Chapter 18- Urinary updated

Urinary System Anatomy Review

• Core components (paired unless noted):

  • Kidneys → renal hilum, cortex–medulla–pelvis, renal artery & vein

  • Ureters → convey urine to bladder by peristalsis

  • Urinary bladder → muscular storage reservoir, trigone area clinically important for infection spread

  • Urethra → terminal conduit; length & course differ in sexes (female-short → ↑UTI risk)

  • Adjacent vasculature/organs as labeled on slide: hepatic veins, aorta, inferior vena cava, adrenal gland, uterus, rectum etc.

  • Nephrons there are about 1 mil they filter the blood. glomeruluis first defense, bowman capsule second defense proximal convuluted tuble reabsorbs good stuff, loop of henley reabsorbs water and salt. Distal convulted tuble one last filter, collecting duct sends it all to the bladder

• Hormonal fine-tuning occurs along the nephron:

  • Antidiuretic hormone (ADH) -produced in the hypothalmus acts on collecting ducts → ↑aquaporins → reabsorbs H₂O, concentrates urine.

Functions of the Urinary System

• Excretory - clean up crew gets rid of waste in the body

  • Removes nitrogenous wastes (urea, creatinine, uric acid), excess hormones, drugs & xenobiotics.

• Homeostatic regulation

  • Maintains water balance, serum osmolality, electrolyte composition (Na⁺, K⁺, Ca²⁺, Cl⁻, HCO₃⁻).

  • Acid–base buffering via secretion/reabsorption of H^+ & HCO_3^-.

• Endocrine

  • Secretes erythropoietin (stimulates red-cell production in bone marrow).

  • Converts vitamin D to active calcitriol \bigl(1,25\text{-(OH)}2\,\text{D}3\bigr).

  • Releases renin, initiating the renin-angiotensin-aldosterone (RAA) cascade → blood-pressure control.

Renin–Angiotensin–Aldosterone (RAA) System

• Trigger: fall in renal perfusion pressure or sympathetic stimulation. kidneys then release Renin that acts on Angio which is a protein

• Sequence (slide 7 graphic):

  • \text{Angiotensinogen} \xrightarrow{\text{Renin}} \text{Ang I} \xrightarrow{\text{ACE}} \text{Ang II}

  • Ang II actions:

  • Potent vasoconstriction → ↑SVR (systemic vascular resistance)

  • Stimulates adrenal cortex → aldosterone release → Na⁺ & H₂O retention in distal nephron.

  • Enhances sympatheangiotension

• et result: restoration of arterial pressure \uparrow BP .

• Angiotensin 1 is inactive, Angiotensin 2 is active ACE (angiotension cangiotensionzyme) comes from the Lungs

Diagnostic Evaluation of the Urinary System

• Urinalysis (non-invasive, inexpensive)

  • pH (acidic ~6.0 normally) → alkalinity may indicate infection. Low PH indicates dehydration

  • Protein (proteinuria = glomerular leakage)

  • Glucose → diabetes screen.

  • Microscopy: bacteria, casts, crystals, RBC/WBC.

  • Specific gravity (1.005–1.030 normal) reflects concentrating ability.

• Blood tests

  • BUN & \text{Creatinine} → glomerular filtration markers. - BUN means waste

  • Electrolytes/acid-base (special note: Ca²⁺ on slide).

• Imaging

  • KUB (Kidney–Ureter–Bladder) X-ray → detect calculi, structural anomalies, obstructions.

• Endoscopic/other

  • Cystoscopy → direct visualization of bladder/urethra.

  • Renal biopsy → histology for GN vs. malignancy.

Disorders of Voiding

Incontinence (loss of voluntary control) - can be casued by pregnancy, spinal injury.

• Stress type → weak pelvic floor; leaks with cough, laugh, lifting.

• Urge type → detrusor overactivity; sudden compelling need.

• Overflow type → urethral obstruction or neurogenic atony; constant dribble.

• Neurogenic → CNS/PNS lesions (spinal cord, MS, diabetic neuropathy). - Spinal Injury

• Pediatric term: enuresis (incontinence after toilet-training age).

Retention

• Inability to empty bladder → painful distention, risk of infection/reflux.

• Causes: BPH, neurogenic bladder, medication side effects.

Urinary Tract Infections (UTIs) -Can be casued by Catheter, Intercourse,

• Urine is ordinarily sterile; becomes a ‘‘buffet’’ for bacteria when stasis or contamination occurs.

• Common pathogen: E.\,coli (≈80 %). Other gram-negatives, enterococci.

• Epidemiology

  • ↑Women (short urethra), post-menopausal, pregnant, sexual activity.

  • Older men: prostate enlargement → stasis; instrumentation (catheters).

• Anatomic terms

  • Cystitis (bladder), urethritis (urethra), pyelonephritis (renal pelvis/parenchyma).

• Clinical picture

  • Local: dysuria, urgency, frequency, nocturia, suprapubic/flank pain.

  • Systemic: fever, leukocytosis if upper-tract.

• Management → culture-guided antibiotics, fluids, address risk factors.

Glomerular Disorders

Acute Post-streptococcal Glomerulonephritis (prototype) - from an infection of strep

• Immune complex deposition after \beta-hemolytic strep infection → inflammation → increased glomerular permeability.

• Pathophysiology linkage: Capillary damage → protein & RBC leakage; reduced GFR triggers renin → fluid retention & hypertension.

• Hallmarks

  • Sudden ‘‘coffee-colored’’ (cola) urine, periorbital edema, elevated BP, flank pain.

  • Oliguria <400{mL\/day}

  • Labs: ↑BUN/Cr, anti-streptolysin-O titres, ↓C3, ↑ESR/CRP.

• Therapy: corticosteroids, limit Na⁺/fluid/protein, manage BP; most children recover.

Nephrotic Syndrome -Secondary to multiple different kidney diseases

• Not a single disease but a pattern of injHypoalbuminemia → ↓plasma oncoticic, etc.).

• Mechanism: massive glomerular basement membrane leak → >3.5\,\text{g\/24h} protein loss.

• Consequences

  • Hypoalbuminemia → ↓plasma oncotic pressure → generalized edema (anasarca), ascites.

  • Hyperlipidemia & lipiduria (‘‘frothy’’ urine) as liver compensates for protein loss.

  • Possible thrombotic risk (loss of antithrombin III).

• Management: high-dose steroids (if minimal-change), ACE/ARBs for protein reductioLasixuretics (Lasix) + IV albumin, salt restriction.

Urolithiasis (Renal & Ureteric Calculi)

• Composition

  • Calcium oxalate/phosphate (≈80 %), struvite, uric acid, cystine.

  • Predisposed by hypercalciuria, dehydration, gout, infection, metabolic disorders.

• Pathogenesis → supersaturation → nucleation → stone growth; can obstruct ureter causing hydronephrosis (urine back-pressure on kidney).

• Presentation: renal colic (excruciating flank radiating to groin), hematuria, reduced urine flow, sandy sediment.

• Therapy

  • Aggressive hydration, analgesia.

  • Extracorporeal shock-wave lithotripsy (ESWL) or percutaneous nephrolithotomy for large/obstructing stones.

  • Preventive: thiazides, allopurinol, dietary oxalate reduction.

Urinary Tract Malignancies

Renal Cell Carcinoma (RCC)

• Adenocarcinoma from renal tubular epithelium; often silent until metastatic.

• Classic triad (rarely all present): painless hematuria, flank mass, flank pain.

• Paraneoplastic syndromes: hypercalcemia (PTHrP), erythrocytosis or anemia, Cushing’s (ACTH), HTN (renin).

• Management → radical nephrectomy; targeted TKIs or immunotherapy if advanced.

Bladder Cancer (mostly transitional-cell)

• Risk: aromatic amines (dye, rubber industry), chronic smoking, schistosomiasis (Squamous type), cyclophosphamide.

• Symptoms: painless gross hematuria, irritative voiding (dysuria, frequency), recurrent UTIs.

• Treatment: transurethral resection ± intravesical BCG/chemo, cystectomy for muscle-invasion; urinary diversion (ileal conduit, neobladder) may be required.

Renal Failure Spectrum Hyper tension and Diabetees are the mpst common causes of renal failure

Acute Kidney Injury (AKI)

• Rapid ↓GFR (<48 h) from prerenal, intrinsic, or postrenal cause.

• Findings: oliguria/anuria, fluid overload edema, metabolic acidosis (↑H⁺), hyperkalaemia >5.5\,\text{mmol\/L} → arrhythmia, confusion (ure