Fluids and Electrolytes pt 2

- usually the result of hyponatremia or elevated bicarbonate concentration
- kidney eleminating hyrdrogen ions
- develops as a result of vomiting and the loss of HCl from stomach acid
- occurs in cystic fibrosis (epidermal loss)
- alters acid-base balance

- major ICF cation
- mostly regulates renal
- concentration maintained by Na/K pump
- regulates intracellular electrical neutrality
- essential for the transmission and conduction of nerve impulses

- changes in pH effect K+ balance
- aldosterone reabsorbs sodium = loss of potassium
- insulin and catecholamines (epi/nepi) cause an intracellular shift
- slower changes are tolerated

- low potassium levels
- causes: malnutrition, increased cell entry, increased loss (GI or renal) Conn's Syndrome (increased aldosterone)
- manifestations: hyperpolarization causes a decrease in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, and bradycardia

- high potassium levels (RARE)
- causes: decreased renal excretion, increased intake, shift of K from ICF to ECF, insulin deficiency, cell trauma/injury
- mild attacks: increased neuromuscular irritability (paresthesias: tingling of lips and fingers; restlessness; cramping/diarrhea)
- severe attacks: cell is not able to repolarize resulting in muscle weakness and V fib
- treatments: bicarbonate, insulinlucose, dialysis

- excreted by kidneys
- Vit D and parathyroid hormone (PTH) causes an increase in gut absorption so that Ca circulates back to the bones
- necessary for bones, blood clotting, hormones, cell function, membrane stability, nerve impulses, muscle contractions

- Causes: nutritional deficiencies, low PTH and vit D, and intestinal absorption
- effects: increased neurmuscular excitability
- severe cases: tetany (muscle contractions), seizures, cardiac insufficiency and arrest

- causes: *hyperparathyroidism, bone metastases with calcium reabsorption, vitamin D overdose
- effects: *kidney stones, bradycardia, bone pain

- most located in the bone
- necessary for high energy bonds located in creatine phosphate and ATP; acts as an anion buffer

- causes: intestinal malabsorption, alc, increased renal excretion of phosphate associated with hyperparathyroidism

- causes: renal failure; long term use of laxatives; hypoparathyroidism; tissue injury