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Small Animal Medicine (GP cert) > Endocrinology AI 2 > Flashcards

Endocrinology AI 2 Flashcards

1
Q

How long does it typically take for animals with partial CDI or psychogenic polydipsia to become dehydrated during the modified water deprivation test?

A

1-3 days.

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2
Q

What is the urine SG range for animals with partial CDI after dehydration in the modified water deprivation test?

A

1.008-1.020.

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3
Q

What is the response to desmopressin therapy for animals with CDI (complete and partial)?

A

Positive.

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4
Q

What is the urine SG range for animals with primary NDI during the modified water deprivation test?

A

<1.008 (no change).

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5
Q

What is the urine SG range for animals with psychogenic polydipsia during the modified water deprivation test?

A

> 1.030.

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6
Q

What should be monitored during the assessment of a clinical response to trial desmopressin therapy?

A

Water intake.

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7
Q

How long is synthetic desmopressin (DDAVP) administered via the conjunctival sac during the trial therapy?

A

Several days.

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8
Q

What is the most common presenting sign in animals with sex predisposition?

A

PU/PD (polyuria/polydipsia)

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9
Q

What are the clinical signs of CDI in animals?

A

Increased water intake, increased urine volume, weight loss, and excessive drinking

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10
Q

What can excessive water consumption in animals with CDI lead to?

A

Vomiting and nocturia

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11
Q

What are the clinical signs of CDI in animals with partial CDI?

A

Less marked clinical signs compared to full CDI

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12
Q

What additional neurological signs can develop in dogs with pituitary or hypothalamic neoplasia?

A

Neurological signs due to invasion or compression of adjacent tissue

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13
Q

What can cause neurological signs in dogs and cats?

A

Head trauma or multifocal/widespread inflammatory, infectious, and developmental structural CNS defects

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14
Q

What are the possible endocrine abnormalities associated with lesions affecting the pituitary gland?

A

Congenital or acquired lesions can cause CDI, pituitary dwarfism, secondary hypothyroidism, secondary hypoadrenocorticism, and decreased GH production

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15
Q

What can indicate the presence of hyperadrenocorticism in dogs with CDI?

A

Dermatological and metabolic changes associated with hyperadrenocorticism

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16
Q

What syndrome can occur if animals with CDI experience severe water restriction?

A

Hypertonic dehydration

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17
Q

What are the clinical signs of hypertonic dehydration in animals with CDI?

A

Anorexia, weakness, disorientation, ataxia, and seizures

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18
Q

Is there a single confirmatory test for CDI in dogs or cats?

A

No, diagnosis requires thorough exclusion of other causes of PU/PD

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19
Q

What are the remaining differential diagnoses if PU/PD cannot be attributed to any other cause?

A

CDI, primary nephrogenic diabetes insipidus, and primary polydipsia

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20
Q

When can a modified water deprivation test or desmopressin trial be performed to distinguish between CDI and other conditions?

A

Only after thorough exclusion of other causes of PU/PD

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21
Q

What abnormalities may be observed in routine clinicopathological findings of dogs or cats with CDI?

A

No significant abnormalities, provided water is not restricted

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22
Q

What can cause reduced serum urea concentrations in dogs or cats with CDI?

A

Renal medullary solute washout and loss of ADH-dependent urea reabsorption

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23
Q

What abnormalities may be observed if water is restricted in animals with CDI?

A

Elevated haematocrit, hyperproteinaemia, hypernatraemia, and prerenal azotaemia

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24
Q

What can cause severe hypernatraemia and serum hyperosmolality in CDI?

A

Hypertonic dehydration

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25
Q

How can serum osmolality be measured in dogs and cats?

A

Direct measurement or calculated using a formula based on Na, K, urea, and glucose concentrations

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26
Q

How does ADH conserve water?

A

By increasing the permeability of the distal renal tubule and collecting duct to water

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27
Q

What other activities does ADH have?

A

Intestinal contractility, platelet aggregation, von Willebrand factor release, and hepatic glycogenolysis

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28
Q

What is the primary cause of polyuria?

A

Inability of the kidney to concentrate urine

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29
Q

What is Central Diabetes Insipidus (DI)?

A

A lack of production or release of ADH from the pituitary gland

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30
Q

What is Nephrogenic Diabetes Insipidus (DI)?

A

Lack of renal tubular sensitivity to ADH

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31
Q

What are some causes of secondary nephrogenic diabetes insipidus?

A

Hypercalcaemia, hyperadrenocorticism, renal failure, hyperthyroidism, hypokalaemia, pyometra, toxaemia, and pyelonephritis

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32
Q

Why can PU/PD improve with a trial of exogenous ADH (DDAVP)?

A

The supra-physiological dose can temporarily overcome the problems caused by the underlying disease

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33
Q

What should be ruled out before water deprivation tests and DDAVP trials?

A

Other causes of secondary nephrogenic diabetes insipidus

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34
Q

What is the systematic approach to the PU/PD patient?

A
  1. Full history, 2. Full clinical examination, 3. Confirm PU/PD and isosthenuria/hyposthenuria, 4. Urinalysis, 5. Routine blood tests, 6. Investigate underlying endocrine disease, 7. Diagnostic imaging, 8. Trial of broad spectrum antibiotics if no obvious abnormalities found
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35
Q

What lab tests should be conducted in PU/PD cases?

A

Cystocentesis sample urinalysis, routine haematology/serum biochemistry/electrolytes, possible endocrine disease tests

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36
Q

What further steps can be taken if no obvious abnormalities are found?

A

Consider CNS imaging, water deprivation test, trial of DDAVP, measurement of serum and urine osmolality, or investigating other clinical signs

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37
Q

What does PU/PD stand for?

A

Polyuria/Polydipsia

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38
Q

What can result from depriving a dog of water without ruling out certain diseases?

A

Serious renal damage

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39
Q

What is the mechanism behind many causes of PU/PD?

A

Secondary NDI

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40
Q

What does excess calcium interfere with in hypercalcaemia?

A

ADH activity

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41
Q

Which hormone is affected by cortisol in hyperadrenocorticism?

A

ADH

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42
Q

In which conditions are the effects of ADH disrupted?

A

Renal failure, hyperthyroidism, hypokalaemia, pyometra, toxaemia, and pyelonephritis

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43
Q

What can cause confusion and misdiagnosis of CDI in animals with PU/PD?

A

Improvement with a trial of desmopressin

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44
Q

What should water deprivation tests and desmopressin trials be reserved for?

A

Dogs who have had other causes of secondary NDI ruled out

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45
Q

What is the rare disorder characterized by the inability of renal tubular cells to respond to ADH?

A

Primary NDI

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46
Q

What causes primary nephrogenic diabetes insipidus in humans?

A

Mutations of the V2 receptor or aquaporin-2

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47
Q

Which breed of dog is associated with a 10-fold reduction in the responsiveness of renal tubular cells to vasopressin?

A

Siberian Huskies

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48
Q

Why are clinical signs reported only in male dogs with congenital nephrogenic diabetes insipidus?

A

Suspected gene mutation on the X chromosome

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49
Q

How is primary NDI diagnosed?

A

Exclude all other causes of PU/PD and failure to concentrate urine after dehydration

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50
Q

What does chlorpropamide do in the treatment of primary NDI?

A

Increases responsiveness of renal tubular principal cells to ADH

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51
Q

What is a potential adverse effect of chlorpropamide?

A

Hypoglycemia

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52
Q

Why are thiazide diuretics occasionally used in the management of human CDI?

A

To decrease water loss by reducing urine output

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53
Q

What effect do thiazide diuretics have in dogs with primary NDI?

A

Variable antidiuretic effect

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54
Q

What is the recommended dose of hydrochlorothiazide for dogs and cats?

A

2.5-5.0 mg/kg orally q12h

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55
Q

What might cause low urea besides liver disease?

A

Renal washout effect

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56
Q

In diabetes insipidus, what is often increased due to the body’s inability to retain water?

A

Serum osmolality or sodium

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57
Q

What occurs in psychogenic polydipsia?

A

Dog is overhydrated and may have decreased serum osmolality or hyponatraemia

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58
Q

What is the urine specific gravity in diabetes insipidus compared to glomerular filtrate?

A

Always below, i.e. <1.008-1.010

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59
Q

When should a water deprivation test be performed?

A

When other diseases have been ruled out

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60
Q

What are the two methods for performing a water deprivation test?

A

Abruptly stopping water or gradual reduction in water intake +/- salt supplementation

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61
Q

What hormone is involved in the control of urinary concentration?

A

Anti-diuretic hormone (ADH or arginine vasopressin)

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62
Q

What does ADH do to conserve water?

A

Increases the permeability of distal renal tubule and collecting duct to water

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63
Q

Name some actions of ADH.

A

Intestinal contractility, platelet aggregation, von Willebrand factor release, hepatic glycogenolysis

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64
Q

What can cause polyuria/polydipsia (PU/PD) if disrupted?

A

Presence of an adequate concentrating gradient of sodium and urea in renal cortex

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65
Q

What is the most common cause of central diabetes insipidus (CDI) in dogs?

A

Neoplasia

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66
Q

What is the most common cause of trauma-induced CDI in cats?

A

Trauma

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67
Q

What are some recognised causes of CDI in dogs?

A

Neoplasia, craniopharyngioma, chromophobe adenoma or adenocarcinoma, metastatic neoplasia, idiopathic, trauma, surgery, developmental structural defects, infection, inflammation, cyst

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68
Q

What are the clinical signs of CDI?

A

Polyuria/polydipsia (PU/PD)

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69
Q

What is the formula for calculating serum osmolality?

A

Serum osmolality = 2 (Na + K) + urea + glucose.

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70
Q

What values are considered normal for osmolality in healthy dogs?

A

Approximately 290-310 mOsm/kg.

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71
Q

What values are considered normal for osmolality in healthy cats?

A

Approximately 290-330 mOsm/kg.

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72
Q

In hypertonic dehydration, what is the largest contributor to hyperosmolality?

A

Sodium.

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73
Q

When is the calculation of osmolality not necessary in markedly hypernatraemic animals?

A

In an emergency setting.

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74
Q

What specific gravity (SG) values are consistent with polyuria/polydipsia (PU/PD) in dogs and cats?

A

<1.030 in dogs and <1.035 in cats.

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75
Q

What urine specific gravity (SG) values are typically found in animals with complete central diabetes insipidus (CDI)?

A

Severe hyposthenuria (SG 1.000-1.006).

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76
Q

What are the additional differentials for animals with marked hyposthenuria?

A

Hyperadrenocorticism in dogs, hyperthyroidism in cats, liver disease, hypercalcaemia, primary polydipsia, and nephrogenic diabetes insipidus.

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77
Q

What diagnostic test should always be performed as part of the investigation of PU/PD?

A

Bacteriological culture of urine.

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78
Q

What percentage of dogs with CDI have urinary tract infections at presentation?

A

Approximately 25%.

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79
Q

What is the indication for the water deprivation test?

A

To distinguish between CDI, primary NDI, and psychogenic polydipsia.

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80
Q

What should be considered before performing the water deprivation test?

A

All other causes of PU/PD should be ruled out.

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81
Q

In which patients is the water deprivation test contraindicated?

A

Azotaemic and/or dehydrated patients and those with known renal disease.

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82
Q

What is the first step of a modified water deprivation test?

A

Gradual water restriction over three days to re-establish the renal medullary concentration gradient.

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83
Q

What is stage two of the water deprivation test?

A

Complete water deprivation.

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84
Q

What is performed in stage three of the water deprivation test?

A

Administration of ADH (if necessary).

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85
Q

What should be done during the period of gradual water restriction in a modified water deprivation test?

A

Owners should feed dry food and monitor the animal’s body weight on a daily basis.

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86
Q

What is the main purpose of the modified water deprivation test?

A

To overcome the problem of renal medullary washout and unreliable urine concentrating ability.

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87
Q

What are the major effects of oxytocin?

A

On smooth muscle cells, especially mammary glands and uterus.

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88
Q

What are the major effects of ADH?

A

On renal tubular cells and collecting ducts, and to increase blood pressure.

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89
Q

How is the release of ADH controlled?

A

Via osmoreceptors, water intake receptors, stretch receptors, and baroreceptors in the hypothalamus.

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90
Q

How is growth hormone (GH) secretion regulated?

A

By the opposing actions of GH-releasing hormone (GHRH) and somatostatin.

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91
Q

What are the rapid catabolic actions of GH?

A

Insulin antagonism resulting in enhanced lipolysis, gluconeogenesis, and restricted glucose transport.

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92
Q

What are the slow anabolic effects of GH?

A

Mediated via insulin-like growth factors (IGFs), promoting protein synthesis, chondrogenesis, and growth.

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93
Q

What is hypopituitarism?

A

A deficiency of one or more hormones from the pituitary gland, resulting in lack of stimulation of the respective endocrine glands.

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94
Q

What is pituitary dwarfism?

A

Congenital growth hormone deficiency, usually seen in German Shepherd dogs with combined deficiency of GH, TSH, and prolactin.

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95
Q

What causes pituitary dwarfism in German Shepherd dogs?

A

An underlying genetic defect, rather than pressure atrophy or cyst formation in the pituitary gland.

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96
Q

What is the mutation associated with pituitary dwarfism in German Shepherd dogs?

A

A mutation of the gene encoding the transcription factor LHX3.

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97
Q

What are the three possible causes of PU/PD after ruling out other causes?

A

CDI, primary NDI, and psychogenic polydipsia.

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98
Q

What are the two conditions that dogs with psychogenic polydipsia and primary NDI fail to respond to?

A

Complete and partial CDI.

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99
Q

What test allows differentiation of CDI and nephrogenic diabetes insipidus?

A

Measurement of plasma ADH concentration.

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100
Q

What hormone is very sensitive to proteolysis and requires immediate chilling, separation, and freezing of samples?

A

ADH.

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101
Q

What can MRI or CT imaging identify in relation to PU/PD?

A

Developmental or acquired structural lesions within the hypothalamus or pituitary.

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102
Q

What is the most widely used treatment for CDI in dogs and cats?

A

Desmopressin (DDAVP).

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103
Q

How is desmopressin administered in cats?

A

Conjunctival treatment or orally.

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104
Q

What is the recommended initial dose of desmopressin for oral therapy?

A

0.1 mg once to twice daily.

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105
Q

Which route of desmopressin administration is ineffective in some animals?

A

Gastrointestinal tract.

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106
Q

What medications are occasionally prescribed for the control of CDI in humans and some canine cases?

A

Thiazide diuretics and chlorpropamide.

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107
Q

How can dietary modification be used to treat CDI?

A

To decrease water loss associated with sodium and protein excretion.

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108
Q

What are the clinical signs of pituitary dwarfs in German Shepherd dogs?

A

Growth retardation, abnormal hair coat, truncal alopecia, hyperpigmented and scaly skin, cryptorchidism in males, persistent oestrus in females.

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109
Q

What are the differential diagnoses for pituitary dwarfism?

A

Congenital hypothyroidism, iatrogenic hypercorticism, hypoadrenocorticism, malnutrition, gastrointestinal disorders, exocrine pancreatic insufficiency, portosystemic shunting, congenital renal disease, and skeletal disorders.

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110
Q

What laboratory findings are commonly seen in pituitary dwarfs?

A

Elevations in creatinine, low circulating thyroxine concentration, low plasma IGF-1 concentration.

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111
Q

How is the diagnosis of pituitary dwarfism usually made?

A

Based on the results of a stimulation test.

112
Q

What are the four parts of the pituitary gland?

A

Pars distalis, pars intermedia, pars nervosa, pars tuberalis

113
Q

What are the other names for the anterior and posterior pituitary glands?

A

Anterior – adenohypophysis, Posterior – neurohypophysis

114
Q

Where does the anterior pituitary arise from?

A

An invagination of the oral ectoderm and forms Rathke’s pouch

115
Q

What are the major releasing hormones produced by the hypothalamus?

A

TRH, GnRH, GHIH, GHRH, CRH, PRF, PIH

116
Q

What are the two major hormones produced by the posterior pituitary gland?

A

Oxytocin and antidiuretic hormone

117
Q

How are secretion from the anterior and posterior pituitary controlled?

A

Anterior pituitary – by hypothalamic releasing hormones, Posterior pituitary – by direct neural stimulation

118
Q

What hormone is produced from the cleavage of corticotropin (ACTH)?

A

Melanocyte stimulating hormone (MSH)

119
Q

What is the mechanism behind many causes of PU/PD?

A

Secondary NDI

120
Q

What can interfere with ADH activity in hypercalcaemia?

A

Excess calcium

121
Q

Which hormone affects ADH actions in hyperadrenocorticism?

A

Cortisol

122
Q

Which conditions disrupt the effects of ADH?

A

Renal failure, hyperthyroidism, hypokalaemia, pyometra, toxaemia, and pyelonephritis

123
Q

What is the reasoning behind animals initially improving with a trial of desmopressin?

A

Supra-physiological dose of desmopressin temporarily over-rides the problems caused by the underlying disease

124
Q

What should be ruled out before conducting water deprivation tests and desmopressin trials?

A

Other causes of secondary NDI

125
Q

What is primary NDI characterized by?

A

The inability of renal tubular cells to respond to adequate plasma concentrations of ADH

126
Q

What causes primary nephrogenic diabetes insipidus in humans?

A

Mutations of either the V2 receptor or aquaporin-2

127
Q

What is a congenital form of NDI associated with in Siberian Huskies?

A

A 10-fold reduction in the responsiveness of renal tubular cells to vasopressin

128
Q

Which gene mutation is suspected in Siberian Huskies with NDI?

A

V2 receptor gene

129
Q

How is primary NDI diagnosed?

A

By excluding all other causes of PU/PD and observing a failure to concentrate urine following dehydration and administration of desmopressin

130
Q

What is the treatment for primary NDI?

A

Chlorpropamide and thiazide diuretics

131
Q

What is the potential effect of chlorpropamide in the treatment of NDI?

A

Increase in the responsiveness of renal tubular principal cells to ADH

132
Q

What is a potential adverse effect of using chlorpropamide?

A

Hypoglycaemia

133
Q

Which natriuretic agent is occasionally used in the management of human CDI?

A

Thiazide diuretics

134
Q

How do thiazide diuretics decrease water loss in primary NDI?

A

By decreasing water delivery to the distal tubule

135
Q

What is the recommended dose of hydrochlorothiazide for dogs and cats?

A

2.5-5.0 mg/kg orally q12h

136
Q

What are some GH stimulants used in the diagnosis of pituitary dwarfism in dogs?

A

GHRH, clonidine, xylazine

137
Q

How are GH concentrations measured in dogs with pituitary dwarfism?

A

Before and after intravenous administration of a stimulant

138
Q

What is the additional test to determine GH response?

A

The ghrelin stimulation test

139
Q

What is the dose of human ghrelin administered intravenously in the ghrelin stimulation test?

A

2 µg/kg

140
Q

What can exclude congenital GH deficiency in dogs?

A

A post-ghrelin plasma GH concentration of >5 µg/l at 20-30 minutes after intravenous administration of the stimulant

141
Q

What can pituitary imaging reveal in dogs with pituitary dwarfism?

A

The presence of pituitary cysts

142
Q

What may cause pituitary cysts in dogs apart from pituitary dwarfism?

A

They can also be seen in healthy dogs, especially in brachycephalic breeds

143
Q

When is it recommended to start therapy for pituitary dwarfism in dogs?

A

As young as possible

144
Q

What are some reported treatments for pituitary dwarfism in dogs?

A

Exogenous bovine, human, or porcine GH

145
Q

What are the potential side effects of GH treatment for pituitary dwarfism?

A

Hypersensitivity reactions to GH and diabetes mellitus

146
Q

What is the recommended subcutaneous dose of GH for pituitary dwarfism in dogs?

A

0.1-0.3 IU per kg bodyweight three times a week

147
Q

What should be monitored every 3 weeks during GH treatment for pituitary dwarfism?

A

Plasma concentrations of glucose

148
Q

What can induce expression of the GH gene in the canine mammary gland?

A

Progestogens

149
Q

What treatment resulted in an increase in body size and the development of a complete adult hair coat in German Shepherd dwarfs?

A

Medroxyprogesterone acetate treatment

150
Q

What hormone replacement should be started for pituitary dwarfs with evidence of hypothyroidism?

A

Thyroid hormone replacement

151
Q

What is used for the long-term treatment of growth failure?

A

Recombinant human IGF-1 (Mecasermin, Increlex)

152
Q

What is the condition called that affects hair growth and skin pigmentation in dogs?

A

Growth hormone-responsive alopecia

153
Q

What is the relationship between growth hormone and growth hormone-responsive alopecia?

A

The relationship is unproven and the etiology remains uncertain.

154
Q

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

A

Bilaterally symmetric alopecia and hyperpigmentation mainly of the trunk.

155
Q

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

A

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

156
Q

What are the diagnostic tests for growth hormone-responsive alopecia?

A

Routine endocrine testing, low GH levels testing, and IGF-1 concentrations testing.

157
Q

What are the histopathological findings in growth hormone-responsive alopecia?

A

Atrophic follicles, dilated and devoid of hair, and follicular dysplasia.

158
Q

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

A

Bovine, porcine, and human growth hormone at a dose of 0.1 IU/kg subcutaneously three times a week.

159
Q

What is another name for growth hormone-responsive alopecia?

A

Castration-responsive alopecia

160
Q

What condition should be considered in a patient with polyuria and polydipsia?

A

Primary diabetes insipidus

161
Q

What is the defining water intake for polyuria and polydipsia?

A

Water intake of >100ml/kg/day

162
Q

What are the possible differential diagnoses for 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

163
Q

What is the cause of primary polyuria in polyuria and polydipsia?

A

Osmotic diuresis caused by glycosuria in diabetes mellitus

164
Q

What is the main action of Anti-diuretic hormone (ADH)?

A

ADH conserves water by increasing the permeability of the distal renal tubule and collecting duct to water.

165
Q

How does ADH exert its actions?

A

ADH allows water channels (aquaporins) to be inserted into cell membranes.

166
Q

What are the other activities of ADH?

A

Intestinal contractility, platelet aggregation, von Willebrand factor release, and hepatic glycogenolysis.

167
Q

What results in primary polyuria?

A

Inability of the kidney to concentrate urine, due to Central or Nephrogenic Diabetes Insipidus [DI].

168
Q

What is Central Diabetes Insipidus (DI) caused by?

A

A lack of production or release of anti-diuretic hormone (ADH) from the pituitary.

169
Q

What is Nephrogenic Diabetes Insipidus (DI) caused by?

A

Lack of renal tubular sensitivity to ADH.

170
Q

What is the difference between primary and secondary nephrogenic diabetes insipidus?

A

Primary disease is rare, while secondary nephrogenic DI is more common and is the mechanism behind many causes of PU/PD.

171
Q

What can disrupt the effects of ADH?

A

Renal failure, hyperthyroidism, hypokalaemia, pyometra, toxaemia, pyelonephritis, and various other diseases.

172
Q

Why can PU/PD initially improve with a trial of exogenous ADH?

A

Supra-physiological doses of ADH can temporarily over-ride the problems caused by underlying disease.

173
Q

When should water deprivation tests and DDAVP trials be reserved for?

A

Dogs who have had other causes of secondary nephrogenic diabetes insipidus systematically ruled out.

174
Q

What should be done before depriving a dog of water?

A

Ruling out diseases that can cause PU/PD, such as hyperadrenocorticism, pyelonephritis, hypercalcaemia, liver disease, etc.

175
Q

What are the initial steps in a systematic approach to the PU/PD patient?

A

1) Full history, 2) Full clinical examination, 3) Confirm PU/PD and isosthenuria/hyposthenuria, 4) Urinalysis of a cystocentesis sample.

176
Q

What should follow up abnormalities found in routine haematology/serum biochemistry?

A

Further investigation and appropriate tests for possible underlying endocrine disease.

177
Q

What diagnostic imaging should be considered?

A

Chest and abdominal radiographs, ultrasound of the abdomen (adrenal glands, urinary tract).

178
Q

If no obvious abnormalities are found, what should be considered?

A

A trial of broad-spectrum antibiotics to rule out low-grade urinary tract/renal infection.

179
Q

What are the further steps to consider?

A

Imaging of the CNS, water deprivation test, trial of DDAVP (ADH), measurement of serum and urine osmolality or following up other clinical signs.

180
Q

What should be noted about interpreting lab tests in PU/PD?

A

It can be difficult to culture bacteria from very dilute urine, so urine culture results should be interpreted with caution.

181
Q

What is the common presenting sign in animals with CDI?

A

PU/PD

182
Q

How do the clinical signs of CDI vary?

A

From acute to chronic over several weeks or months

183
Q

What can excessive water consumption in animals with CDI lead to?

A

Weight loss

184
Q

What are some additional clinical signs that may be present in animals with PU/PD?

A

Vomiting, urinary incontinence, loss of house training

185
Q

What are some causes of neurological signs in dogs with CDI?

A

Pituitary or hypothalamic neoplasia, head trauma, inflammatory/infectious/developmental CNS defects

186
Q

What other endocrine abnormalities can occur in association with lesions affecting the pituitary gland?

A

Hypothyroidism, hypoadrenocorticism, decreased GH production

187
Q

What can be present concurrently with CDI in dogs with chromophobe adenomas or adenocarcinomas?

A

Hyperadrenocorticism

188
Q

What can severe water restriction in animals with CDI lead to?

A

Hypertonic dehydration

189
Q

What are some clinical signs of hypertonic dehydration?

A

Anorexia, weakness, disorientation, ataxia, seizures

190
Q

What is the diagnosis of CDI dependent upon?

A

Thorough exclusion of other causes of PU/PD

191
Q

What are the differential diagnoses for CDI?

A

Primary nephrogenic diabetes insipidus and primary polydipsia

192
Q

What abnormalities in routine clinicopathological findings are associated with CDI?

A

None, provided water is not restricted

193
Q

What happens to serum urea concentrations in dogs or cats with CDI?

A

They are frequently reduced due to renal medullary solute washout

194
Q

What abnormalities can be seen if water is restricted in CDI?

A

Elevated haematocrit, hyperproteinaemia, hypernatraemia, prerenal azotaemia

195
Q

What are the potential effects of severe hypernatraemia and serum hyperosmolality?

A

Hypertonic dehydration

196
Q

How can serum osmolality be measured?

A

Directly or calculated using a formula based on sodium, potassium, urea, and glucose concentrations

197
Q

What is the formula for calculating serum osmolality?

A

Serum osmolality = 2(Na+K) + urea + glucose

198
Q

What are the approximate osmolality ranges for healthy dogs and cats?

A

Approximately 290-310 mOsm/kg for dogs and 290-330 mOsm/kg for cats

199
Q

When is calculation of osmolality not necessary in hypertonic dehydration?

A

In markedly hypernatraemic animals in an emergency setting

200
Q

What values are detected in animals with complete central diabetes insipidus (CDI)?

A

Hyposthenuria (SG 1.000-1.006)

201
Q

What are some additional differentials for marked hyposthenuria?

A

Hyperadrenocorticism, hyperthyroidism, liver disease, hypercalcaemia, primary polydipsia, nephrogenic diabetes insipidus

202
Q

When should bacteriological culture of urine be performed?

A

As part of the diagnostic investigation of PU/PD, regardless of the suspected cause

203
Q

What percentage of dogs with CDI have urinary tract infections at presentation?

A

Approximately 25%

204
Q

What is the indication of the water deprivation test?

A

To distinguish between CDI, primary nephrogenic diabetes insipidus (NDI), and psychogenic polydipsia

205
Q

What can the water deprivation test result in?

A

Rapid alterations of water and electrolyte balance that can be life threatening

206
Q

When is the water deprivation test contraindicated?

A

In azotaemic and/or dehydrated patients, and in patients with known renal disease

207
Q

What should be ruled out before performing the water deprivation test?

A

All other causes of PU/PD, limiting the differential diagnoses to CDI, primary NDI, and psychogenic polydipsia

208
Q

What can happen in animals with PU/PD of any cause during a water deprivation test?

A

Renal medullary washout, limiting urine concentrating ability and ADH production

209
Q

What is the first step in a water deprivation test?

A

Gradual water restriction over three days to re-establish renal medullary concentration gradient

210
Q

What is the protocol for stage 1 of a modified water deprivation test?

A

Gradual restriction of water intake over three days with divided small portions per day

211
Q

What is the protocol for stage 2 of a modified water deprivation test?

A

Complete water deprivation after obtaining exact body weight and emptying the bladder

212
Q

What is the final stage of a modified water deprivation test?

A

The administration of ADH (if necessary)

213
Q

Why should an indwelling urinary catheter be considered in female animals during urethral catheterization?

A

To empty the bladder many times at frequent intervals

214
Q

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

A

At 1-2 hour intervals

215
Q

What are the endpoints for the water deprivation test in dogs and cats?

A

5% loss of body weight or urine SG >1.030 in dogs (>1.035 in cats)

216
Q

What should be monitored in the animal during the water deprivation test?

A

Signs of CNS depression, urine SG, and body weight

217
Q

What should be done if the patient fails to reach the 5% dehydration endpoint by the end of the working day?

A

Transfer the patient to a facility with overnight care or provide overnight access to water in maintenance amounts

218
Q

What are the recommended doses of desmopressin for dogs and cats in the ADH response test?

A

2.0 μg for dogs <15 kg and cats, 4.0 μg for dogs >15 kg

219
Q

What is the maximum response time to intravenous desmopressin in dogs and cats?

A

4-8 hours

220
Q

How can animals with complete CDI or primary NDI be identified?

A

They cannot concentrate urine above a specific gravity (SG) of 1.007 even after severe dehydration

221
Q

How long may it take for animals with partial CDI or psychogenic polydipsia to become dehydrated?

A

1-3 days

222
Q

What is a positive response to desmopressin a sign of?

A

Complete or partial CDI

223
Q

What is the average duration of synthetic desmopressin administration for assessing the response?

A

Several days

224
Q

What happens to water consumption during trial desmopressin therapy?

A

It dramatically decreases

225
Q

Who is the module developer for this course?

A

Nick Bexfield

226
Q

Who is the module tutor for this course?

A

Ann Thompson

227
Q

What are the learning objectives of this module?

A

Describe the structure and function of the pituitary gland, review the hormones produced, recognize clinical signs of pituitary dwarfism and differential diagnoses for polyuria/polydipsia.

228
Q

How many parts is the pituitary gland divided into?

A

4

229
Q

What are the two regions of the pituitary gland?

A

Anterior and posterior

230
Q

From which embryological origin does the posterior pituitary originate?

A

Neuroectoderm

231
Q

What is the name of the hormone produced by the anterior pituitary that stimulates the thyroid gland?

A

Thyroid stimulating hormone

232
Q

What is the name of the hormone produced by the anterior pituitary that stimulates growth?

A

Growth hormone

233
Q

What is the name of the hormone produced by the posterior pituitary that regulates water balance?

A

Antidiuretic hormone

234
Q

What are the major hormones produced by the posterior pituitary?

A

Oxytocin and antidiuretic hormone

235
Q

What are the clinical signs of pituitary dwarfs in German Shepherd dogs?

A

Growth retardation, soft and woolly hair coat, truncal alopecia, hyperpigmented and scaly skin, and other reproductive and dental abnormalities.

236
Q

What are the common findings in male and female pituitary dwarfs?

A

Male: cryptorchidism
Female: persistent oestrus with swelling of the vulva, attractiveness to male dogs, and bloody vaginal discharge.

237
Q

What is a possible cause of a continuous heart murmur in pituitary dwarfs?

A

Patent ductus arteriosus.

238
Q

What are the differential diagnoses for pituitary dwarfism?

A

Congenital hypothyroidism, iatrogenic hypercorticism, hypoadrenocorticism, malnutrition, gastrointestinal disorders, and more.

239
Q

What laboratory findings are commonly seen in pituitary dwarfs?

A

Elevated creatinine levels, low circulating thyroxine concentration, and low circulating IGF-1 concentrations.

240
Q

How is the diagnosis of pituitary dwarfism made?

A

The definitive diagnosis is based on the results of a stimulation test.

241
Q

What is the purpose of measuring plasma IGF-1 concentration in pituitary dwarfs?

A

It can be used to indirectly assess the GH status of an animal.

242
Q

What is the major effect of oxytocin?

A

Effects on smooth muscle cells, especially mammary glands and uterus.

243
Q

What is the major effect of ADH?

A

Effects on renal tubular cells and collecting ducts, with a secondary effect to increase blood pressure.

244
Q

How are ADH and oxytocin synthesized?

A

They are synthesised as pre-pro-hormones and undergo cleavage when released to form pro-hormones and then hormones.

245
Q

How is the release of ADH controlled?

A

Release is controlled by osmoreceptors, water intake receptors in the stomach and oesophagus, stretch receptors in the atria, and baroreceptors in the carotid sinus and aortic arch.

246
Q

What controls the release of growth hormone?

A

The opposing actions of GH-releasing hormone (GHRH) and somatostatin.

247
Q

What are the rapid catabolic actions of growth hormone?

A

Enhanced lipolysis, gluconeogenesis, and restricted glucose transport across the cell membrane.

248
Q

What are the long-lasting anabolic effects of growth hormone?

A

Mediated via insulin-like growth factors (IGFs) which stimulate protein synthesis, chondrogenesis, and growth.

249
Q

Where are insulin-like growth factors (IGFs) produced?

A

IGFs are produced in many different tissues, with the main source of circulating IGF-1 being the liver.

250
Q

What is hypopituitarism?

A

It is a deficiency of one or more hormones from the pituitary gland, resulting in lack of stimulation of the respective endocrine glands.

251
Q

What is pituitary dwarfism?

A

It is a rare disorder of congenital growth hormone (GH) deficiency, resulting in stunted growth.

252
Q

What is the most striking example of pituitary hormone deficiency?

A

Congenital growth hormone (GH) deficiency, or pituitary dwarfism.

253
Q

What causes pituitary dwarfism in German Shepherd dogs?

A

It is thought to be due to an underlying genetic defect, rather than pressure atrophy of the anterior lobe.

254
Q

What gene mutation is associated with pituitary dwarfism in German Shepherd dogs?

A

A mutation of the gene encoding the transcription factor LHX3.

255
Q

What are the possible causes of PU/PD in animals?

A

CDI, primary NDI, psychogenic polydipsia

256
Q

What hormone can be measured to differentiate CDI and nephrogenic diabetes insipidus?

A

ADH

257
Q

What can diagnostic imaging like MRI or CT identify in animals with PU/PD?

A

Structural lesions in the hypothalamus or pituitary

258
Q

What should never be used as a treatment for CDI in animals?

A

Water restriction

259
Q

What is the most widely used treatment for CDI in dogs and cats?

A

Desmopressin (DDAVP)

260
Q

What is the recommended dose for intranasal administration of desmopressin for CDI?

A

1-4 drops (approximately 1.5-4.0 µg/drop) 1-3 times daily

261
Q

What other forms does desmopressin come in?

A

Sterile solution for intravenous administration and tablets

262
Q

What is the success rate of desmopressin therapy in controlling clinical signs in animals?

A

The majority of cases

263
Q

What are some other medications occasionally prescribed for the control of CDI?

A

Thiazide diuretics and chlorpropamide

264
Q

Can dietary modification alone effectively treat CDI in animals?

A

No, it is ineffective as the sole method of treatment

265
Q

What does nephrogenic diabetes insipidus result from?

A

Lack of renal tubular sensitivity to ADH

266
Q

What can primary nephrogenic diabetes insipidus be managed with?

A

Thiazide diuretics and chlorpropamide

267
Q

What is the primary cause of nephrogenic diabetes insipidus?

A

Renal tubular insensitivity to ADH

268
Q

Why might urea be low in patients?

A

Due to renal washout effect

269
Q

What is the effect of diabetes insipidus on serum osmolality?

A

It is often slightly increased

270
Q

What is the effect of psychogenic polydipsia on serum osmolality?

A

It may be decreased or result in hyponatraemia

271
Q

What is the urine specific gravity in diabetes insipidus?

A

Always below that of glomerular filtrate (<1.008-1.010)

272
Q

What is the main function of anti-diuretic hormone?

A

To conserve water by increasing permeability of the renal tubule and collecting duct to water

273
Q

What are the other activities of anti-diuretic hormone?

A

Intestinal contractility, platelet aggregation, von Willebrand factor release, and hepatic glycogenolysis

274
Q

What is central diabetes insipidus?

A

The syndrome resulting from deficiency of ADH

275
Q

What is the most common cause of CDI in dogs?

A

Neoplasia

276
Q

What is the most common cause of CDI in cats?

A

Trauma

277
Q

What are the clinical signs of CDI?

A

Can occur at any age, no apparent breed predisposition

Small Animal Medicine (GP cert) (22 decks)

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