A 55-year-old woman, gravida 3 para 3, comes to the office due to constipation. For the past 6 months, the patient has had increasing constipation associated with mild, crampy abdominal pain and fatigue. She has only 1 or 2 bowel movements every week. Medical history is notable for nephrolithiasis, for which the patient was briefly hospitalized a year ago. She has not undergone colonoscopy. Vital signs are normal. The abdomen is soft. Rectal tone is normal. Deep tendon reflexes are 2+. The remainder of the examination shows no abnormalities. Laboratory results are as follows:
| Serum chemistry | |
| Sodium | 140 mEq/L |
| Potassium | 3.9 mEq/L |
| Creatinine | 0.9 mg/dL |
| Calcium | 11.5 mg/dL |
| Phosphorus (inorganic) | 2.2 mg/dL |
Which of the following is the most likely underlying cause of constipation in this patient?
Hypercalcemia-induced constipation | |
Significant causes |
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Typical symptoms |
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Pathophysiology |
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This patient has constipation associated with hypercalcemia and hypophosphatemia, which is a common presentation of primary hyperparathyroidism (PHPT). PHPT is usually caused by a benign parathyroid adenoma that autonomously secretes parathyroid hormone (PTH), leading to increased bone resorption, increased renal calcium reabsorption, and increased intestinal calcium absorption (due to increased production of 1,25-dihydroxyvitamin D). This patient's history of renal stones also indicates hyperparathyroidism and is due to increased urinary calcium excretion despite maximal renal tubular calcium reabsorption.
Hypercalcemia inhibits nerve depolarization by interfering with sodium movement through voltage-gated sodium channels, leading to impaired smooth muscle contraction and reduced colonic motility. Symptoms include constipation, crampy abdominal pain, and nausea. Other potential gastrointestinal manifestations of hypercalcemia include acute pancreatitis (due to increased conversion of trypsinogen to trypsin) and peptic ulcer (due to increased release of gastrin).
(Choice B) Dyssynergic defecation is characterized by altered passage of stool through the anorectum due to uncoordinated contraction and relaxation of pelvic floor muscles. It is often caused by obstetric complications during vaginal delivery. However, hypercalcemia and hypophosphatemia would not be present, and most patients have either anal sphincter dysfunction or the absence of perianal descent (this patient's rectal tone is normal).
(Choices C and E) Intestinal motor function is generally stimulated by the parasympathetic nervous system and inhibited by the sympathetic nervous system. Although constipation can occur due to autonomic dysfunction from demyelination (eg, multiple sclerosis) or nerve fiber interruption (eg, traumatic spinal cord injury), these disorders would not explain this patient's electrolyte abnormalities.
(Choice D) Colon cancer can cause intestinal obstruction, which can interfere with the passage of stool, and can be associated with hypercalcemia (bone metastasis); however, this would result in PTH suppression, so it is unlikely to cause hypophosphatemia. This patient's history of renal stones also is more consistent with primary hyperparathyroidism.
Educational objective:
Hypercalcemia inhibits nerve depolarization, leading to impaired smooth muscle contraction and reduced colonic motility. Symptoms include constipation, crampy abdominal pain, and nausea.