VMD-421

HYPOTHYROIDISM AND DIABETES IN DOGS

HYPOTHYROIDISM AND DIABETES IN DOGS

Learning objectives

 To study the etiology, pathogenesis, clinical signs, diagnosis, treatment and

control of hypothyroidism in dogs
 To know about the etio-pathogenesis, clinical signs, diagnosis, treatment and
control of Diabetes mellitus and Diabetes insipidus.

DEFINITION ETIO-PATHOGENESIS AND EPIDEMIOLOGY OF

HYPOTHYROIDISM

Definition

 Hypothyroidism is the result of decreased production of thyroxine (T 4) and

Triiodothyronine (T3) by the thyroid gland.

Etio-pathogenesis

 Hypothyroidism may result from dysfunction of any part of the hypothalamic –

pituitary – thyroid axis.
 Primary acquired canine hypothyroidism is due to lymphocytic thyroiditis.
 In idiopathic follicular atropy, there is loss of thyroid parenchyma and
replacement by adipose connective tissue.
 Less commonly, hypothyroidism is caused by bilateral thyroid neoplasia.
 Secondary hypothyroidism (deficiency of TSH) is rarely described in dogs. Causes
of acquired secondary hypothyroidism include pituitary malformations and
pituitary neoplasia.
 Tertiary Hypothyroidism (deficiency of TRH) is yet to be documented in the dog.
 Congenital hypothyroidism (cretinism) is rarely diagnosed in dogs.
 Congenital primary hypothyroidism includes iodine deficiency, thyroid
dysgenesis and dyshormonogenesis.
 Secondary congenital hypothyroidism due to apparent isolated TSH or TRH
deficiency was reported in a family of young giant schnangers and in a young
boxer.
 Iatrogenic causes of hypothyroidism include iodine treatment, administration of
anti-thyroid drugs and surgical thyroidectomy.

Epidemiology

 The reported prevalence of canine hypothyroidism is from 0.2% to 0.8%. Mean

age at diagnosis is 7 years, with range of 0.5 to 15 years. Golden retrievers and

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 Doberman pinschers are among the breeds reported to be at higher risk for
hypothyroidism.
 In one study, Neutered males and females were reported to be at increased risk
for developing hypothyroidism compared with sexually intact animals.

CLINICAL SIGNS AND CLINICO-PATHOLOGICAL CHANGES OF

HYPOTHYROIDISM

Clinical signs

 Clinical signs of hypothyroidism may be non-specific and insidious in onset.

Common clinical signs attributable to decreased metabolic rate include lethargy,
mental dullness, weight gain, unwillingness to exercise and cold intolerance.
Obesity occurs in approximately 40% of hypothyroid dogs.

Dermatological changes

 Dermatologic changes occur in 60% to 80% of hypothyroid dogs. Common

findings include dry scaly skin, changes in hair coat quality or color, alopecia,
seborrhea and superficial pyoderma. Hyperkeratosis, hyperpigmentation,
comedone formation, hypertrichosis, ceruminous otitis, poor wound healing,
increased bruising and myxedema may also occur.
 Alopecia is usually bilaterally symmetric and is first evident in areas of wear and
tear such as the lateral trunk, ventral thorax and tail. The hair is often brittle,
easily epilated and loss of under-coat may result in a coarse appearance or puppy
– like hair coat.
 Signs of decreased metabolic rate in conjunction with dermatologic abnormalities
should increase suspicion of hypothyroidism.
 Hypothyroid dogs are predisposed to recurrent bacterial infections of the skin
such as folliculitis, pyoderma and furunculosis.
 Malassezia spp infections and demodicosis are associated with hypothyroidism.
Pruritus may occur with concurrent infection.

Reproductive abnormalities

 Female reproductive abnormalities attributed to hypothyroidism include

prolonged interestrous interval, silent estrus, failure to cycle, spontaneous
abortion, low-birth weight litters, uterine inertia and stillborn puppies.
 Inappropriate galactorrhea apparently due to hyperprolactinemia has been
reported in sexually intact hypothyroid bitches.
 Male reproductive problems attributed to hypothyroidism include low libido,
testicular atrophy, hypospermia and azoospermia.

Nervous system abnormalities

 Both the peripheral and central nervous systems may be affected by

hypothyroidism. Peripheral neuropathy is the best documented neurologic

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 manifestation. Affected dogs have exercise intolerance, weakness, ataxia,
paralysis, deficits of conscious proprioception and decreased spinal reflexes.
 Unilateral lameness reported in hypothyroid dogs may be a manifestation of
generalized neuromyopathy.
 Dysfunction of multiple cranial nerves and abnormal gait and postural reactions.
 In myxedema, coma, profound mental dullness or stupor is accompanied by non
pitting edema, hypothermia with a lack of shivering, bradycardia, weakness and
inappetence.
 Abnormalities of the cardiovascular system such as sinus bradycardia, weak apex
beat, low QRS voltages and inverted T waves occur in hypothyroid dogs. Reduced
left ventricular pump function has also been documented.
 Ocular abnormalities reported in canine hypothyroidism include corneal
lipidosis, corneal ulceration, uveitis, lipid effusion into the aqueous humor,
secondary glaucoma, lipemia, retinitis, retinal detachment and
keratoconjunctivitis sicca.
 Congenital hypothyroidism results in mental retardation and stunted
disproportionate growth due to epiphyseal dysgenesis and delayed skeletal
maturation. Affected dogs are mentally dull and have large broad heads, short
thick necks, short limbs, macroglossia, hypothermia, delayed dental eruption,
ataxia and abdominal distention. Dermatologic findings are similar to those seen
in the adult hypothyroid dog. Other clinical signs may include gait abnormalities,
stenotic ear canals, sealed eyelids and constipation.

Clinicopathologic changes

 Results of hemogram, biochemical panel and urinalysis often support a diagnosis

of hypothyroidism.
 A mild non regenerative anemia occurs in 30% of hypothyroid dogs
 Fasting hypercholesterolemia occurs in 75% of hypothyroid dogs where as
hypertriglyceridemia occurs in up to 88% cases
 In rare cases hyperlipidemia may lead to atherosclerosis.

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DIAGNOSIS AND TREATMENT OF HYPOTHYROIDISM

Diagnosis

 A complete history
 Physical examination
 Minimum data base: T4 concentration - 1.5 – 3.5 µg/dL; TSH response test ;
TRH response test
 Antithyroglobulin antibody is found in 36% to 50% of hypothyroid dogs.
 Thyroid biopsy

Treatment

 The initial treatment of choice regardless of the underlying cause of the disease is
synthetic sodium L-thyroxine (T4) 0.02 mg/kg P.O, every 12 hr
 In myxedema coma, T4 should be administered initially intravenously (5mg/kg)
because of poor gastrointestinal absorption due to hypo motility. Other
supportive therapy including appropriate fluid therapy, passive rewarming and
ventilatory support may also be necessary.

DIABETES INSIPIDUS

 A functional disturbance of the kidney (decreased tubular reabsorption) due to

pituitary dysfunction so that ADH is not secreted in adequate amount to control
water excretion, leading to watery urine, free from albumin and sugar.

Etiology

 More in horse especially stallion (Bed wetting).

 More in summer than in winter.
 Cats: Cancerous growth of pituitary and injuries to skull.
 Rare in farm animals.

Symptoms

 Polyuria: Horse 40 to 60 liters. Dog 3 to 4 liters.

o Urine: Watery with odour: Low sp. Gr. 1.001 to 1.002.
o In early: Easy voiding.
o In Late: Some what painful.
 Polydipsia: Horse 100 Liters; Dog 10-15 lit/day. When sufficient water not
available – Drink urine.
 Appetite – slowly decrease.
 Mucous membrane and skin – dry.
 Hair: dull and coarse.
 In Dogs: cataract, abscess in the perenial glands and prostate.
 Sooner or later emaciation.

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  Neglected cases: Absolute cachexia.

Differential diagnosis

 Diabetes mellitus.

Treatment

 Horse: Best food free from albumin and salt.

 Reduce water to 20-24 liter / day.
 Pitressin tannate in oil.

DIABETES MELLITUS

 Diabetes mellitus is a complex metabolic disorder as result of insufficient insulin

secretion or excessive insulin antagonism leading to wide aberrations in
carbohydrate, fat and protein metabolism with secondary disturbances in water
and electrolytes.

Insulin non-availability

 Degenerative changes in β cells in pancreatic islets.

 Reduced effectiveness of hormone due to anti-insulin antibodies or inactive
complex.
 Autoimmune mediated islets cytotoxicity.
 Inappropriate secretion of hormones by neoplasms in other organs.

Incidence

 1:200 total canine patients

 Spontaneous in mature dogs (8-9 yrs female more affected than male)
 Susceptibility: miniature Poodle, Dacshunds and Terriers.

Pathogenic mechanism

 Destruction of islet cells due to severe pancreatitis and subsequent replacement

by fibrous tissues. So, the gland becomes firm, multinodular and often has
scattered areas of haemorrhage and necrosis.
 Selective degeneration of Islet cells (more in cats): Stress, obesity, administration of
cortisol.

Causes

 Idiopathic atrophy
 Virus

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Clinical signs

 Onset is insidious – chronic.

 Polydipsia, polyuria, increased food consumption but loss of body weight.
 Bilateral cataract.
 In diabetes increased concentration of glucose in aqueous and vitreous humour.
So glucose penetrates into lens. There, it is metabolized into sorbitol and further
into fructose. The increased concentration in lens leads to entry of water into lens
fiber and causing swelling.
 Weakness.
 Diminished resistance to bacteria and fungal infection. So, recurrent or chronic
infection such as suppurative cystitis, prostatitis, Bronchopneumonia and
dermatitis.
 Hepatomegaly due to cirrhosis or accumulation of fat. Rough palpation leads to
intra abdominal haemorrhage.
 Chronic renal disease.
 Blindness due to microangiopathy.
 Gangrene.
 Ketone bodies accumulate in blood. Loss of sodium through urine – H+
conserved – so, acidosis leading to coma.

Laboratory diagnosis

 Glycosuria (urine more viscid, sweety odour & specific gravity increase.
 Fasting hyperglycemia - increases to 140 mg/ 100ml.
 Glucose tolerance test (GTT) (i/v or oral).
 Ketone in blood and urine and smell in respiratory tract.
 Elevated serum cholesterol and triglycerides.

Differential diagnosis

 Chronic nephritis: urine - Low specific gravity, increased protein, no sugar.

 Diabetes insipidus: Urine - low specific gravity which increase after the
administration of antidiuretic hormone.
 Pyometra: Polyuria, No glucose. Abdominal distension.
 Acute nephritis: Increased temperature, vomition, occasionally urine contains
sugar.
 Adreno cortical hyper function: Alopecia, hyperkeratosis.
 Prolonged steroid therapy.

Treatment

 Uncomplicated - Control hyperglycemia by insulin.

 Complicated - Correction of dehydration with plasma expanders, electrolyte
replacement.
 Infusion of bicarbonate to control acidosis.
 If hypokalemia , 'K' to be given.

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 For obese animal - no insulin.
 In milder cases - Soluble insulin- absorbed quickly, act within 20-30 minutes;
reach peak levels within 4 hrs and maintained at these levels for maximum of 8
hrs
 Protamine Zn insulin s/c : reach peak in 8-12 hrs and this level is maintained for
nearly 24-36 hrs
 Intermediate action: - Lente insulin, Globulin insulin and Isophan insulin. They
start acting in 4 hrs, reach peak in 8hrs and maintained for 18-26 hrs.
 NPH (Neutral Protamine Hagedorn) : 1 unit /kg in morning along with food.
 Stabilize the patient: To start with 2 units of soluble insulin + 2 units of other
types; then 4 + 4; then 6+6 units
 Check the urine daily.
 In advanced case – several hundred units i/v.
 Good grade of canned food and green vegetables + pancreatin – 2 tablet.
 Oral therapy – unsuccessful.