Download Disorders of Sodium and Potassium Metabolism

Disorders of Sodium and
Potassium Metabolism
Outline
1. Review of sodium and potassium
2.
3.
4.
5.
metabolism
Paradigm for analyzing pathophysiology
Abnormalities of potassium balance
Abnormalities of sodium and water
balance
Example cases
Major Mediators of Sodium and
Water Balance
Angiotensin II
Aldosterone
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
tubule
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
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
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
Etiologies of Hyponatremia
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
Decreased Urinary Excretion of Water
Decreased GFR
Increased ADH
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
Vomitting
Diarrhea
Cirrhosis
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
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
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
K 4.4
Cl 95
HCO3 25
BUN 12
Cr 1.4
Glucose 102
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 nonresponsiveness 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
K 4.8
Cl 126
HCO3 28
BUN 50
Cr 2.6
Glucose 98
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
K 2.8
Cl 105
HCO3 32
UA unremarkable.
BUN 12
Cr 0.7
Glucose 102
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
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