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What is the hallmark sign indicative of glomerulonephritis?
What are typical clinical findings in nephrotic syndrome?
Which immune-mediated mechanism involves the formation of antibodies against glomerular structures?
What structural change occurs in the kidneys during the later stages of glomerulonephritis?
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Which complement components are primarily involved in attracting neutrophils during glomerulonephritis?
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What is a notable characteristic of fibrous osteodystrophy associated with mineral metabolism disorders?
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Which complication is most consistent with bilateral renal agenesis postnatally?
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What distinct appearance do polycystic kidneys have when viewed in a gross examination?
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Which finding is indicative of renal hypoplasia?
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What condition involves the fusion of the cranial or caudal poles of the kidneys?
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Which of the following does NOT represent an abnormality found in the kidneys?
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How do the kidneys typically present in individuals with renal dysplasia?
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What is the implication of high levels of parathyroid hormone in this context?
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What occurs after about 3 weeks of complete obstruction in the renal system?
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Which of the following best describes the histological appearance of amyloid deposits?
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What is a major consequence of urinary stasis in the renal system?
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What staining technique reveals amyloid deposits with 'apple green' birefringence?
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Which type of nephritis is classified as 'ascertaining' based on the route of infection?
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What gross finding is commonly associated with organs affected by amyloidosis?
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What histologic feature is indicative of membranous glomerulonephritis?
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What is the most common pathology observed when the kidneys are affected by amyloid?
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What is the consequence of unilateral hydronephrosis on the contralateral kidney if it is functioning normally?
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What kind of glomerulonephritis is characterized by increased cellularity?
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Which mechanism is NOT associated with hypocalcemia?
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Which is a characteristic finding in the kidneys during chronic azotemia?
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Uremic gastritis in the gastrointestinal tract is associated with which of the following?
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What symptom is primarily associated with metabolic acidosis in this context?
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Which physiological process results from increased parathyroid hormone (PTH) due to hypocalcemia?
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Which of the following gastrointestinal symptoms is NOT commonly associated with uremia?
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What causes edema and ascites in hypoproteinemia?
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What is the primary gas exchange issue in pulmonary edema?
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Which option describes a common complication resulting from hypocalcemia over time?
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Which of the following best explains the smell associated with the oral cavity in uremic conditions?
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What type of hemorrhages are specifically noted to occur beneath the capsule in swine diseases?
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Which condition is characterized by local ischemic necrosis due to occlusion of the renal artery?
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Which of the following is a consequence of hydronephrosis?
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What is the primary drug mechanism associated with analgesic nephropathy?
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In cases of renal infarction, what happens to the affected tissue after 2-3 days?
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Which of the following is NOT a cause of hydronephrosis?
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What is the typical appearance of the kidney in advanced cases of hydronephrosis?
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Which of the following conditions is characterized by papillary necrosis or renal crest necrosis?
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What indicates a severe outcome in a case of hydronephrosis if the obstruction is not resolved?
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What differentiates porcine erysipelas from other diseases regarding the size and shape of hemorrhages?
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Study Notes
Clinical Pathology
- Renel failure can lead to anemia due to loss of erythropoietin.
- Hypoproteinemia is a consequence of renal failure and can cause edema, ascites, and protein loss in urine.
- Metabolic acidosis in renal failure is due to loss of bicarbonate.
- Azotemia is a consequence of kidney function decline resulting in a higher concentration of BUN and creatinine in the blood.
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Hypocalcemia is a common feature of chronic renal failure and can occur by:
- Retention of phosphate.
- Metabolic acidosis resulting in decreased serum calcium.
- Decreased renal 1-α-hydroxylase activity, which leads to vitamin D deficiency.
- Hypocalcemia triggers hyperplasia of the parathyroid gland, leading to increased parathyroid hormone (PTH) secretion. PTH causes bone resorption, resulting in fibrous osteodystrophy and pathologic fractures.
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Clinical Findings of renal failure include:
- Polyuria.
- Neurologic abnormalities, specifically uremic encephalopathy, caused by metabolic acidosis and hypocalcemia.
- Gastrointestinal signs including ulcers caused by bacteria and damage to endothelial cells, and vomiting.
- Hypertension.
- Pulmonary edema.
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Gross Findings in renal failure include:
- Kidneys are small, firm, and have an irregular surface.
- The capsule is difficult to remove due to adhesions.
- Cut Surface displays a thinned cortex.
- Gastrointestinal Tract findings include uremic gastritis with ulcerations and marked mineralization in the stomach.
- Oral Cavity manifestations include a foul-smelling odor and ulcers.
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Widespread Soft Tissue Mineralization occurs due to high free calcium levels.
- Lungs can exhibit a "pumice stone" appearance with mineralization beneath the parietal pleura.
- Ulcerative endocarditis can also be present with endocardial mineralization.
- Parathyroid Glands display hyperplasia.
- Bones exhibit fibrous osteodystrophy, also known as "Rubbery Jaw".
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Congenital Anomalies of the kidney include:
- Agenesis: absence of the kidney. Bilateral agenesis is incompatible with postnatal life.
- Renal hypoplasia: underdevelopment of the kidney. Unilateral hypoplasia is often accompanied by contralateral hypertrophy of the other kidney, which compensates for the smaller kidney and can potentially reach a mature size.
- Renal dysplasia: abnormal development of the kidney.
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Polycystic Kidney Disease:
- Gross Findings: Kidneys are large, pale, and contain numerous 1-5 mm diameter cysts. The cut surface has a "Swiss cheese" appearance.
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Horseshoe Kidney:
- Fusion of the cranial or caudal poles of the kidneys.
- Kidney function is usually normal.
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Petechial Hemorrhages beneath the kidney capsule can be an indicator of:
- Classical swine fever (hog cholera)
- African swine fever
- Porcine salmonellosis
- Porcine erysipelas, with larger, irregular hemorrhage
- Porcine circovirus-2
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Renal Infarction results from local ischemic necrosis of the kidney, caused by occlusion of the renal artery or its branches.
- In cats, it can be indicative of hypertrophic cardiomyopathy and distal aortic thromboembolism.
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Gross Findings of Renal Infarction:
- Wedge of tissue is swollen and congested.
- Dehemoglobinization occurs 24 hours later.
- The infarcted area becomes white within 2-3 days.
- It is progressively replaced by fibrous tissue, resulting in pale gray-white scars that are wedge-shaped and depressed.
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Renal Medullary Necrosis: Necrosis of the kidney medulla, frequently caused by analgesic nephropathy.
- Analgesic nephropathy is most commonly caused by nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, phenylbutazone, flunixin, and ibuprofen. These drugs inhibit cyclooxygenase, reducing the production of prostaglandin E2 (PGE2), a vasodilator essential for the juxtamedullary nephrons.
- This loss of vasodilation can lead to papillary necrosis (renal crest necrosis).
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Hydronephrosis: Accumulation of fluid in the kidney, causing dilation of the renal pelvis and progressive atrophy of the kidney parenchyma.
- Mostly caused by urinary obstruction due to:
- Calculi
- Prostatic enlargement (dogs)
- Cystitis
- Compression of the ureters
- Bilateral obstruction can lead to death from uremia.
- Mostly caused by urinary obstruction due to:
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Gross Findings of Hydronephrosis:
- Early stages: Progressive dilation of the pelvis and calyces.
- Advanced stages: Kidney transformed into a thin-walled sac.
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Sequelae of Hydronephrosis:
- If obstruction is removed within a week, renal function can return.
- After 3 weeks of complete obstruction, irreversible renal damage occurs.
- Unilateral hydronephrosis can be compensated by the contralateral kidney if it is normal.
- Urinary stasis predisposes to pyelonephritis (infection).
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Amyloidosis:
- Abnormal protein deposition, amyloid, in tissues, leading to tissue dysfunction and pressure atrophy of adjacent cells.
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Gross Findings of Amyloidosis:
- Enlarged, firm organs.
- Pale gray to yellowish orange color, with a waxy appearance.
- Kidneys have a finely stippled appearance with fine yellow spots representing the glomeruli.
- Iodine staining of the glomeruli results in a red-brown staining, changing to purple upon exposure to acetic acid (vinegar).
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Microscopic Findings of Amyloidosis:
- Glomerular tufts are expanded by amyloid, an acellular, pale eosinophilic, homogenous, extracellular material.
- Congo Red staining of amyloid exhibits "apple green" birefringence.
- Nephritis: Inflammation of the renal parenchyma.
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Classification of Nephritis:
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According to route of infection:
- Ascending (uriniferous): Infection ascends from the lower urinary tract.
- Descending (hematogenous): Infection spreads through the bloodstream to the kidney.
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According to histologic distribution:
- Tubulointerstitial: Affects the tubules and interstitium.
- Glomerulonephritis (GN): Affects the glomeruli.
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According to histologic appearance:
- Suppurative: Pus-forming.
- Non-suppurative: Not pus-forming.
- Proliferative: Characterized by cell proliferation.
- Membranous: Thickening of basement membrane.
- Membranoproliferative (mesangiocapillary): Combination of membranous and proliferative changes.
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According to route of infection:
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Glomerulonephritis (GN) is often immune-mediated, caused by:
- Antibodies targeting antigens in the glomerulus (exogenous).
- Deposition of circulating immune complexes in the glomeruli.
- Antibodies against the glomerular basement membrane.
- Antigen-antibody complexes activate complement components, attracting neutrophils, which release chemokines and oxidants that damage cellular structures.
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Typical Clinical Findings of GN:
- Proteinuria: A hallmark sign.
- Nephrotic syndrome: Characterized by proteinuria, hypoalbuminemia, generalized edema, and hypercholesterolemia.
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Gross Findings of GN:
- Bilateral distribution.
- Early stages: Kidneys are pale, edematous, and enlarged, with a bulge on the cut surface.
- Later stages: Kidneys are shrunken with a granular pitted surface.
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Description
Test your understanding of the clinical consequences of renal failure, including anemia, hypoproteinemia, and metabolic acidosis. This quiz covers key features like hypocalcemia and its impact on parathyroid hormone secretion, as well as clinical findings associated with kidney dysfunction.
