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Flashcards in Urinary tract disease Deck (100)
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Give the USG reference ranges for the "normal", isosthenuria, hypersthenuria and hyposthenuria in the cat

- Normal: 10.015-1.060 (healthy cat usually 1.035)
- Iso: 1.008-1.012
- Hyper: >1.012
- Hypo: <1.008


List the tests that can be used in the examination of urinary tract disease

- Urinalysis
- Clinical pathology (haem, biochem, +/-SDMA, UPCR)
- Imaging: radiography, ultrasound, CT
- Surgical


What lateral radiographic view gives the least superimposition of the kidneys?

Right lateral


What contrast medium is generally used in the investigation of urinary tract disease?

Iodine salts e.g. iohexol


Define azotaemia

Increased concentration of non-protein nitrogenous compounds in the blood


Define uraemia

Clinical syndrome associated with renal failure


Outline the measurement and interpretation of urea in the investigation of urinary tract disease (causes of increase/decrease, when to sample)

- May be elevated if high protein diet or just eaten (wait 12hours after meal ideally)
- Also elevated by GI haemorrhage
- Increases with: fever, starvation, sepsis, burns, dehydration (mild elevation)
- Decreases with: severe hepatic dysfunction, protein restricted diets


Discuss the limitations of urea measurements in the investigation of urinary tract disease

- Reflects gut microbiome more than kidney in ruminants and horses
- Birds/reptiles excrete nitrogen as uric acid rather than urea
- Must be measured in relation to hydration status and urine output
- >70% renal function loss before sustained changes in levels of urea and creatinine


Outline the sources of creatinine in the blood

- Majority from skeletal muscle breakdown (constant rate)
- Increased by increased muscle breakdown
- Small amounts from diet


Outline the use of creatinine in the diagnosis of urinary tract disease

- Used for IRIS staging of CKD
- Less sensitive than urea to changes in plasma concentrations
- Better indicator of renal function due to free filtering at glomerulus and no reabsorption


What may lead to a falsely low pH reading on urine dipstick?

Urine spilling from protein to pH pad (protein pad uses acid)


Give the USG reference ranges for the "normal", isosthenuria, hypersthenuria and hyposthenuria in the dog

- Normal: 10.015-1.050
- Iso: 1.008-1.012
- Hyper: >1.012
- Hypo: <1.008


Give the normal values for UP:CR in dogs and cats

Dogs <0.5
Cats <0.4


What are the indications for use of cystoscopy in the investigation of urinary tract disease?

Recurrent or persistent lower urinary tract disease


List the uses of cystoscopy in the investigation of urinary tract disease

- Visualisation, biopsy/removal of masses/polyps
- Evaluation of recurrent urinary tract infection
- Diagnosis of ectopic ureters
- Localisation of haematuria
- Aid removal of uroliths
- Dilating urethral strictures


Give the indications for renal biopsy

- Suspected neoplasia
- Famillial nephropathy which might have an impact on other animals
- Non-azotaemic PLN
- Haematuria or protenuria
- Diagnosis of glomerular disease/AKI


List the contraindications for renal biopsy

- Hydronephrosis
- Renal cysts
- Pyelonephritis/abscessation


What are the possible complications of renal biopsy?

- Haemorrhage/clots in kidney
- Further compromise of renal function
- If performed blind, risk of rupturing renal artery


Give the options for method of renal biopsy

- Percutaneous ultrasound guided (needle, trucut, spring biopsy needle)
- Surgical methods: laparoscopy, laparotomy


What USG indicates pre-renal azotaemia in a cat and dog?

Cat: >1.045
Dog: >1.035


What USG indicates renal azotaemia in a cat and dog?

Cat: 1.008-1.035
Dog: 1.008-1.029


What USG indicates post-renal azotaemia in a cat and dog?

Variable - decreased elimination of urine rather than alteration in production


Outline the 3 presentations of renal failure

- AKI: renal, pre-renal or post-renal causes
- CKD: renal causes
- Acute decompensation of CKD: underlying renal cause with pre-renal factors causing decompensation
- All will be azotaemic


List potential nephrotoxins

- Organic compounds e.g. ethylene glycol
- Drugs incl. antibiotics, antifungals, amphotericin B, NSAIDs, ACEIs, diuretics, contrast agent, chemotherapy agents, immunosuppressive agents e.g. cyclosporine
- Heavy metals
- Mushroom, grapes/raisins, rodenticides
- Myoglobin, haemoglobin


Which antibiotic is directly nephrotoxic?



Give the possible causes of pre-renal proteinuria

Increased small size plasma proteins e.g. Hb, myoglobin, immunoglobulin Bence Jones light chains


Give the possible causes of post-renal proteinuria

Protein from urinary tract, usually inflammatory disease


Outline the investigation of proteinuria

- Identify as pre, post or intrinsic renal
- Rule out pre and post renal causes
- Aim to identify underlying cause - infectious, endocrine, neoplastic
- Assess sequelae (azotaemia, hypoalbuminaemia, hypertension)
- Do the above using urinalysis, CBC, biochem, test for infectious diseases, immune mediated disorders, DNA mutations


Outline the role of the kidney in acid base balance

- Excrete H+ via Na/H exchange in PCT and active H+ATPase pump in collecting tubules
- Reabsorption of HCO3- in PCT


List the differentials for hyperkalaemia

- Increased intake
- Translocation from ICF to ECF (insulni deficit, tumour lysis syndrome, acidosis, drugs)
- Decreased urinary excretion: renal failure, ruptured bladder, obstruction, GI disease, hypoadrenocorticism


List the main functions of the proximal convoluted tubule

- Reabsorption of water
- Acidification of urine (H+ secreted, Na+ reabsorbed)
- Glucose reabsorption
- Bicarbonate reabsorption


List the main functions of the Loop of Henle

- Formation of countercurrent multiplier and countercurrent exchange
- H2O reabsorption in descending limb
- Na+Cl-K+ reabsorption in thick ascending limb
- Bicarb reabsorption in thick ascending limb
- Calcium reabsorption in thick ascending limb


List the main functions of the distal tubule

- Na+ reabsorption
- K+ secretion
- Cl- reabsorption
- Water reabsorption


List the main functions of the collecting duct

- H+ secretion
- HCO3- reabsorptoin


Give examples of potassium sparing diuretics and state where these act

- Aldosterone antagonists (spironolactone)
- ENaC blockers (amiloride)
- Inhibit Na reabsorption n principle cell of DT and CD


Describe the location, shape and margination of air bubbles in the bladder

- Central in contrast puddle (solitary) or periphery of contrast puddle (multiple)
- Rounded shape (solitary) or polygonal (multiple)
- Distinct margination


Describe the radiographic appearance of acute and chronic cystitis

- Acute: minimal changes
- Chronic: thickening may be localised (cranioventral) or generalised


Describe the radiographic appearance of mucosal tumours in the bladder

- Irregular surface
- Protrude into lumen
- Positive contrast adherence


Describe the radiographic appearance of bladder wall neoplasia

- Fixed wall
- May be no mucosal irregularity or mass and no contrast adherence
- Mucosal irregularity when epithelial layer is eroded
- Area of wall is rigid/fixed, will not distend


What are the main portals of entry for damage to kidney?

- Haematogenous spread
- Ascending from ureter
- Glomerular filtrate (e.g. oxalate crystals, preformed toxins)
- Direct penetration (e.g. heavy metals, drugs with direct toxic action_


Describe the post-mortem appearance of a kidney in a case of ethylene glycol intoxication

- Hyperaemic
- Shiny apperance
- Medulla bulging due to oedema


Describe the post-mortem appearance of a kidney in a case of chronic renal disease

- Multifocal coalescing indented white-tan areas on cortical surface (areas of fibrosis, may represent areas of old, chronic infarcts)
- Small
- Irregular surface


What is meant by horseshoe kidneys?

Congenital abnormality where the cranial or caudal poles of kidneys are fused, may still be functional


Which breeds (of dogs, cats, sheep) are predisposed to polycystic kidney disease?

- Bull terrier, WHWT, Cairn terrier
- Persian cats
- Perendale sheep


Give examples of non-inflammatory nephropathies/uropathies

- Renal haemorrhage
- Renal infarction
- Acute tubular necrosis
- Hydronephrosis/hydroureter
- Amyloidosis


Give the possible causes for renal haemorrhage

- Bacterial: porcine erysipelas, salmonellosis
- Viraemia: classical SF, ASF, CHV1
- Other: coagulopathies, vasculitis, trauma


Give the possible causes of renal infarction

- Thrombotic valvular endocarditis (septic emboli)
- Systemic vasculitis (immune mediated, infectious)
- Mural cardiac thrombosis (feline cardiomyopathy)
Aortic thrombosis


Compare acute vs chronic renal infarction

- Acute: swollen, intensely cyanotic, congested blood, histo shows central area of coagulative necrosis surrounded by haemorrhage and congestion
- Chronic: pale (cream/tan), shrunken and fibrotic, resulting in distortion and depression of renal contour, histo shows tubuarl atrophy, fibrous tissue in interstitium, paler areas of fibrosis


What are the main causes of acute tubular necrosis?

- Hypoxia/ischaemia (hypovolaemic shock, cardiogenic shock, severe dehydration)
- Nephrotoxicity
- Often exacerbated by haemoglobin or myoglobin pigments


Give examples of nephrotoxins that may cause acute tubular necrosis

- Lead
- Aminoglycosides (gentamicin directly nephrotoxic)
- Tetracycleins
- Monensin
- Oak
- Ochratoxin A
- Vit D
- Ethylene glycol
- Cisplatin


What are the consequences of acute tubular necrosis?

Acute renal failure or chronic interstitial nephritis (possible chronic renal failure


What are the possible causes of hydronephrosis/hydroureter?

- Calculi
- Chronic inflammation
- Neoplasia
- Congenital malformation
- Iatrogenic


Which dog and cat breeds are predisposed to amyloidosis?

- Shar-pei
- Abyssinian and Siamese cats


Describe renal amyloidosis (development and consequences)

- Extracellular deposition of amyloid (eosinophilic, homogenous appearance)
- Usually glomerular, but medullary in cats and Shar-peis
- Most commonly reactive systemic amyloidosis (chronic Ag stimulation)
- Clinically causes chronic renal insufficiency and proteinuria (may lead to nephrotic syndrome


Give examples of inflammatory nephropathies/uropathies

- Glomerulonephritis
- Tubulointerstitial nephritis
- Pyelonephritis and cystitis


What is glomerulonephritis? What is the consequence?

Inflammation of glomeruli with secondary tubulointerstitial and vascular changes , leads to PLN and glomerulosclerosis (chronic)


What are the types of glomerulonephritis and in which species do these occur?

Membranous: Cats
Proliferative: horses
Membranoproliferative: dogs


What are the potential causes of glomerulonephritis?

- Immune mediated
- Prolonged antigenaemia


Describe immune mediated disease as a cause of glomerulonephritis

- Either deposition of immune complexes
- Or antibodies directed against the glomerulus (rare)


Describe prolonged antigenaemia as a cause of glomerulonephritis

- Persistent infections/inflammations or other diseases
- Viral: FeLV, FIV, FIP, canine adenovirus 1, EIAV, BVDV, ASFC
- Chronic bacterial infections: pyometra, pyoderma
- Chronic parasitism: dirofilaria, leishmania, trypanosoma, encephalitozoon
- Neoplasia


Compare the appearance of the different types of glomerulonephritis

- Membranous: eosinophilic and white, thickening of glomerular basement membrane
- Membranoproliferative: less cellular vs. proliferative but more than membranous, thickened basement membrane
- Proliferative: proliferation of endothelial, epithelial and mesangial cells, influx of inflammatory cells and/or fibrin
- Glomerulosclerosis (consequence): hypocellular, shrinkage, increased fibrous tissue


What is thyroidisation of the kidney?

Occurs in end-stage renal disease - development of tubular hyaline casts leads to thyroid like histological appearance


What are the portals of entry for tubulointerstitial nephritis?

- Haematogenous
- Urinary


What are the main times of tubulointerstitial nephritis and what are the relevant sources?

- Embolic suppurative (haematogenous)
- Non-suppurative (haematogenous or ascendant)
- Pyelonephritis (ascendant)


Briefly outline embolic suppurative tubulointerstitial nephritis incl. causative agents

- Bacterial
- Forms multiple small abscesses or fewer larger ones
- Horse: Actinobacillus equui
- Swine: Erysipelothrix rhusiopathiae
- Cattle: Trueperella pyogenes
- Sheep and goat: Corynebacterium pseudotuberculosis


What are the possible presentations of non-suppurative intersitial nephritis

- Acute, subacute or chronic presentation (chronic most common in cats and dogs)
- White spotted kidney in calves, incidental finding


Briefly describe chronic interstitial nephritis (cause, agents, consequences, gross appearance)

- Common end stage of chronic glomerulonephritis, acute tubular necrosis, acute pyelonephritis, acute interstitial nephritis
- Granulomatous: infection with Aspergillus, Toxocara, Encephalitozoon, Prototheca, Mycobacteria, FIPV, PCV2
- Causes chronic renal failure
- Irregular surface, smal, pale, may see white nodules with some causes (FIP)


What are the risk factors for pyelonephritis and cystitis?

- Female
- Urine stasis/obstruction
- Diabetes, hyperoestrogenism, congenital malformations


List the possible causative pathogens for pyelonephritis

- Endogenous bacteria of bowel and skin e.g. E coli, Staph, Strep, enterobacteriaeceae
- Specific urinary tract pathogens e.g. Corine bacterial renale (cattle), Actinobaculum suis (swine)


List the possible causative pathogens of cystitis

- Same as pyelonephritis
- Viruses: MCF, classifcal SF, West nile virus
- Toxins: bracken, cyclophosphamide in cats and dogs (sterile haemorrhagic cystitis)


In which species is metastatic lymphoma of the urinary tract more common?

Cats and cattle


Describe the metastasis of urothelial cell tumours

- ~50% metastasise, usually to regional LNs then lungs
- peritoneal implantation or retrograde lymphatic spread to the soft tissue and bones of HLs or vertebrae may occur


List the potential consequences/lesions secdonary to renal failure

- Parathyroid hyperplasia, fibrous osteodystrophy, metastatic mineralisation
- Ulcerative and haemorrhagic gastritis
- Pulmonary oedma and fibrinous pericarditis
- Atrial and vascular thrombosis
- Anaemia
- Hypertension


Briefly outline the pathophysiology of PUPD

- Usually primary PU with compensatory PD
- Controlled by plasma osmolality (esp. plasma sodium), hypothalamic-pituitary-ADH axis (regulates water reabsorption in collecting duct), renal function


List the ddx for primary polydipsia

- Psychogenic (horse > other species)
- Hepatic insufficiency/PSS (leads to hepatic encephalopahy, abnormal mentation seen)
- Central lesion affecting hypothalamus
- Dietary change e.g. wet to dry (will not cause PU!)
- Compensation for increased loss e.g. heat (no compensatory PU)


List the ddx for primary polyuria and identify those most common in dogs

- Renal disease*
- Hepatic disease
- Endocrine (DM*, DI, HAC*, hyperthryoidism)
- Infectious (endotoxins): pyometra* (or any other encapsualted pyogenic infecton), pyelonephritis
- Electrolytes: hypoK, hyperCa*
- Iatrogenic: diuretics, steroids etc., post-obstructive


Outline the ways in which ADH abnormalities can be affected leading to PUPD

- Primary central diabetes insipidus: no ADH produced
- Nephrogenic diabetes insipidus: congenital lack of ADH receptors in DCT
- Reduced sensitivity to ADH: E coli toxins in pyelonephritis, pyometra, also HAC
- Interference with action of ADH at tubule: hyperCa, hypoK
- ADH receptor downregulation: obstruction of ureters/bladder, hypoK


Identify the possible causes of osmotic diuresis leading to PUPD

- Diabetes mellitus (glucose)
- Post-obstructive diuresis
- Liver failure incl. PSS (cortisol and other solutes not broken down)


Identify the possible causes of a reduced medullary concentration gradient leading to PUPD

(unable to concentrate in loop of Henle)
- Long period of PU of any cause (reduced BUN in medulla) e.g. fluid therapy, steroids
- Liver failure (reduced BUN prod.)
- Hypoadrenocorticism (pre-renal azotaemia, loss of sodium, unable to increase USG due to lack of sodium)
- Hyperthyroidism (increased renal blood flow)


Outline your approach to a case of PUPD

- History: change in management, medications, urination characteristics, volume, conscious/unconscious, change to urine
- Drinking more than it should? Able to concentrate urine? If PUPD, or USG low, or both -> dipstick
- Dipstick: glucosuria? Compare with blood to rule out DM
- No glucose, look for evidence of CKD: low BCS, skin tent, small kidneys, uraemic syndrome (halitosis, ulceration), isosthenuria, BUN
- Blood biochem and haem
- Consider history and signalment


List the 5 most common causes of PUPD in cats

- HyperT4
- Lymphoma
- Diabetes
- Hypertension


List the 4 most common causes of PUPD in dogs

- Cushing's
- Neoplasia (paraneoplastic hyperCa)
- Diabetes
- Kidney disease


What test is used to rule in/out liver disease as a cause of PUPD?

Bile acid stimulation test (also biochem showing low urea, liver parameters elevated)


What test is used to rule in/out hyperadrenocorticism/hypoadrenocorticism as a cause of PUPD?

ACTH stim


What test is used to rule in/out pyelonephritis as a cause of PUPD?

- Sediment/urine culture (may be negative)
- Ultrasonography


What test is used to rule in/out diabetes insipidus as a cause of PUPD?

- Water deprivation test previously used
- Now rule out other differentials, then trial treat with DDAVP
- Consider ADH assay with blood and urine osmolality measurements


What USG would be appropriate for an animal showing signs of dehydration?



Outline the clinical signs of congenital/neonatal renal abnormalities

- Signs of renal disease in young animal
- OR may develop later in life due to accumulation of products
- Predisposition to urolithiasis


List the structural renal congenital abnormalities

- Agenesis
- Abnormal connection of ureteric ducts to bladder
- Glomerulopathy due to abnormal collagen in basement membrane


List the functional renal congenital abnormalities

- Impaired tubular reabsorption in Basenjiis
- Hyperuricuria in Dalmatians


When do clinical signs of amyloidosis resulting from a functional renal abnormality generally develop?

1-6years old


Which dog breeds are predisposed to congenital glomerulopathy?

- Bernese mountain dog
- Cockers (autosomal recessive trait)
- Samoyeds (genetic disorder, X linked dominant gene)
- Dobermann's
- Rottweilers


Briefly outline the characteristics of congenital glomerulopathy (consequence, signs, diagnosis)

- Things that should have been filtered end up in urine
- Mainly proteinuria
- Definitive diagnosis made on biopsy


Which dog breed is predisposed to familial nephropathy?

Cocker spaniel


Which dog breeds are predisposed to congenital canine renal dysplasia?

- Lhasa Apso and Shih Tzu main ones
- Also: standard poodle soft coated wheaten terrier, chow chow, alaskan malamute, mini schnauzer


Which breeds are predisosed to Fanconi's syndrome? Describe the pathophysiology

- Basenjii (main one), also Norwegian Elkhound, mini schnauzer
- Impaired tubular reabsorption of ions, channels imparied


Which breeds are predisposed to congenital primary renal glucosuria? Describe the pathophysiology

Scottish terriers
- Reabsorption defect


Which breeds are predisposed to cysteinuria, hyperuricosuria and xanthinuria? Describe the pathophysiology and consequences

- Predisposes to urolithiasis
- Related to absorption, metabolism or secretion of specific minerals
- Dalmatian (hyperuricosuria)
- Newfoundlands (cysteinuria)
- Toy Manchester Terrier, Cavalier King Charles Spaniel, English Cocker Spaniel, Dachshund, Chihuahua (xanthinuria)


Compare intra and extramural ectopic ureters

- Intra: enter bladder wall normally, tunnel distally along wall to urethra/vagina (most common presentation in dogs)
- Extra: bypass bladder to enter more distally (most common presentation in cats)


Discuss the occurence of ectopic ureters in large animals, dogs and cats

- Large: rare, reported in horses, cattle and sheep
- Dogs: mainly mixed larger breeds, e.g. Golden or Labrador retriever
- Cats: no breed/familial predisposition, less common vs. dogs