The excretory system is responsible for eliminating metabolic waste products - substances produced during normal body metabolism that are toxic if allowed to accumulate. Key waste products excreted: Urea (from protein metabolism), Carbon dioxide (from cellular respiration), Water (from metabolic reactions), Salts/ions (excess minerals), Bile pigments (from haemoglobin breakdown). Organs of excretion: Kidneys (urea, salts, water), Lungs (CO2, water), Skin (salts, water - sweat), Liver (bile pigments). The excretory system also helps maintain homeostasis - stable internal environment.

Aldosterone is a mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex. It acts on the DCT and collecting duct: Increases Na+ reabsorption (water follows - increases blood volume and pressure), Increases K+ secretion (into urine), and Increases H+ secretion (alkalinising effect). Stimulated by: Angiotensin II (RAAS system), high blood K+, low blood Na+. Conn's syndrome (primary hyperaldosteronism) = excess aldosterone - hypertension, hypokalaemia. Addison's disease = aldosterone deficiency - low BP, hyperkalaemia.

Erythropoietin (EPO) is a glycoprotein hormone produced by peritubular cells of the renal cortex in response to low oxygen levels (hypoxia) in the blood. EPO stimulates the bone marrow to produce more red blood cells (erythropoiesis), increasing oxygen-carrying capacity. Clinical significance: In Chronic Kidney Disease (CKD) - reduced EPO production - anaemia of chronic disease - treated with recombinant EPO (epoetin). EPO doping - illicitly used by athletes (cyclists, runners) to boost RBC count and endurance. People at high altitude naturally produce more EPO - polycythaemia (more RBCs) - part of acclimatisation.

The RAAS is a critical hormonal system for blood pressure and fluid regulation: Low blood pressure/volume > Juxtaglomerular (JG) cells of kidney secrete Renin > Renin converts Angiotensinogen (liver) to Angiotensin I > ACE (Angiotensin Converting Enzyme) in lungs converts Angiotensin I to Angiotensin II > Angiotensin II causes: Vasoconstriction (increases BP), Stimulates Aldosterone release (Na+/water retention), Stimulates ADH release (water retention), and Stimulates thirst. ACE inhibitors (e.g., ramipril) and ARBs (e.g., losartan) block this system to treat hypertension.

The Countercurrent Mechanism allows the kidney to produce urine more concentrated than plasma. Two components: 1) Countercurrent Multiplier (Loop of Henle) - The descending and ascending limbs run in opposite directions, establishing an increasing osmolarity gradient in the medullary interstitium (from ~300 mOsm in cortex to ~1200 mOsm in deep medulla). 2) Countercurrent Exchanger (Vasa Recta) - The capillaries surrounding the loop of Henle also flow in opposite directions, maintaining the medullary gradient without washing it away. Under ADH influence, the collecting duct becomes permeable to water - water moves out into concentrated medulla - concentrated urine is produced.

The kidneys are the primary organs of excretion in humans. They are a pair of bean-shaped organs located in the retroperitoneal space (behind the peritoneum) in the abdominal cavity, on either side of the vertebral column at the level of T12-L3 vertebrae. The right kidney is slightly lower than the left (due to the liver above it). Each kidney is approximately 10-12 cm long, 5-6 cm wide, and weighs about 150 g. Together, the kidneys filter approximately 180 litres of blood per day, producing about 1.5 litres of urine.

The Ureter is a muscular tube (~25-30 cm long, 3-4 mm diameter) that connects each renal pelvis (of the kidney) to the urinary bladder. There are two ureters - one for each kidney. Structure: three layers - inner mucosa (transitional epithelium), middle muscularis (smooth muscle), outer adventitia (fibrous). Function: carries urine from the kidney to the bladder by peristaltic contractions (wave-like muscular movements). The ureter enters the bladder at the ureterovesical junction (UVJ) - a common site for kidney stones (renal calculi) to get stuck.

Acute Kidney Injury (AKI) (previously called Acute Renal Failure - ARF) is a sudden deterioration in kidney function occurring over hours to days, leading to accumulation of waste products and fluid/electrolyte imbalances. Causes classified as: Pre-renal (most common, ~55%) - reduced blood flow to kidneys (dehydration, shock, heart failure, haemorrhage). Renal (Intrinsic) - direct kidney damage (glomerulonephritis, ATN - acute tubular necrosis - most common intrinsic, nephrotoxic drugs). Post-renal - obstruction to urine outflow (kidney stones, enlarged prostate, tumours). AKI is potentially reversible with treatment. Diagnosis: rising serum creatinine, reduced urine output. Treatment: treat underlying cause, fluid management, dialysis if severe.

The Nephron is the structural and functional unit of the kidney. Each kidney contains approximately 1-1.3 million nephrons. Each nephron consists of: Renal corpuscle (Bowman's capsule + Glomerulus), Proximal Convoluted Tubule (PCT), Loop of Henle (descending and ascending limbs), Distal Convoluted Tubule (DCT), and Collecting Duct. Types of nephrons: Cortical nephrons (85% - short loop of Henle, located mainly in cortex) and Juxtamedullary nephrons (15% - long loop of Henle, important for urine concentration).

The Urinary Bladder is a hollow, distensible (stretchable) muscular organ located in the pelvis that stores urine. Key features: Capacity = 400-600 mL (urge to urinate at ~300 mL), Wall = Detrusor muscle (smooth muscle - three layers) contracts during urination, Lining = Transitional epithelium (urothelium) - can stretch without tearing, Trigone = triangular area at the base of the bladder formed by the two ureteral openings and internal urethral orifice (most sensitive area; common site of infection), and Micturition (urination) = voluntary control via external urethral sphincter (skeletal muscle); involuntary via internal urethral sphincter (smooth muscle).