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8...urinary system
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8...urinary system

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  • 1. 1 Urinary system Renal physiology
  • 2. 2 Urinary system  Maintain homeostasis By maintaining water, electrolyte balance, acid-base regulation and endocrine functions. Component of urinary system: 1. Kidney: formation of urine 2. Ureter: convey urine from kidney 3. Urinary bladder: Reservoir 4. Urethra: excrete urine from bladder to exterior
  • 3. 3
  • 4. 4 Functions of kidney: 1. Formation of urine: regulate water, electrolyte and acid-base balance 2. Endocrine function: a. Formation of erythropoietin b. Conversion of 25 hydroxycholecalciferol to 1, 25 Dihydroxycholecalciferol (active vit D) c. Secretion of renin d. Produce prostaglandin 3.Excretory function: Excretes waste products, e.g., urea, uric acid, creatinine, drugs and toxic substances from body 4. Degradation of several polypeptide hormones, Insulin, glucagons, PTH
  • 5. 5
  • 6. 6 Nephrone  Structural and functional unit of kidney.  About 1 million nephrons in each kidney 1. Glomerulus: Through which large quantity of fluid are filtered from blood 2. Renal tubules: Filtered fluid is converted into urine. It consists of a. Bowman’s’ capsule b. Proximal convoluted tube c. Descending limb d. Loop of Henle e. Ascending limb f. Distal convoluted tubule g. Collecting tubule
  • 7. 7
  • 8. 8 Renal blood flow
  • 9. 9
  • 10. 10 Approximate pressure in circulation of normal kidney 1. Renal artery: 100 mmHg 2. Glomerular capillary: 60 mmHg 3. Peritubular capillary: 18 mmHg 4. Renal vein: 9 mmHg Pressure in renal tubule 1. Proximal convoluted tubule: 18 mmHg 2. DCT: 10 mmHg 3. Collecting tubule: 2 mmHg 4. Renal pelvis: 0 mmHg 5. Interstitial fluid: 6 mmHg
  • 11. 11 Glomerular filtration: The filtration that occurs through glomerular capillary - glomerular filtration How filtration occurs? It occurs due to effective filtration pressure 1. The force that forces the fluid outward Glomerular capillary pressure = 60 mmHg 2. The force that opposes movement of fluid outward Capsular pressure = 18 mmHg Colloidal osmotic pressure in glomerulus: 32 mmHg Total +18+32 = 50 mmHg Effective filtration pressure = Force that forces fluid outward – force that opposes = (60-50) = 10 mmHg This 10 mmHg of effective filtration pressure that causes filtration
  • 12. 12 Glomerular filtrate: Amount 180 lit/day Urine formed is less than 1% of glomerular filtrate 99% of glomerular filtrate is reabsorbed Composition of glomerular filtrate: a. It is isotonic to plasma b. It contains no cellular element c. It contains about 0.03% protein, about 1/240 the protein in plasma d. The electrolyte and other solute composition is similar to that of interstitial fluid
  • 13. 13 The quantity of glomerular filtrate formed each minute by all the nephrons of both kidney is called GFR. It is about 125 ml/min. Factors that effect GFR: A) Major factors: 1. Glomerular capillary pressure: It promotes filtration. 2. Plasma colloidal osmotic pressure: It opposes filtration. 3. Bowman’s capsular pressure: It opposes filtration. 4. Colloidal osmotic pressure of protein in Bowman’s capsule, insignificant. 5. Surface area of filtration. Glomerular filtration rate:
  • 14. 14 B) Other factors: a. Renal blood flow: b. Constriction of afferent arteriole – c. Constriction of efferent arteriole: d. Sympathetic stimulation: Vasoconstriction of afferent arteriole-- -– decrease GFR e. Arterial blood pressure: Increase arterial blood pressure- decrease GFR due to autoregulation
  • 15. 15 Kidney effectively maintains renal blood flow and GFR relatively constant over an arterial pressure range between 80-170 mmHg. This is called auto regulation. Mechanism of autoregulation of GFR: •GFR is autoregulated by tubuloglomerular feedback mechanism •This mechanism has two components that can act together to control GFR. 1. Afferent arteriolar feedback mechanism 2. Efferent arteriolar feedback mechanism The feedback mechanism depends on “JG complex” especially macula densa. Autoregulation of GFR:
  • 16. 16 Afferent arteriolar vasodilator feedback mechanism:
  • 17. 17 Efferent arteriole vasoconstrictor mechanism
  • 18. 18 Formation of urine:  Mechanism of formation of urine: Urine formation takes place by the following three mechanisms:  1. Formation of glomerular filtrate.  2. Reabsorption of glomerular filtrate from tubule  3. Tubular secretion.
  • 19. 19 Urine: Volume: 1000-1500 ml/24 hrs in adult man Specific gravity: 1.010-1.035 Reaction: Usually slight acidic PH 4.5-8 (varies on diet) Color: Yellow due to urochrome Odor: Aromatic (when fresh) Ammonical (bacterial decomposition of urea to ammonia)
  • 20. 20 Obligatory urine volume: The minimal volume of urine that must be excreted to rid the body waste products is obligatory volume. Human kidney can produce a maximal urine concentration of 1200-1400 mosm/l A normal 70 kg human must excrete about 600 mosmole of solute each day to rid the body of waste products of metabolism and ion that are ingested. The minimal volume of urine that must be excreted to rid the body waste products is obligatory volume. If maximal urine concentrating ability is 1200 mosm/l Obligatory volume = 600 MOSM/day = 0.5 L/day 1200 MOSM/L When there is a water deficit in the body, the kidney forms concentrated urine by continuing to excrete solute while increasing water reabsorption and decreasing volume of urine formed.
  • 21. 21 Renal failure
  • 22. 22  Renal failure is a pathological process in which the functions of the both kidneys is severely compromised, leading to the accumulation of metabolic products and disorder of water, electrolyte and acid base balance and endocrine dysfunction.
  • 23. 23  Broadly the causes of renal failure are divided in to two categories. 1. Renal diseases-  Glomerulonephritis , pyelonephritis, renal TB, acute tubular necrosis, polycystic kidney disease. 2. Non-renal diseases  shock, heart failure, diabetes, hypertension, atherosclerosis, SLE, drugs and chemicals, calculus, tumors ect.
  • 24. 24 Basic pathology of renal failure 1. Dysfunction of glomerular filtration 2. Renal tubular dysfunction 3. Renal endocrine dysfunction.
  • 25. 25 A) Dysfunction of glomerular filtration The function of glomerulus is to filtration, the first step in the formation of urine. Its capacity is measured by GFR (glomerular filtration rate). The following mechanisms may be responsible for decreased GFR. 1. Decreased renal blood flow In the condition like shock and HF, the CO and BP decreased leading to decreased blood flow to kidney and decreased GFR. 2. Decreased effective glomerular pressure Effective glomerular filtration is the driving force to form the GFR, if it is decreased due to any cause GFR decreases. Decreased blood pressure renal tubular obstruction, renal interestial edema causes increased tubular hydrostatic pressure resulting in decreased GFR.
  • 26. 26 3. Decreased glomerular capillary surface area- inflammation, destruction or removal of kidney substances causes the surface area to decrease, GN, basement membrane diseases, nephrectomy all lead to renal insufficiency. 4. Alteration of permeability: the glomerular membrane has size barrier and charge barrier. GN damage the membrane and cause hematuria and proteinuria.
  • 27. 27 B) Renal tubular dysfunction : Impaired renal Reabsorption, secretion and excretion. - Ischemia, infection and nephrotoxic drugs damage the renal epithelial cells. The function of cells is modified by Aldosterone, antidiuretic hormone, natriuretic peptide, so presence or absence of these substance and responsiveness of renal tubules to these hormones determines the formation of urine.
  • 28. 28 1. Dysfunction of PCT Reabsorption of most of the filtered glucose, AA, bicarbonate, phosphate, Na occurs in this segment, so its dysfunction causes, glycosuria, aminoaciduria, renal tubular acidosis. 2. Dysfunction of Loop of Henle Ascending loop permeable to Na, Cl but not permeable to water, main contributor of medullary hypertonicity and urinary concentration, so dysfunction causes polyuria, hypotonic urine.
  • 29. 29 3. Dysfunction of DCT Aldosterone – may secret H, K, NH3 in exchange of Na, so its dysfunction cause Na, K and acid base imbalance.
  • 30. 30 C) Renal endocrine dysfunction 1. RAAS –  Renin, regulation of circulatory volume, blood pressure, metabolism of water and sodium.  Inappropriately activated RAAS causes renal hypertension, Na and water retention. 2. Erythropoetin – 90% of EPO source.  Anemia.
  • 31. 31 3. 1, 25 dihydroxycholecalciferol 7- dehydrocholesterol (skin)– hepatic 25 hydroxylation, renal 1 alpha hydroxylation (1, 25 dihydroxy cholecalciferol), it is an active vit-D.  Calcium imbalance.
  • 32. 32 4. Kallikrein– Kinin and prostaglandin  Kallikrein produced by kidney converted in to bradykinin, synthesize prostaglandin E2, A2.  It dilates the renal vessels and promote excretion of Na and water. Analgesic nephropathy.
  • 33. 33 5. Parathyroid hormone and gastrin  kidney deactivates PTH and Gastrin.  PTH mobilizes calcium and phosphorus from bone and promotes phosphate excretion from PCT and DCT.  In CRF these hormones are not deactivated causing renal osteodystrophy and peptic ulcer.
  • 34. 34 Acute renal failure
  • 35. 35  Acute kidney injury (AKI) is defined as an abrupt or rapid decline in renal filtration function.  Renal function deteriorates over hours to days.  Results in fluid and electrolyte derangement and retention of normally excreted substances in the blood
  • 36. 36 In relation to the nature of onset RF is divided into Acute and Chronic RF The pathophysiology, causes, prognosis and the strategy for management of acute and chronic RF is different.
  • 37. 37 Effects of ARF  Failure of the kidney to excrete nitrogenous waste products.  Unable to maintain water and electrolyte balance and homeostasis.  Acid base disorder.
  • 38. 38 Etiology 1. Prerenal - Hypovolemia - Hypotension - Renal artery occlusion/stenosis 2. Intrinsic renal disease  Acute tubular necrosis  Prolonged renal ischemia : Thrombosis, emboli, vasculitis  Exposure to nephrotoxic drugs, heavy metals, and organic solvents  Intratubular obstruction resulting from  Hemoglobinuria, Myoglobinuria, or uric acid casts  Acute renal disease (acute glomerulonephritis,pyelonephritis)  3. Post-renal • Postrenal AKI is a consequence of urinary tract obstruction. • This may be related to • Benign prostatic hyperplasia, • Kidney stones, • Bladder stone, • Bladder, ureteral or renal malignancy.
  • 39. 39 Pathogenesis of ARF The basic changes occurring in ARF are  Renal hemodynamic alteration  Renal glomerular injury  Renal tubular injury
  • 40. 40 A. Renal hemodynamic alteration 1. Decrease renal perfusion pressure-- renal blood flow loses auto regulation if systemic BP is less than 80 mmHg. 2. Renal vasoconstriction: during the initial phase of ARF, the symp. nervous system, RAAS, activated, decrease prostaglandin, kinin, decrease NO secretion -- causes vasoconstriction mainly of afferent arterioles. 3. Renal vascular endothelial swelling– renal-ischemia induced injury 4. Intrarenal DIC
  • 41. 41 B. Renal glomerular injury  In intrinsic diseases of renal glomerulus like Acute glomerulonephritis, glomerular membrane damage occurs leading to increase pore size, loss of electrical polarity, and ultimately fibrosis and loss of glomerulus.  It causes loss of filtration area and ARF.
  • 42. 42 Renal tubular injury  Tubuloglomerular feedback  Regulation of GFR in response to the solute concentration in distal renal tubule is called Tubuloglomerular feedback.  When PCT and loop of Henle are damaged by ischemia during the course of ARF, the Na load is increased and sensed by the macula densa, and activates RAAS.
  • 43. 43 Alteration of metabolism and functions  The course of ARF is divided into 3 stages  The oliguric stage  Diuretic stage  The recovery phase
  • 44. 44 The oliguric stage  Persists days to weeks, significant homeostatic disturbance occurs.  it is marked by 1. Urinary alteration - Oliguria or anuria - Dilute urine sp. Gr. 1.01-1.02 - Increase urinary Na - Hematuria, albuminuria, casts are found in urine.
  • 45. 45 2. Water intoxication: Oliguria, less removal of water from the body causes dilutional hyponatraemia, pulmonary edema and neurological dysfunction 3. Hyperkalaemia – Decreased excretion, leading to VF and cardiac arrest. 4. Metabolic acidosis: Due to decreased GFR and decreased secretion of H+, and decreased HCO3 generation causes acidosis.
  • 46. 46 5. Azotemia- normal BUN is 10-15 mg %  The marked increase of non protein nitrogen (NPN), eg urea, creatinine and uric acid is called azotemia.  More protein degradation, less excretion causes it to accumulate.
  • 47. 47 Diuretic stage  This phase can last for 1~3 weeks.  In Diuretic phase, the urine output in 24 hours can exceed 400 ml and even 2500 ml.  When diuretic phase starts, as the glomerular filtration rate does not recover and the concentration ability of renal tubule is very poor so the urine output is usually very high.  The levels of urea nitrogen, creatinine and potassium in blood will increase further.  Moreover, water and electrolyte disturbance, infections are also very common in this phase.
  • 48. 48 The recovery phase  In recovery phase, the renal tubule grows again and the glomerular filtration rate recovers normal as well as the urea nitrogen level and creatinine level decline to the normal range.  Only few go into CRF due to significant injury to renal epithelium, basement membrane; leading fibrosis.
  • 49. 49 Non-oliguric ARF  In some of the forms of ARF, the renal pathological changes are less and oliguric phase is less marked and urine output is 400- 1000/ day, it is called non-oliguric ARF.  The specific Gravity of urine is low and fixed and urine sodium is low.  Have beter prognosis.
  • 50. 50 How to diagnose  The clinical history  The symptoms  The lab: increased creatinine, BUN, hyperkalaemia, hypercalcaemia, acidosis, decreased HCO3, urine vol and casts, sp gr, low sodium content.
  • 51. 51 A. Symptoms 1. Polyuria, Oliguria or Anuria, hematuria 2. Dysuria 3. Dyspnoea 4. Malaise 5. Flank pain 6. Facial edema 7. Hypertension 8. Uremia a. Symptomatic azotemia b. Acidosis (± tachypnea) c. Mental Status changes d. Hypervolemia / Hypertension e. Hyperkalemia Most of the patients are asymptomic
  • 52. 52 Treatment of ARF  Eliminate the toxic insult  Hemodynamic support  Respiratory support  Fluid management  Electrolyte management  Medication dose adjustment  Dialysis Dialysis or continuous renal replacement therapy (CRRT) may be indicated when nitrogenous wastes and the water and electrolyte balance cannot be kept under control by other means.
  • 53. 53 Chronic renal failure  It is the permanent reduction in glomerular filtration rate (GFR) sufficient to cause sign and symptoms of organ dysfunctions.  This is obvious when GFR is below 15 ml/min.
  • 54. 54 Azotemia - Elevated  blood urea nitrogen (BUN >28mg/dL) and  Creatinine (Cr>1.5mg/dL) • Uremia - azotemia with symptoms or signs of renal failure • Silent phase of CRF; until GFR upto 50 ml/min • Renal insufficiency; GFR 25-50, polyuric, nocturia, mild azetomia, anemia. Definitions
  • 55. 55 • Renal failure; GFR 5-25 ml/ min, clinical evidence of uremia established • End Stage Renal Disease (ESRD) - GFR < 5 ml/min. uremia requiring transplantation or dialysis • Creatinine Clearance (CCr) - the rate of filtration of creatinine by the kidney (GFR marker)
  • 56. 56 Etiology  Common Underlying Causes of CRF a. Diabetes: most common cause ESRD (risk 13x ) b. HTN causes at 23% ESRD cases c. Glomerulonephritis accounts for ~10% cases d. Polycystic Kidney Disease - about 5% of cases e. Rapidly progressive glomerulonephritis (vasculitis) - about 2% of cases f. Renal (glomerular) deposition diseases g. Renal Vascular Disease - renal artery stenosis, atherosclerotic lesion
  • 57. 57
  • 58. 58
  • 59. 59  Chronic renal results from irreversible injuries.  The pathogenesis is not fully understood.  There is evidence of progression of renal failure even if the primary inciting cause is removed.  However it is best tried to explained as following hypothesis: Pathogenesis
  • 60. 60 1. Intact nephrone hypothesis  There is progressive loss of nephrones with remaining nephrones fully functional.  As disease advances the amount of solutes to be excreted does not change, but number of nephrones decrease.  The level of Na and K does not changes until GFR is <5 ml/min and phosphate and urate level remain normal until GFR is below 20 ml/min.
  • 61. 61 2.Trade-off hypothesis  According to this hypothesis in the process of adaptation for one component second component becomes disordered. i.e. acquires a new lesion.  The retention of phosphates in CRF reduces the concentration of Ca++ in blood, there by stimulating the release of PTH.  The PTH stimulates renal phosphate excretion but at the same time release Ca from bone and increases Ca reabsorption from kidney.  This can maintain the Ca and phosphate level but develops parathyroid gland hypertrophy and renal osteodystrophy.  Thus in correcting one abnormality it acquired other disease.
  • 62. 62 3. Glomerular hyperfiltration hypothesis  When the number of nephrones sufficiently reduced, the functioning single nephrone GFR increases which causes intraglomerular hypertension and hyperfiltration, this in turn causes damage to the glomerulus endothelial cells, activation of platelets, increased protein flux, and decreased permeability of glomerulus.  Ultimately it causes sclerosis of glomeruli, atrophy of tubules and interstitial fibrosis.  Thus giving continuity to nephrone loss and aggravating CRF.
  • 63. 63 Metabolic and functional alterations 1. Urine Early polyuria, nocturia, proteinuria, RBC, WBC and casts. But later oligouria develops. it is due to compensatory hyperperfusion and filtration from the intact nephrone, accelerated motion of fluids -- less chance of reabsorption, osmotic diuresis, decreased concentration of solute in the renal interstitium.
  • 64. 64 2.Azotemia - BUN increase 3. Water electrolyte and acid base imbalance - Volume and salt over load-if used deliberately, - Causes dehydration and hyponatraemia if restricted. - If overloaded pulmonary edema, brain edema and heart failure occurs.
  • 65. 65 4. Hyperkalaemia when GFR < 15 ml/min Results in cardiac arrythemia. 5. Disorders of Mg, Ca and phosphorus hypermagnesemia, hyperphosphatemia, hypocalcaemia. 6. Metabolic acidosis 7. Renal HTN 8. Renal osteodystrophy - osteoporosis, osteosclerosis.
  • 66. 66 9. Haemorrhage , bruising, GI hemorrhage, IC hemorrhage due to inhibitory effect of uremic toxin on platelets and deficit of some coagulation factors. 10. Anemia – normochromic normocytic. (Erythropoetin)
  • 67. 67 Uremia  It is a symptom complex due to accumulation of uremic toxins in acute and chronic renal failure.  Different retained products of metabolism, under and overproduction of different hormones results in uremic syndrome.  It is manifested by 1. nervous system- neuropathy, intellectual slow down, or overt encephalopathy with confusion, stupor and coma. 2.Water electrolyte, acid base, accumulated poisons,, vascular spasm, hypoxia all contribute for the symptom.
  • 68. 68 2 Digestive system Early symptoms: nausea, vomotting, diarrhea, mucosal ulcerations and bleeding. 3. CVS- HTN, arrythmia, Cardiac failure. - Uremic pericarditis and pericardial effusion, it is a leading cause of death in CRF
  • 69. 69 4. Respiratory Dyspnoea, kussmaul breathing, pulmonary edema, respiratory failure. 5. Metabolic diseases Proteinuria; leads to cachexia, hypertriglyceridemia
  • 70. 70 1. Treat the primary cause; 2 reversible factors of CRF, HTN, reduced renal perfusion (HF, renal artery stenosis, hypotension due to drugs), UTI, other infection, urinaty tract obstruction. 3. Slow progression of diseases- ACEI if not contraindicated, 4. Renal replacement therapy. - peritoneal dialysis - hemodialysis - renal transplantation 5. Prompt treatment of complication, eg, haemorrhage, anemia, acute and chronic HF, active vitamin D substitute, erythropoetin. Prevention and treatment
  • 71. 71 To be continued…..

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