Neurogenic bladder

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Neurogenic bladder

Renal x2

Renal x2

Anatomy of the abdominal viscera: Kidneys, ureters and suprarenal glands
Anatomy of the urinary organs of the pelvis
Anatomy of the female urogenital triangle
Anatomy clinical correlates: Male pelvis and perineum
Development of the renal system
Ureter, bladder and urethra histology
Kidney histology
Renal system anatomy and physiology
Hydration
Body fluid compartments
Movement of water between body compartments
Renal clearance
Glomerular filtration
TF/Px ratio and TF/Pinulin
Measuring renal plasma flow and renal blood flow
Regulation of renal blood flow
Tubular reabsorption and secretion
Tubular secretion of PAH
Tubular reabsorption of glucose
Urea recycling
Tubular reabsorption and secretion of weak acids and bases
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Renin-angiotensin-aldosterone system
Sodium homeostasis
Potassium homeostasis
Phosphate, calcium and magnesium homeostasis
Osmoregulation
Antidiuretic hormone
Kidney countercurrent multiplication
Free water clearance
Vitamin D
Erythropoietin
Physiologic pH and buffers
Buffering and Henderson-Hasselbalch equation
The role of the kidney in acid-base balance
Acid-base map and compensatory mechanisms
Respiratory acidosis
Metabolic acidosis
Plasma anion gap
Respiratory alkalosis
Metabolic alkalosis
Renal agenesis
Horseshoe kidney
Potter sequence
Hyperphosphatemia
Hypophosphatemia
Hypernatremia
Hyponatremia
Hypermagnesemia
Hypomagnesemia
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Renal tubular acidosis
Minimal change disease
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Amyloidosis
Membranous nephropathy
Lupus nephritis
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
Membranoproliferative glomerulonephritis
IgA nephropathy (NORD)
Alport syndrome
Kidney stones
Hydronephrosis
Acute pyelonephritis
Chronic pyelonephritis
Prerenal azotemia
Renal azotemia
Acute tubular necrosis
Postrenal azotemia
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Angiomyolipoma
Nephroblastoma (Wilms tumor)
WAGR syndrome
Beckwith-Wiedemann syndrome
Posterior urethral valves
Hypospadias and epispadias
Vesicoureteral reflux
Bladder exstrophy
Urinary incontinence
Neurogenic bladder
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Nephritic and nephrotic syndromes: Clinical
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Urinary tract infections: Clinical
Kidney stones: Pathology review
Kidney stones: Clinical
Renal and urinary tract masses: Pathology review
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Potassium sparing diuretics
ACE inhibitors, ARBs and direct renin inhibitors

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Neurogenic bladder

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A 75 year-old African-American male comes to the office because of continuous dribbling of urine which began one month ago. In addition, the patient endorses difficulty initiating and maintaining a urinary stream. Past medical records indicate that he has hypertension and type 2 diabetes mellitus. The patient has a 40-pack-year smoking history. His temperature is 37.0°C (98.6°F), blood pressure is 150/86 mmHg, pulse is 70/min, and respirations are 15/min. Cardiac, pulmonary, and abdominal examinations are non-contributory. Digital rectal exam reveals an enlarged, symmetrical, and smooth prostate. Laboratory study results are as follows:  
 
 Laboratory value  Result 
 Glucose  118 mg/dL 
 HbA1c  6.9% 
 Prostate-specific antigen (PSA)*  3.6 ng/ml 
*Normal PSA < 4.0 ng/ml

Which of the following is the most likely cause of the patient’s urinary symptoms?

External References

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Neurogenic bladder p. 537, 618

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Content Reviewers

With neurogenic bladder, neurogenic means arising from the nervous system, so neurogenic bladder is typically some difficulty emptying the bladder normally, as a result of either damage to the peripheral nerves, brain, or spinal cord.

Normally, urine is held in the bladder, which receives urine from two ureters coming down from the kidneys and then that urine leaves the bladder through the urethra.

As urine flows from the kidney, through the ureters and into the bladder, the bladder starts to expand into the abdomen. The bladder is able to expand and contract because it’s wrapped in a muscular layer, called the detrusor muscle, and within that, lining the bladder itself is a layer of transitional epithelium containing “umbrella cells”. These umbrella cells get their name because they physically stretch out as the bladder fills, just like an umbrella opening in slow-motion.

In a grown adult, the bladder can expand to hold about 750ml, slightly less in women than men because the uterus takes up space which crowds out the bladder a bit.

Okay - so when the urine is collecting in the bladder, there are basically two “doors” that are shut, holding that urine in. The first door is the internal sphincter muscle, which is made of smooth muscle and is under involuntary control, meaning that it opens and closes automatically. Typically, the internal sphincter muscle opens up when the bladder is about half full.

Now the second door is the external sphincter muscle, and it’s made of skeletal muscle and is under voluntary control, meaning that it opens and closes when a person wants it to. This is the reason that it’s possible to stop urine mid-stream by tightening up that muscle, which is called doing kegel exercises. Once urine has passed through the external sphincter muscle, it exits the body, in women the exit is immediate and in men the urine flows through the penis before it exits.

So, when specialized nerves called stretch receptors in the bladder wall sense that the bladder is about half full, they send impulses to the spinal cord, specifically the sacral spinal cord at levels S2 and S3, known as the micturition center, and the brain, specifically two locations in the pons—the pontine storage center and pontine micturition center.

The spinal cord response is part of the micturition reflex. And it causes an increase in parasympathetic stimulation and decrease in sympathetic stimulation which makes the detrusor muscle contract and the internal sphincter relax. It also decreases motor nerve stimulation to the external sphincter allowing it to relax as well.

At this point, urination would occur at this point, if not for the pons. The pons is the region of the brain that we train to voluntarily control urination.

If we want to delay urination, or hold it in, the pontine storage center overrides the micturition reflex, and when we want to urinate, the pontine micturition center allows for the micturition reflex to happen.

Now with neurogenic bladder - the exact pattern of symptoms depends on the nerve that is damaged.

In diabetes mellitus, excess glucose levels in the blood attaches to various proteins - a process called glycation. This process can damage sensory nerve fibers in the bladder wall, in the pelvic nerve, or in dorsal nerve roots entering the spinal cord, all of which interferes with the initial stretch signal that gets sent out as the bladder fills.

Another potential cause is syphilis, this infection can eventually lead to tabes dorsalis—which is inflammation and scarring of those same little dorsal root nerves.

Also, with herpes, the virus takes up a home in the dorsal nerve roots for months to years and it can also disrupt the sensory fibers that they carry within them.

This all means that as the bladder fills to capacity and stretches, that sensory information is not received, and the bladder starts to overflow, drop by drop, out of the urethra. This is called overflow incontinence.

Summary

Neurogenic bladder is a type of bladder dysfunction that is caused by damage to the nerves related to the bladder control. It is characterized by difficulty emptying the bladder normally, as a result of either damage to the peripheral nerves, brain, or spinal cord.

Neurogenic bladder can occur as a result of various conditions, such as spinal cord injuries, multiple sclerosis, and diabetes. Related bladder dysfunctions could be overflow incontinence, where the bladder fills up to capacity and then dribbles out of the urethra, or urge incontinence, where an individual feels frequent urges to urinate.