Urinary -1 Modify 2 PDF

 Renal failure ↑ Acute renal failure (ARF) 24h Chronic renal failure (CRF) 3 - 4 Jays...

 Renal failure ↑ Acute renal failure (ARF) 24h Chronic renal failure (CRF) 3 - 4 Jays -  Acute glomerular or Tubulo-interstitial injury  End result of many chronic renal diseases - -  oliguria or anuria #  Polyuria (Usually irreversible) - -  Azotemia  Uremia T Azotemia Uremia BUN blood urea and creatinine - blood urea and creatinine -- Without clinical manifestations of renal disease. Clinical syndrome & extra-renal lesions (often) - - Smo then one problem  e Low 1- Prerenal azotemia: Renal hypoperfusion (heart failure, shock, or hemorrhage) internal som - - injury Renal injury 2- Renal azotemia: Problem in 3- Postrenal azotemia: Urinary obstruction.  # Clinical Pathology ⑤  Anemia  Hypoproteinemia:  Metabolic acidosis:  Due to loss of erythropoietin  Edema and Ascites Due to loss of Bicarbonate Chronic Unfilteration of Protein t Utemin T m Azotemia  BUN and creatinine  Hypocalcemia (via three mechanisms) ratio disturbance Negative feedback 1- Retention of phosphate 1/2 Calcium 2- Metabolic acidosis > decreased serum calcium o 3-Decreased renal 1-α-hydroxylase activity # Vit D. deficiency -  Hypocalcemia > Parathyroid gland hyperplasia > increased parathyroid hormone (PTH) > bone resorption > fibrous - osteodystrophy and pathologic fractures - -  CLINICAL FINDINGS SymptomsT  Polyuria  Neurologic abnormalities (Uremic encephalopathy) - -  metabolic acidosis  hypocalcemia  Gastrointestinal signs  ULCERS caused by: ↳ Bacteria BacallD1- Urea Ammonia 2- Damage to endothelial cells  Vomiting  Hypertension  Pulmonary edema  GROSS FINDINGS Necesy Kasa  Kidneys: Shin  Small, firm, with irregular surface (usually bilateral) -  Capsule: Difficult to remove from the cortex because of adhesions -  Cut surface: Thinned cortex -  d  Gastrointestinal tract Stomach: “uremic gastritis” Ulcerations Marked mineralization Red-black blood - Oral Cavity ammonium Foul-smelling odor in oral cavity Ulcers (especially at ventral surface of & the tongue)  Widespread soft tissue mineralization · High free calcium 800 & Lungs: “pumice stone” beneath the parietal pleura, “ladder like” ↓ >5) 51 i 9. & Ulcerative endocarditis Endocardial mineralization  Mention the gloss Finding ?  Parathyroid glands  hyperplasia ↳ High D + H  Bone: Fibrous osteodystrophy (Rubbery Jaw) (especially bones of the head) -  T Congenital anomalies  Renal Rine) of Kidney  Agenesis > - Absence ②  Bilateral agenesis is inconsistent with postnatal life  Renal hypoplasia #  Unilateral contralateral hypertrophy is expected Jecense mature size reach Size After zu to Atrophy Anability to teach of agen HypoPosin - nature Size & D Renal dysplasia 1) Abnormal Starte in Kidney  Polycystic kidney - GROSS FINDINGS:  Kidneys are large, pale  contain numerous 1-5 mm diameter cysts contain watery liquid material  “Swiss cheese” appearance on cut surface Dolmal b  Horseshoe kidney Z  fusion of the cranial or caudal poles of the kidneys  Kidneys function normally.  X renal hemorrhages = Petechial hemorrhages occur beneath the capsule: 1) Classical swine fever (hog cholera) 2) African swine fever 3) Porcine salmonellosis 4) Porcine erysipelas (hemorrhages tend to be larger and more irregular in size and shape) 5) Porcine circovirus-2  renal infarction # Haast  Local Ischemic necrosis. Kidney & Spker  Occlusion of the renal artery or of one of its branches (End-artery)  In cats indicator of underlying hypertrophic cardiomyopathy and distal aortic thromboembolism - * be Xine ↓ castic Low output  - - >  Wedge of tissue is swollen & congested -- & &  Dehemoglobinization 24 hours later -  2-3 days infarcted area then becomes white -  Progressively replaced by fibrous tissue ( healed) - & pale gray-white scars, wedge shaped, and depressed renal medullary necrosis => &  Analgesic Nephropathy = 2 Nonsteroidal Anti-inflammatory Drugs (NSAIDs) (Aspirin, Phenylbutazone, Flunixin, Ibuprofen) Inhibit Cyclooxygenase Decreased Production Of PGE2 Loss of its Vasodilatory Effect On Arterioles Of Juxtamedullary Nephrons - Papillary Necrosis (Renal Crest Necrosis) Horse 3 -  hydronephrosis # no medial Accumulation of fluids in kidney  Dilation of the renal pelvis & progressive atrophy renal parenchyma kidney Cause: urinary obstruction (incomplete)  Calculi - &  Prostatic enlargement in the dog  Cystitis  Compression of the ureters  Bilateral obstruction results in early death from uremia  D Early: Progressive dilation of the pelvis and calyces advanced cases: the kidney is transformed into a thin-walled sac  -  Sequel:  If the obstruction is removed within about 1 week, renal function returns.  After about 3 weeks of complete obstruction, irreversible renal damage.  Unilateral hydronephrosis, the contralateral kidney can compensate if it is normal.  Urinary stasis predisposes to infection ( pyelonephritis)  amyloidosis e Abnormal protein  Deposition of amyloid (an amorphous, hyaline substance) #  interfere with normal tissue function + pressure atrophy of adjacent cells plesite Ha  GROSS FINDINGS: ⑤  Enlarged  Firm like muscle  Pale gray to yellowish orange  Waxy organs  Kidney has finely stippled appearance with fine yellow spots representing glomeruli Io  Iodine: Glomeruli stain red-brown with iodine solution and turn purple when subsequently exposed to acetic acid/vinegar b & &  MICROSCOPIC FINDINGS: M sit Congo glomerular tufts are expanded by variable amounts of amorphous, finely fibrillar to waxy, lightly eosinophilic material (amyloid)  Acellular, pale eosinophilic, homogenous, extracellular material T  Congo red staining of amyloid “apple green” birefringence  nephritis = Inflammation of renal parenchyma  CLASSIFICATION OF Nephritis T According to route of infection -- 1- Ascending - (uriniferous) - 2- Descending (hematogenous) > 2614 - -  ⑳ Suppurative Tubulo-intersitial Non-suppurative According to histologic distribution Proliferative Glomerulonephritis Membranous Membranoproliferative  glomerulonephritis (gn) Acute D Classified based on histologic appearance as:  Membranous: Thickening of capillaries of basement membrane -  Proliferative: Increased cellularity due to proliferation of endothelial, mesangial cells and/or epithelial cells.  Membranoproliferative (mesangiocapillary): both membranous and Membranoproliferative proliferative changes & Membranous Proliferative Most cases of GN are immune-mediated: => 1. Antibodies binding antigens in the glomerulus (exogenous) 2. Deposition of circulating immune complexes in glomeruli 3. Formation of antibodies against the glomerular basement membrane Antigen-antibody complexes complement components (C3a, C5a) attract neutrophils & releasing chemokines and oxidants that damage cellular constituents  TYPICAL CLINICAL FINDINGS =>  Proteinuria: hallmark sign  Nephrotic syndrome: proteinuria, hypoalbuminemia; generalized edema; hypercholesterolemia  GROSS FINDINGS &  Bilateral distribution  Early: pale, edematous large kidney , bulge on cut surface  Later: shrunken with granular pitted surface  - & -