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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
tx hypokalemia
tx underlying cause, check hypomagnesemia, 24 hr urine K (20 mEq/d suggests renal loss)
26
if you cant get a hold on a pt low K, what should you check (BOARD)
check Mg
27
rapid correction hypokalemia
IV: cardiac monitor, IV KCl: usually <20mEq/hr *check Stat K q 2-4hr
28
slow correction hypokalemia
Oral or liquid: 20-40 mEq BID-TID kids: 1-2 mEq/kd/d divided dose
29
what are the components of CMP
Glu, BUN, Cr, BUN/Cr, Na, K, Cl, CO2, Total Pro, Alb, Ca, ALK pho, ALT, AST, total bilirubin
30
what are potential additional components of CMP
phos, Mg, anion gap, Globulin, A/G ratio
31
what is total protein composed of and what is the RR
RR = 6.4-8.3 g/dL | composed of Prealbumin, albumin, globulin (PAG for Pro)
32
what is total protein level used for
dx/eval/monitor: | cancer, immune disorders, protein losing enteropathies, impaired ntr, liver dz, edema (ascites, burns etc)
33
What is albumins RR and what percent of total protein does it comprise
RR albumin = 3.5-5 g/dL for adult 4-5.9 g/dL child makes up 60% of total protein (prealb, alb, globulin)
34
functions of albumin?
* transport drugs, hormones and enzymes | * maintain osmotic pressure
35
where is albumin synthesized and what is it a measure of
synthesized in liver, measure of hepatic function and NUTRITIONAL STATUS!!!
36
when might we see decreased ALbumin
* 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)
37
when might we see increased alb
dehydration
38
where are globulins mostly made and what are they used for
mostly made in bone marrow and lymph tissue (few in liver) | *used for antibodies, acute phase reactants (ie CRP for inflammation)
39
what groups of globulins exist
alpha, gamma, beta | *gamma = immunoglobulin
40
when are globulins often elevated
when albumin is low, globulins are often elevated: acute rznz, chronic inflammatory dz, advanced cirrhosis (bc albumin made in liver)
41
What is serum protein electrophoresis (SPEP) and what disease can it be used to dx?
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
42
What is Multiple Myeloma and it's initial sx and what urine component is indicated of the dz
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
43
What is the RR for Ca
RR adult 9-10.5
44
What is total Ca consist of and what is it used to evaluate
Total Ca = free (ionized) + protein bound * measures alb simultaneously * used to eval Parathyroid function
45
What is the critical value for Ca
13 mg/dl
46
who is it important to monitor Ca levels in?
pt with renal failure, hyperparathyroidism and malignancies
47
What is the calcium distribution in the body
99% in bone 1% in cells (.9 in ICF) 0.1% in ECF/serum (50% free, 10% complexed, 40% protein bound)
48
What percentage of serum Ca is ionized/free Ca and what exactly does this mean physiologically
50% of serum Ca is free/ionized. This means that the Ca is free to leave vascular compartment and participate in cell function
49
What cell functions/roles does ionized/free Ca play an important role in?
NMJ activity (eg muscle and heart contractility) enzymatic rxn blood clotting
50
outline the process of Ca entering/exiting body
1. Enters body via GI tract 2. Absorbed into intestine with help from vitamin D 3. Stored in bone 4. Excreted by kidney
51
What is serum Ca regulated by and what happens if there is a decrease in serum Ca
serum Ca regulated by PTH and vit D | *dec in serum Ca causes PTH secretion to increase serum Ca
52
how does PTH increase serum Ca
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
What happens if serum Ca is too high
Thyroid gland releases calcitonin --> stimulates Ca deposition into bone, reduces Ca uptake in intestines and reduces Ca uptake in kidneys
54
Dx of hypercalcemia and most common causes
serum Ca > 10.5 mg/dL = hypercalcemia *most common causes (bone resorption) = hyperparathyroidism**MOST COMMON, malignancy (bone destruction or stimulation of osteoclast activity
55
what are some other not as common causes of hypercalcemia
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
What are some sx of hypercalcemia
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
What is the def of hyperparathyroidism and presentation
(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
What phrase should we remember for hyperparathyroidism/hypercalcemia
"bones, stones, abdominal groans, psychic moans with fatigue overtones"
59
Clinical presentation of hyperparathyroidism
BRAD!!! Bone pain (osteitis fibrosa cystica, osteopenia) Renal stones (ca oxalate or phosphate) Abdominal pain, anorexia, n/v Depression, personality disorders (fatigue)
60
how do you dx hyperparathyroidism
hypercalcemia, hyPOphosphatemia elevated PTH PT scan PT exploration and biops
61
tx for hyperparathyroidism/hypercalcemia
parathyroidectomy
62
what malignancies are associated with hypercalcemia
``` solid tumors (breast w/ mets, lung, kidney) Hematologic malignancies (MM (cancer of WBC), lymphoma, leukemia) ```
63
definition of hypocalcemia
serum Ca <9 mg/dL
64
3 main causes of hypocalcemia (Ca<9) are:
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
what is the most common cause of reported hypocalcemia (not true hypoCa)
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
for every 1 g/dL that albumin is below 4 g/dL, Serum calcium should...
be increased by 1 mg/dL (get adjusted Ca value)
67
Besides hypoalbuminemia, what are other causes of hypocalcemia
hypoPTH, Mg def, renal failure (bc phos retention), Vit D deficiency/rickets, Osteomalacia
68
sx of hypocalcemia
Increased NM excitability: (paresthesias, cramps, hyperactive reflexes, carpopedal spasms, +chvostek and trousseau, tetany) CV effects: hypotension, EKG changes prolonged QT, arrythmia
69
why is tetany associated with hypocalcemia
bc low ca results in lowered threshold for muscular excitability --> spasm *numbness and tingling of lips and fingers/toes may proceed spasm
70
what is carpopedal spasm and what is it assoc with
assoc with hypocalcemia = contraction of hands/feet
71
what is carpal spasm (assoc with hypoCa)
wrist flexion, MCP flexion with ext of IP joints and adduction of hyperextended fingers forming "cone" called "obstetricians hand"
72
what may cause latent tetany/hypoCa tetany
hypoPTH, acute hyperventilation (resp alkalosis) or hypomagnesemia
73
what tests can be done for latent tetany
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
RR for phosphate is..?
RR = 3-4.5 mg/dL
75
what is Phosphate level used for
to investigate Parathyroid and Ca abnormalities | *note: phosphate interchangeable with phosphorus, a component of phosphate
76
where is the majority of phosphorus found
bone (85%)
77
what is the critical value for phosphate
<1 mg/dL (RR is 3 to 4.5 mg/dL)
78
where is phosphate absorbed and what is it decreased with?
absorbed in SI, decreased with antacids
79
regarding phosphate: renal excretion ??? to dietary intake
equals!
80
what does PTH do to phosphate reabsorption
PTH decreases phosphate reabsorption by the kidneys
81
causes of increased phosphate
hypoPTH, renal failure, increased diet intake, acromegaly
82
causes of decreased phosphate
TPN, tx DKA, alcohol withdrawal, hyperPTH
83
RR of Mg
RR adult: 1.3-2.1 mEq/L
84
where is Mg located and what is it's distribution in the body
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
what functions depend on Mg
NM and cardiac function
86
what are the critical values of Mg
3.0 mEq/L
87
what dietary sources of Mg are there
green veggies, grains, nuts, meats, seafood
88
what percent of dietary Mg is absorbed
25-65%
89
Mg level is regulated by.. and when is it decreased
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
dx of hypomagnesemia
Mg<1.3 mg/dL
91
when is hypoMg common and what usually causes it
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
causes of increased Mg
Renal insufficiency addisons hypoTHyroidism ingestion of Mg containing cmpd (antacid, laxative)
93
causes of decreased Mg
``` malnutrition malabsorption alcoholism diarrhea tx DKA CHF hypocalcemia hypokalemia ```
94
what are clinical signs of hypomg
*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
what can hypo Mg cause
hypokalemia and hypocalcemia hypocalcemia prob related to low PTH, need to correct Mg to fix Ca
96
why is hypoMg assoc with hypokalemia
hypoMg impairs ability of kidney to conserve K.. need to correct Mg deficit to fix K level
97
Oral tx of low Mg
Mg Ox 400 mg | *caution if renal dz
98
IV tx of low Mg
MgSO4 infusion followed by additional infusion over 3-7 days | *follow blood levels and DTR
99
dx hypermg
Mg>2.1 mg/dL | RARE bc kidney can usually handle excess Mg, so renal insuff is usually cause of hyperMg
100
what (besides renal insuff) can lead to hyperMg
Mg containing Meds (mylanta, maalox)
101
what are NM and CV effects of HyperMg
NM: hyporeflexia, muscle weakness, resp paralysis, confusion CV: Hypotension (but low Ca = HTN), arrythmia *note: hyPERCa = HTN; hyPERMg = hypotension)
102
RR BUN
10-20 mg/dL
103
what is BUN
rough measurement of renal function and GFR
104
what is urea
by product of liver pro metab
105
if urea is poorly excreted by kidneys, what happens to BUN and what is this called
increase in BUN with poor excretion | this increase in BUN is called axotemia
106
what is the mosby and Meyer critical values for BUN
mosby: >100mg/dL | meyer worrisome: >50mg/dL
107
what causes inadequate excretion of urea and what does this do to BUN
renal dz causes inadequate excretion | this causes BUN to rise (aotemia)
108
effect on BUN: low pro vs high
Low: decreases BUN high: increases
109
hydration status effect on BUN
dehydration: increase BUN
110
Cr RR male and femal
F: 0.5-1.1 mg/dL M: 0.6-1.2 mg/dL
111
what is Cr used for
used in conjunction with bUN to assess renal function | *BEST est of GFR
112
who have lower Cr levels and why
elderly and kids bc decreased muscle mass (Cr is byproduct of Cr phosphate used in skeletal m contraction)
113
critical value for Cr
>4 mg/dL = problem
114
increased levels of Cr due to
renal dz, rhabdomyolysis, acromegaly, gigantism
115
decreased levels Cr due to
debilitation, muscular dystrophy, myasthenia gravis, elderly/kids
116
BUN/Cr ratio.. use and comparison bw BUN and Cr
used as renal function tests | BUN is less accurate indicator BUT provides info about origin of kidney problem (prerenal, renal, postrenal)
117
what is normal ratio BUN/cr
10-20:1
118
pre/renal/postrenal azoemia ratios
pre: >20:1 renal: 10-20:1 Post: variable
119
Prerenal azotemia definition and cuase
BUN increase> Cr increase = >20:1 ratio | Causes: hypovolemia (trauma/burn/hemorrhage, dehydration, diuretic), infection (sepsis), low CO (CHF)
120
tx prerenal azotemia
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
good news about prerenal azotemia
close med monitoring and mgmt can prevent and remedy prerenal azotemia
122
what is renal azotemia
BUN and Cr increase proportionately | normal BUN:Cr ratio 10-20:1
123
renal etiologies of renal azotemia
* 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
tx renal azotemia
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
What is postrenal azotemia
BUN increase, variable Cr thus ratio is nondiagnostic (usually about 10:1)
126
What causes postrenal azotemia
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
tx postrenal azotemia
``` identiy location of obstruction if urethral or bladder --> FOLEY catheter temp correction higher obstruction (ureter or renal pelvis) -> urologist ```
128
RR chloride
98-106
129
what does Cl indicate and what is it's purpose
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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