27 – Polyuria and Polydipsia Flashcards
1
Q
Water homeostasis: hormones
A
- ADH
- Aldosterone
- Need normal secretion in response to appropriate stimuli
- Must have normal renal tubular sensitivity to ADH
- Normal thirst mechanism
- *need medullary concentrating gradient (urea/NH4 recycling and NaCl)
2
Q
ADH synthesis
A
- Synthesized by hypothalamus
- Secreted by posterior pituitary
- Regulated by osmotic and volume stimuli
o Dehydration INCREASES osmolality which ACTIVATES hypothalamic osmoreceptors
o Hypovolemia or low BP=STIMULATES ADH release
3
Q
What are the actions of ADH?
A
- In states of hypovolemia, ADH is secreted even if patient is hypoosmotic
- Reduces free-water clearance by kidney
- If NO ADH: water channels are withdrawn and free water CLEARANCE INCREASES
4
Q
ADH measurement
A
- Do NOT measure it
- *Measure copeptin as a surrogate marker
5
Q
Aldosterone and thirst
A
- Thirst center in hypothalamus is stimulated by decline in plasma volume (10-15%)
o Increase in plasma osmolality (1-2%) - Aldosterone: sustain extracellular fluid volume by conserving body sodium
o Produced by adrenal cortex: RAAS activation (zona glomerulosa)
6
Q
Polyuria and polydipsia
A
- Common problem in SA medicine
- MUST occur together or the animal will DIET from OVERHYDRATION or DEHYDRATION
- Water intake is affected by many things: diet, exercise, environmental temperature, interindividual differences in osmolality set points
7
Q
EXAMPolyuria: values
A
- Increased volume of urination: >2ml/kg/hr
- Ex. 20kg dog: expect at least 40mL urine per hour
8
Q
EXAMPolydipsia: values
A
- > 100mls/kg/day for dog
- > 45ml/kg/day for cat
9
Q
For PU and PD to be a real problem, what do you need to see?
A
- Reliable history or evidence of PU/PD
- Persistently low USG (exception: DM)
o One time low USG is NOT meaningful in an otherwise healthy animal or animal w/o clinical signs of PU/PD
o Cats with diabetes do NOT have dilute urine b/c ADH works and they produce a lot of it - Take into consideration age of the animal, species, diet and medications
10
Q
Isothenuria
A
- USG fixed and between 1.008-1.015
11
Q
Hyposthenuria
A
- USG <1.008
o Does NOT suggest renal failure
o Production of dilute urine is an ACTIVE process performed by renal tubules
12
Q
Hypersthenuria
A
- USG >1.015 but less than threshold values we expect with any degree of dehydration
13
Q
What are the 2 broad categories that PU/PD can be divided into?
A
- Primary polydipsia with compensatory polyuria
- *primary polyuria with compensatory polydipsia=MOST COMMON
**some patients can have BOTH
14
Q
Primary polydipsia with compensatory polyuria
A
- Primary (idiopathic): psychogenic polydipsia
- Secondary polydipsia
a. Fever
b. Pain
c. Overactive thirst center
15
Q
Primary polyuria with compensatory polydipsia: categorization based on mechanism responsible
A
- Lack of production or secretion of ADH: central diabetes insipidus (primary or secondary)
- Renal insensitivity to ADH: nephrogenic diabetes insipidus (primary or secondary)
- Osmotic diuresis
- Disorders associated with renal medullary washout
a. ALWAYS RULE OUT FIRST
16
Q
What are 4 organ systems to consider with polyuria and polydipsia?
A
- Liver: urea, psychogenic
- CNS: hypothalamus, pituitary, cerebral cortex
- Endocrine: pituitary, adrenal glands, pancreas, thyroid, paraneoplastic
- Renal: medullary concentrating gradient, tubular response to ADH and aldosterone, nephron number
17
Q
“CLAMPED RIBS’ (acronym)
A
- Calcium
- Liver insufficiency/disease
- Metabolic: including electrolytes
- Psychogenic, polycythemia, pyelonephritis, pyometra
- Endocrine: hyperadrenocorticism, acromegaly
- Drugs, DM, diabetes insipidus
- Renal insufficiency/failure
- Infection
- Brain
- Salty treats, salty diets
18
Q
Central diabetes insipidus: what is it? What are the causes?
A
- *lack of production of ADH
- Causes
o Primary or metastatic CNS disease
o Infection: sepsis
o *idiopathic (MOST COMMON)
o Granulomatous disease
o Trauma
o Iatrogenic
o High set osmoreceptors
19
Q
Nephrogenic diabetes insipidus
A
- Primary: congenital (RARE)
- Secondary: acquired
o “HOG IN YARD pneumonic
20
Q
HOG IN YARD (nephrogenic diabetes insipidus causes)
A
- Hyper PTH
- Osteomyelitis
- Granulomatous disease
- Idiopathic: cats
- Neoplasia
- Youth/spurious
- **Addison’s
- Renal disease
- D: Vit D toxicosis
21
Q
Medullary washout
A
- Osmotic diuresis
o Probably plays a role in most animals with PU/PD - CRF: not enough nephrons left
- Diabetes mellitus: (USG not that low in cats)
- Diuretic therapy (post obstructive diuresis)
22
Q
Polydipsia types
A
- Idiopathic
- Secondary
o Fever
o Pain
o CNS neoplasia
o Encephalopathies
o GI disease
o Liver disease
23
Q
What are the most common causes of PU/PD in dogs?
A
- CRF
- Hyperadrenocorticism
- DM
- pyometra
24
Q
What are the most common causes of PU/PD in cats?
A
- CRF
- Hyperthyroidism
- DM
25
PU/PD diagnostic approach
- Signalment may provide a clue
- Get a complete history and PE
o Don’t confuse with pollakiuria and incontinence
- Rule out pharmacologic causes
- Minimum data base
- Rule out endocrine diseases
- Imaging
- Perform modified water deprivation test in 3 stages
- GFR determination if renal insufficiency suspected
26
Minimum database (PU/PD diagnostic approach)
- Helps screen for DM, renal disease, liver disease, pyelonephritis, sepsis, hypercalcemia, hyper and hypoadrenocorticism
- SDMA or GFR measurement for renal insufficiency
- Collect multiple UAs
- Psychogenic PD diagnosed by production of concentrated urine on at least some occasions
- USG to help differentiate if something wrong with the kidneys
27
What test can you use to differentiate idiopathic diabetes insipidus from psychogenic polydipsia?
- Modified water deprivation test (MWDT)
28
MWDT
- Typically do last when have failed to find a cause with more practical diagnostic test
- Primary polydipsia: will be able to concentrate urine after the first 2 stages
- Central DI or nephrogenic DI: will NOT be able to concentrate urine
29
How can you use MWDT to also differentiate between central DI and nephrogenic DI?
- give vasopressin in stage III
o central DI=expect a response=USG will increase
o nephrogenic DI=expect NO response=USG will NOT increase
30
What are the contraindications to the MWDT?
- Never perform if dehydrated, sick, hypercalcemic or azotemic
- ONLY perform when all common causes ruled out
- *read the protocol
31
What are some issues with the MWDT?
- Not great at differentiating partial forms of DI from primary polydipsia and ADH resistance in some primary polydipsia patients
32
What is the ‘protocol’ for MWDT in a nutshell?
- Phase I: gradually reduce water intake several days prior to test
o 100mL/kg/d over 2-5 days
- Phase II: hospitalization required for water restriction
o Water restriction > dehydration/hyperosmolarity > release of ADH > concentrated urine produced
o Primary polydipsia if concentration occurs after first phase (partial CDI and PNDI are still possible)
33
What are some alternatives to the MWDT?
- DDAVP trial
o Give it at least 2 weeks
o Needs time to re-establish medullary concentrating gradient
o Expect response with CDI but not with NDI
- ADH measurement with hypertonic saline infusion
- Future:
o Copeptin with and w/o a WDT or saline infusion
o Stimulation test with ADH or copeptin measurement
34
What is diabetes insipidus characterized by?
- *PU/PD
- *Hyposthenuria (USG<1.008)
- Onset of signs are more commonly abrupt
- If due to a CNS mass lesion
o Signs associated with deficiency of other hypothalamic/pituitary hormones
o Neurological signs
- If congenital: signs by 8-12 weeks
35
What might be seen with idiopathic forms of diabetes insipidus?
- CBC, biochem and UA profile normal other than low USG and maybe low to normal urea
36
What might be seen if water is restricted to a patient with diabetes insipidus?
- Erythrocytosis
- Hypernatremia
o *due to thirst centre abnormality could lead to adipsia and we might see a DANGEROUS hypernatremia
- Hyperproteinemia
- Azotemia
37
How might plasma osmolarity provide a clue in patients with diabetes insipidus?
- High in CDI: result of dehydration
- Low in animals with primary polydipsia: result of overhydration
38
Advanced imaging for diabetes insipidus
- MRI to look for intracranial causes or findings suggestive of diabetes insipidus
o Thickening of infundibular stalk
o Loss of normal T1 posterior pituitary bright spot (PPBS)
o *T1 PPBS seen in NORMAL dogs and depletion seen with hypertonic saline infusion
39
How can central DI (idiopathic) be treated?
- Long acting ADH analogue (DDAVP: desmopressin)=expensive
o Topical, oral and injectable forms: titrate to effect (BID or TID)
o Typically continued for life unless it’s a post-operative condition
40
How can nephrogenic DI be treatment?
- Need to ID and treat underlying disease
- *continuous water supply (at risk of severe dehydration)
- If no underlying causes: try administration of THIAZIDE
o Paradoxical reduction in urine volume (increases reabsorption of Na and water)
o Helpful in 50% of patients
o Some cases will response to very high disease of DDAVP
41
Psychogenic polydipsia
- Compulsive drinking
- Boredom in young large breed dogs (also some cases in cats)
- GI disease in dogs: maybe due to pain
- Treatment options limited
o Behaviour modification or medications, water restriction with monitoring (avoid DDAVP as it could lead to dilutional hyponatremia)
- Treatment of dilution natremia may be needed
o If acute/sub acute time frame or symptomatic: 3% saline infusion bolus to reduce risk of herniation from cerebral edema
