Endocrine 3 Flashcards
Accessory/ectopic thyroid tissue does it cause an issue and what are the 3 typical sites
- Common incidental finding many species
- Usually incidental but may become neoplastic
- Typical sites:
○ Ventral neck
○ Mediastinum
○ Heart base
Hypothyroidism what are the 2 main causes and causes within
1) Insufficient functional thyroid tissue
1. thyroid aplasia/hypoplasia - rare
2. thyroid destruction - most common
a. generally immune-mediated - cause unknown
b. neoplasia
c. iatrogenic (thyroidectomy)
3. thyroid atrophy - idiopathic follicular atrophy seen occansionally in dogs
2) Impaired thyroid hormone production
1. iodine deficiency - leads to defect in T3 or T4
2. iodine excess - hyperplastic goiter
3. goitrogenic toxins - interfere with synthesise of thyroid hormones
Congenital dyshormonogenetic goiter
what is it due to, how common, what develops and define it and the 3 types
- Due to genetic defects in enzymes responsible for thyroid hormone synthesis
- Rare
- This type of hypothyroidism typically results in development of GOITER
- Goiter is non-inflammatory and non-neoplastic thyroid enlargement -> enough tissue but can’t produce the thyroid
Three forms:
1) Hyperplastic goiter
2) Colloid goiter
3) nodular hyperplasia
Hyperplastic goiter what reflects, hwo does this occur, how does thyroid look change and is it reversible
- Reflects persistent secretion of TSH due to inadequate thyroid hormone secretion, causing hypertrophy and hyperplasia of thyroid tissue
○ Inadequate T3/T4 causes increased secretion of TRH and TSH -> Inability of thyroid to respond with stimulation results in cellular hypertrophy/ hyperplasia, endocytosis of colloid, hyper cellularity and follicular collapse - Thyroids are diffusely enlarged, firm and dark red with a “meaty” texture due to increased cellularity and blood flow.
○ This colour due to decreased colloid
Colloid goiter what does it reflex and how occur, what does thyroid look like grossly and histology, do you need to treat
- Reflects the resolution stage of hyperplastic goiter once thyroid hormonal function has been restored
○ Restoration of normal T3/T4 -> decreased TSH stimulation of thyroid -> follicular atrophy and accumulation of colloid within follicles - Thyroids are diffusely enlarged pale tan coloured with a waxy appearance on cut surface.
- Histologically, thyroids follicular cells are flattened and follicles are distended with colloid
- Regression occurs gradually over weeks to months
Problem is being resolved -> DON’T TREAT
Nodular hyperplasia what is it also called, what cuased by, where common and what assicatied with
- also called adenomatous hyperplasia multinodular goiter
- Idiopathic hyperplasia of thyroid tissue
- Common in older cats, dogs and horses
- May be associated with hyperthyroidism in cats, but not typically an indicator of hypothyroidism and often incidental findings
Congenital hypothyroidism what species common in, what due to, what are the 3 main clinical signs associated
- Common in lambs, other species affected rarely
○ Typically due to iodine deficiency in lambs
§ Impaired production of thyroid hormone so often present with goiter
○ Weak or stillborn animals with increased thyroid weight:body weight ratio (>0.4g/kg bodyweight) - Congenital cases may display cretinism, but relatively uncommon in domestic species
1. Disproportionate dwarfism caused by retarded epiphyseal growth with long limbs, short bodies, spinal kyphosis, ataxia of the limbs and domed heads with shortened muzzle.
2. Mental impairment common
3. Retention of juvenile hair coat (fine hair)
Adult-onset hypothyroidism what generally caused by, is there goiter, chronic or acute disease and the 5 main areas of clinical signs
- Common in middle-aged and older dogs
- Generally reflects immune-mediated destruction of the thyroids, so no goiter seen
- Disease is slowly progressive, with an insidious course
1) demeanour
2) skin
3) reproductive
4) neurological
5) circulatory
Adult-onset hypothyroidism what occurs to the demeanour, reproductive, neurological and circulatory
Demeanour
- Animals display lethargy, mentral dullness, inactivity, exercise intolerance and cold intolerance, as well as weight gain without increase in food intake
Reproductive
- Hypothyroid males and females may be infertile
Neurological
- associated with neuropathies
- Animals may develop megaesophagus due to neuropathy affecting oesophageal innervation
Circulatory
- Bradycardia due to absence of cardiac stimulating effect of thyroid hormone
○ Severe cases may have hypotension or circulatory shock, hypothermia and become comatose (myxedema coma)
- Hyperlipidaemia predisposes to atherosclerosis
Adult-onset hypothyroidism what occurs in terms of skin clinical signs
1) Alopecia (typically bilaterally symmetrical (similar to hyperadrenocorticisim) affecting the tail, trunk and friction sites (eg. lateral elbows, lateral hocks, under collar)
2) Coat quality is poor (dry, coarse, pale coloured and easily broken hair)
3) Crusting and scaling of skin due to seborrhea sicca and hyperkeratosis
4) Secondary pyoderma, Demodex and otitis externa common - decrease T cell function
5) hyperpigmentation
6) - Myxoedema - different from hyperadrenocorticisim
○ Non-pitting oedematous thickening of the forehead, eyelids and skin folds of the face and neck.
§ Animals have a sad or “tragic” facial expression
Thyroid neoplasia what arise from the two types and list the 2 main neoplasia and their behaviour
- Generally arise from follicular epithelium and may arise in ectopic thyroid tissue
- May be functional (causing hyperthyroidism) or non-functional
1) Adenomas - Usually small, solitary, well-circumscribed and encapsulated white to tan nodules that compress the adjacent parenchyma
- Composed of well-differentiated follicles which may contain colloid
2) Carcinomas - Mainly occur in dogs, especially Beagles, Boxers and Golden Retrievers
- Tumours are locally infiltrative and may damage surrounding structures
○ Affected animals may develop laryngeal paralysis, Horner’s syndrome or dyspnea due to tracheal occlusion - Carcinomas readily invade vessels and metastasize to lungs and beyond
- <10% of canine thyroid carcinomas are functional - typically non-functional
Hyperthyroidism which species most common in and which clinical sign is variable and why
- Most common endocrinopathy in cats, rare in other species
- polyphagia (small percentage decrease appetite), hyperactivity and irritability
Approximately 10% of cats have “apathetic hyperthyroidism” and display anorexia and lethargy
What are the main clinical signs of hyperparathyroidism
RESORPTION OF BONE
- Animals may develop shifting lameness due to microfractures or paresis due to spinal fractures
- Resorbed bone may be replaced by loose fibrous connective tissue (fibrous osteodystrophy) - Bone resorbed by osteoclasts
○ In some cases abundance of fibrous tissue may result in firm swellings, particularly around facial bones
§ Condition called “big head”
§ Mostly seen in cases of nutritional hyperparathyroidism, but not exclusively
○ In other cases, bone resorption may cause maxilla and mandible to become flexible
§ Condition called “rubber jaw”
§ Mostly seen in cases of renal hyperparathyroidism, but not exclusively (rubber jaw common in nutritional hyperparathyroidism in reptiles)
Glucagonoma how common, what develops
- Glucagon-secreting islet neoplasia is rare
- Animals are hyperglycaemic (and may develop diabetes mellitus due to insulin resistance) and display a vacuolar hepatopathy
- Glucagonomas are associated with superficial necrolytic dermatitis (AKA hepatocutaneous syndrome)
Animals display bilaterally symmetrical hyperkeratotic crusting (and sometimes ulcerated) lesions of muzzle, lips, periocular skin, pinnal margins, distal extremities, ventrum, pressure points (eg. hocks) and external genital mucocutaneous margins.
Hypothyroidism what do you see on CBC and blood smear
- Mild normocytic normochromicnon-regenerative anaemia (30%)
○ likely due to decreased erythrocyte production
§ ↓ EPO secretion from reduced peripheral metabolic demand - Increased “target cell” seen on the blood film
Due to increased membrane cholesterol
Hypothyroidism what 2 main changes do you see on serum biochemistry most commonly
1) Hypercholesterolaemia(75%)
○ due to ↓ hepatic LDL receptor and lipoprotein lipase activity
○ fasting hypertriglyceridaemiais also common
○ not pathognomonic for hypoT4
§ but in conjunction with appropriate clinical signs provides supportive evidence
2) Mild elevations in CK, ALP (30%)
§ hypothyroid myopathy, hepatic lipid deposition
Testing for canine hypothyroidism why challenging and the main clinical tests
Challenging
- long pre-clinical phase
- vague clinical signs
- poor specificity of diagnostic test -> no single conclusive test NEED TO USE CLINICAL SIGNS, BIOCHEM, CBC, PHYSICAL EXAM
1. *Total thyroxine(tT4)
2. *Free thyroxine(fT4)
3. *Thyroid stimulating hormone (TSH)
4. Less commonly: TgAA, tT3, fT3
Serum total T4 (TT4) what suggests hypothyroidism and rules it out but what is the issue
- ↓ TT4 and suggestive clinical signs SHOULD support hypothyroidism, but…
○ the test has poor specificity
§ TT4 is commonly lowered by non-thyroidal illness, drugs and some dog breeds (creating false positives) - normal TT4 SHOULD rule out hypothyroidism, but…
○ the test has reasonable sensitivity
§ in a number of cases (< 10%) T4 autoantibodies (T4AA) may cross-react with the assay (creating false negatives)
What are the 3 main factors that may reduce TT4 levels besides hypothyroidism
1) Non-thyroidal illness syndrome (NTIS) oreuthyroidsick syndrome
○ Eg DKA, renal disease, liver disease, cardiac failure, neurologic disease, severe inflammation, neoplasia, hyperA
2) Some drugs
○ Eg glucocorticoids, sulphonamide-containing antibiotics phenobarbital, NSAID
3) Some dog breeds
○ especially Greyhounds (and other sight hounds)
§ have lower TT4 than other dog breeds
§ have their own reference intervals
§ TT3 may be useful
Free T4 (FT4) what should occur with HypoT, how god is it, what is problem and how compare to TT4
○ Should be decreased with hypoT
○ gold stdis to measure via equilibrium dialysis (not in Australia)
§ A lot harder and more expensive to run
○ higher specificity than TT4, but less sensitive
§ unaffected by mild-mod NTIS
§ also unaffected by T4 autoantibodies
Thyroid stimulating hormone (TSH) when should change with what disease, sensitivity and specificity and what needs to be used iwth
- TSH should be increased in cases of primary hypothyroidism
○ the lack of T4 removes -ve feedback
○ test lacks sensitivity (20-40% of hypoT dogs may have normal TSH levels) -> fluctuation
○ high specificity for hypoT4 when TT4 or fT4 is concurrently low
○ Needs to be used co-currently with TT4 and FT4 - TSH should be decreased in cases of 2○hypothyroidism
○ TSH assay cannot differentiate between low and normal levels
Thyroglobulin auto-antibodies (TgAA) what a test for, what used with, how accurate is it and what is the main issue
- Test for lymphocytic thyroiditis
- Needs to be used again co-currently with TT4 and FT4
○ positive in around 50% of hypothyroid dogs
○ gives no information of severity or function of the gland
§ may be positive before clinical disease
□ » not all positive TgAAcases develop hypothyroidism
□ » may be useful to identify possible hereditary disease prior to breeding
§ may be negative in end-stage disease
T4 autoantibodies when produced and therefore what test for and what other test may interfere with
- Produced during immune mediated thyroid disease
○ 10-30% of TgAA+ve dogs - High levels may interfere with TT4 assay
○ suspect when clinical suspicion of hypothyroidism but TT4 normal
TT3 and fT3 how useful and what used for
- Limited diagnostic value
○ Mostly intracellular, minimal secretion from gland - Similar concentrations in healthy, hypoT and NTIS
- May be useful in greyhounds
○ sighthounds have low TT4 and fT4, but ‘normal’ TT3 and fT3
○ may need to use TT3 or fT3 for sighthounds
