Stomach Flashcards
Blood supply to stomach
Greater curve = R/L gastroepiploic arteries
Lesser curve = R/L Gastrics
Pylorus = Gastroduodenal artery
Fundus = Short gastrics
Innervation of stomach
“LARP”
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
Antrum
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?
NSAIDs
Acetazolamide
Alpha blockers
Alcohol
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
Dysphagia
Bleeding
Anemia
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)
N/v
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
Medical:
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?
GAME PAD
Gallstones
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
Type III GU
Prepyloric
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
Vomiting
Associated with blood type A
Dx of GUs
EGD
All GUs are biopsied - 3% are associated with gastric cancer
Tx of GUs
Medical - same as DUs
Surg - by type and indication
Signs of duodenal perforation
Bleeding from the Back (posterior duodenal erosion/perf involving gastroduodenal artery)
Free Air from Anterior duodenal perf
Anterior is more common than posterior
Curling’s ulcer
Gastric stress ulcers in patients with severe burns
Cushing’s ulcer
Gastric stress ulcer related to severe CNS damage
Gastritis
Acute or chronic inflammation of stomach lining
Etiologies similar to PUD; EGD needed to tell the difference
Dx via EGD
Tx is same as medical treatment of gastric ulcers
