Electrolytes 2 Flashcards
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?
- 1st: UA sodium, UA osmolality, serum osmolality, CMP
- 2nd: TSH, serum cortisol
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
- Hospitalize!
- Chronic
- Cerebral pontine myelinolysis (CPM)
- Hypertonic solutions (3% NaCl)
- Demeclocycline / to induce nephrogenic diabetes insipidus
- “Vaptans”
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*****
- 6-12 mEq/L
- 18 mEq/L
- 8 mEq/L
When correcting Hyponatremia, how often should you be checking serum sodium as you are replacing it (to make sure not overcorrecting)?
q2h
- 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
Central Pontine Myelinolysis (CPM)
- Irreversible
- 1-3 days after
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
Hypernatremia
3 causes of Hypernatremia
- Too little dietary water
- Too much dietary salt
- Excessive water loss from the body
4 causes of Hypernatremia
- GI losses: elderly / infants w/ diarrhea
- Skin loss: sweating, fever
- Renal loss
- Drug related: diuretics, lithium (can induce nephrogenic diabetes insipidus)
Clinical features of what condition?
- Often asymptomatic
- Thirst
- AMS / weakness
- Neuromuscular irritability
- Focal neurologic deficits
- Seizures or coma
Hypernatremia
Symptoms of Hypernatremia are related to rate of onset. If hypernatremia develops slowly, sxs will be ____.
Less dramatic
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 _____.
- Create thirst / increase fluid intake
- Maximally concentrate urine to prevent further water loss
- Water loss (GI tract, skin, renal)
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)
Diabetes Insipidus
Which type of diabetes insipidus?
- Due to impaired secretion of antidiuretic hormone (ADH)
- Also called _____.
- Typically treated w/ _____
- Central DI
- Neurogenic DI
- Desmopressin (often an inhaled dDAVP nasal spray or IV DDAVP)
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
Nephrogenic DI
Nephrogenic Diabetes Insipidus can be genetic or acquired.
- Acquired is typically from which 4 things?
- What is the treatment?
- 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)
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?
- Hospitalize
- Oral, NG tube, IV w/ hypotonic fluids
- present for several days (can cause seizures, brain damage, CPM)
- Tx Rapid: If hypernatremia developed acutely
In order to replace free water in hypernatremia, you need to calculate what?
Water deficit
- 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
Serum Potassium
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 ____.
Hypokalemia
Clinical presentation of which condition?
- Weakness, fatigue
- Muscle cramps
- Hyporeflexia
- Flaccid paralysis (ascending)
- Hypercapnia
- Which one is most important (not listed here)****
Hypokalemia
- Cardiac arrhythmias
T/F
- K can be replaced more rapidly than Na
True
4 ECG findings of Hypokalemia
- Flattened T waves
- Prominent U waves
- Premature Ventricular Contractions (PVC’s)
- Depressed ST segments
Hypokalemia mnemonic
hYpOkalemia U CRAMP
- U waves
- Cramping
- Resp failure / rhabdomyolysis
- Anorexia, N/V
- Muscle weakness
- Paralysis
3 mechanisms which cause Hypokalemia
- Transcellular shifts
- Renal losses
- Extrarenal losses
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 _____)
Transcellular Shifts
- K shifts out of blood stream and into the cells
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
- Diuretics
- distal tubules
- What are 3 extrarenal losses causing Hypokalemia?
- Which one causes metabolic alkalosis, which further promotes renal potassium loss?*
- Vomiting & diarrhea
- Burns
- Magnesium deficiency
- *vomiting, NG suction
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!!
- Telemetry
- Oral potassium (better absorption)
- Lidocaine, it burns and can destroy veins
- Push, should be given slowly
How do you replace potassium?
- For every 0.1 mEq/L below 4mEq/L, give ___ mEq/L
10
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
- Hypomagnesemia
- Digoxin
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?
Hyperkalemia
- Potentially life threatening arrhythmias
- Seen in 50% of patients
- Peaked T waves**
- Widened QRS
- Junctional rhythm
- Ventricular fibrillation
Mnemonic for Hyperkalemia
“A FACT”
- Arrhythmias
- Flaccid paralysis
- Ascending muscle weakness
- Conduction abnormalities
- T waves
2 “factitious” causes of Hyperkalemia (Pseudohyperkalemia)
- Hemolysis
- Repeated fist clenching w/ tourniquet in place (poor venipuncture technique)
3 causes of Hyperkalemia from Impaired K excretion
- Renal failure
-
Mineralocorticoid deficiency
- Addison’s Disease
- Hypoaldosteronism
- Renal tubular dysfunction
5 drugs which can cause Hyperkalemia
- K sparing diuretics
- ACE inhibitors
- ARBs
- NSAIDs
- Bactrim
3 ways increased inake of K can cause Hyperkalemia
- Increased dietary intake of K containing foods
- Taking too much PO potassium
- Taking too much IV potassium
Other causes of Hyperkalemia
- 3 conditions which move K from intracellular to extracellular spaces
- Tissue damage (rhabdomyolysis)
- Acidosis
- Decreased insulin
2 emergent treatment options for tx of Hyperkalemia
- IV Calcium
-
Maneuvers to shift K from ECF to ICF
- Sodium bicarbonate (IV push)
- Insulin IV + D50W (given w/ dextrose)
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
IV Calcium
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
Sodium Bicarbonate
(shifts K from ECF to ICF)
Other potential options for emergent tx of Hyperkalemia (3)
- Nebulized albuterol
- IV Lasix
- Dialysis
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?
Kayexalate
- Lasix (and other loop & thiazide diuretics)
- Correct underlying cause
Measure of total Ca is ___ + ____
Free (ionized) + protein bound
Serum calcium is used to evaluate metabolism and monitor patients w/ what 3 things?
- Hyperparathyroidism
- Malignancies
- Renal Failure
Calcium has an inverse relationship with what chemical compound?
Phosphate
- 99% of Ca is located where in the body?
- ECF Calcium
- 50% is ____
- 10% is _____
- 40% is ____
Bone
- 50% is free (ionized)
- 10% is complexed
- 40% is protein bound
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
Ionized
Which form of Calcium?
- Citrate added to blood to prevent clotting
Complexed (chelated with substances such as citrate)
Which form of Calcium?
- When serum albumin is low, Ca level will also be low
- Albumin and Calcium should be measured silmultaneously
Protein - bound (albumin)
Calcium Physiology
- Calcium is absorbed through ____ under influence of _____
- Stored where?
- Excreted by what organ?
- Regulated by what 3 things?
- GI tract / Vitamin D
- Bone
- Kidney
- PTH / Vit D / Calcitonin
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?
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)
An increase in serum Calcium triggers the release of ____ from the thyroid gland, which acts to decrease Ca in blood by doing what?
Calcitonin
- Inhibiting bone resorption
If calcium levels are high, what should you be concerned about?
Malignancy
Sxs of Hypercalcemia
“Has a cute saying to remember”
“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
What 2 things cause 90% of hypercalcemia?
- Malignancy
- Primary hyperparathyroidism
Which 4 medications can cause hypercalcemia?
- Thiazide diuretics
- Lithium
- Antacids
- Vitamin A analogs (accutane)
Evaluation of Hypercalcemia
- PTH is increased with _____
- PTH is suppressed in _____
- Increased in primary hyperparathyroidism
- Suppressed in malignancy
- What is the #1 therapy / tx of Hypercalcemia?
- What are 3 other tx options?
- **#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)
