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gastrointestinal > peptic ulcer disease and gastric carcinoma > Flashcards

peptic ulcer disease and gastric carcinoma Flashcards

1
Q

how is an ulcer different to an erosion

A
  • penetrates the muscularis mucosae

- can be acute or chronic (fibrosis)

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2
Q

prevalence of gastric-duodenal ulcers and m:f ratio, blood group

A

10% population
M:F 5:1
blood group A+

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3
Q

what is more common gastric or duodenal ulcers

A

duodenal ulcers

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4
Q

pathophysiology of peptic ulcer disease

A

produced by imbalance of gastro-mucosal defence mechanisms vs secretions and hormone gastrin

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5
Q

causes of peptic ulcer disease and why

A
  • NSAIDs deplete mucosal defence
  • stress: burn, sepsis
  • smoking: damage and delay healing
  • H.pylori
  • acid pepsin vs mucosal resistance
  • zollinger ellison syndrome get excess gastrin
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6
Q

prevalence of H.pylori in gastric vs duodenal ulcers

A

gastric=70%

duodenal=90%

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7
Q

what type of bacteria is H.pylori

A

spiral shaped gram negative acidophilic bacterium with flagella

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8
Q

where is h.pylori prevalence highest

A

africa and south america

more on socio-economic status

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9
Q

mechanism by which H.pylori isnt destroyed

A
  • oral transmission
  • produces urease to break down urea to bicarbonate and ammonia which buffers the acid
  • adhesions help it to attach onto epithelial cells
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10
Q

where does h.pylori prefer in the body and why

A

lives in stomach next to epithelium in the antrum where it is protected by stomach mucosa

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11
Q

4 cytotoxins it produces h.pylori

A
  • vacuolating cytotoxin (vacA) induction apoptosis, disrupt epithelial junction & block t cell response
  • cytotoxin assoc. genes (cagA) alteration of signalling pathway and alter tight junctions
  • phospholipases
  • LPS induce inflammatory response
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12
Q

4 mechanisms of injury in H.pylori

A

-HYPERGASTRINEMIA
negative feedback for gastrin is blocked
-Antral somatostatin is depleted and increased gastrin release

  • HYPERACIDITIY occurs with mucosal damage
  • DIRECT MUCOSAL INJURY; cytotoxins
  • INFLAMMATORY RESPONSE- mediated by macrophages, neutrophil & T cell
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13
Q

dx of H.pylori 4

A
  1. breath test: H.pylori produces from urea: ammonium and bicarbonate
  2. antibody measurement
  3. stool HP antigen test
  4. urease CLO test: take a biopsy from mucosa and place urea on it and see if it goes yellow to red
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14
Q

Prognosis of untreated H.Pylori infection

A

1.chronic active gastritis: predominantly antrum
(increased risk of duodenal ulcers)
2.chronic active pangastritis with some atrophy ( increased risk of gastric ulcers)
3.Chronic atrophic pangastritis (cancer risk)
4.metaplasia of duodenum
5.MALT gastric marginal B cell lymphoma
6. NSAID induced gastropathy

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15
Q

How do NSAIDS cause mucosal damage

A

affect COX1 also which is the housekeeping protective prostaglandins that protect mucosa

  • increase mucosal blood flow
  • stimulate bicarb and mucus secretion
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16
Q

Risk factors for NSAID induced ulcers 8

A
  • age >60 years (atrophic gastritis)
  • phx of PUD
  • phx of adverse event with NSAID
  • concomitant steroid use
  • high dose NSAID or multiple
  • hereditary predisp
  • o blood group
  • smoking
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17
Q

typical symptoms NSAID peptic ulcer disease

A

-epigastric pain (relief by food)
-nausea
-fullness
-bloating
-hunger pain
-night pain
ALARM S

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18
Q

alarm symptoms of NSAID peptic ulcer disease

A 
anaemia
haematemesis 
mealena
vomiting
anorexia
pain radiation
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19
Q

treatment of benign peptic ulcer disease

A
  • stop smoking
  • avoid aspirin and nsaid
  • PPI or H2 blockers
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20
Q

h.pylori eradication therapy

A

omeprazole 20mg
amoxicillin 1gram
clarithromycin 500mg
all three one week

omeprazole
clarithromycin 500mg
metronidazole 400mg

if fails can use Tripotassium Dicitratobismuthate 120mg or tetracycline

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21
Q

H.pylori eradication side effects

A 
diarrhoea
can get c.diff colitis
metronidazole= metallic taste, flush, vomit
headaches
rash
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22
Q

management for NSAID induced ulcers

A
  • stop NSAID or use lower dose
  • co give with PPI
  • use COX2 specifc eg celecoxib
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23
Q

5types of gastric carcinomas

A
  • gastric adenocarcinoma
  • gastric lymphoma
  • GISTs (mostly benign leiomyomas)
  • carcinoid tumours
  • gastrinomas
24
Q

factors assoc. with gastric carcinoma

some animals have fun playing all day games

A 
smoking
alcohol
HP 
FAP syndromes
pernicious anaemia
Blood group A
Diet rich in nitrosamines or salty and spicy
gastric adenomatous polyps
25
Q

what is Zollinger Ellison syndrome and where

A
  • develop gastrinomas in pancreas and duodenum
  • excess gastrin
  • acts on parietal cells to increase acid secretion
26
Q

which part of the multiple endocrine neoplasia is Zollinger ellsion part of

A

MEN1 but also alone

with parathyroid and pituitary

27
Q

symptoms of Zollinger ellison

A
  • multiple ulcers
  • gi bleeds
  • diarrhoea and steatorrhea as inactivated pancreatic enzymes and bile salts
28
Q

management of ZE 4

A

surgical resection tumour
PPI
Octreotide injections to reduce gastrin levels

29
Q

5 year survival for ze

A

60-75%

30
Q

signs of perforation from peptic ulcer

A 
peritonitis
shock
sudden sever pain
air under diaphragm on x-ray
shoulder tip pain
31
Q

management of gastric outlet obstruction

A
  • NG tube for vomit
  • iv fluids
  • acidosis correction
32
Q

4 types of surgical management or peptic ulcers

A
  • vagotomy
  • pyloroplasty
  • bilroth1
  • bilroth2
33
Q

what is vagotomy

A

cut vagus nerve to reduce gastrin secretion

34
Q

what is pyloroplasty

A

cut the pylorus if the pyloric sphincter has thickened to relieve gastric outlet obstruction

35
Q

what is bilroth 1

A

removal of pylorus to create a duodenal anastamosis

36
Q

what is bilroth2

A

removal of the pylorus to create a jejunm anastomosis

37
Q

where are gist tumours found

A

in the tissue in the interstitial cells of cajal

38
Q

treatment for gist and how it works

A

imatinib bonds to c-kit a tyrosine kinase to prevent signalling

39
Q

sign of gist on biopsy

A

spindle cell pattern

40
Q

what does signet cell ring carcinoma produce

A

mucin

41
Q

what is lintis plastica

A

leather bottle stomach
cancer gastric
fibrotic and rigid stomach that wont distend
see signet cell ring proliferation

42
Q

where are gastric carcinomas most common 4

ccjf

A

china
japan
finland
colombia

43
Q

most common gastric carcinoma

A

adenocarcinoma of mucus secreting cells

44
Q

chemotherapy for gastric carcinom

A

5-fluorouracil

45
Q

what are carcinoid tumous of the stomach assoc. to and where are they found

A

assoc. to chronic pernicious anaemia

seen in fundus

46
Q

2 causes of gastric lymphomas

A

extranodal non Hodgkin lymphoma or

primary

47
Q

what infection is closely assoc. to lymphoma gastric

A

h.pylori

48
Q

what does malt stand for

A

mucosal assoc. lymphoid assoc. tumour most commonly seen in stomach

49
Q

treatment of gastric lymphoma

A
  • h.pylori eradication
  • chemo
  • rituximab
  • resection
50
Q

surgery options for gastric carcinoma

A
  • Those proximal ie 5-10cm from og junction treat with sub total gastrectomy
  • Total gastrectomy if tumour is >5cm from og junction
  • Oseophagastrectomy tumours for type 2
  • Lymphadenectomy should be performed
  • Chemotherapy
51
Q

3 types of gastro-oesophageal carcinoma classifiction

A

1=oesophageal
2=carcinoma of the cardia
3=sub cardial cancers that spread across junction

52
Q

summary of gastric carcinoma treatment

A

total gastrectomy and lymphadenectomy

53
Q

most common place for gastric adenocarcinoma

A

antrum 50%

54
Q

2 types of gastric adenocarcinomas

A

intestinal= from areas with intestinal metaplasia

diffuse=normal gastric mucosa-lintis plastica

55
Q

what do gastric adenocarcinomas arise from

A

mucus secreting cells

gastrointestinal (26 decks)

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