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.
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.
3
Q
What is the response to desmopressin therapy for animals with CDI (complete and partial)?
A
Positive.
4
Q
What is the urine SG range for animals with primary NDI during the modified water deprivation test?
A
<1.008 (no change).
5
Q
What is the urine SG range for animals with psychogenic polydipsia during the modified water deprivation test?
A
> 1.030.
6
Q
What should be monitored during the assessment of a clinical response to trial desmopressin therapy?
A
Water intake.
7
Q
How long is synthetic desmopressin (DDAVP) administered via the conjunctival sac during the trial therapy?
A
Several days.
8
Q
What is the most common presenting sign in animals with sex predisposition?
A
PU/PD (polyuria/polydipsia)
9
Q
What are the clinical signs of CDI in animals?
A
Increased water intake, increased urine volume, weight loss, and excessive drinking
10
Q
What can excessive water consumption in animals with CDI lead to?
A
Vomiting and nocturia
11
Q
What are the clinical signs of CDI in animals with partial CDI?
A
Less marked clinical signs compared to full CDI
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
13
Q
What can cause neurological signs in dogs and cats?
A
Head trauma or multifocal/widespread inflammatory, infectious, and developmental structural CNS defects
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
15
Q
What can indicate the presence of hyperadrenocorticism in dogs with CDI?
A
Dermatological and metabolic changes associated with hyperadrenocorticism
16
Q
What syndrome can occur if animals with CDI experience severe water restriction?
A
Hypertonic dehydration
17
Q
What are the clinical signs of hypertonic dehydration in animals with CDI?
A
Anorexia, weakness, disorientation, ataxia, and seizures
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
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
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
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
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
23
Q
What abnormalities may be observed if water is restricted in animals with CDI?
A
Elevated haematocrit, hyperproteinaemia, hypernatraemia, and prerenal azotaemia
24
Q
What can cause severe hypernatraemia and serum hyperosmolality in CDI?
A
Hypertonic dehydration
25
How can serum osmolality be measured in dogs and cats?
Direct measurement or calculated using a formula based on Na, K, urea, and glucose concentrations
26
How does ADH conserve water?
By increasing the permeability of the distal renal tubule and collecting duct to water
27
What other activities does ADH have?
Intestinal contractility, platelet aggregation, von Willebrand factor release, and hepatic glycogenolysis
28
What is the primary cause of polyuria?
Inability of the kidney to concentrate urine
29
What is Central Diabetes Insipidus (DI)?
A lack of production or release of ADH from the pituitary gland
30
What is Nephrogenic Diabetes Insipidus (DI)?
Lack of renal tubular sensitivity to ADH
31
What are some causes of secondary nephrogenic diabetes insipidus?
Hypercalcaemia, hyperadrenocorticism, renal failure, hyperthyroidism, hypokalaemia, pyometra, toxaemia, and pyelonephritis
32
Why can PU/PD improve with a trial of exogenous ADH (DDAVP)?
The supra-physiological dose can temporarily overcome the problems caused by the underlying disease
33
What should be ruled out before water deprivation tests and DDAVP trials?
Other causes of secondary nephrogenic diabetes insipidus
34
What is the systematic approach to the PU/PD patient?
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
35
What lab tests should be conducted in PU/PD cases?
Cystocentesis sample urinalysis, routine haematology/serum biochemistry/electrolytes, possible endocrine disease tests
36
What further steps can be taken if no obvious abnormalities are found?
Consider CNS imaging, water deprivation test, trial of DDAVP, measurement of serum and urine osmolality, or investigating other clinical signs
37
What does PU/PD stand for?
Polyuria/Polydipsia
38
What can result from depriving a dog of water without ruling out certain diseases?
Serious renal damage
39
What is the mechanism behind many causes of PU/PD?
Secondary NDI
40
What does excess calcium interfere with in hypercalcaemia?
ADH activity
41
Which hormone is affected by cortisol in hyperadrenocorticism?
ADH
42
In which conditions are the effects of ADH disrupted?
Renal failure, hyperthyroidism, hypokalaemia, pyometra, toxaemia, and pyelonephritis
43
What can cause confusion and misdiagnosis of CDI in animals with PU/PD?
Improvement with a trial of desmopressin
44
What should water deprivation tests and desmopressin trials be reserved for?
Dogs who have had other causes of secondary NDI ruled out
45
What is the rare disorder characterized by the inability of renal tubular cells to respond to ADH?
Primary NDI
46
What causes primary nephrogenic diabetes insipidus in humans?
Mutations of the V2 receptor or aquaporin-2
47
Which breed of dog is associated with a 10-fold reduction in the responsiveness of renal tubular cells to vasopressin?
Siberian Huskies
48
Why are clinical signs reported only in male dogs with congenital nephrogenic diabetes insipidus?
Suspected gene mutation on the X chromosome
49
How is primary NDI diagnosed?
Exclude all other causes of PU/PD and failure to concentrate urine after dehydration
50
What does chlorpropamide do in the treatment of primary NDI?
Increases responsiveness of renal tubular principal cells to ADH
51
What is a potential adverse effect of chlorpropamide?
Hypoglycemia
52
Why are thiazide diuretics occasionally used in the management of human CDI?
To decrease water loss by reducing urine output
53
What effect do thiazide diuretics have in dogs with primary NDI?
Variable antidiuretic effect
54
What is the recommended dose of hydrochlorothiazide for dogs and cats?
2.5-5.0 mg/kg orally q12h
55
What might cause low urea besides liver disease?
Renal washout effect
56
In diabetes insipidus, what is often increased due to the body's inability to retain water?
Serum osmolality or sodium
57
What occurs in psychogenic polydipsia?
Dog is overhydrated and may have decreased serum osmolality or hyponatraemia
58
What is the urine specific gravity in diabetes insipidus compared to glomerular filtrate?
Always below, i.e. <1.008-1.010
59
When should a water deprivation test be performed?
When other diseases have been ruled out
60
What are the two methods for performing a water deprivation test?
Abruptly stopping water or gradual reduction in water intake +/- salt supplementation
61
What hormone is involved in the control of urinary concentration?
Anti-diuretic hormone (ADH or arginine vasopressin)
62
What does ADH do to conserve water?
Increases the permeability of distal renal tubule and collecting duct to water
63
Name some actions of ADH.
Intestinal contractility, platelet aggregation, von Willebrand factor release, hepatic glycogenolysis
64
What can cause polyuria/polydipsia (PU/PD) if disrupted?
Presence of an adequate concentrating gradient of sodium and urea in renal cortex
65
What is the most common cause of central diabetes insipidus (CDI) in dogs?
Neoplasia
66
What is the most common cause of trauma-induced CDI in cats?
Trauma
67
What are some recognised causes of CDI in dogs?
Neoplasia, craniopharyngioma, chromophobe adenoma or adenocarcinoma, metastatic neoplasia, idiopathic, trauma, surgery, developmental structural defects, infection, inflammation, cyst
68
What are the clinical signs of CDI?
Polyuria/polydipsia (PU/PD)
69
What is the formula for calculating serum osmolality?
Serum osmolality = 2 (Na + K) + urea + glucose.
70
What values are considered normal for osmolality in healthy dogs?
Approximately 290-310 mOsm/kg.
71
What values are considered normal for osmolality in healthy cats?
Approximately 290-330 mOsm/kg.
72
In hypertonic dehydration, what is the largest contributor to hyperosmolality?
Sodium.
73
When is the calculation of osmolality not necessary in markedly hypernatraemic animals?
In an emergency setting.
74
What specific gravity (SG) values are consistent with polyuria/polydipsia (PU/PD) in dogs and cats?
<1.030 in dogs and <1.035 in cats.
75
What urine specific gravity (SG) values are typically found in animals with complete central diabetes insipidus (CDI)?
Severe hyposthenuria (SG 1.000-1.006).
76
What are the additional differentials for animals with marked hyposthenuria?
Hyperadrenocorticism in dogs, hyperthyroidism in cats, liver disease, hypercalcaemia, primary polydipsia, and nephrogenic diabetes insipidus.
77
What diagnostic test should always be performed as part of the investigation of PU/PD?
Bacteriological culture of urine.
78
What percentage of dogs with CDI have urinary tract infections at presentation?
Approximately 25%.
79
What is the indication for the water deprivation test?
To distinguish between CDI, primary NDI, and psychogenic polydipsia.
80
What should be considered before performing the water deprivation test?
All other causes of PU/PD should be ruled out.
81
In which patients is the water deprivation test contraindicated?
Azotaemic and/or dehydrated patients and those with known renal disease.
82
What is the first step of a modified water deprivation test?
Gradual water restriction over three days to re-establish the renal medullary concentration gradient.
83
What is stage two of the water deprivation test?
Complete water deprivation.
84
What is performed in stage three of the water deprivation test?
Administration of ADH (if necessary).
85
What should be done during the period of gradual water restriction in a modified water deprivation test?
Owners should feed dry food and monitor the animal's body weight on a daily basis.
86
What is the main purpose of the modified water deprivation test?
To overcome the problem of renal medullary washout and unreliable urine concentrating ability.
87
What are the major effects of oxytocin?
On smooth muscle cells, especially mammary glands and uterus.
88
What are the major effects of ADH?
On renal tubular cells and collecting ducts, and to increase blood pressure.
89
How is the release of ADH controlled?
Via osmoreceptors, water intake receptors, stretch receptors, and baroreceptors in the hypothalamus.
90
How is growth hormone (GH) secretion regulated?
By the opposing actions of GH-releasing hormone (GHRH) and somatostatin.
91
What are the rapid catabolic actions of GH?
Insulin antagonism resulting in enhanced lipolysis, gluconeogenesis, and restricted glucose transport.
92
What are the slow anabolic effects of GH?
Mediated via insulin-like growth factors (IGFs), promoting protein synthesis, chondrogenesis, and growth.
93
What is hypopituitarism?
A deficiency of one or more hormones from the pituitary gland, resulting in lack of stimulation of the respective endocrine glands.
94
What is pituitary dwarfism?
Congenital growth hormone deficiency, usually seen in German Shepherd dogs with combined deficiency of GH, TSH, and prolactin.
95
What causes pituitary dwarfism in German Shepherd dogs?
An underlying genetic defect, rather than pressure atrophy or cyst formation in the pituitary gland.
96
What is the mutation associated with pituitary dwarfism in German Shepherd dogs?
A mutation of the gene encoding the transcription factor LHX3.
97
What are the three possible causes of PU/PD after ruling out other causes?
CDI, primary NDI, and psychogenic polydipsia.
98
What are the two conditions that dogs with psychogenic polydipsia and primary NDI fail to respond to?
Complete and partial CDI.
99
What test allows differentiation of CDI and nephrogenic diabetes insipidus?
Measurement of plasma ADH concentration.
100
What hormone is very sensitive to proteolysis and requires immediate chilling, separation, and freezing of samples?
ADH.
101
What can MRI or CT imaging identify in relation to PU/PD?
Developmental or acquired structural lesions within the hypothalamus or pituitary.
102
What is the most widely used treatment for CDI in dogs and cats?
Desmopressin (DDAVP).
103
How is desmopressin administered in cats?
Conjunctival treatment or orally.
104
What is the recommended initial dose of desmopressin for oral therapy?
0.1 mg once to twice daily.
105
Which route of desmopressin administration is ineffective in some animals?
Gastrointestinal tract.
106
What medications are occasionally prescribed for the control of CDI in humans and some canine cases?
Thiazide diuretics and chlorpropamide.
107
How can dietary modification be used to treat CDI?
To decrease water loss associated with sodium and protein excretion.
108
What are the clinical signs of pituitary dwarfs in German Shepherd dogs?
Growth retardation, abnormal hair coat, truncal alopecia, hyperpigmented and scaly skin, cryptorchidism in males, persistent oestrus in females.
109
What are the differential diagnoses for pituitary dwarfism?
Congenital hypothyroidism, iatrogenic hypercorticism, hypoadrenocorticism, malnutrition, gastrointestinal disorders, exocrine pancreatic insufficiency, portosystemic shunting, congenital renal disease, and skeletal disorders.
110
What laboratory findings are commonly seen in pituitary dwarfs?
Elevations in creatinine, low circulating thyroxine concentration, low plasma IGF-1 concentration.
111
How is the diagnosis of pituitary dwarfism usually made?
Based on the results of a stimulation test.
112
What are the four parts of the pituitary gland?
Pars distalis, pars intermedia, pars nervosa, pars tuberalis
113
What are the other names for the anterior and posterior pituitary glands?
Anterior – adenohypophysis, Posterior – neurohypophysis
114
Where does the anterior pituitary arise from?
An invagination of the oral ectoderm and forms Rathke's pouch
115
What are the major releasing hormones produced by the hypothalamus?
TRH, GnRH, GHIH, GHRH, CRH, PRF, PIH
116
What are the two major hormones produced by the posterior pituitary gland?
Oxytocin and antidiuretic hormone
117
How are secretion from the anterior and posterior pituitary controlled?
Anterior pituitary – by hypothalamic releasing hormones, Posterior pituitary – by direct neural stimulation
118
What hormone is produced from the cleavage of corticotropin (ACTH)?
Melanocyte stimulating hormone (MSH)
119
What is the mechanism behind many causes of PU/PD?
Secondary NDI
120
What can interfere with ADH activity in hypercalcaemia?
Excess calcium
121
Which hormone affects ADH actions in hyperadrenocorticism?
Cortisol
122
Which conditions disrupt the effects of ADH?
Renal failure, hyperthyroidism, hypokalaemia, pyometra, toxaemia, and pyelonephritis
123
What is the reasoning behind animals initially improving with a trial of desmopressin?
Supra-physiological dose of desmopressin temporarily over-rides the problems caused by the underlying disease
124
What should be ruled out before conducting water deprivation tests and desmopressin trials?
Other causes of secondary NDI
125
What is primary NDI characterized by?
The inability of renal tubular cells to respond to adequate plasma concentrations of ADH
126
What causes primary nephrogenic diabetes insipidus in humans?
Mutations of either the V2 receptor or aquaporin-2
127
What is a congenital form of NDI associated with in Siberian Huskies?
A 10-fold reduction in the responsiveness of renal tubular cells to vasopressin
128
Which gene mutation is suspected in Siberian Huskies with NDI?
V2 receptor gene
129
How is primary NDI diagnosed?
By excluding all other causes of PU/PD and observing a failure to concentrate urine following dehydration and administration of desmopressin
130
What is the treatment for primary NDI?
Chlorpropamide and thiazide diuretics
131
What is the potential effect of chlorpropamide in the treatment of NDI?
Increase in the responsiveness of renal tubular principal cells to ADH
132
What is a potential adverse effect of using chlorpropamide?
Hypoglycaemia
133
Which natriuretic agent is occasionally used in the management of human CDI?
Thiazide diuretics
134
How do thiazide diuretics decrease water loss in primary NDI?
By decreasing water delivery to the distal tubule
135
What is the recommended dose of hydrochlorothiazide for dogs and cats?
2.5-5.0 mg/kg orally q12h
136
What are some GH stimulants used in the diagnosis of pituitary dwarfism in dogs?
GHRH, clonidine, xylazine
137
How are GH concentrations measured in dogs with pituitary dwarfism?
Before and after intravenous administration of a stimulant
138
What is the additional test to determine GH response?
The ghrelin stimulation test
139
What is the dose of human ghrelin administered intravenously in the ghrelin stimulation test?
2 µg/kg
140
What can exclude congenital GH deficiency in dogs?
A post-ghrelin plasma GH concentration of >5 µg/l at 20-30 minutes after intravenous administration of the stimulant
141
What can pituitary imaging reveal in dogs with pituitary dwarfism?
The presence of pituitary cysts
142
What may cause pituitary cysts in dogs apart from pituitary dwarfism?
They can also be seen in healthy dogs, especially in brachycephalic breeds
143
When is it recommended to start therapy for pituitary dwarfism in dogs?
As young as possible
144
What are some reported treatments for pituitary dwarfism in dogs?
Exogenous bovine, human, or porcine GH
145
What are the potential side effects of GH treatment for pituitary dwarfism?
Hypersensitivity reactions to GH and diabetes mellitus
146
What is the recommended subcutaneous dose of GH for pituitary dwarfism in dogs?
0.1-0.3 IU per kg bodyweight three times a week
147
What should be monitored every 3 weeks during GH treatment for pituitary dwarfism?
Plasma concentrations of glucose
148
What can induce expression of the GH gene in the canine mammary gland?
Progestogens
149
What treatment resulted in an increase in body size and the development of a complete adult hair coat in German Shepherd dwarfs?
Medroxyprogesterone acetate treatment
150
What hormone replacement should be started for pituitary dwarfs with evidence of hypothyroidism?
Thyroid hormone replacement
151
What is used for the long-term treatment of growth failure?
Recombinant human IGF-1 (Mecasermin, Increlex)
152
What is the condition called that affects hair growth and skin pigmentation in dogs?
Growth hormone-responsive alopecia
153
What is the relationship between growth hormone and growth hormone-responsive alopecia?
The relationship is unproven and the etiology remains uncertain.
154
What are the clinical signs of growth hormone-responsive alopecia?
Bilaterally symmetric alopecia and hyperpigmentation mainly of the trunk.
155
Which animals are mainly affected by growth hormone-responsive alopecia?
Poodles, Pomeranians, Chow Chows, Keeshonds, Airedales, and Samoyeds.
156
What are the diagnostic tests for growth hormone-responsive alopecia?
Routine endocrine testing, low GH levels testing, and IGF-1 concentrations testing.
157
What are the histopathological findings in growth hormone-responsive alopecia?
Atrophic follicles, dilated and devoid of hair, and follicular dysplasia.
158
What is the suggested management therapy for growth hormone-responsive alopecia?
Bovine, porcine, and human growth hormone at a dose of 0.1 IU/kg subcutaneously three times a week.
159
What is another name for growth hormone-responsive alopecia?
Castration-responsive alopecia
160
What condition should be considered in a patient with polyuria and polydipsia?
Primary diabetes insipidus
161
What is the defining water intake for polyuria and polydipsia?
Water intake of >100ml/kg/day
162
What are the possible differential diagnoses for 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
163
What is the cause of primary polyuria in polyuria and polydipsia?
Osmotic diuresis caused by glycosuria in diabetes mellitus
164
What is the main action of Anti-diuretic hormone (ADH)?
ADH conserves water by increasing the permeability of the distal renal tubule and collecting duct to water.
165
How does ADH exert its actions?
ADH allows water channels (aquaporins) to be inserted into cell membranes.
166
What are the other activities of ADH?
Intestinal contractility, platelet aggregation, von Willebrand factor release, and hepatic glycogenolysis.
167
What results in primary polyuria?
Inability of the kidney to concentrate urine, due to Central or Nephrogenic Diabetes Insipidus [DI].
168
What is Central Diabetes Insipidus (DI) caused by?
A lack of production or release of anti-diuretic hormone (ADH) from the pituitary.
169
What is Nephrogenic Diabetes Insipidus (DI) caused by?
Lack of renal tubular sensitivity to ADH.
170
What is the difference between primary and secondary nephrogenic diabetes insipidus?
Primary disease is rare, while secondary nephrogenic DI is more common and is the mechanism behind many causes of PU/PD.
171
What can disrupt the effects of ADH?
Renal failure, hyperthyroidism, hypokalaemia, pyometra, toxaemia, pyelonephritis, and various other diseases.
172
Why can PU/PD initially improve with a trial of exogenous ADH?
Supra-physiological doses of ADH can temporarily over-ride the problems caused by underlying disease.
173
When should water deprivation tests and DDAVP trials be reserved for?
Dogs who have had other causes of secondary nephrogenic diabetes insipidus systematically ruled out.
174
What should be done before depriving a dog of water?
Ruling out diseases that can cause PU/PD, such as hyperadrenocorticism, pyelonephritis, hypercalcaemia, liver disease, etc.
175
What are the initial steps in a systematic approach to the PU/PD patient?
1) Full history, 2) Full clinical examination, 3) Confirm PU/PD and isosthenuria/hyposthenuria, 4) Urinalysis of a cystocentesis sample.
176
What should follow up abnormalities found in routine haematology/serum biochemistry?
Further investigation and appropriate tests for possible underlying endocrine disease.
177
What diagnostic imaging should be considered?
Chest and abdominal radiographs, ultrasound of the abdomen (adrenal glands, urinary tract).
178
If no obvious abnormalities are found, what should be considered?
A trial of broad-spectrum antibiotics to rule out low-grade urinary tract/renal infection.
179
What are the further steps to consider?
Imaging of the CNS, water deprivation test, trial of DDAVP (ADH), measurement of serum and urine osmolality or following up other clinical signs.
180
What should be noted about interpreting lab tests in PU/PD?
It can be difficult to culture bacteria from very dilute urine, so urine culture results should be interpreted with caution.
181
What is the common presenting sign in animals with CDI?
PU/PD
182
How do the clinical signs of CDI vary?
From acute to chronic over several weeks or months
183
What can excessive water consumption in animals with CDI lead to?
Weight loss
184
What are some additional clinical signs that may be present in animals with PU/PD?
Vomiting, urinary incontinence, loss of house training
185
What are some causes of neurological signs in dogs with CDI?
Pituitary or hypothalamic neoplasia, head trauma, inflammatory/infectious/developmental CNS defects
186
What other endocrine abnormalities can occur in association with lesions affecting the pituitary gland?
Hypothyroidism, hypoadrenocorticism, decreased GH production
187
What can be present concurrently with CDI in dogs with chromophobe adenomas or adenocarcinomas?
Hyperadrenocorticism
188
What can severe water restriction in animals with CDI lead to?
Hypertonic dehydration
189
What are some clinical signs of hypertonic dehydration?
Anorexia, weakness, disorientation, ataxia, seizures
190
What is the diagnosis of CDI dependent upon?
Thorough exclusion of other causes of PU/PD
191
What are the differential diagnoses for CDI?
Primary nephrogenic diabetes insipidus and primary polydipsia
192
What abnormalities in routine clinicopathological findings are associated with CDI?
None, provided water is not restricted
193
What happens to serum urea concentrations in dogs or cats with CDI?
They are frequently reduced due to renal medullary solute washout
194
What abnormalities can be seen if water is restricted in CDI?
Elevated haematocrit, hyperproteinaemia, hypernatraemia, prerenal azotaemia
195
What are the potential effects of severe hypernatraemia and serum hyperosmolality?
Hypertonic dehydration
196
How can serum osmolality be measured?
Directly or calculated using a formula based on sodium, potassium, urea, and glucose concentrations
197
What is the formula for calculating serum osmolality?
Serum osmolality = 2(Na+K) + urea + glucose
198
What are the approximate osmolality ranges for healthy dogs and cats?
Approximately 290-310 mOsm/kg for dogs and 290-330 mOsm/kg for cats
199
When is calculation of osmolality not necessary in hypertonic dehydration?
In markedly hypernatraemic animals in an emergency setting
200
What values are detected in animals with complete central diabetes insipidus (CDI)?
Hyposthenuria (SG 1.000-1.006)
201
What are some additional differentials for marked hyposthenuria?
Hyperadrenocorticism, hyperthyroidism, liver disease, hypercalcaemia, primary polydipsia, nephrogenic diabetes insipidus
202
When should bacteriological culture of urine be performed?
As part of the diagnostic investigation of PU/PD, regardless of the suspected cause
203
What percentage of dogs with CDI have urinary tract infections at presentation?
Approximately 25%
204
What is the indication of the water deprivation test?
To distinguish between CDI, primary nephrogenic diabetes insipidus (NDI), and psychogenic polydipsia
205
What can the water deprivation test result in?
Rapid alterations of water and electrolyte balance that can be life threatening
206
When is the water deprivation test contraindicated?
In azotaemic and/or dehydrated patients, and in patients with known renal disease
207
What should be ruled out before performing the water deprivation test?
All other causes of PU/PD, limiting the differential diagnoses to CDI, primary NDI, and psychogenic polydipsia
208
What can happen in animals with PU/PD of any cause during a water deprivation test?
Renal medullary washout, limiting urine concentrating ability and ADH production
209
What is the first step in a water deprivation test?
Gradual water restriction over three days to re-establish renal medullary concentration gradient
210
What is the protocol for stage 1 of a modified water deprivation test?
Gradual restriction of water intake over three days with divided small portions per day
211
What is the protocol for stage 2 of a modified water deprivation test?
Complete water deprivation after obtaining exact body weight and emptying the bladder
212
What is the final stage of a modified water deprivation test?
The administration of ADH (if necessary)
213
Why should an indwelling urinary catheter be considered in female animals during urethral catheterization?
To empty the bladder many times at frequent intervals
214
How often should the bladder be completely emptied during the water deprivation test?
At 1-2 hour intervals
215
What are the endpoints for the water deprivation test in dogs and cats?
5% loss of body weight or urine SG >1.030 in dogs (>1.035 in cats)
216
What should be monitored in the animal during the water deprivation test?
Signs of CNS depression, urine SG, and body weight
217
What should be done if the patient fails to reach the 5% dehydration endpoint by the end of the working day?
Transfer the patient to a facility with overnight care or provide overnight access to water in maintenance amounts
218
What are the recommended doses of desmopressin for dogs and cats in the ADH response test?
2.0 μg for dogs <15 kg and cats, 4.0 μg for dogs >15 kg
219
What is the maximum response time to intravenous desmopressin in dogs and cats?
4-8 hours
220
How can animals with complete CDI or primary NDI be identified?
They cannot concentrate urine above a specific gravity (SG) of 1.007 even after severe dehydration
221
How long may it take for animals with partial CDI or psychogenic polydipsia to become dehydrated?
1-3 days
222
What is a positive response to desmopressin a sign of?
Complete or partial CDI
223
What is the average duration of synthetic desmopressin administration for assessing the response?
Several days
224
What happens to water consumption during trial desmopressin therapy?
It dramatically decreases
225
Who is the module developer for this course?
Nick Bexfield
226
Who is the module tutor for this course?
Ann Thompson
227
What are the learning objectives of this module?
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
How many parts is the pituitary gland divided into?
4
229
What are the two regions of the pituitary gland?
Anterior and posterior
230
From which embryological origin does the posterior pituitary originate?
Neuroectoderm
231
What is the name of the hormone produced by the anterior pituitary that stimulates the thyroid gland?
Thyroid stimulating hormone
232
What is the name of the hormone produced by the anterior pituitary that stimulates growth?
Growth hormone
233
What is the name of the hormone produced by the posterior pituitary that regulates water balance?
Antidiuretic hormone
234
What are the major hormones produced by the posterior pituitary?
Oxytocin and antidiuretic hormone
235
What are the clinical signs of pituitary dwarfs in German Shepherd dogs?
Growth retardation, soft and woolly hair coat, truncal alopecia, hyperpigmented and scaly skin, and other reproductive and dental abnormalities.
236
What are the common findings in male and female pituitary dwarfs?
Male: cryptorchidism
Female: persistent oestrus with swelling of the vulva, attractiveness to male dogs, and bloody vaginal discharge.
237
What is a possible cause of a continuous heart murmur in pituitary dwarfs?
Patent ductus arteriosus.
238
What are the differential diagnoses for pituitary dwarfism?
Congenital hypothyroidism, iatrogenic hypercorticism, hypoadrenocorticism, malnutrition, gastrointestinal disorders, and more.
239
What laboratory findings are commonly seen in pituitary dwarfs?
Elevated creatinine levels, low circulating thyroxine concentration, and low circulating IGF-1 concentrations.
240
How is the diagnosis of pituitary dwarfism made?
The definitive diagnosis is based on the results of a stimulation test.
241
What is the purpose of measuring plasma IGF-1 concentration in pituitary dwarfs?
It can be used to indirectly assess the GH status of an animal.
242
What is the major effect of oxytocin?
Effects on smooth muscle cells, especially mammary glands and uterus.
243
What is the major effect of ADH?
Effects on renal tubular cells and collecting ducts, with a secondary effect to increase blood pressure.
244
How are ADH and oxytocin synthesized?
They are synthesised as pre-pro-hormones and undergo cleavage when released to form pro-hormones and then hormones.
245
How is the release of ADH controlled?
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
What controls the release of growth hormone?
The opposing actions of GH-releasing hormone (GHRH) and somatostatin.
247
What are the rapid catabolic actions of growth hormone?
Enhanced lipolysis, gluconeogenesis, and restricted glucose transport across the cell membrane.
248
What are the long-lasting anabolic effects of growth hormone?
Mediated via insulin-like growth factors (IGFs) which stimulate protein synthesis, chondrogenesis, and growth.
249
Where are insulin-like growth factors (IGFs) produced?
IGFs are produced in many different tissues, with the main source of circulating IGF-1 being the liver.
250
What is hypopituitarism?
It is a deficiency of one or more hormones from the pituitary gland, resulting in lack of stimulation of the respective endocrine glands.
251
What is pituitary dwarfism?
It is a rare disorder of congenital growth hormone (GH) deficiency, resulting in stunted growth.
252
What is the most striking example of pituitary hormone deficiency?
Congenital growth hormone (GH) deficiency, or pituitary dwarfism.
253
What causes pituitary dwarfism in German Shepherd dogs?
It is thought to be due to an underlying genetic defect, rather than pressure atrophy of the anterior lobe.
254
What gene mutation is associated with pituitary dwarfism in German Shepherd dogs?
A mutation of the gene encoding the transcription factor LHX3.
255
What are the possible causes of PU/PD in animals?
CDI, primary NDI, psychogenic polydipsia
256
What hormone can be measured to differentiate CDI and nephrogenic diabetes insipidus?
ADH
257
What can diagnostic imaging like MRI or CT identify in animals with PU/PD?
Structural lesions in the hypothalamus or pituitary
258
What should never be used as a treatment for CDI in animals?
Water restriction
259
What is the most widely used treatment for CDI in dogs and cats?
Desmopressin (DDAVP)
260
What is the recommended dose for intranasal administration of desmopressin for CDI?
1-4 drops (approximately 1.5-4.0 µg/drop) 1-3 times daily
261
What other forms does desmopressin come in?
Sterile solution for intravenous administration and tablets
262
What is the success rate of desmopressin therapy in controlling clinical signs in animals?
The majority of cases
263
What are some other medications occasionally prescribed for the control of CDI?
Thiazide diuretics and chlorpropamide
264
Can dietary modification alone effectively treat CDI in animals?
No, it is ineffective as the sole method of treatment
265
What does nephrogenic diabetes insipidus result from?
Lack of renal tubular sensitivity to ADH
266
What can primary nephrogenic diabetes insipidus be managed with?
Thiazide diuretics and chlorpropamide
267
What is the primary cause of nephrogenic diabetes insipidus?
Renal tubular insensitivity to ADH
268
Why might urea be low in patients?
Due to renal washout effect
269
What is the effect of diabetes insipidus on serum osmolality?
It is often slightly increased
270
What is the effect of psychogenic polydipsia on serum osmolality?
It may be decreased or result in hyponatraemia
271
What is the urine specific gravity in diabetes insipidus?
Always below that of glomerular filtrate (<1.008-1.010)
272
What is the main function of anti-diuretic hormone?
To conserve water by increasing permeability of the renal tubule and collecting duct to water
273
What are the other activities of anti-diuretic hormone?
Intestinal contractility, platelet aggregation, von Willebrand factor release, and hepatic glycogenolysis
274
What is central diabetes insipidus?
The syndrome resulting from deficiency of ADH
275
What is the most common cause of CDI in dogs?
Neoplasia
276
What is the most common cause of CDI in cats?
Trauma
277
What are the clinical signs of CDI?
Can occur at any age, no apparent breed predisposition
