Intro and GERD Flashcards
Foregut
(To mid-3rd duodenum)
o Includes liver, biliary tree, pancreas
Blood supply: Celiac artery (from aorta)
2 branches of celiac artery include:
• Gastroduodenal artery (passes behind duodenal bulb, so posterior bulb ulcers can lead to serious bleeding)
• Proper hepatic artery (but liver gets most of blood supply from hepatic portal vein)
Midgut
(To distal transverse colon)
o Includes jejunum, ileum, appendix
Blood supply: Superior mesenteric artery
• With acute blockage → loss of entire small bowel
• Atherosclerosis → pain with eating
Hindgut
(Through rectum)
Blood supply: Inferior mesenteric artery
• Most susceptible to low flow states → ischemic colitis from hypotension
Describe the enteric nervous system and identify its location. Explain its interaction with the central nervous system.
Contains 100 million neurons (vs. brain = 100 billion neurons)
o Functions independently of CNS
o Exhibits simple programeed functions (MMC, peristalsis)
o Intrinsic pacemaker = controls rhythm
But sill connected/communicate = Brain-Gut axis
o Actions modified by vagal and sympathetic extrinsic nerves
Input from ANS:
• Parasympathetic info from vagus nerve and sacral nerves
• Sympathetic info from dorsal root ganglia of spinal nerves
Senses stretch and muscular contractions → refers to midline: • Epigastrium (foregut) • Around umbilicus (midgut) • Above pubic bone (hindgut) • 95% of body’s serotonin receptors
Location within gut wall:
o Myenteric plexus = between longitudinal and circular muscles
o Mucosal plexus = around submucosa
Describe the neuromuscular anatomy of the esophagus
Dual innervation
CNS:
• Controls effector muscles of swallowing from mouth to constrictors of oropharynx and UES
• Originates from swallowing center in medulla oblongata
• Transmitted via vagus nerve
ENS:
• Controls and coordinates peristalsis
• NT’s involved:
• Excitatory NT = Ach → muscle layer contraction
• Inhibitory NT = NO and VIP (vasoactive intestinal peptide) → relaxation of muscle
Explain the pathophysiology of gastroesophageal reflux disease (GERD)
Reflux:
o Physiologic = occurs daily in normal people
o Pathologic = reflux of gastric material into esophagus or oropharynx → symptoms, tissue injury, or both
Prevalence = common
o 40% U.S. population have heartburn at least 1x/month
o 5-10% have heartburn 1x/day
Pathophysiology = multifactorial
o Abnormal LES function → transient relaxation (TLESRs) → reflux and inflammation → weakened LES = eventually fixed open
• Stimuli that increase TLESR frequency: gastric distension, pharyngeal stimulation, stress, posture, sleep
o Hiatal hernia = disrupts diaphragm’s positioning and sphincter integrity
o Poor peristalsis → inadequate clearing of reflux
o Reduced epithelial resistance from HCO3- from saliva and mucosa
o Caustic substances:
• Stomach: HCl
• Other refluxate: deconjugated bile salts, pancreatic enzymes, pepsin, medications, ingested foodstuffs
Recognize the variety of manifestations of GERD: classic, atypical, laryngopharyngeal and non-acid reflux
Classic:
o Note: severity of symptoms ≠ severity of disease or inflammation
• Can be completely asymptomatic (25% cases)
o Heartburn (pyrosis) = most common symptom
o Regurgitation (sense of liquid passing up into chest and sometimes mouth)
• 90% diagnostic when heartburn and regurgitation occur together!
o Water brash = increased salivation from stimulating esophageal reflux
Atypical symptoms o Adult-onset asthma o Chronic cough o Laryngitis o Non-cardiac chest pain o Recurrent pneumonia o Dental erosions
Endoscopic or radiographic signs:
NERD (non-erosive reflux disease)
• Imaging of esophageal mucosa = normal
• Most common pathologic reflux
Erosive reflux disease
• Esophageal erosions of varying severity
• May lead to complications from chronic inflammation
Describe the appropriate diagnostic work-up required for GERD.
Clinical
o 90% sensitive if classic presentation
o 1st step = empiric PPI trial
o Further testing if dysphagia or other “red flag” symptoms or refractory to treatment
Endoscopy
o Gold standard for esophagitis
o Necessary with complicated GERD and Barretts
o Rules out complications
o Able to grade severity of disease
Influence management (?)
• 50% with heartburn do NOT have endoscopic findings
• Severity of heartburn does NOT predict esophagitis
• Lack of esophagitis does NOT predict easier to treat patients
Radiography
o Not sensitive for mild reflux
Ambulatory pH-Impedance testing
o Quantifies reflux (percentage of time reflux is occurring)
o Able to correlate pH to symptoms
o Helpful in patients that aren’t responding to empiric therapy and may have non-acid reflux
Symptoms not responsive to PPI:
• Heartburn
• Atypical chest pain
• Extra-esophageal manifestations of GERD (ex: laryngitis, chronic cough, asthma)
• Considering non-acid reflux
Describe treatment options for GERD: conservative, pharmacologic, or surgical.
Lifestyle changes
o Elevate head of bed at least 4 to 6 inches
o Stop Smoking!
o Decrease alcohol consumption
o Reduce fat intake
o Decrease size of meals
o Avoid bedtime snacks or eating 2 hours before lying down
o Avoid tea, coffee, citrus, chocolate, mint, tomato juice, and cola.
o Avoid these drugs as much as possible: anticholinergics, diazepam, theophylline, calcium channel blockers, and narcotics.
Drug therapy Antacids • Neutralize acid • Ex: Tums, Maalox, Pepto-bismol • OTC H2 receptor antagonists • Decrease acid content of gastric refluxate = less noxious to epithelium • Ex: Cimetidine, ranitidine, famotidine, nizatidine • OTC and by prescription Proton pump inhibitors (PPI) • Block parietal cell H+/K+ ATPase • Ex: Omeprazole, esomeprazole, lansoprazole, rabeprazole, pantoprazole • OTC and by prescription
Surgical therapy = Nissen fundoplication
o Wraps stomach around GEJ
o Corrects hiatal hernia → re-establishes anti-reflux barrier
Describe the complications of reflux disease.
Scarring
Schatzki ring = superficial mucosal scar
Strictures
• Deeper and thicker mucosal and submucosal scarring
• Most often found near GEJ
• Can develop dysphagia
• Most common GERD complication (in up to 25%)
• Due to PPI treatment = decreasing severity
Barrett’s Esophagus (intestinal metaplasia)
o 1/10 GERD patients develop Barrett’s
o Premalignant condition
o Metaplastic intestinal-type (columnar) epithelium replaces damaged esophageal squamous epithelium
o ~0.5% rate per patient/year progression to adenocarcinoma so patients with Barrett’s are monitored
Esophageal cancer
o Poor prognosis (5 year survival: <10%)
o Fastest growing incidence of any solid tumor in U.S.
List the esophageal motility disorders
Hypercontractile -Achalasia -Spastic esophageal motility disorders: • Diffuse esophageal spasm • Nutcracker esophagus • Hypertensive lower esophageal sphincter
Hypocontractile
• Non-specific (Inefficient) Motility Disorders
• Scleroderma esophagus (smooth muscle replaced by scar tissue)
Achalasia: symptoms
o Dysphagia
o Vomiting undigested foods
o Chest pain
o Weight loss
o Regurgitation at night → leading to aspiration
o Pyrosis (represents lactic acid from fermentation of retained food)
Achalasia: pathophysiology
Loss of neurons → LES cannot relax
Pathophysiology
o Best described esophageal motility disorder
o Unknown etiology
Considerations (in a susceptible individual)
• Virus or post-viral
• Other infectious agents
• Autoimmune
Neuropathy
o Loss of myenteric ganglia from LES
o Vagal nerve degeneration
o Decreased intramuscular nerves
o Functional loss of LES’s ability to relax
o Followed by loss of esophageal peristalsis → functional obstruction at GEJ
Achalasia: diagnosis
Barium esophagram
• See dilated esophagus
• Loss of peristaltic wave
• Tightly closed tapering LES that fails to open (“birds beak” GEJ)
Esophageal manometry
• See incompletely relaxing LES and complete loss of esophageal peristalsis
• Also: elevated LES resting pressure, low amplitude simultaneous contractions of esophageal body
Achalasia: treatment
o No cure
o Goal = relieve functional obstruction at LES
Pharmacologic:
Ca2+ channel blockers, nitrates, anticholinergics → relax spastic LES
• But not give prolonged response
Botulinum toxin injection into LES
• Decreases resting LES pressure but needs repeated injections every 6-24 months
Endoscopic intervention
• Balloon dilation of LES
Surgical intervention
• Better and longer lasting efficacy
• Better symptom relief
Dietary issues with achalasia o Liquid or semi-liquid o Small frequent meals o Increased time after meal prior to reclining or exercising o Consideration for PEG tube
Describe gastric motility and regulation
Stomach motility
Gastric pacemakers:
• Interstitial cells of Cajal
• Integrate into ENS and onto smooth muscle
Fed pattern motility:
• Expands to accommodate ingested material = receptive relaxation
• Tonically contracts
• Empties liquids from the stomach
• Moves ingested material into caudad stomach
• Reduces size of stomach
Fasting motility pattern:
• Increasing frequency and strength of sequential muscle contractions
• Maximum cycling of 3 cycles/minute
• Functions to grind, mix, and empty stomach contents
Gastric emptying affected by: Gastric motility • Fed vs. Fasting states • Solids empty after a lag and are reduced in size by retropulsion to 2 mm • Liquids empty quickly • Non-nutrients empty rapidly • Fastest with higher volume Gastroduodenal motility Duodenal motility Chemical composition Duodenal receptors: Reversed or slowed • Feedback Inhibition • Osmotic pressure • Caloric content • Hydrogen ions • Fatty acids
Gastroparesis: causes
o Delay in gastric emptying of a meal in absence of mechanical outlet obstruction
o Cardinal symptoms: early satiety, nausea, vomiting, bloating
Causes:
Diabetes
• Most common cause
• 10% diabetes = symptomatic
• 30-50% diabetics = develop delayed emptying
• Secondary to abnormal nerve conduction from hyperglycemia (often see other signs of peripheral neuropathy)
Other causes:
• Idiopathic
• Chronic renal failure
• Gastric surgeries (post-surgical vagotomy)
Gastroparesis: diagnosis
For impaired gastric emptying = need to rule out mechanical obstruction: • Peptic ulcer disease • Stricture • Gastric cancer • Crohn’s
Scintigraphy:
• Ingest radio-labeled eggs and scan the stomach serially
• Delayed if >50% meal remains at 2 hours; >10% at 4 hours
Less sensitive:
• Barium = delayed emptying of barium
• Endoscopy = retained food or bezoar
Gastroparesis: treatment
Patient education
Dietary manipulation
• Small but frequent (6/day) meals
• Reduced fat (10% wt loss)
Metabolic control (if diabetic)
Pro-kinetic drugs:
• Metoclopramide
• Erythromycin (motilin analog)
Antiemetic agents
Gastric pacemaker
Surgery (partial gastectomy, place a J-tube/venting G-tube)
