90% of urea is excreted through its kidneys

There are some losses through the gastrointestinal tract and skin

Kidney disease shows accumulation of urea in blood

Uremic (azotemic) state: increase in [blood urea] 

Fearon Reaction (chemical method): molecules of diacetyl condense with those of urea to form the chromogen diazine, which absorbs strongly at 540 nm.

Enzymatic Methods: based on preliminary hydrolysis of urea with urease to generate ammonia; use spectrophotometry (Berthelot reaction and enzymatic assays)

Excreted in the urine. 

(note: although it is present in all body fluids and secretions and is freely filtered by the glomerulus)

marker of glomerular filtration rate

implicated in diabetes, hypertension, and congestive heart failure

lack of specificity for creatinine

many compounds have been reported to produce a Jaffe-like chromagen 

30 mmol/L maximum

3 - 16 mmol/L

major product of catabolism of the purine nucleosides adenosine and guanine.

Both endogenous and exogenous nucleic acids are degraded/catabolized into uric acid.

Highly present in the urine and can be found in serum

Did you know that it can be crystallized in the serum and deposited in the joints?

there are more than 20 disorders of purine metabolism that cause hyperuricemia and hypouricemia

suspicious symptoms: kidney failure/stones in children or young adult, unexplained neurological problems in infant - adolescent, gout in man/woman <30 years old

Once eaten, amylase (salivary) breaks down starch into glucose and disaccharides into monosaccharides

Carbohydrates are absorbed in the intestines and liver

structureal components in RNA and DNA

source of energy

1) Decrease in blood [glucose] stimulate α-cells of pancreas to secrete glucagon

2) Glucagon causes lipolysis, glycogenolysis, and gluconeogenesis to occur, yielding normal blood [glucose]

1) An increase in blood [glucose] cause the β-cells of the pancreas to release insulin

2) Insulin causes lipogenesis, glucose uptake, and glycogenesis to occur

Abrupt onset of symptoms: polyuria, polydipsia, and rapid weight loss

Insulinopenia (deficiency of insulin) due to loss of pancreatic β cells; autoantibody may be involved

Peak incidence occurs in childhood and adolescence

Minimal symptoms, not prone to ketosis, and not dependent on insulin

[Insulin] may be normal, decreased, or increased; insulin action may be impaired

Obesity is commonly associated

1) women who have marked hyperglycemia during or soon after pregnancy

2) women who are obese

3) women whose GDM was diagnosed before 24 weeks' gestation

Glucose + H₂O + O₂ →(glucose oxidase)→ Glucaronic Acid + H₂O₂

H₂O₂ + Reducing Dye (color #1) →(peroxidase)→ Oxidized Dye + H₂O

The more oxidied dye there is, the more H₂O₂ produced, thus, the more glucose initially present

Glucose is phosphorylated in presence of hexokinase and forms Glucose-6-phosphate. Glucose-6-phosphate is oxidized by G6PD to another product in the presence of NADP⁺ or NAD⁺

The amount of reduced NADP or NADH produced is directly proportional to the amount of glucose in sample (340 nm ABS)

plasma or serum.

NaF, with an anticoagulant may be used

Hemolyzed specimens containing more than 0.5g of Hgb/dL 

drugs, bilirubin, and lipemia

The dihydroxyboryl group in the cellulose reesin has an affinity to cis-diol groups on simple sugars, thus allowing separation of glycated hemoglobins from non-glycated.

Elution with a basic developer removes non-glycated Hb. The glycated forms are eluted using sorbitol buffer. Then spectrophotometry

1) Patient has 3 days of unrestricted diet

2) Collect blood after patient has fasted for at least 8 hrs

1) Collect patient sample from 8-hour fast

2) Give 75g of glucose

3) Collect blood every half hour (up to 2 hours)

4) Patient is considered diabetic if the 2-hour test tube (and another test tube) is >200 mg/dL

Normally, 7% of blood glucose is lost every hour (cellular glycolysis)

1) sodium-dependent glucose transporter (promote the uptake of glucose and galactose from the lumen of the small bowel and their reabsorption from urine in the kidney)

2) facilitative glucose transporter (located on the surface of all cells)

1) Acetest

2) Ketostix

3) Determination of β-hydroxybutyrate

Benedict's Test

Aldose + Cu(citrate)₂^2- (blue) → carboxylate anion and Cu₂O (brick red ppt)

If the color of the solution changes, glucose is present (spectrophotometry?)

1) High-Performance Liquid Chromatography

2) Immunoassay

3) Affinity Chromatography (*done in lab)

any group of yellow-brownish fatty substances occurring in animal and plant tissues composed of phosphoric acid, choline, fatty acids, glycerol, glycolipids, triglycerides, and phospholipids.

major surfactant found in the lung; used along with sphingomyelin to assess fetal lung maturity

a lipid compound that coats lung cells

substance that occurs widely in brain and nervous tissue, consisting of complex phosphoryl derivatives of sphingosine and choline

protein that together with a prosthetic group forms a particular biochemical molecule such as a hormone or enzyme

apolipoproteins are the major components of lipoproteins

1. a pancreatic enzyme that catalyzes the breakdown of fats to fatty acids and glycerol or other alcohols

Saturated fatty acids have no double bond between their carbons

Monounsaturated fatty acids contain one double bond

Polyunsaturated fatty acids contain multiple double bonds

A microscopically visible particle appearing in the plasma after a fatty meal.

Over 90% of TGL make up chylomicrons

Composition: 50-65% TGL, 15% cholesterol, +proteins

Function: carries endogenous cholesterol and other TGL from liver to tissues

Composition: primarily cholesterol about 50%

Function: primary chosterol transport from liver to tissues; transports most of the TGLs?

Composition: AI & AII apolipoprotein and contains cholesterol ester

Function: "cholesterol scavenger"; esterification of cholesterol and transports cholesterol from tissues to liver, where it is converted to bile acids and excreted.