Each week, Osmosis shares a USMLE® Step 1-style practice question to test your knowledge of medical topics. Today’s case involves a 55 year-old female patient with urinary incontinence. Her past medical history is notable for type 2 diabetes mellitus and hypertension. Can you figure it out?
A 55 year-old female comes to her outpatient physician because of urinary incontinence. The patient reports a sense of fullness in the bladder and continuous dribbling of urine over the past two months. Past medical history is notable for type 2 diabetes mellitus and hypertension. However, the patient reports being inconsistent in taking her medications. Her temperature is 37.1°C (98.8°F), blood pressure is 158/91 mmHg, and pulse is 75/min. Physical exam reveals decreased sensation to soft touch and pinprick in the distal arms and legs. Laboratory results are as follows:
| Laboratory value | Result |
| Glucose | 167 mg/dL |
| HbA1c | 8.1% |
| Postvoid residual volume | 170 ml |
Which of the following best describes the pathophysiology of this patient’s symptoms?
A. Impaired parasympathetic innervation of the bladder
B. Impaired sympathetic innervation of the bladder
C. Peripheral vascular disease causing reduced blood supply to the urethra
D. Abnormal connection between the bladder and vagina
E. Pelvic floor musculature weakness causing hypermobile urethra
Scroll down to find the answer!
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The correct answer to today’s USMLE® Step 1 Question is…
A. Impaired parasympathetic innervation of the bladder
Before we get to the Main Explanation, let’s look at the incorrect answer explanations. Skip to the bottom if you want to see the correct answer right away!
Incorrect answer explanations
The incorrect answers to today’s USMLE® Step 1 Question are…
B. Impaired sympathetic innervation of the bladder
Incorrect: This patient has symptoms of overflow incontinence such as bladder fullness, continuous dribbling of urine, and an ultrasound showing an increased postvoid residual volume. The sympathetic nervous system prevents micturition by contracting the internal urethral sphincter and relaxing the detrusor. As a result, reduced sympathetic innervation would cause increased detrusor activity and reduced sphincter tone, resulting in symptoms more consistent with those of urge incontinence.
C. Peripheral vascular disease causing reduced blood supply to the urethra
Incorrect: Poorly controlled diabetes mellitus can lead to peripheral vascular disease. In healthy patients, increased blood supply to the urethra increases intraurethral pressure and prevents urinary loss. In contrast, reduced blood flow would cause a decrease in intraurethral pressure, ultimately causing symptoms similar to those seen in stress incontinence.
D. Abnormal connection between the bladder and vagina
Incorrect: This describes a vesicovaginal fistula. In patients with this condition, urine from the bladder can pass through the fistula and leak into the vagina, resulting in continuous incontinence. Having an elevated postvoid residual volume or sense of pubic fullness would be atypical in patients with a vesicovaginal fistula.
E. Pelvic floor musculature weakness causing hypermobile urethra
Incorrect: A hypermobile urethra can cause stress incontinence. This is because increases in abdominal pressure will be transmitted more to the bladder and less to the urethra. As a result, pressure within the bladder will exceed that within the urethra, resulting in urine expulsion. Stress incontinence typically presents as loss of urine with activities that increase intra-abdominal pressure (e.g., coughing, sneezing, laughing), which is inconsistent with this patient’s presentation.
Main Explanation
This patient has overflow incontinence secondary to diabetic neuropathy. To understand the mechanism behind the patient’s condition, it is important to first understand urinary tract and pelvic physiology.
The bladder is connected to the urethra via the urethrovesical junction. At the junction are two sphincters, the internal sphincter which is regulated by the autonomic nervous system, and external sphincter which is regulated by the somatic nervous system.
Neurological control of the bladder and internal urethral sphincter is provided by both the sympathetic and parasympathetic nervous system. Sympathetic signals ensure continence by preventing detrusor muscle contraction and promoting internal sphincter contraction (increases bladder outlet resistance). In contrast, parasympathetic signals promote micturition by inducing contraction of the detrusor and relaxing the internal sphincter.
Another line of regulation involves controlling blood flow to the urethra. Increased urethral blood flow increases intraurethral pressure, ultimately preventing urine loss.
In this vignette, the patient has poorly controlled diabetes that has caused somatic and autonomic neuropathy. The patient’s symptoms of suprapubic fullness, continuous dribbling of urine, and increased postvoid residual volume are consistent with those of overflow incontinence. This condition would manifest if parasympathetic signals had difficulty reaching the bladder or urethra, resulting in a lack of detrusor contraction and urethral sphincter relaxation.
Major Takeaway
The detrusor muscle and internal urethral sphincter are innervated by both the sympathetic and parasympathetic nervous systems. Sympathetic activity prevents urination by preventing detrusor contraction and promoting internal urethral sphincter contraction. Parasympathetic activity promotes urination by inducing detrusor contraction and relaxing the internal urethral sphincter.
References
- Blueprints Obstetrics & Gynecology
- Gray’s Anatomy for Students 4th Edition
- Diabetic bladder dysfunction: A review
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The United States Medical Licensing Examination (USMLE®) is a joint program of the Federation of State Medical Boards (FSMB®) and National Board of Medical Examiners (NBME®). Osmosis is not affiliated with NBME nor FSMB.
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