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Clin Lab Med > electrolyte 2 and CMP > Flashcards

electrolyte 2 and CMP Flashcards

1
Q

range Na

A

135-145 mEq/L

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2
Q

range K

A

3.5-5 mEq/L

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3
Q

range Cl

A

98-106 mEq/L

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4
Q

range bicarb

A

22-32 mEq/L

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5
Q

electrolyte panel CPT code

A

80051

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6
Q

EKG hypokalemia

A

prominent U wave

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7
Q

EKG hyperkalemia

A

tall peaked T wave

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8
Q

what is K

A

K: major intracellular CATion, renal excretion, regulated in distal nephron

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9
Q

RAS system aldosterone actions

A

increase renal Na reabsorption and increase renal K excretion

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10
Q

hyperkalemia dx and etiology

A

Hyperkalemia: K>5.0 (>6-6.5 = serious problem)

May be caused by:

  1. false elevation
  2. pseudohyperkalemia
  3. inadequate excretion
  4. redistribution from ICF to ECF
  5. excess administration
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11
Q

clinical features of hyperkalemia

A

Neuro: weakness, numbness, tingling, paralysis, hypoactive DTR
EKG changes, arrythmia, cardiac arrest: early EKG tall peaked T wave, end event: sine wave pattern with arrest

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12
Q

Causes of pseudohyperkalemia

A
  1. hemolysis due to poor venipuncture technique *most common
  2. Thrombocytosis, leukocytosis
    * *repeat K determination to check for artifactual elevation
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13
Q

Inadequate excretion of K etiology cause of hyeperkalemia

A
  1. Renal failure: assess BUN/Cr
  2. Meds blocking K excretion: spironolactone, triamterene, amiloride
  3. Hypoaldosteronism (adrenal insufficiency ie Addisons disease, ACE inhibitors-common, NSAIDS -uncommon, Renal tubular disease)
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14
Q

Etiology redistribution of K cause of hyperkalemia

A

K moves from ICF to ECF:

  • tissue damage ie rhabdomyolysis
  • acidosis (a 0.1 decrease in pH raises serum K+ about 0.5-1.0 mEq/L due to ECF shift)
  • decreased insulin
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15
Q

Etiology of excess K+ admin

A 
K supplement (oral, IV)
K based salt sub
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16
Q

Tx hyperkalemia, rapid

A

r/o pseudohyperkalemia via repeat K+
If K+ is >6.5 send to ER or ICU
*rapid correction: CaCl IV to protect heart; maneuvers to shift K from ECF to ICF (sodium bicarb IV to increase pH, D50W plus insulin IV)

*give dextrose with insulin to prevent hypoglycemia

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17
Q

tx hyperkalemia, slow

A

Slow correction:

  • diuretics (furosemide)
  • kayexalate + sorbitol (po or rectal) - cation exchange resin (Na for K in gut)
  • dialysis

Correct underlying cause:

  • stop K sparing diuretic
  • stop ACE inhibitor, K supp etc
  • mineralcorticoid replacement if Addisons
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18
Q

dx and etiology hypokalemia

A 
Hypokalemia: K< 3.0 is potentially dangerous; 2.0 = ~ 200 mEq deficit in adult
Cause:
1. inadequate intake
2. GI tract loss
3. Renal loss
4. Redistribution ECF to ICF
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19
Q

Clinical features/sx hypokalemia

A

sx:
neuromuscular: malaise, weakness, cramps, constipation, paralysis
polyuria, polydipsia with hyperglycemia
signs:
cardiac: arrythmia, hypotension (EKG - flattened T wave, ST depression , U WAVES, ventricular ectopy)

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20
Q

low potassium is more dangerous when taking what?

A

digoxin

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21
Q

etiology GI loss cause of hypokalemia

A

vomiting, diarrhea (laxative abuse, IBD), fistula, villous adenoma (rectosigmoid tumor)

Upper GI loss (vomiting, NG suction) –> metab alkalosis which promotes renal K loss (*Cl losing diarrhea can cause metab alkalosis as well) however note that lower GI loss ie diarrhea or fistula usually causes metab ACIDosis

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22
Q

Etiology renal loss cause of hypokalemia

A

diruetic*, osmotic diuresis (hyperglycemia or EtOH), renal tubular acidosis (RTA), Bartter’s syndrome (elevated renin and aldosterone)

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23
Q

Causes of K redistribution from ECF to ICF (hypokalemia)

A
  1. Metab alkalosis (each 0.1 increase in pH lowers serum K+ by 0.5-1 mEq/L)
  2. insulin administration
  3. mineralocorticoid excess ie hyperaldosteronism, cushings, steroid
  4. hypokalemic periodic paralysis
  5. B agonist induce cellular uptake of K and promote insulin secretion by pancreas (Albuterol)
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24
Q

Prompt tx of hypokalemia is critical if taking what?

A

Digitalis

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25
Q

tx hypokalemia

A

tx underlying cause, check hypomagnesemia, 24 hr urine K (20 mEq/d suggests renal loss)

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26
Q

if you cant get a hold on a pt low K, what should you check (BOARD)

A

check Mg

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27
Q

rapid correction hypokalemia

A

IV:
cardiac monitor, IV KCl: usually <20mEq/hr
*check Stat K q 2-4hr

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28
Q

slow correction hypokalemia

A

Oral or liquid: 20-40 mEq BID-TID

kids: 1-2 mEq/kd/d divided dose

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29
Q

what are the components of CMP

A

Glu, BUN, Cr, BUN/Cr, Na, K, Cl, CO2, Total Pro, Alb, Ca, ALK pho, ALT, AST, total bilirubin

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30
Q

what are potential additional components of CMP

A

phos, Mg, anion gap, Globulin, A/G ratio

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31
Q

what is total protein composed of and what is the RR

A

RR = 6.4-8.3 g/dL

composed of Prealbumin, albumin, globulin (PAG for Pro)

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32
Q

what is total protein level used for

A

dx/eval/monitor:

cancer, immune disorders, protein losing enteropathies, impaired ntr, liver dz, edema (ascites, burns etc)

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33
Q

What is albumins RR and what percent of total protein does it comprise

A

RR albumin = 3.5-5 g/dL for adult
4-5.9 g/dL child
makes up 60% of total protein (prealb, alb, globulin)

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34
Q

functions of albumin?

A
  • transport drugs, hormones and enzymes

* maintain osmotic pressure

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35
Q

where is albumin synthesized and what is it a measure of

A

synthesized in liver, measure of hepatic function and NUTRITIONAL STATUS!!!

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36
Q

when might we see decreased ALbumin

A
  • malnourished pt
  • protein losing enteropathies (crohn, celiac)
  • protein losing nephropathies (nephrotic syndrome = edema, proteinuria, hyperlipidemia)
  • Liver dz, third spacing (ascites, burns), inflammatory dz (globulins ^ causing alb to dec)
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37
Q

when might we see increased alb

A

dehydration

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38
Q

where are globulins mostly made and what are they used for

A

mostly made in bone marrow and lymph tissue (few in liver)

*used for antibodies, acute phase reactants (ie CRP for inflammation)

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39
Q

what groups of globulins exist

A

alpha, gamma, beta

*gamma = immunoglobulin

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40
Q

when are globulins often elevated

A

when albumin is low, globulins are often elevated: acute rznz, chronic inflammatory dz, advanced cirrhosis (bc albumin made in liver)

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41
Q

What is serum protein electrophoresis (SPEP) and what disease can it be used to dx?

A

SPEP is a process that separates serum components by electrical charge; can reveal patterns characteristic of dz

*Multiple Myeloma (MM) has “M spike” (monoclonal gammopathy) in beta or gamma globulin demonstrated on SPEP

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42
Q

What is Multiple Myeloma and it’s initial sx and what urine component is indicated of the dz

A

MM is cancer of plasma cells usually occurring in 6th decade. Initial sx are back or rib pain and anemia
*BENCE JONES PROTEINS IN URINE

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43
Q

What is the RR for Ca

A

RR adult 9-10.5

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44
Q

What is total Ca consist of and what is it used to evaluate

A

Total Ca = free (ionized) + protein bound

  • measures alb simultaneously
  • used to eval Parathyroid function
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45
Q

What is the critical value for Ca

A

13 mg/dl

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46
Q

who is it important to monitor Ca levels in?

A

pt with renal failure, hyperparathyroidism and malignancies

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47
Q

What is the calcium distribution in the body

A

99% in bone
1% in cells (.9 in ICF)
0.1% in ECF/serum (50% free, 10% complexed, 40% protein bound)

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48
Q

What percentage of serum Ca is ionized/free Ca and what exactly does this mean physiologically

A

50% of serum Ca is free/ionized. This means that the Ca is free to leave vascular compartment and participate in cell function

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49
Q

What cell functions/roles does ionized/free Ca play an important role in?

A

NMJ activity (eg muscle and heart contractility)
enzymatic rxn
blood clotting

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50
Q

outline the process of Ca entering/exiting body

A
  1. Enters body via GI tract
  2. Absorbed into intestine with help from vitamin D
  3. Stored in bone
  4. Excreted by kidney
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51
Q

What is serum Ca regulated by and what happens if there is a decrease in serum Ca

A

serum Ca regulated by PTH and vit D

*dec in serum Ca causes PTH secretion to increase serum Ca

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52
Q

how does PTH increase serum Ca

A

PTH –>

  • increase vit D activation = increase Ca absorption from gut
  • promotes Ca release from bone
  • promotes conservation of Ca by kidneys (and excretion of phosphate)
53
Q

What happens if serum Ca is too high

A

Thyroid gland releases calcitonin –> stimulates Ca deposition into bone, reduces Ca uptake in intestines and reduces Ca uptake in kidneys

54
Q

Dx of hypercalcemia and most common causes

A

serum Ca > 10.5 mg/dL = hypercalcemia
*most common causes (bone resorption) = hyperparathyroidism**MOST COMMON, malignancy (bone destruction or stimulation of osteoclast activity

55
Q

what are some other not as common causes of hypercalcemia

A
  1. pagets dz
  2. prolonged immobilization (bone demineralizes)
  3. Hyperthyroidism
  4. Acromegaly (impaired GH)
  5. Addisons dz
  6. excess vit D or Ca intake (antacid)
  7. Granulomatous dz (sarcoidosis)
  8. Various drugs (lithium, thiazide diuretics) *thiazides enhance Ca reab in DCT
56
Q

What are some sx of hypercalcemia

A

decrease NM excitability (weak, loss of tone, lethargy, stupor, coma)
CV effects (HTN, EKG abnormalities - short QT)
Renal (polyuria, increased thirst, kidney stones)
GI (anorexia, n/v, constipation)

57
Q

What is the def of hyperparathyroidism and presentation

A

(hyperparathyroidism = hypercalcemia)
excess secretion of PTH leads to hypercalcemia; usual cause is PARATHYROID ADENOMA

F>M, >50 yo, often asymptomatic (80%)
“bones, stones, abdominal groans, psychic moans with fatigue overtones”

58
Q

What phrase should we remember for hyperparathyroidism/hypercalcemia

A

“bones, stones, abdominal groans, psychic moans with fatigue overtones”

59
Q

Clinical presentation of hyperparathyroidism

A

BRAD!!!
Bone pain (osteitis fibrosa cystica, osteopenia)
Renal stones (ca oxalate or phosphate)
Abdominal pain, anorexia, n/v
Depression, personality disorders (fatigue)

60
Q

how do you dx hyperparathyroidism

A

hypercalcemia, hyPOphosphatemia
elevated PTH
PT scan
PT exploration and biops

61
Q

tx for hyperparathyroidism/hypercalcemia

A

parathyroidectomy

62
Q

what malignancies are associated with hypercalcemia

A 
solid tumors (breast w/ mets, lung, kidney)
Hematologic malignancies (MM (cancer of WBC), lymphoma, leukemia)
63
Q

definition of hypocalcemia

A

serum Ca <9 mg/dL

64
Q

3 main causes of hypocalcemia (Ca<9) are:

A
  1. inability to mobilize bone stores (hypoPTH, Mg deficiency which causes inhibition of PTH)
  2. excess renal Ca loss (renal failure causes phosphate retention and reciprocal loss of Ca)
  3. Increased Pro binding –> less Ca in ionized form (ie alkalosis)
65
Q

what is the most common cause of reported hypocalcemia (not true hypoCa)

A

HYPOALBUMINEMIA
if serum albumin is low, must mathematically correct Ca
adjusted Ca = serum Ca - serum alb+4
**serum Ca should ^ 1 mg/dL for every 1 g/dL that albumin is below 4 g/dL

66
Q

for every 1 g/dL that albumin is below 4 g/dL, Serum calcium should…

A

be increased by 1 mg/dL (get adjusted Ca value)

67
Q

Besides hypoalbuminemia, what are other causes of hypocalcemia

A

hypoPTH, Mg def, renal failure (bc phos retention), Vit D deficiency/rickets, Osteomalacia

68
Q

sx of hypocalcemia

A

Increased NM excitability: (paresthesias, cramps, hyperactive reflexes, carpopedal spasms, +chvostek and trousseau, tetany)

CV effects: hypotension, EKG changes prolonged QT, arrythmia

69
Q

why is tetany associated with hypocalcemia

A

bc low ca results in lowered threshold for muscular excitability –> spasm
*numbness and tingling of lips and fingers/toes may proceed spasm

70
Q

what is carpopedal spasm and what is it assoc with

A

assoc with hypocalcemia = contraction of hands/feet

71
Q

what is carpal spasm (assoc with hypoCa)

A

wrist flexion, MCP flexion with ext of IP joints and adduction of hyperextended fingers forming “cone” called “obstetricians hand”

72
Q

what may cause latent tetany/hypoCa tetany

A

hypoPTH, acute hyperventilation (resp alkalosis) or hypomagnesemia

73
Q

what tests can be done for latent tetany

A

chvostek sign: tap facial n against bone anterior to ear –> contraction of facial mm

Trousseau’s sign: occlude brachial a for 3 min with cuff induces carpal spasm

74
Q

RR for phosphate is..?

A

RR = 3-4.5 mg/dL

75
Q

what is Phosphate level used for

A

to investigate Parathyroid and Ca abnormalities

*note: phosphate interchangeable with phosphorus, a component of phosphate

76
Q

where is the majority of phosphorus found

A

bone (85%)

77
Q

what is the critical value for phosphate

A

<1 mg/dL (RR is 3 to 4.5 mg/dL)

78
Q

where is phosphate absorbed and what is it decreased with?

A

absorbed in SI, decreased with antacids

79
Q

regarding phosphate: renal excretion ??? to dietary intake

A

equals!

80
Q

what does PTH do to phosphate reabsorption

A

PTH decreases phosphate reabsorption by the kidneys

81
Q

causes of increased phosphate

A

hypoPTH, renal failure, increased diet intake, acromegaly

82
Q

causes of decreased phosphate

A

TPN, tx DKA, alcohol withdrawal, hyperPTH

83
Q

RR of Mg

A

RR adult: 1.3-2.1 mEq/L

84
Q

where is Mg located and what is it’s distribution in the body

A

Mg is 2nd most common ICF cation
50-60% in bone, 39-49% in body cells,
1% in ECF (1/3 bound to pro mainly albumin)

85
Q

what functions depend on Mg

A

NM and cardiac function

86
Q

what are the critical values of Mg

A

3.0 mEq/L

87
Q

what dietary sources of Mg are there

A

green veggies, grains, nuts, meats, seafood

88
Q

what percent of dietary Mg is absorbed

A

25-65%

89
Q

Mg level is regulated by.. and when is it decreased

A

regulated by the kidneys

  • Reabsorption decreased if serum Mg is high or serum Ca is high - neg feedback
  • Mg reab decreased by loop diuretics
90
Q

dx of hypomagnesemia

A

Mg<1.3 mg/dL

91
Q

when is hypoMg common and what usually causes it

A

hypomag common in critical care/ER settings
Usually caused by conditions that limit GI intake, increase GI/Renal loss, cause movement between ECF and ICF (pH change or admin of glucose and insulin)

92
Q

causes of increased Mg

A

Renal insufficiency
addisons
hypoTHyroidism
ingestion of Mg containing cmpd (antacid, laxative)

93
Q

causes of decreased Mg

A 
malnutrition
malabsorption
alcoholism
diarrhea
tx DKA
CHF
hypocalcemia
hypokalemia
94
Q

what are clinical signs of hypomg

A

*note hypoMg clinically more common than hyper

NM: similar to low Ca (hyperactive reflexes, paresthesias, muscle weakness, tremors, tetany with +chvostek and trousseau

CV: HTN (hypocalcemia = hypotension *this is where Mg and Ca differ), tachy and arrythmia

95
Q

what can hypo Mg cause

A

hypokalemia and hypocalcemia

hypocalcemia prob related to low PTH, need to correct Mg to fix Ca

96
Q

why is hypoMg assoc with hypokalemia

A

hypoMg impairs ability of kidney to conserve K.. need to correct Mg deficit to fix K level

97
Q

Oral tx of low Mg

A

Mg Ox 400 mg

*caution if renal dz

98
Q

IV tx of low Mg

A

MgSO4 infusion followed by additional infusion over 3-7 days

*follow blood levels and DTR

99
Q

dx hypermg

A

Mg>2.1 mg/dL

RARE bc kidney can usually handle excess Mg, so renal insuff is usually cause of hyperMg

100
Q

what (besides renal insuff) can lead to hyperMg

A

Mg containing Meds (mylanta, maalox)

101
Q

what are NM and CV effects of HyperMg

A

NM: hyporeflexia, muscle weakness, resp paralysis, confusion

CV: Hypotension (but low Ca = HTN), arrythmia
*note: hyPERCa = HTN; hyPERMg = hypotension)

102
Q

RR BUN

A

10-20 mg/dL

103
Q

what is BUN

A

rough measurement of renal function and GFR

104
Q

what is urea

A

by product of liver pro metab

105
Q

if urea is poorly excreted by kidneys, what happens to BUN and what is this called

A

increase in BUN with poor excretion

this increase in BUN is called axotemia

106
Q

what is the mosby and Meyer critical values for BUN

A

mosby: >100mg/dL

meyer worrisome: >50mg/dL

107
Q

what causes inadequate excretion of urea and what does this do to BUN

A

renal dz causes inadequate excretion

this causes BUN to rise (aotemia)

108
Q

effect on BUN: low pro vs high

A

Low: decreases BUN
high: increases

109
Q

hydration status effect on BUN

A

dehydration: increase BUN

110
Q

Cr RR male and femal

A

F: 0.5-1.1 mg/dL

M: 0.6-1.2 mg/dL

111
Q

what is Cr used for

A

used in conjunction with bUN to assess renal function

*BEST est of GFR

112
Q

who have lower Cr levels and why

A

elderly and kids bc decreased muscle mass (Cr is byproduct of Cr phosphate used in skeletal m contraction)

113
Q

critical value for Cr

A

> 4 mg/dL = problem

114
Q

increased levels of Cr due to

A

renal dz, rhabdomyolysis, acromegaly, gigantism

115
Q

decreased levels Cr due to

A

debilitation, muscular dystrophy, myasthenia gravis, elderly/kids

116
Q

BUN/Cr ratio.. use and comparison bw BUN and Cr

A

used as renal function tests

BUN is less accurate indicator BUT provides info about origin of kidney problem (prerenal, renal, postrenal)

117
Q

what is normal ratio BUN/cr

A

10-20:1

118
Q

pre/renal/postrenal azoemia ratios

A

pre: >20:1
renal: 10-20:1
Post: variable

119
Q

Prerenal azotemia definition and cuase

A

BUN increase> Cr increase = >20:1 ratio

Causes: hypovolemia (trauma/burn/hemorrhage, dehydration, diuretic), infection (sepsis), low CO (CHF)

120
Q

tx prerenal azotemia

A

bc sign of intravascular vol depletion or hypotension thus tx = restore fluid (oral, IV, reduce or dc diuretic)
*watch status esp when changes to meds made

121
Q

good news about prerenal azotemia

A

close med monitoring and mgmt can prevent and remedy prerenal azotemia

122
Q

what is renal azotemia

A

BUN and Cr increase proportionately

normal BUN:Cr ratio 10-20:1

123
Q

renal etiologies of renal azotemia

A
  • acute tubular necrosis (most common cause, secondary to low perfusion or nephrotoxic drugs ie vancomycin or acyclovir)
  • chronic renal dz
  • acute glomerulonephritis (not as common but can follow endocarditis or strep)
124
Q

tx renal azotemia

A

when BUN and Cr both increases suspect intrinsic renal dz –> med mgmt or dialysis
*optimize fluid mgmt and watch in/output to prevent fluid overload

125
Q

What is postrenal azotemia

A

BUN increase, variable Cr thus ratio is nondiagnostic (usually about 10:1)

126
Q

What causes postrenal azotemia

A

obstruction to urine flow
*ureter and renal pelvis: clot, stones, sickle cell
Bladder: BPH or malignancy, neuropathic bladder with urinary retention, clot
*urethral stricture
**SX

127
Q

tx postrenal azotemia

A 
identiy location of obstruction
if urethral or bladder --> FOLEY catheter temp correction
higher obstruction (ureter or renal pelvis) -> urologist
128
Q

RR chloride

A

98-106

129
Q

what does Cl indicate and what is it’s purpose

A

acid base balance and hydration

  • purpose is to maintain electrical neutrality*
  • abnormalities typically accompany shifts in Na and bicarb

Clin Lab Med (6 decks)

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