1. Disorders of Sodium and Potassium Metabolism

2. Outline Review of sodium and potassium metabolism
Paradigm for analyzing pathophysiology
Abnormalities of potassium balance
Abnormalities of sodium and water balance
Example cases

3. Major Mediators of Sodium and Water Balance
Angiotensin II
Aldosterone
Antidiuretic hormone (ADH)

4. 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

5. 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

8. Overview of Biochemical Homeostasis

9. Overview of Potassium Balance

10. Etiologies of Hyperkalemia
Excessive Dietary Intake
Decreased Urinary Excretion
Decreased GFR
Aldosterone deficiency
Adrenal insufficiency
ACE inhibitors
Hyporeninemic hypoaldosteronism
Diabetic nephropathy
Aldosterone resistance
Potassium sparing diuretics
Internal Redistribution
Transmembrane Shift
Acidosis
Exercise
Cell Lysis
Rhabdomyolysis
Tumor lysis syndrome

11. 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

12. Overview of Sodium Balance

13. Etiologies of Hyponatremia
Primary Sodium Loss
Primary Water Excess
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
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).

14. Etiologies of Hypernatremia
Primary Water Loss
Primary Sodium Excess
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)
Excess Intake of Sodium
Decreased Urinary Excretion of Sodium
Hyperaldosteronism

15. 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 BUN 12 Glucose 102
K 4.4 HCO3 25 Cr 1.4
Her CBC shows mild normocytic anemia.

16. 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 50 Glucose 98
K 4.8 HCO3 28 Cr 2.6

17. 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 BUN 12 Glucose 102
K 2.8 HCO3 32 Cr 0.7
UA unremarkable.

18. 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 Cl 89 BUN 32 Glucose 135
K 3.1 HCO3 32 Cr 1.4
2 months ago Na 132 Cl 97 BUN 24 Glucose 128
K 3.8 HCO3 27 Cr 1.2