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74 Cards in this Set
- Front
- Back
Can new nephrons form once renal maturity has been established? |
NO although renal compensation can occur by tubular hypertrophy |
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What is end stage kidney |
Irreversable changes in chronic renal failure |
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Why are kidneys susceptable to toxic injury |
20% of cardiac output Large glomerular capilliary surface area for toxin-endothelial reaction High metabolic rate of PCT and Thick ascending loop of henle |
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How can kidneys be damaged |
Ascending insults Haematogenous Metabolic insults |
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What are the features of an end stage kidney |
Shrunken and fibrosed Pale and firm - difficulty removing the capsule post mortem Non renal changes to the whole body |
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What is an ideal corticomedullary ratio |
1:2 and 1:3 |
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What is azotaemia |
Abnormal increase in non protein nitrogenous substances in the blood Principally urea and creatinine |
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What is uraemia |
Group of clinical signs resulting from azotaemia |
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Pre-renal azotaemia |
Decreased renal perfusion or increased protein catabolism Urea is increased, creatinine is not |
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Why is urea but not creatinine increased in pre-renal azotaemia |
Decreased flow rate in tubules allows increased resorbtion of urea but not creatinine. Creatinine is not absorbed by the renal tubules |
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What is the cause of increased protein catabolism associated with pre-rental azotaemia |
Sepsis Starvation Fever Glucocorticoid administration |
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What is renal azotaemia |
Decreased glomerular filtration rate due to acute or chronic renal disease Both creatinine and urea increase |
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Why does both urea and creatinine increase with renal azotaemia |
Decreased glomerular filtration rate results in decreased clearence of both urea and creatinine |
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How is creatinine cleared |
Glomerular filtration and proximal tubular excretion No reabsorbtion |
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What causes post renal azotaemia |
Obstruction of the urinary tract distal to the kidneys Both urea and creatinine are decreased |
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Increased synthesis of urea is caused by what |
Intestinal haemorrhage High protein diet Protein catabolism
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Hypersthenuric |
USG higher than normal |
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Isosthenuric |
USG normal |
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Features of pre renal azotaemia |
Hypersthenuraemic (1.030 - 1.035) Urine volume decreased Serum urea increased Normal serum creatinine |
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Features of renal azotaemia |
Increased serum volume of creatinine and urea Increased urine volume USUALLY Isosthenuric |
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Features of postrenal azotaemia |
Variable USG Decreased urine volume Increased serum urea / creatinine |
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Features of increased urea synthesis |
Variable USG Variable urine volume Increased serum urea with normal creatinine |
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What are the types of non renal pathology associated with renal failure |
Epithelial lesions CV changes Pulmonary lesions Altered calcium and phosphorus metabolism Abnormal biochemistry |
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What are the 2 causes of epithelial lesions |
Degeneration and necrosis of endothelial cells resulting in vasculitis, leading to thrombosis and infarction Production of ammonia via bacterial action un urea - epithelial damage |
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What are the manifestations of epithelial lesions |
Stomatitis - ulcerative necrotic Gastritis
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Cardiovascular changes associated with renal failure |
Uraemic lesions of the wall of the left auricle, proximal aorta and pulmonary trunk (erosion and thrombi formation) Hypertensive lesions - cardiac hypertrophy (left sided) Fibrinous pericarditis Anaemia |
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WHat can cause anaemia in renal failure |
Multifactorial aetiology Increased RBC fragility |
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What causes increased serum phosphate |
Decreased GFR Decreased clearence - post renal, renal and pre renal disease |
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What causes increased serum calcium? |
Decreased synthesis of calcitriol Result is decreased absorbtion of calcium from intestine and decreased resorbtion from bone Stimulation of PTH - compensatory hyperparathyroidism |
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What is the result of decreased calcium |
Parathyroid hyperplasia Soft tissue mineralisation Osteodystrophy |
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What causes increased serum potassium in renal failure |
Oliguria and decreased potassium output
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oliguria |
lowered urine output |
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Aldosterone action |
Increase potassium absorbtion |
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Metabolic acidosis is caused by? |
Decreased renal hyrogen excretion Increased potassium uptake into cells - cells then lose hyrdogen compensatory to maintain charge balance |
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Congenital renal conditions |
Renal aplasia or agenesis Ectopic kidneys Dysplasia Cysts |
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What is renal aplasia |
Failure to develop Familial condition in the doberman and the beagle |
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What is renal hypoplasia |
Incomplete renal development Clinical manifestations depend on severity |
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What is ectopic kidney |
Anomolous development of kidneys Usually in pigs and dogs Pelvic or inguinal location Incontinence, hyronephrosis, pyelonephritis |
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What is horseshoe kidney |
Fused kidneys One large kidney with 2 ureters Abnormal nephrogenesis |
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What is a congenital renal cyst |
Common incidental finding in pigs and calves Usually solitary |
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Polycystic kidney disease |
Both kidneys contain many cysts and such there is a progressive compromise in renal function Slow development, cysts become numerous and enlarge |
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What are acquired renal cysts |
Sequel to interstitial fibrosis Obstruction of tubules with scar tissue |
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Perinephric pseudocysts |
Between the renal capsule and the renal reflection of the peritoneum |
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What is juvenile nephropathy |
Cause of renal failure in young animals Familialy in the wheaten terrier Not associated with inflammation |
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What are the circulatory disturbances of the kidney |
Hyperaemia Haemorrhage Infarction
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What are the types of hyperaemia |
Active Passive Hypostatic |
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Haemorrhage sequalae |
Gross haemorrhage = Complete renal failure
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Causes of petechial haemorrhages |
Septicaemic disease
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Renal cortical haemorrhages common in= |
Significant in neonatal herpes virus in puppies |
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Consequences of renal artery infart |
Total necrosis |
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Consequences of arcuate artery infarct |
Necrosis of a wedge in the cortex and medulla |
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Arteries in the kidney size order |
Renal artery Interlobar artery Arcuate artery Interlobular arery |
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Where are most infarctsq |
Smaller arteries - most blockages due to smaller size for passage of emboli |
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Consequences of interlobular infarct |
Cortical necrosis only - both tubules and glomeruli |
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Stages of infacts |
Acute stage with swelling and haemorrhage Pallor with surrounding hyperaemia Chroni infarct - shrunken and fibrotic with contour distortion |
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Renal papillary necrosis cause |
Reduced medullary blood flow Primary Disease following NSAID therapy |
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Cause of hydronephrosis |
Obstruction at any level between the pelvis and urethra |
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Sequalae to hydronephrosis |
Ischaemic lesions develop in addition to persistance of glomerular filtration that causes pressure atrophy |
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Renal cortical necrosis cause |
DIC Endotoxaemia G- septicaemia |
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How do nsaids cause medullary necrosis |
decrease in prostaglandins no maintainence of GFR hyertonicity of medulla apoptosis and necrosis |
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What causes haemoglobin pigmentation of kidneys |
Floowing any haemolytic crisis Blakc discolouration - concentrated haemoglobin |
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Haemosiderosis |
Occurs in asscoication with chronic haemoltic anaemia or haemaglobinurea (acute) Brown discolouration |
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How do we demonstrate haemoglobin in the tissues |
Perls prussian blue reaction Ferric iron blue reaction |
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Renal dysplasia Disorganised development of parenchyma |
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Congenital renal cyst Solitary |
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Polycystic kidney disease Both kidneys contain many cysts and there is progressive comporomise Renal function - persian cats and cairn terriers Slowly developing |
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Acquired cysts as a sequel to interstitial fibrosis Tubules obstructed by scar tissue |
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Renal cortical ecchymoses Significant lesion of neonatal herpesvirus of pups |
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Interlobular Arcuate Interlobar Renal |
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Necrotic on the left and normal on the right |
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Hydronephrosis |
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Bladder stones - causing local irritation of the walls/mucosa If one of these caliculi were to become lodged in the ureter (unilateral) or urethra (bilateral) hydronephrosis would result |
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Haemosiderosis |
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Fatty change |