Disorders of Sodium and Potassium Metabolism

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Outline
1. Review of sodium and potassium 2. 3. 4.

5.

metabolism Paradigm for analyzing pathophysiology Abnormalities of potassium balance Abnormalities of sodium and water balance Example cases

Major Mediators of Sodium and Water Balance

Angiotensin II Aldosterone
Antidiuretic hormone (ADH)

Renin-Angiotensin-Aldosterone Axis

Angiotensin II 1. Stimulates production of aldosterone 2. Acts directly on arterioles to cause vasoconstriction 3. Stimulates Na+/H+ exchange in the proximal tubule Aldosterone

1. Stimulates reabsorption of Na+ and excretion of K+ in the late distal tubule 2. Stimulates activity of H+ ATPase pumps in the late distal tubule

Role of ADH (antidiuretic hormone)

Synthesized in the hypothalamus and stored in the posterior pituitary

Released in response to plasma hyperosmolality and decreased effective circulating volume

Actions of ADH 1. Increases the water permeability of the collecting tubule 2. Mildly increases vascular resistance

Overview of Biochemical Homeostasis

Overview of Potassium Balance

Etiologies of Hyperkalemia
Excessive Dietary Intake Internal Redistribution
Transmembrane Shift Acidosis

Decreased Urinary Excretion

Decreased GFR Aldosterone deficiency Adrenal insufficiency ACE inhibitors Hyporeninemic hypoaldosteronism Diabetic nephropathy Aldosterone resistance Potassium sparing diuretics

Exercise

Cell Lysis
Rhabdomyolysis Tumor lysis syndrome

Etiologies of Hypokalemia
Poor Intake Increased GI Losses
Diarrhea Laxative abuse Vomiting / NG drainage

Increased Urinary Excretion

Decreased reabsorption in loop of Henle Furosemide Increased excretion in the late distal tubule Increased delivery of Na+ to the late distal tubule Furosemide, thiazides, and acetazolamide

Increased Transcutaneous Losses

Copious sweating

Proximal RTA
Reduced function of the K+/H+ ATPase Distal RTA Hyperaldosteronism Primary hyperaldosteronism Adrenal adenoma Adrenal hyperplasia Secondary hyperaldosteronism Renovascular hypertension Renin-secreting tumor

Transmembrane Shift
Alkalosis Insulin treatment for DKA High catecholamine states

Overview of Sodium Balance

Etiologies of Hyponatremia
Primary Sodium Loss Poor Intake of Sodium Primary Water Excess Excessive Intake of Water (1 polydipsia)
Psychosis

Increased Urinary Loss of Sodium

Diuretics Proximal RTA Aldosterone deficiency/resistance

Decreased Urinary Excretion of Water

Decreased GFR Increased ADH Decreased effective circulating volume

True volume depletion (any cause)

Increased GI Loss of Sodium (Fluid loss

must be followed by repletion with free water). Vomitting Diarrhea

Apparent volume depletion Heart failure Cirrhosis SIADH Reset osmostat

Increased Transcutaneous Loss of Sodium (Fluid loss must be followed by

repletion with free water).

Transmembrane Shift of Water

Hyperglycemia

Etiologies of Hypernatremia
Primary Sodium Excess Excess Intake of Sodium Primary Water Loss Poor Intake of Water
Impaired access to water (i.e. infants, elderly patients with dementia or whom are bedbound)

Impaired thirst sensation

Decreased Urinary Excretion of Sodium

Hyperaldosteronism

Hypothalamic lesions

Increased Urinary Loss of Water

ADH deficiency (Central DI) ADH resistance (Nephrogenic DI)

Increased GI Loss of Water

Increased Transcutaneous Loss of Water

Transmembrane Shift of Water (most often due to

rapid production of intracellular lactate)

Case 1
Mrs. L is a 62 y/o woman with a past medical history significant only for hypertension. She has a 45 pack year smoking history. She comes to the urgent care clinic today complaining of a cough and shortness of breath for the past week. Her physical exam is notable for both mild wheezing and rhonchi, more pronounced on the right side than the left. Labs include the following: Na 126 K 4.4 Cl 95 HCO3 25 BUN 12 Cr 1.4 Glucose 102

Her CBC shows mild normocytic anemia.

Case 2
Mr. R is an 85 y/o man with advanced dementia who was sent to the ER from his skilled nursing facility for nonresponsiveness since the morning nursing shift started about 8 hours ago. The remainder of his past medical history is unknown. Aside from his mental status, his physical exam is remarkable for a HR of 110 and BP of 100/50. Labs include the following:

Na 164 K 4.8

Cl 126 HCO3 28

BUN 50 Cr 2.6

Glucose 98

Case 3
Miss K is a 28 y/o woman who presents for her first routine clinic visit. She has no complaints, and her medical history is unremarkable. On physical exam you note that her BP is 162/94.

You send her for some routine labs which find the following:
Na 147 K 2.8 Cl 105 HCO3 32 BUN 12 Cr 0.7 Glucose 102

UA unremarkable.

Case 4
Mr. W is a 65 y/o man with a past history significant for CHF secondary from an MI 4 years ago. He comes to general medicine clinic today for a routine appointment. He states that he was complaining of some mild dyspnea on exertion at his cardiology appointment 2 weeks ago. In response, his cardiologist told him to double one of his medications, which the patient did, but at the moment he cant remember which medication this was. He does report that his shortness of breath is now better. Routine fasting labs reveal the following: Today Na 128 K 3.1 Na 132 K 3.8 Cl 89 HCO3 32 Cl 97 HCO3 27 BUN 32 Cr 1.4 BUN 24 Cr 1.2 Glucose 135

2 months ago

Glucose 128