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Evaluation of the medial and lateral collateral ligaments

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Evaluation of the medial and lateral collateral ligaments

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the patient is supine, with the knee flexed about 20° and the hamstring muscles relaxed. The examiner puts one hand over the side of the knee opposite the ligament being tested. With the other hand, the examiner cups the heel and pulls the lower leg outward to test the medial collateral ligament or inward to test the lateral collateral ligament. Moderate instability after acute injury suggests that a meniscus or cruciate ligament is torn as well as the collateral ligament.

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4q25 AF Risk Genotype Test 90948(X) may help predict risk of atrial fibrillation (AF) and cardioembolic (CE) stroke. 4q25 AF Risk carriers may have up to a 1.7x19 increased risk of AF and up to a 1.5x20 increased risk of CE stroke related to AF.* Physicians may benefit from knowledge of their patients’ increased AF risk, and therefore consider additional clinical follow-up for these patients.

Apolipoprotein E (ApoE) Genotype Test 90649(X) may help predict risk of CVD and response to different diets.

9p21 Genotype Test 90648(X) may help predict risk of early onset MI, abdominal aortic aneurysm (AAA), and MI/CHD.† Identification of 9p21 carriers may allow clinicians to take steps to characterize and reduce risk factors that may contribute to the development or progression of disease.

CYP2C19 Genotype Test 90668(X) may help predict response to Plavix® (clopidogrel).‡ Patients carrying one or two copies of nonfunctional alleles may not receive the full benefits of Plavix, and therefore may benefit from alternative dosing strategies or an anti-platelet agent other than Plavix.

Familial Hypercholesterolemia (FH) Panel 94877(X) tests for variants in the genes LDLR, APOB, and PCSK9 to help diagnose FH.

KIF6 Genotype Test 90645(X) may help predict risk of a CHD event and response to Lipitor® (atorvastatin) or Pravachol® (pravastatin).§ In certain studies, atorvastatin and pravastatin therapy was found to reduce CHD event risk more effectively in KIF6 carriers compared with noncarriers.

LPA Aspirin Genotype Test 90553(X) may help predict risk of CVD and response to aspirin therapy.ll In the Women’s Health Study (WHS), low-dose aspirin therapy resulted in a greater reduction of CVD events in LPA Aspirin carriers than in noncarriers.

LPA Intron 25 Genotype Test 90655(X) may help predict risk of CHD, providing additional insight into a patient’s risk for CHD beyond traditional risk factors.

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NT-proBNP 91739(X), or N-terminal pro b-type natriuretic peptide, is an endogenously produced neurohormone secreted from the cardiac ventricular myocytes in response to cardiac stress. Elevated levels indicate the presence of ongoing myocardial stress and potentially an underlying cardiac disorder. As a highly sensitive marker for cardiac dysfunction, elevated NT-proBNP levels are prognostic of future cardiovascular events, even in the setting of undiagnosed, subclinical CVD.

ST2, Soluble (sST2) 91823(X) can be used in risk assessment of patients with acute and chronic heart failure. The sST2 biomarker binds and removes Interleukin-33 from the circulation, thus eliminating the protective effect the IL-33 provides to the cardiac muscle. Patients with HF and elevated sST2 levels are at increased risk for progression, heart transplantation, and possibly death. sST2 is not affected by confounding factors as is BNP/ NT-proBNP. Using sST2 alongside BNP/NT-proBNP may help improve the risk stratification of patients with chronic HF. High levels of both sST2 and BNP/NT-proBNP, compared with high levels of only one, better predict HF progression.

Galectin-3 92768(X) is a carbohydrate-binding lectin that increases collagen production and cardiac fibroblast proliferation. Elevated levels of galectin-3 have been associated with macrophage infiltration, cardiac fibrosis, and cardiac hypertrophy, which contribute to progression of heart failure and poor cardiovascular outcomes. Measuring galectin-3 in conjunction with BNP/NT-proBNP and ST2 may further enhance risk stratification to monitor and treat HF and CVD.

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Cardio IQ® Insulin Resistance Panel with Score 96509(X) combines fasting insulin and Cpeptide measurements to evaluate the likelihood that an individual has insulin resistance. Both analytes are simultaneously quantified by liquid chromatography-tandem mass spectrometry (LC/MS/MS).

Diabetes Risk Panel with Score 92026(X) measures glucose, hemoglobin A1c (HbA1c), and lipids. It also estimates the 8-year risk of developing diabetes using laboratory test results, anthropomorphic data, and family history. The risk algorithm is based on the analysis of 3,453 individuals (ages 30–79) within the Framingham cohort. It is intended to aid in the identification of patients at risk for developing diabetes mellitus, permitting lifestyle or pharmacologic interventions.

Diabetes panel components may be ordered separately: Glucose 91947/483 (CPT 82947); Hemoglobin A1c 91732/496 (CPT 83036); Cholesterol, Total 91717(X)/334 (CPT 82465); HDL Cholesterol 91719(X)/608 (CPT 83718); Triglycerides 91718(X)/896 (CPT 84478). Available with and without score.

Glucose 91947(X) measures serum glucose levels under fasting conditions. Elevated serum glucose (hyperglycemia) is associated with diabetes and insulin resistance. Low levels indicate hypoglycemia.

Cholesterol, Total 91717(X) is useful in the diagnosis of hyperlipoproteinemia, atherosclerosis, hepatic, and thyroid diseases.

Hemoglobin A1c 91732(X) reflects average blood sugar levels over the preceding 90-day period. Elevated levels are associated with prediabetes and diabetes. HbA1c measurement requires no fasting or glucose loading requirement, is less sensitive than glucose to stress and illness, and is more specific for identifying individuals at increased risk for diabetes. Lowering HbA1c levels by 1% reduces the risk of microvascular complications by approximately 40%.17

Insulin 91731(X) is associated with the characterization of an atherogenic lipid profile and metabolic syndrome. Abnormal fasting insulin, especially when combined with other risk factors, identifies patients at significantly higher risk for the development of CVD.

Homocysteine 91733(X) is a metabolic by-product of methionine metabolism. Progressively elevated blood levels of homocysteine are a documented risk marker for CVD events.

Omega-3 and -6 Fatty Acids (FAs) 91734(X)—a diet rich in omega-3 fatty acids is associated with a decreased risk of cardiovascular events, including sudden cardiac death (SCD). The three major omega-3 fatty acids are eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and alpha-linolenic acid. Omega-6 fatty acids are proinflammatory and prothrombotic. The major omega-6 fatty acid is arachidonic acid (AA). The omega-3 index—EPA and DHA expressed as a percentage of phospholipid FAs—is an indicator of risk for SCD and nonfatal cardiovascular events and is used as a therapeutic target. The EPA/AA ratio is a marker of cardiovascular risk, with higher ratios being associated with lower cardiac risk. This test measures omega-3 and -6 fatty acid levels free in serum.

OmegaCheck™ 92701(X) measures the long-chain omega-3 fatty acids: EPA, docosapentaenoic acid (DPA), DHA, and the most abundant forms of omega-6 fatty acids: AA and linoleic acid (LA). Omega-3 fatty acids have anti-oxidant, anti-inflammatory, and antithrombotic effects, and may help reduce triglycerides. Increased levels of omega-3 fatty acids are associated with a lower risk of sudden cardiac death. High ratios of AA/EPA or omega-6/omega-3 are associated with increased CVD and mortality risk. The OmegaCheck test measures omega-3 and -6 fatty acid levels in whole blood.

TMAO 94154(X), or trimethylamine-N-oxide, is a metabolite produced by the gut microbiome following consumption of food products containing the precursors L-carnitine, choline, and phosphatidylcholine (lecithin), which are abundant in various animal-derived products (dairy, egg yolk, and red meat) as well as dietary supplements and energy drinks. TMAO impacts physiological processes that may increase risk of atherosclerosis, enhance platelet hyperreactivity, and increase thrombosis. Elevated TMAO is associated with a 2.5x increased risk of incident major adverse cardiovascular events (MACE). A meta-analysis also demonstrated a 7.6% increase in relative risk for CVD mortality for every 10μmol/L increase in TMAO.18

Vitamin D, 25 Hydroxy, LC/MS/MS 91735(X) at low levels are associated with increased risk of CVD events and death due to heart failure, sudden cardiac death, and stroke. The cardiovascular impact of low vitamin D is via activation of the renin-angiotensin-aldosterone system, as well as via increased parathyroid hormone levels (which predispose individuals to increased insulin resistance associated with diabetes, hypertension, inflammation, and increased cardiovascular risk).

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F2-IsoPs 92771(X), or F2-Isoprostanes, are prostaglandin-like compounds formed from free radical-mediated oxidation of arachidonic acid. F2-IsoPs measure oxidative stress induced by lifestyle risk factors for CVD, which includes smoking, poor diet, high red meat intake, and a sedentary lifestyle. F2-IsoPs contribute to CVD progression through increased vasoconstriction via thromboxane production, platelet aggregation, and thrombus formation. Elevated levels of F2-IsoPs indicate a 2.6x increased risk for CAD and a 1.8x increased risk of CVD mortality.6

OxLDL 92769(X), or oxidized LDL, measures damage of the ApoB protein subunit on the surface of LDL due to oxidative modification. Oxidation of ApoB is an initiating factor in macrophage recruitment, foam cell formation, and vascular inflammation within the arterial wall. Elevated OxLDL levels indicate a 4.3x increased risk of having a coronary heart disease (CHD) event and a 3.5x increased risk of developing metabolic syndrome (MetS).7,8

ADMA/SDMA 94153(X), or asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA), are derivatives of the amino acid L-arginine and are produced via protein degradation. ADMA is a competitive inhibitor of nitric oxide synthase and can reduce the production of nitric oxide. Nitric oxide deficiency is an early manifestation of endothelial dysfunction and atherosclerotic disease. Elevated ADMA indicates a 1.4x increased risk of CVD and CHD and a 1.6x increased risk of stroke. SDMA is primarily excreted in the urine and strongly correlates with reduced renal function.9

Fibrinogen 91743(X) is a plasma glycoprotein that can be transformed into a fibrin clot in response to vascular or tissue injury. The combination of elevated fibrinogen with other CVD risk factors produces an additive risk and may substantially increase disease potential.10

hs-CRP 91737(X) is a highly sensitive measurement of C-reactive protein, an acute-phase reactant protein that increases in response to inflammation. In large epidemiologic studies, elevated levels of CRP have been shown to be a strong indicator of CVD. Patients with high CRP have a 1.5–2.0x increased risk of developing subsequent atherosclerotic disease compared with patients with low CRP levels. It’s also been demonstrated that lowering hs- CRP, independent of lipid levels, results in a 15% risk reduction of recurrent cardiovascular events.11-13

Lp-PLA2 94218(X), or lipoprotein-associated phospholipase A2, is an enzyme produced by macrophages and foam cells within the necrotic core of arterial plaque. Lp-PLA2 measures the disease activity within the arterial wall under the calcified cap of the plaque. Elevated Lp- PLA2 has been associated with a 2.0x increased risk for developing CHD independent of non- HDL cholesterol levels. Also, elevated Lp-PLA2 levels indicate a 2.0x risk of having a CHD event (MI, coronary revascularization or CHD-related death).14

MPO 92814(X), or myeloperoxidase, is an inflammatory enzyme released within the vascular lumen during white blood cell activation in response to fissures, erosions, or degradation of the fibrous cap. MPO is a specific marker of vascular inflammation and is a measure of vulnerable plaque. Elevated levels of MPO independently predict 2.0–2.4x increased risk of future cardiovascular events (MI, coronary revascularization, or CVD-related death).

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ApoB 91726(X),
or apolipoprotein B, is the predominant apoprotein attached to LDL, intermediate-density lipoproteins (IDL), and very-low-density lipoproteins (VLDL). Several decades of scientific literature support the measurement of ApoB for monitoring response to statin therapy. Elevated ApoB is associated with a 2.0–2.5x increased CVD risk.4

Lp(a) 91729(X),
or lipoprotein(a), consists of an inherited protein attached to an LDL particle. Elevated Lp(a) is associated with increased coagulation and a 1.5–5.3x increased incidence of CVD.5 Lp(a) has been linked to the promotion of both early- and advanced-stage atherosclerosis. When the measurement of Lp(a) is combined with other abnormal CVD risk markers, the associated risk increases further.

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Ion Mobility 91604(X)
is a proprietary test methodology for lipoprotein subfractionation. Individual lipoprotein subclasses are separated with high resolution, and direct quantification of lipoproteins provides precise particle counts for each lipoprotein type and subclass. Measurements of LDL or HDL determined as part of the conventional lipid panel may be optimal, while LDL and HDL subclass analysis may indicate increased cardiovascular disease (CVD) risk.
Ion Mobility identifies small- and medium-LDL subclasses, which are highly atherogenic. There is a 1.3x increased CVD risk associated with the small LDL trait and a 1.4x increased risk for the medium LDL trait.¹⁻³ The large HDL subclass is the most efficient cholesterol reabsorbing HDL particle, and best reflects the efficacy of the reverse cholesterol transport system and cholesterol clearance by the liver. Low levels of large HDL are correlated with a 1.8x increased CVD risk.1

HDL2b 36405(X)
consists of the largest and most buoyant particles of the HDL subclasses. A low level of large HDL particles may reduce the efficacy of the reverse cholesterol transport process and increase CVD risk.

sdLDL 36406(X), or small dense LDL, particles
are particularly atherogenic due to their increased affinity for vessel walls, increased susceptibility to oxidation, and reduced ability to be cleared by the liver, increasing the length of time in which these particles remain in circulation.

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Lipid Panel/ASCVD (Atherosclerotic Cardiovascular Disease) Risk Panel

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Lipid Panel/ASCVD (Atherosclerotic Cardiovascular Disease) Risk Panel

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Lipid Panel with Direct LDL Reflex 92061(X) and without Direct LDL Reflex 91716(X) is a panel of blood tests that serves as an initial broad medical assessment tool for abnormalities in total cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol (calculated), and cholesterol/HDL ratio (calculated). A lipid panel is used to identify hyperlipidemia, which may indicate an increased risk for cardiovascular disease. If the triglycerides level is greater than 400 mg/dL, LDL will be directly measured, and not calculated, if direct LDL reflex was chosen.

Lipid Panel/ASCVD Risk Panel Assessment 92052(X) is a lipid panel with a reflex to direct LDL cholesterol (when triglycerides are greater than 400 mg/dL) and a calculation of a 10-year risk of a first ASCVD event—defined as coronary death or nonfatal myocardial infarction (MI), or fatal or nonfatal stroke—using race- and sex-specific pooled cohort evaluations, and as recommended by the 2013 ACC/AHA Guidelines on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Patient information is provided by the ordering physician.

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OxLDL, or oxidized LDL, measures damage of the ApoB protein subunit on the surface of LDL due to oxidative modification. Oxidation of ApoB is an initiating factor in macrophage recruitment, foam cell formation, and vascular inflammation within the arterial wall. Elevated OxLDL levels indicate a 4.3x increased risk of having a CHD event and a 3.5x increased risk of developing metabolic syndrome (MetS).

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What is being tested?

The comprehensive metabolic panel (CMP) is a frequently ordered panel of 14 tests that gives a healthcare provider important information about the current status of a person's metabolism, including the health of the kidneys and liver, electrolyte and acid/base balance as well as levels of blood glucose and blood proteins. Abnormal results, and especially combinations of abnormal results, can indicate a problem that needs to be addressed.

The CMP includes the following tests:

Glucose - energy source for the body; a steady supply must be available for use, and a relatively constant level of glucose must be maintained in the blood.

Calcium - one of the most important minerals in the body; it is essential for the proper functioning of muscles, nerves, and the heart and is required in blood clotting and in the formation of bones.

Proteins

Albumin - a small protein produced in the liver; the major protein in serum

Total Protein - measures albumin as well as all other proteins in serum

Electrolytes

Sodium - vital to normal body processes, including nerve and muscle function

Potassium - vital to cell metabolism and muscle function

CO₂ (carbon dioxide, bicarbonate) - helps to maintain the body's acid-base balance (pH)

Chloride - helps to regulate the amount of fluid in the body and maintain the acid-base balance

Kidney Tests

BUN (blood urea nitrogen) - waste product filtered out of the blood by the kidneys; conditions that affect the kidney have the potential to affect the amount of urea in the blood.

Creatinine - waste product produced in the muscles; it is filtered out of the blood by the kidneys so blood levels are a good indication of how well the kidneys are working.

Liver Tests

ALP (alkaline phosphatase) - enzyme found in the liver and other tissues, bone; elevated levels of ALP in the blood are most commonly caused by liver disease or bone disorders.

ALT (alanine amino transferase, also called SGPT) - enzyme found mostly in the cells of the liver and kidney; a useful test for detecting liver damage

AST (aspartate amino transferase, also called SGOT) - enzyme found especially in cells in the heart and liver; also a useful test for detecting liver damage

Bilirubin - waste product produced by the liver as it breaks down and recycles aged red blood cells

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the patient is prone, and the examiner stabilizes the patient’s thigh. The examiner flexes the patient’s knee 90° and rotates the lower leg while pressing the lower leg downward toward the knee (compression), then rotates the lower leg while pulling it away from the knee (distraction). Pain during compression and rotation suggests a meniscal injury; pain during distraction and rotation suggests a ligamentous or joint capsule injury.

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To help rule out clotting (thrombotic) episodes and to help diagnose conditions related to thrombosis

When you have symptoms of a blood clot or a condition that causes inappropriate blood clots, such as deep vein thrombosis (DVT), pulmonary embolism (PE), or disseminated intravascular coagulation (DIC), and to monitor treatment of DIC and excessive clotting conditions

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Erythrocyte sedimentation rate (ESR or sed rate) is a test that indirectly measures the degree of inflammation present in the body. The test actually measures the rate of fall (sedimentation) of erythrocytes (red blood cells) in a sample of blood that has been placed into a tall, thin, vertical tube. Results are reported as the millimeters of clear fluid (plasma) that are present at the top portion of the tube after one hour.

When a sample of blood is placed in a tube, the red blood cells normally settle out relatively slowly, leaving little clear plasma. The red cells settle at a faster rate in the presence of an increased level of proteins, particularly proteins called acute phase reactants. The level of acute phase reactants such as C-reactive protein (CRP) and fibrinogen increases in the blood in response to inflammation.

Inflammation is part of the body's immune response. It can be acute, developing rapidly after trauma, injury or infection, for example, or can occur over an extended time (chronic) with conditions such as autoimmune diseases or cancer.

The ESR is not diagnostic; it is a non-specific test that may be elevated in a number of these different conditions. It provides general information about the presence or absence of an inflammatory condition.

There have been questions about the usefulness of the ESR in light of newer tests that have come into use that are more specific. However, ESR test is typically indicated for the diagnosis and monitoring of temporal arteritis, systemic vasculitis and polymyalgia rheumatica. Extremely elevated ESR is useful in developing a rheumatic disease differential diagnosis. In addition, ESR may still be a good option in some situations, when, for example, the newer tests are not available in areas with limited resources or when monitoring the course of a disease.

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Thyroid autoantibodies are antibodies that develop when a person's immune system mistakenly targets components of the thyroid gland or thyroid proteins, leading to chronic inflammation of the thyroid (thyroiditis), tissue damage, and/or disruption of thyroid function. Laboratory tests detect the presence and measure the quantity of specific thyroid autoantibodies in the blood.

The thyroid is a small, butterfly-shaped gland that lies flat against the windpipe in the throat. The primary hormones that it produces, thyroxine (T4) and triiodothyronine (T3), are vital in helping to regulate the rate at which the body uses energy (metabolism). The body uses a feedback system in which thyroid stimulating hormone (TSH) stimulates the thyroid to produce T4 and T3 as needed. This system helps maintain a relatively stable amount of the thyroid hormones in the blood. When thyroid antibodies interfere with this process, they can lead to chronic conditions and autoimmune disorders associated with hypothyroidism or hyperthyroidism, such as Graves disease or Hashimoto thyroiditis.

Thyroid antibody tests include:

Thyroid peroxidase antibody (TPO)

Thyroglobulin antibody (TGAb)

Thyroid stimulating hormone receptor antibodies (TSHRAb), including thyroid stimulating immunoglobulin (TSI) and thyroid binding inhibitory immunoglobulin (TBII)

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To identify the presence of inflammation and to monitor response to treatment for an inflammatory disorder

When To Get Tested?

When your healthcare provider suspects that you have an acute condition causing inflammation, such as a serious bacterial or fungal infection or when you are suffering from an inflammatory disorder such as arthritis, an autoimmune disorder, or inflammatory bowel disease

Sample Required?

A blood sample taken from a vein

Test Preparation Needed?

None

What is being tested?

C-reactive protein (CRP) is a protein made by the liver. CRP levels in the blood increase when there is a condition causing inflammation somewhere in the body. A CRP test measures the amount of CRP in the blood to detect inflammation due to acute conditions or to monitor the severity of disease in chronic conditions.

CRP is a non-specific indicator of inflammation and one of the most sensitive acute phase reactants. That means that it is released into the blood within a few hours after an injury, the start of an infection, or other cause of inflammation. Markedly increased levels can occur, for example, after trauma or a heart attack, with active or untreated autoimmune disorders, and with serious bacterial infections, such as in sepsis. The level of CRP can jump as much as a thousand-fold in response to bacterial infection, and its rise in the blood can precede pain, fever, or other signs and symptoms.

The CRP test is not diagnostic, but it provides information to your healthcare practitioner as to whether inflammation is present, without identifying the source of the inflammation. This information can be used in conjunction with other factors such as signs and symptoms, physical exam, and other tests to determine if you have an acute inflammatory condition or are experiencing a flare-up of a chronic inflammatory disease. Your healthcare practitioner may then follow up with further testing and treatment.

This standard CRP test is not to be confused with an hs-CRP test. These are two different tests that measure CRP and each test measures a different range of CRP level in the blood for different purposes:

The standard CRP test measures high levels of the protein observed in diseases that cause significant inflammation. It measures CRP in the range from 8 to 1000 mg/L (or 0.8 to 100 mg/dL).

The hs-CRP test precisely detects lower levels of the protein than that measured by the standard CRP test and is used to evaluate individuals for risk of cardiovascular disease. It measures CRP in the range from 0.3 to 10 mg/L. (See the article on hs-CRP.)

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Antinuclear antibodies (ANA) are a group of autoantibodies produced by a person's immune system when it fails to adequately distinguish between "self" and "nonself." The ANA test detects these autoantibodies in the blood.

ANA react with components of the body's own healthy cells and cause signs and symptoms such as tissue and organ inflammation, joint and muscle pain, and fatigue. ANA specifically target substances found in the nucleus of a cell, hence the name "antinuclear." They probably do not damage living cells because they cannot access their nuclei. However, ANA can cause damage to tissue by reacting with nuclear substances when they are released from injured or dying cells.

The ANA test is one of the primary tests for helping to diagnose a suspected autoimmune disorder or rule out other conditions with similar signs and symptoms. The ANA test may be positive with several autoimmune disorders. Patients with the autoimmune disorder systemic lupus erythematosus (SLE) are almost always positive for ANA, but the percentage of patients with other autoimmune disorders who have positive ANA results varies. Also, a significant number of patients with a variety of other types of disorders (and even some heathy people) may be positive for ANA, especially at low levels.

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Parathyroid hormone (PTH) helps the body maintain stable levels of calcium in the blood. It is part of a feedback loop that includes calcium, PTH, vitamin D, and, to some extent, phosphorus (phosphate) and magnesium. Conditions and diseases that disrupt this feedback loop can cause inappropriate elevations or decreases in calcium and PTH levels and lead to symptoms of hypercalcemia or hypocalcemia. This test measures the amount of PTH in the blood.

PTH is produced by four button-sized parathyroid glands that are located in the neck behind the thyroid gland. Normally, these glands secrete PTH into the bloodstream in response to low blood calcium levels. The hormone works in three ways to help raise blood calcium levels back to normal (two are direct and one is indirect):

PTH directly promotes the release of calcium from bones into the bloodstream.

It directly acts on the kidneys to reduce the elimination of calcium in the urine while promoting the elimination of phosphorus in the urine.

The indirect effect stimulates the kidneys to convert vitamin D from the inactive to the active form, which in turn increases the absorption of calcium from food in the intestines.

As calcium levels begin to increase in the blood, PTH normally decreases.

Parathyroid hormone itself is composed of 84 amino acids (sometimes called PTH (1-84)). Intact and fragmented hormone is present in and secreted by the parathyroid gland. The intact hormone represents a smaller fraction, but its portion is increased when calcium levels are low and decreased when calcium levels are high.

Once released into the bloodstream, PTH has a very short life span; levels fall by half in less than 5 minutes due to uptake and cleavage in the liver and kidneys. The fragments are referred to as C-terminal fragments and are variably sized, missing anywhere from 6 amino acids to more than half the N-terminal portion of the molecule. C-terminal fragments have a longer half-life, exist in much higher concentrations, and are eventually cleared by the kidneys.

Although it was originally thought that the C-terminal fragments were inactive, it now appears that certain fragments may have biologic activities that are able to oppose those of intact PTH.

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A cortisol test may be used to help diagnose Cushing syndrome, a condition associated with excess cortisol, or to help diagnose adrenal insufficiency or Addison disease, conditions associated with deficient cortisol. Cortisol is a hormone that plays a role in the metabolism of proteins, lipids, and carbohydrates, among other functions. Normally, the level of cortisol in the blood rises and falls in a "diurnal variation" pattern, peaking early in the morning, then declining throughout the day and reaching its lowest level about midnight.

Cortisol is produced and secreted by the adrenal glands. Production of the hormone is regulated by the hypothalamus in the brain and by the pituitary gland, a tiny organ located below the brain. When the blood cortisol level falls, the hypothalamus releases corticotropin-releasing hormone (CRH), which directs the pituitary gland to produce ACTH (adrenocorticotropic hormone). ACTH stimulates the adrenal glands to produce and release cortisol. In order for appropriate amounts of cortisol to be made, the hypothalamus, the pituitary, and the adrenal glands must be functioning properly. (See the "What is being tested?" section for more.)

Most cortisol in the blood is bound to a protein; only a small percentage is "free" and biologically active. Blood cortisol testing evaluates both protein-bound and free cortisol while urine and saliva testing evaluate only free cortisol, which should correlate with the levels of free cortisol in the blood. Multiple blood and/or saliva cortisol levels collected at different times, such as at 8 am and 4 pm, can be used to evaluate both cortisol levels and diurnal variation. A 24-hour urine cortisol sample will not show diurnal variation; it will measure the total amount of unbound cortisol excreted in 24 hours.

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A liver panel is a group of tests that are performed together to detect, evaluate, and monitor liver disease or damage. The liver is one of the largest organs in the body and is located in the upper right-hand part of the abdomen and behind the lower ribs. The liver metabolizes and detoxifies drugs and substances that are harmful to the body. It produces blood clotting factors, proteins, and enzymes, helps maintain hormone balances, and stores vitamins and minerals. Bile, a fluid produced by the liver, is transported through ducts directly to the small intestine to help digest fats or to the gallbladder to be stored and concentrated for later use.

A variety of diseases and infections can cause acute or chronic damage to the liver, causing inflammation (hepatitis), scarring (cirrhosis), bile duct obstructions, liver tumors, and liver dysfunction. Alcohol, drugs, some herbal supplements, and toxins can also pose a threat. A significant amount of liver damage may be present before symptoms such as jaundice, dark urine, light-colored stools, itching (pruritus), nausea, fatigue, diarrhea, and unexplained weight loss or gain emerge. Early detection is essential in order to minimize damage and preserve liver function.

The liver panel measures enzymes, proteins, and substances that are produced, processed or eliminated by the liver and are affected by liver injury. Some are released by damaged liver cells and some reflect a decrease in the liver's ability to perform one or more of its functions. When performed together, these tests give a healthcare practitioner a snapshot of the health of a person's liver, an indication of the potential severity of any liver injury, change in liver status over time, and a starting place for further diagnostic testing.

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The Lachman test is the most sensitive physical test for acute anterior cruciate ligament tears (2). With the patient supine, the examiner supports the patient’s thigh and calf, and the patient’s knee is flexed 20°.The lower leg is moved anteriorly. Excessive passive anterior motion of the lower leg from the femur suggests a significant tear.

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Iron is an essential nutrient that, among other functions, is needed in small quantities to help form normal red blood cells (RBCs). It is a critical part of hemoglobin, the protein in RBCs that binds oxygen in the lungs and releases it as blood circulates to other parts of the body. The body cannot produce iron and must absorb it from the foods we eat or from supplements.

Iron tests evaluate the amount of iron in the body by measuring several substances in the blood. These tests are often ordered at the same time and the results interpreted together to help diagnose and/or monitor iron deficiency or iron overload.

Serum iron test—measures the level of iron in the liquid portion of the blood.

Transferrin test—directly measures the level of transferrin in the blood. Transferrin is the protein that transports iron around in the body. Under normal conditions, transferrin is typically one-third saturated with iron. This means that about two-thirds of its capacity is held in reserve.

TIBC (total iron-binding capacity)—measures the total amount of iron that can be bound by proteins in the blood. Since transferrin is the primary iron-binding protein, the TIBC test is a good indirect measurement of transferrin availability.

UIBC (unsaturated iron-binding capacity)—The UIBC test determines the reserve capacity of transferrin, i.e., the portion of transferrin that has not yet been saturated with iron. UIBC also reflects transferrin levels.

Transferrin saturation—a calculation that reflects the percentage of transferrin that is saturated with iron (100 x serum iron/TIBC).

Serum ferritin—reflects the amount of stored iron in the body.

Iron is normally absorbed from food in the small intestine and transported throughout the body by binding to transferrin, a protein produced by the liver. In healthy people, most of the iron transported is incorporated into the production of red blood cell hemoglobin. The remainder is stored in the tissues as ferritin or hemosiderin, with additional small amounts used to produce other proteins such as myoglobin and some enzymes.

When the level of iron is insufficient to meet the body's needs, the level of iron in the blood drops and iron stores are depleted. This may occur because:

There is an increased need for iron, for example during pregnancy or childhood, or due to a condition that causes chronic blood loss (e.g., peptic ulcer, colon cancer)

Not enough iron is consumed (either foods or supplements)

The body is unable to absorb iron from the foods eaten in conditions such as celiac disease

Insufficient levels of circulating and stored iron may eventually lead to iron-deficiency anemia (decreased hemoglobin and hematocrit, smaller and paler red cells). In the early stage of iron deficiency, no physical effects are usually seen and the amount of iron stored may be significantly depleted before any signs or symptoms of iron deficiency develop. If a person is otherwise healthy and anemia develops over a long period of time, symptoms seldom appear before the hemoglobin in the blood drops below the lower limit of normal.

However, as the iron deficiency progresses, symptoms eventually begin to appear. The most common symptoms of anemia include fatigue, weakness, dizziness, headaches and pale skin. Read the article on Anemia to learn more.

Conversely, too much iron can be toxic to the body. Iron storage and ferritin levels increase when more iron is absorbed than the body needs. Absorbing too much iron over time can lead to the progressive buildup of iron compounds in organs and may eventually cause their dysfunction and failure. An example of this is hemochromatosis, a rare genetic disease in which the body absorbs and builds up too much iron, even on a normal diet. Additionally, iron overdose can occur when someone consumes more than the recommended amount of iron.

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*Cholesterol and Triglycerides are transported in the blood by lipoproteins

*Each type of lipoprotein contains a combination of cholesterol, triglyceride, protein, and phospholipid molecules

*Lipid panel consists of:

HDL-C (high density lipoprotein

cholesterol): good because they
take up excess cholesterol and
carries it to the liver for removal.

LDL-C - Bad because it deposits excess cholesterol in walls of blood vessels, which can contribute to atherosclerosis.  Low-density lipoprotein particle number

or concentration (LDL-P). This test measures the number of LDL particles, rather than measuring the amount of LDL-cholesterol. It is thought that this value may more accurately reflect heart disease risk in certain people.

Small LDL subclass particles cause plaque buildup to progress much faster because they enter the artery wall more easily than large LDL particles. A predominance of smaller LDL particles, referred to as Pattern B lipid phenotype, represents an atherogenic lipid profile that is associated with CVD