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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?

A
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2
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A
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2
Q

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

A
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3
Q
A
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4
Q

Fill in the covered part

A
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5
Q

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

A

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?

A

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
Q

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

A

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
Q

Hypokalemia
* What is usually low with potassium?

A

Concomitant hypomagnesemia common
* Both intracellular

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9
Q
A
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10
Q

Hypokalemia:
* Potassium is responsible for what?

A

Responsible for nerve conduction and muscle contraction

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11
Q

What are the sxs of hypokalemia?

A

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?

A
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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
Q

Potassium replacement
* Oral replacement recommended when?
* 10mEq raises potassium level about?
* Decreases complications of what?

A

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?

A

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?

A
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17
Q

What is not recommended to do both for potassium?

A

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?

A
  • 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
Q

Potassium Replacement: hospitalized patients
* When do you give IV replacement? (3)

A
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20
Q

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

A
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21
Q
A
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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?

A

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
Q

Hyperkalemia
* When does redistribution of potassium occur?
* What are different type of drugs?
* What is uncommon?

A
  • 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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25
Q

Hyperkalemia
* What are the signs and symptoms?

A
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26
Q

What are the ECG changes of hyperkalemia?

A
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27
Q

Hyperkalemia
* Urgency / aggressiveness of hyperkalemia treatment depends on what?

A

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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28
Q

Hyperkalemia
* What pts require aggressive treatment? (3)
* What should you discontinue?

A

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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29
Q

Hyperkalemia treatment
* Mild increase in potassium may be treated with what?
* Moderate asymptomatic hyperkalemia (K < 6meq/L) may be treated how?

A

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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30
Q

Hyperkalemia
* Symptomatic / severe hyperkalemia (K ≥ 6meq/L) requires prompt treatment. What are the steps? (4)

A
  • 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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31
Q
A
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32
Q

Hyperkalemia treatment:
* What are the Cardiac membrane stabilization medications? What does it increase?

A
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33
Q

Hyperkalemia - treatment
* What drugs shift potassium into cells? How?

A
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34
Q

What drugs remove potassium from the body?

A
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35
Q
  • Inhaled albuterol dose of 10mg or 20mg decreases K+ by what?
A

0.6mEq or1mEq respectively

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36
Q

Sodium zircomium cyclosilicate

A
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37
Q
A
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38
Q

sodium polystyrene

A
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39
Q

Hyponatremia
* What is the serum sodium?
* What is the hypervolemic type?
* What is the hypovolemic type?

A
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40
Q

Hyponatremia
* What is the euvolemic type?
* What is the pseudohyponatremia type?

A
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41
Q

Hyponatremia symptoms
* What are mild and moderate sxs?

A
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42
Q

Hyponatremia symptoms
* What are severe sxs?

A
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43
Q

Hyponatremia - General approach
* What is acute? What type of patients?
* What is chronic?

A

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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44
Q

hyponatremia: severe acute hyponatremia
* Sodium drops how?
* Immediate txt to do what?

A
  • 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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45
Q

hyponatremia
* What is the txt and what do you need to monitor?

A
  • Intermittent doses of hypertonic (3%) saline
  • Monitor sodium levels frequently
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46
Q

hyponatremia: goals
* Increase serum sodium by what?
* Avoid what?
* What happens when their is rapid correction?

A
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47
Q
A
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48
Q

Non severe Hyponatremia
* What is it?
* Generally what?
* What is true hyponatremia?
* Treatment depends on what?

A
  • 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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49
Q
A
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50
Q

Hypotonic hyponatremia
* Patients with ESRD =
* Patients taking thiazide diuretic=
* What happens if sodium is and is not corrected?

A

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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51
Q

Hypotonic hyponatremia: Assess volume status and treat accordingly
* Hypovolemic –
* Euvolemic –
* Hypervolemic –

A
  • Hypovolemic – normal saline
  • Euvolemic – fluid restriction
  • Hypervolemic – fluid and sodium restriction
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52
Q

KNOW

Euvolemic hyponatremia: SIADh (syndrome of inappropriate antidiuretic hormone)
* What senses changes in osmolality of blood
* What is osmolality?
* Primarily what?
* What is normal?

A

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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53
Q

Normal response to dehydration
* Increases what (2)
* Osmo receptors in the hypothalamus detect what? What does that cause?

A
  • 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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54
Q

long but important

ADH – vasopressin
* What is the MOA?
* What does it reduce?

A
  • 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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55
Q

Normal response to increased fluid
* What happens?

A
  • 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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56
Q

SIADh (syndrome of inappropriate antidiuretic hormone)
* Antidiuretic hormone controls what?
* Produced where? Released by what?
* ADH works where?

A
  • 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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57
Q

What does increase and decrease ADH cause?

A
  • 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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58
Q

SIAdH…too much ADH
* What are causes?
* What are sxs?

A

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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59
Q

SIAdH…too much ADH
* how do you dx it? (serum and urine osmolality/sodium)

A
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60
Q

SIADH
* What happens with increase fluid? (what remains high)
* What does that cause?

A
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61
Q

SIADH
* Increased blood volume=
* What is released? What does that cause? (general)

A

Increased blood volume = increased BP

Natriuretic peptides released
* Vasodilation
* Increase GFR
* Increased blood flow to kidneys

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62
Q

SIADH: Natriuretic peptides released
* Vasodilation =
* What does increase GFR cause?
* What happens when there is an increase blood flow to kidney?

A

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

63
Q

What is the net effect of SIADH and abnormal response to increase fluid?

A

sodium removed from the blood that already has a low concentration of sodium

64
Q

SIAdH - treatment
* What is first line?(3)

A
65
Q

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)

A
  • ± salt tablets
  • ± 3% sodium chloride
  • ± loop diuretics
  • ± demeclocycline
  • ± vasopressin receptor antagonists
66
Q

Vasopressin receptor antagonists
* What is the MOA?

A
  • Block V2 vasopressin receptors
  • DCT and CD remain impermeable to water
  • Increased free water excretion
  • Sodium excretion not increased
  • Serum sodium level increases
67
Q

Vasopressin receptor antagonists
* What are the examples?

A

Tolvaptan (PO), conivaptan (IV)

68
Q

Vasopressin receptor antagonists
* What are the SE?(2)
* What is CI?(3)

A
  • Thirst – may limit increase in serum sodium
  • Hepatotoxicity: Use ≤ 30 days
  • CI patients with liver disease and cirrhosis; autosomal dominant polycystic kidney disease
69
Q

Hypernatremia
* What is the serum sodium?
* What are causes of sodium gain ?

A

Serum sodium > 145 mEq/L

Sodium gain (less common)
* Exogenous administration
* Diet – too much sodium intake

70
Q

Hypernatremia
* What are the causes of increase water loss?

A
  • GI illness / sweating / fever
  • Heat injury
  • Diuretics
  • Diabetes insipidus
  • Hypodipsia
71
Q

Hypernatremia
* What are the sxs?

A
72
Q
A
73
Q

Treatment: Hypernatremia
* Treat what?
* Correct what? Determine what? Rate of correction?

A

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

74
Q

Treatment: Hypovolemia Hypernatremia
* Generally what replacement?
* What should you do if possible?
* Symptomatic?

A
  • Generally free water replacement
  • Oral or enteral free water preferred when possible
  • Symptomatic = water depletion = 5% dextrose in water (D5W)
75
Q

fill in hypernatremia

A
76
Q

Calcium
* Where is most stored?
* Disorders of calcium homeostasis related to what? How is calcium present in our body?

A

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

77
Q

Calcium
* What does the lab report calcium as?
* Proper interpretation of total calcium requires what?
* What happens when there is low albumin?

A

Laboratory reports total body calcium
* Proper interpretation of total calcium requires serum albumin level
* Hypoalbuminemia = less bound calcium = more free, active calcium

78
Q

Calcium
* What happens when calcium decreases (think hormone)?

A

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

79
Q

What happens with the increased renal activation of 1,25 dihydroxy vitamin D3?

A

Increased renal activation of 1, 25-dihydroxy vitamin D3
* Directly increases calcium and phosphorus GI absorption
* Decreases calcium renal excretion

80
Q

Calcium
* What is the corrected calcium calculation?

A

Corrected calcium (mg/dL) = measured calcium (mg/dL) + (0.8 x [4 g/dL – measured albumin)]

81
Q

Calcium
* What lab value of calcium is best for critically ill patients?

A

Ionized or free calcium can also be ordered
* Best for critically ill patients

82
Q

hypocalcemia
* What is the serum level in order to be hypocalcemia? Uncommon where?

A

Corrected serum calcium < 8.6 mg/dL (ionized Ca < 4.6 mg/dL)
* Uncommon in outpatient setting

83
Q

hypocalcemia
* What are reasons for Decreased calcium entering the body? (2)

A
  • Hypoparathyroidism – postsurgical MC
  • Low vitamin D
84
Q

hypocalcemia
* What are causes of increase calcium excretion? (2)

A
  • 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)
85
Q

Causes of Hypocalcemia
* Give the whole acronym of the causes (including the disease states)

A
86
Q

Signs & Symptoms of Hypocalcemia
* What are the sxs?

A

CRAMPS
* Confusion
* Reflexes hyperactive
* Arrhythmias (prolonged QT intervaland ST interval)
* Muscle spasms in calves or feet, tetany, seizures
* Positive Trousseau’s – may be first positive sign
* Sign of Chvostek’s

87
Q

What is the EKG change in hypocalcemia?

A
88
Q

hypocalcemia
* Evaluate and treat what?
* What do you do for symptomatic patients and asymptomatic patients?

A

Evaluate and treat underlying causes
* Symptomatic patients
* IV calcium chloride or calcium gluconate over 10 min

Asymptomatic
* IV calcium gluconate (acute)
* PO calcium (chronic)

89
Q

Fill in for the hypocalcemia treatment

A
90
Q

Fill for the difference between calcium CL and calcium gluconate

A
91
Q

Oral calcium replacement
* What is the initial treatment and dose?

A
  • Calcium carbonate or calcium citrate
  • 1 to 4 gm of elemental calcium / day
92
Q

Oral calcium replacement
* What else can you possibly give a patient with low calcium? Why?

A

Concomitant vitamin D
* Patients with vitamin D deficiency or hypoparathyroidism

93
Q

Oral calcium replacement
* What are the SE?(3)

A
  • Hypercalcemia
  • Hypercalcinuria
  • Constipation
94
Q

Calcium carbonate (Tums, Os Cal)
* What is the dose?
* Highest amount of what?
* Used a lot or little?
* Well what?
* best absorbed when?

A
  • 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
95
Q

Calcium carbonate (Tums, Os Cal)
* Limited with what?
* Fomulation of choice for patients with what?

A
  • Limited solubility and absorption in patients with high gastric pH
  • Formulation of choice for patients with hyperphosphatemia in CKD; good phosphate binding
96
Q

Calcium citrate (Citracal)
* What is the dose?

A

Elemental calcium / 1 gram of salt (210mg)

97
Q

Calcium citrate (Citracal)
* Better absorption with what?
* Can be taken without regards to what?
* More doses needed to do what?
* No what?

A
  • 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
98
Q

Hypercalcemia
* What is the calcium level?
* What are the MCC? (2)

A
  • Corrected serum calcium > 10.5 mg/dL (ionized > 5.3 mg/dL)
  • MCC cancer and hyperparathyroidism
99
Q

Hypercalcemia:Hypercalcemia of malignancy
* How does this happen?
* MC with what/where?

A
  • 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
100
Q

Hypercalcemia
* What is the MCC of chronic hypercalcemia in general population?
* What are some other causes?

A
  • Primary hyperparathyroidism ->MCC chronic hypercalcemia in general population
  • Other – drug induced (lithium, vitamin D, vitamin A, thiazide diuretics)
101
Q

hypercalcemia
* What are the sxs?

A
102
Q

hypercalcemia
* What is the EKG findings?

A
103
Q

hypercalcemia
* Many patients asymptomatic with calcium levels of what?

A

Many patients asymptomatic with calcium levels < 13 mg/dL

104
Q

Hypercalcemia
* How do you tx chronic hypercalemia?
* How do you tx cute hypercalemia?

A
  • Chronic hypercalcemia: Treat underlying disease
  • Acute hypercalcemia: Intervention required if calcium > 12 mg/dL or symptomatic
105
Q
A
106
Q
A
107
Q

Hypercalcemia: Volume expansion / increase calcium excretion
* What fluids do you give and why?

A

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

108
Q

Hypercalcemia: Volume expansion / increase calcium excretion
* What diuretics do you give? Why?

A

Loop diuretics
* Decreases overhydration from IV fluid administration
* Minimal effect on decreasing Ca levels

109
Q

Hypercalcemia:Volume expansion / increase calcium excretion
* What do you tx with if the patient has severe renal insufficiency?

A

Urgent dialysis if severe renal insufficiency

110
Q

Hypercalcemia
* What do for symptomatic patients severely elevated calcium or patients not candidates for fluid resuscitation?

A

Calcitonin

111
Q

Calcitonin
* What does it inhibit?
* What is the onset/duration?
* Minimal decrease in what?
* What will develop with 4+ doses?
* Why is it prohibitve?

A
  • Inhibit osteoclast bone resorption
  • Rapid onset / short duration
  • Minimal decrease in calcium
  • Tachyphylaxis develops with > 4 doses
  • Cost prohibitive
112
Q

Hypercalcemia: IV bisphosphonates
* What does it inhibit?
* What does it stimulate?
* What does it reduce?
* What is the onset and duration?

A
  • Inhibit osteoclast bone resorption
  • Stimulating osteoclast apoptosis
  • Reduce osteoclast function
  • Slow onset / long duration
113
Q

Explain the bone remodeling cycle

A
114
Q

Hypercalcemia

A
115
Q

Hypercalcemia

A
116
Q

hypophosphatemia
* What causes decrease GI absorption?

A
  • Pharmacy – aluminum, calcium, magnesium containing antacids; binds phosphate and decreases absorption
  • Decreased intake – anorexia
117
Q

hypophosphatemia
* What causes reduced tubular reabsorption?

A
  • Hyperparathyroidism – increase in PTH; phosphate not reabsorbed by kidneys
  • Fanconi’s Syndrome – PCT impaired electrolyte absorption
118
Q

Hypophosphatemia
* What are causes of internal redistribution?(4)

A
  • Alcoholism
  • Refeeding syndrome
  • Diabetic ketoacidosis treatment
  • Respiratory alkalosis

DARR

119
Q

hypophosphatemia
* What is the serum level?
* Low phosphate level often associated with what?
* What plays role in absorption of phosphate?

A
  • Serum phosphate < 2.5 mg/dL
  • Low phosphate level often associated with high calcium level
  • Vitamin D plays role in absorption of phosphate
120
Q

hypophosphatemia
* sxs in mild cases?

A

Mild – asymptomatic (1-2 mg/dL)

121
Q

Hypophosphatemia:
* What are the sxs of severe cases?

A

Severe - < 1 mg/dL)
* Muscle weakness
* Osteomalacia
* Rhabdomyolysis
* Mental status changes
* Primary hyperparathyroidism
* See hypercalcemia

PROMM

122
Q

Refeeding syndrome
* When does this occur?

A

Prolonged periods of malnutrition or anorexia

123
Q

Refeeding syndrome
* What happens when you start eating?

A
  • 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
124
Q

Refeeding syndrome
* What should be monitored closely?
* What will help decrease the risk?

A
  • Phosphate levels should be monitored closely
  • Gradual caloric increase will help decrease risk
125
Q

Hypophosphatemia:
* What is the txt for mild to moderate?

A
  • Oral replacement therapy – sodium phosphate/potassium phosphate (K-Phos Neutral)
  • Standard dose = 250 to 500mg 3 to 4 times daily
126
Q

hypophosphatemia
* What is the txt for severe?

A
  • IV sodium or potassium phosphate
  • Dose dependent on phosphate level
127
Q

Hyperphosphatemia
* What is the serum level?
* What is the MCC?
* What about creatinine clearance?

A
  • Serum phosphate > 4.5 mg/dL
  • MCC CKD / ESRD
  • Creatinine clearance < 20ml/min/1.73 m2
128
Q

Hyperphosphatemia
* What are the sxs?

A

Same as hypocalcemia

129
Q
A
130
Q

Hyperphosphatemia treatment
* Manage what?
* Prevent what?
* Avoid what?

A
  • 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)
131
Q

Hyperphosphatemia treatment
* What do you give for nonemergent patients?

A

Phosphate binders
* Calcium salts (calcium carbonate)
* Aluminum salts (aluminum hydroxide)
* Polymer agents (sevelamer)

132
Q

Hyperphosphatemia treatment
* What do you give for severe, symptomatic with hypocalemia?

A

IV calcium gluconate

133
Q

Hyperphosphatemia treatment
* What is the txt for Severe, symptomatic without hypocalcemia?

A

Severe, symptomatic without hypocalcemia
* Stop exogenous phosphate sources
* Phosphate binders

134
Q

Hyperphosphatemia treatment
* What is the txt if symptoms continue despite measures

A

Dialysis

135
Q

Magnesium
* Common or not?
* Found where?
* How is it mainly reabsorbed?

A
  • Second MC intracellular cation
  • Primarily found in bone (67%) and muscle (20%)
  • 95% reabsorbed in the kidney (5% eliminated)
136
Q

Magnesium
* Hypomagnesemia common in who?

A

Hypomagnesemia common in hospitalized patients
* 20% general medicine patients
* 65% ICU patients

137
Q

Magnesium
* What is mag’s primary effects?

A

Magnesium primarily effects the neuromuscular and cardiovascular systems

138
Q

hypomagnesemia
* What is the serum level?
* What is MC cause?

A
  • Serum magnesium < 1.4 meq/L (1.7 mg/dL)
  • Decreased GI absorption MC->Diarrhea, proton pump inhibitors, colitis
139
Q

hypomagnesemia Causes
* Decreased reabsorption where?
* Prolonged what?
* Uncontrolled what?
* What social habit?

A
  • Decrease reabsorption from nephron – loop or thiazide diuretics
  • Prolonged malnutrition
  • Uncontrolled DM
  • Alcoholism (increases renal Mg excretion)
140
Q

Hypomagnesemia is assoicated with what?

A

Associated with decreased potassium

141
Q

What are the neuromuscular sxs of hypomag

A
142
Q

Hypomagnesemia treatments: Oral therapy
* Appropriate for who?
* What is available?
* MC drug?

A
  • Appropriate for magnesium levels > 1meq/L
  • Several salts available
  • MC magnesium oxide or hydroxide
143
Q

Hypomagnesemia treatments: oral therapy
* What are the SE?

A

MC adverse effect = diarrhea
* Dose limiting
* Sustained release products increase compliance and decrease diarrhea

144
Q

Hypomagnesemia treatments
* When is IV therapy appropirate?
* What is the dose? How is it given?

A
145
Q
A
146
Q

Polymorphic VT
* What is teh MCC?
* Always associated with what?
* May spontaneously terminate into what?

A

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

147
Q

Polymorphic VT
* What are the causes?

A
  • Inherited disease – congenital prolonged QT, Brugada, etc
  • Electrolyte related – hypokalemia, hypocalcemia, hypomagnesemia
  • Medications
148
Q

TdP - treatment
* What do you do for hemodynamically unstable patients?
* What do you do for hemodynamically stable patients?

A

Hemodynamically unstable - prompt cardioversion/defibrillation

Hemodynamically stable patient:
* Stop causative medications
* Replace abnormal electrolytes

149
Q

TdP - treatment
* What is first line therapy?
* What is the goal?
* Benefit seen with what?

A
  • 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
150
Q

What do you give for TdP resistant to magnesium? What does it cause?

A

Isoproterenol
* Increases HR and shorten QT interval

151
Q

hypermagnesemia
* What is the serum level?
* MC in who?
* MCC of what?

A
152
Q

hypermagnesemia
* What are the sxs?

A
  • Lethargy
  • Confusion
  • Arrhythmias
  • Muscle weakness
  • Absent / decreased DTRs
153
Q

hypermagnesemia txt:
* Reduce what?
* Enhance what? How (2)?

A

Reduce magnesium intake

Enhance elimination
* Loop diuretic administration
* Dialysis

154
Q

hypermagnesemia
* how do you antagonize physiologic effects?

A
  • 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
155
Q
A
156
Q
A

Pharm II (14 decks)

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