Hypernatremia- Diabetes Insipidus, Polydipsia, Polyuria

Question 1

low plasma osmolality= TBW ____

high plasma osmolality = TBW___

Answer 1

low plasma osmolality= TBW EXCESS

high plasma osmolality = TBW DEFICIT

Question 2

Explain this graph

Answer 2

if the plasma osmolality goes above 280, AVP (ADH) starts to be produced. THIS IS THE OSMOTIC THRESHOLD. Sodium and water starts to be conserved.

at 288, the thirst trigger sets in.

Normal range of 290 of plasma osmolality that describes a healthy condition and healthy water access.

If you have an EXCESS of total body water, the plasma osmolality drops below normal. If there’s a deficit of TBW, plasma osmolality rises to a higher level.

The middle y axis is plasma AVP secretion. With a plasma osmoaltiy of 280, AVP is turned off. You’re not trying to retain water when you’re already on the verge of excess TBW. THIS IS THE OSMOTIC THRESHOLD. Threshold above which your body will begin to take action to preserve TBW. As tbw increases and plasma osmolality increases, you can see that your body makes AVP in an effort to prevent further dehydration.

Once you get to a plasma osmolality 288, the thirst effect starts to manifest. From 280-288, tbw is maintained through AVP. But with progressive levels of dehydration (288+), the body engages thirst as a means of taking in water so as to avoid progressive dehydration.

We can excrete up to 16 laters of water per day if we don’t need it.

As plasma osmolality rises (as we get deficient in tbw), AVP is made, which causes our kidneys to retain water and excrete a more concentrated urine (decreases urine output) as a means of conserving water.

Despite maximal effect of AVP, if we get more dehydrated, thirst kicks in, to prevent ongoing dehydration.

Understanding rapid water lost if there is normal Aexcretion.

Question 3

normal serum osm, normal serum Na+

Answer 3

• “Normal” serum osm: 280-295 mosm/kg
• Normal serum Na: 135-145 mmol/L

• Range of renal concentrating/diluting
capacity: 50 – 1200 mosm/kg

• Not the same as a hemogram! • The numbers are inter-connected!

Question 4

hypernatremia is generally due to ___ TBW. what two broad mechanisms cause this?

Answer 4

due to decreased total body water. usually due to failure to take water in or failure to hold water in.

Question 5

two mechanisms that can result in the failure to take water in

Answer 5

1. absent thirst mechanism- brain trauma
2. no access to water - stranded in dessert, unconscious and cannot get yoursefl water.

Question 7

symptoms of hypernatremia from lack of water intake

Answer 7

Question 8

two broad reasons why someone may fail to HOLD onto water

Answer 8

• osmotic losses (presence of non-sodium solutes) like DM
• renal water losses (failure to make or respond to AVP)– like Diabetes insipidus

Question 9

general MOA of ADH/AVP

Answer 9

Antidiuretic hormone stimulates water reabsorbtion by stimulating insertion of “water channels” or aquaporins into the membranes of kidney tubules. These channels transport solute-free water through tubular (DCT and CD) cells and back into blood, leading to a decrease in plasma osmolarity and an increase osmolarity of urine.

Question 10

hallmark symptom of DI

Answer 10

thirst

Question 11

central vs nephrogenic Di

Answer 11

central; lack of appropriate AVP secretion- something wrong with the hypothalamus or pituitary

nephrogenic (renal); lack of appropriate repsonse to normal circulating AVP

Question 13

central DI is uaully __, where as nephrogenic DI is usually ___

Answer 13

central- ACUIRED

nephrogenic - CONGENITAl

Question 14

symptoms in an infant that could indicate DI

Answer 14

• diapers always soaked (POLYURIA), failure to thrive, dehydration, severe hypernatemia

Question 16

primary polydipsia

Answer 16

lots of drinking.Nothing wrong with AVP secretion, they’re just choosing to drink a lot of water (they could be forcing themselves or something)– there’s nothing necessarily wrong with their water axis, they’re just drinking so much to cause polydipsia-polyuria

Question 17

DDX of someone presenting with polydipsia (drinking waer a lot) and polyuria

Answer 17

1. primary polydipsia
2. central DI
3. nephrogenic DI
4. osmotic diuresis (glucose)

Question 18

key labs to do with someone presenting with polydipsia and polyuria

Answer 18

do a 24 hour urine volume and creatinine. also water fast test would be good.

Question 19

on exam, it’s hard to tell between primary polydipsia and hypernatremia because both result in high urine volume and low urine osmolality. what key differences in the water deprivation test would allow you to differentiate?

Answer 19

primary polydipsics; their body will conserve water.

• no hypernatremia
• progressive urinary concentration
• progressive decrease in U/O

Diabetes inspidus; continued losses

• RISK: dehydration/hypernatremia
• persistent polyuria
• lack of urinary concentration.

Question 20

interpret this water deprivation test result

Answer 20

Urine output decreases and urine osmolality increases. This is a normal response.

Question 21

Persistent high volume urine output. And the osmolality does not increase over time, they are still making a dilute high volume urine despite not drinking. They are getting progressively dehydrated. This is DI

Question 22

this person had DI. they did the water deprivation test and then were given AVP. is this central or nephrogenic

Answer 22

Give them AVP and see what happens. After one hour, the urine osm has been concentrated, and is not becoming more dehydrated. They are thus reposing to AVP. The problem initially was lack of AVP, indicating that this is central diabetes insidipidus.

Question 23

central DI etilogies

Answer 23

post head injury/surgery

• hypothalamic tumor
• hypthalamic infiltrative disease
• Ab to posterior pit which secreretes AVP/ ADH/ DDVAP
• congenital mutation in AVP gene/product.

Question 24

Management of Central DI

Answer 24

Question 25

congenital, drugs and renal diseases that can cause nephrogenic DI

Answer 25

congenital ; X linked and mutation in AQP2– autosomal recessive)

drugs; lithium or emphotericin B

renal diseases; sickle cell, myeloma kidney, others

Question 26

management of nephrogenic DI

Answer 26

Question 27

outline the general algorithm for hypernatremia:

Answer 27

Question 28

severe hypernatremia management

Answer 28

• Volume / hemodynamic management
– ABC’s
– IV normal saline until BP stable

• When stable (or if never unstable):
– Water replacement
• IV • oral

Question 29

How to determine type of IV fluid to give someone with hypernatremia

Answer 29

1. use “water deficit” formulat to estimate the amount of water you must replace
   - deliver the water (hypotonic saline or D5W) over a period of time that is slow enough that won’t cause cerebral edema