Endocrinology AI Flashcards
(500 cards)
1
Q
What are the two main forms of canine hyperadrenocorticism?
A
Pituitary-dependent (PDH) and adrenal-dependent (ADH)
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.
3
Q
What is the normal function of the adrenal cortex?
A
The adrenal cortex synthesizes and secretes steroid hormones, including glucocorticoids and mineralocorticoids.
4
Q
What are the three zones of the adrenal cortex?
A
Zona glomerulosa, zona fasciculata, zona reticularis
5
Q
What hormones are produced by the zona glomerulosa?
A
Mineralocorticoids, such as aldosterone
6
Q
What hormones are produced by the zona fasciculata and zona reticularis?
A
Glucocorticoids and sex hormones
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.
8
Q
What is the initial hormone produced in the synthesis of glucocorticoids and mineralocorticoids?
A
Pregnenolone
9
Q
What is hyperadrenocorticism (HAC)?
A
HAC is a condition characterized by excessive production of steroid hormones, especially glucocorticoids, from the adrenal cortex.
10
Q
What are the two forms of spontaneous HAC?
A
Pituitary-dependent (PDH) and adrenal-dependent (ADH)
11
Q
What percentage of HAC cases are pituitary-dependent?
A
80-90%
12
Q
What causes pituitary-dependent HAC?
A
Excess ACTH secretion and bilateral adrenal hyperplasia
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%)
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.
15
Q
What is adrenal-dependent HAC caused by?
A
Adrenal adenomas or carcinomas
16
Q
What are the two main types of tumors that cause adrenal-dependent HAC?
A
Adrenal adenomas and adrenal carcinomas
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.
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.
19
Q
What is iatrogenic HAC?
A
HAC induced by exogenous prednisolone treatment
20
Q
What is the role of cholesterol in the synthesis of steroid hormones?
A
All steroid hormones are derived from cholesterol.
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.
22
Q
Which enzyme is inhibited by Trilostane in the synthesis of steroids?
A
3 β hydroxysteroid dehydrogenase
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.
24
Q
What is the main cause of pituitary-dependent HAC?
A
Excess ACTH secretion and bilateral adrenal hyperplasia
25
What is the pituitary portal blood system?
The system through which corticotrophin releasing hormone (CRH) travels from the hypothalamus to the anterior pituitary.
26
What is the normal negative feedback mechanism in HAC?
In HAC, the negative feedback mechanism fails and excessive amounts of steroid hormones are produced.
27
What is the role of ACTH in HAC?
ACTH stimulates the production of glucocorticoids from the zona fasciculata and zona reticularis in the adrenal cortex.
28
What do the paraventricular nuclei in the hypothalamus synthesize and release?
Corticotrophin releasing hormone (CRH)
29
What are the clinical signs of hyperadrenocorticism?
Clinical signs relate to abnormal concentrations of steroid hormones and can include polyuria, polydipsia, polyphagia, abdominal distension, muscle wasting, etc.
30
What routine laboratory tests are used in the diagnosis of hyperadrenocorticism?
Routine laboratory tests include measurement of serum alkaline phosphatase (ALP) activity, alanine transaminase (ALT) activity, etc.
31
What screening tests are used for the diagnosis of hyperadrenocorticism?
Screening tests include the low-dose dexamethasone suppression test, the urine cortisol-to-creatinine ratio, and the ACTH stimulation test.
32
What are the two main forms of hyperadrenocorticism in cats?
There are no specific mentions of the two main forms in the given text.
33
What are the two main types of tumors that cause adrenal-dependent HAC in dogs?
Adrenal adenomas and adrenal carcinomas
34
What is the role of the adrenal medulla?
The adrenal medulla synthesizes and secretes amines.
35
What hormones are produced by the adrenal medulla?
Amines
36
What hormone is released by the pituitary gland in response to CRH stimulation?
ACTH
37
What are the clinical signs of pituitary-dependent HAC?
Clinical signs can include polyuria, polydipsia, panting, polyphagia, abdominal distension, muscle wasting, etc.
38
Which cells in the anterior pituitary produce ACTH?
Corticotrophin cells
39
What is the role of aldosterone?
Aldosterone is a mineralocorticoid hormone involved in the regulation of electrolyte balance.
40
What are the complications of canine hyperadrenocorticism?
The given text does not explicitly mention the complications of canine hyperadrenocorticism.
41
What is the role of the brain in accurate planning?
The brain is essential for accurate planning.
42
What can diagnostic imaging be used for in relation to tumours of the adrenal cortex?
Diagnostic imaging can be used to distinguish between benign and malignant tumours of the adrenal cortex.
43
What can happen if malignant tumours of the adrenal cortex invade the caudal vena cava?
Malignant tumours may invade the caudal vena cava.
44
Where can malignant tumours of the adrenal cortex spread to?
Malignant tumours can spread to the liver and lungs.
45
What is the purpose of the high-dose dexamethasone suppression test?
The high-dose dexamethasone suppression test inhibits pituitary ACTH secretion and suppresses cortisol concentrations.
46
How does the high-dose dexamethasone suppression test work in pituitary-dependent hyperadrenocorticism?
The high dose of dexamethasone inhibits pituitary ACTH secretion through negative feedback in pituitary-dependent hyperadrenocorticism thus suppressing cortisol concentrations.
47
Are adrenocortical tumours autonomous?
Yes, adrenocortical tumours are autonomous and thus cortisol is not suppressed.
48
Is the high-dose dexamethasone suppression test a good discriminatory test?
No, approximately 20 to 30 per cent of pituitary-dependent cases will not suppress with this test, making it a poor discriminatory test.
49
What are the potential complications of leaving hyperadrenocorticism (HAC) untreated?
Complications of untreated HAC include pulmonary thromboembolism, diabetes, pancreatitis, and infection.
50
How long can most cases of untreated HAC survive?
Most cases of untreated HAC will live 6-24 months.
51
How long can well-managed cases of HAC live on therapy?
Well-managed cases of HAC can live for several years on therapy.
52
What is the recommended first choice drug for the management of pituitary dependent disease (PDH)?
Trilostane should be the first choice drug for the management of PDH (80-90% of cases).
53
What is trilostane?
Trilostane is a synthetic steroid with no inherent hormonal activity.
54
How does trilostane work in blocking adrenal synthesis of glucocorticoids, mineralocorticoids, and sex hormones?
Trilostane acts as a competitive inhibitor of the 3ß-hydroxysteroid dehydrogenase enzyme system, blocking adrenal synthesis.
55
What factors should be considered when administering trilostane?
Trilostane should not be used in dogs with primary hepatic disease or renal failure.
56
How frequently should clinical examination and laboratory testing be performed in trilostane-treated dogs?
Clinical examination and laboratory testing should be performed at 10 days, 4 weeks, 12 weeks, and every 3 months thereafter.
57
When should the ACTH stimulation test be performed in trilostane-treated dogs?
The ACTH stimulation test should be performed 4-6 hours after dosing with trilostane.
58
What cortisol concentration indicates adequate control 4-6 hours after trilostane administration?
A post-ACTH cortisol concentration of >20 but <150 nmol/l indicates adequate control.
59
What should be considered if the ACTH stimulation test result shows a cortisol value >150 in a trilostane-treated dog?
Consideration should be given to increasing the dose by 50% and re-testing.
60
Do all dogs require once daily dosing of trilostane?
No, some dogs require twice daily dosing to achieve adequate control of clinical signs over a 24-hour period.
61
What should owners be warned about regarding trilostane treatment?
Owners should be warned about the risk of side effects, including sudden death.
62
How quickly may polyuria/polydipsia (PU/PD) resolve after starting trilostane treatment?
PU/PD may resolve within a few days of treatment commencing.
63
How long may it take for other dermatological manifestations of hyperadrenocorticism to improve with trilostane treatment?
Other dermatological manifestations may take several months to improve with trilostane treatment.
64
What percentage of dogs treated with trilostane have resolution of clinical signs of PU/PD?
Approximately 70% of dogs treated with trilostane have resolution of clinical signs of PU/PD.
65
What percentage of dogs treated with trilostane have resolution of skin changes?
Approximately 60% of dogs treated with trilostane have resolution of skin changes.
66
Does the clinical response to trilostane vary among cases?
Yes, some cases require increasing doses of trilostane, while others may show spontaneous remission requiring lower doses or even cessation of treatment.
67
What complications have been reported in trilostane-treated dogs?
Complications reported include diarrhea, acute pancreatitis, and rare cases of sudden death.
68
What does an elevated cortisol production pathway suggest?
An abnormality in the cortisol production pathway.
69
What is the difference between classic 'Cushing's disease' and the abnormal cortisol production seen in recent studies?
Classic 'Cushing's disease' shows overproduction of cortisol, while recent studies suggest an abnormality in the cortisol production pathway.
70
Why doesn't the author recommend the use of the high-dose dexamethasone suppression test?
Its accuracy has been questioned and it is not recommended for differentiating the cause of hyperadrenocorticism.
71
What is the recommended test for differentiating pituitary and adrenal causes of hyperadrenocorticism?
Canine ACTH assays, specifically measuring the plasma ACTH concentration.
72
Which diagnostic imaging technique is sensitive in distinguishing dogs with pituitary-dependent hyperadrenocorticism from those with adrenocortical tumors?
Abdominal ultrasonography.
73
How can dogs with adenomas be distinguished from dogs with carcinomas?
Recognition of metastatic lesions with radiography and/or ultrasonography.
74
What is the use of measuring basal endogenous ACTH concentrations in the diagnosis of hyperadrenocorticism?
It has no value due to episodic secretion of ACTH in normal dogs and overlapping values with those with hyperadrenocorticism.
75
What is the range of endogenous ACTH concentrations in normal dogs?
13 to 46 pg/ml.
76
What do very low endogenous ACTH concentrations (< 5 pg/ml) indicate in dogs with hyperadrenocorticism?
Adrenal tumors.
77
What do high normal to high concentrations (> 28 pg/ml) of endogenous ACTH indicate in dogs with hyperadrenocorticism?
Pituitary-dependent hyperadrenocorticism.
78
Which imaging techniques can be used to differentiate pituitary-dependent hyperadrenocorticism and adrenal-dependent hyperadrenocorticism?
Abdominal radiography, ultrasonography, CT, and MRI.
79
What suggests pituitary-dependent hyperadrenocorticism?
Similar size and normal shape of both adrenal glands.
80
What suggests adrenal-dependent hyperadrenocorticism in a dog with confirmed hyperadrenocorticism?
A mass in the adrenal area.
81
Which imaging technique accurately localized all adrenocortical tumors in a study?
CT.
82
Why is abdominal radiography less accurate than CT in localizing adrenocortical tumors?
Tumors less than 20 mm in diameter cannot be seen on abdominal radiographs.
83
What can CT identify in relation to adrenocortical tumors?
Invasion of the caudal vena cava by the tumor and adhesions between the adrenal gland and the caudal vena cava.
84
Which imaging technique is superior to CT in detecting ACTH-secreting tumors of the pituitary gland in humans?
MRI.
85
How small pituitary tumors can be detected using MRI in dogs and cats?
As small as 3 mm.
86
Are large pituitary tumors associated with neurological signs in dogs?
Not always, as some large tumors have been shown to be present without causing neurological signs.
87
What has been shown in another study regarding pituitary masses and neurological signs?
Pituitary masses ranging in size from 8 to 24 mm were associated with neurological signs.
88
What are some neurological signs associated with a rapid enlargement of a pituitary tumor?
Neurological signs associated with a rapid enlargement of a pituitary tumor can include adrenal necrosis and acute hypoadrenocorticism or thromboembolism.
89
What are the potential adverse effects of trilostane treatment in dogs with hyperadrenocorticism?
Potential adverse effects of trilostane treatment in dogs with hyperadrenocorticism include sudden death and adrenal necrosis.
90
Why is awareness of adrenal necrosis in dogs receiving trilostane treatment important?
Awareness of adrenal necrosis in dogs receiving trilostane treatment is important because prompt treatment is required to correct this life-threatening situation.
91
What is mitotane and how effective is it in the management of hyperadrenocorticism?
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.
92
What were the findings of the study comparing the survival times of dogs treated with mitotane or trilostane for pituitary-dependent hyperadrenocorticism?
The study found no significant difference in survival times between dogs treated with mitotane or trilostane for pituitary-dependent hyperadrenocorticism.
93
What is the best prognosis for dogs with adrenal-dependent hyperadrenocorticism?
Dogs with adrenal-dependent hyperadrenocorticism have the best prognosis if the tumor can be completely removed surgically.
94
What should be included in the pre-operative staging of an adrenal tumor in dogs?
The pre-operative staging of an adrenal tumor in dogs should include thoracic radiographs and abdominal ultrasound to assess vascular invasion and metastatic spread.
95
What are the recommended treatments to control hyperadrenocorticism before surgical adrenalectomy?
Some authors recommend the administration of trilostane or mitotane before surgical adrenalectomy to attempt to control hyperadrenocorticism.
96
What are the requirements for unilateral adrenalectomy in dogs?
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.
97
What was the perioperative mortality rate observed in a study on unilateral adrenalectomy in dogs?
In a study, the perioperative mortality rate for unilateral adrenalectomy in dogs was 30 percent.
98
What is the purpose of trilostane therapy in dogs with adrenal-dependent hyperadrenocorticism?
Trilostane therapy aims to provide symptomatic control of clinical signs without treating the underlying neoplastic disease process.
99
What was the reported survival time in one case using trilostane therapy for an adrenal tumor in dogs?
In one case, an 80-week survival was reported in a dog with an adrenal tumor using trilostane therapy.
100
What is mitotane therapy and how is it used in the treatment of adrenal-dependent hyperadrenocorticism?
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.
101
What is the current status of mitotane's licensing and its usage?
Mitotane is no longer licensed and as a result, it is rarely used in the management of hyperadrenocorticism.
102
What are some common clinical signs of hyperadrenocorticism (HAC)?
Polyuria, polydipsia, polyphagia, panting, abdominal distension
103
What are some hematologic abnormalities commonly observed in HAC?
Eosinopaenia, neutrophilia, monocytosis, erythrocytosis
104
What is the typical urinalysis finding in HAC?
Isosthenuria or hyposthenuria
105
What percentage of HAC cases demonstrate glycosuria?
Approximately 10%
106
What are some common findings on abdominal radiographs of HAC patients?
Good contrast, hepatomegaly, distended bladder, calculi, adrenal enlargement
107
What might be seen on thoracic radiographs of HAC patients?
Tracheal and bronchial wall mineralization, pulmonary metastasis, osteoporosis
108
When should diagnostic tests for HAC be performed?
In animals with consistent histories and clinical signs
109
What is the purpose of performing at least one positive screening test for HAC?
To confirm the need for further diagnostic testing
110
What are some options for diagnostic testing of HAC?
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
111
Which screening test is very sensitive but not very specific for HAC?
Urine Cortisol: Creatinine ratio
112
What is the recommended way to collect urine samples for the cortisol:creatinine ratio test?
In as stress-free a way as possible, usually at home
113
What is the sensitivity of the ACTH stimulation test for detecting PDH?
Approximately 85%
114
When should HAC not be automatically excluded based on the ACTH stimulation test results?
If the ACTH result is within the reference interval
115
What is the preferred test for monitoring mitotane and trilostane treatment?
ACTH stimulation test
116
What is the purpose of the LDDS test in diagnosing HAC?
To induce negative feedback to the pituitary and detect cortisol suppression
117
What does a positive result on the LDDS test indicate?
Resting cortisol > 40 nmol/l at 8 hours (not suppressed)
118
What is the purpose of the 17 alpha-OH progesterone assay?
To detect HAC cases that are negative on other tests
119
What is o.p.' -DDD?
o.p.' -DDD is a medication used in dogs with adrenal-dependent hyperadrenocorticism.
120
Is o.p.' -DDD effective in dogs with adrenal-dependent hyperadrenocorticism?
Yes, o.p.' -DDD is effective in dogs with adrenal-dependent hyperadrenocorticism.
121
Is o.p.' -DDD relatively safe in dogs with adrenal-dependent hyperadrenocorticism?
Yes, o.p.' -DDD is relatively safe in dogs with adrenal-dependent hyperadrenocorticism.
122
Are dogs with adrenal tumours more resistant to mitotane than dogs with pituitary-dependent hyperadrenocorticism?
Yes, dogs with adrenal tumours tend to be more resistant to mitotane than dogs with pituitary-dependent hyperadrenocorticism.
123
What dose range is generally required for dogs with adrenal-dependent hyperadrenocorticism during the induction period?
Dogs with adrenal-dependent hyperadrenocorticism generally require higher daily induction doses of 50-75 mg/kg/day.
124
Is a longer period of induction required for dogs with adrenal-dependent hyperadrenocorticism compared to dogs with pituitary-dependent hyperadrenocorticism?
Yes, dogs with adrenal-dependent hyperadrenocorticism require a longer period of induction (>14 days) than dogs with pituitary-dependent hyperadrenocorticism.
125
What percentage of cases responded successfully to the recommended protocol for pituitary-dependent hyperadrenocorticism?
About 20 percent of cases responded successfully to the recommended protocol for pituitary-dependent hyperadrenocorticism.
126
Why is frequent monitoring of treatment by ACTH stimulation testing important?
Frequent monitoring of treatment by ACTH stimulation testing is important to ensure adequate control of the hyperadrenocorticism.
127
Are maintenance doses generally higher for dogs with adrenal-dependent hyperadrenocorticism?
Yes, maintenance doses are generally higher (75-100 mg/kg/week) for dogs with adrenal-dependent hyperadrenocorticism.
128
Why is frequent monitoring of the cortisol response to ACTH stimulation required for dogs with adrenal-dependent hyperadrenocorticism?
Frequent monitoring of the cortisol response to ACTH stimulation is required to maintain optimal control of the disease.
129
Do dogs requiring higher dose rates of mitotane tend to be more prone to adverse effects?
Yes, dogs requiring higher dose rates of mitotane tend to be more prone to adverse effects.
130
What can happen to the adrenal tumour and metastatic mass during mitotane therapy?
The adrenal tumour and metastatic mass can often reduce in size due to the cytotoxic effects of mitotane.
131
Does the tumour always shrink during mitotane therapy?
No, in some cases the tumour will continue to grow despite increasing doses of mitotane.
132
What was the median survival time in a study of adrenocortical tumours treated using mitotane therapy?
The median survival time was 11 months.
133
What was the range of survival time in a study of adrenocortical tumours treated using mitotane therapy?
The range of survival time was a few weeks to more than 5 years.
134
What are the clinical signs of hyperadrenocorticism (HAC)?
Polyphagia, PU/PD, abdominal enlargement, muscle weakness
135
What are the predisposed breeds for pituitary-dependent hyperadrenocorticism (PDH)?
Poodles, Dachshunds, small Terriers
136
What are the clinical signs of hyperadrenocorticism (HAC) in small breed dogs?
Abdominal enlargement, polyphagia, PU/PD
137
What are the clinical signs of hyperadrenocorticism (HAC) in larger breed dogs?
Abdominal enlargement, hepatomegaly, muscle wasting/weakness
138
What are the clinical signs of hyperadrenocorticism (HAC) in older dogs?
Lethargy/exercise intolerance, skin changes, reproductive changes
139
What is polyphagia?
Excessive hunger or increased appetite
140
What is PU/PD?
Polyuria (excessive urination) and polydipsia (excessive thirst)
141
What are the complications of hyperadrenocorticism (HAC)?
Urinary tract infection, hypertension, glomerulonephropathies, pulmonary thromboembolism, diabetes mellitus
142
What are the biochemical abnormalities associated with hyperadrenocorticism (HAC)?
Elevated ALP, ALT, cholesterol, bile acids, lipids; reduced urea, T4
143
What are the haematological changes consistent with hyperadrenocorticism (HAC)?
Lymphopaenia
144
What is the maximum concentration of desoxycortone?
The maximum concentration of desoxycortone is assessed after 10 days.
145
When should the clinical signs and electrolytes be re-evaluated?
The clinical signs and electrolytes should be re-evaluated after 10 days.
146
What should be done if the clinical signs have worsened or not resolved?
The dose of glucocorticoid should be adjusted and/or other causes of the clinical signs should be investigated.
147
When should the dog be re-evaluated and the Na+/K+ ratio measured?
The dog should be re-evaluated and the Na+/K+ ratio should be measured on Day 25.
148
What should be done if the dog is both clinically normal and has a normal Na+/K+ ratio on Day 25?
The dose should be adjusted based on the Day 10 Na+/K+ ratio using the guidelines on the datasheet.
149
What should be done if the dog is clinically normal and has a Na+/K+ ratio >32 on Day 25?
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.
150
What should be done if the dog is either not clinically normal or if the Na+/K+ ratio is abnormal on Day 25?
The dose of glucocorticoid or Zycortal should be adjusted.
151
How can the dosing interval be prolonged?
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.
152
How often should the electrolytes be evaluated if the dosing interval is prolonged?
The electrolytes should be evaluated every 5-9 days until the Na+/K+ ratio is <32.
153
What should be done once the optimal dose and dosing interval have been determined?
The same regimen should be maintained.
154
What should be done if the dog develops clinical signs of polyuria/polydipsia?
The glucocorticoid dose should be decreased first.
155
What should be done if the polyuria/polydipsia persists and the Na+/K+ ratio is >32?
The dose of Zycortal should be decreased without changing the dosing interval.
156
What should be done if the dog develops clinical signs of depression, lethargy, vomiting, diarrhea, or weakness?
The glucocorticoid dose should be increased.
157
What should be done if the dog has hyperkalemia, hyponatremia, or Na+/K+ ratio <27?
The Zycortal dosing interval should be decreased by 2-3 days or the dose should be increased.
158
What should be done if the dog has hypokalemia, hypernatremia, or Na+/K+ ratio >32?
The Zycortal dose should be decreased.
159
What should be considered prior to a stressful situation?
Temporarily increasing the dose of glucocorticoid should be considered.
160
What was the mean final dose of desoxycortone pivalate in the clinical trial?
The mean final dose of desoxycortone pivalate was 1.9 mg/kg.
161
What was the mean final dosing interval in the clinical trial?
The mean final dosing interval was 38.7 ± 12.7 days.
162
What is the majority of thyroid secretion composed of?
The majority of thyroid secretion is composed of T4.
163
What is the function of the thyroid glands?
The thyroid glands produce thyroid hormone.
164
What are the two thyroid hormones called?
The two thyroid hormones are T3 (Tri-iodothyronine) and T4 (Thyroxine).
165
What is the substance secreted from the cells of the thyroid glands?
Thyroglobulin is the substance secreted from the cells of the thyroid glands.
166
How are thyroid hormones synthesized?
Thyroid hormones are synthesized from 2 connected tyrosine molecules.
167
What is the enzyme involved in incorporating iodine into thyroglobulin?
Thyroid peroxidase is the enzyme involved in incorporating iodine into thyroglobulin.
168
Where do hormones remain until they are required for release?
Hormones remain in the acinar lumen of the thyroid glands until they are required for release.
169
How are the majority of T4 and T3 transported in the circulation?
The majority of T4 and T3 are transported in the circulation attached to binding proteins.
170
What are the biological effects exerted by 'free' T4 and T3?
'Free' T4 and T3 exert the biological effects.
171
What does T4 get converted into in the periphery?
T4 can be converted into the more active T3 in the periphery.
172
What is the normal proportion of T4 and T3 in thyroid secretion?
Approximately 95% of thyroid secretion is T4 and 5% is T3.
173
What is fludrocortisone?
Fludrocortisone is a mineralocorticoid and glucocorticoid replacement medication.
174
How is fludrocortisone administered?
Fludrocortisone is administered orally.
175
Is fludrocortisone licensed?
No, fludrocortisone is not licensed.
176
What is the current cost status of fludrocortisone?
Fludrocortisone is now very expensive.
177
What are the aim(s) of hyperthyroid cat treatment?
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.
178
What are the two curative options for hyperthyroid cat treatment?
Surgical thyroidectomy and radioactive iodine therapy.
179
What is the role of medical management in hyperthyroid cat treatment?
It is an option for many hyperthyroid cats, resulting in a rapid return to euthyroidism.
180
What are the two medical options for hyperthyroid cat treatment?
Carbimazole and methimazole (thiamazole).
181
How do carbimazole and methimazole work in hyperthyroid cat treatment?
They reversibly block iodination of thyroglobulin, effectively suppressing thyroid hormone production.
182
What are the trade names for methimazole?
Felimazole and Thyronorm.
183
What is the trade name for carbimazole?
Vidalta.
184
How is methimazole administered to cats?
Usually administered orally, but it can be administered transdermally as a gel applied to the non-haired part of the ear.
185
What tests are used to monitor cats receiving antithyroid medications?
Serum total T4 is often measured after therapy initiation or dose adjustment, and should be checked every 3-6 months once stability is achieved.
186
When should the serum sample be taken for monitoring cats receiving antithyroid medications?
The time of day is not important.
187
What is the goal of maintaining total T4 levels in cats receiving antithyroid medications?
To keep total T4 within the lower half of the reference interval.
188
Do clinical signs of hypothyroidism typically develop in cats with low total T4 levels?
No, clinical signs of hypothyroidism rarely develop even when total T4 is well below the reference interval.
189
What are the mild adverse effects of antithyroid medications in cats?
Vomiting, with or without anorexia and depression, usually occurring in the first 3 weeks of therapy.
190
Do mild adverse effects of antithyroid medications typically require discontinuation of the treatment?
No, in most cases these adverse effects are transient and self-limiting.
191
What should be done if circulating total T4 is severely depressed in cats receiving antithyroid medications?
The dosage of drugs should be decreased, if possible, and the cat should be re-assessed.
192
Which liver enzymes decline progressively as euthyroidism is achieved in cats receiving antithyroid medications?
Serum ALT and ALP.
193
What potential harmful effect has been associated with induced hypothyroidism in cats?
Renal impairment and shortened survival.
194
What are the advantages of medical management for hyperthyroid cats?
Widely available, requires no specialist facilities, and is recommended as trial therapy for assessing the effects on renal function.
195
What is the difference in potency between 5mg of carbimazole and a similar weight of methimazole?
A 5mg dose of carbimazole is equal to a 3mg dose of methimazole.
196
Does carbimazole or methimazole have a lower incidence of adverse effects?
Carbimazole is often suggested to have a lower incidence of adverse effects than methimazole.
197
What drives the production of thyroid hormone?
Thyroid stimulating hormone (TSH)
198
What is the main purpose of the hypothalamic / pituitary axis?
To regulate free T4 and T3 levels
199
How does thyroid hormone affect metabolism?
It affects basal metabolic rate, protein synthesis, and lipid metabolism
200
What body systems does thyroid hormone affect?
Metabolism, growth, development, osteogenesis, skin and hair growth, cardiovascular system
201
What are the clinical signs of hyperthyroidism in cats?
Weight loss, increased appetite, hyperactivity, gastrointestinal signs, tachycardia
202
What is the average age of onset for hyperthyroidism in cats?
12 years
203
What are some possible causes of hyperthyroidism in cats?
Bilateral thyroid hyperplasia, adenomas, dietary, toxic, geographical influences
204
What percentage of hyperthyroid cats have a palpable goitre?
98%
205
What are some diagnostic indicators of hyperthyroidism in cats?
Weight loss, increased appetite, hyperactivity, gastrointestinal signs, tachycardia
206
What are the haematological changes seen in hyperthyroidism?
Mild to moderate increase in PCV, RBC count, and hemoglobin concentration
207
Which liver enzymes are frequently elevated in hyperthyroid cats?
ALT, AST, and ALP
208
What is the significance of elevated liver enzymes in hyperthyroid cats?
Unknown, may reflect non-specific changes associated with malnutrition and toxic effects of thyroid hormones
209
What is the most common endocrinopathy in cats?
Hyperthyroidism
210
What percentage of hyperthyroidism cases are due to thyroid carcinomas?
5%
211
What are some clinical signs of hyperthyroidism in cats?
Weight loss, increased appetite, hyperactivity, gastrointestinal signs, tachycardia
212
What percentage of hyperthyroid cats present with a palpable goitre?
98%
213
What is a possible sign of congestive heart failure in hyperthyroid cats?
Hypertrophic cardiomyopathy
214
What are some reported clinical signs seen in hyperthyroid cats?
Weight loss, polyphagia, polyuria/polydipsia, tachycardia, hyperactivity
215
What lab test is often used for diagnosing hyperthyroidism?
Total serum T4
216
What are some routine lab test results that may indicate hyperthyroidism?
Mild to moderate increases in liver enzymes ALT, AST, and ALP
217
What is the pathophysiology of canine hypoadrenocorticism?
It is caused by a deficiency in mineralocorticoid and/or glucocorticoid production.
218
How is primary hypoadrenocorticism (Addison’s Disease) different from secondary hypoadrenocorticism?
Primary hypoadrenocorticism is due to immune destruction of adrenal cortices, while secondary hypoadrenocorticism is due to a deficiency of ACTH.
219
What are the causes of primary hypoadrenocorticism?
Causes include idiopathic atrophy, iatrogenic factors such as drugs (mitotane, trilostane) or bilateral adrenalectomy.
220
Which breeds have an increased risk of hypoadrenocorticism?
Standard Poodles, Bearded Collies, Portuguese Water Dog, Great Dane, Rottweiler, WHWT, Soft Coated Wheaten Terrier.
221
What are the clinical signs of chronic hypoadrenocorticism?
Signs can include anorexia, vomiting, lethargy, depression, weakness, shivering, weight loss, PUPD, and abdominal pain.
222
What should be considered as a differential diagnosis in animals with waxing/waning signs and intermittent GI disease/bleeding?
Hypoadrenocorticism.
223
What are the physical findings in hypoadrenocorticism?
Depression, weakness, dehydration, bradycardia, weak pulses, ECG changes, and intermittent signs of GI hemorrhage.
224
What are the clinical signs of acute hypoadrenocorticism?
Hypovolemic shock, relative bradycardia, collapse or extreme weakness, and hypothermia.
225
What is the pathophysiology of feline hyperthyroidism?
Review the pathophysiology of feline hyperthyroidism.
226
What are the clinical features of feline hyperthyroidism?
Recognize the clinical features of feline hyperthyroidism.
227
What can routine laboratory tests help interpret in feline hyperthyroidism?
Routine laboratory tests can help interpret the results of feline hyperthyroidism.
228
What should be discussed in the management of feline hyperthyroidism?
Disease management should be discussed in feline hyperthyroidism.
229
What is the pathophysiology of canine hypothyroidism?
Review the pathophysiology of canine hypothyroidism.
230
What are the clinical features of canine hypothyroidism?
Recognize the clinical features of canine hypothyroidism.
231
What can routine laboratory tests help interpret in canine hypothyroidism?
Routine laboratory tests can help interpret the results of canine hypothyroidism.
232
What should be discussed in the management of canine hypothyroidism?
Management of the disease should be discussed in canine hypothyroidism.
233
What are the physical examination findings in acute hypoadrenocorticism?
Depression, thinness, weakness, dehydration, bradycardia, melena/hematochezia
234
What blood parameter changes reflect the lack of aldosterone and cortisol in hypoadrenocorticism?
Hyperkalemia, hyponatremia, hypochloridemia
235
What are the classic findings in the serum biochemistry of hypoadrenocorticism?
Hyperkalemia, hyponatremia, hypochloridemia, Na:K ratio <23
236
What percentage of cases do not have classical electrolyte changes in hypoadrenocorticism?
10%
237
What are the findings in urinalysis in hypoadrenocorticism?
High urine specific gravity may not always happen
238
What are the ECG changes seen in hypoadrenocorticism?
T wave peaking and Q-T shortening, increased QRS duration, decreased P wave, severe bradycardia
239
What are the radiographic changes usually seen in hypoadrenocorticism?
Microcardia, decreased pulmonary vessel size, reduced caudal vena cava size, microhepatica
240
What is the value of basal cortisol that effectively rules out hypoadrenocorticism?
>55nmol
241
What is the most useful test for diagnosing hypoadrenocorticism?
ACTH stimulation test
242
How can aldosterone pre and post ACTH be used to distinguish primary and secondary causes of hypoadrenocorticism?
Raised post ACTH aldosterone in secondary causes, no response in primary causes
243
What are the steps in the management of the acute crisis in hypoadrenocorticism?
Restore intravascular volume, reversal of hyperkalemia, reversal of hyponatremia, provision of glucocorticoids and mineralocorticoids, correction of any life-threatening arrhythmias
244
What intravenous fluid can be used to restore intravascular volume in a patient with hypoadrenocorticism?
0.9% NaCl or lactated Ringer’s (Hartmann’s) solutions
245
What solution is suggested to be used in hyperkalemic patients?
Hartmann's solution
246
What are the advantages of using Hartmann's solution in hyperkalemic patients?
Large volume fluid provision, diuresis, kaluresis, alkalizing effect
247
What treatments can be used to decrease potassium level in hyperkalemic animals?
Calcium gluconate, sodium bicarbonate, glucose with or without regular insulin
248
How does calcium gluconate help in hyperkalemia reversal?
It is cardioprotective and re-establishes normal resting membrane potential.
249
How does sodium bicarbonate help in hyperkalemia reversal?
It creates a gradient for hydrogen ions to move out of cells, allowing potassium ions to move into the cells.
250
How does glucose with or without regular insulin help in hyperkalemia reversal?
Glucose moves into cells under insulin influence, carrying potassium along.
251
What is the recommended treatment for correcting hyponatremia?
Intravenous fluid therapy
252
What should be considered when correcting hyponatremia with intravenous fluid therapy?
Ensure sodium does not rise too rapidly to avoid central nervous system signs.
253
What is the best way to correct acute glucocorticoid deficiency?
Intravenous administration of rapid-acting glucocorticoid
254
What are the available options for glucocorticoid administration in acute crisis situations?
Dexamethasone, hydrocortisone, methylprednisolone sodium, prednisolone
255
Why is dexamethasone preferred over other corticosteroids for ACTH stimulation test?
It does not cross-react with cortisol measurement.
256
What is Zycortal and how is it administered?
A mineralocorticoid replacement administered by subcutaneous injection.
257
What is the requirement for dogs receiving Zycortal for hypoadrenocorticism treatment?
They must also receive oral glucocorticoids.
258
What is the initial and second dose requirement for Zycortal administration?
Details are available in the data sheet.
259
What are the common clinical signs of hypothyroidism in dogs?
Lethargy, weight gain, alopecia, pyoderma, seborrhoea, cold intolerance, bradycardia, and 'Rat Tail'.
260
What are the common breeds of dogs that are usually affected by hypothyroidism?
Dobermans, Miniature Schnauzers, Cocker Spaniels, and Golden Retrievers.
261
What are the blood abnormalities commonly seen in hypothyroidism?
Increased cholesterol, increased triglycerides, and mild liver enzyme elevation.
262
What are the differential diagnoses for cholesterol elevation in hypothyroidism?
High fat diet, other endocrinopathies (e.g. diabetes mellitus), nephrotic syndrome, cholestasis, or dyslipoproteinaemia.
263
What are the two main diagnostic tests used for hypothyroidism?
Serum T4 and Serum TSH.
264
Why is measuring total T4 alone not enough to diagnose hypothyroidism?
It can be misleading due to factors like certain drugs and systemic disease.
265
What can falsely lower T4 levels in the body?
Phenobarbitone, NSAID's, GA, sedatives, AB's, and frusemide.
266
What is the advantage of using TSH as a diagnostic test for hypothyroidism?
Readily available and not expensive.
267
Why should TSH be used in combination with T4 for diagnosing hypothyroidism?
Approximately 25% of hypothyroid dogs may have TSH values within the reference range.
268
What is the most reliable method to measure free T4?
Equilibrium dialysis.
269
What test is used to detect thyroid autoimmunity?
Testing for anti-thyroglobulin antibodies.
270
What is the advantage of using rhTSH for the stimulation test?
Considered as a gold standard and reliable.
271
What are some potential disadvantages of rhTSH stimulation test?
It takes several hours to perform and anaphylactic reactions have been described with bovine rhTSH.
272
What are some mild and transient haematological abnormalities that can occur in cats during therapy?
Lymphocytosis, eosinophilia, leucopenia
273
What are some more serious haematological complications that can occur in cats during therapy?
Agranulocytosis, thrombocytopenia
274
What is the frequency at which clinicians have recommended assessing haematology during therapy?
Every 2 weeks
275
What percentage of cats may experience hepatopathy during therapy?
<2%
276
What is the recommended action if any serious adverse effects occur during therapy?
Drug withdrawal
277
What is surgical thyroidectomy?
A very effective management strategy for hyperthyroidism
278
What is the most significant post-operative complication of thyroidectomy?
Hypocalcaemia
279
What occurs if the parathyroid glands are removed, damaged, or devascularized during thyroidectomy?
Hypocalcaemia
280
What is the generally considered optimal treatment for most hyperthyroid cats?
Radioactive iodine
281
What is the most commonly used radioisotope for the treatment of hyperthyroid cats?
Iodine-131
282
What is the commercially available diet formulated for the management of hyperthyroid cats?
Hills y/d
283
What does the diet Hills y/d contain in extremely low levels?
Iodine
284
What percentage of hyperthyroid cats exclusively eating y/d will have normal serum total T4 concentrations by 4 weeks on the diet?
About 75%
285
In cats with severe hyperthyroidism, is the diet Hills y/d highly effective?
Not as effective
286
Other than surgery and radioactive iodine treatment, what is another therapy option mentioned in the notes?
Injection of ethanol directly into the thyroid adenomas
287
What is the rough reference range for T4 in hypothyroid, sick euthyroid or drug treatment?
0-15nmol/l
288
What does a T4 value of >25nmol/l indicate?
The dog is probably euthyroid
289
What percentage of hypothyroid dogs have normal TSH?
Approximately 25%
290
What is the reference range for TSH in normal, sick euthyroid, and rarely hypothyroid dogs?
0 - 0.41ng/ml
291
What is the reference range for TSH in hypothyroid dogs?
>0.6ng/ml
292
What are the possible causes for a Total T4 that is normal, cTSH normal, and non-thyroidal illness?
Non-thyroidal illness, euthyroid, drug therapy
293
What is the treatment for hypothyroidism in dogs?
Levothyroxine sodium
294
What are the first clinical signs to improve in response to levothyroxine treatment?
Lethargy and mental demeanour
295
When can dermatological improvement be expected after starting levothyroxine treatment?
By 3 months
296
What should the peak plasma concentration of T4 be in adequately dosed dogs?
Approximately 30 to 47 nmol/l
297
How often can clinical and biochemical monitoring be performed after the optimum replacement dose has been attained?
Every 6-12 months
298
Which drug can cause blunted TSH stimulation test results at high doses and durations?
Glucocorticoids
299
What are the cardiac findings associated with hyperthyroidism in cats?
Left ventricular hypertrophy, left atrial dilation, and interventricular septum hypertrophy.
300
What is the significance of changes in calcium and circulating PTH levels in hyperthyroidism?
The significance of these changes is unknown.
301
What is the most frequently identified echocardiographic abnormality in hyperthyroidism?
Left ventricular hypertrophy.
302
What is the most consistently elevated thyroid hormone in hyperthyroid cats?
Serum free T4.
303
Can hyperthyroidism be excluded based on total T4 within the reference range?
No, because non-thyroidal illness can suppress total T4 concentrations.
304
What is the recommended time frame to retest cats with marginally elevated total T4?
4-6 weeks.
305
What proportion of euthyroid sick cats have an elevation in free T4?
12%.
306
Should free T4 alone be relied upon for diagnosing hyperthyroidism?
No, it should be interpreted alongside total T4.
307
What effect does T3 have on serum total T4 concentration in hyperthyroid cats?
Minimal to no decrease.
308
Is there a species-specific feline TSH assay available?
No, but assays for measuring canine TSH may be useful in cats.
309
What cat population had undetectable circulating cTSH levels?
Hyperthyroid cats.
310
What proportion of feline TSH can the current assay detect?
Approximately 35%.
311
What is the reason for the rare elevation of plasma sodium concentrations in cats with hypokalaemic myopathy?
Water reabsorption secondary to sodium retention.
312
What are the usual serum creatine kinase concentrations in cats with hypokalaemic myopathy?
Markedly elevated.
313
What is the mean potassium concentration at presentation in cats with primary hyperaldosteronism?
2.5 mEq/L.
314
Does normokalaemia exclude the possibility of hyperaldosteronism?
No, it does not.
315
What should be considered if hypertention is unexplained in a cat?
Hyperaldosteronism.
316
How many of the described cases of adrenal hyperplasia were hypokalaemic at initial presentation?
Approximately half.
317
What should prompt suspicion of hyperaldosteronism in cats?
Persistence of hypokalaemia despite potassium supplementation.
318
What was the range of sodium concentration in cats with primary hyperaldosteronism?
148 to 168 mEq/L.
319
What were the mean creatine kinase levels in cats with primary hyperaldosteronism?
6,837 IU/L.
320
How many out of 13 cats with primary hyperaldosteronism were hypertensive?
12
321
What can be evidence of renal disease in cats with primary hyperaldosteronism?
Isosthenuria and elevated serum creatinine and blood urea nitrogen concentrations.
322
Why is imaging necessary in cats suspected of having primary hyperaldosteronism?
To detect adrenal abnormalities and evaluate metastases.
323
What can thoracic radiography detect in cats with primary hyperaldosteronism?
Pulmonary metastases.
324
What are the common ultrasonographic changes observed in the adrenal glands of cats with primary hyperaldosteronism?
Adrenal masses, adrenal calcification, and changes in adrenal echogenicity.
325
What is the median dorsoventral width of the adrenal glands of healthy cats?
3.9 mm.
326
Is finding an enlarged adrenal gland or mass definitive for a diagnosis of primary hyperaldosteronism?
No.
327
What are some other considerations for finding an adrenal gland mass in cats?
Non-functional tumors, phaeochromocytomas, cortisol-secreting tumors, and progesterone-secreting tumors.
328
Are functional tumors and clinically relevant hyperplasia always visible on diagnostic imaging?
No, they may not be large enough to be detected.
329
What were the imaging findings in cats with histologic confirmation of primary hyperaldosteronism?
Absent to minor changes in adrenal gland size and morphology.
330
When should primary hyperaldosteronism be considered as a possibility?
In cases with hypokalaemia, hypertension, adrenal mass, or abnormal regulation of aldosterone production.
331
What are the clinical signs associated with feline hyperaldosteronism?
Increased sodium and water retention, systemic arterial hypertension, and hypokalaemia.
332
How is feline hyperaldosteronism diagnosed?
Through blood tests to measure aldosterone levels and imaging techniques to detect adrenal masses.
333
What are the treatment options available for feline hyperaldosteronism?
Surgical removal of adrenal masses, medication to control blood pressure, and potassium supplementation.
334
What is the role of aldosterone in the body?
Aldosterone regulates sodium and water balance, and potassium excretion.
335
How is aldosterone production regulated?
Through the renin-angiotensin-aldosterone system (RAAS) and direct regulation via potassium ions.
336
What is primary hyperaldosteronism?
Excessive aldosterone production independent of the RAAS, caused by adrenal neoplasia or hyperplasia.
337
What are the causes of secondary hyperaldosteronism?
Stimulation of the RAAS due to dehydration, hypotension, reduced renal perfusion, or sodium deficiency.
338
What are the clinical consequences of excessive aldosterone production?
Systemic arterial hypertension and hypokalaemia.
339
What are the histopathological findings in feline primary hyperaldosteronism?
Unilateral or bilateral adenoma or carcinoma, or bilateral hyperplasia of the zona glomerulosa.
340
How does aldosterone affect the kidney, colon, and salivary gland?
It causes sodium reabsorption, water retention, and potassium and hydrogen ion excretion.
341
What is the main mechanism of aldosterone regulation?
Activation of the renin-angiotensin-aldosterone system (RAAS) due to decreased blood volume and renal blood flow.
342
What is the result of aldosterone binding to mineralocorticoid receptors?
Increased sodium and water reabsorption, leading to increased blood pressure and volume.
343
What are the causes of hypercalcaemia in dogs and cats?
Various underlying disorders, such as primary hyperparathyroidism or malignancies.
344
What is the physiology of calcium balance?
Calcium balance is regulated by parathyroid hormone, vitamin D, and calcitonin.
345
What is primary hyperparathyroidism?
Excessive secretion of parathyroid hormone from a neoplastic parathyroid gland.
346
How do animals with primary hyperaldosteronism differ from those with secondary hyperaldosteronism?
Primary hyperaldosteronism is independent of the RAAS, while secondary hyperaldosteronism is in response to RAAS stimulation.
347
What are the clinical signs associated with primary hyperparathyroidism?
Hypercalcaemia, renal disease, urolithiasis, and soft tissue mineralization.
348
What is the diagnostic plan for investigating hypercalcaemic patients?
Blood tests for calcium and parathyroid hormone levels, imaging techniques, and identification of underlying causes.
349
How is primary hyperparathyroidism treated?
Surgical removal of the affected parathyroid gland or medical management to control calcium levels.
350
What are the effects of primary hyperaldosteronism on sodium, water, and potassium balance?
Increased sodium and water retention, and increased potassium excretion leading to hypokalaemia.
351
What is the main effect of calcitonin on bone?
Calcitonin decreases calcium movement from 'soluble bone' layer into interstitial fluid.
352
What is the main effect of calcitonin on renal excretion?
Calcitonin increases renal excretion of calcium and phosphate.
353
How is vitamin D activated in the kidneys?
Vitamin D is converted to the active form 1,25 dihydroxycholecalciferol (1,25 DHCC) in the kidneys.
354
What hormone controls the conversion of vitamin D to its active form?
Parathyroid hormone (PTH) controls the conversion of vitamin D to its active form.
355
What are the effects of active vitamin D (calcitriol) on the gastrointestinal tract?
Active vitamin D promotes calcium uptake in the gastrointestinal tract.
356
What is the distribution of calcium forms in healthy dogs?
Ionised calcium: 56%, protein-bound calcium: 34%, complexed calcium: 10%.
357
Which form of calcium is biologically active?
Only ionised calcium is biologically active.
358
What can cause artificial lowering of total calcium levels?
Low albumin levels can artificially lower total calcium levels.
359
How can ionised calcium be measured in a laboratory?
Ionised calcium can be measured using an ionic specific electrode or an I-stat or Irma blood gas analyser.
360
What is the preferred method for measuring ionised calcium?
It is preferable to measure ionised calcium immediately using in-house analysers or a local hospital laboratory.
361
How is intact PTH measured?
Intact PTH is measured by immunoradiometric assay.
362
What is the reference range for intact PTH?
The reference range for intact PTH is 10 - 60 pg/ml.
363
What is primary hyperparathyroidism defined by?
Primary hyperparathyroidism is defined by hypercalcaemia with high or high-normal PTH and no other identifiable underlying cause.
364
What is another disease state where PTH may be elevated?
PTH may be elevated in hyperadrenocorticism and in some normocalcaemic dogs with lymphoma.
365
What should be performed to rule out other causes of hypokalaemia and hypertension?
Thorough history, physical examination, blood count, serum chemistry, T4 measurement, urinalysis, and blood pressure measurement.
366
What is the main determinant of aldosterone secretion?
Potassium concentration.
367
What is the confirmation of diagnosis for primary hyperaldosteronism?
Elevated plasma aldosterone concentration.
368
What is the requirement for collection and handling of serum or plasma for aldosterone concentration assay?
Routine collection and handling processes.
369
Is there clear evidence for improved diagnostic performance with ACTH stimulation test for primary hyperaldosteronism?
No, there is no clear evidence.
370
What are the main causes of high plasma aldosterone concentration in primary hyperaldosteronism?
Adrenocortical tumors and chronic renal disease.
371
Is plasma aldosterone concentration alone sufficient to distinguish between primary and secondary hyperaldosteronism?
No, it is not sufficient.
372
What should plasma aldosterone concentration be interpreted together with in cases of primary hyperaldosteronism?
Plasma renin activity.
373
What is required to reliably distinguish primary from secondary hyperaldosteronism?
Measurement of plasma renin activity.
374
What can influence the measurement of plasma renin activity?
Certain drugs (ACE inhibitors, beta-blockers) and dietary salt intake.
375
What pattern of plasma aldosterone concentration and plasma renin activity is consistent with primary hyperaldosteronism?
Elevated plasma aldosterone concentration with low renin activity.
376
In cases of adrenal tumors, what is the expected plasma aldosterone concentration and plasma renin activity?
Markedly elevated aldosterone and completely suppressed renin activity.
377
What is the gold standard for screening for feline primary hyperaldosteronism in humans?
Aldosterone: renin ratio.
378
What are the recommended pre-operative treatments for hypertension and hypokalaemia?
Correcting hypokalaemia and controlling hypertension.
379
What are some reported perioperative complications of surgery for hyperaldosteronism?
Intra-abdominal haemorrhage, acute renal failure, sepsis, and suspected thromboembolism.
380
What should be assessed upon recovery and periodically after surgery for hyperaldosteronism?
Blood pressure and potassium concentration.
381
When should oral therapy be continued in hypertensive or hypokalaemic patients after surgery?
If the patient remains hypertensive or hypokalaemic at the time of discharge.
382
What medications were discontinued the day of surgery in cats surviving surgical intervention for hyperaldosteronism?
Spironolactone and amlodipine therapy.
383
What is the reported survival time for cats with primary hyperaldosteronism treated with potassium supplementation, spironolactone, and amlodipine?
7 to 32 months.
384
What is the prognosis for cats with completely excised unilateral adrenocortical neoplasia and no evidence of metastasis?
Good, with reported survival rates of at least 1 year and some cats alive 3.5 and 5 years postoperatively.
385
What is the relationship between adrenal adenomas and adenocarcinomas in cats?
Adrenal adenocarcinomas do not appear to be associated with a poorer prognosis than adrenal adenomas.
386
What is the function of parathyroid glands in maintaining calcium homeostasis?
They release parathyroid hormone (PTH) to maintain serum calcium and lower serum phosphate.
387
What are the main organs responsible for calcium control in the body?
Bones, gastro-intestinal tract, and kidneys.
388
How is blood calcium controlled in the short term?
By utilizing the calcium reservoir in bone.
389
What percentage of calcium is filtered and re-absorbed by the kidneys?
Less than 2% of the filtered load.
390
What is the role of osteoclasts in maintaining blood calcium levels?
Re-modeling the layer of 'soluble bone' to release calcium into the circulation as required.
391
What triggers the release of parathyroid hormone (PTH)?
A fall in blood ionized calcium.
392
What are the direct effects of PTH on bone and kidney?
Increasing osteoclast activity, decreasing osteoblast activity, and promoting increased calcium absorption in the kidney.
393
What is the immediate effect of PTH on calcium levels?
Increased release of calcium into the circulation.
394
What is the recommended number of parathyroid glands to be removed at one time if multiple glands are enlarged?
Up to three glands may be removed at one time.
395
Why should at least one parathyroid gland be left in situ during surgery?
To maintain calcium homeostasis.
396
What is the likely cause of multiple enlarged parathyroid glands?
Secondary hyperparathyroidism, indicating hyperplastic rather than adenomatous glands.
397
What may occur post-surgery regarding PTH and calcium concentrations?
PTH and calcium concentrations should decrease rapidly; hypocalcaemia may occur in some cases.
398
Under what circumstances is hypocalcaemia more likely to occur?
If pre-treatment calcium has been severely elevated (exceeded 3.5 mmol/l) for more than a few months.
399
What happens to the remaining parathyroid glands when a parathyroid adenoma is functioning autonomously?
They become atrophied and are unable to support normal calcium homeostasis.
400
How can the crisis of atrophied parathyroid glands be avoided?
By giving vitamin D ± oral calcium supplements pre-surgery and in the immediate post-treatment period.
401
What are the two recommended preparations of vitamin D for managing parathyroid adenoma?
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
In combination with vitamin D, what are the different preparations of oral calcium available?
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
What is the short to mid-term prognosis for primary hyperparathyroidism (PHPT) in most breeds?
Excellent prognosis.
404
Is the long-term prognosis for PHPT also good in most breeds?
Yes, except in Keeshonds where recurrence can occur due to genetic drive to develop parathyroid adenomas.
405
What breed requires monitoring throughout life for recurrence of PHPT, especially if the first surgery was done at a young age?
Keeshonds.
406
What are the different forms of hyperfunction of the adrenal glands?
Unilateral adrenocortical adenocarcinomas, unilateral and bilateral adenomas, and bilateral nodular hyperplasia.
407
What is the possible cause of hyperfunction of the zona glomerulosa?
A circulating stimulatory factor, possibly a fragment of pro-opiomelanocortin.
408
Which mediators are responsible for progressive renal disease in cats with hyperaldosteronism?
Aldosterone and angiotensin II.
409
How is chronic renal disease linked to glomerular and tubulointerstitial injury?
Excessive accumulation of the extracellular matrix of the kidney.
410
Which growth factor can mediate the extracellular matrix accumulation in the kidney?
Angiotensin II.
411
Apart from its role in renal disease, what other functions does angiotensin II have?
Peripheral vasoconstriction, regulation of glomerular filtration, and pro-inflammatory cytokine activity.
412
How can aldosterone contribute to the progression of renal damage?
By promoting vascular thrombosis and fibrosis.
413
What organ damage is often found in cats with hyperaldosteronism?
Cardiovascular disease, indicated by heart murmur, cardiomegaly, or ventricular hypertrophy.
414
What are the typical clinical signs of feline hyperaldosteronism?
Potassium depletion (hypokalaemic myopathy) and systemic arterial hypertension.
415
What are the signs of hypokalaemic myopathy?
Episodic or acute muscle weakness, hindlimb plantigrade stance, and cervical ventroflexion.
416
What can acute-onset blindness in cats with hyperaldosteronism indicate?
Intraocular hemorrhage or retinal detachment due to systemic hypertension.
417
Which eye condition is more commonly associated with adrenal hyperplasia in cats?
Retinal detachment or subretinal, intraretinal, and intravitreal hemorrhages.
418
What physical examination findings are reported in cases of primary hyperaldosteronism?
Elevated arterial blood pressure, ocular signs of hypertension, and hypokalaemic myopathy.
419
What are some less specific physical examination findings in cats with hyperaldosteronism?
Polyuria, polydipsia, weight loss, palpable abdominal masses, polyphagia, heart murmur, and irregular cardiac rhythm.
420
What other concurrent diseases should be considered in older cats with hyperaldosteronism?
Chronic kidney disease or hyperthyroidism that may cause hypokalaemia and/or hypertension.
421
What are the typical biochemical abnormalities in cats with hyperaldosteronism?
Moderate to severe hypokalaemia.
422
What are the causes of primary hyperparathyroidism?
Adenoma, carcinoma, or adenomatous hyperplasia of parathyroid glands
423
What is the signalment of dogs with primary hyperparathyroidism?
Older dogs, no known gender predisposition, Keeshonds, German shepherd dogs, Poodles, Golden retrievers
424
What are the clinical signs of primary hyperparathyroidism?
Polyuria, polydipsia, vomiting, inappetence, urinary incontinence, constipation, stranguria, pollakiuria, depression, stiff gait, exercise intolerance, lameness, shivering, facial pain/discomfort when eating
425
Why do dogs with primary hyperparathyroidism develop uroliths?
Increased concentrations of calcium and phosphate in urine leading to calcium phosphate precipitation and stone formation
426
What are the relevant findings on physical examination in dogs with primary hyperparathyroidism?
Stiffness, gait abnormalities, dull mentation, weakness, muscle wastage
427
What is the expected severity of hypercalcemia in dogs with primary hyperparathyroidism?
Dependent on the duration of the disease; mild to severe hypercalcemia
428
What parameters should be measured in animals with primary hyperparathyroidism to characterize the electrolyte disturbance?
Total and ionized calcium, phosphate, PTH, PTHrp
429
What are the expected results in primary hyperparathyroidism?
Elevated PTH above reference interval or inappropriately high for concurrent serum calcium
430
What does the ARR test allow differentiation of?
Primary versus secondary hyperaldosteronism.
431
What is indicated by a high ARR?
Primary hyperaldosteronism.
432
What are some examples of mineralocorticoid function tests (MFTs) used in humans?
Oral sodium loading, saline infusion, fludrocortisone acetate administration with sodium supplementation, and the captopril challenge test.
433
What was assessed in healthy cats to investigate mineralocorticoid function tests?
Changes of the urinary aldosterone: creatinine ratio in response to increased dietary salt or administration of fludrocortisone acetate.
434
What is the initial treatment of primary hyperaldosteronism directed at?
Controlling hypokalaemia and/or hypertension.
435
What is spironolactone?
A competitive aldosterone antagonist.
436
What is the recommended dose of spironolactone?
2-4mg/kg orally q24hours.
437
What is a potential adverse reaction of spironolactone in human patients?
Gynaecomastia and menstrual irregularities.
438
What is the initial treatment of choice for hypertension in cats?
Amlodipine besylate.
439
What monitoring should be performed after every dose adjustment?
Electrolytes and blood pressure.
440
What is the optimal treatment for cats with unilateral aldosterone-secreting adrenal masses and no detectable metastatic disease?
Surgical excision.
441
What is the most common cause of death in cats undergoing surgical excision of adrenal masses?
Severe acute haemorrhage from the caudal vena cava.
442
How is PTHrp measured?
By two-site IRMA and RIA.
443
What is the reference interval for PTHrp in dogs?
<0.5 pmol/l.
444
What is the reference interval for PTHrp in cats?
<0.5 pmol/l.
445
Which breed is predisposed to inherited PHPT?
Keeshond.
446
What is the penetrance of PHPT in Keeshonds?
Partial, age-dependent.
447
What is the purpose of genetic testing in Keeshonds?
To limit the use of mutation-carrying animals.
448
What imaging modality is most useful for investigating parathyroid adenomas?
Ultrasonography.
449
What percentage of parathyroid adenomas are positively identified by ultrasonography?
90-95%.
450
How are parathyroid glands identified on ultrasound when they are abnormal?
Small hypoechoic nodules within thyroid tissue.
451
What is the initial management for hypercalcaemia in PHPT?
Diuresis with intravenous sodium chloride.
452
Which medication may reduce osteoclast activity in PHPT?
Bisphosphonates.
453
What is the treatment of choice for PHPT?
Excision of abnormal parathyroid gland.
454
How is excellent visualisation of the thyroid glands achieved during surgery?
Using a ventral midline cervical approach.
455
How are parathyroid adenomas removed during surgery?
Either by dissection from adjacent thyroid tissue or by partial thyroidectomy.
456
What are the GH stimulants used to measure GH concentrations?
GHRH, clonidine, and xylazine.
457
How are GH concentrations measured after administering the stimulant?
GH concentrations are measured before and 20-30 minutes after intravenous administration of the stimulant.
458
What is the purpose of the ghrelin stimulation test?
To determine GH response, with a post-ghrelin plasma GH concentration of >5 µg/l excluding congenital GH deficiency.
459
What can advanced imaging of the pituitary reveal in dogs with pituitary dwarfism?
The presence of pituitary cysts, which may increase in size as the dog gets older.
460
Which hormones should be replaced if lacking in treatment for pituitary dwarfism?
Thyroxine and other hormones should be replaced if lacking.
461
At what age should therapy for dwarfism ideally be started?
Therapy is best started when the dog is as young as possible, ideally at 4-6 weeks of age.
462
What are the potential side effects of GH treatment?
Hypersensitivity reactions to GH and diabetes mellitus.
463
Why is canine GH not available for therapeutic use?
Antibody formation precludes the use of a human product due to differences between canine and human GH.
464
What is the recommended subcutaneous dose for GH?
0.1-0.3 IU per kg bodyweight three times per week.
465
What improvements can be expected after starting GH therapy?
Beneficial response of the skin and hair coat usually occurs within 6-8 weeks after starting therapy.
466
How can progestogens induce GH expression in the mammary gland?
Progestogens can induce expression of the GH gene in the mammary gland, leading to secretion into the systemic circulation.
467
What treatment can result in an increase in body size and development of an adult hair coat in German Shepherd dwarfs?
Medroxyprogesterone acetate treatment at 2.5-5.0 mg/kg s.c., initially at 3-week intervals and subsequently at 6-week intervals.
468
In addition to GH, what other monitoring is important during treatment?
Monitoring of plasma concentrations of IGF-1, GH, and glucose are important during the treatment.
469
What should be done before starting the progestogen treatment in bitches?
Ovariohysterectomy should be performed before starting the progestogen treatment.
470
When should thyroid hormone replacement be started?
Thyroid hormone replacement should be started as soon as there is evidence of hypothyroidism.
471
What is the long-term treatment for growth failure in dogs with growth hormone deficiency?
Recombinant human IGF-I (Mecasermin, Increlex) is used for long-term treatment of growth failure.
472
What is the condition called where children have severe primary IGF-I deficiency?
Severe primary IGF-I deficiency
473
What is the relationship between insufficient GH and growth hormone-responsive alopecia in dogs?
Unproven
474
What are the clinical signs of growth hormone-responsive alopecia in adult dogs?
Bilaterally symmetric alopecia and hyperpigmentation mainly of the trunk
475
Which breeds are mainly affected by growth hormone-responsive alopecia?
Poodles, Pomeranians, Chow Chows, Keeshonds, Airedales, and Samoyeds
476
What should be performed to rule out other endocrine causes of alopecia in dogs?
Routine endocrine testing
477
What is the management therapy for growth hormone-responsive alopecia in dogs?
Bovine, porcine, and human growth hormone at a dose of 0.1 IU/kg subcutaneously three times a week for 4-6 weeks
478
What is another name for growth hormone-responsive alopecia?
Castration-responsive alopecia
479
What should be considered when investigating a patient with polyuria and polydipsia?
Comprehensive differential diagnosis list
480
What are the possible differential diagnoses for a patient with polyuria and polydipsia?
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
What are the primary polydipsias and primary polyurias associated with PU/PD?
Varies for each condition, depending on the underlying mechanism
482
What is the definition of polyuria and polydipsia?
Water intake of >100ml/kg/day
483
What could be a reason if urine is not hyposthenuric or isosthenuric in a patient with PU/PD?
Fluid loss through another route, dietary change, or improper swallowing
484
What is the mechanism for primary polyuria in diabetes mellitus?
Osmotic diuresis caused by glycosuria
485
What is the mechanism through which endogenous and exogenous glucocorticoids inhibit GH secretion?
Enhanced somatostatin release
486
What should be done to diagnose low GH levels in dogs with growth hormone-responsive alopecia?
Clonidine and xylazine stimulation tests
487
What histopathological findings are seen in dogs with growth hormone-responsive alopecia?
Atrophic follicles, hairless dilated follicles, and reduced dermal elastin
488
What abnormal adrenal sex hormone production has been observed in Pomeranians with growth hormone-responsive alopecia?
Elevated progesterone, 17-hydroxyprogesterone, and androstenedione in response to ACTH stimulation, and elevated plasma ACTH concentrations
489
What is the suggested underlying cause in Pomeranians with abnormal adrenal sex hormone production?
Partial 21-hydroxylase enzyme deficiency
490
What might help manage growth hormone-responsive alopecia in dogs?
Castration, mitotane, and trilostane in case of suspected abnormalities in adrenal sex hormone production
491
What is an exceptionally rare condition that is commonly over-diagnosed in thirsty patients with polyuria and polydipsia?
Primary diabetes insipidus
492
What should be considered when performing urethral catheterisation in female animals?
Consider the use of an indwelling urinary catheter.
493
How often should the bladder be emptied during the water deprivation test?
Every 1-2 hours.
494
What should be measured during the water deprivation test to monitor for dehydration?
Urine specific gravity (SG) or osmolality and body weight.
495
When should the water deprivation test be stopped?
When there is either a 5% loss of body weight or the urine SG is >1.030 in dogs (>1.035 in cats).
496
What should be monitored during the water deprivation test if the 5% dehydration endpoint is not reached by the end of the working day?
Urine SG and body weight can continue to be monitored overnight.
497
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?
Perform an ADH (desmopressin) response test.
498
What is the dose of synthetic analogue of ADH (desmopressin) for dogs weighing less than 15 kg or cats?
2.0 μg (micrograms).
499
What is the maximum response time to intravenous desmopressin after the test is performed?
4-8 hours.
500
What are the urine SG ranges for animals with complete CDI or primary NDI during the modified water deprivation test?
1.001-1.007 (<1.008 after severe dehydration).
