By A. Jerek. Champlain College. 2019.

Irradiation of bone marrow Normal Count and Variations 3 Normal count of platelet is 1 purchase online kamagra super. Hemostasis occurs in two major steps: temporary hemostasis and defini- Thrombocytopenia is defined as the platelet count less 3 tive hemostasis purchase kamagra super 160mg overnight delivery. There- 3 in prevention of bleeding purchase kamagra super with mastercard, which is called temporary fore, platelet count below 50,000/mm of blood is hemostasis. Therefore, splenectomy usually causes thrombocy- Role in Temporary Hemostasis tosis and hypersplenism invariably causes thrombo- cytopenia. Immediate hemostasis following vascular injury is achieved by formation of platelet plug (also called, plate- Thrombocytosis let thrombus) at the site of injury. As platelet thrombus Thrombocytosis commonly occurs in polycythemia vera, can be washed away, unless supported by a clot, this is chronic myeloid leukemia, iron deficiency anemia, sple- called temporary hemostatic plug. Temporary hemostatic nectomy, chronic infection, surgery, and following acute plug formation depends on adhesion, platelet aggrega- hemorrhage. Hematocrit: Increased number of red cells increases platelet aggregation by forcing the platelets to the periphery of the blood stream. This is because red cells disproportionately occupy the axial region of the blood in the blood vessels pushing the leucocytes and thrombocytes to the vessel wall. Speed of blood flow: When blood flow is faster, plate- lets do not get adequate time to interact with vessel wall. Also, the force tending to pull platelet from ves- sel wall and from another platelet is more in fast flow that prevents platelet adhesion and aggregation. Size of blood vessel: This determines the number of platelets passing through the vessel at a given time that influences platelet adhesion to vessel wall. B Platelet Aggregation Platelet adhesion is immediately followed by platelet aggregation at the site of injury (Fig. Simultaneously, platelets are activated, and activated platelets release chemicals from their granules (refer Fig. Note, exposed collagen of the site of vascular injury facilitates the process of tempo- damaged vascular endothelium promote adhesion; (B) Platelet aggregation; (C) Formation of fibrin threads in and around the rary hemostatic plug (platelet thrombus) formation. However, platelet adhesion is also controlled by following factors: Important Note 1. Depth and degree of injury: Deeper and extensive the Use of antiplatelet drugs such as aspirin: Aspirin inhibits platelet aggregation by inhibiting the membrane enzyme cyclooxygenase injury more is the platelet aggregation. Cyclooxygenase facilitates thromboxane A2 formation to release of more quantity of platelet activating fac- that facilitates platelet aggregation and causes vasoconstriction. Site of injury: Injury in mucocutaneous vascular bed of myocardial infarction and stroke. Platelet aggregation is Adhesion of platelets to damaged vascular endothelium more in mucocutaneous tissue. Age of the individual: As composition of vessel wall occurs in activated platelets that results in pseudopodia or changes with age, platelet aggregation alters with age spicules formation. In elderly individuals, the aggrega- tors and chemicals released from granules of the platelets, tion is less. Inhibitors of thrombin generation and action • Arachidonic acid is converted to endoperoxides by cyclooxygenase. Following are the possible mechanisms of • Serotonin released from platelet produces vasocon- platelet release. Through Platelet Activating Factor Through Thrombospondin and Thrombonectin Platelet adhesion activates platelets. Note the factors produced by endothelial cells that promote and inhibit hemostasis. They also facilitate the conversion of X to Xa and pro- Role of Vascular Wall in Hemostasis thrombin to thrombin (Flowchart 20. Thus, platelets Vascular endothelium plays an important role in hemo- accelerate thrombin formation. Endothelial cells of blood vessel synthesize certain substances that are inhibitory and substances that have Role in Clot Retraction facilitatory influence on hemostasis (Fig. If platelets are present in the clot in a test tube, within minutes to hours, the clot contracts, extruding a very large Inhibitors of Hemostasis fraction of serum. The platelet filopodia extends into fibrin clot and fibrin inhibitory influence on hemostasis. Thus, shrinkage of platelet • Thrombomodulin with contraction of filopodia causes internalization of • Protein S fibrin that causes clot retraction. Role in Thrombolysis Heparin: Heparin-like substances on the surface of Role of platelet in fibrinolysis is complex. Endothelial cells also synthesize tis- brinolytic are synthesized and released by platelets. However, antifibrinolytics like plasminogen activator plasmin, and activates fibrinolytic system. Platelets by causing clot retraction decrease the effi- Certain factors synthesized by endothelial cells promote ciency of thrombolysis. It appears that antifibrinolytic effects of platelets pre- and platelet activating factor. Tissue factor or thromboplastin activates extrinsic sys- platelet rich thrombus is known to resist thrombolysis. Platelet activating factor induces aggregation of plate- by estimating the platelet retention in the tube. Another vascular factor promoting hemostasis is vaso- anticoagulant, clotted blood retracts and 50% retrac- constriction of small vessels following injury. Subendothelial collagen promotes platelet adhesion completes at the end of 18 to 24 hours. Platelet count: Decreased platelet count is associated with prolongation of bleeding time. Platelet count is not routinely ordered in which usually occurs due to formation of antibody against clinical practice. Antiplatelet antibodies get attached to platelet hemostatic mechanisms, especially in the diagnosis of membrane glycoproteins, and these platelets are phagocy- a bleeding disorder, platelet count is a must. It is prolonged in severe and occurs equally in both genders that usually thrombocytopenia and thrombasthenia. Thecommon featureof the disease isbleedingthat usu- gate is assessed with the help of aggregometer. Skin is the commonest site test, an aggregating agent is added to a suspension of platelets in plasma and the response is measured of hemorrhage, exhibiting petechiae or ecchymoses. Diagnosis is made by demonstrating thrombocytope- blood is allowed to pass at a constant rate through a nia, anemia, and anti-platelet antibodies in the patient. Note that platelets having antiplatelet antibodies on their surface are destroyed in spleen. The treatment consists of administration of corticos- cytopenia (platelet count less than 50,000/cu mm of teroids, and splenectomy. Thrombocytopenia in Pregnancy Neonatal Autoimmune Thrombocytopenia Thrombocytopenia is common during pregnancy and usu- Sometimes, neonatal autoimmune thrombocytopenia ally asymptomatic. A form, called as gestational thrombocytopenia that 50,000/cu mm of blood in this condition.

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To program proper biostimulation buy generic kamagra super, or points that are: rather skin regeneration with a M edical Device generic 160mg kamagra super with amex, we must 1 order discount kamagra super. The mimetic action of epidermal cholinergic frst understand the biological mechanisms relevant to system the biology of the skin. The reduction processes of skin aging caused by dermo-epidermal regeneration obtained with the use of oxidation of oxygen-free radicals medical devices should lead to the skin: This forced us to treat these two points with differ- 1. An action of stimulation of receptor tyrosine kinase ent drugs, not approved for this treatment (glycerate normally activated by growth factors necessary to choline and reduced glutathione). Action mimetic that improves the epidermal cholin- described above with the addition, in one case, of cho- ergic system line, and in the other, antioxidants. These receptors, once activated induce a metabolic the antioxidants (vitamin C and glutathione) act by activation and dermal–epidermal regeneration with inactivating oxygen-free radicals, escaped from the multiplication. Vitamin C reactivates with its the fbroblasts, of the matrix new components and reversible passage by ascorbic acid to dehydro- collagen lattice [5]. Bicarbonate buffer system that inactivates the release stimulation, allows us to review, for the better, our proto- of H + ions induced by infammation of the skin, col on the heterologous regeneration, incorporating these keeping constant the pH value of 7. Hyaluronic acid and chondroitin-4- skin damage, we keep the classical treatment using sulphte possess antioxidant properties. The times are those based been assigned various physiological functions in the on each mesotherapy treatment: one session a week intercellular matrix, e. Therefore, there is no stimulation of the fnally a maintenance session once a month. In the patient with damage of biological aging hydration and of antioxidant effect. In the patient with epidermal damages we replace the M edical Device Base with one with choline, Nucleic acid is an intercellular component contained always maintaining the same protocol. So the contact of this material with the surface of vides a session with M edical Device Base week for the fbroblast foresees the cellular rupture due to bio- four times. In the derma the fbroblast receives M edical Device with choline and one session every the information of biological damage from the endo- fortnight with the M edical Device with antioxidants. This neocollagenogenesis is relevant to the for- mation of fbrotic collagen characteristic of a repara- M acromolecular hyaluronic acid is a polymer set up tive cicatricial tissue. The adenosine (Purina basis) regulates the infam- lant effect for the macromolecular Hyaluronic acid, mation and the reparation of the tissues. The presence of hyaluronic acid does not have effect pathogen of the dermal fbrosis. The stimulation of the purinergic receptors 2 of the formation of extracellular matrix. Phlogogen stimulus selects some under populations those which are latent in the extracellular matrix of fbroblast with an important role in the formation (M M Ps). The literature confrms that: the best known and publicized radiofrequency tool for 1. Radiofrequency causes movement of charged par- the aging skin is thus presented: “It is a safe, clinically ticles within the tissue, and the resultant molecular proven way to tighten and contour skin, with improve- motion generates heat. The heat in turn causes col- ments in tone contour, and texture occurring naturally lagen shrinkage and new collagen deposition. The physical agents (mechanical, thermal, electri- this case we speak of neocollagenogenesis without cal, radiant, etc. Phlogogen stimulus select some under populations Radiofrequency permits the transformation of cold of fbroblasts with an important role in the forma- energy at high frequency relevant in heat, with an increase tion of the fbrosis. The law of physics at the base of the effects of So, even considering radiofrequency useful for the radiofrequency, is given by the modifcation of the elec- treatment of the aging skin, this technique must be tric feld of the treated zone with a change of the electri- used only for older skins because the biological effect cal charge and of the resistance, and to the movement of is harmful and therefore the results are only aesthetic. Use is made of a the biological effect of the heat produced by the controlled vaporization of thin layers of skin. The light radiofrequency is a denaturation of the collagen fbers emitted by the laser is so intense that in a very short (from 5 to 30% of total fbers), with a consequent time (90 ms) it vaporizes and coagulates a thickness of immediate contraction of the fbers themselves, with a skin between 40 and 60 mm (the thousandth part of a progressive effect in the successive 4–6 months. The protein’s structure is characterized in four Resurfacing with laser will produce very good classes: primary, secondary, tertiary, and quaternary. A source of energy activates the molecules permit the tridimensionality of the protein and their through a tube containing gas so to determine an aton- functions (structure, enzyme, antibody, etc. The weak ics excitement followed by a successive release of bonds break easy with just an increase of the molecular energy which hits the skin bring about a coagulative or kinetics energy (heat). The increase in heat tein denaturalization or the coagulation is followed by beyond the physiological value of 37 °C denatures the a reparative process that is evidenced by a deposit of protein, leading to a loss in biological functions. The damage continues, this results in biological damage and literature confrms that: 140 M. Histological to the deep dermis, avoiding their use on areas of evidence confrms the micro columnar nature of scarce thickness, for example the neck. Phlogogen stimulus select some under populations made of silanoles (onometiltrisilanolo orthohydroxy- of fbroblasts with an important role in the forma- benzoate sodium–silanol salicylate pH:5. These bonds break once This confrms the recognition that, although pro- the substance is inserted in the derma. The prod- an aesthetic improvement of the skin, its use therefore uct is proposed for the treatment of wrinkles, scars, is reserved for older patients. In young people the skin is the tissue that, together with Recently polylactic acid fller has been proposed not the arteries and the thymus, contains more organic sili- only as fller but also as biological stimulus for the reju- con. Polylactic acid is different from This affrmation is real but refers to the silicon intro- other fllers. Simply, its action is based not on the flling duced in the diet as the literature states: of the cutaneous defect, but on the increase in derma’s 1. Silicon is one of the important oligoelements for volume due to the proliferation of neocollagenesis, the regular metabolism of some of our tissues and induced by the stimulus on the fbroblasts provoked by in particular for the bony, cartilaginous and connec- the Polylactic acid itself. The silicon is being introduced nor- because a permanent fller induces a fbrotic response mally in our organism through the diet and it is from a foreign body. Host defense mecha- collagen of Type 1 and in the activity of the proline nisms react differently to the various fller materials. Its defciency is shown with an alteration of the for- process of varying degrees on the biological mate- mation of the bony tissue and with a reduced hepatic rial with damage of the same. The exogenous supplementation of silicon in the of fbroblasts with an important role in the forma- diet allows, through the normalization of the con- tion of the fbrosis. The hydroxilate silicon or oxydated forms (sila- Therefore, the neocollagenogenesis is real but con- noles) are utilized in the analytic medical technol- stituted by fbrotic collagen of type I and therefore ogy (Technologies of selective separation) to stop does not induce a biological rejuvenation but only an hydrophilic molecules at high molecular weight, aesthetic rejuvenation. The dimensions of the perma- such as the Hyaluronic acid, and tying them up, nent fbrotic capsule which forms can be more or less separate them from other components. The particles of organic silicon put into the organ- the toxin can be used in the seborrheic skins to reduce ism induce an infammatory reaction and a response the production of sebocyte and to narrow the pores and of fbrotic character.

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At birth purchase kamagra super online, the concentra­ Er – 2 tion is about one­fifth of concentration in adults order kamagra super from india. Blood group antigens play a critical role in suscepti- and reaches maximum at 15–17 years of life (Application bility to infections by malaria parasites discount kamagra super 160mg mastercard, bacteria and Box 16. Also, few blood groups provide resistance to transfusion, the age of the donor should be minimum of some diseases (see above). Therefore, and acquired diseases are associated with alteration for collection of blood for blood transfusion, the age of the donor should of red cell antigen expression. Medicolegal experts take the help of characterization Blood group antigen A and B are complex oligosaccha- of red cell antigen and antibodies in establishing the rides. For identity of the father in cases of disputed paternities agglutinogen A, terminal sugar is N-acetylgalactosamine, (and also to identity the mother in cases of disputed and for agglutinogen B, terminal sugar is galactose. Specific blood groups have been reported to be associ­ Blood Groups Based on Antigens ated with human behaviors. Therefore, blood groups Based on the presence or absence of A and B antigens on are believed to contribute to the personality of the the red cell membrane individually or in group, four blood individual. A, B and H anti­ Group O : Neither A nor B antigen is present gens may be detected in the saliva and other body fluids also. Such individuals are called secretors, while Subtypes the remaining without it are non-secretors. As A antigen has two sub­types, A and A1, the group A is subdivided into two groups: the group A1 containing A Important Note and A1 antigens, and group A2 containing A antigen alone. These individuals lack the H gene, and therefore A : 27% the basic precursor substance can not be converted into B : 31% H substance. These individuals therefore, should be transfused the expression of A and B antigens are dependent on the with only Bombay blood group. The α agglutinin has two subtypes, α proper their formation starts with basic precursor substances and α1. Basic precursor substance is first converted to H sub- stance (by transferase) under the influence of H gene. H substance is partially converted under the influence antibodies are formed against a particular antigen, when of A and B genes (and specific transferase) into A and they are exposed to that antigen. Some of the H substance remains uncon­ bodies are naturally occurring antibodies as they are verted. They appear in the second O Nil Anti-A and anti-B week of neonatal life and increase very slowly in concen­ tration to attain the peak level at about 10 years of life: Scientist contributed 1. The exact mechanism of formation of agglutinins in Karl Landsteiner discovered isoagglutinin in the absence of their corresponding agglutinogen is human blood in 1900, leading to recognition not clearly known. It has been proposed that intestinal of human blood groups and success of blood bacteria and food contain antigens similar to that of transfusion. Therefore, when the baby of agglutinogen and agglutinin in red cells and plasma in various blood groups is popularly starts eating and food gets absorbed from intestine, known as Landsteiner Law. As these antigens are recognized as non-self antigens Karl Landsteiner (1868–1943) by the body’s immune system, they stimulate antibody production. However, these antigens are present in very low con­ This law states that if a particular agglutinogen is present centration and antibodies against them are produced on the red cell membrane of an individual, the correspond­ very slowly; therefore, antigen­antibody reaction does ing agglutinin must be absent in his plasma. They antibodies in the plasma, and blood group O has no anti­ function efficiently at low temperature, i. Agglutinins Against Blood Groups Blood Grouping Antibodies are directed against the antigens: 1. The individuals with blood group A antigen on the red Blood grouping is performed by suspending the red cells cell membrane do not have anti­A antibody, rather of the person’s blood group to be checked in the anti­A possess anti-B antibody in their plasma. Persons with blood group B do not contain anti­B, rather agglutination (clumping of red cells, as checked under the have anti-A antibody in their plasma (Table 16. Individuals with blood group O have both the anti-A and ant-B antibodies in their plasma. Normally, pres­ These facts were first noted and described by Karl ence of a blood group antigen is a dominant characteristic. Landsteiner in 1900, and his theory is popularly known as Therefore, the antigen is present in the phenotype irres­ Landsteiner’s law. The antigens of Rh system participate in cation trans­ Disputed paternity: the knowledge of inheritance of blood group is useful to solve the cases of disputed paternity. Rh antigens are membrane proteins found in red cell suspicion could have been the father of the child or not. This is because the blood group of the man can be one out of Inheritance several other possible men. Therefore, determination of blood group gene only helps to identify, not confirms the identity. If one of the parents is homozygous positive and the Weiner; hence it is called Rh system (for Rhesus). First, it was other is homozygous negative, all offsprings will be discovered that injection of red cells of Rhesus monkey heterozygous positives (Fig. Chapter 16: Blood Groups and Physiological Basis of Blood Transfusion 121 the similar Rh incompatibility occurs in pregnancies when Rh negative mother bears Rh positive fetus, which leads to erythroblastosis fetalis. Erythroblastosis Fetalis Etiopathogenesis This is a hemolytic disease of the newborn which occurs Fig. Similarly, if the father and mother are homozygous ever, at the time of delivery during placental sepa- negatives, all offsprings will be homozygous negatives, ration, a small amount of fetal blood leaks into the and when one of the parents is heterozygous positive maternal circulation. This induces formation of anti­Rh and the other homozygous negative, 50% of offsprings agglutinins in the mother. In third and subsequent pregnancies, the degree of which is produced only when an Rh negative individual hemolysis becomes severe. These antibodies develop very slowly in the first encoun­ Clinical Features ter, but form rapidly following subsequent encounters. Hemolysis leads Rh antibody is of Ig G type, which can cross placental to anemia, extramedullary hemopoiesis and neonatal barrier. Hence, if antibodies are present in mother’s blood, can may die in utero or if the fetus is born alive, he may have be transferred to the fetus. Anemia: Anemia is proportionate to the degree of therefore, designated as warm antibody. Serum Rh Incompatibility bilirubin level may be more than 25 mg% in severe Rh incompatibility occurs when an Rh negative individual cases. Normally, when an Rh negative person receives Rh due to anemia and hypoproteinemia. This is called positive blood, there will be no immediate reactions hydrops fetalis. Hyperbilirubinemia occurs response in the recipient to synthesize anti­Rh anti­ due to hemolysis.

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Enzymes for lipid digestion are pancreatic lipase (triacyl- glycerol hydrolase purchase generic kamagra super pills, cholesterol ester hydrolase order kamagra super 160 mg with visa, and phos- Enzymes for Carbohydrate Digestion pholipase A ) purchase 160 mg kamagra super with amex, colipase and phospholipases. Pancreatic secretion contains enzymes that help in Enzymes for protein digestion are trypsin, chymotrypsin, digestion of fat, protein and carbohydrate as listed carboxypeptidase, procollagenase, proelastase, and nucle- in Table 40. These proteolytic enzymes are secreted in the inac- pancreatic deficiency leads to severe malabsorption tive forms like trypsinogen, chymotrypsinogen, pro- syndrome. The first step in the process of activation is the activa- Thus, it prevents formation of duodenal ulcer (Clinical tion of trypsinogen to trypsin, which is mediated by the Box 40. Once trypsin is formed, it converts other proenzymes Upper part of duodenum is the commonest site for duodenal ulcer: to their active forms (Flowchart 40. Therefore, once it is However, as acidic chyme in the 1st part of duodenum (part above the activated in the pancreas, it digests the pancreatic tis- ampulla of Vater, the site of opening of major pancreatic duct) remains sue (Clinical Box 40. However, normally it remains mostly unaffected by alkaline pancreatic secretion, it is the commonest inactivated in pancreas. In the resting state (interdigestive phase), the secre- tion of aqueous component occurs mainly from inter- calated and intralobular ducts, but in the stimulated state (after eating) the secretion occurs additionally Fig. The primary secre‑ – tion from acinus is modified by the exchange of ions in the duct. Defect in the chloride channel causes thick exocrine secretion in the duct (Clinical Box 40. The granules are produced by the columnar epithelial cells that line the located toward the apical region of the cells. Pancreatic juice is nearly isotonic with plasma at any exocytosis into the lumen of acinus. The Na and K concentration of pan- cells and duct epithelial cells via voltage gated Cl– channels. The primary 3 – defect in cystic fibrosis is the mutation of the gene that encodes for creatic juice is similar to that of plasma. Cystic fibrosis gene is located on chromosome 7, mutation and Cl concentration varies according to the rate of of which alters the function of its product, cystic fibrosis transmembrane secretion. As − At higher rate of secretion, their concentration is a result, the secretion becomes thick causing duct obstruction which more than 100% of plasma (Fig. The aqueous component secreted by the duct cell is severe pancreatic deficiency causing severe impairment of absorption – of important nutrients. Stimuli Mechanisms Effects Cephalic phase Sight, smell, thought, and taste of food. It is secreted from I cells located in upper small intestine in response to fatty foods. Secretin: Secretin is secreted from S cells of upper small intestine in response to acidic chyme. Cholecystokinin stimulates enzymatic pancreatic secretion, whereas secretin stimulates There are three phases of pancreatic secretion: cephalic, pancreatic secretion rich in water and bicarbonate. The neural factors are sympathetic and parasympa- are different in different phases of secretion (Table 40. Parasympathetic stimulation increases secretion whereas sympathetic stimulation decreases secretion. Cephalic Phase However, the control mechanism varies according to the cephalic phase is induced by smell, sight, thought and the phases of secretion (described below). The effer- Hormonal Factors ent impulses originating from brain directly stimu- 1. The vagovagal reflex also mediates pancreatic secre- stimulates pancreatic secretion. Presence of amino acids and peptides in the gastric content stimulate gastrin release from stomach that in turn stimulate pancreatic secretion (Fig. This is a serious condition of acute abdomen that occurs Intestinal Phase due to inflammation of the pancreas. The disease is characterized by severe pain in the epi- When chyme enters the duodenum, intestinal phase starts. The physiological alteration in the disease is the activa- Secretin stimulates pancreatic juice rich in aqueous tion of trypsin inside the pancreatic tissue that causes (water and bicarbonate) component. Trypsin also activates phospholipase-A which forms 2 amino acids and peptides, and the products of fat lysolecithin from fatty acid of lecithin. Lysolecithin damages pancreatic tissue and produces evoke pancreatic secretion rich in enzymes, which is necrosis of surrounding fat. Classification Diagnosis Pancreatic function tests are described in detail in bio- Acute pancreatitis is diagnosed by its typical presentation chemistry books. However, in this section, we describe of abdominal pain associated with increased plasma level the physiological principles of these tests. First type uses stimulation of pancreatic secretion by blood is collected from abdominal cavity of the patient meals such as Lundh meal or duodenal infusion of and filtered, abdomen is thoroughly washed, bleeding amino acids. It may be due to improper recovery from pancreatitis increases rate of formation and flow, and aqueous compo- or persistence of low grade acute pancreatitis. Meal Stimulation Test Cystic Fibrosis the test meal is called Lundh meal (Lundh and Borgstrom, 1962). This is an autosomal recessive monogenic disorder, in Following ingestion of the meal, duodenal content is aspi- – which the major defect is in the Cl channel. Lung is the most common organ affected and decreased as sensitive and specific as the invasive tests. First type includes estimations in stool for food parti- obstruction and exocrine pancreatic deficiency. Second type includes estimations in blood, urine and Exocrine pancreatic function tests are based on assess- breath for products of digested food due to action of ment of pancreatic secretion in response to hormonal pancreatic enzymes that are absorbed into systemic stimulation, or a meal or measurement of production of circulation. Third type includes estimations in plasma or blood for absorption) and jejunal (low absorption) insufficiencies. It hormones (Schilling test) and enzymes, amino acids, also helps evaluate response to therapy. Schilling Test Fecal Estimation of Fat It is done to assess the absorption of vitamin B12 which requires intrinsic factor. Vitamin B12 deficiency is seen in Normally, about 5 g of fat is excreted per day in the feces. Serum Amylase Estimation Fecal Estimation of Nitrogen Normal level of serum amylase is 60–120 units per liter. In acute pancreatitis, serum amylase concentration becomes About 7 g of nitrogen is excreted in stool per day in very high. Cholangiopancreatography This is a special radiodiagnostic investigation in which the D Xylose Absorption Test details of the contour of hepatopancreatic duct system are A pentose sugar called xylose is administered (25 g, usu- visualized by introducing an endoscope.