Disorders of Sodium and Potassium Metabolism

Disorders of Sodium and Potassium Metabolism - Disorders of...

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Unformatted text preview: Disorders of Sodium and Potassium Metabolism Potassium Outline Outline 1. Review of sodium and potassium Review 2. 3. 4. 5. metabolism metabolism Paradigm for analyzing pathophysiology Abnormalities of potassium balance Abnormalities of sodium and water Abnormalities balance balance Example cases Major Mediators of Sodium and Water Balance Water Angiotensin II Aldosterone Antidiuretic hormone (ADH) Renin-Angiotensin-Aldosterone Axis Renin-Angiotensin-Aldosterone 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) Role Synthesized in the hypothalamus and stored in the Synthesized posterior pituitary posterior Released in response to plasma hyperosmolality and Released decreased effective circulating volume decreased Actions of ADH 1. Increases the water permeability of Actions the collecting tubule the 2. Mildly increases vascular resistance Overview of Biochemical Homeostasis Overview Overview of Potassium Balance Overview Etiologies of Hyperkalemia Etiologies 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 Etiologies 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 Overview Etiologies of Hyponatremia Etiologies 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 Cirrhosis Vomitting Diarrhea 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 Etiologies 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 Case Mrs. L is a 62 y/o woman with a past medical history Mrs. 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. 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 Case Mr. R is an 85 y/o man with advanced dementia who was Mr. sent to the ER from his skilled nursing facility for nonsent responsiveness since the morning nursing shift started responsiveness 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. 100/50. Labs include the following: Na 164 K 4.8 Cl 126 HCO3 28 BUN 50 Cr 2.6 Glucose 98 Case 3 Case Miss K is a 28 y/o woman who presents for her first routine Miss 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: following: Na 147 K 2.8 Cl 105 HCO3 32 UA unremarkable. BUN 12 Cr 0.7 Glucose 102 Case 4 Case Mr. W is a 65 y/o man with a past history significant for CHF secondary from an Mr. 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. that Routine fasting labs reveal the following: Today Today Na 128 Na K 3.1 Cl 89 HCO3 32 BUN 32 Cr 1.4 Glucose 135 2 months ago Na 132 K 3.8 Cl 97 HCO3 27 BUN 24 Cr 1.2 Glucose 128 ...
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