigen test
-CLO test - rapid urease test which is done in lab
-need to not take PPI for two weeks with test

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Barrett caused by what

GORD

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what is Barrett s

metaplasia from a stratified squamous to a columnar epithelium

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Mx of GORD

absence of red flags,
1) lifestyle + review medications
2) trial a PPI for 4 weeks
3) refer to gastro for consideration of surgery

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Ix for GORD

if no red flags - 24hr pH monitor and may do barium swallow to rule out a hiatus hernia

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complications of GORD

barrets, strictures, cancer (adenocarcinoma in lower 1/3 of oesophagus)

is H pylori involved in GORD

NO! no role for testing or Tx

what is boerhaave syndrome

oesophageal rupture secondary to forceful vomiting (or in rare cases can get it from endoscopy)

triad of symptoms in boerhaave syndrome

epigastric pain, vomiting, subcutaneous emphysema

Mx of boerhaave syndrome

surgical correction but mortality is high

Dx for barrets

diagnosis is based on histology for biopsy

any dysplastic changes on barrets require what

endoscopic intervention

surveillance for barrets

OGD every 3-5 years and high dose PPI

what kind of oesophageal cancer do you get in bottom 1/3

adenocarcinoma (from barrets)

staging for oesophageal cancer

CT CAP, PET and staging laparoscopy to look for intraperitoneal mets

what causes oesophageal varies

dilation of the porto-systemic anastomosis (which have thin walls) due to portal hypertension

venous drainage of the oesophagus

lower 1/3 left gastric vein --> portal vein Upper 2/3 --> oesophogeal vein --> azygous --> SVC

what kind of dysphagia do you get in achalasia

dysphagia to liquids and solids

why do you get achalasia

failure of peristalsis and failure of the LOS to relax

Ix for achalasia

high resolution manometry to show info on muscle contraction barium swallow - birds beak appearance

Mx for achalasia

balloon dilation and botulin injections (limited role for CCB)

where do peptic ulcers normally occur

lesser curvature of the stomach or proximal part of duodenum

RF for PUD

H pylori, alcohol, GORD, smoking, stress

pathophysiology of PUD

normally stomach protected by HCO3 and surface mucous production. peptic ulcer disease is causes when these protective mechanisms are off. Eg NSAID (stop PGE2 prostaglandin) and H pylori

what does PGE2 do in stomach

HCO3 and mucous production

presenting symptom of PUD

epigastric pain (stomach - worse after eating, duodenum - worse hour later), early satiety, dyspepsia, malaena

Ix for PUD

urease breath test, do OGD if Tx doesn't work (if H pylori done on samples taken from biopsy this is a CLO test) and biopsy as all ulcers have malignant potential

MX of PUD

1) conservative - weight loss, less spicy food 2) PPI for 4-8 weeks 3) triple therapy if H pylori + 4) rare but surgery - bilroth 1 and bilroth 2

complications of PUD

strictures (GOO), pyloric stenosis, bleeding, perforation

what is a bilroth I vs a bilroth II

I = part of stomach remove and duodenum rejoined II = part of stomach removed and jejunum rejoined

in the acute setting how is a bleeding ulcer treated

normally adrenaline injection in endoscopy

most common type of oesophageal cancer is

squamous

what kind of oesophageal cancer is hard to operate on and normally results in having chemo/radio

squamous

generalised vs localised peritonitis

generalised = perforation of an abdominal organ localised = underlying organ infection

main causes of acute vs chronic gastritis

acute --> NSAID, chemo, alcohol --> get more angry vasodilation/epithelial damage chronic --> autoimmune / H pylori--> get more atrophic changes (and pernicious anaemia)

Mx of gastritis

avoid triggers and treat any underlying cause (eg H pylori eradication therapy)

what is the only test recommended for post pylori eradication therapy testing

urease breath test