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GI Pathology > Esophagus > Flashcards

Esophagus Flashcards

1
Q

Atresia

A

Incomplete development

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2
Q

Tracheoesophageal fistula

A

Abnormal connection b/w 2 tubes (this case = esophagus and trachea)

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3
Q

What is TE fistula?

A

Congential defect w/connection b/w esophagus and trachea

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4
Q

Most common variant of TE fistula?

A

Proximal esophageal atresia w/distal esophagus arising from stomach

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5
Q

Presentation of TE fistula?

A

Vomiting, polyhydramnios (excess amniotic fluid b/c baby can’t remove any via swallowing), abdominal distension (air entering stomach), and aspiration (gastric contents coming up into trachea)

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6
Q

Esophageal web?

A

Thin protrusion of esophageal mucosa

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7
Q

What is esophageal web found?

A

Most often upper esophagus

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8
Q

Presentation of esophageal web?

A

Dysphagia w/poorly chewed food

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9
Q

Esophageal web increases risk of?

A

Esophageal squamous cell carcinoma

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10
Q

Plummer-Vinson Syndrome/Patterson-Brown-Kelly Syndrome? (4)

A

Severe iron deficiency anemia
Esophageal web
Beefy red tongue due to atrophic glossitis and exposed BV
Cheilosis (inflammation at corners of mouth)

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11
Q

Esophageal rings - Schatzki A and B

A

Similar to webs but circumferential and thicker

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12
Q

Rings include…

A

Mucosa and submucosa (and sometimes hypertrophic muscularis propria)

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13
Q

A rings

A

Above gastroesophageal junction (GEJ) - A (squamous mucosa)

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14
Q

B rings

A

Below gastroesophageal junction - B (gastric cardia-type mucosa)

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15
Q

Diverticulae

A

Outpouching of pharyngeal mucosa thru an acquired defect in muscular wall

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16
Q

Esophageal diverticula

A

FALSE diverticulae b/c lack true muscularis involvement

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17
Q

How to get diverticulae

A

Disordered swallowing

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18
Q

Presentation of diverticula

A

Dysphagia, obstruction, and halitosis (due to rotting food stuck in throat)

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19
Q

Types of esophageal diverticula

A

Zenker (above UES)
Epiphrenic (above LES)
Traction (midpoint of esophagus)

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20
Q

Esophageal lacerations/Mallory Weiss tears

Mallory-Weiss Syndrome

A

Longitudinal laceration of mucosa at GEJ

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21
Q

Lacerations caused by

A

Severe vomiting

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22
Q

Presentation of lacerations

A

Painful hematemesis

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23
Q

Expect w/lacerations (2 diseases)

A

Alcoholism or bulimia

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24
Q

Pathophys of Mallory Weiss Syndrome?

A

Reflex relaxation of GE musculature precedes antiperistaltic contractile wave associated w/ vomiting –> this fails during prolonged vomiting and gastric contents overwhelm gastric inlet –> esophageal wall stretches and then tears

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25
Q

Achalasia

A

A = w/out
Chalasis = relaxation
Disordered esophageal motility w/inability to relax LES

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26
Q

Cause of achalasia

A

Damaged ganglion cells in myenteric plexus (b/w IC and OL of ME, important for regulating bowel motility and LES relaxation)

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27
Q

Damage to myenteric plexus ganglion cells is…

A 
Primary = idiopathic 
Secondary = Chagas disease (caused by Trypanosoma cruzi)
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28
Q

Clinical features of Achalasia (5)

A
  1. Dysphagia for solids and liquids (b/c need peristalsis to move both down esophagus)
  2. Putrid breath (accumulation of rotten food in esophagus)
  3. High LES pressure on esophageal manometry
  4. Bird break sign on barium swallow study (inability to relax LES –> dilation of esophageal wall as food/liquid build up in esophagus)
  5. Increased risk for esophageal squamous cell carcinoma
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29
Q

Tx for Achalasia

A

Botox, laparoscopic myotomy, pneumatic balloon dilation

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30
Q

Pathophys for achalasia

A

Increased tone of LES because of impaired smooth muscle relaxation. Normally NO and VIP are released from inhibitory cells and cholinergic signaling is interrupted to allow for LES relaxation.

31
Q

Hiatal hernia - definition

A

Protrusion of stomach through diaphragmatic hiatus into thorax

32
Q

2 types of hiatal hernia

A

Sliding and paraesophageal

33
Q

Sliding hiatal hernia

A

Most common type

Stomach herniates into esophagus so there is reflux into esophagus and increases risk for GERD

34
Q

Paraesophageal hiatal hernia

A

Part of stomach herniates into thorax beside the esophagus
Less common
Classic Sx: bowel sounds in lower lung fields
If congenital –> less space for lung to develop so there is lung hypoplasia

35
Q

Cause of GERD

A

Reflux of acid from stomach due to decreased LES tone

36
Q

Risk factors for GERD (6)

A

Alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal hernia (sliding type)

37
Q

Clinical fx for GERD (5)

A
  1. Heartburn (mimics cardiac chest pain)
  2. Asthma (due to airway irritation from gastric reflux) and cough
  3. Damage to enamel of teeth
  4. Ulceration w/stricture and Barrett esophagus (late complications) as well as melena and hematemesis
  5. Noticeable regurgitation of sour-tasting gastric contents
38
Q

Why do you see stricture as complication of GERD?

A

Acid erosion –> ulceration (taking out a chunk of mucosa and a bit of submucosa) –> kills stem cells –> healing then involves fibrosis –> thickening of wall –> narrows lumen

39
Q

Pathophys of GERD?

A

Nonkeratinized SSE of esophagus has a very linear epi w/LP and is resistant to food abrasion but sensitive to acid
Increased submucosal glands production will secrete mucin and bicarb
LES tone keeps gastric contents out of esophagus so anything that decreases LES tone (risk factors!) or increase abdominal pressure (b/c gastric contents are under + pressure)

40
Q

Tx for GERD

A

Proton pump inhibitors (PPI) or H2 R antagonists

41
Q

Z line

A

Line b/w gastric mucosa (cardia) and esophageal mucosa

42
Q

Normal esophageal mucosa

A

White b/c it doesn’t have metabolically active mucosa (unlike say the stomach)

43
Q

Early mucosal changes in GERD (5)

A

Thickening of SSE, prominence of lamina propria papillae, and intraepithelial inflammation

44
Q

Intestinal (Barrett) metaplasia (2)

A

Increased glandular production in submucosa that secrete mucin and bicarb
Change from SSE to nonciliated columnar epi (NCCE) w/goblet cells

45
Q

What causes the intestinal metaplasia?

A

Esophageal stem cells to acidic stress

46
Q

Why called specialized intestinal metaplasia?

A

Goblet cells + mucous cells –> acid mucus (normal gastric mucous cells produce neutral mucus
Full features of intestinal mucosa (e.g. Paneth cells) not seen

47
Q

Barrett’s Esophagus can progress to….

A

Dysplasia and adenocarcinoma

48
Q

Dysplasia (3)

A 
Increased nuclear size, disordered
nuclear polarity (linear basal region of epi becomes more chaotic), and prominent mitotic figures
49
Q

Classic presentation of Barrett’s

A

White males b/w 40-60

50
Q

Morphology of Barrett’s Esophagus

A

Red velvety mucosa alternating w/normal smooth, pale SSE mucosa and light brown columnar (gastric) mucosa

51
Q

Other complications of Barrett’s Esophagus

A 
Peptic ulcer (normally only seen in stomach and duodenum) 
Stricture
52
Q

Esophageal varices

A

Dilated submucosal veins in lower esophagus

53
Q

Esophageal varices arise secondary to…

A

portal HTN

54
Q

Portal HTN

A

Distal esophageal vein normally drains into portal vein via L gastric vein. L gastric vein gets backed up into esophageal vein w/portal HTN so as a result the esophageal veins dilate

55
Q

Associate esophageal varices w/

A

Alcoholics and cirrhosis (thus portal HTN)

56
Q

Sx of esophageal varices

A

Painless hematemesis w/rupture, otherwise is ASx

57
Q

Most common cause of death in pts w/cirrhosis

A

Ruptured esophageal varices

58
Q

Pathophys behind death from ruptured esophageal varices and cirrhosis

A

Liver isn’t functioning so not producing adequate coagulation factors –> have a functional coagulopathy and so if hemorrhage occurs (b/c varices rupture) then it is a bleed w/out ability to seal it

59
Q

Sx of hemorrhage from ruptured varice

A

Pain, anemia, tarry vomit/stool (melena) (thus bleeding Sx)

60
Q

Tx of hemorrhage from ruptured varice

A

Band ligation of sclerotherapy (endoscopic injection of thrombotic agents), octreotide (inhibits vasodilation), and ceftriaxone

61
Q

Adenocarcinoma of esophagus

A

Malignant proliferation of glands (produce acidic mucin)

62
Q

Are glands normal in esophagus?

A

NO!

63
Q

Most common esophageal carcinoma in West

A

Adenocarcinoma

Think white, men, developed countries

64
Q

Cause of esophageal carcinoma?

A

Preexisting Barrett’s esophagus

65
Q

In what part of esophagus is esophageal carcinoma found?

A

Lower 1/3 of esophagus (and may invade gastric cardia)

66
Q

Squamous Cell Carcinoma (in esophagus)

A

Malignant proliferation of squamous cells

67
Q

Most common esophageal carcinoma WW

A

Squamous cell carcinoma

Think AA, men, >45 (for West)

68
Q

In what part of esophagus is esophageal squamous cell carcinoma found?

A

Upper or middle 1/3 of esophagus

69
Q

Risk factors for squamous cell carcinoma (5) –> all irritate mucosa

A
  1. Alcohol and tobacco (most common causes)
  2. Very hot tea/beverages
  3. Achalasia
  4. Esophageal web (e.g. Plummer-Vinson Syndrome)
  5. Esophageal injury (e.g. lye ingestion)
70
Q

Microscopic features of squamous cell carcinoma (well-differentiated)

A

Keratin pearls and intercellular bridges

71
Q

Prognosis for esophageal carcinoma

A

Presents late –> poor

72
Q

Sx for esophageal carcinoma (squamous cell or adenocarcinoma) (4)

A
  1. Progressive dysphagia (solids to liquids)
  2. Wt loss
  3. Odynophagia (pain w/swallowing)
  4. Hematemesis
73
Q

2 more Sx for sqamous cell carcinoma

A
  1. Hoarse voice (b/c of recurrent laryngeal n involvement, seen in upper part of esophagus)
  2. Cough (b/c of tracheal involvement)
74
Q

Location of lymph node spread depends on level of esophagus involved –> 3 levels

A

Upper 1/3 = cervical nodes
Middle 1/3 = mediastinal or tracheobronchial nodes
Lower 1/3 = celiac and gastric nodes

GI Pathology (5 decks)

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