Clinical Signs:
Metabolic
Lethargy
Reproductive
Prolonged parturition
Hypothyroidism
Mental dullness Reduced fertility
Inactivity Low birth weight puppies Aetiology of Aquired Primary Hypothyroidism
Inappropriate weight gain Ophthamologic Lymphocytic thyroiditis
I.e. feed amount hasn’t changed but Corneal lipid deposits Idiopathic atrophy
they are suddenly putting on weight Cardiovascular Neoplastic destruction
Cold intolerance Bradycardia Miscellaneous
Dermatological Cardiac arrhythmias Iodine deficiency
Symmetrical alopecia Neurological Removal of the thyroid
Dry, brittle hair coat Vestibular signs Anti-thyroid medication, chronic TMPS
Pyoderma, otitis externa Polyneuropathy
Myxodema Facial nerve paralysis
Hyperpigmentation
Diagnosis:
Haematology
Non-regenerative anaemia (mild)
Biochemistry
Inappropriate weight gain
Fasting hypercholesterolemia “Rat tail” Myxoedema
Mild to moderate increase in ALT and ALKP
Total T4 Treatment
Low with hypothyroidism Sodium levothyroxine
Must interpret in conjunction with TSH, never on it’s own! Monitoring
TSH 6-8 wks after starting therapy
Expected to be high Measure TT4 and TSH 4-6hrs after medicine given
Can be normal in 40% of cases so do additional tests Improvement in clinical signs
Free T4 (fT4) by equilibrium dialysis Metabolic signs improve within days
Low TT4, normal TSH, low fT4 = hypothyroidism Dermatological signs improve within 4-6 weeks
Very expensive, hard to run and easy to do wrong Hair loss may worsen at first
Thyrogobulin antibiodies (TgAAs) Titrate dose up and down depending on findings
Positive result = presence of thyroiditis When stable recheck every 6 months
Negative = early hypothyroid OR end-stage lymphocytic thyroiditis
, Hyperthyroidism in Dogs - RARE
Associated with functional thyroid carcinoma Hyperthyroidism
Clinical presentation:
Aetiology
Mass in neck ⟶ metastasise to local LNs and pulmonary parenchyma
Mostly due to adenoma / adenomatous hyperplasia
Signs of hyperthryoidism similar to cats
Some are due to malignant thyroid carcinoma
Diagnosis
Cytology and Advanced Imaging
The Kidneys
TT4
Untreated hyperthyroidism state:
Treatment
Increased renal blood flow and GFR can make
Thyroidectomy for local disease
suboptimal renal function look normal
Radiotherapy
Protein catabolism so increased BUN
Loss of muscle mass meaning decreased creatinine
Clinical Signs Hyperthyroidism being treated
Weight loss and increased appetite (polyphagia) Renal blood flow and GFR fall back to normal levels
Behavioural changes True renal function unmasked
Polyuria and polydipsia May become azotemic if not already
Unkempt hair coat or hair loss
Gastrointestinal signs Treatment:
Vomiting, Diarrhoea Anti-thyroid drugs (long term)
Heat and stress intolerance Methimazole/thiamizole and carbimazole
Palpable thyroid goitre Inhibits thyroid peroxidase enzyme
Cardiac disturbances Iodine restricted diet
Tachycardia, gallop rhythm, heart murmur Markedly restricted iodine content
Systemic hypertension Must be the only food source!
Must not be given alongside anti-thyroid drugs
Diagnosis: Urinalysis Thyroidectomy
Haematology Decreased USG +/- glycosuria Curative +/- risk of reoccurance/complications
Erythrocytosis Thyroid Hormones Radioactive iodine
Heinz bodies on blood smear Elevated TT4 Gold standard
Mildly increased PCV Imaging Thyroid cells concentrate radioactive iodine
Biochemistry Schintigraphy Transported to thyroid follicular cells and
Increased liver enzymes Inject radionuclide iodine isotope incorporated into thyroglobin.
High ALT and ALKP Cardiac Assessment Beta ionising radiation occurs ⟶ follicular death
Azotaemia Echocardiography and ECG Hospitalised for a period of time as “radioactive”
, Hyperadrenocortisim (Cushings disease)
Cushings in Cats Pituitary dependent hyperadrenocorticsm
Most with pituitary dependent 80-85% of cases
Clinical signs Tumour of anterior pituitary gland causing autonomous production of ACTH
PU/PD/PP and pot belly Adrenal glands continually stimulated by ACTH leading to bilateral adrenal
Thin fragile skin that easily tears hyperplasia and chronic, excessive cortisol production
Diagnostics Despite high cortisol levels, ACTH secretion remains high as tumour keeps
Most have concurrent insulin resistant DM producing it
ACTHst or dexamethosine suppression test Adrenal dependent hyperadrenocorticism
15-20% of cases
Diagnosis: Tumour of adrenal gland causing autonomous production of cortisol
Contralateral, unaffected gland undergoes atrophy
Haematology
Persistent high cortisol level has negative feedback on hypothalamus and
Stress leukogram
anterior pituitary
High neutrophils and monocytes
CRH and ACTH suppressed
Low eosinophils and lymphocytes
Thrombocytosis
Biochemistry Clinical signs: Pyoderma and seborrhoea
Increased ALKP, ALT, Cholesterol, triglycerides PU/PD/PP Calcinosis cutis
Mild hyperglycaemia Panting + Pot belly Reduced mentation
Urinalysis Endocrine alopecia Circling and seizure
Proteinuria Hyperpigmentation Increased risk of thromboembolism
BP
Systemic hypertension Treatment
Urine cortisol:creatinie ratio (UCCR) Surgery
Screening test to rule OUT cushings Gold standard is remove tumour causing excess
Highly influenced by stress - collect urine at home PDH = hypophysectomy Monitoring
ACTH Stimulation test ADH = adrenalectomy ACTH stimulation test
Tests adrenocorticol reserve Long term medical therapy Pre-pill cortisol test
Can’t differentiate between PDH and ADH Trilostane Signs of over-suppression
Low-dose dexamethasone suppression test (LDDST) Inhibits HSD enzyme in steroid synthesis Inappetence
Tests response to negative glucocorticoid feedback pathway GI signs
Dex causes a decrease in cortisol levels when normal Reversible Lethargy
Allows differentiation between PDH and ADH Does not affect tumour growth Collapse
Metabolic
Lethargy
Reproductive
Prolonged parturition
Hypothyroidism
Mental dullness Reduced fertility
Inactivity Low birth weight puppies Aetiology of Aquired Primary Hypothyroidism
Inappropriate weight gain Ophthamologic Lymphocytic thyroiditis
I.e. feed amount hasn’t changed but Corneal lipid deposits Idiopathic atrophy
they are suddenly putting on weight Cardiovascular Neoplastic destruction
Cold intolerance Bradycardia Miscellaneous
Dermatological Cardiac arrhythmias Iodine deficiency
Symmetrical alopecia Neurological Removal of the thyroid
Dry, brittle hair coat Vestibular signs Anti-thyroid medication, chronic TMPS
Pyoderma, otitis externa Polyneuropathy
Myxodema Facial nerve paralysis
Hyperpigmentation
Diagnosis:
Haematology
Non-regenerative anaemia (mild)
Biochemistry
Inappropriate weight gain
Fasting hypercholesterolemia “Rat tail” Myxoedema
Mild to moderate increase in ALT and ALKP
Total T4 Treatment
Low with hypothyroidism Sodium levothyroxine
Must interpret in conjunction with TSH, never on it’s own! Monitoring
TSH 6-8 wks after starting therapy
Expected to be high Measure TT4 and TSH 4-6hrs after medicine given
Can be normal in 40% of cases so do additional tests Improvement in clinical signs
Free T4 (fT4) by equilibrium dialysis Metabolic signs improve within days
Low TT4, normal TSH, low fT4 = hypothyroidism Dermatological signs improve within 4-6 weeks
Very expensive, hard to run and easy to do wrong Hair loss may worsen at first
Thyrogobulin antibiodies (TgAAs) Titrate dose up and down depending on findings
Positive result = presence of thyroiditis When stable recheck every 6 months
Negative = early hypothyroid OR end-stage lymphocytic thyroiditis
, Hyperthyroidism in Dogs - RARE
Associated with functional thyroid carcinoma Hyperthyroidism
Clinical presentation:
Aetiology
Mass in neck ⟶ metastasise to local LNs and pulmonary parenchyma
Mostly due to adenoma / adenomatous hyperplasia
Signs of hyperthryoidism similar to cats
Some are due to malignant thyroid carcinoma
Diagnosis
Cytology and Advanced Imaging
The Kidneys
TT4
Untreated hyperthyroidism state:
Treatment
Increased renal blood flow and GFR can make
Thyroidectomy for local disease
suboptimal renal function look normal
Radiotherapy
Protein catabolism so increased BUN
Loss of muscle mass meaning decreased creatinine
Clinical Signs Hyperthyroidism being treated
Weight loss and increased appetite (polyphagia) Renal blood flow and GFR fall back to normal levels
Behavioural changes True renal function unmasked
Polyuria and polydipsia May become azotemic if not already
Unkempt hair coat or hair loss
Gastrointestinal signs Treatment:
Vomiting, Diarrhoea Anti-thyroid drugs (long term)
Heat and stress intolerance Methimazole/thiamizole and carbimazole
Palpable thyroid goitre Inhibits thyroid peroxidase enzyme
Cardiac disturbances Iodine restricted diet
Tachycardia, gallop rhythm, heart murmur Markedly restricted iodine content
Systemic hypertension Must be the only food source!
Must not be given alongside anti-thyroid drugs
Diagnosis: Urinalysis Thyroidectomy
Haematology Decreased USG +/- glycosuria Curative +/- risk of reoccurance/complications
Erythrocytosis Thyroid Hormones Radioactive iodine
Heinz bodies on blood smear Elevated TT4 Gold standard
Mildly increased PCV Imaging Thyroid cells concentrate radioactive iodine
Biochemistry Schintigraphy Transported to thyroid follicular cells and
Increased liver enzymes Inject radionuclide iodine isotope incorporated into thyroglobin.
High ALT and ALKP Cardiac Assessment Beta ionising radiation occurs ⟶ follicular death
Azotaemia Echocardiography and ECG Hospitalised for a period of time as “radioactive”
, Hyperadrenocortisim (Cushings disease)
Cushings in Cats Pituitary dependent hyperadrenocorticsm
Most with pituitary dependent 80-85% of cases
Clinical signs Tumour of anterior pituitary gland causing autonomous production of ACTH
PU/PD/PP and pot belly Adrenal glands continually stimulated by ACTH leading to bilateral adrenal
Thin fragile skin that easily tears hyperplasia and chronic, excessive cortisol production
Diagnostics Despite high cortisol levels, ACTH secretion remains high as tumour keeps
Most have concurrent insulin resistant DM producing it
ACTHst or dexamethosine suppression test Adrenal dependent hyperadrenocorticism
15-20% of cases
Diagnosis: Tumour of adrenal gland causing autonomous production of cortisol
Contralateral, unaffected gland undergoes atrophy
Haematology
Persistent high cortisol level has negative feedback on hypothalamus and
Stress leukogram
anterior pituitary
High neutrophils and monocytes
CRH and ACTH suppressed
Low eosinophils and lymphocytes
Thrombocytosis
Biochemistry Clinical signs: Pyoderma and seborrhoea
Increased ALKP, ALT, Cholesterol, triglycerides PU/PD/PP Calcinosis cutis
Mild hyperglycaemia Panting + Pot belly Reduced mentation
Urinalysis Endocrine alopecia Circling and seizure
Proteinuria Hyperpigmentation Increased risk of thromboembolism
BP
Systemic hypertension Treatment
Urine cortisol:creatinie ratio (UCCR) Surgery
Screening test to rule OUT cushings Gold standard is remove tumour causing excess
Highly influenced by stress - collect urine at home PDH = hypophysectomy Monitoring
ACTH Stimulation test ADH = adrenalectomy ACTH stimulation test
Tests adrenocorticol reserve Long term medical therapy Pre-pill cortisol test
Can’t differentiate between PDH and ADH Trilostane Signs of over-suppression
Low-dose dexamethasone suppression test (LDDST) Inhibits HSD enzyme in steroid synthesis Inappetence
Tests response to negative glucocorticoid feedback pathway GI signs
Dex causes a decrease in cortisol levels when normal Reversible Lethargy
Allows differentiation between PDH and ADH Does not affect tumour growth Collapse
