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CVSOH 4 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are 2 mechanisms of increased functional effects of hormones in endocrine disease?

A

Hyperfunction – excess production of hormone

New source of hormone other than expected endocrine gland

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2
Q

What are the mechanisms of primary hyperfunction?

A
  • Functional hyperplastic or neoplastic disease of endocrine gland – these cells have the ability to produce and secrete functional hormone
  • Autonomous secretion of excess hormone, independent of a stimulus and cells may have reduced sensitivity/insensitivity to negative feedback mechanisms
  • Hormone secretion above homeostatic control
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3
Q

Distinguish primary and secondary hyperfunction.

A

If this lesion occurs within the endocrine gland, it is primary hyperfunction.

If a lesion occurs outside the endocrine gland producing the excess hormone this is secondary hyperfunction

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4
Q

Outline the steps of secondary hyperfunction.

A
  1. Functional lesion in endocrine gland 2
  2. Excess stimulatory hormone
  3. Endocrine gland 1
  4. Excess hormone from endocrine gland 1
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5
Q

Explain 1 example of non-hormonal signals causing secondary hyperfunction.

A

Endocrine glands can also be stimulated by non-hormonal signals, such as electrolytes like calcium. Primary disease causing hypercalcaemia, causing excess stimulation at endocrine gland 1 and meaning excess hormone is produced

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6
Q

Outline the normal pituitary axis.

A
  1. Pituitary
  2. ACTH/adrenocorticotropic hormone
  3. Adrenal cortex
  4. Cortisol
  5. Negative feedback on pituitary
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7
Q

If an animal had excess production of cortisol by the adrenal glands (adrenal hyperfunction) caused by a functional neoplastic lesion, where might this neoplasm be present?

A

Could have a functional neoplasm in the adrenal cortex, producing cortisol. Could have functional neoplasm in the anterior pituitary gland producing ACTH, causing excessive stimulation of the adrenal cortices and excess secretion of cortisol as a result.

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8
Q

How would you classify the adrenal hyperfunction arising from tumours at the pituitary and at the adrenal cortex?

A

Adrenal = primary, pituitary = secondary

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9
Q

If there were no abnormalities present in the adrenal glands or pituitary to account for a state of excess circulating cortisol, how else might this state have arisen?

A

Most common way is exogenous source of cortisol/administration of glucocorticoids. In rare cases, can get ACTH being produced from a site that is not the pituitary gland – ectopic production of ACTH by a non-pituitary tumour. The hypothalamus produces corticotropin releasing hormone that stimulates ACTH production and very rarely can ectopic production of CRH by a tumour occur.

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10
Q

How are hyperplastic lesions, benign tumours, and malignant endocrine tumours differentiated?

A

Hyperplastic lesions on endocrine glands may result in nodular hyperplasia. Tumours are often larger than hyperplasia and carcinomas are larger than adenomas. Presence of a capsule is often used to differentiate nodular hyperplasia. Local tissue invasion and metastases is used to differentiate carcinomas.

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11
Q

What are the mechanisms that cause decreased functional effects of hormones?

A
  • Hypofunction – insufficient production of hormone
  • Lack of response to a hormone
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12
Q

What is primary hypofunction?

A
  • Endocrine gland has impaired ability or lack of ability to produce hormone
  • Leads to insufficient circulating hormone
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13
Q

What are the possible congenital causes of primary hypofunction?

A
  • Genetic mutation – biochemical defect in hormone synthesis or activation pathways
  • Development anomaly – hypoplasia or aplasia of endocrine glands
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14
Q

What might cause destruction of functional cells in acquired primary hypofunction?

A
  • Infections
  • Immune-mediated disease
  • Neoplastic disease
  • Vascular disease, such as infarctions
  • Treatments - surgical excision, radiotherapy, drugs
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15
Q

Outline the 2 mechanisms causing secondary hypofunction.

A

Diseased endocrine gland – primary hypofunction > reduced stimulatory signal > endocrine gland – secondary hypofunction > subnormal hormone secretion

Nutritional deficient or intestinal disease > decreased absorption of nutrients > lack of substrate for hormone synthesis > endocrine gland – secondary hypofunction > subnormal hormone secretion

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16
Q

What might cause lack of response to hormones?

A
  • Primary disease, such as an abnormal receptor or failure of a component of a signalling cascade
  • Dysfunction caused secondary to another disease condition in the body
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17
Q

What basic mechanisms could affect this system and result in persistent excessively high blood glucose levels (hyperglycaemia)?

A

May have a state of hypofunction with inadequate production of insulin – this may be primary (congenital with beta-cell hypoplasia or acquired with pancreatitis and immune mediate degeneration of beta-cells). Another mechanism could be lack of response to insulin/insulin resistance, factors that contribute to this is obesity and other endocrine diseases.

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18
Q

What do the different parts of the adrenal gland produce?

A
  • Zona glomerulosa – mineralocorticoids, such as aldosterone
  • Zona fasciculata – glucocorticoids, such as cortisol
  • Zona reticularis – sex steroids
  • Medulla – catecholamines
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19
Q

Diseases affecting the adrenal gland are more common in which part?

A

Adrenal cortex > adrenal medulla

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20
Q

How do functional tumours cause atrophy of the adrenal glands?

A

Functional tumour arising in the adrenal cortex and causing autonomous production of cortisol, which negatively feedbacks on the hypothalamus and the pituitary > decreased CRH > decreased ACTH. This will cause atrophy of the adrenal cortices.

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21
Q

What are the characteristics of adrenal cortical tumours?

A
  • Most common in dogs
  • May be functional or non-functional
  • Bilateral or unilateral
  • Adenoma > carcinoma
  • Obliterate effect of the adrenal gland
  • Local invasion metastatic spread – liver, kidneys, lungs, lymph nodes
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22
Q

What is the clinical significance of adrenal cortical nodular hyperplasia?

A

Does not cause signs of hyperadrenocorticism so are incidental findings of no clinical significance.

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23
Q

Describe secondary (pituitary dependent) hyperadrenocorticism.

A

Pituitary tumour, usually adenoma) with autonomous production of ACTH, in secondary hyperfunction of the adrenal glands. Excess production of cortisol and bilateral hypertrophy of the adrenal cortices. Cortisol has a negative feedback to the hypothalamus causing a decreased CRH but pituitary tumour is insensitive to the negative feedback.

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24
Q

What neoplastic changes can cause hyperadrenocorticism in dogs?

A
  • 85% secondary hyperadrenocorticism (functional pituitary tumours), pituitary dependent
  • 15% primary hyperadrenocorticism (functional adrenocortical tumours)
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25
Q

What is iatrogenic hyperadrenocorticism?

A
  1. Glucocorticoids administration
  2. Negative feedback on hypothalamus and pituitary glands
  3. Decreased CRH to pituitary glands and decreased ACTH to adrenals
  4. Bilateral adrenal cortex atrophy
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26
Q

What is the end effect of primary hypoadrenocorticism?

A

Bilateral adrenocortical atrophy/destruction

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27
Q

What are the causes of primary hypoadrenocorticism?

A
  • Idiopathic (immune-mediated?)
  • Adrenal inflammation (adrenalitis)
  • Vascular disease e.g. adrenal gland infarction, haemorrhage and necrosis
  • Metastatic tumour spread to the adrenals
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28
Q

What do disturbances in mineralocorticoids, such as aldosterone, cause?

A
  • Disturbances in potassium, sodium and chloride
  • Hyperkalaemia and hyponatraemia
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29
Q

What are the causes of secondary hypoadrenocorticism?

A
  • Pituitary disease – infections, neoplasia
  • Loss of ACTH
  • Bilateral adrenal cortical atrophy with sparing of the zona glomerulosa, as ACTH mostly affects the production and release of glucocorticoids
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30
Q

What is iatrogenic secondary hypoadrenocorticism?

A
  1. Rapid withdrawal o glucocorticoids
  2. ACTH decrease
  3. Atrophied cortex unable to produce sufficient cortisol to compensate for withdrawal of exogenous glucocorticoids
  4. Hypoadrenocorticism
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31
Q

What are the characteristics of phaeochromocytomas?

A
  • Benign or malignant
  • Local invasion and metastatic spread
  • Occasionally function and can produce catecholamines, such as adrenaline and noradrenaline, and when this happens, they cause cardiovascular disease – tachycardia and hypertension
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32
Q

Explain why loss of insulin causes persistent hyperglycaemia.

A
  • Insulin suppresses hepatic glucose production and enhances uptake of glucose by peripheral tissues, particularly striated muscles and adipose tissue.
  • Other roles of insulin include breakdown of fat and glycogen synthesis.
  • So loss of insulin action loses regulatory control of blood glucose levels and so persistent hyperglycaemia develops.
  • This is because of over-production of glucose by the liver and a reduction in uptake of glucose by skeletal muscle (and adipose tissue).
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33
Q

What are the main 2 mechanisms of diabetes mellitus?

A
  • Pancreatic beta-cell hypofunction resulting in insufficient insulin production
  • Insulin resistance – reduced response to insulin by target cells or antagonism of insulin
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34
Q

Distinguish the human based classification of type 1, type 2 and type S of diabetes mellitus.

A

Type 1
- Deficiency of insulin
- Primary immune-mediated or idiopathic loss of beta-cells

Type 2
- Complex multifactorial disease
- Inadequate insulin production and resistance to insulin in tissues

Other causes/type S
- Destruction of beta-cells by exocrine pancreatic disease
- Antagonism of insulin by other hormones or drugs

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35
Q

What are the 4 causes of diabetes mellitus in dogs?

A
  • Beta-cell destruction – pancreatitis, pancreatic necrosis
  • Immune-mediated destruction of beta-cells
  • Insulin antagonism/insulin resistance
  • Congenital/juvenile disease – uncommon
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36
Q

What causes insulin antagonism/resistance in dogs?

A
  • Progesterone and growth-hormone – dioestrus and pregnancy
  • Cortisol – hyperadrenocorticism
  • Exogenous glucocorticoids and progestogens
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37
Q

What is the onset of juvenile disease causing diabetes mellitus in dogs?

A

Onset at birth – Keeshond

Juvenile onset – islet cell hypoplasia, juvenile pancreatic atrophy, greyhounds

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38
Q

What are the causes of diabetes mellitus in cats?

A
  • Type 2 diabetes – reduced insulin production and insulin resistance
  • Beta-cell exhaustion and glucotoxicity
  • Beta-cell destruction – pancreatitis
  • Insulin antagonism/insulin resistance - growth hormone/acromegaly, cortisol
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39
Q

What are the risk factors of diabetes mellitus in cats?

A
  • Age (> 10 years old)
  • Obesity
  • Male
  • Burmese breed
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40
Q

Describe the histological appearance of cats with disturbances to beta cells.

A

Cats with disturbances beta cell function often develop amyloid deposition/accumulation in the pancreatic islets - pale pink

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41
Q

Explain how beta cell exhaustion and glucotoxicity causes diabetes mellitus in cats.

A

Insulin resistance and hyperglycaemia can result in persistent stimulation of beta cells to produce insulin, leading to cell exhaustion and decrease in beta cell function. This then leads to decreased insulin secretion and exacerbation of chronic hyperglycaemia. Initially reversible but over time irreversible injury and loss of beat cells

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42
Q

What are 2 causes of diabetes mellitus in cattle?

A

Immune-mediated

Associated with some viral infections
- Persistent foot and mouth disease virus
- Bovine viral diarrhoea virus?

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43
Q

What are 2 causes of beta cell hyperfunction?

A

Excess insulin production > hypoglycaemia

Functional insulin secreting beta-cell tumour/insulinoma

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44
Q

Name the 2 hormones that the thyroid gland produces.

A

Triiodothyronine/T3
Thyroxin/T4

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45
Q

What is the cause of primary hyperthyroidism?

A

Functional nodular hyperplasia or neoplasia of one or both thyroids.

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46
Q

What does T3 and T4 production by functional lesions cause?

A

Negatively feedback that will cause a reduction in TRH and TSH but does not affect the autonomous production of thyroid hormones by the functional lesions in the thyroid glands, so the overproduction f thyroid hormones continues.

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47
Q

What is the cause of feline hyperthyroidism?

A
  • Multinodular hyperplasia/adenomatous hyperplasia and/or follicular adenomas
  • Cause enlargement of the thyroid
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48
Q

What are the characteristics of thyroid neoplasia in dogs?

A
  • Carcinomas are more common than adenomas
  • May invade local tissues
  • Metastatic spread to lungs and local lymph nodes
  • Clinical signs of hyperthyroidism are uncommon in dogs
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49
Q

What is primary hypothyroidism?

A

Destruction of thyroid follicular cells

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50
Q

What are the causes of primary hypothyroidism in dogs?

A
  • Lymphocytic thyroiditis
  • Idiopathic follicular atrophy
  • Thyroid neoplastic disease - destruction of the thyroids, uncommon
  • Pituitary lesions causing insufficient release of TSH - secondary hypothyroidism, uncommon
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51
Q

How does lymphocytic thyroiditis cause primary hypothyroidism?

A

Autoantibodies against thyroid follicular cell antigens. Causes degeneration of the thyroid follicles and associated with lymphocytic inflammatory cell infiltrate. Over time, functional thyroid tissue becomes replaced by fibrous connective tissue that separates residual small follicles.

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52
Q

How does idiopathic follicular atrophy cause primary hypothyroidism?

A

Progressive loss of thyroid follicular epithelium and replaced with adipose tissue = loss of functional tissue

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53
Q

Where does parathyroid hormone act and what is its effect at each site?

A
  • Kidney – increases calcium reabsorption and decreases phosphorus reabsorption. Activation of calcitriol (active form of vitamin D) synthesis
  • Bone – bone resorption by osteoclasts for mobilisation of calcium
  • GI tract – promotes absorption of calcium
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54
Q

What is the effect of calcitriol on parathyroid hormone?

A

Calcitriol has a suppressive regulatory action on PTH, which contributes to the reduction of PTH secretion.

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55
Q

What are the mechanisms of hyperparathyroidism?

A
  • Primary hyperparathyroidism
  • Parathyroid hormone related protein production by neoplasms/pseudohyperparathyroidism
  • Hyperparathyroidism secondary to chronic kidney disease
  • Hyperparathyroidism secondary to nutritional imbalances
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56
Q

Explain how primary hyperparathyroidism causes hypercalcaemia.

A
  • Functional chief cell adenoma or focal/multifocal nodular hyperplasia or chief cell carcinoma (rare)
  • Autonomous secretes PTH
  • Hypercalcemia
  • Negative feedback on normal chief cells
  • Reduced PTH secretion from normal chief cells
  • Atrophy of normal chief cells and atrophy of remaining parathyroid glands over time
  • Functional lesion is insensitivity to the negative feedback and so persistent state of hypercalcaemia
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57
Q

Which neoplasms can release parathyroid hormone related protein?

A
  • Anal sac apocrine gland carcinoma
  • Multiple myeloma
  • Lymphoma
  • Some carcinomas
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58
Q

What is the effect of parathyroid hormone related protein production by neoplasms?

A
  • Binds to PTH receptors in bone and kidney
  • Hypercalcaemia
  • Persistent hypercalcaemia will cause atrophy of the parathyroid glands
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59
Q

Explain how hyperparathyroidism occurs secondary to chronic kidney disease.

A
  • In CKD, there is reduced GFR and retention of phosphate, resulting in hyperphosphatemia
  • Hyperphosphatemia stimulates fibroblast growth factors-23, which causes a reduced calcitriol synthesis by renal tubules
  • So there is increased blood phosphate and decreased calcitriol
  • Phosphorus binds bioavailable calcium
  • Reduced calcium uptake by the GI tract
  • Decreased blood calcium
  • This stimulates chief cells in the thyroid to secrete PTH
  • Decreased regulatory effect of calcitriol on PTH synthesis
  • Increased PTH – diffuse chief cell hypertrophy and hyperplasia in all parathyroid glands
  • Renal osteodystrophy – increased PTH causes increased osteoclastic action of bone and replacement with fibrous tissue.
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60
Q

Explain how hyperparathyroidism occurs secondary to nutritional imbalances.

A
  • Dietary calcium: phosphate imbalance – low calcium or high phosphate with low or normal calcium
  • Vitamin D deficiency
  • Decreased blood calcium concentration
  • Diffuse chief cell hypertrophy and hyperplasia in all parathyroid glands
  • Increased PTH
  • Fibrous osteodystrophy
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61
Q

Distinguish the adenohypophysis and neurohypophysis/pars nervosa that encompass the pituitary.

A

Pars nervosa contains external processes extending from the hypothalamus and hormones that are produced in the hypothalamus are transported to the pars nervosa for storage and secretion into the blood.

The adenohypophysis contains the pars distalis and the pars intermedia, which contain a variety of cell populations that can secrete a number of hormones, including growth hormone, TSH, ACTH and melanocyte stimulating hormone.

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62
Q

Describe the activity of the cells in the pars intermedia.

A

Cells in the pars intermedia are mainly melanotropes which synthesise POMCs, which is processed to produce a range of hormones, such as melanocyte stimulating hormone, beta-endorphin an corticotrophin-like intermediate peptide. The activity of the cells in the pars intermedia are regulated by dopamine, produced by neurones extending from the hypothalamus. Dopamine acts to inhibit activity of these cells.

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63
Q

What is PPID?

A

Thought to be an age related degeneration of dopaminergic neurones. The loss of the inhibitory effect resulting the cells of the pars intermedia causes increased synthesis and secretion of POMC and so MSH, CLIP and beta-endorphin. Additionally it can cause neoplasia/adenomas in the pars intermedia, which are often functional tumours

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64
Q

What are the clinical manifestations of PPID?

A
  • Hirsutism (fail to shed hair)
  • Hyperhidrosis (sweating)
  • Muscle weakness
  • Increased appetite
  • PUPD
  • Lethargy/docile
  • Laminitis
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65
Q

What is diabetes insipidus?

A

Inability of the kidneys to concentrate urine due to loss of function effects of ADH

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66
Q

What are the mechanisms of diabetes insipidus?

A
  • Insufficient ADH production or release from the hypothalamus/pituitary - central diabetes insipidus
  • Renal tubules insensitive to ADH - nephrogenic diabetes insipidus
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67
Q

How does central diabetes insipidus arise?

A

Injury/destruction of the hypothalamus or pituitary

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68
Q

Distinguish primary and secondary nephrogenic diabetes insipidus.

A

Primary NDI rare congenital disease, such as mutation affecting the ADH receptor

Secondary (acquired) NDI can be associated with various diseases, such as pyometra, pyelonephritis, hyperadrenocorticism, hypercalcaemia

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69
Q

What is acromegaly the result of?

A

Hypersomatotropism caused by growth-hormone (somatotropin) secretion by a functional pituitary tumour - adenoma and slow growing

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70
Q

What does acromegaly cause?

A
  • Pituitary is greatly enlarged
  • Can have enlarged skull and face with broadened facial changes
  • May also have enlargement of the feet, liver and kidneys
  • Myocardial hypertrophy
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71
Q

How are POMCs produced?

A

Hypothalamus > dopamine > positive feedback > pituitary > pro-opiomelanocortins (POMCs)

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72
Q

What happens to the production of POMCs in PPID in horses?

A
  • Decrease in production of dopamine from hypothalamus
  • Decrease in inhibition of pituitary
  • Pituitary adenoma
  • Overproduction of POMCs
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73
Q

What are the clinical signs of PPID in horses?

A
  • Long curly coat, unknown cause
  • Laminitis – insulin resistant
  • PUPD – decreased secretion of vasopressin?
  • Weight loss – cortisol production, associated other disease, parasites
  • Docile – increase in B-endorphin in CSF
  • Neurological impairment – compression from adenoma
  • Hyperhidrosis
  • Change in fat distribution, bulging fat pads
  • Infertility
  • Skin disease
  • Periodontal disease
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74
Q

How is PPID diagnosed in horses?

A
  • Clinical signs and signalment
  • Post mortem
  • Individual variation in POMC production
  • Pars intermedia more active in Autumn - adjust reference ranges
  • ACTH test
  • Overnight dexamethasone suppression test/ONDST
  • THR stimulation
  • Combined dex suppression and THR test
  • Insulin concentration
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75
Q

How is an ACTH test done in order to diagnose PPID in horses?

A
  • Best first-line test
  • Resting plasma ACTH concentration
  • Should not be stressed
  • Collect blood – cold plastic EDTA tube
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76
Q

How is an THR stimulation test done in order to diagnose PPID in horses?

A
  • Better than ACTH – more sensitive
  • Inject TRH
  • Blood for ACTH at 10 and 30 mins
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77
Q

How useful is combined dex suppression and TRH tests to diagnose PPID in horses?

A

May be the best test but expensive and multiple sample collections

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78
Q

How useful is insulin concentration to diagnose PPID in horses?

A

Often insulin resistant, may have EMS instead/as well, may help management but not firm diagnosis

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79
Q

What is done if PPID diagnosis has a positive test result?

A
  • Remember risk of false positives due to Autumn
  • Start treatment
  • Repeat the test in 4-6 weeks to check dose
  • Repeat annually as disease progresses
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80
Q

What is done if PPID diagnosis has a negative test result?

A
  • But high clinical suspicion?
  • Start treatment anyway?
  • Assess clinical response
  • Routine checking of aged horses?
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81
Q

How is PPID treated in horses?

A
  • Farriery
  • Clipping
  • Parasite control
  • Dental care
  • Feeding
  • Dopamine agonist
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82
Q

Describe the anatomy of the thyroid in horses.

A
  • 2 lobes over position of proximal trachea
  • Usually palpable but not visible
  • Thyroid hormones for cell growth, differentiation, metabolism in nearly all tissues
  • Thyroid disease in horses rare
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83
Q

What are the factors affecting thyroid gland function and testing in horses?

A

Age
Gender
Breed
Hormones
Season
Disease
Activity
Feeding
Iodine supplementation
Medication

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84
Q

Describe hyperthyroidism in foals.

A
  • Major cause is nutritional during gestation
  • Inadequate or excessive iodine intake by the mare
  • Low TH > lack of pituitary inhibition > excess TSH secretion > thyroid enlargement
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85
Q

What are the clinical signs of hyperthyroidism in foals?

A
  • Thyroid enlargement (goitre) – but not in all
  • Stillbirth, weakness, defective ossification
  • Can be born normal, develop skeletal lesions when weeks old
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86
Q

How is hyperthyroidism in foals diagnosed?

A
  • TH concentrations vary in foals
  • TSH/TRH stim tests
  • But thyroid gland function may be normal once the foal is born
  • Look at mare’s diet – beware seaweed supplementation
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87
Q

Why is prognosis of hyperthyroidism in foals poor?

A

Because the problem happened during development so cannot be reversed

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88
Q

What are the clinical signs of hyperthyroidism in adult horses?

A

Anaemia
Irregular oestrous cycle
Poor performance
TH low, TRH, TSH high
High T3 and T4
Tremors
Excitability
Tachycardia
Sweating

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89
Q

How is hyperthyroidism in adult horses treated?

A

Levothyroxine
Anti-thyroid therapy with potassium iodide

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90
Q

What are the characteristics of thyroid adenomas in horses?

A
  • Enlarged thyroid, often unilateral
  • Usually no thyroid dysfunction
  • Biopsy – benign
  • Hemithyroidectomy if size interfering
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91
Q

What are the characteristics and clinical signs of thyroid granulosa-theca cell tumours in horses?

A
  • Benign tumours
  • Poor fertility
  • Abdominal discomfort
  • Stallion-like behaviour
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92
Q

How are thyroid granulosa-theca cell tumours in horses diagnosed?

A
  • Rectal – enlarged ovary
  • Usually unilateral and other often small
  • Ultrasound multiloculated
  • Anti-mullerian hormone newest and best test
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93
Q

How are thyroid granulosa-theca cell tumours in horses surgically removed?

A
  • Standing laparoscopic assisted if possible
  • Or laparotomy if very large (but long recovery)
  • Usually only need to remove 1 ovary
  • Histopathology
  • Surgery and histopathology even if AMH negative
  • Fertility should return
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94
Q

You see a severely overweight 10 year old pony for vaccinations. What test should you take for EMS and why would you?

A

OGTT as risk laminitis, lipomas, hyperlipaemia if starved

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95
Q

You see a 14 year old pony with laminitis. What underlying disease process do you test him for?

A

EMS and PPID

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96
Q

You see a lean 21 year old pony with his first bout of laminitis. What do you test him for and how?

A

PPID - TRH stimulation test or ACTH

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97
Q

You test ACTH when diagnosing PPID in a horse and get a borderline result. What test do you do now?

A

TRH stimulation test

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98
Q

You diagnose PPID in the pony. What treatment is used?

A

Pergolide and management

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99
Q

When do you re-test for PPID diagnosis in horses?

A

4-6 weeks after starting treatment, then every year. May want to test again before going on lush grass, which would increase insulin in the blood due to sugars in the grass.

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100
Q

Why is a re-test done when diagnosing PPID in horses?

A

Check pergolide dosage

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101
Q

What is pergolide’s mechanism of action?

A

Dopamine agonist

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102
Q

What is the most common side effect of pergolide?

A

Going off feed

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103
Q

What are the common downsides of pergolide?

A

Can’t compete, cost, might not be able to work/enough/be too late

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104
Q

What metabolic processes do thyroid hormones affect?

A
  • Concentration/activity of various enzymes
  • Metabolism of proteins, carbohydrates, lipids, minerals, vitamins
  • Secretion/degradation of and regulate response to many other hormones
  • The heart – positive chronotropy/positive inotropy
  • Enhance responsiveness to catecholamines
  • Foetal development
  • Stimulate erythropoiesis
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105
Q

How are thyroid hormones produced in the thyroid gland?

A
  • Thyroid glands are follicular structures containing large reservoir of thyroglobulin (Tg)
  • Iodination of tyrosine residues of Tg creates thyroid hormones
  • So production requires adequate dietary iodide
  • Iodide is actively transported from extracellular fluid to the thyroid gland
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106
Q

How do thyroid hormones circulate?

A

Primarily circulate in protein bound state as reservoir, only the free portion is metabolically active

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107
Q

What is euthyroid sick syndrome?

A
  • Suppresses production of T4
  • Many sick patients will have measurably low T4 levels
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108
Q

What is the most common acquired cause of canine hypothyroidism?

A

Most commonly immune mediated lymphocytic thyroiditis progressing to idiopathic atrophy

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109
Q

What are the dermatological clinical signs of canine hypothyroidism?

A
  • Truncal alopecia, often spares the limbs and head but can vary from mild to severe
  • May have secondary yeast or bacterial infections
  • May have thickened skin particularly on the skin that is non-pitting but gives a depressed look due to myxoedema – hyaluronic acid in the skin
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110
Q

What are the clinical manifestations of canine hypothyroidism?

A
  • Lethargy/weight gain
  • Bradycardia
  • Neuromuscular
  • Rare - reproductive failures, corneal lipid deposition, megaoesophagus
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111
Q

How is canine hypothyroidism diagnosed?

A
  • Sick dogs will have low T4 so only test when we are really suspicious
  • Concurrent illness suppresses serum thyroid hormone concentrations
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112
Q

How are bloods used to diagnose canine hypothyroidism?

A
  • Mild, non-regenerative anaemia – normocytic, normochromic anaemia of chronic disease
  • Hyperlipaemia common – over 75% have hypercholesterolaemia and/or hypertriglyceridaemia. Ideally evaluate on fasted sample
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113
Q

Describe the levels of TSH and T4 if hypothyroid.

A

Hypothyroid – high TSH to attempt to stimulate the low T4

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114
Q

What does it mean if both T4 and TSH are normal?

A

Not hypothyroid

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115
Q

What does it mean if T4 is low and TSH is normal?

A

Non-thyroidal illness, such as inflammatory, body is trying to reduce metabolism and pituitary recognises this as appropriate so has normal TSH

116
Q

What does it mean if TSH is high and T4 is normal?

A

Early hypothyroidism or non-thyroidal illness, so re-test in 1-3 months

117
Q

How can free T4 be used to diagnose hypothyroidism?

A
  • More accurately reflects thyroid function as it reflects the biologically active fraction
  • Need to use validated (equilibrium dialysis) methodology
  • May be less affected by non-thyroidal illness – however, severe illness may also suppress free T4
118
Q

When is lymphocytic thyroiditis clinical significant?

A

Lymphocytic thyroiditis is gradually progressive – clinically significant hypofunction does not occur until 80% of the gland is destroyed

119
Q

How can thyroglobulin antibody assays be used to diagnose lymphocytic thyroiditis hypothyroidism?

A
  • Present during the destructive phase
  • Not when destruction is complete
  • Antibodies = thyroiditis (not hypothyroidism)
120
Q

What are the pitfalls in thyroid profiles?

A
  • Identify/treat the non-thyroidal illness first
  • Greyhound T4 is lower than other breeds
  • TMPS and phenobarbitone mimic hypothyroidism (decreased fT4/TT4 and increased TSH) – never test while on these
  • Glucocorticoids and NSAIDs cause decreased fT4/TT4
  • Anti-thyroid hormone antibodies (rare)
121
Q

How is canine hypothyroidism treated?

A

Synthetic levothyroxine sodium - dose much higher than in people as they do not absorb oral version very well. Ideally with food as food decreases bioavailability. Be consistent

122
Q

How is levothyroxine replacement monitored in canine hypothyroidism treatment?

A

If giving once daily – trough T4/TSH (T4 should be low normal, TSH should be normal)

123
Q

Why might treatment of canine hypothyroidism fail?

A

-Incorrect diagnosis
- Insufficient time
- Expired drug
- Inadequate dose/frequency
- Owner/dog compliance
- Poor absorption (with food, concurrent GI disease)
- Concurrent disease

124
Q

What is congenital hypothyroidism/cretinism?

A
  • Disproportionate dwarfism and impaired mental development
  • Comparison to growth hormone deficiency which causes proportionate dwarfism
125
Q

What are the characteristics of canine thyroid neoplasia?

A
  • Usually non-secretory
  • Unilateral
  • Carcinomas
  • Adherence and local lymph nodes
126
Q

How is canine thyroid neoplasia diagnosed?

A
  • Diagnostic imaging
  • Thyroid panel
  • Cytology usually avoided
  • Histology - part of curative intent surgery
127
Q

What are the risk factors for feline hyperthyroidism?

A
  • Increasing age
  • Non-Siamese breeds
  • Female
  • Canned food – iodine deficiency or excess, various other factors
  • Indoor?
  • Litter tray use?
  • Exposure to chemical products
128
Q

What are the clinical signs of feline hyperthyroidism?

A
  • Weight loss, polyphagia and hyperactivity
  • Polyuria/polydipsia
  • Vomiting and/or diarrhoea
  • Cardiorespiratory signs - including CHF
  • Apathetic hyperthyroidism – weight loss, inappetence/anorexia, lethargy
129
Q

What are the findings on clinical examination of a patient with feline hyperthyroidism?

A
  • Restless/irritable during examination
  • Palpable goitre
  • Poor BCS/poor coat quality
  • Bad skin flexibility so tenting without being dehydrated
  • Tachy/dyspnoea
  • Tachycardia
  • Heart murmur
  • Gallop sound
130
Q

How is feline hyperthyroidism diagnosed?

A
  • Increased total T4 – high sensitivity and specificity
  • Free T4 may be useful – higher sensitivity, poorer – some euthyroid sick cats have high fT4
131
Q

What is hyperthyroidism a common cause of in cats?

A

HCM

132
Q

Why are complementary diagnostic tests for feline hyperthyroidism important?

A
  • Because hyperthyroidism is multisystemic
  • Baseline prior to treatment
  • Older cats commonly have comorbidities
133
Q

What are the important complementary diagnostic tests for feline hyperthyroidism?

A
  • Systolic blood pressure and retinal examination
  • Haematology
  • Serum biochemistry
  • Urinalysis – might unmask renal disease
  • With/without echocardiography
134
Q

What is the classic haematological finding of feline hyperthyroidism?

A

HCT higher than you would expect in a cat with chronic disease

135
Q

What are the biochemical findings of feline hyperthyroidism?

A
  • Increased liver enzymes (reactive hepatopathy), typically commensurate with T4 level
  • Hyperphosphataemia
  • Concurrent CKD
136
Q

What is the effect of initial medical management of feline hyperthyroidism?

A

Reversibly inhibits thyroid hormone synthesis – no impact on underlying hyperplasia/neoplasia

Expect creatinine to increase – unmasking of chronic renal disease. Avoid biochemical hypothyroidism

137
Q

What is the initial medical management for feline hyperthyroidism?

A

Carbimazole (pro-drug), then methimazole

138
Q

What is the aim of initial medical management of feline hyperthyroidism?

A

Total T4 in the lower half of the reference interval

139
Q

How is the effect of initial medical management of feline hyperthyroidism monitored?

A

Haematology, biochemistry, total T4, BP:

  • 3 weeks after starting/changing dose
  • Every 3 weeks for first 3 months
  • Every 3-6 monthly during stable dosing
  • Anytime clinical concerns
140
Q

What are the adverse clinical signs of initial medical treatment of feline hyperthyroidism?

A

Anorexia, vomiting and lethargy - transient

Facial excoriation - usually require drug discontinuation and alternative

141
Q

When should you discontinue initial medical treatment for feline hyperthyroidism?

A

Blood dyscrasias – discontinue treatment
- Thrombocytopenia with/without bleeding
- Neutropenia with/without clinical signs of secondary infections

Acute toxic hepatopathy – discontinue treatment

142
Q

How is concurrent chronic kidney disease managed with feline hyperthyroidism?

A
  • Avoid hypothyroidism
  • Institute appropriate management for the stage of CKD present
  • Ensure hypertension is appropriately managed
142
Q

Why is azotaemia not an adverse effect of initial medical treatment of feline hyperthyroidism?

A

Not an adverse effect, just unmasking disease that is already there

143
Q

Started oral methimazole 3 weeks ago. Resolved presenting signs (hyperactivity, polyphagia). 1 week of marked facial excoriations. Normal haematology, biochemistry Total T4 22nmol/l (ref. 15-60nmol/l). Hyperthyroid patient on medical therapy, what should I do with the dose?

A

Discontinue – cat is well controlled but facial excoriation requires a non-medical treatment

144
Q

Started oral carbimazole 4 weeks ago. Improved presenting signs (restlessness, vomiting, weight loss). Normal haematology. Biochemistry – creatinine 242umol/l (from 163umol/l pre-treatment); ref. Hyperthyroid patient on medical therapy, what should I do with the dose?

A

Stay the same – unmasked kidney disease so needs management

145
Q

Started transdermal methimazole 4 weeks ago. Improved presenting signs (polyphagia, weight loss). Normal haematology, biochemistry - total T4 48nmol/l (ref. 15-60nmol/l). Hyperthyroid patient on medical therapy, what should I do with the dose?

A

Increase and re-check in 4 weeks time

146
Q

What is the gold standard treatment option for feline hyperthyroidism?

A

Subcutaneous administration of radioiodine causes concentration in thyroid gland - radiation causes follicular cell death and so kills thyroid tissue regardless of location

147
Q

What are the advantages of radioiodine treatment of feline hyperthyroidism?

A
  • Curative – addresses non-cervical thyroid tissue as well as metastatic disease
  • No/limited long term need for treatment/monitoring
  • No anaesthesia
148
Q

What are the disadvantages of radioiodine treatment of feline hyperthyroidism?

A
  • Expense
  • Period of isolation from owner
  • Period of handling restrictions
  • Irreversible – if iatrogenic hypothyroidism sometimes need to supplement levothyroxine
149
Q

Why is surgery a semi-curative option for feline hyperthyroidism?

A
  • Greater risk of leaving some tissue behind
  • Stabilisation with medical therapy
  • Risk of recurrence
150
Q

What are the advantages of surgical management of feline hyperthyroidism?

A
  • Often curative
  • Readily available
  • No/limited ongoing treatment/monitoring
151
Q

What are the disadvantages of surgical management of feline hyperthyroidism?

A
  • Short-term expense
  • Period of hospitalisation
  • Risk of anaesthesia
  • Risk of surgical trauma/damage to local structures
  • Risk of post-operative hypoparathyroidism
  • Irreversible
152
Q

How can you get post-operative hypoparathyroidism when surgically managing feline hyperthyroidism?

A
  • Parathyroid glands closely anatomically related to thyroid glands
  • Primarily a risk in bilateral thyroidectomy
  • After bilateral thyroidectomy, monitor ionised calcium at least once daily for 4-7 days
153
Q

How is post-operative hypoparathyroidism when surgically managing feline hyperthyroidism managed?

A
  • Mild, transient hypocalcaemia is common and may not require treatment
  • Marked or clinical signs of hypocalcaemia, requires treatment – calcium and vitamin D supplementation
154
Q

What is iodine restricted dietary management for feline hyperthyroidism?

A
  • The principles are chronic dietary iodine restriction – limits thyroid hormone production
  • Possibility of goitre developing
  • Diet must be fed exclusively – not with drugs
155
Q

What are the advantages of iodine restricted dietary management for feline hyperthyroidism?

A
  • No pills, no surgery, no isolation
  • Relatively affordable
156
Q

What are the disadvantages of iodine restricted dietary management for feline hyperthyroidism?

A
  • Takes longer to respond to treatment
  • Does not typically achieve T4 in lower half of reference range
  • Submaximal clinical improvement
157
Q

What are the uses of glucocorticoids in the body?

A
  • Regulation of metabolism
  • Modulation of the stress response
  • Anti-inflammatory and immune function
  • Influence blood pressure and gastrointestinal function
158
Q

What is the effect of steroids such as prednisolone on cortisol secretion?

A

Steroids/prednisolone usage suppresses CRH and ACTH production so can’t stop suddenly after giving for more than 1-2 months as they have down regulated this so need to taper this so they can upregulate endogenous production of cortisol.

159
Q

Describe pituitary dependent hyperadrenocorticism.

A

Autonomously functioning pituitary tumour causes excessive ACTH secretion and so leads to bilateral adrenocortical hypertrophy and excessive cortisol secretion. Macroademonas may additionally cause primary neurological signs.

160
Q

Describe adrenal dependent hyperadrenocorticism.

A

Unregulated cortisol secretion, independent of ACTH. Excess cortisol causes suppressed ACTH, CRH and leads to contralateral adrenal atrophy. Broadly, PDH more likely in smaller, ADH more likely in larger (>20kg)

161
Q

What are the clinical signs of hyperadrenocorticism?

A
  • Profound PUPD is exceptionally common with/without nocturia
  • Polyphagia
  • Bilateral symmetrical flank/generalised alopecia
  • Secondary pyoderma, hyperpigmentation, comedomes, thin skin, calcinosis cutis
  • Pot-bellied/pendulous abdomen
  • Muscle wastage with/without weakness causes lethargy and exercise intolerance
  • Muscle loss and fat gain from catabolic steroids
  • Panting – underlying reduced pulmonary function
162
Q

How is hyperadrenocorticism diagnosed?

A

In the presence of a justified clinical suspicion, start with haematology, serum biochemistry, urinalysis and blood pressure – common haematological findings are mild increase HCT, thrombocytosis, features of a stress leukogram (due to presence of cortisol).

163
Q

Describe the blood biochemistry results for a dog with hyperadrenocorticism.

A
  • Moderate markedly increased ALP activity
  • With/without concurrent ALT (lesser)
  • Hypercholesterolaemia
  • Hypertriglyceridaemia
164
Q

Describe the urinalysis of a dog with hyperadrenocorticism.

A
  • Poorly concentrated urine due to PUPD – USG 1.014
  • Proteinuria – UPC 1.26, with a quiescent sediment
  • Many cases may have bacteriuria – asymptomatic bacteria so not do treat
165
Q

Why do we have to be very certain about diagnosing hyperadrenocorticism?

A

Drugs we give to treat are very potent

166
Q

How does cortisol:creatinine ration relate to hyperadrenocorticism diagnosis?

A

A normal urine cortisol:creatinine ratio (UCCR) essentially excludes HAC

High ratio indicates HAC

167
Q

How are ACTH stimulation tests done to diagnose hypoadrenocorticism?

A

Measure serum cortisol pre and 1 hour post a single intravenous injection of synthetic ACTH

NAI/non-adrenal illness may mimic any of these patterns – a dog with cancer could have high cortisol level due to the metabolic strain from the cancer

168
Q

How can non-adrenal illness be distinguished from PDH and ADH patterns?

A

Give dexamethasone after measuring baseline, then 3-4 and then 8 hours later remeasure. Dex should suppress ability to produced cortisol for at least 8 hours, so normal dog would be suppressed. HAC dogs would produce cortisol regardless, would transiently decreased at 3-4 hours but spike again at 8 hours

169
Q

How useful is diagnostic imaging in diagnosing hyperadrenocorticism?

A
  • Useful to differentiate PDH vs ADH and identify concurrent disease
  • Abdominal ultrasound - adrenal size, except hepatomegaly, concurrent gall bladder mucocoeles
  • May facilitate surgical planning
  • CT to evaluate for pituitary mass
170
Q

What is the gold standard management for hyperadrenocorticism?

A

Surgery is gold standard. Can give medical therapy, radiotherapy or do nothing (these are happy dogs, PUPD is often more of an issue for owners than the dogs).

171
Q

What is trilostane treatment of hyperadrenocorticism?

A
  • Synthetic steroid analogue
  • Inhibits 3β-hydroxysteroid dehydrogenase - required in production of cortisol and aldosterone
  • Typically reversible suppression of steroid hormone synthesis
172
Q

What is done if trilostane treatment of hyperadrenocorticism causes adverse effects?

A
  • Provide supportive management and withdraw trilostane until clinically (and laboratory) recovered
  • Re-start trilostane at a lower dose
173
Q

What is the optimal dosing for trilostane?

A

Twice daily dosing – lower total daily dose (cheaper, less risk of adverse events as they will start to peak again by the end of the day on 1 dose) and better clinical control, (Better survival?)

Start 1mg/kg twice daily

174
Q

What do endocrinologically active incidentalomas produce and cause?

A

Cortisol producing – i.e. hyperadrenocorticism

Mineralocorticoid producing – i.e. hyperaldosteronism (Conn’s syndrome)

Catecholamine producing – i.e. phaeochromocytoma

175
Q

What are the electrolyte disturbances caused by Conn’s syndrome/phaeochromocytoma?

A

Hypertensive and hypokalaemia as they retain sodium

176
Q

What are the clinical signs of Conn’s syndrome/phaeochromocytoma?

A

Often episodic
- Lethargy
- Weakness
- Collapse
- Irritability
- Hypertension
- Arrythmias
- PUPD

177
Q

What causes PUPD in feline hyperadrenocorticism/feline cushing’s?

A

Secondary diabetes mellitus which causes the PUPD, not directly from HAC

178
Q

What are the clinical signs of feline hyperadrenocorticism?

A

Skin fragility
Alopecia - failed regrowth instead of specific pattern

179
Q

What is the normal RAAS stimulation in health?

A

Low bp = RAAS stimulation = aldosterone production = sodium resorption, potassium excretion, vasoconstriction

180
Q

How is primary hyperaldosteronism diagnosed?

A
  • Hypokalaemia and/or hypertension causing raised suspicion
  • Exclude chronic kidney disease, diabetes mellitus, vomiting/diarrhoea, inappetence/anorexia
  • Abdominal ultrasound – typically unilateral adrenal mass
  • Serum aldosterone concentration
181
Q

How is primary hyperaldosteronism treated?

A

Adrenalectomy

When surgery not an option:
- Spironolactone – aldosterone antagonist
- Chronic potassium supplementation
- Medical management of hypertension

182
Q

What is diabetes mellitus?

A
  • Insulin deficiency and/or insulin resistance through a lack of insulin action or hyperglycaemia
  • Osmotic polyuria with compensatory polydipsia – owners may misperceive nocturia as incontinence
  • Lack of intracellular glucose may be perceived as starvation through polyphagia and weight loss
183
Q

What is type 1 diabetes mellitus?

A

Insulin dependent DM. Absolute insulin deficiency due to irreversible loss of beta cell function – necessity of exogenous insulin for treatment/survival, gestational diabetes is an exception

184
Q

What are the multifactorial aetiologies of type 1 diabetes mellitus?

A
  • Breed predispositions
  • Immune mediated
  • Environmental factors – obesity, steroids, progestogens, pancreatitis, chronic insulin antagonistic diseases
185
Q

What are the findings on clinical examination of diabetes mellitus?

A

Almost all dogs are presented due to PUPD, PP and weight loss

Examination findings are often normal, but may include diabetic cataracts with/without uveitis and visual impairment, hepatomegaly and poor coat quality

186
Q

Why does diabetes mellitus result in glucosuria?

A
  • Diabetes mellitus causes persistent hyperglycaemia
  • ‘Renal threshold’ for glucose >10-12mmol/l (blood) causing glucosuria
  • Persistent hyperglycaemia with glucosuria = DM
187
Q

What is transient and/or mild hyperglycaemia the result of?

A

Below renal threshold without glucosuria can happen with stress and insulin resistant states

188
Q

What is glucosuria without hyperglycaemia the result of?

A

Renal tubular disorder

189
Q

What are the laboratory findings of diabetes mellitus from haematology, biochemistry, urinalysis and blood pressure?

A
  • Hyperglycaemia with glucosuria
  • Mild-moderate (typically cholestatic) hepatopathy
  • Hyperlipaemia (cholesterol/triglycerides)
  • Urine retains reasonable USG despite PU, due to impact of glucose
  • With/without ketonuria
  • With/without evidence of bacteriuria
  • Hypertensive
190
Q

You are presented with a 7 year old female entire border collie, with a 3 week history of PUPD and weight loss. A urine sample demonstrates glucosuria (++++) but is otherwise unremarkable. Is this sufficient to make a diagnosis of diabetes mellitus?

A

No, have to check if she is hyperglycaemic first

191
Q

Her fasting blood glucose is 4.8mmol/l (ref. 3.5-5.0mmol/l). What is the cause of her glucosuria?

A

Tubulopathy

192
Q

Which concurrent diseases contribute to insulin resistance?

A
  • Chronic infections – dermatological, dental
  • Chronic inflammatory disease – pancreatic, intestinal
  • Endocrinopathies – hyperadrenocorticism, hypothyroidism
  • Neoplasia
193
Q

What is the cornerstone of therapy for diabetes mellitus?

A
  • Exogenous insulin
  • Starting dose 0.25iu/kg (per dose)
  • Every 12 hours, subcutaneously at mealtimes
  • Ensure patient eating first
194
Q

What is the adjunctive management used for diabetes mellitus?

A
  • Dietary modification - high fibre, high complex carbohydrates. low simple sugar
  • Exercise - daily consistency
  • Neutering entire female bitches (cautious of ovarian remnant)
  • Discontinue any insulin antagonistic
195
Q

What is the primary goal of therapy of diabetes mellitus?

A

The primary goal of therapy is to achieve a good patient/owner quality of life – clinical signs are more important than numbers – animals do not live for decades with this disease to suffer the consequences of the effects of mild hyperglycaemia long term unlike humans

196
Q

What are the principles of glucose curves?

A
  • Only test that can determine peak and duration of insulin action, and presence of hypoglycaemia, insulin resistance or Somogyi overswing
  • Time 0 (pre-insulin) and q2 hour samples
  • Subject to error – ear prick samples, stress/anxiety
197
Q

Describe ideal glucose curves.

A
  • Glucose ranges from 4.5-17mmol/l throughout the day
  • Mean across all readings of 14mmol/l
  • Nadir (lowest glucose) 4.5-7.3mmol/l – around 8 hours post injection
198
Q

Describe glucose curves that are too short.

A
  • Initial blood glucose >17mmol/l
  • And nadir occurs within 6 hours of injection
  • And post-nadir glucose increase to >17mmol/l
199
Q

Describe glucose curves that are too long.

A

Glucose nadir occurring >12 hours post-injection, consider changing insulin type or frequency

200
Q

What is Somogyi overswing?

A
  • Physiologic response to impending hypoglycaemia, occurs when Nadir is too low
  • Rapid drop in glucose, regardless of specific value (nadir within 2-3 hours of injection
  • Consequential rebound ‘protective’ period of seemingly insulin resistant hyperglycaemia
201
Q

How are GI complications of diabetes mellitus managed?

A

Inappetance:
- If eat >50% meal – insulin as usual
- If eat 0-50% meal – half dose insulin
- If persists more than a few days, or other signs – investigate

Vomiting – if bright, appetent = manage as above

202
Q

What is hypoglycaemia as a complication of diabetes mellitus usually associated with?

A
  • Inappetance/anorexia and ongoing insulin administration
  • Erratic exercise/feeding regime
  • Resolution/fluctuation of disease causing insulin resistance
203
Q

What is hypoglycaemia as a complication of diabetes mellitus managed?

A

Decrease future insulin doses by 25-50% - repeat glucose curve after 1 week of the new dose

204
Q

What are 4 mechanisms of hypoglycaemia?

A
  • Inadequate synthesis
  • Excessive consumption - sepsis
  • Excessive hypoglycaemic agents
  • Paraneoplastic, insulinoma, hepatomas, IGF-2 producing tumours
205
Q

What are 3 differentials of inadequate synthesis causing hypoglycaemia?

A
  • Hepatic dysfunction/portosystemic shunting
  • Toy dog hypoglycaemia – inadequate glycogen stores
  • Hypoadrenocorticism
206
Q

What other causes of hyperglycaemia occur in dogs?

A

Stress/anxiety can theoretically cause stress related hyperglycaemia – rarely observed in dogs – can exclude by confirming concurrent glucosuria and/or elevated fructoasmine

Diseases causing insulin resistance may cause mild ‘pre-diabetic’ hyperglycaemia

207
Q

When do cataracts occur in diabetes mellitus?

A

Poorly controlled dogs at most risk
Irreversible

208
Q

How is feline diabetes mellitus different from canine diabetes mellitus?

A
  • Cats typically experience type 2 (non-insulin dependent) DM
  • More susceptible to stress induced hyperglycaemia
  • Diabetes in cats can go into remission
  • Insulin and dietary recommendations differ in cats
209
Q

Why doe cats experience type 2 diabetes mellitus?

A
  • Relative insulin insufficiency due to beta-cell dysfunction and/or
  • Concurrent diseases causing insulin resistance - exogenous glucocorticoids or progestogens, chronic inflammatory diseases, hyperthyroidism, acromegaly
210
Q

What is done because cats are more susceptible to stress induced hyperglycaemia?

A
  • Essential to evaluate for concurrent glucosuria and/or increased fructosamine to confirm diagnosis
  • This adds complexity to interpretation of hospital based glucose curves
  • Cats also have a higher renal threshold for glucose
211
Q

Describe insulin diets for cats.

A
  • In the UK, protamine zinc insulin
  • Elsewhere, glargine – not preferred as this is peakless and does not produce a normal glucose curve
  • Optimal diabetic diets are high protein, low carbohydrate (do not od well with high fibre like dogs do)
212
Q

What oral therapy is available for cats with diabetes mellitus?

A
  • Velaglifozin; sodium-glucose co-transporter inhibitor – senvelgo
  • If develop DK/A – are usually euglycaemic, very hard to detect diabetic ketoacidosis as they will never be hyperglycaemic again
  • An option for owners not able to inject
213
Q

When is remission more likely in cats with diabetes mellitus?

A
  • Recent steroid treatment - easy removal of source of insulin resistance
  • Lack of concurrent diseases causing insulin resistance
  • Excellent diabetic control
  • Newer insulins
  • Prescription diabetic diets
214
Q

What are the complications of diabetes mellitus in cats?

A
  • Rarely, if ever, get diabetic cataracts
  • Diabetic neuropathy - typically hindlimbs, manifesting as plantigrade stance, weakness, ataxia, reduced ability to jump with/without reluctance to have feet handled
  • Diabetic nephropathy vs. coexisting CKD
215
Q

What is the consequence of insulin deficiency being a carbohydrate depleted state?

A
  • Cells are glucose depleted
  • Hepatic gluconeogenesis (synthesis of glucose from non-CHOate sources) acts to maintain glucose supply
  • Lipolysis liberates free fatty acids as an alternative energy supply
216
Q

How do ketone bodies form during carbohydrate depletion?

A
  • Liberation of excess Acetyl CoA from fat breakdown
  • Cannot enter the Kreb’s cycle – oxaloacetate is CHOate origin
  • Oxidation of acetyl CoA produces ketone bodies/‘ketosis’ – pear drop smell
  • Ketone bodies are an energy source especially in CHOate depleted states
217
Q

What is the clinical significance of ketone bodies?

A
  • Indicate lipolysis as provision of energy substrate at times of Kreb’s cycle (CHOate provision) failure
  • Due to cellular CHOate deficiency – starvation in puppy toy breeds, DM, failure to uptake into cells
218
Q

When does diabetic ketoacidosis present?

A

Often, especially in novel diabetics presenting with DKA, there is a concurrent disease process – inflammatory, infectious, neoplastic, endocrine

In pre-existing diabetics, chronic sub-optimal insulin therapy may contribute

219
Q

What primary differential needs excluding, in a vomiting patient, with concurrent hyponatraemia, hypochloraemia and hypokalaemia?

A

Upper GI obstruction

220
Q

How is diabetic ketoacidosis diagnosed?

A
  • Dipstix will detect acetone and acetoacetate in the serum or urine
  • Need to measure BHB at lab – the predominant ketone body in canine and feline DK/A patients
221
Q

Distinguish diabetic ketotics and diabetic ketoacidotics.

A

Diabetic ketotics are well patients and treated as per standard DM management. Diabetic ketoacidotics are sick patients and treated with neutral insulin and supportive management as needed.

222
Q

How are diabetic ketotics and diabetic ketoacidotics distinguished on diagnosis?

A
  • Using blood gas analysis
  • Bright, no fluid deficits, eating – treat as standard DM
  • Inappetant, fluid deficits, other signs (vomiting, collapse etc.) – treat as DKA
223
Q

Why is fPLI important to have as additional diagnostics in DKA cases?

A

Feline pancreatic lipase immunoreactivity - important as if he had chronic pancreatitis, scarring and loss of functional tissue, that might be the issue for his beta cell dysfunction, this tells us exocrine pancreatic function

224
Q

How is diabetic ketoacidosis managed?

A

Once euvolaemic and ongoing fluid therapy is being provided to correct interstitial deficit and electrolyte derangements, commence neutral insulin therapy

Monitor blood gas hourly, aim is <14mmol/L, then reduce intensity of insulin therapy. Preferably over a minimum of 8 hours, avoids large osmolarity shifts.

Supplement glucose CSL to mainatin BG 8-17mmol/L

225
Q

How often do we monitor blood gas/glucose/electrolytes in DKA?

A

Every 2-12 hours

226
Q

How are electrolyte derangements caused by DKA corrected?

A

Hypokalaemia – supplement fluids as needed with KCl

Hypophosphataemia
- Severe = haemolysis
- Monitor every 12-48h
- Supplement half of potassium requirement with K phosphate

Sodium – correct no faster than 0.5mmol/l/h

227
Q

An equine patient has a raised ACTH indicating PPID. With what pharmaceutical do you treat him?

A

Pergolide

228
Q

What blood test do you do to see if hyperlipaemic?

A

Triglycerides

229
Q

What organ is often the first to be affected insulin dysregulation?

A

Liver

230
Q

What blood test do you take initially to check liver for function and damage in insulin dysregulation in horses?

A

GGT and bile acids

231
Q

What electrolyte derangement can cause flattened P, wide QRS and spiked T ECG changes?

A

Hyperkalaemia

232
Q

What intravenous therapy can be used to stabilise the cardiomyocyte membranes in hyperkalaemia?

A

Calcium gluconate – has opposite effect than potassium, stabilises the heart

233
Q

What are the differentials diagnoses for hyperkalaemia?

A
  • Inappropriate retention/failed excretion - Addison’s disease, olig/anuric acute kidney injury, urinary tract obstruction/rupture
  • Fluid shifts (e.g. effusions/gastrointestinal sequestration), (massive) cell lysis
  • EDTA contamination
234
Q

How is hypoadrenocorticism diagnosed?

A
  • ACTH stimulation test – evaluate pre and 1 hour post synthetic ACTH IV
  • Failure of stimulation – exclude iatrogenic
  • Causes hypoadrenocorticism (addison’s)
  • Basal cortisol >55nmol/l essentially excludes hypoadrenocorticism
235
Q

What is addison’s disease/hypoadrenocorticism?

A
  • Adrenocortical failure – typically due to idiopathic immune mediated adrenalitis and subsequent atrophy
  • Typically affects the whole adrenal cortex
  • Clinically may see mineralocorticoid (aldosterone) and/or glucocorticoid (cortisol) deficiency
236
Q

How does mineralocorticoid/aldosterone deficiency present on clinical examination?

A
  • Hypovolaemic shock/collapse
  • Hyperkalaemia/hyponatraemia with inappropriate bradycardia for poor perfusion state
237
Q

How does mineralocorticoid/aldosterone deficiency present on laboratory findings?

A
  • Hyperkalaemia with hyponatraemia and hypochloraemia
  • Azotaemia
  • With/without hypercalcaemia (total adn/or ionised)
238
Q

How does glucocorticoid/cortisol deficiency present on clinical examination?

A
  • Waxing/waning GI signs or GI haemorrhage
  • Inappetance, lethargy, weight loss
  • Collapse, exercise intolerance
239
Q

How does glucocorticoid/cortisol deficiency present on laboratory findings?

A
  • With/without lack of or a reverse stress leukogram
  • Lymphocytosis/eosinophilia
  • Neutropenia/monocytopenia
  • With/without anaemia of chronic disease, non-regenerative unless due to GI haemorrhage
  • With/without hypoalbuminaemia, hypocholesterolaemia and hypoglycaemia
240
Q

What is typical and atypical hypoadrenocorticism?

A

Mineralocorticoid deficiency = typical

Glucocorticoid deficiency = atypical

241
Q

How is typical hypoadrenocorticism diagnosed?

A
  • Cortisol pre/post ACTH stimulation test is used to diagnose hypoadrenocorticism
  • Haematological/biochemical findings are utilised to support whether sole (MC or GC) or combined deficiency – if sodium/potassium derangements > MC deficiency present
242
Q

How is hypoadrenocorticism managed?

A
  • Fluid therapy and management of hyperkalaemia is the cornerstone of initial management – avoid correcting Na+ more rapidly than 0.5mmol/l/hour
  • Perform your ACTH stimulation test prior
  • Glucocorticoid therapy is required lifelong
  • Mineralocorticoid therapy is required lifelong hypoadrenocorticoid in patients presenting with evidence of MC deficiency
243
Q

What is glucocorticoid replacement therapy used to treat hypoadrenocorticism?

A
  • All hypoadrenocorticoid dogs require glucocorticoid replacement
  • Once fluid deficits corrected/patient can tolerate oral therapy transition to maintenance therapy. Prednisolone – commence at 0.2-0.25mg/kg/day
  • Taper to lowest effective daily dose
244
Q

What is mineralocorticoid replacement therapy used to treat hypoadrenocorticism?

A
  • Desoxycortone pivalate - start at 1.2mg/kg subcutaneously, every 25 days
  • Monitor Na:K at 10 days post-injection to establish peak effect of DOCP, and at 25 days post-injection to establish duration of DOCP activity
245
Q

What are the characteristics of feline hypoadrenocorticism?

A
  • Rare
  • Most common signs in cats are lethargy and anorexia
  • Cats are slower to respond to treatment
246
Q

Describe calcium and phosphate regulation.

A
  • Low calcium > PTH release > 2 actions – directly released calcium from bone and absorption of calcium In kidney and excretion of phosphate in the kidney > net effect is to increase calcium and reduced phosphate.
  • Some tumours release PTH related PTH peptide that works the same way as PTH autonomously produced from these tumours somewhere else in the body.
  • PTH activates vitamin D in the kidneys > renal calcium and phosphate reabsorption, GI calcium and phosphate reabsorption, and calcium and phosphate mobilisation from bone.
  • High calcium inhibits PTH release in negative feedback loop.
  • But if a tumour that is autonomously producing PTH this is not turned off by the negative feedback loop.
  • Inhibited PTH release through negative feedback causes calcitonin release > renal calcium excretion and storage of calcium intracellularly and in bone > decreased calcium.
247
Q

What are the differential diagnoses of hypercalcaemia using HARDIONSG?

A
  • Primary hyperparathyroidism
  • Addison’s disease (hypoadrenocorticism)
  • Renal disease
  • Hypervitaminosis D
  • Idiopathic (cats)
  • Osteolytic
  • Neoplastic – (PTHrp) anal sac adenocarcinoma, lymphoma, other carcinomas
  • Spurious (lipaemia)
  • Granulomatous (inflammation) / Growth
248
Q

What are the clinical signs of hypercalcaemia?

A

Inappetance
Lethargy
Vomiting
Diarrhoea
Related to primary disease process

249
Q

What is the net effect of parathyroid related protein mediated hypercalcaemia?

A

Calcium increase and phosphate decrease

250
Q

What are the differential diagnoses of parathyroid related protein mediated hypercalcaemia?

A
  • Primary hyperparathyroidism
  • Renal disease
  • Neoplastic – anal sac adenocarcinoma, lymphoma, other carcinomas
251
Q

What is the net effect of vitamin D mediated hypercalcaemia?

A

Increased calcium and increased phosphate

252
Q

What are the differential diagnoses of vitamin D mediated hypercalcaemia?

A
  • Hypervitaminosis D
  • Granulomatous (inflammation)/growth
253
Q

If examination, haem, chem do not elucidate a diagnosis, how is a PTH/rp pattern established?

A

Clinically well dog – primary hyperparathyroidism likely

Clinically unwell dog – neoplasia highly likely

254
Q

If examination, haem, chem do not elucidate a diagnosis, how is vitamin D/analogue pattern established?

A
  • Vitamin D related intoxication – diet, supplements, fish/omega3 oils, psoriasis cream, some houseplants, some rodenticides
  • Granulomatous inflammation - mycobacterial, fungal, other infections
  • Osteolysis
255
Q

How is idiopathic hypercalcaemia in cats diagnosed?

A
  • Haematology, serum biochemistry with/without urinalysis and ACTH stimulation
  • Thoracic, abdominal imaging
  • Sampling of any abnormalities, where appropriate (lymph nodes, structural disease in other organs)
  • Measurement of PTH, PTHrp, vitamin D metabolites
256
Q

How is hypercalcaemia treated?

A
  • Ideally identify and treat the underlying disease
  • 0.9% NaCl (i.e. normal saline) diuresis
  • With/without frusemide
  • With/without glucocorticoids
  • Hypercalcaemia with concurrent hyperphosphataemia
  • Irreversible tissue - mineralisation and renal failure
257
Q

How is idiopathic hypercalcaemia in cats managed effectively without drug therapy?

A
  • Encourage water intake
  • Dietary modification
  • Dietary fibre supplementation
  • Glucocorticoids (prednisolone)
  • Bisphosphonates (aledronate)
258
Q

What are the differential diagnoses of hypocalcaemia?

A
  • True - concurrent hyperkalaemia (EDTA contamination?), concurrent hypoalbuminaemia (check ionised calcium)
  • Pregnancy/lactation
  • Hypoparathyroidism
  • Acute kidney injury
  • Pancreatitis
  • Sepsis
  • Nutritional secondary hyperparathyroidism
  • Hypovitaminosis
259
Q

What are the clinical signs of hypocalcaemia?

A
  • Anorexia, restlessness, behavioural change
  • Facial rubbing, lip-licking – itching nerve endings around the face
  • Twitching, tremors
  • Stiffness, tetany
  • Seizures
259
Q

How is clinically significant hypocalcaemia managed?

A
  • Tolerate mild hypocalcaemia
  • Calcium gluconate bolus IV
  • Oral vitamin D
  • With oral calcium carbonate for first week of therapy
260
Q

What can give high indication for pituitary dependent hyperadrenocorticism?

A

If UCCR over 100

261
Q

What are the most likely causes of chylothorax?

A

CHF, neoplasia, traumatic or idiopathic

262
Q

How would you confirm the cause of chylothorax?

A

Looking for pulmonary oedema so need to do chest x-rays. On echo, look for large LA which implies pulmonary venous congestions (which results in pulmonary oedema)

263
Q

What treatment is given to a cat with CHF causing chylothorax?

A

Frusemide and clopidogrel – prevent formation of saddle thrombus, frusemide not enough to resolve pleural effusion so need to drain too.

264
Q

Quantify polydipsia and polyuria.

A

Polydipsia = water intake >100ml/kg/day
Polyuria = urine production >50ml/kg/day

265
Q

What are the majority of small animal PUPD cases due to?

A

Due to polyuria, with compensatory polydipsia. Water restriction as a control mechanism is absolutely contraindicated

266
Q

Outline the homeostatic mechanism that acts to maintain plasma osmolarity and volume.

A
  1. Increased plasma osmolarity detected by CNS osmoreceptors
  2. Decreased blood pressure detected by baroreceptors
  3. AVP release by the posterior pituitary increased renal water resorption
  4. RAAS stimulated to stimulate thirst and water acquisition via angiotensin II and renal sodium and water conservation by aldosterone.
  5. Decreased plasma osmolarity and increased blood volume
267
Q

What is the physiology of urine production?

A
  • Production of concentrated urine relies upon a hyperosmolar medullary interstitium
  • Vasopressin increases permeability of the collecting duct to water by inserting pores into the collecting duct
  • Leads to osmotic water reabsorption and reduced volume, concentrated urine produced
267
Q

Name 7 mechanisms of PUPD.

A
  • Central diabetes insipidus
  • Primary nephrogenic diabetes mellitus
  • Secondary nephrogenic diabetes insipidus
  • Intrinsic renal disease
  • Osmotic diuresis
  • Psychogenic polydipsia
  • Medullary washout
268
Q

How does central diabetes insipidus cause PUPD?

A
  • Lack of AVP (or ADH) production
  • Markedly dilute urine (even in the presence of dehydration)
  • Secondary to hypothalamic/pituitary lesion
269
Q

How does primary nephrogenic diabetes mellitus cause PUPD?

A
  • Rare
  • Congenital inability of collecting duct to respond to AVP
  • Dogs
270
Q

How does secondary nephrogenic diabetes insipidus cause PUPD?

A
  • Submaximal response of the kidney to AVP/ADH
  • Electrolyte disturbances – hypercalcaemia, hypokalaemia
  • Endocrinopathies
  • Drugs – steroids, phenobarbitone
  • Endotoxins – pyometra, pyelonephritis
  • Metabolic disease
271
Q

How does intrinsic renal disease cause PUPD?

A
  • Nephron loss, resulting in reduced renal concentrating ability, leads to production of dilute urine
  • May be temporary/AKI or permanent/CKD
  • Post-obstructive diuresis
272
Q

How does osmotic diuresis cause PUPD?

A
  • Loss of osmotic substances in urine, with related water loss
  • Diabetes mellitus is the most common example
  • Fanconi syndrome
  • Primary renal glucosuria
  • Iatrogenic - mannitol
273
Q

How does psychogenic polydipsia cause PUPD?

A
  • Primary polydipsia, with compensatory polyuria
  • Bored (often young) dogs
  • Likely other behavioural problems – in clinic might be drinking normally as there is enough going on around them to stimulate them
274
Q

How does medullary washout cause PUPD?

A

Loss of the medullary concentration gradient of the kidneys – urea and or sodium deficit

Another underlying pathophysiological process
- Hyponatraemia, as with hypoadrenocorticism
- Low urea, as in hepatic insufficiency
- Can occur secondary to chronic PUPD of any cause

275
Q

How are PUPD cases approached?

A
  • Confirm the presence of PUPD
  • Be guided by other presenting findings and your clinical examination
  • Start with urinalysis
  • Next step is haematology and biochemistry
  • Abdominal imaging
276
Q

Which drugs may cause PUPD?

A

Diuretics, steroids, phenobarbitone

277
Q

What things on clinical examination must be ruled out when diagnosing PUPD?

A

Exclude pyometra
Young dog – congenital disease

278
Q

How can diagnostics be prioritised using concurrent signs?

A
  • Polyphagia, weight loss – diabetes mellitus, hyperthyroidism
  • Polyphagia, alopecia – hyperadrenocorticism
  • Lymphadenopathy – possible concurrent hypercalcaemia
  • Inappetant/gastrointestinal signs – hypercalcaemia/hypokalaemia, renal disease, liver disease, infection (pyometra, pyelonephritis), hypoadrenocorticism, diabetic ketoacidosis
279
Q

How is urinalysis used to diagnose the cause of PUPD?

A
  • Glucosuria presence = the cause of the PUPD. Diabetes mellitus, tubulopathy, basenji (likely Fanconi). Rule out antibiotics, jerky treats, leptospirosis
  • Asymptomatic bacteriuria – pyelonephritis has to be present to cause PUPD
280
Q

If investigation has not elucidated a cause of PUPD, what are the remaining differentials of PUPD?

A

Central diabetes insipidus (CDI)
Primary nephrogenic diabetes insipidus (NDI)
Psychogenic polydipsia

281
Q

How are central and nephrogenic diabetes insipidus and psychogenic polydipsia differentiated?

A

Quantify in-clinic vs. at home water intake

Measuring serum osmolality can be valuable
- Primary polydipsia (PP) results in hypo-osmolality
- Primary polyuria (CDI, NDI) results in hyper-osmolality

282
Q

How can DDAVP be a valuable diagnostic and therapeutic trial for central and nephrogenic diabetes insipidus and psychogenic polydipsia?

A
  • Dogs with CDI have a notable improvement with DDAVP
  • Dogs with PP may partially improve with DDAVP
  • Primary NDI cannot respond to DDAVP, secondary NDI can partially respond

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