Fluid and Electrolytes

Question 1

Main electrolytes inside the cell? Outside the cell?

Answer 1

Inside: K, Mg, PO4, Proteins
Outside: Na, HCO3, Cl, Ca

Question 2

Describe the relationship between hydrogen and potassium? What happens in increased H? Decreased H?

Answer 2

Exchanged for one another across cell membrane. When increased H+ occurs, H moved into ICF and K moves into ECF = hyperkalemia and vice versa. Acidosis = hyperkalemia. Alkalosis = hypokalemia.

Question 3

What is the relationship of glucose, insulin, K, PO4, and Na?

Answer 3

When insulin moves glucose into a cell it takes K with it and PO4 and Mg is used for the Na/K pump/PO4 goes into cell with glucose. Na moves out of the cell.

Question 4

What is ionized Ca? Describe the relationship between albumin, pH and ionized Ca?

Answer 4

Small percentage of Ca available. Ca is otherwise bound to albumin. Ca competes with H for binding sites on albumin. In presence of alkalosis (dec H) there are MORE binding sites available on albumin so we will have DECREASED ionized calcium levels and true is for the opposite.

Question 5

What is the relationship between Chloride and pH?

Answer 5

Decreased Cl levels are seen in presence of metabolic alkalosis and increased Cl levels are seen in presence of metabolic acidosis.

Question 6

What metabolic abnormality can occur as a result of rapid NaCl infusion? Why?

Answer 6

Hyperchloremic metabolic acidosis. It results in excessive renal excretion of HCo3

Question 7

What type of volume and concentration imbalance would rapidly bleeding patient experience?

Answer 7

isotonic hypovolemia

Question 8

What type of vol and conc imbalance would an over-resuscitated pt receiving isotonic fluid experience?

Answer 8

isotonic hypervolemia

Question 9

SIADH will cause what type of vol and conc imbalance?

Answer 9

hypotonic hypervolemia / hypervolemic hyponatremia

Question 10

DI will cause what type of vol and conc imbalance?

Answer 10

hypertonic hypovolemia

Question 11

An elderly person living in LTC who cannot make needs known is at risk for what type of vol and conc imbalance?

Answer 11

hypertonic hypovolemia

Question 12

What are three causes of metb acidosis? What does metb acidosis result in? What are things to consider when a patient is receiving vasoactive drugs?

Answer 12

• lactic acidosis
• renal dysfx
• loss of hco3
  results in decreased myocardial contractility and dec CO as well as arterial vasodilation and v/q mismatch deadspace like
  when pH is below 7.2 vasoactive drugs are less effective

Question 13

What are normal functions of the liver in CHO metb? What will we see in liver failure that corresponds to these functions?

Answer 13

Convert glucose for glycogen to store (glycogenesis), convert stored glycogen back into glucose for use (glycogenolysis), convert non-CHO into energy when glycogen isn’t avaiable (gluconeogenesis). Dec BG.

Question 14

Normal liver fx in protein metb and synthesis of clotting factors? What will we see in liver failure?

Answer 14

Convert AA, lipids to glucose. Plasma protein formation: albumin, globulins (immune function), clotting factors. Will see bleeding, poor immune fx, edema

Question 15

Normal liver fx in lipid metb? What medications do we need to be cautious with using?

Answer 15

converts excess CHO and protein into fatty acids and triglycerides, stores in adipose tissue. Lipid based meds will cause increased triglycerides (propofol)

Question 16

Normal liver fx in bile production. What will we see in liver failure?

Answer 16

Produces bile. Bile necessary for absorption of fat soluble vitamins (A D E K) and digestion/absorption of fat. Makes stool brown. We will see bleeding issues as Vit k cannot be absorbed and pale coloured stool.

Question 17

Normal liver fx with bilirubin? What will we see in liver failure?

Answer 17

Converts unconj bili to conj bili to be excreted by gall bladder/GIT. Will see inc unconj bili levels in liver failure, or inc conj bili levels if blockage present.

Question 18

Normal liver fx in detoxifying, bacterial removal, cell clean up. What will we see in liver failure?

Answer 18

Kuppfer cells remove bacteria, toxins, drugs (make up 70% of body’s macrophages). Drugs will take a lot longer to clear, increased infection risk, lactate levels will take longer to go down, liver unable to convert ammonia to urea for excretion = neurotoxic = hepatic encephalopathy/dec LOC

Question 19

what is the treatment for hepatic encephalopathy?

Answer 19

lactulose PO/PR clears ammonia via gut and low protein diet

Question 20

When does refeeding syndrome occur? Why does it occur?

Answer 20

12-72 hours after nutrition is introduced. Malnourished patient metabolism has changed to use fat, protein and AA for energy and intracellular electrolytes become depleted. when nutrition is introduced CHO is now used for energy and insulin levels spike and cause a further dangerous shift in electrolytes

Question 21

describe the electrolyte shifts that occur in refeeding?why?

Answer 21

Na moves out of the cell because glucose and K move into the cell from insulin = edema, fluid overload, hypernatremia. K moves into the cell causing hypokalemia. PO4 moves into cell with glucose = hypophosphatemia. Mg is used for Na/K pump = hypomagnesemia. Thiamine is used for ATP = decreased thiamine levels

Question 22

What are the hallmark signs of refeeding

Answer 22

dec PO4, abn fluid balance (Na shifts out of cell to ECF), vitamin deficiency (thiamine/B12), dec Mg, dec K (which are both associated with cardiac, respiratory and neuromuscular dysfunction)

Question 23

What is the treatment for refeeding?

Answer 23

start low and feed slow (trickle), replace electrolytes per protocols, be aware of risk factors, monitor BW closely