Achalasia/hiatal herna/gastritis Flashcards

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
Q

Regions of the stomach

A

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
Q

Wall of the Stomach

A

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

27
Q

Secretory Cells of the Gastric Glands

Chief cells

A

Secretes pepsinogen, the inactive proenzyme of pepsin

28
Q

stomach

Parietal cells

A

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?

29
Q

stomach

Mucous neck cells

A

Secrete alkaline mucus

30
Q

stomach

Enteroendocrine cells

A

D cells secrete somatostatin – inhibitory
G cells secrete gastrin stimulates parietal cells

31
Q

Mucosal Barrier of the Stomach

Protection from self-digestion

A

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
Q

Gastritis

general and types

A

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

33
Q

Erosive Gastritis

general

A

Gastric mucosal erosion caused by damage to the mucosal defenses
Superficial erosions and punctate mucosal lesions
Typically occur in the body of the stomach

34
Q

Erosive Gastritis

Common causes:

A

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

35
Q

Erosive Gastritis

S/Sx

A

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
Q

erosive gastritis

EndoscopyDx
When is it performed

A

Most sensitive method for diagnosis
Performed within 24 hours of upper GI bleeding

37
Q

erosive gastritis

Tx

A

Removal of the offending agent
Bleeding
Endoscopic hemostasis

Acid suppression
H2 blocker or proton pump inhibitor
4-8 week trial

38
Q

Nonerosive Gastritis

types

A

type A=autoimmune. Type B=bacteria. Type C=precancerous.

39
Q

Non erosive gastritis

Helicobacter pylori

A

Spiral gram-negative bacterium that resides beneath the gastric mucosa layer causing mucosal inflammation with PMNs (neutrophils) and lymphocytes

40
Q

H pylori

Mechanism for surviving the acidic environment of the stomach

A

Ammonia that erodes the mucus barrier
Cytotoxins and mucolytic enzymes cause mucosal damage and lead to ulcerogenesis

41
Q

H pylori

common causes

A

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
Q

H. pylori gastritis

acute vs chronic infection

A

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
Q

Chronic H. pylori gastritis

types

A

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
Q

H pylori gastritis

Dx

3 options

A

Screening of asymptomatic patients is not indicated

initial Dx:
1. Stool (fecal) antigen immunoassay
Similar sensitivity and specificity to that of urea breath test

  1. Urea breath test
  2. 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

45
Q

H Pylori gastritis

Endoscopy

A

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)

46
Q

H pylori

Tx

A

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

47
Q
A
48
Q

Pernicious anemia gastritis

general

A

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

49
Q
A
50
Q

Pernicious anemia gastritis

Dx

A

Diagnosis
Measuring anti-parietal cell and anti-intrinsic factor antibodies
Serum gastrin
Serum pepsinogen
Endoscopic biopsy