Disorders Of Sodium And Potassium Metabolism

Disorders of Sodium and Potassium Metabolism

Outline 1. 2. 3. 4. 5.

Review of sodium and potassium 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

Exercise Cell Lysis

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

Rhabdomyolysis Tumor lysis syndrome

Etiologies of Hypokalemia Poor Intake

Increased GI Losses Diarrhea

Increased Urinary Excretion Decreased reabsorption in loop of Henle

Laxative abuse Vomiting / NG drainage

Furosemide Increased excretion in the late distal tubule Increased delivery of Na+ to the late distal tubule Furosemide, thiazides, and acetazolamide Proximal RTA

Increased Transcutaneous Losses Copious sweating

Reduced function of the K+/H+ ATPase Distal RTA Hyperaldosteronism Primary hyperaldosteronism

Transmembrane Shift Alkalosis

Adrenal adenoma

Insulin treatment for DKA

Adrenal hyperplasia

High catecholamine states

Secondary hyperaldosteronism Renovascular hypertension Renin-secreting tumor

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

Increased GI Loss of Sodium (Fluid loss must be followed by repletion with free water).

Decreased Urinary Excretion of Water Decreased GFR Increased ADH Decreased effective circulating volume True volume depletion (any cause) Apparent volume depletion Heart failure

Vomitting Diarrhea

Increased Transcutaneous Loss of Sodium (Fluid loss must be followed by repletion with free water).

Cirrhosis SIADH Reset osmostat

Transmembrane Shift of Water Hyperglycemia

Etiologies of Hypernatremia Primary Sodium Excess

Primary Water Loss Poor Intake of Water

Excess Intake of Sodium

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 Cl 95 K 4.4

BUN 12Glucose 102 HCO3 25 Cr 1.4

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 non-responsiveness 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 Cl 126 BUN 50Glucose 98 K 4.8 HCO3 28 Cr 2.6

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 Cl 105 K 2.8 HCO3 UA unremarkable.

BUN 12Glucose 102 32 Cr 0.7

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 can’t 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

Cl 89 HCO3 32Cr 1.4

BUN 32

Glucose 135

2 months ago

Na 132 K 3.8

Cl 97 HCO3 27Cr 1.2

BUN 24

Glucose 128