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132 Cards in this Set
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- Back
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Urine is formed by filtration of plasma through the "filtration barrier" of the glomerulus and tubules. It helps to keep the good things in the blood and excrete the excess. Describe what the "barrier" is composed of |
- gaps between endothelial cells - basement membrane - gaps between podocytes (visceral epithelial cells) |
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Explain how the renal glomerulus, tubules and osmotic balance aid in the production of urine
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Plasma flows through the glomerulus and products are filtered out. Because of this the fluid in the bowman's capsule (surrounding the glomerulus) (in the cortex) is the same conc as plasma. The fluid flows through the proximal convoluted tubule (cortex) and down the proximal straight tubule (in cortex then medulla which is hypertonic). In the proximal straight tubule Na+ leaves the tubule and enters the interstitium in the medulla (maintaining hypertonic sol.) As the fluid passes through the loop on Henle (medulla) urea is excreted into the interstitium also. Because the medulla is hypertonic water follows the solutes leaving the tubules so urine is concentrated. In the thin ascending tubule (medulla) and the thick ascending limb (cortex) the mermbrane is impermeable to water and only Na+ can be excreted into the interstitium. The distal convoluted tubule (cortex) and the collecting duct (medulla mostly) are also impermeable meaning only a small amount of urea can be excreted into the medulla at the very end of the collecting duct before the urine production process is finished. |
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How does aldosterone act on the kidney tubules and what effect does it have? |
Modifies Na+ pumps in distal tubule so more Na+ moved into the interstitium. This causes water to follow |
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Describe the action of ADH (antidiuretic hormone) on the kidney tubules |
It makes the collecting duct more permeable so more water can leave the ducts and the urine can become more concentrated (ie. it acts as an antidiuretic) |
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Which part of the kidney (medulla or cortex) is most evolved as the zone of 'concentration'? |
The medulla |
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Fill in the blanks: Collecting ducts converge at medulla to form a _____. Each lobe has ________. Lobes may be fused to form single papilla such as in _______________. Some species don't fuse, resulting in ___________ (cattle/pigs) |
Lobe; papilla; cats/dogs; multilobar kidney |
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What percentage of cardiac output do the kidneys receive? |
20-30% |
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Describe the consequences of the kidneys characteristic 'end artery' pattern |
If it gets obstructed - get infarction of whole wedge |
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At what percentage of nephron damage will renal insufficiency and renal failure occur respectively |
2/3rd damaged; 75% damaged; kidneys can cope with loss/damage to <1/2 - 2/3 without compromise of renal function |
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Describe a consequence of renal failure on the body fluid balace |
if in renal failure can't concentrate urine or dilute it. So get polyuria and polydipsia and an inability to handle high fluid loads. This causes a decreased excretion of metabolic wastes resulting in azotemia |
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Describe the consequences of renal failure on phosphate homeostasis |
Decreased homeostasis - can't excrete enough P. -> hyperphosphataemia. Combines with calcium > precipitates > metastatic calcification. This is known as secondary renal hyperparathyroidism. See normal/low Ca on biochem (jaw resorbtion -> rubber jaw in young animals) -> potentiates renal failure -> also get precipitation in lung vessels and parathyroid glad enlargement too (indicative). (Parathyroid hormone regulates Ca conc -> acts on bone and gut (also releases more P) and acts on kidneys to retain Ca -> retain Ca -> but kidneys in failure |
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Describe how renal failure can affect acid-base balance and cause metabolic acidosis |
In general with renal failure -> can't excrete bicarbonate well etc |
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Describe how renal failure can affect electrolyte balance |
decreased electrolyte balance -> can cause lots of issues. K excreted in tubules, increased with increased flow. If acute renal failure, oligonuria and anuria -> hyperkalaemia (can't actively excrete potassium. Polyuria can lead to hypokalaemia |
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Describe how renal failure can affect hormone production |
Decreased EPO (leading to regenerative anaemia) and reduced active vitamin D. More imp in chronic renal failure -> acute -> some reservoirs |
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List the clinical pathology abnormalities in renal failure |
- Azotemia - Polydipsia/polyuria (chronic) OR oligouria/anuria (cells block tubules -> damage -> acute renal failure) - Isosthenuria -> if chronic make lots of urine - Hyperphosphataemia (not horses) -> tend to get rid of Ca and P together - Hyperkalaemia (acute) - Metabolic acidosis - Anaemia (in chronic renal failure) Collectively known as uraemia |
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Define azotemia |
increased serum creatinine and urea. - urea - from protein breakdown -> input depends on diet, catabolic state - creatinine - from muscle phosphocreatine -> constant input - tends to be relatively steady - excreted via glomerular filtration |
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Describe the mechanism of Pre-Renal azotemia |
- decreased blood flow to kidneys - dehydration -> most common cause - decreased cardiac ouput -> shock; congestive heart failure (other possible causes) - prolonged decreased blood flow can lead to renal azotemia (renal tubules start to die) - highly conc urine - likely this is azo and conc urine - Can become renal if ongoing |
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Describe the mechanism of Renal Azotemia |
- occurs with compromised renal function - seen once >75% nephrons affected - not very sensitive indicator of renal function - usually accompanied by polyuria BUT depending on cause and stage may see oliguria or anuria - cant be this if really conc urine - due to decreased excretion of urea + creatinine by damaged - mild to severe azo and less than optimally conc urine |
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Describe the mechanism of Post Renal Azotemia |
- obstruction of excretion of urine (urethral obstruction (increased pressure); bladder rupture) - prolonged obstruction of the urinary tract can lead to renal azotemia - can have conc urine - variable USG + oliguria/anuria + hyperkalaemia - can be caused by FLUTD (blocked cats), peripartum bladder rupture in foals, Trauma e.g. RTA, urolithiasis in ruminants |
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Describe the mechanism of Non-Renal azotemia |
- increased input into system (incr. urea prod. not decr. excretion) - associated with extra-renal disease, and not involving decreased glomerular filtration - usually mild - no concurrent increase in creatinine - can have conc urine - caused = Incr. protein catabolism - Incr. dietary intake; incr. catabolism of body tissues; GIT haemorrhage; some drugs; post-prandial |
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Describe the non-renal changes associated with uraemia |
- loss of concentrating ability (e.g. PU/PD) - loss of excretory function (azotemia, hyperkalaemia) - loss of normal hormone activity (anaemia; renal secondary hyperparathyroidism) - can sometimes distinguish between acute and chronic renal failure |
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Describe the possible gross lesions associated with uraemia |
- Endothelial damage - leakage of protein rich fluid into body cavities - thrombosis and infarction - caustic effect on mucosal surfaces (mucosal ulcers -> oral cavity and stomach) - bleeding diathesis - decreased platelet function occurs with uraemia, prolonged bleeding after trauma or surgery |
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True or false: CRF tends to have more non-renal gross lesions than ARF |
True |
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Decide whether the following clinical signs are associated with acute or chronic renal failure: - Petechial haemorrhages in oral cavity - pale mucous membranes - ulceration of the gums - "uraemic" breath - enlarged painful kidneys - black tarry faeces - shrunken firm kidneys - PU/PD |
1. Both 2. CRF 3. Both 4. ARF/both 5. ARF 6. Both 7. Both 8. CRF -> due to fibrosis 9. CRF (sometimes acute) |
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What are two important parameters you must know/measure to accurately interpret a USG |
Hydration status + azotemia |
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True or false: Renal failure is the only cause of azotemia |
FALSE (RLLY IMP) |
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Which USG would be suggestive of NOT renal failure and which USG ranges would be suggestive OF renal failure |
USG <1.008 - kidneys have some function as failing kidneys can't dilute NOT RENAL FAILURE
USG >1.030(dogs) - > 1.035(cats) - kidneys have adequate concentrating ability NOT RENAL FAILURE USG 1.008-1.029 (dogs) or 1.008-1.034 (cats) + dehydration +/- azotemia - IMPAIRED RENAL CONC ABILITY (could be renal dz) USG 1.008-1.012 + dehydration + azotemia - LIKELY RENAL FAILURE |
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Define renal aplasia |
Failure to develop one or more kidneys |
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Describe progressive juvenile nephropathy |
Early onset renal failure with no underlying cause |
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True or false: Ectopic and fused (horseshoe) kidneys can still work fine as long as they are attached to ureter |
True. Develop like this in embryo |
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Describe congenitally cystic kidney characteristics |
Many urine filled cysts; Cysts can develop at any level of nephron; single or multiple; polycystic; +/- bile duct cysts; associated with the developement of ciliated cells |
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Describe the cause of leaky filtration barrier in the glomerulus |
Damage to filtration barrier causes leakiness causing loss of proteins into urine (protein loss from blood = hypoalbuminaemia -> oedema) |
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What syndrome does a protein losing nephropathy cause? |
Nephrotic syndrome -> peeing albumin and low albumin |
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Describe the pathogenesis of immune mediated glomerulonephritis |
Immune complexes are formed on or deposited in the basement membrane (its not complex being there its what the complex causes) -> causes activation of complement -> attracts neutrophils -> produces proteases, free radicals -> membrane damage |
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List and describe the two forms of immune mediated glomerulonephritis |
1. Anti-basement membrane disease - immune complex formed in situ - most common form in primates 2. Pre-formed complexes trapped in BM - associated with underlying chronic disease - formation of soluble immune complexes - deposited in various BM e.g. eye, synovium of joints, glomerulus - e.g. chronic bacterial or viral infections, neoplasms - many cases are idiopathic |
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Describe amyloidosis |
Amyloid deposited in: - glomerulus (dogs) - medullary interstitium (cats) Glomerular deposition causes disruption of filtration barrier -> proteinuria, hypoalbuminaemia |
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Describe the components of nephrotic syndrome |
- Occurs in forms of kidney disease where glomerular filtration barrier is severly disrupted - loss of excessive amounts of albumin - decreased colloid osmotic pressure (oedema, ascites) - proteinuria - thrombosis (due to loss of anti-thrombin III) - hypercholesterolaemia (can be strong indicator of nephrotic syndrome) (path not fully understood) Nephrotic syndrome is not always assoc. with chronic renal failure |
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Bacteria in blood can localise in glomerular and/or interstitial capillaries causing acute glomerulitis. How would this present on PM and how would this change as the glomerulitis became more chronic |
Acute - see red spots in the cortex due to vasodilation (as part of inflammatory response) Chronic - get accumulation of neutrophils (suppurative glomerulitis) causing white spots. Later will get infiltration of lymphocytes, plasma cells, macrophages |
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What causes sleepy foal disease (an example of suppurative glomerulitis) and what are the clinical signs |
Actinobacillus equuli. Foal presents with pyrexia, lethargy, swollen joints, associated with bacteraemia/septicaemia. Gains entry via umbilicus, ingestion, inhalation. Get rapid deterioration and often fatal. |
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Describe what the interstitium of the kidney is made up of |
Everything in between tubules and glomeruli, including fibroblasts, matrix, cells, vessels. |
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List and describe the pathogenesis and clinical signs of 2 causes of interstitial nephritis |
a) Leptospirosis - bacteria enter blood vessels and travel throughout the body; localise in kidneys (also uterus, liver); exit into interstitium; migrate to renal tubules; localise in tubular epithelium; shed in urine. Clinical signs vary with species. b) E coli septicaemia in cattle - "white spotted kidney disease" - follows acute septicaemia due to E coli infection |
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How would you diagnose leptospirosis in a histological preparation (using stain?) |
Leptospires stain black with silver stains |
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List some causes of interstitial fibrosis of the kidney |
Infarcts, pyelonephritis, glomerulonephritis. Commonly seen in CRF - can be part of idiopathic chronic renal failure in cats |
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Describe the pathogenesis and cause of Ischaemic tubular necrosis |
Disruption of blood (oxygen) supply to kidney -haemolytic disease (severe anaemia) -renal vasoconstriction (hypovolemia, NSAIDs) -severe hypoxia |
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List some causes of haemolytic disease that can then result in Ischaemic nephrosis (tubular necrosis) |
- copper toxicity in sheep - leptospirosis in calves - immune mediated haemolytic anaemia in dog - various toxins (onions, brassica crops, zinc in small animals, crude oil in marine species) |
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Describe the characteristics of Toxic tubular necrosis and some possible causes |
Histologically similar to ischaemic nephrosis. Toxins may act directly on tubular epithelium (agents excreted in urine) or can act indirectly via disrupting blood or oxygen supply (e.g. NSAIDs) - Heavy metals (arsenic, lead; diagnose by tissue analysis or lead has inclusions in kidney tubules on histo) - plants (grapes, raisins, lillies, oak buds/acorns) -Antibiotics (older generation; ok if hydrated) - NSAIDs - Oxalates - Vit D - mycotoxins - therapeutic drugs |
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Describe how NSAIDs can result in toxic tubular necrosis |
Causes acute renal failure in small animals - inhibit prostaglandin production (some PGs specific to renal arterioles) -> decreased levels of PGs cause renal vasoconstriction -> ischaemic damage. Toxicity more likely with concurrent renal disease, cardiac disease or dehydration Causes renal papillary necrosis in horses |
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Describe how oxalates can cause toxic tubular necrosis |
Often seen in prod. animals (often not enough to cause lesions but are in SA) - Chelating agents -> sticks to Ca -> forms crystals -> precipitate out in vessels and excreted and damage tubules. Found in plants (sorrel, dock, rhubarb) - Absorbed from GIT - Also cause hypocalcaemia -> neuromuscular dysfunction - Animals present initially with trembling and weakness and later develop renal failure (not common in LA but very common in SA) |
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Give an example of an oxalate that commonly causes acute toxic tubular necrosis in animals |
Ethylene glycol - metabolised in the liver; metabolites excreted in urine; some metabolites cause direct epithelial cell damage; calcium oxalate crystals precipitate in urine. They look like dumbells or hay stacks |
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List the signs of ethylene glycol toxicity |
- Painful kidneys - Azotemia - Oligouria/dysuria - Isosthenuria ? - Haematuria/blood in urine |
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Define pyelonephritis and its cause |
Inflammation of the renal pelvis and renal parenchyma -> ascends from lower urinary tract -> travels via ureter (vesiculoureteral reflex; bacterial contamination of urine) |
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Give predisposing factors to Pyelonephritis |
- urethral obstruction - bacterial cystitis -> allows damage to sphincters and bacteria and urine can migrate up to kidneys - congenital malformation of ureter or sphincter - specific gram -ve infectionc (endotoxins -> inhibited peristalsis) - bacterial adhesion factors (some E coli) - shape of female urethra |
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In what circumstance would you see Haemoglobin in the kidney epithelial cells and describe the gross and histological appearances of the kidney |
Usually in assoc. with intravascular haemolysis Metabolised to haemosiderin over time See dark red/brown/black kidney if chronic See haemosiderin in the tubular epithelium on histo |
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Describe briefly how amyloidosis affects the kidney and the gross and histological appearances of the affected kidney |
Damages the filtration mechanism - protein losing nephropathy and lead to nephrotic syndrome (glomerulus in dogs, medulla in cats). Grossly kidneys are pale and waxy. When stained with Congo red the amyloid appears orangey/red in the glomerular tissue or the medulla. Usually asymptomatic in cats but can cause compression of the vessels -> medullary necrosis (papillary necrosis) |
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Describe hydronephrosis and its possible cause(s) |
Dilation of the renal pelvis (water in the kidney) Usually follows obstruction of urine flow in lower urinary tract Can be acquired (e.g. blocked ureter (tumour, crystal, stone)) Can be congenital (ectopic ureters) Can be unilateral or bilateral |
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Which two diseases of cats can look very similar with white spots on the kidney? |
Lymphoma and FIP |
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Describe and give the possible consequences of the congenital anomaly, ectopic ureters |
Implanting at 90 degree angle -> constant reflux -> could lead to hydronephrosis or pylonephritis if bladder infection too |
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Define a patent urachus and give some possible consequences of this congenital anomaly |
Foetal connection between the bladder and the umbilicus remains resulting in constant urine dribbling from the umbilicus (can get urine scald on the belly). Sometimes closure of the urachus is only partial, causing development of a diverticulum -> urine stasis -> predisposes to urinary tract infection (can use contrast medium cytography to diagnose) |
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List some possible causes of bladder rupture |
- Foals at parturition (lots of pressure from mares pushing) - can get swollen abdomen and uroperitoneum - Road traffic accidents in small animals - Urethral obstruction (male cats, dogs, small ruminants) |
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Define cystitis, give its clinical signs and possible causes |
- Inflammation of the urinary bladder - Similar clinical signs no matter what the underlying cause is: behavioural changes, frequent/painful urination, haematuria (whole RBCs), incontinence - Chemical agents and natural toxins (cyclophosphamide; blister beetles - found in horses hay, has toxin which causes necrosis on contact with mucosal surfaces -> causes GI ulcers; bracken fern - cattle) as well as uroliths, tumours and bacterial infection |
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True or false: Bacteria are a common cause of cystitis |
False. Not often are they the cause of cystitis surprisingly |
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List some protective mechanisms employed by the bladder to combat bacterial infections and cystitis |
Urinary tract is sterile (except distal urethra) Frequent voiding (physically removes bacteria) Urine pH Local antibody Dissolved solutes and organic acids |
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List some predisposing factors to UTI |
- Female urethra - wider than males -> easier for bacteria to enter - Trauma (uroliths, catheterisation) - Glucosuria (diabetes mellitus - great growth medium for bacteria) - Urine stasis - Dilute urine - Urinary pH changes |
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List some predisposing factors of urolithiasis |
- Urinary stasis - dehydration - urinary tract infection (changes pH) - high mineral content in urine (due to diet?) - pH of urine affects solubility of minerals (can feed food to change pH and stop formation of crystals) - males predisposed to obstruction (thin urethra) - almost never occurs in females |
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Give the most common sites of urolithiasis obstructions in the following animals: - Bulls/steers - Rams/wethers - Cats - Dogs |
1. Ischial arch; signmoid flexure 2. Urethral process 3. Entire urethra 4. proximal end of os penis |
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Which type of uroliths predominate in feline urolithiasis |
- Struvite crystals - Usually tiny sand-like grains - Can get increased numbers of calcium phosphate crystals (just because crystals are present doesn't mean cause of cystitis -> lots of cats have crystals and are asymptomatic) |
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What % of crystals are struvite and what % of crystals are calcium oxalate in dog urolithiasis |
50% are struvite (most due to UTI with urease producing bacteria (e.g. staph aureus) 30% are calcium oxalate (diff. to toxic form) |
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What causes urolithiasis in sheep? |
- pastures high in oxalates (e.g. sorrel, dock) - also high phosphate or oestrogens (e.g. subterranean clover) - housed sheep on concentrates or hay - common incidental finding |
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Define the following: - Dysuria - Stranguria - Haematuria - Pollakiuria |
- Dysuria = difficulty urinating - Stranguria = straining - Haematuria = Whole blood in urine - Pollakiuria = increased frequency of urination |
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List the clinical signs of NON obstructed urolithiasis |
- Dysuria - Stranguria - Haematuria - Pollakiurua (due to pain -> decreased vol too) - Behavioural changes - Inappropriate urination |
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List the clinical signs of OBSTRUCTED urolithiasis |
Dysuria, stranguria, behavioural changes PLUS uraemia, shock. Uraemia often distinguishing factor. Rock hard bladder on palpation (can feel really solid, dont confuse for tumour), brick red OR pale mm (shock). Post renal azotemia (at least initially). Hyperkalaemia (can cause arrythmias + tachycardia) |
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List some possible causes of Urinary Tract Obstruction and what you would expect clinically
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- masses (neoplasms, polyps) - inflammatory disease (e.g. FLUTD) - scarring (trauma, catheterisation) - uroliths - urethral plugs (made up of proteinaceous matrix, dericed from protein produced by inflamed bladder wall, matrix plugs can cause obstruction) - See straining, dripping urine, post-renal azotemia |
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List the 4 general caused of FLUTD in order of most to least likely and give possible clinical signs |
1. idiopathic (usually self limiting, common in fat, lazy indoor young to middle aged neutered males) 2. urolithiasis 3. bacterial cystitis (rare cause) 4. neoplasia (transitional cell carcinoma) - dysuria, pollakiuria, haematuria, vocalisation, inappropriate urination |
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Which components of the urine dipstick are useful; have limited use and are useless |
Useful: Blood, protein (only reliably predicts albumin), glucose, ketones, bilirubin Limited use: Urobilinogen, pH Do not use: Nitrates, leukocytes, SG (use refractometer) |
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Describe and give the causes of PRE-RENAL proteinuria |
"overflow" proteinuria -> increased protein delivered to glomerulus Causes = often transient - Hb (intravascular haemolysis) - Myoglobin (muscle damage) - Bence Jones proteins (multiple myeloma) |
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Describe and give the cause(s) of RENAL proteinuria |
Due to either glomerular or tubular disease. - Glomerular disease is clinically more severe/important (immune-mediated glomerulonephritis or glomerular amyloidosis; magnitude of protein loss usually grater than for tubular disease; also results in hypoalbuminaemia; nephrotic syndrome) - Tubular disease (e.g. inflammatory disease involving tubules) |
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Describe and give the causes of POST RENAL proteinuria |
Protein added to urine AFTER it exits the renal pelvis. No hypoalbuminaemia. Usually mild. |
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How can you quantify more closely the amount of protein in urine |
Using urinary protein:creatinine ratio (UPCR) - not affected by vol of urine produced. Single sample required. Do sediment exam first (will tell you if proteinuria is post-renal). Should be <0.5. If >1 then likely glomerular disease. If in between likely tubular. |
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What 3 things could be in the urine if the blood pad on a dipstick detects 'blood' |
Whole blood, Hb, and myoglobin. Very sensitive, will even give +ve result in slight contamination (e.g. cystocentesis) |
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What must you never forget to do as part of your urinalysis work up? |
Sediment exam! - see stuff in sediment! (cells - RBCs, WBCs, epithelial cells; casts, crystals, bacteria, etc) |
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What would you be thinking if you saw increased large, abnormally shaped transitional cells in a urine sediment exam? |
Transitional cell carcinoma. Stain slide or send to lab to confirm |
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What can bilirubin crystals indicate in a urine sediment sample in the dog and in the cat respectively? |
Common in concentrated urine of the dog, not significant. In Cats, usually an indicator of cholestatic liver disease |
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What quaitities would constitute Polyuria and Polydipsia in an animal? |
PD: >100ml/kg/day PU: >50ml/kg/day |
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Describe the normal function of ADH (vasopressin) |
Produced in hypothalamus; stored in posterior pituitary; released with decreased blood volume or increased plasma osmolality; acts on collecting ducts -> increases permeability (urine becomes more concentrated aka anti diuresis)
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Define Diabetes insipidus and give the two general causes |
Deficiency in production of or response to ADH. Central DI = problem in CNS. Nephrogenic DI = problem with the kidneys' response to ADH (but not due to primary renal disease). (Tumours and trauma most common cause) |
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What is the most common cause of PU/PD and give the mechanism? |
Renal disease. Idiopathic chronic renal disease where >66% nephrons lost. See PU/PD before azotemia. Mech: Decreased nephrons -> decreased ability to concentrate urine -> Primary PU -> Secondary PD |
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True or false: PU/PD can be seen in liver disease but it an uncommon cause of PU/PD. |
True. Sometimes seen in chronic (not acute) disease. Mechanism uncertain. |
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Describe the mechanism of PU/PD in association with diabetes mellitus |
COMMON cause. Hyperglycaemia -> exceeds renal threshold for resorption -> glucosuria -> osmotic diuresis -> Primary PU -> secondary PD |
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True or false: Central diabetes insipidus is RARE. |
True. It causes marked hyposthenuria |
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Describe the prevalence, mechanism and clinical signs of the two types of Nephrogenic Diabetes insipidus |
Mech: ADH produced but tubules don't respond to it -> structural or functional abnormality in distal tubules and collecting ducts. Primary (congenital) = VERY RARE. Marked PU/PD + hyposthenuric (USG <1.008) from early age. May pee inside or get very dehydrated easily if waterbowl not topped up. Secondary (acquired) = MORE COMMON. Many different causes (hypercalcaemia - inhibits the action of ADH in collecting ducts; E. coli - endotoxin causes decreased ADH sensitivity (reversible)) |
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Describe the mechanism and consequences of medullary solute washout |
Decrease hypertonicity of the medulla. Causes decreased ability to concentraet urine. Urea and sodium important. Decreased urea -> liver disease. Decreased sodium -> systemic hyponatremia. Decreased both -> sustained high urine flow -> fluid overload (iatrogenic). Can lose more solutes by peeing a lot of dilute urine -> makes production of dilute urine worse. |
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Which tubes would you use to collect blood for the following: - CBC - Serum biochemistry - Endocrine testing |
1. Purple top (EDTA) 2. Red top (plain) 3. Red top (plain) |
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Describe how a UTI can cause PU/PD and state whether or not this is a common cause of PU/PD |
Common cause. Mech = E. coli endotoxin -> decreased tubular sensitivity to ADH. More common in dogs and females. |
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Name the gray cells shown in this image and name the single purple stained cell in the centre |
1. Erythrocytes (RBCs) 2. Neutrophil (Leukocyte -> granulocyte) |
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Name the cell in the centre of this image. Note its pink granules and polymorphinc neuclues |
Eosinophil |
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Name the two prominent cells in the centre of this image |
Lymphocytes |
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True or false: Bone marrow is involved in producing lymphocytes |
False |
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How will a reticulocyte present on a NMB stain? |
Like a blue RBC but with blue dots or granules on it |
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Define MCV, macrocytosis and microcytosis and anisocytosis |
MCV - mean corpuscular volume (ie. RBC size) Macrocytosis = increased MCV (think IMHA, reticulocytosis, poodles, FeLV) Microcytosis = decreased MCV (think Iron def. anaemia (almost always), liver dz, japanese akitas) Anisocytosis = variation in cell size (usually indicative of regen. anaemia. Mild anisocytosis = normal in cats |
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Define MCHC, hypochromasia, hyperchromasia and polychromasia |
MCHC = amount of Hb (ie. colour of RBC) Hypochromasia = decreased MCHC -> increased central pallor (think iron def. or reticulocytosis) Hyperchromasia = Increased MCHC -> usually artefactual. (think haemolysis, heinz bodies, marked spherocytosis, lipaemias) |
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Describe the cause and possible diseases associated with spherocytes |
Small dark spherical RBC, lack central pallor. Cell gets bitten and closes bite. Due to Ab attachement? Suggestive of IMHA, |
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Define poikilocytosis |
abnormally shaped RBC |
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Define the following types of RBC shapes: - Acanthocytes - Echinocytes - Schistocytes - Keratocytes - Eccentrocytes - Codocytes or Leptocytes |
1. Spur cells - irregular projections. Mech. unknown. Cause: Cats: hepatic lipidosis; Dogs: haemangiosarcoma 2. Burr cell - short, evenly spaced, uniform projections. Often artefactual. Common in cat blood smears. Less commonly due to: renal dz, lymphoma, chemotherapy, post exercise in horses, rattlesnake bite 3. Fragmented RBC. Caused by intravascular trauma: DIC - fibrin strands, vascular neoplasms, Iron def. 4. Helmet or blister cell. Caused by Iron def. or intravascular trauma (DIC - fibrin strands, vascular neoplasms, Iron def.) 5. Hb shifted to one side of cell lacking central pallor. Oxidative damage; can be found in conjunction with Heinz bodies 6. Target cells - excessive membrane resulting in folding and a ring of pallor. Artefactual: increased EDTA. Can be caused by hepatic or lipid disorders. Little diagnostic significance |
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Describe the difference between Heinz bodies and Howell-jolly bodies |
Heinz bodies = denatured Hb beneath cell membrane - blebs on cell edge. Caused by oxidative damage to Hb (onions, brassicas, paracetamol) Can be normal in cats. Increased in HyperT and lymphoma Howell-Jolly = small, deeply basophilic inclusions. Retained nuclear material. Suggestive of regen. anaemia, chronic steroid therapy or reduced splenic function |
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Describe metarubricytes and their possible cause |
Last nucleated RBC stage. Normally seen in peripheral blood. Caused by: regen. anaemia, nonfunctioning spleen, haemangiosarcoma, lead tox, increased corticosteroids
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Define siderocytes and their cause(s) |
Erythrocytes with iron containing (siderotic) cytoplasmic inclusions; stain blue with prussian blue. Assoc. with Taranaki anaemia (decreased Mg) and lead toxH |
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How would you differentiate between Rouleaux and Agglutinated cells |
Pour saline on - if disperse then rouleaux (can be caused by hyperfibrinogenemia (acute inflamm.) or hyperglobulinaemia (plasma cell myeloma)). If dont then agglutinate as caused by Ag-Ab complex (suggestive of IMHA) |
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Describe the 3 mechanisms of Erythrocytosis and their pathogenesis and their causes |
- Relative = most common, actual RBC mass the same - decreased plasma vol. due to dehydration. - Physiologic = true but transient increase in RBC level (up to 2hr). Caused by: Splenic contraction, adrenalin mediated; from fear, pain, excitement. Most common in horses.Possibly concurrent physiological leukocytosis. Non pathogenic and no clin. sign. - Absolute = RBC mass is truly increased (long term). Due to: Primary erythrocytosis - regulatory defects, independent of EPO (myeloproliferative dz - neoplasm); Secondary erythrocytosis - normal regulatory mechanisms, increased EPO -> can be appropriate (due to decreased O2 conc - hypoxia, cardiopulmonary dz, high altitude, CV shunts); or inappropriate (EPO prod. not due to hypoxia (rare) - renal lesions (hydronephrosis, cysts, infarcts etc), hyperAC, anabolic steroids) |
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What blood smear characteristics are typical of regenerative anaemia? |
Anisocytosis and polychromasia |
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How would preregenerative anaemia appear on a blood smear? |
Normal. So Normocytic, normochromic. |
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Describe the mechanism involved in regenerative anaemia |
Decreased RBC mass -> hypoxia -> increased EPO from kidneys -> BM make RBC |
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What two mechanisms of anaemia can cause regenerative anaemia |
1. blood loss - haemorrhage. External or internal, acute vs. chronic. 2. blood destruction - haemolysis. Intravascular vs extravascular |
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true or false: Haemolytic anaemia generally gives a larger regenerative response than haemorrhage or external blood loss |
True |
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Describe how chronic renal disease can cause anaemia |
Decreased EPO production by the kidney |
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True or false: myelocytes (immature leukocytes) must mature for one week before they can be stored |
True |
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What is the most common cause of Leukocytosis
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Neutrophilia >> lymphocytosis > monocytosis, eosinophilia, basophilia (leukopenia usually due to neutropenia too) |
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Who has the largest storage pool or neutrophils out of large and small animals? |
Small - if get inflammation start off neutropenic because have such a small store. Then become neutrophilic |
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List the 3 main causes of Neutrophilis and describe them |
1. Physiologic response (fear/excitement) - mature neuts with no left shift; transient; may also see mild polycythaemia (splenic contraction) and lymphocytosis. No clin. sign. 2. Corticosteroid response (aka "stress response") - can be endog or exog. Mature neuts with no left shift. Decreased adhesion so more in circulating pool. May also see lymphopenia +/- monocytosis +/- eosinopenia (stress leukogram) 3. Inflammation (also in assoc, with IMHA and leukaemia) - increased demand for neuts. Get left shift -> immature cells such as bands, metamyelocytes +/- myelocytes |
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What are some possible causes of an inflammatory neutrophil response?
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The "p's" - pyometra. penumonia, pancreatitis, pleuritis/pyothorax, peritonitis, +/- prostatitis, pyelonephritis
generally caused by pyogenic bacteria |
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What is the most common cause of neutropenia? |
Acute inflammation causing mass emigration and N release from BM. Small animals have increased storage so neutropenia more concerning |
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What can cause decreased neutrophil production leading to neutropenia (aka granulocytic hypoplasia) |
Stem cell damage due to: infection - quite common, parvoviruses, erhlichiosis toxicity - oestrogens, PBZ, chloramphenicol myelopthisis - neoplasia, fibrous tissue congenital - rare, cyclic haematopoiesis of grey collies - get neutropenia at 12d intervals |
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True or false: Immune mediated neutropenia is quite common |
False
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What can cause transient sequestration of neuts causing neutropenia? |
anaphylaxis, endotoxaemia |
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Describe the changes seen in neuts with toxic change (accelerated maturation) |
Cytoplasmic basophilia and vacuolation; doehle bodies; toxic granulation |
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What are some causes of Eosinopenia? |
1. Increased corticosteroid levels (endog = hyperAC, stress; exog = glucocorticoid therapy) 2. Acute inflammation |
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What are some causes of Eosinophilia? |
1. Hypersensitivity/allergic reaction 2. Parasitism (LA>SA) 3. Other: Eosinophilic leukaemia; hypereosinophilic syndrome; idiopathic |
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List and describe the possible causes of Lymphocytosis |
1. Physiologic - mainly horses and cats; transient, +/- neutrophilia & erythrocytosis 2. Chronic inflammation - increased lymphopoiesis; reactive lymphs (bigger + incr. cytoplasmic basophilia) +/- rare blasts 3. Neoplasa - lymphoid leukamia - massive incr. 4. Others: BLV infx; Addisons |
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List and describe the possible causes of Lymphopenia |
1. Corticosteroid induced (most common) - stress leukogram, move from circ. to other pools - sequestration in LN, lympholysis 2. Acute viral infx - also common 3. Reduced lymphopoiesis - radiation, chemo 4. Loss, sequestration, lymph blockage - protein losing enteropathy etc |
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How would you differentiate between Neuts and monocytes? |
Monocytes bigger, more basophilic, often vacuolated cytoplasm, non lobed nuclei (horseshoe or bean shaped) |
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List and describe possible causes of monocytosis |
1. Chronic inflamm - responds like neuts but slower response - more chronic 2. Corticosteroid excess (dog) |
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Describe the significance of monocytopenia |
Not significant |
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Describe the Stress leukogram or corticosteroid response in the blood |
1. Mature neutrophilia 2. Lymphopenia 3. Eosinopenia (+/-) 4. Monocytosis (dog) If dog doesnt have stress leukogram and is sick or has "antistress leukogram" (lymphocytosis, eosinophilia etc) think Addisons (hypoAC) |
