11.13.2025 - SAM2 - part 1

Overview of Lecture on Maturation Disorders and Prostatic Disease

  • Discussion of maturation disorders for the first two-thirds of the lecture, followed by prostatic disease. These two areas are often linked due to their impact on the urinary system, particularly in older male animals where prostatic disease can lead to secondary urinary issues.

Aims of the Lecture

  • Understand components involved in normal maturation process.

  • Formulate diagnostic plans for patients experiencing urinary incontinence and urinary retention.

  • Understand treatment indications for incontinence and urinary retention.

  • Discuss differential diagnoses for disorders affecting the prostate gland.

Maturation Disorders

  • Definition: Maturation is the controlled, voluntary voiding of urine, involving complex neurological and muscular coordination.

  • Bladder Function:

    • Stores urine for 99% of the time and voids urine for only 1% of the time. This dual function of storage and voiding is regulated by a balanced interplay of the autonomic and somatic nervous systems.

    • Abnormalities may lead to:

      • Inability to store urine, affecting continence, often manifesting as involuntary leakage or dribbling.

      • Problems in initiating or completing urination, leading to urinary retention, where the bladder cannot effectively empty.

Control of Urination

  • Central Nervous System Control:

    • Conscious awareness and voluntary control are required for urination. Signals from higher brain centers (e.g., cerebral cortex, brainstem) travel down the spinal cord to the sacral micturition center (S1-S3), which coordinates bladder and sphincter activity.

    • The cerebral cortex provides voluntary inhibition of urination, while the brainstem coordinates detrusor and sphincter synergy.

  • **Nervous System Control:

    • Sympathetic Input:**

      • Provided by the hypogastric nerve from spinal cord segments L1-L5. This input promotes urine storage by:

      • Relaxing the detrusor muscle (smooth muscle of the bladder) via β2β2​ adrenergic receptors.

      • Contracting the internal urethral sphincter muscle (smooth muscle) via α1α1​ adrenergic receptors.

    • Parasympathetic Control:

      • Via the pelvic nerve (S1-S3), promoting urination by:

      • Causing contraction of the detrusor muscle through muscarinic cholinergic receptors (predominantly M3M3​ receptors), which is essential for initiating and sustaining bladder voiding.

      • Inhibiting the internal urethral sphincter.

    • Somatic Input:

      • Via the pudendal nerve (S1-S3), which controls the external urethral sphincter (skeletal muscle) through nicotinic cholinergic receptors.

      • Contraction of the external sphincter provides voluntary retention of urine, allowing for conscious control over continence.

Phases of Urination

  • Storage Phase:

    • The bladder neck and urethra are closed, and the detrusor muscle relaxes (sympathetic stimulation, parasympathetic inhibition).

    • The internal (sympathetic α1α1​ adrenergic) and external (somatic pudendal nerve) sphincter muscles contract to retain urine.

  • Voiding Phase:

    • The detrusor muscle contracts (parasympathetic stimulation via pelvic nerve and muscarinic receptors).

    • The internal and external sphincter muscles relax, allowing urine passage. This coordination is essential for efficient bladder emptying.

Diagnostic Approach to Urination Disorders

  • Evaluate nervous system control relating to urination, including:

    • Level of consciousness and awareness (central issues), which impact the ability to voluntarily control micturition.

    • Anal tone and sensation (assessed via rectal examination), which are indirect indicators of sacral spinal cord segments (S1-S3) function, often correlating with bladder innervation.

      • Bobble Covered Noses Reflex: This refers to a perineal reflex assessment common in veterinary neurology. Pinching the lips in female dogs and bulbous glands in males is used to assess the anal sphincter reflex response, which similarly evaluates sacral nerve integrity. A positive response indicates a functional reflex arc.

  • Urethral sphincter tone can be assessed by compressing the bladder to gauge emptying ease and the resistance felt. This provides a subjective measure of urethral resistance.

    • Monitor for residual volumes after urination using catheterization or ultrasound to determine the efficiency of bladder emptying and identify retention.

    • Care is needed to avoid exacerbating any underlying conditions (e.g., obstruction) during bladder expression or catheterization, as it could lead to bladder trauma or infection.

Storage Disorders (Incontinence) and Causes

  • Conditions labeled by clients as

    • "incontinence" where urine is dribbling, not retained, signifying involuntary leakage rather than normal voiding.

  • Causes include:

    • Anatomical abnormalities: These are structural defects in the urinary tract.

      • Congenital Issues: Ectopic ureters (incorrect ureter insertion location). These can be intramural (within the bladder wall but bypass the trigone) or extramural (insert directly into the urethra or vagina), often presenting as continuous urine leakage from birth.

      • Genital Urinary Dysplasia: Rare congenital abnormality involving malformation of parts of the urogenital system.

    • Acquired disorders: These develop over time due to disease or intervention.

      • Permanent urethral procedures leading to incontinence (e.g., urethrostomy after obstruction), where normal sphincter function may be compromised.

      • Urethral stents resulting in incontinence post-neoplasm treatment, as the stent might interfere with sphincter closure or cause irritation.

    • Functional Disorders: The internal anatomy appears normal, but the sphincter mechanism is ineffective or bladder instability is present.

      • Examples include urethral sphincter mechanism incompetence (USMI), where the sphincter lacks adequate tone, and detrusor hyper-reflexia (overactive bladder), where the detrusor contracts involuntarily at low bladder volumes.

Urethral Sphincter Mechanism Incompetence (USMI)

  • Most common in large-breed, spayed female dogs (e.g., neutered before first season), where estrogen deficiency is a predisposing factor.

  • Predisposed Breeds: Dobermans, Giant Schnauzers, Old English Sheepdogs, Rottweilers, Boxers, among others. Reduced urethral tone is thought to be multi-factorial, also involving anatomical position of the bladder or urethra.

  • Symptoms include incontinence primarily while lying down, sleeping, or relaxed, as urine flows easier when horizontal and urethral resistance is reduced.

  • Diagnosis: Physical exam usually shows minimal effects, often a normal urinalysis expected, as the problem is functional rather than inflammatory or infectious. However, concurrent urinary tract infection is common due to urine pooling.

  • Conditions affecting concurrent issues:

    • Chronic kidney disease or conditions creating increased urine volume (e.g., Cushing's disease, diabetes mellitus), causing overflow incontinence when the bladder's capacity is exceeded due to excessive urine production, overwhelming even a competent sphincter.

Diagnostic Procedures

  • Pressure Profiling: Urodynamic studies, including urethral pressure profilometry and cystometrography, are technically challenging and not typically performed in awake animals due to feasibility issues, cost, and the need for specialized equipment and expertise.

  • Ideal diagnosis made based on a thorough clinical history, physical examination, exclusion of other conditions (e.g., UTI, ectopic ureters via contrast radiography), and response to specific medical therapy.

Treatment Options for Incontinence

  • Estrogen Therapy: Given to spayed females to counter estrogen deficiency, which contributes to USMI.

    • Mechanism: Estrogen increases the number and sensitivity of α1α1​ adrenergic receptors in the urethral smooth muscle, thereby enhancing responsiveness to endogenous catecholamines and increasing urethral tone. Effective in about 65% of treated cases.

    • Commonly used agents include diethylstilbestrol (DES) or estriol. Possible side effects include vulvar swelling, attractiveness to male dogs, and rarely, bone marrow suppression with overdose.

  • Phenylpropanolamine (PPA): A sympathomimetic agent with a 75-90% efficacy rate.

    • Mechanism: PPA is an α1α1​ adrenergic agonist that directly stimulates adrenergic receptors in the smooth muscle of the internal urethral sphincter, leading to increased urethral tone.

    • Administration Frequency: Higher doses are often prescribed for twice daily administration, or lower doses for thrice daily application to maintain consistent urethral resistance. Side effects include hypertension, restlessness, panting, and anxiety, particularly in sensitive individuals.

  • Surgical Interventions: Reserved for cases refractory to medical management.

    • Procedures like urethral plication (tightening the urethra), colposuspension (repositioning the bladder neck), or artificial sphincters utilize hydraulic cuffs implanted around the urethra to manually manage urine flow effectively by increasing resistance.

Prostatic Disorders

  • Understanding disorders affecting the prostate is critical due to their high prevalence in intact male dogs and potential for severe clinical signs.

  • Physical Examination of Prostate:

    • Palpation via digital rectal examination should reveal the prostate's size (normally 3-4 cm in a medium-sized dog, or up to the width of the pelvis), symmetry, and a distinct median relief (sulcus).

    • Abnormal features include loss of symmetry, pain upon palpation, enlargement (hyperplasia, cyst, neoplasia), firmness (fibrosis, neoplasia), or fluctuance (abscess, cyst), indicative of various conditions requiring further investigation.

Benign Prostatic Hyperplasia (BPH)

  • The most common prostatic disorder in entire male dogs, affecting >90% by 8 years of age. It is an age-related, hormonally-mediated enlargement.

  • Hormonal Basis: BPH is androgen-dependent. Testosterone produced by the testes converts to dihydrotestosterone (DHT) within prostate cells by the enzyme 5α5α-reductase. DHT is a potent androgen that stimulates prostatic cell growth (hyperplasia and hypertrophy).

    • Upregulation of androgen receptors under the influence of estrogen further sensitizes the prostate to DHT, exacerbating the glandular enlargement.

  • Symptoms include:

    • Urinary obstruction, manifesting as stranguria, tenesmus, or dysuria, due to the enlarged prostate compressing the urethra.

    • Hematuria (blood in urine), which can be terminal (at the end of urination) or sporadic, often due to prostatic bleeding.

    • Fecal tenesmus (difficulty passing stool) and flattened stools because the enlarged prostate exerts pressure on the rectum, hindering defecation.

    • Other signs may include small prostatic cysts or asymptomatic hemorrhage.

  • Examination Characteristics:

    • Rectal palpation typically reveals a symmetrically enlarged, non-painful, and non-sensitive prostate with a normal consistency. It may be displaced cranially due to its size.

    • On ultrasound, BPH presents with a homogenous, often hyperechoic appearance, sometimes with small cysts.

Treatment of BPH

  • Surgical Castration: The definitive and most effective treatment. Permanent removal of the testosterone source leads to rapid and significant prostatic regression (up to 70% reduction in size within 2-3 weeks).

  • Medical Options: For owners who wish to maintain breeding potential or avoid surgery.

    • Hormonal implants inhibiting testosterone production for temporary relief (e.g., deslorelin, a GnRH-agonist implant causing down-regulation of GnRH receptors and temporary suppression of gonadal steroids) for 6-12 months.

    • Medications like finasteride inhibit 5α5α-reductase, preventing the conversion of testosterone to DHT. This gradually reduces prostatic size over several weeks to months, making it slower-acting but effective.

    • Anti-androgen steroids (e.g., osaterone acetate) for rapid shrinkage by directly blocking androgen receptors; however, potential side effects (e.g., temporary infertility, adrenal suppression) and the need for reinjections every 5 months are considerations.