Lecture 10.5: Fluid + Electrolytes Part 2 Flashcards

1
Q

Where do I generally find potassium in the body?

A

ICF!

Note:
Serum potassium is normally 3.5-5, which is low, so you know its all inside the cell. Another way to remember potassium is inside is that you can eat 3-5 bananas, so the range is 3.5-5 and the low number means potassium is inside the cell.

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2
Q

How does potassium move in/out of the cell?

A

Na/K/ATPase pump.

3 Na+ out
2 K+ in
1 ATP

Note: Na+ and out are 3 letters
K+ and in are 2 letters
Potassium is lowest outside the cell, so it must be going in.

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3
Q

What ion is the cell membrane generally impermeable to?

A

K

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4
Q

Why is K+ so important for our body?

A

Acid-base balance, as it is exchanged for H+! (hyperkalemia and metabolic acidosis are generally linked)

Muscle cell excitability
Nerve impulses

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5
Q

What kind of medications/things cause K+ to shift into a cell?

A

Insulin, Catecholamines, and B-agonists.

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6
Q

What kind of inhaled medication can help reduce serum potassium?

A

Nebulizing treatments.

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7
Q

What 4 factors promote LOWER serum potassium?

A

Aldosterone (Sodium retention means we get rid of potassium instead)
Insulin
B-agonists
Alkalosis (in order to get back to neutral, we need to exchange our potassium for H+)

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8
Q

What 4 factors promote HIGHER serum potassium?

A

Cell lysis (Think tourniquets)
Strenuous exercise
Alpha agonists
Acidosis (in order to get back to neutral, we need to exchange our excess H+ for more potassium)

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9
Q

Why are K+, H+, and Na+ all linked?

A

Na+ and K+ are linked via cell membrane pumps, aka they exchange for one another.

H+/K+ are exchanged with Na+ in the DCT of the nephron. If we have low H+, we need to retain and kick something else out, so we kick out Na+/K+, which is why acidosis/alkalosis can be linked often with hyper/hypokalemia.

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10
Q

What 3 factors are responsible for modulating our urinary excretion of potassium?

A

Changes in ECF concentration
Changes in pH
Aldosterone levels

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11
Q

What does increased ECF concentration of potassium cause in terms of potassium secretion?

A

Increased secretion of potassium.

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12
Q

What does low pH cause in terms of potassium secretion?

A

Lower secretion of potassium, increased secretion of H+.
Note:
every 0.1 decrease of pH in acidosis = increase of potassium by 0.7 mEq.

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13
Q

What does increased aldosterone cause in terms of potassium secretion?

A

Increased secretion of potassium as we retain sodium preferentially.

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14
Q

What kind of medications can block the secretion of potassium? What is the mechanism?

A

ACEI/ARBs/Aldosterone antagonists.

All of which block aldosterone, so we get rid of sodium instead of potassium.

Note:
This is why the side effect of all 3 is hyperkalemia and aldosterone antagonists are known as K+ sparing diuretics.

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15
Q

What are the 4 ways hypokalemia is caused?

A

Renal loss
GI loss
Poor intake
Transcompartmental shift

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16
Q

What ways does renal loss cause hypokalemia?

A

Diuretics
Renal disease
Elevated aldosterone/corticosteroids

Renal syndromes: Bartter syndrome, Liddle syndrome, Gitelman syndrome

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17
Q

What ways does GI loss cause hypokalemia?

A

Vomiting or diarrhea

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18
Q

What 3 things cause transcompartmental shifts of potassium into the cell?

A

Beta-adrenergic agonists
Insulin
Alkalosis

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19
Q

What are the lab abnormalities we would expect in hypokalemia?

A

Low serum potassium < 3.5 mEq/L
Blood pH increase (alkalosis)
Decreased urine osmolality
Decreased urine specific gravity
EKG abnormalities (QT prolongation and presence of a U wave)

Note:
A U wave appears in after a T wave and before a P wave. Normally not visible.

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20
Q

What happens to our urine in hypokalemia?

A

Polydipsia
Polyuria

AKA we can’t concentrate our urine well.

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21
Q

What neuro symptoms do I expect in hypokalemia?

A

Paresthesias
Paralysis
Irritability/Confusion
Drowsiness

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22
Q

What muscular symptoms do I expect in hypokalemia?

A

Weakness
Fatigue/Lethargy
Cramps or tenderness

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23
Q

What GI symptoms do I expect in hypokalemia?

A

Constipation
Ileus
Abdominal distension

Note:
AKA abdominal weakness. Food isn’t moving well cause muscles are weak/fatigued.

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24
Q

What cardiac symptoms do I expect in hypokalemia?

A

Hypotension
Palpitations
Dysrhythmias
Weak, thready pulse

Note:
Imagine a heart that is getting weaker ):

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25
Q

What does potassium do to the T wave in an EKG?

A

Low K = low T
High K = high T

Note:
Normal would have a T wave and maybe a tiny U wave.
Hypo would have a shallow T wave with a big U wave.

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26
Q

What is the acronym for hypokalemia symptoms?

A

I am

Alkalosis

Shallow respirations
Irritability
Confusion/drowsiness

Weakness/fatigue
Arrthymias (tachy and/or brady)
Lethargy
Thready pulse

Also
Decreased intestinal motility, nausea, vomiting, and ileus.

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27
Q

How do I manage hypokalemia?

A

Treat underlying cause!!!!!!!!!
AND
check for hypomagnesemia!!

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28
Q

How do I treat acute hypokalemia?

A

Potassium replacement via oral/IV KCl at 10-20 mEq/hr.

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29
Q

How do I treat chronic hypokalemia?

A

Eat more potassium-rich foods
Check for other predisposing conditions (such as chronic metabolic acidosis)
Consider oral potassium (CONSIDER!!! not automatic)

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30
Q

What lab value is hyperkalemia?

A

> 5.0 mEq/L

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31
Q

What generally causes hyperkalemia?

A

Excess intake
Inadequate elimination
Release from ICF

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32
Q

What is the main cause for excess intake of potassium?

A

IVs

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33
Q

What can cause impaired/inadequate elimination of K+?

A

CKD, adrenal insufficiency, meds

Note:
Addison’s causes hyperkalemia by impairing aldosterone production.

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34
Q

What can cause K+ to be released from cells?

A

Cell damage, excessive/severe muscle contractions

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35
Q

What can cause pseudohyperkalemia?

A

Hemoylsis of samples, prolonged tourniquet time, traumatic stick

Note:
All of these cause cells to explode, and most of our potassium is contained in cells! If you retake the labs properly, potassium will be different by a decent amt.

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36
Q

What meds can cause hyperkalemia?

A

ACEI/ARBs/K+ sparing diuretics
NSAIDs
Trimethoprim
Heparin

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37
Q

What conditions can cause hypoaldosteronism?

A

Addison’s
Congenital adrenal hyperplasia
Hyporeninemic state
Severe dehydration
SLE (Systemic lupus erythematosus)
Type 4 renal tubular acidosis

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38
Q

What cause cause an extracellular shift of potassium?

A

Hemolysis
Tissue damage (both of these generally need renal failure to actually cause hyperkalemia)

Acute acidosis (decreased insulin or digoxin OD)
Beta-blockers
Hyperosmolar state (think diabetes)

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39
Q

What lab abnormalities do I expect in hyperkalemia?

A

Serum potassium > 5.0 mEq/L
EKG changes (wide QRS, huge, peaked T wave)

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40
Q

What neuro symptoms do I expect in hyperkalemia?

A

Paresthesia
Weakness
Dizziness/drowsiness

Note:
Weakness and dizziness are the distinct symptoms.
Paresthesia and drowsiness is found in both kalemias.

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41
Q

What muscle symptoms do I expect in hyperkalemia?

A

Weakness
Cramps

Note:
Overlaps with hypokalemia, but hypokalemia also includes fatigue.

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42
Q

What GI symptoms do I expect in hyperkalemia?

A

Diarrhea
Abdominal cramps
Nausea/vomiting

Note:
No overlap with hypokalemia!

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43
Q

What cardiac symptoms do I expect in hyperkalemia?

A

Palpitations
Dysrhythmias
Cardiac arrest
Hypotension

Note:
Only difference is cardiac arrest.
In hypokalemia, its a weak and thready pulse.

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44
Q

What EKG changes do I expect in hyperkalemia?

A

High K = high T, so I would see a tall, peaked T wave.

I would also see a wide QRS with ST depression.

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45
Q

What are the summarized hyperkalemia symptoms?

A

Muscle twitches = cramps = paresthesias
Irritability & anxiety
Low BP
EKG changes
Dysrhythmias
Abdominal cramping
Diarrhea

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46
Q

How do I treat hyperkalemia?

A

Treat UNDERLYING cause!!!!!

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47
Q

What is the process of treating hyperkalemia that has associated EKG changes?

A

IV calcium gluconate
IV insulin + glucose
+/- inhaled albuterol therapy (adjunct)
+/- urgent diuresis (if kidney dysfunction is present)

Note:
IV calcium gluconate is given because calcium salts can stabilize cell membranes. AKA it’s to help with the EKG changes so we don’t have a cardiac arrest or dysrhythmia. Calcium will also cause an intracellular shift of potassium.

Insulin can cause shift of potassium back into the cell. Glucose is given to make sure blood glucose doesn’t crash.

Nebulizing tx, as mentioned earlier, is an beta agonist, which also brings potassium back into the cell.

48
Q

What treatment steps do I give for ALL hyperkalemic patients?

A

DC all meds that can increase K+
Educate on low-K diet
CONSIDER meds to lower potassium (diuretics, cation exchange agents, potassium binders)

49
Q

What is the preferred diuretic for hyperkalemia treatment? What SE do I look out for?

A

Loops.

Look out for hypokalemia, hypovolemia, hyponatremia, metaboic alkalosis, hypocalcemia.

Also note any ototoxicity, allergic rxns, and hyperuricemia.

50
Q

What should I look out for when giving thiazide diuretics for hyperkalemia?

A

HCTZ, chlorthalidone, metolazone may be better tolerated than loops.

Look out for hypokalemia, hyponatremia, metabolic alkalosis, hypomagnesemia, and hypercalcemia

May also see hyperlipidemia, hyperuricemia, sleep disturbances.

51
Q

What side effects are opposites of each other between thiazides and loops?

A

Thiazides cause HYPERcalcemia
Loops cause HYPOcalcemia

52
Q

What are the two cation exchange agents?

A

Patiromer (veltassa): binds K in gut for Ca.

Sodium zirconium cyclosilicate (Lokelma): binds K in gut for Na and H.

53
Q

What are the SE of the cation exchange agents? Contraindications?

A

Patiromer/veltassa = hypokalemia, hypomagnesemia, constipation/diarrhea.

Sodium zirconium cyclosilicate (Lokelma) = hypokalemia, edema.

CI: Allergy to the med itself.

Also, watch out for the med binding to other meds in the GI tract!!

54
Q

What is the potassium binding resin?

A

Sodium Polystyrene sulfonate (Kayexelate) binds K in gut.

Takes 24 hrs to lower K.

SE: Hypernatremia, hypokalemia, hypocalcemia, hypomagnesemia

Causes SIGNIFICANT GI SE: Constipation, vomiting, intestinal necrosis.

CI: Hypokalemia, allergy, neonatal age, bowel obstruction.

Note: No longer recommended.
Brand name sounds like K is exiting!

55
Q

What are the 3 bone minerals?

A

Calcium
Phosphorus
Magnesium

56
Q

Where do I find calcium and magnesium in the body?

A

Calcium is found 99% in bone, 0.8 in ICF, 0.2 in ECF.
Magnesium is found 50-60 in bone, 40-50 in ICF, 1 in ECF.

57
Q

What are the 3 kinds of calcium in the ECF?

A

Protein-bound calcium (40% of ECF calcium)
Chelated calcium (10% of ECF calcium)
Ionized calcium (50% of ECF, aka UNBOUND)

58
Q

What is protein-bound calcium usually bound to?

A

Albumin, so it can’t move in/out of cells.

59
Q

Which calcium can freely move?

A

Ionized calcium (often considered the metabolically active form)

60
Q

What can cause pseudohypocalcemia?

A

Low serum albumin.

Note:
This is because serum calcium calculations don’t differentiate between ionized and protein-bound. However, your body will shift calcium elsewhere if there is not enough albumin to bind it. This effectively lowers serum calcium with no effect on ionized calcium.

Must calculate corrected calcium if hypoalbuminemia and hypocalcemia is present!!!

61
Q

How much of our magnesium is protein-bound?

A

20-30% of ECF Mg

Note:
If hypoalbuminemia present, consider Mg correction.

62
Q

What is the most important vitamin when it comes to calcium!!!!

A

Vitamin D, which is synthesized by skin from UV exposure OR diet.

Activated once processed in the liver/kidney.

Increases C and P absorption from the intestine.
Needed for normal bone formation.

63
Q

What two hormones in the body regulate calcium levels?

A

PTH by the paraythyroid glands.
Calcitonin by the thyroid.

64
Q

How does PTH regulate serum calcium?

A

Released when serum calcium is LOW.

Promotes release of calcium from bone, increases vit D activation, stimulates renal conservation of calcium, and increases phosphate excretion.

Note:
Mg is important because it is a cofactor for PTH synthesis and release.

65
Q

How does calcitonin regulate serum calcium?

A

Release when serum calcium is HIGH.
Opposes PTH actions.

66
Q

What are the functions of calcium in the body?

A

Muscular and Neuro
Blood clotting
Enzymatic reactions
Second messengers
Generating APs

67
Q

What are the functions of magnesium in the body?

A

Enzymatic reactions
ATP generation
Calcium transport
Potassium reabsorption
PTH release

68
Q

What lab value is hypocalcemia?

A

<8.5 mg/dL

Note:
It is actually very rare, seen only in critically ill patients.

69
Q

What are the potential causes of hypocalcemia?

A

Impaired ability to mobilize stored calcium
Decreased intake/reabsorption
Abnormal renal losses
Increased binding/chelation

70
Q

What can impair our ability to mobilize our stored calcium?

A

Hypoparathyrodism (main one)
Hypomagnesemia (needed for PTH synthesis)
Resistance to PTH

71
Q

What can impair our calcium intake/absorption?

A

Malabsorption (AKA something happening to our SI)
Vit D deficiency

72
Q

What conditions cause increased the binding/chelation of calcium?

A

Hyperphosphatemia (causes calcium to be leeched from bones and blood to precipitate into tissues)
Acidosis (We will use Ca to maintain acid-base balance?)

73
Q

What happens to our AP threshold in hypocalcemia?

A

DECREASED thresholds for excitation, AKA easy to excite a cell.

74
Q

What lab abnormality do I expect in hypocalcemia?

A

< 8.5 mg/dL

75
Q

What neuro symptoms do I expect in hypocalcemia?

A

Anxiety, irritability
Seizures
Hyperactive reflexes
Paresthesias (especially periORAL)
Death

76
Q

What muscular symptoms do I expect in hypocalcemia?

A

Cramps (skeletal and abdominal)
Laryngeal spasms (stridor)
Carpopedal spasm
Chvostek and Trosseau signs

77
Q

What cardiac symptoms do I expect in hypocalcemia?

A

Cardiac dysrhythmias
Prolonged QT INTERVAL

78
Q

What skeletal symptoms do I expect in hypocalcemia?

A

Osteomalacia (weakness of the bones, but better described as softness)
Bone pain
Deformities
Fractures

79
Q

What is the acronym for hypocalcemia?

A

Convulsions
Arrhythmias
Tetany
Stridor and spasms

80
Q

How do I treat acute hypocalcemia?

A

IV infusion of calcium solution

81
Q

How do I treat chronic hypocalcemia?

A

Calcium replacement via diet/supplements
Vit D supplements (maybe)
Synthetic PTH

82
Q

What lab value is hypercalcemia?

A

> 10.5 mg/dL
(sometimes falsely elevated if lab draw is prolonged with a tight tourniquet)

83
Q

What are some potential causes of hypercalcemia?

A

Increased bone resorption
Increased intake/absorption
Decreased renal elimination

84
Q

What mnemonic sums up hypercalcemia symptoms?

A

Stones, bones, abdominal moans, and psychic groans

85
Q

What conditions would cause increased bone resorption?

A

Hyperparathyroidism, cancer (previous MOD lecture!)

Note:
Cancer can cause increased PTH!!! One of the main symptoms of paraneoplastic syndrome.

86
Q

What can cause increased calcium intake/absorption?

A

Excessive Vit D or calcium
Milk-alkali syndrome (AKA lots of TUMs and milk)

87
Q

What can cause decreased renal elimination of calcium?

A

Thiazides
Lithium

Note:
This is why thiazides are used to treat hypercalciURIA.

88
Q

What does hypercalcemia do to membrane thresholds?

A

Increases the threshold for excitation, AKA harder to excite the cell.

89
Q

What lab abnormality do I expect in hypercalcemia?

A

> 10.5 mg/dL

90
Q

What neuro symptoms do I expect in hypercalcemia?

A

Lethargy
Personality and behavior changes
Diminished reflexes
Coma

Note:
AKA all of these sound like a very exhausted person. Neurons firing slow.

91
Q

What muscular symptoms do I expect in hypercalcemia?

A

Muscle weakness and low tone
Muscle atrophy

92
Q

What skeletal symptoms do I expect in hypercalcemia?

A

Bone pain
Osteopenia (Low bone density)
Osteoporosis (Low bone mass)

93
Q

What GI symptoms do I expect in hypercalcemia?

A

Anorexia
Nausea/vomiting
Constipation

94
Q

What renal symptoms do I expect in hypercalcemia?

A

Inability to concentrate urine (polydipsia, polyuria)
Flank pain
Kidney stones

95
Q

What cardiac symptoms do I expect in hypercalcemia?

A

SHORT QT interval

96
Q

How do I treat hypercalcemia?

A

Managing the UNDERLYING cause!!!!

Rehydration (if indicated)
Increased renal excretion of calcium via loop diuretics (think pharmacology. Loops + IV fluids)

Limit release of new calcium from bone stores
Bisphosphonate (prevents calcium leeching off bones)
Calcitonin

Dialysis (if needed)

97
Q

What lab value corresponds to hypomagnesemia?

A

< 1.8 mg/dL

98
Q

What is hypomagnesemia typically seen with?

A

Combination with hypokalemia and/or hypocalcemia

99
Q

What are the potential causes of hypomagnesemia?

A

Impaired intake/absorption
Increased Mg loss

100
Q

What causes impaired intake/absorption of magnesium?

A

Malnutrition/alcoholism
PPIs (proton pump inhibitors)
Loop diuretics

101
Q

What causes increased Mg loss?

A

Diuretics (loops)
Severe burns
Hyperparathyroidism
Hyperaldosteronism
DKA

Note:
Kidneys are only good at getting rid of Mg, not keeping it.

For hyperparathyroidism, the increased load of calcium (hypercalcemia is caused by hyperparathyroidism) causes us to get rid off more Mg.

Essentially, the minor increased reabsorption of Mg from PTH is overriden by the ensuing hypercalcemia.

102
Q

What does hypomagnesemia do to membrane thresholds?

A

Decreased thresholds for excitation, AKA easy to excite the cells.

103
Q

What lab abnormalities do I expect in hypomagnesemia?

A

Serum Mg < 1.8 mg/dL
low K and Ca are often seen as well.

104
Q

What neuro symptoms do I expect in hypomagnesemia?

A

Personality change
Anxiety, depression, apathy
Tremor
Nystagmus
Seizures
Death

105
Q

What muscular symptoms do I expect in hypomagnesemia?

A

Weakness
Cramps
Involuntary movements (athetoid or choreiform)
Tetany
Babinski/Chvostek/Trosseau signs

106
Q

What cardiac symptoms do I expect in hypomagnesemia?

A

Cardiac dysrhythmias
Tachycardia
PROLONGED QT interval

107
Q

How do I treat acute hypomagnesemia?

A

IV infusion of magnesium solution

108
Q

How do I treat chronic hypomagnesemia?

A

Mg replacement therapy (diet/oral supplements)
Address other underlying electrolyte disorders too!

109
Q

What lab value do I see in hypermagnesemia?

A

> 3.0 mg/dL

Note:
VERY RARE

110
Q

What are the potential causes of hypermagnesemia?

A

Excessive intake (IV, oral)
Decreased excretion (AKI, CKD)

Note:
kidneys are very good at getting rid of Mg, so its hard for us to build up a lot.

111
Q

How does hypermagnesemia affect membrane thresholds?

A

Increased threshold for excitation AKA hard to excite!

112
Q

What can happen in hypermagnesemia to PTH?

A

Suppressed PTH secretion

Note:
You need Mg all the way up to > 4.8 mg/dL for this to occur.

113
Q

What are the muscular symptoms of hypermagnesemia?

A

Muscle weakness and low tone
Flaccid paralysis

114
Q

What are the cardiac symptoms of hypermagnesemia?

A

Bradycardia
Hypotension
SHORTENED QT intervals

115
Q

What are the neuro symptoms of hypermagnesemia?

A

Lethargy
Confusion
Diminished reflexes
Coma

Note:
Slow neurons due to increased threshold requirement.

116
Q

How do I treat hypermagnesemia?

A

DC Mg therapy. (IV calcium can antagonize Mg)

Dialysis if AKI/CKD is present (kidneys are primary way for getting rid of Mg)