Calcium metabolism and lytes Flashcards

1
Q

What % of calcium is bound to proteins like albumin?

A

~50%

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2
Q

Etiology of hypocalcemia

A

Can be due to hypoparathyroidism, vitamin D deficiency, hyperphosphatemia, malabsorption, acute pancreatitis, and renal disease.

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3
Q

The severity of clinical signs for hypocalcemia depend upon?

A

How rapidly levels fall.

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4
Q

What happens when the calcium levels fall?

A

neutonal membranes become increasingly more permeable to sodium, enhancing excitation. K & Mg ions have an antagonizing effect on this excitation.
Decreased myocardial contractility..
^PTH

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5
Q

S/S of hypocalcemia

A

Primarily d/t neuromuscular irritabiliy.

-tetany, mental irritability, muscle weakness, mental depression and anxiety. Prolonged Q-T interval.

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6
Q

Dx of hypocalcemia

A

Serum calium and ionized calcium.

Further testing required to determine cause of hypocalcemia.

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7
Q

H+ ___________ ionized Ca

A

increases

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8
Q

Alkalosis ________ ionized Ca

A

decreases

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9
Q

Hypercalcemia is defined as:

A

Total serum calcium > 12mg/dl

Ionized >1.42 mmol/L

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10
Q

Causes of hypercalemia

A
hypercalcemia of malignancy
Primary hyperparathyroidism
Osteolytic 
Granulomatous
Hyper vit D
secondary renay hyperPTH
Addison's
Idiopathic
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11
Q

Signs of hypercalcemia

A
Anorexia
Vomiting
Depression
Weakness
PU/PD
dehyration
Abdominal discomfort
Constipation
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12
Q

Objectives of tx hypercalcemia

A

Correct dehydration
Promote calciuresis
Inhibit bone reabsorption
Treat underlying disorder

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13
Q

Causes of HYPOcalcemia

A
Primary hypoPTH
Postpartum lactation
Hyperphosphatemia (acute)
Hypovitamin D
Hypoalbuminemia
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14
Q

ER treatment of HYPOcalcemia

A

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.

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15
Q

Normal range for potassium

A

3.5-5.5 mEq/L

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16
Q

What are the 4 major categories of hypokalemia?

A
  • Dilutional & decreased intake
  • Transcellular maldistribution
  • Loss via GIT
  • Loss via urine
17
Q

What is dilutional hypokalemia?

A

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.

18
Q

What is transcellular maldistribution hypokalemia?

A

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).

19
Q

How is hypokalemia caused by renal loss?

A

Many conditions can allow:

  • high sodium intake
  • alkalosis
  • renal failure
  • diuretics
  • hyperaldosteronism
20
Q

S/S of hypokalemia

A

Muscle weakness is primary sign.

May also see, lethargy, confusion, PU/PD, carb intolerance, ileus, and EKG changes.

21
Q

When replacing potassium what is the rate it should be administered?

A

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.

22
Q

What is an oral form of potassium supplementation?

A

Tumil K

23
Q

S/S of HYPERkalemia

A

Muscle weakness due to deplorization.

Cardiac excitation and conduction abnormalities

24
Q

What conduction abnormalities can be noted on an ECG from a hyperkalemia patient?

A

Loss of P waves.
High peaked or deep T waves, prolonged QRS complexes, complete heart block, bradycardia, atrial standstill, and ventricular fibrillation or standstill.

25
Q

What are the possible mechanisms of causing hyperkalemia?

A

Too much intake.
Impaired excretion (ARF, addison’s).
Shifting.
Other less common means: cell death, severe exercise, medications, hypertonic plasma, lack of insulin, acidemia.

26
Q

Tx for hyperkalemia

A
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!

27
Q

Why would you give 10% calcium gluconate to a hyperkalemic patient?

A

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.

28
Q

What are the 2 main causes of hyponatremia?

A

Water gain - common

Sodium loss

29
Q

S/S of hyponatremia

A
Weakness
Dementia
Stupor/coma
Absense of thirst
Decreased skin elasticity
Hypotension/hypothermia
Shock
Seizures
Myoclonus
30
Q

How do you treat acute hyponatremia?

A

If it occurs in <24hr, remove causative factors and can correct rapidly over 24h period.
Replacement rate of at least 1 mEq/L/hr

31
Q

How do you treat chronic hyponatremia?

A

“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

32
Q

How high does semur sodium need to be before signs are seen?

A

> 170 mEq/L

33
Q

What are the two main causes of hypernatremia?

A

Na+ gain

H20 loss - common

34
Q

What effects does hyperosmolality cause on neurons?

A

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.

35
Q

What happens to the brain size with acute hypernatremia?

A

Brain shrinks due to water loss to try and match serum osmolality.

36
Q

S/S of hypernatremia

A
Fever
Nausea/vomiting
Seizures
Coma
Array of neuro signs
Hypotension
Tachycardia
Oliguria (unless DI)
37
Q

What are the 3 types of hypernatremia and their causes?

A

Hypovolemic - renal, GI
Hypervolemia - hypertonic saline Rx
Euvolemic - DI

38
Q

How do you tx hypernatremia?

A

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.

39
Q

What is central pontine myelinosis?

A

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.