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ICMLPS - Electrolytes - April 4
Terms in this set (15)
Symptoms and Signs
• Asymptomatic, i.e., a lab diagnosis. Usually when hyponatremia is chronic and occurred gradually
• General symptoms: fatigue, weakness and muscle cramps
• CNS: headache, agitation, lethargy, disorientation, seizures, and death
• GI (due to CNS edema): anorexia, N/V
Think water = too much or too little water
Plasma Osmolality = 2 Na + glucose/18 + BUN/2.8
due to space-occupying compounds in the plasma (solids), i.e., high level of triglycerides or paraprotein (multiple myeloma).
In these cases, the blood will be isotonic*.
Plasma water = 99.1 - (0.1 x L) - (0.07 x P)
Chol = 200, Protein 7
Plasma = 99.1 - 0.4 - 4.9 = 93.8%
Plasma Na = 140
True plasma "water" = 149
(dilutional hyponatremia): due to water shifting from intracellular stores to extracellular compartment.
Usually due to the presence of a large amount of high- osmolality molecules in the blood,
- glycerol, etc.
In these cases, the blood will be hypertonic.
due to loss of sodium in excess of water (or replacement of
isotonic Na loss with Na-poor solutions).
Volume overrules osmolality: ADH is increased despite hypoosmolality.
- Renal loss (urine Na > 10 mmol/L):
• diuretics, commonly seen in elderly and especially with thiazide diuretics • renal tubular diseases, i.e., renal tubular acidosis (RTA)
• mineralocorticoid deficiency
• osmotic diuresis: mannitol, hyperglycemia
- Nonrenal loss (urine Na < 10 mmol/L):
• GI loss: diarrhea, vomiting
• skin: burns
• abdominal cavity and soft tissue (third-space): pancreatitis, peritonitis
due to the retention of water in excess of sodium:
Volume rules over osmolality: ADH is increased despite hypoosmolality.
The body senses hypovolemia despite increased interstitial volume.
- Congestive heart failure
- Cirrhosis (d/t vasodilation)
- Renal disease: renal failure, nephrotic syndrome.
Important clinical clues:
Due to inappropriate ADH secretion.
Syndrome of Inappropriate ADH Secretion (SIADH):
-carcinoma: particularly small-cell lung cancer
-pulmonary disease: pneumonia, TB, tumor, pneumothorax, atelectasis
-CNS disorders: trauma, tumors, CVA, infection
-drugs: oral hypoglycemics,
chemotherapy, psychotropic, anticonvulsants, NSAID, and clofibrate.
Symptoms and Signs
mostly due to aberrations in membrane polarization that affect the function of excitable tissue.
The threshold for provoking an action potential is increased when Ki/Ke ratio is increased.
Also, high ratio interferes with the termination of the action potential and subsequent repolarization.
• Cardiac: ventricular premature contractions (increased susceptibility to epinephrine), abnormal EKG (decreased amplitude, flattened T, U-waves), predisposition to digitalis toxicity (increased Na-K pump affinity to ouabain inhibitory effect)
• Musculoskeletal: fatigue, weakness, and cramps. Severe hypokalemia may cause paralysis, tetany and rhabdomyolysis.
• GI: reduced motility (constipation, ileus)
• Renal: polyuria and polydipsia due to renal concentrating defect
Important clinical clues of SIADH:
• Head or chest lesions
• No symptoms or signs of hypo- or hypervolemia
• High urinary sodium concentration (> 20 meq/L)
• Urine not maximally diluted (> 100 mOsm/kg)
• No clinical or biochemical evidence of hypothyroidism or
Treatment - Demeclocycline, fluid restriction, vaspressin receptor blockade
• history of cardiac, liver or kidney disease
• symptoms and signs of increased volume:
- increased JVP
- crackles or pleural effusion
- S3 gallop
- hepatic congestion
Treatment - Fluid restriction, Vasopressin receptor blockade, treat underlying cause
Important clinical clues:
• history of diuretics use or GI loss
• the presence of symptoms and signs of volume depletion:
- orthostatic symptoms
- orthostatic hypotension
- poor skin turgor and dry mucous membrane - flat jugular venous veins
Treatment - Saline, Correct the cause
-Hypokalemic periodic paralysis
-Renal potassium losses
-Extrarenal potassium loses
Renal Potassium Losses
(Urine K>20 meq/L)
The patient is alkalotic
- Excess mineralocorticoid
- Bartter's syndrome (no NaKCC)
- Vomiting/NG suction (low urine chloride):**
--Secondary hyperaldosteronism (volume depletion)
--Alkalosis promotes K+ secretion by the distal tubule
--Hypochloremia promotes K+ secretion by the distal tubule
The patient is acidotic
- Renal tubular acidosis (RTA)
- Carbonic anhydrase inhibitors
- Diabetic ketoacidosis
Extrarenal Potassium Losses
(Urine K<20 meq/L):
- GI fistulas
- Villous adenoma
- Geophagia (clay ingestion)
- Laxative abuse
- Copious perspiration (9 mEq/L)
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