Disorders of sodium and potassium metabolismPresentation Transcript
Disorders of Sodium and Potassium Metabolism Electrolyte disbalance
Review of sodium and potassium metabolism
Paradigm for analyzing pathophysiology
Abnormalities of potassium balance
Abnormalities of sodium and water balance
Major Mediators of Sodium and Water Balance
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
Etiologies of Hypokalemia Poor Intake 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 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 Increased GI Losses Diarrhea Laxative abuse Vomiting / NG drainage Increased Transcutaneous Losses Copious sweating Transmembrane Shift Alkalosis Insulin treatment for DKA High catecholamine states
Overview of Sodium Balance
Etiologies of Hyponatremia Poor Intake of Sodium 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). Vomitting Diarrhea Increased Transcutaneous Loss of Sodium (Fluid loss must be followed by repletion with free water). Excessive Intake of Water (1 ° polydipsia) Psychosis Decreased Urinary Excretion of Water Decreased GFR Increased ADH Decreased effective circulating volume True volume depletion (any cause) Apparent volume depletion Heart failure Cirrhosis SIADH Reset osmostat Transmembrane Shift of Water Hyperglycemia Primary Sodium Loss Primary Water Excess
Etiologies of Hypernatremia Primary Sodium Excess Excess Intake of Sodium Decreased Urinary Excretion of Sodium Hyperaldosteronism 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 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)
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 BUN 12 Glucose 102
K 4.4 HCO 3 25 Cr 1.4
Her CBC shows mild normocytic anemia.
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 50 Glucose 98
K 4.8 HCO 3 28 Cr 2.6
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 BUN 12 Glucose 102
K 2.8 HCO 3 32 Cr 0.7
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.