Fluid and Electrolytes. Large Group 1 -Barnes

Question 1

What 3 things need to be evaluated in a pt with hyponatremia?

Answer 1

plasma osmolality, volume status and urine osmolality

Question 2

How is serum osmolality calculated?

Answer 2

Sosm= 2x[Na+] + (BUN/2.8) + (glucose/18)

Question 3

what is Isotonic-pseudo hyponatremia due to?

Answer 3

inaccurate lab results

if a lab does not calculate the osmolality in the aqueous form, hyperlipidemia or hyperproteinemia can make it appear that the Na+ is low

Question 4

What is the most common way a person can get hypertonic hyponatremia?

Answer 4

hyperglycemia

Question 5

How can a pt get hypotonic hyponatremia? Is this a Na+ problem, a water problem, or both?

Answer 5

this is a sodium problem

lose Na+ > H2O

vomiting or diarrhea

Question 6

What will be found on physical exam of a HYPOvolemic pt?

Answer 6

skin tenting

dry mucous membranes of tongue/mouth

flat JVP

Question 7

What are some signs of HYPERvolemia?

Answer 7

pitting edema

ascites

elevated JVP

Question 8

What is SIADH? What cancer can cause this?

Answer 8

vasopressin is secreted from the metastasis causing an increase in free water absorption and Na+ to remain at the same level–> leads to hyponatremia

Small cell lung carcinoma

Question 9

What does ADH do? Where does it have an effect on the kidney?

Answer 9

ADH induces the insertion of AQP2 channels on the membrane of the cortical collecting duct, the outer medullary collecting duct and the inner medullary collecting duct

leads to increased H2O reabsorption without changes in Na+ reabsorption

Question 10

Is SIADH a water or a Na+ problem or both?

Answer 10

water!!!

Question 11

What drugs can cause SIADH?

Answer 11

SSRI

Carbamazepine

platinum compounds

proton pump inhibitors

alkylating agents

Question 12

Which class of drugs is a vasopressin antagonist? Where do they act?

Answer 12

vaptans

act on the principal cells in the cortical collecting duct to block the V2 receptors so ADH cannot bind–> decrease water reabsorption b/c less AQP2 insertion

Question 13

How do Lithium and Demeclocycline help in SIADH?

Answer 13

block the increase in cAMP in the principal cells of the CCD–> cannot insert AQP 2 channels into the membrane

Question 14

What can result from rapid correction of hyponatremia? How?

Answer 14

Osmotic demyelination syndrome

in hyponatremia, the cells will initially swell and then the cell will force electrolytes and osmolytes out of the cell (with water following) to decrease the water and swelling in the cell.

at this point, if you add Na+ too fast, the concentration OUTSIDE of the cell will increase way too much leading to more water leaving the cell and ODS

Question 15

What should be checked in a pt that is hyponatremic, hypotonic and euvolemic?

Answer 15

thyroid and adrenals for low functioning

Question 16

What are the steps for evaluating hyponatremia (7)?

Answer 16

Identify there is a Low Serum Sodium level

Obtain Serum and Urine Osmolality

Identify the Serum Osmolality as low, as majority of the time it is low

Evaluate the patient’s volume status

Based on the patient’s volume status identify the source

Intervene on the source of the patient’s hyponatremia for correction or utilize fluid restriction, isotonic saline, or hypertonic saline as indicated.

If recurrent hyponatremia, consider the use of a “vaptan” or demeclocycline.

Question 17

What can result from untreated hyponatremia?

Answer 17

cerebral edema

the higher osmotic P inside the cells causes water to move in–> cerebral edema

Question 18

Is hypertonic hypernatremia a water problem, Na+ problem, or both? What is the most common cause of this?

Answer 18

water problem

water is decreasing and Na+ is remaining the same

*diabetes insipidus

Question 19

What is the difference between neurogenic and nephrogenic diabetes insipidus? How do these affect Na+ levels?

Answer 19

neurogenic=brain is not producing AVP ==> no AQP 2 channels

nephrogenic=kidneys (V2 receptors) are not responding to AVP–> no AQP2 channels

both lead to hypernatremia due to an increase in loss of H2O

Question 20

How can you distinguish between nephrogenic and neurogenic DI?

Answer 20

Timed water deprivation test

deprive the person of water and then administer AVP

in neurogenic–> urine osmolality will increase (decrease in SERUM osmolality)

in nephrogenic, urine osmolality will not increase—> still get dilute urine–> still high serum osmolality

Question 21

What are some causes of neurogenic DI?

Answer 21

head trauma

pituitary surgery

aneurysm

CVA

sheehan’s syndrome

meningitis

sarcoidosis

syphyillis

TB

Question 22

What are the 3 main medications that can cause nephrogenic DI?

Answer 22

Lithium

Demeclocycline

vaptans

Question 23

What is the acute treatment for hypernatremia?

Answer 23

free water

Question 24

Does the rate of treatment matter in hypernatremia?

Answer 24

yes!!!

rapid correction can result in a lot of water moving into the cells–> cellular swelling, damage and death

*cerebral edema

Question 25

What medications can be given for chronic Neurogenic DI? Nephrogenic DI?

Answer 25

chronic neurogenic:
-DDAVP

Nephrogenic:

• Thiazides
• NSAIDS
• Amiloride for Lithium toxicity

Question 26

What are Barnes’ Steps to Hypernatremia? (7)

Answer 26

Identify there is an Elevated Serum Sodium level

Evaluate the patient’s volume status

Calculate a Free Water Deficit

Consider use of Free Water infusions or oral administration of free water

For Euvolemic (as most cases are) perform a water deprivation test to differentiate between Central DI or Nephrogenic DI

Attempt to identify the source of DI and correct

Consider DDAVP for Central DI vs. thiazides+ low Na diet or NSAIDs for Nephrogenic DI

Question 27

How do you calculate a water deficit?

Answer 27

Water Deficit (L)=0.6 x (body weight in kg) x ([Na+]/140-1)

Question 28

How do you determine the hourly water replacement rate in treatment of DI?

Answer 28

Hourly water replacement rate=(water deficit mL) x ([Na+] -140) + ongoing water loss in mL

Question 29

What are the 4 possible causes of low potassium?

Answer 29

decreased intake

potassium loss (renal loss or extra-renal loss)

increased cellular uptake

Question 30

How can you determine if the kidneys are causing a hypokalemia or reacting to it?

Answer 30

TTKG equation (trans-tubular K+ gradient)=(K+urine/K+ blood) x (blood osm/urine osm)

-normally, if there is a low serum K+, we expect the urine K+ to also be low (unless the kidneys are not functioning properly, which will be seen by an elevated urine K+)

if TTKG>3 –> there is a renal loss of K+

Question 31

In which portion of the kidney should compensation for low K+ be taking place?

Answer 31

in the distal nephron

Question 32

What 3 findings point towards hyperaldosteronism?

Answer 32

hypertension

hypokalemia

metabolic alkalosis

Question 33

Where does Aldosterone act on the kidney? What does it do?

Answer 33

aldosterone –> increase ENaC on the Principal cells of the CCD

allows for increased Na+ and water reabsorption

this also leads to a secretion of K+ through the ROMK (renal outer medullary K+ channel) –> lose K+ in the urine

Question 34

What are Barnes’ steps to hypokalemia? (5)

Answer 34

Identify the low Potassium

Obtain an Electrocardiogram

Implement Acute management as indicated

Consider three major sources of Hypokalemia; (Transcellular shifts, decreased intake, increased renal excretion/secretion) Consider Calculating a TTKG

Once source identified, Institute chronic management of Hypokalemia as indicated. Consider use of K+ sparing diuretics or chronic K+ supplementation

Question 35

What are the causes of high Potassium?

Answer 35

increased intake (with abnormal renal excretion)

decreased cellular uptake

decreased renal excretion (low aldosterone states)

Question 36

What medications can cause hyperkalemia?

Answer 36

Impaired renin release: NSAIDs, beta blockers

Ace inhibitors

ARBs

sodium channel inhibitors (amiloride, triamterene, trimethoprim, pentamidine) –> block ENaC –> prevent K+ excretion

Question 37

What is the first thing you should give to a pt with K+ >6? why?

What else should be given?

Answer 37

Calcium gluconate or calcium chloride

stabilize the cardiac membranes to protect the heart from the high K+

then give bicarb and insulin with glucose to get the K+ into the cell

can also give Na+ polystyrene sulfonate (kayexalate) to get the K+ in the gut into the stool

loop diuretics to increase K+ excretion

or dialysis to get the K+ out

Question 38

What are Barnes’ steps to hyperkalemia? (6)

Answer 38

Identify an elevated Potassium

Consider an evaluation for Pseudohyperkalemia

Obtain an Electrocardiogram

Implement Acute management as indicated

Consider three major sources of Hyperkalemia; (Transcellular shifts, Increased intake, Decreased renal excretion i.e. Aldosterone deficiency)
Consider Calculating a TTKG

Once source identified, Institute chronic management of Hyperkalemia if indicated

Question 39

How can you increase K+ excretion?

Answer 39

Aldosterone

High sodium delivery to the distal tubule (eg, diuretics)

High urine flow (eg, osmotic diuresis)

High serum potassium level

Delivery of negatively charged ions to the distal tubule (eg, bicarbonate)