Esophageal Motility Flashcards

1
Q

Describe the control of GI motility

A

It is the controlled by the interaction of the CNS, ANS, and the ENS (neurons located in the gut wall) as well as other factors including neurotransmitters, and neurohumoral factors such as serotonin, food, and mechanical stretch

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2
Q
A
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3
Q

Describe the ENS

A

It is present all the way from the esophagus to the rectum and is comprised of two components, the myenteric (between the circular and longitudinal muscle layers) and Meissner (in the submucosa) Plexuses

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4
Q

How does peristalsis of the GI tract occur in basic terms?

A

It results from pacing set by the pacemaker cells of the ENS, the interstitial cells of Cajal in the myenteric plexus

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5
Q

Describe interstitial cells of cajal

A

These are located in the ENS throughout the entire length of the GI tract, and generate rythmic slow waves which lead to peristalsis at variables depending on their location in the tract

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6
Q

Describe esophageal motility

A

The upper esophageal sphincter consists of striated muscle so it is under voluntary control (i.e.problems in things like muscular dystrophy) and the muscle transitions to smooth muscle along the length

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7
Q

What controls relaxation of the lower esophageal sphincter?

A

NO released from the vagus nerve

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8
Q

What are some conditions/diseases that primarily affect the upper regions of the esophagus?

A

skeletal muscle diseases such as myasthenia gravis, muscular dystrophy, polymyositis, etc.

whereas smooth muscle involved conditions such as scleroderma and achlasia mostly affect the lower parts

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9
Q

What are the different phases of peristalsis in the esophagus?

A

primary peristalsis- the reflex initial peristaltic contractive wave associated with swallowing

secondary peristalsis- peristaltic waves assoicated with clearing residual food

tertiary peristalsis- nonperistaltic contractions associated with pathology such as GERD

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10
Q

How does the fundus of the stomach react to a bolus of food from the LES?

A

it undergoes receptive relaxation to accomodate food entry (pts. that dont have this can experience bloating and early satiety) and waves press food into the pyloric region until it is small enough (1mm) to pass into the duodenum

NOTE: The gastric pacemaker is set as 3 cycles/min

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11
Q

Describe the motor pattern of the small bowel during fasting states

A

During fasting the main function of the contractions of the small bowel is maintainence to keep it as sterile as possible. It is comprised of four distinct, but connected phases and is governed by migrating motor complexes

  • Phase 1-motor quiescence (40-60%)
  • Phase II-increasing but irregular contraction (20-30%)
  • Phase III-intense rhythmic contraction (10%)
  • Phase IV-is a transition from phase III to I (0-5%)
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12
Q

What would lack of MMCs in the small bowel, as commonly seen in old age or with neuropathy, cause?

A

risk of bacterial overgrowth which can lead to diarrhea

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13
Q

What is achlasia?

A

failure of the LES to relax upon swallowing resulting in dysphagia

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14
Q

What causes achalasia?

A

It has unknown etiology (possible autoimmune, degenerative, or infectious) but results from selective loss of post-ganglionic inhibitory neurons (no NO)

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15
Q

How does achalasia present histologically?

A

lymphocytic infiltrate in the myenteric plexus with loss of ganglion cells

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16
Q

What are the symptoms of achalasia?

A

Primarily dysphagia for both solids and liquids, and commonly:

chest pain in the xiphoid process area (40%)- food will become fermented to lactic acid causing inflammation and esophagitis

heart burn (40%)

weight loss (60%)

-regurgitation of food

17
Q

What is Allgrove syndrome?

A

Individuals affected by AAA have adrenal insufficiency/Addison’s disease due to ACTH resistance, alacrima (absence of tear secretion), and achalasia (a failure of a ring of muscle fibers, such as a sphincter, to relax) of the lower esophageal sphincter at the cardia which delays food going to the stomach and causes dilation of the thoracic esophagus.

There may also be signs of autonomic dysfunction with AAA, such as pupillary abnormalities, an abnormal reaction to intradermal histamine, abnormal sweating, orthostatic hypotension, and disturbances of the heart rate.[5] Hypoglycemia (low blood sugar) is often mentioned as an early sign.[4]The disorder has also been associated with mild mental retardation.[4]

The syndrome is highly variable. Managed effectively, affected individuals can have a normal lifespan and bear children.

18
Q

How is achalasia diagnosed?

A

start with an H&P and then move to endoscopy to rule out any inflammation, malignancy, or stricture. Once that occurs, perform a barium radiography. Confirm with a manometry

19
Q

Notice the esophageal dilation– in acute causes of dysphagia such as malignancy, the esophagus does not have enough time to dilate proximal to the stricture

A
20
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21
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22
Q

What is classic appearance of the lwoer esophagus on barium testing?

A
  • Can be use as primary screening test (diagnostic accuracy 95%)
  • Dilated esophagus with bird beak appearance of distal part
  • Severe dilatation can lead to sigmoid esophagus
  • Poor peristalsis on fluoroscopy
23
Q
A
24
Q

What are the 2 manometric requirements for confirmation of achalasia?

A
  • Incomplete LES relaxation (LES fail to relax in response to swallow)
  • Aperistalsis in the body of esophagus (distal 2/3)

Supportive feature hypertensive LES, Low amplitude esophgeal contraction

25
Q
A

Figure 6-7. Manometric tracing from a patient with achalasia of the esophagus. Simultaneous pressure measurements were made in the stomach, lower esophageal sphincter (LES), at three sites in the distal esophagus (5 cm apart), and at the pharynx. The subject was asked to swallow 5 mL of water for each of the three wet swallows (WS) shown in the tracing. Each swallow results in a pharyngeal contraction followed by a simultaneous pressure wave throughout the distal esophagus. The LES pressure is high (> 40 mm Hg), and there is incomplete relaxation of the LES in response to each of the swallows.

26
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27
Q

Note that medical tx does not work well and that botox does but only lasts for about 6-9 months and is less effective each time its given

A

There is also an ednoscopic tx called PERM

28
Q

Describe the difference between Heller’s Myotomy and PERM

A

Heller’s involved entering the peritoneum and cutting the muscular layers of the esophagus from the exterior while leaving the mucosal layers in tact, while PERM is more an endoscopic procedure which involves splicing the mucosa to make an incision in the muscular layers from the interior of the esophagus

29
Q

Describe how balloon dilation works with achalasia?

A

a balloon is inflated in/near the LES which causes tearing of the muscular layers (risk for perforation)

30
Q

What are some complications of achalasia?

A
  • Malnutrition
  • Aspiration
  • Malignancy: Untreated achalasia is associated with an increased risk of squamous cell esophageal cancer
31
Q

What are some diseases associated with achalasia-like motility disorder?

A
  • Malignancy, especially gastric carcinoma
  • Chagas disease, secondary to Trypanosoma cruzi infection
  • Amyloidosis
  • Sarcoidosis
  • Neurofibromatosis
32
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33
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