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Clinical Chemistry Review > Laboratory Result Interpretations > Flashcards

Laboratory Result Interpretations Flashcards

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1
Q

psychogenic polydipsia

A

Overhydration

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2
Q

serum sodium is reduced below 135 mEq/L

A

Overhydration

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3
Q

Because the consumed water is excreted by the kidneys, the urine is also dilute in this ion.

A

Overhydration

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4
Q

In fact, the osmolality of urine will be low—that is, less than 300 mOsm/kg.

A

Overhydration

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5
Q

Often accompanying hyponatremia are low values of the hematocrit and low values of BUN

A

Overhydration

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6
Q

Urinalysis in the fluid-restricted patient will reveal urinary sodium of less than 25 mEq/L and low osmolalities.

A

Overhydration

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7
Q

The potassium may also be low, although it often remains within the reference range.

A

Overhydration

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8
Q

Because mainly water is excreted in urine in this condition, the total 24-hour sodium excre- tion will be low

A

Overhydration

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9
Q

block the chloride pump in the loop of Henle, thereby blocking the formation of the ion gra- dients via the countercurrent multiplier, necessary for water conservation. Thus, water is lost.

A

Diuretics

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10
Q

Also, because sodium is no longer retained because it follows chloride in the loop, it also is depleted from serum.

A

Diuretics

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11
Q

Thus, unlike in overhydration, the total 24-hour sodium excretion is high

A

Diuretics

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12
Q

pattern resembles overhydration (dilute serum and urine), except that loop diuretics cause severe potassium deple- tion unless the diuretic is combined with a potassium-sparing diuretic such as triamterene.

A

Diuretics

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13
Q

Combined hyponatremia and hypokalemia with a high uri- nary sodium and potassium 24-hour excretion point to diuretic use.

A

Diuretics

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14
Q

In this condition, secondary to head trauma, seizures, other CNS diseases, and neoplastic conditions, espe- cially lung, breast, and ovarian cancers that secrete ADH-like hormones, the serum sodium is depressed due to the excess retention of water in the collecting ducts.

A

SIADH

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15
Q

This results in depletion of water in the renal tubules, thereby concentrating the urine.

A

SIADH

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16
Q

Therefore, while the serum is dilute in sodium (hypotonic), the urine is concentrated to levels of over 40 mEq/L and the urine osmolality exceeds 300 mOsm/kg, while the serum osmolal- ity is less than 280 mOsm/kg.

A

SIADH

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17
Q

This condition is second- ary to Addison disease and AIDS-related hypoadrenalism.

A

Aldosterone Deficit

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18
Q

Without aldo- sterone, the Na+–K+ and Na+–H+ exchange in the distal convoluted tubules and collecting ducts does not occur.

A

Aldosterone Deficit

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19
Q

Therefore, serum sodium concentra- tion is reduced, while serum potassium concentration increases, and there is a mild metabolic acidosis.

A

Aldosterone Deficit

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20
Q

Urinary sodium increases but not to the high levels seen in SIADH, and the osmolality of urine is also not so elevated as in SIADH.

A

Aldosterone Deficit

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21
Q

This rare condition resem- bles diuretic use except that the hyponatremia is not corrected with fluid restriction.

A

Bartter Syndrome

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22
Q

This syndrome is actually a complex of diseases, each of which is caused by mutations of genes that encode ion transporter proteins in the thick portion of the ascending loop of Henle.

A

Bartter Syndrome

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23
Q

caused by absence or mutations of the Na-K-2Cl symporter protein (SLC12A2 or NKCC2 gene) or the ROMK/KCNJ1- encoded potassium channel protein.

A

Bartter Syndrome

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24
Q

the CLCNKB gene–encoded chloride channel protein is defective.

A

classic Bartter syndrome

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25
Q

associated with hearing loss (sensorimotor loss–associated), the BSND gene–encoded accessory chlo- ride channel protein is dysfunctional.

A

Bartter syndrome

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26
Q

the CASR (calcium-sensing receptor) gene–encoded calcium transporter protein is defective, leading to superimposed hypocalcemia.

A

Bartter Syndrome

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27
Q

In Gitelman syndrome, which parallels this syndrome but is a milder form of disease, mutations in the NCC gene–encoded sodium-chloride symporter protein, also termed the thiazide-sensitive Na+-Cl− cotransporter protein (Ped- ersen et al., 2010), cause malfunction of reabsorption of sodium and chloride ions from the tubular fluid into the cells of the distal convoluted tubule.

A

Bartter Syndrome

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28
Q

In all forms of this disease, as in diuretic use, there is a high 24-hour sodium and potassium excretion.

A

Bartter Syndrome

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29
Q

In patients with diabetes mellitus, if they are in a hyperosmolar state—that is, in which the serum glucose is markedly elevated (say, around 700 mg/dL)—the hyperosmolarity of serum causes efflux of cellular water, with a conse- quent osmotic dilution of serum sodium.

A

Diabetic Hyperosmolar State

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30
Q

Roughly, for each 100 mg/dL increase in serum glucose, there is a 1.6 mEq/L decrease in the serum Na+ concentration.

A

Diabetic Hyperosmolar State

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31
Q

Because transport of glucose into cells is accompanied by concurrent transport of potassium into cells, low insulin levels also cause high serum potassium.

A

Diabetic Hyperosmolar State

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32
Q

Thus, the net effect of diabetic hyperosmolar states is a low serum sodium and a high serum potassium.

A

Diabetic Hyperosmolar State

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33
Q

This resembles hypoal- dosteronism, but the presence of abnormally high glucose levels signals the possibility of diabetes mellitus as the cause.

A

Diabetic Hyperosmolar State

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34
Q

This condition is usually caused by the presence of excess lipids in serum.

A

Pseudohyponatremia

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35
Q

No sodium ions are dissolved in lipids, which can take up a considerable volume of serum.

A

Pseudohyponatremia

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36
Q

If the absolute amount of sodium in a given volume of serum is determined, as is performed when using such methods of sodium determination as flame photometry, this value is divided by the sample vol- ume to get the concentration.

A

Pseudohyponatremia

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37
Q

However, part of this volume is lipid that has no sodium; thus, a falsely low value of sodium can be obtained.

A

Pseudohyponatremia

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38
Q

This artifact is eliminated by the use of ion-selective electrodes that directly determine the concentration of sodium and do not depend on knowledge of the vol- ume of serum.

A

Pseudohyponatremia

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39
Q

Note that although most modern, high-throughput chem- istry analyzers measure serum sodium using ion-selective electrodes, they perform a predilution (dilution prior to analysis) of the specimen (so-called indirect potentiometry); thus, the measurement is relative to volume and is susceptible to

A

Pseudohyponatremia

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40
Q

This can be caused by excess renal loss with high positive free water clearance (i.e., loss of water in excess of NaCl), excess sweating, and low water intake.

A

Dehydration

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41
Q

The serum sodium is ele- vated, as is the hematocrit (possibly masking a true anemia), and the urine sodium is also high due to increased renal excretion of NaCl.

A

Dehydration

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42
Q

may be central (neurogenic; i.e., due to decreased vasopressin secretion) or nephrogenic (i.e., due to decreased renal response).

A

Diabetes Insipidus

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43
Q

Functionally, this condition is the reverse of SIADH—that is, water retention in the tubules is not adequate.

A

Diabetes Insipidus

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44
Q

Although this condition is not completely understood and may be multi- factorial, current research suggests that either mutation and/or changes in protein expression of “water channel molecules” (renal aquaporins) and/ or the vasopressin V2 renal collecting tubule cell receptor may play a role in both pathologic water loss, such as in nephrogenic DI, and pathologic water retention, such as in SIADH

A

Diabetes Insipidus

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45
Q

The pat- tern is elevated serum sodium but dilute urinary sodium due to the func- tionally inadequate levels of ADH.

A

Diabetes Insipidus

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46
Q

This condition may result from adrenal hyperplasia, Cushing syndrome, Cushing disease (see endocrine section to come) and Conn syndrome, in which there is hyper- secretion of aldosterone from the zona glomerulosa.

A

Hyperaldosteronism

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47
Q

The levels of circulat- ing aldosterone are inappropriately high, causing excessive reabsorption of Na+ and excretion of K+ and H+ ions.

A

Hyperaldosteronism

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48
Q

The patient will be hypernatremic and hypokalemic and exhibit a mild metabolic alkalosis.

A

Hyperaldosteronism

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49
Q

Many of the causes overlap with those of hyponatremia, including overhydration; use of loop diuretics; SIADH; and Bartter syn- drome, as discussed earlier.

A

hypokalemia

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50
Q

Infusion of insulin to diabetics.

A

hypokalemia

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51
Q

This results in rather large influxes of potassium into cells, lowering its concentration in serum.

A

hypokalemia

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52
Q

Alkalosis.

A

hypokalemia

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53
Q

Red blood cells are themselves excellent buffers.

A

hypokalemia

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54
Q

They are capable of exchanging potassium for hydrogen ions.

A

hypokalemia

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55
Q

Thus, in acidosis, H+ ions enter red cells in exchange for K+ ions.

A

hypokalemia

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56
Q

Conversely, in alkalosis, H+ ions leave red cells (to neutralize excess base), while K+ ions enter the red cells.

A

hypokalemia

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57
Q

Vomiting.

A

Hypokalemia

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58
Q

The major loss is both H+ and K+ from the stomach.

A

Hypokalemia

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59
Q

Loss of K+ in gastric fluid may be less important than the overall fluid loss, which causes activation of aldosterone and renal wasting of K+.

A

Hypokalemia

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60
Q

Among the major causes are those that also cause hypernatremia—for exam- ple, dehydration and DI—acidosis and diabetes mellitus (as discussed earlier), and hemolysis.

A

Hyperkalemia

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61
Q

Hypoadrenalism resulting in low levels of aldosterone

A

Hyperkalemia

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62
Q

Any kind of cell damage, such as rhabdomyolysis, and especially hemolysis of erythrocytes

A

Hyperkalemia

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63
Q

In hemolysis, all of the intracellular K+ is extruded into plasma.

A

Hyperkalemia

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64
Q

Another analyte that is con- centrated in red cells that rises with K+ in hemolysis is LD.

A

Hyperkalemia

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65
Q

Concomitant elevations of potassium and LD in serum should be taken as indications of hemolysis either artifactually after a blood sample has been taken from the patient or, less commonly, hemolysis from an underlying hemolytic condition.

A

Hyperkalemia

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66
Q

must be neutralized by counterions, most of which, in blood, are constituted by chloride and bicarbonate ions, and, to a lesser degree, by phosphate, sulfate, and protein carboxylate groups.

A

sodium ions

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67
Q

Normal serum sodium

A

140 mEq/L

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68
Q

Normal serum chloride

A

100 mEq/L

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69
Q

Normal serum bicarbonate

A

24 mEq/L

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70
Q

defined as Na+ − (Cl− + HCO3−), which, for normal individuals, is around 16

A

Anion Gap

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71
Q

comprises the other counterions that neutralize sodium but are not measured in serum

A

16 mEq/L

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72
Q

the acid will be buffered by bicarbonate (converted to H2CO3)

A

metabolic acidosis (rise in H+ ion concentration is accompanied by a corresponding rise in Cl− ions)

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73
Q

The bicarbonate value will therefore decrease, but there will be a 1 : 1 increase in chloride ion. Thus, there will be no change in the anion gap.

A

metabolic acidosis (rise in H+ ion concentration is accompanied by a corresponding rise in Cl− ions)

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74
Q

bicarbonate is reduced but there is no corresponding increase in Cl−

A

metabolic acidosis (acetoacetic acid/lactic acid/non-chloride-containing acid)

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75
Q

there is an increase in the anion gap that can reach values of 25 to 30 mEq/L

A

metabolic acidosis (acetoacetic acid/lactic acid/non-chloride-containing acid)

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76
Q

diabetic acidosis

A

acetoacetic acid

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77
Q

sepsis or hypoperfusion

A

lactic acid

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78
Q

signify the presence of high levels of basic protein, often a monoclonal paraprotein as occurs in plasma cell dyscrasias

A

Low Anion Gaps (1 to 3 mEq/L)

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79
Q

Basic protein contains ammonium ions, the counterions for which are

A

chloride and bicarbonate.

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80
Q

Now the “invisible” ion is ammonium, while there is a measurable increase in chloride and bicarbonate ions.

A

Low Anion Gaps (1 to 3 mEq/L)

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81
Q

serious sign of possible malignancy—for example, multiple myeloma. 

A

Low Anion Gaps (1 to 3 mEq/L)

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82
Q

The four analytes that aid in the diagnosis of this condition are

A

BUN, creatinine, calcium, and phosphate.

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83
Q

neither is produced in the kidneys, yet both are excellent indicators of renal conditions

A

BUN or creatinine

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84
Q

Urea nitrogen is generally measured in plasma or serum, but it has historically been referred to as

A

BUN

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85
Q

The formula for urea is

A

H2N—CO—NH2.

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86
Q

per mole of urea

A

two moles of nitrogen

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87
Q

This is the end product of NH3 metabolism in the liver

A

BUN

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88
Q

is excreted by the renal tubules at a rate that is roughly proportional to the glomerular filtration rate (GFR).

A

Urea

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89
Q

Note, therefore, that the retained urea—that is, plasma or serum urea or BUN— is approximately inversely proportional to the GFR—that is,

A

BUN∝1/GFR

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90
Q

is secreted but is also reabsorbed to an approximately equal extent over a rather wide range for the GFR so that the net effect is that the amount filtered is the amount excreted.

A

Creatinine

91
Q

The total amount of creatinine filtered then is its urinary concentration, Ucr × the volume of urine, V, over a given time. The total plasma volume that delivered this quantity of creatinine to the glomerulus in a given time period is the GFR and is the total amount of creatinine filtered divided by the plasma concentration, Pcr. This quantity is also the creatinine clearance, Ccr. Thus, the GFR is:

A

GFR=Ccr=Ucr×V/Pcr

92
Q

BUN reference range =

A

10–20 mg/mL

93
Q

BUN is abnormally high

A

Prerenal

Renal and Postrenal

94
Q

renal plasma flow is reduced from such lesions

A

Pre renal

95
Q

renal artery stenosis

A

Pre renal

96
Q

renal vein thrombosis

A

Pre renal

97
Q

↓ GFR = ↑ BUN

A

Pre renal

Renal and Postrenal

98
Q

Normal or mildly elevated CREATININE

A

Pre renal

99
Q

CREATININE reference range

A

0.5 to 1.0 mg/dL

100
Q

↓GFR = ↓ Urine Volume/Flow

A

Prerenal

101
Q

NORMAL Pcr and Ucr

A

Prerenal

102
Q

disproportionate rise in BUN over creatinine

A

Prerenal

103
Q

normal BUN/creatinine ratio

A

10:1 to 20 : 1

104
Q

BUN/creatinine ratio above 20 : 1

A

Prerenal

105
Q

creatinine filtration will be compromised so that its serum level will rise correspondingly

A

Renal

106
Q

both BUN and creatinine rise together, maintaining the BUN/creatinine at 10:1 to 20 : 1

A

Renal

107
Q

obstructive uropathy

A

Postrenal

108
Q

renal or ureteral stones (nephro- or urolithiasis)

A

Postrenal

109
Q

prostatic enlargement from benign prostatic hypertrophy or prostatic carcinoma

A

Postrenal

110
Q

urinary tract infection

A

Postrenal

111
Q

bladder stasis

A

Postrenal

112
Q

urothelial carcinomas

A

Postrenal

113
Q

BUN: 60 mg/dL
Creatinine: 3.5 mg/dL

A

True renal failure

114
Q

iltration compartment

A

glomerulus

115
Q

concentration compartment

A

renal tubules

116
Q

to conserve fluids or to concentrate the urine

A

kidneys

117
Q

fluid- restricted diet: higher than the osmolality of plasma (Posm)

A

osmolality of urine (Uosm)

118
Q

Uosm/Posm normal

A

higher than 1.2

119
Q

If a 24- hour urine specimen collection from this patient on a fluid- restricted diet is measured for [?], we can determine where the lesion has occurred.

A

Uosm

120
Q

urine is not being concentrated

A

Uosm/Posm: <1.2

121
Q

tubular lesion

A

Uosm/Posm: <1.2

122
Q

glomerular lesion

A

Uosm/Posm: >1.2

123
Q

Confirmation can be performed by urinalysis

A

glomerular lesions

124
Q

The presence of [?] in urine suggests compromise of the filtration function of the glomerulus.

A

albumin and/or globulins

125
Q

glomerulonephritis
glomerular lesions pyelonephritis
glomerular lesions lupus nephritis
glomerular lesions crescentic disease such as Goodpasture syndrome
glomerular lesions immune complex disease
glomerular lesions pauci- immune crescentic disease
glomerular lesions/tubular lesions diabetes
glomerular lesions/tubular lesions infarction

tubular lesions pyelonephritis
tubular lesions papillary necrosis
tubular lesions acute tubular necrosis (ATN)
tubular lesions shock
tubular lesions ischemia

A

glomerular lesions

126
Q

It is remarkable that from a blood specimen of only [?] and several urine aliquots, not only can we determine the presence of renal failure, but we can localize the lesion, and all of this virtually noninvasively. 

A

100 μL

127
Q

filtration mechanisms become nonfunctional such that proteins are filtered and consequently are present in urine; urinalysis should reveal elevated protein concentrations.

A

glomerular disease

128
Q

Assay of urine for albumin should likewise be performed.

A

glomerular disease

129
Q

Albumin = Total Protein = only albumin was filtered in the glomerulus

This condition is termed and has sometimes been termed

A

nephrosis or the nephrotic pattern /lipoid nephrosis

130
Q

β- lipoprotein is often concurrently elevated in serum

A

lipoid nephrosis

131
Q

This condition is also termed minimal change disease because there is little morphologic change in the glomerulus histopathologically.

A

lipoid nephrosis

132
Q

If the albumin level is elevated but is significantly less than that for total protein in urine, then many proteins, besides albumin, pass through the glomerulus, which, in contrast to the glomerulus in [?], is morphologically damaged.

A

minimal change disease

133
Q

The presence of multiple proteins in urine is called the

A

nephritic pattern

134
Q

can also be diagnosed by observing the patterns of urine protein electrophoresis

A

nephritic pattern

135
Q

only albumin is present; if multiple protein bands, that is, albumin and α, and/or β, and/or γ are present

A

nephrotic pattern; nephritic pattern

136
Q

can now be diagnosed by ELISA on sera

A

glomerular disease

137
Q

Glomerular diseases often have immunological causes that are of two types:

A

immune complex disease

autoimmune disease

138
Q

immune complexes are present as subendothelial or subepithelial deposits in the glomerulus

A

immune complex disease

139
Q

specific antibodies to components of the glomerulus, such as the glomerular basement membrane, are present

A

autoimmune disease

140
Q

can be identified in immunohistochemical studies on renal biopsies

A

Immune complex
Autoimmune

141
Q

the same antibodies in the [?] and in [?] are frequently present in the circulation where they can be identified in ELISA in serum.

A

immune complexes

glomerular tissue

142
Q

In fact, due to improved ELISA techniques, there is currently a major trend for relying on these assays on patients’ sera to determine the cause of glomerulopathies. This approach has the advantage that it allows avoidance of performing renal biopsies, which are invasive procedures. In addition, there are studies suggesting that assays for specific proteins in urine samples of patients with glomerular and tubular diseases may result in direct diagnosis of these diseases and can be used to monitor progress in disease treatment such as for diabetes mellitus. Here, we focus on serologic markers for specific proteins that have been validated as markers for specific glomerular diseases. While there are numerous conditions for which these assays are now available, we list the most prominent among them.

A
143
Q

common cause: deposition of polymeric IgA1 in the mesangium of the glomerulus

A

primary glomerulonephritis

144
Q

The cause of this condition appears to be antibodies to this immunoglobulin.

A

primary glomerulonephritis

145
Q

An important component of this condition is a defect in the posttranslational modification of IgA1 in that there is the absence of O- glycosylation by galactose of the hinge region of this antibody, resulting in galactose- deficient IgA1 (Gd- IgA1).
opathies have high serum titers of circulating antibodies to a membrane receptor for phospholipase A2 on podocytes (glomerular visceral epithelial cells), the so- called PLA- 2 antigen.

A

primary glomerulonephritis

146
Q

This results in an unexpected antigenic determinant that provokes an immune response.

A

primary glomerulonephritis

147
Q

However, other antibodies against IgA1 are also required for full expression of this disease.

A

primary glomerulonephritis

148
Q

Expression in serum of both antiglycan antibodies and of Gd- IgA1 in the presence of proteinuria appear to identify glomerulonephritis at an early stage.

A

primary glomerulonephritis

149
Q

high serum titers of circulating antibodies to a membrane receptor for phospholipase A2 on podocytes (glomerular visceral epithelial cells), the so- called PLA- 2 antigen.

A

membranoproliferative glomerulonephritis

150
Q

a major finding is subendothelial deposition of immune complexes, containing high levels of C3 from the primary complement cascade that may result from concurrent infectious or other diseases provoking an immune response.

A

membranoproliferative glomerulonephritis

151
Q

A diagnostic serologic finding is depletion of circulating levels of C3.

A

membranoproliferative glomerulonephritis

152
Q

do not seem to have an immunologic component

A

minimal change disease and focal segmental glomerulosclerosis

153
Q

here are elevated serum levels of a soluble (non- membrane- bound) form of the urokinase receptor, called suPAR, suggesting that both conditions are manifestations of the same underlying disease, although this view is not universally accepted.

A

minimal change disease and focal segmental glomerulosclerosis

154
Q

A current hypothesis is that binding of suPAR to integrin 3 on the membrane surface of podocytes seems to induce changes in overall cell- cell orientation, resulting in abnormal spacing between cells.

A

minimal change disease and focal segmental glomerulosclerosis

155
Q

cytotoxic antibodies to glomerular cells result from [?] that are not confined to the kidneys

A

autoimmune systemic diseases

156
Q

antinuclear antibodies (ANAs) circulate and cause polysystemic disease, including renal nephropathy

A

systemic lupus erythematosus

157
Q

It appears that two prominent antibodies that cause direct glomerular damage are ANAs and antinucleosome antibodies.

A

systemic lupus erythematosus

158
Q

Circulating antibodies against neutrophil cytoplasmic antigen (ANCA)

A

Wegener granulomatosis

159
Q

serodiagnostic: affecting both lung and kidney, with a specificity for myeloperoxidase (ANCA- MPO)

A

Wegener granulomatosis

160
Q

These antibodies have been identified as occurring in so- called pauci- immune complex disease identified in the immunohistochemistry on renal biopsies on patients with this disease.

A

Wegener granulomatosis

161
Q

Anti- glomerular basement membrane (anti-GBM) antibody has been identified as a prominent causative factor

A

Goodpasture syndrome

162
Q

is a systemic disease affecting both kidney and lung

A

Goodpasture syndrome

163
Q

about 20% of patients who have high titers of anti- GBM antibodies also have high titers of ANCA- MPO.

A

Goodpasture syndrome

164
Q

Thus, serodiagnostic markers for renal disease can not only indicate the presence of renal disease but can further identify the location of the disease in the kidneys and further identify the cause of the disease in a virtually noninvasive manner. 

A

Goodpasture syndrome

165
Q

play an important role in the regulation of calcium levels

A

kidneys

166
Q

↓ calcium = ↑ phosphate

A

renal failure

167
Q

calcium is the most abundant cation in the body, most of it stored in bone as a

A

calcium hydroxyphosphate in hydroxyapatite crystal

168
Q

complexes with phosphate in several different forms, depending on the ionization state of phosphate

A

Calcium

169
Q

The most insoluble calcium phosphate forms are those with the most

A

basic phosphates

170
Q

promote calcium deposition in bone

A

alkaline conditions

171
Q

promote leaching of calcium from bone

A

acidic conditions

172
Q

alkalosis promote
acidosis promotes

A

hypocalcemia

hypercalcemia

173
Q

Note also that there is an equilibrium between soluble calcium phosphate and insoluble calcium phosphate in bone. We represent this equilibrium as:

where P represents all ionic phosphate forms and where the left side is all soluble calcium phosphate salts and the right side is the insoluble salt forms.

A

Ca+P↔(CaP)

174
Q

The equilibrium constant, Ksp, for this equilibrium is:

A

Ksp=(Ca)×(P)/(CaP)insoluble

175
Q

Because (CaP) insoluble is constant in concentration, the product of soluble Ca × soluble P is a constant, called the (?). Thus, there is an (?) relationship between Ca and P.

A

solubility constant or Ksp

inverse

176
Q

are almost always accompanied by hyperphosphatemic states and vice versa.

A

Hypocalcemic states

177
Q

Of the soluble calcium, in the numerator of Equation 9.7, there are two forms

A

calcium bound to albumin and globulin, and small molecules in chelate form, and so- called ionized or nonchelated calcium.

178
Q

is in the ionized form

A

active calcium

179
Q

are considered to be the best measure of hypocalcemia, normocalcemia, or hypercalcemia.

A

serum levels of ionized calcium

180
Q

stimulates the renal tubules to excrete phosphate.

level must then rise

A

parathyroid hormone (PTH)

serum calcium

181
Q

kidneys are vital to the formation of active vitamin D in the synthesis of (?), which is necessary for the absorption of calcium in the gut.

A

1,25- dihydroxycholecalciferol

182
Q

tubular failure = phosphate excretion is inhibited due to the nonresponsiveness of the tubules to PTH.

A

renal disease

183
Q

phosphate levels rise, while calcium levels fall

A

renal disease

184
Q

is reduced, lowering absorbed calcium

A

active vitamin D production

185
Q

in the face of elevated BUN and creatinine, indicative of renal disease, strongly suggest tubular failure.

A

Hypocalcemia and hyperphosphatemia

186
Q

alkalosis and renal failure

A

hypocalcemia

187
Q

hypoparathyroidism, also leading to hyperphosphatemia.

A

hypocalcemia

188
Q

medullary thyroid carcinomas

A

hypocalcemia

189
Q

amine precursor uptake and decarboxylase (APUD) activity cell tumors

A

hypocalcemia

190
Q

medullary thyroid carcinomas and other amine precursor uptake and decarboxylase (APUD) activity cell tumors

A

Hypocalcemia.

191
Q

the elaboration of calcitonin, a well- known calcium- lowering hormone

A

Hypocalcemia.

192
Q

vitamin D levels may be low, resulting in diminished reabsorption of calcium for the gut

A

Hypocalcemia.

193
Q

These causes may be encapsulated in the acronym CHARD (Calcitonin, Hypoparathyroidism, Alkalosis, Renal failure, and vitamin D deficit)

A

Hypocalcemia.

194
Q

Besides acidosis, the possible causes of this condition may be summarized by Bakerman’s CHIMPS mnemonic (Bakerman & Strausbauch, 1994)

A

Hypercalcemia.

195
Q

Cancer

A

Hypercalcemia.

196
Q

Hypercalcemia. Multiple myeloma
Hypercalcemia. Hyperparathyroidism
Hypercalcemia. Sarcoidosis. 

A

Hypercalcemia.

197
Q

Hyperthyroidism

A

Hypercalcemia.

198
Q

Iatrogenic causes

A

Hypercalcemia.

199
Q

Multiple myeloma

A

Hypercalcemia.

200
Q

Hyperparathyroidism

A

Hypercalcemia.

201
Q

Sarcoidosis. 

A

Hypercalcemia.

202
Q

Calcitonin

A

Hypocalcemia

203
Q

Hypoparathyroidism

A

Hypocalcemia

204
Q

Alkalosis

A

Hypocalcemia

205
Q

Alkalosis

A

Hypocalcemia

206
Q

Renal failure

A

Hypocalcemia

207
Q

vitamin D deficit

A

Hypocalcemia

208
Q

Normal albumin

A

4 g/dL

209
Q

diabetic ketoacidosis

A

metabolic acidosis

210
Q

lactic acidosis (e.g., from gram- negative sepsis)

A

metabolic acidosis

211
Q

renal failure

A

metabolic acidosis

212
Q

diarrhea

A

metabolic acidosis

213
Q

most common cause: vomiting, with a loss of HCl from the stomach and an attendant rise in bicarbonate

A

metabolic alkalosis

214
Q

myasthenia gravis, in which there is partial paralysis of the accessory muscles of breathing

A

Respiratory Acidosis

215
Q

pneumonia

A

Respiratory Acidosis

216
Q

CNS diseases affecting the brainstem in areas involved in respiratory control

A

Respiratory Acidosis

217
Q

is due mainly to hyperventilation, often of psychogenic origin

A

Respiratory alkalosis

218
Q

pain from trauma or underlying disease, especially inflammation

A

Respiratory alkalosis

219
Q

Here, the PCO2 is reduced because of the rapidity of breathing.

A

Respiratory alkalosis

220
Q

This condition is seen mainly in the pediatric population when a child swallows multiple aspirin tablets.

A

“Overcompensation” of metabolic acidosis in salicylic acid overdose.

221
Q

Since aspirin is salicylic acid, the first manifestation of this condition is metabolic acidosis with a partially compensated reduced PCO2 and an increased anion gap.

A

“Overcompensation” of metabolic acidosis in salicylic acid overdose.

222
Q

However, salicylate anion induces increased respiratory rates, causing lowering of the PCO2 to levels significantly lower than those in the normal compensatory process, resulting in a respiratory alkalosis that masks the fundamental metabolic acidosis.

A

“Overcompensation” of metabolic acidosis in salicylic acid overdose.

223
Q

results from the independent action of salicylate anion on respiratory centers in the CNS.

A

“Overcompensation” of metabolic acidosis in salicylic acid overdose.

224
Q

“Overcompensation” of metabolic acidosis in salicylic acid overdose.

A

Clinical Chemistry Review (15 decks)

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