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Endocrine Disease Part 1 > Water Metabolism and Diabetes Insipidus > Flashcards

Water Metabolism and Diabetes Insipidus Flashcards

1
Q

Water consumption and urine production are controlled by complex interactions between…

6 Answers

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Plasma osmolality
  2. Fluid volume in the vascular compartment
  3. Thirst centre
  4. Kidney
  5. Pituitary gland
  6. Hypothalamus
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2
Q

Diabetes insipidus results from…

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Deficiencies in secretion of vasopression OR its ability to interact normally with receptors located in the distal and collecting tubular cells

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3
Q

Diabetes insipidis results from either a deficiency in secretion of vasopression OR its ability to interact normally with receptors in the kidney. What is the result of either of these scenarios clinically?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

This results in an impaired ability to conserve water and concentrate urine

Which results in the production of large volumes of hypotonic dilute urine

Which results in compensatory polydipsia to minimise dehydration

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4
Q

The physiologic regulation of vasopressin synthesis and secretion is governed by which two major factors?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Extracellular fluid osmolality
  2. Blood pressure and volume

Extracellular fluid osmolality (and water homeostasis) is primarily regulated by ADH
Blood pressure and volume are in a large part regulated by the RAAS

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5
Q

Vasopressin is the main hormone involved in the regulation of…

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Water homeostasis and osmolality

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6
Q

Water homeostasis and osmolality are primarily regulated by which hormone?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Vasopressin

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7
Q

What is the system that has a large responsibility in regulating blood pressure and volume?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

The RAAS system

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8
Q

How does vasopressin secretion respond to changes in plasma osmolality?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Small increases in osmolality result in increased production and secretion of vasopressin

Small decreases in osmolality result in decreased production and secretion of vasopressin

Changes occur in parallel

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9
Q

The neurohypophysis contains a set of hypothalamic nuclei (supraoptic and paraventricular) responsible for the synthesis and secretion of oxytocin and vasopressin. These nuclei are composed of…

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. The magnocellular neurons
  2. Axonal cell processes (form the supraopticohypophysial tract)
  3. The termini within the posterior lobe of the pituitary
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10
Q

What is the function of the magnocellular nuclei?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

They secrete vasopressin and oxytocin in response to appropriate stimuli

Stimulus comes from high pressure baroreceptors in the carotic sinus and aortic arch and low pressure volume receptors in the atria and pulmonary venous system

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11
Q

Vasopressin and oxytocin are produced by which structure?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

The magnocellular neurons in the neurohypophysis

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12
Q

Describe how neurogenic input from high pressure arterial baroreceptors and low pressure volume receptors affect the release of vasopressin

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Baroreceptors and volume receptors normally inhibit the magnocellular neurons. Decrease in this tonic inhibition results in the release of vasopressin

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13
Q

Decreased tonic inhibition of high pressure baroreceptors and low pressure volume receptors results in the release of vasopressin the action of which is…

Chapter 1: Textbook of Canine and Feline Endocrinology

A

To stimulate V1a receptors on blood vessels, the result of which is vasoconstriction. The purpose of this is the effectively increase circulating plasma volume

ADH also acts on the kidneys to retain water but the main hormonal regulator of blood volume is the RAAS (stimulates renal sodium resorption)

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14
Q

What is the general molecular composition of arginine vasopressin?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Six member disulfide ring with a three membered tail on which the terminal carboxyl group is amidated

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15
Q

What is the difference in structure between arginine vasopressin and the synthetic compound desmopressin acetate (DDAVP)

Chapter 1: Textbook of Canine and Feline Endocrinology

A

D-arginine is substituted for L-arginine at position 8
The terminal amino group is removed from cysteine

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16
Q

What is DDAVP?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Desmopressin acetate (synthetic form of ADH)
AKA Deamino D-arginine vasopressin

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17
Q

The production of vasopressin (and oxytocin) is associated with specific binding proteins called…

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Neurophysins

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18
Q

The neurophysin peptide (vasopressin / oxytocin) combination is often referred as…

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Neurosecretory material

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19
Q

Describe the transport and release of vasopressin starting at the magnocellular neurones

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. One molecule of neurophysin II binds one molecule of vasopressin (neurosecertory material)
  2. Neurosecretory material is transported along the the axons of the hypothalamo-neurohypophyseal nerve tract
  3. Stored in granules in nerve terminals in the posterior pituitary
  4. Electrical stimulation of magnocellular neurons results of release into the blood stream via exocytosis
  5. Neurophysin-vasopressin combination dissociates in plasma releasing free vasopressin (the majority of this hormone exists unbound in plasma)
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20
Q

What are the mechanisms by which vasopressin is metablised and excreted?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. AVP binds to specific receptors after which they undergo proteolytic degradation
  2. Renal excretion is a secondary method (approx 1/4 of metabolic clearance)
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21
Q

The actions of AVP are mediated via the binding of receptors on the end organs of response. What are these receptors, what are the resulting actions, and how are these results acheived?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. V2 cAMP dependent receptors on the epithelia of the renal collecting duct. This mediates the diuretic action of AVP. It also stimulates the production of factor VIII and von Willebrand factor
  2. V1a phosphatidylinositol dependent receptors on blood vessels. This mediates the vasoconstrictive actions of ADH
  3. V3/V1b stimulates the secretion of ACTH from the anterior pituitary
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21
Q

Where are the primary cells that sense changes to osmolality located?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

In the brain. Specifically cells in the organum vasculosum of the lamina terminalis and in areas near the anterior wall of the third cerebral ventricle

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22
Q

The primary cells that sense change to osmolality are located in the brain. What is anatomically significant about the cells of this region?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

The cells in this region are perfused by fenestrated capillaries. Thus the blood brain barrier at this stie is deficient. The cells are therefore influenced by the composition of plasma rather than cerebrospinal fluid. Thus they are able to respond rapidly to changes in osmolality by increasing/reducing the production / secretion of vasopressin.

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23
Q

How large must be the change in plasma osmolality to change the secretion of vasopressin?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

As little as a 1% increase or decrease in plasma osmolality is sufficient to stimuate and increase or decrease in AVP release from the store of hormone in the posterior pituitary

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24
Q

What is the half life of AVP?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Approximately 15 minutes

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25
Q

Describe how AVP leads to the insertion of aquaporins in the apical membrane of the renal tubular epithelial cells

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. AVP binds V2 receptors on the basolateral surface of the cell
  2. Activation of the V2 receptor triggers membrane adenylate cyclase function. This enxyme converts ATP to cAMP
  3. cAMP activates protien kinase A
  4. PKA triggers the insertion of aquaporins into the luminal surface of the renal tubular epithelial cells
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26
Q

What is the result of aquaporin insertion into the apical membrane of renal epithelial tubular cells?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Water permeability is increased.
This allows osmotic water flow (not active water flow) from the tubular lumen into the hypertonic medullary interstitium

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27
Q

AVP increases osmotic water flow from the tubular fluid of the collecting duct into the medullary interstitium. In this circumstance, how is medullary hypertonicity maintained?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

The vasa recta resorbs this water from the medullary interstitium thereby maintaining the osmotic gradient / hypertonicity of the renal medulla

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28
Q

What are the factors that impact the amount of water reabsorbed from the distal nephron?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Plasma AVP concentration
  2. Existence of a significant osmotic gradient in the renal interstitium (i.e. adequate renal medullary hypertonicity)
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29
Q

How does a reduction in / loss of renal medullary hypertonicity affect the action of AVP?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Movement of water from the distal tubular lumen into the renal interstitium is passive. A reduction in medullary hypertonicity reduces the osmotic gradient required for this passive resoprtion of water. This means that a loss of renal medullary hypertonicity may inhibit vasopressin’s antidiuretic effects.

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30
Q

Why does medullary washout alone rarely result in significant polyuria?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

This is because a majority of the fluid coming from the loop of Henle can still be resorbed isotonically in the distal convoluted tubule and proximal collecting duct

31
Q

What is solute diuresis?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

This is a process that occurs when large volumes of filtered solutes reduce impair the ability of fluid to be reabsorbed in the proximal tubule. The resulting large amount of fluid presented to the distal nephron then overwhelms its capacity for water reabsorption resulting in diuresis even in the presence of large concentrations of vasopressin.
This can occur in the presence of high dietary intakes of sodium, or in the presence of poorly reasborbed solutes such as mannitol, urea, or glucose.

32
Q

What are mechanisms that stimulate thirst?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Increased ECF osmolality (via osmoreceptors in the anterior hypothalamus)
  2. Decreases in intravascular volume (via high and low baroreceptors in the thorax)
  3. Angiotensin II
33
Q

By how much must plasma osmolality increase to stimulate thirst?

This value is from a study in humans

Chapter 1: Textbook of Canine and Feline Endocrinology

A

2-3%

34
Q

What satiates thirst?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

This requires restoration of normal plasma osmolality (major role) and blood volume

35
Q

What defines polyuria and polydipsia clinically?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Polydipsia: water intake > 100ml/kg/day
Polyuria: Urine output > 2ml/kg/hr (>50ml/kg/24hrs)
Keeping in mind there is potential for urine production to be abnormal within the normal reference ranges in some individuals

36
Q

What are the classifications of primary polyuric disorders?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Primary pituitary and nephrogenic diabetes insipidus (NDI)
  2. Secondary NDI
  3. Osmotic diuresis induced polyuria
  4. Intereference with the hypothalamic-pituitary secretion of AVP
37
Q

What is the most common form of diabetes insipidus?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Acquired secondary NDI

38
Q

What are the mechanisms by which secondary NDI can occur?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Interference with the normal interaction of AVP and renal tubular AVP receptors
  2. Problems with the generation of intracellular cAMP
  3. Problems with renal tubular cell function
  4. Loss of the renal medullary interstitial concentration gradient
39
Q

Chapter 1: Textbook of Canine and Feline Endocrinology

A
40
Q

What is the mechanism by which diabetes mellitus stimulates osmotic diuresis and compensatory polydipsia?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Relative or absolute insulin deficiency results in hyperglycaemia
  2. Capacity for renal tubular reabsorption of glucose is exceeded
  3. Glucose appears in the urine and acts as an osmotic diuretic causing increased water loss into the urine
  4. Water loss results in hypovolaemia
  5. Hypovolaemia stimulates thirst and increased water intake
41
Q

What is renal tubular glycosuria?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

A rare congenital tubular disorder in which there is an inability for glucose to be reabsorbed from the ultrafiltrate

42
Q

What are the clinical findings that would increase the suspicion of renal tubular glycosuria?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Polyuria and polydipsia
  2. Persistent glycosuria
  3. Normal blood glucose and serum fructosamine concentrations
43
Q

What are the potential reasons for the development of polyuria in patients with pyometra?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Bacterial endotoxins may
1. Compete with AVP for V2 receptor binding sites
2. Interfere with the insertion of aquaporin-2 water channels into the apical membrane of renal tubular epithelial cells
3. Cause reversible renal tubular cell lesions

44
Q

Why does hypercalcaemia result in polyuria?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Increased calcium is associated with down regulation of aquaporin-2 water channels and decreased function of AVP. It results in:
1. Inhibited binding of AVP to its receptor binding site
2. Damage to AVP receptors in the renal tubules
3. Inactivation of adenylate cyclase
4. Decreased transport of sodium and chloride into the renal medullary interstitium

45
Q

How do glucocorticoids affect the production of AVP at the level of the hypothalamus?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Glucocorticoids work at the level of the hypothalamus and / or neurohypophysis to inhibit AVP release. They do this by:
1. Increasing the osmotic threshold for for AVP release
2. Decreasing the sensitivity of the AVP response to increasing osmolality

46
Q

Besides its action at the level of the hypothalamus, what are potential mechanisms by which glucocorticoids cause polyuria?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Increase GFR (potentially via altered renal autoregulation - not from this reference)
  2. Altered proximal tubular epithelial sodium transport
  3. Increased free water clearance
  4. Cause resistance to the effects of AVP in the kidney
47
Q

Besides the increase in circulating steroid hormones, how might a pituitary tumour present in Cushing’s disease result in polyuria?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

There is potential that the presence of a pituitary macrotumor may directly compress the magnocellular neurons resulting in a deficiency of AVP

48
Q

What are the potential mechanisms by which polyuria occurs in pyelonephritis?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Direct destruction of renal tissue (and thus the countercurrent mechanism in the renal medulla) via infection and inflammation
  2. Bacterial endotoxins may compete for AVP binding sites (as with pyometra)
49
Q

How does hyperaldosteronism result in polyuria?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

The mechanism for this is not clear

50
Q

What is CDI?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Central diabetes insipidus
It is a polyuric syndrome that results from a lack of sufficient AVP to concentrate urine for water conservation

51
Q

What is the result of an absolute deficiency in AVP (compared to partial deficiency)?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Persistent hyposthenuria
Severe diuresis
USG remains </= 1.006 even with severe dehydration

52
Q

What is the result of a partial deficiency in AVP (compared to an absolute deficiency)?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

This is known as partial CDI
Persistent hyposthenuria and severe diuresis as long as there is unlimited water access
USG can increase into the isosthenuric range (1.008 - 1.015) with water restriction but cannot generally concentrate above 1.015 - 1.020 (even with severe dehydration)

53
Q

What is the relationship between AVP and USG in patients with partial CDI?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Maximum USG in periods of dehydration is inversely related to the severity of the deficiency in AVP secretion

54
Q

What us the pathophysiology of CDI?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

This requires destruction of AVP production sites (the supraoptic or paraventricular nuclei of the hypothalamus) and/or the major ducts (axons) that carry AVP to the axon terminals in the posterior pituitary (neurohypophysis)

55
Q

What is the aetiology of CDI?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

It can result from any condition that damages the neurohypophyseal system
D: Hypothalamic pituitary malformation
A: Cysts
N: Neoplasia
I: Idiopathic (most common),Inflammation, Parasite migration, Transsphenoidal hypophysectomy
T: Head trauma

56
Q

What is the common signalment for the development of CDI?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Appears at any age in any breed of any gender

57
Q

Trauma induced transection of the pituitary stalk often results in transient CDI. What affects the duration of CDI in this circumstance?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Duration depends on the location of the transection of the hypophyseal stalk relative to the hypothalamus. Transections more proximally (closer to the median eminence) results in a longer duration because it is associated with a longer time frame for the hypothalamic axons to undergo regeneration and begin secreting AVP again.

58
Q

When should trauma induced CDI be suspected?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. When severe polydipsia and polyuria develop within 48 hours of head trauma
  2. When hypernatraemia, hyposthenuria, and hypertonic dehydration develop in a traumatised patient being treated with IV fluids
59
Q

Transient or permanent DI is a common result of transsphenoidal hypophysectomy performed for the treatment of pituitary dependent hyperA in dogs. What are the statistics cited in this chapter for this outcome?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

One study evaluating 127 dogs with pituitary dependent hyperA
1. Postoperative CDI was transient in 78% of dogs with DDAVP discontinued 2 weeks after surgery in 47% and eventually discontinued in 31% (THESE NUMBERS DO NOT MAKE SENSE TO ME > LOOK UP ORIGINAL ARTICLE)
2. CDI was present until death or final follow up in 22% of dogs

60
Q

Neoplastic destruction of the magnocellular neurons may cause CDI. What percentage destruction must occur for DI symptoms to become apparent?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

90% of the magnocellular neurons must be destroyed

61
Q

In one study, what influence the incidence of postoperative permanent CDI in dogs undergoing transsphenoidal surgery for hyperA?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Occurence was strongly influenced by the size of the tumour; larger tumour = more likely

62
Q

Does CDI have a hereditary component?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Though it is well established in puppies and kittens, a hereditary link has not been documented

63
Q

Define NDI

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Nephrogenic diabetes insipidus
This is a polyuric disorder that results from impaired responsiveness of the nephron to the actions of AVP

64
Q

Describe the general concentrations of plasma AVP in cases of NDI

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Plasma AVP concentrations are normal or increased in NDI

65
Q

How would you establish a diagnosis of congenital NDI?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Findings of high plasma AVP concentrations in the presence of hypotonic polyuria and a lack of responsiveness to DDAVP

66
Q

How common is primary NDI in cats and dogs?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

It is rare. There have only been a few reports in the dog and none in the cat

67
Q

Familia NDI has been reported in a family of Huskies. What was the underlying mechanism for the disease in this case?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

The affected puppies had normal V2 receptor numbers, but there was a tenfold decrease in their binding affinity for AVP

68
Q

When can primary NDI be considered as a differential diagnosis in older patients?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Only when polyuria and polydipsia has been present for the animals entire life

69
Q

Define primary polydipsia

Chapter 1: Textbook of Canine and Feline Endocrinology

A

(Compulsive water consumption) Syndrome characterised by ingestion of excess water. It results in compensatory polyuria to prevent water intoxication

70
Q

What is the aeitology of primary polydipsia in the dog and cat?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

There appears to be a psychogenic basis in dogs (this is uncommon). This has not been reported in cats.
Hypothalamic lesions affecting the thirst centre have not been documented in dogs or cats

71
Q

Describe the urine concentrating ability if dogs with primary polydipsia

Chapter 1: Textbook of Canine and Feline Endocrinology

A

Urine concentration can exceed 1.030 during water deprivation

72
Q

Why might it take a prolonged period for dogs with primary polydipsia to show an increase in USG during water deprivation?

Chapter 1: Textbook of Canine and Feline Endocrinology

A

This is because primary polydipsia results in concurrent renal medullary solute washout

73
Q

What does the identification of concentrated urine imply about the mechanism of action of AVP?

Chapter 1: Textbook of Canine and Feline Endocrinology

A
  1. Hypothalamic AVP production
  2. Pituitary AVP secretion
  3. Renal tubular responsiveness to AVP
74
Q
A
75
Q
A

Endocrine Disease Part 1 (3 decks)

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