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
2
Q
What may develop secondary to ectopic ureters?
A
- Hyroureter/hydronephrosis
- Urine scald
- UTI
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
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
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
6
Q
List the differentials for umbilical swellings in the neonate/young animal
A
- Umbilical hernia
- Umbilical abscess
- Patent urachus
7
Q
Describe the typical appearance of umbilical hernias
A
- Soft tissue swelling in ventral abdomen
- Usually present since birth
- May be fluctuant
- Reducible
8
Q
How are umbilical hernias diagnosed?
A
Ultrasonography demonstrating intestine, omentum, other abdominal organs
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
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)
11
Q
Outline the signs of umbilical infection
A
- Heat, pain, oedema, cellulitis
- Other systemic signs e.g. pyrexia, joint infection
- +/- discharge
12
Q
Describe the ultrasonographic appearance of umbilical infection
A
Encapsulated soft tissue mass with flocculent fluid (pus) or gas
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
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)
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
16
Q
List causes of uroperitoneum
A
- Patent urachus
- Damage to ureters or urethra
- Bladder rupture or perforation
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
18
Q
Discuss the occurrence uroperitoneum in adults
A
- Bladder rupture secondary to trauma
- Bladder rupture secondary to obstruction
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
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
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
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
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
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)
25
What disease may be transmitted by rabbit urine? Zoonotic?
- Encephalitozoon cuniculi
| - May affect severely immunocompromised people
26
Compare leptospirosis in cattle and dogs
- Cattle: mainly reproductive disease
| - Dogs: AKI, liver disease, acutely ill
27
Describe the clinical signs of Clostridium perfringens type D in cattle
- Neuro signs, depresson, sudden death
| - Pulpy kidney on PM (not pathognomic)
28
Outline the treatment and prevention of Clostridium perfringens type D in cattle
- Antibiotics not usually effective, toxins causing disease, often fatal
- Vaccinate pregnant dam with general clostridial vaccine
- Prevent animals gorging on lush pasture
29
Outline the prevention of Clostridium perfringens type D in sheep
- Vaccinate lambs before 2 months old, booster 1 month later
| - Care moving lams from milk to concentrate, prevent gorging
30
Compare the prevalence of Clostridium perfringens type D and Clostridium haemolyticum
- Common in UK
| - C. haemolytic ~15% of clostridial disease
31
Outline the clinical signs of Clostridium haemolyticum in cattle
- Haemoglobinuria
- Sudden death
- Sudden onset depression, pyrexia, abdominal pain, dyspnoea, dysentery
- Anaemia and jaundice variable
- +/- Oedema of brisket
- Mortality 95%
32
Describe the post mortem findings in a case of Clostridium haemolyticum in a cow
- Hepatic necrosis (ischaemic infarct)
- Bloody fluid in abdominal and thoracic cavities, trachea contains bloody froth
- Kidneys dark, friable
- +/- small and large intestinal haemorrhage
33
Outline the treatment of C haemolyticum in cattle
- Early treatment with penicillin or tetracyclines
| - Whole blood transfusions in early disease (before excessive liver damage)
34
Outline the prevention of C haemolyticum in cattle
- 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
35
How is Babesia transmitted?
Tick borne protozoan, not shed in urine
36
Describe the prevalence of Babesia in the UK
Endemic in south west in cattle, sporadic in dogs related to travel
37
Describe the clinical signs of babesiosis in dogs and cattle
- Dogs: anaemia, MODS, SIRS
| - Cattle: pyrexia, anaemia, neuro signs, haemoglobinuria, anorexia
38
Outline the treatment of babesiosis
- Imidocarb dipropionate licensed for cattle, off license in dogs
- Supportive care e.g. blood transfusion
39
Outline the control of babesiosis in dogs and cattle
- 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
40
Outline the clinical signs of malignant catarrhal fever in cattle
- 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)
41
Describe the transmission of MCF
Transmitted directly or via fomites from sheep to cattle
42
Outline the treatment and control of MCF in cattle
- 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
How is E cuniculi transmitted?
Can be transmitted in the urine of rabbits and other affected animals
44
Outline the clinical signs of E cuniculi in rabbits
- Neuro signs e.g. head tilt, collapse, paresis/paralysis, fitting
- Urinary incontinence
- Renal failure
45
Outline the treatment and control of E cuniculi
- 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
List plant toxins affecting the renal and urinary system and give the species affected
- Calcinogenic glycosides: livestock
- Lily: cats
- Oak: cattle, sheep
- Oxalates: Livestock
- Pigweed: swine, cattle
- Ptaquiloside (Bracken): mostly cattle, but also other ruminants
47
List mycotoxins affecting the renal and urinary system and give the species affected
- Citrinin: all
- Ochratoxin: all
- Oosporein: chickens, turkeys
48
List metal toxins affecting the renal and urinary system and give the species affected
- Arsenic: all
| - Mercurial salts: all
49
List pesticide toxins affecting the renal and urinary system and give the species affected
- 3-chloro-p-toludidine hydrochloride: birds
- Cholecalciferol rodenticide: all
- Diquat: all
- Paraquat: all
50
List household and industrial toxins affecting the renal and urinary system and give the species affected
- Ethylene glycol: all
- Phenols: cats mostly
- Pine oil: cats mostly
- Toluene: all
51
List pharmaceutical toxins affecting the renal and urinary system and give the species affected
- 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
List animal toxins affecting the renal and urinary system and give the species affected
Snake venom, esp. rattlers: all
53
Which toxins affect the glomerulus?
Snake venom
54
Which toxins affect the renal tubules?
- Antimicrobials
- Antineoplastic drugs
- Anaesthetics
- Chlorinated hydrocarbons
- Herbicides
- Immunosuppressants
- Solvents
- Metals
- Mycotoxins
- Oxalate containing plants
- Endogenous nephrotoxins
55
Which toxins cause renal mineralisation?
- Vit D
- Cholecalciferol type rodenticides
- Plants with vit D like activity
56
Which toxins affect the renal papilla?
NSAIDs
57
Which toxins affect the renal pelvis and lower urinary tract by
a: contact irritation
b: haemorrhage and neoplasia?
A: cantharidin
B: bracken
58
Outline the mechanisms of action of the renal toxic side effects of NSAIDs
- 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
Outline the mechanisms of action of the renal toxic side effects of aminoglycosides
- 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
What is a key contraindication for the use of aminoglycosides?
Do not give close to administration of alpha-2 blocking sedatives
61
Give examples of conditions that are renally toxic due to pigmenturia
- Equine rhabdomyolysis
- White muscle disease
- Exertional muscle myopathy
- Snake bites
62
Outline the sources and mechanisms of oak poisoning
- 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
What are the risk factors for oak poisoning?
- Cattle more at risk than other species
- Lack of alternative food
- Heavy storms leading to large fall of acorns
64
Outline the clinical signs of oak poisoning
- Constipation
- Brown urine lasting 24 hours (may be missed)
- Anorexia, depression, dehydration, rumen atony +/- haemorrhagic diarrhoea
65
Outline the clinical pathology seen with oak poisoning
- Elevated BUN, creatinine, AST
| - Proteinuria, haematuria, glucosuria
66
Outline the post mortem findings in a case of oak poisoning
- 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
Outline the treatment and prevention of oak poisoning
- Supportive treatment only
| - Prevent by avoidance
68
Identify sources of oxalates
Docks, sorrel, rhubarb, leaves of sugar beet
69
Outline the mechanism of action of oxalate poisoning
- 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
Outline the clinical signs of oxalate poisoning
- 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
Describe the clinical pathology resulting from oxalate poisoning
- HypoCa
- Azotaemia
- HyperK
- If bladder rupture: hypoNa, hypoCl, hyperP (free urine in abdo cavity)
- Haematuria
- Crystals in urine
72
Describe the post mortem findings with oxalate poisoning
- 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
Outline the treatment and prevention of oxalate poisoning
- 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
List the sources of brassica poisoning
- Kale
- Rape
- Chow
75
List the toxic conditions that may result from brassica ingestion
- Conversion of SMCO into dimethyl disulphide in rumen
- Goitrogens
- Nitrate poisoning
- Photosensitisation
- (dirty crop, increased risk of clostridial disease)
76
Outline the mechanisms of action and clinical signs resulting from conversion of SMCO into dimethyl disulphide in rumen with brassica poisoning
- Oxidation of erythrocytes producing Heinz bodies
| - Haemoglobinuira, pallor, weakness, jaundice, tachycardia, diarrhoea, collapse, death
77
Outline the management of Heinz body anaemia resulting from brassica poisoning
- Stop feeding brassica (usually kale)
- Blood transfusion
- Supportive care
78
Outline the mechanisms of action and clinical signs resulting from goitrogens with brassica poisoning
- 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
Outline the management of goitrogen toxicity from feeding brassicas
- Iodine supplementation limited benefit - is the conversion that is blocked
- Stop feeding brassica
80
Outline the mechanisms of action and clinical signs resulting from conversion of nitrate poisoning with brassica feeding
- 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
Outline the management of nitrate poisoning resulting from brassica feeding
- 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
List the sources of bracken
- May be used as bedding
| - Sparse pastures
83
Outline the mechanisms of acton of bracken poisoning
- 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
Outline the clinical signs of bracken poisoning
- 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
Outline the post mortem findings of bracken poisoning
- Ulceration of bladder, GIT
| - Cerebro-corticonecrosis in calves
86
Outline the treatment and prevention of bracken poisoning
- Supportive +/- blood transfusion
- Prognosis guarded if bone marrow suppression
- Prevent by limiting exposure
87
Outline the mechanism of action of lamb nephrosis
- 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
Outline the clinical signs of lamb nephrosis
- Non-specific renal failure: depression, inappetance, abdominal pain
- No enlargement of bladder/accumulation of urine
89
Outline the clinical pathology seen with lamb nephrosis
- Indicative of renal failure
- Elevated BUN, creatinine, AST
- Proteinuria, haematuria, glucosuria
90
Outline the post mortem pathology seen with lamb nephrosis
- Kidneys enlarged and pale
| - No pooling of urine within renal pelvis, normal ureters and bladder
91
Outline the prevention of lamb nephrosis
No recognised preventative measures that are effective
92
List the large animal differentials for haemturia
- 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
List the differentials for large animal haemoglobinuria
- Babesiosis
- Bacillary haemoglobinuria
- Copper toxicity
- Brassica poisoning (esp. rape, kale)
- Leptospira icterohaemorrhagiae
- Post parturient haemoglobinuria
94
List the differentials for large animal myglobinuria
- Equine rhabdomyolysis
| - White muscle disease and exertional myopathy in cattle associated with vit E/Se deficiency
95
Give examples of the natural barriers to infection in the urinary tract
- 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
Outline the risk factors for UTIs
- Females > males (short wide urethra)
- Physical defects e.g. ectopic ureters, spay incontinence
- Catheterisation
- Immunocompromise e.g. HAC, systemic disease
- Calculi
97
List the bacteria typically involved in UTIs
- 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
Compare UTIs in large and small animals
- 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
What is by sabulous cystitis?
Accumulation of sand of CaCO3 crystals in the bladder, often concurrent with bacterial infection
100
Which bacteria are classed are urease positive?
Proteus, Staphylococcus, Klebsiella
