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Endocrine & Diabetes > Body Water Balance & Diabetes Insipidus > Flashcards

Body Water Balance & Diabetes Insipidus Flashcards

1
Q

What is hypo and hypernatraemia (values)?

A

Plasma sodium [Na+] or [Na+]p normal 135-145 mmol/l
=Hypernatraemia [Na+] > 145 mmol/l
=Hyponatraemia [Na+] < 135 mmol/l

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2
Q

What is plasma osmolarity in terms of hyper and hypotonic?

A

Plasma osmolality p normal ~ 282-296mosmol/kg
calculated approximation: p  2x[Na+] + [urea] + [glucose]
hypertonic = hyperosmolar p > 296 (>299 often used)
hypotonic = hyposmolar p < 282

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3
Q

ADH

A

antidiuretic hormone = vasopressin

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4
Q

SIADH

A

syndrome of inappropriate ADH

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5
Q

Polyuria

A

excessive urine volume (>2ml/kg/hr, or 3litres/day)

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6
Q

Polydipsia

A

excessive fluid intake (usual defn by assoc polyuria)

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7
Q

Diabetes insipidus

A
  • deficiency of ADH action, (hypotonic polyuria)

- with inability concentrate urine

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8
Q

Diabetes mellitus

A
  • deficiency of insulin action with raised plasma

glucose which can drive an osmotic diuresis

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9
Q

DDAVP

A

= a synthetic ADH with little pressor activity
= 1-deamino-8-D-arginine vasopressin
=longer half-life

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10
Q

Oedema

A

-Expansion of extracellular spaces with fluid which
collects in dependent areas (ankles, sacral), typical causes are:
=heart failure, liver failure, nephrotic syndrome.
-Usually indicates increase in body water, Na+ and ECF vol.

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11
Q

Why do we need appropriate levels of ADH?

A
  • retain to replace losses
  • excrete sufficient to allow renal function
  • excrete excess water
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12
Q

Describe body water balance

A

-Water used in all cells continuously
-Water lost continuously:
=kidney > 400ml/day
=Normal urine volume 0.6-1.5 litres
=skin, respiration, gut  500ml/day

  • Need to take in water regularly= Thirst
  • Normal intake, adult, temperate climate 0.9 to 2-2.5 litres
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13
Q

Describe how thirst is linked to ADH release

A

-Coordinated in diencephalon, hypothalamus nuclei= supraoptic and paraventricular nuclei, make ADP, trickles down in nerve terminals to posterior pituitary, released to circulation
=Stimulated from osmo sensor, third ventricle
=Thirst centre nearby
=Coordinate with each other for water balance

-Ascending tracts= baroreceptor afferents (blood pressure) and SNA pain afferents
=High level stimulation= change ADH by feeding into system

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14
Q

How does thirst occur?

A
  • Feedback loop
  • If plasma osmolarity rises= thirst= stimulates desire to drink water at higher CNS= decreased plasma osmolarity as plasma fluids diluted= closes off feedback loop
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15
Q

What does thirst require?

A
  • Sufficient alertness

- Access to water

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16
Q

Why is thirst important?

A

•Important when fluid intake has been inadequate
=e.g. high insensible losses (traveller in desert)
=e.g. high GI tract losses ( esp. GI infections)
•Important in high urinary losses (polyuria)
=e.g. untreated diabetes mellitus
=or diabetes insipidus
-Dangerous when thirst is not intact, when intake is inadequate as risk of hypernatraemia

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17
Q

How can we measure thirst?

A
  • Semi quantitatively
  • 10 scale, marking how relatively thirsty they are
  • Can plot how thirst rises with plasma osmolarity
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18
Q

What is loss of thirst?

A
  • Loss of thirst (adipsia) can occur with hypothalamic damage
  • Difficult to treat – often use fixed fluid intake
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19
Q

What are the 2 key mechanisms in regulating body water balance?

A
  • Thirst feedback loop, linear response as thirst rises with plasma osmolarity
  • ADH feedback loop, as plasma osmolarity rises ADH release rises, need to be able to make and release and kidneys need to be responsive (V2 receptors, urine concentrated so water retained) and feedback loop needs to be able to switch off and on
20
Q

What are the causes of polydipsia and polyuria?

A

-Hypothalamus
=Damage to primary stimulation of thirst centre and osmo-sensors, inhibitory or excitatory lesions (primary polydipsia= excess, inadequate= adipsia)
-Pituitary
=Lack of ADH (cranial diabetes insipidus)
-Kidney
=Resistance to ADH (nephrogenic diabetes insipidus)

21
Q

Describe Vasopressin

A

-Short peptide
-Derived from large precursor peptide (pre-pro-vasopressin)
=contains component called neurophysin and c-terminal glycopeptide that are cleaved off during processing
-Moves down axons in vesicles, processing
=Arginine vasopressin, 9 amino acids with cysteine bond, short half-life

22
Q

Where does vasopressin act?

A
  • V1A= maintain blood volume and circulation (role at high AVP)- constrict vessels= much higher levels needed
  • V1B= role in ACTH release and stress response, pituitary
  • V2= cAMP, kidneys, appropriate retention of water, maintain osmolality, vaptan inhibits receptors, very little levels up to 6
  • Low affinity to oxytocin receptors in uterus
23
Q

Where is the actin of vasopressin in the kidneys?

A
  • Distal tubule, final adjustment (second half and whole of collecting ducts)
  • Aquaporin 2 in apical cells, highly sensitive, channel rare when ADH turns off so water permeability drops

=Intermedullary concentration gradient in kidney
=Thick ascending limb sodium chloride channels (pull water out)
=Inner medulla loop of Henle for urea channels

24
Q

What factors affect ADH release?

A 
-Non-osmotic stimuli 
=low BP, pain
-Pressor action
=V1 receptors
-Increased plasma osmolality
25
Q

What are the problems with ADH action?

A

-Problems arise from both:-
=inadequate ADH action (Diabetes Insipidus, DI)
-ADH in excess of needs of water balance
=non-osmotic ADH release
=physiologically appropriate (haemorrhage)
=physiologically inappropriate (SIADH)

26
Q

How is disorders of thirst and ADH linked to natremia?

A

-Thirst= hypernatraemia
-ADH= hyponatraemia
-Effective lower normal p determined by [ADH] low enough for max urine dilution
=Gives water excretion > 15ml/min = > 21L/day
-Effective upper normal p determined by threshold for thirst to drive persistent water seeking
=Occurs when ADH also driving max urine concentration (u>1000mosmol/kg

27
Q

Describe excess water loss

A

-Polyuria - if loss is renal
-Thirsty, “drinking to keep up with output”
-If intake inadequate [Na+] increases, plasma osmolality increases ± BP
=presents as polyuria,
If cannot “drink to keep up” then collapse + confusion

28
Q

Describe excess water retention

A

-Usually little symptoms initially
-Later [Na+] decreases and plasma osmolality decreases
=Confusion, drowsiness, nausea, even fits
=presents as unexplained confusion

29
Q

Describe excessive polyuria

A

excessive = >2ml/kg/hr =70kg person > 3.36 litres
= inappropriately high and causing negative fluid balance
 if > 2 litres when [Na]p > 145mmol/l or persistently thirsty (inc during night)

30
Q

What are the causes of polyuria?

A

(i) Diabetes insipidus (cranial or nephrogenic)
(ii) Habitual/psycogenic polydipsia
(iii) Osmotic diuresis e.g. glucose (diabetes mellitus)
mannitol, hypercalcaemia
(iv) Renal impairment (unusual)

31
Q

How do you investigate polyuria?

A

(1)accurate fluid balance to determine if polyuria >2ml/kg/hr, urine volume high and persistent thirst/ [Na]p>145mmol/l so high
(2)check glucose, Ca2+, urea, creatinine - identify cases of osmotic diuresis or renal impairment, inability to concentrate urine
(3)check urine never normally concentrated
=random urine samples including early morning- less than 600mosmol/kg so dilute
(4) water deprivation test - show if unable to concentrate urine
=p and [Na]p rise as negative water balance
DI if u still < 600mosmol/kg when p >300 mosmol/kg
+/or [Na]p > 145mmol/l
(5) if DI, give DDAVP (1µg im) - if no effect - nephrogenic DI
=if u rises so > 600mosmol/kg, then cranial DI

32
Q

How is a water deprivation test performed?

A

-12 hours prior to test
=Can have fluids overnight + breakfast
-During test (up to 8hrs) – no fluids, dry snacks
=Patient supervised
=Hourly weight, BP, urine sample (vol +πu)
=2 hourly blood (Na+, πp, ± AVP)
-Stop test if πu>600, of if danger (weight loss>3%, hypotensive+ dizzy etc)
when water depleted (πp>296 or[Na+]>145) give DDAVP

33
Q

What are the types of diabetes insipidus and the results of the water deprivation test?

A
  • Cranial DI= <300 initially and after dehydration but >600 after DDAVP
  • Nephrogenic DI= all <300
  • Partial DI/ Habitual /Psychogenic polydipsia= 300-600 initially and after dehydration but <600 after DDAVP (wash out medullary concentration gradient)
34
Q

What is hypertonic saline test?

A
  • Infuse with saline solution more concentrated than blood
  • Plasma osmolality rises
  • Measure blood samples and check ADH levels
  • Graph
  • If it responds= rises, flat= abnormal so diabetes insipidus
35
Q

What are the causes of cranial diabetes insipidus?

A

-Neurosurgery – pituitary or hypothalamus
-Head injury
-“Idiopathic”
-Other Hypothalamic/pituitary disease
=large pituitary tumour
=cyaniopharyngoma
=histiocytosis X
=sarcoidosis
=metastasis
-Major Haemorrhage =postpartum (Sheehan’s syndrome)
=aneurysm
-Genetic
=isolated AVP gene (A.Dom, secondary loss of post
pit cells-delayed dom negative)
=DIDMOAD (Diabetes Insipidus, Diabetes Mellitus, Optic, Atrophy, Deafness)

36
Q

Describe gestational DI (in pregnancy)

A 
-Vasopressinases in placenta – degrade AVP, little effect on DDAVP,
resolve 1st week post partum
=Sub-clinical DI
 overt DI
=?others limited synthetic capacity
 overt DI
37
Q

What are the causes of nephrogenic diabetes insipidus?

A

-Inherited
=majority V2R X-linked, reports of v mild DI in females (variable X inactivation)
=others AQP2 Ch12 – A.Recessive or A.Dom (C-term mutat→basolat in A.Dom)

-Acquired
=hypercalcaemia
=hypokalaemia
=resolution after urinary tract obstructive
=secondary effect of psychogenic polydipsia
=Lithium therapy effect
=Demeclocycline

38
Q

What is the overall treatment for diabetes insipidus?

A

•Cranial DI – replace AVP – use dDAVP
=dDAVP = long acting, can give just x2/day, more selective for V2R renal effects
-peptide – intranasal spray/drops
–tablets (desmopressin)
–injections (inpatients, diagnosis)
•Nephrogenic DI – other measures to ↓polyuria

39
Q

Describe cranial diabetes insipidus treatment

A

1) Treat other hypothalamo-pituitary deficiencies
=(cortisol, thyroxine, sex steroids, ?GH)
2) Give replacement for vasopressin = Desmopressin/DDAVP
=Desmopressin spray (nasal 10μg/spray: 1-2sprays bd)
=Desmotabs tablets (oral typically 100-200μg tds)
=DDAVP injection (rarely long-term, caution
typically - initially 1μg sc/IM, wait until wears off
then 1-4 μg sc/IM/day over 1-2 doses
=to diagnose diabetes insipidus - 2μg DDAVP sc, warn < 500ml fluid/next 8hrs
=(Similar treatment may be useful in troublesome gestational DI.)

40
Q

Describe nephrogenic diabetes insipidus treatment

A

1)Think of causes – treat them if possible
?[K+]↓, [Ca2+]↑, Lithium or demeclocycline treatment…..
2) Some treatment of partial benefit, consider
- thiazide/amilorids diuretics paradoxically lower urine volumes
- indomethacin – limit renal prostaglandins
- lower salt diet limit urinary osmotic load
± lower protein diet
=In partial DI ± occasionally try drugs with SIADH tendency, (eg chlorpropamide may ↑renal receptors and response to ADH

41
Q

How is SIADH diagnosed?

A 
(1) Is the patient dehydrated?
=If so Na+ and water loss,
identify if urine is site of excess salt loss
(2) Is the patient oedematous?
=If so treat the cause of the oedema
(3) If neither (1) nor (2) check for
=thyroid or adrenal/ACTH deficiency

SIADH - show inappropriately concentrated urine
show urine osmolality>500 or >2x plasma osmolality when plasma [Na+]<135 and/or plasma osmolality < 280
-Hyponatraemia with normal ECF (kidney adaptions to reduce water reabsorption from PCT), urine sodium >20mmol, not on diuretics and adrenal glands normal

42
Q

What are the causes of SIADH?

A

•Intracranial Lesions/disease - of diverse kinds (interfere with feedback= trauma, surgery, CNS infection, Stroke)
•Intrathoracic disease, especially infections, pneumonia (affect baroreceptor feedback)
•Neoplasms, especially lung/mediastinal/ pancreatic (secrete ADH ectopically)
•Drugs
antipsychotics e.g. phenothiazines
sedatives e.g. morphine, barbiturates
-CARDISH= chemotherapy, antidepressants, recreational, diuretics, inhibitors (ACE, SSRI), sulfonylurea, hormones (desmopressin)
5 C’s chlorpropamide,
clofibrate
chlorpromazine
carbamazepine
chlorthiazide (and other thiazides)
•Miscellaneous
nicotene, pain (especially post-op)

43
Q

What is the treatment for SIADH?

A

-confirm diagnosis
-fluid restrict (1000ml/d, then < 800ml/d if needed)
-occasionally require demeclocycline (cause partial nephrogenic DI)
-normalise [Na+] slowly ( <10mmol/l/day)
-New options = aquaretics – V2 receptor antagonists e.g. Tolvaptan (may also reduces decline in PKD)
- combined V2-V1a antagonists e.g. conivaptan
(roles in SIADH, heart failure etc, less effective in cirrhosis)

44
Q

How does Addison’s Disease lead to hyponatraemia?

A

-Loose mineralocorticoids and glucocorticoids
-1-Aldosterone↓ (+/- adrenaline), ADH not↓=imbalance, salt wasting leads to dehydration and reduced blood pressure, increases K+, acidosis
2-non-osmotic ADH stimuli –↓vol, nausea, pain
3-↓GC effects – impair water loss

45
Q

How does ACTH/ GC deficiency lead to hyponatraemia?

A

-Thyroid hormone, sex steroids, GH
-Decreased GC effects- impair water loss
=central effect increased ADH at given plasma osmolality
=renal effect decreased renal water excretion
=decreased glucose so non-osmotic ADH stimulus

46
Q

What is the triple phase response after pituitary surgery?

A
  • Cranial DI followed by SIADH followed by cranial DI again-Urine output fluctuates massively
  • Usually then remains as cranial DI
  • Damage to pituitary stalk allows partially processed forms are released= have long half life so dont get cleared from blood quickly, released for several days mean there is too much then is cleared
47
Q

What happens to serum and urine osmolality?

A
  • Urine has low sodium level due to excess of water= low osmolality
  • Serum has high sodium and so high osmolality (lack of water being reabsorbed into blood)

Endocrine & Diabetes (45 decks)

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