ILE U4 D3

Question 1

What is the primary intracellular cation?

Answer 1

K

Question 2

Functions of K

Answer 2

1. Regulates protein synthesis
2. Regulates intracellular volume
3. Responsible for regulation of nerve excitability (especially cardiac muscle!)
4. Carbohydrate metabolism

Question 3

How is dietary K absorbed?

Answer 3

Passively, through upper GI tract

Question 4

What regulates K balance?

Answer 4

Na-K-ATPase pump (Mag is cofactor)

Question 5

Low mag -> hypomagnesia ->

Answer 5

refractory hypokalemia

Question 6

When too much K exists in extracellular cardiac space,

Answer 6

arrhythmia occurs

Question 7

K is eliminated

Answer 7

renally

Question 8

K is filtered freely at _, and is _ before reaching tubules

Answer 8

glomerulus, reabsorbed

Question 9

What happens to K in the distal tubule?

Answer 9

K is secreted into the tubule and Na is reabosrbed

Question 10

Aldosterone effect in regards to K

Answer 10

increases K secretion into the urine, in response to K concentrations

Question 11

What happens to K when large amounts of Na into tubule?

Answer 11

K is excreted

Question 12

Metabolic alkalosis

Answer 12

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

Question 13

Metabolic alkalosis: does serum K increase or decrease?

Answer 13

Decrease

Question 14

Metabolic acidosis

Answer 14

Extracellular shift of K due to intracellular shift of hydrogen ions

Question 15

Metabolic acidosis: does serum K increase or decrease?

Answer 15

Increase

Question 16

Causes of hypokalemia

Answer 16

1. Intracellular shifting
2. True deficits
   2a. Decreased intake (alcoholism, anorexia, etc.)
   2b. Increased output (GI losses, corticosteroids, loop/thiazide diuretics)

Question 17

Signs of hypokalemia

Answer 17

1. Skeletal muscle weakness
2. Lethargy
3. GI
4. Ascending paralysis
5. Cardiac arrhythmia

Question 18

When do you administer PO K? IV?

Answer 18

PO: When patient is largely asymptomatic
IV: When GI isn’t functioning, otherwise symptomatic patients

Question 19

Problems with PO K?

Answer 19

1. unpleasant taste

2. GI upset

Question 20

PO K dose

Answer 20

20 –40 mEq every 2 –4 hours to decrease GI side effects

Question 21

IV K dose

Answer 21

every 10 mEq KCl increases serum K+by 0.1 mEq/L (if normal renal function)

Question 22

IV K dose in renal failure

Answer 22

50% of normal dose

Question 23

When do you see hyperkalemia?

Answer 23

Renal failure, extracellular shifting

Question 24

Medications that cause hyperkalemia

Answer 24

K sparing diuretics
ACEIs, 
ARBs, 
NSAIDs, 
trimethoprim (Bactrim)
heparin

Question 25

Causes of hyperkalemia

Answer 25

1. Meds 2. Increased K intake 3. Adrenal steroid deficiency 4. Addison's disease

Question 26

ECG changes associated with hyperkalemia

Answer 26

peaked T waves

Question 27

ECG changes associated with hypokalemia

Answer 27

Flattened T waves, elevated U

Question 28

Mag predominately exists in

Answer 28

Predominantly in intracellular space; 50 –60% in bones

Question 29

Mag is involved in enzymatic reactions like

Answer 29

Cofactor in Na+-K+-ATPase pump Involved in glucose metabolism, fatty acid synthesis/breakdown, DNA and protein metabolism

Question 30

How much mag is normally reabsorbed?

Answer 30

~97%

Question 31

Where is mag reabsorbed?

Answer 31

ascending LoH, proximal tubule, and distal tubule

Question 32

Which drugs significantly affect Mag wasting

Answer 32

loop diuretics (furosemide)

Question 33

Causes of hypomagnesia

Answer 33

Renal wasting, GI losses, protein-calorie malnutrition, refeeding syndrome, alcohol abuse

Question 34

Which medications cause hypomagnesia

Answer 34

Loop diuretics Amphotericin B Cisplatin Aminoglycoside antibiotics

Question 35

Signs of hypomagnesia

Answer 35

1. Twitching 2. Weakness 3. Increased reflexes

Question 36

PO mag isn't preferred because

Answer 36

PO takes a log time, poor absorption, IV preferred

Question 37

Max mag dose for asymptomatic patients

Answer 37

1 g/hr

Question 38

Severe mag dose

Answer 38

4-8 g

Question 39

Mild mag dose

Answer 39

1-4 g

Question 40

How long does it take for mag to fully distribute to tissue?

Answer 40

2 days

Question 41

Dose for mag for patient with renal impairment

Answer 41

Reduce normal dose by 50%

Question 42

Hypermagnesemia signs

Answer 42

Fatigue, lethargy, confusion, cardiac arrest

Question 43

Hypermagnesemia treatment

Answer 43

IV Ca gluconate to stabilize membrane, reverse cardiac and NM effects, diuretics to increase renal elimination, dialysis (last line)

Question 44

Hypermagnesemia occurence

Answer 44

really rare - usually seen with cardiac arrest

Question 45

Phos is mostly found in

Answer 45

Primary INTRACELLULAR anion | Mainly found in bones, soft tissues; <1% in serum

Question 46

Phos functions

Answer 46

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

Question 47

Where does Phos get absorbed?

Answer 47

2/3 - small intestine (increased with active vit. D)

Question 48

How does phos get eliminated?

Answer 48

Renally

Question 49

Hypophosphatemia causes

Answer 49

``` Intracellular shifting Decreased phosphate or vitamin D intake Malnutrition Alcoholism Refeeding syndrome Meds Critical illness Metabolic alkalosis ```

Question 50

Meds that cause hypophosphatemia

Answer 50

1. Sucralfate 2. Calcium carbonate 3. Al/Mag antacids 4. Sevelamer 5. Lanthanum carbonate

Question 51

When to use PO phos

Answer 51

when asymptomatic, causes diarrhea, erratic absorption

Question 52

When to use IV phos

Answer 52

when symptomatic or unable to tolerate oral formulations

Question 53

IV phos dose for renal impairment

Answer 53

50% of normal dose

Question 54

Hyperphosphatemia causes

Answer 54

``` renal dysfunction (common) extracellular shifting (esp during acidosis) Increased phos or vit D intake (phos containing enemas) ```

Question 55

Signs of hyperphosphatemia

Answer 55

nausea, vomiting, dehydration, NM irritability

Question 56

Complications of hyperphosphatemia

Answer 56

Soft tissue and vascular calcification, renal osteodystrophy

Question 57

Refeeding Syndrome

Answer 57

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))

Question 58

Refeeding syndrome mechanism

Answer 58

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

Question 59

Hallmark sign of referring syndrome

Answer 59

hypophosphatemia

Question 60

K and Mag also shift in response to ___ and ___ in referring syndrome

Answer 60

anabolism and insulin release

Question 61

ISMP High-Alert Medications

Answer 61

Must be monitored closely due to high potential for adverse effects if used incorrectly

Question 62

Electrolytes considered high-alert by ISMP

Answer 62

All forms of K and Mag