CMS- urinary and hepatic + reproductive and endocrine

Question 1

primary vs secondary causes of vomiting

Answer 1

Gastrointestinal – e.g dietary change/indiscretion, food intolerance/allergy, obstruction (foreign body or other), IBD, volvulus
Other abdominal causes, e.g pancreatitis, renal disease, pyometra
Metabolic/endocrine, e.g diabetic ketoacidosis, hypoadrenocorticism
Infectious, e.g parvovirus, feline panelukopaenia, giardia, helminths
Central/CNS, e.g vestibular disease
Toxins, e.g raisins/grapes (dogs), lilies
Drugs, e.g NSAIDs, cephalosporins

Question 2

Prioritising diagnostic tests for vomiting

Answer 2

Blood sampling Biochemistry
Electrolytes
Haematology
Pancreatic lipase

Endocrine testing
ACTH stimulation test
Thyroid (cats)

Urinalysis- Diabetic ketoacidosis

Infectious disease testing
Parvovirus, feline panelukopaenia
Giardia

Imaging
Radiography (+/- contrast)
Ultrasonography
CT

When do we need to do further diagnostic tests?-
Mild acute vomiting, history unconcerning and clinical exam unremarkable - probably not, adopt a ‘watch, wait and see’.

Severe acute vomiting, history concerning and/or clinical exam abnormal – most likely yes.

Chronic vomiting – further investigation is warranted.

Do I need to perform diagnostics straight away? Think about severity of clinical signs and information obtained from history.

Question 3

create a problem lsit and differentails for this case-

History: Bramble, a 10 week old mixed breed, ME puppy. Had his first DHPPiL vaccination and deworming 2 weeks ago. In the last 24 hours, he has stopped eating and drinking, and has vomited on 3 occasions. The owner reports that he is quieter than usual, but still wants to play a little. He is not on any medications and has not had any access to toxins.
Physical exam: QAR. He has a slight loss of skin turgor and his mucous membranes are semi-dry, pulse rate and quality are normal, suggesting 5% (mild) dehydration. Rectal temperature is elevated (39.3). The rest of the clinical exam is normal.

Answer 3

Problem list? Acute vomiting
Dehydration
Inappetant and quiet/lethargic

Ddx? Infectious – parvovirus, giardia
GI – dietary indiscretion/scavenging (even if not apparent from history)
GI – intussusception (although often palpable)
Other abdominal – renal disease

Tests? – biochemistry, haematology, electrolytes: haematology results identify a leukopaenia (neutropaenia and lymponpaenia) and a mild elevation in haematocrit. Biochem and electrolytes are normal.

Revised differential diagnosis list: leukopaenia makes parvovirus more likely and renal disease ruled out.

Parvovirus SNAP test: positive

Question 4

create a problem list, differentila and test recomendations for this case-

History: Molly, a 3 year old, female entire Labrador retriever. She was in season 6 weeks ago. She is fully vaccinated with no history of travel outside the UK and she is not on any medications. The owner is concerned about intermittent history of vomiting, lethargy and increased thirst over the past few weeks.

Physical exam: QAR. She has a skin tent and tacky mucous membranes (estimated dehydration 6-8%). HR 90 bpm. Rectal temperature 38.3.

biochem= high urea
high creatinine
high sdma

low tp
low albumin
low globulin
low cholesterol

heamotology-
low wbc
low neutrophils
low monocytes

Urinalysis (free catch) – SG 1.019, leukocytes ++, protein +

Answer 4

Problem list: chronic intermittent vomiting
polydipsia
lethargy

Ddx vomiting: GI – dietary indiscretion, partial obstruction; other abdominal – pyometra; renal disease; hepatic disease; metabolic/endocrine – hypoadrenocorticism; diabetic ketoacidosis
Ddx polydipsia: e.g pyometra, hypoadrenocorticism, diabetes/diabetic ketoacidosis.

Revised ddx list after blood results for vomiting: hypoadrenocorticism and renal disease more likely, pyometra and partial obstruction not ruled out, hepatic disease unlikely, diabetic ketoacidosis ruled out
Next step: imaging and ACTH stimulation test (beware of concurrent disease)

Diagnosis: hypoadrenocorticism

Question 5

create a problem list, differentila and test recomendations for this case-

History: Dora, a 16 year old, fully vaccinated, indoor only, female neutered DSH cat. She has a progressive history over the past few months of vomiting, polyphagia and weight loss.

Physical exam: BAR. Hydration status is normal. Rectal temperature is 38.1. HR is 240 with normal rhythm. Body condition score 3/9. She has a reduced range of motion and discomfort on examination of her hips. The rest of the exam is unremarkable.

Answer 5

Problem list: chronic vomiting
polyphagia
reduced ROM and discomfort hips
weight loss

Ddx vomiting: GI – neoplasia; other abdominal – pancreatitis, renal or hepatic disease; metabolic/endocrine – hyperthyroidism
Ddx polyphagia – hyperthyroidism
Ddx reduced ROM hips – osteoarthritis, other

Tests? Biochemistry including T4, haematology

Result – elevated T4
Urinalysis
Blood pressure

Diagnosis – hyperthyroidism.

Question 6

Interventions for common causes of vomiting

Answer 6

Specific (based on diagnosis) vs supportive
Supportive care considerations – dehydration (fluid support), age, severity
Avoid prokinetics (e.g metoclopramide) unless you have ruled out an obstruction
Will often include antiemetics (maropitant)
NSAIDs are contraindicated
Bland diet
Short period of not feeding?
Gastroprotectants (evidence?) Reference ACVIM consensus statement 2018: support for rational administration of gastrointestinal protectants to dogs and cats

Antimicrobials are NOT indicated for acute vomiting (unless a specific diagnosis tells you otherwise, e.g parvovirus due to neutropaenia).

Question 7

History: Bear, a 3yo MN miniature schnauzer. Fully vaccinated with no history of travel outside of the UK. Ran off on walk for about 20 minutes two days ago. 24 hour history of vomiting and lethargy.

Physical exam: Dull. Moderate dehydration. Rectal temperature is 39.1. HR is 120 with normal rhythm. Body condition score 4/9. He tries to bite when palpating his abdomen.

Answer 7

Problem list: abdominal pain
acute vomiting
lethargy/dull
Ddx abdominal pain: obstruction (foreign body); pancreatitis; injury; gaseous distension; torsion; peritonitis
Ddx vomiting: GI – dietary indiscretion, obstruction; other abdominal – pyometra; renal disease; hepatic disease; metabolic/endocrine – hypoadrenocorticism; diabetic ketoacidosis
Lethary/dullness are considered to be secondary problems

You perform biochemistry including electrolytes and haematology. Results from haematology show an increased RBC and haematocrit, which is likely to be a result of dehydration and an inflammatory leukogram. Biochemistry shows a mild elevation in urea which is likely to be a result of dehydration and a mild hypokalaemia which is likely a result of vomiting. Urinalysis is unremarkable, USG 1.038.

You perform a SNAP cPL (vs SNAP fPL in cats)
which shows an abnormal result. Is
pancreatitis your diagnosis?

The abnormal SNAP cPL is strongly suggestive of pancreatitis
A normal SNAP cPL does not rule out pancreatitis (false negatives)

But ……..how can you be sure if it is a primary or secondary process?

It is important to rule out pancreatitis as a secondary problem (e.g a concurrent duodenal foreign body). You perform abdominal ultrasonography which supports your finding of pancreatitis and does not identify other abnormalities. In this case, it is a primary pancreatitis.

Ideally, follow up your SNAP cPL with a SPEC cPL because the SNAP cPL has a grey zone which mean false positives are possible.

Question 8

Interventions for abdominal pain

Answer 8

Considering again pancreatitis: dogs vs cats
Our case of primary pancreatitis in a dog: IVFT to address dehydration and hypokalaemia
Analgesia: opioids (methadone, buprenorphine); paracetamol. Can also consider gabapentin, CRIs lidocaine and ketamine
Antiemetics: maropitant. If inadequate consider ondansetron or metoclopramide
Feeding: early enteral nutrition is important (nasogastric or oesophagostomy tube are often required).
NSAIDs are contraindicated
Antimicrobials are not indicated (unless high index of suspicion of infection).

Question 9

Causes of vomiting and abdominal pain that require surgical intervention

Answer 9

Critical, immediate -
Gastric dilation and volvulus
Intestinal volvulus
Diaphragmatic hernia
Acute peritonitis (abdomincentesis
required for diagnosis)
Linear foreign body
Complete high FB obstruction
Ischaemic bowel
Surgical complete urinary tract
obstruction, e.g urolithiasis

Critical, surgery once stable-

GD without volvulus
Gastric obstruction
Partial or distal intestinal
obstruction
Intussusception
Pyometra
Pancreatic mass/abscess

For further diagnostics-
E.g for small bowel biopsy beyond reach of endoscope in cases of chronic vomiting

Question 10

What are the different causes of discoloured (“red”) urine?

Answer 10

Haemoglobinuria
Myoglobinuria
Haematuria
(Oxidation causes darkening of urine after exposure to air or snow)
Plant-derived pigmentation

Red maple causes hemoglobinuria
Sycamore causes myoglobinuria
Oak causes renal failure and hematuria

Plant-derived pigmentation
White clover
Oxidising agents in normal urine
Pyrocatechins
Usually darkens urine AFTER storage/standing
Natural pigments in normal urine
Darkens or turns urine red after contact with air or snow
Drug-induced
Rifampin, phenothiazine, nitazoxanide -> bright orange/red
Doxycycline -> dark brown or black

Question 11

what tests can be run on red urine to determine ehat is present

Answer 11

sedement exam- clear urine= hematuria: urinary or repro dource
Red urine after spinning- hemoglobinuria/ myoglobinuria- look at complete blood count

Dipstick- test for haem

Question 12

causes of heamatureia

Answer 12

Urethral rents
Urethritis
Bacterial cystitis
Urolithiasis
Pyelonephritis
Idiopathic haematuria
Verminous nephritis
Renal and vesicular neoplasia

Question 13

causes of Myoglobinuria

Answer 13

Muscle damage/necrosis
Trauma
Exertional rhabdomyolosis
Polysaccharide storage myopathy
Toxicity
Idiopathic

Question 14

causes of Haemoglobinuria

Answer 14

Intravascular haemolysis due to:
Infectious disease of the haemopoietic system
Toxicity
Immune-mediated disease

Question 15

paramenters of PUPD in horses

Answer 15

Polydipsia is defined as = >100ml/kg daily (>10% BWT)
Normal water intake is 40-60ml/kg daily (4-6% BWT)

Note variations:
In grazing horses as low as 2% BWT
In lactating mares as high as 8-9% BWT

Polyuria is usually defined as urine production >50ml/kg daily (harder to measure than PD)
Normal urine production is between 15-30ml/kg daily

Question 16

Causes of PUPD in horses

Answer 16

Before investigations rule out physiological explanations:
Hot weather/ hard work/ lactation/ excess dietary protein/ excess salt/ administration of glucocorticoids/ diuretics

Causes:
PSYCHOGENIC POLYDIPSIA
PPID (Cushing’s Disease)
Chronic Renal Failure
Hepatic insufficiency
Diabetes Melitus
Diabetes Insipidus

Question 17

confirming pd in horses

Answer 17

1. Quantify and confirm the presence of PD
   Stable the horse for 24hours and measure PD
   If water intake is >100 ml/kg/day (>10% BWT) then PD is confirmed (and PU is almost inevitable).
   If water intake is 70-100 ml/kg/day (7-10% BWT) then PD may be suspected if there are no apparent physiologic causes (see above).
   If water intake is <70ml/kg/day (<7% BWT) then PD is not confirmed.

Question 18

diagnosis of pupd in horses

Answer 18

1. Quantify and confirm the presence of PD
2. Initial blood and urine tests
   Blood tests-
   Haematology:
   Anaemia common with CRF
   Neutrophilia may indicate glucorticoid response or inflammatory disease
   Basal plasma ACTH or TRH stimulation test – for PPID

Creatinine and Urea-
Very high in CRF: urea>15mmol/L and creatinine >300umol/L
Moderate more commonly indicates dehydration or acute kidney injury (compare to urine creatinine)
Low: urea <4mmol/L and creatinine <75umol/L may occur in hepatic insufficiency or in cases of primary (psychogenic) PD with washout.

Glucose-
Persistent hyperglycaemia indicates DM – due to PPID (transient hyperglycaemic occurs with alpha 2 agonists and pain/stress

Hypercalcaemia-
In CRF – ddx for hypercalcaemia: paraneoplastic disease

GGT/AST-
Rule out liver disease

Urine test-
USG
Low (1.002, hypersthenuria) is not really compatible with persistent PUPD and confirms renal concentrating ability.
Medium (1.008-1.012, isosthenuria) suggests that the kidney is neither actively concentrating nor diluting the filtrate and is consistent with (but not diagnostic for) chronic renal failure (check serum urea and creatinine)
High (>1.020, hypersthenuria) is not really compatible with persistent PUPD and confirms renal concentrating ability.

Glycosuria:
DM (usually caused by PPID)
Acute stress, pain, transport
Alpha-2 agonists

water restriction test- diabetes insipitus or physcogenic polydipsia

Question 19

low usg in horses

Answer 19

Low (1.020, hypersthenuria) is not really compatible with persistent PUPD and confirms renal concentrating ability.

Question 20

medium usg in horses

Answer 20

Medium (1.008-1.012, isosthenuria) suggests that the kidney is neither actively concentrating nor diluting the filtrate and is consistent with (but not diagnostic for) chronic renal failure (check serum urea and creatinine)

Question 21

high usg in horses

Answer 21

High (>1.020, hypersthenuria) is not really compatible with persistent PUPD and confirms renal concentrating ability.

Question 22

interpretation of water restriction test in horses

Answer 22

If SG rises above 1.020 this confirms renal concentrating ability is present and therefore rules-out diabetes insipidus. This indicates psychogenic polydipsia.
If the horse fails to concentrate the urine and urine SG stays <1.020, or the horse becomes dehydrated or loses 5%BWT, this suggests diabetes insipidus.

Further tests to classify diabetes insipidus (for interest)
Measure serum vasopressin at end of water restriction period
Vasopressin > 5 pmol/L – indicates normal vasopressin secretion
Vasopressin < 5 pmol/L – indicates central diabetes insipidus

Question 23

physiologic causes of pu/pd in dogs

Answer 23

Diet change (wet to dry food)
Following increased activity
During hot weather

Question 24

causes of polyuria in dogs

Answer 24

Renal disease-
Chronic kidney disease
Pyelonephritis
Acute kidney injury
Post obstructive diuresis
Renal glycosuria/Fanconi’s syndrome

Hepatic disease-
Endocrine disease=
Hyperadrenocorticism
Hypoadrenocorticism
Diabetes mellitus
Diabetes insipidus (central or nephrogenic)
Primary hyperaldosteronism
Metabolic abnormalities=
Hypercalcaemia
Hypokalaemia

Pyometra-
Polycythaemia (hyperviscosity syndrome)
Iatrogenic (drug or fluid administration)

Question 25

causes of polydipsia in dogs

Answer 25

Psychogenic!

Hepatic encephalopathy
Gastrointestinal disease (compensatory)

Question 26

pysiological caused of PU/PD in cats

Answer 26

Diet change (wet to dry food)
2o to increased grooming
Following increased activity
Playing with water

Question 27

caused of Polyuria

Answer 27

Renal disease-
Chronic kidney disease
Pyelonephritis
Acute kidney injury
Post obstructive diuresis

Hepatic disease

Endocrine disease-
Diabetes mellitus
Diabetes insipidus (central only)
Primary hyperaldosteronism
Hypersomatotropism (acromegaly)
Hyperadrenocorticism
Hypoadrenocorticism

Metabolic abnormalities-
Hypercalcaemia

Iatrogenic (drug or fluid administration)

Question 28

xauses of polydipsai in cats

Answer 28

Hyperthyroidism
Hepatic encephalopathy
Gastrointestinal disease (compensatory)

bengals love of water may cause itr

Question 29

causes of polyurea in ferrets

Answer 29

Renal disease
Hyperadrenocorticism
Diabetes mellitus

Question 30

physioogical causes of pu/pd in rabbits

Answer 30

Diet change (hay to grass in the spring)

Question 31

causes of polyurea in rabbits

Answer 31

Renal disease-
Chronic kidney disease
Pyelonephritus
Post obstructive diuresis

Hepatic disease

Metabolic disease-
Hypercalcaemia
Hypokalaemia

Pyometra
Pregnancy toxaemia (+/-ketoacidosis)
Hypervicosity syndrome (polycythaemia, hyperproteinaemia)
Itatrogenic (drug or fluid administration)

Question 32

causes of polydipsia in rabbits

Answer 32

Psychogenic
Pain related

Question 33

physiological causes of pu/pd in birds

Answer 33

During egg laying
Diet change (conversion to pelleted diet from seed)

Question 34

causes of polyurea in birds

Answer 34

Renal disease
Hepatic disease
Pancreatic disease
Diabetes mellitus
Toxins (heavy metals, aflatoxins)
pituitary adenoma

Question 35

causes of polydipsia in birds

Answer 35

Stress/fear

Question 36

clinical approch to pupd in small animals

Answer 36

History and clinical examination- Young animals – congenital, infectious, psychogenic etc. more common
Older animals – endocrine, chronic disease processes, neoplasia etc. more common.
Entire female animals – reproductive disorders

Mentation/neuro exam:
Hepatic encephalopathy -> altered mentation

Hyperactivity -> primary PD, or as a result of hyperthyroidism

Ocular exam:
Icterus (hepatic disease)
Cataracts (DM)
Retinal changes (hypertension 2o to CKD, AKI, hyperT4, HAC etc.)

Cervical palpation-
Goitre (hyperthyroidism)

Oral exam:
Mucous membranes - Icteric (hepatic disease), congested (polycythaemia, systemic inflammatory response), pale (anaemia of chronic disease/neoplasia)
Lingual ulceration and/or halitosis in advanced CKD

Thoracic auscultation-
Tachycardia (hyperthyroidism, phaeochromocytoma, sepsis), vs bradycardia (hypoadrenocorticism)
Panting (HAC), tachypnoea (pulmonary neoplasia/metastases)

Dermatological exam:
Skin thinning, alopecia, pigmentation change, comedones, calcinosis cutis (HAC)
Hepatocutaneous syndrome.

Reproductive examination:
History of egg laying – physiological PD
Pregnancy – toxaemia, gestational diabetes
Discharge – open pyometra

Confirm the presence- of PU/PD
Fluid intake
Urine output
Urine specific gravity

Urinalysis
Blood tests
Imaging
Further tests

Question 37

Hypersthenuric

Answer 37

(urine osmolarity is above blood osmolarity) – rarely used term, usually reserved for USG at the upper end of the reference range.

Question 38

Isosthenuric

Answer 38

(urine osmolarity is the same as blood osmolarity). Occurs when kidneys are completely incapable of concentrating the urine.- diabetes, phycogenic polydipsia

Question 39

Hyposthenuric

Answer 39

(urine osmolarity is lower than blood osmolarity) – indicates that kidneys are functioning as they are actively diluting the urine.

Question 40

normal fluid levels and usg in dogs

Answer 40

Normal fluid intake: 20–90 ml/ kg/day (depending on the moisture content of the diet)

Normal urine output: 20-45 ml/kg/day

Normal USG: >1.030

To confirm the presence of PU/PD
Fluid intake >100 ml/kg/day
Urine output >50 ml/kg/day
USG consistently < 1.030

Question 41

normal fluid levels and usg in cats

Answer 41

Normal fluid intake: 20–50 ml/ kg/day (depending on the moisture content of the diet)

Normal USG: >1.040

To confirm the presence of PU/PD
Fluid intake >100 ml/kg/day
USG consistently < 1.040

Question 42

normal fluid levels and usg in ferrets

Answer 42

Normal fluid intake: 75–100 ml/kg/day

Normal urine output: Poorly defined. Ranges of 8-140 ml/day reported.

Normal USG: Males 1.034 to 1.070, females 1.026 to 1.060.

To confirm the presence of PU/PD
Poorly defined.
Generally based on owners reporting a change from normal

Question 43

normal fluid levels and usg in rabbits

Answer 43

Much more variable than cats and dogs
Normal fluid intake: 50–150ml/kg/day
Normal urine output: 20-130ml/kg/day
Diet plays an important role.
Normal USG: 1.003 – 1.036

To confirm the presence of PU/PD:
Poorly defined
Water intake >120ml/kg/day considered suspicious.

Question 44

normal fluid levels and usg in birds

Answer 44

Normal fluid intake: Highly variable between species and individuals
Normal urine output: Highly variable between species and individuals; very difficult to quantify
Diet plays an important role.
Normal USG: Not enough data

To confirm the presence of PU/PD:
Subjectively larger urine portion of the droppings

Question 45

urinalysis in small animals

Answer 45

USG – As above
Dipstick
Glucose (+/- ketones)
Blood
Protein
Urine sediment (+/- UPCr)
Urine culture
Urine creatinine:cortisol ratio

Question 46

Glucosuria in small animals differentails

Answer 46

Stress
Contaminated sample
Diabetes mellitus
Fanconi’s syndrome

Question 47

Ketonuria
in small animals differentails

Answer 47

Diabetes mellitus

Question 48

Haematuria
in small animals differentails

Answer 48

Contaminated (cystocentesis; in season bitch) sample
Renal disease
Pyometra

Question 49

Proteinuria
in small animals differentails

Answer 49

Renal disease
UTI
Hyperadrenocorticism

Question 50

Pyuria (active sediment)
in small animals differentails

Answer 50

UTI
Pyometra

Question 51

Positive culture
from urinein small animals differentails

Answer 51

Contaminated/free catch sample
UTI
Pyometra

Question 52

blood tests for pupd in smal animals

Answer 52

Haematology and biochemistry

Question 53

blood results for renal disease in mall animals

Answer 53

Increased urea, creatinine +/- phosphate
Other electrolyte changes (K, Ca, Mg)
Non-regenerative anaemia (chronic)

targeted test- SDMA

Question 54

blood results for Hepatic disease in small animals

Answer 54

Increased liver enzymes (ALP, ALT, AST, GGT, bile acids)
Decreased albumin, glucose, and/or urea

targeted test- Bile acid stimulation test

Question 55

blood results for Diabetes mellitus
in small animals

Answer 55

Increased glucose
Increased ALP, bilirubin and cholesterol
Hypokalaemia

targeted test- Fructosamine
HBA1C?

Question 56

blood results for Hyper-adrenocorticism
in small animals

Answer 56

Increased cholesterol, ALP and BA
Decreased urea
Stress leukogram

targeted test- ACTH Stimulation test
Low dose dexamethasone test

Question 57

blood results for Hyperthyroidism
in small animals

Answer 57

Increased RBC indices; stress leukogram
Increased glucose, renal enzymes, and/or phosphate.
Decreased creatine

targeted test- Total T4, free T4

Question 58

blood results for Hypercalcaemia
in small animals

Answer 58

Increased total and ionised calcium

Question 59

blood results for Pyometra

in small animals

Answer 59

Neutrophilia +/- mild-moderate anaemia
Increased globulins, liver and kidney enzymes.
Decreased glucose

Question 60

ultrasound for pupd

Answer 60

most useful imiging

Liver
Kidneys
Adrenal glands
Reproductive tract

Question 61

Water restriction test in small animals

Answer 61

further test (exlude other differentials) for pupd

Differentiates between psychogenic polydipsia and diabetes insipidus.

Consider water reduction and/or in hospital serial USG in first instance.

Water reduction:
Owner measures free water intake at home.
Water availability then slowly reduced to 100ml/kg/day over 2-5 days prior to hospitalization.
USG should be monitored at home, and if >1.035 then water restriction test not needed.

Serial USG:
New environment i.e. hospital can reduce psychogenic polydipsia due to boredom, therefore may be able to rule out psychogenic PD without water restriction.

Ideally done in a hospital setting.
Method:
Fast for 12 hours prior to test.
Collect initial samples: Urine +/- plasma.
Withhold fluid and food, weigh hourly, collect urine 1-2 hourly (empty bladder each time) and collect blood 2-4 hourly.

!!!!Stop test when ANY of the following conditions are met:
Animal produces hypersthenuric urine (SG >1.030 dog, >1.040 cat).
Animal loses 5% or more of its bodyweight.
Animal becomes azotemic.
[Animal becomes hyperosmolemic (plasma osmolarity >320 mOsm/kg)]
[Urine osmolality 3 x serum osmolality]

Question 62

ADH response test in small animals

Answer 62

further test (exlude other differentials) for pupd

Differentiates between nephrogenic and central diabetes insipidus.

Desmopressin = synthetic form of antidiuretic hormone without the vasoconstricting effects of vasopressin.

Central diabetes insipidus:
Nephrons should respond to exogenous ADH and urine concentration will occur within 1-2 hours.

Nephrogenic diabetes insipidus-
Animal will be unable to respond to exogenous ADH and urine remains unconcentrated.
Reintroduced water slowly 10-20 ml/kg every 30 min for 2hr then allow ad lib access

Question 63

Psychogenic polydipsia

Answer 63

Mainly dogs, occasionally reported in cats, rabbits, birds, and ferrets.
Usually boredom response, occasionally stress/fear.
Treatment:
Slowly restrict water to a normal volume (species dependant).
Address underlying issue

Boredom-
Provide enrichment – puzzle feeders, toys, conspecifics (if appropriate).
Increase exercise.
Increase owner interaction/play.
Dogs suffering from psychogenic polydipsia often respond well to being given a hobby- fly ball, sheep dog training ect.

Stress/fear-
Most common in prey species.
Identify trigger and remove if possible.
General support – provide places to hide, ensure correct husbandry, calming supplements etc.

Question 64

Renal amyloidosis in cattle

Answer 64

Amyloidoses are rare disorders caused by the synthesis and deposition of misfolded proteins in tissues – create insoluble fibrils called amyloid

In humans it can affect and damage the heart, kidneys, liver, nerves or digestive system, and cause red-purple blotching around the eyes and lips (see photo)

At least 36 proteins have been identified in humans as being linked to amyloidosis

AL amyloidosis is most common type in people - linked to bone marrow problems and myeloma

AA amyloidosis is also common and linked to long-term inflammatory conditions e.g. rheumatoid arthritis, Crohn’s disease, ulcerative colitis, tuberculosis (TB) (AA form most common in cattle)

Rare condition of adult cattle - typically at least 3 yrs old, usually older

Deposition of amyloid in renal glomeruli – can also be deposited in other organs

Profuse diarrhoea, subcutaneous oedema and renal enlargement, weight loss

Protein-losing nephropathy: protein lost in urine – can be foamy

Hypoalbuminaemia (severe), proteinuria, uraemia (terminally)

Diarrhoea due to intestinal oedema and deposition of amyloid in intestines affecting absorption of fluid

NO TREATMENT – euthanasia; very likely to be condemned at slaughter in abattoir

Turkish study looking at cases of mastitis, metritis etc: finding an association with the AA form of amyloidosis, which is also linked to inflammation/infection in humans

Question 65

Pyelonephritis – pigs

Answer 65

Actinobaculum suis is in the same family of bacteria as Trueperella pyogenes (acute mastitis and metritis in cattle) and Actinomyces bovis (‘lumpy jaw’ in cattle)

A. suis is anaerobic - found in prepuce and preputial diverticulum of boars

Infected through natural service by the boar – infection of urinary tract of gilt/sow

Cystitis and pyelonephritis – urinary tract infections quite common cause of culling of sows

clinical signs-
May die suddenly – acute pyelonephritis – sows found dead or develop clinical signs rapidly – purulent bloody urine – could die in 2-3 days

Chronic pyelonephritis - hunched backs, anorexia, drinking more, lose condition, may be vulval discharge, coloured urine

Likely to see first clinical signs 2-3 wks after natural service with boar – could affect more than one animal

Test urine - presence of blood, bacteriology for A. suis

Treatment: antibiotics – sensitivity; likelihood of success depends on stage of infection

e.coli- clinical signs-
Ascending infection by E. coli from faecal contamination of vulva – dirty environment (used to be contaminated back ends of dry sow crates pre-1999)

Restricted water intake will allow infection to set in rather than bacteria being flushed from urinary tract

Cystitis and pyelonephritis both seen – simple bladder infection, or both?

Increased frequency urination – little and often, blood/pus in urine

Treatment – Abx; but if pyelonephritis established, kidney damage may be irreparable

Prevention - hygienic environment (outdoor challenges) and unrestricted water access

Question 66

Pyelonephritis in cattle

Answer 66

Not that common – but more common in older beef cows

Range of bacteria involved – ascending infection to kidneys – calving, insemination, coitus

Acute: abdominal pain – arched back, kicking at abdomen, tail twitching, dull, frequent urination of discoloured urine (blood, pus), pyrexia, left kidney may feel enlarged at rectal exam – may elicit discomfort touching it, may die

Chronic form – loss of condition and dropping milk yield, frequent urination bloody urine (haematuria) with pus

diagnosis and treatment-
Diagnosis – collect urine for culture – rub perineal area for sample collection; ultrasound examination of kidneys – uni- or bilateral

Treatment – Abx unlikely to have effect, procaine penicillin 3 weeks?; relapse likely. Consider antimicrobial stewardship – justified?

Post-mortem meat inspection – total condemnation of carcass if signs of systemic infection, poor condition

Question 67

Acute tubular necrosis in ruminants

Answer 67

Clinical signs:
Depression, inappetence, mild bloat, acute diarrhoea

Treatment:
Remove toxic source/treat septic focus – fluid therapy, antimicrobials if appropriate

nephrotoxins-
Oak poisoning
Oxalates e.g. from brassicas (weaned lambs), rhubarb, ethylene glycol (antifreeze)
NSAIDs
Heavy metals e.g. lead, cadmium
Aminglycosides
Tetracyclines

renal ischeamia-
Acute mastitis
Septic metritis
Abomasal torsion
Salmonellosis

Question 68

Nephrosis in lambs

Answer 68

Occurs sporadically in lambs up to about 4 months old, often much younger

May appear after coccidiosis or Nematodirus infection in older lambs; may also see cryptosporidiosis in younger lambs

First described around late 1980s

Clinically – dull, temperature normal, not eating, losing weight, die

Swollen, pale kidneys at PM – nephrosis seen on histopath

Angell et al. (2013) associate nephrosis with Drunken Lamb Syndrome (DLS):

D-lactic acidosis of intestinal microbial origin linked to DLS; significance of nephrosis unknown

Oral bicarbonate solution and long-acting parenteral amoxicillin suggested as treatment by Angell et al

Question 69

enterotoxaemic clostridial diseases

Answer 69

Black disease (C. novyi B)
Braxy (C. septicum)
Pulpy kidney (C. perfringens D)

Question 70

Muscle or tissue damage / toxaemia clostridial diseases

Answer 70

Blackleg (C. chauvoei)
Malignant oedema (C. novyi A) - (‘big head’ rams)

Question 71

Nervous system Clostridial diseases

Answer 71

Tetanus (C. tetani)
Botulism (C. botulinum)

Question 72

Black disease

Answer 72

Clostridium novyi type B
Clostridial disease

Black disease resulting in necrotic liver tissue – more often sheep – multifocal areas in liver, often associated with areas of liver fluke damage

Question 73

Blackleg

Answer 73

Clostridium chauvoei
Clostridial disease

will result in “black leg”- damaged muscle tissue

Question 74

Tetanus

Answer 74

Clostridium tetani
Clostridial disease
Extensor rigidity in limbs

e.g. after castration, infection of open wound

Question 75

Botulism

Answer 75

Clostridium botulinum

Clostridial disease

collapse, paralysis- non rigid

Question 76

‘Pulpy kidney’ in lambs

Answer 76

C. perfringens Type D

1. Occurs in young 4–10-week-old lambs born from unvaccinated dams
2. Also in unvaccinated older weaned lambs at around 6 months of age
   when maternal antibodies have worn off

Major feature – sudden death, often some of the best lambs

Results in enterotoxaemia (NOT renal disease) from epsilon (ETX) toxin produced by multiplying bacteria in gut: fermentation of lush grass or concentrate; often triggered by move onto better pasture or introduction of supp. feeding

Name comes from the friability of kidneys post-mortem – but brain oedema, cardiac and pulmonary lesions were produced by the ETX toxin, not renal pathology in this recent study:

Prevention: Vaccinate pregnant ewes – primary course and annual booster; then vaccinate lambs s/c twice before weaning at 4-6 weeks apart e.g. Heptavac® P Plus (noahcompendium.co.uk)

Question 77

Leptospirosis in cattle

Answer 77

Global problem – significant zoonosis and economic impact in livestock farming

Leptospira borgpetersenii serovar Hardjo

Leptospira interrogans serovar Hardjo

Abortion, stillbirths, weak calves, infertility most common problems in European cattle

Milk drop syndrome – sudden decrease in yield with high pyrexia – thick milk like colostrum with soft, flabby udder

Leptospires colonize the proximal renal tubules - intermittently excreted in the urine of carrier animals – then ingested or inhaled to infect other cattle

Infected watercourses often seem to be a source of infection – think biosecurity

controle and prevention-
Serology for diagnosis – MAT (microscopic agglutination test), ELISA, PCR

Vaccination should prevent urine shedding following exposure and will protect against milk drop and abortion

UK cattle vaccines: e.g. Spirovac (Zoetis UK); Bovilis Leptavoid (MSD Animal Health)

Vaccination programmes important to protect both cattle and human health

Consider source of environmental contamination to cattle (water & soil), closed herd

Handling of aborted material and infected urine splash – high risk for humans

a significant zoonosis

Question 78

Redwater fever in cattle

Answer 78

Babesiosis
Protozoal parasite Babesia divergens in northern Europe – zoonotic (rare but dangerous in humans)

Transmitted by the tick Ixodes ricinus (definitive host) to cattle and red deer (intermediate hosts)

Seen in hilly regions where tick habitat is abundant – heather, fern, tall grass

Seasonal – 2 peak tick feeding seasons – Spring and Autumn, but cases can be seen in Summer

Clinical signs: most signs seen in adults –
Dull, not eating, pyrexia, very loud heart sounds, haematuria (coffee-coloured), ‘pipe-stem’ faeces – ‘hosepipe’ due to spasm of anal sphincter – then constipation

Key factors: (i) Tick habitats (ii) Seasonal tick activity (iii) % of ticks infected with B. divergens (iv) Immune status of host

Young animals under 6-9 months tend not to show clinical signs

Exposure early in life provides immunity in herds in endemic areas

Biggest risk is for bought-in cows coming in from clear areas – very susceptible to infection – outbreaks can occur in these immunologically naïve cattle

Question 79

Redwater fever in cattle (Babesiosis) - treatment

Answer 79

Imidocarb - Licensed treatment (and for prophylactic): Imizol® 85 mg/ml Solution for Injection (noahcompendium.co.uk)

Note extremely long withdrawal period for imidocarb: 213 days for meat! Tang et al. (2022): ‘The slow elimination of IMD in bovine tissues is conducive to protozoa elimination, but it poses risks and challenges to food safety.’

Blood transfusion to increase blood volume: Soldan (1999): Blood transfusions in cattle (wiley.com)

Laxative for constipation

Good prognosis if early treatment instituted

Be conscious of whether in an endemic area for redwater fever

Question 80

Causes of AKI/ ARF in horses

Answer 80

Haemodynamic / Vasomotor- reduced blood supply to kidney= dehydration ect

Nephrotoxic

rare!-
Obstructive nephropathy- urinary tract obstruction
Interstitial nephritis- secondary to bacterial infection

Question 81

Haemodynamic/ Vasomotor
(Hypotension/ hypoxia) causes of AKI/ARF in horses

Answer 81

Colic
Sepsis
Acute severe D++
PAS/HIE (Foals)
Haemorrhage
Pigmenturia (myopathy/haemolysis)
Acute Heart Failure

Question 82

Nephrotoxic / acute tubular necrosis
(especially in dehydrated/ hypotensive patients)
causes of AKI/ARF in horses

Answer 82

Aminoglycosides
Oxytetracycline
NSAID’s
Bisphosphonates
Immune mediated drug reactions
Pigmenturia (myopathy/haemolysis)
Leptospirosis (foals)
Heavy metal (lead/mercury)
Acorn

Question 83

Obstructive/ Rupture
causes of AKI/ARF in horses

Answer 83

Obstruction of Urethra
Obstruction of Ureters

Question 84

Clinical Signs of AKI/ARF in horses

Answer 84

Often the result of the predisposing disease (sepsis/ colitis etc.)
Some adults with oliguric RF present with colic (restless, frequent pawing ? Increased pressure in renal capsule)
Uraemia causes anorexia and depression and v rarely uremic encephalopathy, (blood ammonia is elevated)
Clinical findings due to obstructive renal failure or rupture of the urinary tract also include stranguria, abdominal distention, colic.
Acute septic nephritis (rare) – pyrexia may be present.

Question 85

diagnosis of AKI/AKF in horses

Answer 85

History and clinical signs

Azotaemia (abnormally high serum concentrations of urea, creatinine or more recently, symmetric dimethylarginine (SDMA).

Concurrent isosthenuria (1.008-1.014= isosthenuria)- kidney is neither concentrating or diluting

Electrolyte abnormalities hypochloraemia and hyponatraemia (most common)

Potassium concentrations can be variable in azotaemic horses.

Reduced dietary intake can compensate for decreased excretion.

If potassium is elevated consider ARF, prerenal azotaemia, obstructive nephropathy and uroabdomen

In ARF high K might indicate that the renal failure is oliguric or anuric or at least not just prerenal azotaemia

K levels usually decrease quickly following fluid therapy with prerenal azotaemia

Occasionally be dangerously high (>5.5 mEq/L) and require specific medical treatment (glucose/insulin) to decrease potassium concentrations.Serum magnesium can be high with either renal or prerenal azotaemia as kidney is primary organ controlling magnesium excretion

Serum calcium can be decreased or increased in ARF, although increased levels more commonly found with chronic renal failure.

Ultrasound findings of the kidneys are often unremarkable with AKI/ARF unless obstruction is the cause. Occasional oedema – poor prognostic sign

urinalysis–
In cases of pigmenturia urine will be discoloured +ve for blood on dipstick

Proteinuria is generally minimal ( unless acute glomerulopathy –rare)

Bacteriuria is uncommon in horses with ARF since acute septic nephritis is rare in adult horses.

Question 86

Separating prerenal azotaemia from intrinsic renal disease

Answer 86

Best and most practical test is urine specific gravity (USG).
Ability to dilute or concentrate urine is lost when approximately two-thirds of tubular function is lost
Urine osmolarity will then be comparable to serum osmolarity (between 1.008 and 1.016)
If the azotemic horse has a USG greater than 1.025, prerenal azotemia is the most likely cause.
But some degree of prerenal azotemia is often present in patients with ARF.

Question 87

treatment of AKI/ARF in horses

Answer 87

Aims
Treat the initiating disease
Correct Prerenal factors (dehydration and hypotension)
Tailor treatment of primary disease to avoid nephrotoxic drugs (alternate analgesics or antimicrobials as necessary)
Obstructive causes of ARF are mostly treated by surgical removal of the obstruction

Horses with ARF (if not already hospitalised for the primary condition) usually require hospitalisation for appropriate treatment and monitoring.

fluid therapy

Prognosis is usually good, as much of the pathology will be reversible (if primary disease can be treated).
Renal enzymes may not decrease significantly for 2-4 days but continued improvement possible for up to 6 months as less injured nephrons hypertrophy.
Early recognition and intervention will improve prognosis
Polyuria good prognostic finding compared with oliguria or anuria (as allows standard treatment to continue)
Therapy may be prolonged and expensive in severe AKI

Question 88

fluid therapry for aki/arf in horses

Answer 88

First line of treatment in most cases (crystalloids)

Determine if the patient is anuric, oliguric, or polyuric.

For the polyuric ARF patient, fluid therapy is the “gold standard” treatment.

IVFT re-establishes renal blood flow & glomerular pressures, flushes out tubular debris improving glomerular function, and corrects electrolyte abnormalities.

If the horse urinates a moderate to large volume after receiving fluids, can assume intravascular volume and systemic pressures are adequate for kidney function.

If the horse has not produced urine after an adequate fluid challenge, the bladder should be rectally palpated or visualised by ultrasound to exclude obstructive nephropathy.

If the patient is oliguric (or even worse, anuric) after correction of prerenal factors, the prognosis is guarded.

Fluid therapy alone is certainly not the “gold” standard in these cases and overhydration will lead to an earlier demise!

Easiest and earliest treatment to try in hopes of causing polyuria is a single dose of furosemide

These horses may need vasopressor drugs to try to improve urine production.

Question 89

chronic renal faluire in horses

Answer 89

Chronic, irreversible progressive disease of the kidneys, with a duration greater than 3 months.
Functional or structural change which leads to a chronic reduction in the glomerular filtration rate (GFR).
Much less common than ARF in horses

Primary Glomerulopathies-
Glomerulonephritis (following streptococcal infection/ stem cell treatment/ EIA/ Purpura: immune complex deposition)

Primary tubulointerstitial disease (chronic interstitial nephritis)-
Incomplete recovery from acute tubular necrosis

Nephrolithiasis, pyelonephritis, renal dysplasia

Question 90

CRF clinical signs in horses

Answer 90

Not specific
Weight loss
Polyuria / Polydipsia
Peripheral oedema (due to hypoproteinaemia)
Dull hair coat
Poor performance (anaemia)
Poor appetite
Oral changes (gingivitis, dental tartar, uremic ulcers)
Changes in mentation
Mild diarrhoea
Uremic encephalopathy (rare)

Question 91

diagnosis of crf in horses

Answer 91

Azotaemia
Mild anaemia (due to reduced production of erythropoietin)
Hypoalbuminemia
Hypercalcaemia often identified as a distinct feature in horses with CRF
Associated with high dietary intake and altered renal excretion
Not due to hyperparathyroidism as it often is in dogs
Often accompanied by hypophosphatemia (contrast with small animals)

A horse with increased creatinine and hypercalcemia should be highly suspect for CRF

Urinalysis-
Renal casts and renal tubular epithelial cells (tubular damage)
May see erythrocytes and leucocytes (pyuria- pyelonephritis? perform culture) or even neoplastic cells
Trace protein often detected in normal alkaline equine urine
Marked proteinuria is considered a hallmark of equine glomerulonephritis.

Ultrasound-
Hydronephrosis
Poor corticomedullary definition ( sign of chronic renal disease)
Nephroliths / uroliths – may or may not be obstructive – result of chronic inflammation or cause?
Biopsy – may cause haemorrhage and can be fatal. Not often performed.
Can be very hard to establish inciting cause even with biopsy

Question 92

treatment of crf in horses

Answer 92

CRF is a progressive and irreversible condition
Generally symptomatic except for rare cases of chronic septic pyelonephritis – abx therapy
Postinfectious glomerulonephritis – corticosteroids for controlled, immunosuppressive therapy +/- concurrent abx
Avoid dehydration and use of toxic drugs.
High energy diets with, moderate protein, low calcium.
Can use vegetable oil to increase caloric intake.
Ureterolithiasis/nephrolithiasis - shock wave lithotripsy or nephrotomy for stone removal.
Prognosis for long term survival is poor.