2 Outline Review of sodium and potassium metabolism Paradigm for analyzing pathophysiologyAbnormalities of potassium balanceAbnormalities of sodium and water balanceExample cases
3 Major Mediators of Sodium and Water Balance Angiotensin IIAldosteroneAntidiuretic hormone (ADH)
4 Renin-Angiotensin-Aldosterone Axis Angiotensin II 1. Stimulates production of aldosterone2. Acts directly on arterioles to cause vasoconstriction3. Stimulates Na+/H+ exchange in the proximal tubuleAldosterone 1. Stimulates reabsorption of Na+ and excretion of K+ in the late distal tubule2. Stimulates activity of H+ ATPase pumps in the late distal tubule
5 Role of ADH (antidiuretic hormone) Synthesized in the hypothalamus and stored in the posterior pituitaryReleased in response to plasma hyperosmolality and decreased effective circulating volumeActions of ADH 1. Increases the water permeability of the collecting tubule2. Mildly increases vascular resistance
11 Etiologies of Hypokalemia Poor IntakeIncreased Urinary ExcretionDecreased reabsorption in loop of HenleFurosemideIncreased excretion in the late distal tubuleIncreased delivery of Na+ to the late distal tubuleFurosemide, thiazides, and acetazolamideProximal RTAReduced function of the K+/H+ ATPaseDistal RTAHyperaldosteronismPrimary hyperaldosteronismAdrenal adenomaAdrenal hyperplasiaSecondary hyperaldosteronismRenovascular hypertensionRenin-secreting tumorIncreased GI LossesDiarrheaLaxative abuseVomiting / NG drainageIncreased Transcutaneous LossesCopious sweatingTransmembrane ShiftAlkalosisInsulin treatment for DKAHigh catecholamine states
13 Etiologies of Hyponatremia Primary Sodium LossPrimary Water ExcessExcessive Intake of Water (1° polydipsia)PsychosisDecreased Urinary Excretion of WaterDecreased GFRIncreased ADHDecreased effective circulating volumeTrue volume depletion (any cause)Apparent volume depletionHeart failureCirrhosisSIADHReset osmostatTransmembrane Shift of WaterHyperglycemiaPoor Intake of SodiumIncreased Urinary Loss of SodiumDiureticsProximal RTAAldosterone deficiency/resistanceIncreased GI Loss of Sodium (Fluid loss must be followed by repletion with free water).VomittingDiarrheaIncreased Transcutaneous Loss of Sodium (Fluid loss must be followed by repletion with free water).
14 Etiologies of Hypernatremia Primary Water LossPrimary Sodium ExcessPoor Intake of WaterImpaired access to water (i.e. infants, elderly patients with dementia or whom are bedbound)Impaired thirst sensationHypothalamic lesionsIncreased Urinary Loss of WaterADH deficiency (Central DI)ADH resistance (Nephrogenic DI)Increased GI Loss of WaterIncreased Transcutaneous Loss of WaterTransmembrane Shift of Water (most often due to rapid production of intracellular lactate)Excess Intake of SodiumDecreased Urinary Excretion of SodiumHyperaldosteronism
15 Case 1Mrs. 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 102K 4.4 HCO3 25 Cr 1.4Her CBC shows mild normocytic anemia.
16 Case 2Mr. 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 98K 4.8 HCO3 28 Cr 2.6
17 Case 3Miss 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 102K 2.8 HCO3 32 Cr 0.7UA unremarkable.
18 Case 4Mr. 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 Cl 89 BUN 32 Glucose 135K 3.1 HCO3 32 Cr 1.42 months ago Na 132 Cl 97 BUN 24 Glucose 128K 3.8 HCO3 27 Cr 1.2
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