Achalasia/hiatal herna/gastritis Flashcards
Esophagus
general
Made up of an outer longitudinal muscle layer and an inner circular muscle layer
Circular muscle fibers: allowperistalsis
Upper ⅓ ofesophagus: predominantlyskeletal muscles
Lower ⅔ ofesophagus:smooth muscles become more dominant from the middle to the distalesophagus
Auerbach plexus (Myenteric plexus)
general
Between the circular muscle layer and the longitudinal muscle layer in the loweresophagus, stomach, and intestines
Responsible for the peristaltic movement of the bowels
Can act independently from the central nervous system
achalasia
general
Difference between major and minor
Rare, neurogenic esophageal motility disorder
Age 25-60 years
Male = female
Pathological features:
Failed relaxation in the lower esophageal sphincter (LES) during swallowing (MAJOR)
Impaired peristalsis in the lower 2/3 of the esophagus (minor)
achalasia
causes
Degeneration of myenteric plexus ganglia in the lower esophagus
Viral and autoimmune factors are suspected; appear there is a genetic predisposition (familial cases)
achalaisa
complications
Aspiration pneumonia: from regurgitation
Megaesophagus in 10% of cases
Increase in size affects the transport of food
Increased risk ofesophageal cancer
Food stasis, bacterial overgrowth, and chronic inflammation
achalasia
primary vs secondary
Primary – no known cause
Secondary
Due to diseases that cause esophageal motor abnormalities
Malignancy (esophageal, gastric, or other extraesophageal cancers) by mass effect
Chagas disease
Caused by a protozoan parasite(Trypanosoma cruzi)
Seen in Central and South America
Infiltrative disorders: amyloidosis, sarcoidosis
Eosinophilic esophagitis
MEN type 2B
achalasia
S/Sx
Onset is insidious
Dysphagia (progressive)
Major symptom
Solids → liquids
Nocturnal regurgitation of undigested food
May cause a nocturnal cough or lead to aspiration pneumonia
Heartburn (pyrosis)
Retrosternal pain
Spontaneous or with swallowing
Weight loss (mild to moderate)
Vomiting
achalasia
Upper endoscopy
Upper endoscopy – performed first
Esophageal dilation
Rule out any obstructing lesions or malignancy
Classic “pop” when the endoscope passes into the stomach
achalasia
High-resolution manometry with esophageal pressure topography (EPT)
Gold standard test
Pressure: represented by color (↑ intensity of color = ↑ pressure)
Demonstrates the following:
Incomplete relaxation of the LES after swallowing
High LES resting pressure
Aperistalsis in the lower 2/3 of the esophagus
achalasia
Barium swallow
Barium swallow
Complementary test in equivocal manometric findings
May show the absence of progressive peristaltic contractions during swallowing
Upper esophagus is dilated, but is narrowed and “beak-like” at the LES
Pathognomonic
Delayed emptying of the barium
achalasia
Tx goal
No therapy will restore peristalsis
Goal of treatment is to reduce the pressure at the LES and allow for the passage of ingested material
achalasia Tx options
Pneumatic balloon dilation of the LES
circumferential stretching
achalsia Tx options
Surgical myotomy of the LES
Muscles of the LES are cut to allow food and liquids to pass to the stomach (relieves pressure)
Complication of treatment – esophageal perforation and/or gastroesophageal reflux
Hiatal hernia
general
Protrusion of the stomach through the diaphragmatic hiatus
Common condition
Increased incidence with advancing age
two types:
Sliding
Paraesophageal
Sliding hiatal hernia
Most common (~95%)
Gastroesophageal junction and a portion of the stomach are above the diaphragm
Paraesophageal hiatal hernia
Higher risk condition
Gastroesophageal junction is in the normal location, but a portion of the stomach is adjacent to the esophagus in the diaphragmatic hiatus
hiatal hernia
Pathogenesis
The distal end of the esophagus is anchored to the diaphragm by the phrenoesophageal membrane
hiatal hernia
Causes
Repetitive stress (swallowing, abdominal straining, vomiting) causes wear and tear on the phrenoesophageal membrane
Tonic contraction of the esophageal longitudinal muscle induced by gastroesophageal reflux and mucosal acidification causing stress on the phrenoesophageal membrane
Hiatal hernia
S/Sx
Majority of patients are asymptomatic
Symptoms:
Chest pain
Dysphagia
Reflex symptoms – heartburn, cough, belching
Incidental finding on x-ray in >40% of the population
hiatal hernia
Dx
3 options
Barium swallow
Best study for discovering a small hiatal hernia
Chest x-ray- Incidental finding on x-ray in >40% of the population
Upper endoscopy
hiatal hernia
Tx
ASx/sliding/paraesophageal
Asymptomatic sliding hiatal hernia requires no treatment
Sliding hiatal hernia with associated GERD → proton pump inhibitor (PPI)
Sliding hiatal hernia with persistent symptoms → offer surgical repair
Paraesophageal hiatal hernia → surgical repair due to risk of strangulation
Hiatal hernia
Nissen fundoplication
Procedure for the treatment of hiatal hernia and GERD
Top of the stomach is wrapped around the lower esophagus; this reinforces the lower esophageal sphincter, making it less likely that acid will back up in the esophagus
A 44-year-old woman presents for follow-up of GERD. She was started on pantoprazole 8 weeks ago when she first presented with heartburn. She has had improvement in her heartburn symptoms during the day but continues to have heartburn causing awakenings at night. She takes her pantoprazole 30 minutes before breakfast as directed.
Vitals are normal and exam is unremarkable. Her chest x-ray is shown.
What is the next best step in management?
Refer for surgery. She has not had improvement, persistant systems.
(Pic has hiatal hernia)
stomach
J-shaped muscle organ located in the left upper abdominal cavity inferior to the diaphragm
Contribute to mechanical and chemical digestion of food from the esophagus before releasing it, as chyme, to the small intestine
Structures:
Greater curvature
Convex lateral surface of the stomach
Lesser curvature
Concave medial surface the stomach
Stomach is held in place by:
Greater omentum
Runs from the greater curvature to the posterior abdominal wall
Lesser omentum
Extends from the liver to the lesser curvature
Regions of the stomach
Region of the stomach:
Cardia
Region where food passes from the esophagus and into the stomach
Fundus
Dome-shaped region located above and to the left of the cardia
Stores undigested food and gases
Body
Largest region of the stomach
Pylorus
Funnel-shaped region that connects to the duodenum
Pyloric antrum: wider end
Pyloric canal: narrow end
Pyloric sphincter: smooth muscle that controls gastric emptying
Wall of the Stomach
Mucosa
Forms large folds when the stomach is empty known as rugae
Contains a protective alkaline mucus
Gastric pits are depressions that mark entry to gastric glands
Submucosa
Contains the blood vessels, lymphatic vessels, and nerves
Muscularis externa
Responsible for mechanically breaking down food into smaller particles
Layers:
Inner oblique layer
Middle circular layer
Outer longitudinal layer
Secretory Cells of the Gastric Glands
Chief cells
Secretes pepsinogen, the inactive proenzyme of pepsin
stomach
Parietal cells
Produce hydrochloric acid (HCl)
High acidity (pH 1.5-3.5) of the stomach
Kill ingested bacteria
Denatures proteins
Activates the digestive enzyme, pepsin
Produces intrinsic factor
Glycoprotein necessary for the absorption of vitamin B12 in the small intestine
Why is vitamin B12 vital to survival?
stomach
Mucous neck cells
Secrete alkaline mucus
stomach
Enteroendocrine cells
D cells secrete somatostatin – inhibitory
G cells secrete gastrin stimulates parietal cells
Mucosal Barrier of the Stomach
Protection from self-digestion
Gastric enzymes have the potential to digest the stomach itself!
Mucosal barrier
Thick coating of bicarbonate-rich mucus
Acts as a physical barrier
Bicarbonate ions neutralize acid
Tight junctions
Block gastric juice from penetrating underlying tissues
Stem cells
Located at the junction of the gastric pits and gastric glands
Replace damaged epithelial mucosal cells
Surface epithelium of the stomach is completely replaced every 3-6 days
Gastritis
general and types
General term for a group of conditions in which there is histologic evidence of inflammation, irritation, or erosion of the lining of the stomach
Acute (neutrophilic infiltration) or chronic (lymphocyte and plasma cell infiltration)
Types:
Erosive gastritis
Nonerosive gastritis
Erosive Gastritis
general
Gastric mucosal erosion caused by damage to the mucosal defenses
Superficial erosions and punctate mucosal lesions
Typically occur in the body of the stomach
Erosive Gastritis
Common causes:
NSAIDs, ASA, bisphosphonates
Alcohol
Physiological stress
Severe medical or surgical illness
5% of critically ill patients
Incidence increases with duration of intensive care unit stay and length of time the patient is not receiving enteral feeding
Erosive Gastritis
S/Sx
Mild erosive gastritis – asymptomatic
Moderate or severe erosive gastritis
Develop within 2-5 days of the inciting event
Dyspepsia (indigestion)
Nausea and/or vomiting
Epigastric pain
GI bleeding
Mild-moderate
Hematemesis, “coffee grounds” emesis, and/or melena
erosive gastritis
EndoscopyDx
When is it performed
Most sensitive method for diagnosis
Performed within 24 hours of upper GI bleeding
erosive gastritis
Tx
Removal of the offending agent
Bleeding
Endoscopic hemostasis
Acid suppression
H2 blocker or proton pump inhibitor
4-8 week trial
Nonerosive Gastritis
types
type A=autoimmune. Type B=bacteria. Type C=precancerous.
Non erosive gastritis
Helicobacter pylori
Spiral gram-negative bacterium that resides beneath the gastric mucosa layer causing mucosal inflammation with PMNs (neutrophils) and lymphocytes
H pylori
Mechanism for surviving the acidic environment of the stomach
Ammonia that erodes the mucus barrier
Cytotoxins and mucolytic enzymes cause mucosal damage and lead to ulcerogenesis
H pylori
common causes
Gastritis
Peptic ulcer disease
Gastric adenocarcinoma
Low-grade B-cell gastric lymphoma
Infection
Increases with age
50% over the age of 60 infected
Most common among blacks, Hispanics, and Asians
Transmission
Oral-oral or fecal-oral route
H. pylori gastritis
acute vs chronic infection
Also known as Type B gastritis
Acute infection
Transient illness for several days
Nausea
Abdominal pain - epigastric
Chronic infection
Most patients are asymptomatic (80%)
Dyspepsia:
Early satiety
Postprandial fullness
Gnawing or burning upper abdominal discomfort
Chronic H. pylori gastritis
types
Types:
Mild diffuse gastritis
Antral-predominant gastritis
Increased gastrin production
Gastrin: stimulates secretion of gastric acid (HCl) by the parietal cells
Resultant hypersecretion of acid predisposes patients to developing peptic ulcers and gastric adenocarcinoma
Body-predominant gastritis
Destruction of acid-secreting glands resulting in gastric atrophy and decreased acid production
Predisposes patients to neuroendocrine tumors
H pylori gastritis
Dx
3 options
Screening of asymptomatic patients is not indicated
initial Dx:
1. Stool (fecal) antigen immunoassay
Similar sensitivity and specificity to that of urea breath test
- Urea breath test
- Oral dose of 13C or 14C-labeled urea (capsule)
Infected patient – H. pylori will metabolize the urea and liberate labeled CO2 which is exhaled and quantified in breath samples taken 20-30 minutes after ingestion of the urea
Prior to testing, proton pump inhibitors should be discontinued for 14 days and antibiotics should be discontinued for 28 days
H Pylori gastritis
Endoscopy
Not recommended solely for the diagnosis of H. pylori
Performed in patients with symptoms suggestive of upper gastrointestinal disease
Gastric mucosal biopsy for histology and rapid urease test (RUT)
H pylori
Tx
Due to the role of H. pylori in gastric cancer, all positive patients should be treated
Infected patient with duodenal or gastric ulcers require continuation of acid suppression for at least 4 weeks
Eradication can be confirmed with a urea breath test, stool antigen test, or endoscopy ≥ 4 weeks after completion of therapy
Pernicious anemia gastritis
general
Also known as Type A gastritis
Rare autoimmune disease
Parietal cells antibodies (PCA) and intrinsic factor antibodies (IFA)
Achlorhydria
Impaired iron absorption
Hyperplasia of G-cells → ↑ gastrin secretion
Vitamin B12 malabsorption
Destruction of chief cells → ↓ pepsinogen
Typically restricted to the fundus and body of the stomach
Pernicious anemia gastritis
Dx
Diagnosis
Measuring anti-parietal cell and anti-intrinsic factor antibodies
Serum gastrin
Serum pepsinogen
Endoscopic biopsy
