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ILE I > ILE U4 D3 > Flashcards

ILE U4 D3 Flashcards

1
Q

What is the primary intracellular cation?

A

K

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2
Q

Functions of K

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

How is dietary K absorbed?

A

Passively, through upper GI tract

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4
Q

What regulates K balance?

A

Na-K-ATPase pump (Mag is cofactor)

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5
Q

Low mag -> hypomagnesia ->

A

refractory hypokalemia

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6
Q

When too much K exists in extracellular cardiac space,

A

arrhythmia occurs

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7
Q

K is eliminated

A

renally

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8
Q

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

A

glomerulus, reabsorbed

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9
Q

What happens to K in the distal tubule?

A

K is secreted into the tubule and Na is reabosrbed

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10
Q

Aldosterone effect in regards to K

A

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

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11
Q

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

A

K is excreted

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12
Q

Metabolic alkalosis

A

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

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13
Q

Metabolic alkalosis: does serum K increase or decrease?

A

Decrease

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14
Q

Metabolic acidosis

A

Extracellular shift of K due to intracellular shift of hydrogen ions

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15
Q

Metabolic acidosis: does serum K increase or decrease?

A

Increase

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16
Q

Causes of hypokalemia

A
  1. Intracellular shifting
  2. True deficits
    2a. Decreased intake (alcoholism, anorexia, etc.)
    2b. Increased output (GI losses, corticosteroids, loop/thiazide diuretics)
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17
Q

Signs of hypokalemia

A
  1. Skeletal muscle weakness
  2. Lethargy
  3. GI
  4. Ascending paralysis
  5. Cardiac arrhythmia
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18
Q

When do you administer PO K? IV?

A

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

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19
Q

Problems with PO K?

A
  1. unpleasant taste

2. GI upset

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20
Q

PO K dose

A

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

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21
Q

IV K dose

A

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

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22
Q

IV K dose in renal failure

A

50% of normal dose

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23
Q

When do you see hyperkalemia?

A

Renal failure, extracellular shifting

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24
Q

Medications that cause hyperkalemia

A 
K sparing diuretics
ACEIs, 
ARBs, 
NSAIDs, 
trimethoprim (Bactrim)
heparin
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25
Q

Causes of hyperkalemia

A
  1. Meds
  2. Increased K intake
  3. Adrenal steroid deficiency
  4. Addison’s disease
26
Q

ECG changes associated with hyperkalemia

A

peaked T waves

27
Q

ECG changes associated with hypokalemia

A

Flattened T waves, elevated U

28
Q

Mag predominately exists in

A

Predominantly in intracellular space; 50 –60% in bones

29
Q

Mag is involved in enzymatic reactions like

A

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

30
Q

How much mag is normally reabsorbed?

A

~97%

31
Q

Where is mag reabsorbed?

A

ascending LoH, proximal tubule, and distal tubule

32
Q

Which drugs significantly affect Mag wasting

A

loop diuretics (furosemide)

33
Q

Causes of hypomagnesia

A

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

34
Q

Which medications cause hypomagnesia

A

Loop diuretics
Amphotericin B
Cisplatin
Aminoglycoside antibiotics

35
Q

Signs of hypomagnesia

A
  1. Twitching
  2. Weakness
  3. Increased reflexes
36
Q

PO mag isn’t preferred because

A

PO takes a log time, poor absorption, IV preferred

37
Q

Max mag dose for asymptomatic patients

A

1 g/hr

38
Q

Severe mag dose

A

4-8 g

39
Q

Mild mag dose

A

1-4 g

40
Q

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

A

2 days

41
Q

Dose for mag for patient with renal impairment

A

Reduce normal dose by 50%

42
Q

Hypermagnesemia signs

A

Fatigue, lethargy, confusion, cardiac arrest

43
Q

Hypermagnesemia treatment

A

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

44
Q

Hypermagnesemia occurence

A

really rare - usually seen with cardiac arrest

45
Q

Phos is mostly found in

A

Primary INTRACELLULAR anion

Mainly found in bones, soft tissues; <1% in serum

46
Q

Phos functions

A

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

47
Q

Where does Phos get absorbed?

A

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

48
Q

How does phos get eliminated?

A

Renally

49
Q

Hypophosphatemia causes

A 
Intracellular shifting
Decreased phosphate or vitamin D intake
Malnutrition
Alcoholism
Refeeding syndrome
Meds
Critical illness
Metabolic alkalosis
50
Q

Meds that cause hypophosphatemia

A
  1. Sucralfate
  2. Calcium carbonate
  3. Al/Mag antacids
  4. Sevelamer
  5. Lanthanum carbonate
51
Q

When to use PO phos

A

when asymptomatic, causes diarrhea, erratic absorption

52
Q

When to use IV phos

A

when symptomatic or unable to tolerate oral formulations

53
Q

IV phos dose for renal impairment

A

50% of normal dose

54
Q

Hyperphosphatemia causes

A 
renal dysfunction (common)
extracellular shifting (esp during acidosis)
Increased phos or vit D intake (phos containing enemas)
55
Q

Signs of hyperphosphatemia

A

nausea, vomiting, dehydration, NM irritability

56
Q

Complications of hyperphosphatemia

A

Soft tissue and vascular calcification, renal osteodystrophy

57
Q

Refeeding Syndrome

A

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))

58
Q

Refeeding syndrome mechanism

A

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

59
Q

Hallmark sign of referring syndrome

A

hypophosphatemia

60
Q

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

A

anabolism and insulin release

61
Q

ISMP High-Alert Medications

A

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

62
Q

Electrolytes considered high-alert by ISMP

A

All forms of K and Mag

ILE I (18 decks)

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