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Alterations in Gastrointestinal and Obesity Assignment.

Alterations in Gastrointestinal and Obesity Assignment.

All nutrients are absorbed in the gastrointestinal (GI) system, and GI motility plays a very critical role in the consumption of foods, digestion, and absorption of nutrients. Various segments of the GI tract (esophagus, stomach, and intestines) coordinate in a complex yet precise way to control the process of food consumption, digestion, and absorption of nutrients. Alterations in Gastrointestinal and Obesity Assignment.GI motility not only regulates the rates at which nutrients are processed and absorbed in the gut but also participates in the control of appetite and satiety. Altered GI motility has been associated with various disease conditions (gastroparesis, etc.) and has been frequently observed in obese patients. The significance of these GI motility alterations in obesity is not fully understood, but they have been considered as potential contributing factors in the development and maintenance of obesity and changed eating behavior. Therapies aimed at regulating GI motility are being actively explored and applied clinically for the management of obese patients. To better understand the pathophysiology of obesity, we systematically reviewed GI motility changes observed in obese conditions. The relationship and pathological significance of these findings, as well as the potential therapies by modification of GI motility, are also discussed.Alterations in Gastrointestinal and Obesity Assignment.



Patient’s Chief Complaints “I’ve been nauseated again and have thrown up several times since yesterday. I also have a constant aching in my stomach and I feel really bloated again.”   HPI J.A. is an 83-year-old man who is a five-day post-status surgical patient for elective repair of an abdominal aortic aneurysm. After nearly nine hours of uncomplicated surgery the patient was transferred to the surgical intensive care unit.Alterations in Gastrointestinal and Obesity Assignment. Intravenous methyldopa was used to maintain the patient’s systolic blood pressure below 160 mm Hg. He awoke one hour later and was drowsy from the IV morphine sulfate that he was receiving every 90–120 minutes for pain. Vital signs were stable for the next five hours (BP 148/85, P 91, RR 21, Hct 39%) on 40% oxygen by face mask. Then, his abdomen became moderately distended but soft. No bowel sounds were heard during a prolonged period of auscultation. There was no fever or elevated white blood cell count, but there was mild abdominal tenderness with palpation. Plain film radiographs demonstrated a cecal diameter of 10.5 cm (the upper limit of normal cecal size is 9.0 cm) and a diagnosis of acute colonic pseudo-obstruction secondary to surgery was made. Nasogastric and rectal tubes were inserted and low constant suction provided to ensure gastric decompensation. The patient was periodically rolled from side to side and to the prone position in an effort to promote expulsion of colonic gas. Nasogastric output was replaced mL for mL with IV 0.45% saline and 20 meq/L potassium chloride. On post-operative day 1, repeat abdominal radiographs revealed that cecal diameter remained at 10.5 cm. The patient continued to feel nauseous and vomited twice. Nasogastric output was measured every 4–4½ hours and fluctuated from 50 to 175 mL of green drainage fluid.


Patient Case Question 1. Determine the grade of vomiting during the last 24 hours.

On post-operative day 2, analgesia was maintained with 8 mg morphine IM every 4 hours. Abdominal radiographs showed that cecal diameter had increased to 11.5 cm. Two more episodes of vomiting occurred. A single dose of 2 mg neostigmine was given IV and significant colonic decompression occurred within 20 minutes. The patient was monitored for possible neostigmine-induced bradycardia, but no adverse effects developed. On post-operative day 3, cecal diameter was measured at 9.5 cm, a decrease of 2.0 cm from post-operative day 2. The patient felt considerably less nauseated and had not vomited in the past 12 hours. Nasogastric output had slowed to 60 mL/8 hours. He remained on IV saline and KCl, however, and orders of “nothing by mouth.” His abdomen was only mildly distended and soft. Bowel sounds were audible by auscultation in all four quadrants. A decision was made to maintain his tubes in place for one more day. On post-operative day 4, the patient’s tubes were removed and he began taking in a clear liquid diet by mouth in the early morning. By noon, however, he began to complain of increasing abdominal discomfort, feeling bloated and nauseous, and suffered three episodes of vomiting a greenish fluid. Respiration rate was 28/minute, heart rate was 105/minute, and both blood pressure and temperature were normal. Bowel sounds, which had been nor-moactive upon rising, were now absent. The patient did not respond to neostigmine this time, but responded well to placement of a decompression tube. Within 18 hours, however, symptoms had returned once again.  Alterations in Gastrointestinal and Obesity Assignment.


HTN × 20 years OA × 18 years Type 2 DM Hyperlipidemia


Right nephrectomy for “benign” renal disease, 23 years ago Partial colectomy for polyposis, 14 years ago Total right hip replacement for worsening hip pain from OA unresponsive to analgesic treatments, 5 years ago


Mother and younger sister (both deceased) had “high blood pressure” Father died from AMI at age 78 History of AMI and stroke at young ages in maternal grandparents

SH Patient lives with wife of 55 years, is a retired civil engineer (retired at age 65), and enjoys gardening and travel No tobacco × 15 years No EtOH × 15 years


(+) nausea, retching, vomiting, epigastric discomfort, dry mouth, and fatigue (−) headache, stiff neck, fever, abdominal pain, diarrhea, melena, urinary frequency/ urgency/discomfort, weakness, SOB, numbness/tingling in extremities


Amlodipine 10 mg po Q AM Glyburide 10 mg po Q AM, 5 mg po Q PM EC ASA 325 mg po QD Gemfibrozil 600 mg po BID

Patient Case Question 2. How does amlodipine work to relieve hypertension? Alterations in Gastrointestinal and Obesity Assignment.

Patient Case Question 3. How does glyburide work to control blood sugar in type 2 diabetes mellitus?

Patient Case Question 4. What are the two major contributing factors for nausea and vomiting in this patient?

All No known drug or food allergies

PE and Lab Tests


White male who looks his stated age in moderate distress Ill-appearing and slightly lethargic in his hospital bed The patient’s face is ashen and the eyes are noticeably sunken VS See Patient Case Table 26.1

Skin Color: gray Temperature: cold Turgor: poor, some skin tenting noted Feel: dry No rash, petechiae, or lesions


PERRLA EOMI Fundi benign Sclera without icterus TMs intact Mucous membranes dry


Supple Thyroid WNL (−) adenopathy bruits, and JVD


Tachypnea prominent Lungs clear to auscultation


Sinus tachycardia (−) murmurs, rubs, and gallops


Soft and moderately distended with hypoactive BS Pain is elicited on light palpation of RLQ (−) HSM, rebound tenderness, and masses Genit/Rect

Genital exam not performed Normal sphincter tone Rectal exam WNL No bright red blood or masses visible Stool guaiac-negative


Extremities are cold and gray Pulses hypoactive at 1 + throughout

(−) edema and clubbing

Neuro (+) lethargy (−) visual abnormalities Cranial nerves intact DTRs 2 + Strength is equal bilaterally in all extremities

Laboratory Blood Test Results See Patient Case Table 26.2

Patient Case Question 5. List twelve clinical manifestations in this patient that are consistent with a diagnosis of dehydration.

Patient Case Question 6. Has the patient developed hypokalemia?

Patient Case Question 7. Why can acute pancreatitis be ruled out as a cause of nausea and vomiting in this patient?

Patient Case Question 8. Perforation of the cecum often occurs when cecal diameter > 10 cm. Severe abdominal pain, fever, and leukocytosis are clinical manifestations of perforation. Has the cecum perforated in this patient?

Patient Case Question 9. What is believed to be the pathophysiologic mechanism that underlies acute colonic pseudo-obstruction?

Patient Case Question 10. Are respiratory and reflex signs consistent or inconsistent with metabolic alkalosis?


Explain the pathogenesis with common clinical presentation of celiac’s disease
Analyze the pathophysiology Crohn’s disease and relate genetic issues
Differentiate between hepatitis A, B, C, and viral hepatitis
Elaborate on the pathogenesis and pathophysiology of pancreatic cancer
Complete Case Study #26 (nausea and vomiting) in the Bruyere textbook.

Alterations in Gastrointestinal and Obesity Assignment.

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