GERD Flashcards
Describe the innervation for the upper and lower esophagus.
upper: from the nucleus ambiguus, vagus innervation motor fibers go to striated muscle
lower: from the dorsal motor nucleus, vagus innervation parasympathetic fibers release Ach onto enteric nerves controlling the smooth muscle fibers
Anatomically speaking where is the enteric system located in the layers of gut tissue?
between circular and longitudinal muscle layers
Contrast physiologic and pathologic reflux
physiologic reflux occurs daily in normal people
pathologic reflux causes symptoms, tissue injury or both (due to acid, bile, pepsin and pancreatic enzymes)
Name the classic and atypical presentations of GERD
classic: heartburn and regurgitation (90% diagnostic)
atypical: adult onset asthma, chronic cough, laryngitis, non-cardiac chest pain, recurrent pneumonia, dental erosions
25% are asymptomatic
Heartburn may be aggravated by…
alcohol, caffeine, chocolate, citrus, fat, peppermint, spicy foods, tomatoes
bending, lifting, meals at bed, meds, obesity, pregnancy, running, smoking, tight clothing
List the “multifactorial” causes of GERD that contribute to the disease.
dysfunction of anti-reflux mechanisms (transient LES relaxation, hiatal hernia)
caustic reflux
sufficient duration of contact (clearance mechanism)
What might you use to diagnose GERD?
empiric PPI trial
endoscopy is gold standard for esophagitis
ambulatory pH-impedance testing can quantify reflux (can rule out non-acid reflux)
How does endoscopy effect GERD management?
50% with heartburn have no endscopic findings and lack of esophagitis does not predict easier to treat patients, can be used to rule out complications and grade disease severity if signs are present
How do cholinergic, pro kinetics, motility stimulating drugs and PPIs help to treat GERD?
cholinergic: enhance salivation
pro kinetics: enhance clearance/ gastric emptying
motility stimulating drugs: strengthen antireflux barrier
PPI- decrease acid and pepsin
Give examples of hyper contractile and hypo contractile motility disorders of the esophagus.
hyper contractile: achalasia, spastic esophageal motility disorders (diffuse esophageal spasm, nutcracker esophagus and hypertensive LES)
hypo contractile: inefficient motility disorders, scleroderma esophagus
Describe the pathophysiology of achalasia.
loss of myenteric ganglia and vagal nerve degeneration causes decreased innervation
(results in “bird’s beak” appearance on GEJ)
What are possible alternative diagnoses that present similar to achalasia?
maligancy, esp. of gastric cardia Chaga's Disease amyloidosis post-radiotherapy end stage GERD
requires endoscopy (rule out tumor) and manometry to confirm diagnosis (document peristalsis and abnormal LES
What treatments are available for achalasia?
drugs: nitrates, CCB, botulinum toxin
pneumatic dilation
myotomy (surgical myotome is more efficacious and has lower risk for subsequent intervention)
Contrast fasting and fed motility of the stomach
fasting to feeding: receptive relaxation
fed: tonically contracts for emptying
What factors do the duodenal receptors read in order to provide feedback to gastric emptying?
osmotic pressure, caloric content, hydrogen ions, fatty acids
