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Disease of Urinary System.pptx
- 1. Dr. Fahmida Parveen Associate Professor Veterinary Pathology SAU Tandojam
- 2. Urinary System â«The urinary system consists of the two kidneys, two ureters, the urinary bladder, and the urethra. â«Blood flows through the kidneys as they filter out waste such as urea. The urine produced by the kidneys goes through the ureters. It then waits in the urinary bladder, until it goes out from body â« Each kidney contains millions of tiny filtering units called Nephron
- 3. kidney
- 4. Functions of Kidney â«Excretion- remove waste products from the blood â«Regulation of blood volume and pressure- kidneys control amount of extracellular fluid, can make dilute or very concentrated urine â«Regulation of the concentration of solutes in the blood- kidneys regulate molecules and ions like glucose, sodium, hydrogen carbonate
- 5. Functions of Kidney â«Regulation of red blood cell synthesis- kidneys secrete erythropoietin, which regulates blood cell production in bone marrow â«Vitamin D synthesis- kidneys control blood levels of calcium by regulation synthesis of vitamin D.
- 6. Functional Disturbance And Consequences Of Urinary Disease
- 7. Functional Disturbance And Consequences Of Urinary Disease â« Retention of excretory wastes â« Azotemia â« Uremia â« Abnormal urination â«Anuria â«Oliguria â«Pollakiuria â«Dysuria â«Polyuria â«Abnormal urine contents â«Proteinuria â«Hematuria â« Hemoglobinuria â«Myoglobinuria â«Glucosuria â«Pyuria
- 8. Retention of excretory wastes â«Azotemia: â« Presence of excessive urea or creatinine in the blood. â« Azotemia may be due to several causes â renal failure is not the only cause! â«Uremia: â« Presence of urinary constituents in the blood AND the toxic condition produced by those constituents. â«Thus uremic animals would be azotemic â«AND have clinical signs or systemic lesions caused by the retained waste products
- 9. Abnormal urination â«Anuria â«Absence of urine excretion. â«Renal or post-renal lesions may result in anuria
- 10. Abnormal urination â«Oliguria: â«Reduction in the amount of urine excreted. â«The causes include renal, post-renal and pre- renal factors. â«It occurs due to glomerulonephritis, obstruction in urinary passage, dehydration, low blood pressure and tubular damage.
- 11. Abnormal urination â«Pollakiuria; â«Increased frequency of urination â«(the amount may be normal).
- 12. Abnormal urination â«Dysuria: â«Painful or difficult urination. â«Stranguria â«Slow and painful discharge of urine due to spasm of the urethra or bladder.
- 13. Abnormal urination â«Polyuria â«The passage of abnormally large amounts of urine. â«This may be verified by catheterization and collection, so the amount may be quantitated. â«Polyuria, increased amount of urine leading to frequent urination caused due to diabetes insipidus, hormonal imbalance and polydypsia. â«In this condition, waste products are successfully eliminated.
- 16. Proteinuria â«Presence of excess protein particularly albumin in urine. â«The presence of albumin in urine is indicative of damage in glomeruli. â«It is also characterized by oedema due to protein deficiency.
- 17. Proteinuria
- 18. Hematuria â«Presence of blood (RBCs) in urine giving bright red color. â«It may occur due to damage in glomeruli, tubule or hemorrhage anywhere from glomeruli to urethra. â«The most important cause of hematuria is bracken fern toxicity.
- 19. Hemoglobinuria â«When hemoglobin is present in urine without erythrocytes due to intravascular hemolysis. The urine becomes brownish red in color. â«It must be differentiated from hematuria in which intact erythrocytes are present and settle down after some time leaving clear urine as supernatant. â«Hemoglobinuria is caused by various infections such as leptospira sp., Babesia sp. Or phosphorus deficiency in animals.
- 20. Myoglobinuria â«Presence of myoglobin in the urine. â«This results from damage to skeletal muscle with release of myoglobin into the blood (myoglobinemia) and subsequent excretion in the urine (myoglobinuria).
- 21. Pyuria â«The presence of pus in the urine - or the presence of inflammatory cells in the urine sediment (neutrophils as seen here). â«Presence of pus in urine due to suppurative inflammation in urinary tract
- 22. Renal cysts
- 23. Renal cysts â«Enlargement of kidney due to clear fluid or blood mixed fluid containing cysts. â«Three mechanisms are now considered possible: â«Obstruction of the nephron may cause elevated luminal pressure and secondary dilatation â«Defective tubular basement membranes allow saccular dilatation of tubules â«Focal tubular epithelial hyperplasia with production of new basement membranes causes development of enlarged, dilated tubules.
- 24. Renal cysts â«Multiple small prominent cysts in the cortex, due to dilation of parts of the nephrons â«(Bowman's capsules and/or tubules) associated with accumulation of glomerular filtrate.
- 25. Renal cysts â«A single large cyst in the medulla. The cysts may be multiple and smaller.
- 26. Renal cysts â«Cysts may arise anywhere along the nephron, be located in cortex or medulla, and vary from barely visible to several centimeters in diameter. â«They contain clear watery fluid
- 27. Renal cysts â«Polycystic kidneys contain many cysts that involve many nephrons giving the kidney a cheese like appearance. â«As the cysts enlarge and compress the parenchyma renal function may be compromised.
- 29. Glomerulus â«Glomerulus...Filters toxins out of the blood." When there is glomerular disease, the filtration function is altered. â«So, instead of just very small ions and water passing through the glomerulus into the tubules, bigger molecules that are supposed to stay in the blood (!) get passed through into the urine. â«This is bad!
- 30. Glomerulus â«When the glomerulus is altered, the blood flow to the tubules changes. All the blood to the kidney goes through the glomerulus first, so if there is a problem in the glomerulus, the tubules donât get enough blood, and they eventually die too! â«The two important glomerular diseases of domestic animals are â«Glomerulonephritis â«Glomerular amyloidosis.
- 31. Glomerulitis â«Glomerulitis is inflammation of the glomerulus only. â«The reaction is limited to the glomerulus and the rest of the nephron is not affected.
- 32. Glomerulonephritis (glomerulus + nephron) â«The glomerulus and other parts of the nephron are damaged or have inflammatory lesions. â«Glomerular damage usually induces tubular or interstitial damage too. â«One reason for this is that blood flow to the tubules goes through the glomerulus first, therefore inflammatory mediators will be carried to tubules. â«Damage to the glomerulus results in increased permeability, allowing protein to escape from the blood into the glomerular filtrate, results in hypoproteinemia with subsequent edema formation.
- 33. Glomerular amyloidosis â«Results from the build up of misfolded proteins known as amyloids â«Abnormal proteins that can settle in body tissue, forming deposits and causing disease. Abnormal proteins were first discovered, called amyloid, and the disease process amyloidosis. â«It totally disturb the filtration and all the protein in the blood just spills out into the urine.
- 35. Glomerular amyloidosis â«As an extracellular deposit, it may cause ENLARGEMENT of affected organs such as in kidney, spleen and liver. â«Amyloid can be deposited in glomeruli or in the interstitium, but glomerular deposition is most common in dogs.
- 36. Glomerular amyloidosis â«Amyloid proteins may be deposited in a localized cause damage by displacing normal cells. â«If critical organs such as the kidneys, liver, or heart are extensively disrupted, the disease may be fatal. â«Amyloidosis develops as a inflammatory diseases, result of chronic chronic bacterial infections, and malignant tumors.
- 37. Tubulo-interstitial disease â«It is overlap between inflammatory diseases that affect the tubules and the interstitium, because damage to on component triggers' a response in the other. â«Interstitial inflammation and fibrosis results in tubular atrophy and degeneration with secondary damage to glomeruli and vessels. â«Similarly, tubular damage stimulates inflammation, which spills over into the interstitium, with end result of an kidney failure.
- 38. Tubulo-interstitial disease â«Some organisms (E.coli cause white spot kidney in cattle; â«Actinobacillus equi in horses) localize in the kidney â«Either hematogenous route like bacteremia OR in infected emboli. â«Pyogenic organisms result in the formation of foci of pus / abscesses scattered through the kidney.
- 39. Pyelonephritis â«Pyelitis- inflammation of renal pelvis alone â«Pyonephritis- severe suppuration of whole kidney â«PYELONEPHRITIS is inflammation of the RENAL PARENCHYMA and the RENAL PELVIS. â«Pyelonephritis usually results from an ascending urinary tract infection. â«Urinary obstruction from any cause (pregnancy, urolithiasis etc.) Will lead to urinary stasis, which predisposes the animal to bacterial cystitis.
- 40. Pyelonephritis
- 41. Pyelonephritis â«Once an infection is established in the bladder, It may ascend up the ureters via vesicoureteral reflux. â«Once the renal pelvis is infected, bacteria probably gain access to the parenchyma via the collecting ducts and by direct invasion across erosions in the pelvic urothelium. â«In severe cases of reflux, bacteria laden urine flows up into the tubules via the collecting ducts, carrying bacteria as far as the urinary space of glomeruli. This is intrarenal reflux
- 42. Renal failure
- 46. Acute renal failure â«Injury resulting in the death of tubular epithelial cells is termed acute tubular necrosis (nephrosis) and is the result of toxic or ischemic damage. â«The lesion is characterized by coagulative necrosis of tubular epithelial cells dilated hypo cellular tubules and intratubular debris.
- 47. Acute renal failure â«What mechanisms are involved in acute renal failure secondary to tubular damage? â«Back leak and tubular obstruction are at least two mechanisms â«In both mechanisms, filtrate (urine) is not excreted and azotemia results
- 48. Acute renal failure â«With back leak, the filtrate produced by the glomerulus is not contained in injured tubules. it "leaks back" into the interstitium and is reabsorbed into blood vessels. Wastes are not eliminated and the animal dies of renal failure â«The tubule may be obstructed (plugged) and prevent passage of the filtrate. If many tubules are obstructed, azotemia results. â«Activation of the renin-angiotensin system due to tubular damage, intrarenal vasoconstriction occurs resulting in decreased glomerular blood flow and filtration.
- 50. Which part of the tubule is most often injured? â«The 3 segments of the PROXIMAL TUBULE are most often injured. â«The agents that injure this area usually by toxic or ischemic action. â«The convoluted segments, S1 and S2, are most susceptible to toxic injury and â«S3 most susceptible to ischemic injury. However, the major take home message is that toxic and ischemic damage usually involves the proximal tubules.
- 53. Yes, toxins generally cause epithelial necrosis whereas ischemia causes necrosis AND RUPTURE of the basement membrane (TUBULORRHEXIS). Thus ischemic lesions are more severe since fibrosis rather than regeneration occurs.
- 54. Yes, one example is the microvilli ("brush border") which is sensitive to certain toxins and may disappear completely resulting in less absorption and resultant Polyuria. Other organelles (i.e. mitochondria) and enzymes may also be selectively injured with other agents
- 55. Urolithiasis
- 56. Urolithiasis â«Calcus or stone formation in any part of Urinary System is called Urolithiasis. â«The Stone is called Urolith or Urinary Calcus.
- 57. Caprine urinary bladder urolithiasis
- 59. Urine â«The fluid produced by the kidneys. It consists of excess water and the toxic waste products from food. â«If there is any disturbance in the excretion of these wastes they remain in body & cause various problems, urolithiasis is one of them.
- 60. Formation of calculi â«For the formation of calculi there must be a nidus or nucleus around which salts may be deposited. â«Nidus or nucleus are found in following condition. â«Bacteria â«Leucocytes â«Degenerated cells â«Muco-protein.
- 61. How urolithiasis occurs â«Genetics: â«The physiology of some animals causes their bodies to produce higher levels of the substances that form the crystals; these are then excreted or formed in the urine. â«Gender: â«Crystals and stones occur in both male and female dogs but, because the urethra of the male is longer and narrower than the femaleâs, urethral obstruction is more common in males.
- 62. How urolithiasis occurs â«High mineral intake: â«The higher the urine concentration of minerals that make up the stones, the higher the risk that stones will form. â«Diet: â«High levels of some minerals in the diet, such as magnesium, phosphorus, and calcium, have been directly linked to canine urinary bladder stone formation. A diet with excess protein can also contribute to stone formation. Diet can also influence the acidity or alkalinity of the urine.
- 63. How urolithiasis occurs â«Urine pH: â«The acidity or alkalinity of the urine can influence the formation of crystals and stones. Some crystals, such as struvite, form in alkaline urine, whereas others form in acidic urine. The urine pH is largely influenced by diet. â«Bacterial Infections: â«Bacterial infections of the bladder can play the major role in struvite stone formation. They make the urine more alkaline which enhances the formation of struvite crystals and the by- products of bacterial metabolism may also enhance crystal formation.
- 64. How urolithiasis occurs â«Holding urine for long periods: â«Animals that have been confined or have a lack of regular exercise and are unable to pass urine on a regular basis are more likely to develop this disease â«Low water intake: â«Dogs that do not drink enough may also be more likely to develop this disease
- 65. Size and Shape â«Size of Calculi depends upon its location. â«E.g.: â« Renal calculi are microscopic. â« Pelvis calculi up to 8cm. â« Cystic calculi may vary from grain of sand up to a tennis ball.
- 66. Size & shape: (Cont) â«They may have smooth or rough surface, sometimes they may have spine like projections.
- 67. Composition â«The composition of Calculi depends upon the diet of animal. â«Calculi are different in chemical composition in different species of animals.
- 68. Composition (Cont.) â«The stone from herbivorous contain predominance of silicates. Sometimes it contains phosphate, carbonates oxalates, calcium and magnesium. â«Important amount of protein always found with these minerals.
- 69. Composition (Cont.) â«In Carnivorous & omnivorous animals the chemical constituents of urolith is quite different. â«They resembles much like with the stones of humans b/c of acidic urine. â«Stone contain oxalates, urates, and cystine.
- 70. Types of calculi â«Different names are given to different calculi due to their composition. e.g: â«Oxalate calculi. â«Uric acid calculi. â«Phosphate calculi. â«Cystine calculi.
- 71. Oxalate calculi â«Most common stone type in humans. â«They are hard, white or light yellow in color, covered with sharp spines.
- 72. Oxalate calculi â«Composed of calcium oxalate monohydrate (whewellite) or calcium oxalate dihydrate (weddelite)
- 73. Oxalate calculi â«They usually found as single stone in urinary bladder. â«They are radio opaque. â«High recurrence rate (25 to 48%)
- 74. Uric acid calculi â«They are yellow to brown in color. â«They are formed by ammonium sodium urates & uric acid.
- 75. Urate urolithiasis â Defectiveâ uric acid metabolism in Dalmatian is a predisposing factor rather than primary cause. They are spherical or irregular in shape & are formed in acidic urine.
- 76. Struvite urolithiasis â«They are white or gray in color, chalky in consistency, can be crushed with mild pressure. â«High recurrence rate (> 20%) â«Younger animals
- 77. Struvite urolithiasis â«Bladder is most common site in dogs and cats â«They are composed of magnesium ammonium phosphate (struvite). â«It can be occur as a result of bacterial infection.
- 78. Cystine urolithiasis â«They are small, soft with shiny or greasy appearance. â«They are yellow in color which become darken on exposure to air. â« Usually in bladder and urethra â«High recurrence rate (47 to 75%)
- 79. Cystine urolithiasis â«They are caused by insoluble amino acid cystine participates in urine. â«Cystinuria is an inherited defect in renal tubular transport of cystine or cystine and other amino acids (e.g. COLA group)
- 80. Incidences: â«Both male & female animals are infected with urolithiasis, but urinary obstruction occur mostly in males due to narrow urethral diameter & long urethra. â«In females obstruction is mostly occur due to large calculi.
- 81. Causes: â«Infection. â«Concentration of salts. â«Deficiency of green fodder. â«Sulfonamide medication. â«Hormones. â«Prolonged confinement.
- 82. Causes: (cont ) â«Dietary mineral imbalance in calcium, magnesium imbalance.e.g:High in Ash & phosphates may lead to urolithiasis. â«Dehyderation.Individually it doesn't cause urolithiasis but if diet is high in silicates or other minerals or other predisposing factors are present it favors stone formation. â«Hereditary defects.e.g:cystineurea.
- 83. Symptoms: â«Blood in urine. â«Difficulty and pain in urination. â«Small and frequent urination. â«Vommition. â«Depression.
- 84. Microscopic feature: â«Inflammation & hemorrhage of lower urinary tract. â«Mucosa is ulcerated. â«Degeneration & necrosis of smooth muscles.