Motility Disorders of the Stomach and Small Bowel Flashcards
(197 cards)
1
Q
What controls the contractile activities of the stomach and small intestine?
A
The enteric (autonomic) neuromuscular system within the wall of the gut.
2
Q
What role do the parasympathetic/vagal nerves and sympathetic/paravertebral nerves play in gut motility?
A
They do not control or initiate motility but can influence motor patterns
3
Q
What are the two basic patterns of contractile activity in the stomach and small intestine?
A
One during fasting (interdigestive period) and another after feeding (postprandial period)
4
Q
What generates the contractile activity in the gut?
A
Spontaneously active neuromotor cells within the gut wall.
5
Q
What occurs during the interdigestive period in the stomach and small intestine?
A
Intense contractions cycle peristaltically, beginning in the stomach and moving slowly down the small intestine over 90 minutes to clear undigested food and debris.
6
Q
How do contractile patterns change during the postprandial period?
A
The stomach mixes and breaks down food particles for digestion, while the small intestine slows transit to maximize absorption
7
Q
What prevents larger food particles from leaving the stomach during the postprandial period
A
The antropyloric pump controls the size of the pylorus, only allowing particles smaller than 1 cm to pass.
8
Q
What role does the proximal stomach play in gastric emptying?
A
It controls the emptying of liquids through slow, continuous tonic activity and vagally mediated “receptive relaxation.”
9
Q
What type of contractions occur in the distal stomach?
A
Phasic contractions (2–4 per minute) arise from a pacemaker region in the mid-stomach and propagate distally to aid in the mechanical breakdown of food
10
Q
How do injuries to the vagus nerves affect gastric motility?
A
They can impair the relaxation of the proximal stomach (emptying of liquids) and disrupt the coordination of contractions of the distal stomach (emptying of solids)
11
Q
Where is the pacemaker region located in the small intestine, and what does it control?
A
It is in the proximal duodenum and controls the rate and direction of small intestinal contractions
12
Q
What is the length of a true peristaltic contraction in the small intestine after a meal?
A
It typically migrates only 5 to 10 cm.
13
Q
What is the purpose of the segmenting contraction pattern in the small intestine?
A
It increases contact of the luminal content with the mucosa, slows transit, and enhances absorption.
14
Q
What role does the sympathetic system play in small intestinal contractions?
A
It has modulatory (primarily inhibitory) effects, as seen in conditions like postoperative ileus (POI) or adynamic ileus caused by retroperitoneal trauma or infection
15
Q
What are common causes of gastric dysmotility seen by surgeons?
A
Operations that cut or injure the vagus nerves, such as gastrectomy, esophagectomy, and hiatal herniorrhaphy
16
Q
How can chronic illness contribute to gastric dysmotility?
A
Neuropathy from chronic conditions like poorly controlled diabetes can damage the vagus nerves
17
Q
What was a consequence of truncal vagotomy in past duodenal ulcer surgeries?
A
Rapid emptying of liquids leading to dumping syndrome and disrupted emptying of solids due to loss of vagally mediated relaxation
18
Q
What syndrome can occur after the creation of a Roux-en-Y limb?
A
Roux stasis syndrome, characterized by delayed gastric emptying due to erratic, noncoordinated contractions.
19
Q
What disrupts myoelectric continuity in a Roux-en-Y limb?
A
Transection of the jejunum, which affects the coordination of contractions with the duodenal pacemaker
20
Q
What is “gastroparesis-like syndrome” and who typically experiences it?
A
A poorly understood condition with symptoms similar to gastroparesis, usually occurring in young females, often without objective delay in gastric emptying.
21
Q
What are the two main types of true gastric motility disorders?
A
Delayed emptying (gastroparesis) and too rapid emptying (dumping syndrome)
22
Q
What role does the proximal stomach play in digestion?
A
It provides vagally mediated receptive relaxation for temporary storage and starts the enzymatic and mechanical breakdown of ingested content.
23
Q
How does the presence of amino acids in the duodenum affect the proximal stomach?
A
It triggers hormonal signaling that leads to a slow tonic contraction, increasing intraluminal pressure and emptying chyme into the duodenum.
24
Q
How do fats in the duodenum impact gastric emptying?
A
They slow gastric emptying by prolonging the relaxation of the proximal stomach
25
What factors can disrupt gastric emptying mediated by the enteric nervous system?
Surgical procedures, diabetes, hypothyroidism, chronic narcotic use, and cancer.
26
How does aging affect gastric emptying?
The rate of gastric emptying decreases with age, making older patients more susceptible to gastric motility disorders
27
What types of operations can lead to delayed gastric emptying?
Operations on the distal esophagus or stomach, including known or inadvertent vagotomy, Roux-en-Y gastrojejunostomy, and antireflux procedures.
28
How does the risk of delayed gastric emptying change after a gastrectomy with a truncal vagotomy?
The risk increases twofold
29
What is the rate of delayed gastric emptying after a classic pancreatoduodenectomy with Roux-en-Y reconstruction?
Up to 30%
30
What are key contributors to delayed gastric emptying after certain surgeries?
Vagus nerve dysfunction and disruption of the continuity between the proximal jejunum and the duodenal pacemaker
31
How can truncal vagotomy affect gastric motility?
It can disrupt afferent vagal signaling to the brain, leading to gastric stasis or atony.
32
What is a potential outcome of vagus nerve dysfunction after gastric surgery?
Incomplete gastric emptying or gastric stasis
33
What symptoms are commonly associated with true gastroparesis?
Epigastric fullness, early satiety, nausea, and vomiting, usually of solids more than liquids, with delayed vomiting of undigested food
34
What symptom is virtually pathognomonic of gastroparesis if there is no mechanical obstruction?
Delayed vomiting of undigested food hours or a day after ingestion.
35
What are the typical effects of gastroparesis on liquid and solid intake?
Liquids are better tolerated than solids, but early satiety and anorexia can still limit calorie intake, potentially leading to dehydration, weight loss, or malnutrition.
36
What risk factors should be evaluated in a patient with suspected gastroparesis?
Prior upper abdominal surgery and metabolic disturbances like diabetes or hypothyroidism
37
What physical exam finding may suggest delayed gastric emptying from mechanical obstruction?
A succussion splash
38
What mechanical obstructions should be excluded in the diagnostic phase of suspected gastroparesis?
Efferent limb syndrome, anastomotic stricture, or post-gastroenterostomy intussusception
39
What nutritional marker may be helpful in evaluating the nutritional state in gastroparesis?
Prealbumin, due to its shorter half-life compared to albumin
40
Why is it important to rule out NSAID or aspirin use in patients with an anastomotic stricture?
Because NSAIDs and aspirin can cause ulceration and anastomotic inflammation, which can contribute to stricture formation
41
What imaging technique can help rule out mechanical obstruction in suspected gastroparesis?
Abdominal x-rays with contrast.
42
Why is gastric distension uncommon in gastroparesis associated with vagal dysfunction?
Because it involves loss of proximal gastric relaxation rather than obstruction.
43
What is the gold standard test for diagnosing gastroparesis?
The 4-hour scintigraphic gastric emptying test for solids.
44
How is gastroparesis severity graded in the 4-hour scintigraphic gastric emptying test?
Based on percent retention at 4 hours: mild (<15%), moderate (16%-35%), and severe (>35%).
45
What alternative test to scintigraphy avoids radiation but is primarily used experimentally?
Wireless motility capsule (WMC).
46
What other test used in Japan is experimental for measuring gastric emptying in the United States?
Carbon breath testing.
47
Why is a barium swallow not recommended for assessing gastric emptying?
It is not a good measure of gastric emptying.
48
What is the initial step in treating gastroparesis?
Management of contributing factors, such as better glucose control or treatment of hypothyroidism.
49
What dietary modifications are recommended for patients with gastroparesis?
Ingesting more liquids than solids
eating smaller and more frequent meals (ideally six or more per day)
and following a low-residue, softer food diet
50
What types of liquid formulations are suggested for patients with nutritional challenges in gastroparesis?
High-calorie, high-protein, low-fat small particle liquid formulations, unless associated with problematic dumping syndrome > give high Protein Formula for Dumping
51
What prokinetic drugs may be tried if dietary changes do not alleviate gastroparesis symptoms?
Metoclopramide, domperidone (for patients with an antrum), and low-dose erythromycin (125 mg).
52
What is a key side effect of metoclopramide that physicians need to warn patients about?
Extrapyramidal side effects, such as spasmodic dystonias and tardive dyskinesia, especially in the elderly.
53
What are the concerns associated with domperidone, which is used outside the US?
Cardiovascular proarrhythmic risks, such as QT prolongation and tachyphylaxis
54
Why might erythromycin be used short-term for gastroparesis?
It can improve gastric emptying but may develop tachyphylaxis, requiring “drug holidays.”
55
What role do tricyclic antidepressants play in treating gastroparesis?
They may be considered for refractory nausea and vomiting, but they can potentially worsen symptoms due to their anticholinergic effects
56
When might total parenteral nutrition (TPN) or enteral nutrition be necessary for gastroparesis patients?
In severe and life-threatening cases of malnutrition; enteral nutrition should be tried before TPN.
57
What is a limitation of the newer 5HT3 antagonists and 5HT4 receptor agonists in gastroparesis treatment?
They may help with nausea and vomiting but do not increase effective gastric emptying.
58
When should operative intervention for gastroparesis be considered?
For patients with severe, medically refractory symptoms affecting quality of life and nutritional health.
59
What is essential before placing a jejunal feeding tube in gastroparesis patients?
A trial of nasoenteric feeding to evaluate tolerance
60
What indicates a poor prognosis for successful enteric feedings in gastroparesis patients?
Inability to tolerate feedings due to severe bloating or exacerbation of abdominal pain
61
What might be the only viable option for severe refractory gastroparesis when enteric feedings fail?
Total parenteral nutrition (TPN).
62
What is the purpose of a venting gastrostomy tube in gastroparesis?
To relieve gastric fullness or persistent vomiting.
63
Why should the volume loss from a gastrostomy tube be monitored?
To ensure volume replacement and prevent loss of bile salts, which may require reinfusion
64
What surgical approach might be considered for patients with postsurgical gastroparesis after a total vagotomy?
Near total or completion gastrectomy, but only in selected patients who tolerate enteric feedings
65
What recent interest has emerged in surgical treatments for gastroparesis?
Pyloroplasty and endoscopic procedures like G-POEM or per-oral pyloromyotomy (POP)
66
What preoperative measure should be considered before a pyloroplasty in gastroparesis patients?
Injection of botulinum toxin into the pylorus as a trial.
67
What is the potential role of sleeve gastrectomy in gastroparesis treatment?
It may increase gastric emptying, especially in patients with obesity or diabetes, but data are limited.
68
What is gastric electrical stimulation (GES), and who might it benefit?
A treatment involving an electrical stimulator implanted in the stomach wall, suggested for severe gastroparesis patients, particularly with diabetes or predominant nausea/vomiting
69
Does gastric electrical stimulation (GES) reliably increase gastric emptying?
No, GES may help with nausea and vomiting but does not reliably increase effective gastric emptying
70
Why is the use of gastric electrical stimulation (GES) considered controversial?
Success rates vary significantly among different groups, and it does not function like a cardiac pacemaker to “pace” the stomach.
71
What are symptoms of gastroparesis-like syndromes, and who is most affected?
Early satiety, nausea, and vomiting, often seen in young females in their 20s or 30s
72
How do symptoms of gastroparesis-like syndromes relate to objective gastric emptying results?
There is often poor correlation, with many patients having normal gastric emptying despite significant symptoms.
73
What alternative mechanisms might contribute to gastroparesis-like syndromes?
Impaired gastric accommodation and sensitization of vagal afferent pathways.
74
What is the initial step in diagnosing gastroparesis-like syndromes?
Excluding true gastroparesis with a formal radionuclide gastric emptying study.
75
What is the primary treatment focus for patients with gastroparesis-like syndromes?
Symptomatic treatment for nausea and vomiting, starting with antiemetics and antinausea medications.
76
Which antiemetic medications are typically used first for treating nausea in these patients?
Metoclopramide and 5HT3 receptor antagonists like ondansetron or granisetron.
77
What neuromodulator has been used for gastroparesis-like syndrome, and what were its results in studies
Tricyclic antidepressants, like nortriptyline, showed no improvement in nausea in a randomized controlled study.
78
Which agent has shown promise for treating nausea and improving appetite in gastroparesis-like syndromes?
Mirtazapine, due to its 5HT3 receptor antagonism.
79
What role does buspirone play in treating gastroparesis-like symptoms?
It may improve gastric accommodation, useful for patients with early satiety.
anxiolytic that is an agonist of the 5HT1A receptor
80
What is Gastric Electrical Stimulation (GES), and for whom is it FDA-approved?
A technique using serosal electrodes on the gastric antrum for "drug refractory disease.
81
What is the presumed mechanism of action for GES?
Modulation of vagal signaling, not improved gastric emptying.
82
What is diabetic gastroparesis primarily related to?
Poor glucose control and its effects on vagal nerve function.
83
How does the symptomatology of diabetic gastroparesis typically present?
It waxes and wanes in severity, making irreversible interventions usually inadvisable.
84
What initial steps are recommended for managing diabetic gastroparesis?
Better control of glucose intolerance and dietary modifications, along with pharmacologic agents used for other forms of gastroparesis.
85
How might insulin pumps benefit patients with diabetic gastroparesis?
They can lead to fewer hyperglycemic events, a decrease in HbA1c, and symptom improvement.
86
What is the role of a venting gastrostomy in diabetic gastroparesis?
It can relieve bloating symptoms, but continuous drainage should be avoided to prevent dehydration and bile salt loss
87
How should gastric resection be considered for diabetic gastroparesis?
It should be avoided in most patients, except in highly unusual and severe cases.
88
What role might Gastric Electrical Stimulation (GES) play in treating diabetic gastroparesis?
It may help with symptoms of vomiting and nausea, although it may not necessarily improve gastric emptying.
89
What is dumping syndrome, and how does it occur?
It is the overly rapid emptying of gastric contents into the duodenum or jejunum, commonly occurring after gastric operations involving a vagotomy.
90
What types of meals exacerbate symptoms of dumping?
Carbohydrate-rich or hyperosmolar liquid meals.
91
What was disproven as the primary cause of dumping symptoms?
The old theory that a rapid fluid shift into the gut causes relative hypovolemia.
92
What symptoms are commonly associated with early dumping syndrome?
Abdominal bloating, nausea, and the need to lie down after eating; diarrhea may occur but is not universal.
93
Which type of gastric surgery most frequently results in dumping syndrome?
Subtotal gastrectomy with vagotomy.
94
When do early dumping symptoms typically occur?
Within 30 minutes of eating.
95
How does late dumping differ from early dumping?
Late dumping occurs 90 minutes to 3 hours after eating and often involves symptoms of hypoglycemia and potentially diarrhea.
96
What causes hypoglycemia in late dumping syndrome?
High-calorie meals overwhelming insulin regulation, leading to a delayed insulin release and rapid reactive hypoglycemia
97
What are severe symptoms that can result from hypoglycemia in late dumping?
Disturbed thinking, seizures, and coma
98
What modern bariatric syndrome is similar to late dumping?
Noninsulinoma postprandial pancreatogenous hypoglycemia syndrome (NIPPS)
99
After which surgery is dumping syndrome most commonly seen today?
Roux-en-Y gastric bypass surgery.
100
Is dumping syndrome usually permanent after gastric bypass?
No, most patients do not have prominent or persistent symptoms after the first 3 months.
101
What percentage of patients with dumping syndrome present with early symptoms?
About 75%.
102
What should be included in the differential diagnosis for dumping syndrome?
Afferent loop syndrome
pancreatic insufficiency
and bowel obstruction after prior gastric surgery.
103
What symptoms are associated with early dumping syndrome?
Early satiety, abdominal pain, nausea, and autonomic dysfunction (e.g., racing heartbeat, sweating, dizziness, and tremors)
104
Is diarrhea common with early dumping syndrome?
No, diarrhea is not commonly associated with early dumping
105
How long do symptoms of early dumping typically last?
About an hour.
106
What triggers the release of vasoactive substances in early dumping syndrome?
The high osmolarity of the gastric contents.
107
What are the characteristic symptoms of late dumping syndrome?
Similar to early dumping but also include fatigue, mental changes, and fainting due to reactive hypoglycemia.
108
When does late dumping syndrome typically occur after a meal?
Approximately 90 minutes to 3 hours after eating
109
What test can be used to help confirm late dumping syndrome?
Provocative testing with 50 g of orally administered glucose followed by measurements of glucose, plasma insulin, heart rate, and symptoms.
110
What is the sensitivity and specificity of the heart rate increase and hydrogen breath excretion test for late dumping syndrome?
Sensitivity of 94% and specificity of 92%.
111
Is an upper GI series typically necessary for diagnosing dumping syndrome?
No, it may help define anatomy but is often not necessary, as the diagnosis is usually evident from patient symptoms and clinical context.
112
What is the primary treatment for dumping syndrome?
Dietary modification.
113
Which types of foods should patients with dumping syndrome avoid?
Simple sugars, alcohol, and most dessert-type food items
114
What simple dietary measure can help minimize dumping syndrome symptoms?
Avoiding drinking fluids 30 minutes before, during, and after meals
115
How can fiber supplements and complex carbohydrates benefit patients with dumping syndrome?
They help slow transit and alleviate symptoms.
116
What postural advice should be given to patients with dumping syndrome?
Patients should avoid an upright posture while eating and recline after meals
117
What medication may be used for patients with refractory dumping syndrome symptoms?
Octreotide
118
How should subcutaneous octreotide be administered for optimal effect?
30 minutes before a meal.
119
What side effect may occur with long-acting octreotide, and how can it be managed?
Steatorrhea, which can be managed with pancreatic enzyme replacement.
120
What outdated surgical procedure for severe diarrhea due to rapid gastric emptying is no longer recommended?
The use of a 10-cm reversed jejunal limb
121
What endoscopic procedure may benefit patients with late dumping syndrome and hypoglycemia after Roux-en-Y gastric bypass?
Endoscopic transoral outlet reduction (TORe)
122
What are potential surgical options for severe cases of late dumping syndrome?
Reversing the gastric bypass or redirecting the Roux limb into the duodenum
123
Why is subtotal pancreatectomy not recommended for hypoglycemia associated with late dumping?
It has proven to be ineffective in long-term outcomes
124
What is a true small intestinal “ileus,” and how common is it after intraabdominal operations?
It is very unusual and not commonly seen after intraabdominal operations.
125
What is a “physiologic ileus,” and when does it typically occur?
It is a transient form of ileus, occurring in the first 1 to 4 days postoperatively, often referred to as “postoperative ileus.”
126
What causes the transient postoperative ileus?
It is primarily a gastric and colonic response to abdominal wall trauma from a laparotomy
127
Is postoperative ileus a result of small bowel dysmotility?
No, small intestinal contractile activity is present during and after the operation
128
How can small intestinal contractile activity be demonstrated intraoperatively?
By “tweaking” the small bowel and observing it contract, unlike the stomach and colon
129
Can intraintestinal feeding be administered postoperatively?
Yes, it can be administered immediately as the small intestine functions relatively normally.
130
What causes the absence of “bowel sounds” in the early postoperative period?
The loss of gastric emptying of swallowed gas, which leads to the absence of the gas/liquid interface that produces bowel sound
131
What is adynamic ileus, and how does it differ from physiologic ileus?
Adynamic ileus is a rare, generalized motor disorder affecting the entire gut, involving the stomach, small intestine, and colon.
132
What are common causes of adynamic ileus?
Systemic inflammatory disorders (e.g., sepsis), retroperitoneal operations (e.g., kidney transplantation), or retroperitoneal conditions (e.g., trauma, hematoma)
133
What is isolated colonic ileus (colonic pseudo-obstruction), and what does it involve?
It involves only the colon, not the stomach or small bowel, and can complicate procedures like total hip arthroplasty or retroperitoneal operations
134
What symptoms are indicative of adynamic ileus?
Vomiting, bloating, abdominal distention, obstipation of stool and gas, and tinkling bowel sounds.
135
What is distinctly unusual in adynamic ileus compared to a mechanical small bowel obstruction?
Crampy abdominal pain
136
What imaging can confirm the diagnosis of adynamic ileus?
A simple abdominal radiograph showing dilation of the stomach, small intestine, and entire colon
137
What should be included in the differential diagnosis for adynamic ileus?
Exclusion of an obstructing rectal lesion, which may require proctoscopy or a transrectal contrast radiograph.
138
What is the primary treatment focus for adynamic ileus?
Treating the underlying cause, most commonly sepsis.
139
Are pharmacologic or operative interventions effective for adynamic ileus?
No, they are neither needed nor effective
140
What conservative management approach is commonly used for adynamic ileus?
The use of a nasogastric tube
141
Are prokinetic agents effective in treating adynamic ileus?
No, prokinetic agents are not effective.
142
What is the prognosis for adynamic ileus once the systemic cause is controlled?
It is transient and resolves when the underlying cause is treated.
143
What is the primary difference between POI and adynamic ileus?
POI is a physiologic response to abdominal wall trauma, while adynamic ileus is a pathologic response to conditions like infection.
144
Which parts of the gut are affected by POI?
POI involves the stomach and colon but not the small intestine.
145
Which parts of the gut are involved in adynamic ileus?
Adynamic ileus affects the entire gut, including the stomach, small intestine, and colon
146
How significant is POI in modern surgical practice, especially with the increase in laparoscopic operations?
POI is considered less relevant or problematic with the rise of laparoscopic surgeries
147
What has recent work with enhanced recovery after surgery (ERAS) shown about postoperative feeding?
Early postoperative feeding of the stomach or small intestine is beneficial and reinforces the lesser importance of POI
148
What common belief about POI has been disproven by studies?
The belief that POI is related to the extent of handling of the intestine has been disproven; it is more related to abdominal wall trauma and factors like opioid medications.
149
Which types of surgeries are less susceptible to POI?
Laparoscopic surgeries, such as laparoscopic colectomy.
150
What is a notable exception where gastric emptying recovery can be delayed postoperatively
After a distal gastrectomy when there has been mechanical obstruction of the gastric outlet and stomach dilation.
151
Are prokinetic medications effective for treating POI? after distal gastrectomy for gastric obstruction
Most prokinetic medications, including erythromycin, domperidone, and prucalopride, have minimal or no benefit for POI
152
What should be avoided when treating rare cases of delayed gastric emptying after distal gastrectomy?
Reoperation to “redo” the gastroenteric anastomosis should be avoided
153
What is chronic idiopathic pseudo-obstruction?
A family of rare heritable disorders that mimic mechanical small bowel obstruction with progressive and disorganized motility patterns.
154
What are the three most common forms of chronic idiopathic pseudo-obstruction?
Histopathologic myopathy of smooth muscle, histopathologic neuropathy, and neuromotor dysmotility without definitive histopathologic findings.
155
What is mitochondrial neurogastrointestinal encephalopathy disease (MNGIE)?
An extremely rare genetic cause of GI pseudo-obstruction with peripheral and GI dysfunction and associated neurological symptoms (e.g., ptosis/ophthalmoplegia, peripheral neuropathy, leukoencephalopathy), caused by a mutation in the thymidine phosphorylase gene
156
What characterizes the motility patterns in chronic idiopathic pseudo-obstruction?
Ineffective, uncoordinated contractile activity leading to intestinal distention and stasis.
157
Which organs can be initially affected by chronic idiopathic pseudo-obstruction?
The esophagus (megaesophagus), duodenum (megaduodenum), colon (megacolon), or urinary system (megaureter).
158
How does chronic idiopathic pseudo-obstruction progress over time?
It eventually affects all smooth muscle in the gut and genitourinary system to varying extents.
159
What type of biopsy is needed to diagnose chronic idiopathic pseudo-obstruction?
A full-thickness biopsy, not just an endoscopic biopsy, requiring specialized staining and reading.
160
What role does the autonomic nervous system play in chronic idiopathic pseudo-obstruction?
It leads to discoordinated contractile activity and ineffective transit in the gut
161
Can chronic idiopathic pseudo-obstruction be associated with neoplasms?
Yes, it is rare but possible as a paraneoplastic phenomenon mediated by an uncharacterized humoral agent
162
What is a common initial presentation of hereditary dysmotility syndromes?
Severe constipation, which may progress to involve the small intestine over time.
163
What inappropriate treatment have some patients with hereditary dysmotility syndromes received?
Colectomy for a diagnosis of colonic inertia
164
How can hereditary dysmotility syndromes mimic achalasia?
Patients may present with isolated megaesophagus, which eventually involves the distal gut over time
165
What is a common presentation of pseudo-obstruction in teenagers?
Megaduodenum of the first and second portion of the duodenum, often confused with superior mesenteric artery syndrome
166
What key aspect differentiates SMA syndrome from pseudo-obstruction?
SMA syndrome usually follows marked weight loss rather than preceding it.
167
Why should a family history be considered in patients with hereditary dysmotility syndromes?
These disorders are often familial and heritable, so there should be a history of esophageal, colonic, or genitourinary issues unless it is a new mutation
168
At what age do symptoms of intestinal pseudo-obstruction typically begin?
Symptoms often start in late childhood/early teenage years or may appear in the 20s and 30s.
169
What are common early symptoms of hereditary dysmotility syndromes?
Vague, chronic GI complaints such as substantial constipation, dysphagia, gastroesophageal reflux, or intermittent abdominal distention/cramping
170
What is a clinical clue that a patient may have a hereditary dysmotility syndrome?
A history of surgery for presumed mechanical small bowel obstruction without convincing evidence of such obstruction during exploration
171
How do the symptoms of hereditary dysmotility syndromes often behave over time?
They frequently wax and wane, raising questions about whether current symptoms are due to dysmotility or adhesions from prior surgery
172
How is the diagnosis of chronic idiopathic intestinal pseudo-obstruction typically made?
It is most often a diagnosis of exclusion, unless there is a strong family history
173
What is a key radiographic finding that suggests chronic idiopathic intestinal pseudo-obstruction?
Small intestinal and often gastric distention extending to the cecum without a clear transition point.
174
What should raise suspicion for chronic idiopathic intestinal pseudo-obstruction in younger patients?
A prior history of negative laparotomy
recurrent childhood complaints of abdominal distention or constipation
and no history of potential mechanical obstruction
175
Why is diagnosing chronic idiopathic intestinal pseudo-obstruction challenging?
Because it mimics mechanical obstruction, and delaying necessary operative treatment is a concern
176
What is a key finding during laparoscopic exploration that confirms the diagnosis of chronic idiopathic intestinal pseudo-obstruction?
Distention of the entire small intestine down to the cecum without any convincing site of obstruction
177
What might a previous operative note imply if a patient is suspected of chronic idiopathic intestinal pseudo-obstruction?
It may reveal the surgeon’s attempt to justify an obstruction that was not clearly identified, hinting at pseudo-obstruction
178
What has proven unreliable in diagnosing chronic idiopathic intestinal pseudo-obstruction?
Characterizing the motor (contractile) pattern and measuring the amplitude of contractions
179
What preoperative diagnostic tool is considered most reliable for chronic idiopathic intestinal pseudo-obstruction?
Diagnostic laparoscopic exploration for visualizing the distended bowel.
no signs of concurrent or prior obstruction, such as adhesions, hernia, or intraluminal mass.
180
What type of treatment is available for intestinal pseudo-obstruction?
Only symptomatic and supportive treatment.
181
Why should resections and internal bypasses be avoided in patients with intestinal pseudo-obstruction?
Because it is a progressive disorder involving the entire small intestine, making resections or bypasses ineffective
182
Is a full-thickness biopsy usually helpful in diagnosing intestinal pseudo-obstruction?
No, it is often debatable and most centers lack the expertise for specialized neuromuscular staining
183
Why should nonreversible treatments be avoided in the early course of intestinal pseudo-obstruction?
Because symptoms and severity tend to wax and wane, making irreversible procedures risky.
184
What supportive measure can be used when the disease affects the esophagus, stomach, and/or duodenum?
Intrajejunal feedings, to delay the need for chronic parenteral feeding
185
What becomes the mainstay of treatment in advanced stages of intestinal pseudo-obstruction?
Chronic parenteral nutrition
186
What procedure might be considered for chronic and symptomatic abdominal distention?
Decompressive tube enterostomy (not a formal enterostoma due to risk of stomal prolapse)
187
What alternative feeding measure can be taken if vomiting is problematic?
A venting tube gastrostomy, with careful fluid replacement
188
What is a potential treatment option for highly selected individuals with severe intestinal pseudo-obstruction?
Intestinal transplantation
189
When does small bowel involvement typically occur in the course of scleroderma?
Usually later in the disease course
190
Which part of the gastrointestinal tract is more commonly involved in scleroderma?
The esophagus, often presenting with gastroesophageal reflux.
191
What is the most prevalent finding in the small bowel wall of scleroderma patients?
myopathy with hypoplasia of the intestinal wall muscles.
leads to poor amplitude contractions and dyscoordination of contractile patterns, resulting in poor propulsion of luminal content.
192
What treatments have been attempted for small bowel dysmotility in scleroderma?
Pyridostigmine
octreotide
oral antibiotics for bacterial overgrowth
193
How common is postvagotomy diarrhea?
It is a very rare form of dysmotility with no known effective treatment.
194
What is believed to be the underlying pathophysiology of postvagotomy diarrhea?
Dysmotility causing rapid transit through the small intestine rather than malabsorption
195
What are the primary symptoms of postvagotomy diarrhea?
Diarrhea and cramping after eating, without symptoms between meals.
196
What is a key diagnostic feature of postvagotomy diarrhea when analyzing the stool?
The diarrhea is watery, and the presence of undigested foodstuffs indicates rapid transit.
197
How is postvagotomy diarrhea diagnosed? and Tx
It is a diagnosis of exclusion
Supportive treatment.
