A Case Study on Urinalysis and Body Fluids

A Rotational Case Study Presented to the Faculty of Medical Laboratory Science Department San Pedro College Davao City

In Partial Fulfilment of the Requirements for the Completion of Clinical Chemistry Rotation

RICHARD GLYNN D. ESTOMATA JOMARIE EVE D. ENRIQUEZ KURT RUSSEL A. JUMUAD JESSA MAE C. MENDOZA Group 5 Subgroup 3 17 February 2011

Objectives of the Study

General Objective

To formulate specific, measurable, attainable realistic and time bounded differential diagnosis toward the case to the patient. Specific Objectives To be able to: y y y y y y y y Give adequate developmental data of the patient in relation to diagnosis and the case. Present a sufficient history of the illness, including precipitating and predisposing factors. Explain well the salient anatomy physiology and pathophysiology of the case of the patient. Interpret laboratory results accurately yet precisely. Discuss the rationale of the laboratory results to the clinical diagnosis of the case patient. Identify the etiology of the disease of the patient. Determine the immediate preventive management care of the patient s case. Know the action, mechanism, preparation and side effects of the drugs, if there are any, used by the patient prior to admission.

Chapter I Introduction to the Case A 75-year-old woman with a history of hypertension and temporal arthritis was admitted for evaluation of 6 weeks of worsening abdominal pain. The pain was described as an intermittent, sharp, right upper quadrant discomfort that lasted 15 to 45 minutes. There were no clear precipitating or relieving factors. During the past 24 hours, the pain had increased in severity and was associated with nausea and vomiting. She denied fever, chills, melena, hematochezia, change in character of stool and urine, and weight loss. Her medication regimen included nifedipine, 30 mg qd, and prednisone, 2 mg qd. She drank approximately 2 alcohol- containing beverages a month. There was no significant family medical history. Significant findings on physical examination included a temperature o 37C, stable vital signs, anicteric sclerae, regular heart rate, clear lungs, and right upper quadrant abdominal tenderness with voluntary guarding but no rebound tenderness. Laboratory Studies: White blood cell count White cell differential Hemoglobin Hematocrit Sodium Potassium Chloride Bicarbonate Blood Urea Nitrogen Creatinine Glucose Calcium Amylase Lipase Aspartate aminotransferase (AST) Alanine aminotrasferase (ALT) Alkaline phosphatase Total Bilirubin Albumin Cholesterol Triglycerides 13.3 x 103 (Normal: 44.8 10.8 x 103) 87% polys, 10% bands, 1% lymphocytes 12.4 g/dL (Normal: 12 16 g/dL) 39.3 % (Normal: 37% - 447 %) 132 mmol/L (Normal: 135-145 mmol/L) 4.2 mmol/L (Normal: 3.5 5.0 mmol/L) 100 mmol/L (Normal: 95- 105 mmol/L) 22 mmol/L (Normal: 22-30 mmol/L) 12 mg/dL (Normal: 7-17 mg/dL) 0.7 mg/dL (Normal: 0.7 1.2 mg/dL) 139 mg/dL (Normal: 65 105 mg/dL) 8.5 mg/dL (Normal: 8.5 10.5 mg/dL) 1153 U/L (Normal: <109 mmol/L) 6173 U/L (Normal: 25 -300 mmol/L) 502 U/L (Normal: 15 45 mmol/L) 257 U/L (Normal: 10 50 U/L) 298 U/L (Normal: 40-125 U/L) 1.2 mg/dL (Normal: 0.2 1.3 mg/dL) 4.9 g/dL (Normal: 3.5 5.0 g/dL) 245 mg/dL (Normal: 190-260 mg/dL) 120 mg/dL (Normal: 10-160 mg/dL)

Ultrasound of the hepatobiliary tree reveals multiple gallstones in the gallbladder.

Chapter II Patient s Data with History The following data are categorized according to the standard nursing assessment by Delaune and Ladner (2006). More so, according to them, assessment s purpose is to establish a database concerning a client s physical, psychosocial, and emotional health in order to identify health promoting behaviours as well as actual and potential health problems. PRE-EXAMINATION I. Subjective Self-reported denial of the following: -elevation of temperature above the normal range of 98.6 F (37 degree Celsius) -sensation of coldness -black tarry faeces -passage of fresh blood per anus -change in stool and urine characteristic -reduction of the total body mass Intermittent, sharp, right upper quadrant abdominal pain lasting 15 45 minutes Sensation of unease and discomfort in the upper stomach with an involuntary urge to vomit Forceful expulsion of the contents of one s stomach through the mouth and sometimes the nose (emesis) II. Objective Not available III. History High blood pressure Palpation of the head shows scalp sensitivity and shows a tender, thick, palpable artery on one side of the head A. Current Medications Nifedipine, 30 mg qd. Prednisone, 2 mg qd. B. Personal Habits Drinks approximately 2 alcohol-containing beverages a month C. Genetics No genetic history defined PHYSICAL EXAMINATION I. General Appearance A 75-year old hypertensive woman with no clear precipitating or relieving factors A. Organs A1. Lungs Clear A2. Sclerae Anicteric, unrelated to jaundice A3. Abdominal region Right upper quadrant abdominal tenderness with voluntary guarding but no rebound tenderness II. Physical Tests A. Heart Rate Regular (probably 60-80 beats per minute)

III.

B. Temperature 37 degrees Celsius (98.6 F) C. Vital signs Stable Laboratory Examinations Department of Pathology and Laboratories 1. Haematology A. Complete Blood Count White blood cell count 13.3 x 103 (Normal: 44.8 10.8 x 103) White cell differential 87% polys, 10% bands, 1% lymphocytes Hemoglobin 12.4 g/dL (Normal: 12 16 g/dL) Hematocrit 39.3 % (Normal: 37% - 447 %) 2. Clinical Chemistry A. Electrolytes Sodium 132 mmol/L (Normal: 135-145 mmol/L) Potassium 4.2 mmol/L (Normal: 3.5 5.0 mmol/L) Chloride 100 mmol/L (Normal: 95- 105 mmol/L) Bicarbonate 22 mmol/L (Normal: 22-30 mmol/L) Calcium 8.5 mg/dL (Normal: 8.5 10.5 mg/dL) B. Non-Protein Nitrogen Compounds Blood Urea Nitrogen 12 mg/dL (Normal: 7-17 mg/dL) Creatinine 0.7 mg/dL (Normal: 0.7 1.2 mg/dL) C. Sugars, Proteins and Liver Function Tests Glucose 139 mg/dL (Normal: 65 105 mg/dL) Total Bilirubin 1.2 mg/dL (Normal: 0.2 1.3 mg/dL) Albumin 4.9 g/dL (Normal: 3.5 5.0 g/dL) Cholesterol 245 mg/dL (Normal: 190-260 mg/dL) Triglycerides 120 mg/dL (Normal: 10-160 mg/dL) D. Enzymes Amylase 1153 U/L (Normal: <109 mmol/L) Lipase 6173 U/L (Normal: 25 -300 mmol/L) Aspartate aminotransferase (AST) 502 U/L (Normal: 15 45 mmol/L) Alanine aminotrasferase (ALT) 257 U/L (Normal: 10 50 U/L) Alkaline phosphatase 298 U/L (Normal: 40-125 U/L) Department of Radiology Ultrasound:

Presence of gallstones in the gallbladder

Chapter III A. Definition of the Case ACUTE GALLSTONE PANCREATITIS

The case of the 75-year old woman is identified as Acute Gallstone Pancreatitis. Pancreatitis encompasses a group of disorders characterized by inflammation of the pancreas. The clinical manifestations can range in severity from a mild, self-limited disease to a life-threatening acute inflammatory process, and the duration of the disease can range from a transient attack to an irreversible loss of function. By definition, in acute pancreatitis, the gland can return to normal if the underlying cause of the pancreatitis is removed. By contrast, chronic pancreatitis is defined by the presence of irreversible destruction of exocrine pancreatic parenchyma. According to our Anatomy and Physiology, the pancreas is an organ that produces hormones, such as insulin, as well as digestive juices. It is located in the back middle part of the abdomen. When something causes the pancreas to become inflamed it is usually referred to as having acute pancreatic. Acute pancreatic can be caused by different things but is normally curable with proper medical care. It can be caused by several different things. Alcohol consumption over a prolonged amount of time, medications, infections, surgery, injury or gallstones can all cause the pancreas to become inflamed. Nearly 70% of all pancreatitis occurrences are due to either consuming too much alcohol or from gallstones. Of course there are the other 30% of sufferers that have an underlying cause of pancreatitis that may be more serious. Since gallstones cause a good portion of the cases of pancreatitis it is a good idea to discuss what causes this to happen and what exactly gallstones are. Gall stones are hard substances similar to rocks that form inside the gallbladder. The gallbladder is there to store bile until it is needed for digestion of foods. The bile that the gallbladder stores consists of bile salts, proteins and water, cholesterol and bilirubin. When the bile contains too much salt, bilirubin and cholesterol , they can form into a gallstone. These pebble-like formations can be as small as a grain of sand or as large as a golf ball. The gallbladder may produce one of these stones or up to a hundred at a time. Since the pancreas and the gallbladder share the same drainage duct, often times a small sized gallstone can become lodge inside the duct. When this happens it causes all the digestive juices, enzymes and hormones inside the pancreas to become trapped inside the pancreas. The flow of these juices becomes irregular and this causes acute pancreatitis. Framework and composition of these organs are discussed on Anatomy and Physiology later. In-depth discussion of the above paragraphs including laboratory rationale will be at the pathophysiology and in the presentation of data. The case study also presents distinguishing features of the differences between Gallstone Pancreatitis from other types of pancreatitis, their divergence on diagnosis and their resemblance in terms of prognosis. Inclusive also of the case study are the precipitating and underlying predisposing factors of the patient, if available, that may otherwise be correlated to the construction of the disease. Thus, its pathogenesis may be also linked to these factors. Recommendation, immediate management goals and treatment are embraced on the next contexts.

B. Anatomy and Physiology

4 . 5 f 2 e . e 5 t i l n o c n h g e , s 2 w . i 5 d e i , n c a h n e d s i w s i d a e , m u a s n c d u l i a s r a t u m

GALLBLADDER The gallbladder is a pear shaped organ located on the liver that stores about 50 ml of bile until the body needs it for digestion. The gallbladder is about 7-10cm long in humans and is dark green in appearance due to its contents (bile), not its tissue. It is connected to the intestinal system by the cystic duct which in turn empties into the common bile duct. When we eat a large or fatty meal, nerve and chemical signals cause our gallbladder to contract thereby adding bile into our digestive system. The gallbladder stores bile, which is released when food containing fat enters the digestive tract, stimulating the secretion of cholecystokinin (CCK). The bile emulsifies fats and neutralizes acids in partly digested food. Normally we make 1000 to 1500cc of bile a day. It is constantly produced. As a result, there is always a steady amount of bile entering our intestinal tract. Some of it goes into the gallbladder as it comes down the duct. After being stored in the gallbladder, the bile becomes more concentrated than when it left the liver, increasing its potency and intensifying its effect in fats. Bile is a complex fluid composed of bile salts, cholesterol and other molecules (phospholipids and lecithin). The bile salts are the breakdown products of hemoglobin, the oxygen carrying pigment of red blood cells. Bile salts and bile itself are formed in the liver and excreted into bile ducts which converge in the liver to form the main bile ducts. Just as there is a left and right liver lobe, there is a left and a right hepatic (liver) bile duct which join to form a single bile duct, the common hepatic or common bile duct. The common bile duct enters the duodenum, the earliest part of the small intestine where digestion and absorption of food begins. PANCREAS The pancreas is a large gland that is involved in the digestive process, but located outside of the gastrointestinal system. As a digestive gland, the pancreas is only second in size to the liver, weighing about 70-150 g. It is located behind the peritoneal cavity across the upper abdomen at about the level of

the first and second lumbar vertebrae, about 1-2 inches above the umbilicus. It is located in the curve made by the duodenum. The pancreatic duct system is highly variable. The main pancreatic duct, also known as the duct of Wirsung, most commonly drains into the duodenum at the papilla of Vater, whereas the accessory pancreatic duct, also known as the duct of Santorini, most often drains into the duodenum through a separate minor papilla approximately 2 cm cephalad (proximal) to the major papilla of Vater. In many adults, the main pancreatic duct merges with the common bile duct proximal to the papilla of Vater, thus creating the ampulla of Vater, a common channel for biliary and pancreatic drainage. Although the organ gets its name from the Greek pankreas, meaning "all flesh," the pancreas is, in fact, a complex lobulated organ with distinct endocrine and exocrine components. The endocrine portion is composed of about 1 million clusters of cells, the islets of Langerhans. The islet cells secrete hormones that constitute only 1% to 2% of the organ. The exocrine portion of the gland, which produces digestive enzymes, constitutes 80% to 85% of the pancreas. The endocrine (hormone-releasing) component is by far the smaller of the two which are welldelineated, spherical or ovoid clusters composed of at least for different cell types. The islet cells secrete at least three hormones into blood: insulin, glucagon, and somatostatin. The larger, exocrine pancreatic component (enzyme-secreting) secretes about 1.5-2 L/day of fluid, which is rich in digestive enzymes, into ducts that ultimately empty into the duodenum. This digestive fluid is produce by pancreatic acinar cells, which line the pancreas and are connected by small ducts. Normal, protein-rich, pancreatic fluid is clear, colorless, and watery with an alkaline pH that can reach up to 8.3. This alkalinity is caused by the high concentration of sodium bicarbonate present in pancreatic fluid, which is used eventually to neutralize to neutralize the hydrochloric acid in gastric fluid from the stomach as it enters the duodenum. The bicarbonate and chloride concentrations vary reciprocally so that they total about 150 mmol/L. Pancreatic fluid has about the same concentrations of potassium and sodium in serum. The digestive enzymes, or their proenzymes secreted by the pancreas, are capable of digesting the three major classes of food substances (proteins, carbohydrates, and fats) and include: (1) the proteolytic enzymes trypsin, chymotrypsin, elastase, collagenase, leucine aminopeptidase, and some carboxypeptidases; (2) lipid-digesting enzymes, primarily lipase and lecithinase; (3) carbohydratesplitting pancreatic amylase; and (4) several nucleases, which separate the nitrogen-containing bases from their sugar-phosphate strands. Pancreatic activity is under both nervous and endocrine control. Branches of the vagus nerve can cause a small amount of pancreatic fluid secretion when food is smelled or seen, and these secretions may increase as the bolus of food reaches the stomach. Most of the pancreatic action, however, is under hormonal control of scretin and cholecystokinin (CCK). Secretin is responsible for the production of bicarbonate-rich and, therefore, alkaline pancreatic fluid, which protects the lining of the intestine from damage. Secretin is synthesized in response to the acidic contents of the stomach reaching the duodenum. It can also affect gastrin activity in the stomach. This pancreatic fluid contains few digestive enzymes. CCK, in the presence of fats and amino acids in the duodenum, is produced by the cells of intestinal mucosa and is responsible for the release of enzymes from the acinar cells by the pancreas into pancreatic fluid.

C. Pathophysiology

Our definitive diagnosis is Acute Gallstone Pancreatitis. Hence, there are evidences that provided us in the diagnosis of the patient. But there are differentials diagnoses and clinical trials to be consider in arriving a concrete diagnosis. This chapter will discuss on the etiology, mechanism of the disease and how we end up in this diagnosis. The succeeding page presents a concept map of which tackles the summary of this entire pathophysiology. There are several common causes of the acute pancreatitis these are idiopathic, chronic alcohol intake, trauma, autoimmune and drugs. In the case of the patient Gallstones is the cause of pancreatitis that travel down to her common bile duct and which subsequently get stuck in the Ampulla of Vater that causes obstruction in the outflow of pancreatic juices from the pancreas into the duodenum this condition is called Choledocothiasis. The gallbladder has one purpose only: to store bile, which helps digest fats in the small intestine. But the bile become concentrated and thicken. Eventually, bile salts can combined with cholesterol to form (stones) gallstones are composed of a combination of crystallized cholesterol deposits or calcium crystals ionized with bilirubin. These stones block the flow of bile from the gallbladder; this is typically manifested as pain in the upper right quadrant of the abdomen. Gallstone pancreatitis is caused when a migrating gallstone obstructs the ampulla of Vater. The precise mechanism by which obstruction of the sphincter by a gallstone or microlithiasis (sludge) causes pancreatitis is unclear, although it probably involves increased ductal pressure. Ductal obstruction by these protein plugs may cause premature activation of pancreatic enzymes. Then the exocrine of pancreas produces a variety of enzymes, such as proteases, lipases, and saccharidases. These enzymes contribute to food digestion by breaking down food tissues. In this condition it is the worst offender among these enzymes may well be the protease trypsinogen which converts to the active trypsin. Trypsin is most responsible for auto-digestion of the pancreas which in turn causes the pain and complications of the patient. These enzymes can damage tissue and activate complement and the inflammatory cascade, producing cytokines. This process causes inflammation, edema, and sometimes necrosis. In mild pancreatitis, inflammation is confined to the pancreas.In severe pancreatitis, there is significant inflammation, with necrosis and hemorrhage of the gland and a systemic inflammatory response. Activated enzymes and cytokines that enter the peritoneal cavity cause a chemical burn and third spacing of fluid; those that enter the systemic circulation cause a systemic inflammatory response that can result in acute respiratory distress syndrome and renal failure. The systemic effects are mainly the result of increased capillary permeability and decreased vascular tone, which result from the released cytokines and chemokines. Phospholipase A2 is thought to injure alveolar membranes of the lungs. In the milder form, acute interstitial pancreatitis, histologic alterations are limited to interstitial edema and focal areas of fat necrosis in the pancreatic substance and peripancreatic fat. Fat necrosis, as we have seen, results from enzymatic destruction of fat cells. The released fatty acids combine with calcium to form insoluble salts that precipitate in situ. The anatomic changes of acute pancreatic strongly suggest autodigestion of the pancreatic substance by inappropriately activated pancreatic enzymes. This hypothesis is supported by the hereditary forms of pancreatitis described above. Here we focus on the more common, acquired forms of acute pancreatis. As has been discussed, pancreatic enzymes are present in acinar cells in the proenzyme form and have to be activated to fulfill their enzymatic potential. A major role is attributed to trypsin, which itself is synthesized as the proenzyme trypsinogen. Once trypsin is generated, it can in turn activate other proenzymes such as prophospholipase and proelastase, which then take part in the process of autodigestion. The activated enzymes that are so generated cause disintegration of fat cells and damage the elastic fibers of blood vessels, respectively. Trypsin also converts prekallikrein to its activated form,

Precipitating Factors
History of hypertension and temporal arthritis Personal Habit: Drinks approximately 2 alcohol-containing beverages a month

Acute Gallstone Pancreatitis

Predisposing Factors
Age: 75 year old Sex: Female Genetics: No genetic history defined

Gallbladder Multiple Gallstones (Cholelithiasis) Loose gallstones in Oddi sphincter/Common Bile Duct Nausea Emesis

Pancreas Multiple Gallstones in Common Bile Duct (Choledocolithiasis)

Obstruction

Right upper quadrant discomfort

Trypsin

Entrapped Pancreatic Enzymes Reflux Inappropriately Activated Pancreatic Enzymes Pancreatic Autodigestion

Prekallikrein Kallikrein Complement Cascade Increased WBC Count Clotting Cascade

Proelastase

Prophospolipase

Disintegration of fat cells

Damage of elastic fibers in blood vessels

Important triggering event of inflammation

Calcium levels already at lower limit

Increased Glucose

Increased Glucagon release

Increased alpha cells destruction

Fat necrosis

Released fatty acids + Calcium = Insoluble salt in situ

Increased ALT

Increased ALP

Increased AST

Increased Lipase

Increased Amylase

Plate 1. Pathophysiology of the case of the patient. Shadowed boxes connote patient s subjective preexamination whereas rhomboid figures signify laboratory results.

thus bringing into play the kinin system and, by activation of Hageman factor, the clotting and complement systems as well. In this way, inflammation and small-vessel thromboses (which may lead to congestion and rupture of already weakened vessels) are amplified. Thus, activation of trypsinogen is an important triggering event in acute pancreatitis. In about 40% of patients, collections of enzyme-rich pancreatic fluid and tissue debris form in and around the pancreas. In about half, the collections resolve spontaneously. In others, the collections become infected or form pseudocysts. Pseudocysts have a fibrous capsule without an epithelial lining. Pseudocysts may hemorrhage, rupture, or become infected. Death during the first several days is usually caused by cardiovascular instability (with refractory shock and renal failure) or respiratory failure (with hypoxemia and at times adult respiratory distress syndrome). Occasionally, death results from heart failure secondary to an unidentified myocardial depressant factor. Death after the first week is usually caused by multiorgan system failure. Presented elevated serum amylase, lipase and LDH levels which are contributed in the enzymatic activity of the pancreas, in combination with severe abdominal pain, often trigger the initial diagnosis of acute pancreatitis. "It is usually not necessary to measure both serum amylase and lipase. Serum lipase may be preferable because it remains normal in some nonpancreatic conditions that increase serum amylase including macroamylasemia, parotitis, and some carcinomas. In general, serum lipase is thought to be more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis."Although amylase is widely available and provides acceptable accuracy of diagnosis, where lipase is available it is preferred for the diagnosis of acute pancreatitis. Serum amylase and lipase levels are not the only indicators of acute pancreatitis; C-reactive protein, leukocyte elastase, trypsinogenactivating peptides and lactate dehydrogenase are also gauges but are rarely tested by clinicians. A urinary trypsinogen-II assay can be performed at the bedside; the 3-minute dipstick test is "highly sensitive and specific in detecting acute pancreatitis," but it is not currently licensed for use in the United States.

Chapter IV Presentation of Data A. Laboratory Results

Requested test

Normal Values

Test Values

Interpretation

Rationale in relation to the Diagnosis

A. Haematology
CBC Hemoglobin Hematocrit 12-16 g/dL 37%-47%
3

12.4 g/dL 39.3%

3

Normal Normal
Enzymes damage tissues and also activate complement cascade and the inflammatory cascade. indicating Acute inflammation Shift to the left Immature PMNs are released in the circulation because of chemical signals from the site of inflammation

White blood cell count

4.8-10.8 x 10

13.3 x 10

Increased

a. Neutrophils

40%-60%

87%

Increased

b. Bands

0%-3%

10%

Increased

c. Lymphocytes

20%-40% 135-145 mmol/L 3.5-5.0 mmol/L 95-105 mmol/L 22-30 mmol/L

1% 132 mmol/L 4.2 mmol/L 100 mmol/L 22 mmol/L

Decreased Slightly decreased Normal Normal Normal

B. Clinical Chemistry
Sodium Potassium Chloride Bicarbonate

Blood Urea Nitrogen

7-17 mg/dL

12 mg/dL

Normal

Glucose

65-105 mg/dL

139 mg/dL

Increased

Calcium

8.5-10.5

8.5 mg/dL

Normal

Amylase

<109 U/L

1153U/L

Increased

Lipase

35-300 U/L

6173 U/L

Increased

Increased Glucagon release from the destruction of alpha cells. Already at lower limit, calcium combined with liberated fatty acids from fat necrosis to form insoluble salt in situ. Found at the acinar cells of the pancreas and the salivary glands. Damage cells in the pancreas causes this enzyme to leak in the bloodstream. Lipase concentration is found primarily in the pancreas, therefore tissue damage liberates lipase into the circulation.
Increased transaminase activity is not entirely dependent on pancreatic necrosis, but related to increased intrabiliary pressure and associated obstruction of the biliary tract.

Aspartate aminotransferase (AST)

15-45 U/L

502 U/L

Increased

Alanine aminotransferase (ALT)

10-50 U/L

257 U/L

Increased

Alkaline Phosphatase

40-125 U/L

298 U/L

Increased

Increases are primarily a result of increased synthesis of the enzyme induced by cholestasis.

Total Bilirubin Albumin Cholesterol Triglycerides

0.2 1.3 mg/dL 3.5-5.0 g/dL 190-260 mg/dL 10-160 mg/dL

1.2 mg/dL 4.9 g/dL 245 mg/dL 120 mg/dL

Normal Normal Normal Normal

GENERIC Nifedipine

B. Drug Regimen DRUGS MODE OF ACTION ADVERSE EFFECTS Belongs to the class of y worsening angina; dihydropyridine derivative y feeling like you might pass out; selective calcium-channel y feeling short of breath, blockers with mainly vascular swelling in your hands or effects. Used in the treatment of feet; cardiovascular diseases. y fast or pounding heartbeats; y numbness or tingly feeling; y jaundice (yellowing of the skin or eyes); or y chest pain or heavy feeling, pain spreading to the arm or shoulder, nausea, sweating, general ill feeling.

Prednisone

belongs to the class of glucocorticoids. Used in systemic corticosteroid preparations; prevents the release of substances in the body that cause inflammation.

y y y y y y y y y y

liver disease (such as cirrhosis); kidney disease; a thyroid disorder; diabetes; a history of malaria; tuberculosis; osteoporosis; a muscle disorder such as myasthenia gravis; glaucoma or cataracts; herpes infection of the eyes;

y y y

stomach ulcers, ulcerative colitis, or diverticulitis; depression or mental illness; congestive heart failure; or high blood pressure

Chapter V A. Summary Many signs of acute gallstone pancreatitis can be detected by simple laboratory results, like increased enzyme levels, to wit, amylase, lipase, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase. Furthermore, the straightforward physical observation such as right upper quadrant discomfort including nausea and emesis escort us to the diagnosis of a gallstone-induced pancreatitis. We further classify it as acute, rather than chronic, is that the reversible impairment of the pancreatic function, rather than an irreversible impairment. Moreover, it does not come to a point where there is an extent of fibrosis ang long-standing bile duct obstruction plus excessive calcium carbonate precipitates. Perhaps, the reason why, the physician of the 75-year old woman ordered different tests ranging much on clinical chemistry tests towards haematology, is that, it aims to exhaust all the different cryptogram of the case of the patient to arrive on a sure-ball diagnosis. The ultrasound in this patient that revealed multiple shadowing stones in the gallbladder, the patient s elevated alkaline phosphatase which is suggestive of ductal obstruction, the increased transaminase (AST and ALT) levels, all support gallstone-induced pancreatitis. An ALT of 150 U/L can have a 95% specificity and a 96% positive predictive value for gallstone-induced pancreatitis. Additionally, biliary pancreatitis causes a rapid rise in serum amylase to levels >1000 IU/L. This level of amylase is seldom seen in alcohol-induced or other forms of pancreatitis. B. Conclusion Deliberation of differential diagnosis is very difficult especially if you are not familiarized with a one-big-signs-and-symptoms book. A lot of disease can be drawn. Hence, a need for elimination is to be drawn (Ancheta, 2010). Moreover, as medical laboratory scientist, we should practice a scientific method of solving a case study. It more likely a murder case, you see on TV, where you endeavour to fabricate the true story to solve a missing puzzle delicate for its completion (Ancheta, 2010). In this case study, we draw out many conclusions from the predisposing and precipitating factors, symptoms and signs present in the patient.. Hence, these would conclude us how important gallbladder and pancreas is to our system, performing the most complicated and enigmatic functions; like storage of bile and the production of pancreatic enzymes respectively. The patient s history presumptively suggests this disease, as it has shown on the different areas of the laboratory the consistency of the flow on its pathogenesis. Hence, we considered hypertension as a precipitating factor (a factor that could have been changed n the course of the case) because it contributes somehow to the pancreatitis of the patient.

C. Recommendations Computerized tomography (CT) is one choice for imaging the pancreas. CT allows the identification of pancreatic edema, fluid or cysts, and it allows the severity of pancreatitis to be graded. Later in the disease, it may also be of use in recognizing complications. But literature states that CT scanning should only be done if the diagnosis is uncertain, if severe pancreatitis is expected, or if the pancreatitis worsens or does not resolve. Transabdominal ultrasonography (TUS) can be used to identify cholelithiasis and dilatation of the extrahepatic biliary tree, but in detecting bile duct stones, it is 95 percent specific and 60 percent sensitive. TUS seldom visualizes the pancreas in patients with acute pancreatitis due to air in the distended loops of the small bowel. If TUS is utilized, the quality of the results relies heavily on the expertise of the technician, who should scan the entire abdomen in case abdominal pain has a nonbiliary, nonpancreatic source. Other imaging options include ultrasonography and MR cholangiography, which is noninvasive and does not require contrast. MR cholangiography is especially useful for common bile duct stones. Endoscopic ultrasound is more accurate than transabdominal ultrasound but is an invasive endoscopic procedure which requires sedation. How can gallstone pancreatitis be treated? The use of ERCP in patients with gallstone pancreatitis is controversial. The literature indicates that in patients without biliary obstruction, ERCP does not benefit them and may even produce complications that make the disease worse. Overall, Baillie says, experts recommend urgent ERCP for biliary compression only for patients with progressive biliary obstruction (who have progressive jaundice with or without cholangitis). It is not necessary to perform preoperative ERCP in all patients undergoing laparoscopic cholecystectomy; the surgeon should, alternatively, perform intraoperative cholangiography, with ERCP incorporated if bile duct stones are found. However, patients with a suspected or known surgical reconstruction of the gut should undergo preoperative ERCP, which may help the surgeon plan her approach. Preoperative ERCP should also be performed in patients with persistent or progressive biliary obstruction (regardless of choledocholithiasis); surgery should then follow the bile duct clearing to prevent any additional migration of stones from the gallbladder. Because ERCP and sphincterotomy combined are associated with much higher morbidity and mortality than is laparoscopic cholecystectomy -- partly owing to the large number (more than 500,000) of cholecystectomy procedures performed annually in the U.S. alone -- endoscopists performing ERCP prior to laparoscopic cholecystectomy must consider the medicolegal consequences in the event of a severe complication (usually severe pancreatitis) related to the procedure. Typically, if gallstones are confirmed but are not symptomatic, removal of the gallbladder is not recommended. Diabetic patients are an exception to the "wait and see" theory; they may be better candidates for surgical removal of the gallbladder because they can lack "clear-cut pain signals" and therefore may not recognize a gallbladder attack. Diagnostic endoscopic retrograde cholangiopancreatography (ERCP) does increase morbidity in severe pancreatitis patients and is contraindicated unless expertise is available for therapeutic options. The therapeutic ERCP with endoscopic sphincterotomy and drainage of the bile duct with extraction of gallstones is of primary importance in the therapy of cholangitis. Even though pancreatitis may occur with endoscopic sphincterotomy, the procedure does not exacerbate the pancreatitis or have a higher incidence of perforation or hemorrhage in patients with gallstone pancreatitis. If drainage is not possible by therapeutic ERCP or the patient is unable to be sedated, percutaneous transhepatic cholangiography is a possible consideration, especially with dilated intrahepatic ducts.

The gold standard for treatment is laparoscopic cholecystectomy, according to many physicians. Richard A. Kozarek, a physician at Virginia Mason Medical Center in Seattle, expresses concern over potential overuse of ERCP and recommends laparoscopic cholecystectomy and mandatory intraoperative cholangiography for patients who have mild gallstone pancreatitis. In his response to a study published in the American Journal of Gastroenterology, Kozarek writes that ERCP and other actions that have traditionally been to treat pancreatitis should be reserved only for patients with severe forms of the malady, not utilized in those with milder forms. Overall, both procedures (ERCP and laparoscopic cholecystectomy) are safe and effective when they are clinically indicated; ERCP, when performed selectively (not routinely) before laparoscopic cholecystectomy is cost-effective. Endoscopic sphincterotomy can shorten the hospital stay and allow laparoscopic cholecystectomy earlier. The management of gallstone pancreatitis is variable. Laparoscopic cholecystectomy is considered the procedure of choice to prevent recurrent pancreatitis and to evaluate the bile duct. An early therapeutic ERCP may prevent recurrence of pancreatitis or prevent the complications of cholangitis and necrotizing pancreatitis. Routine preoperative ERCP is not indicated since gallstone pancreatitis usually responds to conservative therapy and subsequent laparoscopic cholecystectomy. Chapter VI Bibliography Albanese, C., et al., (2006) Current Surgical Diagnosis and Treatment, 12th Edition, Chapter 26 Ancheta, Jiau (2010) Personal Communication, Southern Philippines Medical Center (SPMC), Davao City Bishop, Michael L., Fody, Edward P., Schoeff, Larry E. (2005) Lippincott Williams and Wilkins Clinical Chemistry: Principles, Procedures, Correlations, 5th Edition, pp. 220-221, 243-258, 317-338 Buchamp, R.D., Evers, B.M., Mattox, K. (2007) Biston Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 18th Edition, Section 8, Chapter 38 DeLaune, Sue C., Ladner, Patricia K., (2006) Thomson Delmar Learning Fundamentals of Practice: Standards and Practice, 3rd Edition, pp. 101 Fauci, A., et al. (2008) Harrison s Principles of Internal Medicine, 17th Edition, Part 13, Section 3 Kumar, V., Abbas A., Nelson F., (2004) Robbins and Cotran s Pathologic Basis of Disease, 7th Edition, Chapter 19 McPherson, Richard A., Pincus, Matthew R., (2007) Saunders, Elseviers, Inc., Henry s Clinical Diagnosis and Management by Laboratory Methods, 21st Edition, pp. 460 Webliography http://www.endonurse.com/articles/2002/12/gallstone-pancreatitis.aspx http://www.mims.com/Page.aspx http://www.wikipedia.org/gallstonepancreatitis