Small Animal Medicine

Disorder of CHO, protein and fat metabolism caused by an absolute or relative insulin deficiency.

When there is primary beta cell loss. Can also be classed as IDDM (but early in type I diabetes insulin may not be required).

Peripheral insulin resistance and dysfunctional beta cells.

Virtually all dogs and the majority of cats are type I.

Immune-mediated destruction
Pancreatitis
Obesity
Genetic susceptibility
Endocrinopathies (Cushing's, diestrus, hypoT) and certain drugs.

Amyloidosis
Pancreatitis
Obesity

Causes a reversible insulin resistance that results from insulin receptor downregulation, impaired receptor binding affinity for insulin and post receptor defects in insulin action. Persistent hyperglycaemia leads to glucose toxicity, with eventual irreversible beta cell destruction and IDDM.

Quick control of newly diagnosed diabetic cats may lead to resolution.

An absolute or relative insulin deficiency leads to decreased tissue utilisation of glucose, AA's and TG's. This results in a lack of inhibition of the satiety centre of the brain and thus polyphagia. The liver increases gluconeogenesis and glycogenolysis in an effort to rectify this, resulting in hyperglycaemia, glucosuria and thus diuresis and primary PU/secondary PD.

Dogs - entire females 7-9 years

Cats - majority older than 6 with peak at 10yo. Male neutered.

PU,PD, polyphagia and weight loss.

Hepatomegaly
Infections such as UTIs
+/- Cataracts in dogs

Vomiting
Dehydration
Weakness
Depression
Tachypnoea or slow, deep breathing
Acetone breath

Hyperglycaemia leads to increased glucose in the lens. The high level of glucose exceeds the normal metabolic pathway and the excess is metabolised to sorbitol and in turn fructose which isn't able to move out of the lens. Water moves in via osmotic drag leading to lens oedma.

Appropriate clinical signs
Demonstration of both hyperglycaemia and glucosuria

Fructosamine is a glycosylated plasma protein and is a marker of mean blood glucose level. Useful for evaluating glucose in the face of stress-induced hyperglycaemia in cats and general monitoring.

Leukocytosis (d/t concurrent infections/inflammation)
inc. liver enzymes (d/t hepatic lipidosis)
Lipaemia
inc. cholesterol
low USG
+/- bacteruria, ketonuria and pyuria

Alleviation of owner-observed clinical signs.

Insulin
Diet
Controlled exercise
Routines

Correct obesity gradually.
If not obese feed them 150% caloric requirement initially and adjust from there.
Maintain consistency in the timing and energy content of meals.
Don't feed food high in simple sugars or propylene glycol.
Dogs do well on high fibre diets, while cats do well on high protein diets (essentially Atkins).

Is used in cats to increase insulin secretion. Response to treatment is slow and most cats eventually relpase anyway. Not to be used in dogs as they don't have any beta cells left to increase insulin secretion from.

Take a thorough history regarding insulin dose, feeding regimen and any signs of hyper or hypoglycaemia. Thoroughly examine the animal - weight, body condition, hydration, concurrent illness or complications.

Insulin overdose
Unusually strenuous activity
Inappetance
Decreased insulin need

Lethargy
Behaviour changes
Tremors
Weakness/ataxia
Collapse/seizures

Persistent hyperglycaemia (>16mmol/L) despite insulin dose over 2U/kg.

Biologically inactive insulin (outdated, overheated, poor mixing technique, diluted etc)
Inappropriate syringes
Inappropriate administration technique.

Occurs due to relative insulin overdose, release of gluconeogenic hormones leads to rebound hyperglycaemia and insulin resistance for 24-72 hours after

Hyperadrenocorticism, diestrus, obesity, pancreatitis, infection, CHF

Compounds such as glucocorticoids, catecholamines, TH, GH, progesterone

SPAY

Cataracts
Pancreatitis
Hepatic lipidosis
Ketoacidosis
Bacterial infections
Neuropathy (rare)

Absolute or relative nsulin deficiency causes increased lipolysis - with the products of lipolysis used to produced excessive amounts of ketone bodies. This in conjunction with decreased peripheral utilisation of KBs.
Accumulation of KBs leads acidosis, osmotic diuresis, nausea/vomiting and obtundation. The dehydration/hypotension produced via the vomiting and diuresis leads to decreased GFR and H+ excretion - worsening the acidosis.

Fluids
Insulin
Potassium
Phosphate
+/- Bicarbonate
Antibiotics/Anitemetics
Monitoring

Ketonuric patients may not be vomiting and may still be eating - such patients don't require as intensive treatment as sick DKA patients. Insulin should be provided to these animals as soon as possible.

Helps replace the fluid deficit caused by vomiting and diuresis - this increases GFR and thus H+ excretion which helps rectify acidosis. Fluids also directly reduce acidosis (bicarbonate).

0.9% saline, or 0.45% if hypernatremia
Add potassium
Add glucose if blood glucose is less than 13 mmol/L

Use regular/crystalline insulin as either CRI or intermittent IM.

Move the patient to intermediate insulin once they're bright, eating well and off IV fluids.

If blood glucose falls too low, stress hormones are secreted (which are insulin antagonistic) and thus further worsen the ketoacidotic state.

Decreases serum potassium since insulin acts on the glucose-potassium cotransporter to increase cellular uptake of both.

Potassium therapy is MANDATORY unless the patient is anuric.

Diuresis increase phosphate excretion (since the kidneys are designed to excrete phosphate) and so DKA patients have lowered phosphate. Therapy lowers it further.

Because phosphorous is an essential component of ATP low serum phosphorous conc. can cause ATP depletion which primarily affects cells that are high energy users such as RBCs, skeletal muscle cells and neurones.

Pallor due to haemolytic anaemia
Haemoglobinuria
Tachypnoea, dyspnoea or rapid shallow breathing due to decreased respiratory muscle function
Muscle weakness
Mental depression

Provide half of the potassium as potassium chloride and half as potassium phosphate.

Generally not necessary because fluid therapy, electrolyte replacement and insulin correct the acidosis.

May be required if there is an enormous abberation from normal as measured by blood bicarb or pH.

Diabetic patients are prone to UTIs. Take a urine sample for culture, and then use empirical broad spec bacteriocidal antibiotics.

Fluid administration rates
Hydration status
Urine output
Electrolyte level
Blood glucose

Search for underlying disease processes such as Cushing's, pancreatitis and hyperT.

Deficient production of glucocorticoids and/or mineralocorticoids which occurs with a loss of 85-90% of the adrenal cortex.

Stimulates gluconeogenesis and glycogenolysis
Stimulates erythrocytosis
Counteracts the effects of stress
Plays a vital role in the maintenance of vascular tone, endothelial integrity and vascular permability
Potentiates the vasoconstrictor action of catecholamines

RAS system activation leads to increased aldosterone release.

Decreased perfusion through the juxtaglomerular apparatus leads to renin secretion. Renin cleaves angiotensinogen to angiotensin I. ACE acts on angiotensin I to produce angiotensin II.
Angiotensin II has many effects including:
constricts efferent glomerular arterioles (forces blood to build up in the glomerulus which increases GFR despite lowered renal perfusion)
stimulates aldosterone release from the adrenal cortex.

Tubular reabsorption of Na/Cl and K excretion at the DCT and CD.

Increases salt appetite and leads to the sensation of thirst.

Stimulates release of ADH which increases the permeability of the CD leading to increases water absorption.

Very small increases lead to aldosterone secretion

Primary
immune-mediated adrenocortical destruction by lymphocytic/plasmacytic infiltration
atrophy
mitotane overdose, tumor mets or infarctions (rare)

Secondary
iatrogenic via chronic cortisol administration or progestagen therapy
destructive pituitary lesions (rare)

GI signs = anorexia, vomiting, abdominal pain, weight loss, melaena/haematochezia
Fasting hyperglycaemia = dec. gluconeogenesis, dec. fat utilisation, depletion of liver glycogen stores
Diminished vigour and lethargy
Impaired tolerance to stress
Anaemia
Hypotension

All occur because glucocorticoids are essential for maintenance of vascular tone and integrity, CHO/P metabolism and erythrocytosis

Hyponatraemia and hypochloraemia = impaired ability to conserve Na/Cl. Consequences may not occur if dietary salt is adequate. Inappetance, vomiting, diarrhoea may lead to rapid depletion

Hypovolaemia = loss of Na,Cl means hypovolaemia, hypotension, dec. CO, GFR, azotaemia. Loss of renal medullary hypertonicity reduces renal concentrating ability resulting in further water loss. ADH secretion dec. because osmolality is dec. Seen as PU/PD
Hyperkalaemia = d/t dec. GFR and acidosis leads to cardiac problems

Acidosis = d/t decreased tissue perfusion and HCO3 and Cl resorption in tubules.

Generally young to middle aged, mean 4-5 yo. Can be less than 1 or up to 12.
Majority are female.
No breed predilection but may be familial in certain dogs.

Lethargy, depression, anorexia
Vomiting, regurgitation, weight loss, meleana/haematochezia, PU/PD, weakness, shivering/shaking, collapse, dehydration, weak pulse, bradycardia and hypothermia.

Very vague clinical signs, duration may be from a few days to several months. Typically chronic progressive disease which may wax and wane. CS may suggest GI, renal or infectious disease. CS may resovle with fluid therapy and steroids.

Collapse, shock, dehydration, lethargy, weakness, vomiting, trembling, anorexia and GI signs.

Anaemia, eosinophilia and lymphocytosis with a lack of a stress leukogram. VERY SUSPICIOUS if there isn't a stress leukogram in a clinically unwell patient.
HypoNa and hypoCl
HyperK and hyperCa
Azotaemia (pre- or renal)
Inappropriately low USG in a clinically dehydrated animal - Na in urine filtrate impairs the ability to retain water (medullary washout)

Absolute or relative nsulin deficiency causes increased lipolysis - with the products of lipolysis used to produced excessive amounts of ketone bodies. This in conjunction with decreased peripheral utilisation of KBs.
Accumulation of KBs leads acidosis, osmotic diuresis, nausea/vomiting and obtundation. The dehydration/hypotension produced via the vomiting and diuresis leads to decreased GFR and H+ excretion - worsening the acidosis.

Fluids
Insulin
Potassium
Phosphate
+/- Bicarbonate
Antibiotics/Anitemetics
Monitoring

Ketonuric patients may not be vomiting and may still be eating - such patients don't require as intensive treatment as sick DKA patients. Insulin should be provided to these animals as soon as possible.

Helps replace the fluid deficit caused by vomiting and diuresis - this increases GFR and thus H+ excretion which helps rectify acidosis. Fluids also directly reduce acidosis (bicarbonate).

0.9% saline, or 0.45% if hypernatremia
Add potassium
Add glucose if blood glucose is less than 13 mmol/L

Use regular/crystalline insulin as either CRI or intermittent IM.

Move the patient to intermediate insulin once they're bright, eating well and off IV fluids.

If blood glucose falls too low, stress hormones are secreted (which are insulin antagonistic) and thus further worsen the ketoacidotic state.

Decreases serum potassium since insulin acts on the glucose-potassium cotransporter to increase cellular uptake of both.

Potassium therapy is MANDATORY unless the patient is anuric.

Diuresis increase phosphate excretion (since the kidneys are designed to excrete phosphate) and so DKA patients have lowered phosphate. Therapy lowers it further.

Because phosphorous is an essential component of ATP low serum phosphorous conc. can cause ATP depletion which primarily affects cells that are high energy users such as RBCs, skeletal muscle cells and neurones.

Pallor due to haemolytic anaemia
Haemoglobinuria
Tachypnoea, dyspnoea or rapid shallow breathing due to decreased respiratory muscle function
Muscle weakness
Mental depression

Provide half of the potassium as potassium chloride and half as potassium phosphate.

Generally not necessary because fluid therapy, electrolyte replacement and insulin correct the acidosis.

May be required if there is an enormous abberation from normal as measured by blood bicarb or pH.

Diabetic patients are prone to UTIs. Take a urine sample for culture, and then use empirical broad spec bacteriocidal antibiotics.

Fluid administration rates
Hydration status
Urine output
Electrolyte level
Blood glucose

Checking for secondary disease processes such as Cushing's, hyperT or pancreatitis.

Deficiency of glucocorticoids and/or mineralocorticoids that occurs with 85-90% loss of the the adrenal cortex.

Primary = immune mediated destruction via lymphocytic/plasmacytic infiltration
Atrophy
Mitotane overdose, tumor mets, infarction (rare)

Secondary = iatrogenic due to chronic cortisol admin or progestagen therapy.
Destructive pituitary lesions (rare)

When perfusion through the JGA falls renin is secreted. Renin cleaves angiotensinogen to angiotensin I, which ACE acts on to produce angiotensin II. Angiotensin II has a number of effects in the body - including constrictive effects on the efferent glomerular arterioles which leads to blood build up in the glomerulus and inc. GFR despite dec. renal perfusion.
It also stimulates aldosterone release from the adrenal cortex via tubular Na/Cl reabsorption and K excretion at DCT/CD.
Aldosterone stimulates the release of ADH which increases the permeability of the CD which increases water reabsorption.

HypoNa
HypoCl
Hypovolaemia
HyperK
Acidosis

Inappetance, vomiting or diarrhoea.

When dietary salt is adequate.

Dec. CO leads to dec. GFR and azotaemia.

Dec. GFR promotes hyperK and predisposes to cardiac problems.

Stimulates gluconeogenesis and glycogenolysis
Stimulates erythrocytosis
Offsets the effects of stress
Vital role in the maintenance of vascular tone and permeability as well as endothelial integrity
Potentiates vasoconstrictive effects of catecholamines

Decreased tolerance of stress
Lethargy
Hypoglycaemia
Hypotension
Anaemia
GI bleeding
Vomiting

PU/PD
Azotaemia
Heart problems

Majority are female, around 4-5yo although HAC can occur less than 1yo and upwards of 12yo. Any breed although poodles, WHWT, great danes and collies are more common.

Generally vague, may wax and wane for a while. Disease course may be a few days or many months.

Very, very sick dog. Shock, collapse, weakness, vomiting and other GI signs.

Anaemia
Eosinohilia
Lymphocytosis
Lack of a stress leukogram in a clinically unwell dog is VERY SUSPICIOUS

HyperK and Ca
HypoNa and Cl
Azotaemia (pre-renal and renal poss.)
Inappropriately low USG in a clinically dehydrated animal
Acidosis
Hypoalbuminaemia
Hypoglycaemia

Bradycardia
Peaked T waves
Widened GRS
Little or no P waves
Ventricular asystole

Renal failure
DM
HyperT
Pyometra
Pyelonephritis
Malignancy-induced hyperCa

Ulcerative/erosive GI neoplasia
Parasites
Helicobacter
Foreign body
Gastritis
NSAIDs
Renal failure
Pancreatitis
Thrombocytopenia

Artifact
Urinary obstruction/rupture
Anuric/olliguric renal failure
Severe GI disease
Acidosis

Electrolyte abnormalities (not always present)
Lack of stress leukogram in a clinically ill patient
Young dog with chronic history of illness

ACTH stim test. Demonstration of undetectable-to-low serum cortisol conc. that fail to increase after administration of ACTH.

Sensitive and specific if no previous steroid admin.

Hypotension/hypovolaemia = 0.9% saline at shock rates. Monitor urine output and blood pressure. Add glucose if hypoglycaemic
Electrolyte imbalance = dextrose +/- regular insulin
+/- Ca gluconate (give if no P waves)
Acidosis = +/- bicarbonate but shock fluids normally take care of this anyway
Glucocorticoid deficiency = give any formulation IV after samples are taken

Fludrocortisone PO BID - minimal glucocorticoid activity and thus may cause signs of Cushings

Prenisolone = double the dose of pred prior to stressful events

DOCP isn't available in NZ

PU/PD, polyphagia and alopecia (iatrogenic Cushings)

Excessive production of cortisol from the adrenal cortex due to pituitary tumors, adrenal tumors or iatrogenic causes.

85-90% of cases of spontaneous Cusings are caused by pituitary tumors.

The pituitary tumor secretes excessive amounts of ACTH - resulting in bilateral adrenal hyperplasia and subsequent excessive cortisol secretion. Vast majority of dogs have a microadenoma, with 10-20% having a macroadenoma.

2 big adrenals

10-20% of cases of spontaneous Cushings are caused by adrenal tumors - 50% are adenomas and 50% are sarcomas.

The adrenal tumor is function and secretes excessive cortisol which provokes negative feedback on the pituitary - resulting in decreased ACTH secretion and the unaffected adrenal gland becomes atrophied due to a lack of stimulation.

1 big and one small adrenal

Longterm, exogenous corticosteroids will result in suppression of the HPA axis and iatrogenic HAC.

2 small adrenals.

Disease of middle aged/older dogs.
ATH 11yo
PDH 10yo

Females are at an increased risk of ATH, no predilection in PDH.

Risk factors for PDH - affected dogs generally weigh less than 20kg. Breeds include poodles, dachshunds, terriers and beagles.

Risk factors for ATH - have a tendancy to weigh more than 20%. Breeds include poodles, german shepherds, labs and dachshunds.

No - patients are rarely acutely ill and will present for chronic illness with slowly progressive clinical signs.

PU
PD
Polyphagia
Pot-bellied appearance

Primary polyuria occurs due to excess cortisol interfering with the action of ADH on the CD leading to diuresis and secondary polydipsia

Direct metabolic effect of glucocorticoids and the anti-insulin effect.

Redistribution of abdominal fat and abdominal muscle wasting.
Lethargy is also common and occurs due to muscle weakness and wasting.

DJD - due to presence of anti-inflammatory levels of corticosteroids. Cruciate ligament rupture can occur.

Bilaterally symmetrical alopecia
Pruritis isn't a feature of Cushings
Thin skin, pyoderma, seborrhoea and demodicosis
Bruising
Calcinosis cutis

Hypertension
UTIs
Pyelonephritis
Urinary calculi
Pulmonary thromboembolism
DM
Pituitary macroadenoma

Volume retention via hypernatremia (inc. mineralocorticoids), activation of renin-angiotensin system and decreased synthesis of vasodilatory prostaglandins.

Immunosuppression and low USG allowing microbrial proliferation.

Increased urinary Ca excretion.

Hypercoagulable state
Vascular fragility and exposure of subendothelial collagen, increase in certain clotting factors and a decrease in antithrombin III.

Dullness
Obtundation
Ataxia
Tetraparesis
Nystagmus
Circling
Head pressing
Blindness

Stress leukogram with thrombocytosis
Increased liver enzymes (due to hepatocellular damage and direct effect of cortisol on ALP isoenzyme)
Decreased BUN d/t diuresis
Hyperglycaemia
Hypercholesterolaemia
Lipaemia
Low USG
+/- glucosuria
proteinuria
+/- Ca oxalate crystals

Hepatomegaly
Osteopenia
Enlarged bladder
Dystrophic mineralization
Calcified adrenal mass
Mass effect
Presence of mets (with adrenal adenocarcinoma)
Presence of pulmonary thromboembolic disease

PDH will demonstrate bilaterally symmetrical adrenomegaly +/- nodular hyperplasia

ATH will demonstrate unilateral adrenomegaly +/- invasion of local structures such as liver, kidney and great vessels.

ACTH stim
LDDS
Urine cortisol:creatinine
Combined ACTH stim/dex suppression test

LDDS
HDDS
Combine ACTH stim/dex suppression test
Endogenous ACTH assay
Imaging of pituitary/adrenals

Quick and easy
Preferred test for patients with concurrent non-adrenal disease
Can diagnose iatrogenic Cushings
Most specific

550nmol/L is suspicious - LDDS should be run for borderline results. 650nmol/L is diagnostic for Cushings.

80% of PDH
60% of ATH
30% of iatrogenic

Chronic, non-adrenal disease may produce a false positive

Can be used as a confirmatory and discriminatory test for Cushings
More sensitive than ACTH stim but is more likely to be affected by non-adrenal disease

No suppression what-so-ever = straight line = either ATH or the small percentage of PDH which fail to suppress

ie a flat line isn't diagnostic for ATH but DOES INDICATE CUSHINGS

"Suppress-and-escape" = cup shaped line = majority of PDH

HDDS - dogs with PDH should suppress at higher dex concentrations.

Additional imaging diagnostics can also be employed.

To RULE OUT Cushings

Medicine

Medicine is the treatment of choice when there is:
tumor invasion of the great vessels
evidence of mets
unacceptable surgical risk

Medicinal treatment can be used to decrease surgical risk for patients where that is an option.

Mitotane
Trilostane
L-Deprenyl
Ketaconazole

Adrenocorticolytic drug which leads to progressive necrosis of the zona fasiculata and reticularis.

Prior to therapy client must record appetite and water intake. Feed one third of the normal food twice daily commencing the day before the first mitotane dose.
An initial loading dose during the induction phase of 30-50mg/kg/day is dispensed.
Dispense prednisone and instruct owner to give only in the advent of pred toxicity.
Have the owner bring the patient back for ACTH stim test in 5-7 days or earlier if decreased water consumption/appetite.

Pre and post stim cortisol should be in basal reference range.

50mg/kg/WEEK divided into 4 treatments to prevent the GI signs associated with large mitotane doses. ACTH stim every 3 months to evaluate control.

PDH about a year
ATH 20-29 months

Decreased appetite/anorexia
Decreased water consumption (less than 40mL/kg/day)
Vomiting
Diarrhoea
Lethargy
Weakness

Competitive inhibitor of an enzyme in cortisol synthesis.

Good response in PDH dogs
Generally few side effects, but all dogs develop adrenomegaly
Can be sourced from human pharmacies in NZ but there's not an animal formulation licensed.

Adrenal necrosis and Addisons may occur at any stage during therapy

Irreversible inhibitor of monoamine oxidase type B which increase dopaminergic tone in the brain. This decreases ACTH secretion

Generally not recommended - variability in the results of clinical trials. Not indicated for the treatment of ATH, and generally a poor response seen with PDH.

Hypophysectomy - not a viable option as requires enormous technical skill.
Bilateral adrenalectomy - provides a cure for PDH but medical therapy is easily accomplished so use is debatable. Necessitates treatment for Addisons.

Bilateral adrenalectomy - excellent prognosis for adenoma, good prognosis for non-invasive carcinoma. Survival post surgery 18-36 months.

A patient should not be treated for Cushings if there aren't any clinical signs consistent with the disorder.

Clinical condition which results from inadequate production and release of T4 and T3.

Primary occurs as a result of problems with the thyroid gland such as lymphocytic thyroiditis, idiopathic atrophy, neoplastic destruction, follicular cell hyperplasia or iatrogenic causes

Secondary occurs from impaired secretion of TSH from the pituitary as a result of neoplasia or suppression of TSH by glucocorticoids.

Tertiary hypoT hasn't been documented, congenital hypothyroidism is quite rare in small animals.

Relatively common endocrine disease of dogs. Predisposed breeds include dobermans, golden retrievers, labs, cocker spaniels, dachshunds and poodles.
No sex predilection, most common in middle aged to older dogs - mean of 7yo.

Tend to be vague, diffuse, gradual and aren't pathognomonic for any disease. Clinical signs may vary between the breeds due to different hair cycles - dermatological and metabolic signs generally predominate in most cases.

Lethargy, dullness, inactivity, weight gain, cold intolerance
Bilaterally symmetrical alopecia, dry scaly skin, course coat, puppy coat, hyperpigmentation, seborrhoea, pyoderma
Weakness, ataxia
Bradycardia

Mild normocytic, normochromic nonregenerative anaemia
Hypercholesterolaemia

Measurement of total T4 and free T4 in conjunction with TSH concentration

Consider havine a test run for lymphocytic thyroiditis or testing for thyroglobulin antibodies.

0.02mg/kg PO q12h using name brand levothyroxine. Start patients with cardiovascular disease on 1/2 dose.

T4 levels checked 4 weeks after start of therapy. Pre-pill level recommended for those animals on once daily. Serum sample 4-6 hours post pill is submitted for analysis. T4 levels should be monitored during the first 8 months every 6-8 weeks.

Increased serum T3 and T4, which in cats is most commonly due to benign adenomatous hyperplasia, with 2% due to thyroid carcinomas.

Age range 4-22, but mean age around 13yo.
Siamese and Himalayan are at decreased risk - no other breed predilection. Neither sex is predisposed.

Weight loss
PU/PD
Polyphagia
Hyperactivity
GI disease
Tachycardia
Tachypnoea/panting

Mild/moderate erythrocytosis in early phase of the disease
Macrocytosis
Heinz bodies
Stress leukogram
Normocytic, normochromic non-regenerative anaemia may occur in chronic cases due to bone marrow exhaustion or iron deficiency
Increased liver enzymes
Increased phosphorous +/- azotemia (inc. P can occur without azotemia)
Decreased creatinine
Hypocalcaemia

HyperT causes hypertension which protects the kidneys by maintaining GFR - thus renal failure patients may not be azotemic. So if an aged cat comes in with a low USG this could be due to renal failure or hyperT.

Is possible to measure GFR via nuclear scintigraphy or iohexol clearance

Fundic examination to check for retinal haemorrhages/tortuous vessels.

Low body condition score
Tachycardia
Unkempt coat
Heart murmur/gallop rhythm
Restlessness
Agression
Signs of CHF
Ocular lesions due to hypertension
Ventroflexion of the head
Dehydration

Evaluate the cardiac silhouette/great vessels for signs of HCM, mets, lung pathology indicating heart failure

Echocardiography needed to confirm nature of cardiomyopathy

TT4 - cheap and picks up the majority of patients with hyperT.

Normal diurnal variation in T4 concentration - mildly hyperT cats may show up as 'normal' on the test

Non-thyroidal illness can suppress T4 into the reference range in mildly affected hyperT cats

Based on the uptake of radioactive iodine isotopes or technetium 99m as pertechnetate.
Radioactive compounds are concentrated in hyperplastic and neoplastic tissue regardless of location. Normal tissue is spared due to atrophy.

Provides a permanent cure - 96-98% effective
Determines benign vs. malignant disease
Destroys neoplastic ectopic tissue
Identifies metastatic disease
Procedure doesn't require anaesthesia
Owner doesn't need to pill the cat for the rest of its life

Quite expensive
Requires referral facilities (can't be done in general practice)
Not appropriate for patients which require daily medication for life-threatening conditions
Small percentage become hypothyroid
Small percentage initial treatment doesn't kill all of the hyperplastic/neoplastic tissue so retreatment required

TRH test and T3 suppression test.

5mg PO BID

Renal parameters and TT4 should be re-evaluated in 10-14 days. If TT4 is within reference range and renal parameters aren't increasing continue with current dose.
If renal parameters are up, decrease dose (will have to accept less control over T4 - recommended protocol for CRF patients)

Cheap
Effective in reducing clinical signs
Reversible
Small tablets
No anaesthesia or specialist facilities required

Monitoring (TT4 and CBC every 2-4 weeks for first 3 months then every 3-4 months) can be very expensive
Adverse GI signs associated with drug admin
Serious side effects include drug eruption, hepatotoxicity, thrombocytopenia, leucopenia
Need to pill a cat twice a day for the rest of its life
Not a permanent cure

Pretreatment with carbimazole to minimize complications
Thyroid scan recommended prior to surgery to identify unilateral, bilateral or ectopic disease

Relatively quick and simple
Permanent cure
Thyroid gland is easily accessible

Anaesthetic risk in elderly/compromised patients
Iatrogenic hypothyroidism
Iatrogenic hypoparathyroidism
Recurrent laryngeal nerve damage
Recurrence of hyperT if all neoplastic tissue isn't removed
Recurrence rate regardless of removal
Permanent cure

Water consumption of more than 100ml/kg/day

Urine production of more than 50ml/kg/day

Behavioural
Physiologic
CNS lesion
Hepatic encephalopathy
Hyperthyroidsim

Primary polyuria

Lack of ADH - central diabetes insipidus
Lack of response to ADH - nephrogenic diabetes insipidus
Osmotic diuresis

Congenital
CNS lesions
Idiopathic

Primary and secondary

Congenital defect in the mechanism which increases water permeability of tubules. Very rare

Consequence of dysfunctional ADH/receptor interactions, dysfunctional renal tubular cells or medullary solute washout.

E. coli endotoxin cause reversible renal tubular insensitivity to ADH

Infection/inflammation in the renal pelvis can destroy the counter current mechanism in the renal medulla. This results in isosthenuria, PU/PD and eventually renal failure.

Precise pathogenesis not understood but thought to occur through reduced medullary hypertonicity through impaired urea production by the liver.

Addisons = mineralocorticoid deficiency results in sodium loss and renal medullary solute washout

Cushings = interference with the action of ADH at the CD

Hypercalcaemia = Ca damages ADH receptors in the renal tubules

Hypokalaemia = reduces sensitivity to ADH

Increased medullary blood flow increases GFR.

DM
Addisons
Primary renal glucosuria

The ability to concentrate urine normally is reliant on the interaction between ADH, ADH-receptor and hypertonic medullary interstitium.
Interference with the synthesis, action or release of ADH, damage to the renal tubule or alterations in the medullary tonicity can cause hyposthenuria.

Advanced renal failure.

Addisons
Cushings
Diabetes insipidus
Early renal failure
Hypercalcaemia
Hypokalaemia
Primary liver disease
Primary polydipsia
Pyelonephritis
Pyometra

High ALP suggests Cushings or primary liver disease
High cholesterol is commonly high in Cushings patients
Serum bile acids can be used to evaluate liver function - but some Cushings patients will have mild elevations
Leucocytosis with left shift may occur in patients with pyometra or pyelonephritis
Inflammatory sediment or bacteruria consistent with pyelonephritis
Hyponatremi in conjunction with hyperkalaemia suggests Addisons
Proteinuria is common in patients with pyelonephritis, pyometra and Cushings

Ionized 55%
Protein-bound 35%
Complexed 10%

Ionized is the active form and is the most important in determining whether a patient is hypercalcaemic

The precise signalment depends on the aetiology - numerous conditions may cause hypercalcaemia.

PU/PD - acquired nephrogenic diabetes insipidus
Muscle weakness, vomiting, constipation, anorexia, brady cardia all due to decreased neural/muscular excitability
Depression, coma, seizures
Urolith formation

Renal failure can cause hypercalcaemia and hypercalcaemia can cause renal failure.

Hypercalcaemia causes polydipsia, vomiting and anorexia. This results in dehydration, renal vasoconstriction (in an effort to preserve perfusion pressure) and a decrease in GFR. Ca deposition in the kidneys leads to tubular mineralization, degeneration and necrosis.

Renal failure
Tissue mineralization
Bone resorption/FOD

HOGS IN YARD
Hyperparathyroidism
Osteolytic
Granulomatous
Spurious
Idiopathic (cats only)
Neoplastic
Young, growing animal
Addisons
Renal Disease
D-vitamin D toxicosis

Cancer, CANCER, CANCER

Lymphosarcoma (leukaemia, plasma cell myeloma)
Apocrine gland adenocarcinoma of anal sac origin
Carcinomas (mammary, nasal, SCC, pulmonary, thyroid, nasal)

Renal failure, neoplasia and idiopathic.

Young to middle aged cats with no obvious aetiology. Total and iCa are high, low to normal PTH with normal phosphorous and vitamin D.
Non-azotaemic but frequently have crystalluria

Potentially due to decreased renal Ca excretion, haemoconcentration and increased protein binding

Solitary adenoma in 85-90% of cases
Hyperplasia or carcinoma in 15% of cases

Neoplastic/hyperplastic tissue fails to respond to normal regulatory factors.

10-20% of cases - clinical signs are associated with renal failure as hypercalcaemia isn't the primary disease process.

Confirm that the patient is indeed hypercalcaemic - ensure a fasted, non-lipaemic and non-haemolysed sample

Evaluate iCa (not just total calcium), phosphorous, degree of azotaemia.

Renal parameters up may indicate renal secondary hyperparathyroidism.

Hyponatraemia/hyperkalaemia may indicate Addisons = do an ACTH stim test

PTH, PTHrp and vitamin D assay to determine if there is primary hyperparathyroidism, hypercalcaemia of malignancy or vitamin D toxicosis

a) low-normal
b) high-normal

Thorough neoplasia hunt - repeat lymph node, anal gland and mammary gland palpation.

Thoracic and abdominal rads, ultrasound

Lymph node, liver, bone marrow and spleen biopsies

Precise nature depends on the cause (ie vitamin D toxicosis vs. malignancy).

Always treat the primary problem and provide symptomatic care:
-saline diuresis
-+/-potassium supplementation where appropriate
-furosemide once fluid deficit is corrected to increase Ca excretion. DON'T use thiazides
-+/-glucocorticoids. DON'T give if lymphoma is suspected or prior to ACTH stim test
-phosphonates

Bleeding due to lesions in the urogenital tract
Clotting factor deficiency
Thrombocytopenia

Prostate or bladder trigone.

Perhaps a genital lesion.

Bilirubin
Porphyrins
Drugs
Dyes etc

Urine sediement.

Haematuria/myoglobinuria.

+/- thrombocytopenia
Azotemia in patients with bilateral renal disease
+/- crystaluria in patients with urolithiasis
+/- inflammatory leukogram in patients with UTI (also +/- bacteruria)

+/- blood transfusion if animal is severely anaemic
Crystalloids for dehydration
Antibiotics for UTI
Heparin for DIC (causing thrombocytopenia)

40 mL/kg/day in cats
60 mL/kg/day in dogs

Greater than 100 mL/kg/day is considered PD

Renal/hepatic failure/insufficiency
Cushings
Addisons
HyperT
HyperCa
HypoK
Diabetes mellitus
Primary renal glucosuria
Post-obstructive diuresis
Pyometra/pyelonephritis

Renal failure, DM, hyperT, hepatic failure, pyometra/pyelonephritis and malignancy-induced hypercalcaemia.

DM, hyperT and Cushings

Elevation of non-protein nitrogenous waste in the blood.

Clinical signs due to azotaemia.

Pre renal
Renal
Post renal

Anything which elevates BUN/creatinine prior to metabolism in the kidney.

Increased protein in the diet
GI bleeding
Accelerated catabolism of endogenous protein
Decreased GFR

ARF or CRF

Urinary tract obstruction
Bladder rupture

Obtain initial blood work and urinalysis
Estimate degree of dehydration
Rehydrate the patient over 4-12 hours
Monitor hydration status, urine output, body weight, PCV/TS
Repeat bloodwork after 24-48 hours.

Degree of dehydration was underestimated
Ongoing losses

Renal or post renal component

First correct live-threatening metabolic derangements

Relieve urinary obstruction or repair bladder

Anticipate post obstruction diuresis and treat/monitor accordingly

Urine:serum creatinine
More than 20:1 with pre renal
Less than 10:1 with ARF

The onset of clinical signs with ARF are quick, generally no weight loss or anaemia, kidneys are enlarged and electrolytes are markedly abnormal (high K)

Clinical signs associated with CRF are insidious in onset, associated with weightloss, kidneys are small/nobbly, anaemic with mildly abnormal electrolytes (relatively normal K)
Parathyroid glands are enlarged compared to ARF.

Depression
Anorexia
Vomiting/diarrhoea
Dehydration
Uraemic odor on breath
Really big or really small kidneys
PU/PD or oliguria/anuria
Uraemic stomatitis
Hypertension

Ishcaemic
Toxic
Infectious
Obstructive

Kidneys receive 20% of CO - delivery of toxins is increased
Proximal tubules and thick ascending loop of Henle receive majority of renal blood flow and are even more susceptible due to their transport functions and high metabolic rate.

Resorption of water electrolytes from the glomerular filtrate may increase toxin exposure, as well as the countercurrent system may concentrate toxins

Hyperkalaemia leads to a decreased potassium concentration across myocytes - this reduces the membrane potential and makes the cell more excitable.

Direct effect of uraemic toxins on the CNS causing lethargy, coma and seizures.

Direct necrosis of GI mucosae as well as causing a necrotising vasculitis, thrombosis and thus ischaemic damage.

Anaemia of ARF isn't due to decreased EPO - time course isn't long enough for this to occur. Anaemia occurs due to haemorrhage due to the uraemic thrombocytophathy (uraemic toxins inhibit the release of PF3 and thus cannot form a functional haemostatic plug).
Vasculopathy occurs as a result of necrotising vasculitis.

Acidosis, hyperkalaemia and hyperphosphataemia due to the kidneys no longer being able to excrete hydrogen ions, potassium and phosphate.

Tubular obstruction
Back leaking of urine
Renal vasoconstriction
Decreased glomerular permeability
Or mixtures of the above

Identify underlying cause
Prevent further exposure to toxins/cause
Establish and maintain haemodynamic stability
Provide fluids
Correct metabolic derangements
Provide nutritional support

Establish degree of dehydration. Assume 5% dehydrated if no clinical signs of dehydration. Use 0.9% saline or LRS. Rehydrate over 4-8 hours, then give 2x maintenance. If fluids don't take care of the acidosis, administer Nabicarb.

Monitor hydration status, urine output, body weight, PCV/TS. Urine output should be more than 1 mL/kg/hour

Once rehydrated, use mannitol, 10-20% dextrose or furosemide to induce diuresis.

Optimise renal perfusions using dopamine infusion

Use antiemetics where appropriate - metoclopramide, chlorpromazine or mariopitant.

H2 receptor antagonists - cimetidine, ranitidine

Gastric protectants eg sucralfate

Yes - 70-100 cal/kg/day

Can occur as a progressive condition as a result of ARF or due to idiopathic causes that result in a loss of a critical number of nephrons and the self-perpetuation of renal failure. Many times the exact cause is impossible to determine - even with biopsy. Histo changes are generally non-specific, but primary glomerular disorders are thought to be a leading cause.

Renal lymphoma

Mean age of FeLV + cats 3 yo
Mean age of FeLV - cats 7 yo
Approx half of renal lymphoma cases are FeLV+.
Kidneys are enlarged and may be smooth or irregular.

Dx made by radiographs/US
FNA of kidneys

NSAIDs are COX inhibitors and thus reduce the production of prostaglandins. Prostaglandins are involved in a number of pathways in the body - vasodilatory prostaglandins play a role in maintaining perfusion to the kidneys in response to hypovolaemia.

HyperCa of malignancy
Hypervitaminosis D
Renal failure
Primary hyperparathyroidism

Lhasa apso, chow chow, Shi tzu

Himalayans
Persians

Shar pei
Abyssinian

English cocker spaniels
Soft-coated Wheaton terriers
Samoyeds

Non regenerative anaemia
Azotaemia
Hyperphosphatemia
Hypokalaemia
Acidosis
Inc. or dec. calcium

NEPHRON

Important to maintain body condition and prevent protein catabolism. Oesophageal feeding tubes may be helpful.

Low protein, low phosphorous diet. Phosphate binders may be useful

Omega-3 in the ration decreases intraglomerular hypertension, lipaemia, increases GFR and vasodilatory PGs and reduces inflammation

Anitemetics, H2 blockers, proton pump inhibitors and sucralfate where indicated

Hypokalaemia is common in cats with CRF.

RMP is increased - cell membrane is less sensitive to stimuli.
Clinical signs include:
ventroflexion of neck
stiff, stilted gait
generalized weakness
anorexia

Renal diets usually have Kcitrate added. Otherwise oral supplementation with KCl or Kgluconate

Metabolic acidosis is common.
Due to decreased hydrogen ion excretion, bicarb wasting and chloride retention, decreased filtration of phosphate and increased protein catabolism.

Anorexia, hypokalaemia, and muscle weakness. Metabolic acidosis causes a shift of potassium into the extracellular space which can then be vomited out.

Decrease signs of uraemic acidosis
Decreases protein catabolism due to acidosis.
Limits demineralization via buffering
Minimises adverse effects of acidosis on the cardiovascular system

Low protein diets reduce the production of organic acids.
Many renal diets have Kcitrate to act as an alkalinizer
Administer Nabicarb if bicarbonate is less than 15mmol/L. Issues with Na retention worsening hypertension.

Provide constant access to water. Add low-Na broth if they'd like it.
SQ fluids 75-150mL q24-72 hours using low Na or LRS

Kidneys are unable to eliminate nitrogenous waste - low protein diet.
High soluble fibre in the diet promotes bacterial proliferation which requires nitrogen

Avoid at all costs:
Hypotension, dehydration and hypovolaemia
Nephrotoxic meds
UTI

Anaemia occurs due to dec. EPO and blood loss through uraemic gastritis.
Fix by providing excellent nutrition, minimizing losses and giving transfusion if necessary.
+/- various forms of EPO and EPO analogues

Used to minimise the effects of the condition
Prevents tissue mineralization

Extensive monitoring required, hyperCa common

Dec GFR leads to activation of the RAS and Na retention.

Blindness
Cardiomyopathy
Proteinuria
Seizures
Progressive glomerular disease

Na restriction
ACE inhibitors produce systemic vasodilation but also selectively dilate the renal efferent arteriole
Ca channel blockers are associated with fewer side effects

Leads to proteinuria in conjunction with the existing disease process and chronic inflammation.
Proteinuria is very bad because in itself leads to more progressive renal disease

Pre renal
Renal
Post renal

Colorimetric, and mainly pick up albumin - ie don't pick up Bence Jones proteins

Prolonged contact
Contamination
Alkaluria

Dilute urine
Aciduria
Abnormal proteins

Urine sediment exam

24hr urinary protein
UPC
Microabluminuria

Quick and convenient.

Doesn't localize the proteinuria
Influenced by haemorrhage, inflammation/infection
Doesn't differentiate between the causes of glomerular disease

Immune mediated and non-immune mediated glomerulopathies

Immune mediated and non-immune mediated amyloidosis

Any infectious, inflammatory, parasitic, neoplastic, or degenerative disease process that results in sustained antigenic stimulation can lead to subsequent immune-mediated glomerular damage

Familial
• Neoplastic
– LSA, MCT
• Infectious
– ICH, brucella,
leishmania
– heartworms heartworms, ,
Ehrlichia, RMSF RMSF, ,
fungal, FIP, FeLV
• Inflammatory
– SLE SLE, , pancreatitis,
chronic pyoderma,
chronic otitis externa externa, ,
polyarthritis
• Miscellaneous
– Cushing Cushing’s, DM, , chronic
steroids steroids, systemic
, arterial hypertension,
idiopathic

Immune complexes lodge in basement membrane of glomerulus and activate complement. This leads to neutrophil chemotaxis and production of inflammatory mediators which produce glomerular damage.

Membranous
Proliferative
Membranoproliferative

Familial (Dobermans) or disease processes which produce intraglomerular hypertension such as
- Cushing’s
– Chronic glucocorticoids
– Diabetes mellitus
– Systemic arterial hypertension
– Renal failure

Excess serum amyloid A accumulates as beta pleated fibrils in the extracellular matrix of various tissues througout the body - notably the kidney. Uniformly progressive and results in renal failure. Can be primary or secondary.

Usually in the glomerulus, although in certain familial amyloidosis deposition is in the tubulointerstitium without glomerular involvement.

Tubulointerstitium

Shar peis and Abyssinian cats.
Onset generally less than 5yo with variable disease progression.

Lugol's iodine and Congo Red

Often none, but...
PU/PD
Weight loss
Lethargy
Thromboembolism (lameness/respiratory distress)
Hypoalbuminaemia (oedema/ascites)
Systemic arterial hypertension

1) Treat underlying cause
2)Dietary management
3)ACE inhibitor
4)NSAID’s
5)Omega-3 fatty acids
6)Immunosuppressive drugs
7)Diuretics

Renal failure diet - low protein and sodium but calorically dense with lots of vitamins/minerals and fish oil.

They dilate efferent arteriole, decreasing intraglomerular pressure which decreases proteinuria. BUT also decreases GFR which may worsen azotemia.
Possibly use specific anti-hypertensives such as amlodipine

Aspirin 0.25-0.5 mg/kg PO q12-24hr inhibits platelet activation without causing
vasoconstriction or decreased renal
medullary perfusion.
Decrease dose with hypoalbuminaemia.

Anti-inflammatory

Lower urinary tract infection
and urethral obstruction

Bacterial infections
iFLUTD
Cystic calculi
Bladder/urethral neoplasia

Urolithiasis
iFLUTD causing mucus plug formation
Neoplasia
Functional obstruction

Pass a catheter.

Palpate bladder
Rectal exam before and after urine voiding to feel for calculi, masses
Urine sample via cystocentesis for UA
+/- imaging

Old femal dogs

E.col, Staph, Strep, Proteus, Klebsiella, Pseudomonas and Enterobacter

May be mixed infection. Infection almost exclusively aerobes that ascend urethra

Diseases which cause urine stasis or incomplete emptying of the bladder
Diseases which act as a nidus of infection (vaginitis, calculi, neoplasis)
Diseases which produce systemic immunosuppression (DM, Cushings, systemic neoplasia, chemotherapy, inherited immunodeficiency etc etc)

Stranguria
Pollakiuria
Haematuria
Inappropriate urination

Fever
Anorexia
Signs of uraemia

Cystocentesis with a urine sediment to check for pyuria/bacteruria

C & S

CBC/biochem would indicate an inflammatory leukogram and azotemia

UA would indicate pyuria/bacteruria/haematuria
+/- leukocyte casts

Radiography and US

Offer the client C & S - choose Ab based on results.
If client won't allow C & S choose Ab based on the sediment exam/most likely species involved - good choices include amoxycillin-clavulanic acid
DON'T use aminoglycosides

Treat lower UTIs for 14 days and upper for 4-8 weeks. Check urine a week after treatment cessation to ensure resolution.

Fever
Anorexia
Signs of uraemia

Dysuria
Pollakiuria
Haematuria

Dysuria
Stranguria
Anuria
Abdominal discomfort
Signs of uraemia

Magnesium ammonium phosphate

Chalky yellow/white-ish. Radiopaque

Less

Urine must be super-saturated with struvite to allow precipitation and thus urolithiasis. A number of processes result in super-saturation of struvite including infection with urease-producing bacteria, alkaline urine, genetic predisposition and diet.

Yes

Generally not infected.

Use Abs to treat the UTI
Calculolytic diet - Hill's s/d. May take quite some time - monitor every 4-6 weeks and feed diet 4 weeks post resolution

Use Abs to treat any UTI prior to surgery. Culture any that are apparently sterile. Any that are apparently sterile should be maintained on Hill's c/d or equivalent.

Monitor all cases for reccurence

Protein restrictive diet
Constant UTI watch
Encourage plenty of water intake

White/cream quartz-like appearance.
Radiopaque

Hypercalciuria
Increased urinary oxalate
Decreased urinary citrate
Acidic urine

Older male cats and dogs

No

Surgical removal and correction of underlying cause of hypercalcuria (NB steroids and furosemide)
Avoid high Na foods
+/- oral Kcitrate (alkalinizer and chelates Ca)
+/- thiazides (promotes Ca excretion)

Yes

Radiopaque

Dalmations and English bulldogs

Impaired conversion of uric acid to allantoin causes hight conc. of uric acid in serum and urine.

This may be due to a genetic defect, PSS or liver failure.
Urease producing UTIs predispose by increasing available ammonia.

Cystotomy, urethrotomy or nephrotomy to remove stone.
PSS ligation if necessary.

Treat any UTIs promptly
Low purine diet (Hill's u/d + salt or Hill's s/d + alkali)
Allopurinol (decreases the formation of uric acid from precursor compounds)

Generally small, yellow and easily crushed. Often radiolucent.

Formed in acid urine

Defect in cystine resorption

Low protein diet such as Hill's u/d (alkalinises the urine and reduces renal cystine concentrating ability)

Nabicarb or potassium citrate to alkalinise the urine

Males - dachshund, English bulldog, staffies and Welsh corgis

MPG
Forms disulphide bond with cysteine, leads to a soluble
product
5-10 mg/kg q12h

D-penicillamine
– Forms a disulphide bond with cysteine to form a soluble
product
Reduces conversion of cysteine to cystine
Dosage 15 mg/kg q12h

Cats 1-5yo, equally affects males and females

Dysuria
Pollakiuria
Haematuria
Inappropriate urination
Licking the penis/vulva

The above signs as well as post renal azotemia, hyperphosphatemia and hyperkalaemia
Enlarged, turgid and painful bladder

Clinical signs and CBC finding (haematuria)

C & S
Radiography
US

Tincture of time for first occurence cases
Abs only indicated if infection is documented

Recurrent bouts should be treated according to the underlying disease mechanism (if known) - otherwise treat as idiopathic

Propantheline or amitriptyline

Relieve the obstruction
Place a catheter, relieve the bladder and thoroughly lavage
Surgery may be indicated
Manage post-obstructive diuresis

Feed wet food/encourage water consumption - flushing action of increased urine output reduces the concentration of toxins, inflammatory mediators or whatever it is that causes this disease
Likewise encourage regular and frequent urination to get rid of nasties in the urine

Old intact male dogs

Tenesmus
Dysuria
Urinary incontinence
Urethral discharge - purulent etc
Abdominal distension
Stiff gait
Painful caudal abdomen
Fever, depression

Often none, but....
Bloody urethral discharge
Haematuria
Tenesmus
Ribbon-like stools
Dysuria

Symmetrically enlarged non-painful prostate

Castration or finasteride

Lethargy/depression
Anorexia
Tenesmus
Dysuria
Pyrexia
Painful caudal abdomen/prostate
Prostate normal/enlarged

Inflammatory leukogram or neutropenia (due to enormous neutrophil requirement)
Haematuria
Pyuria
Bacteruria
Findings may indicate a UTI but this isn't the case

Prostatic lavage or ejaculation and fluid analysis and culture

E. coli, Staph, Strep, Proteus, Klebsiella, Enterobacter, Pseudomonas

Variably sized, symmetrical prostate which is firm and generally not painful
UA may demonstrate findings similar to UTI
Prostatic fluid is positive on culture
Prostatic biopsy indicates chronic inflammation

21 days

Reculture approx a week after treatment has started to ensure it's working.
Reculture one month or so after therapy to ensure no reinfection.

Yes

Good gram negative spectrum
Issues with penetration into the prostate (blood-prostate barrier)
Ideally want a bacteriocidal one for acute prostatitis, this isn't as big of a concern with chronic prostatitis.
Fluoroquinolones
Trimethoprim sulfa
Cephalosporin

Enlarged, assymetric prostate

Neutrophilic leukocytosis

Infected prostate acts as a nidus of infection which then gets into the bladder.

Massage and biopsies-may rupture the abscess leading to septic peritonitis.

Antibiotics following similar protocol as to that for prostatitis.
Surgery to lance and drain the abscess.
Castration

Intraprostatic with BPH
Retention
Paraprostatic

Assymetric fluctuant prostate or a separate mass with paraprostatic cysts.

Radiography may indicate prostatomegaly. US may indicate fluid-filled structures.

Surgical drainage/excision
Castration

Adenocarcinoma
TCC

Dysuria
Rear limb weakness
Weight loss
Uraemic signs associated with renal failure

Assymetrically enlarged prostate which may be painful

Lumbar vertebral osteolysis

Mineralization of the prostate.

Inflammatory leukogram
Post renal azotaemia
UA-inflammation, UTI or neoplastic cells

Cytology or biopsy

Surgical excision is not usually undertaken-difficult to excise neoplasm without damaging the urethra
No proven protocl for chemotherapy and radiation has variable results.
Castration may have a palliative effect

Neurogenic
Non-neurogenic

UMN dz
LMN dz
Detrusor-urethral dyssnergia

Hormone responsive incontinence
Stress
Urge incontinence
Ectopic ureters

Hypogastric nerve L1-4

Beta receptros

Suppression of contraction of the detrusor ie bladder RELAXATION

Alpha receptors

Contraction of the internal sphincter

Sympathetic

Pudendal nerve S1-3

Cholinergic receptors located in the external sphincter

Contraction of the sphincter to maintain contenance - predominates during storage/filling of the bladder

Pelvic nerve S1-3

Cholinergic receptors located in the body of the bladder.

Contraction of the detrusor and voiding of bladder

Puppy excitement
Submissive behaviour
Inadequate house breaking
Kept inside too long

LMN
UMN
Detrusor-urethral dyssynergia
Partial obstruction

ie there is something stopping that bladder being expressed

Hormone-relate
Urge incontinence
Congenital

ie there is something stopping that bladder from filling properly

Spinal cord segments or pelvic nerve

Detrusor and sphincter areflexia.

Large, easily expressed bladder
Overflow incontinence
Loss of other reflexes

Manually express the bladder
Bethanecol (parasympathomimetic)

Above the spinal cord somewhere in the CNS.

Incomplete detrusor contraction
Spasticity of the urethral sphincter

Large, turgid bladder which is difficult to express
Unable to urinate
Concomitant pareisis/paralysis

No pharmacological therapy is able to be used-daily expression of the bladder required.

The contraction of the bladder isn't co-ordinated with the relaxation of the sphincter to enable micturition.

Reticulospinal tract or caudal mesenteric ganglion.

Initiation of voiding followed by abrupt cessation of urine stream
Large non-expressable bladder
Bladder easily catheterized

Treatment is targeted at the sphinters.
Either alpha blockers to prevent continual contraction eg oxybutin chloride and propantheline
OR muscle relaxants eg diazepam and dantrolene

Hormones upregulate the number of adrenergic receptors in the urethral sphincter and enhance urethral defence mechanisms.
Pathogenesis is most likely multifactorial

Usually older spayed bitches, although can occur in male dogs.
Often associated with early spaying with the development of intermittent incontinence subsequently.
+/- UTI

Oestrogens and phenylpropranolamine in female dogs

Testosterone and phenylpropranolamine in males.

Intermittent incontinence when the animal is at rest or stressed, but still maintains a degree of voluntary urination.
UTIs aren't a feature of the disease

Intra-pelvic bladder and tortuous urethra.

Phenylpropranolamine and ephedrine

Separation of tight junctions between the cells in the detrusor muscle from a functional or mechanical obstruction. Excessive sympathetic stimulation

Large flaccid bladder
Intact reflexes
Large residual urine volumes

Indwelling urinary catheter
Cholinergic agonists - bethanecol
Alpha adrenergic blockers - prazosin