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URI2 > Urinary tract disease > Flashcards

Urinary tract disease Flashcards

1
Q

Give the USG reference ranges for the “normal”, isosthenuria, hypersthenuria and hyposthenuria in the cat

A
  • Normal: 10.015-1.060 (healthy cat usually 1.035)
  • Iso: 1.008-1.012
  • Hyper: >1.012
  • Hypo: <1.008
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2
Q

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

A
  • Urinalysis
  • Clinical pathology (haem, biochem, +/-SDMA, UPCR)
  • Imaging: radiography, ultrasound, CT
  • Surgical
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3
Q

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

A

Right lateral

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4
Q

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

A

Iodine salts e.g. iohexol

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5
Q

Define azotaemia

A

Increased concentration of non-protein nitrogenous compounds in the blood

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6
Q

Define uraemia

A

Clinical syndrome associated with renal failure

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7
Q

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

A
  • 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
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8
Q

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

A
  • 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
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9
Q

Outline the sources of creatinine in the blood

A
  • Majority from skeletal muscle breakdown (constant rate)
  • Increased by increased muscle breakdown
  • Small amounts from diet
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10
Q

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

A
  • 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
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11
Q

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

A

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

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12
Q

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

A
  • Normal: 10.015-1.050
  • Iso: 1.008-1.012
  • Hyper: >1.012
  • Hypo: <1.008
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13
Q

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

A

Dogs <0.5

Cats <0.4

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14
Q

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

A

Recurrent or persistent lower urinary tract disease

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15
Q

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

A
  • 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
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16
Q

Give the indications for renal biopsy

A
  • Suspected neoplasia
  • Famillial nephropathy which might have an impact on other animals
  • Non-azotaemic PLN
  • Haematuria or protenuria
  • Diagnosis of glomerular disease/AKI
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17
Q

List the contraindications for renal biopsy

A
  • Hydronephrosis
  • Renal cysts
  • Pyelonephritis/abscessation
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18
Q

What are the possible complications of renal biopsy?

A
  • Haemorrhage/clots in kidney
  • Further compromise of renal function
  • If performed blind, risk of rupturing renal artery
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19
Q

Give the options for method of renal biopsy

A
  • Percutaneous ultrasound guided (needle, trucut, spring biopsy needle)
  • Surgical methods: laparoscopy, laparotomy
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20
Q

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

A

Cat: >1.045
Dog: >1.035

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21
Q

What USG indicates renal azotaemia in a cat and dog?

A

Cat: 1.008-1.035
Dog: 1.008-1.029

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22
Q

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

A

Variable - decreased elimination of urine rather than alteration in production

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23
Q

Outline the 3 presentations of renal failure

A
  • 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
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24
Q

List potential nephrotoxins

A
  • 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
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25
Q

Which antibiotic is directly nephrotoxic?

A

Gentamicin

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26
Q

Give the possible causes of pre-renal proteinuria

A

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

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27
Q

Give the possible causes of post-renal proteinuria

A

Protein from urinary tract, usually inflammatory disease

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28
Q

Outline the investigation of proteinuria

A
  • 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
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29
Q

Outline the role of the kidney in acid base balance

A
  • Excrete H+ via Na/H exchange in PCT and active H+ATPase pump in collecting tubules
  • Reabsorption of HCO3- in PCT
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30
Q

List the differentials for hyperkalaemia

A
  • 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
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31
Q

List the main functions of the proximal convoluted tubule

A
  • Reabsorption of water
  • Acidification of urine (H+ secreted, Na+ reabsorbed)
  • Glucose reabsorption
  • Bicarbonate reabsorption
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32
Q

List the main functions of the Loop of Henle

A
  • 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
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33
Q

List the main functions of the distal tubule

A
  • Na+ reabsorption
  • K+ secretion
  • Cl- reabsorption
  • Water reabsorption
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34
Q

List the main functions of the collecting duct

A
  • H+ secretion

- HCO3- reabsorptoin

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35
Q

Give examples of potassium sparing diuretics and state where these act

A
  • Aldosterone antagonists (spironolactone)
  • ENaC blockers (amiloride)
  • Inhibit Na reabsorption n principle cell of DT and CD
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36
Q

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

A
  • Central in contrast puddle (solitary) or periphery of contrast puddle (multiple)
  • Rounded shape (solitary) or polygonal (multiple)
  • Distinct margination
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37
Q

Describe the radiographic appearance of acute and chronic cystitis

A
  • Acute: minimal changes

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

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38
Q

Describe the radiographic appearance of mucosal tumours in the bladder

A
  • Irregular surface
  • Protrude into lumen
  • Positive contrast adherence
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39
Q

Describe the radiographic appearance of bladder wall neoplasia

A
  • 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
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40
Q

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

A
  • Haematogenous spread
  • Ascending from ureter
  • Glomerular filtrate (e.g. oxalate crystals, preformed toxins)
  • Direct penetration (e.g. heavy metals, drugs with direct toxic action_
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41
Q

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

A
  • Hyperaemic
  • Shiny apperance
  • Medulla bulging due to oedema
42
Q

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

A
  • Multifocal coalescing indented white-tan areas on cortical surface (areas of fibrosis, may represent areas of old, chronic infarcts)
  • Small
  • Irregular surface
43
Q

What is meant by horseshoe kidneys?

A

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

44
Q

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

A
  • Bull terrier, WHWT, Cairn terrier
  • Persian cats
  • Perendale sheep
45
Q

Give examples of non-inflammatory nephropathies/uropathies

A
  • Renal haemorrhage
  • Renal infarction
  • Acute tubular necrosis
  • Hydronephrosis/hydroureter
  • Amyloidosis
46
Q

Give the possible causes for renal haemorrhage

A
  • Bacterial: porcine erysipelas, salmonellosis
  • Viraemia: classical SF, ASF, CHV1
  • Other: coagulopathies, vasculitis, trauma
47
Q

Give the possible causes of renal infarction

A
  • Thrombotic valvular endocarditis (septic emboli)
  • Systemic vasculitis (immune mediated, infectious)
  • Mural cardiac thrombosis (feline cardiomyopathy)
    Aortic thrombosis
48
Q

Compare acute vs chronic renal infarction

A
  • 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
49
Q

What are the main causes of acute tubular necrosis?

A
  • Hypoxia/ischaemia (hypovolaemic shock, cardiogenic shock, severe dehydration)
  • Nephrotoxicity
  • Often exacerbated by haemoglobin or myoglobin pigments
50
Q

Give examples of nephrotoxins that may cause acute tubular necrosis

A
  • Lead
  • Aminoglycosides (gentamicin directly nephrotoxic)
  • Tetracycleins
  • Monensin
  • NSAIDs
  • Oak
  • Ochratoxin A
  • Vit D
  • Ethylene glycol
  • Cisplatin
51
Q

What are the consequences of acute tubular necrosis?

A

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

52
Q

What are the possible causes of hydronephrosis/hydroureter?

A
  • Calculi
  • Chronic inflammation
  • Neoplasia
  • Congenital malformation
  • Iatrogenic
53
Q

Which dog and cat breeds are predisposed to amyloidosis?

A
  • Shar-pei

- Abyssinian and Siamese cats

54
Q

Describe renal amyloidosis (development and consequences)

A
  • 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
55
Q

Give examples of inflammatory nephropathies/uropathies

A
  • Glomerulonephritis
  • Tubulointerstitial nephritis
  • Pyelonephritis and cystitis
56
Q

What is glomerulonephritis? What is the consequence?

A

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

57
Q

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

A

Membranous: Cats
Proliferative: horses
Membranoproliferative: dogs

58
Q

What are the potential causes of glomerulonephritis?

A
  • Immune mediated

- Prolonged antigenaemia

59
Q

Describe immune mediated disease as a cause of glomerulonephritis

A
  • Either deposition of immune complexes

- Or antibodies directed against the glomerulus (rare)

60
Q

Describe prolonged antigenaemia as a cause of glomerulonephritis

A
  • 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
61
Q

Compare the appearance of the different types of glomerulonephritis

A
  • 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
62
Q

What is thyroidisation of the kidney?

A

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

63
Q

What are the portals of entry for tubulointerstitial nephritis?

A
  • Haematogenous

- Urinary

64
Q

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

A
  • Embolic suppurative (haematogenous)
  • Non-suppurative (haematogenous or ascendant)
  • Pyelonephritis (ascendant)
65
Q

Briefly outline embolic suppurative tubulointerstitial nephritis incl. causative agents

A
  • Bacterial
  • Forms multiple small abscesses or fewer larger ones
  • Horse: Actinobacillus equui
  • Swine: Erysipelothrix rhusiopathiae
  • Cattle: Trueperella pyogenes
  • Sheep and goat: Corynebacterium pseudotuberculosis
66
Q

What are the possible presentations of non-suppurative intersitial nephritis

A
  • Acute, subacute or chronic presentation (chronic most common in cats and dogs)
  • White spotted kidney in calves, incidental finding
67
Q

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

A
  • 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)
68
Q

What are the risk factors for pyelonephritis and cystitis?

A
  • Female
  • Urine stasis/obstruction
  • Diabetes, hyperoestrogenism, congenital malformations
69
Q

List the possible causative pathogens for pyelonephritis

A
  • 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)
70
Q

List the possible causative pathogens of cystitis

A
  • Same as pyelonephritis
  • Viruses: MCF, classifcal SF, West nile virus
  • Toxins: bracken, cyclophosphamide in cats and dogs (sterile haemorrhagic cystitis)
71
Q

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

A

Cats and cattle

72
Q

Describe the metastasis of urothelial cell tumours

A
  • ~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

73
Q

List the potential consequences/lesions secdonary to renal failure

A
  • Parathyroid hyperplasia, fibrous osteodystrophy, metastatic mineralisation
  • Ulcerative and haemorrhagic gastritis
  • Pulmonary oedma and fibrinous pericarditis
  • Atrial and vascular thrombosis
  • Anaemia
  • PUPD
  • Hypertension
74
Q

Briefly outline the pathophysiology of PUPD

A
  • 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
75
Q

List the ddx for primary polydipsia

A
  • 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)
76
Q

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

A
  • 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
77
Q

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

A
  • 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
78
Q

Identify the possible causes of osmotic diuresis leading to PUPD

A
  • Diabetes mellitus (glucose)
  • CKD (BUN)
  • Post-obstructive diuresis
  • Liver failure incl. PSS (cortisol and other solutes not broken down)
79
Q

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

A

(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)
80
Q

Outline your approach to a case of PUPD

A
  • 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
81
Q

List the 5 most common causes of PUPD in cats

A
  • CKD
  • HyperT4
  • Lymphoma
  • Diabetes
  • Hypertension
82
Q

List the 4 most common causes of PUPD in dogs

A
  • Cushing’s
  • Neoplasia (paraneoplastic hyperCa)
  • Diabetes
  • Kidney disease
83
Q

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

A

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

84
Q

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

A

ACTH stim

85
Q

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

A
  • Sediment/urine culture (may be negative)

- Ultrasonography

86
Q

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

A
  • Water deprivation test previously used
  • Now rule out other differentials, then trial treat with DDAVP
  • Consider ADH assay with blood and urine osmolality measurements
87
Q

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

A

> 1.035

88
Q

Outline the clinical signs of congenital/neonatal renal abnormalities

A
  • Signs of renal disease in young animal
  • OR may develop later in life due to accumulation of products
  • Predisposition to urolithiasis
89
Q

List the structural renal congenital abnormalities

A
  • Agenesis
  • Abnormal connection of ureteric ducts to bladder
  • Glomerulopathy due to abnormal collagen in basement membrane
90
Q

List the functional renal congenital abnormalities

A
  • Impaired tubular reabsorption in Basenjiis

- Hyperuricuria in Dalmatians

91
Q

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

A

1-6years old

92
Q

Which dog breeds are predisposed to congenital glomerulopathy?

A
  • Bernese mountain dog
  • Cockers (autosomal recessive trait)
  • Samoyeds (genetic disorder, X linked dominant gene)
  • Dobermann’s
  • Rottweilers
93
Q

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

A
  • Things that should have been filtered end up in urine
  • Mainly proteinuria
  • Definitive diagnosis made on biopsy
94
Q

Which dog breed is predisposed to familial nephropathy?

A

Cocker spaniel

95
Q

Which dog breeds are predisposed to congenital canine renal dysplasia?

A
  • Lhasa Apso and Shih Tzu main ones

- Also: standard poodle soft coated wheaten terrier, chow chow, alaskan malamute, mini schnauzer

96
Q

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

A
  • Basenjii (main one), also Norwegian Elkhound, mini schnauzer
  • Impaired tubular reabsorption of ions, channels imparied
97
Q

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

A

Scottish terriers

- Reabsorption defect

98
Q

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

A
  • 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)
99
Q

Compare intra and extramural ectopic ureters

A
  • 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)
100
Q

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

A
  • 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

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