Electrolytes 2- SG Flashcards

1
Q

Evaluation of Hyponatremia

  • After initial steps of a thorough H&P, evaluate fluid status and then get which 4 labs first?
  • Which 2 labs second?
A
  • 1st: UA sodium, UA osmolality, serum osmolality, CMP
  • 2nd: TSH, serum cortisol
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2
Q

Tx of Hyponatremia

  • If Na is <125 or symptomatic, what is the tx?
  • ___ hyponatremia must be managed w/ extreme care
  • Rapid increase in serum sodium can lead to _______
  • Use of _____ is reserved for severe symptomatic cases
  • What is the “traditional” treatment of chronic hyponatremia? to induce what?
  • _____ are a newer class of tx agents which are vasopressin receptor antagonists
A
  • Hospitalize!
  • Chronic
  • Cerebral pontine myelinolysis (CPM)
  • Hypertonic solutions (3% NaCl)
  • Demeclocycline / to induce nephrogenic diabetes insipidus
  • “Vaptans”
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3
Q

Tx of Hyponatremia

  • In pts w/ severe symptomatic hyponatremia, the rate of sodium correction should be ____ in the first 24 hrs and ___ or less in 48 hours.
  • ****If CHRONIC hyponatremia, should try to keep it ___ or less in the first 24 hours*****
A
  • 6-12 mEq/L
  • 18 mEq/L
  • 8 mEq/L
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4
Q

When correcting Hyponatremia, how often should you be checking serum sodium as you are replacing it (to make sure not overcorrecting)?

A

q2h

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5
Q
  • Poorly understood entity characterized by focal demyelination in the pons and extra-pontine areas
  • Is it reversible?
  • Dysarthria, dysphagia, seizures, AMS, quadriparesis, hypotension begin ___ after over-correction of hyponatremia
A

Central Pontine Myelinolysis (CPM)

  • Irreversible
  • 1-3 days after
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6
Q

Which condition?

  • A hypertonic disorder due to serum sodium >145 mEqL
  • “Too little water relative to salt”
  • Clinical features due to brain shrinkage secondary to increased ECF osmolality
A

Hypernatremia

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7
Q

3 causes of Hypernatremia

A
  • Too little dietary water
  • Too much dietary salt
  • Excessive water loss from the body
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8
Q

4 causes of Hypernatremia

A
  • GI losses: elderly / infants w/ diarrhea
  • Skin loss: sweating, fever
  • Renal loss
  • Drug related: diuretics, lithium (can induce nephrogenic diabetes insipidus)
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9
Q

Clinical features of what condition?

  • Often asymptomatic
  • Thirst
  • AMS / weakness
  • Neuromuscular irritability
  • Focal neurologic deficits
  • Seizures or coma
A

Hypernatremia

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10
Q

Symptoms of Hypernatremia are related to rate of onset. If hypernatremia develops slowly, sxs will be ____.

A

Less dramatic

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11
Q

Normal Response to Hypernatremia

  • In response to hypernatremia, the body’s homeostatic mechanisms will normally do what 2 things?
  • The vast majority of cases of hypernatremia are due to _____.
A
  1. Create thirst / increase fluid intake
  2. Maximally concentrate urine to prevent further water loss
  • Water loss (GI tract, skin, renal)
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12
Q

Which condition?

  • Non-osmotic urinary water loss in setting of elevated serum sodium: urine is dilute when it should be concentrated (the collecting ducts are impermeable to water - water is not reabsorbed)
A

Diabetes Insipidus

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13
Q

Which type of diabetes insipidus?

  • Due to impaired secretion of antidiuretic hormone (ADH)
  • Also called _____.
  • Typically treated w/ _____
A
  • Central DI
  • Neurogenic DI
  • Desmopressin (often an inhaled dDAVP nasal spray or IV DDAVP)
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14
Q

Which type of diabetes insipidus?

  • Lack of kidney response to ADH, causing continued water loss even though patient is low on water.
  • Adequate ADH is present
A

Nephrogenic DI

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15
Q

Nephrogenic Diabetes Insipidus can be genetic or acquired.

  • Acquired is typically from which 4 things?
  • What is the treatment?
A
  • Chronic renal insufficiency
  • Tubulointerstitial renal disease
  • Amyloidosis
  • Lithium toxicity

Tx:

  • Thiazide diuretic
  • Amiloride (K sparing diuretic)
  • Chlorpropamide (antidiabetic oral agent)
  • NSAIDs have been tried (including Indomethacin)
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16
Q

Tx of Hypernatremia

  • ____ if severe
  • Stop water loss
  • Replace water deficit in what 3 ways? w/ what fluid?
  • Do not replace too rapidly, especially is the hypernatremia is _____. Why?
  • It is okay to correct rapidy if what?
A
  • Hospitalize
  • Oral, NG tube, IV w/ hypotonic fluids
  • present for several days (can cause seizures, brain damage, CPM)
  • Tx Rapid: If hypernatremia developed acutely
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17
Q

In order to replace free water in hypernatremia, you need to calculate what?

A

Water deficit

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18
Q
  • Major intracellular cation
  • Renal excretion is the major route of elimination
  • Regulation of renal ___ excretion and total body ___ balance occurs in the distal nephron
  • Aldosterone causes increased renal excretion
A

Serum Potassium

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19
Q

Which condition?

  • Nearly 98% of body’s K is intracellular
  • Total body K stores of approximately 50 mEq/kg
  • 20% of hospitalized pts are _____
  • 80% of pts who are receiving diuretics become ____.
A

Hypokalemia

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20
Q

Clinical presentation of which condition?

  • Weakness, fatigue
  • Muscle cramps
  • Hyporeflexia
  • Flaccid paralysis (ascending)
  • Hypercapnia
  • Which one is most important (not listed here)****
A

Hypokalemia

  • Cardiac arrhythmias
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21
Q

T/F

  • K can be replaced more rapidly than Na
A

True

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22
Q

4 ECG findings of Hypokalemia

A
  • Flattened T waves
  • Prominent U waves
  • Premature Ventricular Contractions (PVC’s)
  • Depressed ST segments
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23
Q

Hypokalemia mnemonic

hYpOkalemia U CRAMP

A
  • U waves
  • Cramping
  • Resp failure / rhabdomyolysis
  • Anorexia, N/V
  • Muscle weakness
  • Paralysis
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24
Q

3 mechanisms which cause Hypokalemia

A
  • Transcellular shifts
  • Renal losses
  • Extrarenal losses
25
Q

Which mechanism causing Hypokalemia?

  • Drugs: insulin, caffeine, bronchodilators, theophylline
  • Delirium tremens
  • Hyperthyroidism
  • Metabolic alkalosis

(all lead to increase beta-adrenergic activity which causes K to shift _____)

A

Transcellular Shifts

  • K shifts out of blood stream and into the cells
26
Q

Renal Losses causing Hypokalemia

  • ___ are the most common cause
  • Aldosterone facilitates K excretion in the _____ therefore, high aldosterone states such as Hyperaldosteronism and Cushing’s can lead to hypokalemia
  • Renal tubular acidosis types 1&2
A
  • Diuretics
  • distal tubules
27
Q
  • What are 3 extrarenal losses causing Hypokalemia?
  • Which one causes metabolic alkalosis, which further promotes renal potassium loss?*
A
  • Vomiting & diarrhea
  • Burns
  • Magnesium deficiency
  • *vomiting, NG suction
28
Q

Tx of Hypokalemia

  • Replace K and if possible tx underlying cause
  • ___ monitoring if inpatient
  • ____ replacement is preferred method
  • IV reserved for those not able to eat
    • If giving IV potassium via peripheral IV (not central line), include ____ with it because why?
    • Never ____ IV potassium!!
A
  • Telemetry
  • Oral potassium (better absorption)
  • Lidocaine, it burns and can destroy veins
  • Push, should be given slowly
29
Q

How do you replace potassium?

  • For every 0.1 mEq/L below 4mEq/L, give ___ mEq/L
A

10

30
Q

Special Circumstances of Tx of Hypokalemia

  • ______ is important in potassium reuptake, and if low can hinder replacement of potassium
    • draw Mg if hypokalemia is severe/resistant
  • Hypokalemia precipitates ____ toxicity
A
  • Hypomagnesemia
  • Digoxin
31
Q

Which condition?

  • In absence of renal failure or other identifiable causes, is actually quite rare
  • Relatively asymptomatic
  • Muscle weakness
    • begins in legs, acsends to trunk/arms
    • “ascending flaccid paralysis”
  • ECG changes show what?
A

Hyperkalemia

  • Potentially life threatening arrhythmias
  • Seen in 50% of patients
    • Peaked T waves**
    • Widened QRS
    • Junctional rhythm
    • Ventricular fibrillation
32
Q

Mnemonic for Hyperkalemia

“A FACT”

A
  • Arrhythmias
  • Flaccid paralysis
  • Ascending muscle weakness
  • Conduction abnormalities
  • T waves
33
Q

2 “factitious” causes of Hyperkalemia (Pseudohyperkalemia)

A
  • Hemolysis
  • Repeated fist clenching w/ tourniquet in place (poor venipuncture technique)
34
Q

3 causes of Hyperkalemia from Impaired K excretion

A
  • Renal failure
  • Mineralocorticoid deficiency
    • Addison’s Disease
    • Hypoaldosteronism
  • Renal tubular dysfunction
35
Q

5 drugs which can cause Hyperkalemia

A
  • K sparing diuretics
  • ACE inhibitors
  • ARBs
  • NSAIDs
  • Bactrim
36
Q

3 ways increased inake of K can cause Hyperkalemia

A
  • Increased dietary intake of K containing foods
  • Taking too much PO potassium
  • Taking too much IV potassium
37
Q

Other causes of Hyperkalemia

  • 3 conditions which move K from intracellular to extracellular spaces
A
  • Tissue damage (rhabdomyolysis)
  • Acidosis
  • Decreased insulin
38
Q

2 emergent treatment options for tx of Hyperkalemia

A
  • IV Calcium
  • Maneuvers to shift K from ECF to ICF
    • Sodium bicarbonate (IV push)
    • Insulin IV + D50W (given w/ dextrose)
39
Q

Which emergent tx of Hyperkalemia?

  • Less than 5 mins onset of action
  • Lasts 60 minutes
  • Reduces threshold potential of cardiac myocytes, restoring the normal gradient with the resting membrane potential which is distorted by hyperkalemia
A

IV Calcium

40
Q

Which emergent tx of Hyperkalemia?

  • IV push to increase pH
  • Action within 5 mins
  • Lasts 15-30 mins
  • Typically start with 1 amp = 50 mEq
A

Sodium Bicarbonate

(shifts K from ECF to ICF)

41
Q

Other potential options for emergent tx of Hyperkalemia (3)

A
  • Nebulized albuterol
  • IV Lasix
  • Dialysis
42
Q

Which “less urgent” tx of Hyperkalemia?

  • Exchanges Na for K in the gut
  • Decreases total body K
  • Causes lots of horrible diarrhea
  • Onset 2-12 hours, available PO or PR
  • Lowers K level by 0.5 for every gram given

What are 2 other less urgent tx options?

A

Kayexalate

  • Lasix (and other loop & thiazide diuretics)
  • Correct underlying cause
43
Q

Measure of total Ca is ___ + ____

A

Free (ionized) + protein bound

44
Q

Serum calcium is used to evaluate metabolism and monitor patients w/ what 3 things?

A
  • Hyperparathyroidism
  • Malignancies
  • Renal Failure
45
Q

Calcium has an inverse relationship with what chemical compound?

A

Phosphate

46
Q
  • 99% of Ca is located where in the body?
  • ECF Calcium
    • 50% is ____
    • 10% is _____
    • 40% is ____
A

Bone

  • 50% is free (ionized)
  • 10% is complexed
  • 40% is protein bound
47
Q

Which form of calcium?

  • Physiological active form, unaffected by serum albumin levels
  • Free to participate in cellular function
    • role in neuromuscular activity, cardiac function, and blood clotting
A

Ionized

48
Q

Which form of Calcium?

  • Citrate added to blood to prevent clotting
A

Complexed (chelated with substances such as citrate)

49
Q

Which form of Calcium?

  • When serum albumin is low, Ca level will also be low
    • Albumin and Calcium should be measured silmultaneously
A

Protein - bound (albumin)

50
Q

Calcium Physiology

  • Calcium is absorbed through ____ under influence of _____
  • Stored where?
  • Excreted by what organ?
  • Regulated by what 3 things?
A
  • GI tract / Vitamin D
  • Bone
  • Kidney
  • PTH / Vit D / Calcitonin
51
Q

A decrease in serum Calcium triggers the release of ___ from the parathyroid gland, which acts to increase Ca in the blood by doing what 3 things?

A

PTH

  • Activating Vit D (to increase Ca absorption in gut)
  • Promoting bone resorption (release Ca from bone)
  • Increasing Ca uptake in the kidneys (Promotes conservation)
52
Q

An increase in serum Calcium triggers the release of ____ from the thyroid gland, which acts to decrease Ca in blood by doing what?

A

Calcitonin

  • Inhibiting bone resorption
53
Q

If calcium levels are high, what should you be concerned about?

A

Malignancy

54
Q

Sxs of Hypercalcemia

“Has a cute saying to remember”

A

“Stones, bones, abdominal moans, and psychiatric groans”

  • Kidney stones
  • Bone pain
  • Abd pain, N/V, anorexia, constipation
  • Effects of nervous system, lethargy, fatigue, memory loss, psychosis, depression
55
Q

What 2 things cause 90% of hypercalcemia?

A
  • Malignancy
  • Primary hyperparathyroidism
56
Q

Which 4 medications can cause hypercalcemia?

A
  • Thiazide diuretics
  • Lithium
  • Antacids
  • Vitamin A analogs (accutane)
57
Q

Evaluation of Hypercalcemia

  • PTH is increased with _____
  • PTH is suppressed in _____
A
  • Increased in primary hyperparathyroidism
  • Suppressed in malignancy
58
Q
  • What is the #1 therapy / tx of Hypercalcemia?
  • What are 3 other tx options?
A
  • **#1: Volume expansion (normal saline)
  • Calcitonin (used to lower levels rapidly)
  • Pamidronate (usually given to cancer pts)
  • Zoledronic Acid (Zometra - replaced Pamidronate as a 1st line therapy for malignancy)