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Renal Pathology
SGU/SVM Renal Path
| Question | Answer |
|---|---|
| In what species are ectopic ureters most common | Ectopic ureters are most common in bitches. They are rare in horses, but are the most common developmental anomaly in the urinary tract of horses. |
| What is the minimum percentage of nephrons required to maintain normal kidney function | As long as 35% of all nephrons are functioning, normal kidney function remains. |
| What is the first kidney function to be lost when more than 70% of the nephrons are non-functional | The ability to concentrate urine is lost when 70% of the nephrons are damaged. The first sign of kidney disease is isosthenuria. |
| What results from a loss of 70-75% of nephrons | The glomerular filtration rate will remain normal until 70-75% of nephrons stop functioning. So, first comes isosthenuria (at 70%), then azotemia. |
| What clinical syndrome occurs when 75% of nephrons are non-functional | Renal failure/insufficiency and uremia occur when more than 75% of nephrons become non-functional. |
| What is the first protein seen in the urine when the filtration barrier (glomerulus and Bowman's capsule) is damaged, In what species is it normal to see trace protein | largest protein that can pass through filtration barrier-albumin,but albumin neg charge norm prevents this,When the barrier is damaged,albumin is the first protein seen in the urine,Norm dog have trace albumin in the urine, other species should have none. |
| What is the only place in the nephron where protein reabsorption occurs | The proximal tubule is the only site of protein reabsorption. |
| How much of the filtrate is reabsorbed in the proximal tubule | The obligatory reabsorption in the proximal tubule is about 65% of the filtrate. |
| T/F The distal tubule is often the first part of the nephron to be injured by hypoxia, toxins, etc | FALSE, The proximal tubule is usually the first part of the nephron to be injured by hypoxia, toxins, etc. This may indicate acute injury. |
| Give the three primary functions of the loop of Henle | The loop of Henle reabsorbs water (only in the descending part), Na+, Cl-, and maintains the concentration gradient of the interstitium (which is required for concentrating urine). |
| What part of the nephron becomes permeable to water in the presence of ADH | ADH is required for the reabsorption of water in the distal tubule and cortical collecting tubules. |
| What does aldosterone do | Aldosterone increases the reabsorption of Na+ and secretion of K+ from the principal cells in the cortical collecting tubules. It is secreted from the adrenal cortex in response to angiotensin II, increased plasma K+ concentration, and ACTH. |
| Cortical blood flow is (high, low) and medullary is (high, low) | Cortical blood flow is high, medullary is low. |
| Put these in order of blood flow: glomerular capillary bed, efferent arteriole, afferent arteriole, peritubular capillary bed | Blood flow order: afferent arteriole, glomerular capillary bed, efferent arteriole, peritubular capillary bed. So the blood nourishing the tubules has already been filtered. |
| Give five general functions of the kidney and the primary mechanisms of each | The kidney is involved in elimination of metab waste,acid-base balance,extracell K+ conc,water conservation and endocrine functions (parathyroid hormone degredation, erythropoietin for RBC formation, renin, calcitriol for intestinal Ca+ absorption) |
| What does renin do and where is it made | Renin is made in the juxtaglomerular apparatus in response to low blood pressure, It stimulates angiotensin,which (angiotensin II)causes preferential effrent arteriolar constriction,stimulates aldosterone release,& increases water & Na+ reabsorption. |
| T/F Proteinuria and hematuria can occur without renal dysfunction | TRUE. |
| T/F Azotemia is a clicinal sign resulting from a decrease in glomerular filtration rate | FALSE, Azotemia is a high BUN and creatinine level generally caused by low glomerular filtration. It is NOT a clinical sign (but it may or may not be associated with clinical signs). |
| What blood chemistry value is used to estimate glomerular filtration rate, Why | Creatinin level can be used as a good estimate of GFR because it is normally almost completely cleared (no maximum filtration rate) and very few things would cause values to vary besides a change in GFR. |
| Give three possible causes of increased urea values | An increase in urea may be due to increased production, urine leakage into body cavities, or most likey decreased filtration. |
| T/F Because creatinine is breakdown product of muscle, damaged myocytes and high meat intake could cause azotemia in a normal animal | FALSE, Because creatinine is rapidly cleared and has no maximum clearance rate, only a change in GFR can change creatinine levels. |
| Give reasons for pre-renal, renal, and post-renal reduced glomerular filtration, What findings can be shown for each | Reduced renal blood flow can be a pre-renal cause for low GFR,findings inc azotemia & NORM urine conc. Renal insuff causes reduced GFR,leading to azotemia,isosthenuria,Post-renal dec GFR may be caused by obstruct of urinary outflow,there will be azotemia |
| T/F Clinical signs will always accompany azotemia | FALSE, Presence and type of clinical signs will depend on the cause of azotemia. |
| T/F Clinical signs will always accompany uremia | TRUE, By definition, uremia is a clinical syndrome resulting from renal insufficiency. It is seen in both acute and chronic renal failure. |
| Is it possible to have severe uremia without having high azotemia | YES, A sudden loss of renal function can cause severe uremia without equally severe azotemia. |
| What information must be evaluated to understand the significance of urine specific gravity | The hydration status, BUN, and creatinine levels should be all be considered when evaluating urine specific gravity. |
| What are the three requirements for concentrating urine | Concentrating urine requires presence of ADH, a response to ADH, and a concentration gradient between the interstitium and tubules. |
| What are the signs of urine concentration dysfunction | Polyuria and accompanying polydipsia, and isosthenuria may indicate inability to concentrate urine. |
| T/F Isosthenuria without azotemia is physiological and can be ignored | FALSE, Low specific gravity can be normal if there is no azotemia and the animal is well hydrated, but it can be a sign of initial renal damage, so the problem should be monitored. |
| Give reasons for pre-renal, renal, and post-renal proteinuria, Which is most common | Pre-renal causes of proteinuria:plasma conc of small proteins exceed ability to reabsorb them,Renal causes:reduced ability to reabsorb protein(tubular proteinuria)or damaged filtration barrier(glomerular proteinuria)Post-renal causes:hemorrhage into or in |
| T/F Hemoglobinuria, myoglobinuria, bilirubinuria, and ketonuria are signs of renal dysfunction | FALSE, Hemoglobinuria, myoglobinuria, ketonuria, bilirubinuria are always pre-renal in origin. They do not indicate renal dysfunction. |
| What are two possibe reasons (in general) for glucosuria | Glucosuria can be caused by glucose in excess of the maximum capacity for resorption (hyperglycemic glucosuria), or by defective resorption (renal glucosuria). |
| What type of casts might be found in healthy animals, What type of casts reflect active tubular degeneration or necrosis | Healthy animals may have a small number of fine granular or hyaline casts. Fatty, cellular, or granular casts may reflect active tubular degeneration or necrosis. |
| How does chronic renal failure cause hypocalcemia | The kidney makes the active form of vit D(calcitriol)without it,intest absorp of Ca is low,If Ca reabsorp from the kid is also low, this will stim PTH, causing calcium to be released from bones & the cycle continues,The hyperphosphatemia ass wth renal ins |
| How does chronic renal failure cause non-regenerative anemia | If erythropoietin can't be made, neither can new red blood cells, hence non-regenerative anemia. |
| What causes hyperkalemia in renal disease | Hyperkalemia in renal disease is caused by inability to excrete K+(either because of a blockage or because of tubular insufficiency). Even though renin stimulates K+ secretion, a lack of renin is NOT the cause for hyperkalemia during renal disease. |
| Define renal disease | Renal disease is any morphologic or functional lesion in one or both kidneys (regardless of extent). |
| What is renal failure | Renal failure (the same as renal insufficiency) is a clinical syndrome in which the kidneys can no longer maintain their regulatory, excretory, and endocrine functions. |
| What defines end-stage kidney, What is the gross appearance of end-stage kidneys | End-stage kidney results from chronic, progressive disease. There is no recovery. The kidneys are reduced in size, distroted and firm (due to scarring) and pale. |
| If irreversible damage is done to the proximal tubule, will the rest of the nephron maintain function | NO, nephrons are a functional unit and partial (irreversible) damage will leave the entire nephron non-functional. |
| What type of acute changes can occur in the glomerulus, What do chronic injuries do to the glomerulus | The glomerulus can respond to acute injury with proliferation or necrosis; rupture or thickening of the basement membrane; infiltration of inflammatory cells. Chronic injuries cause fibrosis and atrophy (followed by atrophy of renal tubular epithelium) |
| T/F Renal tubules are non-regenerative | FALSE, Renal tubular epithelium CAN regenerate, but only if the basement membrane is intact. |
| Give possible signs of acute damage in renal interstitium | Inflammation, hemorrhage or edema may be signs of acute injury in renal interstitium. |
| What might be seen in renal interstitium after chronic injuries | Inflammation and fibrosis indicate chronic injury. |
| List three major pre/extra-renal categories or causes for renal lesions/dysfunction | Pre-renal disorders are related to disorders of circulation, ADH, or aldosterone. |
| What is most common pre-renal cause of renal lesions | Circulatory disturbances are the most common pre-renal cause of renal disorders. |
| Describe the normal blood flow to the kidney | The renal artery splits into interlobar arteries, to arcuate arteries, to interlobular, to afferent arterioles, to glomerular capillary tufts, to efferent arterioles, to the peritubular capillary plexus. |
| How does underperfusion lead to renal damage, What signs are associated with this | Low bloodflow causes low GFR, which leads to azotemia. The response to low blood flow is conservation of water and sodium, so there will be oliguria and conced urine.Severe, prolonged reduced perfusion causes ischemic necrosis and primary renal failure |
| Describe the appearance of a hyperemic kidney, What might cause this | Hyperemic kidneys are swollen, dark red, and ooze blood from the cut surface. This can be caused by acute septicemia, but may be physiologic. If an animal dies in lateral recumbancy there may be unilateral renal hypostatic congestion. |
| Give reasons for renal cortical hemorrhages | Renal cortical hemorrhages may be associated with septicemia due to vasculitis, vascular necrosis, or thromboemboli of DIC. |
| What might cause large intrarenal or subcapsular hemorrhages | A large area of intrarenal hemorrhage can be caused by trauma, biopsy, bleeding disorders, or DIC. |
| What is the most typical appearance of renal infarctions, Why are red and some pale, How do they heal | Renal infarctions tend to be pyrimidal shaped (with the base at the cortex and apex toward the medulla)They start out red if they are caused by arterial occlusion (and nearly all are) and become pale white 2-3 days after the occlusion. Pale infarcts have |
| Under what circumstances is cortical necrosis seen, What is it associated with | Cortical necrosis is the result of widespread thrombosis in the small renal arteries and arterioles, caused by DIC. It's often associatecd with gram negative septicemias or endotoxemias. |
| T/F Cortical necrosis is usually bilateral | TRUE. |
| What areas of the kidney are most prone to hypoxia | The proximal tubules have a high metabolic rate, so at the edge of an infarct, these will be necrotic but glomeruli may not be. The inner medulla is the least well-perfused, making it more prone to hypoxia. |
| What type of renal damage is caused by overuse of NSAIDs, Give specific examples | Papillary/medullary necrosis is caused by overuse of NSAIDs,especially phenylbutazone & flunixin in horses,They cause direct damage to medullary interstitial cells & the reduction in prostaglandin synthesis reduces blood flow.Dogs and cats are susceptible |
| What is neurogenic diabetes insipidus, What is the primary clinical sign | Neurogenic diabetes inspidus is caused by a deficiency in ADH production. The primary sign is PU/PD and isosthenuria. |
| What is nephrogenic diabetes insipidus | Nephrogenic diabetes insipidus is when the kidney can't respond to ADH. |
| Aldosterone deficiency results in loss of __ and retention of __ | Aldosterone deficiency results in a loss of Na+ and retention of K+ (hyperkalemia). So excess aldosterone causes hypokalemia and retention of sodium. |
| What is the most common cause of excessive aldosterone | Excessive aldosterone is usually secondary to congestive heart failure, Low blood pressure stimulates renin, which leads to angiotensin II, which leads to aldosterone. Sodium retention causes hypervolemia and edema. |
| What do the terms diffuse and global lesions refer to with respect to glomerulopathies | Diffuse means that many glomeruli are affected throughout the kidney, A global lesion is one in which the entire glomerular tuft is damaged. |
| What is the hallmark of glomerular disease | Proteinuria is the hallmark of glomerular disease (usually albumin), After a while, hypoalbuminemia may be seen. |
| T/F Azotemia and glomerular disease go hand-in-hand | FALSE, It is possible to have severe glomerular disease without a change in GFR (at least for a while). |
| T/F If the glomerulus is irreversibly damaged, the entire nephron will become non-functional | TRUE. |
| What three signs define nephrotic syndrome, What other sign may also be present | Nephrotic syndrome consists of edema, proteinuria, and hypoalbuminemia. Hypercholesterolemia may also be present. |
| Describe the pathogenesis of nephrotic syndrome | The glomerular filtration barrier becomes more permeable when it is damaged; albumin will be the first protein lost (because of its small size). The tubules become overloaded and cannot reabsorb the excess albumin. This results in proteinuria. Becau |
| What causes hypercholesterolemia associated with nephrotic syndrome | Hypoalbuminemia triggers increased synthesis of lipoproteins in the liver, There is also a decrease in lipolysis and processing of intravascular lipoproteins (for unknown reasons). |
| Why might thrombosis result from glomerular disease | Anti-thrombin III can be lost in the urine (like albumin), leading to thrombosis. |
| What are the two main glomerular disease entities | Glomerulonephritis and glomerular amyloidosis are the two main glomerular disease. |
| T/F Inflammatory cells are a key characteristic of glomerulonephritis | FALSE, There may be inflammatory cells involved in glomerulonephritis, but some forms of the disease cause very little inflammation. |
| T/F Patients with glomerulonephritis can’t concentrate urine | FALSE, In the early stages of acute severe glomerulonephritis, urine concentrating ability is preserved and tubular function is intact. If disease progresses, the tubules will be damaged, eventually resulting in renal failure. |
| What causes most cases of glomerulonephritis | Most cases of glomerulonephritis are caused by deposits of immune complexes. |
| T/F Glomerulonephritis is the most common cause of chronic renal failure in cats | FALSE, Glomerulonephritis is the most common cause of renal failure in dogs. |
| T/F Glomerulonephritis is common in ruminants | FALSE, Glomerulonephritis may be seen in ewes with pregnancy toxemia, but is otherwise rare. |
| The antigens involved in immune-complex glomerulonephritis are (exogenous, endogenous, both, neither) | The antigens involved in immune-complex glomerulonephritis can be either exogenous or endogenous. |
| Antigen/antibody complexes are most likely to form when (Ag>Ab, Ab>Ag, Ab=Ag, none of the above), Why | Antigen/antibody complexes are most likely to form when the amount of antigen and antibody are about equal (slight excess of antigen). If the antigen greatly exceeds the antibody level, injury caused by compliment fixation is unlikely. If the antibody |
| Describe the pathogenesis of immune-complex glomerulonephritis | Immune-complex glomerulonephritis is associated with prolonged moderate antigen excess, These complexes become trapped in the glomerulus (or antibodies form against the glomerulus resulting in true autoimmune glomerulonephritis). Immune complexes stimu |
| Immune-complex glomerulonephritis is often associated with what conditions, What antigens are usually involved | Immune-complex glomerulonephritis is often associated with chronic inflammation, persistent infections and neoplasia. The antigens involved are usually not identified. |
| What species and breed is prone to a genetic form of glomerulonephritis | Finnish Landrace lambs are prone to a genetic form of glomerulonephritis. |
| Describe the gross appearance of acute glomerulonephritis | Acute glomerulonephritis causes the kidney to be pale and slightly swollen with pinpoint red dots on the cut surface (the glomeruli). |
| Describe the gross appearance of chronic glomerulonephritis | Chronic glomerulonephritis causes the renal cortex to be slightly shrunken, the capsule may be finely granular and glomeruli appear as pale grey pinpoint dots. |
| What cellular changes occur with glomerulonephritis | Glomerulonephritis causes cellular proliferation with thickening of the basement membrane, which also becomes much more porous. |
| What is the end stage of glomerulonephritis called | Glomerulosclerosis is the end stage of glomerulonephritis. |
| What is the most common histologic type of glomerulonephritis, What other types are there | Diffuse membranous glomerulonephritis is the most common histologic type in cats and membranoproliferative is most common in dogs (p. 257 of text). Other types include membrano-proliferative, exudative, and necrotizing. |
| Diffuse membranous glomerulonephritis is associated with what infections in dogs, In cats | Diffuse membranous glomerulonephritis is associated with FIV and FeLV in cats and Dirofilaria immitis in dogs, Systemic lupus may also be a contributing factor. |
| How is glomerulonephritis diagnosed, What is the key feature | Glomerulonephritis is diagnosed by a prolonged proteinuria of renal origin, Other blood chemistry values may vary depending on the severity of disease, A renal biopsy is recommended. |
| List four possible consequences of glomerulonephritis | Glomerulonephritis may spontaneously resolve, may cause nephrotic syndrome, may progress to renal failure, and may cause a hypercoagulable state (because of loss of anti-thrombin III) which could lead to thrombosis and renal infarction. |
| Which is more common, glomerular amyloidosis or glomerulonephritis | Glomerulonephritis is much more common than glomerular amyloidosis. |
| In what species is glomerular amyloidosis usually diagnosed | Glomerular amyloidosis is most often diagnosed in dogs. |
| T/F If diagnosed early, amyloidosis has a good prognosis | FALSE, Glomerular amyloidosis is ALWAYS chronic, progressive, irreversible and incurable. |
| Dogs with glomerular amyloidosis usually present with what condition | Dogs with glomerular amyloidosis usually present with chronic renal failure, but may present with nephrotic syndrome. |
| What is the most common site of amyloid deposits in dogs (be specific), Where else can it be deposited | In dogs, amyloid usually gets deposited in the glomeruli in the mesangium between the endothelial cells and basement membrane. It can be deposited just about anywhere though. |
| Where is amyloid usually deposited in cats | Amyloid is deposited in the renal papilla and outer medulla in cats. |
| What breeds of cats and dogs have a familial predisposition to glomerular amyloidosis | Abyssinian, Siamese, Oriental shorthair cats, and shar pei dogs have a familial predisposition to glomerular amyloidosis. |
| What are the two forms of amyloidosis, Which is more common | Amyloidosis is classified as idiopathic (diagnosed most often) or reactive, which is associated with chronic inflammatory disease or neoplasia. |
| Describe the gross lesions of glomerular amyloidosis as the disease progresses | In early glomerular amyloidosis there may not be any visible changes, As it progresses, the surface of the kidney becomes irregularly depressed, mottled, and firm. The kidneys can be enlarged, pale tan to yellow. |
| What stain can be used to make a presumptive diagnosis of amyloidosis, What stain is used on histologic specimens for a more definitive diagnosis, Describe the appearance of both | An iodine solution will turn glomeruli brown if there is enough amyloid in them (used on a gross specimen). These will turn purple when exposed to dilute sulfuric acid. Amyloid can be observed as a green birefrigence (green sheen in light) when staine |
| Where is amyloid deposited in cattle, How do they present | Amyloid is deposited in the kidney, liver, GI tract and adrenal glands in cattle, They present with chronic wasting disease. |
| When is renal amyloidosis seen in horses | Renal amyloidosis has only been seen in horses used for antiserum production. |
| How is renal amyloidosis differentiated from glomerulonephritis in patients | A biopsy must be done to distinguish glomerulonephritis from amyloidosis, This will aid in prognosis, but the treatment is the same. |
| What test should be done before a renal biopsy, What part of the kidney is biopsied | A clotting test should always be done before a renal biopsy, Biopsy the cortex, because that’s where the glomeruli are. |
| What causes uremia (be specific) | Uremia is a syndrome associated with multisystemic clinical signs and lesions due to renal failure, caused by the build-up of toxins (including urea, creatinine and ammonia). |
| What is the pathogenesis of the mucosal hemorrhage that often occurs in animals with renal failure | Platelet secretion, adhesion, aggregation and prostaglandin metabolism, are impaired in uremia, and are responsible for the mucosal hemorrhage that may occur with renal failure (p. 356). The accumulation of toxins also promotes endothelial damages that |
| Why does thrombosis and infarction occur with renal failure | Thrombosis (and resulting infarction) is related to increased endothelial damage with loss of anti-thrombin III in the urine and impaired platelet function.. |
| Why does dehydration occur with uremia | The kidneys are unable to retain water and uremia may cause vomiting and diarrhea, leading to further loss of fluids. |
| Why does edema develop with uremia | Uremia causes endothelial damage, which increases permeability, causing edema, The hypoproteinemia prevents the extracellular fluid from being reabsorbed. |
| T/F Ruminants in renal failure will commonly have a metabolic acidosis | FALSE, Ruminants (unlike other domestic animals) tend to have a metabolic alkalosis associated with renal failure because they have GI atony and sequestration of HCL in the abomasum. |
| Why does metabolic acidosis occur with uremia | The tubules can’t produce ammonia (to get rid of excess H+), there is increased retention of H+, and bicarbonate reabsorption is limited when there is renal failure. |
| Describe the pathogenesis of renal secondary hyperparathyroidism, Under what circumstances does it occur | Renal secondary hyperparathyroidism occurs in chronic renal failure (NOT acute). Phosphate levels increase because of reduced glomerular filtration (decreased excretion and secretion). The increased inorganic phosphate binds to the free ionized calci |
| What are the consequences of hyperparathyroidism, Which are most common | Hyperparathyroidism can cause osteodystrophy because it stimulates osteoclastic bone resorption. However, clinically important renal osteodystraphy is rare, but may be seen in the skull bones of young dogs. A characteristic lesion in dogs is calcifica |
| Why is non-regenerative anemia possible with uremia | Non-regenerative anemia can occur in uremic states because of reduced erythropoietin. |
| What causes vomiting and weight loss related to uremic syndrome | Gastric ulcers and high levels of toxins (metabolic waste) may cause vomiting. Weight loss may occur from vomiting, diarrhea, and they probably just feel like crap. |
| Explain the pathogenesis of ulcerative necrotic stomatitis and gastritis related to uremia | The high levels of ammonia cause endothelial damage and necrosis leading to ulcers in the mouth and stomach. |
| In what species and under what circumstances is hyperkalemia seen | Hyperkalemia is seen in dogs, cats, and horses with chronic renal failure or oliguric/anuric acute renal failure. It is due to impaired renal excretion of potassium and is also associated with acidosis (caused by impaired H+ excretion and low bicarbona |
| Why do cattle with renal failure sometimes have hypokalemia | Cattle tend to have hypokalemia because they go into alkalosis. They also have increased excretion in saliva. |
| What would you expect the level of phosphate to be in uremic animals, Explain species differences | Dogs, cats, and horses have hyperphosphatemia because of impaired excretion (from low GFR). Cattle may or may not have hyperphosphatemia because saliva and ruminal excretion of phosphate are more significant than renal excretion. |
| What species in renal failure is often hypercalcemic | Horses are usually hypercalcemic because vitamin D (calcitriol) does not have a large role in calcium absorption from the gut, so they take a lot in but can’t get it out (poor renal clearance). |
| Serum Ca++ is usually (very low, low-normal, normal, high, very high) in uremic dogs, cats, and cattle | Uremic dogs, cats and cattle tend to have mild hypocalcemia. Levels can be low, normal, or high (PTH usually keeps it right about normal). |
| Why do animals usually die of renal failure | Animals that die of renal failure do so because of the cardiotoxicity of increased serum K+, metabolic acidosis, and pulmonary edema. |
| What is another term for acute tubular necrosis | Nephrosis is acute tubular necrosis. |
| T/F Acute tubular necrosis is the most common cause of acute renal failure | TRUE. |
| What is the difference between nephrosis, nephritis, and nephrotic syndrome | Nephrosis is acute tubular necrosis; nephritis is inflammation of the nephrons (or part of the nephron; i.e. glomerulonephritis); and nephrotic syndrome is hypoalbuminemia + proteinuria + edema +/- hypercholesterolemia. |
| What causes intratubular obstruction associated with nephrosis | Intratubular obstruction occurs when sloughed tubular epithelial cells get stuck in the tubules. |
| Why does nephrosis cause a reduced GFR | The reduction in GFR is a result of vasoconstriction brought on by rennin release due to damaged tubular epithelium. |
| Give a pre- and post-renal cause for nephrosis, and two renal causes | Ischemia (pre-renal), obstruction (post-renal), nephrotoxins and severe acute glomerulonephritis may all cause nephrosis. |
| What is the pre-requisite for tubular regeneration to occur | Tubular epithelium can regenerate if the basement membrane is intact. |
| What three things occur (in order) as a response to tubule insult | Injury to tubules causes tubular degeneration, tubular necrosis, and desquamation into lumen. |
| What is the key feature of interstitial nephritis | Inflammatory cells are present with interstitial nephritis. |
| T/F Inflammatory and degenerative changes in the tubules often accompany interstitial nephritis | TRUE. |
| What usually causes suppurative interstitial nephritis | Suppurative interstitial nephritis is usually caused by hematogenous spread of systemic bacterial infection. |
| Give two causes of non-suppurative interstitial nephritis | Non-suppurative interstitial nephritis can be secondary to glomerular disease or infection (usually viruses, some bacteria). |
| T/F Interstitial fibrosis occurs with acute damage to the interstitium | FALSE, Fibrosis is always a chronic change. |
| What is the most common cause of chronic renal failure in horses | Chronic interstitial nephritis may be the most common cause of chronic renal failure in horses. |
| What usually causes acute tubular necrosis in horses | Nephrosis in horses is often caused by exposure to nephrotoxins or hypoperfusion. |
| Pyelonephritis is (suppurative, non-suppurative) (tubular, glomerular, interstitial, tubulointerstitial) disease (with, without) inflammation centered in and around what area of the kidney | Pyelonephritis is suppurative tubulointerstitial disease with inflammation centered in and around the renal pelvis and deep medullary tissues. |
| Pyelonephritis is usually caused by (ascending, descending) infection and is usually (unilateral, bilateral) | Pyelonephritis is usually caused by ascending infection and is usually bilateral. |
| Give five signs of pyelonephritis that might be seen in a urinalysis | Pyelonephritis might cause casts, hematuria, proteinuria, bacteruria, and pyuria. |
| T/F As long as urine can still get through, obstruction will not increase the risk of pyelonephritis | FALSE, Anything that impedes (does not have to cause complete obstruction) urine flow increases risk of pyelonephritis. |
| T/F Cats most commonly get amyloid deposits in the glomeruli | FALSE, Cats usually get amyloid deposits in the medullary interstitium, leading to chronic renal failure. |
| Granulomatous nephritis is associated with what type of disease, Give a specific example in cats, Give a differential diagnosis for granulomatous nephritis | Granulomatous nephritis is associated with chronic diseases, like FIP in cats. Renal lymphoma is a differential for granulomatous nephritis. |
| Primary renal tumors are (common, uncommon) and (unilateral, bilateral) | Primary renal tumors are rare, and usually unilateral. |
| What is the most common type of primary renal neoplasm, What species is it seen in most often | Renal adenocarcinomas are the most common primary renal neoplasm. They occur most often in dogs and cattle. |
| What is the most common site of renal adenocarcinoma metastasis | Renal adenocarcinomas usually metastasize to the lungs (can also go to liver, opposite kidney, and adrenals). |
| In what part of the kidney do transitional cell papillomas and carcinomas arise | Treansitional cell papillomas and carcinomas arise in the renal pelvis and lower urinary tract. |
| T/F Generally lymphosarcomas have no effect on total renal function and clinical signs are related to pain or blood loss from hemorrhage (not renal failure) | TRUE, Except in cats. |
| What is the first sign of lymphosarcoma in cats, What is a major differential diagnosis | Cats with lymphosarcoma usually present with signs of renal failure (lymphosarcomas can be bilateral). The differential diagnosis would be granulomas of FIP. |
| T/F Metastatic lesions to the kidneys are common and nearly always unilateral | FALSE, Metastatic lesions to the kidneys are not as common as to the lung and liver, but they are more common than primary renal tumors. They may be unilateral or bilateral. |
| Which are more common, metastatic tumors in the kidney or primary renal tumors | Metastatic renal tumors are more common than primary renal tumors. |
| Nephroblastomas are (benign, malignant) | Nephroblastomas are benign. |
| T/F Renal aplasia, hypoplasia, and dysplasia have all been noted in animals | TRUE. |
| What species are more likely to have ectopic kidneys, Is it usually unilateral or bilateral | Functional or non functional |
| In what species are renal cysts often an incidental finding | Renal cysts may be seen in pigs and calves as an incidental finding. |
| T/F Polycystic kidneys are often an incidental finding, since they don’t impair renal function | FALSE, Polycystic kidneys compress the parenchyma and may impair renal function. |
| In what species/breeds can polycystic kidneys be inherited | Polycystic kidneys can be inherited in cairn terriers, west highland white terriers, collies, Persian cats, pigs, and lambs. |
| What worm is found in the kidney of dogs | Dioctophyma renale is the kidney worm of dogs. |
| What kind of damage can Dioctophyma renale cause | Dioctophyma renale can cause severe hemorrhagic or purulent pyelitis and urethral obstruction. |
| What is the kidney worm of pigs | Stephanurus dentatus is the kidney worm of pigs. |
| T/F Stephanurus dentatus passes eggs through the feces | False, Eggs of Stephanurus dentatus are passed in the urine. |
| What word means increased frequency of urination (and is a sign of post-renal dysfunction) | Pollakiuria is an increase in urination frequency |
| What bacteria are usually found in urinary tract infections, What is their origin | E. coli, Staphylococcus, Streptococcus, Klebsiella, Pasteurella, and others may be found in the urinary tract and they are usually of fecal origin. |
| T/F Cystitis is common in dogs and cats | TRUE, Very common. |
| T/F It is rare to have ureteritis or urethritis without cystitis | TRUE. |
| Rate the ability of the bladder to heal itself after injury | The bladder has very good ability to repair itself if the cause of the inflammation is removed. |
| What is the most common cause of acute cystitis | Acute cystitis is usually caused by a bacterial infection. |
| Chronic ingestion of what toxin causes enzootic hematuria if cattle, What else is it associated with | Chronic ingestion of bracken fern causes enzootic hematuria of cattle and bladder neoplasia. |
| Name two toxins, besides bracken fern, that cause acute cystitis | Cyclophosphamide (a cancer drug) and cantharidin (from blister beetles) both cause hemorrhagic, cystitis. |
| What allows bacteria to colonize the bladder mucosa | Normally bacteria will only attach to and colonize the mucosa when the defense mechanisms are altered. |
| What causes the thickened bladder wall with acute cystitis | Edema and cellular infiltrate cause thickening of the bladder wall in acute cystitis. |
| Why does thickening of the bladder wall occur with chronic cystitis (4 reasons) | Chronic cystitis causes thickening of the bladder wall because of fibrosis of lamina propria, hyperplastic mucosa, lymphoplasmacytic infiltrate, and hypertrophy of muscularis. |
| T/F Mycotic cystitis may occur secondary to chronic bacterial cystitis | TRUE, Opportunist fungi can invade due to a long course of antibacterial therapy and immunosuppression. |
| T/F Urinary calculi are microscopic precipitates that form in urine | FALSE, Urinary calculi are macroscopic. |
| T/F Urolithiasis results when there is over saturation of substances eliminated in urine | TRUE, Can come from a wide variety of sources. |
| What might result from urolithiasis in the renal pelvis | Urolithiasis in the renal pelvis can cause hydronephrosis. |
| T/F Uroliths are more common in horses than other large animals | FALSE, Uroliths are common in cattle, sheep, and goats, but less common in horses. |
| What are the possible consequences of urolithiasis | Urolithiasis can cause obstruction, irritation, disruption of urine flow, predisposes to UTIs, they may pass, dissolve, or remain without causing clinical signs. |
| What is another name for feline urologic syndrome | Feline urologic syndrome = lower urinary tract disease of cats. |
| What is FUS | FUS is a group of diseases with multiple causes and clinical signs relate to lower urinary tract disease. |
| What results from LUTD if obstruction is present | Obstructed FUS causes uremia within 24 hours and death within 48-72 hours if not treated. |
| T/F Most cats with LUTD have sterile urine | TRUE. |
| What is the most common disorder of the bladder of otherwise healthy newborn foals | Some foals have ruptured bladders, due to unknown causes. |
| What is the first step in treating a ruptured bladder in foals | Correct the electrolyte abnormalities, then treat surgically. |
| What are urinary tract tumors associated with in cattle | Bracken fern causes urinary tract tumors in cattle. |
| What is the most common type of epithelial tumor in the lower urinary tract, What is the exception | Most epithelial tumors in the lower urinary tract are transitional cell carcinomas, but in horses squamous cell carcinomas are more common. |
| What is the most common type of mesenchymal tumor in the lower urinary tract | Leiomyomas are the most common type of mesenchymal tumor in the lower urinary tract. |
| What is the most common malformation of the urinary bladder, In what species is it seen | Patent urachus is the most common malformation of the urinary bladder and it occurs in foals. |
| T/F Clinical signs of renal lesions indicate a loss of renal function | FALSE, Clinical signs associated with renal damage do not always indicate a loss of function (ex: unilateral pylonephritis can cause pain and fever, but no loss of kidney function). |
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alljacks
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