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Flashcards in Stomach Deck (85)
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Blood supply to stomach

Greater curve = R/L gastroepiploic arteries

Lesser curve = R/L Gastrics

Pylorus = Gastroduodenal artery

Fundus = Short gastrics


Innervation of stomach


Anterior = L Vagus nerve (gives branch to liver)

Posterior = R Vagus nerve (gives Celiac branch and the "criminal nerve of Grassi")

Gastroduodenal pain = sensation via sympathetic afferents from level T5 (below nips) to T10 (umbilicus)


What are the causes of B12 deficiency?

1) Gastrectomy - loss of intrinsic factor-secreting tissue

2) Disease or resection of terminal ileum - malabsorption of B12

3) Pernicious anemia - AI destruction of parietal cells

4) Insufficient dietary intake - B12 is in most foods of animal origin


Parietal cells

Fundus and body

"oxyntic cells"

Secrete HCl and intrinsic factor


Chief cells

"peptic cells"

Fundus and body

Secrete pepsinogen. Pepsinogen is activated by HCl to form pepsin which digests proteins


G cells


Secrete Gastrin - stimulates gastric acid secretion, pepsin secretion, and mucosal growth of GI tract (trophic action)


What stimulates acid secretion by parietal cells?

Vagus nerve (ACh via M3 receptors)

Histamine (H2 receptors)

Gastrin (via gastrin receptors)

Proton pump (H/K ATPase) is final common pathway


What stimulates release of gastrin from G cells?

Gastrin-releasing peptide (GRP)

Presence of digested protein products (AAs) in stomach

Inhibited by somatostatin and low antral pH (


What affects gastric mucosal barrier?

NSAIDs - damage it

Prostaglandin E - enhances it


What inhibits gastric HCO3 secretion into the mucosal barrier?



Alpha blockers



PUD epi

H pylori, NSAIDs, smoking

FHx of ulcers, Z-E (gastrinoma), corticosteroids (high dose or longterm)

Ulcer incidence increases with age for both GUs and DUs

DU emerges two decades earlier than GU, particularly in men


Complications of PUD

1) Bleeding - 20% incidence
- hemorrhage: dizziness, syncope, hematemesis, melena

2) Perforation - 7% incidence - sudden severe midepigastric pain radiating to R shoulder with peritoneal signs and free peritoneal air

Posterior perf of a DU will cause pain that radiates to back and can cause pancreatitis or cause GI bleeding (erosion of gastroduodenal artery). Chest or abdominal film may not show free air bc the posterior duodenum is retroperitoneal

Anterior perf will show free air under diaphragm 70% of the time

3) Obstruction (gastric outlet) - due to scarring and edema; early satiety, anorexia, vomiting, weight loss


What are some alarm symptoms that indicate an EGD is needed

Weight loss

Recurrent vomiting





Duodenal Ulcer pathophys

Increased acid production (different from gastric ulcers)

H Pylori may weaken mucosal defenses


Causes of Duodenal Ulcers

1) H Pylori - makes urease which breaks down protective mucous lining of stomach. 10-20% of people with H Pylori develop PUD (H pylori may colonize 90% of us though so infection does not necessarily mean PUD)

2) NSAIDs/steroids - inhibit production of prostaglandin E, which stimulates mucosal barrier production

3) ZE syndrome - Gastrinoma (gastrin secreting tumor near pancreas - 2/3 are malignant). 20% of ZE patients have associated MEN1 (parathyroid hyperplasia, pancreatic islet tumors, pituitary tumors); diarrhea is common

ZE accounts of 0.1-1% of patients with ulcer, but over 90% of ZE patients have PUD (you can even see jejunal ulcers)


Clinical signs of Duodenal ulcers

Burning, gnawing epigastric pain that occurs with an empty stomach and is relieved by food or antacids

Nighttime awakening (when stomach empties)


Associated with blood type O


Dx of DUs

DU: EGD, but most symptomatic cases of DU are easily diagnosed clinically

H Pylori
1) EGD with bx - allows culture and sensitivity (very hard organism to culture - multiple specimens needed during bx)

2) Serology - Anti-Hpylori IgG indicates current or prior infection

Urease breath test: C-13/C-14 labeled urea ingested. If gastric urease is present, the carbon isotope can be detected as CO2 isotopes in breath

ZE - fasting serum gastrin > 1000.
- Secretin stimulation test: Secretin (gastrin inhibitor) is delivered parenterally usually with calcium and its effect on gastrin secretion is measured. In ZE, there is a paradoxical astronomic rise in serum gastrin


Tx for DUs

1) Risk mods
- D/C NSAIDs, steroids, smoking
- Prostaglandin analogues (misoprostol)

2) Acid reduction
- PPI: 90% cure rate after 4 weeks
- H2 blockers (cimetidine, ranitidine, famotidine, nizatidine): 85-95% cure rate after 8w
- Antacids

3) Eradication of H Pylori
- Triple therapy (2w regimen with BID dosing) - PPI + Amoxicilin + Clarithromycin - 70-85% eradication rate
- If allergic to penicillin, can use metronidazole for amoxacillin
- If patient fails 1 course of therapy, can try alternate regimen using dif combo or quad therapy (2w PPI + bismuth + tetracycline + metronidazole) - 75-90% eradication rate

Surgical - indicated when ulcer is refractory to 12w of medical tx or if hemorrhage, obstruction or perf is present
1) Truncal vagotomy and selective vagotomy - high morbidity (Dumping syndrome) but successful just not used much anymore

2)*** procedure of choice is highly selective vagotomy - parietal cell vagotomy/prox gastric vagotomy
- individual branches of anterior and posterior nerves of Latarjet in gastrohepatic ligament going to lesser curve of stomach are divided. Terminal branches to pylorus and antrum are spared - NO NEED FOR GASTRIC DRAINAGE
- lowest rate of dumping, but higher recurrence rate
- Recurrence depends on site of ulcer preop. Prepyloric = 30% recurrence. Lowest recurrence is with vagotomy + antrectomy


Most common location for DU

Posterior duodenal wall within 2cm of pylorus


What are some complications that are specific to surgery for PUD?


Afferent loop syndrome
Marginal ulcer
Efferent loop obstruction

Postvagotomy diarrhea (#1)
Alkaline reflux gastritis
Dumping syndrome


Gastric ulcer pathophys

Decreased protection against acid; acid protection may not even be elevated (can even occur with achlorhydria)

Can be caused by reflux of duodenal contents (pyloric sphincter dysfunction) and decreased mucus and HCO3 production


Causes of GUs

NSAIDs and steroids inhibit PGE (PGE stimulates production of protective mucus barrier)

H Pylori - makes urease which breaks down gastric mucosal barrier

Obviously smoking is a risk factor


Classification of GUs

Location determines classification and is important for treatment

"One is Less, Two has Two, Three is Pre, Four is by the Door"


Type I GU

Most common

Near angularis incisura on lesser curvature

From normal/decreased acid secretion; decreased mucosal defense

Surg tx = distal gastrectomy with ulcer excision


Type II GU

Associated with DU (active or quiescent)

From normal or increased acid secretion

Surg tx = Antrectomy with truncal vagotomy and ulcer excision




From normal or increased acid secretion

Surg tx = Antrectomy with truncal vagotomy and ulcer excision


Type IV GU

Near GEJ

Normal or subnormal acid secretion; decreased mucosal defense

Surg tx = distal gastrectomy with ulcer excision and esophagogastrojejunostomy


Signs/symptoms of GUs

Burning, gnawing epigastric pain that occurs with anything in the stomach; pain is worst after eating

Anorexia/weight loss


Associated with blood type A


Dx of GUs


All GUs are biopsied - 3% are associated with gastric cancer


Tx of GUs

Medical - same as DUs

Surg - by type and indication