GENITOURINARY DISORDERS with nursing care.pptx

this ppt will bw helpfull for BSN generic students for making better diagnosis and outstanding nursing care. the most common genitourinary tract infections are discussed here and eleborated for their diagnosis and treatment line along with nursing care. hope people who will learn from this ppt, do proper handling of pts in clinical areas

1. GENITOURINARY DISORDERS AHN 1 PRESENTER: NEELAM DILDAR TIME: 60MINUTES REFERENCE BOOK:BRUNNER’S AND suddarth

2. UTI UTI is an infection of any part of the urinary tract (kidneys, ureters, bladder, urethra) caused mostly by bacteria , leading to inflammation and urinary symptoms. Lower UTI: Cystitis (bladder), Urethritis (urethra ). Upper UTI: Pyelonephritis (kidney).

3. Causes / Risk Factors Bacteria (most common): Escherichia coli (70–90%). Klebsiella , Proteus , Enterococcus . Risk factors: Female gender (short urethra, proximity to anus). Poor hygiene. Sexual activity ("honeymoon cystitis"). Pregnancy. Diabetes mellitus. Indwelling catheters (CAUTI). Urinary obstruction (stones, enlarged prostate). Immunosuppression.

4. Pathophysiology Bacteria colonize periurethral area. Ascend through urethra → bladder → ureters → kidneys. Host defense failure (low immunity, obstruction) → infection spreads. Leads to inflammation, mucosal edema, and systemic symptoms if upper tract involved.

5. Clinical manifestation Lower UTI (Cystitis, Urethritis) Dysuria (burning urination). Frequency & urgency. Suprapubic pain. Hematuria (blood in urine). Cloudy, foul-smelling urine. Upper UTI (Pyelonephritis) Fever, chills. Flank pain (costovertebral angle tenderness). Nausea, vomiting. Malaise. Possible sepsis in severe cases.

6. Diagnostic Evaluation Urine analysis (UA): Pyuria (WBCs in urine). Bacteriuria. Nitrite test positive (Gram-negative bacteria). Leukocyte esterase positive. Urine culture & sensitivity: Gold standard. CBC: ↑ WBC count. Imaging (if complicated): Ultrasound, CT scan for obstruction/abscess.

7. Medical management Pharmacological Antibiotics (based on culture): Trimethoprim-sulfamethoxazole (TMP-SMX). Nitrofurantoin. Fluoroquinolones (ciprofloxacin, levofloxacin). Cephalosporins . Analgesics: Phenazopyridine (for burning urination). Antipyretics: Paracetamol for fever. Supportive Increased fluid intake (2–3 liters/day). Cranberry juice (acidifies urine, reduces bacterial adherence). Strict perineal hygiene.

8. Surgical / Interventional Management Correction of urinary obstruction (stones, prostate enlargement). Removal/replacement of infected catheter. Complications Pyelonephritis (kidney infection). Recurrent/chronic UTI. Urosepsis (life-threatening). Renal abscess, scarring, chronic kidney disease.

9. Nursing Care Plan / Interventions Assessment : Monitor urinary symptoms, fever, pain. Pain relief: Provide warm sitz baths, analgesics. Hydration: Encourage fluids to flush bacteria. Hygiene: Teach perineal cleaning (front to back in females). Monitor labs & culture reports. Catheter care: Strict asepsis, minimize indwelling catheter use. Health education: Void after intercourse. Avoid irritants (tight clothing, perfumed sprays). Complete full antibiotic course.

10. Renal abscess and tuberculosis

11. Renal abcess A renal abscess is a localized collection of pus in the kidney due to infection, usually from untreated or complicated urinary tract infection (UTI ). Causes / Risk Factors Ascending infection: Complicated UTI, pyelonephritis. Hematogenous spread: From Staphylococcus aureus bacteremia. Urinary tract obstruction (stones, strictures, prostate enlargement). Diabetes mellitus. Immunosuppression. Recent urinary instrumentation (catheter, surgery).

12. Pathophysiology Bacteria invade renal tissue → inflammation. Pus collects in localized area → abscess formation. Abscess enlarges → compresses renal tissue → risk of rupture into perinephric space → perinephric abscess/sepsis . Clinical Manifestations Persistent fever, chills, night sweats . Flank or abdominal pain. Dysuria, frequency, hematuria. Weight loss, malaise. Tenderness at costovertebral angle (CVA). In severe cases: septicemia, hypotension.

13. Diagnostic Evaluation/management CBC : ↑ WBC count. Urine culture: May or may not be positive. Blood culture: Detects bacteremia. Ultrasound / CT scan: Gold standard for detecting abscess size & location . Management Antibiotics: Broad spectrum initially, then according to culture. Percutaneous drainage (ultrasound/CT-guided needle aspiration). Surgical drainage or nephrectomy if abscess does not resolve. Supportive care: fluids, analgesics, antipyretics.

14. Complications Perinephric abscess. Sepsis, septic shock. Chronic renal failure if bilateral and untreated.

15. Renal tuberculosis Renal tuberculosis is a chronic granulomatous infection of the kidney caused by Mycobacterium tuberculosis , usually secondary to pulmonary TB. It is the most common form of extrapulmonary tuberculosis in the genitourinary tract . c auses / Risk Factors Hematogenous spread from pulmonary TB. Immunosuppression (HIV, steroid therapy). Previous history of TB. Poor living conditions / endemic areas.

16. Pathophysiology M . tuberculosis spreads to renal cortex via bloodstream. Granulomas form → caseating necrosis. Progressive destruction of renal tissue → cavitation, fibrosis. Infection may extend to ureters, bladder, epididymis → genitourinary TB .

17. Clinical Manifestations Initially asymptomatic (early disease). Urinary symptoms: Dysuria, frequency, urgency. Hematuria (often microscopic). Sterile pyuria (pus cells but no bacterial growth). Flank pain. Constitutional symptoms: Low-grade fever, night sweats, weight loss. Advanced cases: Renal colic, obstruction, renal failure.

18. Diagnostic Evaluation Urine tests: Persistent sterile pyuria. Acid-fast bacilli (AFB) in urine (3 consecutive morning samples). Urine culture for M. tuberculosis (Gold standard). Imaging: IVP (Intravenous pyelogram) → "moth-eaten calyces", strictures. CT scan, MRI → detects cavitations & scarring. Tuberculin skin test ( Mantoux ).

19. Management Anti-tubercular therapy (ATT): Standard regimen (HRZE: Isoniazid, Rifampicin, Pyrazinamide, Ethambutol) for 6–9 months. Surgical options: Nephrectomy if kidney is nonfunctional or severely destroyed. Ureteral reconstruction if strictures present. Supportive care: fluids, nutrition, monitoring renal function.

20. Complications Ureteric strictures. Hydronephrosis . Renal failure (bilateral disease). Infertility in males ( epididymal involvement).

21. glomerulonephritis Glomerulonephritis is an immunologic disorder of the kidney characterized by inflammation of the glomerular capillaries . It is often the result of an antigen–antibody immune response to an infection elsewhere in the body (commonly streptococcal infection of the throat).

22. Pathophysiology After an infection (commonly group A β- hemolytic streptococcus ), immune complexes are formed and deposited in the glomeruli. This triggers an inflammatory response → leukocyte infiltration → glomerular injury. The glomerular basement membrane thickens and becomes permeable to proteins and red blood cells . Results in proteinuria, hematuria, decreased GFR, and edema .

23. Types Acute post-streptococcal glomerulonephritis (APSGN). Chronic glomerulonephritis. Rapidly progressive glomerulonephritis (RPGN).

24. Clinical Manifestations Urinary findings: Hematuria (cola- or tea-colored urine). Proteinuria. Oliguria. Edema: Periorbital and dependent edema. Hypertension. General symptoms: Headache, malaise, flank pain. In severe cases → encephalopathy, pulmonary edema, heart failure.

25. Diagnostic Evaluation Urinalysis : Proteinuria, hematuria, red blood cell casts. Blood tests: Elevated BUN and creatinine, ↓ GFR. ASO titer: Evidence of recent streptococcal infection. Renal biopsy: To confirm diagnosis & type. Electrolytes: Hyperkalemia, metabolic acidosis in advanced cases.

26. Medical Management Antibiotics : To treat underlying infection (e.g., penicillin for streptococcus). Corticosteroids / Immunosuppressants : In severe or rapidly progressive cases. Antihypertensives & diuretics: To control blood pressure and edema. Dietary restrictions: Sodium restriction (for edema & hypertension). Protein restriction (if azotemia severe). Potassium restriction (if hyperkalemia present). Dialysis: For renal failure.

27. Nursing Management Monitor vital signs (especially BP). Assess fluid balance : intake–output, daily weight, edema. Monitor labs: BUN, creatinine, electrolytes, urinalysis. Provide rest in acute phase. Administer prescribed medications. Patient teaching: Importance of completing antibiotics. Low-sodium, adequate rest. Monitoring urine output and follow-up.

28. Complications Hypertensive encephalopathy. Heart failure. Pulmonary edema. Chronic glomerulonephritis → End-stage renal disease (ESRD).

29. Urethral stricture

30. Urethral stricture Narrowing of the urethra due to scar tissue formation → obstructs urine flow. Causes Congenital. Trauma or instrumentation (catheterization, surgery). Infections (especially sexually transmitted). Post-inflammatory scarring (e.g., urethritis). Pathophysiology Scar tissue → narrowing → bladder outflow obstruction. Leads to urinary retention , infections, and secondary complications ( hydronephrosis if severe).

31. Clinical Manifestations Weak or diminished urine stream. Straining during urination. Dribbling after voiding. Urinary retention, recurrent UTIs. Diagnostic Evaluation Urethrography . Cystoscopy. Uroflowmetry (↓ flow rate). Management Dilation of stricture. Urethrotomy (endoscopic incision). Urethroplasty (surgical reconstruction for recurrent cases).

32. Hydroureter and hydronephrosis

33. hydroureter Dilation of the ureter due to obstruction of urine outflow. Causes Urethral stricture, ureteral calculi, tumors, congenital anomalies. Neurogenic bladder. Pathophysiology Obstruction → urine accumulates in ureter → ureter dilates. May progress to hydronephrosis if pressure transmitted to renal pelvis.

34. Clinical Manifestations Often asymptomatic initially. Flank or abdominal pain. Recurrent urinary tract infections. Signs of obstruction (oliguria, retention). Diagnostic Evaluation Ultrasound of kidney & ureter. Intravenous pyelography (IVP). CT scan. Management Identify & relieve obstruction (stone removal, stricture dilation, tumor excision). Stent placement to restore flow. Antibiotics for infection.

35. hydronephrosis Dilation of the renal pelvis and calyces due to obstruction of urine flow. Causes Urethral strictures, calculi, tumors, congenital obstruction (UPJ stenosis). Pregnancy (physiologic hydronephrosis ). Prostatic hypertrophy. Pathophysiology Obstruction → urine backs up into kidney → ↑ hydrostatic pressure. Leads to progressive atrophy of renal tissue and impaired renal function. Prolonged obstruction → chronic kidney disease.

36. Clinical Manifestations May be asymptomatic (if slow onset). Dull flank pain, may radiate. Palpable renal mass. Recurrent UTIs, hematuria. Hypertension (due to renin–angiotensin activation). Diagnostic Evaluation Ultrasound (best initial test). CT scan or MRI (to locate cause of obstruction). IVP (shows delayed excretion, dilated system). Renal function tests (BUN, creatinine).

37. Management Relieve obstruction (stone removal, tumor resection, ureteric stent, nephrostomy tube). Antibiotics for infection. Nephrectomy if kidney is severely damaged and nonfunctional .

38. Nursing management Monitor urine output, color, and stream. Assess for flank pain, bladder distention. Strict intake–output chart. Administer prescribed antibiotics and analgesics. Prepare for surgical intervention if needed. Patient education: hydration, infection prevention, follow-up care.

39. Urinary incontinence Involuntary loss of urine → social or hygienic problem. Types Stress incontinence – leakage with coughing, sneezing, lifting (weakened pelvic floor). Urge incontinence – strong urge, cannot hold urine (overactive bladder). Overflow incontinence – bladder overdistended (e.g., BPH, diabetes neuropathy). Functional incontinence – impaired cognition/mobility prevents reaching toilet. Mixed incontinence – combination (usually stress + urge).

40. Causes Aging, childbirth, menopause (↓ estrogen). Neurologic disorders (stroke, Parkinson’s, spinal cord injury). Prostate enlargement. Medications (diuretics, sedatives). Clinical Manifestations Dribbling, urgency, frequency. Leakage with exertion or urge. Nocturia . Diagnosis Voiding diary. Urinalysis (rule out UTI). Post-void residual volume (ultrasound, bladder scan).

41. Management Behavioral : Bladder training, Kegel’s exercises, fluid schedule. Pharmacological : Anticholinergics (oxybutynin, tolterodine ), estrogen therapy. Surgical : Sling procedures, artificial urinary sphincter. Devices : Pessaries, absorbent pads.

42. Urinary Retention Definition Inability to completely empty the bladder. Types Acute retention : sudden painful inability to void (emergency). Chronic retention : gradual bladder distension, incomplete emptying. Causes Obstructive: BPH, strictures, stones. Neurogenic: spinal cord injury, diabetes neuropathy. Medications: anticholinergics, opioids. Postoperative retention (anesthesia).

43. Pathophysiology Obstruction/neurologic dysfunction → incomplete bladder emptying → overdistention → ↑ risk of infection & hydronephrosis . Clinical Manifestations Inability to urinate. Distended bladder, suprapubic discomfort. Overflow incontinence (dribbling). Restlessness.

44. Diagnosis Bladder scan (post-void residual). Catheterization (diagnostic + therapeutic). Management Immediate catheterization (Foley or intermittent). Treat underlying cause (BPH meds/surgery, remove stricture/stone). Intermittent self-catheterization for chronic cases. Cholinergic drugs ( bethanechol ) if neurogenic.

45. Renal Calculi ( Urolithiasis / Nephrolithiasis) Definition Formation of stones in urinary tract (kidney, ureter, bladder). Types of Stones Calcium oxalate/phosphate (most common). Uric acid (gout, high purine diet). Struvite (infection stones) – associated with UTI by urease-producing bacteria. Cystine – rare, genetic defect.

46. Risk Factors Dehydration, hot climate. High intake of calcium, oxalate, purines. Hyperparathyroidism. Recurrent UTIs. Family history. Pathophysiology Supersaturation of urine with crystals → aggregation → stone formation. Stones obstruct urinary flow → hydronephrosis , infection, renal damage.

47. Clinical Manifestations Severe colicky flank pain → radiates to groin/genitals. Hematuria. Nausea, vomiting. Urinary frequency, urgency (if stone in bladder). Oliguria/anuria (if bilateral obstruction). Diagnosis Urinalysis (hematuria, crystals). Non-contrast CT scan (gold standard). Ultrasound (especially in pregnancy). KUB X-ray (calcium stones visible).

48. Management Conservative : Analgesics (NSAIDs, opioids). Hydration (2–3 L/day). Medical expulsive therapy ( tamsulosin ). Interventional : Extracorporeal shock wave lithotripsy (ESWL). Ureteroscopy . Percutaneous nephrolithotomy (for large stones). Surgical removal if refractory. Prevention : Increase fluids. Dietary modification (low oxalate/purine, adequate calcium). Thiazide diuretics for hypercalciuria . Allopurinol for uric acid stones.

49. Nursing Considerations (Common) Monitor urine output & characteristics. Pain management. Encourage fluids. Strain urine to detect stones/fragments. Teach lifestyle/dietary modifications. Prevent infection (aseptic catheter care if needed).

50. Acute Renal Failure (ARF) / Acute Kidney Injury (AKI) Definition : A sudden, rapid decline in kidney function , leading to accumulation of waste products (urea, creatinine) and disturbances in fluid/electrolytes. Potentially reversible if treated promptly.

51. Causes (Etiology) Prerenal causes (↓ blood supply to kidneys): Hypovolemia (hemorrhage, dehydration, burns) Shock (septic, cardiogenic) Heart failure Intrarenal causes (damage to kidney tissue): Acute tubular necrosis (ischemia, nephrotoxic drugs like aminoglycosides, contrast agents) Glomerulonephritis Infection (pyelonephritis) Postrenal causes (obstruction of urine flow): Kidney stones, tumors Prostatic hypertrophy/stricture

52. Pathophysiology ↓ Renal perfusion or direct damage → impaired filtration → retention of nitrogenous wastes ( azotemia ). Disruption of fluid, electrolyte, and acid–base balance (↑ potassium, metabolic acidosis). Untreated ARF may progress to end-stage renal disease .

53. Clinical Manifestations Oliguria (<400 mL/day) or anuria Fluid overload (edema, hypertension, pulmonary congestion) Electrolyte imbalances: hyperkalemia, hyponatremia, hypocalcemia Uremic symptoms: nausea, vomiting, confusion, fatigue Metabolic acidosis

54. Diagnostic Evaluation Serum creatinine ↑ BUN ↑ Hyperkalemia, metabolic acidosis on ABG Urinalysis (proteinuria, casts, specific gravity changes) Imaging: Ultrasound/CT (obstruction)

55. Medical & Nursing Management Identify and treat cause (e.g., fluid resuscitation, remove obstruction, stop nephrotoxic drugs). Fluid & electrolyte management : Strict I&O Restrict potassium & protein IV glucose/insulin or calcium gluconate for hyperkalemia Dialysis if unresponsive. Nursing Care : Monitor vitals, urine output, weight Dietary: low potassium, low protein, high carbs Prevent infection, skin care

56. Chronic Renal Failure (CRF) / Chronic Kidney Disease (CKD) Definition : Progressive, irreversible destruction of kidney function , lasting more than 3 months. Leads to end-stage renal disease (ESRD) requiring dialysis or transplantation.

57. Causes (Etiology) Diabetes mellitus (leading cause) Hypertension Chronic glomerulonephritis Polycystic kidney disease Recurrent infections (pyelonephritis) Obstructive uropathy

58. Pathophysiology Progressive nephron destruction → compensatory hyperfiltration of remaining nephrons → sclerosis and further damage. Gradual buildup of uremic toxins → multi-system involvement.

59. Clinical Manifestations (Uremic Syndrome) Fluid & Electrolytes: edema, hypertension, pulmonary edema Electrolyte: hyperkalemia, hypocalcemia, hyperphosphatemia, metabolic acidosis Gastrointestinal: nausea, anorexia, uremic fetor Neurological: confusion, seizures, peripheral neuropathy Hematologic: anemia (↓ erythropoietin), bleeding tendency Skeletal: renal osteodystrophy (bone pain, fractures) Skin: pruritus, uremic frost

60. Stage GFR (mL/min/1.73 m²) Description Clinical Features Stage 1 ≥90 (with evidence of kidney damage such as proteinuria, hematuria, or abnormal imaging) Kidney damage with normal or increased GFR Often asymptomatic, early changes detectable only via labs/urine tests. Stage 2 60–89 Mild decrease in GFR with kidney damage Usually asymptomatic, may have subtle lab changes. Stage 3a 45–59 Mild to moderate decrease in GFR Fatigue, anemia, mild HTN, early bone disease. Stage 3b 30–44 Moderate to severe decrease in GFR Increased creatinine, edema, metabolic acidosis, worsening HTN. Stage 4 15–29 Severe decrease in GFR Severe symptoms: anemia, hyperkalemia, metabolic acidosis, bone/mineral disorders, uremic symptoms. Preparation for dialysis/transplant. Stage 5 (ESRD) <15 (or on dialysis) Kidney failure Uremic symptoms: nausea, vomiting, confusion, pruritus, severe fluid/electrolyte imbalance. Requires renal replacement therapy (dialysis/transplant).

61. Diagnostic Evaluation ↑ BUN, creatinine ↓ GFR (<60 mL/min/1.73 m² for ≥3 months) Electrolyte disturbances Anemia (low Hb , Hct ) Imaging: small, shrunken kidneys on ultrasound

62. Medical & Nursing Management Slow progression & treat cause (control BP, manage diabetes). Dietary management: Low protein, potassium, sodium, phosphorus High carbohydrate, vitamins Medications: Antihypertensives Diuretics (careful use) Phosphate binders (calcium carbonate, sevelamer ) Erythropoietin injections for anemia Vitamin D analogs for bone disease Dialysis (hemodialysis or peritoneal dialysis). Renal transplantation for ESRD.

63. Nursing Considerations Monitor fluid balance, electrolytes, daily weight Educate on diet & medication adherence Provide emotional support (chronic illness, dialysis stress) Prevent infection and complications

64. Feature Acute Renal Failure (ARF/AKI) Chronic Renal Failure (CRF/CKD) Onset Sudden, hours–days Gradual, months–years Duration Usually reversible Irreversible Cause Prerenal, intrarenal, postrenal Diabetes, HTN, GN, PKD Clinical Oliguria, azotemia, hyperkalemia Uremic syndrome, anemia, bone disease Treatment Remove cause, dialysis (short-term) Long-term dialysis, transplant Prognosis Good if treated early Progressive, ESRD

65. Urinary bladder carcinoma Bladder cancer is a malignant tumor of the urinary bladder mucosa , most commonly transitional cell carci noma (urothelial carcinoma ) . Causes & Risk Factors Cigarette smoking (most significant) Occupational exposure to dyes, rubber, leather, chemicals Chronic bladder irritation/infections Radiation therapy to pelvis Long-term catheterization

66. Pathophysiology Usually arises from urothelial cells lining the bladder. May spread by direct invasion → muscle wall → perivesical tissue → lymph nodes → distant metastasis (lungs, liver, bones).

67. Clinical Manifestations Painless hematuria (most common) Dysuria, frequency, urgency Pelvic/back pain (advanced disease ) Diagnostic Evaluation Urine cytology (malignant cells in urine) Cystoscopy with biopsy (gold standard ✅) CT / MRI for staging IV urography / Ultrasound

68. Management Medical / Non-surgical Intravesical therapy: BCG vaccine, mitomycin C (for superficial tumors) Chemotherapy / immunotherapy (systemic for advanced cases) Surgical Transurethral resection (TURBT) for small superficial tumors Cystectomy (partial or radical with urinary diversion in invasive cancer) Urinary diversions : Ileal conduit, continent reservoir, orthotopic neobladder Nursing Care Monitor urine output, bleeding, infection Educate about stoma care (if diversion) Support body image, lifestyle adjustments

69. Renal Carcinoma (Renal Cell Carcinoma) Definition Renal cell carcinoma (RCC) is the most common kidney cancer , arising from the renal cortex (proximal tubular epithelium ) . Risk Factors Smoking Obesity Chronic kidney disease / long-term dialysis Family history, genetic syndromes (von Hippel-Lindau) Male gender, age >50

70. Pathophysiology Tumor originates in renal cortex → invades renal vein → IVC → can spread to lungs, liver, bones, brain. Produces paraneoplastic syndromes (due to abnormal hormone secretion: erythropoietin, renin, PTH-like hormone).

71. Clinical Manifestations Classic triad (rare, late finding): Hematuria Flank pain Palpable abdominal mass Weight loss, fever, hypertension Anemia or polycythemia (due to EPO production) Metastatic symptoms (cough, bone pain)

72. Diagnostic Evaluation Ultrasound / CT scan (preferred imaging) MRI (for vascular invasion) IV urography, renal angiography (less common) Biopsy (rare, only if diagnosis uncertain)

73. Management Surgical (main treatment) Radical nephrectomy (kidney + adrenal gland + fat + lymph nodes) Partial nephrectomy (for small localized tumors, nephron-sparing) Medical RCC is resistant to chemo/radiation Targeted therapy: Tyrosine kinase inhibitors ( sunitinib , sorafenib ), immunotherapy (interleukin-2, checkpoint inhibitors). Nursing Care Pre/post-op care for nephrectomy (monitor urine, bleeding, infection) Monitor renal function (BUN, creatinine, electrolytes) Psychosocial support, smoking cessation, nutrition

74. Key point Bladder cancer → usually detected early due to hematuria; treated with TURBT & intravesical therapy. Renal carcinoma → often silent until advanced; treated mainly with nephrectomy.