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  • 1. Disease/ Disorder Brief Description Epidemiology Pathogenesis Clinical Signs Lesions Diagnosis Differential Diagnosis Treatment Control and Prevention DISEASES OF THE BLADDER, URETERS AND URETHRA UroperitoneuminFoals Accumulation of urine into the peritoneal cavity. It occurs as a result of variety of situations: *Congenital rupture of the bladder *Bladder rupture associated with sepsis *Rupture of urachus Avulsion of the bladder from its urachal attachment Some studies indicate a higher incidence of bladder rupture in males than in females, possibly because the narrower pelvis and the longer, narrower urethra of colts is a predisposing factor. The pathophysiology is that of postrenal azotemia. Accumulation of urine within the peritoneal cavity results in substantial electrolyte, acid-base and cardiovascular effects in affected foals. Foals are unable to excrete waste products and are unable to maintain water and electrolyte balance. Lethargy, decreased appetite, mild abdominal distension, and abdominal distension (2-4 days old) Hypokalemia Foals with this condition usually appear normal at birth, but gradually become ill over 1 to 2 days. They are weak, lack energy and interest in their surroundings, and have an increased heart rate. Most of these foals attempt to urinate often, but only produce a small amount of urine. Necropsy examination confirms the presence of uroperitoneum and the structural defect allowing leakage of urine into the abdomen. The defect can have signs of healing, which can make it readily confused with a malformation, because affected foals can survive for days after the rupture occurs- sufficient time for partial healing of the defect. Ultrasonographi c abdominal examination Physical exam (ballottement) Blood and peritoneal fluid analysis Septicemia, hypoxic ischemic encephalopathy /neonatal encephalopathy Persistent meconium impaction or colic Primary renal disease Surgery Peritoneal drainage There are no recognized means of prevention and control. Minimize the risk of foals developing septic disease.
  • 2. Urolithiasis Urolithiasis is an obstruction to the urinary tract. The mechanism of urolith formation in horses is unknown, although the alkaline pH and high mineral content of normal equine urine may favor crystal formation and precipitation. Normal equine urine also contains large amounts of mucoproteins, which may serve as a cementing substance to adhere crystals. Consumption of feed and water high in mineral content may increase urinary solute concentrations and thereby promote crystallization and precipitation. Multiple nephroliths may develop in horses with renal papillary necrosis (associated with NSAID administration while dehydrated) and mineralization of the papillae. Occurs sporadically in horses, the prevalence is low at about 0.04%-0.5% of all horse accessions or diagnoses. Animals from 5-15 years of age are most commonly affected and 76% males are (27% intact, 49% gelding) and 24% are females. Equine uroliths have a diameter of 0.5–21 cm, weigh as much as 6.5 kg, and are found most often within the bladder. Obstruction of one ureter may cause unilateral hydronephrosis, with compensation by the contralateral kidney. Rupture of the urethra or bladder is more likely to occur with a spherical, smooth calculus and causes complete obstruction of the urethra. Most equine uroliths are composed of calcium carbonate, in various hydrated forms, with either calcium phosphate or struvite uroliths occasionally noted. Weight loss, Anorexia, Stranguria. Most uroliths are located in the bladder and cause dysuria, pollakiuria, and hematuria. Hematuria is most evident after exercise and toward the end of a voided urine stream. Affected horses frequently stretch out to urinate and may maintain this posture for variable periods before and after micturition. Additional signs may include scalding of the perineum in females or of the medial aspect of the hindlimbs in males. Geldings and stallions may protrude the penis flaccidly for prolonged periods while intermittently dribbling urine. Affected horses may occasionally exhibit recurrent bouts of colic or an altered hindlimb gait. Urethral perforation Hydronephrosis Urinary bladder rupture Transrectalultras onography Urinalysis Rectal palpation Clinical signs, and History Surgical removal of the calculus and correction of any defects in the bladder. Midline or paramedian laparotomy and cystotomy, Pararectal cystotomy, Subischial urethrostomy, Urethral sphincterotomy Laser or shock wave lithotripsy Ammonium chloride (200 mg/kg BW) twice daily. Increase urinary chloride excretion, decrease urine pH, and provide calcium: phosphorus ratio of 2:1 in the complete ration. Adding sodium chloride up to 4% of the total ration
  • 3. RuptureoftheBladder(Uroperitoneum) This occurs most commonly in castrated males as a sequel to obstruction of the urethra by calculi. Rare cases are recorded in cows as a sequel to a difficult parturition and in mares after normal parturition, possibly because of compression of a full bladder during foaling. After the bladder ruptures, uroperitoneum results in a series of abnormalities that arise from failure of the excretory process combined with solute and fluid redistribution between the peritoneal fluid and extracellular fluid. Bladder rupture leads to gradual development of ascites from uroperitoneum, ruminal stasis, constipation, and depression. Depression, anorexia, colic, abdominal distension, and uremia develop within 1-2 days following rupture. Ruptured urinary bladder Ultrasonographi c abdominal examination Physical exam (ballottement) Blood and peritoneal fluid analysis Ascites Urinary tract obstruction Surgery with a goal of bladder repair. To avoid costs of laparotomy in feedlot animals, urethrostomy is created or an indwelling catheter is placed and the rupture is allowed to repair itself.
  • 4. Cystitis Inflammation of the bladder usually associated with bacterial infection and is characterized clinically by frequent, painful urination and hematuria, inflammatory cells and bacteria in the blood. It is likely to be the result of an obstruction in the urinary tract or paralysis of the bladder (which may be the result of nerve damage). Occurs also in mares with chronic inflammation of the vagina. Bacteria frequently gain entrance to the bladder but are usually removed by flushing action of voided urine before they invade the mucosa. Mucosal injury facilitates invasion but stagnation of urine is the most important predisposing cause. Loss of control over urination, frequent urination, urine dribbling, urine scalding, and straining to urinate. Hyperemia,hem orrhage and edema of the mucosa Complete blood test Urinalysis Rectal examination Based on Clinical signs Pyelonephritis Presence of calculi in the bladder Urethral obstruction Antimicrobial therapy for 7-14 days. Although there is no fool-proof way to prevent cystitis, the environment, diet, and on-going attention to the physical condition of each horse can help owners and handlers to catch the infection in its earliest stages to ensure proper treatment. Given the fact that certain grasses can cause cystitis, horses should not be pastured in pastures where Sudan grass, sorghum of sorghum-sudan hybrid grasses are grown, nor should they be fed cuttings from such pastures.
  • 5. Paralysisofthebladder Paralysis of the bladder is uncommon in large animals. This usually occurs as a result of neurological diseases affecting the lumbosacral spinal cord such as equine herpes myelopathy and cauda equine syndrome, and particularly ascending spinal meningitis in lambs after tail docking. Spinal cord degeneration following consumption of sorghum can lead to bladder paralysis in horses. Iatrogenic bladder paralysis occurs in horses in which there has been epidural injection of excessive quantity of alcohol. In some horses, idiopathic bladder paralysis and overflow incontinence may occur sporadically in the absence of other neurological or systemic signs. Compression of the lumbar spinal cord by neoplasia (lymphosarcoma, melanoma) or infected tissue (vertebral osteomyelitis) causes paralysis in bladder. Chronic distention of the bladder leads to accumulation of a sludge of calcium carbonate crystals. Urine stasis produces ideal conditions for bacterial growth. Incontinence with constant or intermittent dribbling of urine. Urine flow is often increased during exercise. Large bladder, often displaced cranioventrally, detected on rectal examination. Physical examination (manual bladder compression) Non- neurogenic, non-myogenic causes of apparent incontinence. Myogenic problems of the bladder such as cystic calculi. Supportive and aimed at relieving bladder distension by regular catherization and lavage. Parasympathomi metic drug ( bethanicol) and sympatholytic ( prazosin,phenoxy benzamine) Regular catheterization is essential in conjunction with a prophylactic dose of antibiotic.
  • 6. Urethraltearsinstallionsandgeldings Urethral rents are lesions in the convex and surface at the level of the ischial arc in geldings and stallions. The lesions communicate with the corpus spongiosum and cause hemorrhage at the end of urination in geldings or during ejaculation by stallions. The disease is apparently caused by contraction of the bulbospongiosis muscle at the end of urination, with a consequent increase in pressure in the corpus spongiosum and expulsion of blood through the rent. Urethral tears typically result in hematuria at the end of urination, in association with urethral contraction. Affected horses generally void a normal volume of urine that is not discolored. At the end of urination, affected geldings have a series of urethral contractions resulting in squirts of bright red blood. Occasionally, a smaller amount of darker blood may be passed at the start of urination. With hematuria of several weeks duration, the lesion may appear as a fistula communicating with the vasculature of the corpus spongiosum penis (cavernous vascular tissue surrounding the urethra). Endoscopic examination of the urethra with visualization of the rent in the urethral mucosa. Urethritis or hemorrhage from "varicosities" of the urethral vasculature. Breeding rest is recommended for stallions. Subischial urethrostomy or subischial incision into the spongiosum penis reduces vascular pressure in the corpus spongiosum during urination, allowing the defect to heal. A buccal mucosal graft was used to repair the defect in a stallion. CONGENITAL DEFECTS OF THE URINARY TRACT Renalhypoplasia A decrease in total renal parenchyma of one-third or more, with a proportionately greater loss of medullary than cortical tissue. Lethargy, shivering, depression, anorexia, and a slow rate of growth. Polydipsia, polyuria, as well as other signs of kidney disease such as weakness, lack of appetite, abdominal pain, fever, or swelling of the legs. Evidence of chronic renal failure on clinicopathologi cal examination Transrectal and transabdominal ultrasonography reveal small renal medulla and pelves. Renal dysplasia There is no treatment for renal hypoplasia. Care for affected dogs consists of managing the problems associated with the kidney failure that results from this condition.
  • 7. Renaldysplasia It is defined as disorganized development of the renal parenchyma due to anomalous differentiation. This is common in dogs but rare in cats, lambs, and horses. In pigs, renal dysplasia may be idiopathic or associated with nutritional avitaminosis A. Renal dysplasia may be unilateral or bilateral. When these conditions occur, the kidneys are usually small, firm, and pale. The outer portion of the kidney that contains glomeruli may be smaller than normal in size. Renal failure, nephromegaly and in some instances hematuria and colic. Polydipsia, polyuria, as well as other signs of kidney disease such as weakness, lack of appetite, abdominal pain, fever, or swelling of the legs. Azotemia, increased serum phosphorus concentrations and oliguria. Characterized by persistence of abnormal mesenchymal structures, including undifferentiated cells, cartilage, immature collecting ductules, and abnormal lobar organization. Animals affected bilaterally generally die in the early neonatal period, whereas animals affected unilaterally typically develop hypertrophy of the contralateral kidney. Ultrasonographi c examination of the kidneys may reveal a poor distinction between the cortex and medulla due to a hyperechoic medulla, which was due to fibrosis. Renal biopsy confirms dysplasia Other causes of chronic renal failure including renal hypoplasia. Renal neoplasia. Other intra- abdominal neoplasia. Interstitial nephritis. Glomeruloneph ritis. Pyelonephritis. Treatment is aimed at managing the associated chronic renal failure.
  • 8. Polycystickidneys The kidneys are usually grossly enlarged on palpation. Horses with this condition sometimes also have cysts in the bile ducts of the liver. Polycystic kidneys are rare in cattle and horses and very rare in sheep. It is commonly recorded in dogs. In adult horses, polycystic disease may also be acquired rather than congenital. Renal failure, nephromegaly and in some instances hematuria and colic. Polycystic kidneys may cause no clinical signs or lead to progressive renal failure. If it is extensive and bilateral the affected animal is usually stillborn or dies soon after birth. Based on physical and radiographic findings, ultrasonic examination, or exploratory laparotomy. Other causes of chronic renal failure , including renal hypoplasia. Pyelonephritis Ectopicureter The ectopic ureter opens into the urogenital tract at a place Other than the bladder such as cervix, urethra or vagina. The condition may be unilateral with urinary incontinence from birth as major clinical sign In horses, ectopic ureter is the most common congenital anomaly affecting the urinary tract; as in dogs, it is significantly more common in fillies than in colts. Ectopic ureters generally result from disruption of development of the mesonephric and metanephric duct systems. Continual dripping of urine is the classic sign, although animals with unilateral ectopic ureter may void normally; the inability to void normally suggests bilateral ectopic ureters. A low-grade vaginitis or vulvitis may also be present due to urine scalding. Definite diagnosis requires excretory urography or endoscopy; visualization of the ureteral openings during endoscopy can be assisted by intravenous administration of phenolsulfonpht halein (0.01 mg/kg BW) or indigo carmine (0.25 mg/kg BW) to impart a red or blue color, respectively, to the urine being produced. Surgical treatment involving ureterovesical anastomosis or unilateral nephrectomy has been successful. Successful surgical treatments usually involve transplantation of affected ureters into the bladder, or ureteronephrecto my.
  • 9. Patenturachus The urachus is the tube within the umbilical cord through which urine from the unborn foal travels from its bladder to the allantois (a fluid filled sac surrounding the unborn foal). Patent urachus occurs as three syndromes in foals: congenital and present at birth; acquired and secondary to urachal infection or inflammation; or secondary to severe systemic illness, usually sepsis. Failure of the urachus to close at birth occurs most commonly in foals. As a result of the patent urachus, which during intra-uterine life drains urine into the allantoic fluid, urine leaks from the umbilicus. Early signs of infection may include an enlarged navel that is painful to the touch and discharge of pus from the navel opening. Fever, Depression, loss of appetite, and signs of serious systemic illness such as respiratory difficulty, lameness and swollen joints. Patent urachus is typically associated with continuous urinary incontinence, urine scalding of the ventral abdomen, and development of bacterial urinary tract infections. Foals with patent urachus secondary to umbilical disease usually have enlarged umbilicus and some have purulent discharge. Ultrasonographi c examination of the umbilicus of foals with patent urachus is essential to determine the extent of disease and presence of intra-abdominal disease. Cystitis Surgical resection and 2–4 wks. of appropriate antibiotic therapy when indicated. Surgical resection is the standard treatment for umbilical urachal sinuses and intra- abdominal urachal cysts. Bibliography American College of Veterinary Surgeon. (n.d.). Retrieved January 8, 2014, from https://www.acvs.org/large-animal/patent-urachus-foals II, H. C. (2009, April 1). Retrieved January 6, 2014, from dvm360.com: http://veterinarycalendar.dvm360.com/avhc/article/articleDetail.jsp?id=675274&sk=&date=&pageID=2 Moses, S. E. (n.d.). The Merck Veterinary Manual . Retrieved january 9, 2014, from The Merck Veterinary Mnual Online: http://www.merckmanuals.com/vet/index.html O.M. Radostits, C. C. (2007). Veterinary Medicine A Textbook of the diseases in cattle, horses, sheep,pigs and goats 10th Edition. Philadelphia, USA: Elsevier Limited.
  • 10. DISEASES OF THE KIDNEYS DISEASE OTHER NAME BRIEF DESCRIPTION ETIOLOGY CLINICAL SIGNS LESIONS DIAGNOSIS DIFFERENTIAL DIAGNOSIS TREATMENT CONTROL AND PREVENTION GLOMERULO NEPHRITIS Chronic nephritis -can occur as a primary disease or as a component of diseases affecting several body systems -equine infectious anemia -amyloidosis -streptococci infection -weight loss -anorexia -polyuria -kidneys are shrunken and fibrous -ulceration in the GI tract -acute renal failure -pre-eclamtic toxemia -remove the causative agent -restore normal fluid balance There is no specific prevention for most cases of chronic glomerulonephritis. Some cases may be prevented by avoiding or limiting exposure to organic solvents, mercury, and nonsteroidal anti- inflammatory analgesics. RENAL ISCHEMIA -reduced blood flow through the kidneys -usually from general circulatory failure ACUTE -general circulatory emergencies such as shock, dehydration, acute hemorrhagic anemia, acute heart failure CHRONIC -congestive heart failure -masked by the clinical signs of the primary disease -oliguria and azotemia will go unnoticed in most cases -proteinuria-early indication -primary cortex is pale and swollen -distinct line of necrosis at the corticomedullary junction -necrosis of tubular epithelium and/ or glomeruli -urinalysis with urea nitrogen and creatinine concentration used as indices -serum biochemistry on urine -Nonoliguric Acute Renal Failure -correction of fluid, electrolyte and acid-base balance TOXIC NEPHROSIS -direct action of toxins -metals - antimicrobials -vit. K via IM or IV -vit. D2 and D3 -NSAID - benzimidazole -may not be referable to urinary system -colic, stranguria -depression, dehydration, anorexia, hypothermia, slow or elevated heart rate and weak pulse -diarrhea may be present ACUTE CASES -kidney is swollen and wet on the cut surface -edema may be present -necrosis and desquamation of tubular epithelium -hyaline casts -urinalysis with proteinuria, glucosuria, enzymuria and hematuria as initial changes -detection of the proximal tubule enzyme GGT in urine -pulmonary adenomatosis - mycotoxicoses -nutritional or metabolic disorders (eg, selenium, vitamin E, or copper deficiency) -removal of the toxin identified -anti-toxins -hemodialysis for foals with oxytetracyclinenephrotoxicosis -controlled secondary diseases
  • 11. -chlorinated naphthalene -oxalate in mushrooms -mycotoxins are present in the dilated tubules DISTAL RENAL TUBULAR ACIDOSIS(TYPE 1) - characterized by normal glomerular function but abnormal tubular function -detect in the ability to secrete H ions in the distal convoluted tubules against a concentration gradient -profound strong ion acidosis due to hyperchloremia -alkaline urine pH(>8) -increased fractional clearance of sodium -examining the ability of the distal convoluted tubules to excrete H ions by oral administration of ammonium chloride - uroperitoneum - renal calculi -symptomatic -focuses sodium bicarbonate PO or IV administration -The goal is to restore the normal pH (acid-base level) and electrolyte balance. EMBOLIC NEPHRITIS -any septicemia or bacteremia when bacteria is lodged in the renal tissue -toxemia -kidney may be enlarged on rectal examination -small gray spots in cortex -develop into large abcesses -extensive scarring -microscopic exam of urine -hematology -amyloidosis -nephritis -antimicrobials -avoid use of nephrotoxic drugs -supportive care, including hydrotherapy of accessible veins, anti-inflammatory agents, and systemic antimicrobials to control secondary sepsis PYELONEPHRITIS -develops by ascending infection from lower urinary tract -secondary to bacterial infections of the lower urinary tract -septicemia -secondary to anatomical abnormalities of the kidneys or distal convoluted structures -hematuria with pyelonephritis -presence of abnormality shaped kidneys with loss of corticomedullary gradient -hyper echoic abnormalities in the renal cortex -increased echogenicity -erythrocytes, leukocytes and cell debris are present in the urine upon microscopic examination -ultra sonography of the kidneys based on the lesions described -Azotemia -Chronic Renal Failure - Nephrolithiasis -unilateral nephrectomy(only in non-azotemic patients) -includes longterm antibiotics (4 to 6 weeks), sometimes at high dosages -alteration of the urinary pH(reduce the ability of the bacteria to attach to the epithelial cells HYDRONEPHROSIS -dilation of the renal pelvis with -obstruction of the ureter -congenital or -anuria, dysuria or stranguria - ultrasonography -unilateral -Urinary stones -Urinary reflux -hydroureter is aimed at restoring urine flow
  • 12. progressive atrophy of the renal parenchyma acquired obstruction may be detectable on palpation per rectum of a grossly distended kidney -UTI -restoration of fluid balance RENAL NEOPLASMS -primary tumors are uncommon -carcinomas occur in horse -unknown -enlargement of the kidneys(characteristic sign) -weight loss, reduced appetite, intermittent bouts of abdominal pain -massive ascites, hemoperitonium, hematuria - ultrasunographic examination of the kidneys -renal biopsy -surgical removal of the neoplasms -chemotherapy -nephrectomy