stomach power point
TRANSCRIPT
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StomachSurgery Review, Fairfax Residency
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Stomach: Basic Anatomy
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Blood Supply
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Innervation
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HSV
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Parietal Cell Secretes acid and IF
Regulated by Ach, gastrin, histamine
Basal acid secretion 10% of maximal
Food bolus gastrin acid production luminal acid
inhibits gastrin
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Cell Types & Locations
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Abnormal Motility:
Gastroparesis Vagotomy
Hyperglycemia
H pylori
Common s/p Whipple
Anorexia & Bulimia
Connective tissue disorders
(Ehlers Danlos,
Scleroderma, parkinsons)
Tobacco?
1st line: treat with pro-kinetics
(reglan, erythro)
Dietary changes (plus
glucose control in DM)
Surgical (reversible):
jejunostomy, TPN, gastric
pacers, botulin
Surgical (irreversible):
Antrectomy, Distalgastrectomy
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Vagotomy Loss of receptive relaxation and accommodation
Early satiety, bloating, accelerated emptying of liquids,
delayed emptying of solids
Pyloroplasty cuts pylorus, allows easier emptying of
food into duo (high incidence of recurrent ulcer)
Antrectomy removes gastrin-producing cells (less
chance of recurrent ulcer)
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H pylori Found in 90% of duodenal ulcers & 75% of gastric
ulcers
Gram negative, microaerophilic bacteria
1st-line tx: PPI (Omeprazole = Prilosec) +Clarithromycin + Amoxicillin (or Flagyl if PCN-allergic)
Treat x 7 days
If refractory, add Bismuth (= Peptol Bismol)
Once eradicated, rarely recurs
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Gastric Ulcers I: Lesser curve at incisura
(low to normal acid)
II: Gastric body with duo
ulcer (increased acidity)
III: Pre-pyloric (incr. acidity)
IV: High on lesser curve
(normal acidity)
V: Anywhere (normal acidity,NSAID-induced)
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Gastric Ulcer Treatment
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Gastric Cancer
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Q1 68 yof on high-dose NSAIDs
from chronic low back pain,
early satiety, nausea,
vomiting; narrowing of lumen
at 1st portion of duo, almost
occluded; CT shows no
mass
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Treatment? Pneumatic dilation
Anti-secretory meds
PEG Gastrojejunostomy
H pylori treatment
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Whats Going On? Gastric outlet obstruction
Most likely cause: previous generations, ulceration
would have been most likely, now canceris most likely
Has cancer been ruled out? (CT negative)
High-dose NSAIDs, think ulcer (Type V)
Anti-secretory meds & H pylori eradication necessarybut not the firststep
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Pneumatic Dilation Ulceration leads to
inflammation, scarring &
edema of pyloroduodenal
channel
90% success, can attempt x3, but if fails, proceed with
gastrojejunosomty
NEXT step is tx with anti-
secretory meds & H pylori
eradication
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Treatment? Pneumatic dilation
Anti-secretory meds
PEG Gastrojejunostomy
H pylori treatment
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Q2: Regarding gastroparesis:
Which is true?
More common in Type 2 than Type 1 diabetes?
Gastric electrical stimulation does not cause directcontraction of smooth muscle or entrain normal gastricelectrical rhythm
Receptive relaxation of fundus in diabetic patients is normal
Gastric electrical stimulation improves sx in idiopathic butnot diabetic gastroparesis
Idiopathic gastroparesis most common secondary tobacterial gastroenteritis
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Gastroparesis Sx: slow emptying, nausea, vomiting, abd pain,
bloating, anorexia, weight loss; due to abnormalmyoelectrical activity
Seen in diabetics and after truncal vagotomy
In diabetics, 50% of Type I, 30% of Type II
Tx with reglan and erythro
40% of pts cannot tolerate pro-kinetic meds; anti-emetics are 2nd line
Medical success rate ~ 50%
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Gastroparesis Surgical treatment includes gastro electric stimulation
Low-energy pulses delivered to greater curve 10 cm from
pylorus
Small amt of stimulation, not enough to cause directcontraction of smooth muscle
Does not always normalize emptying, but improves sx of
N&V and QOL.
Equally effective for diabetic and idiopathic gastroparesis
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Q2: Regarding gastroparesis:
Which is true?
More common in Type 2 than Type 1 diabetes?
Gastric electrical stimulation does not cause directcontraction of smooth muscle or entrain normal gastricelectrical rhythm
Receptive relaxation of fundus in diabetic patients is normal
Gastric electrical stimulation improves sx in idiopathic butnot diabetic gastroparesis
Idiopathic gastroparesis most common secondary tobacterial gastroenteritis
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Q348 yom, etoh abuse, presents with massive UGI bleed,endoscopy shows linear disruption of gastric mucosa high onlesser curvature at GE jct. Endoscopic treatment cannot controlbleeding. Pt gets 6 u PRBCs, HR is 115, SBP in 85.Treatment?
Embolize L gastric A.
Place Blakemore tube and inflate balloon
Anterior gastrostomy & oversewing bleeding site
Vagotomy, Antrectomy & biopsy of bleeding site
Total gastrectomy
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Whats Going On? Mallory-Weiss Tear, pt unstable
Source of ~ 10% of admission for UGI bleed
Endoscopy 1st line
If pt unstable, tx is proximal anterior gastrostomy withoversewing of tear
Bleeding stops in 90% with resuscitation only. LGA
embolization and vasopressin useful if pt not opcandidate
Lesion not malignant, not due to incr acid
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Q348 yom, etoh abuse, presents with massive UI bleed,endoscopy shows linear disruption of gastric mucosa high onlesser curvature at GE jct. Endoscopic treatment cannot controlbleeding. Pt gets 6 u PRBCs, HR is 115, SBP in 85.Treatment?
Embolize L gastric A.
Place Blakemore tube and inflate balloon
Anterior gastrostomy & oversewing bleeding site
Vagotomy, Antrectomy & biopsy of bleeding site
Total gastrectomy
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Q4: Pathology of stress-related gastric
mucosal injury
Elevated gastric acid
Bile reflux
Reduced gastric blood flow
H pylori infection
NSAIDs
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Stress related gastric injury ICU patients
Seen in fundus and body of stomach
Rarely in distal stomach
Diagnose with endoscopy
Tx: Resuscitate, correct coagulopathy, NG lavage, H2
blockers (Ranitidine = Zantac)
Source is reduced mucosal perfusion acid damages
gastric mucosa
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Q4: Pathology of stress-related gastric
mucosal injury
Elevated gastric acid
Bile reflux
Reduced gastric blood flow
H pylori infection
NSAIDs