Week 7: BMP (not done)

Question 1

1) What is BMP also called? How many tests?
2) List the tests
3) What is the test that’s freq. included?

Answer 1

1) AKA BMP, chem 7, or chemistry panel
7 tests
2) Sodium, potassium, chloride, bicarb(onate), BUN, creatinine, glucose
3) Also frequently has eighth test: calcium

Question 2

Creatinine:
1) Where does it come from?
2) What excretes it? What are levels directly proportional to?
3) Where is it found? Are levels stable?

Answer 2

1) Byproduct of skeletal muscle activity
2) Excreted primarily by the kidneys
Levels directly proportional to renal excretory function
3) Abundant in the body and stable
Skeletal volume and dietary patterns are relatively stable

Question 3

slide 5

Answer 3

Therefore, it is a useful filtration marker to estimate GFR
Doubling of serum creatinine suggests 50% reduction in GFR

Answer 4

Urea formed in the liver as a metabolic byproduct
Ingested proteins broken down into amino acids
Amino acids catabolized to form ammonia
Ammonia converted into urea

Answer 5

BUN is excreted by the kidneys
Levels reflect metabolic health of the liver and excretory health of the kidneys

Question 6

Glucose

Answer 6

Regulated via insulin and glucagon
Must be evaluated in relation to mealtime
Example: 135 is high in fasted state but not abnormal 1 hour post-prandial (PP)
Follow up testing with glycosylated hemoglobin (HbA1c)

Question 7

Glucose

Answer 7

Increased
DM, Cushing’s, pancreatitis, steroids, physiologic stress (CVA, MI, shock)
Decreased
Starvation, hypothyroidism, excess insulin administration

Question 8

Bicarbonate

Answer 8

AKA CO2 or total CO2 (different from pCO2)
Most of the body’s CO2 is in the form of bicarbonate (HCO3-)
CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3-
CO2 itself is a metabolic byproduct

Question 9

Bicarbonate

Answer 9

Used in the evaluation of pH status
Technically bicarb can act as an acid or a base but in acid-base/blood gas analysis it acts as a base
Normal range of HCO3: 22-26 mEq/L

Question 10

1) List the extracellular electrolytes
2) List the intracellular ones

Answer 10

1) Sodium
Calcium
Chloride
Bicarbonate
2) Potassium
Magnesium
Phosphate

Question 11

Electrolytes:
1) What are they?
2) What are they important from?
3) What regulates their concentration throughout the body?

Answer 11

Minerals with electric charges that dissociate in a solution into + or – ions
Maintenance of physiologic body fx, cellular metabolism, neuromuscular fx, osmotic equilibrium.
3) Homeostatic mechanisms

Answer 12

Electrolytes
Serum electrolytes are maintained within a narrow range by the kidneys
May not correlate with total body levels due to shifting of water or electrolytes in and out of cells

Answer 13

Urine concentration of an electrolyte is helpful when compared to serum levels
Can determine if kidneys are excreting/retaining electrolyte in response to high/low serum levels
Gold-standard – 24-hour urine collection to monitor electrolyte excretion
Can be cumbersome and challenging
Fractional excretion (FE) of an electrolyte is more convenient

Question 14

Fractional excretion (FEx)

Answer 14

Compares a substance in a spot urine sample to the serum levels and also to creatinine
Low fractional excretion indicates ________
High fractional excretion indicates ________
Can be used to determine if kidneys are responding appropriately to a specific electrolyte disorder

Question 15

True or false: osmolarity and osmolality are used interchangeably in clinical med

Answer 15

True

Answer 16

Osmolality of all solutes (electrolytes and others) in plasma is 280-295 mmol/kg
Water moves from region of low osmolality to high osmolal

Question 17

What are the major fluid compartments?

Answer 17

Intracellular (ICF): inside cell
Extracellular (ECF):
Interstitial (surrounding cells)
Plasma (intravascular)

Question 18

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Answer 18

Water is balanced between the intracellular compartment and extracellular compartment (including serum)
Water will move (towards compartment with higher solute concentration) to balance the concentrations until there is equilibrium

Question 19

Sodium

Answer 19

The main extracellular cation
Main determinant of extracellular osmolality (affects fluid shifts)
Balanced between dietary intake and renal excretion
Hyponatremia is the most common electrolyte abnormality

Question 20

Describe what ADH does

Answer 20

Actions: Kidney reabsorbs water (concentrates urine)
Consequently dilutes serum Na+ (lowering concentration)
-Main stimulators are increased plasma osmolality and decreased blood volume

Question 21

Describe what aldosterone does and what causes it to be released

Answer 21

Actions: Increases tubular reabsorption of Na+ (excretes K+ and H+); water is also reabsorbed (follows Na+)
Stimulators of Release:
Most powerful stimulator is angiotensin II (e.g., renin-angiotensin-aldosterone [RAAS] system)

Question 22

Natriuretic peptide hormones

Answer 22

Actions: Increase Na+ excretion (sodium lost in urine); water is also excreted (follows Na+)
Stimulators of Release: Myocardial stretch

Question 23

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Answer 23

Closely related to body’s fluid status
Disorders of sodium are (generally) disorders of water (see following slides)

Question 24

Hyponatremia (low serum Na+):
1) What does it represent?
2) What is it usually due to? Give an example

Answer 24

1) Represents an excess of water relative to sodium in the serum
Usually due to an excess of total body water diluting serum Na+, rather than a deficiency in total body Na+
Example: increased PO or IV water

Question 25

Hyponatremia (low serum Na+): 1)

Answer 25

Serum osmolality: Usually low (hypotonic), but sometimes normal (pseudohyponatremia) or increased (hypertonic) Water moves to compartment with greater solute concentration (cells) Cells will swell (can cause cerebral edema, seizures, brain herniation)

Question 26

Hypernatremia (high serum Na+)

Answer 26

Usually due to water loss > intake (i.e. rarely due to too much Na+ except when too much hypertonic fluid is given) Too little water relative to Na+ in the serum (concentrating serum Na+)

Question 27

Hypernatremia (high serum Na+)

Answer 27

Water moves to compartment with greater solute concentration (the blood) Cells shrink Serum osmolality: always high (unlike hyponatremia, which can be variable)

Question 28

Hyponatremia: 1) Describe the acute Sx 2) Describe the chronic Sx 3) When may the chronic Sx be different?

Answer 28

1) headache, difficulty concentrating, disorientation, nausea (early)  progressing to vomiting, LOC, seizure, brainstem herniation, death 2) usually asymptomatic (brain cells adapt to hypotonicity); may be found on routine testing -May have subtle sxs like mild concentration deficit, nausea, gait issues Quickly reversing chronic hyponatremia can lead to neurologic complications (osmotic demyelination syndrome)

Question 29

Hypernatremia 1) What are the clinical features? 2) When are there going to be acute features? List them

Answer 29

1) Signs of volume depletion (e.g., dry mouth and mucous membranes, lack of tears, tachycardia, hypotension, oliguria/anuria) 2) Acute and severe symptoms with Na+ >160: lethargy, irritability, weakness, hyperreflexia  progressing to hyperthermia, delirium, seizures, coma (irreversible neurologic damage if untreated)

Answer 30

Overhydration status (oral or IV) More water is ingested than the kidney can excrete (often due to ADH)

Question 31

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Answer 31

: (Measure serum osmolality) Pseudohyponatremia (normal serum osmolality) – rarer as lab technology improves Severe hypertriglyceridemia or hypergammaglobulinemia throws off sodium reading Hypertonic (hyperosmolar) hyponatremia Hyperglycemia and (less common) mannitol infusion Increase osmolality of ECF which pulls fluid from cells Hypertonicity will still stimulate thirst and ADH secretion, contributing to water retention

Question 32

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Answer 32

Calculate “corrected” sodium if hyperglycemia: Increase sodium by 1.6 for every 100mg/dL rise in plasma glucose above normal (100 mg/dL) (See example on later slide)

Question 33

What is the most common hyponatremia? What are its 2 categories?

Answer 33

Hypotonic (hypo-osmolar) hyponatremia  most common (water intake exceeds kidney’s excretional capacity) Further divided into ADH independent and ADH dependent (measure urine osmolality)

Question 34

slide 26 chart

Question 35

slide 26 chart

Answer 36

ADH independent causes – ADH is appropriately suppressed; kidney’s ability to excrete water is intact (urine osm <100, dilute urine)* i.e. The problem is not due to ADH causing water retention. Pt cannot excrete enough of the excess water for another reason.

Question 37

List Hyponatremia: Etiologies (con.)Hypotonic – ADH Independent

Question 38

slide 28

Question 39

slide 28

Answer 40

) ADH dependent causes: most common category of hypotonic hyponatremias (urine osm >100, concentrated urine) involve failure to suppress ADH; water is retained This is the appropriate response to hypovolemia or reduced effective arterial volume (e.g., hypervolemic states like cirrhosis or heart failure)

Question 41

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Answer 41

Can be inappropriate in the absence of hypovolemia or edematous states Aka syndrome of inappropriate ADH secretion (SIADH) Categorized by pt volume status (hypo-, eu-, or hypervolemic) (also evaluate urine sodium)

Question 42

Hyponatremia: Etiologies (con.)Hypotonic – ADH Dependent - Hypovolemic 1) When does it occur?

Answer 42

Occurs with renal or extrarenal volume loss (various causes) and subsequent hypotonic fluid replacement Fluid loss happens (water and sodium is lost) Then pituitary secretes ADH to limit water excretion to maintain blood pressure (sacrifices serum osmolality to preserve intravascular volume) Water retained, remaining sodium diluted Then hypotonic fluids are given, further diluting the sodium

Question 43

Hyponatremia: Etiologies (con.)Hypotonic – ADH Dependent - Hypervolemic

Answer 43

Usually occurs in the setting of edematous states (cirrhosis, heart failure, rarely nephrotic syndrome) Cirrhosis – systemic vasodilation (primary cause; multifactorial) Heart failure – reduced cardiac output Nephrotic syndrome – urinary loss of albumin leads to third spacing of fluid outside of vessels

Answer 44

Decreased effective circulating volume (e.g., to kidneys) triggers ADH secretion and RAAS activation, even though there is already excess extracellular fluid (edema) Because of RAAS activation and increased aldosterone, urine sodium is low

Question 45

Hyponatremia: Etiologies (con.)Hypotonic – ADH Dependent - Euvolemic SIADH – syndrome of inappropriate ADH secretion

Answer 45

ADH secreted in the absence of appropriate physiologic stimuli (e.g., decreased effective circulating volume, hyperosmolality) Other issue (e.g., CNS or lung disorders [cancer/infections], medications) leads to ADH secretion

Question 46

Hyponatremia: Etiologies (con.)Hypotonic – ADH Dependent - Euvolemic SIADH – syndrome of inappropriate ADH secretion

Answer 46

Diagnosis of exclusion after ruling out other causes of hyponatremia Hyponatremia with decreased plasma osmolality, high urine sodium; no heart/kidney/liver disease, normal thyroid and adrenal function

Question 47

Reset osmostat: Rare condition in which pts regulate ADH release around a lower (hypotonic) set point (mild form occurs in pregnancy) Adrenal insufficiency and severe hypothyroidism: Cortisol normally inhibits ADH release (negative feedback) Deficiency of cortisol means more ADH is released (disruption of ADH “off-switch”)  can lead to hyponatremia

Question 48

Adrenal insufficiency and severe hypothyroidism:

Answer 48

Myxedema coma (in hypothyroidism) may cause hyponatremia May be due to reduced cardiac output and concurrent adrenal insufficiency increasing ADH activity

Question 49

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Question 50

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Question 51

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Answer 51

Lab considerations Serum and urine electrolytes (specifically Na+) Serum and urine osmolality Urine osmolality is used as a surrogate for ADH activity (ADH is typically not directly measured in hyponatremia) Others as indicated (renal function, thyroid function, etc.)

Question 53

Hypernatremia: oliguria

Answer 53

(urine flow <0.5 mL/minute, low)* Reduced water intake – patients with inability to communicate or access water for themselves Nonrenal water loss – sweat, vomiting/diarrhea, respiratory losses (ventilator) Water shifted into cells due to gain of intracellular osmole – rare, seizures or rhabdomyolysis

Question 54

Hypernatremia: nonoliguria

Answer 54

Assess urine osmolality Low (<250 mOsm/kg) [dilute urine] Diabetes insipidus central (not producing enough ADH) or nephrogenic (not responding to ADH) or release of a vasopressinase High (>300 mOsm/kg) [concentrated urine] Hypernatremia with high urine volume and osmolality have osmotic diuresis likely too much glucose or urea spilling into urine, pulling water with it

Question 55

slide 41

Answer 55

Urine osmolality will generally be high for the causes listed here

Question 56

“Third spacing” 1) What is it? What can cause it? 2) What are some S/Sx? 3)

Answer 56

Outdated term Can be caused by hyponatremia (solute concentration in intravascular space < interstitial space) Fluid moves out of intravascular spaces to interstitial fluid Fluid is unavailable for circulatory system S/sx Weight gain Edema Hypotension Tachycardia Decreased Urine output (Uo) Example: ascites

Answer 57

Factors affecting serum K+ concentration include: Aldosterone: tends to increase renal losses of K+ (while retaining Na+ and water in blood) Sodium resorption: as sodium is resorbed, K+ is lost Acid–base balance: Alkalotic states/ Metabolic acidosis

Question 58

Alkalotic states (less H+ in serum) tend to lower serum K+ levels by causing a shift of K+ into the cell (as H+ is shifted out of cell); a similar shift also occurs in renal tubules Metabolic acidosis (except for organic acidoses) tends to raise serum K+ levels (reverse the H+/K+ shift)

Question 59

Hypokalemia: Etiologies

Answer 59

Insufficient intake (diet) Usually not the issue as kidneys can lower excretion to very low levels Certain diet patterns that are extremely low in K+ (e.g., anorexia nervosa, alcoholism) can deplete stores

Question 60

Hypokalemia: Etiologies

Answer 60

Potassium shifted into cells Insulin, beta-adrenergic agonists (e.g., albuterol), alkalosis GI losses/wasting Diarrhea, vomiting

Question 61

Hypokalemia: What are 4 etiologies of renal losses/wasting?

Answer 61

1) Loop diuretics: Can cause substantial potassium and magnesium excretion -Most common cause of potassium wasting 2) Increased aldosterone 3) Hypomagnesemia (Magnesium is important in regulating potassium excretion) 4) Others (renal tubulopathies/tubular acidosis, etc.)

Question 62

Assessing urine potassium can help distinguish renal from non-renal causes of hypokalemia: 1) What is ideal? 2) What is convenient?

Answer 62

Ideal: 24-hour urine collection Convenient: urine potassium to creatinine ratio (Uk/UCr)

Answer 63

Convenient: urine potassium to creatinine ratio (Uk/UCr) Comparing the potassium in spot urine sample to the creatinine Low (kidneys are appropriately preserving K+ in blood)  likely nonrenal cause Evaluate for GI losses (e.g., diarrhea), intracellular K+ shifts, inadequate dietary intake High (more K+ in urine)  likely renal cause Renal K+ wasting (may be related to acid-base disorder, diuretics, hyperaldosteronism, low magnesium, etc.)

Question 65

Hyperkalemia (Serum K+ >5.0 mEq/L): Clinical Features

Answer 65

Impairs neuromuscular transmission Serious manifestations (usually when K+ ≥7.0 mEq/L if chronic or lower if acute) Ascending muscle weakness or paralysis Cardiac conduction abnormalities and cardiac arrhythmias (bradycardias, blocks, VT, VF, asystole, etc.)  eventual cardiac arrest

Question 66

Hyperkalemia (Serum K+ >5.0 mEq/L): Clinical Features 1) What are some other potential Sx? 2) What may it directly cause?

Answer 66

Other potential symptoms include: GI (nausea, vomiting, diarrhea), areflexia, paresthesias May cause metabolic acidosis (interferes with renal NH4+ excretion)

Question 67

Hyperkalemia: Etiologies

Answer 67

Increased K+ intake (not a common cause alone unless acute) Increased net K+ release from cells (can cause transient hyperkalemia) Reduced urinary K+ excretion (can cause persistent hyperkalemia) Medications (multiple mechanisms)

Answer 68

Pseudohyperkalemia Issues during blood collection, storage, handling (fist clenching, tourniquet, shaking the tube) Should be suspected when there is no apparent cause in an asymptomatic patient (repeat lab test) Tissue breakdown Tissue damage releases intracellular K+ Trauma/crush injuries, tumor lysis syndrome, severe hemolysis, rhabdomyolysis, hypothermia

Answer 69

Hyperglycemia Uncontrolled diabetes can cause hyperkalemia Combination of insulin deficiency and hyperglycemic hyperosmolarity (pulling water and K+ into vessels) Metabolic acidosis (other than organic acidosis [lactic/keto-acidosis]) H+ moves from blood into cells, whereas K+ moves opposite direction (from cells into blood) to maintain electroneutrality

Question 70

Beta blockers, digitalis, exercise, RBC transfusion, hyperkalemic periodic paralysis can all cause what?

Answer 70

Increased net K+ release from cells (causing hyperkalemia)

Question 71

Impaired renal elimination of K+

Answer 71

1) **CKD:** Usually able to maintain normal K+ until GFR <20-30 (unless other contributing factors) 2) **Reduced aldosterone action** (deficiency or lack of response) Aldosterone increases Na+ and water reabsorption, K+ and H+ secretion Hypoaldosteronism (e.g., Addison disease), meds (e.g., potassium-sparing diuretics), etc.

Question 72

Impaired renal elimination of K+

Answer 72

1) AKI Especially in oliguric AKI 2) Low effective circulating volume E.g., hypovolemia, heart failure, cirrhosis Reduced Na+ and water delivery to the distal nephron tubule For K+ to be effectively secreted, there needs to be sufficient Na+ and water in the tubule that can be reabsorbed (exchanged for K+)

Question 73

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Answer 73

Medications It is vital to carefully review the pt’s med list Many potential drug causes of hyperkalemia Some of the more common ones:

Question 74

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Question 75

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Answer 75

Consider repeat testing to confirm hyperkalemia (do not delay emergent treatment though) Especially in patients without kidney disease or medications that cause hyperkalemia

Question 76

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Answer 76

Make sure to assess renal function (e.g, Creatinine, BUN), acid-base status (e.g, ABG), glucose (e.g., hyperglycemia) Labs for work-up include BMP (electrolytes, renal function), Mg2+, Ca2+, CBC (e.g., hemolysis), +/- serum osmolality and urine studies (pH, osmolality, creatinine, electrolytes). Others as directed at suspected etiology.

Question 77

Chloride: 1) What is it?

Answer 77

1) Major extracellular anion Neuron action potentials and extracellular fluid tonicity Not useful by itself, interpreted with other electrolytes for acid-base and hydration status Hypo/hyperchloremia doesn’t usually occur in isolation Involves shifts in sodium and/or bicarbonate

Question 78

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Question 79

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Answer 79

Serum calcium (total) is often included on BMP (may need to order separately) 99% of the body’s calcium is in bone Serum calcium is split between free (ionized) calcium and albumin-bound Total serum calcium = ionized + albumin-bound

Question 80

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Answer 80

Total serum calcium: 8.5-10.5 mg/dL (normal) Ionized calcium Physiologically active portion of calcium Necessary for muscle contraction and nerve function Low ionized Ca2+ = true hypocalcemia  implies insufficient action of PTH or active vitamin D

Question 81

Ionized vs. Total Calcium & Effect of Albumin

Answer 81

Usually measuring total serum calcium is sufficient because changes in total mirror those in ionized fraction Exceptions (total calcium is low but ionized may be normal) include: hypoalbuminemia, certain acid-base disorders -When serum albumin is <4 g/dL, serum Ca2+ is reduced by ~0.8 mg/dL* for every 1 g/dL of albumin below normal (4)

Answer 82

If albumin is low, total calcium is expected to be low  measure both when evaluating calcium (Albumin is part of the CMP)

Question 83

Calcium & Phosphorus

Answer 83

Inversely related in the body as one rises, the other falls (generally) PTH causes kidneys to reabsorb calcium but excrete phosphate in urine (raising serum calcium and lowering serum phosphate) When serum phosphate is high (hyperphosphatemia): calcium-phosphate complexes precipitate in tissues, lowering serum calcium (hypocalcemia) also induces PTH secretion to raise calcium and lower phosphate towards normal

Question 84

Hypocalcemia: Clinical Manifestations

Answer 84

Signs/sxs: depend on severity and chronicity May be asymptomatic (if not severe) Hallmark of acute/severe hypocalcemia = tetany (due to neuromuscular irritability) Symptoms range from mild paresthesias to carpopedal spasm to seizures

Question 85

Hypocalcemia: Clinical Manifestations

Answer 85

Classic physical findings include: Chvostek sign, Trousseau sign ECG: QT prolongation predisposes to ventricular arrhythmias, though serious dysrhythmias are rare

Answer 86

Hypoalbuminemia is most common cause of decreased total serum Ca2+ (but ionized Ca2+ may be normal) Causes of low albumin include malnutrition, alcoholism, large volume IV infusion Advanced CKD is most common cause of true hypocalcemia (due to decreased production of calcitriol and hyperphosphatemia)

Answer 87

Hypomagnesemia: reduces PTH release and tissue responsiveness to PTH Vitamin D deficiency: low serum calcium and phosphate, +/- high PTH

Question 88

1) What does primary hypoparathyroidism cause? 2) List some other causes of hypocalcemia

Answer 88

1) **low serum calcium**, high phosphate, low PTH 2) alkalosis (increased pH promotes protein binding, lowering free calcium levels, and vice versa), malabsorption, pancreatitis, diuretics…

Question 89

Hypercalcemia: Clinical Manifestations

Answer 89

May affect GI, kidney, and neurologic function ECG: shortened QT interval (if acute), clinically relevant arrhythmias are rare

Question 90

Hypercalcemia: 1) Common Sx? 2) Complications? (3)

Answer 90

1) Constipation, anorexia, anxiety, cognitive changes (lethargy and stupor if severe) 2) a) Pancreatitis (calcium deposition in pancreatic ducts) b) Impaired renal concentrating ability: Polyuria and dehydration c) Nephrolithiasis (due to hypercalciuria): renal colic, hematuria

Question 91

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Answer 91

Most common causes (90%): Asymptomatic, mild hypercalcemia: usually primary hyperparathyroidism PTH increases GI absorption of calcium, increases urinary reabsorption, increases bone resorption Symptomatic, severe hypercalcemia: usually malignancy-associated hypercalcemia Myeloma, breast, lung, renal cell metastases destroy bone and release calcium into blood Various cancers produce PTH-like substance

Question 93

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Answer 93

Elevated serum total and ionized calcium May have hypophosphatemia Serum PTH levels: used to determine if hypercalcemia is PTH-mediated or not High: primary hyperparathyroidism is the most likely cause Low: eval for non-PTH-mediated cause (malignancy, Vit. D intoxication, etc.)

Answer 94

Most magnesium is stored in bones and muscles Physiologic effects on nervous system are similar to Ca2+ Both hypo- and hypermagnesemia can decrease PTH secretion/action and provoke hypocalcemia

Question 95

Hypermagnesemia

Answer 95

Advanced CKD (impaired excretion) Chronic intake of Mg-containing drugs (Antacids, laxatives) Pregnant pts receiving IV Mg for preeclampsia/ eclampsia 2) Decreased DTRs (earliest finding)  weakness, somnolence, confusion, bradycardia, hypotension  respiratory muscle paralysis, cardiac arrest

Question 96

Hypomagnesemia common etiologies?

Answer 96

GI losses (diarrhea, malabsorption, small bowel bypass surgery, pancreatitis, PPIs) Urinary losses (loop/thiazide diuretics, alcohol abuse, hypercalcemia, uncontrolled DM)

Question 97

Hypomagnesemia Clinical Manifestations Include what?

Answer 97

Neuromuscular and CNS hyperirritability (may be from low K+/Ca2+)  tremors, cramps, Trousseau/Chvostek signs, confusion, disorientation, convulsions, coma; weakness; hypertension, tachycardia, arrhythmias (e.g., torsades de pointes) Can cause hypokalemia and hypocalcemia that are refractory to treatment until Mg is fixed

Answer 98

Hypophosphatemia: Etiologies include: Diminished absorption (e.g., antacids), refeeding syndrome, vitamin D deficiency, hyperparathyroidism Clinical manifestations related to ATP deficiency (phosphorus is a key ingredient of ATP) Sx - Muscle weakness, hemolysis. Severe  rhabdomyolysis, paresthesia, encephalopathy

Answer 99

Hyperphosphatemia: Etiologies include: advanced CKD (most common); phosphate-containing laxatives; rapid cell breakdown releasing intracellular phosphate (tumor lysis syndrome, rhabdomyolysis, hemolysis) Can cause concurrent hypocalcemia Sx - Usually asymptomatic (may have sxs from hypocalcemia and underlying disorder)