Disorders of Sodium and Potassium Metabolism

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Disorders of Sodium and Potassium Metabolism
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Outline

1. Review of sodium and potassium metabolism
2. Paradigm for analyzing pathophysiology
3. Abnormalities of potassium balance
4. Abnormalities of sodium and water balance
5. Example cases

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Major Mediators of Sodium and Water Balance

• Angiotensin II
• Aldosterone
• Antidiuretic hormone (ADH)

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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
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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

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Overview of Biochemical Homeostasis
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Overview of Potassium Balance
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Etiologies of Hyperkalemia
Excessive Dietary Intake Decreased Urinary
Excretion Decreased GFR Aldosterone
deficiency Adrenal insufficiency ACE
inhibitors Hyporeninemic hypoaldosteronism Di
abetic nephropathy Aldosterone
resistance Potassium sparing diuretics
Internal Redistribution Transmembrane Shift
Acidosis Exercise Cell Lysis
Rhabdomyolysis Tumor lysis
syndrome
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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 Transmem
brane Shift Alkalosis Insulin treatment for
DKA High catecholamine states
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Overview of Sodium Balance
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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 I
ncreased 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).
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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
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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.

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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

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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.

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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 cant 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