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Gland: Digestive
Fibrinogen
- FIBRINOGEN- BLOOD TEST RANGES 200 and 400 mg/dL (2.0 to 4.0 g/L)
(coagulation factor I) is a glycoprotein complex that is synthesized by the liver and circulates in the blood stream. During tissue and or vascular injury, it is converted enzymatically by thrombin to fibrin which creates a blood clot The primary function is to occlude blood vessels thus stopping bleeding. Fibrin also binds and reduces the activity of thrombin. This activity referred to as antithrombin I, which limits clot formation. Fibrin also mediates and is important in blood platelet, endothelial cell spreading, capillary tube formation, tissue fibroblast proliferation, and angiogenesis thereby promoting revascularization and wound healing. Thrombin is synthesized in the liver and secreted into the general circulation in an inactive zymogen form (prothrombin), a complex multidomain glycoprotein that is activated to yield thrombin at sites of vascular injury by limited proteolysis following upstream activation of the coagulation cascade.
Chloride
ELECTROLYTES
The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion.
Sodium, potassium, and chloride enter the body via ingestion of food.
Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins.
Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes.
Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body.
There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate.
The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site.
Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites.
Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids.
Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell.
Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport.
CHLORIDE
Chloride a blood electrolyte, and is the major anion and exists in the extracellular spaces as part of the sodium chloride or HCl molecules.
Chloride is used for assessing pH, and electrolyte balance.
From a physiologic perspective, the primary purpose of chloride is to regulate the quantity of carbohydrates and proteins entering into the cells, by inhibiting the exchange of mineral controlled substances across the cell membrane and responds to the oxidative power of potassium.
Chloride the major anion is predominantly found in the extracellular spaces as part of sodium chloride or in the stomach as hydrochloric acid.
Chloride maintains cellular integrity by its influence on acid-base and water balance as well as osmotic pressure. Chloride has a reciprocal power with other anions by decreasing or increasing when there are too many or not enough anions. Aldosterone has a direct effect of reabsorption of sodium and an indirect effect on the increased absorption of chloride.
Chlorides are lost via the GI tract through vomiting or diarrhea and thru the kidneys during times of diuresis.
Chloride also responds to the antioxidant media (cell membrane) by mobilizing, and collecting sodium/food aggregates on a selectively permeable basis. This reaction is under the influence of the adrenal medulla/epinephrine/norepinephrine thereby maintaining energy stores.
Chloride also assists in the production of HCl via the chief cells in the stomach.
In the bowel, chloride is important in preventing the passage of water out of the body. Therefore, chloride literally blocks the flow of water/gas exchange across a cell membrane. This is extremely important in the intestines and bladder.
Chloride plays a vital role during the conduction of a neurological impulse where sodium lines up on the outside of a cell membrane, and potassium on the inside of the cell membrane, during the resting stage or polarized state. In a normal nerve fiber, the permeability of the membrane to potassium is about 100 times that of sodium. The sodium-potassium pump moves three sodium ions to the exterior of the cell, for every two potassium ions that are moved to the interior of the cell, creating a net positive charge to the outside of the cell membrane for each revolution of the sodium-potassium pump. This creates a positively charged external membrane and a negatively charged internal membrane, which sets up a membrane electrical potential. As a neurological impulse is transmitted down the nerve, (which is the excitation phase of an impulse), sodium crosses the cell membrane, and enters into the cell, while potassium moves to the external portion of the membrane.
This then creates the depolarization of the cell membrane, thereby creating a negative charge on the outside, and a positive charge on the inside. The transmission of each impulse along the nerve fiber reduces infinitesimally as the concentration differences of sodium and potassium between the inside and outside of the cell membrane change slightly. In so doing allows the nerve fiber to transmit between 100, 000 to 50, 000, 000 impulses before the concentration differences are rundown.
As the neurological impulse passes, the sodium-potassium ATPase pump re-establishes the sodium-potassium ratio back to normal (repolarization). The pumping activity is dramatically increased approximately eightfold to restore the membrane back to the polarized state.
The chloride shift to the inside of the cell membrane during the final stages makes the inside of the cell, even more, negative, which further helps repolarize the cell.
Chloride generally increases and decreases with plasma or serum sodium levels.
CHLORIDE IS HIGH WHEN
General considerations:
¬ Drink plenty of water
¬ Decrease sodium levels
¬ Increase fat-soluble vitamins D, E, K, and A
Calcium
CALCIUM
Calcium is the largest most nonpolar, alkaline and most abundant of all minerals with 99% of all calcium found in the bones and teeth.
Calcium exists in the ionized state 55 percent of the time and 45 percent of the time in the non-diffusible state, bound to either albumin, prealbumin or thyroglobulin. Therefore, if there is a decrease in serum albumin then there will be a decrease in serum calcium.
Calcium has many functions:
¬ Provides the mobilizing factor in trauma, infections and stress for tissue repair, along with vitamins A, C, manganese, phosphorus, and fatty acids.
¬ Causes vasoconstriction, while potassium, sodium, magnesium, hydrogen ions, and carbon dioxide cause vasodilatation.
¬ Is necessary for bone formation along with phosphorus, collagen, hydroxyapatite (gives bone its hardness) and bone salts of magnesium, sodium, potassium, carbonate, uranium, plutonium, and strontium.
¬ Calcium is used to create action potentials across smooth and striated muscles leading to contraction.
¬ Calcium is used as an intracellular communicator via calcium ion gated channels.
¬ Calcium collects and gather up lipoproteins, and move them across the intestinal membrane. Attaches to oils, fats, fatty acids and waxes. Calcium is absorbed in the upper portion of the small intestines (duodeneum), and the amount absorbed depends on the "acidity" of the intestinal content, via phosphorylation and protein content. When the ratio of calcium to magnesium (which is found in the intestinal membrane as well as cell membranes) is greater than 2-1, fat is drawn through the intestinal and cell membranes. Calcium also requires vitamin D. and HCl for optimal metabolism.
The glands involved with calcium are:
1. The stomach via the release of HCL, which affects the preparation and absorption of calcium.
2. The parathyroids- via parathormone control of calcium ion concentration by controlling intestinal absorption, excretion via the kidneys and the release of calcium from the bones.
3. The liver/gallbladder- via bile emulsification of lipoproteins, preparing them for intestinal absorption.
4. The spleen- which stores and ages fats or lipoproteins.
5. The parotids- due to their ability to program foodstuffs.
6. The thyroid glands-via "calcitonin", promoting deposition of calcium in the bones, while decreasing calcium concentration in the extra-cellular fluids and the blood.
7. The anterior pituitary via its control of magnesium regulating calcium uptake, which regulates protein transport thru the cell membranes.
8. The pancreas- via its ability to oxidize fatty acids
Therefore, any of the above glands or organs or combinations thereof has a great impact on calcium levels.
CALCIUM IS HIGH WHEN
General considerations
¬ Your patient should drink plenty of water
¬ Make sure they are not hypervitaminosis on Vitamins A or D
¬ Very high protein diets may increase calcium levels
¬ Magnesium and phosphates may also increase calcium levels
¬ Using sea salt can help to reduce calcium levels.
CALCIUM IS LOW WHEN
General considerations:
¬ Increase Vitamin A and D intake
¬ Increase albumin and protein intake
¬ Increase magnesium intake
¬ Increase phosphorus
Phosphorus
PHOSPHORUS
85% of the total phosphorus exists as phosphates or esters in the body and is found chiefly in the skeleton and is combined with calcium. 14% of the phosphorus is found in intracellular tissues and 1 % is found in the extracellular fluid. Therefore phosphorus levels are a poor indicator of levels of phosphates in the body.
Phosphorus runs inversely to calcium levels in the body at a calcium to phosphorus ratio of 10 to 4. Therefore, calcium can be a great indicator for phosphorus as well.
As calcium levels increase in the serum, phosphorus levels decrease, and when calcium levels decrease phosphorus levels increase. In fact, causes of high calcium also cause low phosphorus. The controlling factor of phosphorus is parathormone (PTH), which is also the calcium-controlling factor. Phosphorus helps calcium through the cell membrane by increasing the permeability of the cell membrane via oxygen displacement.
1. Phosphorus is responsible for growth and development by way of:
✓ bonding
✓ polymer function
✓ hydration
✓ chemical transport, and
✓ buffering
2. Phosphorus is also responsible for bone formation
3. Phosphorus and metabolism of glucose
Phosphorus is also required for the metabolism of glucose via phosphorylation. Phosphorylation is when a phosphate radical promoted by glucokinase in the liver, or hexokinase in other cells captures the glucose and once inside the cells keeps it there. The exception to this occurs in the liver, the kidneys, and the intestinal epithelial cells.
Ingestion of carbohydrates causes phosphorus to enter RBC’s with glucose causing a reduction of serum phosphorus levels and lipids.
Phosphorus also works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation.
Phosphorylation and its counterpart, dephosphorylation, turn many protein enzymes on and off, thereby altering their function and activity.
By altering pepsin/HCL levels phosphorus can:
a. Stabilize simple sugars-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage.
b. Activation of starches- HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust). Thus making them readily available for oxidation.
The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion.
The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates, as well as proteins for further digestion in the small intestines.
4. The regulation and maintenance of the acid-base balance in the body by maintaining glandular acidity.
5. The storage and transfer of energy from one part of the body to the other.
6. Used in the Production of phospholipids (90 % produced by the liver): lecithin, A cephalin, and sphingomyelin
Phospholipids are necessary for:
Proper brain function (sphingomyelins)
Phospholipids are a major constituent of lipoproteins which can affect function, formation and transport of these lipoproteins causing serious cholesterol abnormalities
Production of cell membranes
Thromboplastin production produced from A cephalin
7. Intracellular phosphorus is used for:
Energy transport formation of ATP from ADP and creatine phosphate via oxidative phosphorylation.
Major constituent of plasma membranes (phospholipids)
Major constituent of DNA and RNA (nucleic acids)
Calcium transport and osmotic fluid pressure
General nutritional considerations when phosphorus is high:
1. Patient should increase water intake
2. Reduce fat intake
3. Reduce Vitamin D intake if overdosing
4. An isotonic saline solution (sea salt) will decrease phosphorus levels
5. Also, decrease phosphorus in the diet and add calcium carbonate to your diet
General considerations when phosphorous is low:
1. Vitamin D deficiency
2. Calcium deficiency
3. Magnesium deficiency
4. Patient needs a high protein diet
Bilirubin, Total
TOTAL BILIRUBIN
Bilirubin comes from the breakdown of hemoglobin and is the byproduct of hemolysis. Bilirubin is produced by the RE portion of the liver and is excreted with the bile.
Pathologically elevations in total bilirubin occur when there is a massive amount of destruction of RBC’s, or the liver is congested and unable to excrete bilirubin.
From a physiologic perspective, the components of bile are inositol, choline, lecithin, cholesterol, and bilirubin/biliverdin. Cholesterol, which is produced by the liver, is converted into bile salts via the influence of the adrenal glands.
The bile salts are converted into cholic acid or chenodeoxycholic acid equally. Approximately 60 percent of all cholesterol is converted into these two acids.
These acids then combine with glycine and taurine to form glyco and tauro conjugated bile acids. The salts of these acids are secreted in the bile.
These salts do two things:
1. They act like "soap" creating saponification and emulsification of fat. This decreases the surface tension of the fat allowing agitation to break the fat up into smaller sizes.
2. Bile salts help absorb fatty acids, monoglycerides, cholesterol, and other lipids, by
forming minute complexes called micelles. Micelles are highly soluble, highly charged, and easily absorbed, increasing absorption by 40 percent.
The liver secretes about 600-1,200 milliliters of bile per day.
The purpose of bile is to:
1. Digest, emulsify and absorb fats.
2. To excrete waste products, such as excessive cholesterol, and bilirubin, which is the end product of hemoglobin degradation.
Bilirubin is the predominant pigment of bile, and is formed from hemoglobin, and destroyed red blood cells. The red blood cells are destroyed by the reticulo-endothelial system (liver and spleen), including the kupfer cells of the liver.
If the spleen/liver are hyperactive, the bile production is increased.
This allows the passive function of bile production to elevate.
As the spleen, liver, and bone marrow destroy hemoglobin it passes into the bloodstream with a protein creating a colloidal state. This creates hemolytic jaundice when there is excessive destruction or impaired production of red blood cells, leading to excessive amounts of prehepatic bilirubin.
The liver cells are unable to withdraw the bilirubin from the blood as fast as it is formed. Therefore consequently there is an increase in prehepatic bilirubin (indirect form).
Remember total bilirubin = the direct and indirect forms.
The direct is elevated in biliary obstruction, which is conjugated and reacted on by the liver.
The indirect form is elevated in liver failure, which is unconjugated and not reacted on by the liver.
Since the liver, spleen, adrenals and diet play a role in total bilirubin production from a physiologic perspective we must evaluate those glands as well.
LDH
LACTIC ACID DEHYDROGENASE
Lactic acid dehydrogenase is found chiefly in the heart, skeletal muscles, kidneys, and liver, as well as all cells.
In pathological states, elevated levels indicate damage to the above areas and is used to determine myocardial and pulmonary infarction.
In physiological states, LDH catalyzes the conversion of pyruvate ( the final step in glycolysis) to lactate and back, as it converts NADH to NAD+ and back.
A dehydrogenase is an enzyme that transfers a hydride from one molecule to another.
When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, a by-product called lactic acid is produced.
When lactic acid combines with the carbon dioxide of the venous blood you have a hydrogen displacement. Lactic acid now becomes lactic acid dehydrogenase.
Lactic acid dehydrogenase, therefore, is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism to produce energy.
The pancreas via insulin and the posterior pituitary via ADH are responsible for this sugar and water exchange across the muscle cell interface. Lactic acid dehydrogenase indicates the active exchange of sugar across the membrane (muscle cell interface) utilizing chloride, zinc, and selenium.
The utilization of these minerals creates glycolysis.
LDH then from a physiological perspective determines pancreatic function regulating the amount of glucose into muscle.
It is also important to note that sugar metabolism is very complex and does involve a series of other organs.
Ranges for LDH are between 0-220; again it is rather obvious that LDH is a by-product of sugar metabolism and a 0 figure could not be construed as a low normal range. I feel that the range should start at 80.
You will find many patients with a low LDH having problems with decreased function causing heart, skeletal muscle (weakness, loss of strength, muscle wasting), kidney and liver dysfunction, and eventual wasting away of these organs.
ALT (SGPT)
SERUM GLUTAMIC PYRUVIC TRANSAMINASE (SGPT) (ALT)
SGPT is primarily a liver function test. It has a maximum concentration in the liver (fatty membranes) sinusoids. Low concentrations of SGPT are also found in the kidneys, heart, and skeletal muscle.
In pathological states, elevations indicate liver disease.
ALT is found in serum and in various bodily tissues but is most commonly associated with the liver. It catalyzes the transfer of an amino group from alanine to alpha-ketoglutarate, and the products of this reversible transamination reaction being pyruvate and glutamate.
glutamate + pyruvate ⇌ alpha-ketoglutarate + alanine
Alanine transaminase delivers skeletal muscle carbon and nitrogen in the form of alanine to the liver.
In skeletal muscle, pyruvate is transaminated to alanine, thus affording an additional route of nitrogen transport from muscle to liver. In the liver, alanine transaminase transfers the ammonia to A-KG and regenerates pyruvate. The pyruvate can then be diverted into gluconeogenesis. This process is referred to as the glucose-alanine cycle. The glucose-alanine cycle is used primarily as a mechanism for skeletal muscle to eliminate nitrogen as the muscles replenish their energy supply. Within the liver, alanine is converted back to pyruvate and is then a source of carbon atoms for gluconeogenesis. The newly formed glucose can then enter the bloodstream for delivery back to the muscle. The amino group transported from the muscle to the liver, in the form of alanine, is converted to urea in the urea cycle and then excreted.
In physiological states SGPT is a primary kreb cycle expressant and as a result causes the release of catabolic fats. SGPT occurs in serum as a consequence of substances being released by the fatty membranes of the liver sinusoids, and lymphatic ducts. The liver sinusoids store food, and the lymphatic ducts house toxins.
Picture a layer of fat that holds foods or toxins in the cell. Now as that layer of fat is being burned off, foods and toxins are being released in a controlled manner. This allows foods or toxins to be directed to their next destination.
Please note that most lab ranges for this test start at 0, which in actuality is false since this is a measurement of liver function, and 0 would mean that the liver was not functioning at all. A low range then should be around 15.
Therefore, from a physiological perspective, a low SGPT between 15-20 would indicate a sluggish liver causing many metabolic disturbances.
Typically these people have no energy, get sick a lot, cannot tolerate food well and have a slow metabolism.
GGT
GAMMA GLUTAMYL TRANSPEPTIDASE (GGT)
Is a biliary enzyme useful in the diagnosis of obstructive jaundice, intrahepatic cholestasis and pancreatitis. GGT is more responsive to biliary obstruction than are aspartate aminotransferase (AST) (SGOT) and alanine aminotransferase (ALT) (SGPT). 1. GGT is increased in hepatoma and carcinoma of the pancreas and useful in the diagnosis of metastatic carcinoma of the liver. Increasing levels in carcinoma patients relate to tumor progression and a dubious outcome.
1. CEA, alkaline phosphatase and GGT together are useful markers for hepatic metastasis from the breast and colon.
2. May be useful in the diagnosis of chronic alcoholic liver disease. Follow-up blood chemistries of serum GGT, AST and ALT levels can distinguish recovering alcoholics who resume drinking from those who do not.
3. Increase in body mass correlates with increased GGT levels.
4. GGT along with MCV is a useful test for alcoholism.
5. GGT is the test of choice for pregnant females who may have cholestasis.
6. GGT levels are elevated in cirrhosis and hepatitis.
7. The transaminases, AST and ALT rise higher in acute viral hepatitis; then GGT.
8. Increased in systemic lupus erythematosus
GGT IS HIGH WHEN
General considerations:
If patient has been on a very low-fat diet for long periods of time then increase fat intake
Total Iron
Total Iron Binding Capacity (TBIC)—measures the amount of transferrin,
which is a blood protein that transports iron from the digestive system to cells that
will be utilizing the iron. Your body produces transferrin in relationship to the
body’s need for iron. When iron stores are low, transferrin levels will increase
and when transferrin levels are low, too much iron is present. Usually, about one
third of the transferrin is being used to transport iron at any one time. Because of
this, your blood serum has considerable extra iron-binding capacity, which is
called the Unsaturated Iron Biding Capacity (UIBC). The TIBC then equals
UIBC plus serum iron measurement. Some laboratories may measure UIBC,
some measure TIBC and others measure transferrin. TIBC is increased in iron-
deficiency, acute hepatitis, during pregnancy or when oral contraceptives are
used. TIBC is decreased in hypoproteinemia from many causes, cirrhosis of the
liver, nephrosis and thalassemia or from a number of inflammatory states.
TOTAL IRON
IRON
Men 65-175ug/dL 11.6-31.3 umol/L
Women 50-170ug/dL 9.0 -30.4 umol/L
Children 50-120ug/dL 9.0-21.5 umol/L
Newborns 100-250 ug/dL 17.9-44.8 umol/L