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Y5 colorectal > stomach > Flashcards

stomach Flashcards

1
Q

what kind of bacteria is H pylori

A

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

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2
Q

what do parietal cells produce

A

HCL

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3
Q

what do chief cells produce

A

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

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4
Q

what is the lining of the stomach made of

A

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

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5
Q

RF of gastric cancer

A

H pylori, male, smoking, pernicious anaemia

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6
Q

how does h pylori cause its problems

A

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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7
Q

O/E of gastric cancer

A

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

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8
Q

gold standard Ix for upper GI cancer

A

OGD with biopsy

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9
Q

staging for GI cancer

A

staging CT CAP and a staging laparoscopy

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10
Q

surgical option for a proximal gastric cancer

A

total gastrectomy

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11
Q

surgical option for a distal gastric cancer

A

subtotal gastrectomy

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12
Q

surgical option for a T1 gastric tumour

A

endoscopic mucosal resection

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13
Q

reconstruction surgery after a gastrectomy

A

roux en Y

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14
Q

Complications of gastrectomy

A

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

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15
Q

what are the 2WW criteria for upper GI

A

ANYONE with dysphagia
-anyone over 55 with new upper abdo pain, reflux, dyspepsia

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16
Q

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

A

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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17
Q

Barrett caused by what

A

GORD

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18
Q

what is Barrett s

A

metaplasia from a stratified squamous to a columnar epithelium

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19
Q

Mx of GORD

A

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

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20
Q

Ix for GORD

A

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

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21
Q

complications of GORD

A

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

22
Q

is H pylori involved in GORD

A

NO! no role for testing or Tx

23
Q

what is boerhaave syndrome

A

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

24
Q

triad of symptoms in boerhaave syndrome

A

epigastric pain, vomiting, subcutaneous emphysema

25
Q

Mx of boerhaave syndrome

A

surgical correction but mortality is high

26
Q

Dx for barrets

A

diagnosis is based on histology for biopsy

27
Q

any dysplastic changes on barrets require what

A

endoscopic intervention

28
Q

surveillance for barrets

A

OGD every 3-5 years and high dose PPI

29
Q

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

A

adenocarcinoma (from barrets)

30
Q

staging for oesophageal cancer

A

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

31
Q

what causes oesophageal varies

A

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

32
Q

venous drainage of the oesophagus

A

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

33
Q

what kind of dysphagia do you get in achalasia

A

dysphagia to liquids and solids

34
Q

why do you get achalasia

A

failure of peristalsis and failure of the LOS to relax

35
Q

Ix for achalasia

A

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

36
Q

Mx for achalasia

A

balloon dilation and botulin injections (limited role for CCB)

37
Q

where do peptic ulcers normally occur

A

lesser curvature of the stomach or proximal part of duodenum

38
Q

RF for PUD

A

H pylori, alcohol, GORD, smoking, stress

39
Q

pathophysiology of PUD

A

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

40
Q

what does PGE2 do in stomach

A

HCO3 and mucous production

41
Q

presenting symptom of PUD

A

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

42
Q

Ix for PUD

A

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

43
Q

MX of PUD

A

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

44
Q

complications of PUD

A

strictures (GOO), pyloric stenosis, bleeding, perforation

45
Q

what is a bilroth I vs a bilroth II

A

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

46
Q

in the acute setting how is a bleeding ulcer treated

A

normally adrenaline injection in endoscopy

47
Q

most common type of oesophageal cancer is

A

squamous

48
Q

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

A

squamous

49
Q

generalised vs localised peritonitis

A

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

50
Q

main causes of acute vs chronic gastritis

A

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

51
Q

Mx of gastritis

A

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

52
Q

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

A

urease breath test

Y5 colorectal (8 decks)

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