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Cardio-Renal I FINAL > Hughes - Fluid and Electrolytes Part 2 > Flashcards

Hughes - Fluid and Electrolytes Part 2 Flashcards

1
Q

2 general causes of hyperkalemia

A

-efflux and release of potassium out of cells

-decreased elimination

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2
Q

___glycemia can cause the efflux of potassium from cells and thus be a cause of hyperkalemia

A

hyper

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3
Q

true or false

high levels of aldosterone can lead to hyperkalemia

A

FALSE - low levels

aldosterone helps to excrete potassium

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4
Q

true or false

a patient can get hyperkalemia by consuming too much potassium

A

FALSE - not possible

pt must also have some renal impairment

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5
Q

true or false

hyperkalemia is considered asymptomatic until catastrophe

A

TRUE

dont really notice anything until ventricular fibrillation and asystole — like pulseless rhythms. die immediately

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6
Q

HOW does hyperkalemia increase the risk of arrythmias like ventricular fibrillation

A

bc the membrane potential is less negative – closer to excitatory potential

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7
Q

3 general categories of treatment for hyperkalemia

A

-agents that antagonize the cardiac effects – move FURTHER from excitatory potential

-agents that shift potassium to the intracellular space

-agents that enhance the clearance of potassium

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8
Q

as mentioned, agents that antagonize cardiac effects can be used in hyperkalemia

explain further how they work and when they’re used

A

they do NOT actually lower the potassium levels – are only used when EKG changes are present – save lives by shifting potential further from excitement

cardiac protective but do NOT actually get rid of potassium

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9
Q

name the medication that is used in hyperkalemia as a cardioprotective agent (only given when EKG changes are present)

important consideration when using

A

calcium gluconate (10% 10mL IV push) can repeat again in 5 mins if EKG doesnt resolve

only lasts for 1 hour, and also if the pt has overdosed on digoxin, it can make the cardiotoxicity worse (so use cautiously or not at all in this case)

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10
Q

name some agents that are used in hyperkalemia to shift potassium to the intracellular space

is this effect permanent?

A

insulin and glucose, b2 agonists, albuterol, sodium bicarb

NOT PERMANENT - works quick but is def temporary

ultimately in hyperkalemia - we need to give agents that ENHANCE THE ELIMINATION OF POTASSIUM - need to just get it out of the body

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11
Q

___________is best to use if the patient has hyperkalemia and metabolic acidosis

A

sodium bicarb

shifts potassium to intracellular space

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12
Q

sodium bicarb may take ___ to work

A

4 hours

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13
Q

name 4 agents that are used in hyperkalemia to enhance the clearance of potassium

A

sodium polystyrene sulfate
patiromer
sodium zirconium cyclosilicate
hemodialysis and loop diuretics

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14
Q

brand name sodium polystyrene sulfonate

A

kayexalate

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15
Q

brand name patiromer

A

veltessa

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16
Q

brand name sodium zirconium cyclosilicate

A

lokelma

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17
Q

3 agents that enhance the excretion of potassium through the GI tract that are used in hyperkalemia

A

veltessa (patiromer)
lokelma (sodium zirconium cyclosilicate)
sodium polystyrene sulfonate (kayexalate)

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18
Q

2 things used in hyperkalemia to enhance the clearance of potassium through the KIDNEYS

A

hemodialysis and loop diuretics

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19
Q

3 risks when using sodium polystyrene sulfonate for hyperkalemia

A

sodium overload
diarrhea
intestinal necrosis

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20
Q

which 2 agents that enhance the excretion of potassium are technically only indicated for chronic use and not for emergencies?

A

paritromer (veltessa)
sodium zirconium cyclosilicate (lokelma)

however, often used “off label” anyway for emergencies

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21
Q

true or false

hemodialysis is a more reliable way to remove potassium than through a loop diuretic in cases of severe renal diseas

A

true

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22
Q

99% of total body calcium is located where

A

the bone

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23
Q

calcium located where?? is actually important for things like nerves and muscle contraction

A

in the plasma – not in the bone

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24
Q

when looking at calcium levels, it is important to do what

A

adjust for albumin deficiencies

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25
Q

some absorption of calcium from the GI tract requires….

A

vitamin D

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26
Q

3 general things that can cause hypercalcemia

A

-movement of calcium from the bone (ie - destruction, malignancy, hyperparathyroidism)

-vitamin D toxicity

-drugs

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27
Q

true or false

low levels of vitamin D cause hypercalcemia

A

FALSE - high levels

bc vitamin D helps the body to absorb calcium from the GI tract and into the blood

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28
Q

name 4 general systems affected by hypercalcemia

A

neurologic
cardiac
renal
GI

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29
Q

for the treatment of hypercalcemia, we generally target…

A

THE CAUSE

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30
Q

name 5 drugs that can cause hypercalcemia

A

calcium supplements
thiazides
lithium
estrogens
tamoxifen

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31
Q

drugs that can cause hyperkalemia

A

ACE/ARB
B-blockers
lithium
heparin
K sparing diuretics
cyclosporine
tacrolimus
digoxin

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32
Q

what is always done FIRST in treating hypercalcemia?

is there anything to be aware of with this?

A

give FLUID – 1-2 liters of IV normal saline

have to be careful if the pt has renal or heart failure (fluid overload)

33
Q

why is fluid always given 1st for hypercalcemia

A

most pts are volume depleted - have to expand

also, giving more fluid will increase the GFR and decrease the reabsorption of calcium through the kidney

34
Q

what is given AFTER fluids are given for hypercalcemia?

A

loop diuretics - to increase the release of calcium in the urine (monitor fluid loss and electrolyte disturbances!)

35
Q

if fluid + loop diuretic dont work for hypercalcemia, what is done next?

A

calcitonin-salmon is given. (considered second line)

36
Q

onset of calcitonin-salmon and any concerns with it

A

starts working very quickly - within hours - but has short duration

also, tachyphylaxis also occurs quickly - within 1-3 days

basically the body adjusts to it and it wont do anything anymore

ALSO hypersensitivity concerns bc it’s a protein

37
Q

true or false

thiazides cannot be used for hypercalcemia

A

TRUE - thiazides increase calcium

ONLY LOOPS!!

38
Q

in treating hypercalcemia, what is considered like the “bridge” for bisphosphanates

A

calcitonin-salmon

39
Q

name 3 bisphosphanates that can be used for hypercalcemia

A

etidronate
pamidronate
zoledronic acid

40
Q

true or false

bisphosphanates are not very effective in treating hypercalcemia

A

FALSE - they’re very effective in getting to normal calcium levels – but kidney injury is possible

41
Q

onset and redosing for bisphosphanates

A

onset is slow – 2 days – also has very long duration so can redose but after a week

42
Q

most potent and preferred bisphosphanate for hypercalcemia

A

zoledronic acid

43
Q

name 4 things that can possibly be used for hypercalcemia but are RARELY used

A

gallium
phosphate
corticosteroids
NSAIDS

44
Q

issue with gallium for hypercalcemia

A

causes nephrotixicity - it’s a heavy metal

45
Q

how does phosphate work in hypercalcemia

any AE?

A

makes a complex with calcium and deposits in the bone – given PO only – for chronic use

issue - GI adverse events

46
Q

which potential drug class used to treat hypercalcemia can be useful if the hypercalcemia is vitamin-D induced?

A

CORTICOSTEROIDS - bc they impair the vitamin D-mediated absorption of calcium

47
Q

NSAIDS are mainly used in which patients for hypercalcemia

A

cancer patients (PGE-mediated)

48
Q

most phosphorus is intracellular or extracellular?
specifically where?

A

intracellular
mainly in the bone

BARELY extracellular at all

49
Q

true or false

most phosphorus that we eat gets absorbed

also - which foods have high phosphorus

A

TRUE

milk, meat, veggies

50
Q

what can REDUCE the absorption of dietary phosphorus?

A

Ca/Mg/Al antacids

iron supplements

51
Q

true or false

hypophosphatemia due to low dietary intake is rare

A

TRUE – phosphate is found in so many things

52
Q

give a specific scenario in which hypophosphatemia can occur

A

refeeding syndrome – givin a malnourished pt a high calories diet without supplementing phosphate

53
Q

the symptoms seen in hypophosphatemia is mostly related to….

A

impaired cellular energy stores (the P in ATP is phosphorus!!)

54
Q

explain the treatment for hypophosphatemia (include drug names)

A

may just need to eat more phosphate – resolve on its own

can also give PO supplements (potassium phosphate + sodium phosphate) “K-phos” or “neutra phos”

if the hypophosphatemia is SEVERE or the patient cant take PO - use IV potassium phosphate or sodium phosphate “K-phos” = potassium phosphate

55
Q

cautions when using K-phos, neutra-phos, etc, for hypophosphatemia

A

they have varying amounts of potassium and salt - be careful if either of these are a concern

56
Q

when giving IV phosphate… be careful to consider what

A

each mmol of phosphate also delivers 1.5mmol of potassium!!! watch the rate of infusion

57
Q

AE of IV phosphate

A

tissue calcification
hypotension
K/na/fluid overload

58
Q

magnesium is mostly intracellular or extracellular?

A

like potassium - intracellular

59
Q

the serum magnesium levels have _____ correlation with the total body stores

A

poor

60
Q

what kind of things is magnesium important for

A

metabolism, RNA and DNA handling, operation of electrolyte pumps and channels

61
Q

the dietary absorption of magnesium depends on…

A

the body’s need for it

62
Q

how is magnesium mainly eliminated?

A

kidney

63
Q

the reabsorption of magnesium is parallel with _______

A

sodium

64
Q

general causes of hypomagnesia

A

decreased intake
diarrhea
increased renal elimination
increased requirements for magnesium

65
Q

which patients have increased requirements for magnesium and are thus prone to hypomagnesium

A

pregnant ppl and infants

66
Q

a lot of patients with hypokalemia also have —-

A

hypomagnesium

67
Q

true or false

there is no defining symptom to diagnose hypomagnesium

A

TRUE – all very vague symptoms

need to see CMP

68
Q

when deciding to treat hypomagnesium, ___ is more important than ____

A

symptoms and EKG findings are more important than the levels themselves

69
Q

ORAL treatment for hypomagnesium for an asymptomatic patient with mild depletion

A

Slow Mag (Mg chloride) – sustained release

preferred over Mg antacids, milk magnesia, mg oxide

also give foods with Mg!! - vegetables, nuts, meat, fruit, etc

70
Q

preferred parenteral route for hypomagnesium

A

IV preferred over IM

71
Q

IV treatment for hypomagnesium

include any concerns

A

Mg sulfate. around half is eliminated by the kidneys right away — so give a prolonged infusion over SEVERAL HOURS!!!!!

also, monitor for EKG changes, hypotension (due to vasodilation) and respiratory changes

72
Q

as mentioned, giving IV Mg sulfate for hypomagnesium can cause hypotension

how do you look out for this

A

caused by vasodilation - so watch for flushing of the skin, and warmth – monitor

73
Q

the cause of hypermagnesium is almost always what??

A

renal insufficiency + taking Mg-containing meds and supplements

74
Q

name 2 OTC products that contain magnesium, making it easy to have too much

A

antacids
laxatives

75
Q

explain the presentaiton of hypermagnesium

A

gets worse as concentration increases

starts with bad tendon reflexes, and progresses to complete heart block

76
Q

explain the treatment for hypermagnesium

A

d/c mg-containing meds

if pt has renal impairment – consider hemodialysis - the kidney will get rid of excess

can give loop + 0.45% NaCl to replace volume

77
Q

if life-threatening complications from hypermagnesium occur, what should be given?

(heart block, loss of tendon reflexes, quadraplegia)

A

IV calcium!!!! to antagonize the respiratory and cardiac effects

(same as for hyperkalemia)

78
Q
A

Cardio-Renal I FINAL (13 decks)

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