Final Exam: Electrolytes and Acid Base Imbalances Flashcards
Normal serum electrolyte levels
Sodium: 135 – 145 mEq/L
Potassium: 3.5 – 5.0 mEq/L
Calcium: 4.5 – 5.5 mEq/L
Magnesium: 1.5 – 2.5 mEq/L
Phosphate: 2.5 – 4.5 mg/dL
What is hypokalemia?
Denotes a decreased ion concentration in the EXTRAcellular fluid
What are some factors that may cause hypokalemia?
- Alodsterone increases potassium excretion in the DCT (followed by compensated heart failure and cirrhosis by increased aldosterone levels)
- Black licorice
- Potassium sparing diuretics (prednisone and furosemide)
What are factors that shift K+ from ECF to ICF?
Insulin
B adrenergic stimulation
Alkalosis (hypokalemia)
What are factors that shift K+ from ICF to ECF?
Insulin deficiency
B blockers
Acidosis (hyperkalemia)
Cell lysis
Strenuous exercisie
What are clinical manifestations of hypokalemia?
N&V, weakness, muscle cramps, constipation
Severe: arrhythmias, muscle necrosis, rarely paralysis with respiratory failure
Describe the etiology of Calcium ions/ hypocalcemia
- Calcium ions play a role in speed of ion fluxes through nerve and muscle cell membranes
- Therefore, calcium imbalances alter normal neuromuscular excitability
Increased NM excitability is caused by a decrease in threshold potential of excitable cells so AP are generated more easily
What are some causes of hypocalcemia?
Hypoparathyroidism
Renal Failure
Vitamin D deficiency
Pancreatitis
Chronic diarrhea
Clinical manifestations of Hypocalcemia
Positive Trousseau’s sign: BP cuff and thumb to wrist
Positive Chvostek’s sign: Nerve excitability, touch face and face should twitch
Paresthesia
Hyperactive reflexes
Tetany
Laryngospasm
Cardiac dysrhythmias
Seizures
How would you improve Hypocalcemia?
Treat underlying cause
Increase dietary Ca2+
Severe: IV calcium gluconate
Etiology of Hypercalcemia
Primary hyperparathyroidism
- common in later stages of lung, renal, breast, lymphoma and multiple myeloma
Hypercalcemia causes DECREASED NM excitability, where threshold is now elevated
Clinical manifestations of Hypercalcemia
“Bones, stones, groans and psychiatric overtones”
Weakness
Nausea and Vomiting
Constipation
Psychosis
Bone pain
Treatment of hypercalcemia?
Increase urinary excretion (furosemide)
Diminish bone resorption (biphosphonate drugs)
Decrease GI absorption (corticosteroids)
Last resort (dyalisis)
What are factors that cause hypophophatemia?
Starvation
Malabsorption
Antacid use
Renal loss: Hyperparathyroidisim and diuretics
Etiology and pathogenesis of Hypophosphatemia
Phosphate plays important component in ATP, the major source of energy. Signs and symptoms relate to decreased amounts of ATP
Clinical manifestations of Hypophosphatemia
Anorexia
Malaise
Paresthesias
Diminshed refleces
Muscle aches
Confusion
Respiratory failure
Impaired cardiac function
Treatment of Hypophosphatemia
Oral or IV phosphate
What may cause hyperphosphatemia? This condition is common in what individuals?
Increased intake of phosphate
Common in individuals with Renal Disease
What are the signs and symptoms of Hyperphosphatemia?
Increased neuromuscular excitability because oftentimes it causes hypocalcemia
- Some patients it will cause deposition of calcium leading to things like aching and stiffness of the joints
What are causes of Hypomagnesemia?
Chronic alcoholism (decreased MG intake)
Starvation/ malabsorption
Excess renal loss: Hypokalemia, hypercalcemia
Clinical manifestations of Hypomagnesemia?
Mg ions in ECF depress relase of ACH at NM junctions, if not enough Mg ions present excessive amounts of ACH are released.
- CM are those of increased NM excitability
- Hyperactive refexes, muscle cramps, twitching, Chovstek andd Trousseau sign
Clinical manifestations of Hypermagnesemia?
Too many Mg ions in ECF depress NM function by decreasing release of ACH at NM junction
- deep tendon reflexes, lethargy, hypotension, flushing drowsiness, respiratory depressio, etc
