ILE U4 D3 Flashcards
What is the primary intracellular cation?
K
Functions of K
- Regulates protein synthesis
- Regulates intracellular volume
- Responsible for regulation of nerve excitability (especially cardiac muscle!)
- Carbohydrate metabolism
How is dietary K absorbed?
Passively, through upper GI tract
What regulates K balance?
Na-K-ATPase pump (Mag is cofactor)
Low mag -> hypomagnesia ->
refractory hypokalemia
When too much K exists in extracellular cardiac space,
arrhythmia occurs
K is eliminated
renally
K is filtered freely at _, and is _ before reaching tubules
glomerulus, reabsorbed
What happens to K in the distal tubule?
K is secreted into the tubule and Na is reabosrbed
Aldosterone effect in regards to K
increases K secretion into the urine, in response to K concentrations
What happens to K when large amounts of Na into tubule?
K is excreted
Metabolic alkalosis
Compensatory efflux of hydrogen ions from cells into the extracellular fluid occurs w/ concurrent influx of K into the cells to maintain an electropotential gradient
Metabolic alkalosis: does serum K increase or decrease?
Decrease
Metabolic acidosis
Extracellular shift of K due to intracellular shift of hydrogen ions
Metabolic acidosis: does serum K increase or decrease?
Increase
Causes of hypokalemia
- Intracellular shifting
- True deficits
2a. Decreased intake (alcoholism, anorexia, etc.)
2b. Increased output (GI losses, corticosteroids, loop/thiazide diuretics)
Signs of hypokalemia
- Skeletal muscle weakness
- Lethargy
- GI
- Ascending paralysis
- Cardiac arrhythmia
When do you administer PO K? IV?
PO: When patient is largely asymptomatic
IV: When GI isn’t functioning, otherwise symptomatic patients
Problems with PO K?
- unpleasant taste
2. GI upset
PO K dose
20 –40 mEq every 2 –4 hours to decrease GI side effects
IV K dose
every 10 mEq KCl increases serum K+by 0.1 mEq/L (if normal renal function)
IV K dose in renal failure
50% of normal dose
When do you see hyperkalemia?
Renal failure, extracellular shifting
Medications that cause hyperkalemia
K sparing diuretics ACEIs, ARBs, NSAIDs, trimethoprim (Bactrim) heparin
Causes of hyperkalemia
- Meds
- Increased K intake
- Adrenal steroid deficiency
- Addison’s disease
ECG changes associated with hyperkalemia
peaked T waves
ECG changes associated with hypokalemia
Flattened T waves, elevated U
Mag predominately exists in
Predominantly in intracellular space; 50 –60% in bones
Mag is involved in enzymatic reactions like
Cofactor in Na+-K+-ATPase pump
Involved in glucose metabolism,
fatty acid synthesis/breakdown,
DNA and protein metabolism
How much mag is normally reabsorbed?
~97%
Where is mag reabsorbed?
ascending LoH, proximal tubule, and distal tubule
Which drugs significantly affect Mag wasting
loop diuretics (furosemide)
Causes of hypomagnesia
Renal wasting, GI losses, protein-calorie malnutrition, refeeding syndrome, alcohol abuse
Which medications cause hypomagnesia
Loop diuretics
Amphotericin B
Cisplatin
Aminoglycoside antibiotics
Signs of hypomagnesia
- Twitching
- Weakness
- Increased reflexes
PO mag isn’t preferred because
PO takes a log time, poor absorption, IV preferred
Max mag dose for asymptomatic patients
1 g/hr
Severe mag dose
4-8 g
Mild mag dose
1-4 g
How long does it take for mag to fully distribute to tissue?
2 days
Dose for mag for patient with renal impairment
Reduce normal dose by 50%
Hypermagnesemia signs
Fatigue, lethargy, confusion, cardiac arrest
Hypermagnesemia treatment
IV Ca gluconate to stabilize membrane, reverse cardiac and NM effects, diuretics to increase renal elimination, dialysis (last line)
Hypermagnesemia occurence
really rare - usually seen with cardiac arrest
Phos is mostly found in
Primary INTRACELLULAR anion
Mainly found in bones, soft tissues; <1% in serum
Phos functions
ntracellular metabolism of proteins, lipids, carbs
Major component of phospholipid membrane
Maintaining pHFormation of phosphorylated bonds to make ATP
MUSCULAR FUNCTION - ESP MYOCARDIUM AND DIAPHRAGM
Where does Phos get absorbed?
2/3 - small intestine (increased with active vit. D)
How does phos get eliminated?
Renally
Hypophosphatemia causes
Intracellular shifting Decreased phosphate or vitamin D intake Malnutrition Alcoholism Refeeding syndrome Meds Critical illness Metabolic alkalosis
Meds that cause hypophosphatemia
- Sucralfate
- Calcium carbonate
- Al/Mag antacids
- Sevelamer
- Lanthanum carbonate
When to use PO phos
when asymptomatic, causes diarrhea, erratic absorption
When to use IV phos
when symptomatic or unable to tolerate oral formulations
IV phos dose for renal impairment
50% of normal dose
Hyperphosphatemia causes
renal dysfunction (common) extracellular shifting (esp during acidosis) Increased phos or vit D intake (phos containing enemas)
Signs of hyperphosphatemia
nausea, vomiting, dehydration, NM irritability
Complications of hyperphosphatemia
Soft tissue and vascular calcification, renal osteodystrophy
Refeeding Syndrome
Fluid and electrolyte abnormalities that occur with re-introduction of carbohydrates after periods of starvation (mostly occurs in patients with eating disorders, alcoholics, critically ill (NPO))
Refeeding syndrome mechanism
Body derives energy from ketone production from free fatty acid oxidation, when carbs are reintroduced, a sudden shift back to glucose as main fuel causes shift for phosphorylated ATP
Hallmark sign of referring syndrome
hypophosphatemia
K and Mag also shift in response to ___ and ___ in referring syndrome
anabolism and insulin release
ISMP High-Alert Medications
Must be monitored closely due to high potential for adverse effects if used incorrectly
Electrolytes considered high-alert by ISMP
All forms of K and Mag
