TRIPASS XR تري باس

 molality can be measured by the freezing point depression

method, or estimated by the following equation, which takes

into account the osmotic effect of sodium, glucose, and uosm = 2(Na)(mmol/L) + Glucose (mg/dL)

18

+ BUN (mg/dL)

2.8

(Eq. 10-1)

This equation predicts the measured plasma osmolality within

5 to 10 mOsm/kg. Although urea contributes to the measured

osmolality, it is an ineffective osmole because it readily traverses

cell membranes and, therefore, does not cause significant fluid

shift within the body. Hence, the effective plasma osmolality

(synonymous with tonicity, the portion of total osmolality that

has the potential to induce transmembrane water movement)

can be estimated by the following equation:

Posm = 2(Na)(mmol/L) + Glucose (mg/dL)

18 (Eq. 10-2)

An osmolal gap exists when the measured and calculated values differ by greater than 10 mOsm/kg4; it signifies the presence

of unidentified particles. When the individual solute has been

identified, its contribution to the measured osmolality can be

estimated by dividing its concentration (mg/dL) by one-tenth of

its molecular weight. Calculating the osmolal gap is used to detect

the presence of substances, such as ethanol, methanol, and ethylene glycol, that have high osmolality. Occasionally, the osmolal

gap can also result from an artificial decrease in the serum sodium

secondary to severe hyperlipidemia or hyperproteinemia.

CASE 10-1

QUESTION 1: J.F., a 31-year-old man, is admitted to the

inpatient medicine service for methanol intoxication. Routine laboratory analysis reveals the following:

Sodium (Na), 145 mEq/L

Potassium (K), 3.4 mEq/L

Blood urea nitrogen (BUN), 10 mg/dL

Creatinine, 1.1 mg/dL

Glucose, 90 mg/dL

The blood methanol concentration was 108 mg/dL, and

the measured plasma osmolality was 333 mOsm/kg. What is

J.F.’s calculated osmolality? Are other unidentified osmoles

present?

Using Equation 10-1, J.F.’s total calculated osmolality is

Posm = 2(145 mEq/L) + 90 mg/dL

18

+ 10 mg/dL

2.8

= 290 + 5 + 3.6

= 299 mOsm/kg (Eq. 10-3)

Osmolal gap = 333 mOsm/kg − 299 mOsm/kg

= 34 mOsm/kg (Eq. 10-4)

In J.F., the entire osmolal gap can be accounted for by the

presence of the methanol (because 108 mg/dL of methanol

will provide 108/3.2 = 33.7 mOsm/kg). It is unlikely, therefore,

that other unmeasured osmoles are present (e.g., ethylene glycol, isopropanol, and ethanol). The laboratory determination

of osmolality measures the total number of osmotically active

particles but not their permeability across the cell membrane.

Methanol increases plasma osmolality but not tonicity because

the cell membrane is permeable to methanol. Therefore, no net

water shift occurs between the intracellular and extracellular

compartments. Conversely, mannitol, which is confined to the

extracellular space, contributes to both plasma osmolality and

tonicity.

Tubular Function of Nephron

The kidney plays an important role in maintaining a constant

extracellular environment by regulating the excretion of water

191Fluid and Electrolyte Disorders Chapter 10

and various electrolytes. The volume and composition of fluid

filtered across the glomerulus are modified as the fluid passes

through the tubules of the nephron.

The renal tubule is composed of a series of segments with heterogeneous structures and functions: the proximal tubule, the

medullary and cortical thick ascending limb of Henle’s loop, the

distal convoluted tubule, and the cortical and medullary collecting duct2 (Fig. 10-1). The mechanism for sodium reabsorption is

different for each nephron segment, but is generally mediated by

carrier proteins or channels located on the luminal membrane of

the tubule cell.2 Na+/K+ ATPase (sodium-potassium adenosine

triphosphatase) actively pumps sodium out of the renal tubule

cell in exchange for potassium in a 3:2 ratio. Hence, the intracellular sodium concentration is kept at a low level. The potassium

that is pumped into the cell leaks back out through potassium

channels in the membrane, rendering the cell interior electronegative. The low intracellular sodium concentration and a negative

intracellular potential produce a favorable gradient for passive

sodium entry into the cell.3 Na+/K+ ATPase also indirectly provides the energy for active sodium transport and the reabsorption

and secretion of other solutes across the luminal membrane of

the renal tubule. The distal segments are mainly involved in the

reabsorption of sodium and chloride ions and the secretion of

hydrogen and potassium ions.2

Iso-osmotic reabsorption of the glomerular filtrate occurs in

the proximal tubule such that two-thirds of the filtered sodium

and water and 90% of the filtered bicarbonate are reabsorbed.

The Na+/H+ antiporter (exchanger) in the luminal membrane

is instrumental in the reabsorption of sodium chloride, sodium

bicarbonate, and water. The reabsorption of most nonelectrolyte

solutes, such as glucose, amino acids, and phosphates, are coupled to sodium transport.2,5

Both the thick ascending limb of Henle’s loop and the distal

convoluted tubule serve as the diluting segments of the nephron

because they are impermeable to water. Sodium chloride is

extracted from the filtrate without water. Sodium transport in

both of these segments is flow-dependent and varies with the

amount of sodium ions delivered from the proximal segments

of the nephron. Decreased sodium ions in the tubular fluid will

limit sodium transport in the thick ascending limb of Henle’s

loop and the distal convoluted tubule.2,6

Reabsorption of sodium in the thick ascending limb of Henle’s

loop accounts for approximately 25% of the total sodium reabsorption. Sodium, chloride, and potassium are reabsorbed by

H2O

H2O

H2O

Descending Limb

Cortex

Medulla

Urea

Pars Recta

Organic Acids

Glucose

NaHCO3

Proximal

Convoluted

Tubule

Amino Acids

+ +

+

+

+

+

+

+

+

+

+

+

+

+

–

–

–

– – –

–

–

–

– –

–

ADH H2O

Sensitive

Urea

ADH

Sensitive

NaCl

Henle's Loop

Urea

Medullary Thick

Ascending Limb

2Cl–

Na+

K+

2Cl–

Na+

K+

Cortical Thick

Ascending Limb

ADH

Sensitive

ADH

Sensitive

H2O

H+

Na+

Aldosterone

Sensitive

Na+

K+

H+ Distal

Convoluted

Tubule

FIGURE 10-1 Sites of tubule salt and water absorption. Sodium is reabsorbed with inorganic anions, amino acids,

and glucose in the proximal tubule against an electrical gradient that is lumen-negative. In the distal part of the

proximal tubule (pars recta), sodium and water are reabsorbed to a lesser extent and organic acids (hippurate, urate)

and urea are secreted into the urine. The electrical potential is lumen-positive in the pars recta. Water, but not salt, is

removed from tubule fluid in the thin descending limb of Henle’s loop, but in the ascending portion salt is reabsorbed

without water, rendering the tubule fluid hyposmotic with respect to the interstitium. Sodium, chloride, and potassium

are reabsorbed by the medullary and cortical portions of the ascending limb; the lumen potential is positive. Sodium

is reabsorbed and potassium and hydrogen ions are secreted in the distal tubule and collecting ducts. Water

absorption in these segments is regulated by antidiuretic hormone (ADH). The electrical potential is lumen-negative in

the cortical sections and positive in the medullary segments. Urea is concentrated in the interstitium of the medulla

and assists in the generation of maximally concentrated urine. (Reprinted with permission from Chonko AM et al.

Treatment of edema states. In: Narins RG, ed. Maxwell & Kleeman’s Clinical Disorders of Fluid and Electrolyte

Metabolism. 5th ed. New York, NY: McGraw-Hill; 1994:545.)

192 Section 1 General Care

the medullary and cortical portions of the ascending limb, but

the leakage of reabsorbed potassium ions back into the tubular lumen, via potassium channels, makes the tubular lumen

electropositive. This electrical gradient promotes the passive

reabsorption of cations, such as sodium, calcium, and magnesium, in the distal convoluted tubules. Because the thick ascending limb of Henle’s loop is impermeable to water, it contributes

to the interstitial osmolality in the medulla. This high osmolality is key to the reabsorption of water by the medullary portion

of the collecting duct under the influence of antidiuretic hormone (ADH, vasopressin). Therefore, the thick ascending limb

of Henle’s loop is important for both urinary concentration and

dilution.6

Because, as noted previously, the distal convoluted tubule also

is impermeable to water, the osmolality of the filtrate continues

to decline as sodium is being reabsorbed. In the distal convoluted

tubule and collecting duct, sodium is reabsorbed in exchange

for hydrogen ions and potassium. When sodium ions are reabsorbed, the tubule lumen becomes electronegative, which promotes potassium secretion in the lumen via potassium channels.

Aldosterone enhances sodium reabsorption in the collecting duct

by increasing the number of opened sodium channels.2,7

The collecting duct is usually impermeable to water. Under

the influence of ADH, however, water permeability is increased

through an increase in the number of water channels along the

luminal membrane. The amount of water reabsorbed depends on

the tonicity of the medullary interstitium, which is determined

by the sodium reabsorbed in the thick ascending limb of Henle’s

loop and urea.2,7,8

Osmoregulation

An increase in the effective plasma osmolality often reduces intracellular volume; conversely, decreased effective plasma osmolality is associated with cellular hydration. Water homeostasis is

important in the regulation of plasma osmolality, and plasma

tonicity is maintained within normal limits through a delicate

balance between the rates of water intake and excretion.

The amount of daily water intake includes the volume of

water ingested (sensible intake), the water content of ingested

food, and the metabolic production of water (insensible intake).2

To maintain homeostasis, these should be equal to the amount of

water excreted by the kidney and the gastrointestinal (GI) tract

(sensible loss) plus water lost from the skin and respiratory tract

(insensible loss).2,3

Changes in plasma tonicity are detected by osmoreceptors

in the hypothalamus, which also houses the thirst center and is

the site for ADH synthesis.9,10 When the plasma tonicity falls

below 280 mOsm/kg as a result of water ingestion, ADH release

is inhibited,2 water is no longer reabsorbed in the collecting

duct, and a large volume of dilute urine is excreted. Conversely,

when the osmoreceptors in the hypothalamus sense an increased

plasma osmolality, ADH is released to increase water reabsorption. A small volume of concentrated urine is then excreted. The

threshold for ADH release is 280 mOsm/kg, and maximal ADH

secretion occurs when the plasma osmolality is 295 mOsm/kg.9

Thus, urine osmolality varies from 50 mOsm/kg in the absence of

ADH to 1,200 mOsm/kg during maximal ADH release. The volume of urine produced depends on the solute load to be excreted,

as well as the urine osmolality2,3,9,10:

Urine volume (L) =

 Solute load (mOsm)

Urine osmolality (mOsm/kg)

×

 1

Density of water (kg/L)

(Eq. 10-5)

Therefore, for a typical daily solute load of 600 mOsm:

=

 600 mOsm

50 mOsm/kg  1

1 kg/L

= 12 L (No ADH) (Eq. 10-6)

=

 600 mOsm

1,200 mOsm/kg 1

1 kg/L

= 0.5 L (Max ADH) (Eq. 10-7)

Although the kidney has a remarkable ability to excrete free

water, it is not as efficient in conserving water. ADH minimizes

further water loss, but it cannot correct water deficits. Therefore, optimal osmoregulation requires increased water intake

stimulated by thirst. Both ADH and thirst can be stimulated by

nonosmotic stimuli. For example, volume depletion is such a

strong nonosmotic stimulus for ADH release that it can override

the response to changes in plasma osmolality. Nausea, pain, and

hypoxia are also potent stimuli for ADH secretion.11

Volume Regulation

Sodium resides almost exclusively in the extracellular fluid; the

amount of total body sodium, therefore, determines the extracellular volume.2,11 Because daily sodium intake varies from

100 to 250 mEq, the body must rely on adjustments in urinary

sodium excretion to maintain the extracellular volume and tissue perfusion.2,11 The ability of the kidney to retain sodium is so

remarkable that a person can survive with a daily sodium intake

as low as 20 to 30 mEq.

The afferent sensors for the changes in the effective circulating

volume are the intrathoracic volume receptors, the baroreceptors in the carotid sinus and aortic arch, and the afferent arteriole

in the glomerulus.11

When the effective circulating volume is decreased, both

the renin-angiotensin-aldosterone and the sympathetic nervous

systems are activated.2,11 Angiotensin type 2 (AT2) and norepinephrine enhance sodium reabsorption at the proximal convoluted tubule. In addition, aldosterone stimulates sodium reabsorption at the collecting tubule. The decrease in effective arterial

volume also stimulates ADH release, which enhances water reabsorption at the collecting duct. Conversely, after a salt load, the

increases in atrial pressure and renal perfusion pressure suppress

the production of renin and, subsequently, AT2 and aldosterone.

The release of atrial natriuretic peptide secondary to increased

atrial filling pressure and intrarenal production of urodilators

increase urinary excretion of the excess sodium.12,13

Although the kidney can excrete a 20-mL/kg water load in 4

hours, only 50% of the excess sodium is excreted in the first day.3

Sodium excretion continues to increase until a new steady state

is reached after 3 to 4 days, when intake equals output.3,12 It is

important to recognize that osmoregulation and volume regulation occur independently of each other.2,3 The two homeostatic

systems regulate different parameters and possess different sensors and effectors. Both systems can be activated simultaneously,

however.

DISORDERS IN VOLUME REGULATION

Sodium Depletion

CASE 10-2

QUESTION 1: A.B., a 17-year-old girl, presented to the

emergency department (ED) with complaints of anorexia,

nausea, vomiting, and generalized weakness for the past

6 Section 2 Cardiac and Vascular Disorders

TABLE 13-5

Randomized End Point Trials With Triglyceride-Lowering Therapies

Trial Intervention Lipids: Initial (on Rx) Lipid Changes (%) Placebo CHD Rate (%) CHD Event Reduction (%)

HHS118 Gemfibrozil LDL-C: 189 (170 ↓10

TG: 178 (116) ↓35 4 ↓34

HDL-C: 47 (52) ↑11

VA-HIT119 Gemfibrozil LDL-C: 111 (113) 0

TG: 161 (115) ↓31 22 ↓22

HDL-C: 32 (34) ↑6

BIP120 Bezafibrate LDL-C: 148 (138) ↓7

TG: 145 (115) ↓21 15 ↓9.4

HDL-C: 35 (41) ↑18

FIELD121 Fenofibrate LDL-C: 119 (94) ↓6

TG: 154 (130) ↓22 6 ↓11

HDL-C: 42 (44) ↑1

ACCORD122 Fenofibrate +

Simvastatin

LDL-C: 100 (30)

TG: 164a

HDL-C: 38 (8)

↓19

↓22

↑8

2.4 ↓8

CDP123 Niacin TC: 250 (235) ↓10 30 ↓13

TG: 480 (354) ↓26

a Median.

CHD, coronary heart disease; HDL, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; Rx, drug therapy; TG, triglyceride.

patients who generally had baseline TG levels of 150 to 500

mg/dL and HDL-C levels less than 40 mg/dL (Table 13-5).118–123

The Helsinki Heart Study studied 4,081 men without CHD and

found a 34% reduction in CHD death and nonfatal MI after 5

years of gemfibrozil therapy compared with placebo.118 Post hoc

analysis of this study showed that the group of patients with TG

levels greater than 200 mg/dL and an LDL to HDL ratio greater

than 5.0 (generally with LDL-C >194 mg/dL and HDL-C <40

mg/dL) accounted for 71% of the CHD reduction achieved in

the entire study, although this group represented only 10% of

the total study population124 (Table 13-5). The VA-HIT (HDL

Intervention Trial) studied 2,531 men with a history of CHD and

low HDL-C levels (mean HDL-C level, 32 mg/dL) and reported

a 22% reduction in CHD events with gemfibrozil therapy. The

authors reported that approximately 25% of this risk reduction

resulted from the 6% increase in HDL-C.125 The Bezafibrate

Infarction Prevention (BIP) trial studied CHD patients with a

lipid profile similar to the patients in the AFCAPS/TexCAPS

trial (high LDL-C, low HDL-C, normal TGs) and reported an

insignificant 9% reduction in CHD events associated with an

18% increase in HDL-C and a 21% reduction in TGs.120 A post

hoc analysis of this trial found that patients who had TG levels

of greater than 175 and 200 mg/dL had significant CHD event

reductions of 22% and 40%, respectively. The FIELD study investigated the effects of fenofibrate versus placebo with an average follow-up of 5 years on CHD events in patients with type 2

diabetes with a mean baseline LDL-C, HDL-C, and triglyceride

level of 119 mg/dL, 42 mg/dL, and 153 mg/dL, respectively.121

Similar to the BIP trial, this trial failed to demonstrate a significant reduction in major coronary events (11% reduction in risk;

p = 0.16) in patients randomly assigned to receive fenofibrate.

Because this trial allowed changes in therapy at the discretion of

the patient’s primary-care physician, significantly more patients

receiving placebo (17%) compared with fenofibrate (8%) were

taking nonstudy lipid-lowering agents. This may have partially

accounted for the study results.

The current outcome evidence for fenofibrate and gemfibrozil

(bezafibrate is not available in the United States) reasonably supports their use as second-line agents as an alternative to statin

therapy when a statin is contraindicated or not tolerated in type

2 diabetes and secondary prevention with low HDL-C, respectively. In addition, post hoc analyses suggest that patients with

atherogenic dyslipidemia obtain CHD risk reduction with fibrate

therapy. Unlike statins, however, which have been associated

with a reduction in total mortality,87,88,90,105 fibrates appear not

to reduce all-cause mortality.126 The risk reduction in coronary

events may be in line with that achieved with statins, although

no head-to-head trials exist to refute or affirm this. This presents

a dilemma for the clinician: When presented with a patient who

has atherogenic dyslipidemia, which is the drug of choice, a statin

or fibrate? Some guidance to this question will be provided during the case discussions that follow. Moreover, the question of the

incremental CHD risk reduction benefits of adding a fibrate to

background statin therapy in patients with mixed hyperlipidemia

will be covered later.

Only one placebo-controlled end point study is available for

niacin (Table 13-5). The study was completed in men who had

a prior MI and mixed hyperlipidemia. After 5 years of niacin

therapy, the CHD event rate was reduced by 13%.123 Fifteen

years after the start of the study, and 9 years after the study was

terminated, the investigators reported that total mortality was

11% lower in the men in the niacin arm, suggesting that any

period of lipid-modifying treatment may translate into a longterm benefit.123 Combination therapy with niacin plus a statin has

been studied in patients with CHD with low HDL-C and normal

LDL-C.127 Compared with a mean 3.9% progression in coronary

stenosis with placebo, niacin–simvastatin therapy was associated

with a mean regression of 0.4% (p <0.001). The authors posited

that event reduction with this combination should be equivalent

to the sum of the LDL-C reduction and the HDL-C increase. In

the study, LDL-C was reduced by 42% and HDL-C was increased

by 26%, and the composite end point of death from coronary

causes, MI, stroke, or revascularization for worsening ischemia

was reduced 60% with the niacin–statin combination (p = 0.02).

In addition, the results of the Arterial Biology for the Investigation

of the Treatment Effects of Reducing Cholesterol (ARBITER-2)

trial showed significant slowing of the progression of atherosclerosis by measuring carotid intima–media thickness in patients

with known CHD treated with statin and niacin compared with

those treated with a statin alone.128

Niacin has long been an intriguing drug to clinicians. It is one

of the few drugs that positively affects each component of the

267Dyslipidemias, Atherosclerosis, and Coronary Heart Disease Chapter 13

lipid profile (LDL-C, TGs, and HDL-C). It is the best therapy

available to raise HDL-C and one of the best at lowering TGs. It

is logical to expect that these effects would translate into substantial CHD risk reduction. It is especially interesting to speculate

on how these effects may combine to offer better risk reduction,

especially when combined with one of the statins. This hypothesis is being evaluated in the ongoing AIM HIGH study and

the HPS2-THRIVE study in combination with an investigational

antiflushing drug Laropiprant.

Mechanisms of Coronary Heart Disease

Risk Reduction

Given the consistent relationship between lowering blood cholesterol and reducing CHD events, the question arises, “what is the

mechanism of this protection?” Scientists are offering many new

and exciting answers to this question. At present, it appears that

the reduction in CHD with lipid-altering therapy is mediated

through, or at least tracked by, a reduction in cholesterol levels

and serum lipoproteins. In addition to lowering blood cholesterol

levels, statins and other lipid-altering therapies produce other,

so-called pleiotropic effects that may partly explain their CHDreducing capability.129

One way in which cholesterol lowering may reduce CHD is

by changing atherosclerotic plaque from high-risk lesions with

a large lipid core, thin fibrous cap, and many cholesterol-filled

macrophage cells along the shoulders of the lesion to lower-risk

lesions with a small lipid core and much connective tissue and

smooth muscle matrix throughout. The lesion does not appear to

change much in size, or at least not in ways that can be visualized

on an arteriogram. The harder lesion created with lipid lowering

is much less likely to rupture or erode, however, thus reducing

the risk of forming an occluding clot and producing CHD events.

Lipid lowering may also affect endothelial function. Evidence

indicates that high LDL-C levels cause endothelial dysfunction,

as evidenced by a lowered ability of coronary arteries to dilate.

Cholesterol lowering by practically any means restores endothelial function. Many studies have demonstrated improvement

in brachial artery reactivity and coronary artery dilation when

cholesterol levels are reduced.130–135 Positron emission tomography scans demonstrate improved blood flow and reduced areas of

ischemia throughout the myocardium in patients receiving lipidaltering therapy.132,133 These effects may have important clinical

benefits. In patients with CAD, cholesterol lowering reduces the

number of ST-segment depressions recorded during a 48-hour

electrocardiogram (ECG) Holter monitor study.136,137 Therapy

with a statin can also reduce ischemic events requiring acute management, a potential effect of restored endothelial function.97

Cholesterol lowering might also combat the inflammation

that accompanies atherogenesis. Early in the development of

plaques, monocyte-derived macrophages are recruited to engulf

modified LDL particles, and in every stage of the disease, specific

subtypes of T lymphocytes are present.40,46 At various stages,

cytokines, chemokines, and growth factors are released. Inflammatory processes may be especially active just before or after

the plaque ruptures. Several investigators have attempted to

identify markers of inflammation that may signal an increased

risk of a CHD event. As discussed previously, one promising

marker is hs-CRP. An elevated hs-CRP level predicts a high risk

of future CHD events and appears to add to the risk predicted by

LDL-C alone.110,138 A subanalysis of the CARE trial reported

that high levels of hs-CRP forecast CHD risk in patients on

placebo, but this was attenuated and not significant in patients

assigned to receive pravastatin, suggesting that statin treatment

has an anti-inflammatory effect.139 The American Heart Association (AHA),140 alone and more recently in conjunction with

the American College of Cardiology Foundation, continues to

recommended that measurement of the hs-CRP level in asymptomatic adults (men ≥50 years and women ≥60 years) with

LDL-C less than 130 mg/dL or in asymptomatic adults (men ≤50

years and women ≤60 years) who are intermediate-risk (generally those with two or more CHD risk factors) as a way to further

characterize the patient’s future CHD risk and detect candidates

for drug therapy.141 As mentioned previously, however, the role

of hs-CRP as a therapeutic target has not been defined.

HYPERCHOLESTEROLEMIA

Evaluation of the Lipoprotein Profile

CASE 13-1

QUESTION 1: T.A., a 43-year-old premenopausal woman,

is screened with a lipid profile during an annual medical

evaluation. She has never taken cholesterol-lowering medication and currently takes only a multivitamin daily. She has

had no symptoms of coronary, carotid, or peripheral vascular disease. She has a 20–pack-year history of smoking and

exercises four times a week, without physical limitations.

T.A. states that she follows a low-fat, low-cholesterol diet.

Her father is alive and well at age 71, with a normal cholesterol level. Her mother had an MI at age 47 and died at

age 57 from a second event. Her grandfather died of an

MI at age 52; a sister has hypercholesterolemia and is taking simvastatin. Pertinent physical findings are weight, 125

pounds; height, 63 inches; blood pressure (BP), 120/82 mm

Hg; pulse, 66 beats/minute and regular; carotid pulses symmetric bilaterally without bruits; no neck masses; no abdominal bruit; and no evidence of tendon xanthomas. Pertinent

laboratory findings, obtained after a 12-hour fast, show the

following results:

Total cholesterol, 290 mg/dL

TG, 55 mg/dL

HDL-C, 55 mg/dL

LDL-C, 224 mg/dL

Non–HDL-C, 235 mg/dL

Plasma glucose, 96 mg/dL

Thyroid-stimulating hormone (TSH), 0.92 international

units/mL

Alanine aminotransferase (ALT), 11 units/L

Aspartate aminotransferase (AST), 8 units/L

Blood urea nitrogen, 12 mg/dL

Creatinine, 1.0 mg/dL

Urinalysis, negative

What is your assessment of T.A.’s lipid panel results?

T.A.’s LDL-C is considered very high (>190 mg/dL); NCEP

defines the optimal LDL-C as less than 100 mg/dL.8 Her HDL-C

is right at the average HDL-C for a woman, and her TG is normal

(<150 mg/dL) (Table 13-6). In most cases, it is wise to repeat the

lipid profile to be sure the first results are not atypical. However,

T.A.’s LDL-C is so high a repeat test is not likely to change the

assessment. Thus, in this case, a second test is optional.