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Esophagus Flashcards

1
Q

How much can the esophageal lumen expand with distention?

A

2-3 cm

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2
Q

What are the 4 layers of the esophageal wall (according to lecture)?

A

Mucosa
Submucosa
Muscularis propria
Adventitia

**All of which reach 2-4 mm in thickness

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3
Q

How does the upper esophagus differ from the lower esophagus?

A

The upper is composed of striated skeletal muscle

The lower is composed of smooth muscle

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4
Q

What is the name of the muscle that helps support the LES?

A

Crural Diaphragm

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5
Q

What is primary (proximal) esophageal peristalsis?

A

Caused by direct innervation but vagal efferents
Ca2+ is released from sarcoplasmic reticulum via T-tubules
Generated by the swallowing central pattern generator (nucleus ambiguous) of the brain stem

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6
Q

What is secondary (distal) esophageal peristalsis?

A

Peristaltic wave by intrinsic neurons that are activated by vagal efferents – wave of inhibition followed by wave of excitation
Ca2+ influx from outside

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7
Q

Explain the vagal efferents that synapse on excitatory myenteric neurons. How do they differ from those that synapse on inhibitory myenteric neurons?

A

Excitatory: ACh –> Ca2+ release –> depolarization –> 2nd messenger (Substance P)

Inhibitory: NO –> cGMP dependent pathway –> inhibition of Ca2+ entry –> hyper polarization (VIP)

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8
Q

How will esophageal dysphagia present? What about pharyngeal dysphagia?

A

Esophageal: Sticks or hangs up after swallow, may have chest pain

Pharyngeal: difficulty initiating swallow; coughing, choking and nasal regurgitation

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9
Q

What are some common mechanical causes of dysphagia?

A
  1. peptic stricture
  2. esophageal ring
  3. cancer
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10
Q

What are some common neuromuscular causes of dysphagia?

A
  1. achalasia
  2. esophageal spasm
  3. dysmotility
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11
Q

What can be a neuromuscular or mechanical cause of dysphagia?

A

Eosinophilic esophagitis

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12
Q

What are some common mechanical causes of obstruction seen when eating solids only?

A
  1. progression: age > 50 think cancer
  2. chronic heartburn: peptic stricture
  3. intermittent: esophageal ring
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13
Q

What are some common neurmusular causes of obstruction seen when eating solids or liquids?

A
  1. progressive with heartburn/regurg: scleroderma or achalasia
  2. intermittent and chest pain: spasm
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14
Q

Name 3 diagnostic approches to esophageal disorders.

A
  1. Upper GI endoscopy
  2. Esophageal Manometry
  3. Radiograph – Esophagram
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15
Q

During primary peristalsis, how long does the UES relax for?
How long is the peristaltic duration?
How long does the LES relax for?

A

UES = 1/2 second
Peristaltic duration = 3-7 sec (travels 3-5 cm/sec)
LES = 3-8 seconds

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16
Q

Name the three things that define Achalasia.

A
  1. Impaired LES relaxation
  2. Increased LES tone
  3. loss of peristalsis
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17
Q

What is the pathophysiology behind achalasia?

A

Impaired and loss of inhibitory NO activity

Degeneration of ganglion cells in myenteric plexus, inflammatory lymphocytic infiltration

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18
Q

When and how does Achalasia typically present?

A

7th decade (and 20-30s)
Dysphagia with both solids and liquids
Chest pain, heart burn, regard and weight loss

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19
Q

What are some causes of secondary achalasia?

A
  1. Malignancy – adenocarcinoma
  2. Other infiltrative disorders – amyloidosis, sarcoidosis
  3. Chagas disease – trypanosoma cruzi, diffuse enteric myenteric destruction
  4. Para-neoplastic syndromes – small cell carcinoma of lung
  5. Autonomic nerve damage – diabetes, polio or surgical
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20
Q

What are some available treatments for Achalasia?

A
  1. NO donors, anticholinergic agents
  2. Endoscopic therapy – Botox, Pneumatic dilation
  3. Operative therapy
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21
Q

How does esophageal spasm differ from achalasia?

A

An esophageal spasm is characterized by discoordinated contraction of the muscularis layer – not the LES like in achalasia
A spasm just interferes with efficient delivery of food and fluids to the stomach

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22
Q

What is the most important barrier against reflux?

A

Constant LES tone –prevents reflux of acidic gastric contents that are under constant positive abdominal pressure

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23
Q

Explain the pathophysiology behind GERD.

A

Reflux of gastric juices –> mucosal injury –> inflammation and IL-6 production –> increase in H2O2 –> H2O2 causes increase in PAF and PGE2 –> PAF and PGE2 reduce ACh release and LES tone

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24
Q

What is a hiatal hernia?

A

Separation of the diaphragmatic crura and LES –> protrusion of stomach into thorax

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25
Q

What is the most common type of hiatal hernia?

A

Sliding – asymptomatic in 90% of cases

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26
Q

How does a hiatal hernia change morphology?

A

It causes basal zone hyperplasia and elongation of lamina propria, also eosinophils are recruited, followed by neutrophils

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27
Q

What will you see on endoscopy with reflux esophagitis?

A

Simple hyperemia may be the only alteration

More damage may be seen (erosions)

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28
Q

What is the most common cause of esophagitis?

A

Reflux esophagitis = reflux of gastric contents into lower esophagus

29
Q

What is the common presentation of reflux esophagitis?

A

Adults over 40, obesity, heartburn, regurgitation, dysphagia
Possibly atypical chest pain, chronic cough, hoarseness

30
Q

What are some diagnostic modalities for esophagitis?

A
  1. Endoscopy
  2. Ambulatory reflux monitoring (90% specific, 50% sensitive)
  3. Radiography (70% sensitive)
31
Q

What are some GERD associated “alarm symptoms”?

A 
Dysphagia
Anemia
Weight loss
Abdominal mass
Vomiting
32
Q

What are some lifestyle modification that may improve GERD symptoms?

A

Weight loss
Avoiding late meals
Avoiding trigger foods (ETOH, caffeine, chocolate, greasy foods, citrus or carbonated drinks)

33
Q

What are some other therapies for GERD?

A

PPI
H2 bockeres
Fundoplication (operation)
Substitute devices to enforce LES (LINX and stimulator)

34
Q

What are some possible complications of GERD?

A

Esophageal ulcer
Esophageal stricture
Bleeding
Barrett’s esophagus

35
Q

What are some possible causes of an esophageal stricture?

A

Most often due to inflammation and scarring possibly from:

  1. Chronic GERD
  2. Radiation
  3. Caustic injury

– Usually have problems with solids before liquids

36
Q

What is the pathophysiology of esophageal structuring?

A

Narrowing of esophageal lumen by fibrous thickening of the submucosa, atrophy of the muscularis propria, or secondary epithelial damage.

37
Q

What is the cardinal feature of eosinophilic esophagitis?

A

Epithelial infiltration by large numbers of eosinophils, particularly superficially

38
Q

How does presentation of eosinophilic esophagitis present in adults vs children?

A

In adults: dysphagia, most common cause of food impaction, less common to show heart burn and nausea

In children: nausea, burning and food intolerance

**will also have failure of acid suppressive treatment

39
Q

What is something else to look for when suspecting eosinophilic esophagitis?

A

Personal or family history of utopia (atopic dermatitis, rhinitis or asthma)

40
Q

How is eosinophilic esophagitis causes?

A

Allergic immune reaction to inhaled allergens that involves T-cell mediated hypersensitivity
This leads to eosinophil infiltration and activation –> cytokine release from eosinophils –> MBP deposited and IL-5, IL-13 increase –> tissue remodeling/fibrosis and change in mechanical properties of the esophagus

41
Q

What confirms a diagnosis of eosinophilic esophagitis?

A

> 15 eosinophils per high power field in esophageal mucosa

42
Q

What are some treatments for eosinophilic esophagitis?

A
  1. Elimination diet (no seafood, wheat, soy, nuts, milk or eggs)
  2. Topical steroids
  3. Systemic steroids
  4. Endoscopic dilation
43
Q

What are some other types of esophagitis?

A

Chemical esophagitis
Infectious
Iatrogenic
Skin disorder associated

44
Q

What can cause chemical esophagitis?

A

Medicinal pills that lodge and dissolve in the esophagus instead of passing into the stomach

45
Q

What are some things that can cause infectious esophagitis?

A

Viral: CMV, HSV
Fungal: candida, mucormycosis, aspergillosis
Bacterial: invades lamina propria and causes necrosis

46
Q

How does CMV vs HSV appear in viral esophagitis?

A 
CMV = cytoplasmic and nuclear inclusions within capillary endothelium and storm, Shallow ulcerations
HSV = nuclear inclusions within a rim of degenerating epithelial cells at the ulcer edge, punched out ulcers
47
Q

What are some examples of things that can cause iatrogenic esophagitis?

A

Cytotoxic chemotherapy
GVHD
Radiation

48
Q

What are some skin disorders that can cause esophagitis?

A

Desquamative skin disease (bullous pemphigoid, epidermolysis bullosa)
Lichen planus
Crohn’s disease

49
Q

What is Barrett’s esophagus?

A

When normal esophageal squamous epithelium is replaces by intestinal metaplasia.

50
Q

What type of cell is indicative of intestinal metaplasia?

A

Goblet cells

51
Q

How many GERD patients get BE? How many BE patients get a malignant lesion?

A

10% get BE

0.2-1% get malignant lesion (adenocarcinoma)

52
Q

What are some genetic events that may play a role in BE?

A

Cdx gene in 100% of specimens that is not found in normal esophagus or stomach
Cdx2 above specialized intestinal metaplasia
Abnormalities in p53 and cyclin D1

53
Q

What characterizes intramucosal carcinoma?

A

Invasion of neoplastic epithelial cells into the lamina propria

54
Q

What is BE morphology?

A

Tongues or patches of red, velvety mucosa extending upward from the GE junction

55
Q

What is required for diagnosis of BE?

A

Both endoscopic evidence of abnormal mucosa AND histologically documented metaplasia

56
Q

What is a common presentation of BE?

A

White adult male, between 40-60 yo, with long term reflux

But often BE is asymptomatic

57
Q

What population is esophageal adenocarcinoma highest?

A

white middle age male

developed western countries

58
Q

What are some risk factors for esophageal adenocarcinoma?

A

Dysplasia in BE
Tobacco use
Obesity
Radiation therapy

59
Q

What are some things that lead to adenocarcinoma?

A

Acquisition of genetic and epigenetic changes:

  • p53 (early stages)
  • amplification of c-ERB-B2, cyclin D1 and cyclin E
  • increased TNF and NF-kB
60
Q

Where does esophageal adenocarcinoma usually occur?

A

In the distal 1/3 of the esophagus

May invade adjacent gastric cardia

61
Q

What do adenocarcinoma tumors generally produce?

A

Mucin and form dense glands

62
Q

What population is common affected by squamous cell carcinoma of the esophagus?

A

African american, male, older than 45

63
Q

What are some risk factors of squamous cell carcinoma?

A 
Alcohol and tobacco
Poverty
History of caustic esophageal injury 
Achalasia and Plummer-Vinson Syndrome 
Previous radiation 
Frequent consumption of hot beverages

Endemic risk factors = nutritional deficiency, mutagenic compounds, fungus-contaminated foods, HPV infection

64
Q

Where in the esophagus does squamous cell carcinoma generally occur?

A

Middle 1/3

65
Q

How does squamous cell carcinoma progress?

A

Early lesions are small, gray white plaque-like thickenings

Over months they grow into tumor masses that protrude and obstruct the lumen

66
Q

What are some symptoms of esophageal squamous cell carcinoma?

A
  • symptomatic tumors are generally large at diagnosis
    1. dysphagia
    2. odynophagia
    3. obstruction
  • weight loss, debilitation
67
Q

What is the prognosis like for esophageal squamous cell carcinoma?

A

5 year survival 75% for superficial
Lymph node metastasis – poor prognosis
Overall 5 year survival is 9%

68
Q

What is the prognosis for adenocarcinoma of the esophagus?

A

5 year survival 80% with superficial

Overall survival is 25% d/t advanced stage at time of diagnosis

GI (34 decks)

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