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Small Animal Medicine (GP cert) > Endocrinology AI > Flashcards

Endocrinology AI Flashcards

1
Q

What are the two main forms of canine hyperadrenocorticism?

A

Pituitary-dependent (PDH) and adrenal-dependent (ADH)

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2
Q

What is the difference between pituitary-dependent and adrenal-dependent hyperadrenocorticism?

A

PDH is caused by excess ACTH secretion and bilateral adrenal hyperplasia, while ADH is caused by adrenal adenomas or carcinomas independent of pituitary control.

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3
Q

What is the normal function of the adrenal cortex?

A

The adrenal cortex synthesizes and secretes steroid hormones, including glucocorticoids and mineralocorticoids.

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4
Q

What are the three zones of the adrenal cortex?

A

Zona glomerulosa, zona fasciculata, zona reticularis

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5
Q

What hormones are produced by the zona glomerulosa?

A

Mineralocorticoids, such as aldosterone

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6
Q

What hormones are produced by the zona fasciculata and zona reticularis?

A

Glucocorticoids and sex hormones

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7
Q

What is the role of corticotrophin releasing hormone (CRH)?

A

CRH is synthesized and released by the paraventricular nuclei in the hypothalamus and travels to the anterior pituitary to stimulate the production of ACTH.

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8
Q

What is the initial hormone produced in the synthesis of glucocorticoids and mineralocorticoids?

A

Pregnenolone

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9
Q

What is hyperadrenocorticism (HAC)?

A

HAC is a condition characterized by excessive production of steroid hormones, especially glucocorticoids, from the adrenal cortex.

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10
Q

What are the two forms of spontaneous HAC?

A

Pituitary-dependent (PDH) and adrenal-dependent (ADH)

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11
Q

What percentage of HAC cases are pituitary-dependent?

A

80-90%

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12
Q

What causes pituitary-dependent HAC?

A

Excess ACTH secretion and bilateral adrenal hyperplasia

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13
Q

What are microadenomas and where do they arise from in pituitary-dependent HAC?

A

Microadenomas are tumors <10mm diameter and arise from the pars distalis (70%) or pars intermedia (30%)

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14
Q

What are macroadenomas and what are their characteristics?

A

Macroadenomas are tumors >10mm diameter, slow growing, and do not always produce neurological signs.

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15
Q

What is adrenal-dependent HAC caused by?

A

Adrenal adenomas or carcinomas

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16
Q

What are the two main types of tumors that cause adrenal-dependent HAC?

A

Adrenal adenomas and adrenal carcinomas

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17
Q

What are the differences between microadenomas and macroadenomas?

A

Microadenomas are smaller (<10mm diameter) and more common, while macroadenomas are larger (>10mm diameter) and slower-growing.

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18
Q

What is Cushing’s disease?

A

An alternate name for hyperadrenocorticism (HAC) in reference to the MD who first described the condition in people.

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19
Q

What is iatrogenic HAC?

A

HAC induced by exogenous prednisolone treatment

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20
Q

What is the role of cholesterol in the synthesis of steroid hormones?

A

All steroid hormones are derived from cholesterol.

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21
Q

How are steroid hormones transported in the blood?

A

Steroid hormones are transported in association with proteins such as transcortin due to their lipophilic nature.

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22
Q

Which enzyme is inhibited by Trilostane in the synthesis of steroids?

A

3 β hydroxysteroid dehydrogenase

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23
Q

What hormone is involved in the regulation of electrolyte balance?

A

Aldosterone, which is produced by the zona glomerulosa in the adrenal cortex.

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24
Q

What is the main cause of pituitary-dependent HAC?

A

Excess ACTH secretion and bilateral adrenal hyperplasia

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25
Q

What is the pituitary portal blood system?

A

The system through which corticotrophin releasing hormone (CRH) travels from the hypothalamus to the anterior pituitary.

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26
Q

What is the normal negative feedback mechanism in HAC?

A

In HAC, the negative feedback mechanism fails and excessive amounts of steroid hormones are produced.

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27
Q

What is the role of ACTH in HAC?

A

ACTH stimulates the production of glucocorticoids from the zona fasciculata and zona reticularis in the adrenal cortex.

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28
Q

What do the paraventricular nuclei in the hypothalamus synthesize and release?

A

Corticotrophin releasing hormone (CRH)

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29
Q

What are the clinical signs of hyperadrenocorticism?

A

Clinical signs relate to abnormal concentrations of steroid hormones and can include polyuria, polydipsia, polyphagia, abdominal distension, muscle wasting, etc.

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30
Q

What routine laboratory tests are used in the diagnosis of hyperadrenocorticism?

A

Routine laboratory tests include measurement of serum alkaline phosphatase (ALP) activity, alanine transaminase (ALT) activity, etc.

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31
Q

What screening tests are used for the diagnosis of hyperadrenocorticism?

A

Screening tests include the low-dose dexamethasone suppression test, the urine cortisol-to-creatinine ratio, and the ACTH stimulation test.

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32
Q

What are the two main forms of hyperadrenocorticism in cats?

A

There are no specific mentions of the two main forms in the given text.

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33
Q

What are the two main types of tumors that cause adrenal-dependent HAC in dogs?

A

Adrenal adenomas and adrenal carcinomas

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34
Q

What is the role of the adrenal medulla?

A

The adrenal medulla synthesizes and secretes amines.

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35
Q

What hormones are produced by the adrenal medulla?

A

Amines

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36
Q

What hormone is released by the pituitary gland in response to CRH stimulation?

A

ACTH

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37
Q

What are the clinical signs of pituitary-dependent HAC?

A

Clinical signs can include polyuria, polydipsia, panting, polyphagia, abdominal distension, muscle wasting, etc.

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38
Q

Which cells in the anterior pituitary produce ACTH?

A

Corticotrophin cells

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39
Q

What is the role of aldosterone?

A

Aldosterone is a mineralocorticoid hormone involved in the regulation of electrolyte balance.

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40
Q

What are the complications of canine hyperadrenocorticism?

A

The given text does not explicitly mention the complications of canine hyperadrenocorticism.

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41
Q

What is the role of the brain in accurate planning?

A

The brain is essential for accurate planning.

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42
Q

What can diagnostic imaging be used for in relation to tumours of the adrenal cortex?

A

Diagnostic imaging can be used to distinguish between benign and malignant tumours of the adrenal cortex.

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43
Q

What can happen if malignant tumours of the adrenal cortex invade the caudal vena cava?

A

Malignant tumours may invade the caudal vena cava.

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44
Q

Where can malignant tumours of the adrenal cortex spread to?

A

Malignant tumours can spread to the liver and lungs.

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45
Q

What is the purpose of the high-dose dexamethasone suppression test?

A

The high-dose dexamethasone suppression test inhibits pituitary ACTH secretion and suppresses cortisol concentrations.

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46
Q

How does the high-dose dexamethasone suppression test work in pituitary-dependent hyperadrenocorticism?

A

The high dose of dexamethasone inhibits pituitary ACTH secretion through negative feedback in pituitary-dependent hyperadrenocorticism thus suppressing cortisol concentrations.

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47
Q

Are adrenocortical tumours autonomous?

A

Yes, adrenocortical tumours are autonomous and thus cortisol is not suppressed.

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48
Q

Is the high-dose dexamethasone suppression test a good discriminatory test?

A

No, approximately 20 to 30 per cent of pituitary-dependent cases will not suppress with this test, making it a poor discriminatory test.

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49
Q

What are the potential complications of leaving hyperadrenocorticism (HAC) untreated?

A

Complications of untreated HAC include pulmonary thromboembolism, diabetes, pancreatitis, and infection.

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50
Q

How long can most cases of untreated HAC survive?

A

Most cases of untreated HAC will live 6-24 months.

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51
Q

How long can well-managed cases of HAC live on therapy?

A

Well-managed cases of HAC can live for several years on therapy.

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52
Q

What is the recommended first choice drug for the management of pituitary dependent disease (PDH)?

A

Trilostane should be the first choice drug for the management of PDH (80-90% of cases).

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53
Q

What is trilostane?

A

Trilostane is a synthetic steroid with no inherent hormonal activity.

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54
Q

How does trilostane work in blocking adrenal synthesis of glucocorticoids, mineralocorticoids, and sex hormones?

A

Trilostane acts as a competitive inhibitor of the 3ß-hydroxysteroid dehydrogenase enzyme system, blocking adrenal synthesis.

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55
Q

What factors should be considered when administering trilostane?

A

Trilostane should not be used in dogs with primary hepatic disease or renal failure.

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56
Q

How frequently should clinical examination and laboratory testing be performed in trilostane-treated dogs?

A

Clinical examination and laboratory testing should be performed at 10 days, 4 weeks, 12 weeks, and every 3 months thereafter.

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57
Q

When should the ACTH stimulation test be performed in trilostane-treated dogs?

A

The ACTH stimulation test should be performed 4-6 hours after dosing with trilostane.

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58
Q

What cortisol concentration indicates adequate control 4-6 hours after trilostane administration?

A

A post-ACTH cortisol concentration of >20 but <150 nmol/l indicates adequate control.

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59
Q

What should be considered if the ACTH stimulation test result shows a cortisol value >150 in a trilostane-treated dog?

A

Consideration should be given to increasing the dose by 50% and re-testing.

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60
Q

Do all dogs require once daily dosing of trilostane?

A

No, some dogs require twice daily dosing to achieve adequate control of clinical signs over a 24-hour period.

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61
Q

What should owners be warned about regarding trilostane treatment?

A

Owners should be warned about the risk of side effects, including sudden death.

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62
Q

How quickly may polyuria/polydipsia (PU/PD) resolve after starting trilostane treatment?

A

PU/PD may resolve within a few days of treatment commencing.

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63
Q

How long may it take for other dermatological manifestations of hyperadrenocorticism to improve with trilostane treatment?

A

Other dermatological manifestations may take several months to improve with trilostane treatment.

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64
Q

What percentage of dogs treated with trilostane have resolution of clinical signs of PU/PD?

A

Approximately 70% of dogs treated with trilostane have resolution of clinical signs of PU/PD.

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65
Q

What percentage of dogs treated with trilostane have resolution of skin changes?

A

Approximately 60% of dogs treated with trilostane have resolution of skin changes.

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66
Q

Does the clinical response to trilostane vary among cases?

A

Yes, some cases require increasing doses of trilostane, while others may show spontaneous remission requiring lower doses or even cessation of treatment.

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67
Q

What complications have been reported in trilostane-treated dogs?

A

Complications reported include diarrhea, acute pancreatitis, and rare cases of sudden death.

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68
Q

What does an elevated cortisol production pathway suggest?

A

An abnormality in the cortisol production pathway.

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69
Q

What is the difference between classic ‘Cushing’s disease’ and the abnormal cortisol production seen in recent studies?

A

Classic ‘Cushing’s disease’ shows overproduction of cortisol, while recent studies suggest an abnormality in the cortisol production pathway.

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70
Q

Why doesn’t the author recommend the use of the high-dose dexamethasone suppression test?

A

Its accuracy has been questioned and it is not recommended for differentiating the cause of hyperadrenocorticism.

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71
Q

What is the recommended test for differentiating pituitary and adrenal causes of hyperadrenocorticism?

A

Canine ACTH assays, specifically measuring the plasma ACTH concentration.

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72
Q

Which diagnostic imaging technique is sensitive in distinguishing dogs with pituitary-dependent hyperadrenocorticism from those with adrenocortical tumors?

A

Abdominal ultrasonography.

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73
Q

How can dogs with adenomas be distinguished from dogs with carcinomas?

A

Recognition of metastatic lesions with radiography and/or ultrasonography.

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74
Q

What is the use of measuring basal endogenous ACTH concentrations in the diagnosis of hyperadrenocorticism?

A

It has no value due to episodic secretion of ACTH in normal dogs and overlapping values with those with hyperadrenocorticism.

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75
Q

What is the range of endogenous ACTH concentrations in normal dogs?

A

13 to 46 pg/ml.

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76
Q

What do very low endogenous ACTH concentrations (< 5 pg/ml) indicate in dogs with hyperadrenocorticism?

A

Adrenal tumors.

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77
Q

What do high normal to high concentrations (> 28 pg/ml) of endogenous ACTH indicate in dogs with hyperadrenocorticism?

A

Pituitary-dependent hyperadrenocorticism.

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78
Q

Which imaging techniques can be used to differentiate pituitary-dependent hyperadrenocorticism and adrenal-dependent hyperadrenocorticism?

A

Abdominal radiography, ultrasonography, CT, and MRI.

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79
Q

What suggests pituitary-dependent hyperadrenocorticism?

A

Similar size and normal shape of both adrenal glands.

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80
Q

What suggests adrenal-dependent hyperadrenocorticism in a dog with confirmed hyperadrenocorticism?

A

A mass in the adrenal area.

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81
Q

Which imaging technique accurately localized all adrenocortical tumors in a study?

A

CT.

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82
Q

Why is abdominal radiography less accurate than CT in localizing adrenocortical tumors?

A

Tumors less than 20 mm in diameter cannot be seen on abdominal radiographs.

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83
Q

What can CT identify in relation to adrenocortical tumors?

A

Invasion of the caudal vena cava by the tumor and adhesions between the adrenal gland and the caudal vena cava.

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84
Q

Which imaging technique is superior to CT in detecting ACTH-secreting tumors of the pituitary gland in humans?

A

MRI.

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85
Q

How small pituitary tumors can be detected using MRI in dogs and cats?

A

As small as 3 mm.

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86
Q

Are large pituitary tumors associated with neurological signs in dogs?

A

Not always, as some large tumors have been shown to be present without causing neurological signs.

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87
Q

What has been shown in another study regarding pituitary masses and neurological signs?

A

Pituitary masses ranging in size from 8 to 24 mm were associated with neurological signs.

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88
Q

What are some neurological signs associated with a rapid enlargement of a pituitary tumor?

A

Neurological signs associated with a rapid enlargement of a pituitary tumor can include adrenal necrosis and acute hypoadrenocorticism or thromboembolism.

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89
Q

What are the potential adverse effects of trilostane treatment in dogs with hyperadrenocorticism?

A

Potential adverse effects of trilostane treatment in dogs with hyperadrenocorticism include sudden death and adrenal necrosis.

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90
Q

Why is awareness of adrenal necrosis in dogs receiving trilostane treatment important?

A

Awareness of adrenal necrosis in dogs receiving trilostane treatment is important because prompt treatment is required to correct this life-threatening situation.

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91
Q

What is mitotane and how effective is it in the management of hyperadrenocorticism?

A

Mitotane is a drug used in the management of hyperadrenocorticism and it remains a very effective drug, although it can have potentially fatal side effects.

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92
Q

What were the findings of the study comparing the survival times of dogs treated with mitotane or trilostane for pituitary-dependent hyperadrenocorticism?

A

The study found no significant difference in survival times between dogs treated with mitotane or trilostane for pituitary-dependent hyperadrenocorticism.

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93
Q

What is the best prognosis for dogs with adrenal-dependent hyperadrenocorticism?

A

Dogs with adrenal-dependent hyperadrenocorticism have the best prognosis if the tumor can be completely removed surgically.

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94
Q

What should be included in the pre-operative staging of an adrenal tumor in dogs?

A

The pre-operative staging of an adrenal tumor in dogs should include thoracic radiographs and abdominal ultrasound to assess vascular invasion and metastatic spread.

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95
Q

What are the recommended treatments to control hyperadrenocorticism before surgical adrenalectomy?

A

Some authors recommend the administration of trilostane or mitotane before surgical adrenalectomy to attempt to control hyperadrenocorticism.

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96
Q

What are the requirements for unilateral adrenalectomy in dogs?

A

Unilateral adrenalectomy in dogs requires considerable experience and expertise due to the complex anatomy. Glucocorticoid and mineralocorticoid supplementation are necessary during and after the surgery.

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97
Q

What was the perioperative mortality rate observed in a study on unilateral adrenalectomy in dogs?

A

In a study, the perioperative mortality rate for unilateral adrenalectomy in dogs was 30 percent.

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98
Q

What is the purpose of trilostane therapy in dogs with adrenal-dependent hyperadrenocorticism?

A

Trilostane therapy aims to provide symptomatic control of clinical signs without treating the underlying neoplastic disease process.

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99
Q

What was the reported survival time in one case using trilostane therapy for an adrenal tumor in dogs?

A

In one case, an 80-week survival was reported in a dog with an adrenal tumor using trilostane therapy.

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100
Q

What is mitotane therapy and how is it used in the treatment of adrenal-dependent hyperadrenocorticism?

A

Mitotane therapy is used in the treatment of adrenal-dependent hyperadrenocorticism and it has been recommended for this condition with similar results to surgical treatment.

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101
Q

What is the current status of mitotane’s licensing and its usage?

A

Mitotane is no longer licensed and as a result, it is rarely used in the management of hyperadrenocorticism.

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102
Q

What are some common clinical signs of hyperadrenocorticism (HAC)?

A

Polyuria, polydipsia, polyphagia, panting, abdominal distension

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103
Q

What are some hematologic abnormalities commonly observed in HAC?

A

Eosinopaenia, neutrophilia, monocytosis, erythrocytosis

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104
Q

What is the typical urinalysis finding in HAC?

A

Isosthenuria or hyposthenuria

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105
Q

What percentage of HAC cases demonstrate glycosuria?

A

Approximately 10%

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106
Q

What are some common findings on abdominal radiographs of HAC patients?

A

Good contrast, hepatomegaly, distended bladder, calculi, adrenal enlargement

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107
Q

What might be seen on thoracic radiographs of HAC patients?

A

Tracheal and bronchial wall mineralization, pulmonary metastasis, osteoporosis

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108
Q

When should diagnostic tests for HAC be performed?

A

In animals with consistent histories and clinical signs

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109
Q

What is the purpose of performing at least one positive screening test for HAC?

A

To confirm the need for further diagnostic testing

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110
Q

What are some options for diagnostic testing of HAC?

A

ACTH stimulation test, Low Dose Dexamethasone Suppression (LDDS) test, High Dose Dexamethasone Suppression (HDDS) test, Endogenous ACTH assay, 17 alpha-OH progesterone assay, Urinary cortisol: creatinine ratio

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111
Q

Which screening test is very sensitive but not very specific for HAC?

A

Urine Cortisol: Creatinine ratio

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112
Q

What is the recommended way to collect urine samples for the cortisol:creatinine ratio test?

A

In as stress-free a way as possible, usually at home

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113
Q

What is the sensitivity of the ACTH stimulation test for detecting PDH?

A

Approximately 85%

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114
Q

When should HAC not be automatically excluded based on the ACTH stimulation test results?

A

If the ACTH result is within the reference interval

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115
Q

What is the preferred test for monitoring mitotane and trilostane treatment?

A

ACTH stimulation test

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116
Q

What is the purpose of the LDDS test in diagnosing HAC?

A

To induce negative feedback to the pituitary and detect cortisol suppression

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117
Q

What does a positive result on the LDDS test indicate?

A

Resting cortisol > 40 nmol/l at 8 hours (not suppressed)

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118
Q

What is the purpose of the 17 alpha-OH progesterone assay?

A

To detect HAC cases that are negative on other tests

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119
Q

What is o.p.’ -DDD?

A

o.p.’ -DDD is a medication used in dogs with adrenal-dependent hyperadrenocorticism.

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120
Q

Is o.p.’ -DDD effective in dogs with adrenal-dependent hyperadrenocorticism?

A

Yes, o.p.’ -DDD is effective in dogs with adrenal-dependent hyperadrenocorticism.

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121
Q

Is o.p.’ -DDD relatively safe in dogs with adrenal-dependent hyperadrenocorticism?

A

Yes, o.p.’ -DDD is relatively safe in dogs with adrenal-dependent hyperadrenocorticism.

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122
Q

Are dogs with adrenal tumours more resistant to mitotane than dogs with pituitary-dependent hyperadrenocorticism?

A

Yes, dogs with adrenal tumours tend to be more resistant to mitotane than dogs with pituitary-dependent hyperadrenocorticism.

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123
Q

What dose range is generally required for dogs with adrenal-dependent hyperadrenocorticism during the induction period?

A

Dogs with adrenal-dependent hyperadrenocorticism generally require higher daily induction doses of 50-75 mg/kg/day.

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124
Q

Is a longer period of induction required for dogs with adrenal-dependent hyperadrenocorticism compared to dogs with pituitary-dependent hyperadrenocorticism?

A

Yes, dogs with adrenal-dependent hyperadrenocorticism require a longer period of induction (>14 days) than dogs with pituitary-dependent hyperadrenocorticism.

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125
Q

What percentage of cases responded successfully to the recommended protocol for pituitary-dependent hyperadrenocorticism?

A

About 20 percent of cases responded successfully to the recommended protocol for pituitary-dependent hyperadrenocorticism.

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126
Q

Why is frequent monitoring of treatment by ACTH stimulation testing important?

A

Frequent monitoring of treatment by ACTH stimulation testing is important to ensure adequate control of the hyperadrenocorticism.

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127
Q

Are maintenance doses generally higher for dogs with adrenal-dependent hyperadrenocorticism?

A

Yes, maintenance doses are generally higher (75-100 mg/kg/week) for dogs with adrenal-dependent hyperadrenocorticism.

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128
Q

Why is frequent monitoring of the cortisol response to ACTH stimulation required for dogs with adrenal-dependent hyperadrenocorticism?

A

Frequent monitoring of the cortisol response to ACTH stimulation is required to maintain optimal control of the disease.

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129
Q

Do dogs requiring higher dose rates of mitotane tend to be more prone to adverse effects?

A

Yes, dogs requiring higher dose rates of mitotane tend to be more prone to adverse effects.

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130
Q

What can happen to the adrenal tumour and metastatic mass during mitotane therapy?

A

The adrenal tumour and metastatic mass can often reduce in size due to the cytotoxic effects of mitotane.

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131
Q

Does the tumour always shrink during mitotane therapy?

A

No, in some cases the tumour will continue to grow despite increasing doses of mitotane.

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132
Q

What was the median survival time in a study of adrenocortical tumours treated using mitotane therapy?

A

The median survival time was 11 months.

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133
Q

What was the range of survival time in a study of adrenocortical tumours treated using mitotane therapy?

A

The range of survival time was a few weeks to more than 5 years.

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134
Q

What are the clinical signs of hyperadrenocorticism (HAC)?

A

Polyphagia, PU/PD, abdominal enlargement, muscle weakness

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135
Q

What are the predisposed breeds for pituitary-dependent hyperadrenocorticism (PDH)?

A

Poodles, Dachshunds, small Terriers

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136
Q

What are the clinical signs of hyperadrenocorticism (HAC) in small breed dogs?

A

Abdominal enlargement, polyphagia, PU/PD

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137
Q

What are the clinical signs of hyperadrenocorticism (HAC) in larger breed dogs?

A

Abdominal enlargement, hepatomegaly, muscle wasting/weakness

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138
Q

What are the clinical signs of hyperadrenocorticism (HAC) in older dogs?

A

Lethargy/exercise intolerance, skin changes, reproductive changes

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139
Q

What is polyphagia?

A

Excessive hunger or increased appetite

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140
Q

What is PU/PD?

A

Polyuria (excessive urination) and polydipsia (excessive thirst)

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141
Q

What are the complications of hyperadrenocorticism (HAC)?

A

Urinary tract infection, hypertension, glomerulonephropathies, pulmonary thromboembolism, diabetes mellitus

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142
Q

What are the biochemical abnormalities associated with hyperadrenocorticism (HAC)?

A

Elevated ALP, ALT, cholesterol, bile acids, lipids; reduced urea, T4

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143
Q

What are the haematological changes consistent with hyperadrenocorticism (HAC)?

A

Lymphopaenia

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144
Q

What is the maximum concentration of desoxycortone?

A

The maximum concentration of desoxycortone is assessed after 10 days.

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145
Q

When should the clinical signs and electrolytes be re-evaluated?

A

The clinical signs and electrolytes should be re-evaluated after 10 days.

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146
Q

What should be done if the clinical signs have worsened or not resolved?

A

The dose of glucocorticoid should be adjusted and/or other causes of the clinical signs should be investigated.

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147
Q

When should the dog be re-evaluated and the Na+/K+ ratio measured?

A

The dog should be re-evaluated and the Na+/K+ ratio should be measured on Day 25.

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148
Q

What should be done if the dog is both clinically normal and has a normal Na+/K+ ratio on Day 25?

A

The dose should be adjusted based on the Day 10 Na+/K+ ratio using the guidelines on the datasheet.

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149
Q

What should be done if the dog is clinically normal and has a Na+/K+ ratio >32 on Day 25?

A

The dose should be adjusted based on the Day 10 Na+/K+ ratio according to the guidelines on the datasheet or the dose can be delayed.

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150
Q

What should be done if the dog is either not clinically normal or if the Na+/K+ ratio is abnormal on Day 25?

A

The dose of glucocorticoid or Zycortal should be adjusted.

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151
Q

How can the dosing interval be prolonged?

A

If the dog is clinically normal and the Day 25 Na+/K+ ratio is >32, the dosing interval can be prolonged instead of adjusting the dose.

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152
Q

How often should the electrolytes be evaluated if the dosing interval is prolonged?

A

The electrolytes should be evaluated every 5-9 days until the Na+/K+ ratio is <32.

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153
Q

What should be done once the optimal dose and dosing interval have been determined?

A

The same regimen should be maintained.

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154
Q

What should be done if the dog develops clinical signs of polyuria/polydipsia?

A

The glucocorticoid dose should be decreased first.

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155
Q

What should be done if the polyuria/polydipsia persists and the Na+/K+ ratio is >32?

A

The dose of Zycortal should be decreased without changing the dosing interval.

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156
Q

What should be done if the dog develops clinical signs of depression, lethargy, vomiting, diarrhea, or weakness?

A

The glucocorticoid dose should be increased.

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157
Q

What should be done if the dog has hyperkalemia, hyponatremia, or Na+/K+ ratio <27?

A

The Zycortal dosing interval should be decreased by 2-3 days or the dose should be increased.

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158
Q

What should be done if the dog has hypokalemia, hypernatremia, or Na+/K+ ratio >32?

A

The Zycortal dose should be decreased.

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159
Q

What should be considered prior to a stressful situation?

A

Temporarily increasing the dose of glucocorticoid should be considered.

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160
Q

What was the mean final dose of desoxycortone pivalate in the clinical trial?

A

The mean final dose of desoxycortone pivalate was 1.9 mg/kg.

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161
Q

What was the mean final dosing interval in the clinical trial?

A

The mean final dosing interval was 38.7 ± 12.7 days.

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162
Q

What is the majority of thyroid secretion composed of?

A

The majority of thyroid secretion is composed of T4.

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163
Q

What is the function of the thyroid glands?

A

The thyroid glands produce thyroid hormone.

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164
Q

What are the two thyroid hormones called?

A

The two thyroid hormones are T3 (Tri-iodothyronine) and T4 (Thyroxine).

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165
Q

What is the substance secreted from the cells of the thyroid glands?

A

Thyroglobulin is the substance secreted from the cells of the thyroid glands.

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166
Q

How are thyroid hormones synthesized?

A

Thyroid hormones are synthesized from 2 connected tyrosine molecules.

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167
Q

What is the enzyme involved in incorporating iodine into thyroglobulin?

A

Thyroid peroxidase is the enzyme involved in incorporating iodine into thyroglobulin.

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168
Q

Where do hormones remain until they are required for release?

A

Hormones remain in the acinar lumen of the thyroid glands until they are required for release.

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169
Q

How are the majority of T4 and T3 transported in the circulation?

A

The majority of T4 and T3 are transported in the circulation attached to binding proteins.

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170
Q

What are the biological effects exerted by ‘free’ T4 and T3?

A

‘Free’ T4 and T3 exert the biological effects.

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171
Q

What does T4 get converted into in the periphery?

A

T4 can be converted into the more active T3 in the periphery.

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172
Q

What is the normal proportion of T4 and T3 in thyroid secretion?

A

Approximately 95% of thyroid secretion is T4 and 5% is T3.

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173
Q

What is fludrocortisone?

A

Fludrocortisone is a mineralocorticoid and glucocorticoid replacement medication.

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174
Q

How is fludrocortisone administered?

A

Fludrocortisone is administered orally.

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175
Q

Is fludrocortisone licensed?

A

No, fludrocortisone is not licensed.

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176
Q

What is the current cost status of fludrocortisone?

A

Fludrocortisone is now very expensive.

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177
Q

What are the aim(s) of hyperthyroid cat treatment?

A

The aim of treatment is to remove or destroy abnormally functioning thyroid tissue, inhibit thyroid hormone synthesis, or reduce the effects of excess thyroid hormone on peripheral tissues.

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178
Q

What are the two curative options for hyperthyroid cat treatment?

A

Surgical thyroidectomy and radioactive iodine therapy.

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179
Q

What is the role of medical management in hyperthyroid cat treatment?

A

It is an option for many hyperthyroid cats, resulting in a rapid return to euthyroidism.

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180
Q

What are the two medical options for hyperthyroid cat treatment?

A

Carbimazole and methimazole (thiamazole).

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181
Q

How do carbimazole and methimazole work in hyperthyroid cat treatment?

A

They reversibly block iodination of thyroglobulin, effectively suppressing thyroid hormone production.

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182
Q

What are the trade names for methimazole?

A

Felimazole and Thyronorm.

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183
Q

What is the trade name for carbimazole?

A

Vidalta.

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184
Q

How is methimazole administered to cats?

A

Usually administered orally, but it can be administered transdermally as a gel applied to the non-haired part of the ear.

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185
Q

What tests are used to monitor cats receiving antithyroid medications?

A

Serum total T4 is often measured after therapy initiation or dose adjustment, and should be checked every 3-6 months once stability is achieved.

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186
Q

When should the serum sample be taken for monitoring cats receiving antithyroid medications?

A

The time of day is not important.

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187
Q

What is the goal of maintaining total T4 levels in cats receiving antithyroid medications?

A

To keep total T4 within the lower half of the reference interval.

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188
Q

Do clinical signs of hypothyroidism typically develop in cats with low total T4 levels?

A

No, clinical signs of hypothyroidism rarely develop even when total T4 is well below the reference interval.

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189
Q

What are the mild adverse effects of antithyroid medications in cats?

A

Vomiting, with or without anorexia and depression, usually occurring in the first 3 weeks of therapy.

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190
Q

Do mild adverse effects of antithyroid medications typically require discontinuation of the treatment?

A

No, in most cases these adverse effects are transient and self-limiting.

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191
Q

What should be done if circulating total T4 is severely depressed in cats receiving antithyroid medications?

A

The dosage of drugs should be decreased, if possible, and the cat should be re-assessed.

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192
Q

Which liver enzymes decline progressively as euthyroidism is achieved in cats receiving antithyroid medications?

A

Serum ALT and ALP.

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193
Q

What potential harmful effect has been associated with induced hypothyroidism in cats?

A

Renal impairment and shortened survival.

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194
Q

What are the advantages of medical management for hyperthyroid cats?

A

Widely available, requires no specialist facilities, and is recommended as trial therapy for assessing the effects on renal function.

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195
Q

What is the difference in potency between 5mg of carbimazole and a similar weight of methimazole?

A

A 5mg dose of carbimazole is equal to a 3mg dose of methimazole.

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196
Q

Does carbimazole or methimazole have a lower incidence of adverse effects?

A

Carbimazole is often suggested to have a lower incidence of adverse effects than methimazole.

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197
Q

What drives the production of thyroid hormone?

A

Thyroid stimulating hormone (TSH)

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198
Q

What is the main purpose of the hypothalamic / pituitary axis?

A

To regulate free T4 and T3 levels

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199
Q

How does thyroid hormone affect metabolism?

A

It affects basal metabolic rate, protein synthesis, and lipid metabolism

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200
Q

What body systems does thyroid hormone affect?

A

Metabolism, growth, development, osteogenesis, skin and hair growth, cardiovascular system

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201
Q

What are the clinical signs of hyperthyroidism in cats?

A

Weight loss, increased appetite, hyperactivity, gastrointestinal signs, tachycardia

202
Q

What is the average age of onset for hyperthyroidism in cats?

A

12 years

203
Q

What are some possible causes of hyperthyroidism in cats?

A

Bilateral thyroid hyperplasia, adenomas, dietary, toxic, geographical influences

204
Q

What percentage of hyperthyroid cats have a palpable goitre?

A

98%

205
Q

What are some diagnostic indicators of hyperthyroidism in cats?

A

Weight loss, increased appetite, hyperactivity, gastrointestinal signs, tachycardia

206
Q

What are the haematological changes seen in hyperthyroidism?

A

Mild to moderate increase in PCV, RBC count, and hemoglobin concentration

207
Q

Which liver enzymes are frequently elevated in hyperthyroid cats?

A

ALT, AST, and ALP

208
Q

What is the significance of elevated liver enzymes in hyperthyroid cats?

A

Unknown, may reflect non-specific changes associated with malnutrition and toxic effects of thyroid hormones

209
Q

What is the most common endocrinopathy in cats?

A

Hyperthyroidism

210
Q

What percentage of hyperthyroidism cases are due to thyroid carcinomas?

A

5%

211
Q

What are some clinical signs of hyperthyroidism in cats?

A

Weight loss, increased appetite, hyperactivity, gastrointestinal signs, tachycardia

212
Q

What percentage of hyperthyroid cats present with a palpable goitre?

A

98%

213
Q

What is a possible sign of congestive heart failure in hyperthyroid cats?

A

Hypertrophic cardiomyopathy

214
Q

What are some reported clinical signs seen in hyperthyroid cats?

A

Weight loss, polyphagia, polyuria/polydipsia, tachycardia, hyperactivity

215
Q

What lab test is often used for diagnosing hyperthyroidism?

A

Total serum T4

216
Q

What are some routine lab test results that may indicate hyperthyroidism?

A

Mild to moderate increases in liver enzymes ALT, AST, and ALP

217
Q

What is the pathophysiology of canine hypoadrenocorticism?

A

It is caused by a deficiency in mineralocorticoid and/or glucocorticoid production.

218
Q

How is primary hypoadrenocorticism (Addison’s Disease) different from secondary hypoadrenocorticism?

A

Primary hypoadrenocorticism is due to immune destruction of adrenal cortices, while secondary hypoadrenocorticism is due to a deficiency of ACTH.

219
Q

What are the causes of primary hypoadrenocorticism?

A

Causes include idiopathic atrophy, iatrogenic factors such as drugs (mitotane, trilostane) or bilateral adrenalectomy.

220
Q

Which breeds have an increased risk of hypoadrenocorticism?

A

Standard Poodles, Bearded Collies, Portuguese Water Dog, Great Dane, Rottweiler, WHWT, Soft Coated Wheaten Terrier.

221
Q

What are the clinical signs of chronic hypoadrenocorticism?

A

Signs can include anorexia, vomiting, lethargy, depression, weakness, shivering, weight loss, PUPD, and abdominal pain.

222
Q

What should be considered as a differential diagnosis in animals with waxing/waning signs and intermittent GI disease/bleeding?

A

Hypoadrenocorticism.

223
Q

What are the physical findings in hypoadrenocorticism?

A

Depression, weakness, dehydration, bradycardia, weak pulses, ECG changes, and intermittent signs of GI hemorrhage.

224
Q

What are the clinical signs of acute hypoadrenocorticism?

A

Hypovolemic shock, relative bradycardia, collapse or extreme weakness, and hypothermia.

225
Q

What is the pathophysiology of feline hyperthyroidism?

A

Review the pathophysiology of feline hyperthyroidism.

226
Q

What are the clinical features of feline hyperthyroidism?

A

Recognize the clinical features of feline hyperthyroidism.

227
Q

What can routine laboratory tests help interpret in feline hyperthyroidism?

A

Routine laboratory tests can help interpret the results of feline hyperthyroidism.

228
Q

What should be discussed in the management of feline hyperthyroidism?

A

Disease management should be discussed in feline hyperthyroidism.

229
Q

What is the pathophysiology of canine hypothyroidism?

A

Review the pathophysiology of canine hypothyroidism.

230
Q

What are the clinical features of canine hypothyroidism?

A

Recognize the clinical features of canine hypothyroidism.

231
Q

What can routine laboratory tests help interpret in canine hypothyroidism?

A

Routine laboratory tests can help interpret the results of canine hypothyroidism.

232
Q

What should be discussed in the management of canine hypothyroidism?

A

Management of the disease should be discussed in canine hypothyroidism.

233
Q

What are the physical examination findings in acute hypoadrenocorticism?

A

Depression, thinness, weakness, dehydration, bradycardia, melena/hematochezia

234
Q

What blood parameter changes reflect the lack of aldosterone and cortisol in hypoadrenocorticism?

A

Hyperkalemia, hyponatremia, hypochloridemia

235
Q

What are the classic findings in the serum biochemistry of hypoadrenocorticism?

A

Hyperkalemia, hyponatremia, hypochloridemia, Na:K ratio <23

236
Q

What percentage of cases do not have classical electrolyte changes in hypoadrenocorticism?

A

10%

237
Q

What are the findings in urinalysis in hypoadrenocorticism?

A

High urine specific gravity may not always happen

238
Q

What are the ECG changes seen in hypoadrenocorticism?

A

T wave peaking and Q-T shortening, increased QRS duration, decreased P wave, severe bradycardia

239
Q

What are the radiographic changes usually seen in hypoadrenocorticism?

A

Microcardia, decreased pulmonary vessel size, reduced caudal vena cava size, microhepatica

240
Q

What is the value of basal cortisol that effectively rules out hypoadrenocorticism?

A

> 55nmol

241
Q

What is the most useful test for diagnosing hypoadrenocorticism?

A

ACTH stimulation test

242
Q

How can aldosterone pre and post ACTH be used to distinguish primary and secondary causes of hypoadrenocorticism?

A

Raised post ACTH aldosterone in secondary causes, no response in primary causes

243
Q

What are the steps in the management of the acute crisis in hypoadrenocorticism?

A

Restore intravascular volume, reversal of hyperkalemia, reversal of hyponatremia, provision of glucocorticoids and mineralocorticoids, correction of any life-threatening arrhythmias

244
Q

What intravenous fluid can be used to restore intravascular volume in a patient with hypoadrenocorticism?

A

0.9% NaCl or lactated Ringer’s (Hartmann’s) solutions

245
Q

What solution is suggested to be used in hyperkalemic patients?

A

Hartmann’s solution

246
Q

What are the advantages of using Hartmann’s solution in hyperkalemic patients?

A

Large volume fluid provision, diuresis, kaluresis, alkalizing effect

247
Q

What treatments can be used to decrease potassium level in hyperkalemic animals?

A

Calcium gluconate, sodium bicarbonate, glucose with or without regular insulin

248
Q

How does calcium gluconate help in hyperkalemia reversal?

A

It is cardioprotective and re-establishes normal resting membrane potential.

249
Q

How does sodium bicarbonate help in hyperkalemia reversal?

A

It creates a gradient for hydrogen ions to move out of cells, allowing potassium ions to move into the cells.

250
Q

How does glucose with or without regular insulin help in hyperkalemia reversal?

A

Glucose moves into cells under insulin influence, carrying potassium along.

251
Q

What is the recommended treatment for correcting hyponatremia?

A

Intravenous fluid therapy

252
Q

What should be considered when correcting hyponatremia with intravenous fluid therapy?

A

Ensure sodium does not rise too rapidly to avoid central nervous system signs.

253
Q

What is the best way to correct acute glucocorticoid deficiency?

A

Intravenous administration of rapid-acting glucocorticoid

254
Q

What are the available options for glucocorticoid administration in acute crisis situations?

A

Dexamethasone, hydrocortisone, methylprednisolone sodium, prednisolone

255
Q

Why is dexamethasone preferred over other corticosteroids for ACTH stimulation test?

A

It does not cross-react with cortisol measurement.

256
Q

What is Zycortal and how is it administered?

A

A mineralocorticoid replacement administered by subcutaneous injection.

257
Q

What is the requirement for dogs receiving Zycortal for hypoadrenocorticism treatment?

A

They must also receive oral glucocorticoids.

258
Q

What is the initial and second dose requirement for Zycortal administration?

A

Details are available in the data sheet.

259
Q

What are the common clinical signs of hypothyroidism in dogs?

A

Lethargy, weight gain, alopecia, pyoderma, seborrhoea, cold intolerance, bradycardia, and ‘Rat Tail’.

260
Q

What are the common breeds of dogs that are usually affected by hypothyroidism?

A

Dobermans, Miniature Schnauzers, Cocker Spaniels, and Golden Retrievers.

261
Q

What are the blood abnormalities commonly seen in hypothyroidism?

A

Increased cholesterol, increased triglycerides, and mild liver enzyme elevation.

262
Q

What are the differential diagnoses for cholesterol elevation in hypothyroidism?

A

High fat diet, other endocrinopathies (e.g. diabetes mellitus), nephrotic syndrome, cholestasis, or dyslipoproteinaemia.

263
Q

What are the two main diagnostic tests used for hypothyroidism?

A

Serum T4 and Serum TSH.

264
Q

Why is measuring total T4 alone not enough to diagnose hypothyroidism?

A

It can be misleading due to factors like certain drugs and systemic disease.

265
Q

What can falsely lower T4 levels in the body?

A

Phenobarbitone, NSAID’s, GA, sedatives, AB’s, and frusemide.

266
Q

What is the advantage of using TSH as a diagnostic test for hypothyroidism?

A

Readily available and not expensive.

267
Q

Why should TSH be used in combination with T4 for diagnosing hypothyroidism?

A

Approximately 25% of hypothyroid dogs may have TSH values within the reference range.

268
Q

What is the most reliable method to measure free T4?

A

Equilibrium dialysis.

269
Q

What test is used to detect thyroid autoimmunity?

A

Testing for anti-thyroglobulin antibodies.

270
Q

What is the advantage of using rhTSH for the stimulation test?

A

Considered as a gold standard and reliable.

271
Q

What are some potential disadvantages of rhTSH stimulation test?

A

It takes several hours to perform and anaphylactic reactions have been described with bovine rhTSH.

272
Q

What are some mild and transient haematological abnormalities that can occur in cats during therapy?

A

Lymphocytosis, eosinophilia, leucopenia

273
Q

What are some more serious haematological complications that can occur in cats during therapy?

A

Agranulocytosis, thrombocytopenia

274
Q

What is the frequency at which clinicians have recommended assessing haematology during therapy?

A

Every 2 weeks

275
Q

What percentage of cats may experience hepatopathy during therapy?

A

<2%

276
Q

What is the recommended action if any serious adverse effects occur during therapy?

A

Drug withdrawal

277
Q

What is surgical thyroidectomy?

A

A very effective management strategy for hyperthyroidism

278
Q

What is the most significant post-operative complication of thyroidectomy?

A

Hypocalcaemia

279
Q

What occurs if the parathyroid glands are removed, damaged, or devascularized during thyroidectomy?

A

Hypocalcaemia

280
Q

What is the generally considered optimal treatment for most hyperthyroid cats?

A

Radioactive iodine

281
Q

What is the most commonly used radioisotope for the treatment of hyperthyroid cats?

A

Iodine-131

282
Q

What is the commercially available diet formulated for the management of hyperthyroid cats?

A

Hills y/d

283
Q

What does the diet Hills y/d contain in extremely low levels?

A

Iodine

284
Q

What percentage of hyperthyroid cats exclusively eating y/d will have normal serum total T4 concentrations by 4 weeks on the diet?

A

About 75%

285
Q

In cats with severe hyperthyroidism, is the diet Hills y/d highly effective?

A

Not as effective

286
Q

Other than surgery and radioactive iodine treatment, what is another therapy option mentioned in the notes?

A

Injection of ethanol directly into the thyroid adenomas

287
Q

What is the rough reference range for T4 in hypothyroid, sick euthyroid or drug treatment?

A

0-15nmol/l

288
Q

What does a T4 value of >25nmol/l indicate?

A

The dog is probably euthyroid

289
Q

What percentage of hypothyroid dogs have normal TSH?

A

Approximately 25%

290
Q

What is the reference range for TSH in normal, sick euthyroid, and rarely hypothyroid dogs?

A

0 - 0.41ng/ml

291
Q

What is the reference range for TSH in hypothyroid dogs?

A

> 0.6ng/ml

292
Q

What are the possible causes for a Total T4 that is normal, cTSH normal, and non-thyroidal illness?

A

Non-thyroidal illness, euthyroid, drug therapy

293
Q

What is the treatment for hypothyroidism in dogs?

A

Levothyroxine sodium

294
Q

What are the first clinical signs to improve in response to levothyroxine treatment?

A

Lethargy and mental demeanour

295
Q

When can dermatological improvement be expected after starting levothyroxine treatment?

A

By 3 months

296
Q

What should the peak plasma concentration of T4 be in adequately dosed dogs?

A

Approximately 30 to 47 nmol/l

297
Q

How often can clinical and biochemical monitoring be performed after the optimum replacement dose has been attained?

A

Every 6-12 months

298
Q

Which drug can cause blunted TSH stimulation test results at high doses and durations?

A

Glucocorticoids

299
Q

What are the cardiac findings associated with hyperthyroidism in cats?

A

Left ventricular hypertrophy, left atrial dilation, and interventricular septum hypertrophy.

300
Q

What is the significance of changes in calcium and circulating PTH levels in hyperthyroidism?

A

The significance of these changes is unknown.

301
Q

What is the most frequently identified echocardiographic abnormality in hyperthyroidism?

A

Left ventricular hypertrophy.

302
Q

What is the most consistently elevated thyroid hormone in hyperthyroid cats?

A

Serum free T4.

303
Q

Can hyperthyroidism be excluded based on total T4 within the reference range?

A

No, because non-thyroidal illness can suppress total T4 concentrations.

304
Q

What is the recommended time frame to retest cats with marginally elevated total T4?

A

4-6 weeks.

305
Q

What proportion of euthyroid sick cats have an elevation in free T4?

A

12%.

306
Q

Should free T4 alone be relied upon for diagnosing hyperthyroidism?

A

No, it should be interpreted alongside total T4.

307
Q

What effect does T3 have on serum total T4 concentration in hyperthyroid cats?

A

Minimal to no decrease.

308
Q

Is there a species-specific feline TSH assay available?

A

No, but assays for measuring canine TSH may be useful in cats.

309
Q

What cat population had undetectable circulating cTSH levels?

A

Hyperthyroid cats.

310
Q

What proportion of feline TSH can the current assay detect?

A

Approximately 35%.

311
Q

What is the reason for the rare elevation of plasma sodium concentrations in cats with hypokalaemic myopathy?

A

Water reabsorption secondary to sodium retention.

312
Q

What are the usual serum creatine kinase concentrations in cats with hypokalaemic myopathy?

A

Markedly elevated.

313
Q

What is the mean potassium concentration at presentation in cats with primary hyperaldosteronism?

A

2.5 mEq/L.

314
Q

Does normokalaemia exclude the possibility of hyperaldosteronism?

A

No, it does not.

315
Q

What should be considered if hypertention is unexplained in a cat?

A

Hyperaldosteronism.

316
Q

How many of the described cases of adrenal hyperplasia were hypokalaemic at initial presentation?

A

Approximately half.

317
Q

What should prompt suspicion of hyperaldosteronism in cats?

A

Persistence of hypokalaemia despite potassium supplementation.

318
Q

What was the range of sodium concentration in cats with primary hyperaldosteronism?

A

148 to 168 mEq/L.

319
Q

What were the mean creatine kinase levels in cats with primary hyperaldosteronism?

A

6,837 IU/L.

320
Q

How many out of 13 cats with primary hyperaldosteronism were hypertensive?

A

12

321
Q

What can be evidence of renal disease in cats with primary hyperaldosteronism?

A

Isosthenuria and elevated serum creatinine and blood urea nitrogen concentrations.

322
Q

Why is imaging necessary in cats suspected of having primary hyperaldosteronism?

A

To detect adrenal abnormalities and evaluate metastases.

323
Q

What can thoracic radiography detect in cats with primary hyperaldosteronism?

A

Pulmonary metastases.

324
Q

What are the common ultrasonographic changes observed in the adrenal glands of cats with primary hyperaldosteronism?

A

Adrenal masses, adrenal calcification, and changes in adrenal echogenicity.

325
Q

What is the median dorsoventral width of the adrenal glands of healthy cats?

A

3.9 mm.

326
Q

Is finding an enlarged adrenal gland or mass definitive for a diagnosis of primary hyperaldosteronism?

A

No.

327
Q

What are some other considerations for finding an adrenal gland mass in cats?

A

Non-functional tumors, phaeochromocytomas, cortisol-secreting tumors, and progesterone-secreting tumors.

328
Q

Are functional tumors and clinically relevant hyperplasia always visible on diagnostic imaging?

A

No, they may not be large enough to be detected.

329
Q

What were the imaging findings in cats with histologic confirmation of primary hyperaldosteronism?

A

Absent to minor changes in adrenal gland size and morphology.

330
Q

When should primary hyperaldosteronism be considered as a possibility?

A

In cases with hypokalaemia, hypertension, adrenal mass, or abnormal regulation of aldosterone production.

331
Q

What are the clinical signs associated with feline hyperaldosteronism?

A

Increased sodium and water retention, systemic arterial hypertension, and hypokalaemia.

332
Q

How is feline hyperaldosteronism diagnosed?

A

Through blood tests to measure aldosterone levels and imaging techniques to detect adrenal masses.

333
Q

What are the treatment options available for feline hyperaldosteronism?

A

Surgical removal of adrenal masses, medication to control blood pressure, and potassium supplementation.

334
Q

What is the role of aldosterone in the body?

A

Aldosterone regulates sodium and water balance, and potassium excretion.

335
Q

How is aldosterone production regulated?

A

Through the renin-angiotensin-aldosterone system (RAAS) and direct regulation via potassium ions.

336
Q

What is primary hyperaldosteronism?

A

Excessive aldosterone production independent of the RAAS, caused by adrenal neoplasia or hyperplasia.

337
Q

What are the causes of secondary hyperaldosteronism?

A

Stimulation of the RAAS due to dehydration, hypotension, reduced renal perfusion, or sodium deficiency.

338
Q

What are the clinical consequences of excessive aldosterone production?

A

Systemic arterial hypertension and hypokalaemia.

339
Q

What are the histopathological findings in feline primary hyperaldosteronism?

A

Unilateral or bilateral adenoma or carcinoma, or bilateral hyperplasia of the zona glomerulosa.

340
Q

How does aldosterone affect the kidney, colon, and salivary gland?

A

It causes sodium reabsorption, water retention, and potassium and hydrogen ion excretion.

341
Q

What is the main mechanism of aldosterone regulation?

A

Activation of the renin-angiotensin-aldosterone system (RAAS) due to decreased blood volume and renal blood flow.

342
Q

What is the result of aldosterone binding to mineralocorticoid receptors?

A

Increased sodium and water reabsorption, leading to increased blood pressure and volume.

343
Q

What are the causes of hypercalcaemia in dogs and cats?

A

Various underlying disorders, such as primary hyperparathyroidism or malignancies.

344
Q

What is the physiology of calcium balance?

A

Calcium balance is regulated by parathyroid hormone, vitamin D, and calcitonin.

345
Q

What is primary hyperparathyroidism?

A

Excessive secretion of parathyroid hormone from a neoplastic parathyroid gland.

346
Q

How do animals with primary hyperaldosteronism differ from those with secondary hyperaldosteronism?

A

Primary hyperaldosteronism is independent of the RAAS, while secondary hyperaldosteronism is in response to RAAS stimulation.

347
Q

What are the clinical signs associated with primary hyperparathyroidism?

A

Hypercalcaemia, renal disease, urolithiasis, and soft tissue mineralization.

348
Q

What is the diagnostic plan for investigating hypercalcaemic patients?

A

Blood tests for calcium and parathyroid hormone levels, imaging techniques, and identification of underlying causes.

349
Q

How is primary hyperparathyroidism treated?

A

Surgical removal of the affected parathyroid gland or medical management to control calcium levels.

350
Q

What are the effects of primary hyperaldosteronism on sodium, water, and potassium balance?

A

Increased sodium and water retention, and increased potassium excretion leading to hypokalaemia.

351
Q

What is the main effect of calcitonin on bone?

A

Calcitonin decreases calcium movement from ‘soluble bone’ layer into interstitial fluid.

352
Q

What is the main effect of calcitonin on renal excretion?

A

Calcitonin increases renal excretion of calcium and phosphate.

353
Q

How is vitamin D activated in the kidneys?

A

Vitamin D is converted to the active form 1,25 dihydroxycholecalciferol (1,25 DHCC) in the kidneys.

354
Q

What hormone controls the conversion of vitamin D to its active form?

A

Parathyroid hormone (PTH) controls the conversion of vitamin D to its active form.

355
Q

What are the effects of active vitamin D (calcitriol) on the gastrointestinal tract?

A

Active vitamin D promotes calcium uptake in the gastrointestinal tract.

356
Q

What is the distribution of calcium forms in healthy dogs?

A

Ionised calcium: 56%, protein-bound calcium: 34%, complexed calcium: 10%.

357
Q

Which form of calcium is biologically active?

A

Only ionised calcium is biologically active.

358
Q

What can cause artificial lowering of total calcium levels?

A

Low albumin levels can artificially lower total calcium levels.

359
Q

How can ionised calcium be measured in a laboratory?

A

Ionised calcium can be measured using an ionic specific electrode or an I-stat or Irma blood gas analyser.

360
Q

What is the preferred method for measuring ionised calcium?

A

It is preferable to measure ionised calcium immediately using in-house analysers or a local hospital laboratory.

361
Q

How is intact PTH measured?

A

Intact PTH is measured by immunoradiometric assay.

362
Q

What is the reference range for intact PTH?

A

The reference range for intact PTH is 10 - 60 pg/ml.

363
Q

What is primary hyperparathyroidism defined by?

A

Primary hyperparathyroidism is defined by hypercalcaemia with high or high-normal PTH and no other identifiable underlying cause.

364
Q

What is another disease state where PTH may be elevated?

A

PTH may be elevated in hyperadrenocorticism and in some normocalcaemic dogs with lymphoma.

365
Q

What should be performed to rule out other causes of hypokalaemia and hypertension?

A

Thorough history, physical examination, blood count, serum chemistry, T4 measurement, urinalysis, and blood pressure measurement.

366
Q

What is the main determinant of aldosterone secretion?

A

Potassium concentration.

367
Q

What is the confirmation of diagnosis for primary hyperaldosteronism?

A

Elevated plasma aldosterone concentration.

368
Q

What is the requirement for collection and handling of serum or plasma for aldosterone concentration assay?

A

Routine collection and handling processes.

369
Q

Is there clear evidence for improved diagnostic performance with ACTH stimulation test for primary hyperaldosteronism?

A

No, there is no clear evidence.

370
Q

What are the main causes of high plasma aldosterone concentration in primary hyperaldosteronism?

A

Adrenocortical tumors and chronic renal disease.

371
Q

Is plasma aldosterone concentration alone sufficient to distinguish between primary and secondary hyperaldosteronism?

A

No, it is not sufficient.

372
Q

What should plasma aldosterone concentration be interpreted together with in cases of primary hyperaldosteronism?

A

Plasma renin activity.

373
Q

What is required to reliably distinguish primary from secondary hyperaldosteronism?

A

Measurement of plasma renin activity.

374
Q

What can influence the measurement of plasma renin activity?

A

Certain drugs (ACE inhibitors, beta-blockers) and dietary salt intake.

375
Q

What pattern of plasma aldosterone concentration and plasma renin activity is consistent with primary hyperaldosteronism?

A

Elevated plasma aldosterone concentration with low renin activity.

376
Q

In cases of adrenal tumors, what is the expected plasma aldosterone concentration and plasma renin activity?

A

Markedly elevated aldosterone and completely suppressed renin activity.

377
Q

What is the gold standard for screening for feline primary hyperaldosteronism in humans?

A

Aldosterone: renin ratio.

378
Q

What are the recommended pre-operative treatments for hypertension and hypokalaemia?

A

Correcting hypokalaemia and controlling hypertension.

379
Q

What are some reported perioperative complications of surgery for hyperaldosteronism?

A

Intra-abdominal haemorrhage, acute renal failure, sepsis, and suspected thromboembolism.

380
Q

What should be assessed upon recovery and periodically after surgery for hyperaldosteronism?

A

Blood pressure and potassium concentration.

381
Q

When should oral therapy be continued in hypertensive or hypokalaemic patients after surgery?

A

If the patient remains hypertensive or hypokalaemic at the time of discharge.

382
Q

What medications were discontinued the day of surgery in cats surviving surgical intervention for hyperaldosteronism?

A

Spironolactone and amlodipine therapy.

383
Q

What is the reported survival time for cats with primary hyperaldosteronism treated with potassium supplementation, spironolactone, and amlodipine?

A

7 to 32 months.

384
Q

What is the prognosis for cats with completely excised unilateral adrenocortical neoplasia and no evidence of metastasis?

A

Good, with reported survival rates of at least 1 year and some cats alive 3.5 and 5 years postoperatively.

385
Q

What is the relationship between adrenal adenomas and adenocarcinomas in cats?

A

Adrenal adenocarcinomas do not appear to be associated with a poorer prognosis than adrenal adenomas.

386
Q

What is the function of parathyroid glands in maintaining calcium homeostasis?

A

They release parathyroid hormone (PTH) to maintain serum calcium and lower serum phosphate.

387
Q

What are the main organs responsible for calcium control in the body?

A

Bones, gastro-intestinal tract, and kidneys.

388
Q

How is blood calcium controlled in the short term?

A

By utilizing the calcium reservoir in bone.

389
Q

What percentage of calcium is filtered and re-absorbed by the kidneys?

A

Less than 2% of the filtered load.

390
Q

What is the role of osteoclasts in maintaining blood calcium levels?

A

Re-modeling the layer of ‘soluble bone’ to release calcium into the circulation as required.

391
Q

What triggers the release of parathyroid hormone (PTH)?

A

A fall in blood ionized calcium.

392
Q

What are the direct effects of PTH on bone and kidney?

A

Increasing osteoclast activity, decreasing osteoblast activity, and promoting increased calcium absorption in the kidney.

393
Q

What is the immediate effect of PTH on calcium levels?

A

Increased release of calcium into the circulation.

394
Q

What is the recommended number of parathyroid glands to be removed at one time if multiple glands are enlarged?

A

Up to three glands may be removed at one time.

395
Q

Why should at least one parathyroid gland be left in situ during surgery?

A

To maintain calcium homeostasis.

396
Q

What is the likely cause of multiple enlarged parathyroid glands?

A

Secondary hyperparathyroidism, indicating hyperplastic rather than adenomatous glands.

397
Q

What may occur post-surgery regarding PTH and calcium concentrations?

A

PTH and calcium concentrations should decrease rapidly; hypocalcaemia may occur in some cases.

398
Q

Under what circumstances is hypocalcaemia more likely to occur?

A

If pre-treatment calcium has been severely elevated (exceeded 3.5 mmol/l) for more than a few months.

399
Q

What happens to the remaining parathyroid glands when a parathyroid adenoma is functioning autonomously?

A

They become atrophied and are unable to support normal calcium homeostasis.

400
Q

How can the crisis of atrophied parathyroid glands be avoided?

A

By giving vitamin D ± oral calcium supplements pre-surgery and in the immediate post-treatment period.

401
Q

What are the two recommended preparations of vitamin D for managing parathyroid adenoma?

A
  1. Calcitriol (active form) - capsules of 0.25 or 0.5 µg, at dose rate of 20-30 ng/kg orally q12h. 2. Alfacalcidol - capsules or drops, at dose rate of 0.01-0.03 µg/kg q24h.
402
Q

In combination with vitamin D, what are the different preparations of oral calcium available?

A
  1. Calcium gluconate at 25-50 mg/kg/day divided twice or three times daily. 2. Calcium lactate at 25-50 mg/kg/day divided twice or three times daily. 3. Calcium carbonate at 25-50 mg/kg/day divided twice daily.
403
Q

What is the short to mid-term prognosis for primary hyperparathyroidism (PHPT) in most breeds?

A

Excellent prognosis.

404
Q

Is the long-term prognosis for PHPT also good in most breeds?

A

Yes, except in Keeshonds where recurrence can occur due to genetic drive to develop parathyroid adenomas.

405
Q

What breed requires monitoring throughout life for recurrence of PHPT, especially if the first surgery was done at a young age?

A

Keeshonds.

406
Q

What are the different forms of hyperfunction of the adrenal glands?

A

Unilateral adrenocortical adenocarcinomas, unilateral and bilateral adenomas, and bilateral nodular hyperplasia.

407
Q

What is the possible cause of hyperfunction of the zona glomerulosa?

A

A circulating stimulatory factor, possibly a fragment of pro-opiomelanocortin.

408
Q

Which mediators are responsible for progressive renal disease in cats with hyperaldosteronism?

A

Aldosterone and angiotensin II.

409
Q

How is chronic renal disease linked to glomerular and tubulointerstitial injury?

A

Excessive accumulation of the extracellular matrix of the kidney.

410
Q

Which growth factor can mediate the extracellular matrix accumulation in the kidney?

A

Angiotensin II.

411
Q

Apart from its role in renal disease, what other functions does angiotensin II have?

A

Peripheral vasoconstriction, regulation of glomerular filtration, and pro-inflammatory cytokine activity.

412
Q

How can aldosterone contribute to the progression of renal damage?

A

By promoting vascular thrombosis and fibrosis.

413
Q

What organ damage is often found in cats with hyperaldosteronism?

A

Cardiovascular disease, indicated by heart murmur, cardiomegaly, or ventricular hypertrophy.

414
Q

What are the typical clinical signs of feline hyperaldosteronism?

A

Potassium depletion (hypokalaemic myopathy) and systemic arterial hypertension.

415
Q

What are the signs of hypokalaemic myopathy?

A

Episodic or acute muscle weakness, hindlimb plantigrade stance, and cervical ventroflexion.

416
Q

What can acute-onset blindness in cats with hyperaldosteronism indicate?

A

Intraocular hemorrhage or retinal detachment due to systemic hypertension.

417
Q

Which eye condition is more commonly associated with adrenal hyperplasia in cats?

A

Retinal detachment or subretinal, intraretinal, and intravitreal hemorrhages.

418
Q

What physical examination findings are reported in cases of primary hyperaldosteronism?

A

Elevated arterial blood pressure, ocular signs of hypertension, and hypokalaemic myopathy.

419
Q

What are some less specific physical examination findings in cats with hyperaldosteronism?

A

Polyuria, polydipsia, weight loss, palpable abdominal masses, polyphagia, heart murmur, and irregular cardiac rhythm.

420
Q

What other concurrent diseases should be considered in older cats with hyperaldosteronism?

A

Chronic kidney disease or hyperthyroidism that may cause hypokalaemia and/or hypertension.

421
Q

What are the typical biochemical abnormalities in cats with hyperaldosteronism?

A

Moderate to severe hypokalaemia.

422
Q

What are the causes of primary hyperparathyroidism?

A

Adenoma, carcinoma, or adenomatous hyperplasia of parathyroid glands

423
Q

What is the signalment of dogs with primary hyperparathyroidism?

A

Older dogs, no known gender predisposition, Keeshonds, German shepherd dogs, Poodles, Golden retrievers

424
Q

What are the clinical signs of primary hyperparathyroidism?

A

Polyuria, polydipsia, vomiting, inappetence, urinary incontinence, constipation, stranguria, pollakiuria, depression, stiff gait, exercise intolerance, lameness, shivering, facial pain/discomfort when eating

425
Q

Why do dogs with primary hyperparathyroidism develop uroliths?

A

Increased concentrations of calcium and phosphate in urine leading to calcium phosphate precipitation and stone formation

426
Q

What are the relevant findings on physical examination in dogs with primary hyperparathyroidism?

A

Stiffness, gait abnormalities, dull mentation, weakness, muscle wastage

427
Q

What is the expected severity of hypercalcemia in dogs with primary hyperparathyroidism?

A

Dependent on the duration of the disease; mild to severe hypercalcemia

428
Q

What parameters should be measured in animals with primary hyperparathyroidism to characterize the electrolyte disturbance?

A

Total and ionized calcium, phosphate, PTH, PTHrp

429
Q

What are the expected results in primary hyperparathyroidism?

A

Elevated PTH above reference interval or inappropriately high for concurrent serum calcium

430
Q

What does the ARR test allow differentiation of?

A

Primary versus secondary hyperaldosteronism.

431
Q

What is indicated by a high ARR?

A

Primary hyperaldosteronism.

432
Q

What are some examples of mineralocorticoid function tests (MFTs) used in humans?

A

Oral sodium loading, saline infusion, fludrocortisone acetate administration with sodium supplementation, and the captopril challenge test.

433
Q

What was assessed in healthy cats to investigate mineralocorticoid function tests?

A

Changes of the urinary aldosterone: creatinine ratio in response to increased dietary salt or administration of fludrocortisone acetate.

434
Q

What is the initial treatment of primary hyperaldosteronism directed at?

A

Controlling hypokalaemia and/or hypertension.

435
Q

What is spironolactone?

A

A competitive aldosterone antagonist.

436
Q

What is the recommended dose of spironolactone?

A

2-4mg/kg orally q24hours.

437
Q

What is a potential adverse reaction of spironolactone in human patients?

A

Gynaecomastia and menstrual irregularities.

438
Q

What is the initial treatment of choice for hypertension in cats?

A

Amlodipine besylate.

439
Q

What monitoring should be performed after every dose adjustment?

A

Electrolytes and blood pressure.

440
Q

What is the optimal treatment for cats with unilateral aldosterone-secreting adrenal masses and no detectable metastatic disease?

A

Surgical excision.

441
Q

What is the most common cause of death in cats undergoing surgical excision of adrenal masses?

A

Severe acute haemorrhage from the caudal vena cava.

442
Q

How is PTHrp measured?

A

By two-site IRMA and RIA.

443
Q

What is the reference interval for PTHrp in dogs?

A

<0.5 pmol/l.

444
Q

What is the reference interval for PTHrp in cats?

A

<0.5 pmol/l.

445
Q

Which breed is predisposed to inherited PHPT?

A

Keeshond.

446
Q

What is the penetrance of PHPT in Keeshonds?

A

Partial, age-dependent.

447
Q

What is the purpose of genetic testing in Keeshonds?

A

To limit the use of mutation-carrying animals.

448
Q

What imaging modality is most useful for investigating parathyroid adenomas?

A

Ultrasonography.

449
Q

What percentage of parathyroid adenomas are positively identified by ultrasonography?

A

90-95%.

450
Q

How are parathyroid glands identified on ultrasound when they are abnormal?

A

Small hypoechoic nodules within thyroid tissue.

451
Q

What is the initial management for hypercalcaemia in PHPT?

A

Diuresis with intravenous sodium chloride.

452
Q

Which medication may reduce osteoclast activity in PHPT?

A

Bisphosphonates.

453
Q

What is the treatment of choice for PHPT?

A

Excision of abnormal parathyroid gland.

454
Q

How is excellent visualisation of the thyroid glands achieved during surgery?

A

Using a ventral midline cervical approach.

455
Q

How are parathyroid adenomas removed during surgery?

A

Either by dissection from adjacent thyroid tissue or by partial thyroidectomy.

456
Q

What are the GH stimulants used to measure GH concentrations?

A

GHRH, clonidine, and xylazine.

457
Q

How are GH concentrations measured after administering the stimulant?

A

GH concentrations are measured before and 20-30 minutes after intravenous administration of the stimulant.

458
Q

What is the purpose of the ghrelin stimulation test?

A

To determine GH response, with a post-ghrelin plasma GH concentration of >5 µg/l excluding congenital GH deficiency.

459
Q

What can advanced imaging of the pituitary reveal in dogs with pituitary dwarfism?

A

The presence of pituitary cysts, which may increase in size as the dog gets older.

460
Q

Which hormones should be replaced if lacking in treatment for pituitary dwarfism?

A

Thyroxine and other hormones should be replaced if lacking.

461
Q

At what age should therapy for dwarfism ideally be started?

A

Therapy is best started when the dog is as young as possible, ideally at 4-6 weeks of age.

462
Q

What are the potential side effects of GH treatment?

A

Hypersensitivity reactions to GH and diabetes mellitus.

463
Q

Why is canine GH not available for therapeutic use?

A

Antibody formation precludes the use of a human product due to differences between canine and human GH.

464
Q

What is the recommended subcutaneous dose for GH?

A

0.1-0.3 IU per kg bodyweight three times per week.

465
Q

What improvements can be expected after starting GH therapy?

A

Beneficial response of the skin and hair coat usually occurs within 6-8 weeks after starting therapy.

466
Q

How can progestogens induce GH expression in the mammary gland?

A

Progestogens can induce expression of the GH gene in the mammary gland, leading to secretion into the systemic circulation.

467
Q

What treatment can result in an increase in body size and development of an adult hair coat in German Shepherd dwarfs?

A

Medroxyprogesterone acetate treatment at 2.5-5.0 mg/kg s.c., initially at 3-week intervals and subsequently at 6-week intervals.

468
Q

In addition to GH, what other monitoring is important during treatment?

A

Monitoring of plasma concentrations of IGF-1, GH, and glucose are important during the treatment.

469
Q

What should be done before starting the progestogen treatment in bitches?

A

Ovariohysterectomy should be performed before starting the progestogen treatment.

470
Q

When should thyroid hormone replacement be started?

A

Thyroid hormone replacement should be started as soon as there is evidence of hypothyroidism.

471
Q

What is the long-term treatment for growth failure in dogs with growth hormone deficiency?

A

Recombinant human IGF-I (Mecasermin, Increlex) is used for long-term treatment of growth failure.

472
Q

What is the condition called where children have severe primary IGF-I deficiency?

A

Severe primary IGF-I deficiency

473
Q

What is the relationship between insufficient GH and growth hormone-responsive alopecia in dogs?

A

Unproven

474
Q

What are the clinical signs of growth hormone-responsive alopecia in adult dogs?

A

Bilaterally symmetric alopecia and hyperpigmentation mainly of the trunk

475
Q

Which breeds are mainly affected by growth hormone-responsive alopecia?

A

Poodles, Pomeranians, Chow Chows, Keeshonds, Airedales, and Samoyeds

476
Q

What should be performed to rule out other endocrine causes of alopecia in dogs?

A

Routine endocrine testing

477
Q

What is the management therapy for growth hormone-responsive alopecia in dogs?

A

Bovine, porcine, and human growth hormone at a dose of 0.1 IU/kg subcutaneously three times a week for 4-6 weeks

478
Q

What is another name for growth hormone-responsive alopecia?

A

Castration-responsive alopecia

479
Q

What should be considered when investigating a patient with polyuria and polydipsia?

A

Comprehensive differential diagnosis list

480
Q

What are the possible differential diagnoses for a patient with polyuria and polydipsia?

A

Diabetes mellitus, Hyperadrenocorticism, Hypoadrenocorticism, Diabetes insipidus, Hypercalcaemia, Hypokalaemia, Liver disease, Renal failure, Toxaemia, Pyelonephritis / urinary tract infection, Psychogenic polydipsia, Drug treatment, CNS disease, Gastrointestinal disease

481
Q

What are the primary polydipsias and primary polyurias associated with PU/PD?

A

Varies for each condition, depending on the underlying mechanism

482
Q

What is the definition of polyuria and polydipsia?

A

Water intake of >100ml/kg/day

483
Q

What could be a reason if urine is not hyposthenuric or isosthenuric in a patient with PU/PD?

A

Fluid loss through another route, dietary change, or improper swallowing

484
Q

What is the mechanism for primary polyuria in diabetes mellitus?

A

Osmotic diuresis caused by glycosuria

485
Q

What is the mechanism through which endogenous and exogenous glucocorticoids inhibit GH secretion?

A

Enhanced somatostatin release

486
Q

What should be done to diagnose low GH levels in dogs with growth hormone-responsive alopecia?

A

Clonidine and xylazine stimulation tests

487
Q

What histopathological findings are seen in dogs with growth hormone-responsive alopecia?

A

Atrophic follicles, hairless dilated follicles, and reduced dermal elastin

488
Q

What abnormal adrenal sex hormone production has been observed in Pomeranians with growth hormone-responsive alopecia?

A

Elevated progesterone, 17-hydroxyprogesterone, and androstenedione in response to ACTH stimulation, and elevated plasma ACTH concentrations

489
Q

What is the suggested underlying cause in Pomeranians with abnormal adrenal sex hormone production?

A

Partial 21-hydroxylase enzyme deficiency

490
Q

What might help manage growth hormone-responsive alopecia in dogs?

A

Castration, mitotane, and trilostane in case of suspected abnormalities in adrenal sex hormone production

491
Q

What is an exceptionally rare condition that is commonly over-diagnosed in thirsty patients with polyuria and polydipsia?

A

Primary diabetes insipidus

492
Q

What should be considered when performing urethral catheterisation in female animals?

A

Consider the use of an indwelling urinary catheter.

493
Q

How often should the bladder be emptied during the water deprivation test?

A

Every 1-2 hours.

494
Q

What should be measured during the water deprivation test to monitor for dehydration?

A

Urine specific gravity (SG) or osmolality and body weight.

495
Q

When should the water deprivation test be stopped?

A

When there is either a 5% loss of body weight or the urine SG is >1.030 in dogs (>1.035 in cats).

496
Q

What should be monitored during the water deprivation test if the 5% dehydration endpoint is not reached by the end of the working day?

A

Urine SG and body weight can continue to be monitored overnight.

497
Q

What should be done if the urine SG remains <1.015 after a 5% or more loss of body weight in the water deprivation test?

A

Perform an ADH (desmopressin) response test.

498
Q

What is the dose of synthetic analogue of ADH (desmopressin) for dogs weighing less than 15 kg or cats?

A

2.0 μg (micrograms).

499
Q

What is the maximum response time to intravenous desmopressin after the test is performed?

A

4-8 hours.

500
Q

What are the urine SG ranges for animals with complete CDI or primary NDI during the modified water deprivation test?

A

1.001-1.007 (<1.008 after severe dehydration).

Small Animal Medicine (GP cert) (22 decks)

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