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Pharm II > Lecture 10 (Renal)-Exam 5 > Flashcards

Lecture 10 (Renal)-Exam 5 Flashcards

1
Q

Acid-base disturbance treatments
* How do you tx metabolic acidosis and metabolic alkalosis?

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2
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Acid-base disturbance treatments
* How do you treat respiratary acidosis and respiratory alkalosis

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4
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Fill in the covered part

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5
Q

Hypokalemia:
* What is the serum concentration? What are the different levels (3)

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Serum potassium concentration of < 3.5 mEq/L
* Mild 3.1 to 3.5 mEq/L
* Moderate 2.5 to 3 mEq/L
* Severe < 2.5 mEq/L

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6
Q

Hypokalemia:
* What is the MCC? Explain what happens?

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MCC – diuretic therapy (loop, thiazide)
* Decrease Na+ reabsorption
* Increases delivery of Na+ to DCT
* DCT reabsorbs Na+ and excretes K+

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7
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Hypokalemia:
* What is the 2nd MCC? Explain what happens

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2nd MCC – loss of potassium-rich GI fluid from vomiting and/or diarrhea
* Metabolic alkalosis can also occur -> shifts potassium into the cell

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8
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Hypokalemia
* What is usually low with potassium?

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Concomitant hypomagnesemia common
* Both intracellular

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10
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Hypokalemia:
* Potassium is responsible for what?

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Responsible for nerve conduction and muscle contraction

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11
Q

What are the sxs of hypokalemia?

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Low levels cause body responses to be LOW and SLOW
* Lethargic
* Low, shallow respirations
* Less stool
* Leg cramps
* Limp muscles (decreases DTRs)
* Lethal arrythmias

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12
Q

What is the EKG changes with hypokalemia?

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13
Q

Potassium replacement:
* Corrent what if present?
* Increase intake of what?

A
  • Correct hypomagnesemia if present
  • Increase intake of foods high in potassium
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14
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Potassium replacement
* Oral replacement recommended when?
* 10mEq raises potassium level about?
* Decreases complications of what?

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Oral replacement recommended when possible / for outpatient therapy
* 10mEq raises potassium level about 0.1 mEq/L
* Decreased complications associated with IV potassium infusion->Thrombophlebitis / potential for EKG changes

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15
Q

Potassium replacement
* What is MC used?
* What is the typical dose?
* Monitor levels when?

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Multiple salts available – potassium chloride MC used
* Tablets, liquids, effervescent tablets
* Typical dose: 20 to 80mEq/day (daily to BID)

Monitor levels a minimum of every 4 weeks initially

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16
Q

Potassium Sparing Diuretics-Alternative to potassium replacement:
* What are the MC examples?
* Often combined with what?

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17
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What is not recommended to do both for potassium?

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Concomitant administration with potassium supplementation not recommended

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18
Q

Potassium replacement: Patient educaiton
* Avoiding what?
* What are common symptoms?
* What type of diet?
* What do they need to look out for?

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  • Avoiding concomitant use with potassium sparing diuretics unless specifically prescribed
  • GI symptoms common: abdominal cramping and pain (dose limiting problem)
  • Potassium rich diet
  • Signs and symptoms of low potassium
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19
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Potassium Replacement: hospitalized patients
* When do you give IV replacement? (3)

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20
Q

Potassium replacement
* What is IV replacement associated with?
* What does it recommend?

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21
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22
Q

Hyperkalemia:
* What is the potassium level?
* What should be 1st thought?
* Less common than what?

A
  • Serum potassium level > 5 mEq/L
  • 1st thought – is it REAL?
  • Less common than hypokalemia
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23
Q

Hyperkalemia
* What are the causes?

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Decreased excretion
* MCC is chronic kidney disease - 90% potassium eliminated via kidneys
* Severe hyperkalemia MC with AKI
* Addison’s disease – low aldosterone decreases K excretion

hemolysis, CKD, renal failure

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24
Hyperkalemia * When does redistribution of potassium occur? * What are different type of drugs? * What is uncommon?
* Redistribution of potassium into extracellular space – hemolysis, metabolic acidosis, burns * Drugs – ACEI, ARBS, K-sparing diuretics, NSAIDS * Tubular unresponsiveness to aldosterone – uncommon
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Hyperkalemia * What are the signs and symptoms?
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What are the ECG changes of hyperkalemia?
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Hyperkalemia * Urgency / aggressiveness of hyperkalemia treatment depends on what?
Urgency / aggressiveness of hyperkalemia treatment depends the cause, rapidity of onset, absolute serum potassium level, the degree of symptoms, and the underlying cause
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Hyperkalemia * What pts require aggressive treatment? (3) * What should you discontinue?
Need treatment * Neuromuscular weakness, paralysis, or ECG changes * Potassium level >5.5 mEq/L at risk for ongoing hyperkalemia * Confirmed hyperkalemia of > 6.5 mEq/L Discontinue Exogenous sources of potassium
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Hyperkalemia treatment * Mild increase in potassium may be treated with what? * Moderate asymptomatic hyperkalemia (K < 6meq/L) may be treated how?
Mild increase in potassium may be treated with dietary restriction and close monitoring Moderate asymptomatic hyperkalemia (K < 6meq/L) may be treated conservatively * Diet restriction * Furosemide
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Hyperkalemia * Symptomatic / severe hyperkalemia (K ≥ 6meq/L) requires prompt treatment. What are the steps? (4)
* First priority – antagonize cardiac effects of potassium * Second priority – promote movement of potassium from extracellular space to intracellular space * Third priority – enhance total body removal * Fourth priority – identify and treat underlying cause
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Hyperkalemia treatment: * What are the Cardiac membrane stabilization medications? What does it increase?
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Hyperkalemia - treatment * What drugs shift potassium into cells? How?
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What drugs remove potassium from the body?
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* Inhaled albuterol dose of 10mg or 20mg decreases K+ by what?
0.6mEq or1mEq respectively
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Sodium zircomium cyclosilicate
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sodium polystyrene
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Hyponatremia * What is the serum sodium? * What is the hypervolemic type? * What is the hypovolemic type?
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Hyponatremia * What is the euvolemic type? * What is the pseudohyponatremia type?
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Hyponatremia symptoms * What are mild and moderate sxs?
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Hyponatremia symptoms * What are severe sxs?
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Hyponatremia - General approach * What is acute? What type of patients? * What is chronic?
Acute – patients typically symptomatic with significant history * Surgical patient * Polydipsia – Runners, psychiatric disorders, ecstasy users Chronic: Known hyponatremia for > 48 hours or unknown time frame – ambulatory patients
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hyponatremia: severe acute hyponatremia * Sodium drops how? * Immediate txt to do what?
* Sodium drops abruptly over < 24 hours; associated with seizures, coma * Immediate treatment to prevent cerebral edema and irreversible neurologic damage, brainstem herniation and death
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hyponatremia * What is the txt and what do you need to monitor?
* Intermittent doses of hypertonic (3%) saline * Monitor sodium levels frequently
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hyponatremia: goals * Increase serum sodium by what? * Avoid what? * What happens when their is rapid correction?
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Non severe Hyponatremia * What is it? * Generally what? * What is true hyponatremia? * Treatment depends on what?
* Patients with serum sodium < 135 mEq/L in the absence of severe symptoms * Generally progressive over time * True hyponatremia = hypotonic hypernatremia * Low serum osmolality * Treatment depends on volume status of patient
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Hypotonic hyponatremia * Patients with ESRD = * Patients taking thiazide diuretic= * What happens if sodium is and is not corrected?
Patients with ESRD = nephrology consult Patients taking thiazide diuretic = hold thiazide diuretic and re check sodium * If sodium corrected – consider alternative diuretic * If sodium did not correct assess volume status
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Hypotonic hyponatremia: Assess volume status and treat accordingly * Hypovolemic – * Euvolemic – * Hypervolemic –
* Hypovolemic – normal saline * Euvolemic – fluid restriction * Hypervolemic – fluid and sodium restriction
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# KNOW Euvolemic hyponatremia: SIADh (syndrome of inappropriate antidiuretic hormone) * What senses changes in osmolality of blood * What is osmolality? * Primarily what? * What is normal?
Osmo receptors in the hypothalamus sense changes in osmolality of blood * Osmolality = concentration of dissolved particles in the blood * Primarily Na, glucose, BUN * Normal = 285 to 295 mOsm/kg
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Normal response to dehydration * Increases what (2) * Osmo receptors in the hypothalamus detect what? What does that cause?
* Increased particles in blood * Increases osmolality * Osmo receptors in the hypothalamus detect increase in blood osmolality * Trigger thirst and signal pituitary to release ADH
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# long but important ADH – vasopressin * What is the MOA? * What does it reduce?
* Increased osmolality triggers the hypothalamus to release more ADH into the blood * ADH travels to the kidneys to act on vasopressin receptors on the principal cells in the DCT and collecting duct of the nephron * Increases aquaporin production * Stimulates vesicles containing aquaporin to fuse to the apical side cell membrane * Allows H20 to move from the renal tubule into the blood * Reducing blood osmolality
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Normal response to increased fluid * What happens?
* Fluid intake increases water in the blood * Decreases osmolality of blood * Signals the pituitary to decrease ADH * Decreases aquaporins * More water excreted as more dilute urine
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SIADh (syndrome of inappropriate antidiuretic hormone) * Antidiuretic hormone controls what? * Produced where? Released by what? * ADH works where?
* Antidiuretic hormone controls water retention in the body and causes vasoconstriction * Produced in the hypothalamus; released by the pituitary * ADH works in the DCT and CD of the nephron
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What does increase and decrease ADH cause?
* increase ADH = increase aquaporins = fluid moves into blood = dilute blood * decrease ADH = decrease aquaporins = fluid stays in the CD = dilute urine
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SIAdH…too much ADH * What are causes? * What are sxs?
Causes: medications, malignancy, CNS disorders (stroke, bleeding, trauma) Symptoms of SIADH due to low serum sodium * HA, N, V, muscle cramps, tremors * Cerebral edema – confusion, coma, seizures
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SIAdH…too much ADH * how do you dx it? (serum and urine osmolality/sodium)
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SIADH * What happens with increase fluid? (what remains high) * What does that cause?
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SIADH * Increased blood volume= * What is released? What does that cause? (general)
Increased blood volume = increased BP Natriuretic peptides released * Vasodilation * Increase GFR * Increased blood flow to kidneys
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SIADH: Natriuretic peptides released * Vasodilation = * What does increase GFR cause? * What happens when there is an increase blood flow to kidney?
Vasodilation = help decrease BP Increase GFR * More water and sodium filtered through kidneys and excreted into urine Increased blood flow to kidneys * Decreased renin * Decreased ATII and aldosterone * More water and sodium excretion
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What is the net effect of SIADH and abnormal response to increase fluid?
sodium removed from the blood that already has a low concentration of sodium
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SIAdH - treatment * What is first line?(3)
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SIAdH - treatment * If no improvement in sodium levels after 24 to 48 hours or for more severe SIADH: What are the other adjuvant txt?(5)
* ± salt tablets * ± 3% sodium chloride * ± loop diuretics * ± demeclocycline * ± vasopressin receptor antagonists
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Vasopressin receptor antagonists * What is the MOA?
* Block V2 vasopressin receptors * DCT and CD remain impermeable to water * Increased free water excretion * Sodium excretion not increased * Serum sodium level increases
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Vasopressin receptor antagonists * What are the examples?
Tolvaptan (PO), conivaptan (IV)
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Vasopressin receptor antagonists * What are the SE?(2) * What is CI?(3)
* Thirst – may limit increase in serum sodium * Hepatotoxicity: Use ≤ 30 days * CI patients with liver disease and cirrhosis; autosomal dominant polycystic kidney disease
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Hypernatremia * What is the serum sodium? * What are causes of sodium gain ?
Serum sodium > 145 mEq/L Sodium gain (less common) * Exogenous administration * Diet – too much sodium intake
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Hypernatremia * What are the causes of increase water loss?
* GI illness / sweating / fever * Heat injury * Diuretics * Diabetes insipidus * Hypodipsia
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Hypernatremia * What are the sxs?
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Treatment: Hypernatremia * Treat what? * Correct what? Determine what? Rate of correction?
Treat underlying cause Correct water deficit * Determine patient volume status, water deficit, on-going losses * Rate of correction ≤0.5 mEq/L/hr to prevent cerebral edema
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Treatment: Hypovolemia Hypernatremia * Generally what replacement? * What should you do if possible? * Symptomatic?
* Generally free water replacement * Oral or enteral free water preferred when possible * Symptomatic = water depletion = 5% dextrose in water (D5W)
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fill in hypernatremia
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Calcium * Where is most stored? * Disorders of calcium homeostasis related to what? How is calcium present in our body?
99% stored in bone Disorders of calcium homeostasis related to calcium in extracellular fluid * < 0.5% of total body stores * 40% protein bound (albumin) * 60% unbound / ionized -> physiologically active
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Calcium * What does the lab report calcium as? * Proper interpretation of total calcium requires what? * What happens when there is low albumin?
Laboratory reports total body calcium * Proper interpretation of total calcium requires serum albumin level * Hypoalbuminemia = less bound calcium = more free, active calcium
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Calcium * What happens when calcium decreases (think hormone)?
PTH released – increases serum calcium * Stimulates calcium release from bone * Increases renal tubule reabsorption * Increases GI absorption through increased production of 1, 25 dihydroxy vitamin D3
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What happens with the increased renal activation of 1,25 dihydroxy vitamin D3?
Increased renal activation of 1, 25-dihydroxy vitamin D3 * Directly increases calcium and phosphorus GI absorption * Decreases calcium renal excretion
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Calcium * What is the corrected calcium calculation?
Corrected calcium (mg/dL) = measured calcium (mg/dL) + (0.8 x [4 g/dL – measured albumin)]
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Calcium * What lab value of calcium is best for critically ill patients?
Ionized or free calcium can also be ordered * Best for critically ill patients
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hypocalcemia * What is the serum level in order to be hypocalcemia? Uncommon where?
Corrected serum calcium < 8.6 mg/dL (ionized Ca < 4.6 mg/dL) * Uncommon in outpatient setting
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hypocalcemia * What are reasons for Decreased calcium entering the body? (2)
* Hypoparathyroidism – postsurgical MC * Low vitamin D
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hypocalcemia * What are causes of increase calcium excretion? (2)
* Ca not reabsorbed effectively in kidney failure * Cell lysis (burns, rhabdomyolysis, tumor lysis syndrome); increased phosphorus release as cell lyse; binds calcium (calcium phosphorus insoluble and excreted)
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Causes of Hypocalcemia * Give the whole acronym of the causes (including the disease states)
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Signs & Symptoms of Hypocalcemia * What are the sxs?
CRAMPS * **C**onfusion * **R**eflexes hyperactive * **A**rrhythmias (prolonged QT interval and ST interval) * **M**uscle spasms in calves or feet, tetany, seizures * **P**ositive Trousseau’s – may be first positive sign * **S**ign of Chvostek's
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What is the EKG change in hypocalcemia?
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hypocalcemia * Evaluate and treat what? * What do you do for symptomatic patients and asymptomatic patients?
Evaluate and treat underlying causes * Symptomatic patients * IV calcium chloride or calcium gluconate over 10 min Asymptomatic * IV calcium gluconate (acute) * PO calcium (chronic)
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Fill in for the hypocalcemia treatment
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Fill for the difference between calcium CL and calcium gluconate
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Oral calcium replacement * What is the initial treatment and dose?
* Calcium carbonate or calcium citrate * 1 to 4 gm of elemental calcium / day
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Oral calcium replacement * What else can you possibly give a patient with low calcium? Why?
Concomitant vitamin D * Patients with vitamin D deficiency or hypoparathyroidism
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Oral calcium replacement * What are the SE?(3)
* Hypercalcemia * Hypercalcinuria * Constipation
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Calcium carbonate (Tums, Os Cal) * What is the dose? * Highest amount of what? * Used a lot or little? * Well what? * best absorbed when?
* Elemental calcium/1 gram of salt (400mg) * Highest amount of elemental calcium * Most widely used * Well absorbed and well tolerated * Best absorbed when taken with meals
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Calcium carbonate (Tums, Os Cal) * Limited with what? * Fomulation of choice for patients with what?
* Limited solubility and absorption in patients with high gastric pH * Formulation of choice for patients with hyperphosphatemia in CKD; good phosphate binding
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Calcium citrate (Citracal) * What is the dose?
Elemental calcium / 1 gram of salt (210mg)
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Calcium citrate (Citracal) * Better absorption with what? * Can be taken without regards to what? * More doses needed to do what? * No what?
* Better absorption that calcium carbonate in patients with higher gastric pH or achlorhydria * Can be taken without regards to meals * More doses needed to gt the equivalent elemental calcium compared to calcium carbonate * No phosphate binding
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Hypercalcemia * What is the calcium level? * What are the MCC? (2)
* Corrected serum calcium > 10.5 mg/dL (ionized > 5.3 mg/dL) * MCC cancer and hyperparathyroidism
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Hypercalcemia:Hypercalcemia of malignancy * How does this happen? * MC with what/where?
* Tumors secrete PTH – related protein which bind PTH receptors in bone and renal tissues; increased bone and renal tubular calcium reabsorption * MC with carcinomas of lung and breast
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Hypercalcemia * What is the MCC of chronic hypercalcemia in general population? * What are some other causes?
* Primary hyperparathyroidism ->MCC chronic hypercalcemia in general population * Other – drug induced (lithium, vitamin D, vitamin A, thiazide diuretics)
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hypercalcemia * What are the sxs?
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hypercalcemia * What is the EKG findings?
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hypercalcemia * Many patients asymptomatic with calcium levels of what?
Many patients asymptomatic with calcium levels < 13 mg/dL
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Hypercalcemia * How do you tx chronic hypercalemia? * How do you tx cute hypercalemia?
* Chronic hypercalcemia: Treat underlying disease * Acute hypercalcemia: Intervention required if calcium > 12 mg/dL or symptomatic
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Hypercalcemia: Volume expansion / increase calcium excretion * What fluids do you give and why?
IV fluids * Normal saline volume expansion first-line therapy * Many patients are volume depleted – vomiting / polyuria * Rehydration interrupts the stimulus for sodium and calcium reabsorption in the renal tubule
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Hypercalcemia: Volume expansion / increase calcium excretion * What diuretics do you give? Why?
Loop diuretics * Decreases overhydration from IV fluid administration * Minimal effect on decreasing Ca levels
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Hypercalcemia:Volume expansion / increase calcium excretion * What do you tx with if the patient has severe renal insufficiency?
Urgent dialysis if severe renal insufficiency
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Hypercalcemia * What do for symptomatic patients severely elevated calcium or patients not candidates for fluid resuscitation?
Calcitonin
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Calcitonin * What does it inhibit? * What is the onset/duration? * Minimal decrease in what? * What will develop with 4+ doses? * Why is it prohibitve?
* Inhibit osteoclast bone resorption * Rapid onset / short duration * Minimal decrease in calcium * Tachyphylaxis develops with > 4 doses * Cost prohibitive
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Hypercalcemia: IV bisphosphonates * What does it inhibit? * What does it stimulate? * What does it reduce? * What is the onset and duration?
* Inhibit osteoclast bone resorption * Stimulating osteoclast apoptosis * Reduce osteoclast function * Slow onset / long duration
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Explain the bone remodeling cycle
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Hypercalcemia
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Hypercalcemia
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hypophosphatemia * What causes decrease GI absorption?
* Pharmacy – aluminum, calcium, magnesium containing antacids; binds phosphate and decreases absorption * Decreased intake – anorexia
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hypophosphatemia * What causes reduced tubular reabsorption?
* Hyperparathyroidism – increase in PTH; phosphate not reabsorbed by kidneys * Fanconi’s Syndrome – PCT impaired electrolyte absorption
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Hypophosphatemia * What are causes of internal redistribution?(4)
* Alcoholism * Refeeding syndrome * Diabetic ketoacidosis treatment * Respiratory alkalosis | DARR
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hypophosphatemia * What is the serum level? * Low phosphate level often associated with what? * What plays role in absorption of phosphate?
* Serum phosphate < 2.5 mg/dL * Low phosphate level often associated with high calcium level * Vitamin D plays role in absorption of phosphate
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hypophosphatemia * sxs in mild cases?
Mild – asymptomatic (1-2 mg/dL)
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Hypophosphatemia: * What are the sxs of severe cases?
Severe - < 1 mg/dL) * Muscle weakness * Osteomalacia * Rhabdomyolysis * Mental status changes * Primary hyperparathyroidism * See hypercalcemia | PROMM
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Refeeding syndrome * When does this occur?
Prolonged periods of malnutrition or anorexia
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Refeeding syndrome * What happens when you start eating?
* Glucose levels are low and cellular metabolism is slowed * Increased intake -> increase glucose in blood -> insulin levels increase to push glucose into cells * Cellular demand for phosphate increases because first step of glucose metabolism attaches phosphate to glucose * ATP also requires phosphate * Phosphate is removed from the blood and levels drop drastically; risk for cardiac arrythmias and neurologic problems
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Refeeding syndrome * What should be monitored closely? * What will help decrease the risk?
* Phosphate levels should be monitored closely * Gradual caloric increase will help decrease risk
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Hypophosphatemia: * What is the txt for mild to moderate?
* Oral replacement therapy – sodium phosphate/potassium phosphate (K-Phos Neutral) * Standard dose = 250 to 500mg 3 to 4 times daily
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hypophosphatemia * What is the txt for severe?
* IV sodium or potassium phosphate * Dose dependent on phosphate level
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Hyperphosphatemia * What is the serum level? * What is the MCC? * What about creatinine clearance?
* Serum phosphate > 4.5 mg/dL * MCC CKD / ESRD * Creatinine clearance < 20ml/min/1.73 m2
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Hyperphosphatemia * What are the sxs?
Same as hypocalcemia
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Hyperphosphatemia treatment * Manage what? * Prevent what? * Avoid what?
* Manage GI and neurologic symptoms * Prevent phosphate deposition into urinary tract to avoid AKI * Avoid cardiac complications of calcium-phosphate crystal deposition in the vasculature * Keep calcium – phosphate “product” < 55mg2/dL2 (Calcium X phosphate should be less than 55)
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Hyperphosphatemia treatment * What do you give for nonemergent patients?
Phosphate binders * Calcium salts (calcium carbonate) * Aluminum salts (aluminum hydroxide) * Polymer agents (sevelamer)
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Hyperphosphatemia treatment * What do you give for severe, symptomatic with hypocalemia?
IV calcium gluconate
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Hyperphosphatemia treatment * What is the txt for Severe, symptomatic without hypocalcemia?
Severe, symptomatic without hypocalcemia * Stop exogenous phosphate sources * Phosphate binders
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Hyperphosphatemia treatment * What is the txt if symptoms continue despite measures
Dialysis
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Magnesium * Common or not? * Found where? * How is it mainly reabsorbed?
* Second MC intracellular cation * Primarily found in bone (67%) and muscle (20%) * 95% reabsorbed in the kidney (5% eliminated)
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Magnesium * Hypomagnesemia common in who?
Hypomagnesemia common in hospitalized patients * 20% general medicine patients * 65% ICU patients
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Magnesium * What is mag's primary effects?
Magnesium primarily effects the neuromuscular and cardiovascular systems
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hypomagnesemia * What is the serum level? * What is MC cause?
* Serum magnesium < 1.4 meq/L (1.7 mg/dL) * Decreased GI absorption MC->Diarrhea, proton pump inhibitors, colitis
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hypomagnesemia Causes * Decreased reabsorption where? * Prolonged what? * Uncontrolled what? * What social habit?
* Decrease reabsorption from nephron – loop or thiazide diuretics * Prolonged malnutrition * Uncontrolled DM * Alcoholism (increases renal Mg excretion)
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Hypomagnesemia is assoicated with what?
Associated with decreased potassium
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What are the neuromuscular sxs of hypomag
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Hypomagnesemia treatments: Oral therapy * Appropriate for who? * What is available? * MC drug?
* Appropriate for magnesium levels > 1meq/L * Several salts available * MC magnesium oxide or hydroxide
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Hypomagnesemia treatments: oral therapy * What are the SE?
MC adverse effect = diarrhea * Dose limiting * Sustained release products increase compliance and decrease diarrhea
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Hypomagnesemia treatments * When is IV therapy appropirate? * What is the dose? How is it given?
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Polymorphic VT * What is teh MCC? * Always associated with what? * May spontaneously terminate into what?
MCC Torsades de Pointes * Always associated with prolonged QT interval * QTc > 460 ms in females, > 450 ms in males * > 500 ms = 2-to-3-fold increase in TdP risk * May spontaneously terminate or degenerate into VF
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Polymorphic VT * What are the causes?
* Inherited disease – congenital prolonged QT, Brugada, etc * Electrolyte related – hypokalemia, hypocalcemia, **hypomagnesemia** * Medications
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TdP - treatment * What do you do for hemodynamically unstable patients? * What do you do for hemodynamically stable patients?
Hemodynamically unstable - prompt cardioversion/defibrillation Hemodynamically stable patient: * Stop causative medications * Replace abnormal electrolytes
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TdP - treatment * What is first line therapy? * What is the goal? * Benefit seen with what?
* Magnesium sulfate 2 grams IV over 15 minutes; followed by continuous infusion magnesium * Goal = magnesium level > 2 mEq/L * Benefit seen with normal magnesium levels
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What do you give for TdP resistant to magnesium? What does it cause?
Isoproterenol * Increases HR and shorten QT interval
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hypermagnesemia * What is the serum level? * MC in who? * MCC of what?
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hypermagnesemia * What are the sxs?
* Lethargy * Confusion * Arrhythmias * Muscle weakness * Absent / decreased DTRs
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hypermagnesemia txt: * Reduce what? * Enhance what? How (2)?
Reduce magnesium intake Enhance elimination * Loop diuretic administration * Dialysis
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hypermagnesemia * how do you antagonize physiologic effects?
* IV calcium gluconate * 2 grams IV over 1 hour * Antidote for toxic magnesium levels * Antagonizes the cardiovascular and neuromuscular effects * Repeat doses needed until magnesium levels normalize
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Pharm II (14 decks)

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