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
Complications of chronic gastritis
Gastric atrophy
Gastric metaplasia
Pernicious anemia (lower production of IF from parietal cells due to idiopathic atrophy of gastric mucosa and later malabsorption of B12)
Etiologies of gastritis
GNASHING
Gastric reflux (bile or pancreatic secretions) Nicotine Alcohol Stress H Pylori and other infx Ischemia NSAIDs Glucocorticoids (longterm)
What are the 2 types of chronic gastritis?
A (fundal) - pernicious anemia, parietal cell antibodies, achlorhydria, autoimmune disease
B (antral) - Bug (H pylori in almost all)
Which H2 blocker is known to be a P450 inhibitor?
Cimetidine
Prolongs action of drugs cleared by this system
Postvagotomy diarrhea
1 complication of vagotomy
A common postgastrectomy complication
Self-limited
Symptomatic tx with motility-reducing agents (kaolin-pectin, loperamide, diphenoxylate)
Refractory cases may respond to cholestyramine (bile-salt binding agent)
Dumping syndromes
Complciation postgastrectomy
Complication of gastric surgery thought to come from unregulated movement of gastric contents from stomach to SI
Symptoms usually 5-15mins postprandially (early dumping) due to high osmolar load reaching SI or 2-4hrs postprandial (late dumping) due to hypoglycemia
N/v, belching, diarrhea, tachycardia, palpitations, flushing, diaphoresis, dizziness, syncope
Treated by dietary mods - small, multiple low-carb/fat meals; avoid excess liquid intake
Severe cases (1%) that do not respond to dietary mods can be treated with octreotide (synthetic somatostatin - helps delay gastric emptying time and transit through SI)
Alkaline reflux gastritis
Another postgastrectomy complication
Diagnosis of exclusion after recurrent ulcer has been ruled out; nonspecific EGD and bx findings (edematous, inflamed gastric mucosa)
p/w postprandial pain and bilious vomiting
Surg management (medical is difficult) = RY gastojejunostomy with a long (50cm) Roux limb. Bilious vomiting may improve, but symptoms (early satiety, bloating) may persist
Afferent loop syndrome
Another postgastrectomy complication
Obstruction of afferent limb following gastrojejunostomy (Billroth II). 2/3 present in postop week 1
Symptoms = postprandial RUQ pain, bilious vomiting, steatorrhea (with concomitant malabsorption of fats, B12), anemia
Dx = afferent loop will be devoid of contrast in UGI series
Tx = endoscopic balloon dilation or surgical revision of loop if that fails
Nutritional deficiencies following gastrectomy
B12
Fe
Osteoporosis (reduced calcium absorption)
Common causes of Gastric outlet obstruction
Malignant tumors of stomach and head of pancreas
Obstructing gastric or duodenal ulcers
Usually with duodenal ulcer
Chronic ulcer causes secondary edema or scarring, which occludes lumen
Symptoms of GOO
Early
- early satiety
- gastric reflux
- abdominal distention
Late
- vomiting
- dehydration
- hypochloremic, hypokalemic metabolic alkalosis with paradoxical aciduria
- weight loss
Dx of GOO
EGD or Barium swallow
Tx of GOO
Truncal vagotomy and pyloroplasty or gastrojejunostomy after 7d of NG decompression and antisecretory treatment
NG decompression is necessary to normalize the size of the dilated stomach
Causes of upper GI hemorrhage
Ulcer (peptic) Varices Gastritis AV malformation Mallory-Weiss tear
Signs/symptoms of upper GI hemorrhage
Hematemesis (bright red or coffee grounds)
Hypotension
Tachy
Bleeding that produces 60cc of blood or more will produce black, tarry stool (melena)
Very brisk upper GI bleeds can be associated with bright red blood per rectum (hematochezia) and hypotension
Diagnosis of upper GI hemorrhage
Gastric lavage with NS or free water to assess severity of bleeding (old v new)
Rectal exam
CBC
EGD
Bleeding scan - detects active bleeding by infusing Tc-labeled RBCs and watching their collection in GI tract. It can be done in about an hour and can detect bleeds as slow as 0.1 ml/min, but location specificity is only 60-70%. CTA is faster and detects bleeds up to 0.5 ml/min
Arteriography
Tx of upper GI bleed
Depends on etiology and severity
Bleeding varices are ligated, or sclerosed via EGD
Most M-W tears resolve on own
For severe bleeds:
- IVF and blood needed
- Somatostatin (inhibits gastric, intestinal, and biliary motility, decreases visceral blood flow)
- Consider balloon tamponade for varices
Surgery
- About 5% of the time, upper GI bleeding cannot be controlled via endoscopic or other methods and emergent laparotomy will be needed
- For DUs, a longitudinal incision is made across pylorus and prox duodenum. Bleeding is controlled by undersewing the vessel on either side of the bleed
Risk of ulcers rebleeding
In hospital = 33%
GUs are 3x more likely to rebleed than DUs
Prereq to bariatric surgery
Participation in supervised dietary program without success
Adenocarcinoma Epi
Gastric cancer is in general a disease of the elderly (age over 60), men>women, blacks>whites
Adeno is 95% of malignant gastric cancer
Leading cause of cancer death in Japan
Risk factors for adenocarcinoma of stomach
FAP
Chronic atrophic gastritis
H Pylori (6x risk)
Post-partial gastrectomy (15+ years)
Pernicious anemia
Diet (foods high in nitrites - preserved, smoked, cured)
Cigarette smoking
Pathology of gastric adeno
Polyploid: 25-50%, no real necrosis or ulceration
Ulcerative: 25-50%, sharp margins
Superficial spreading: 3-10%, involves mucosa and submucosa only - BEST PROGNOSIS
Linitis plastica: 7-10%, “leather bottle” type, involves all layers, extremely poor prognosis
Signs/symptoms gastric adeno
Early: Mostly asymptomatic
Late: Anorexia/weight loss, nausea, vomiting, dysphagia, melena, hematemesis; pain is constant, nonradiating, and worse with food.
Anemia - from blood loss, pernicious
Krukenberg tumor
Metastasis to ovaries
Blumer’s shelf
Metastasis to pelvic cul-de-sac, felt on digital rectal exam
Virchow’s node
Metastasis to lymph node palpable in L supraclavicular fossa
Sister Mary Joseph nodule
Periumbilical metastatic nodules
Dx of gastric adeno
Upper GI EGD - best method. allows for bx. definitive > 95% sensitivity and specificity
Upper GI series - with double contrast. 80-96% sens, 90% spec (operator dependent). excellent method in skilled hands
Abdominal CT - good for detecting distant mets, also used for preop staging, but suboptimal
Endoscopic US - good for detecting depth of invasion
Staging of gastric adenocarcinoma
T1s = carcinoma in situ - intraepithelial tumor without invasion of lamina propria
T1 = invades lamina propria or submucosa
T2a = invades muscularis propria
T2b = invades subserosa
T3 = penetrates serosa (visceral peritoneum) without invasion of adjacent structures
T4 = Invades adjacent structures (spleen, colon, liver, diaphragm, pancreas, abdominal wall, adrenals, kidney, SI, retroperitoneum)
N1 = mets to 1-6 regional LNs N2 = 7-15 N3 = >15
Stage 1A = T1N0M0 (70-80% 5yr)
Stage 1B = T1N1M0 or T2a/2bN0M0 (55-70%)
Stage 2 = T1N2M0 or T2N1M0 or T3N0M0 (40-50%)
Stage 3a = T2N2M0 or T3N1M0 or T4N0M0 (10-20%)
Stage 3b = T3N2M0 (10-20%)
Stage 4 = T1-3N3M0 or T4N1-3M0 or AnyTAnyNM1 (
Tx of gastric adenocarcinoma
Radical subtotal gastrectomy can be curative in early disease confined to superficial layers of stomach (less than 1/3 of all patients due to late presentations)
Chemo - sometimes used palliatively for nonsurg candidates; no role for adjuvant chemo
Prognosis of gastric adenocarcinoma
Tx is major prognostic factor - patients who are not resected have worse prognosis
Location - prox gastric cancer is worse than distal lesions
Tumor markers - high preOp levels of CEA and CA19-9 have worse outcomes
Other factors = histo, regional LN spread
Gastric lymphoma epi
#2 most common malignant gastric cancer Stomach is most common site of primary GI lymphoma (majority are B cell non hodgkin) but lymphoma comprises only 4% of all gastric tumors
Increased risk with H pylori
Signs of gastric lymphoma
Nonspecific; include abdominal discomfort, nausea, vomiting, anorexia, weight loss, and hemorrhage, occult bleeding and anemia (half of patients)
Dx of gastric lymphoma
Made by endoscopic bx, nor readily distinguishable from adenocarcinoma by simple inspection
Bone marrow aspiration and gallium bone scans can diagnose mets
Tx of gastric lymphoma
MALT (low grade) - treat H pylori
MALT (high grade) or non-MALT - radiation/chemo +/- surg resection
Resection reserved for patients with bleeding or perforation
Prognosis of gastric lymphoma
Poor factors are:
Involving lesser curvature of stomach
Large tumor size
Advanced stage
GI stomal tumor
Mesenchymal tumors arising from gastric stroma; submucosal and slow growing
Stomach is #1 site
Dif histologies - from spindle cell tumors to epithelioid to pleomorphic
95% of GIST have c-kit (CD117) expression
All are malignant
Treated by surgical resection and Gleevec (imatinib)
Prognosis depends on completeness of resection, presence of mets, and the mitotic index
Benign tumors/adenomatous polyps
10-20% of all gastric polyps
The only ones with any real malignant potential - others are mostly asymptomatic and uncommon
Biopsy if > 5mm to check for neoplasia
Menetrier’s Disease definition
Hypertrophic gastropathy (enlarged, tortuous gastric rugae)
Protein-losing enteropathy
Mucosal thickening secondary to hyperplasia of glandular cells replacing chief and parietal cells
Low grade inflammatory infiltrate - not a form of gastritis
Signs of Menetrier’s
Most commonly middle aged man who presents with epigastric pain, weight loss, diarrhea, hypoproteinemia
Less common is n/v, anorexia, occult GI bleed
Gastric acid secretion can be high, normal or low
Dx of Menetrier’s
EGD with deep mucosal bx is definitive
Barium swallow will reveal large gastric folds and thickened rugae
May look like gastric cancer on barium swallow
Complications of Menetrier’s
Gastric ulcer Gastric cancer (increased incidence so monitor closely)
Tx of Menetrier’s
Anticholinergics
H2 blockers to reduce protein loss
High protein diet
Treatment of ulcers/cancers if present and eradication of H pylori
Severe disease may require gastrectomy
Bezoars definition
Concretions of nondigestible matter that accumulate in stomach.
May consist of hair (trichobezoar), vegetable matter (phytobezoar - esp in people who may have eaten persimmon), or charcoal (used in management of toxic ingestions)
May develop after gastric surgery
Symptoms of Bezoars
Similar to GOO
Occasionally causes ulceration and bleeding
Dx of Bezoars
EGD
Tx of Bezoars
Proteolytic enzymes - papain
Mechanical fragmentation with endoscope
Surg removal
Dieulafoy’s Lesion
Mucosal end artery that causes pressure necrosis and erodes into stomach and ruptures
Massive, recurrent painless hematemesis
Dx = EGD
Tx = endoscopic sclerosing therapy or electrocoagulation
Wedge resection
Gastric volvulus definition
Torsion/twisting of stomach typically along long axis. Often linked with paraesophageal hernia.
May be acute, must usually chronic
Gastric volvulus symptoms
Brochardt’s triad
1) Intermittent severe epigastric pain and distention
2) Inability to vomit
3) Difficult passage of NG tube
Gastric volvulus dx and tx
Upper GI contrast study
Surgical repair of accompanying hernia
Gastropexy - fixes stomach to anterior abdominal wall
Gastric resection if there is necrosis
