Gastroesophageal reflux disease (GERD)

66,758views

Gastroesophageal reflux disease (GERD)

GI

GI

Anatomy of the gastrointestinal organs of the pelvis and perineum
Anatomy of the oral cavity (dentistry)
Anatomy of the pharynx and esophagus
Anatomy of the anterolateral abdominal wall
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Anatomy of the abdominal viscera: Esophagus and stomach
Anatomy of the abdominal viscera: Small intestine
Anatomy of the abdominal viscera: Large intestine
Anatomy of the abdominal viscera: Pancreas and spleen
Anatomy clinical correlates: Anterior and posterior abdominal wall
Abdominal quadrants, regions and planes
Development of the digestive system and body cavities
Development of the gastrointestinal system
Development of the teeth
Development of the tongue
Gallbladder histology
Esophagus histology
Stomach histology
Small intestine histology
Colon histology
Liver histology
Pancreas histology
Gastrointestinal system anatomy and physiology
Anatomy and physiology of the teeth
Liver anatomy and physiology
Escherichia coli
Salmonella (non-typhoidal)
Yersinia enterocolitica
Clostridium difficile (Pseudomembranous colitis)
Enterobacter
Salmonella typhi (typhoid fever)
Clostridium perfringens
Vibrio cholerae (Cholera)
Shigella
Norovirus
Bacillus cereus (Food poisoning)
Campylobacter jejuni
Bacteroides fragilis
Rotavirus
Enteric nervous system
Esophageal motility
Gastric motility
Gastrointestinal hormones
Chewing and swallowing
Carbohydrates and sugars
Fats and lipids
Proteins
Vitamins and minerals
Intestinal fluid balance
Pancreatic secretion
Bile secretion and enterohepatic circulation
Prebiotics and probiotics
Cleft lip and palate
Sialadenitis
Parotitis
Oral candidiasis
Aphthous ulcers
Ludwig angina
Warthin tumor
Oral cancer
Dental caries disease
Dental abscess
Gingivitis and periodontitis
Temporomandibular joint dysfunction
Nasal, oral and pharyngeal diseases: Pathology review
Esophageal disorders: Pathology review
Esophageal web
Esophagitis: Clinical
Barrett esophagus
Achalasia
Zenker diverticulum
Diffuse esophageal spasm
Esophageal cancer
Esophageal disorders: Clinical
Boerhaave syndrome
Plummer-Vinson syndrome
Tracheoesophageal fistula
Mallory-Weiss syndrome
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Gastroesophageal reflux disease (GERD)
Peptic ulcer
Helicobacter pylori
Gastritis
Peptic ulcers and stomach cancer: Clinical
Pyloric stenosis
Zollinger-Ellison syndrome
Gastric dumping syndrome
Gastroparesis
Gastric cancer
Gastroenteritis
Small bowel bacterial overgrowth syndrome
Irritable bowel syndrome
Celiac disease
Small bowel ischemia and infarction
Tropical sprue
Short bowel syndrome (NORD)
Malabsorption syndromes: Pathology review
Malabsorption: Clinical
Zinc deficiency and protein-energy malnutrition: Pathology review
Whipple's disease
Appendicitis: Pathology review
Appendicitis
Appendicitis: Clinical
Lactose intolerance
Protein losing enteropathy
Microscopic colitis
Inflammatory bowel disease: Pathology review
Crohn disease
Ulcerative colitis
Inflammatory bowel disease: Clinical
Bowel obstruction
Bowel obstruction: Clinical
Volvulus
Familial adenomatous polyposis
Juvenile polyposis syndrome
Gardner syndrome
Colorectal polyps and cancer: Pathology review
Colorectal polyps
Colorectal cancer
Colorectal cancer: Clinical
Peutz-Jeghers syndrome
Diverticulosis and diverticulitis
Diverticular disease: Pathology review
Diverticular disease: Clinical
Intestinal adhesions
Ischemic colitis
Peritonitis
Pneumoperitoneum
Cyclic vomiting syndrome
Abdominal hernias
Femoral hernia
Inguinal hernia
Hernias: Clinical
Congenital gastrointestinal disorders: Pathology review
Congenital diaphragmatic hernia
Imperforate anus
Gastroschisis
Omphalocele
Meckel diverticulum
Intestinal atresia
Hirschsprung disease
Intestinal malrotation
Necrotizing enterocolitis
Intussusception
Anal conditions: Clinical
Anal fissure
Anal fistula
Hemorrhoid
Rectal prolapse
Carcinoid syndrome
Crigler-Najjar syndrome
Biliary atresia
Gilbert's syndrome
Dubin-Johnson syndrome
Rotor syndrome
Jaundice: Pathology review
Jaundice
Cirrhosis
Cirrhosis: Pathology review
Cirrhosis: Clinical
Portal hypertension
Hepatic encephalopathy
Hemochromatosis
Wilson disease
Budd-Chiari syndrome
Non-alcoholic fatty liver disease
Cholestatic liver disease
Hepatocellular adenoma
Alcohol-associated liver disease
Alpha 1-antitrypsin deficiency
Primary biliary cholangitis
Viral hepatitis
Hepatitis A and Hepatitis E virus
Hepatitis B and Hepatitis D virus
Viral hepatitis: Pathology review
Viral hepatitis: Clinical
Autoimmune hepatitis
Primary sclerosing cholangitis
Neonatal hepatitis
Reye syndrome
Benign liver tumors
Hepatocellular carcinoma
Gallbladder disorders: Pathology review
Gallstones
Gallstone ileus
Biliary colic
Acute cholecystitis
Ascending cholangitis
Chronic cholecystitis
Gallbladder carcinoma
Gallbladder disorders: Clinical
Cholangiocarcinoma
Pancreatic pseudocyst
Acute pancreatitis
Chronic pancreatitis
Pancreatitis: Clinical
Pancreatic cancer
Pancreatic neuroendocrine neoplasms
Pancreatitis: Pathology review
Abdominal trauma: Clinical
Gastrointestinal bleeding: Pathology review
Gastrointestinal bleeding: Clinical
Pediatric gastrointestinal bleeding: Clinical
Abdominal pain: Clinical
Disorders of carbohydrate metabolism: Pathology review
Glycogen storage disorders: Pathology review
Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Environmental and chemical toxicities: Pathology review
Medication overdoses and toxicities: Pathology review
Laxatives and cathartics
Antidiarrheals
Acid reducing medications

Transcript

Watch video only

Gastro- refers to the stomach, esophageal stands for esophagus, and reflux means “to flow back”.

So gastroesophageal reflux disease, or GERD, is when stomach acid flows back into the esophagus.

The presence of acid in the esophagus can lead to Barrett’s esophagus, a serious complication of GERD where the normal mucosa of the esophagus is replaced by one that’s similar to that of the intestines.

Barrett’s esophagus poses a higher risk of developing esophageal adenocarcinoma.

Normally, the wall of the entire gastrointestinal tract is made of 4 layers: the inner mucosa, the submucosa, a muscular layer, and an outer layer called the adventitia.

The mucosa is further divided into three layers - an innermost epithelial layer, a middle layer called the lamina propria, and an outermost layer, in contact with the submucosa, called the muscularis mucosae, which is made up of smooth muscle that contracts and helps with the breakdown of food.

Now, the stomach mucosa is different from the esophageal mucosa.

Inside the stomach, the epithelial layer is made up of cylindrical cells, which dive into the lamina propria, forming pits.

These pits are the gastric glands, and there are many of them scattered throughout the stomach.

Distributed among the cylindrical gland cells, there’s different types of secretory cells.

First, there’s G cells, which are a type of neuroendocrine cells that secrete a hormone called gastrin in response to food entering the stomach.

Gastrin stimulates another type of cells, the parietal cells, to release hydrochloric acid.

And then, there’s chief cells, which secrete an enzyme called pepsinogen.

Hydrochloric acid and pepsinogen are useful for digestion, but they can be quite aggressive for the delicate mucosa.

Luckily though, the stomach also has some defense mechanism in place.

First, the gastric glands also have foveolar cells, also called surface mucus cells, because they are closer to the surface of the stomach, and they secrete mucus.

Mucus is mostly made up of water and glycoproteins, and also bicarbonate ions which are also secreted by foveolar cells.

This bicarbonate-rich mucus protects the gastric mucosa from our own gastric acid, so it won’t get digested along with food.

Lastly the gastric mucosa is highly vascularized, which helps deliver oxygen and bicarbonate and carry away acid that makes it through into the lamina propria.

The esophagus, on the other hand, is better adapted for the passage of food. So its mucosa is made up of stratified squamous epithelium, which is better equipped to resist abrasion from food going down.

The downside is that this kind of epithelium doesn’t have defense mechanisms, like the stomach - so it’s more susceptible to acid damage.

So to protect the esophageal mucosa, at the lower end of the esophagus there's the lower esophageal sphincter - or LES, which is a circular muscle that relaxes when we swallow, to allow the passage of food, and closes between meals to prevent acid reflux.

The lower esophageal sphincter has a resting pressure of 10 to 45 millimeters of mercury. When the pressure is lower than normal, which means the sphincter becomes looser, gastric acid reaches the esophagus and the pH of the esophagus drops from to around 4 - which is called acid reflux.

Some esophageal defense mechanisms against acid reflux are the primary and secondary peristaltic waves.

Some degree of acid reflux is normal, especially after meals, but it doesn’t last long, since secondary peristaltic waves, which are contractions of the esophageal muscular layer that happen a while after we’ve already swallowed, push the gastric acid back into the stomach.

Finally, saliva also helps neutralize the acidic gastric content.

Now, when the pressure of the lower esophageal gets lower for some reason, reflux persists for longer, becoming pathological.

Persistent acid reflux damages the esophageal mucosa, causing local inflammation, or esophagitis.

Esophagitis, in turn, causes edema and erosion of the mucosa, which leads to more complications.

First off, every time the epithelium and the underlying tissue is damaged, it’s replaced by a scar.

Since this is continuously happening, the scar becomes bigger and bigger, and together with the edema, they turn the wall thicker, and the lumen through which the food passes becomes smaller - which is called esophageal stenosis.

Also, when the epithelium is continuously damaged and replaced, the new epithelium of the lower esophagus is gradually replaced by a single layer of columnar cells, similar to intestinal cells, that are more adapted to withstand the reflux.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Objective Documentation of the Link between Gastroesophageal Reflux Disease and Obesity" American Journal of Gastroenterology (2007)
  6. "Guidelines for the Diagnosis and Management of Gastroesophageal Reflux Disease" American Journal of Gastroenterology (2013)
  7. "Overprescribing proton pump inhibitors" BMJ (2008)