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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
Q

Dysphagia for solids only

A

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.

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26
Q

Dysphagia for solids and liquids

A

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

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27
Q

What is the first step in the evaluation of dysphagia

A

Structural study – endoscopy or barium swallow

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28
Q

Achalasia

A

Loss of inhibitory ganglion cells to myenteric plexus, this causes tonic contraction of the LES.

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29
Q

What eventually happens in achalasia if severe

A

Aperistalsis due to prolonged contraction against hypertonic LES

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30
Q

Symptoms of Achalasia?

A

Dysphagia, regurgitation, chest pain

31
Q

Barium swallow for achalasia? How about if severe?

A

Bird Beak in distal esophagus. Shows air fluid level if severe due to aperistalsis

32
Q

Manometry for achalasia

A

No receptive relaxation, high tone (+60) instead of 20.

33
Q

How to treat achalasia

A

Botox, pneumatic dilation with balloon, myotomy to cut muscles

34
Q

What causes pseudo-achalasia?

A

Chagas’ Disease

Cancer of the GE junction

35
Q

Scleroderma

A

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
Q

Manometry of scleroderma

A

Low amplitude tracings with no rhyme or reason, low LES p and poor motility.

37
Q

Diffuse esophageal spasm

A

Can cause chest pain, odynophagia. Corkscrew esophagus on x-ray. LES is usually normal. Treat with muscle relaxants or CCBs.

38
Q

Manometry of diffuse esophageal spasm

A

Simultaneous prolonged contractions that are repetitive even without a swallow.

39
Q

nutcracker esophagus

A

Pressures of swallow can reach 400! Normal peristalsis and LES

40
Q

Histological layers of the esophagus

A

Mucosa, submucosa/muscularis mucosae (shock absorber between mucosa and smooth muscle, contains glands/ducts and meissner’s plexus), muscularis propria with myenteric plexus

41
Q

How are esophageal squamous cells generated?

A

They arise from basal cells which desquamate and keratinize as they move up.

42
Q

Z line

A

Gastoesophageal junction.

43
Q

Chemical esophagitis

A

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
Q

Steps of immediate damage in chemical esophagitis

A

Necrosis, saponification, perforation, can lead to death

45
Q

1 month consequences post chemical ingestion?

A

Ulcer, scarring, stricture

All leading to dysphagia

46
Q

Worst consequence long term of chemical esophagitis?

A

Squamous cell carcinoma

47
Q

Pill esophagitis

A

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
Q

Bisphosphonate damage to esophagus

A

Things like fosamax and cause huge ulcers and strictures in lower esophagus

49
Q

Common sites of corrosive injury

A

Where esophagus is consticted due to regional anatomy like aortic arch, left main bronchus, Left atrium.

50
Q

Candida esophagitis

A

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
Q

CMV esophagitis

A

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
Q

Herpes esophagitis

A

Can happen in immunocompetent or immunocompromised hosts. Infects squamous cells and causes vesicles/ulcers.

53
Q

Histologic signs of herpes esophagitis

A

Cell-cell detachment, multinucleation, and ground class nuclei.

54
Q

Best place to biopsy if viral esophagitis suspected?

A

At the border between squamous epithelium and ulcer. Get both CMV and herpes.

55
Q

Histology of Reflux esophagitis

A

Congested capillaries as a reaction to acid. Edema between squamous cells, ballooned squamous cells, basal cell hyperplasia and eosinophils

56
Q

Peptic (reflux associated) ulcer

A

Necrotic tissue, fibrosis, and granulation tissue in biopsy

57
Q

Complications of reflux esophagitis

A

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
Q

Eosinophilic esophagitis

A

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
Q

Gross appearance of eosinophilic esophagitis

A

Transverse rings (trachealization) longitudinal furrows, tiny white mucosal plaques that are made up of eosinophils

60
Q

Histology of eosinophilic esophagitis?

A

Eosinophil aggregates near the surface. Mucosa gets bound down to muscle and fibrosis occurs

61
Q

Site of Eoe? How does this compare to gerd?

A

Pan-esophageal. Gerd is distal.

62
Q

Are there symptoms of Barrett esophagus?

A

No

63
Q

What is considered short segment BE?

A

<3 cm

64
Q

How does cancer develop from barrett

A

Progression from intestinal metaplasia to increasingly dysplastic mucosa finally to malignancy. This takes many years. Must be monitored with biopsies

65
Q

See slide deck for histology of dysplasia

A

Do it

66
Q

Barrett adenocarcinoma survival rate?

A

5 year survival is 15%.

Incidence has been increasing in last 30 years.

67
Q

Squamous cell carcinoma risk factors

A

Dietary deficiency/toxins/biomass burning in developing countries. Alcohol and smoking in developed countries. Males&raquo_space; females. African Americans

68
Q

What do symptoms of squamous cell carcinoma suggest?

A

Advanced disease. Progressive dysphagia (solids -> liquids) Weight loss, hemoptysis

69
Q

Gross appearance of squamous cell carcinoma

A

Ulcer on top of mass lesion

70
Q

Gross appearance of adenocarcinoma

A

Ulcerating stricturing mass

71
Q

Slide of squamous cells invading tissues together

A

Know this. It’s SCC

72
Q

Most death from SCC due to?

A

Local complications, not mets. Can compress mediastinal structures.

73
Q

Know slide of squamous cell dysplasia

A

Do it

GI/Liver Pathology (1 decks)

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