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DVM 2 - 2 > Endocrine 3 > Flashcards

Endocrine 3 Flashcards

1
Q

Accessory/ectopic thyroid tissue does it cause an issue and what are the 3 typical sites

A
  • Common incidental finding many species
  • Usually incidental but may become neoplastic
  • Typical sites:
    ○ Ventral neck
    ○ Mediastinum
    ○ Heart base
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2
Q

Hypothyroidism what are the 2 main causes and causes within

A

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

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3
Q

Congenital dyshormonogenetic goiter

what is it due to, how common, what develops and define it and the 3 types

A
  • 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
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4
Q

Hyperplastic goiter what reflects, hwo does this occur, how does thyroid look change and is it reversible

A
  • 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
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5
Q

Colloid goiter what does it reflex and how occur, what does thyroid look like grossly and histology, do you need to treat

A
  • 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
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6
Q

Nodular hyperplasia what is it also called, what cuased by, where common and what assicatied with

A
  • 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
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7
Q

Congenital hypothyroidism what species common in, what due to, what are the 3 main clinical signs associated

A
  • 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)
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8
Q

Adult-onset hypothyroidism what generally caused by, is there goiter, chronic or acute disease and the 5 main areas of clinical signs

A
  • 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
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9
Q

Adult-onset hypothyroidism what occurs to the demeanour, reproductive, neurological and circulatory

A

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

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10
Q

Adult-onset hypothyroidism what occurs in terms of skin clinical signs

A

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

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11
Q

Thyroid neoplasia what arise from the two types and list the 2 main neoplasia and their behaviour

A
  • 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
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12
Q

Hyperthyroidism which species most common in and which clinical sign is variable and why

A
  • 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
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13
Q

What are the main clinical signs of hyperparathyroidism

A

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)

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14
Q

Glucagonoma how common, what develops

A
  • 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.
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15
Q

Hypothyroidism what do you see on CBC and blood smear

A
  • 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
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16
Q

Hypothyroidism what 2 main changes do you see on serum biochemistry most commonly

A

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

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17
Q

Testing for canine hypothyroidism why challenging and the main clinical tests

A

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
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18
Q

Serum total T4 (TT4) what suggests hypothyroidism and rules it out but what is the issue

A
  • ↓ 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)
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19
Q

What are the 3 main factors that may reduce TT4 levels besides hypothyroidism

A

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

20
Q

Free T4 (FT4) what should occur with HypoT, how god is it, what is problem and how compare to TT4

A

○ 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

21
Q

Thyroid stimulating hormone (TSH) when should change with what disease, sensitivity and specificity and what needs to be used iwth

A
  • 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
22
Q

Thyroglobulin auto-antibodies (TgAA) what a test for, what used with, how accurate is it and what is the main issue

A
  • 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
23
Q

T4 autoantibodies when produced and therefore what test for and what other test may interfere with

A
  • 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
24
Q

TT3 and fT3 how useful and what used for

A
  • 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
25
Q

Give test results that would pretty much confirm hypothyroidism

A

1) TT4 -> if low
2) FT4 -> if low
3) TSH -> if high
4) Probably don’t need TgAA% at this point but if want to and high then further evidence

26
Q

Hyperthyroidism what CBC and blood smear results are expected

A
  • Mild erythrocytosis(~50%)
    ○ increased erythropoiesis +/-dehydration
  • Leukogram usually normal
    ○ may have a stress leukogram(20%)
    § mild neutrophilia, lymphopenia, eosinopenia
  • Increased Heinz bodies seen on the blood film due to endogenous oxidative stress
27
Q

What are the 3 main serum biochemistry results expected with hyperthyroidism and what percentage display these

A

1) Mild to moderate increases in liver enzymes
○ Over 75% of cases will have increased ALT and ALP
§ ALT +/-AST: primary or secondary hepatocellular injury
§ ALP: increase bone turnover and hepatic isoenzymes
- May return to normal with successful management of hyperT4
2) Azotaemia (10 -25%)
○ concurrent renal disease (sometimes), dehydration, muscle catabolism
3) Hyperglycaemia (~5%)
○ stress, insulin resistance
§ suspect concurrent diabetes mellitus if persistent hyperglycaemia *fructosamine levels are not reliable in hyperT4 cats!

28
Q

What 2 urinalysis results expected with hyperthyroidism

A
  • proteinuria is common (~75%) due to hypertension

- Lower USG: concurrent CKD, primary polydipsia

29
Q

What is the main test used to confirm hyperT, what results suggest hyperT and what can mask this

A

Serum total T4 (TT4):
- > 90% of hyperthyroid cats will have elevated TT4 - DIAGNOSIS at this point
○ initial screening test of choice
- Occasionally TT4 can be normal in hyperthyroidism
1. early or mild hyperthyroidism with normal fluctuations
2. concurrent non-thyroidal illness syndrome (NTIS)
§ Eg CKD, DM, liver disease, GI disease, systemic neoplasia

30
Q

What are the steps to take if cat appears to be HyperT but normal TT4

A

1) Repeat TT4 at later date
2) Measure free T4 (fT4)
□ elevated fT4 expected with hyperthyroidism
□ higher sensitivity; less affected by NTIS
□ reduced specificity (6-12% false positives in euthyroidcats)
3) If repeat tests fail to confirm hyperthyroidism:
1. Thyroid scintigraphy (radionucleotideimaging) - not commonly done
○ Used in diagnosis, staging and management of hyperthyroidism
2. T3 suppression test (takes 3 days to complete) - not commonly done
○ In hyperT4, administration of T3 should not suppress TT4 levels
○ NB: T3 and TSH measurements are rarely useful.

31
Q

In summary what are the steps in confirming/ testing for hyperT

A
  • Suspicion from clinical signs and examination (thyroid palpation)
  • High TT4 confirms hyperT
  • Normal T4 may indicate early disease or NTIS
    ○ Consider repeat testing at a later date
    ○ If still normal at later date, consider T3 suppression test or scintigraphy
32
Q

What is important about feline hyperthryoidism and renal function

A
  • Renal disease can mask hyperthyroidism
    ○ via NTIS (non-thyroidal illness syndrome); reducing TT4 concentration
    ○ measure freeT4 to help identify effect of NTIS
  • Hyperthyroidism can mask chronic kidney disease
    ○ via increased renal perfusion - may lead to renal disease after treat hyperthyroidism - azotaemia
    ○ many cats have a modest increase in creat/BUN post treatment
    § may or may not result in azotaemia
    □ May have azotaemia for a few months after treatment even if don’t have renal disease -> after this point it goes down
    § small number may develop overt CKD post treatment
33
Q

Hypoadrenocorticism and hyperadrenocorticism what are the general characteristics for diagnosis

A 
HYPOADRENOCORTICISM 
- Generally get deficiency in BOTH 
ALDESTERONE -> electrolyte imbalance 
CORTISOL -> non-stress leukogram and vomiting 
Hyperadrenocorticisim -> leukopenia
34
Q

Azotaemia what do you need to thing of and what characterises each and causes

A

Pre-renal, renal, post-renal
Pre-renal -> maxillary concentrated urine - dehydration
Renal -> not maxillary concentrated - problem with nephron number/function, renal medulla tonicity, ADH secretion and function
Post-renal - urinary obstruction, failure to excrete urine - stranguira or dysuria, variable urine concetration, imaging -> leaking into abdomen or distended bladder, hyperkalaemia

35
Q

Phosphate levels at what level are you worries about arrhythmia and list 5 things that could increase

A

anything above 7.5 is high risk for arrhythmia - high in this case

  • Urinary obstruction
  • Acute urinary disease (anuric)
  • Spurious (incorrect - false)
  • Hypoadrenocorticisim
  • Tissue damage
36
Q

What 4 things could lead to hypoglycaemia

A

1) Insulinoma
2) Sepsis
3) Hypoadrenocorticisim
a. Low sodium potassium ratio -> good indication that it is hypo
4) Liver disease (makes glucose)

37
Q

Why would you get a renal azotaemia with hypoadrenocorticism

A
  • Aldosterone deficit (hypoadrenocorticisim) -> dehydration -> reduced renal perfusion -> azotaemia
    ○ Medullary wash out -> due to the large amount of electrolytes in urine and osmotic effect of dragging water into the urine
    OR co-current renal disease -> secondary renal insufficiency
38
Q

What are 5 differentials for hyperglycaemia

A

1) Cortisol
2) Diabetes
3) Sepsis
4) Stress response
5) Hyperadrenocorticisim

39
Q

What are 4 differentials for hypercholesterolaemia

A

1) Hypothyroidism
2) Post-prandial - just after eating - THINK FIRST
3) Diabetes
4) Hyperadrenocorticisim

40
Q

What are 2 differentials for low TT4

A

1) Euthyroid sick syndrome (common finding in hyperadrenocorticism)
2) Hypothyroidism -> not so common in dogs but if cat likely

41
Q

What are 8 differentials for hypercalcaemia

A

1) Hyperparathyroidism
2) Addisons(dogs)
3) Renal failure (esphorses)
4) D vitamin D toxicosis - high phospahte
5) Idiopathic (cats)
6) Osteolysis - tumours, infection in the bone
7) Neoplasia - MOST COMMON IN CATS AND DOGS
8) Spurious - second most common

42
Q

What are the 2 main differentials for hypophosphataemia

A

1) Malignancy - paraneoplastic - MOST LIKELY

2) Hyperparathyroidism

43
Q

What are the 3 main differentials for PD/PU

A
  • Hypercalcaemia -> inhibit ADH action on the kidney
  • Hyperadrenocorticisim
  • Hyperparathyroidism
44
Q

Ketoacidosis diabetes mellitus when develops, how develop and treatment

A
  • Develops as a result of uncontrolled diabetes mellitus
    ○ Diabetes may have developed due to diabetogenic hormone -> progesterone (not spayed)
    § Ketones are produced as fatty acids are oxidized to form acetoacetate with is reduced to acetone -> excessive production -> accumulation -> osmotic diuresis
    Treatment: initial stage of intensive treatment to stabilize the patient, maintenance stage to manage the diabetes over a long term
45
Q

Describe why in diabete mellitus you get polyuria, weight loss and polyphagia

A
  • Polyuria -> osmotic diuresis secondary to glucosuria
    ○ Compensatory polydipsia
  • Weight loss -> loss of glucose in the urine, reduced peripheral tissue anabolism
  • Polyphagia -> circulating glucose not entering the cells activate the satiety centre in the hypothalamus as this is insulin dependent therefore it fails to inhibit the hunger centre resulting in increased appetite
46
Q

What are the normal USG values for cats, dogs, cows/horses

A

Normal range for following species - top of the range is concentrated - normal kidney function
Cat USG >1.035
Dog USG >1.030
Cows, horses USG >1.025

DVM 2 - 2 (27 decks)

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