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GI/Liver Pathology > Esophagus > Flashcards

Esophagus Flashcards

1
Q

Upper esophageal sphincter

A

Is a true sphincter, has skeletal muscle. Bounded by the inferior pharyngeal constrictor and the cricopharyngeus. Tonically closed at rest, relaxes during a swallow.

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2
Q

Physiology of Swallowing

A

Oral phase (voluntary): bolus is propelled backward by tongue, tongue squeezes against palate

Pharyngeal phase: soft palate elevates to close off nasopharynx, larynx moves antero-superiorly to bring the larynx away from the path of the bolus and open the UES.
Larynx closes and the ues relaxes, the bolus is then propelled into the esophageal inlet by pharyngeal muscles.

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3
Q

What does manometry of swallowing look like?

A

Swallowing causes immediate pressure drop from ~70 mmHg in the UES, then pressure increases, then returns to normal. Distally, the rest of the esophagus contracts to push the food down. Rest of esophagus sits at 0 and contracts up to 60ish. Unique thing though, the LES will engage in receptive relaxation upon swallowing, then will contract after the food moves through.

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4
Q

Receptive relaxation

A

LES will relax at a swallow. Ensure that whatever eventually reaches the LES can pass into stomach.

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5
Q

LES

A

Not a true sphincter – just a high pressure zone created by the crural diaphragm and the smooth muscle of the esophagus.

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6
Q

Why is the esophagus under slighly negative pressure?

A

Because the thoracic cavity is pulling outwards.

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7
Q

Factors that decrease LESp

A

Cholinergic antagonists, alpha-adrenergic blockers, beta-adrenergic agonists, nitric oxide, secretin, cck, somatostatin, progesterone, fats, chocolate, peppermint, protein, theophylline, calcium channel blockers, morphine, serotonin.

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8
Q

Dysphagia

A

Trouble swallowing.

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9
Q

Pyrosis

A

Heartburn - due to the reflux of acid or bile, worse with bending

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10
Q

Odynophagia

A

Pain on swallowing

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11
Q

Diagnostic tests for esophageal disorders

A

Barium esophagram - evaluates a structural lesion, can sometimes demonstrate GE reflux

Endoscopy with biopsy - enables tissue diagnosis

Endoscopic ultrasound – Useful for imaging lesions that are in the esophageal wall or immediately adjacent to the esophagus.

Manometry- pressure reading, can demonstrate the tendency for GE reflux.

Acid studies – measures esophageal pH

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12
Q

GERD Caused by

A

Caused by reflux of gastric contents into the esophagus. Note: not all reflux causes disease and not all reflex is acid

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13
Q

Symptoms of GERD

A

Heartburn – worse with food, laying down, better with antacids.

Also chest pain, dysphagia, hoarseness

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14
Q

How to diagnose GERD

A

24 hour pH monitoring, endoscopy shows the effects of reflux

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15
Q

Pathogenesis of GERD

A

Aggressive (acid) vs defensive factors like anti-reflux barrier. LES is most important. Crural diaphragm is next most important. Also dependent on esophageal acid clearance (saliva, esophageal peristalsis, gastric empyting, hiatal hernia).

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16
Q

Hitatal hernea

A

Stomach moves into chest, this increases transient LES relaxations and creates an acid pocket within proximal stomach. Loss of pinch at GE junction.

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17
Q

Two types of hiatal hernia

A

Sliding type, paraesophageal (where fundus moves around esophagus)

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18
Q

Surgical treatment for GERD

A

Fundoplication, where fundus is wrapped around the esophagus

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19
Q

How does defective esophageal clearance cause GERD

A

Ineffective peristalsis causes prolonged acid content

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20
Q

Complications of GERD

A

Mucosal injury: causes esophagitis or ulceration

Stricture

Barrett’s Metaplasia: squamous epithelium changes to columnar epithelium, premalignant and can turn into esophageal adenocarcinoma.

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21
Q

Los angeles classification of erosive esophagitis

A

Grade A: Almost no ulceration
B: Slightly more
C: visible ulceration
D severe ulceration

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22
Q

Peptic stricture

A

Healing of esophagus can cause fibrosis and constriction

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23
Q

Barrett’s Esophagus

A

Salmon colored macroscopically reveals columnar epithelium. Goblet cells proliferate – looks like intestine.

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24
Q

Esophageal adenocarcinoma

A

A big mass blocks the esophagus

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25
Dysphagia for solids only
Structural disorder. If progressive and rapid, carcinoma If progressive and gradual with a history of gerd, peptic stricture. If intermittent, usually reveals a web or ring.
26
Dysphagia for solids and liquids
Reveals a motility disorder. If progressive with heartburn, then scleroderma (causes low LESp). If progressive without heartburn, then achalasia (high lesp) If intermittent with chest pain, then spasm
27
What is the first step in the evaluation of dysphagia
Structural study -- endoscopy or barium swallow
28
Achalasia
Loss of inhibitory ganglion cells to myenteric plexus, this causes tonic contraction of the LES.
29
What eventually happens in achalasia if severe
Aperistalsis due to prolonged contraction against hypertonic LES
30
Symptoms of Achalasia?
Dysphagia, regurgitation, chest pain
31
Barium swallow for achalasia? How about if severe?
Bird Beak in distal esophagus. Shows air fluid level if severe due to aperistalsis
32
Manometry for achalasia
No receptive relaxation, high tone (+60) instead of 20.
33
How to treat achalasia
Botox, pneumatic dilation with balloon, myotomy to cut muscles
34
What causes pseudo-achalasia?
Chagas' Disease | Cancer of the GE junction
35
Scleroderma
Connective tissue disorder where smooth muscle is replaced by fibrosis. Loss of LES function, poor esophageal peristalsis. This causes GE reflux. Widely patent LES
36
Manometry of scleroderma
Low amplitude tracings with no rhyme or reason, low LES p and poor motility.
37
Diffuse esophageal spasm
Can cause chest pain, odynophagia. Corkscrew esophagus on x-ray. LES is usually normal. Treat with muscle relaxants or CCBs.
38
Manometry of diffuse esophageal spasm
Simultaneous prolonged contractions that are repetitive even without a swallow.
39
nutcracker esophagus
Pressures of swallow can reach 400! Normal peristalsis and LES
40
Histological layers of the esophagus
Mucosa, submucosa/muscularis mucosae (shock absorber between mucosa and smooth muscle, contains glands/ducts and meissner's plexus), muscularis propria with myenteric plexus
41
How are esophageal squamous cells generated?
They arise from basal cells which desquamate and keratinize as they move up.
42
Z line
Gastoesophageal junction.
43
Chemical esophagitis
Injury and complications depend on type, quantity, and duration of exposure. Alkalis are especially dangerous because they are tasteless/odorless and cause rapid injury
44
Steps of immediate damage in chemical esophagitis
Necrosis, saponification, perforation, can lead to death
45
1 month consequences post chemical ingestion?
Ulcer, scarring, stricture All leading to dysphagia
46
Worst consequence long term of chemical esophagitis?
Squamous cell carcinoma
47
Pill esophagitis
When a pull gets stuck and forms kissing ulcers. Iron is especially bad. Bad during sleep because pill can be sandwiched in collapsed esopagus with minimal secretions
48
Bisphosphonate damage to esophagus
Things like fosamax and cause huge ulcers and strictures in lower esophagus
49
Common sites of corrosive injury
Where esophagus is consticted due to regional anatomy like aortic arch, left main bronchus, Left atrium.
50
Candida esophagitis
Early sign of immunocompromised states. Major symptom is odynophagia and oral thrush. On endoscopy there are whitish plaques with desequamated cells and spores/pseudohyphae.
51
CMV esophagitis
Immunocompromised states and indicates viremia. CMV infects mesenchymal cells, NOT squamous cells. So damage is due to thrombus formation in esophageal vessels which cause ischemia and ulceration.
52
Herpes esophagitis
Can happen in immunocompetent or immunocompromised hosts. Infects squamous cells and causes vesicles/ulcers.
53
Histologic signs of herpes esophagitis
Cell-cell detachment, multinucleation, and ground class nuclei.
54
Best place to biopsy if viral esophagitis suspected?
At the border between squamous epithelium and ulcer. Get both CMV and herpes.
55
Histology of Reflux esophagitis
Congested capillaries as a reaction to acid. Edema between squamous cells, ballooned squamous cells, basal cell hyperplasia and eosinophils
56
Peptic (reflux associated) ulcer
Necrotic tissue, fibrosis, and granulation tissue in biopsy
57
Complications of reflux esophagitis
Inflammation causes ulceration (odynophagia and hematemesis). Regeneration of the ulceration can cause barrett esophagus. Ulceration can also proceed to scarring and stricture which causes dysphagia.
58
Eosinophilic esophagitis
Second most common esophagitis, main symptoms are dysphagia and food impaction. Driven by antigen (75% of patients have atopy). Treat with dietary restriction and steroids
59
Gross appearance of eosinophilic esophagitis
Transverse rings (trachealization) longitudinal furrows, tiny white mucosal plaques that are made up of eosinophils
60
Histology of eosinophilic esophagitis?
Eosinophil aggregates near the surface. Mucosa gets bound down to muscle and fibrosis occurs
61
Site of Eoe? How does this compare to gerd?
Pan-esophageal. Gerd is distal.
62
Are there symptoms of Barrett esophagus?
No
63
What is considered short segment BE?
<3 cm
64
How does cancer develop from barrett
Progression from intestinal metaplasia to increasingly dysplastic mucosa finally to malignancy. This takes many years. Must be monitored with biopsies
65
See slide deck for histology of dysplasia
Do it
66
Barrett adenocarcinoma survival rate?
5 year survival is 15%. Incidence has been increasing in last 30 years.
67
Squamous cell carcinoma risk factors
Dietary deficiency/toxins/biomass burning in developing countries. Alcohol and smoking in developed countries. Males >> females. African Americans
68
What do symptoms of squamous cell carcinoma suggest?
Advanced disease. Progressive dysphagia (solids -> liquids) Weight loss, hemoptysis
69
Gross appearance of squamous cell carcinoma
Ulcer on top of mass lesion
70
Gross appearance of adenocarcinoma
Ulcerating stricturing mass
71
Slide of squamous cells invading tissues together
Know this. It's SCC
72
Most death from SCC due to?
Local complications, not mets. Can compress mediastinal structures.
73
Know slide of squamous cell dysplasia
Do it

GI/Liver Pathology (1 decks)

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