Feline Hyperthyroidism Flashcards
What human disease does feline hyperthyroidism clinically resemble?
Toxic Adenomatous Goitre.
- single multinodular autonomously functioning follicles within the thyroid gland (multinodular adenomatous hyperplasia/adenomas).
- less commonly due to functional thyroid carcinoma.
– can metastasise so more challenging and less likely to respond to treatments.
–> should treat with radio-iodine.
Risk factors for hyperthyroidism.
Increasing age (middle to older).
Non-Siamese breeds.
Female.
Canned food.
- iodine deficiency or excess.
- various other factors.
Indoor?
Litter tray use?
Exposure to chemical products (flea / pest control, garden / household products).
Signs of hyperthyroidism?
Weight loss.
Polyphagia.
Hyperactivity.
PUPD.
V+/D+.
CR signs (incl. CHF).
- increased chronotropy.
– increased rate and contractility.
–> develop HCM.
—> can be reversed.
10% present with ‘apathetic hyperthyroidism’ - weight loss, inappetence/anorexia, lethargy.
– diagnostic pathway exactly the same and so is treatment.
Common differential diagnoses for presenting signs.
Polyphagia with weight loss:
- hyperthyroidism.
- DM.
- SI disease.
- EPI.
Polyuria/polydipsia with weight loss:
- hyperthyroidism.
- DM.
- CKD.
Polyphagia with polyuria/polydipsia:
- hyperthyroidism.
- DM.
V+/D+, inappetence, weight loss:
- hyperthyroidism.
- chronic enteropathies.
Clinical exam findings in the hyperthyroid patient.
Restless/irritation during exam.
Poor BCS/poor coat quality/poor skin elasticity.
Palpable goitre.
- may not as may drop into thoracic inlet.
Cardiothoracic:
- tachy/dyspnoea.
- tachycardia.
- heart murmur.
- gallop sound.
Goitre palpation.
Not palpable in normal cats.
Approx. 70% hyperthyroid cats have bilateral disease.
Thyroid tissue may reside anywhere from base of tongue to base of heart.
With carcinoma, local invasion / metastasis (typically pulmonary) may occur.
Dx feline hyperthyroidism.
Relatively straightforward.
Increased TT4 has high sensitivity / specificity.
- interpret T4 in upper half of normal reference range in light of clinical suspicion.
– early disease vs hyperthyroidism and concurrent NTI.
Free T4 may be useful with a higher sensitivity.
- specificity poorer.
– some euthyroid sick cats have high fT4.
Important complementary diagnostics.
Hyperthyroidism is a multisystemic disease.
Flags for suspecting hyperthyroidism.
Baseline prior to treatment.
Older feline patients commonly have comorbidities.
Systolic BP and retinal exam as absolute minimum.
- ~1/3 hyperthyroid cats will have high BP.
Haematology.
Serum biochemistry.
Urinalysis.
- increased CO state created by hyperthyroidism, increased renal perfusion, so falsely increase GFR, so azotaemia falsely reduced.
– bringing animal back to a euthyroid state will bring their GF back to normal and may unmask an azotaemia e.g. CKD.
+/- echocardiography.
- for hypertrophic change.
Classic haematological finding in a cat with hyperthyroidism.
Thyroid hormone stimulates erythropoietin production and ultimately erythropoiesis so see higher haematocrit than would be expected in a cat with chronic disease - high end of normal or higher than top of reference range.
Classic biochemical changes in a cat with hyperthyroidism.
Hepatic enzyme changes.
- reactive hepatopathy due to hypermetabolic state.
– multifactorial.
- proportionate to elevation in thyroid level.
– reduce back to normal with appropriate treatment.
- if marked increase with minor T4 increase, suspect intercurrent liver disease.
– see bilirubin increase too.
Increase phosphate due to increased bone turnover.
No azotaemia at diagnosis.
- creatinine usually slightly low.
– falsely increased GFR.
– muscle mass loss.
Initial medical management.
Enables rapid effective control of hyperthyroidism.
- reverses adverse multisystemic effects.
– improves patient morbidity and QoL.
- enables evaluation (unmasking) of concurrent renal disease.
Can be used for short term stabilisation prior to longer term management (surgery or radioiodine).
Can be used long term.
Medical management options?
Reversibly inhibits thyroid hormone synthesis.
- no impact on underlying hyperplasia/neoplasia.
- take 2-4w to work as thyroid has a store of a few weeks worth of thyroid hormones in it.
Carbimazole (pro-drug) is converted in the body to methimazole (thiamazole).
- start carbimazole (sustained release) 10-15mg SID.
OR
- start methimazole/thiamazole 1.25-2.5mg BID.
Should not be directly handled by pregnant women.
Methimazole comes as a transdermal cream applied to internal pinnae.
- Aim of medical therapy?
- Monitoring of the hyperthyroid patient.
- Total T4 in lower half of reference interval.
- Haematology, biochemistry, TT4, BP.
- 3w (4w for transdermal) after starting/changing dose.
- every 3w for first 3m (in case of adverse effects).
- every 3-6m during stable dosing.
- anytime clinical concerns.
No specific sampling time in relation to meds.
EXPECT creatinine to increase:
- unmaking CKD.
- avoid biochemical hypothyroidism.
Adverse effects associated with medical therapy.
Typically within 1-2m.
Anorexia, v+, lethargy.
- may be transient (or improve with dose reduction).
– discontinue, restart at lower dose after 1w.
- may be ameliorated by using transdermal rather than oral options.
Facial excoriation.
- usually require drug discontinuation and alternative (non-medical) treatment of hyperthyroidism.
Other adverse laboratory findings associated with medical therapy.
Blood dyscrasias - discontinue tx.
- thrombocytopenia +/- bleeding.
- neutropenia +/- clinical signs of secondary infections.
Acute toxic hepatopathy.
- discontinue tx.
- typically would expect hyperthyroid associated enzyme elevations to resolve commensurate with T4 level.
Azotaemia - not adverse effect, just unmasking disease that is already there.
