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Urinary tract disease 2 Flashcards

1
Q

List the methods used for the diagnosis of ectopic ureters and give the treatment

A
  • Diagnosis: contrast radiography, urethroscopy, caginoscopy, cystoscopy in large animals
  • Treatment
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2
Q

What may develop secondary to ectopic ureters?

A
  • Hyroureter/hydronephrosis
  • Urine scald
  • UTI
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3
Q

Give the foetal role and adult structure of the umbilical vein

A
  • Source of oxygentated blood from dam to foetus via liver

- Forms falciform ligament/round ligament of liver

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4
Q

Give the foetal role and adult structure of the umbilical arteries

A
  • Branches of external iliac arteries carrying waste material from foetus to dam
  • Forms round ligaments of the bladder
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5
Q

Give the foetal role and adult structure of the urachus

A
  • Connection from foetal bladder to allantoic sac

- Forms scar on apex of bladder

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6
Q

List the differentials for umbilical swellings in the neonate/young animal

A
  • Umbilical hernia
  • Umbilical abscess
  • Patent urachus
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7
Q

Describe the typical appearance of umbilical hernias

A
  • Soft tissue swelling in ventral abdomen
  • Usually present since birth
  • May be fluctuant
  • Reducible
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8
Q

How are umbilical hernias diagnosed?

A

Ultrasonography demonstrating intestine, omentum, other abdominal organs

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9
Q

Discuss the prognosis for umbilical hernias

A
  • Small: good prognosis, may spontaneously regress, less likely to contain abdominal contents
  • Medium: may contain intestines, more concerning if more than 2-3 fingers wide, risk of strangulation
  • Large: least likely to seal up with conservative treatment, but less likely to strangulate (material can get in, can probably get out)
  • Simple hernias have no effect on animal except cosmetic appearance
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10
Q

Describe the possible types of umbilical infection

A
  • Omphalophlebitis: sepsis of umbilical veins (tracks to liver)
  • Omphaloarteritis: sepsis of umbilical arteries (tracks along round ligaments)
  • Urachal sepsis (sepsis of urachus, tracks to bladder)
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11
Q

Outline the signs of umbilical infection

A
  • Heat, pain, oedema, cellulitis
  • Other systemic signs e.g. pyrexia, joint infection
  • +/- discharge
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12
Q

Describe the ultrasonographic appearance of umbilical infection

A

Encapsulated soft tissue mass with flocculent fluid (pus) or gas

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13
Q

Outline the treatment of umbilical infection

A
  • Asses and correct underlying cause (e.g. failure of passive transfer, hygiene)
  • Medical treatment: systemic antibiotics
  • Surgical: where infection has spread (esp. to abdo organs) or not responding to medical treatment. Must excise or marsupialise entire extent of infection
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14
Q

Outline the signs and diagnosis of patent urachus

A
  • Present at birth
  • Dribble urine from umbilicus
  • Umbilical infection
  • Frequent posturing/straining to urinate
  • Diagnosis: ultrasound or contrast radiography (in dogs and cats)
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15
Q

Outline the treatment of a patent urachus

A
  • Leave to resolve if very young
  • Local treatment if non-infected: clamps, astringents (e.g. 7% iodine, silver nitrate)
  • Medical management: broad spec antibiotic treatment/prophylaxis based on C+S
  • Surgical: resection of urachus back to bladder, close over apex scar
  • Treat scondary problems
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16
Q

List causes of uroperitoneum

A
  • Patent urachus
  • Damage to ureters or urethra
  • Bladder rupture or perforation
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17
Q

Discuss the occurrence uroperitoneum in neonates

A
  • Bladder rupture most common in large animals, usually dorsal bladder, can be spontaneous or trauma
  • Patent urachus discharging into peritoneal cavity
  • Urachal infection compromising bladder wall
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18
Q

Discuss the occurrence uroperitoneum in adults

A
  • Bladder rupture secondary to trauma

- Bladder rupture secondary to obstruction

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19
Q

Outline the clinical signs of uroperitoneum

A
  • Fluid distension, fluid thrill
  • Unable to palpate bladder
  • Peritonitis (abdo pain, ileus)
  • Dehydration
  • Acid-base and electrolyte abnormalities (cardiac arrhythmias)
  • Decreased urination
  • Neonate: lethargy, not suckling, collapse, sepsis
  • Some animals may still pass small vols of urine and small bladder may be visible on imaging
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20
Q

Outline the diagnosis of uroperitoneum

A
  • Aspiration of fluid
  • Ultrasonography/contrast radiogrpahy to confirm peritoneal effusion and defect in bladder
  • Biochem: uraemia, dehydration, hyperK, hypoNa, hypoCl
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21
Q

Discuss hyperK associated with bladder rupture

A
  • Reduced/no excretion = hyper K, reabsorbed through peritoneal membrane
  • Causes bradycardia
  • Must be corrected and stabilised as an emergency, must be dealt with prior to surgery
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22
Q

Outline the treatment of uroperitoneum and bladder rupture

A
  • Correct hydration and electrolyte imbalance
  • Calcium gluconate to correct potassium in emergency, dextrose and insulin
  • Treat uroperitoneum, drain with care, flush
  • Surgical repair of bladder
  • Post-op fluids (0.9% saline, bolus admin indicated), NSAIDs and antibiotics
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23
Q

Compare the fluid therapy of a neonate to that in an adult

A
  • Neonate has limited ability to alter renal function
  • GFR and RBF reduced in neonate
  • Limited ability to respond to changes in ECF or acid base imblances
  • Neonate has high body water due to small amounts of fat
  • Predisposed to hypovol
  • Fluids need to be accurate and regularly monitored
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24
Q

List pathogenic causes of urinary tract disease that may occur in cattle, and indicate other species that may be affected and whether they are shed in the urine

A
  • Leptospirosis (dogs, people, most mammals), shed in urine
  • Clostridium perfringens type D
  • Clostridium haemolyticum (sheep, rarely in dogs), canbe shed in urine
  • Babesia spp. (dogs)
  • MCF (pigs, exotics, ruminants, deer, transmitted asymptomatically by sheep)
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25
Q

What disease may be transmitted by rabbit urine? Zoonotic?

A
  • Encephalitozoon cuniculi

- May affect severely immunocompromised people

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26
Q

Compare leptospirosis in cattle and dogs

A
  • Cattle: mainly reproductive disease

- Dogs: AKI, liver disease, acutely ill

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27
Q

Describe the clinical signs of Clostridium perfringens type D in cattle

A
  • Neuro signs, depresson, sudden death

- Pulpy kidney on PM (not pathognomic)

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28
Q

Outline the treatment and prevention of Clostridium perfringens type D in cattle

A
  • Antibiotics not usually effective, toxins causing disease, often fatal
  • Vaccinate pregnant dam with general clostridial vaccine
  • Prevent animals gorging on lush pasture
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29
Q

Outline the prevention of Clostridium perfringens type D in sheep

A
  • Vaccinate lambs before 2 months old, booster 1 month later

- Care moving lams from milk to concentrate, prevent gorging

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30
Q

Compare the prevalence of Clostridium perfringens type D and Clostridium haemolyticum

A
  • Common in UK

- C. haemolytic ~15% of clostridial disease

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31
Q

Outline the clinical signs of Clostridium haemolyticum in cattle

A
  • Haemoglobinuria
  • Sudden death
  • Sudden onset depression, pyrexia, abdominal pain, dyspnoea, dysentery
  • Anaemia and jaundice variable
  • +/- Oedema of brisket
  • Mortality 95%
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32
Q

Describe the post mortem findings in a case of Clostridium haemolyticum in a cow

A
  • Hepatic necrosis (ischaemic infarct)
  • Bloody fluid in abdominal and thoracic cavities, trachea contains bloody froth
  • Kidneys dark, friable
  • +/- small and large intestinal haemorrhage
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33
Q

Outline the treatment of C haemolyticum in cattle

A
  • Early treatment with penicillin or tetracyclines

- Whole blood transfusions in early disease (before excessive liver damage)

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34
Q

Outline the prevention of C haemolyticum in cattle

A
  • Present in 4 vaccines: Tribovax T, Bravoxin 10, Covexin 8, covexin 10 (only licensed in cattle)
  • Spores activated by liver damage therefore fluke control important (e.g. albendazole, triclabendazole), quarantine new animals, fence off wet areas
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35
Q

How is Babesia transmitted?

A

Tick borne protozoan, not shed in urine

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36
Q

Describe the prevalence of Babesia in the UK

A

Endemic in south west in cattle, sporadic in dogs related to travel

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37
Q

Describe the clinical signs of babesiosis in dogs and cattle

A
  • Dogs: anaemia, MODS, SIRS

- Cattle: pyrexia, anaemia, neuro signs, haemoglobinuria, anorexia

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38
Q

Outline the treatment of babesiosis

A
  • Imidocarb dipropionate licensed for cattle, off license in dogs
  • Supportive care e.g. blood transfusion
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39
Q

Outline the control of babesiosis in dogs and cattle

A
  • No vaccine in dogs
  • Vaccine available for cattle
  • Dogs: control ticks e.g. flurolaner collar, avoid tick areas, check after walks
  • Cattle: topical pyrethroid, OPs before and during challenge period
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40
Q

Outline the clinical signs of malignant catarrhal fever in cattle

A
  • Peracute: non signs/depression, diarrhoea, dysentery 12-24 hours before death
  • General: pyrexia >40, profuse mucopurulent discharge, inappetance, decreased milk yields
  • Skin ulceration
  • Nervous signs, ocular signs (corneal opacity)
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41
Q

Describe the transmission of MCF

A

Transmitted directly or via fomites from sheep to cattle

42
Q

Outline the treatment and control of MCF in cattle

A
  • No specific treatment, Abs to control secondary infection but usually fatal
  • No vaccine
  • Separate sheep, change PPE between lambing and cows
  • Separate susceptible animals in an outbreak
43
Q

How is E cuniculi transmitted?

A

Can be transmitted in the urine of rabbits and other affected animals

44
Q

Outline the clinical signs of E cuniculi in rabbits

A
  • Neuro signs e.g. head tilt, collapse, paresis/paralysis, fitting
  • Urinary incontinence
  • Renal failure
45
Q

Outline the treatment and control of E cuniculi

A
  • Poor prognosis if neurological
  • Albendazole/fenbendazole to get rid of protozoan
  • Can remove ocular lens
  • No vaccine
  • Control: raise food off floor, use sipper bottles, fenbendazole 20mg/kg PO SID for 4 weeks before risk period e.g. introduction of new animal
46
Q

List plant toxins affecting the renal and urinary system and give the species affected

A
  • Calcinogenic glycosides: livestock
  • Lily: cats
  • Oak: cattle, sheep
  • Oxalates: Livestock
  • Pigweed: swine, cattle
  • Ptaquiloside (Bracken): mostly cattle, but also other ruminants
47
Q

List mycotoxins affecting the renal and urinary system and give the species affected

A
  • Citrinin: all
  • Ochratoxin: all
  • Oosporein: chickens, turkeys
48
Q

List metal toxins affecting the renal and urinary system and give the species affected

A
  • Arsenic: all

- Mercurial salts: all

49
Q

List pesticide toxins affecting the renal and urinary system and give the species affected

A
  • 3-chloro-p-toludidine hydrochloride: birds
  • Cholecalciferol rodenticide: all
  • Diquat: all
  • Paraquat: all
50
Q

List household and industrial toxins affecting the renal and urinary system and give the species affected

A
  • Ethylene glycol: all
  • Phenols: cats mostly
  • Pine oil: cats mostly
  • Toluene: all
51
Q

List pharmaceutical toxins affecting the renal and urinary system and give the species affected

A
  • Alkylating antieneoplastics (cyclophosphamide, chlorambucil, lomustine): all
  • Aminoglycosides (gent): all
  • Amphotericin B: all
  • NSAIDs: all
  • Cisplatin; all
  • Sulphonamides: all
  • Tetracyclines: all
  • Vit D: all
  • Vit K3: horses
52
Q

List animal toxins affecting the renal and urinary system and give the species affected

A

Snake venom, esp. rattlers: all

53
Q

Which toxins affect the glomerulus?

A

Snake venom

54
Q

Which toxins affect the renal tubules?

A
  • Antimicrobials
  • Antineoplastic drugs
  • Anaesthetics
  • Chlorinated hydrocarbons
  • Herbicides
  • Immunosuppressants
  • Solvents
  • Metals
  • Mycotoxins
  • Oxalate containing plants
  • Endogenous nephrotoxins
55
Q

Which toxins cause renal mineralisation?

A
  • Vit D
  • Cholecalciferol type rodenticides
  • Plants with vit D like activity
56
Q

Which toxins affect the renal papilla?

A

NSAIDs

57
Q

Which toxins affect the renal pelvis and lower urinary tract by

a: contact irritation
b: haemorrhage and neoplasia?

A

A: cantharidin
B: bracken

58
Q

Outline the mechanisms of action of the renal toxic side effects of NSAIDs

A
  • Inhibit PG synthesis, leads to vasoconstriction if poorly perfused renal pelvis
  • Leads to ischaemia and necrosis of renal papillae and medulla
  • Irreversible necrosis of medullary loops of Henle and associated capillaries if repeated exposure
59
Q

Outline the mechanisms of action of the renal toxic side effects of aminoglycosides

A
  • Excreted largely unchanged in the urine
  • Renal nephrosis by inhibiting phospholipases, leading to lysosomal dysfunction and lysis in renal tubules and proximal tubule epithelium
60
Q

What is a key contraindication for the use of aminoglycosides?

A

Do not give close to administration of alpha-2 blocking sedatives

61
Q

Give examples of conditions that are renally toxic due to pigmenturia

A
  • Equine rhabdomyolysis
  • White muscle disease
  • Exertional muscle myopathy
  • Snake bites
62
Q

Outline the sources and mechanisms of oak poisoning

A
  • All parts of oak treee potentially poisonous, mostly ingestion of fresh green leaves or acorns
  • Mechanism of renal toxicity unknown, tannic acid is a hepatotoxin and causes methaemoglobinaemia
63
Q

What are the risk factors for oak poisoning?

A
  • Cattle more at risk than other species
  • Lack of alternative food
  • Heavy storms leading to large fall of acorns
64
Q

Outline the clinical signs of oak poisoning

A
  • Constipation
  • Brown urine lasting 24 hours (may be missed)
  • Anorexia, depression, dehydration, rumen atony +/- haemorrhagic diarrhoea
65
Q

Outline the clinical pathology seen with oak poisoning

A
  • Elevated BUN, creatinine, AST

- Proteinuria, haematuria, glucosuria

66
Q

Outline the post mortem findings in a case of oak poisoning

A
  • Mucoid and haemorrhagic enteritis, sub-serosal petechial adn ecchymotic haemorrhages
  • Oedema of distal limbs and ventral abdomen, oedema of kidneys
  • Kidneys enlarged, apile, contain numerous haemorrhages with coagulative necrosis of PCT (pink staining solid mass of epithelial cells and protein in tubule lumen)
67
Q

Outline the treatment and prevention of oak poisoning

A
  • Supportive treatment only

- Prevent by avoidance

68
Q

Identify sources of oxalates

A

Docks, sorrel, rhubarb, leaves of sugar beet

69
Q

Outline the mechanism of action of oxalate poisoning

A
  • Formation of calcium oxalate crystals following metabolism in rumen
  • depends on rate of consumption, amounf of other food eaten concurrently, total amount consumed
  • If absorbed form GIT, toxicity signs occur within 1-2 hours of ingestion
  • leads to calcium depletion, and crystallisation of calcium oxalate in kidneys with associated tubular necrosis, and in the vasculature leading to vascular necrosis and haemorrhage
70
Q

Outline the clinical signs of oxalate poisoning

A
  • HypoCa (within 4-6 hours of ingestion)
  • Muscle fasciculations, dullness, ruminal atony, constipation etc.
  • Urolithiasis: inappetance, mild pyrexia, mild tachycardia, tooth grinding, abdominal pain, straining, anuria
  • Crystals may be found on preputial hairs
  • Abdominal distention or ventral oedema (bladder rupture)
71
Q

Describe the clinical pathology resulting from oxalate poisoning

A
  • HypoCa
  • Azotaemia
  • HyperK
  • If bladder rupture: hypoNa, hypoCl, hyperP (free urine in abdo cavity)
  • Haematuria
  • Crystals in urine
72
Q

Describe the post mortem findings with oxalate poisoning

A
  • Excessive abdominal and thoracic fluid
  • Diffuse petechial haemorhage in digestive tract and on serosal memrbanes around heart
  • Kidneys pale, enlarged, swollen pelvises and ureters
  • Cut surface at corticomedullary junction yellow striated appearance, gritty feel
73
Q

Outline the treatment and prevention of oxalate poisoning

A
  • treatment: symptomatic for hypoCa with calclium IV. Dicalcium phsophate and sodium chloride may bind oxalate in rumen
  • Prevention: limit exposure, urinary acidifiers probably not that effective
74
Q

List the sources of brassica poisoning

A
  • Kale
  • Rape
  • Chow
75
Q

List the toxic conditions that may result from brassica ingestion

A
  • Conversion of SMCO into dimethyl disulphide in rumen
  • Goitrogens
  • Nitrate poisoning
  • Photosensitisation
  • (dirty crop, increased risk of clostridial disease)
76
Q

Outline the mechanisms of action and clinical signs resulting from conversion of SMCO into dimethyl disulphide in rumen with brassica poisoning

A
  • Oxidation of erythrocytes producing Heinz bodies

- Haemoglobinuira, pallor, weakness, jaundice, tachycardia, diarrhoea, collapse, death

77
Q

Outline the management of Heinz body anaemia resulting from brassica poisoning

A
  • Stop feeding brassica (usually kale)
  • Blood transfusion
  • Supportive care
78
Q

Outline the mechanisms of action and clinical signs resulting from goitrogens with brassica poisoning

A
  • Block gonversion from T3 to T4 leading to hypoT4 and goitre
  • Effects on neonates when dam fed on this in last third of pregnancy
  • Signs: mental retardation, dyspnoea, poor wiry/fluffy hair coat, higher mortality
79
Q

Outline the management of goitrogen toxicity from feeding brassicas

A
  • Iodine supplementation limited benefit - is the conversion that is blocked
  • Stop feeding brassica
80
Q

Outline the mechanisms of action and clinical signs resulting from conversion of nitrate poisoning with brassica feeding

A
  • Nitrite formation leading to methaemoglobin formation
  • Nephrotoxic
  • Signs: colic, exercise intolerance, staggering initially, then cyanosis and brown MM, collapse,panting, tachycardia, death, methaemoglobinuria, abortion storms
81
Q

Outline the management of nitrate poisoning resulting from brassica feeding

A
  • 1% soln methylene blue Iv at 2-4ml/kg, repeat to effect
  • Prevent by avoidance and gradual introduction of suspect crops (can build tolerance)
  • Test crops for nitrate levels
  • ## Ensiling
82
Q

List the sources of bracken

A
  • May be used as bedding

- Sparse pastures

83
Q

Outline the mechanisms of acton of bracken poisoning

A
  • Thiaminase, breaks down to thiamne in rumen
  • Ptaquiloside causes death of precursor cells in bone marrow causing pancytopaenia and thrombocytopanenia
  • Contains multiple carcinogens acting on bladder and GIT
84
Q

Outline the clinical signs of bracken poisoning

A
  • Anorexia
  • Depression
  • lethargy
  • Dysentery
  • Mucosal petechaei
  • Bleeding from orifices
  • Death
  • Enzootic haematuria
  • Tumour signs depend on location: drooling, loss of condition, diarrhoea, haematuria, rumianl tympani, stasis, anuria/oliguria
  • Bright blindness in sheep
85
Q

Outline the post mortem findings of bracken poisoning

A
  • Ulceration of bladder, GIT

- Cerebro-corticonecrosis in calves

86
Q

Outline the treatment and prevention of bracken poisoning

A
  • Supportive +/- blood transfusion
  • Prognosis guarded if bone marrow suppression
  • Prevent by limiting exposure
87
Q

Outline the mechanism of action of lamb nephrosis

A
  • Unkwnon toxin leading to sporadicoutbreaks of nephrosis in lambs 2-4 mo
  • May be related to previous outbreaks of coccidiosis or nematodirus in older lambs
88
Q

Outline the clinical signs of lamb nephrosis

A
  • Non-specific renal failure: depression, inappetance, abdominal pain
  • No enlargement of bladder/accumulation of urine
89
Q

Outline the clinical pathology seen with lamb nephrosis

A
  • Indicative of renal failure
  • Elevated BUN, creatinine, AST
  • Proteinuria, haematuria, glucosuria
90
Q

Outline the post mortem pathology seen with lamb nephrosis

A
  • Kidneys enlarged and pale

- No pooling of urine within renal pelvis, normal ureters and bladder

91
Q

Outline the prevention of lamb nephrosis

A

No recognised preventative measures that are effective

92
Q

List the large animal differentials for haemturia

A
  • Toxic nephrosis from oak, bracken, lamb nephrosis
  • Enzootic haematuria (chronic bracken poisoning and TCC)
  • Pyelonephritis
  • Urolithiasis/calculi
  • Neoplasia other than when associated with bracken
  • Vascular damage e.g. septicaemia, DIC
  • Renal infarction (v rare)
93
Q

List the differentials for large animal haemoglobinuria

A
  • Babesiosis
  • Bacillary haemoglobinuria
  • Copper toxicity
  • Brassica poisoning (esp. rape, kale)
  • Leptospira icterohaemorrhagiae
  • Post parturient haemoglobinuria
94
Q

List the differentials for large animal myglobinuria

A
  • Equine rhabdomyolysis

- White muscle disease and exertional myopathy in cattle associated with vit E/Se deficiency

95
Q

Give examples of the natural barriers to infection in the urinary tract

A
  • Flushing effect of urine
  • Resident normal flora in lower urogenital tract
  • Urine hostile to bacteria
  • Physical barriers e.g. bladder sphincter
  • Epithelial cell layer
  • Mucosal immune system
96
Q

Outline the risk factors for UTIs

A
  • Females > males (short wide urethra)
  • Physical defects e.g. ectopic ureters, spay incontinence
  • Catheterisation
  • Immunocompromise e.g. HAC, systemic disease
  • Calculi
97
Q

List the bacteria typically involved in UTIs

A
  • G-ve rods: E coli, Proteus spp, Enterbacter spp, Klebsiella spp, pseudomonas spp
  • G+ve cocci: Staph, Strep
  • Large animals: Corynebacterium spp., Actinobacillus spp., Arcanobacter spp.
98
Q

Compare UTIs in large and small animals

A
  • Cattle, sheep, pigs: pyelonephritis more common, secondary to uterine infection e.g. metritis
  • Horses: often secondary to other problems e.g. trauma, anatomical defects
  • Horses and rabbits have sabulous cystitis
99
Q

What is by sabulous cystitis?

A

Accumulation of sand of CaCO3 crystals in the bladder, often concurrent with bacterial infection

100
Q

Which bacteria are classed are urease positive?

A

Proteus, Staphylococcus, Klebsiella

URI2 (9 decks)

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