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Flashcards in Na/K Disorders Deck (20):

A 49‐year‐old woman presented to the emergency department with nausea and vomiting that had occurred for 5 days and slurred speech for 1 day prior to presentation.

Na 101
Osmolality 209
Glucose 3.5

Urine: Na 95
Osmo 812

SIADH is suspected.
Fluid restriction DOES NOT lead to increased serum Na.



Side effect of acute hyponatremia?

cerebral edema


side effect of chronic hyponatremia?

osmotic demyelination


How do we assess ADH activity?

Urine osmolality is a good surrogate marker for renal actions of ADH.

If urine osmo > serum osmo indicates increased ADH


What is ADH?

• Vasopressin or water
conservation hormone
• Synthesized in hypothalamus, which also synthesizes CRH
• Part of the hypothalamic– pituitary–adrenal (HPA) axis
• Negatively regulated by adrenal cortisol


What is aldosterone?

• Aldosterone is a hormone for sodium conservation.
• Aldosterone is synthesized by the adrenal gland.
• Increased aldosterone incresaes Na resorption which leads to decrased Na in urine, but incresae in K excretion in urine. Aldosteronecanbemeasuredclinically.


What can cause high urine osmo with high urine Na?

1. diuretic use (typically hypokalemia)
2. Primary or secondary adrenal insufficiency
3. Cerebral salt wasting (typically present with CNS diseases)
4. Salt‐wasting nephropathy (abnormal serum creatinine)
5. SIADH (a diagnosis of exclusion)


How do you determine if a pt has SIADH or adrenal insufficiency?

1. Look at random cortisol
2. Plasma ACTH (elevated)
3. ACTH stimulation (no change from baseline, should be > 500 if normal response)

Adrenal insufficiency!


What is the treatment for adrenal insufficiency?


• Intravenous hydrocortisone was administered (bolus 100 mg followed by 200 mg/24 h), which corrected serum sodium.
• It important to emphasize that hyponatremia may correct quickly once hydrocortisone is instituted.
• To avoid osmotic demyelination, the correction of hyponatremia should be limited to 8 mmol/L per day.
• After a sodium concentration within the reference interval was achieved, the patient was switched to oral hydrocortisone (10–5–5 mg daily) and L‐thyroxine (50 μg).


What is autoimmune polyglandular syndrome type 2?

Abs form against:
adrenal cortex
thyroid peroxidase
parietal cells
intrinsic factor


What is the MC form of hte polyglandular failure syndromes? who does it affect?

APS type II
women (75%) > men


Why does a pt with APS type II not have hypotension?

• Isolatedhypocortisolism
– Only affected cortisol‐producing zona fasciculata, but not aldosterone‐producing zona glomerulosa
• AngiotensinIIisamorepotentorlonger‐lasting secretagogue for aldosterone than ACTH is for cortisol.
•Therewasadeficiencyofaldosterone,butthat hypotension and hyperkalemia were prevented by other mechanisms.


Primary adrenal insufficiency can present without...

pigmentation, orthostatic hypotension, hyperkalemia, hypoglycemia, and hypercalcemia.


SIADH is a diagnosis of exclusion that can be established onily if...

diuretic use and adrenal, thyroid, and pituitary insufficiency are excluded.


Primary adrenal insufficiency can be confirmed by low random cortisol concentrations but normal concentrations require...

ACTH stimulation test for exxclusion


How does cortisol deficiency cause hyponatremia compared to aldosterone def?

Increase in CRH which stimulates vasopressin release

aldosterone def causes hyponatremia b/c of renal Na loss


A 43‐year‐old woman with a medical history significant for hypertension, depression, and primary biliary cirrhosis (PBC) was admitted to the hospital after outpatient laboratory tests showed hyponatremia.
• Her complaints on admission included blurry vision, nausea, and significant pruritus. Her review of systems was otherwise negative. She declared no family history of hypercholesterolemia or premature heart disease.
• She was taking multiple medications including azathioprine, prednisone, amlodipine, losartan, prochlorperazine, sertraline, trazodone, fenofibrate, ranitidine, hydroxyzine, ursodiol, and cholestyramine.
• Physical exam was remarkable for scleral icterus and mild jaundice; no xanthomas were noted.

Na 121
K 3
Cl 87

• The patient was started on intravenous fluids (0.9% sodium chloride).
• Her most recent total cholesterol (TC) value, measured 1.5 years prior, was 322 mg/dL (8.3 mmol/L).
• Current testing revealed a markedly increased plasma TC concentration of 2156 mg/dL (55.8 mmol/L).
• Furthermore, the sample appearance was clear and not grossly viscous or lipemic.
• An investigation took place to determine if this was an erroneous result.

• Given the possibility that the patient's hyperlipidemia was interfering with her electrolyte measurements, the clinical team stopped treatment with intravenous fluids.
• Direct ion‐selective electrode (ISE) measurement of the initial sample on a Radiometer ABL825 Flex® analyzer showed the following results:
–sodium concentration of 141 mmol/L (referencerange137–145); – potassium, 4.4mmol/L(3.6–5.5)
– chloride,105mmol/L(101–111).
• The patient was discharged after the correct electrolyte results were obtained.


What is the electrolyte exclusion effect?

• Volume of solids in plasma is about 7%.
• So water volume in plasma is 93%.
• Indirect ISE (dilution of specimens) and flame photometry measurements give lower values for electrolytes, because they are based on total sample volume, not water volume.
• Electrolyte exclusion effect does not affect direct ISE measurement (without dilution of specimens).


How do you treat hyperkalemia?

K+ > 6.5 or ECG changes require emergent treatment
• Calcium gluconate given for prevent arrhythmias
• Bicarbonate and/or insulin and glucose to shift K+ into cells
• Kayexalate and/or furosemide with hydrogen given to remove K+ in exchange for Na+
• Restrict K+ intake and discontinue drugs that contribute to hyperkalemia
• Dialysis


What causes pseudohyperkalemia?

• EDTA contamination (confirm with serum calcium conc.)
• Fistpumping/relaxingduringdraw
• Thrombocytosis(plateletsreleasepotassium
during clotting)
• Lymphocytosis (release of potassium due to white blood cell consumption of glucose)