FDU FMPC GU.pptx

Christina Bottiglierie, MS PA-C PHAS Family Medicine and Primary Care GU system  NCCPA topics Balanitis Hernias Benign prostatic Nephrolithiasis hyperplasia Orchitis Chlamydia...

Christina Bottiglierie, MS PA-C PHAS Family Medicine and Primary Care GU system  NCCPA topics Balanitis Hernias Benign prostatic Nephrolithiasis hyperplasia Orchitis Chlamydia Prostatitis Epididymitis Pyelonephritis Glomerulonephritis Testicular cancer Gonorrhea Urethritis Anatomy Lower Urinary Tract Symptoms Normal voiding. Obstructed Voiding  Cause of Obstruction BPH Prostate cancer Prostatitis  Benign Prostatic Hypertrophy Prostate hyperplasia of the TRANSITION ZONE Cause Aging (over 40 years old) Presentation Some have no symptoms Those with symptoms have: Urinary frequency Urgency Decreased force of urinary stream Incomplete bladder emptying Nocturia Hesitancy Dribbling at end Straining Diagnosis Uniformly enlarged smooth prostate Benign Prostatic Hypertrophy – Management  BPH meds: Alpha blockers “-osin” Rapid relief of symptoms No effect on the clinical course of BPH Tamsulosin (Flomax) Alfuzosin -> use in younger men Doxazosin Terazosin Alpha blocker A/E BPH Meds: 5-Alpha-Reductase Inhibitors No effect on immediate relief of symptoms Suppresses prostate growth by converting testosterone into DHT “astride” Finasteride Dutasteride Side effects: ED/decreased libido Breast tenderness/enlargement Hair growth.. Bladder overactivity Urge Incontinence  Anticholinergics “Can't see, can't pee, can't sit, can't SH%@” Side effects: Dry mouth Dry eye Constipation Memory loss / confusion Urinary retention Post void residual: have patient urinate and then do bladder scan to see if there is urine retained (>500 ml= urinary retention) Contraindications: Glaucoma (closed angle) narrows angles; worsens Hx of urinary retention Pupils dilate Bladder Underactivity Overflow Incontinence External Causes of Incontinence  Stress Incontinence Leakage of urine with ↑’s intra-abdominal pressures Causes: Laxity of pelvic floor muscle due to pregnancy, menopausal changes due to estrogen loss Presentation: Leakage of urine with sneezing laughing etc. Management: Pelvic floor exercises Kegal  Functional Incontinence Leakage of urine Causes: Not being able to get to bathroom in time Walker Post op Urinary Incontinence  Prostate Cancer Usually a slow growing cancer Risk factors: Diagnosis: Family history PSA 0-4 over or velocity increase 0.75 in 1 yr (2->3) African American descent DRE -> only inferior posterior is felt Transrectal u/s guided bx (core – 12) Aging Presentation: Pathology: Adenocarcinoma Asymptomatic Obstructive sx: Management: Depends on aggression, age and mets Frequency Gleason scale and age determines tx Younger -> radical prostatectomy Urgency Older -> Active surveillance -> bx once per yr Incomplete bladder emptying Gleason 7-10, radiation therapy and androgen therapy Rare back/bone pain, wt loss (mets) and chemotherapy if mets to bone.  Prostate Screening Ethically: promotes patient autonomy, protecting the integrity of the patient as an independent and rational decisionmaker capable of self-determination. Interpersonal perspective: promotes trust in the patient-clinician relationship and may enhance the confidence of patients to participate in their health care. Educational perspective: improves knowledge about screening and chemoprevention options, creates more realistic expectations about benefits and harms, and reduces the decisional conflict associated with feeling uninformed. Gleason scale  Hematuria Causes Upper GU Kidney or ureteral stones Ureteral mass or cancer Lower GU UTI BPH Bladder CA Dx CT urogram shows how the urine is flowing (upper tract) bladder ca can be missed Cystoscopy with possible bx (lower) Urine testing (U/A and cx) Cytology risk of bladder ca  Bladder Cancer 90% transitional cell Diagnosis: carcinoma Cystoscopy with bx Ct urogram to see if Causes: spread MC Smoking Occupational exposure Management: (dyes) Local – transurethral Cyclophosphamide resection Invasive (muscle) Presentation: cystectomy Recurrent BCG immune Painless hematuria therapy Irritative voiding sx  Testicular Cancer Most common cancer in males aged 15-34 years old (5/100,000 males) Risk Factor: Cryptorchidism Types: Germinal Cell Tumors (95%) Nongerminal Cell Tumors (5%) Leydig Cell Sertoli Cell Gonadoblastoma Testicular Lymphoma Seminoma (60%) Non seminoma (40%0 Embryonal Cell Teratoma Choriocarcinoma (worst prognosis)  Testicular Cancer Presentation: Painless testicular nodule Hydrocele (10%) Gynecomastia (Sertoli or Leydig tumor) -> secrete estrogen Diagnosis: Scrotal US Serum Studies HCG Alpha-feta protein (AFP) LDH Management: Orchiectomy +/- Radiation / Chemotherapy Renal Cell Carcinoma Nephrolithiasis vs Ureterolithiasis  Nephrolithiasis / Ureterolithiasis Causes: Calcium Oxalate Most common Uric acid Seen in more acidic urine Patients may have increased uric acid secretion Struvite Stone Staghorn calculi Offending organism -> Proteus Cystine  Nephrolithiasis Stone formation in the kidney Causes: Low urine volume Other dietary factors Medication induced Presentation: Usually asymptomatic but if stone is stuck in ureter, they will have pain. Diagnosis: Labs Urinalysis +/- RBCs If pH > 7.2 (alkaline)  struvite stone Imaging Renal US Non-contrast CT Scan (radiopaque stones are same color as contrast and would be missed if using contrast) KUB (Kidney, Ureter, Bladder x-ray) Calcium & struvite stones are visible  Nephrolithiasis Management: Stones < 5mm 80% chance of passage Stones > 7mm 20% chance of passage Usually uric acid stones Alkalize the urine to dissolve the stone May need to be treated with allopurinol if recalcitrant uric acid stones Elective Surgical Intervention: Shock wave lithotripsy If stone visible on KUB Ureteroscopy + stent placement Percutaneous nephrolithotomy Large stones (>10mm) Extracorporeal Shock Wave Lithotripsy (ESWL) Ureteroscopy  Ureterolithiasis Stone in ureter Presentation Renal colic Radiation to groin Nausea / vomiting Diagnosis Non contrast CT  Ureterolithiasis Management Dependent on size and duration Emergent ER -> Intractable pain Nausea / vomiting Conservative Cannot tolerate PO Increase fluids Fever Pain medication ~Stent placement~ Tamsulosin Elective surgery Shock wave lithotripsy Ureteroscopy + stent placement  Preventing Stone Formation Preventing Stone Formation: 24 hour urine For everyone: Increase fluid intake  Hydrocele Presence of fluid in the tunica vaginalis Abnormal amount of fluid secretion Presentation: NON painful Testicular edema Will transilluminate Can be seen with: Indirect inguinal hernia Injury and inflammation of epididymis Systemic conditions like CHF and ascites Management: Small – Observe Large – Operate  Varicocele Dilation of pampiniform plexus Most commonly occurs on the LEFT side Presentation: BAG of WORM ↑ dilation: when sitting or standing upright or during valsalva ↓ dilation: when lying supine or if teste is elevated Management: Usually, no intervention necessary If TTC -> causes infertility due to increased blood flow; correct with surgery Note: Sudden onset of LEFT sided varicocele, especially older male, R/O RCC  Testicular Torsion Torsion of the spermatic cord Torsion obstructs the penniform plexus -> edema & hemorrhage -> arterial obstruction of testicular artery Causes: Congenital malformation Bell clapper deformity (teste free to rotate) Presentation: True emergency! SEVERE sudden unilateral scrotal pain Nausea / vomiting Lower abdominal and inguinal pain Examination: Swollen, tender and retracted testicle AKA high riding horizontal testicle NEGATIVE Prehn sign (lifting does NOT relieve pain) Absent cremasteric reflex (superficial reflex -> inner part of the thigh is stroked. Causes the cremaster muscle to contract and pull up the ipsilateral testicle toward the inguinal canal) Testicular Torsion Testicular Torsion  Epididymitis Pain and swelling thought to be secondary to retrograde infection or reflux of urine. Usually bacterial cause Etiologies Males 14-35: Chlamydia MCC then Gonorrhea, Ureaplasma, E coli Males > 35: E coli MCC then Klebsiella, Pseudomonas and Proteus Prepubertal: viruses then bacterial Symptoms Gradual onset (hours to days) Epididymal tenderness and induration May have fever, chills, irritative symptoms (dysuria, urgency or frequency)  Epididymitis PE: Scrotal swelling and tenderness Epididymal tenderness and swelling (posterior and superior to teste) + Prehn sign - relief of pain with scrotal elevation + Cremasteric reflex – elevation of testicle after strking the inner thigh Diagnosis Scrotal u/s best initial test (enlarged epididymis and increased testicular blood flow) U/A, NAAT for G/C Management Elevation, cool compresses, NSAID’s 35, low risk for STI – enteric pathogen Fluroquinolone. TMP/SMX is alternative Bacterial in children – Cepalex or Amoxil  Erectile Dysfunction Inability to generate or maintain an erection Causes: Psychogenic Neurologic DM Vascular Atherosclerosis Endocrine disorder Prolactinoma (decrease T) Medications Beta blockers Diagnosis: Hormone testing Duplex US -> ↓ blood flow to penis Management: Phosphodiesterase - 5 inhibitor -> Contraindicated with NTG Side effects: headache & flushing Sildenafil (Viagra) Tadalafil (Cialis)  Balanitis Inflammation of the head of the penis Most frequent in uncircumcised men, usually caused by Candida. RF: Morbid obesity Condom catheter use Uncontrolled diabetes mellitus Poverty Poor hygiene Chemicals in soap Certain meds (abx, SGLT2) Presentation: Tight, shiny skin on the glans Redness around the glans Inflammation, soreness, itchiness, or irritation of the glans A thick cheesy white discharge under the foreskin (smegma) Small, eroded, itchy spots/plaques may be present with a white cheese-like matter, which can be rubbed off easily Difficulty pulling back the foreskin (phimosis)  Balanitis Treatment: Topical nystatin ointment is the initial treatment if the lesions are mildly erythematous or superficially erosive. Soaking with dilute 5% aluminum acetate for 15 minutes twice daily may quickly relieve burning or itching. Chronicity and relapses, especially after sexual contact, suggest reinfection from a sexual partner who should be treated. Severe purulent balanitis is usually due to bacteria. If it is so severe that phimosis occurs, oral antibiotics—some with activity against anaerobes—are required; if rapid improvement does not occur, urologic consultation is indicated.  Hypospadias & Epispadias Hypospadias Epispadias Congenital condition Congenital condition Urethra located on upper Urethra located on under side of penis aspect of penis  Phimosis and Paraphimosis Phimosis Paraphimosis Inability to retract foreskin past Foreskin becomes trapped glans behind corona of glans & Not emergent constricts penile tissue Urologic emergency! Presentation: Presentation: Inability to retract skin SEVERE pain Discomfort Iatrogenic Management: Management: Steroid cream Circumcision Circumcision Phimosis and Paraphimosis  Peyronie Disease Buildup of scar tissue under the skin of the penis, that causes a bend with a bump in the erection that can be felt Causes Trauma This can occur during athletic activities, an accident, or sex. During vigorous sex especially, the penis can bend and become injured Genetics Men with family members who have PD or other related conditions may be more likely to get it. Genetic issues may cause problems with healing after an injury Age Older men are more likely to have less firm erections that bend more easily, which may put them at higher risk for injury  Peyronie Disease Symptoms A bend in the erection with or without pain Some men report they feel pain in their erection as the bend develops for the first 12 to 18 months A Peyronie's plaque This is a bump of scar tissue under the skin of the penis. It's most commonly found on the top side of the penis. Some men can feel it, while others don't notice it Erection problems- problems getting or maintaining an erection Shortening of the penis Pain In the penis e. Peyronie Disease Treatment Surgical Plication - Tissue inside of the penis is removed or pinched together on the opposite side of the penis bend to help straighten the erectile curvature. Grafting – The scar tissue that makes up the Peyronie’s plaque is cut or partially removed. The scarred tissue is then replaced or expanded with healthy tissue. Implants - A bendable or inflatable cylinder device is permanently inserted inside the penis to help correct erectile curvature. If the implant doesn't help straighten the penis on its own, this procedure may be combined with another surgery. Men who get implants can only have an erection by using this device. Nonsurgical XIAFLEX (collagenase clostridium histolyticum) involves a series of in-office, enzyme injections, given by a urologist into the Peyronie's plaque The enzymes work to help break down the plaque, and along with daily penile exercises, may help reduce the bend in the erection.  Cystitis Infection of the bladder Pathogens: Most common: E coli Other gram-neg pathogens: Proteus, Klebsiella, Pseudomonas Risk Factors: Female: Intercourse Pregnancy Post menopausal -> loss of estrogen -> vaginal atrophy Male: Incomplete bladder emptying Presentation: Afebrile Dysuria Frequency Urgency Suprapubic tenderness Hematuria  Cystitis Midstream catch By definition, UTI = > 100,000 colonies Diagnosis Urinalysis + WBC + RBC +/- Nitrite Urine Culture Definitive diagnosis Treat symptomatic patients Do not treat asymptomatic patients, except if pregnant  Cystitis – Management Uncomplicated cases Complicated cases Men (from BPH so treat BPH as well) Immunocompetent female Immunosuppressed female Trimethoprim- Fluroquinolones po or IV sulfamethoxazole (Bactrim) Pregnant Nitrofurantoin (Macrobid) Tx is normally for 10 days Fosfomycin – expensive Cephalexin (Keflex) Fosfomycin – expensive Amoxicillin-Clavulanate (Augmentin) Cefixime Cefpodoxime Ceftin (Cefuroxime) Urine culture Pyelonephritis Orchitis  Acute Prostatitis Inflammation of the prostate d/t ascent of infection up the urethra or reflux of infected urine into the prostatic ducts Cause: Gram negative rods Most commonly: E coli (men > 35) G/C (men + for organism of suspicion Most likely E coli Prostatic massage is contraindicated! Why? Cause bacteremia Management: If cx suggestive of G or C, treat accordingly If over 35 yo or gram NEG bacteria grows, TMP- SMX is 1st line of treatment Quinolones have black box warning and should only be used for very ill or those who 1st and 2nd line deemed inappropriate Hospitalization may be required if febrile and septic appearing After afebrile for 48 hours -> oral ABX  Chronic Prostatitis MCC organism – E coli (80%) THEN Proteus, Enterococci, Trichomonas, HIV Causes Structural abnormality or recurrent UTI’s Acute may progress to chronic (>3 months) Symptoms Irritative – frequency, urgency, and dysuria. Cloudy urine Obstructive – hesitancy, poor or interrupted stream, straining to void and incomplete emptying. Malaise, arthralgia PE Non tender, boggy prostate Management Fluoroquinolones or TMP/SMX x 6-12 weeks Alpha blockers can help with chronic pain BPH vs Chronic Prostatis  Urethritis Inflammation of the urethra Pathogens: Gonococcal Non-gonococcal (MCC- chlamydia) Presentation: Asymptomatic, incidental on screening Dysuria Urethral discharge Diagnosis: Urethral swab PCR Treatment: Present as a co-infection! Treat both Retest 3 mo due to high rate of reinfection Sexual partners must be identified and treated! Gonococcal Ceftriaxone 250mg IM x 1 dose Non-gonococcal Doxycycline 100mg BID x 7 days (Azith is alternative - 1 g po x 1 dose) Urethritis – Complication  Glomerulonephritis Acute glomerulonephritis is an uncommon cause of AKI, accounting for about 5% of cases. The larger the percentage of glomeruli involved and the more severe the lesion, the higher the risk of a poor clinical outcome. Classified into five pathophysiologic processes, which are characterized by serologic analysis. Immune complex glomerulonephritis occurs when autoantibodies develop and combine with antigens to form immune complexes that deposit within glomeruli. There are several distinct immune complex glomerulonephritides, including IgA nephropathy, infection-related glomerulonephritis, lupus nephritis, and cryoglobulinemic glomerulonephritis (often associated with hepatitis C virus [HCV]). Anti-GBM–associated acute glomerulonephritis is either confined to the kidney or associated with pulmonary hemorrhage. The latter is called “Goodpasture syndrome” Injury is related to autoantibodies against type IV collagen in the GBM Pauci-immune acute glomerulonephritis is a form of small-vessel vasculitis associated with ANCAs, causing kidney disease without direct immune complex deposition or antibody binding. Tissue injury is believed to be due to cell-mediated immune processes. An example is granulomatosis with polyangiitis, a systemic necrotizing vasculitis of small arteries and veins associated with intravascular and extravascular granuloma formation. In addition to glomerulonephritis, these patients can have upper airway, pulmonary, and skin manifestations. Cytoplasmic ANCA (c-ANCA) is the common staining pattern. Microscopic polyangiitis is another pauci-immune vasculitis causing glomerulonephritis and is more commonly associated with perinuclear staining (p-ANCA). ANCA-associated and anti-GBM–associated acute glomerulonephritides have poor outcomes unless treatment is started early. Monoclonal immunoglobulin–mediated glomerulonephritis is characterized by the deposition of a monoclonal immunoglobulin in glomeruli, the tubular basement membrane, or both. Immunofluorescent or immunohistochemical staining of kidney biopsies detects monotypic immunoglobulin deposits. Many cases occur in the setting of an identifiable monoclonal gammopathy, but this is not always the case. Serum protein electrophoresis, immunofixation, and free light chain analysis are important diagnostic tests to perform when monoclonal immunoglobulin–mediated glomerulonephritis is suspected or confirmed. C3 glomerulopathy results from predominant C3 deposition in the glomeruli with or without minimal deposition of immunoglobulins. It is also identified by immunofluorescence or immunohistochemistry. The pathogenesis of C3 glomerulonephropathy stems from abnormalities in regulation of the alternative pathway of complement. Measurement of serum C3 levels may be helpful, but normal levels do not rule out C3 glomerulopathy. Other vascular causes of glomerulonephritis include hypertensive emergencies and the thrombotic microangiopathies such as hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura  Glomerulonephritis Symptoms and Signs Patients with acute glomerulonephritis are often hypertensive and edematous with an abnormal urinary sediment. Patients may experience extrarenal signs that reflect systemic manifestations of their disease (eg, rash in patients with lupus; coughing or sinus congestion in patients with ANCA glomerulonephritis). Macroscopic hematuria is uncommon (in contrast to microscopic hematuria), but may occur in select cases (eg, IgA nephropathy). Laboratory Findings Serum creatinine can rise over days to months, depending on the rapidity of the underlying process. Dipstick and microscopic evaluation reveal evidence of hematuria and subnephrotic proteinuria; there may be cellular elements such as dysmorphic red cells, red cell casts, and white cells. Red cell casts are specific for glomerulonephritis. Serum complement levels (C3, C4) may be low in immune complex glomerulonephritis (except for IgA nephropathy) or C3 glomerulopathy and normal in pauci-immune, anti-GBM–related, and most monoclonal immunoglobulin–mediated glomerulonephritides. Other tests that may be appropriate include ASO titers, anti-GBM antibody levels, ANCAs, antinuclear antibody titers, cryoglobulins, hepatitis serologies, serum protein electrophoresis, immunofixation, serum free light chains, blood cultures, and renal ultrasound. With few exceptions, a kidney biopsy is ultimately necessary to confirm the diagnosis, irrespective of laboratory data. Treatment Tailored to the specific type and severity of glomerulonephritis. It may include high-dose corticosteroids, rituximab, cytotoxic agents (such as cyclophosphamide), antiproliferative agents (eg, mycophenolate), and calcineurin inhibitors (eg, tacrolimus). Plasma exchange can be used in Goodpasture syndrome as a temporizing measure until chemotherapy can take effect. Glomerulonephritis Glomerulonephritis Hernias