Achalasia/hiatal herna/gastritis Flashcards

(50 cards)

1
Q

Esophagus

general

A

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

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2
Q

Auerbach plexus (Myenteric plexus)

general

A

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

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3
Q

achalasia

general
Difference between major and minor

A

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)

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4
Q

achalasia

causes

A

Degeneration of myenteric plexus ganglia in the lower esophagus
Viral and autoimmune factors are suspected; appear there is a genetic predisposition (familial cases)

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5
Q

achalaisa

complications

A

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

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6
Q

achalasia

primary vs secondary

A

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

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7
Q

achalasia

S/Sx

A

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

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8
Q

achalasia

Upper endoscopy

A

Upper endoscopy – performed first
Esophageal dilation
Rule out any obstructing lesions or malignancy
Classic “pop” when the endoscope passes into the stomach

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9
Q

achalasia

High-resolution manometry with esophageal pressure topography (EPT)

A

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

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10
Q

achalasia

Barium swallow

A

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

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11
Q

achalasia

Tx goal

A

No therapy will restore peristalsis

Goal of treatment is to reduce the pressure at the LES and allow for the passage of ingested material

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12
Q

achalasia Tx options

Pneumatic balloon dilation of the LES

A

circumferential stretching

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13
Q

achalsia Tx options

Surgical myotomy of the LES

A

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

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14
Q

Hiatal hernia

general

A

Protrusion of the stomach through the diaphragmatic hiatus
Common condition
Increased incidence with advancing age

two types:
Sliding
Paraesophageal

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15
Q

Sliding hiatal hernia

A

Most common (~95%)
Gastroesophageal junction and a portion of the stomach are above the diaphragm

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16
Q

Paraesophageal hiatal hernia

A

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

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17
Q

hiatal hernia

Pathogenesis

A

The distal end of the esophagus is anchored to the diaphragm by the phrenoesophageal membrane

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18
Q

hiatal hernia

Causes

A

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

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19
Q

Hiatal hernia

S/Sx

A

Majority of patients are asymptomatic
Symptoms:
Chest pain
Dysphagia
Reflex symptoms – heartburn, cough, belching

Incidental finding on x-ray in >40% of the population

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20
Q

hiatal hernia

Dx

3 options

A

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

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21
Q

hiatal hernia

Tx

ASx/sliding/paraesophageal

A

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

22
Q

Hiatal hernia

Nissen fundoplication

A

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

23
Q

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?

A

Refer for surgery. She has not had improvement, persistant systems.
(Pic has hiatal hernia)

24
Q

stomach

A

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

25
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
26
# 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
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# Secretory Cells of the Gastric Glands Chief cells
Secretes pepsinogen, the inactive proenzyme of pepsin
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# 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?
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# stomach Mucous neck cells
Secrete alkaline mucus
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# stomach Enteroendocrine cells
D cells secrete somatostatin – inhibitory G cells secrete gastrin stimulates parietal cells
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# 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**
32
# 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
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# 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
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# 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
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# 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
36
# erosive gastritis EndoscopyDx When is it performed
**Most sensitive** method for diagnosis Performed within 24 hours of upper GI bleeding
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# erosive gastritis Tx
Removal of the offending agent Bleeding Endoscopic hemostasis Acid suppression H2 blocker or proton pump inhibitor 4-8 week trial
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# Nonerosive Gastritis types
## Footnote type A=autoimmune. Type B=bacteria. Type C=precancerous.
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# Non erosive gastritis Helicobacter pylori
**Spiral gram-negative** bacterium that resides beneath the gastric mucosa layer causing mucosal inflammation with PMNs (neutrophils) and lymphocytes
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# 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
41
# 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
42
# 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
43
# 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**
44
# 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 2. Urea breath test 3. 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 ## Footnote Prior to testing, proton pump inhibitors should be discontinued for 14 days and antibiotics should be discontinued for 28 days
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# 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)
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# H pylori Tx
Due to the role of H. pylori in gastric cancer, all positive patients should be treated ## Footnote 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
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# 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
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# Pernicious anemia gastritis Dx
Diagnosis Measuring anti-parietal cell and anti-intrinsic factor antibodies Serum gastrin Serum pepsinogen Endoscopic biopsy