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CS endocrinology > PU/PD > Flashcards

PU/PD Flashcards

1
Q

Define PU/PD

A

PU - >50ml/kg/day

PD - >100 ml/kg/day

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2
Q

Pathophysiology osmotic diuresis

A

Osmotically active particles in the urine

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3
Q

Causes of osmotic diuresis (5)

A 
Diabetes mellitus
Renal glycosuria
Mannitol
CKD (decreased reabsorption of osmotically active substrates e.g. urea)
Post obstruction diuresis
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4
Q

Pathophysiology diabetes insipidus (3)

A

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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5
Q

Causes of secondary nephrogenic diabetes insipidus (9)

A 
Bacterial endotoxins (E.coli)
Hypokalaemia
Hypercalcaemia
Primary hyperaldosteronism
Hyperadrenocorticsm
Hypoadrenocorticism
Polycythaemia
Hyperthryoidism
Hepatic insufficiency
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6
Q

4 possible pathophysiologic mechanisms for polydipsia with hepatic insufficiency

A

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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7
Q

Pathophysiology polydipsia secondary to hypercalcaemia (4)

A

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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8
Q

Pathophysiology polydipsia secondary to hyperadrenocorticism (3)

A

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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9
Q

Primary hypoaldosteronism pathophysiology for polydipsia (2)

A

1) mineralcorticoid induced resistance to ADH

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

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10
Q

Pathophysiology polydipsia and hypoadrenocorticism (2)

A

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

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11
Q

Pathophysiology polydipsia and hyperthyroidism

A

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

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12
Q

Pathophysiology polydipsia and polycythaemia

A

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

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13
Q

Pathophysiology polydipsia with phaeochromocytoma, SIADH, AKI

A

Increased intravascular volume/pressure

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14
Q

Conditions associated with primary polydipsia (4)

A

Idiopathic, hyperthryoidism, liver insuffificiency, GIT disease

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15
Q

Define primary polydipsia

A

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

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16
Q

Diagnostic tests for primary hyperaldosteronism

A

Electrolytes, blood pressure, baseline aldosterone, plasma renin activity

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17
Q

Drugs associated with PU/PD (name 5)

A

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

18
Q

DDX (broad groups) polydipsia (6)

A

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

19
Q

Paraneoplastic causes of polydipsia (2)

A

Leimyosarcoma, splenic mass

20
Q

Osmolality with primary polydipsia

A

Low - dilutional effect of increased water intake

21
Q

Breed reported to have primary central DI (4)

A

Afghan hound littermates

Reported in LR, Boxer and GSD

22
Q

Breed reported to have primary nephrogenic DI (3)

A

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

23
Q

Causes of CDI (5)

A

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

24
Q

Phases of modified water deprivation test (2)

A

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.

25
Q

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

A

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.

26
Q

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

A

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

27
Q

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

A

If safe to do so prior to IVFT:

1) empty bladder - USG and urine osmolality
2) Serum - electrolytes, BUN and vasopressin concentrations

28
Q

What is isotonic dehydration

A

ECF water and electrolyte loss isosmotic (295 mOsm/kg) to total body water

No fluid shift

29
Q

What is hypotonic dehydration

A

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

ECF fluid flows to ICF

30
Q

What is hypertonic dehydration

A

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

ICF fluid to ECF

31
Q

Causes of hypernatraemia (3)

A

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)

32
Q

Urine osmolality after modified water deprevation test in CDI, NDI, primary polydipsia

Initial urine osmolality, after dehydration, after vasopressin

A

CDI - reduced, no change, increase

NDI - reduced, no change, no change

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

33
Q

Stimulus for AVP release

A

Increase plasma osomolality (1%) - osmoreceptors

10-15% decrease blood volume/pressre - loss of inhibitory input from baroreceptors

Angiotensin II

34
Q

AVP receptors (4) - location

A

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

35
Q

Role of V1a receptors (3)

A

Arterioles - Vasoconstriction
Liver - glycogenolysis
Platelets - platelet aggregation

36
Q

Role of V1b receptors

A

Pituritary - ACTH secretion

37
Q

Role of V2 receptors

A

Principle cells - increase aquaporin 2 vesicles to apical membranes&raquo_space; enhanced permeability and water resoprtion

Vascular endothelium - vWF release and increase ANP

38
Q

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

A

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

39
Q

Treatment of NDI

A

Thiazide diruretics
Decrease sodium in diet
NSAIDs have synergistic effect

40
Q

MOA Thiazide diuretics for treatment of NDI

A

1) decrease Na absoprtion from ascending loop of henle&raquo_space; contraction ECF
2) decreased GFR&raquo_space; 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

CS endocrinology (4 decks)

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