Upper GI Flashcards
Achalasia
failure of LES relaxation d/t loss of Auerbach plexus (aka myenteric plexus)
uncoordinated peristalsis
dysphagia to solids and liquids
Barium swallow - bird beak
Chagas disease
secondary achalasia
Trypanosoma cruzi infection
Cardiomegaly
megaesophagus
Extra hepatic biliary atresia
incomplete recanalization of bile duct during development
presents shortly after birth
- dark urine
- clay colored stools
- jaundice
Annular pancreas
failure of ventral pancreatic bud to rotate properly
–> constricting ring around duodenum
-non billious vomiting
presents shortly after birth
Malrotation of midgut
normally 270 degree rotation not completed –> cecum and appendix lie in upper abdomen
assoc w/ volvulus - twisting of intestine –> obstruction
CREST
E = esophageal dysmotility
lower pressure proximal to LES
Esophageal varices
d/t portal HTN generally d/t alcoholic cirrhosis
hematemesis
caput medusa
ascites
Tx: vasopressin
dx: endoscopy
Boerhaave syndrome
Full thickness rupture of esophagus d/t severe retching
pneumomediastinum
GERD predisposes
Mallory Weiss Tear
laceration of gastroesophageal junction - mucosal tear, not as severe as Boerhaave
severe retching or coughing
alcoholics and bulimics
Hiatal hernias
–> Increased incidence of GERD
Sliding: most common
GE junction displaced upward
Barium study: hour glass stomach
Paraesophageal (“rolling”):
upper stomach herniates upward, lies next to esophagus
no displacement of GE junction
GERD
d/t obesity, overeating
tx: H2 blockers, proton pump inhibitors
Barrett esophagus
d/t chronic GERD
Metaplasia in cells of lower esophagus
Normal squamous epithelium –> columnar epithelium and goblet cells
-response to chronic exposure to acid
assoc w/ esophageal adenocarcinoma
Esophagitis
Causes:
GERD
Candida - immunosuppressed, hyphae organism
CMV - enlarged cells w/ intranuclear and cytoplasmic inclusions, clear nuclear halo
HSV - large pink intranuclear inclusion, chromatin pushed to edge
Omphalocele
cele - “has a seal”
OM - “Oh My it’s worse”
Extruding viscera covered by sac composed of peritoneum and amnion
Liver often found protruding
50% have other anomalies - GI, GU, CV, CNS, MS
Gastroschisis
Extruding viscera not covered by sac
Liver NEVER found protruding
10-15% have other anomalies - less common
Defect lateral to umbilicus - R>L
Esophageal strictures
GERD
Caustic substance
Dx: barium swallow
Tx: dilation by endoscopy
Zenker diverticulum
immediately above upper esophageal sphincter
false diverticulum - only mucosa and submucosa
Traction diverticulum
near midpoint of esophagus
true diverticulum - all layers involved
Epiphrenic diverticulum
Phrenic - on top of diaphragm
Immediately above lower esophageal sphincter
false diverticulum
Plummer vinson sn
dysphagia d/t esophageal webs - upper esophagus
Glossitis
Iron deficiency anemia
Post menopausal
Tx: esophageal dilation
Esophageal adenocarcinoma
Assoc w/ Barrett esophagus
-distal 1/3 esophagus metaplastic columnar epithelium w/ goblet cells
MC in whites, MC esophageal cancer in US
Risk: GERD Smoking Obesity Nitrosamine
Dysphagia, pain
Esophageal squamous cell carcinoma
assoc w/ alcohol and tobacco use
MC esophageal CA worldwide
dysphagia, pain
Specialized columnar epithelium seen in biopsy from distal esophagus
Barrett Esophagus
Bx of pt w/ esophagitis reveals large, pink intranuclear inclusions and host cell chromatin pushed to edge of nucleus
HSV esophagitis
Bx of pt w/ esophagitis reveals enlarged cells, intranuclear and cytoplasmic inclusions, clear perinuclear halo
CMV esophagitis
esophageal bx reveals lack of ganglion cells between inner and outer muscular layers
achalasia
protrusion of mucosa in the upper esophagus
esophageal web - Plummer Vinson Syndrome
out pouching of esophagus found just above LES
epiphrenic diverticulum
Goblet cells seen in distal esophagus
Barrett esophagus
PAS stain on bx obtained from patient w/ esophagitis reveals hyphate organism
candida esophagitis
Esophageal pouch found in upper esophagus
Zenker diverticulum
Products secreted by parietal cells
H+ (gastric acid)
Intrinsic factor
Product secreted by chief cells
Pepsinogen
cleaved by gastric acid –> pepsin - digests proteins
Sites of Bicarbonate secretion
Mucosal cells of stomach - in mucus stimulated by prostaglandins (why COX1 inhibitors –> ulcer)
Brunner’s glands - duodenum
Salivary glands
Pancreatic ducts
Secretin stimulates bicarb secretion
Gastrin in gastric acid regulation
Secreted into circulation by G cells in antrum of stomach
Stimulated by:
-phenylalanine, tryptophan, calcium
-Vagus N. via gastrin-releasing peptide (GRP)
“pro gastric”
- acid secretion
- growth of gastric mucosa
- stimulates gastric motility
Stimulates ECL cells to secrete histamine –> stimuate parietal cells to make HCl via H2 receptors - Gs
-blocked by H2 blockers: cimetidine, ranitidine, famotidine
Vagus N in gastric acid regulation
stimulates parietal cells direcly via M3 AChR
-inhibited by antimuscarinic drugs (atropine)
Indirectly stimulates parietal cells via G cell stimulation by gastrin-releasing peptide
-not susceptible to antimuscarinics
Prostaglandins role in gastric acid regulation
stimulates Gi inhibiting adenylyl cyclase stimulated by H2 receptor on parietal cells
Somatostatin role in gastric acid regulation
octreotide - drug analog
inhibit parietal cells via Gi
Parietal cell proton pump
H/K ATPase pumps K into cell against gradient, H+ out into lumen of stomach
Site of PPI activity - omeprazole
H+ into lumen countered by secreting HCO3- into circulation –> alkaline tide
Zollinger Ellison Syndrome
Tumor secretes gastrin - gastrinoma
-usually in pancreas
excess gastric acid –> recurrent duodenal ulcers
Tx: PPI (omeprazole) +/- octreotide
Assoc w/ MEN1
Acute gastritis
inflammation of stomach
break down of mucosal lining
-too much acid or not enough mucus production
Causes: NSAIDs and aspirin Alcohol Burns - Curling ulcer Brain injury - cushing ulcer
Chronic gastritis
H. pylori
Histo: neutrophils invade glands
Lymphocytes invade tissue –> MALT lymphoma
Increased risk of gastric cancer
Peptic ulcer
acid erodes through mucosa to submucosa
stomach –> gastric ulcer
duodenum
Duodenal ulcers
pain relieved by eating d/t bicarb production
pain returns several hours after eating
Wt gain
90-95% H. pylori
Clean smooth borders w/ organisms
Hypertrophy of brunner glands
Rarely caused by Zollinger Ellison Sn
Gastric ulcer
upper abdominal and epigastric pain after eating
wt loss
70% H pylori
NSAIDs use
increased risk of gastric cancer
Ulcer complications
pain
wt loss/gain
hemorrhage
tx: somatostatin (octreotide) - reduces splanchnic blood flow
Perforation - esp duodenum –> peritonitis
H. pylori tx
triple tx:
PPI + clarithromycin + amox
PPI + clarithromycin + metronidazole (if amox allergy)
Quad tx if resistent to clarithromycin:
PPI + bismuth + metronidazole + tetracycline
Antacids
Calcium carbonate (tums) --> hypercalcemia --> G cells stimulated to secrete gastrin --> rebound excess acid
Magnesium hydroxide (rolaids)
- sm.m. relaxer –> diarrhea
- -> hyporeflexia, hypotension, cardiac arrest
Aluminum hydroxide
- constipation
- hypophosphatemia
- proximal m. weakness
- seizures
- osteodystrophy
All can cause hypokalemia
-neutralizing acid –> metabolic alkalosis
H/K ATPase puts H in blood and K into cell
H2Blockers
Cimetidine
Famotidine
Nizatidine
Ranitidine
Inhibit H2 receptor on parietal cells
Cimetidine Side effects:
Inhibit CYP450
Antiandrogen: impotence, decreased libido, gynecomastia
decrease methemoglobin levles
All H2 blockers –> thrombocytopenia
Proton pump inhibitors
“-prazole”
Omeprazole
Esomeprazole
Pantoprazole
Inhibit H/K ATPase - no back door signal can stimulate acid production
Uses: severe GERD Zollinger Ellison Sn erosive esophagitis PUD Gastritis H pylori triple tx
Bismuth
binds tissue at base of ulcer forming protective barrier
–> healing ulcer
good for traveler’s diarrhea
Sucralfate
requires acidic environment to polymerize
binds to base of ulcer
heals ulcer
travelers diarrhea
Misoprostol
prostaglandin analog
generation of gastric mucosa barrier
can use w/ NSAIDs
SE: increased uterine tone –> abortion
Diarrhea
Congenital hypertrophic pyloric stenosis
1:600 births
pyloris hypertrophy –> narrow gastric outlet
impaired stomach emptying
palpable olive mass in epigastric region
–> nonbiliious projectile vomiting
2-6 weeks of age
MC condition requiring surgery in first mo of life
First born males
Electrolyte changes:
Hypocholemic metabolic alkalosis
-days to weeks of vomiting
hypokalemia (H/K exchanger)
Signet ring cells
Gastric adenoma
Krukenburg (ovarian met of gastric adenoma)
Lobular CIS or invasive lobular carcinoma of breast
Serotonin 5-HT3 receptor antagonists
Ondasterone
Granisetron
Chemo
Post op N/V
pregnancy
SE: vasodilation –> HA
Constipation
Menetrier Disease
hypertrophy of mucus producing cells –> hypertrophied rugae that look like gyri of brain
atrophy of parietal cells –> decreased gastric acid production
–> enteric protein loss (can’t cleave pepsinogen) –> hypoalbuminemia –> edema
increased gastric adenocarcinoma risk
Gastric adenocarcinioma
Risk factors: H pylori, chronic gastritis, diet high in nitrosamines (cured/smoked foods, hot dogs)
Men >50
Japanese people IN Japan
Mets:
Left supraclavicular node - Virchow node
Periumbilical node - Sister Mary Joseph nodule
Met to ovary - Krukenburg tumor
Acanthosis nigricans - underlying malignancy
Histo: signet ring cells - mucin filled cells w/ peripheral nucleus
