Calcium metabolism and lytes Flashcards
What % of calcium is bound to proteins like albumin?
~50%
Etiology of hypocalcemia
Can be due to hypoparathyroidism, vitamin D deficiency, hyperphosphatemia, malabsorption, acute pancreatitis, and renal disease.
The severity of clinical signs for hypocalcemia depend upon?
How rapidly levels fall.
What happens when the calcium levels fall?
neutonal membranes become increasingly more permeable to sodium, enhancing excitation. K & Mg ions have an antagonizing effect on this excitation.
Decreased myocardial contractility..
^PTH
S/S of hypocalcemia
Primarily d/t neuromuscular irritabiliy.
-tetany, mental irritability, muscle weakness, mental depression and anxiety. Prolonged Q-T interval.
Dx of hypocalcemia
Serum calium and ionized calcium.
Further testing required to determine cause of hypocalcemia.
H+ ___________ ionized Ca
increases
Alkalosis ________ ionized Ca
decreases
Hypercalcemia is defined as:
Total serum calcium > 12mg/dl
Ionized >1.42 mmol/L
Causes of hypercalemia
hypercalcemia of malignancy Primary hyperparathyroidism Osteolytic Granulomatous Hyper vit D secondary renay hyperPTH Addison's Idiopathic
Signs of hypercalcemia
Anorexia Vomiting Depression Weakness PU/PD dehyration Abdominal discomfort Constipation
Objectives of tx hypercalcemia
Correct dehydration
Promote calciuresis
Inhibit bone reabsorption
Treat underlying disorder
Causes of HYPOcalcemia
Primary hypoPTH Postpartum lactation Hyperphosphatemia (acute) Hypovitamin D Hypoalbuminemia
ER treatment of HYPOcalcemia
Calcium gluconate 10% - 0.5-1.5 ml/kg/IV over several minutes, monitor ECG during.
Maintain - 2ml/kg slowlt over 6-8hr. 5ml/kg slowly per 24hr.
Normal range for potassium
3.5-5.5 mEq/L
What are the 4 major categories of hypokalemia?
- Dilutional & decreased intake
- Transcellular maldistribution
- Loss via GIT
- Loss via urine
What is dilutional hypokalemia?
Usually acquired iatrogenically when given IV /SQ fluids that do now contain appropriate amounts of K+. Note: the 4 mEq/L of K+ in LRS is inadequate for maintenance and almost all maintenance fluids require K supplementation.
What is transcellular maldistribution hypokalemia?
A common cause is metabolic alkalosis, which allows transfer of K+ from ECF to the ICF in attempts to to correct alkalosis.
Hormones can cause similar shift (insulin, epi, and aldosterone).
How is hypokalemia caused by renal loss?
Many conditions can allow:
- high sodium intake
- alkalosis
- renal failure
- diuretics
- hyperaldosteronism
S/S of hypokalemia
Muscle weakness is primary sign.
May also see, lethargy, confusion, PU/PD, carb intolerance, ileus, and EKG changes.
When replacing potassium what is the rate it should be administered?
Should not exceed 0.5 mEq/kg/hr.
In extreme cases in patients with normal renal function up to 1.5 mEq/kg/hr can be given with close EGC monitoring.
What is an oral form of potassium supplementation?
Tumil K
S/S of HYPERkalemia
Muscle weakness due to deplorization.
Cardiac excitation and conduction abnormalities
What conduction abnormalities can be noted on an ECG from a hyperkalemia patient?
Loss of P waves.
High peaked or deep T waves, prolonged QRS complexes, complete heart block, bradycardia, atrial standstill, and ventricular fibrillation or standstill.
What are the possible mechanisms of causing hyperkalemia?
Too much intake.
Impaired excretion (ARF, addison’s).
Shifting.
Other less common means: cell death, severe exercise, medications, hypertonic plasma, lack of insulin, acidemia.
Tx for hyperkalemia
NaHCO3 - ion exchange Insulin/dextrose to drive K+ intracellularly. Diuresis w/ furosemide. Dialysis. Terbutaline, albuterol, aminophylline.
NOTE - try to address the inciting cause…. if patient is ‘blocked’, unblock them!
Why would you give 10% calcium gluconate to a hyperkalemic patient?
Ca gluconate will NOT lower serum K+, but it will counteract the cardiotoxic effects of the hyperkalemia by causing a decreased membrane potential and decreased cardiac membrane excitability.
What are the 2 main causes of hyponatremia?
Water gain - common
Sodium loss
S/S of hyponatremia
Weakness Dementia Stupor/coma Absense of thirst Decreased skin elasticity Hypotension/hypothermia Shock Seizures Myoclonus
How do you treat acute hyponatremia?
If it occurs in <24hr, remove causative factors and can correct rapidly over 24h period.
Replacement rate of at least 1 mEq/L/hr
How do you treat chronic hyponatremia?
“Chronic natremia” occurs over 24h or more. Levels <120mEq/L must be corrected SLOWLY over 48hrs.
Rate of correction should NOT exceed 8-12mEq/L in 24 hours. Give furosemide while giving NaCl helps prevent brain issues.
Addison’s may require most than 48hrs to correct Na levels
How high does semur sodium need to be before signs are seen?
> 170 mEq/L
What are the two main causes of hypernatremia?
Na+ gain
H20 loss - common
What effects does hyperosmolality cause on neurons?
Intracellular water moves to the ECF space, neuron dehydrates and can tear meningeal vessels. CNS hemorrhage and dehydration causes neuron dysfunction and pt can die.
What happens to the brain size with acute hypernatremia?
Brain shrinks due to water loss to try and match serum osmolality.
S/S of hypernatremia
Fever Nausea/vomiting Seizures Coma Array of neuro signs Hypotension Tachycardia Oliguria (unless DI)
What are the 3 types of hypernatremia and their causes?
Hypovolemic - renal, GI
Hypervolemia - hypertonic saline Rx
Euvolemic - DI
How do you tx hypernatremia?
Stop water diuresis by giving ADH to DI patients.
Stop any hypertonic fluids.
Give 0.45% NaCl or D5W IV.
Rate of correction dependent upon rate of accumulation.
What is central pontine myelinosis?
Iatrogenic brain demyelination from too rapid correction of hypoNa. Causes brain to shrink. Rapidly raising sodium levels causes the brain to lose water too rapidly.
