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M2 GI/Nutrition > Esophagus - Babaei > Flashcards

Esophagus - Babaei Flashcards

1
Q

Desribe the measures taken by digestive epithelium to protect it from acid. (Hint: 2 classes)

Why is the esophagus susceptible to damage from acid?

A

Pre-epithelial defense: Secrete a mucus coating to obstruct activated pepsin, and bicarbonate ion to neutralize acid.

Epithelial defense: Intracellular buffering, acid extrusion processes, and structural barriers (membrane, stratification, tight junctions)

The esophagus lacks the described pre-epithelial defense.

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2
Q

Describe the pathogenesis of GERD.

A

Loss of LES tone causes and is exacerbated by esophageal acid reflux.

Damage from acid (and bile) induce IL-6, which increase H2O2, which increase PAF/PGE2, which reduces ACh and LES tone.

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3
Q

T/F: A LES tone of 0mm Hg will always produce gastroesophageal reflux.

A

True; the stomach is constantly under positive pressure.

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4
Q

Compare and contrast spontaneous (transient) LES relaxation and strain insufficiency.

A

In transient LES relaxation, the LES inappropriate relaxes, allowing reflux in the absence of increased gastric pressure.

In strain insufficiency, gastric pressure simply overcomes a usually weakened LES.

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5
Q

Describe the neural circuit that facilitates esophageal peristalsis.

A

Sensory stimulus is transmitted to the nucleus tractus solitarius. Motor efferent signals originating from the dorsal vagal nucleus (and/or nucleus ambiguus) control peristalsis by the postganglionic transmitters ACh and NO/VIP.

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6
Q

What controls the tone of the LES?

A

The LES is controlled by the same vagal circuit as the rest of the esophagus, but contributions are also made by the diaphragmatic crura. These are controlled by the respiratory center in the brainstem which signals along the phrenic nerves (cholinergic)

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7
Q

Give the type of hernia (I vs II) that matches the description.

  1. Para-esophageal
  2. Common
  3. Asymptomatic
  4. Associated with bowel sounds in lung field
A
  1. II
  2. I
  3. I
  4. II (from pathoma)
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8
Q

Describe the histologic appearance of injured esophageal tissue in GERD.

A

There is hyperplasia of the basal zone (regeneration secondary to injury) and elongation of the lamina propria papillae.

Eosinophilic, followed by neutrophilic infiltration.

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9
Q

Describe the gross appearance of injured esophageal tissue in GERD.

A

Redness and mucosal breaks (erosions) mainly in the lower 1/3 of the esophagus. The erosions have visible depth and may feature exudate.

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10
Q

Patients with GERD generally do not report symptoms until it progresses to reflux esophagitis. Describe the epidemiology of this disorder.

A

Usually affects older, obese adults. #1 cause of esophagitis, and #1 outpatient GI diagnosis in the US.

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11
Q

What are the 3 classic symptoms of reflux esophagitis?

What are 3 less common symptoms?

A

Heartburn (substernal, radiating retrosternally), regurgitation (feeling contents of stomach in throat), dysphagia.

Chest pain, chronic cough, hoarseness.

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12
Q

How is GERD diagnosed? When are these modalities indicated?

A
  1. Endoscopy (especially with alarm symptoms: dysphagia, anemia, weight loss, abdominal mass, vomiting)
  2. Ambulatory reflux monitoring (more sensitive than endoscopy)

(don’t bother with radiography)

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13
Q

How is GERD treated?

A
  1. Lifestyle modifications (weight loss, bed elevation, diet)
  2. Anti-secretory drugs (PPI > H2 blocker)
  3. Operative management (fundoplication, LINX?)
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14
Q

Name 4 possible complications of GERD.

A

Ulcer, stricture, bleeding, and Barrett’s Esophagus.

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15
Q

Describe how esophageal strictures are generated.

A

Chronic inflammation and scarring causes progressive dysphagia as the submucosa undergoes fibrous thickening and the muscularis propria atrophies.

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16
Q

Describe the pathogenesis of eosinophilic esophagitis.

A

T-cell mediated hypersensitivity reaction causes eosinophilic infiltration; subsequent deposition of MBP and IL-5/13 cause tissue remodeling/fibrosis.

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17
Q

Describe the clinical presentation of eosinophilic esophagitis. How are adults and children affected differently?

A

Adults experience dysphagia and food impaction (more often than nausea or heartburn)

Children experience nausea, burning, and food intolerance.

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18
Q

What are significant historical findings in the diagnosis of eosinophilic esophagitis?

A

A personal or family history of atopia (rhinitis, asthma, dermatitis)

Failure of acid suppressive treatment or symptoms of GERD without any actual reflux.

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19
Q

Describe the gross and microscopic findings needed to diagnose eosinophilic esophagitis.

A

Histologic: >15 eosinophils per HPF in esophageal mucosa.

Gross: Corrupted esophagus, “felinization”, longitudinal furrows, white abscesses.

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20
Q

How is eosinophilic esophagitis treated?

A

Since it is a hypersensitivity reaction, avoid allergen-rich foods (seafood, wheat, soy, nuts, milk, eggs). Topical & systemic steroids, endoscopic dilation.

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21
Q

What are the causes and possible consequences of chemical esophagitis?

A

Caused by ingestion of corrosives, alcohol, very hot fluids, and smoking, as well as lodging of pills in the esophagus (NSAIDs, Doxycycline, fosomax)

Consequences usually limited to pain, but also what naturally follows chemical injuries: hemorrhage, stricture, and perforation.

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22
Q

Distinguish between HSV and CMV viral esophagites.

A

HSV: Punched-out ulcers with nuclear inclusions at their rims (within epithelial cells).

CMV: Shallow ulcers with cytoplasmic AND nuclear inclusions (within capillary endothelium and stroma)

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23
Q

What agents are usually responsible for fungal esophagitis?

A

Candida is most common, but also mucor and aspergillosis.

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24
Q

How frequent is bacterial esophagitis?

Describe the nature of this infection.

A

Not common at all; only 10% of infectious esophagites.

Bacteria can invade the lamina propria and cause overlying necrosis. Primary or secondary to an existing ulcer.

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25
Q

What can cause iatrogenic esophagitis?

Describe its morphology.

A

Chemo, GVHD, radiation.

Generally non-specific; note that radiation causes blood vessel thickening >> ischemia.

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26
Q

What are the significance of diseases like Lichen planus, bullous pemphigoid, and epidermolysis bullosa in the context of esophageal pathology?

A

These are all conditions which usually affect the skin; many of the same epithelial components are present in the esophagus (or GI tract in general) and so they may have manifestations there.

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27
Q

Define:

dysphagia

heartburn

regurgitation

odynophagia

A

Dysphagia = difficulty swallowing

heartburn = burning feeling typically epigastric rising to the chest

regurgitation = effortless upward return of gastric contents

odynophagia = pain during swallowing and bolus transit

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28
Q

Differentiate esophageal vs. pharyngeal dysphagia

A
  • Esophageal
    • may have chest pain, may refer upwards to the throat
    • ‘sticking’ or ‘hanging up’ after swallowing
  • Pharyngeal
    • difficulty initiating swallowing
    • generally does not refer downwards
    • coughing, choking, nasal regurgitation
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29
Q

Common etiologies of dysphagia: mechanical or neuromuscular?

  1. Peptic stricture
  2. achalasia
  3. dysmotility
  4. esophageal ring
  5. cancer
  6. esophageal spasm
  7. eosinophilic esophagitis
A
  1. mechanical
  2. neuromuscular
  3. neuromuscular
  4. mechanical
  5. cancer
  6. neuromuscular
  7. both
30
Q

Uncommon etiologies of dysphagia: mechanical or neuromuscular?

  1. Esophageal web
  2. Diverticulum
  3. collagen vascular disorders
  4. Chagas disease
  5. Scleroderma
  6. Foreign body
  7. Benign tumors
  8. Extrinsic tumors
  9. SLE
A
  1. mechanical
  2. mechanical
  3. neuromuscular
  4. neuromuscular
  5. neuromuscular
  6. mechanical
  7. mechanical
  8. mechanical
  9. neuromuscular
31
Q

In a patient complaining of dysphagia with solid food only, what is the leading differential for:

  1. Progressive dysphagia, >50 years old
  2. Intermittent dysphagia
  3. Dysphagia with chronic heartburn
A
  1. Cancer
  2. Esophageal ring
  3. Peptic stricture (intermittency due to variable or compensatory eating behaviors)
32
Q

In a patient complaining of dysphagia with** solid or liquid food**, what is the leading differential for:

  1. Progressive dysphagia with heartburn/regurgitation
  2. Intermittent dysphagia with chest pain
A
  1. Scleroderma or achalasia
  2. Esophageal spasm
33
Q

Why is liquid dysphagia almost always neuromuscular in origin?

A

Mechanical obstruction usually does not completely occlude the lumen, allowing liquid to pass. Neuromuscular dysphagia can potentially obstruct or constrict the entire lumen, making it difficult to pass solids or liquids.

34
Q

Can the espohagus be evaluated by physical exam alone?

Name 3 modalities commonly used to evaluate esophageal function

A

No, but some limited eval can be done by looking for deviation of the cricoid cartilage.

  • Upper GI endoscopy (visual inspection)
  • Esophageal manometery (pressure-time measurement)
  • Radiography (indirect visualization)
35
Q

What is the gold standard test for diagnosis of esophageal motor disorders?

A

Esophageal manometry

36
Q

During primary peristalsis, approximately how long does the UES relax?

The primary peristaltic wave lasts how long? How fast does it move?

How long does the LES relax during primary peristalsis?

A

~500ms

Duration: 3-7 seconds, speed: 3-5cm/s

LES relaxes for 3-8 seconds

37
Q

Give the (2) major defining characteristics of achalasia

A
  1. Impaired relaxation of the LES and increased LES tone
  2. Loss of peristalsis in the body of the esophagus
38
Q

Name this sign. What does it indicate?

A

Bird beak sign

Associated with achalasia (not sufficient for diagnosis alone, however - 2-3 modalities are generally required for diagnosis)

39
Q

Explain briefly the pathophysiology of achalasia

A

Abnormal function of the LES and the esophageal body is due to progressive impairment, then loss of inhibitory neurons (ganglion cells) in the myenteric plexus. Loss of inhibitory action is especially apparent in the increased LES tone.

Ultimately, all neurons (inhibitory and excitatory) of the myenteric plexus may be lost.

40
Q

Give some characteristics of the clinical presentaiton of achalasia

A
  • Age: 7th decade (or 20-30)
  • Dysphagia (>90%), solids and liquids
  • Chest pain, heartburn, regurgitation, weight loss (60%)
  • Esophagitis and heartburn (due to food stasis)
  • Bad breath (rotting/fermenting food)
  • Slow progression (progressive damage, accomodative eating behaviors)
41
Q

Chagas disease (trypanosome cruzi) is associated with what disorder of the esophagus?

What other symptoms/disorders might be seen?

A

achalasia

Megacolon, heart disease (most common presentation), neurologic disorders, diffuse myenteric destruction (not just the esophagus)

42
Q

Describe 3 general treatment categories for achalasia

A
  1. Pharmacotherapy - including NO donors and anticholinergic agents
  2. Endoscopic therapy (usually botox or pneumatic dilation)
  3. Surgery
43
Q

Describe esophagel spasm

A

Dyscoordinated contraction of the muscularis layer of the esophagus, leading to inefficient delivery of food and fluids to the stomach.

44
Q

What is the meain feature of Scleroderma Esophagus?

How is its manometric findings different than achalasia?

A

Complete aperistalsis

No LES tone is observed (unlike achalasia, which has increased LES tone)

45
Q

What is Barrett’s Esophagus?

A

Replacement of normal esophageal squamous epithelium with metaplastic columnar epithelium

46
Q

What is the relationship between Barrett’s esophagus, GERD, and dysplasia?

A

Barrett’s esophagus is a complication of GERD. 10% of patients with GERD have Barrett’s esophagus.

Dysplasia is a complication of Barrett’s esophagus; 0.2-1% of people with Barrett’s esophagus each year have dysplasia

47
Q

What genes are involved in Barrett’s esophagus?

What genes are involved in dysplasia and carcinogenesis?

A

CDX2 is found in BE, but not in normal tissue

P53 and cyclin D1 mutations are associated with dysplasia and carcinogenesis

48
Q

What is Barrett’s esophagus similar to molecularly?

A

Adenocarcinoma

49
Q

How is BE typically diagnosed?

Who is the typical patient?

A

BE is diagnosed by endoscope showing abnormal mucosa above the GE junction AND biopsy showing metaplasia

The typical patient is a middle-aged white male with a long history of reflux

50
Q

What symptoms does BE present with?

What is standard of care for BE?

A

BE is asymptomatic, but it presents with reflux symptoms

typically treatment of the reflux, but also periodic endoscopy with biopsy to look for dysplasia

51
Q

Who is the typical esophageal adenocarcinoma patient?

What are risk factors for esophageal adenocarcinoma?

A

A white, middle-aged male from a developed western country

Tobacco use, obesity, radiation therapy, and dysplasia in BE

52
Q

What molecules contribute to the pathogenesis of esophageal adenocarcinoma?

A

P53 is an early mutation

c-ERB, cyclin D1, and cyclin E are amplified

TNF-alpha and NF-KB levels are increased and contribute to inflammation

53
Q

Where does esophageal adenocarcinoma typically present?

What does it look like grossly?

A

distal third of the esophagus, often including the gastric cardia

early lesions look like a flat or raised patch on intact mucosa; later lesions can be very diverse

54
Q

Who is the typical squamous cell carincoma patient?

What are risk factors for squamous cell carcinoma?

What countries have the highest incidence of SCC?

A

African-american, middle-aged male

alcohol use, tobacco use, poverty, caustic esophageal injury, achalasia, plummer vinson syndrome, radiation therapy, food contamination, nutritional deficiencies, HPV infection

Iran, China, Turkmenistan, and Hong Kong

55
Q

Where does squamous cell carcinoma typically present?

What does it look like grossly?

A

typically presents in the mid-esophagus, but late stages can spread to the aorta or respiratory tree

early lesions look lik gray-white plaques, but later stages lesions grow quickly and can occlude the lumen

56
Q

What are some symptoms of squamous cell carcinoma?

A

typically diagnosed in later stages after tumors have grown to occlude the lumen

dysphagia

odynophagia

obstruction

weight loss

tracheo-esophageal fistulas

57
Q

What is the prognosis for squamous cell carcinoma?

Where is SCC most likely to spread?

A

if found early, 75% 5-year survival rate, but overall 9% 5-year survival rate

lymph nodes!

Upper third- cervical lymph nodes

middle third- mediastinal, paratracheal, and tracheobronchial lymph nodes

lower third- gastric and celiac lymph nodes

58
Q

What is the prognosis for adenocarcinoma?

A

80% 5-year survival if caught early, but overal less than 25% 5-year survival

59
Q

What are the two major phases of the swallowing reflex?

About how many muscles are involved in the act of swallowing?

A
  1. Voluntary - initial phase where bolus is pushed toward the hypopharynx
  2. Involuntary - as the bolus meets the hypopharynx, this phase is triggered
  • >50 muscles (oral, pharyngeal, laryngeal, esophageal, diaphragmatic)
60
Q
  1. About how long is a typical adult esophagus?
  2. About how thick is the esophageal wall in a typical adult?
A
  1. 18-26cm
  2. 2-4mm
61
Q
  1. What is the resting appearance of the esophageal lumen?
  2. How much can the lumen expand up to during distention?
A
  1. Collapsed
  2. Expansion of up to 2-3cm
62
Q

What are the orientation of the muscle layers in the esophageal muscularis propria?

What type(s) of muscle make(s) up the esophagus and its sphincters?

A
  1. Inner circular
  2. Outer longitudinal
  • Upper 1/4 and UES is striated muscle
  • Lower 1/2 and LES is smooth muscle
63
Q

What is the zigzag (Z) line?

A

The line demarcating the juncture of esophageal and gastric mucosa (a.k.a. at the gastroesophageal junction.)

64
Q

Describe the process of esophageal peristalsis (characteristics of the muscle contractions & relaxations.)

A
  • Mechanism by which esophagus propels food into the stomach
    • Muscle contractions that are:
      • Coordinated
      • Propulsive
      • Sequential
    • In concert with appropriately times relaxation of UES and LES
65
Q

What triggers primary peristalsis vs. secondary peristalsis?

A
  • Primary: Triggered by swallow
  • Secondary: Triggered by esophageal distention
    • Note: Contractions starts proximal to the distension
66
Q

Name an intrinsic and an extrinsic neural generator of peristalsis.

A
  • Intrinsic: Enteric neural plexus
  • Extrinsic: Vagus nerve
67
Q

What is the difference between the contractions of striated vs. smooth muscle along the esophagus?

A

Striated: Simultaneous electrical activation of all vagal efferent neurons directly produces simultaneous contractions of all of the esophageal striated muscle.

Smooth: Intrinsic neurons activated by the vagal efferents induce sequential activation of the smooth muscle along the esophagus (the true peristaltic contractions.)

68
Q

Ca2+ released to produce contraction in striated esophageal muscle originates from where?

What about the Ca2+ for smooth muscle contraction?

A

Striated: Sarcoplasmic Reticulum, via T-tubules

Smooth: From “the outside” [general ECF?]

69
Q

What type of nerve terminals are found at their interface with esophageal striated muscle?

What type of terminals are found with smooth muscle?

A

Striated: Motor End Plate

Smooth: Varicose nerve endings, gap junctions

70
Q

From the physiological standpoint of nervous control, how is peristalsis in smooth muscle regulated?

A

A wave of inhibition followed by a wave of excitation.

71
Q

What two major motor neuron types within esophageal smooth muscle do vagal efferents synapse onto?

What major neurotransmitter is used in each case?

A
  1. Excitatory motor neurons
    • Ach
  2. **Inhibitory **motor neurons
    • NO
72
Q
A

M2 GI/Nutrition (43 decks)

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