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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
What is the most common type of hiatal hernia?
Sliding -- asymptomatic in 90% of cases
26
How does a hiatal hernia change morphology?
It causes basal zone hyperplasia and elongation of lamina propria, also eosinophils are recruited, followed by neutrophils
27
What will you see on endoscopy with reflux esophagitis?
Simple hyperemia may be the only alteration | More damage may be seen (erosions)
28
What is the most common cause of esophagitis?
Reflux esophagitis = reflux of gastric contents into lower esophagus
29
What is the common presentation of reflux esophagitis?
Adults over 40, obesity, heartburn, regurgitation, dysphagia Possibly atypical chest pain, chronic cough, hoarseness
30
What are some diagnostic modalities for esophagitis?
1. Endoscopy 2. Ambulatory reflux monitoring (90% specific, 50% sensitive) 3. Radiography (70% sensitive)
31
What are some GERD associated "alarm symptoms"?
``` Dysphagia Anemia Weight loss Abdominal mass Vomiting ```
32
What are some lifestyle modification that may improve GERD symptoms?
Weight loss Avoiding late meals Avoiding trigger foods (ETOH, caffeine, chocolate, greasy foods, citrus or carbonated drinks)
33
What are some other therapies for GERD?
PPI H2 bockeres Fundoplication (operation) Substitute devices to enforce LES (LINX and stimulator)
34
What are some possible complications of GERD?
Esophageal ulcer Esophageal stricture Bleeding Barrett's esophagus
35
What are some possible causes of an esophageal stricture?
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
What is the pathophysiology of esophageal structuring?
Narrowing of esophageal lumen by fibrous thickening of the submucosa, atrophy of the muscularis propria, or secondary epithelial damage.
37
What is the cardinal feature of eosinophilic esophagitis?
Epithelial infiltration by large numbers of eosinophils, particularly superficially
38
How does presentation of eosinophilic esophagitis present in adults vs children?
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
What is something else to look for when suspecting eosinophilic esophagitis?
Personal or family history of utopia (atopic dermatitis, rhinitis or asthma)
40
How is eosinophilic esophagitis causes?
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
What confirms a diagnosis of eosinophilic esophagitis?
>15 eosinophils per high power field in esophageal mucosa
42
What are some treatments for eosinophilic esophagitis?
1. Elimination diet (no seafood, wheat, soy, nuts, milk or eggs) 2. Topical steroids 3. Systemic steroids 4. Endoscopic dilation
43
What are some other types of esophagitis?
Chemical esophagitis Infectious Iatrogenic Skin disorder associated
44
What can cause chemical esophagitis?
Medicinal pills that lodge and dissolve in the esophagus instead of passing into the stomach
45
What are some things that can cause infectious esophagitis?
Viral: CMV, HSV Fungal: candida, mucormycosis, aspergillosis Bacterial: invades lamina propria and causes necrosis
46
How does CMV vs HSV appear in viral esophagitis?
``` 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
What are some examples of things that can cause iatrogenic esophagitis?
Cytotoxic chemotherapy GVHD Radiation
48
What are some skin disorders that can cause esophagitis?
Desquamative skin disease (bullous pemphigoid, epidermolysis bullosa) Lichen planus Crohn's disease
49
What is Barrett's esophagus?
When normal esophageal squamous epithelium is replaces by intestinal metaplasia.
50
What type of cell is indicative of intestinal metaplasia?
Goblet cells
51
How many GERD patients get BE? How many BE patients get a malignant lesion?
10% get BE | 0.2-1% get malignant lesion (adenocarcinoma)
52
What are some genetic events that may play a role in BE?
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
What characterizes intramucosal carcinoma?
Invasion of neoplastic epithelial cells into the lamina propria
54
What is BE morphology?
Tongues or patches of red, velvety mucosa extending upward from the GE junction
55
What is required for diagnosis of BE?
Both endoscopic evidence of abnormal mucosa AND histologically documented metaplasia
56
What is a common presentation of BE?
White adult male, between 40-60 yo, with long term reflux | But often BE is asymptomatic
57
What population is esophageal adenocarcinoma highest?
white middle age male | developed western countries
58
What are some risk factors for esophageal adenocarcinoma?
Dysplasia in BE Tobacco use Obesity Radiation therapy
59
What are some things that lead to adenocarcinoma?
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
Where does esophageal adenocarcinoma usually occur?
In the distal 1/3 of the esophagus | May invade adjacent gastric cardia
61
What do adenocarcinoma tumors generally produce?
Mucin and form dense glands
62
What population is common affected by squamous cell carcinoma of the esophagus?
African american, male, older than 45
63
What are some risk factors of squamous cell carcinoma?
``` 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
Where in the esophagus does squamous cell carcinoma generally occur?
Middle 1/3
65
How does squamous cell carcinoma progress?
Early lesions are small, gray white plaque-like thickenings | Over months they grow into tumor masses that protrude and obstruct the lumen
66
What are some symptoms of esophageal squamous cell carcinoma?
* symptomatic tumors are generally large at diagnosis 1. dysphagia 2. odynophagia 3. obstruction - weight loss, debilitation
67
What is the prognosis like for esophageal squamous cell carcinoma?
5 year survival 75% for superficial Lymph node metastasis -- poor prognosis Overall 5 year survival is 9%
68
What is the prognosis for adenocarcinoma of the esophagus?
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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