Disorders of Sodium and Potassium Metabolism

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					Disorders of Sodium and
 Potassium Metabolism
1. Review of sodium and potassium
2.   Paradigm for analyzing pathophysiology
3.   Abnormalities of potassium balance
4.   Abnormalities of sodium and water
5.   Example cases
Major Mediators of Sodium and
       Water Balance

 Angiotensin II


 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
                 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
Decreased Urinary Excretion
                                                            Cell Lysis
        Decreased GFR
        Aldosterone deficiency
                                                                  Tumor lysis syndrome
                 Adrenal insufficiency
                 ACE inhibitors
                 Hyporeninemic hypoaldosteronism
                           Diabetic nephropathy
        Aldosterone resistance
                 Potassium sparing diuretics
                      Etiologies of Hypokalemia
Poor Intake                                                    Increased GI Losses

Increased Urinary Excretion                                            Laxative abuse
                                                                       Vomiting / NG drainage
    Decreased reabsorption in loop of Henle
    Increased excretion in the late distal tubule
         Increased delivery of Na+ to the late distal tubule   Increased Transcutaneous
                Furosemide, thiazides, and acetazolamide       Losses
                Proximal RTA                                           Copious sweating

         Reduced function of the K+/H+ ATPase
                Distal RTA
         Hyperaldosteronism                                    Transmembrane Shift
                Primary hyperaldosteronism                             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                                  Primary Water Excess

Poor Intake of Sodium                             Excessive Intake of Water (1° polydipsia)

Increased Urinary Loss of Sodium
                                                  Decreased Urinary Excretion of Water
                                                      Decreased GFR
      Proximal RTA
                                                      Increased ADH
      Aldosterone deficiency/resistance
                                                           Decreased effective circulating volume
                                                                  True volume depletion (any cause)
Increased GI Loss of Sodium (Fluid loss                           Apparent volume depletion
must be followed by repletion with free water).
                                                                        Heart failure
                                                           Reset osmostat
Increased Transcutaneous Loss of
Sodium (Fluid loss must be followed by
repletion with free water).                       Transmembrane Shift of Water
                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               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

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.
                       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

Labs include the following:

Na 164       Cl 126           BUN 50    Glucose 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

You send her for some routine labs which find the

Na 147       Cl 105        BUN 12        Glucose 102
K 2.8        HCO3 32       Cr 0.7

UA unremarkable.
                                 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

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