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G.I & Nutrition > Esophageal Pathophysiology > Flashcards

Esophageal Pathophysiology Flashcards

1
Q

3 functions of esophagus

A

propel swallowed food into stomach, prevent gastroesophageal reflux/clear refluxed material back into stomach, vomiting and belching

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2
Q

What does the upper esophageal sphincter separate?

A

pharynx from esophagus –> high pressure zone

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3
Q

3 muscles of esophageal sphincter

A

inferior pharyngeal sphincter, cricopharyngeus, cervical/proximal esophagus

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4
Q

Is the esophageal sphincter smooth or striated?

A

striated muscle

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5
Q

Functions of upper esophageal sphincter

A

barrier between pharynx and esophagus, prevents air entry into GI tract, and prevents reflux of gastric contents into pharynx

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6
Q

What structure anchors the gastroesophageal junction?

A

phreno-esophageal ligament

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7
Q

2 sphincters of the gastroesophageal junction

A

lower esophageal sphincter, diaphragm

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8
Q

Barrier between esophagus and stomach

A

gastroesophageal junction and its two sphincters

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9
Q

Is the lower esophageal sphincter smooth or striated?

A

smooth

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10
Q

Expansion of the chest by contraction of the diaphragm leads to increase/decrease in pressure on the LES?

A

increase

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11
Q

In what condition does LES pressure not depend on diaphragmatic contraction?

A

hiatal hernia

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12
Q

What condition is the most common cause of compromise of the phrenoesophageal ligament?

A

obesity

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13
Q

What kind of epithelial lining is there in the esophagus?

A

squamous epithelia

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14
Q

Does the esophagus have a serosal layer?

A

no, just an adventitia

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15
Q

What anatomic feature of the esophagus makes esophageal cancer so bad?

A

lymphatics in the esophagus come up to the surface epithelium –> easy cancer spread

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16
Q

Voluntary component of swallowing

A

voluntary bolus movement into pharynx –> everything past upper esophageal sphincter is involuntary

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17
Q

What is the initiator of involuntary esophageal activity?

A

act of swallowing voluntarily

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18
Q

What brain area controls voluntary component of swallowing?

A

cortex

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19
Q

What afferent nerve pathway brings information from the esophagus to the brain?

A

nucleus tractus solitarius (NTS)

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20
Q

Which brain nucleus controls the skeletal muscle of the upper esophagus and the diaphragm?

A

nucleus ambiguus

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21
Q

Which brain nucleus controls the smooth muscle of the esophagus?

A

dorsal motor nucleus

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22
Q

What is the functional difference in innervation of esophageal smooth vs striated muscle?

A

smooth muscle has an intermediate connection in the myenteric plexi before connecting with tracts; striated muscle has a direct neural connection

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23
Q

What 2 kinds of neural pathways originate in the dorsal motor nucleus?

A

caudal inhibitory and rostral excitatory pathways

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24
Q

Which neural pathway from the dorsal motor nucleus is activated first upon swallowing?

A

inhibitor pathways –> simultaneous inhibition of the entire smooth muscle esophagus (distal > upper)

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25
Q

Which neural pathway from the dorsal motor nucleus is activated second upon swallowing?

A

sequential activation of excitatory pathways –> variable inhibition of the esophagus means that the proximal part of the esophagus will start contracting when excited before the distal esophagus –> peristalsis

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26
Q

Are there more noncholinergic nerves in the distal esophagus or the proximal esophagus?

A

More noncholinergic in the distal esophagus to ensure more inhibition in the first phase of swallowing

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27
Q

Is the lower esophageal sphincter open or closed at rest?

A

tonically closed at rest

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28
Q

After swallowing, does pressure on the LES increase or decrease?

A

pressure falls within 1.5-2.5 seconds of swallowing –> stays low for 5-6 seconds until bolus arrives

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29
Q

What molecule mediates the inhibitory pathways in the esophageal smooth muscle?

A

NO

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30
Q

What molecule mediates the excitatory pathways in the esophageal smooth muscle?

A

ACh

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31
Q

What are the three mechanisms involved in regulation of LES tone?

A
  1. basal tone of the muscle, 2. NO inhibition, 3. ACh excitation
32
Q

Relaxation of the lower esophageal sphincter in response to gastric distension, lasting for 10 to 30 seconds and resulting in gastroesophageal reflux or belching.

A

Transient LES relaxation

33
Q

What is the trigger for TLESR?

A

distension of the stomach leads to vagal afferent stimulation which results in transient esophageal sphincter relaxation

34
Q

Perception that there is an impediment to the normal passage of swallowed material.

A

dysphagia

35
Q

Sensation of pain on swallowing.

A

odynophagia

36
Q

Sensation of an object in esophagus when there is non.

A

globus

37
Q

Is globus associated with difficulty swallowing?

A

no

38
Q

Effortless return of gastric contents into chest or mouth.

A

regurgitation

39
Q

Burning feeling rising from stomach or lower chest up towards neck.

A

heartburn

40
Q

Classic barium xray sign of achalasia.

A

bird’s beak

41
Q

What does manometry on achalasia look like?

A

LES contraction but no contraction along rest of esophagus or gastroesophageal junction

42
Q

Pathogenesis of achalasia

A

decrease in myenteric neurons in distal esophagus, especially NO releasing neurons –> no initial inhibition of esophagus

43
Q

2 pathologic features of achalasia on histology

A

inflammation of myenteric nerves and ganglion, scarring of nerve with minimal residual inflammation

44
Q

Gender preference for achalasia

A

none –> both M/F

45
Q

Peak age group for achalasia

A

30-60

46
Q

Incidence of achalsia

A

1/100,000

47
Q

Etiology of achalasia

A

unclear –> maybe viral, autoimmune, neurodegenerative

48
Q

Pseudoachalasia

A

looks like achalasia but due to primary GEJ cancer, metastases of lung, breast, pancreatic cancer, or benign mesenchymal tumors, pseudocysts, or amyloid

49
Q

Are medications effective in achalsia?

A

no

50
Q

What are the endoscopic/surgical treatments for achalasia and are they effective?

A

botulinum, pneumatic dilation, Heller myotomy, POEM –> temporary fixes with drop in success during years after surgery

51
Q

What is a Heller myotomy?

A

basically a fundoplication of the LES to resolve achalasia

52
Q

What is POEM?

A

In this procedure, performed in the operating room under general anesthesia, a flexible endoscope is passed into the esophagus, a mucosal flap and a submucosal tunnel is created. This tunnel extends onto the stomach. The inner circular muscle layer of the lower esophagus and sphincter (LES) is identified and a myotomy is started 3-4cm distal to the mucosal flap and carried all the way onto the stomach. –> basically separate the two muscle layers to keep the GEJ open

53
Q

A condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications.

A

GERD: Gastroesophageal reflux disease

54
Q

Criteria for GERD (2)

A

> =2 heartburn episodes/week and adversely affecting individual’s well being

55
Q

Elements of body that protect against GERD

A

saliva in esophagus, diaphragm, LES, peristalsis

56
Q

Pathogenesis of GERD

A

Loss of “defense”: any compromise of the elements that protect against GERD –> reduced saliva, decreased resting LES tone, peristalsis inhibition, impaired esophageal clearance, impaired tissue resistance
or
Increased “offense”: hernia, increased distension of stomach and TLESR, delayed gastric emptying, bile reflux

57
Q

In absence of hiatal hernia, what is the primary etiology of GERD?

A

transient LES relaxation (TLESR) > low LES pressure > strain + low LES pressure (e.g. bending over with weakened LES)

58
Q

2 mechanistic links between obesity and GERD

A
  1. increased pressure in abdomen

2. separation of diaphragm from GEJ

59
Q

What does GERD look like under endoscopy?

A

looks like a normal esophagus most of the time but can have mucosal breaks, scarring, Barrett’s segment

60
Q

Tx for GERD

A

lifestyle measures (most effective), antisecretory therapy (H2 blockers or PPIs), antireflux surgery

61
Q

The major precursor to Barrett’s esophagus

A

GERD

62
Q

What is the key histologic feature of Barrett’s esophagus?

A

metaplasia of esophageal lining from squamous to columnar

63
Q

Risk factors for Barrett’s

A

Males, Caucasians, increasing age, GERD, smoking, central obesity

64
Q

Pathophysiology of Barrett’s

A

Increased permeability of esophagus due to toxicity from reflux contents results in dilated intercellular spaces –> contact of noxious substances with the basal cells induces metaplasia (unclear whether it is trans-differentiation of existing cells, change in stem cells, or other etiology)

65
Q

What transcription factors are suspected to be the key modulators of Barrett’s metaplasia?

A

basal cell CDX and BMP4

66
Q

How does Barrett’s turn into cancer?

A

the usual way –> inflammation, lots of proliferation, oxidative stress –> DNA damage –> cancer

67
Q

Can esophageal cancer be resolved via endoscopic surgery?

A

if early stage –> endoscopic mucosal resection +/- radiotherapy ablation of mucosa is effective

68
Q

Endoscopic signs of eosinophilic esophagitis

A

rings, linear furrows, food obstruction, white exudate/eosinophilic pus

69
Q

Diagnostic criteria for eosinophilic esophagitis

A

esophageal and/or upper GI symptoms with >= 15 eosinophils/hpf in >=1 biopsy specimen in the absence of GERD (failure to respond to PPI or normal pH monitoring)

70
Q

Risk factors for eosinophilic esophagitis

A

Males, average age either 9 or 38

71
Q

Clinical presentation of eosinophilic esophagitis in adults

A

dysphagia, food impaction, heartburn/regurgitation, chest pain, abdominal pain, odynophagia

72
Q

Etiology of eosinophilic esophagitis

A

Th2 mediated allergic response to inhaled or consumed allergens –> IL4, 5, 13 –> production of eotaxin3 –> signals eosinophils and mast cells to esophagus

73
Q

What kind of cell type is implicated in eosinophilic esophagitis?

A

Th2 cells

74
Q

Main complication of eosinophilic esophagitis

A

fibrosis and scarring of esophagus

75
Q

What is the primary signaling protein implicated in eosinophilic esophagitis?

A

eotaxin 3

76
Q

Tx of eosinophilic esophagitis

A

dietary (get rid of allergen foods like milk, gluten), dilation, PPI, topical steroids,

G.I & Nutrition (43 decks)

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