PU/PD Flashcards by C Sealion

Define PU/PD

PU - >50ml/kg/day

PD - >100 ml/kg/day

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Pathophysiology osmotic diuresis

Osmotically active particles in the urine

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Causes of osmotic diuresis (5)

Diabetes mellitus
Renal glycosuria
Mannitol
CKD (decreased reabsorption of osmotically active substrates e.g. urea)
Post obstruction diuresis

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Pathophysiology diabetes insipidus (3)

1) Central - lack of ADH production
2) Primary nephrogenic - lack of ADH receptors
3) Secondary nephrogenic - interference normal interaction ADH and ADH receptors in renal tubule –> loss of hypertonic renal medullary gradient

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Causes of secondary nephrogenic diabetes insipidus (9)

Bacterial endotoxins (E.coli)
Hypokalaemia
Hypercalcaemia
Primary hyperaldosteronism
Hyperadrenocorticsm
Hypoadrenocorticism
Polycythaemia
Hyperthryoidism
Hepatic insufficiency

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4 possible pathophysiologic mechanisms for polydipsia with hepatic insufficiency

1) Loss of medullary tonicity due to impaired production of urea or altered renal blood flow
2) Increased GFR and ultrafiltrate volume
3) hypokalaemia
4) Impaired metabolism of cortisol

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Pathophysiology polydipsia secondary to hypercalcaemia (4)

1) Downregulation of aquaporin 2 water channels
2) Inhibitied binding with ADH receptors
3) Inactivation adenyl cyclase
4) Reduced transport Na and Cl in the renal medullar interstitium

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Pathophysiology polydipsia secondary to hyperadrenocorticism (3)

1) Reduced ADH release (increase osmotic threshold, decreased sensitivity to ADH response increasing osmolality)
2) Increased GFR
3) Interfere ADH action at level if renal tubules/interfere with renal tubular permeability to water

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Primary hypoaldosteronism pathophysiology for polydipsia (2)

1) mineralcorticoid induced resistance to ADH

2) hypokalaemia associated with reduction aquaporin-2 channels and urea transporters

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Pathophysiology polydipsia and hypoadrenocorticism (2)

1) Mineralcorticoid deficiency –> chronic sodium wasting and renal medullary washout –> loss of renal medullar hypertonic gradient
2) +/- effects of hypercalcaemia

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Pathophysiology polydipsia and hyperthyroidism

1) increased renal blood blow may decrease medullary hypertonicity and impair water resoprtion from distal portion of the nephron

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Pathophysiology polydipsia and polycythaemia

Increased osmostic threhold to ADH, likely secondary to increased blood volume which stimulates AND and barore receptors

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Pathophysiology polydipsia with phaeochromocytoma, SIADH, AKI

Increased intravascular volume/pressure

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Conditions associated with primary polydipsia (4)

Idiopathic, hyperthryoidism, liver insuffificiency, GIT disease

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Define primary polydipsia

Marked increase in water intake, not due to compensatiory mechanisms for excessive fluid loss

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Diagnostic tests for primary hyperaldosteronism

Electrolytes, blood pressure, baseline aldosterone, plasma renin activity

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Drugs associated with PU/PD (name 5)

Phenobarbital, diuretics, coritcosteroids, sodium bicarbonate, vitamin D toxicity

DDX (broad groups) polydipsia (6)

Osmotic diuresis, primary central DI, primary nephrogenic DI, Secondary DI, increased plasma volume/pressure, iatrogenic, paraneoplastic

Paraneoplastic causes of polydipsia (2)

Leimyosarcoma, splenic mass

Osmolality with primary polydipsia

Low - dilutional effect of increased water intake

Breed reported to have primary central DI (4)

Afghan hound littermates

Reported in LR, Boxer and GSD

Breed reported to have primary nephrogenic DI (3)

Siberian Husky (litter) - altered aquaporin-2 expression
GSD (13 wk)
Minature poodle *18 mo)

Causes of CDI (5)

1) Idiopathic
2) Head trauma
3) Neoplasia (meningioma, adenoma, mets)
4) Transphenoidal hypophysectomy
5) Cysts

Phases of modified water deprivation test (2)

Phase I - AVP secretory capabilities and renal distal tubules responsiveness to AVP are evaluated by assessing effects of deydration (water restriction till 3% bwt loss) USG should be >1.030/1.035 in normal dog/cat

Phase II - Determines effects of exogenous AVP has on renal tubular concentrating ability in the face of dehydration. Differentiates impaired secretion from impaired responsiveness.

Responses to Modified water deprevation test - how to differentiate between normal, complete CDI, partial CDI and nephrogenic DI.

Normal dogs - 24 hours to dehydrate. urine osmolatity >1100 uOsm and USG >1.030 after dehydration, suggesting AVP secretion and responsiveness is intact. Complete CDI - can not concentrate urine to greater than plama osmolality (280-310 mOsm/kg) even when dehydrated. 50-600% increase in osmolality follwoing administration AVP. Partial CDI - urine osmolality >300 mOsm/kg after dehydration and further 10-50% increase follwoing vasopressin administration. Nephrogenic DI - can not concentrate urine to greater than plasma osmolality (280-310 mOsm/kg) and there is minimal increase in urine osmolality and USG follwoing vasporessin injection.

USG complete CDI, partial CDI, primary NDI and primary polydipsia initially, after 5% dehydrtation and post ADH

Complete CDI - <1.006, <1.006, >1.010 Partial CDI - <1.006, 1.008-1.020, >1.015 Primary NDI - <1.006, <1.006, <1.006 Primary polydipsia - 1.1002-1.020, >1.030, NA

Approach to polydipsic dog with dehydration (e.g. owner withheld water)

If safe to do so prior to IVFT: 1) empty bladder - USG and urine osmolality 2) Serum - electrolytes, BUN and vasopressin concentrations

What is isotonic dehydration

ECF water and electrolyte loss isosmotic (295 mOsm/kg) to total body water No fluid shift

What is hypotonic dehydration

ECF loss of water and electrolytes is hyperosmotic (>310 mOsm/kg) to total body water. ECF fluid flows to ICF

What is hypertonic dehydration

ECF loss of water and electrolytes hyposomotic (<280 mOsm/kg) to the total body water ICF fluid to ECF

Causes of hypernatraemia (3)

1) Pure water loss - CDI, NDI 2) Hypotonic fluid loss - GI fluid loss, CKD, polyuric AKI 3) Excess sodium retention - primary hyperaldosteronism, Itarogenic (sodium bicarb/sodium phosphate enema)

Urine osmolality after modified water deprevation test in CDI, NDI, primary polydipsia Initial urine osmolality, after dehydration, after vasopressin

CDI - reduced, no change, increase NDI - reduced, no change, no change Primary polydipsia - reduced, increase, no change/ mild increase

Stimulus for AVP release

Increase plasma osomolality (1%) - osmoreceptors 10-15% decrease blood volume/pressre - loss of inhibitory input from baroreceptors Angiotensin II

AVP receptors (4) - location

V1b - anterior pituritary V1a - arterioles, liver and platelets V2 - basolateral membrane of principle cell, vascular endothelium

Role of V1a receptors (3)

Arterioles - Vasoconstriction Liver - glycogenolysis Platelets - platelet aggregation

Role of V1b receptors

Pituritary - ACTH secretion

Role of V2 receptors

Principle cells - increase aquaporin 2 vesicles to apical membranes >> enhanced permeability and water resoprtion Vascular endothelium - vWF release and increase ANP

Movement of water in the distal renal tubules in response to AVP

Increased permeability results in passive movement of water from low osmolality tublar lumen through the aquaporin 2 channels and exiting aquaporin 3 and 4 channels to the high osmolarity medullay interstitium and into circulation

Treatment of NDI

Thiazide diruretics Decrease sodium in diet NSAIDs have synergistic effect

MOA Thiazide diuretics for treatment of NDI

1) decrease Na absoprtion from ascending loop of henle >> contraction ECF 2) decreased GFR >> increase sodium and water resoprtion in proximal tubule 3) decreased water to distal tubule and decreased water loss Also upregulation of aquaporin 2 channels and distal sodium transport expression