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EM - Exam 2 > Electrolyte Abnormalities > Flashcards

Electrolyte Abnormalities Flashcards

1
Q

What is the most abundant intracellular cation?

A

K

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2
Q

Importance of potassium?

A

Cell metabolism, neuromuscular and cardiac electrical transmission

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3
Q

Etiology of K imbalances

A

Renal dysfunction
Dietary
Meds side effects (diuretics)

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4
Q

Causes of hypokalemia

A
  • Loss: renal excretion via diuretics, vomiting, diarrhea, hyperaldosteronism, hypomag
  • Shift: insulin, dobutamine, epi
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5
Q

S/s of hypokalemia

A
  • Weakness, fatigue, constipation, palpitations

- EKG: flat T, ST depression, U waves

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6
Q

Tx of mild hypokalemia

A

PO KCl (K-Dur, K-Lor, K-Tab)

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7
Q

Tx of mod-severe hypokalemia

A

IV KCl at 10 mEq/hr

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8
Q

10 mEq of KCl raises serum K by:

A

0.1 mEq/L

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9
Q

Causes of hyperkalemia

A
  • Absolute: renal insufficiency, meds (ACE, ARB, digoxin)

- Pseudo: DKA, hemolysis

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10
Q

S/s of hyperkalemia

A
  • Weakness, cramping, paresthesias

- EKG: peaked T, wide QRS, loss of P, sine wave

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11
Q

Sine wave on EKG is a late sign of:

A

Hyperkalemia

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12
Q

What is a late sign of hyperkalemia?

A

Sine wave on EKG

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13
Q

Tx of hyperkalemia

A
  • ALWAYS on cardiac monitor
  • Ca gluconate (stabilize myocytes)
  • Regular insulin
  • Albuterol nebulizer
  • Lasix
  • Na polystyrene sulfonate (Kayexalate)
  • Dialysis
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14
Q

Importance of Na in the body

A

Indirect measure of free water in serum

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15
Q

Define osmolarity

A

Concentration of solutes per L of solution

  • HIGH = fluid depletion
  • LOW = fluid retention
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16
Q

Etiology of Na imbalances

A
  • Hormonal (SIADH)

- Free water excess or loss

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17
Q

Causes of hyponatremia

A
  • Hypovolemic: diuretics, DM, adrenal insufficiency, sweat, burns, vomiting, diarrhea
  • Hypervolemic: CHF, cirrhosis, nephrotic synrome, preg, excess IVF
  • Euvolemic: SIADH, Ca, water intoxication
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18
Q

S/s of hyponatremia

A

HA, N/V, lethargy, confusion, seizure, coma

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19
Q

What are the symptoms of hyponatremia determined by?

A

Degree and rapidity of development

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20
Q

Causes of hypernatremia

A
  • Hypovolemic: sweating, vomiting, diarrhea, DI

- Hypervolemic: excess IV hydration, hyperaldosteronism

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21
Q

Tx of mild (asymp) hyponatremia

A

Fluid restriction

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22
Q

Tx of mod-severe hyponatremia

A
  • Acute/severe: 3% hypertonic saline 100 ml over 10 min

- Chronic: 0.5 ml/kg/hr or less

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23
Q

Why is correction of chronic hyponatremia slow?

A

Avoid central pontine myelinolysis (flaccid paralysis, seizures)

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24
Q

S/s of hypernatremia

A

AMS, seizures, hyperreflexia, spasticity, lethargy

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25
Q

Tx of hypernatremia

A

Gradual correction w/hypotonic or isotonic fluids (to avoid cerebral herniation)

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26
Q

Importance of Ca in body

A
  • Blood coagulation
  • Nerve conduction
  • Osteoclast bone activity
  • APs for muscle contractions
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27
Q

Etiologies of Ca imbalance

A

Regulated via PTH, calcitonin (thyroid), calcitriol (kidneys)

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28
Q

What Ca level is most accurate?

A

Ionized Ca level

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29
Q

Causes of hypocalcemia?

A

Hypothyroid
HypoPTH
Thyroidectomy
CKD

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30
Q

S/S of hypocalcemia

A
  • Paresthesias, hyperreflexia, tetany, Chvostek/Trousseau

- EKG: QT prolonged leading to Torsades

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31
Q

Tx of hypocalcemia

A
  • Asymp: oral Ca carbonate (or citrate)
  • 10% Ca gluconate IV
  • Replace Mg 1st if deficient
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32
Q

Causes of hypercalcemia

A
  • HyperPTH
  • Bone cancer
  • Prolonged immobilization
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33
Q

S/s of hypercalcemia

A
  • Stones, bones, moans, psychic groans and fatigue overtones

- EKG: short QT

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34
Q

Tx of mild-mod hypercalcemia

A

Increased oral hydration or IVF with or w/o diuretic

35
Q

Tx of mod-severe hypercalcemia

A

Bisphosphonates IV OR calcitonin IM/SC OR dialysis

36
Q

Importance of Mg in the body

A
  • Energy metabolism and neuromuscular transmission

- Necessary in facilitating replacement of K and Ca

37
Q

Etiologies of Mg imbalance

A
  • GI absorption
  • Renal excretion
  • Tubular reabsorption
38
Q

Causes of hypomagnesemia

A
  • Alcoholism (poor diet, decreased intestinal absorption, increased renal excretion)
  • Vomiting
  • Diarreha
39
Q

S/s of hypomagnesemia

A

Lethargy, confusion, tremors, seizures, paresthesias, hyperreflexia

40
Q

Tx of mild/chronic hypomagnesemia

A

Mg oxide PO 1-2x a day

41
Q

Tx of mod/symptomatic hypomagnesemia

A

Mg sulfate IV over 15-60 mins

42
Q

Causes of hypermagnesemia

A
  • Renal failure
  • Supratherapeutic replacement
  • Antacid abuse
43
Q

S/s of hypermagnesemia

A
  • Hyporeflexia
  • Bradycardia
  • Hypotension
  • Cardiac arrest
44
Q

Tx of hypermagnesemia

A
  • Stop any Mg supplements

- Give loop diuretics, CaCl IV, dialysis

45
Q

What conditions use Mg therapeutically?

A
  • Asthma
  • AF, torsades, dig toxicity
  • Preeclampsia
  • Migraine/cluster HAs
  • Constipation
46
Q

MOA of Mg therapy in asthma?

A

Pulm smooth muscle relaxation at bronchial level (improves FEV1)

47
Q

MOA of Mg therapy in AF/torsades/dig tox?

A

Prolongs sinus node recovery time and reduces AV node/accessory pathway conductions

48
Q

MOA of Mg therapy in preeclampsia?

A
  • Ca antagonist effect for seizure activity or to slow uterine contractions
  • Stimulates PG release, potent vasodilatory effect for BP control
49
Q

MOA of Mg therapy in migraine/cluster HAs?

A

Decrease vasospasm and pain transmitting chemicals

50
Q

MOA of Mg therapy in constipation?

A

Osmotic effect - causes H2O retention in GI lumen

51
Q

What is the normal BUN:Cr ration?

52
Q

Elevated BUN alone indicates?

A 
RBC hemolysis (GIB)
Excess protein intake
Corticosteroids
53
Q

Elevated BUN and Cr with ratio over 20:1 indicates?

A

Prerenal azotemia (dehydration)

54
Q

Elevated BUN and Cr with ration less than 20:1 indicates?

A

Azotemia (CKD, GN, post-renal obstruction)

55
Q

Abnormalities of Cl and CO2 MC reflect:

A

Compensations of acid-base secondary to pulm (respiratory) or renal (metabolic) disorders

56
Q

Causes of hypochloremia

A
  • Primary metabolic alkalosis (GI losses)

- Compensated respiratory acidosis

57
Q

Causes of hyperchloremia

A
  • Primary metabolic acidosis (excess NS)

- Compensated resp alkalosis

58
Q

Causes of hypobicarbonatemia

A
  • Primary met acidosis (renal failure)

- Compensated resp alkalosis

59
Q

Causes of hyperbicarbonatemia

A
  • Metabolic alkalosis (hypovolemia)

- Compensated chronic resp acidosis

60
Q

CV effects of acidosis

A

Decreased contractility

Hypotension

61
Q

Metabolic effects of acidosis

A

Insulin resistance

Hyperkalemia

62
Q

Neuro effects of acidosis

A

Somnolence

Coma

63
Q

Respiratory effects of acidosis

A

Compensatory hyperventilation resulting in respiratory muscle fatigue

64
Q

What is the use of anion gap?

A

Used to determine a metabolic acidosis state and to figure out its etiology (esp in setting of AMS or unknown exposures)

65
Q

How to calculate anion gap

A

AG = Na - (Cl+HCO3)

Normal is 8-16

66
Q

DDx of an elevated anion gap acidosis?

A
  • MUDPILES (methanol, uremia, DKA, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates)
  • GOLDMARK (glycols, oxoproline, lactate, D-lactate, methanol, aspirin, renal failure, ketoacidosis)
67
Q

Etiologies of euglycemic ketoacidosis

A
  • Fasting diabetic
  • Hypertriglyceridemia
  • Low carb/high fat diet
  • Gestational DM
68
Q

How does a fasting diabetic develop euglycemic ketoacidosis?

A

Depletion of their glycogen stores which ultimately results in decreased glucose production

69
Q

How does hypertriglyceridemia cause euglycemic ketoacidosis?

A

Causes volume displacement that can result in patient’s glucose level to appear normal or near-normal

70
Q

How does a low carb/high fat diet cause euglycemic ketoacidosis?

A

Decreases insulin levels and increases glucagon

71
Q

How does gestational DM cause euglycemic ketoacidosis?

A
  • Glucose utilization by fetus
  • Decreased carb intake from hyperemesis
  • Insulin levels that prohibit glycogenolysis but still alter glucagon:insulin ration
72
Q

Treatment of euglycemic ketoacidosis

A

Aggressive administration of NS solution, insulin, maintaining K levels, treating underlying conditions

73
Q

What is the only means by which ketoacidosis can be reversed?

A

Insulin therapy - but induces an intracellular shift of K resulting in hypokalemia

74
Q

How is insulin therapy used to treat ketoacidosis?

A
  • Reverses it but induces hypokalemia

- Treatment should be coupled with glucose and potassium

75
Q

Etiology of alcoholic ketoacidosis

A
  • Abd pain and/or vomiting causes decreased dietary intake (starvation)
  • Development of increased ketoacid production
  • Body decreases insulin to combat starvation
76
Q

Treatment of alcoholic ketoacidosis

A
  • ABCDEs
  • Hydration with D5NS
  • Bicarb (ONLY for severe acidosis and if not responding to D5NS)
77
Q

How to treat someone who comes into ED with AMS and unclear etiology?

A 
DONT
Dextrose (if hypoglycemic)
O2
Naloxone
Thiamine
78
Q

Onset of salicylate toxicity?

A

May begin 4-6 hrs after ingestion in a young infant, 24 hr or more in adolescent/adult

79
Q

Pathophys of salicylate toxicity

A
  • Inhibits Krebs cycle and AA synthesis which triggers fatty acid metabolism leading to ketonemia
  • Respiratory alkalosis
  • Renal insufficiency possible
80
Q

Earliest signs of salicylate toxicity

A

N/V, diaphoresis, tinnitus

81
Q

Treatment of salicylate toxicity

A
  • ABCs
  • Dextrose w/AMS
  • Gastric lavage and charcoal if early presentation
  • Na bicarb
  • Dialysis
82
Q

Describe pathophys of starvation/fasting and how to treat it

A
  • Similar to alcoholic ketoacidosis but less severe ketonemia
  • Treatment with D5NS, counseling
83
Q

Pathophys of uremia

A
  • Chronic decline in tubular functions of kidney
  • H excretion reduced
  • HCO3 excretion increased
  • Attempted buffering releases Ca salts from bone and their excretion in urine
84
Q

Treatment of uremia

A

Na bicarb to keep serum HCO3 greater than 20, nephrology consult

EM - Exam 2 (7 decks)

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