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PU/PD Flashcards

1
Q

Polydipsia definition

A
  • Drinking more than 100 mLs/kg/day (grey zone is 50-100 mgs/kg/day)
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2
Q

Polyuria definition

A
  • producing more than 50 mLs/kg/day of urine
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3
Q

Where is antidiuretic hormone produced and released?

A
  • Produced by the hypothalamus

- Released by the posterior pituitary

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4
Q

What two things control water balance in the body?

A
  • Osmolarity of plasma

- Circulating volume

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5
Q

What happens with osmolarity is increased?

A
  • Thirst is stimulated

- ADH is produced

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6
Q

ADH action

A
  • Works on the collecting tubules and duct of the kidney to increase
  • Stimulates formation of aquaporins to move water into the renal medullary interstitium
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7
Q

How much of water filtered by the kidneys is reabsorbed?

A

> 99%

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8
Q

Kidneys and water balance during state of dehydration

A
  • Can produce urine 7-8x the osmolality of plasma
  • Plasma is 300 mOsm/L
  • Concentrated urine is >2000 mOsm/L
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9
Q

Hypersthenuria urine concentration in dogs and cats

A
  • Dog: >1.030

- Cat: >1.035 (closer to >1.050)

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10
Q

Isosthenuria urine concentration

A

1.008-1.012

But definitely be considering it still if USG is <1.017

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11
Q

Hyposthenuria urine concentration

A
  • <1.008
  • A little bit of a gray zone but <1.008 usually
  • Resorption of solute > water
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12
Q

Gray zone of being minimally concentrated

A
  • 1.012-1.030
  • 1.030 is more of a cat thing
  • 1.020 is more of a dog thing
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13
Q

When is isothenuria appropriate?

A
  • If the patient needs to excrete water

- Primary polydipsia

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14
Q

What type of urine should a dehydrated patient have?

A
  • Concentrated urine
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15
Q

DfDx for PU/PD (I don’t think we need to memorize this…yet)

A
  1. Diabetes mellitus
  2. Hyperthyroidism
  3. Hyperadrenocorticism
  4. Hypoadrenocorticism
  5. Acromegaly
  6. Primary hyperaldosteronism
  7. Diabetes insipidus - central
  8. Diabetes insipidus - nephrogenic
  9. Pheochromocytoma
  10. Hypercalcemia
  11. Neoplastic (intestinal leiomyosarcoma)
  12. Pyometra
  13. E. coli infections (urinary, sepsis)
  14. Hepatic disease
  15. Fanconi’s Syndrome
  16. Renal disease
  17. Hyperviscosity syndrome
  18. Polycythemia
  19. Post-obstructive diuresis
  20. Pyelonephritis
  21. Hypokalemia
  22. Hyponatremia
  23. Drugs (steroids, diuretics, anticonvulsants
  24. Psychogenic polydipsia
  25. Pain, heat, stress
  26. Hyperthermia
  27. Very low protein diets
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16
Q

Which diseases antagonize ADH to cause PU/PD?

A
  • Cushing’s
  • Primary Hyperaldosteronism
  • Pheochromocytoma
  • Hypercalcemia
  • Neoplasia
  • Pyometra/endotoxemia
  • Hyperviscosity/endotoxemia
  • Polycythemia
  • Hypokalemia
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17
Q

Which diseases cause a loss of medullary gradient/osmotic diuresis to cause PU/PD?

A
  • Diabetes mellitus
  • Addison’s (losing so much sodium)
  • Acromegaly
  • Pyometra/endotoxemia
  • Hepatic disease
  • Fanconi’s
  • Renal failure
  • Post-obstructive diuresis
  • Pyelonephritis
  • Hyponatremia
  • Low protein diet
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18
Q

Diseases with other or unclear causes of PU/PD

A
  • Hyperthyroidism
  • Psychogenic
  • Pain, heat, stress
  • Hyperthermia
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19
Q

Mechanism of PU/PD in Diabetes mellitus

A
  • Glucose in urine causes osmotic diuresis leading to hypovolemia thus stimulating drinking
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20
Q

Mechanism of PU/PD in hyperthyroidism

A
  • unclear

- Decrease medullary tonicity due to increased blood flow, psychogenic, concurrent renal insufficiency

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21
Q

Mechanism of PU/PD in Cushing’s

A
  • glucocorticoids inhibit ADH release and renal response to ADH
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22
Q

Mechanism of PU/PD in Addison’s

A
  • Mineralocorticoid deficiency causes chronic Na wasting, loss of medullary gradient
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23
Q

Mechanism of PU/PD in acromegaly

A
  • Due to concurrent DM; glomerulonephropathy from Dr or excess GH
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24
Q

Mechanism of PU/PD in Primary hyperaldosteronism

A
  • Unclear
  • ADH resistance
  • Hypokalemia
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25
Mechanism of PU/PD in pheochromocytoma
- catecholamine induced inhibition of ADH release and renal ADH response
26
Mechanism of PU/PD in hypercalcemia
- Downregulation of aquaporin water channels and ADH inhibition
27
Mechanism of PU/PD in Neoplasia
- Paraneopalstic nephrogenic diabetes insipidus
28
Mechanism of PU/PD in pyometra/bacterial infections
- Bacterial (E. coli) endotoxin production competes with ADH at renal receptors, damages renal receptors, inactivation of adenylate cyclase, decrease Na and Cl transport into renal medullary interstitium
29
Mechanism of PU/PD in Hepatic disease (PSS)
- Unknown | - Loss of medullary gradient due to impaired urea nitrogen production
30
Mechanism of PU/PD in Fanconi's syndrome
- Renal glucosuria causing osmotic diuresis
31
Mechanism of PU/PD in renal disease
- nephron dysfunction and compensatory increases in GFR to surviving nephrons - Increased tubular fluid volume, decreased absorption of solutes leading to an osmotic diuresis and loss of medullary gradient
32
Mechanism of PU/PD in hyperviscosity syndrome/polycythemia
- increased blood volume and viscosity trigger release of atrial natriuretic peptide (ANP) secretion and stimulate baroreceptors - ANP inhibits ADH release
33
Mechanism of PU/PD in post-obstructive diuresis
- Osmotic diuresis
34
Mechanism of PU/PD in pyelonephritis
- Destruction of countercurrent mechanisms and loss of medullary gradient; endotoxemia
35
Mechanism of PU/PD in hypokalemia
- Decreased renal ADH response, loss of medullary gradient
36
Mechanism of PU/PD in Hyponatremia
- Loss of medullary gradient
37
Mechanism of PU/PD in psychogenic PD
- Primary polydipsia resulting in pecondary polyuria
38
Mechanism of PU/PD in pain, heat, stress, hyperthermia
- Polydipsia resulting in secondary polyuria
39
Mechanism of PU/PD in very low protein diet
- Decreased urea nitrogen and resulting loss of medullary gradient
40
Diabetes insipidus overview
- Both a secondary condition and a primary disease - Includes all alterations in ADH production and functionality - Includes all of the PU/PD dfdx that affect ADH
41
Central DI
- ADH not being made
42
Nephrogenic DI
- Kidneys are not responding to ADH | - Receptors are not present or not responsive
43
Central diabetes insipidus
- Partial or complete deficiency of ADH - Results in decreased ability or inability of the kidneys to conserve water and concentrate urine in response to increases in plasma osmolality - Polyuria causes increased plasma osmolality because fluid is lost in excess of solute - Increased osmolality stimulates thirst (polydipsia)
44
How common is central DI?
- Super rare
45
USG in Central DI
- USG is hyposthenuric, unless it's partial | - if partial can be isosthenuric
46
Causes o fCentral DI
- Congenital, acquired, idiopathic - Surgery, trauma, neoplasia - e.g. pituitary surgery
47
Nephrogenic DI
- Lack of or impaired renal tubular responsiveness to ADH | - Primary or secondary
48
Primary nephrogenic DI
- Congenital defect in the nephron - Mutation in ADH receptor or aquaporin - RARE - Hyposthenuric
49
Secondary nephrogenic DI
- MORE COMMON - Causes are any conditions that affect ADH binding and function in the renal tubules, causing loss of medullary gradient, or causing osmotic diuresis
50
Approach to PU/PD
- Confirm it's occurring - Perform simple, high yield tests first - Rule out causes of secondary NDI - Then...and only then...consider CDI or primary NDI
51
How to confirm PU/PD?
- Water intake - USG (first urination of the day) - If you measure USG in the morning try to find out if the animal is drinking at night
52
Clues for underlying cause of PU/PD
- Look for clues based on patient history, PE, diet, drug history - Basic lab work - Ultrasound - Evaluate for infection - Additional endocrine testing - Additional organ testing
53
Basic lab work screening
- Evaluate PCV, protein levels, electrolytes, calcium (iCa), renal values, liver values, glucosuria, pyuria, bacteriuria
54
Ultrasound
- Look for pyelonephritis, pyometra, hepatic, renal, endocrine, neoplasia
55
Infectious disease evaluation
- Cultures, Lepto serology
56
Additional endocrine testing
- LDDS, ACTH stim, thyroid levels (if cat)
57
Additional organ function testing for PU/PD
- Bile acids | - GFR study
58
Further possible clues for PU/PD
- Liver aspirate or biopsy, lymph node aspirates, bone marrow biopsy, etc.
59
If all of your testing is normal but you still have PU/PD, now what?
- Left with psychogenic vs primary DI
60
How to assess for Diabetes insipidus?
- Modified water deprivation test - DDAVP response - Remember that CDI or primary NDI is rare - Psychogenic is MUCH MORE likely
61
Serum osmolality testing CDI vs psychogenic
- With CDI should be in the high-normal range or above normal (280-320 mOsm/kg) - With psychogenic polydipsia would have a low-normal to below-normal serum osmolality (<275 mOsm/kg) caused by ingestion of water in excess of the kidneys' ability to excrete it appropriately
62
Exogenous DDAVP
- Acts like ADH
63
Exogenous DDAVP Administration Response supportive of DI
- Increase in USG of at least 50% compared with pretreatment USG by day 5 to 7 or a specific gravity >1.030 supports the diagnosis of CDI - May also result in concentrated urine with other disorders (psychogenic polydipsia, hyperadrenocorticism) - You have to have ruled out everything else first
64
Modified water deprivation
- Used to determine whetehr endogenous ADH is appropriately released in response to dehydration and whether the kidneys can appropriately respond to ADH
65
What are drawbacks to modified water deprivation?
- Time consuming and labor intensive - If done wrong, useless (need u cath, adequate staff to perform everything on time, in-house lab machines) - If done wrong, dangerous (YOU CAN KILL PATIENTS).
66
Who is at risk of death in modified water deprivation?
- Hypernatremia, hyperosmolar, azotemia - They keep urinating because they can't stop - Then you give them no water - May be inhumane - Monitor closely
67
Modified Water Deprivation Test procedures
1. Gradually limit water intake over 3-5 days (dangerous) 2. Then hospitalize and remove water completely. Monitor weight, PCV, TP, BUN, Na every 1-2 hours. If no concentration is reached, move to the next step. 3. Give DAVP and monitor urine USG or urine osmolality. Offer small amounts of water 2 hours after administration. CDI is diagnosed when USG or urine osmolality increases by 50% or more.
68
Endpoint of water deprivation
- 5% dehydration of USG >1.025 | - Either they have functional receptors and can produce
69
How not to do a water deprivation test?
- Take away water overnight then check a morning urine - Take water away from the dog in hospital and just check a USG at the end of the day - Start a modified water deprivation test without first gradually limiting water consumption for several days
70
Treatment for Acquired NDI
- Address the underlying cause!
71
Treatment for Central Diabetes insipidus
- Lifelong therapy! - DDAVP (Desmopressin) - Oral or nasal formulation, given as an eye drop or SC. - Very expensive
72
Treatment for congenital Nephrogenic Diabetes insipidus
- Low-sodium diet - Thiazide diuretics - Free-choice water with NO RESTRICTION - Allow constant access to water - Ensure outside access to prevent accidents in the house
73
Thiazide diuretics and treatment of congenital nephrogenic diabetes insipidus
- Inhibit distal sodium resorption - Causes volume contraction - Increased proximal tubular sodium and water resorption
74
Prognosis of acquired NDI
- Depends on underlying disease
75
Prognosis of Congenital NDI
- good with constant water availability
76
Prognosis of acquired central DI
- Dependent on lesion | - If secondary to trauma, resolves within 2 weeks usually
77
Prognosis of congenital central DI
- Great with treatment
78
Endocrine diseases that do NOT cause PU/PD
- Hypothyroidism - Primary hyperparathyroidism (if not hypercalcemic) - Hypoparathyroidism
79
Endocrine diseases that DO cause PU/PD
- Diabetes mellitus - Hyperthyroidism - Hyperadrenocorticism - Hypoadrenocorticism - Primary hyperaldosteronism - Acromegaly - Diabetes insipidus - Primary hyperparathyroidism (if hypercalcemic)

SA Medicine Endocrine (8 decks)

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