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METABOLISM AND NUTRITION MODULE B SCENARIO PROBLEM BASED LEARNING

PRESENTED BY: GROUP 16th

FACULTY OF MEDICINE AIRLANGGA UNIVERSITY

METABOLISM AND NUTRITION MODULE 16th Group

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3rd SEMESTER – 2010 METABOLISM AND NUTRITION MODULE B SCENARIO PROBLEM BASED LEARNING

Scenario Creator Prof. Dr. Suhartati, dr., MS Edhi Rianto, dr., MS

METABOLISM AND NUTRITION MODULE 16th Group

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16th Group Members
Leader : Shaleh Muhammad D Members: Muhammad Achdiar R Filipus Michael Yofrido Togar Erkasan Sitorus Christopher Njotokusgito Karin Dhia Fahmita Dini Nur Aini Wirawan Indra P. Rizal Constantino Susilo Agnes Candra Pradhita 010911152 010911154 010911155 010911157 010911158 010911163 010911169 010911170 010911172 010911171

Tutor : dr. Subagio

METABOLISM AND NUTRITION MODULE 16th Group

.....................................................................................................................9 1............................................................6 1........................................................................8 1...................................................................................................................................................................................2 The Answer of Learning Issue 1......................................4 Final Mind Mapping...........................................................................................................................................79 3..6 1.............................3 Final Hypothesis ............5 Early Hypothesis .................3 Learning Issue II ...................................2 Group Members ..........................................................11 2........................................................................................7 1......................69 3................................................................................................................3 Keywords ..............................6 1.........11 2...........................................................................................................................................................................6 Obstacles...........4 Additional Information...............................................4 Instructional Objectives ....................................................1 Scenario Creator....................................................................................................1 Methods and Steps to Find the Information............................................................................80 EBL & Critical Appraisal ..............................6 Early Mind Mapping .........................................5 Chapter I : 1st Tutorial .1 Scenario....................................................................................11 2...................................................................5 Group Opinion....................................................83 Appendix (Journal Appraisal) ...................................................................................42 3.........................................................................10 Chapter II : 2nd Tutorial ........................................................4 CONTENTS Cover ................79 References .....2 Main Problem .76 3..............................................................7 Learning Issue 1..................3 Contents .........1 The Answer of Learning Issue 1I.............................................6 1.............................41 Chapter III : 3rd Tutorial ...............42 3.............2 Analysis ...................................................................................97 METABOLISM AND NUTRITION MODULE 16th Group ................77 3.....................................................................91 Journal .......................................................................................................

5 EIGHTH MODULE HUMAN FUNCTION MODULE PROBLEM BASED LEARNING INSTRUCTIONAL OBJECTIVES After finishing this module. METABOLISM AND NUTRITION MODULE 16th Group . students of Airlangga university.School of Medicine in third semester can explain the patophysiology of health problem through understanding the intermediate metabolism.

Female 1.3. sometimes feel tingling in both feet.3. came to the outpatient polyclinic with complaints often sleepy.3 Key Words 1.3. Numbness in both lower extremities 1. Main Problem A woman. Outpatient treatment 1.3.2.1.1 Scenario 1.3. • • Often feels sleepy Often feels sleepy and numbness 1. Sleepy METABOLISM AND NUTRITION MODULE 16th Group .6 CHAPTER I FIRST TUTORIAL 1.4.2.

Occupation: Housewive 1.7. Husband’s occupation: Private Company Officer 1.4.8.4.4.3.4. Surabaya 1.1.4.5.4.4.9.4. age: 41 years old 1.4. Medical Record: No hypertension Body weight has decreased 3 kg recently 1.4 Additional Information 1.7 1. Status: Married with 1 child 1. Woman.4. Almost every night wakes up to go to the toilet 1.6. Physical Examination: Body weight: 89 kg Height: Pulse: RR: 157 cm 80 times per minute 20 times per minute Blood Pressure:120/80 mmHg Body temperature: 37ºC No anemic sign No cyanotic sign No icterus sign Heart and Lung: Normal condition Hepar and Spleen: cannot be sense Abdomen Circle measurement 92 cm No acytes sign No extremity abnormality METABOLISM AND NUTRITION MODULE 16th Group .10. Family Medical Record: Her father passed away due to complication Her brother passed away in the age of 40 years old with smelly and can-not-heal wound in his leg 1. Address: Kupang Indah.4.2. She has been feeling numbness for 1 month 1.

8 1.6 Early Mind Mapping FINANCIAL METABOLISM AND NUTRITION MODULE CONDITION 16th Group .5 Early Hypothesis • • • • • • • Diabetes Mellitus Malnutrition deficiency Anemia Neuron disorders Cardio-vascular disorders Lipid metabolism disorders Hypoxia 1.

cyanotic. 41 y.9 Female.1.o Anamnesis: Tingling Sleepy Weight Loss Physical Examination: Weight 89 kg Height 157cm BP 120/80 mmHg PP 80 tpm RR 20 tpm Temperature 37 ºC Supporting Exam: Hepar & Spleen normal Heart & Lung normal No anemic.7 Learning Issue 1 1. icterus Early hypothesis: DM Malnutrition Deficiency Neuron Disorders 1. What are the causes of drowsiness? METABOLISM AND NUTRITION MODULE 16th Group .7.

7.7.7.7.13 How is the mechanism of numbness/tingling? How is the patophysiology of Diabetes Mellitus? What are the symptoms of Diabetes Mellitus? What is normal stomach circumference of human? What are the risk factors of Diabetes Mellitus? What are the complications of Diabetes Mellitus? What is blood gas analysis? How is the normal blood glucose measurement? How is the normal rate of TG? How is the normal rate of Haemoglobin? What is anion gap? What are the symptoms of anemia? METABOLISM AND NUTRITION MODULE 16th Group .2 1.8 1.3 1.7.7 1.4 1.10 1.9 1.5 1.7.7.7.6 1.11 1.7.7.7.12 1.7.10 1.

1 METHODS AND STEPS TO FIND THE INFORMATION To get the information we need. hypercalcemia. antihistamines) Medical conditions (such as hypothyroidism. Internet We got information from internet in the form of scientific journals and articles. and hyponatremia /hypernatremia) Not sleeping for long enough Sleep disorders (such as sleep apnea syndrome and narcolepsy) METABOLISM AND NUTRITION MODULE 16th Group . our relative’s books. 2. sleeping pills.2 THE ANSWERS OF LEARNING ISSUES I 2.1 • • • • • What are the causes of drowsiness? Having to work long hours or different shifts (nights. Sources in English are cited directly into this report but sources in Indonesian are translated into English first. we got much information both in English and in Indonesian.2. 2. weekends) Medications (tranquilizers. We also bought some books to get more information.11 CHAPTER II SECOND TUTORIAL 2. Text Books We used text books from library. such as: 1. By typing the keywords in the search engine. we use some sources.

The pathophysiology of diabetes mellitus in all forms is related to the insulin hormone. feet. and it passes as soon as you move around a bit.12 2. 2. persistent tingling is a troubling symptom that requires a thorough medical workup. This results in elevated levels of glucose in METABOLISM AND NUTRITION MODULE 16th Group . fats.2. This feeling results from temporary nerve compression and diminished blood flow.2 How is the mechanism of numbness/tingling? Any time you remain still for a long period. particularly if you're leaning on your arm or sitting cross-legged. or ineffective use of. In general. It also aids the body in breaking down the glucose to be used as energy. the body does not break down the glucose in the blood as a result of abnormal insulin metabolism.2. others are based primarily in different parts of the body. cause a persistent tingling sensation — usually in the hands. and proteins because of a lack of. formerly known as "borderline diabetes" is a degree of hyperglycemia that may precede type 2 diabetes. While several of these conditions originate in the peripheral nervous system (the network of nerves branching out from the spinal cord to the extremities). Impaired glucose tolerance. When someone suffers from diabetes. Many medical conditions. the hormone insulin. Insulin is secreted by cells in the pancreas and is responsible for regulating the level of glucose in the bloodstream. however. or legs — that is unrelated to posture and unrelieved by movement. you are bound to develop a pins-and-needles sensation in one or more limbs. however. Diabetes is classified into three primary types that are different disease entities but share the symptoms and complications of hyperglycemia (high blood glucose). arms.3 What are the patophysiologies of Diabetes Melitus? Diabetes is a chronic metabolic disorder in which the body cannot metabolize carbohydrates.

and fatigue. Monitoring II. Type 1 (previously called insulin dependent diabetes mellitus (IDDM) or juvenile onset diabetes) A. B. stress. Exercise 4. and nerve problems can occur. kidney damage. 3. Diet 3.type 1. frequent urination. around 10-12 years of age in girls and 12-14 years in boys. Characteristics 1. Ketosis prone. Causes 1.13 the blood. When 80-90% of the beta-cells are destroyed. Environmental exposure: virus. 2. overt symptoms occur. When glucose levels remain high over an extended period of time. Treatment 1. Diabetes Facts. type 2. eye disorders. * Source: American Diabetes Association. Causes METABOLISM AND NUTRITION MODULE 16th Group . Abrupt onset of signs and symptoms of hyperglycemia: increased thirst and hunger. or adult onset diabetes) A. toxin.* 2. which is known as hyperglycemia. but can occur at any age. Peak incidence occurs during puberty. Type 2 (previously called non-insulin-dependent diabetes mellitus. and gestational. severe complications including cardiovascular disease. Genetic predisposition. Diabetes mellitus occurs in three different forms . Education 5. I. November. Usually occurs before 30 years of age. NIDDM. C. weight loss. Autoimmune reaction: beta-cells that produce insulin in the pancreas are destroyed. 3. 2003. Insulin by injection with syringes or pumps 2.

Frequently obese. 5. Signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans [dirty-neck syndrome]. numbness and tingling of hands and feet. Asian Americans.. Strong genetic predisposition. 2. recurring yeast infection. African Americans. 8. Decreased insulin secretion: pancreas does not secrete enough insulin in response to glucose levels. May also have extreme tiredness. Insulin resistance: unable to utilize insulin that the body makes because of cell-receptor defect. dyslipidemia [lipoproteins inbalance]. Not prone to ketoacidosis until late in course or with prolonged hyperglycemia. May or may not have symptoms of hyperglycemia.14 1.2. Excess production of glucose from the liver: result of defective insulin secretor response. 4. 3. Increased prevalence in some ethnic groups. Characteristics 1. e. but is now occurring in children and adolescents. and Pacific Islanders. Children between the ages of 10-19 that have one or more of the following are at an increased risk: • • • • • • Family history Member of certain ethnic populations listed above in B.g. delayed healing. B. glucose is unable to be absorbed into cells for fuel. METABOLISM AND NUTRITION MODULE 16th Group . Hispanic/Latino. 7. dawn phenomenon (see glossary) is an example. 3. Usually occurs after 30 years of age. hypertension [high blood pressure]. blurred vision. Overweight Sedentary lifestyle Pre-puberty. polycystic ovarian syndrome [PCOS]). 2. 6. Native Americans.

3 mmol/ l) and <140 mg/dl (<7. Education 5. Causes 1. Treatment 1.15 C. C. Monitoring 6. insulin sensitizers. METABOLISM AND NUTRITION MODULE 16th Group . Diet/weight management 2.g. Exercise: program that does not cause fetal distress. Characteristics 1. 3-hour oral glucose tolerance test (OGTT) is indicated. lipid abnormalities) III. Genetic predisposition B. Insulin: if unable to consistently maintain blood glucose <95 mg/dl fasting (<5.8 mmol/l).7 mmol/l) 2 hours postprandial. 3. Gestational Diabetes Mellitus (GDM) A.. Diet: provide adequate calories without hyperglycemia or ketonemia 2. Exercise/increase physical activity 3.8 mmol/l) 1 hour postprandial and <120 mg/dl (<6. a full diagnostic 100-g. hypertension. or hypertension (>140/90 mmHg). contractions. or insulin 4. If the 1-hour screen for glucose is >140 mg/dl (>7. Oral hypoglycemic/antihyperglycemic agents. Insulin resistance due to pregnancy 2. Carbohydrate intolerance during pregnancy identified via 1-hour screen using a 50-g oral glucose load (performed between 24th and 28th week of gestation unless otherwise indicated). Treatment of co morbid conditions (e. Treatment 1.

which may leave you dehydrated. 2. They include dehydration from increased urination and your body's inability to function properly. Presence of ketones may indicate starvation rather than hyperglycemic ketosis. When you lose sugar through frequent urination. If your kidneys can't keep up. you'll urinate even more. including the lenses of your eyes.4 What are the symptoms of Diabetes Mellitus? Excessive thirst and increased urination Excessive thirst and increased urination are classic diabetes signs and symptoms. At the same time. Blurred vision Diabetes symptoms sometimes involve your vision.2. you also lose calories. diabetes can cause new blood vessels to form in your retina — the back part of your eye — as well as damage established vessels. excess sugar (glucose) builds up in your blood. High levels of blood sugar pull fluid from your tissues. Weight loss Weight fluctuations also fall under the umbrella of possible diabetes signs and symptoms. especially if you have type 1 diabetes. Your kidneys are forced to work overtime to filter and absorb the excess sugar.16 D. Many factors can contribute to this. the excess sugar is excreted into your urine along with fluids drawn from your tissues. For most METABOLISM AND NUTRITION MODULE 16th Group . As you drink more fluids to quench your thirst. Blood glucose: required to determine effectiveness of treatment and possible need for insulin. diabetes may keep the sugar from your food from reaching your cells — leading to constant hunger. Left untreated. Monitoring 1. since it's less able to use sugar for energy needs. Fatigue You may feel fatigued. This triggers more frequent urination. 2. The combined effect is potentially rapid weight loss. When you have diabetes. Ketones: test for ketones using first morning urine sample. Glucose should be checked fasting and 1-2 hours postprandial. This affects your ability to focus.

stage 1 has been ongoing since early 1990. It may be that high levels of blood sugar impair your body's natural healing process and your ability to fight infections. hands. Red. In fact. swollen. these early changes do not cause vision problems. has not proved whether this is entirely true. You may notice tingling and loss of sensation in your hands and feet. bladder and vaginal infections are especially common. Slow-healing sores or frequent infections Doctors and people with diabetes have observed that infections seem more common if you have diabetes. legs and feet. Since then the Indonesian people begin to experience obesity. more cases of abdominal fat due to diet and an increasingly unbalanced motion. particularly in urban areas. This will trigger the spread of various diseases metabolic disorders. If more than that. For women. then it could be said he was experiencing abdominal obesity. If someone has abdominal circumference more than the normal number. nor why. unhealthy lifestyle diseases (metabolic syndrome). if these changes progress undetected. Your gums may pull away from your teeth.5 What is normal stomach circumference of human? To determine whether suffering abdominal obesity or not. Tingling hands and feet Excess sugar in your blood can lead to nerve damage. they sign congested hormone bad fats in the stomach. they can lead to vision loss and blindness. Especially since the fast-food METABOLISM AND NUTRITION MODULE 16th Group . which increases the risk of infection in your gums and in the bones that hold your teeth in place.17 people. women's waist size 90 inches biggest meter and men's 80 inch meter. tender gums Diabetes may weaken your ability to fight germs. 2.2. What causes obesity? It is said that there are two factors causing the genetic and lifestyle factors. your teeth may become loose. as well as burning pain in your arms. However. Research in this area. however. the people of Indonesia have the ideal waist size. or you may develop sores or pockets of pus in your gums — especially if you have a gum infection before diabetes develops. However. Usually.

thickened skin around the neck or armpits METABOLISM AND NUTRITION MODULE 16th Group . Furthermore. and bearing.6 What are the risk factors of Diabetes Mellitus? You have a higher risk for diabetes if you have any of the following: • • • • • • • • • • • • Age greater than 45 years Diabetes during a previous pregnancy Excess body weight (especially around the waist) Family history of diabetes Given birth to a baby weighing more than 9 pounds HDL cholesterol under 35 mg/dL High blood levels of triglycerides. because the fat inside the abdomen. 2. Meanwhile. there are a lot of the mobility of free fatty acids to the liver and muscles. the hormone is more dangerous. a type of fat molecule (250 High blood pressure (greater than or equal to 140/90 mmHg) Impaired glucose tolerance Low activity level (exercising less than 3 times a week) Metabolic syndrome Polycystic ovarian syndrome mg/dL or more) A condition called acanthosis nigricans. The hormone estrogen source of fat in the thighs. the center of power. the pattern of motion (sports) in the stomach the less.18 restaurants to grow and increasingly giving kemudahkan for people to eat all the time.2. rather than under a layer of skin. on the contrary in the stomach. Whereas most high mobility of fat in the abdomen and the nature of fat is more dangerous than the fat in the thighs or in other organs. which causes dark. it will affect the fatty acid metabolism and pancreatic work. Also explained that the fat can not be removed through liposuction. and in abdominal fat.

and Native Americans. If too much lactic acid stays in the METABOLISM AND NUTRITION MODULE 16th Group .7 What are the complications of Diabetes Mellitus? Without proper management it can lead to various complications such as cardiovascular disease. blindness and nerve damage. have exercised more than anticipated or have not eaten enough). Cells make lactic acid when they use glucose for energy. It mainly affects people with type 1 diabetes. Hypoglycaemia can be corrected rapidly by eating some sugar. (MedlinePlus. kidney failure. Short-term complications: • Low blood sugar (hypoglycaemia) A person who takes insulin is going to face the problem of their blood sugar falling too low at some point (because they have overestimated the insulin they need. have a higher risk for diabetes. • Lactic acidosis Lactic acidosis is the build up of lactic acid in the body. It is important that the person with diabetes recognises the signs of hypoglycaemia.19 Persons from certain ethnic groups. If it is not corrected it can lead to the person losing consciousness. The body cannot tolerate large amounts of ketones and will try to get rid of them through the urine. • Ketoacidosis When the body breaks down fats. causing ketoacidosis. Ketoacidosis is a severe condition caused by lack of insulin. acidic waste products called ketones are produced. 2010) 2. Hispanic Americans. the body cannot release all the ketones and they build up in your blood. Regular testing of blood sugar levels should begin at a younger age. Everyone over 45 should have a blood sugar (glucose) test at least every 3 years. and be performed more often if you are at higher risk for diabetes.2. However. including African Americans. Asian Americans.

Long-term complications: • Eye disease (retinopathy) Eye disease. the eye. pain in the foot and problems with the functioning of different parts of the body including the heart. These injuries can lead to ulcers and possibly amputation. ringworm and vaginal infections. About 2% of all people who have had diabetes for 15 years become blind. There are different types of nerve disease which can result in a loss of sensation in the feet or in some cases the hands.20 body. • Bacterial/fungal infections People with diabetes are more prone to bacterial and fungal infections. Bacterial infections include sties and boils. Lactic acidosis is rare and mainly affects people with type 2 diabetes. or neuropathy affects at least half of all people with diabetes. IDF fact sheet on diabetes and kidney disease • Nerve disease (neuropathy) Diabetic nerve disease. the bladder and the penis. Fungal infections include athlete’s foot. or retinopathy. IDF fact sheet on diabetes and eye disease • Kidney disease (nephropathy) Diabetes is the leading cause of kidney disease (nephropathy). while about 10% develop a severe visual impairment. A lack of sensation in the feet can lead to people with diabetes injuring their feet without realising it. is the leading cause of blindness and visual impairment in adults in developed societies. • Diseases of the circulatory system METABOLISM AND NUTRITION MODULE 16th Group . About one third of all people with diabetes develop kidney disease and approximately 20% of people with type 1 diabetes develop kidney failure. the stomach. the balance tips and the person begins to feel ill.

SI Units pH Adults Panic values Children Birth to 2 months 2 months to 2 years >2 years PaCO2 Panic values 7.7–5.2. Must be corrected for body temperature. 2010) 2.49 7. People with diabetes are 15 to 40 times more likely to require lower-limb amputation compared to the general population. (International Diabetes Federation.46 7.32–7. It is the main cause of disability and death for people with type 2 diabetes in industrialized countries.35–7.2 and >7. accounts for 75% of all deaths among people with diabetes of European origin.2 and >7.34–7.3 kPa <2.35–7.6 7.35–7.45 ≤7.8 What is the blood gas analysis? Blood Gases.6 METABOLISM AND NUTRITION MODULE 16th Group .32–7.45 ≤7. corony heart disease is present in between 8% and 20% of people with diabetes over 45 years of age.7 kPa 7.46 7.35–7. IDF fact sheet on diabetes and cardiovascular disease • Amputation Diabetes is the most common cause of amputation that is not the result of an accident.49 7.21 Disease of the circulatory system.34–7.45 4. Arterial (ABG)—Blood Norm. In the USA. or cardiovascular disease. Their risk of heart disease is 2-4 times higher than those who do not have diabetes.45 35–40 mm Hg <20 mm Hg 7.

metolazone. sodium bicarbonate. emphysema. ethacrynic acid. pleurisy. duodenal). metabolic alkalosis. prednisone. asthma (late stage).4 kPa <5. pneumonia. Drugs include sodium bicarbonate. pleural effusion. near drowning. hyperemesis. intestinal obstruction (pyloric. hysteria.96–1. aminoglycoside toxicity. shock. Cushing's disease. brain death. empyema. renal disease. diarrhea. Acute intermittent porphyria. renal disorders. hypoventilation (alveolar). pulmonary infection. Increased PaO2. tetralogy of Fallot. peptic ulcer therapy. salicylate intoxication.22 SI Units >70 mm Hg PaO2 Panic values HCO3Panic values O2 Saturation Panic value <40 mm Hg 22–31 mEq/L <10 mEq/L >40 mEq/L 96%–100% <60% >9. and thiazides.7–13. respiratory alkalosis. Increased PaCO2. Drugs include aldosterone. pulmonary edema. poisoning.00 <0. hyperventilation.3 kPa 22–31 mmol/L <10 mmol/L >40 mmol/L 0. and vomiting. hyaline membrane disease. electrolyte disturbance (severe). METABOLISM AND NUTRITION MODULE 16th Group . congestive heart failure. Hyperbaric oxygenation and hyperventilation. hypothyroidism (severe).3 kPa Oxyhemoglobin Dissociation Curve No shift Increased pH. pneumothorax. respiratory acidosis. metabolic alkalosis. fever.60 80–100 mm Hg 10. Alkali ingestion. coarctation of the aorta. respiratory failure. transposition of the great vessels. high altitude. and vomiting (excessive).

diabetes mellitus. Addison's disease. fever. high altitude. diabetic ketoacidosis. asthma. pulmonary edema. Hamman-Rich syndrome. increased oxygen affinity for hemoglobin. High altitudes. Dysrhythmias. hypocapnia. pickwickian syndrome. respiratory alkalosis. METABOLISM AND NUTRITION MODULE 16th Group . head injury. myocardial infarction. Acute respiratory distress syndrome. dimercaprol. pulmonary infection. hyperbaric oxygenation. coarctation of the aorta. nitrofurantoin. hyaline membrane disease. Decreased PaCO2. nephritis. cerebrovascular accident. positive end-expiratory pressure (PEEP) added to mechanical ventilation. Increased O2 Saturation. methicillin sodium. renal disease. Decreased PaO2. hypercapnia. nephrosis. nitrofurantoin sodium. Drugs include acetazolamide. tetracycline. sepsis. berylliosis. atrial septal defect. hyperventilation. flail chest. and triamterene. diarrhea. metabolic alkalosis. asthma. atelectasis. diabetic ketoacidosis. anoxia. pneumonia. lymphangitic carcinomatosis. hypothermia.23 Increased HCO3-. dysrhythmias. Anoxia. emphysema. phrenic nerve paralysis. respiratory alkalosis. metabolic acidosis. carbon monoxide poisoning. and respiratory acidosis. cardiac disease. hypercapnia. and shock. pulmonary embolism. respiratory acidosis (also caused by large volumes of lactated Ringer's). oxygen therapy. near drowning. arteriovenous shunt. malignant hyperthermia. metabolic acidosis. respiratory failure. anesthesia. pulmonary obstructive disease. hypoventilation. aortic valve stenosis. Decreased pH. pulmonary malignancy. emphysema. asthma (early stage). hypoventilation. and salicylate intoxication. increased cardiac output. lung resection. hepatic disease.

pneumonia. pleural effusion. decreased cardiac output. head injury. pneumothorax. pulmonic stenosis. hypoventilation. pulmonary pulmonary hemangioma. See diagram. pickwickian syndrome. pulmonary adenomatosis. carbon monoxide poisoning. congenital heart defects. transposition of the great vessels. pleural effusion. pain causing restricted diaphragmatic breathing. hypercapnia. 2. flail chest. Shift to Left. hypocapnia. and ventricular septal defect. atelectasis. berylliosis. shock. pulmonary embolism. metabolic acidosis. Decreased HCO3-. anesthesia. hypothermia. pulmonic stenosis. near drowning. pulmonary poisoning. coarctation of the aorta. aortic valve stenosis. infection. poliomyelitis pulmonary (acute). tetanus. cerebrovascular accident. fever. shock. respiratory failure. tricuspid atresia. tricuspid atresia. METABOLISM AND NUTRITION MODULE 16th Group . decreased oxygen affinity for hemoglobin. lymphangitic carcinomatosis. smoke inhalation. Hypocapnia. and ventricular septal defect. respiratory failure. poisoning. respiratory acidosis.24 pain causing restricted diaphragmatic breathing. tetanus. status epilepticus. sarcoidosis. hypoxia.3-DPG deficiency. transposition of the great vessels. Oxyhemoglobin Dissociation Curve. pulmonary hemangioma. pneumonia. high altitude. pneumothorax. pulmonary infection. asthma. anoxia. poliomyelitis (acute). arteriovenous shunt. hyaline membrane disease. phrenic nerve paralysis. embolism. smoke inhalation. emphysema. adenomatosis. Hamman-Rich syndrome. Decreased O2 Saturation. and respiratory alkalosis. and respiratory alkalosis. atrial septal defect. sarcoidosis. lung resection. anorexia. status epilepticus. Acute respiratory distress syndrome.

Any alteration in the ratio between bicarbonate and carbonic acid will cause a reciprocal change in release or uptake of free H+. The partial pressure of oxygen (pO 2. counteracting the pH reduction and increasing the breathing rate. more CO2 dissociates from carbonic acid and is exhaled through the lungs. and respiratory acidosis. Significant deviations in pH can be life threatening. SaO 2 applies to arterial hemoglobin saturation: The oxyhemoglobin dissociation curve represents the affinity of hemoglobin for oxygen by demonstrating the normal levels of arterial oxygen saturation (O2Sat. increased production of 2. The kidneys and lungs regulate pH by preserving the ratio of acid to base. which are buffered as either an acid (HCO3-) or a base (H2CO3). thereby altering pH value. fever.3DPG. Description. The arterial blood gas test measures the dissolved oxygen and carbon dioxide in the arterial blood and reveals the acid-base state and how well the oxygen is being carried to the body. emphysema.25 Shift to Right. SaO2) of hemoglobin at varying partial pressures of oxygen. The partial pressure of carbon dioxide (pCO2. Cluster headaches. The METABOLISM AND NUTRITION MODULE 16th Group . Intracellular metabolism results in the continuous production of hydrogen ions. P-50 is the partial pressure of oxygen at which the given hemoglobin sample is 50% saturated. Oxygen saturation (O2Sat) is the amount of oxygen actually bound to hemoglobin (as a percentage of the maximum amount that could be bound) and available for transport throughout the body. The body demands that pH remain constant. hypercapnia. The pH is the measurement of free H+ ion concentration in circulating blood. Both bicarbonate (HCO3-) and carbonic acid (H2CO3) are components of the body's acid-base system that influence pH. PaO2) is the amount of oxygen dissolved in plasma and represents the status of alveolar gas exchange with inspired air. When pH decreases. PaCO2) is the amount of carbon dioxide in the blood based on the pressure it exerts in the bloodstream and represents the degree of alveolar ventilation occurring.

2 or >7.32–7. Arterial—Blood .5 kPa 17–23 mEq/L 17–23 mmol/L <10 mEq/L >40 mEq/L <10 mmol/L >40 mEq/L 0. less oxygen is delivered to the tissues. SI Units pH Panic value pCO2 pO2 HCO3Panic values 7.6 35–45 mm Hg 4.6–6. Must be corrected for body temperature. Increased HCO3-. Interpretation of oxygen levels is not appropriate on venous blood specimens.80 O2 Saturation 60%–80% Increased pH. When the curve is shifted to the left.6 7.6–6.32–7. Blood Gases. Increased pO2. See Blood gases.43 <7.2 or >7. Increased pCO2. when the shift is to the right.60–0. Generally. Arterial—Blood . Venous—Blood Norm. METABOLISM AND NUTRITION MODULE 16th Group .0 kPa 20–49 mm Hg 2.26 Hem-O-Scan machine analyzes and plots the hemoglobin-oxygen dissociation on a curve. more oxygen is delivered to the tissues for a given partial pressure of oxygen. See Blood gases.43 <7. decreased oxygen saturation to less than 90%–92% must be addressed by thorough assessment of the client and clinical status.

Arterial— Blood for complete descriptions of the test components.27 See Blood gases. Decreased O2 Saturation.6 METABOLISM AND NUTRITION MODULE 16th Group . Interpretation of oxygen saturation is not appropriate on venous blood specimens. Venous blood gases may be used in situations where assessment of oxygenation is unnecessary. See Blood gases.2 or >7.) Blood Gases. Decreased pO2. Arterial—Blood . Decreased HCO3-. A method for assessing acid-base status and for cellular hypoxia without performing an arterial puncture.35–7. Description. Interpretation of oxygen levels is not appropriate on venous blood specimens.6 7. Interpretation of oxygen saturation is not appropriate on venous blood specimens. See Blood gases. Decreased pCO2. Increased O2 Saturation.45 <7. Must be corrected for body temperature.45 <7.2 or >7. SI Units pH Adults Panic values 7. Capillary—Blood Norm. Arterial—Blood .35–7. Arterial—Blood . (See Blood gases. See Blood gases. Decreased pH. Arterial—Blood .

60 2 months to 2 years 7. Arterial—Blood .28 SI Units Children (arterialized capillary sample) Birth to 2 months >2 years pCO2 Panic values pO2 Panic values HCO3Panic values O2 Saturation Panic value 7.45 <2. Increased O2 Saturation.45 <20 mm Hg >70 mm Hg 75–100 mm Hg <40 mm Hg 22–26 mEq/L <10 mEq/L >40 mEq/L 96%–100% <60% 7. METABOLISM AND NUTRITION MODULE 16th Group .35–7.7 kPa >9.3 kPa <5. Increased pCO2. See Blood gases.49 7.2 mm Hg 3. Increased HCO3-.3 kPa 22–26 mmol/L <10 mmol/L >40 mmol/L 0.0–13. See Blood gases.00 <0. Arterial—Blood .4–41.34–7.4 kPa 10.34–7. Arterial—Blood . Arterial—Blood . Increased pO2.5–5. See Blood gases. Arterial—Blood .46 26.35–7.4 kPa Increased pH.96–1. Decreased pH.49 7. See Blood gases. See Blood gases.32–7.32–7.46 7.

In normal clients. Dependent on time and content of last meal. Arterial—Blood .4 mmol/L METABOLISM AND NUTRITION MODULE 16th Group . See Blood gases. Decreased pO2.9 mmol/L 3.8 mmol/L 60–89 mg/dL 68–98 mg/dL 3. glucose levels return to the fasting level (given in these norms) within 2 hours after the last meal. Arterial—Blood .8–5. Arterial—Blood .1–4.9 How is the normal blood glucose measurement? Glucose—Blood Norm.2. 2008) 2. Arterial—Blood . Decreased HCO3-. for complete description of the test components.29 See Blood gases.9–2. Arterial .6 mmol/L 0. Decreased O2 Saturation. SI Units Whole Blood Adults >60 years Children Cord blood Premature infant 38–82 mg/dL 17–51 mg/dL 2. Capillary pO2 interpretation is limited to assessment for hypoxia. Used mostly in infants to assess pH and pCO2. Description.) (Chernecky & Berger. See Blood gases.3–4. Decreased pCO2. See Blood gases. A method for determining acid-base status from a heel stick for capillary blood. (See Blood gases.

5 mmol/L 65–100 mg/dL 80–115 mg/dL 3.8–4.4 mmol/L 25–51 mg/dL 34–51 mg/dL 42–68 mg/dL 51–85 mg/dL 1. cerebrovascular accident.30 SI Units Neonate Newborn to 24 hours Newborn >24 hours Child Serum Adults >60 years Children Cord blood Premature infants Neonates Newborn to 24 hours Newborn >24 hours Child 45–96 mg/dL 20–60 mg/dL 30–60 mg/dL 40–60 mg/dL 50–80 mg/dL 60–100 mg/dL 2. hypervitaminosis A (chronic).8–4.3 mmol/L 2. carbon monoxide poisoning. burns. pancreatic carcinoma. convulsions.4–2.5 mmol/L 4.6–5. hemorrhage. encephalitis. Panic Levels Adults Neonates <40 mg/dL or >700 mg/dL <2.8 mmol/L 2. myocardial infarction.5–5.3 mmol/L 2. malnutrition (chronic). cystic fibrosis. gigantism. infections.3–3.3 mmol/L 1. hyperadrenalism. hyperpituitarism. injury. erectile dysfunction.3–5. eclampsia.2–3.1–3.8 mmol/L 2. meningitis. hyperthyroidism. obesity.0 mmol/L Increased. hemochromatosis. Cushing's disease.9–2.8 mmol/L 1.2 mmol/L or >38.6 mmol/L >16. hyperosmolar hyperglycemic nonketotic coma (HHNK). diabetes mellitus.4 mmol/L 3. Cushing's syndrome. pancreatic METABOLISM AND NUTRITION MODULE 16th Group .6 mmol/L <30 mg/dL or >300 mg/dL <1.7 mmol/L NOTE: Whole-blood glucose values are about 15% less than serum glucose values because of greater dilution.7–3. Acromegaly.3 mmol/L 1. anesthesia. hypertension.4–6.

haloperidol. metronidazole. stress. hepatic phosphorylase deficiency (type VI glycogen storage disease). hydralazine hydrochloride. risperidone. epinephrine hydrochloride. reserpine. corticosteroids. fructose intolerance. hypothyroidism. glucose infusions. insulinoma. lithium carbonate. asparaginase. sodium. exercise. muscle phosphofructokinase deficiency (type VII glycogen storage disease). atenolol. corticotropin. hydrochlorothiazide. thiazides/thiazide diuretics. tetracyclines. levodopa. thyroglobulin. nalidixic acid. carcinoma (adrenal gland. phenytoin oxazepam. pancreatic islet cell tumor. maple syrup urine disease. Drugs include anabolic steroids. isoniazid. chlorthalidone. insulin overdose (factitious hypoglycemia).31 insufficiency. cretinism. acid. hypopituitarism. methyldopate (hydrochloride). pituitary adenoma. ethacrynic acid. Forbes' disease (type III glycogen deposition disease). methyldopa. postoperatively (after gastrectomy or METABOLISM AND NUTRITION MODULE 16th Group . nicotinic acid. estrogens. glucagon deficiency. androgens. alcoholism. terbutaline sulfate. propranolol (in diabetic clients). kwashiorkor. mercaptopurine. cimetidine. baclofen. pancreatitis (chronic). phenolphthalein. Addison's disease. sildenafil. benzodiazepines. hepatitis. methimazole. epinephrine. and Wernicke's encephalopathy. subarachnoid hemorrhage. isoproterenol hydrochloride. dextran. disopyramide phosphate. pancreatitis. cirrhosis. myxedema. hyperinsulinemia. imipramine. levothyroxine sodium/T4. protease inhibitors. leucine sensitivity. arginine. pregnancy. Decreased. adrenal medulla unresponsiveness. p-aminosalicyclic progestins. dumping syndrome. infant of diabetic mother. stomach. pheochromocytoma. niacin. propylthiouracil. epinephrine bitartrate. ritodrine hydrochloride. ascorbic acid. nicotine. diabetes mellitus (early). meperidine. thyroid medications. oral contraceptives. magnesium hydroxide (prolonged high doses). dextrothyroxine. diazoxide. clonidine. bisacodyl (prolonged use). indomethacin. phenytoin. malnutrition. chlorpromazine. promethazine hydrochloride. tolbutamide (SMA methodology). rifampin. heparin sodium. furosemide. heparin calcium. galactosemia. shock. fever. hypothermia. trauma. aspirin. fibrosarcoma). epinephrine borate. and triamterene.

phenelzine sulfate. propranolol (in diabetics). gypsum) taken in combination. isoniazid. vomiting. clofibrate. mesha shringi. and Zetterstrom syndrome. isocarboxazid. syzigium cumini (jamun). guar gum. It is also formed from the digestion of carbohydrates and the conversion of glycogen by the liver and is the body's main source of cellular energy. thyroxine. Excess glucose is stored as glycogen in the liver and muscle cells. Herbs or natural remedies include teas (decoctions. Hormones influencing glucose metabolism include insulin. A randomly timed test for glucose is usually performed for routine screening and nonspecific evaluation of METABOLISM AND NUTRITION MODULE 16th Group .' Scrophularia ningpoensis. pargyline hydrochloride. aspirin. caffeine. Reye's syndrome. potato yam) and huang qi (‘yellow-old 60. postprandial hypoglycemia. glucagon. cerivastatin. Description. Glucose is essential for brain and erythrocyte function. tundika (Coccinia indica). allopurinol. guanethidine sulfate. Fasting glucose levels are used to help diagnose diabetes mellitus and hypoglycemia.' Astragalus reflexistipulus.32 gastroenterostomy). nitrazepam.' Atractylodes lancea. shan yao (‘mountainmedicine. ovata) taken in combination. p-aminosalicylic acid. xuan shen (‘black ginseng. and epinephrine. figwort) and cang zhu (‘green-shu/zhu herb. ginseng. Herbs or natural remedies include zhi mu (‘knowmother. var. methi (fenugreek leaves).' calcium sulfate. chlorpropamide. hoantchy. balsam apple) taken in combination with chlorpropamide.' Anemarrhena asphodeloides. Waterhouse-Friderichsen syndrome. cortisol. Glucose is a monosaccharide found naturally occurring in fruits. amphetamines. phenformin. beta-adrenergic blockers. theophylline. gatifloxacin. Drugs include acetaminophen. Simmonds' disease. and tranylcypromine sulfate. somatostatin. oral hypoglycemic agents. phenacetin. or A.' Dioscorea batatas. tetracyclines. von Gierke's disease (type I glycogen storage disease). an herb) and shi gao (‘stone-plaster. ethyl alcohol (ethanol). marijuana. atenolol. karela. Indian milkweed vine). edetate disodium. infusions) containing chromium. insulin. meshasringi (Gymnema sylvestre. yellow vetch) taken in combination. phenazopyridine. and karela (Momordica charantia.

Cushing's syndromea. cerebral).7 mmol/L 3. pheochromocytoma. 2-Hour Postprandial—Serum Norm.6–7. dumping syndrome (after gastrectomy). Decreased. sepsis. lipoproteinemias. infarction (myocardial. pancreatitis.8 mmol/L American Diabetes Association diagnosis of diabetes >200 mg/dL >11 mmol/L (after 75-g glucose load) Usage. cirrhosis. METABOLISM AND NUTRITION MODULE 16th Group . Glucose. brain tumor.33 carbohydrate metabolism. malignancy. emotional). Increased. hepatic disease (chronic). nephrotic syndrome. preeclampsia. Screening for diabetes mellitus and assessing control of hyperglycemia.6–8.3 mmol/L 3. pregnancy. anxiety. SI Units Newborn to 50 years 50–60 years >60 years 65–140 mg/dL 65–150 mg/dL 65–160 mg/dL 3. anoxia. hyperlipoproteinemia. malnutrition. and stress (physical. Drugs include those discussed under Glucose—Blood. hyperthyroidism. diabetes mellitus. Acromegaly. convulsive disorders. The American Diabetes Association criteria for diagnosis of diabetes mellitus include a fasting plasma glucose level of >126 mg/dL (7 mmol/L).6–8. Cushing's disease.

11–1.11–2.66 mmol/L SI Units METABOLISM AND NUTRITION MODULE 16th Group . hypoglycemia.38 mmol/L 0. insulinoma. hypothyroidism. Drugs include those discussed under Glucose—Blood.24 mmol/L 10–100 mg/dL 10–110 mg/dL 10–122 mg/dL 10–134 mg/dL 10–147 mg/dL 0.11–1. anterior pituitary insufficiency.11–2.11–1. hyperinsulinism. malabsorption syndrome.51 mmol/L 0.34 Addison's disease.11–2.77 mmol/L 0.2.24 mmol/L 0. myxedema.11–1. congenital adrenal hyperplasia.11–1.11–2.10 How is the normal rate of TG? Triglycerides—Blood Norm. steatorrhea.05 mmol/L 0. and von Gierke's disease.22 mmol/L 0. glucose should return to fasting levels within 2 hours after the ingestion of the test meal.11–1. hypopituitarism. adrenal insufficiency. In normal clients.13 mmol/L 0. (Chernecky & Berger. 2008) 2. Serum Values Adult Females 20–29 years 30–39 years 40–49 years 50–59 years >59 years Adult Males 20–29 years 30–39 years 40–49 years 50–59 years >59 years 10–157 mg/dL 10–182 mg/dL 10–193 mg/dL 10–197 mg/dL 10–199 mg/dL 0.18 mmol/L 0. islet cell adenoma. The 2-hour postprandial glucose test is the measurement of serum glucose level 2 hours from the beginning of a meal containing a specific amount of carbohydrate. hepatic insufficiency. Description.

35 Serum Values Children Female: 1–19 years Male: 1–19 years 10–121 mg/dL 10–103 mg/dL SI Units 0. Decreased. pancreatitis. nephrotic syndrome. asparaginase. metformin. gemfibrozil. chronic obstructive pulmonary disease. niacin.5 mmol/L >11. obesity.3–4. Tangier disease. and soy.11–1. hyperalimentation. heparin. pravastatin. arteriosclerosis. garlic (aged extract taken over time). Abetalipoproteinemia. prolonged high-fat). aortitis. starvation (early). myxedema.16 mmol/L NOTE: Plasma values are lower by about 3%. hepatic cholesterol ester storage disease. clofibrate.11–1. aortic aneurysm. renal insufficiency (chronic). miconazole (intravenous). and spironolactone. hypercholesterolemia. hyperthyroidism. ethyl alcohol (ethanol). myocardial infarction (for up to 1 year).3 mmol/L 400–1000 mg/dL 4. diet (recent high-carbohydrate.5–11. Tobacco use. glycogen storage diseases. diabetes mellitus. gout. stress. and malnutrition. oral contraceptives. metabolic syndrome (>150 mg/dL). Drugs include cholestyramine. hypothyroidism.36 mmol/L 0. and sulfonylureas. and von Gierke's disease. phenformin. Herbal or natural remedies include Cordyceps sinensis. estrogens. lovastatin. dextrothyroxine. corticosteroids. cirrhosis (portal). familial hypertriglyceridemia. malabsorption. fat embolism. pregnancy. acanthocytosis.3 mmol/L >1000 mg/dL . Classification of Triglyceride Levels Borderline high 200–400 mg/dL High Very high Increased. METABOLISM AND NUTRITION MODULE 16th Group 2. Alcoholism. Drugs include ascorbic acid. hyperlipoproteinemia.

and chylomicron levels when categorizing a client's serum into lipoprotein phenotypes that represent genetic lipoprotein abnormal-ities. SI Units Females Pregnant Males Children Neonates 3 months 1–2 years 6–10 years 14–27 g/dL 10–17 g/dL 9–15 g/dL 11–16 g/dL >20 g/dL 8. Dietary triglycerides are carried as part of chylomicrons through the lymphatic system and bloodstream to adipose tissue. They may be later retrieved and formed into glucose through gluconeogenesis when needed by the body.58–9.76 mmol/L 6.3–9.6–18.90 mmol/L 6. where they are released for storage.10 mmol/L >12. Triglyceride levels are taken into consideration with total cholesterol.44–11.31 mmol/L 6. Triglycerides are also synthesized in the liver from fatty acids and from protein and glucose above the body's current needs and then stored in adipose tissue.17 mmol/L Panic Levels <5 g/dL METABOLISM AND NUTRITION MODULE 16th Group .0 g/dL 8. (Chernecky & Berger.45–9.2. Treatments differ for the different phenotypes.55 mmol/L 5. Also known as “fat.41 mmol/L 12–16 g/dL 10–15 g/dL 7.82–9.92 mmol/L <3.11 How is the normal rate of Haemoglobin? Hemoglobin (Hb.36 Description. Hgb) Norm.21–10. high-density lipoprotein cholesterol.9 mmol/L 13.69–16.” triglyceride is a compound consisting of fatty acid or glycerol ester that constitutes a major part (up to 70%) of very-low-density lipoproteins (VLDLs) and a small part (<10%) of low-density lipoproteins (LDLs) in fasting serum samples. 2008) 2.

platelet apheresis. Drugs include gentamicin. lymphoma. polycythemia vera. tetralogy of Fallot. hyperthyroidism. Decreased. monoamine oxidase inhibitors. hemolytic reaction to chemicals or drugs or prosthetics. hypothyroidism. severe hemorrhage. hydantoin derivatives. Burns (severe). and zidovudine (AZT). antineoplastic agents. fluid retention. renal cortical necrosis. pregnancy. Each erythrocyte contains approximately 300 million molecules of hemoglobin.” Heme contains iron atoms and the red pigment porphyrin. systemic lupus erythematosus. fatty liver. diarrhea. and pentoxifylline. fat emboli. aspirin. sulfonamides. Andersen's disease. indomethacin. chronic obstructive pulmonary disease (COPD). 2008) 2. erythrocytosis. dehydration.12 What is anion gap? METABOLISM AND NUTRITION MODULE 16th Group . methyldopa.2. hydremia of pregnancy. carcinomatosis. primaquine. cirrhosis. high altitudes.37 Increased. anemia (iron deficiency). It is composed of amino acids that form a single protein called “globin” and a compound called “heme. rifampin. hemolysis. hemoconcentration. vegetarian diet. intravenous overload. Description. snorers. hypervitaminosis A. sarcoidosis. cystic fibrosis. congestive heart failure. (Chernecky & Berger. Drugs include antibiotics. leukemia. idiopathic steatorrhea. Also conditions that increase red blood cells (RBCs). tridione. Apresoline (hydralazine HCl with hydrochlorothiazide). Hodgkin's disease. and transfusion of incompatible blood. hemorrhage. Hemoglobin is the oxygen-carrying pigment of the RBCs. hemorrhage. intestinal obstruction (late). and thrombotic thrombocytopenic purpura. conditions that decrease RBCs. Also.

38 Definition & Clinical Use The term anion gap (AG) represents the concentration of all the unmeasured anions in the plasma. The acid anions (eg lactate. K+ can vary over a wider range and have more effect on the measured Anion Gap.[Cl-] . In Renal Units.[Cl-] .[HCO3-] Reference range is 8 to 16 mmol/l. This alternative formula is: AG = [Na+] + [K+] . The H+ produced reacts with bicarbonate anions (buffering) and the CO2 produced is excreted via the lungs (respiratory compensation). AG is calculated from the following formula: Anion gap = [Na+] . Major Clinical Uses of the Anion Gap • To signal the presence of a metabolic acidosis and confirm other findings METABOLISM AND NUTRITION MODULE 16th Group . An alternative formula which includes K+ is sometimes used particularly by Nephrologists. The negatively charged proteins account for about 10% of plasma anions and make up the majority of the unmeasured anion represented by the anion gap under normal circumstances.[HCO3-] The reference range is slightly higher with this alternative formula. sulphate) produced during a metabolic acidosis are not measured as part of the usual laboratory biochemical profile. The [K+] is low relative to the other three ions and it typically does not change much so omitting it from the equation doesn’t have much clinical significance. The net effect is a decrease in the concentration of measured anions (ie HCO3) and an increase in the concentration of unmeasured anions (the acid anions) so the anion gap increases. acetoacetate.

39

Help differentiate between causes of a metabolic acidosis: high anion gap versus normal anion gap metabolic acidosis. In an inorganic metabolic acidosis (eg due HCl infusion), the infused Cl- replaces HCO3 and the anion gap remains normal. In an organic acidosis, the lost bicarbonate is replaced by the acid anion which is not normally measured. This means that the AG is increased.

To assist in assessing the biochemical severity of the acidosis and follow the response to treatment

The Anion Gap can be Misleading It is determined from a calculation involving 3 other measured ions, so the error with an AG is much higher than that of a single electrolyte determination. The commonest cause of a low anion gap is laboratory error in the electrolyte determinations. The 95% error range for the AG is about +/- 5 mmol/l (ie a 10mmols/l range!) If the AG is greater than 30 mmol/l, than it invariably means that a metabolic acidosis is present. If the AG is in the range 20 to 29 mmol/l, than about one third of these patients will not have a metabolic acidosis. Other clinical guides should also be used in deciding on the presence and severity of a metabolic acidosis. Significant lactic acidosis may be associated with an anion gap which remains in the reference range. Lactate levels of 5 to 10 mmols/litre are associated with a high mortality if associated with sepsis, but the AG may be reported as within the reference range in as many as 50% of these cases! (Dorwart & Chalmers 1975). The anion gap is useful especially if very elevated or used to confirm other findings. Causes of a high anion gap acidosis can be sorted out more specifically by using other investigations in addition to the history and examination of the patient. Investigations which may be very useful are:

METABOLISM AND NUTRITION MODULE 16th Group

40

• • • •

Lactate Creatinine Plasma glucose Urine ketone test

Key Fact: Hypoalbuminaemia causes a low anion gap
Albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. Every one gram decrease in albumin will decrease anion gap by 2.5 to 3 mmoles. A normally high anion gap acidosis in a patient with hypoalbuminaemia may appear as a normal anion gap acidosis. This is particularly relevant in Intensive Care patients where lower albumin levels are common. A lactic acidosis in a hypoalbuminaemic ICU patient will commonly be associated with a normal anion gap. 2.2.13 What are the symptoms of anemia? The severities of the clinical features are dependent not only on the degree of anemia, but on the rapidity of its development. Common symptoms are general fatigue and lassitude, breathlessness on exertion, giddiness, dimness of vision, headache, insomnia, pallor of the skin and, much more important for diagnosis, of mucous membranes, palpitation, functional anorexia and dyspepsia, tingling and ‘pins and needles’ in the fingers and toes (paraesthesiae). Angina pectoris (due to myocardial hypoxia), is often present in elderly patients. Physical signs include tachycardia, functional systolic murmurs, evidence of cardiac dilatation and, in severe cases oedema of the ankles and crepitations at the bases of the lungs. In addition to these general features of anemia there may be signs of nutritional deficiency, particularly angular stomatitis, koilonychias and glossitis. Atrophy of the papillae and mucous membrane gives the tongue a smooth glazed appearance (chronic atrophic glossitis). The atrophy begins at the edges and later affects the whole tongue. As a result the tongue appears moist and exceptionally clean. Koilonychia is the name given to certain changes in the nails; first there is

METABOLISM AND NUTRITION MODULE 16th Group

41

brittleness and dryness: later there is flattening and thinning and finally concavity (spoon-shaped nails).

2.3 LEARNING ISSUES II 2.3.1 2.3.2 What is the connection between Diabetes Mellitus and drowsiness? How is the pathogenesys of Neuropathy? polyfagia, and polyuria? 2.3.4 What is the connection between Diabetes Mellitus and body weight? 2.3.5 2.3.6 2.3.7 What are the causes of Diabetes Mellitus Type 2? What is the connection between DM Type 2 with Carbohydrate Metabolism? What is the connection between DM Type 2 with Lipid Metabolism? 2.3.8 What is the connection between DM Type 2 with Protein Metabolism? 2.3.9 What is the normal rate of Insulin, Haematocrit, and Creatinin? 2.3.10 What is the solution of this problem?

2.3.3 What is the connection between Diabetes Mellitus and polydipsi,

METABOLISM AND NUTRITION MODULE 16th Group

The lipid deposits plus the cellular proliferation can become so large that the plaque bulges into the lumen of the artery and greatly reduces blood flow. sclerosis (fibrosis) becomes so great that the arteries become stiff and unyielding. Still later. and the surrounding fibrous and smooth muscle tissues proliferate to form larger and larger plaques. the fibroblasts of the plaque eventually deposit extensive amounts of dense connective tissue. the macrophages release substances that cause inflammation and further proliferation of smooth muscle and fibrous tissue on the inside surfaces of the arterial wall. With time.1 THE ANSWERS OF LEARNING ISSUES II 3.1. the fatty streaks grow larger and coalesce. Atherosclerotic arteries lose most of their dispensability. leading to bony-hard calcifications that can make the arteries rigid tubes. calcium salts often precipitate with the cholesterol and other lipids of the plaques. Even without occlusion. Also. METABOLISM AND NUTRITION MODULE 16th Group . sometimes completely occluding the vessel.1 What is the connection between Diabetes Mellitus and drowsiness? Two possible causes are often sleepy at this woman is atherosclerosis and sleep apnea.42 CHAPTER III THIRD TUTORIAL 3.

then it cause of this woman is easy sleepy during the day.2 How is the pathogenesys of Neuropathy? The most common form of neuropathy associated with diabetes mellitus is distal symmetric sensorimotor polyneuropathy. METABOLISM AND NUTRITION MODULE 16th Group . Neuropathy may also contribute to the significant reduction in quality of life for patients. Recently it has become clear that sleep disturbances (e.. leading to a sudden blockage of all blood flow in the artery. chronic insomnia. it can also decrease blood flow to the brain.e. cardiovascular disease). 3.g. other thing that easily allows the woman drowsy is sleep apnea. in some cases. The indiscriminate use of sleeping pills may further disrupt the sleep-wake cycle and contribute to stress in patients with sleep disorders. and paranodal demyelination and blunted nerve fiber regeneration.. the majority of diabetic patients continue to die from macrovascular complications (i.43 and because of the degenerative areas in their walls. often accompanied by autonomic neuropathy.1. short-term disturbances of sleep may evolve into chronic conditions. So because this woman's quality of sleep less. it is this which is the reason why women are often sleepy. and even when sleep is enough. sleep disturbances are believed to be common and have been attributed to impaired glucose metabolism and general physical distress. With the obstructive on the artery. segmental. their rough surfaces can cause blood clots to develop. with resultant thrombusor embolus formation. In type 2 diabetes. furthermore. Besides atherosclerosis. These problems are frequently overlooked on routine medical interviews. Also. This disorder is characterized by striking atrophy and loss of myelinated and unmyelinated fibers accompanied by Wallerian degeneration. they are easily ruptured. although much progress has been made in therapy. sleep apnea) have an impact on health and quality of life. All values for nerve conduction velocity in sensory and motor nerves were slower. and. Most patients develop diabetes after age 40 years. where the plaques protrude into the flowing blood.

polyuria. Metabolic dysfunction in diabetic nerve is accompanied by vascular insufficiency and nerve hypoxia that may contribute to nerve fiber loss and damage. activation of the polyol pathway by glucose via AR. this progressive nerve fiber damage and loss parallels the degree and/or duration of hyperglycemia. (Greene. Several metabolic mechanisms have been proposed to explain the relationship between the extent and severity of hyperglycemia and the development of diabetic neuropathy.44 and the sensory amplitude of the radial nerve and the motor amplitude of the median nerve were lower. 1995) In both humans and laboratory animals. which overwhelms the kidney's ability to reabsorb the sugar as the blood is filtered to make urine. superoxide radical formation. which normalize nerve myo-inositol and nerve conduction slowing. METABOLISM AND NUTRITION MODULE 16th Group ..3 What is the connection between Diabetes Mellitus and polydipsi.1. et al. is a prominent metabolic feature of diabetic rat peripheral nerve. where it promotes sorbitol and fructose accumulation. 1992) 3. The body encourages more water consumption to dilute the high blood sugar back to normal levels and to compensate for the water lost by excessive urination. protein glycation. One mechanism. or potential blunting of normal neurotrophic responses. ARIs. Other specific metabolic abnormalities that may play a role in the pathogenesis of diabetic neuropathy include abnormal lipid or amino acid metabolism. are currently the focus of clinical trials. and slowing of nerve conduction by alteration of neural Na(+)K(+)-ATPase activity or perturbation of normal physiological osmoregulatory mechanisms. (Partanen et al. which translates into thirst. and polyfagia?? Excessive thirst (polydipsia): A person with diabetes develops high blood sugar levels. The body tries to counteract this by sending a signal to the brain to dilute the blood. myoinositol depletion. Excessive urine is made as the kidney spills the excess sugar.

the person may gain very little weight and may even lose weight. 2005). Adipocytes secrete a number of biologic products (leptin. Obesity.4 What is the connection between Diabetes Mellitus and body weight? Obesity can increase risk factor to type 2 diabetes mellitus. and body weight and may contribute to the insulin resistance. TNF-α. higher insulin levels lead to increased hunger and eating.45 Excessive urination (polyuria): Another way the body tries to get rid of the extra sugar in the blood is to excrete it in the urine. glucose tolerance METABOLISM AND NUTRITION MODULE 16th Group . 3.1. In the early stages of the disorder. This can also lead to dehydration because excreting the sugar carries a large amount of water out of the body along with it. particularly visceral or central (as evidenced by the hip-waist ratio). insulin resistance is often associated with abdominal obesity (as opposed to hip and thigh obesity) and hypertriglyceridemia (Kasper. Moreover. insulin action. Type 2 DM is characterized by three pathophysiologic abnormalities: impaired insulin secretion. resistin. and excessive hepatic glucose production. One of the functions of insulin is to stimulate hunger. peripheral insulin resistance. Excessive eating (polyphagia): If the body is able. free fatty acids. Therefore. it will secrete more insulin in order to try to deal with the excessive blood sugar levels. and adiponectin) that modulate insulin secretion. is very common in type 2 DM. Despite increased caloric intake. In type 2 DM. the body is resistant to the action of insulin in type 2 diabetes.

Another emerging theory proposes that elevated levels of free fatty acids. acetyl CoA. because the pancreatic β cells compensate by increasing insulin output. characterized by elevations in postprandial glucose. β cell failure may ensue. despite insulin resistance. The decreased ability of insulin to act effectively on peripheral target tissues (especially muscle and liver) is a prominent feature of type 2 DM and results from a combination of genetic susceptibility and obesity (Kasper. However. triacylglicerol stored will be split into 3 fatty acids and 1 glycerol. promote glucose production by the liver. As insulin resistance and compensatory hyperinsulinemia progress. the pancreatic islets in certain individuals are unable to sustain the hyperinsulinemic state. A further decline in insulin secretion and an increase in hepatic glucose production lead to overt diabetes with fasting hyperglycemia. Diabetes mellitus can reduce body weight. Acetyl-CoA will enter the Krebs cycle which produces nucleoside phosphate compounds-energy high (Murray. IGT. 2005). may contribute to the pathogenesis of type 2 DM. 2005). Ultimately. Body weight is dynamic due to fat accumulation (triacylglicerol) in adipocytes cells.46 remains normal. then develops. Markers of inflammation such as IL-6 and C-reactive protein are often elevated in type 2 diabetes (Kasper. Fatty acids will be distributed and to enter into the lane on the mitochondrial oxidation β cells that would produce. the food material will be deflected into the path of formation triacylglicerol. 2003). if someone experienced hunger. Free fatty acids can impair glucose utilization in skeletal muscle. Fat is dynamic because the amount of fat follow the energy situation in one's body. a common feature of obesity. 2005). METABOLISM AND NUTRITION MODULE 16th Group . If someone is having excess energy. and impair β cell function (Kasper.

METABOLISM AND NUTRITION MODULE 16th Group . The number of reserves will result in triacylglycerol lipolysis in adipocytes cells is reduced. 2003). Thus. the inhibition of lipolysis is greatly reduced. the rate of formation of fatty acids will increase. if too many will lead to many complications associated blood acidosis (Murray. The enzyme is inhibited by insulin. low levels of insulin will lead to lower the barriers for hormonesensitive lipase. Swift fatty acids will result in the number of acetyl-CoA resulting in β oxidation. if insulin levels are decreased (as in diabetes). Thus. so that the process of lipolysis will go well.47 In solving triacylglycerol (lipolysis) is required enzyme hormone-sensitive lipase enzyme which is sensitive to insulin levels. so that the weight will decrease. Fatty acid that increases will shift the use of glucose as energy to the use of fatty acids for energy. However. Acetyl-CoA which many will be deflected towards the formation of ketone compounds which.

in the early stages will not cause disruption to the blood glucose levels. then at the stage of decompensation. this disease is progressive travel and tend to involve too fat or protein metabolism disorders. the body that may be deficient in relative terms. In impaired glucose tolerance (IGT) was found postprandial blood glucose levels. especially in adults and older age groups in all socio-economic status. ranged between 140-200 mg / METABOLISM AND NUTRITION MODULE 16th Group . hypertension. although the known negative impact thereof large enough between. system nerve. eyes and kidneys. fats and proteins and is characterized by high blood sugar levels (hyperglycemia) and in urine. Although no national survey.1. Currently. This disease affects not only individually. but the health system a country. liver. in line with changes lifestyle.5 What are the causes of Diabetes Mellitus Type 2? Diabetes Mellitus (DM) is one health problem impact on productivity and can lower the Human Resources. DM is increasing. To obtain a normal glucose levels in the blood necessary drugs that can stimulate beta cells to increase insulin secretion (insulin secretagogue) or when required by the substitution of insulin. an increase in postprandial blood glucose levels. where an interruption occurs metabolism of carbohydrates. DM is a degenerative disease. efforts to control disease DM has not occupied the main priorities in health care.48 3. including eating patterns of Indonesian society is estimated patient. or after being fed a solution of 75 g glucose load with Oral Glucose Tolerance Test (oral glucose tolerance). which is then followed by performance improvement phase 2 insulin secretion. brain. Clinically. other chronic complications in chronic heart disease. in addition to efficacious drugs that reduce insulin resistance (insulin sensitizers). Clinically. At this stage of compensatory mechanisms have started no longer adequate. Inadequate phase 1. Increased blood glucose levels because of utilization that are not going perfectly in turn often led to the clinical abnormalities of blood lipid levels. can be detected condition called impaired glucose tolerance which is also called as a prediabetic state.

WATER normal lasting. Increasing levels of insulin resistance can be seen also from increased levels of fasting and postprandial blood glucose. Performance of a rapid and adequate water is essential for normal glucose regulation because pasa turn contribute significantly in controlling postprandial blood glucose levels. both at the stage of chronic diabetes. has negative long-term tissue complications of chronic diabetes. beneficial in METABOLISM AND NUTRITION MODULE 16th Group . We have to know that. This is evident from the fact that in the early stages DMT2. Secretion of phase 1 (AIR) usually have a relatively high peak. at the higher levels of hepatic insulin resistance. particularly microvascular. Thus. Accordingly. the presence of normal water needed to sustain the process of physiological glucose metabolism. immediately after eating. which is also known as Fasting Blood Glucose Disturbed (GDPT). increased dramatically at this stage of diabetes. causing the higher the level of hepatic glucose production. Insulin resistance from prominent role since the change or conversion into DMT2 TGT phase. although the serum insulin levels are high enough. and widespread process of glycosylation.Tingginya blood glucose levels (glucotoxicity) which followed by dyslipidemia (lipotoxicity) is responsible for tissue damage both directly through oxidative stress. Secreation of phase (Acute insulin secretion responce = AIR) is the secretion of insulin that occurs immediately after stimulation of beta cells. the lower the ability of inhibition to the process of glycogenolysis and gluconeogenesis. arise quickly and ended too quickly. Also known as prediabetes. when fasting blood glucose levels between 100126 mg / dl. but hyperglycemia can still occur. It is said that at the start of dominant factor of insulin resistance as a cause of hyperglycemia as well as a variety of tissue damage. or acute postprandial hyperglycemia that occurred were ulangkali every day since the stage of IGT. because it is necessary to anticipate the blood glucose levels typically rise sharply.49 dl. whereas macrovascular disorders have emerged since prediabetes. State of hyperglycemia that occurs. Tissue damage occurs.

Increased insulin production is essentially aimed at meeting the needs of the body for blood glucose levels (postprandial) remained within normal limits. METABOLISM AND NUTRITION MODULE 16th Group . If the phase 1 secretion is inadequate. the task of blood glucose regulation subsequently taken over by the secretion phase 2. after the secretion phase 1 ended. Insulin secretion phase 2. where insulin secretion increased again slowly and survive in a relatively longer time. there was a mechanism of compensation in the form of increased secretion of insulin in Phase 2. So. insulin secretion phase 2 will be heavily influenced by phase 1. accompanied also by the action of insulin which is also normal in the network (without insulin resistance).50 preventing the occurrence of acute hyperglycemia after a meal or postprandial blood glucose spikes (postprandial spike) with all consequences thereof including compensed inemia.In the figure below (Fig. latent phase). After the end of phase 1. appear secretion phase 2 (sustained phase. the secretion of phase 2 will also be normal. which lasted relatively long. In the prospective course of the disease. and Type 2 Diabetes Mellitus. 2) demonstrated the dynamics of insulin secretion in normal circumstances. a kind of adjustment mechanism of secretion of phase 2 to phase 1 previous performance. Thus no additional need (extra) synthesis and secretion of insulin in Phase 2 above normal in order to maintain the state of normoglycaemia. also without hyperinsulinemia with various negative impacts. Usually. Furthermore. in addition to insulin resistance factor.This is a physiological condition which is ideal for without raising blood glucose levels that may impact glucotoxicity. with a normal phase 1 performance. Disturbed Glucose Tolerance (IGT = Impaired Glucose Tolerance). how high the peak (quantitative) will be determined by how much the blood glucose level at the end of phase 1.

initially determined by the performance of Phase 1 which then gives a negative impact on the performance of phase 2. often leading to a collection of symptoms called metabolic syndrome.51 Intravenous glucose stimulation First-Phase Second Phase IGT Normal Type 2DM Insulin Secretion Basal So. it can be concluded trip DMT2 disease. and a direct result of elevated levels of blood glucose (hyperglycemia).Disruption or environmental influences such as lifestyle or obesity will accelerate progression of the disease. other than intolerance to glucose and its various consequences. Hyperglycemia occurs not only due to impaired insulin secretion (insulin deficiency). but at the same time also by the low response of body tissues to insulin (insulin resistance). METABOLISM AND NUTRITION MODULE 16th Group . Impaired glucose metabolism will continue in fat and protein metabolism disorders and the damage to various body tissues. The series of disorders that are motivated by insulin resistance.

1.52 3. excess glucose is converted into glycogen and stored in the liver due to the action of insulin. This causes glucose in human blood cannot be converted into glycogen by hepar’s cells (glycogenesys doesn’t work). insulin. This mechanism body.6 What is the connection between Diabetes Mellitus Type 2 and Carbohydrate Metabolism? With type 2 diabetes. the impairment of glucose metabolism arises as a result of a decreased sensitivity to insulin by the body’s cells. Overlap point with lipogenesys: Upon consuming foods. Any remaining glucose may be converted for fat storage. This is known as insulin resistance. the body’s cells and liver do not respond to insulin. leading to inappropriate amount of insulin in human METABOLISM AND NUTRITION MODULE 16th Group . Glucose then enters the blood stream where it is transported to cells throughout the body. This means that the cells do not respond to insulin to take up glucose from the bloodstream and utilize it. the digestive system along with the liver. break down the food into simple sugars like glucose. particularly carbohydrates. seen in impaired glucose tolerance (or pre-diabetes). Compensatory mechanism: The insulin levels in the blood are elevated. And also other kind of cells do not use blood glucose due to its insensitivity caused by the malfunction of beta cells of islets of Langerhans. This blood glucose regulating mechanism is primarily controlled by the hormone. Excess glucose is converted to glycogen and stored in the liver and muscles. which is secreted by the pancreas (beta cells in the islets of Langerhan’s). above the norm (hyperinsulinemia) as the pancreas secretes higher amounts of glucose in an attempt to overcome this resistance (compensatory mechanism). Insulin triggers cells to take up glucose from the blood so that individual cells can burn this glucose for energy. Alternatively. In insulin resistance. Excess glucose builds up in the blood stream causes hyperinsulinemia until bile is overworked and malfunctioned as well.

insulin resistance and pre-diabetes will lead to type 2 diabetes. Thus. The nutritional state of the organism is the main factor regulating the rate of lipogenesis. Insulin stimulates lipogenesis by several other mechanisms as well as by increasing acetyl-CoA carboxylase activity. or when there is a deficiency of insulin. leading to severe metabolic derangement. the rate is high in the well-fed animal whose diet contains a high proportion of carbohydrate. In the starving state. In diabetes mellitus there is either impaired synthesis and secretion of insulin (type 1 diabetes mellitus) or impaired sensitivity of tissues to insulin action (type 2 diabetes mellitus).7 What is the connection between Diabetes Mellitys Type 2 with lipid metabolism? After a normal meal there is an ample supply of carbohydrate. It increases the transport of glucose into the cell (eg.53 and the pancreas attempts to secrete more insulin. This excess insulin secretion may not always trigger the desired effect resulting higher than normal blood glucose levels. on a fat diet. increasing the availability of both pyruvate for fatty acid synthesis and glycerol 3-phosphate for esterification of the newly METABOLISM AND NUTRITION MODULE 16th Group . These events are largely controlled by the hormones insulin and glucagon. These latter conditions are associated with increased concentrations of plasma free fatty acids. in adipose tissue). Over time. glucose must be spared for use by the central nervous system (which is largely dependent on glucose) and the erythrocytes (which are wholly reliant on glucose). as in diabetes mellitus. 3. also known as adult-onset diabetes or non-insulin dependent diabetes. Other tissues can utilize alternative fuels such as fatty acids and ketone bodies. As glycogen reserves become depleted. It is depressed under conditions of restricted caloric intake.1. and the fuel for most tissues is glucose. so amino acids arising from protein turnover and glycerol arising from lipolysis are used for gluconeogenesis. and an inverse relationship has been demonstrated between hepatic lipogenesis and the concentration of serum-free fatty acids.

Insulin inhibits the release of free fatty acids from adipose tissue. and their esterification. In poorly controlled type 1 diabetes mellitus. as in diabetes. It enhances lipogenesis and the synthesis of acylglycerol and increases the oxidation of glucose to CO2 via the pentose phosphate pathway. Free fatty acids from the circulation are the main source during starvation. patients may become hyperglycemic. Lipid is mobilized from adipose tissue as free fatty acids (FFA) attached to serum albumin. and also converts the inactive form of pyruvate dehydrogenase to the active form in adipose tissue but not in liver.CoA. insulin stimulates glucose uptake. which is ultimately fatal. At the same time. Abnormalities of lipoprotein metabolism cause various hypo. the feeding of high-fat diets. The most common of these is diabetes mellitus.54 formed fatty acids. where insulin deficiency causes excessive mobilization of FFA and underutilization of chylomicrons and VLDL.or hyperlipoproteinemias. Increased fatty acid oxidation is a characteristic of starvation and of diabetes mellitus. partly as a result of lack of insulin to stimulate uptake and utilization of glucose and partly because of increased gluconeogenesis from amino acids in the liver. leading to ketone body production by the liver (ketosis). In adipose tissue. Insulin also—by its ability to depress the level of intracellular cAMP—inhibits lipolysis in adipose tissue and thereby reduces the concentration of plasma free fatty acids and therefore longchain acyl. an inhibitor of lipogenesis. Ketosis is mild in starvation but severe in diabetes mellitus and ruminant ketosis. Ketone bodies are acidic and when produced in excess over long periods. when hepatic lipogenesis is inhibited. and the resultant free fatty acids are substrates for ketogenesis in the liver. and inhibits intracellular lipolysis and the release of free fatty acids. cause ketoacidosis. Most other pathologic conditions affecting lipid transport are due primarily to inherited METABOLISM AND NUTRITION MODULE 16th Group . which is followed by a fall in circulating plasma free fatty acids. its conversion to fatty acids. the lack of insulin results in increased lipolysis in adipose tissue. leading to hypertriacylglycerolemia. or in diabetes mellitus.

the ribosomes simply stop working. Insulin stimulates transport of many of the amino acids into the cells. isoleucine. and phenylalanine. (Murray. the amino acids affected are not necessarily the same ones. thus forming new proteins. 3. and premature atherosclerosis. The manner in which insulin causes protein storage is not as well understood as the mechanisms for both glucose and fat storage. In the absence of insulin. some of which cause hypercholesterolemia.8 What is the connection between Diabetes Mellitus Type 2 with protein metabolism? During the few hours after a meal when excess quantities of nutrients are available in the circulating blood. Presumably this results from the ability of insulin to diminish he normal degradation of proteins by the cellular lysosomes. insulin also increases the rate of transcription of selected DNA genetic sequences in the cell nuclei. 2. In some unexplained way. Insulin increases the translation of messenger RNA. insulin “turns on” the ribosomal machinery. METABOLISM AND NUTRITION MODULE 16th Group . insulin is required for this to occur. Some of the facts follow. However. thus forming increased quantities of RNA and still more protein synthesis— especially promoting a vast array of enzymes for storage of carbohydrates. Over a longer period of time. especially from the muscle cells. Thus. leucine. almost as if insulin operates an “on-off” mechanism. 2003) 3.1. and proteins. Insulin inhibits the catabolism of proteins. fats. insulin shares with growth hormone the capability of increasing the uptake of amino acids into cells.55 defects. Among the amino acids most strongly transported are valine. 4. not only carbohydrates and fats but proteins as well are stored in the tissues. tyrosine. 1. thus decreasing the rate of amino acid release from the cells.

Free insulin: fasting ≤25 IU/mL (<172. (Guyton and Hall.1. Virtually all protein storage comes to a halt when insulin is not available. In the liver. The resulting protein wasting is one of the most serious of all the effects of severe diabetes mellitus.00 mg/L <117 pmol/L 3–20 μIU/mL 21–139 pmol/L METABOLISM AND NUTRITION MODULE 16th Group . insulin depresses the rate of gluconeogenesis. This degradation of the amino acids also leads to enhanced urea excretion in the urine. 2006) 3.9 What is the normal rate of Insulin. SI units). The plasma amino acid concentration rises considerably.56 5. The catabolism of proteins increases. and large quantities of amino acids are dumped into the plasma.) Insulin Level via Radioimmunoassay: SI Units Adult. Because the substrates most used for synthesis of glucose by gluconeogenesis are the plasma amino acids. In summary. fasting level Newborn <17 μIU/mL or 1.5 pmol/L. and Creatinin? Insulin and Insulin Antibodies—Blood Norm. Insulin Lack Causes Protein Depletion and Increased Plasma Amino Acids. and most of the excess amino acids are used either directly for energy or as substrates for gluconeogenesis. this suppression of gluconeogenesis conserves the amino acids in the protein stores of the body. Haematocrit. It does this by decreasing the activity of the enzymes that promote gluconeogenesis. (Norms and standardization of the test method vary widely by laboratory. It can lead to extreme weakness as well as many deranged functions of the organs. insulin promotes protein formation and prevents the degradation of proteins. protein synthesis stops.

and thiazide diuretics. calcium gluconate in the newborn. quinine. Diabetes mellitus. Drugs include albuterol. hyperinsulinism. pancreatic islet cell lesion. amniotic fluid 11. beta-cell adenoma. and pheochromocytoma. Insulin antibodies have been shown to occur more frequently with aging and more in females than in males. Increased Insulin. Cushing's syndrome. ethyl alcohol (ethanol). calcitonin. Decreased Insulin. medroxyprogesterone. sucrose. levodopa. quinidine. nifedipine. Undetectable to less than 4% when using either bovine or porcine insulin as a reagent. insulin-resistance syndromes. nesidioblastosis. Acromegaly. furosemide. hypopituitarism. cimetidine. hypoglycemia. and tolbutamide. hyperglycemia. insulinoma. oral contraceptives. phenformin. liver disease. diazoxide. ethacrynic acid.57 SI Units Infant Prepubertal child Panic levels <13 μIU/mL <13 μIU/mL >30 μIU/mL ≤89 pmol/L ≤89 pmol/L >207 pmol/L 78 pmol/L Last trimester. tolazamide.3 μIU/mL Insulin Antibodies. metformin. phenytoin. spironolactone. overdose of insulin. non–insulin-dependent diabetes mellitus. familial fructose and galactose intolerance. Beckwith-Wiedemann syndrome. fructose. glucose. prednisolone. terbutaline. METABOLISM AND NUTRITION MODULE 16th Group . ether. asparaginase. glucagon. phenobarbital. and pancreatectomy-induced diabetes. insulin. metabolic syndrome. dystrophia myotonica. Drugs include beta-adrenergic blockers. Positive Insulin Antibodies. estrogen. obesity.

control. Insulin antibodies. Also negative in insulinoma. Insulin is a hormone that regulates carbohydrate metabolism. It is produced in the pancreas by the beta cells of the islets of Langerhans. Insulin antibodies are transferred through the placenta and are present in 30%–50% of children at the time of diagnosis before beginning insulin therapy. this test may be used with C-peptide to determine whether hypoglycemia is caused by insulin abuse. Description. The percentage of antigen bound to antibody is related to the total antigen present and is reflected by the distribution of a radioactive label. These antibodies may also be present in persons who have never received insulin but have autoimmune insulin syndrome (AIS). may be present in diabetic clients treated for several weeks or more with conventional insulin. and dyslipidemia. and its rate of secretion is determined primarily by the level of blood glucose. hypertension.47 METABOLISM AND NUTRITION MODULE 16th Group . Low immunoreactive insulin levels have been associated with a higher risk of developing degenerative diseases such as atherosclerosis. a rare condition characterized by hyperinsulinemia and hypoglycemia.58 Factitious hypoglycemia. For diabetic clients. SI Units Females Adult 37%–47% 0. Negative Insulin Antibodies. or unknown. also referred to as anti–insulin-Ab. autoimmune insulin syndrome (AIS).37–0. Normal finding. The client's unlabeled antigen in the blood competes with labeled antigen for antibody-binding sites. Hematocrit (Hct)—Blood Norm. The radioimmunoassay test measures endogenous insulin by using a series of tubes containing a fixed amount of antibody label and an aliquot of standard.

Monitor hematocrit. thirst and weakness Extremity pain and redness. anasarca decreasing QRS voltage with severe fluid overload Possible Treatments Administer IV fluids. restlessness. tachycardia. and shortness of breath Administer diuretics. decreased skin turgor. Administer oxygen. decreased venous filling. Restrict fluids. True polycythemia overtransfusion Panic Level Symptoms and Treatment—Decreased Cause Symptoms Possible Treatments Hemodilution Rales.29–0.54 0. Perform bloodletting by venipuncture (phlebotomy). anxiety. orthostatic hypotension.46 0.15 or >0. METABOLISM AND NUTRITION MODULE 16th Group . dry mucous membranes.35–0.45 30%–46% 0. Cause Hemoconcentration Symptoms Decreased pulse pressure and volume.31–0. monitor hematocrit. jugular venous distention. Observe for signs of thrombosis. Monitor hematocrit and intake and output.44 0.40–0. hypertension.30–0.54 Adult Males 40%–54% Panic Levels <15% or >60% <0. facial flushing.40–0. low central venous pressure. Stop or reduce dose of diuretics if they are contributors to condition.59 SI Units Pregnant Children Neonates 3 months 1–2 years 6–10 years 40%–68% 29%–54% 35%–44% 31%–45% 0.60 Panic Level Symptoms and Treatment—Increased NOTE: Treatment choice(s) depend(s) on client's history and condition and episode history. edema. Administer IV fluids.68 0. irritability. Restrict sodium.

antibiotics. hydremia of pregnancy. oxyphenbutazone. dehydration (severe). or phosphate. Decreased. cardiac decompensation. idiopathic steatorrhea. fatty liver. and tetralogy of Fallot. acetohexamide.60 Cause Blood loss Symptoms Hypotension. leukemia. Protect airways. hydrochloride. chloramphenicol. hemoconcentration. hydralazine indomethacin. diabetes mellitus. and pregnancy. burns (severe). isoniazid. haloperidol. pancreatitis (hemorrhagic). Addison's disease. cystic fibrosis. cirrhosis. methyldopate hydrochloride. polycythemia. shock. bleeding. mefenamic mephenytoin. mercurial diuretics. novobiocin sodium. hemorrhage. conditions that decrease RBCs. doxapram acid. Drugs include acetaminophen. overhydration. methaqualone. Give isotonic fluids. bone marrow hyperplasia. ethotoin. amphotericin. furazolidone. pancreatitis (acute). Any condition that increases red blood cells (RBCs). aminosalicylic acid. Anemia. methsuximide. Increased. diarrhea. congestive heart failure. hemolytic reactions to chemicals or drugs or prosthetics. Administer omeprazole (if blood loss is caused by bleeding esophageal varices). Also. metaxalone. oleandomycin. atabrine hydrochloride. hypothyroidism. paramethadione. chloroquine hydrochloride isocarboxazid. nitrates. eclampsia. hemorrhage. antimony potassium tartrate. blood doping (autologous transfusion to improve athletic performance). hydrochloride. ethosuximide. methyldopa. nitrofurantoin. erythrocytosis. pargyline METABOLISM AND NUTRITION MODULE 16th Group . Perform blood transfusion. fluid overload. antineoplastic agents. hypoxia Possible Treatments Identify and treat cause of bleeding. hyperthyroidism. administer oxygen as needed. burns (severe). pneumonia. intestinal obstruction (late).

thiocyanates.7–1.61 hydrochloride. and zidovudine (AZT).7 mg/dL ≤0. vegetarian diet. phenobarbital.7 mg/dL 62–150 μmol/L ≤0.5–1. radioactive agents. female 1 year.7 mg/dL ≤0. Kinetic or Enzymatic Method Adults Females Males Elderly Children Cord blood Newborn Infant 1 year.6 mg/dL ≤0. sulfonamides. trimethadione. female 0. male 4–7 years. phenylbutazone. phenytoin sodium. tripelennamine hydrochloride.6–1. Manual Method Jaffe. primidone.6–1. phenacemide. tranylcypromine sulfate. rifampin. Creatinine—Serum Norm. spectinomycin hydrochloride. SI Units Jaffe.2 mg/dL 53–105 μmol/L 0. male 8–10 years.8 mg/dL ≤0.2 mg/dL 53–105 μmol/L May be lower May be lower 0.4 mg/dL 71–124 μmol/L 0. penicillins.6–1. male 2–3 years. phytonadione. troleandomycin. Hematocrit is the percentage of red blood cells in a volume of whole blood. Description. tolbutamide. vitamin A.6 mg/dL 52–142 μmol/day METABOLISM AND NUTRITION MODULE 16th Group . female 2–3 years. tetracyclines.5 mg/dL ≤0. tolazamide.8–1.8 mg/dL ≤44 μmol/L ≤53 μmol/L ≤53 μmol/L ≤62 μmol/L ≤62 μmol/L ≤71 μmol/L ≤71 μmol/L 0. phensuximide. thiosemicarbazones.6 mg/dL ≤0.1 mg/dL 44–97 μmol/L 0. phenelzine sulfate. valproic acid. female 4–7 years. thiazide diuretics.

gentamicin sulfate. male ≤0. systemic lupus erythematosus. Acromegaly. pancreatitis (necrotizing). renal cortical necrosis. cephalexin). azotemia (prerenal. metal poisoning. disopyramide phosphate. hypovolemic shock. female 13–17 years. hydroxyurea. clofibrate. congestive heart failure. intestinal obstruction. micro albuminemia. glucose. allergic purpura. diacetic acid. fenofibrate. uremia. mannitol.2 mg/dL ≤1. corticosteroids. amphotericin B. Drugs include acetohexamide. captopril.9 mg/dL ≤1. polyarteritis nodosa. METABOLISM AND NUTRITION MODULE 16th Group . subacute bacterial endocarditis. preeclampsia. renal artery stenosis or thrombosis. nephrosclerosis. acyclovir. hypokalemic). urinary obstruction. amyloidosis. Bromsulphalein. congenital hypoplastic kidneys. multiple myeloma.0 mg/dL ≤1. Goodpasture's syndrome. pyelonephritis. diuretics. female 11–12 years. cinchophen. toxic shock syndrome. rheumatoid arthritis (active).2 mg/dL ≤1. bleomycin-induced pulmonary toxicity. testosterone therapy. scleroderma. nephritis. losartan.9 mg/dL ≤0. Lipomul. lithium carbonate. fosinopril. dopamine. diabetes mellitus. renal failure.1 mg/dL ≤1. fructose. postrenal). male 13–17 years. KimmelstielWilson syndrome. gout. and vomiting. female 18–20 years. renal tuberculosis. arginine. glomerulonephritis (chronic).3 mg/dL ≤80 μmol/L ≤80 μmol/L ≤88 μmol/L ≤97 μmol/L ≤106 μmol/L ≤106 μmol/L ≤115 μmol/L Increased. hypothyroidism. diet (high meat content). cephalosporins (Cefoxitin. hemoglobinuria. muscle destruction. cimetidine. renal vein thrombosis. male 18–20 years.62 SI Units 8–10 years. gigantism. infants (first 2 weeks of life). sickle cell anemia. ammonia (inhaled). high dietary intake. nephropathy (hypercalcemic. analgesic abuse. Values are 20–40% higher in the late afternoon than in the morning. male 11–12 years. polycystic disease. hydralazine hydrochloride. androgens.

A diurnal variation in creatinine may be related to meals. Mokutsu.. Asarum spp. mithramycin.. chlorpromazine. Menispernum spp. birthwort. and viomycin. Clematis spp. Creatinine is produced continuously as a nonprotein end product of anaerobic energy-producing creatine phosphate metabolism in skeletal muscle. marijuana. testosterone triamterene. SI Units Lipids.).0–8. See individual test listings for age-specific norms. streptokinase. Diabetic ketoacidosis (artifactual decrease) and muscular dystrophy. methicillin sodium. cypionate. Bragantia spp. Description.63 meclofenamate sodium. pyruvate. Dutchman's pipe. propionate. with troughs occurring around 0700 (7 AM) and peaks occurring around 1900 (7 PM).. cimetidine. Diploclisia spp. metoprolol tartrate. Herbal or natural remedies include Cordyceps sinensis. Cocculus spp. and Stephania spp. Decreased. testosterone sulfobromophthalein. Fang chi.. nitrofurantoin. Because it is continually and easily excreted by the renal system. including norms for children. total 400–800 mg/dL 4. and vancomycin.. propranolol. thiazide diuretics. Creatinine is thus a very specific indicator of renal function. increased levels indicate a slowing of the glomerular filtration rate.. revealing the balance between creatinine formation and excretion.. Drugs include cefoxitin sodium. nitrogen oxide (inhaled).. Fang ji. Mu tong.0 g/L METABOLISM AND NUTRITION MODULE 16th Group . chlorprothixene. Guang Kan-Mokutsu. Lipid Profile—Blood Norm. protein. Aristolochia spp. enanthate. testosterone testosterone. Sinomenium spp. sulfonamides. Herbal or natural remedies include products containing aristolochic acids (Akebia spp.. minoxidil.

8 mmol/L VLDL cholesterol (calculated) ≤30 mg/dL Total-to-HDL cholesterol ratio Median = 5 Condition Alcoholism Aortic aneurysm Aortitis Arteriosclerosis Diabetes mellitus Glycogen storage Hyperalimentation Triglycerides Total Cholesterol HDL Increase Increase Increase Increase Increase Increase Decrease Increase Increase Increase Increase Increase — Decrease Increase Increase — Decrease Increase Increase Increase LDL Increase Increase Increase Increase Increase Increase Decrease Increase Increase Increase — — Increase Increase Decrease Decrease Increase Increase Decrease — Decrease Decrease Increase Increase Increase Increase Increase Increase Hypercholesterolemia Increase Hyperlipoproteinemia Increase Hypothyroid Malabsorption Myxedema Nephrotic syndrome Pancreatitis Description. and phospholipids.0–4.78 mmol/L 10–190 mg/dL 0. Fasting lipid profiles are recommended every 5 years in clients older than age 19.7 mmol/L 2.9 mmol/L <0. Blood lipids comprise cholesterol.64 SI Units Triglycerides HDL cholesterol Females Males LDL cholesterol 35–85 mg/dL 30–65 mg/dL 80–190 mg/dL 0.2 mmol/L 0. See individual test sections for further descriptions of the METABOLISM AND NUTRITION MODULE 16th Group .8–1.9–2. triglycerides.2–4. Increase Decrease Increase Increase Increase Lipid profile is a battery of laboratory studies to help determine the risk factors in coronary artery disease.

18–6.59– 3.15 High Risk mg/dL SI Units mmol/L ≥240 ≥200 ≥6.4 11.12 High 160–189 4.37– 4.16 <35 <0.65 components of the lipid profile.4 9.14– 4.91–1.0 4.92 SI Units mg/dL SI Units METABOLISM AND NUTRITION MODULE 16th Group .19 4.53 35–45 0. as well as levels for which lifestyle changes and therapeutic drug regimens are recommended.554 45–59 1.40 Borderline High Risk mg/dL SI Units mmol/L 200– 239 170– 199 5.16–1.18 HDL Cholesterol—Coronary Heart Disease Risk Very Low Risk Low Risk Moderate Risk High Risk mg/dL SI Units mg/dL SI Units mg/dL SI Units mg/dL SI Units mmol/L mmol/L mmol/L mmol/L Adults >60 >1.6 7.18 <4.22 ≥25.1 3 × Average Risk 23.91 Total to HDL Ratio Coronary Heart Disease Risk Male Female Average Risk 2 × Average Risk 5.89 SI Units mg/dL SI Units mg/dL High Risk Very High >190 >4.34 mg/dL SI Units mg/dL Moderate Risk Borderline High 130–159 3.40–5. (Chernecky & Berger.0 LDL Cholesterol—Coronary Heart Disease Risk Low Risk Optima <100 <2. 2008) Total Cholesterol—Coronary Heart Disease Risk Desirable Norm mg/dL Adult <200 Child <170 SI Units mmol/L <5.59 Near Optimal 100–129 2.

Insulin pump has the advantage that is not needed injection. In people with type 2 diabetes. especially children. there is danger of infection given the interruption of blood flow and decreased immune system that occurs in most patients with diabetes. • Insulin: Type 1 diabetes requires insulin therapy. Insulin also vary in aspects of work. This objective is achieved through a variety of ways. In addition.10 What is the solution of this problem? The aim of treatment of diabetes mellitus is consistently normalize blood glucose levels with minimum variation. then the pump can be programmed to increase or reduce the amount of insulin secreted. If the planned changes to the regular schedule.1. The pump is also very expensive. People with type 2 diabetes. although considered not insulin dependent. and length of work. an important consideration for all people with diabetes. may occur insulin deficiency or insulin release produced less effective because METABOLISM AND NUTRITION MODULE 16th Group . Recent studies suggest that maintaining blood glucose levels as normal and as often as possible to reduce morbidity and mortality. Available subcutaneous insulin pump that can be programmed for release a certain amount of insulin within a certain time interval per day. each of which is adjusted individually. Lack of programming failure pump is likely causing hypoglycemia or hyperglycemia. the peak time of work. Although the injection of subcutaneous insulin is usually given 3-4 times a day after the basal blood glucose levels measured.66 3. can also benefit from insulin therapy. but treatment for people with type 1 diabetes in the future will most likely be directed toward a more frequent injections. There are various types of insulin with the origin and purity of different. as well as damage to the pump which caused the death.

These medications can be used effectively only if the individual shows insulin secretion. Drugs are contraindicated for individuals with kidney disease. and length of work. and mineral. • Education and adherence to the diet: Another important component in the treatment of diabetes type 1 and 2. Diabetes diet plan is calculated on an individual basis depending on the needs of growing. 20% from protein. • Sports programs. These drugs also appear to reduce gluconeogenesis by the liver. vitamins. Exercise also can increase the sensitivity of cells to insulin. and activity level. Diet also includes fiber. especially for people with type 2 diabetes. will promote weight loss can improve insulin sensitivity distinction.67 a slight change. It is the third therapeutic interventions for diabetes mellitus. weight loss plan (typically for patients with type 2 diabetes). exercise is proven to increase the use of glucose by the cells so that blood glucose levels down. Oral hypoglycemic medications vary in aspects of work. especially on the sata-time stress or illness. due to a decline in blood glucose that triggers hypoglycemia. Exercise. Most patients with type 2 diabetes recovering near-normal blood glucose levels with dietary intervention only because of the role of obesity factor. People with type 2 diabetes can be treated with oral hypoglycemic drugs. this form of monitoring of blood glucose levels carefully and diet. For both types of diabetes. If present. METABOLISM AND NUTRITION MODULE 16th Group . the most important aspect of treatment is prevention. then the diabetic ketoacidosis treated with insulin and measures for balancing fluid and electrolytes. and 30% from fat. combined with the liberation of the diet. People with type 1 diabetes must be careful when exercising. • Prevention: for diabetic ketoacidosis. Distribution is usually 50-60% of calories from complex carbohydrates. These drugs appear to work by stimulating pancreatic beta cells to increase insulin release and increased sensitivity to insulin receptor cells. time fatherly reached peak employment. This right is especially true if insulin is not adapted to the exercise program.

• Replacement of the island of Langerhans cells: recent advances in the techniques of replacement cells of Langerhans islands enables more than 3000 people worldwide were treated with the island of Langerhans cell transplantation. • Insertion of genes for insulin: is currently also being carried out preliminary experiments designed to allow insertion of the insulin gene to type 1 diabetes. In future. Treatment in this manner gives hope for diabetes cure in the future.68 • Fluid: nonkelotik hiperglikemik hyperosmolar coma treated by giving fluids in bulk and slow correction of potassium deficit. compared with drug therapy. This incident can be prevented by good diet control. • Pharmacological interventions that can be considered to be given to patients with diabetes are antihypertensive medications. METABOLISM AND NUTRITION MODULE 16th Group . Anti-hypertensive medications have been proven to reduce hypertension in patients with diabetes and kidney disease awitan slow. this procedure is to provide hope for healing diabetes.

have 1 child Address : Kupang Indah Surabaya Job : Housewife She has tingling since 1 month ago. Diabetes : unknown Hypertension : disputed Family history : Her father dead from complication METABOLISM AND NUTRITION MODULE 16th Group . She often wakes up at night for micturing. She losses 3 kg of her weight. series of anamnestic question. physical examination.69 3.2 ANALYSIS A woman came with problems of her drowsiness and her tingling. and laboratory test should be done Anamnesis • • • • • • • • • • • • Age : 41 years Marital status : Married. She often fell sleepy. In order to get the diagnosis and the possible patophysiology of her problems. all the time and progressive.

She often feel hungry too. Anemia. Icterus = Negative (-) Ascites = negative (-) Palpation: • Hepar and Lien cannot be felt METABOLISM AND NUTRITION MODULE 16th Group . She rarely.70 • Her eldest sister dead in 40th years old with a wound in her leg which cannot be healed and nasty smell • • • • She hasn’t received any treatments before. practically never. She often feels thirsty and drinks much. does any sports Physical Examination • • • • • • • • • General condition : good Blood pressure : 120/80 mmHg Pulse pressure : 80 times/minute Respiratory Rate : 20 times/minute Temperature : 37o Celsius Weight : 89 kg Height : 157 cm Waist Circumference : 93 cm No bad smell in her breath Inspection : • • Cyanosis.

" and excessive muscle loss in the ancient world. Besides.71 Percussion : Thorax : • Heart and Lungs = Normal Laboratory Result • • • • • • Fasting Glucose : 199 mg/dL 2-h PP Glucose : 317 mg/dL Triachilglicerol 278 mg/dL Hemoglobin : 12 g/dL Creatinin Level : 0. Total Cholesterol : 171 mg/dl From the data above. LDL : 94 mg/dL. or both. hence the term sweet urine. commonly referred to as diabetes was first identified as a disease associated with "sweet urine. When the blood glucose elevates (for example. the absence or insufficient production of insulin causes hyperglycemia. In this patient. Normally. METABOLISM AND NUTRITION MODULE 16th Group . In patients with diabetes. Diabetes mellitus. Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine.7 mg/dL HDL : 38 mg/dL . blood glucose levels are tightly controlled by insulin. polydipsia (increased thirst) and polyphagia (increased hunger). we think of the most possible disease called Diabetes Mellitus. after eating food). insulin is released from the pancreas to normalize the glucose level. we found some conditions fit these symptomps. there is a losing in the body weight. Insulin lowers the blood glucose level. Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels that result from defects in insulin secretion. or action. This high blood sugar produces the classical symptoms of polyuria (frequent urination). a hormone produced by the pancreas.

and other large blood vessel diseases. She drinks much in order to fulfill her thirst. patient also complains about her being sleepy easily recently. coronary heart disease. It will be manifested in her drowsiness at day. This drowsiness may be a result from the fatigued cells and the bad quality of sleep. Because the glucose can’t enter the cells well. This tingling may come from the damage of the small vessels which supply nerves which inervates the specific location.specifically nocturia). This kind of damage may occur in the patient above. atherosclerosis made by the high glucose in diabetic patient will make the cells receive oxygen less or we called it (hypoxia). Besides. a condition which someone never gets satisfied with their intake. Over time. It is well known as neuropathy. Somehow. This polyphagia may occurs because diabetic patient can’t make much energy from the glucose so it will force the diabetic patient to eat more in order to make some energies. diabetes can lead to blindness. Diabetic patient has 2 requirements becoming often sleepy. the brain will compensate it by making a thirst signal that insist person to drink more and more (polydipsia). The damage may occur because high blood glucose will make the glucose enters endothelial cells easier because it doesn’t need any insulin. nocturia and sleep apnea often occur and make the patient has a bad quality of sleep at night. because of the more lipolysis and muscle (protein) degradation. Also. METABOLISM AND NUTRITION MODULE 16th Group .72 First. kidney failure. in diabetic patient. This is what we called polyphagia. referred to as micro vascular disease. Because of losing many water from the body by polyuria. the body will feel weaker because it lacks of energy. leading to strokes. These types of damage are the result of damage to small vessels. especially at night (polyuria. and nerve damage. This is referred to as macro vascular disease. the patient has an increase frequency in urination. She often feels hungry too. She has tingling since 1 month ago. Diabetes is also an important factor in accelerating the hardening and narrowing of the arteries (atherosclerosis). She also starts losing her body weight. This damage will make the nerve supplied by the damaged vessels starving and then damaged as well. and this patient also often feel thirsty.

Glucose is an essential nutrient that provides energy for the proper functioning of the body cells.18 kg/m2) put into the condition of obesity class II. The Insulin Resistance can be occurred in this patient in some ways. This obesity can increase the possibility to the damage of insulin receptor in body cells someway. In addition her waist circumference (93 cm) exceed female’s waist circumference standard. is the main disorder in type 1 diabetes. According to Asia standard. The absolute lack of insulin. and results in a condition known as "insulin resistance. the cells' inability to utilize glucose gives rise to the ironic situation of "starvation in the METABOLISM AND NUTRITION MODULE 16th Group . production of defective insulin (which is uncommon). or the inability of cells to use insulin properly and efficiently leads to hyperglycemia and diabetes. the body can. glucose cannot enter the cells alone and needs insulin to aid in its transport into the cells. After time. Essentially. Carbohydrates are broken down in the small intestine and the glucose in digested food is then absorbed by the intestinal cells into the bloodstream. In certain types of diabetes. and it is very dangerous to our health. Without insulin. to some degree. increase production of insulin and overcome the level of resistance. When it happens for a long time.73 Insufficient production of insulin (either absolutely or relative to the body's needs). usually secondary to a destructive process affecting the insulin producing beta cells in the pancreas." This is the primary problem in type 2 diabetes. if production decreases and insulin cannot be released as vigorously. It is called Central Obesity. In type 2 diabetes. her BMI (36. This latter condition affects mostly the cells of muscle and fat tissues. and is carried by the bloodstream to all the cells in the body where it is utilized. sensitivity of the body cells toward insulin will be more decrease and finally it is called Insulin Resistance. the cells become starved of glucose energy despite the presence of abundant glucose in the bloodstream. there also is a steady decline of beta cells that adds to the process of elevated blood sugars. if someone is resistant to insulin. Glucose is a simple sugar found in food. hyperglycemia develops. However.

In normal individuals.) In addition to helping glucose enter the cells. or not used properly by the body. As outlined above. but in the range of 100-126mg/dl. and is addressed elsewhere. When fasting blood glucose stays above 100mg/dl. The abundant. insulin is also important in tightly regulating the level of glucose in the blood. After a meal. A blood glucose level of 200 mg/dl or higher indicates diabetes. the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. the blood glucose level rises. All of these factors cause elevated levels of blood glucose (hyperglycemia). in patients with diabetes. • Fasting plasma glucose levels of more than 126 mg/dl on two or more tests on different days indicate diabetes. this condition carries with it its own risks and concerns. unutilized glucose is wastefully excreted in the urine. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. • A random blood glucose test can also be used to diagnose diabetes.74 midst of plenty". While patients with IFG do not have the diagnosis of diabetes. METABOLISM AND NUTRITION MODULE 16th Group . this is known as impaired fasting glucose (IFG). (The pancreas is a deep-seated organ in the abdomen located behind the stomach. The fasting blood glucose (sugar) test is the preferred way to diagnose diabetes. When the blood glucose levels are lowered. relatively insufficient for the body's needs. In response to the increased glucose level. the insulin is either absent. • Normal fasting plasma glucose levels are less than 100 milligrams per deciliter (mg/dl). the insulin release from the pancreas is turned down. such a regulatory system helps to keep blood glucose levels in a tightly controlled range.

before we learn more about DM. 16th Edition. Likewise. we think that she is suffered from type 2 Diabetes Mellitus. particularly in obese adolescents. an autoimmune beta cell destructive process can develop at any age. After that we get a data that explain about the onset. but it also occurs in children. In that time. Her 2-h PP plasma glucose are 317 mg/dL and it exceeds the normal 2-h PP plasma glucose which is less than 200 mg/dL.75 We try to compare the patient’s blood glucose level with the standard itself. we think that type 2 DM develop with increasing age and type 1 DM develop in younger age. type 2 DM more typically develops with increasing age.2005 by Kasper. METABOLISM AND NUTRITION MODULE 16th Group .2005) So we should analyze more from other data. Those conditions above tell us that this patient truly suffers from hyperglycemia. because from the anamneses we know that she is 41 years old. “ Although type 1 DM most commonly develops before the age of 30. In the first. Her fasting plasma glucose are 199 mg/dL and the normal fasting plasma glucose are less then 100 mg/dL. which is one of the characteristics of Diabetes Mellitus. We got a data about the risk factors for type 2 Diabetes Mellitus from Harrison's Principles Of Internal Medicine. It is estimated that between 5 and 10% of individuals who develop DM after age 30 have type 1A DM.” (Kasper.

Second. The first factor is she is obese (the BMI is about 36. 3.3 FINAL HYPOTHESIS Miss X . Third.1). because uncontrolled diabetes can make complication problem and diabetic patient often have wound that hard to be healed (ulcer). 41 years old.76 In this patient. has the symptoms of Diabetes Mellitus Type 2 with hyperglycemia. we find some risk factors for type 2 Diabetes Mellitus in this patient. From anamneses we know that her father dead from complication and her eldest brother dead in 40 th years old with a wound in her leg which cannot be healed and nasty smell. We think that her father and her brother had suffered from diabetes. she is habitual physical inactivity. That is she have family history of diabetes. There is one more risk factor that maybe she have but we aren’t sure about that. triglyceride level is > 250 mg/dL (278 mg/dL). dysllipidemia due to the decreasing of sensitivity of insulin receptor in cells caused by her obesity METABOLISM AND NUTRITION MODULE 16th Group .

polydipsia.7 mg/dL HDL: 38 mg/dL . practically never. LDL: 94 mg/dL. polyphagia. tingling.4 FINAL MIND MAPPING Sensitivity of insulin receptor is decreased Palpation. Total Cholesterol: 171 mg/dl High lipotoxic from rarely. Anemia. and other progressive complication like atherosclerosis. does adipocyte any sports 3. Mellitus . 41 years old vital sign examination: Pulse : 80/min RR : 20/min Temp: 37 oC Blood pressure : 120/80 mmHg Weight: 89 kgs Height: 157 cms Waist circumference: 93 cms Examination Inspections: Cyanosis. percussion. & auscultation : Ascites (-) Hepar & Lien normal Compensated by pancreas to produce more insulin Decompensation of β cell of pancreas High level of blood glucose Other complications: Polyuria. METABOLISM AND NUTRITION MODULE 16th Group Type 2 Diabetes sleepy.77 Anamnesis: Tingling all time since a month ago Wake up at night for micturing Often feel sleepy 3 kgs weight losses Family sick: father dead from complication and eldest sister dead in 40 years old with a wound in her leg which can’t be healed and nasty smell Often feels thirsty and drinks much Often feel hungry too Hasn’t received any treatments before A Female. Icterus (-) Ascites (-) Extremity deformities (-) Obese Laboratory results: Fasting Glucose: 199 mg/dL 2-h PP Glucose: 317 mg/dL Triachilglicerol 278 mg/dL Hemoglobin: 12 g/dL Creatinin Level: 0.

78 Obese Large amount of adipocytes Others factor High lypotoxic Sensivity of insulin receptor decreased Polyphagya polydypsea polyuria Chardiovascula r disease Glucose can not enter into cells with GLUT-4 CASE MAPPING Blood glucose increase Complication of diabetes melitus Renal disease Neuropaty Other complication Type 2 diabetes mellitus Compensated by pancreas to increase the insulin production Sensivity of insulin receptor decrease progressively High level of blood glucose METABOLISM AND NUTRITION MODULE 16th Group Decompensation of beta cell of pancreas Low level of insulin .

oral glucose-lowering agents are subdivided into agents that increase insulin secretion.79 3. reduce glucose production. etc without METABOLISM AND NUTRITION MODULE 16th Group . which make glucose can be absorbed by the cells like skeleton muscle. oral glucose-lowering agents can be given to this woman. She should start to exercise.5 GROUP OPINION Knowing that this woman has type 2 diabetic diseases which cells unable to use insulin although insulin is produce. or increase insulin sensitivity so it can decrease the level of blood glucose. We also suggest that this woman should seriously change her habit.

this woman should have diet.S.80 insulin. Since all of us are involved in medical science held by the students of Airlangga University Medical Faculty. Peripheral Neuropathy Fact Sheet. 2010. she should has a struggle to restrain her apatite.nlm. because if she is not change her diet.gov/medlineplus/ency/article/003208.nih. 2010. Difficult for gathering the members of our group because of our bustle. so it can help the insulin’s receptor activity to fulfill the cell needs for glucose. We are lack to ask more completely about patient examination so it’s hard for us in making decision of analysis and final mind-map. And the most important. 3. we do not have enough time to gather and discuss References U. Available at: METABOLISM AND NUTRITION MODULE 16th Group . National Institute of Neurological Disorders and Stroke. 3.6 OBSTACLES 1.htm on November 6th 2010) National Institute of Neurological Disorders and Stroke. National Library of Medicine. 2. Drowsiness. Available at: (Accessed http://www. Department of Health and Human Services. She must be decrease carbohydrate intake. her glucose level will always be high that have many risk for her health.

gov/disorders/peripheralneuropathy/detail_peripheral neuropathy. Available at: http://www.nih. Available at: http://www. A service of the U. Pathophysiology Of Diabetes Mellitus. [online] (Updated 12 Oct 2010).2010. Type 2 Diabetes – risk factors. National Library of Medicine National Institutes of Health (Online). Available at: METABOLISM AND NUTRITION MODULE 16th Group .html (Accessed November 7th 2010) Unknown author. [internet] Diabetes Manegement in School Setting. 2010. [online] (Updated 12 Oct 2010). 2010. International Diabetes Federation (Online). [Online] (unknown updated date). Phatophysiology of Diabetes.mo.dhss. Diabetes symptoms: When diabetes symptoms are a concern.81 http://www.ninds. Lingkar Perut Membesar dan Kegemukan.mayoclinic. Available at: http://www.com/index. . Available at: http://www. Available at: http://www.com/health/diabetessymptoms/DA00125/NSECTIONGROUP=2 (Accessed 7 November 2010) Hani L.gov/medlineplus/ency/article/002072.co.htm (Accessed on November 11th 2010) Pathophysiology Of Diabetes Mellitus. Available at http://www.htm (Accessed on Nopember 10th 2010) International Diabetes Federation. Diabetes symptoms: When diabetes symptoms are a concern.mayoclinic. 2009. unknown year.S.com/health/diabetes-symptoms/DA00125 (Accessed 7 November 2010) Mayo Clinic.nlm. 2010.id/index.nih.gov/diabetes/DMOverview.pdf (Accessed on November 7th 2010) Mayo Clinic. 2010.pathophysiologyofdiabetesmellitus.indonesiapower. Complications of diabetes.php? option=com_content&view=article&id=1145:lingkar-perut-membesardan-kegemukan (Accesed on November 17th 2010) MedlinePlus.

2003.com/diabetes/page3_em.USA: Lange Medical Lopes et al. 2005. Diabetes Care December 1992 Vol..unand.htm (Accessed November 17th 2010) Kasper. (Accessed on November 10th 2010) Chernecky & Berger. Restless Legs Syndrome and Quality of Sleep in Type 2 Diabetes Greene et al. 2005. Robert K. Available at http://www.ac. pathogenetic considerations. MEKANISME SEKRESI DAN ASPEK METABOLISME. 2010.id/url? sa=t&source=web&cd=2&ved=0CBkQFjAB&url=http%3A%2F %2Frepository.org/content/15/12/1902 (Accessed on November 11th 2010) eMedicineHealth. Human Nutritions and Dietetics. Edinburgh: English Language Book Society.anaesthesiamcq. eds. twenty six edition. Availablet at http://www.google. S. 2003. New York: Lange Medical Books Manaf. 15 no. 2007.php (Accessed on November 8th 2010) Davidson.com/AcidBaseBook/ab3_2. et al. New York: McGraw-Hill Companies Murray.org/complications-diabetes. Harper’s Illustrated Biochemistry. Diabetes Symptoms. 1992.diabetesjournals. 5th Edition. 12.co.82 http://www. Robert et al. Dennis L.. et al. A.idf. 1973. Laboratory Tests and Diagnostic Procedures. et al. Harrison’s Principles of Internal Medicine 16th ed.emedicinehealth.id %2F96%2F1%2FINSULIN__MEKANISME_SEKRESI_DAN_ASPEK_ METABOLISM AND NUTRITION MODULE 16th Group . Acid-base Physiology. Missouri: Saunders Elvesier Brandis. 2008. Avalable at: http://care.. Available at http://www. Kerry. Harper’s Illustrated Biochemistry 26th ed. Complications: neuropathy.

1980. Lange Medical Books/McGraw-Hill Medical Publishing Division.Harper’s Illustrated Biochemistry. Hall.full. 2003.83 METABOLISME. Vol.gizi. Missisipi : Elsevier Inc. Insulin release. EGC Penerbit Buku METABOLISM AND NUTRITION MODULE 16th Group . 2006.pnas. Available at http://www.12. Guyton. Textbook of Medical Physiology 11th Ed. p. Jakarta. Kedokteran Pathophysiology. insulin sensitivity. et al. and glucose intolerance.org/content/77/12/7425. PERAN DIIT DALAM PENANGGULANGAN DIABETES. No. Departemen Kesehatan RI. Robert K. (Online).net/makalah/Makalah%20Pekan%20DM.2003. Twenty-Sixth Edition.966 .PDF (Accesed on November 17th 2010) Efendic.pdf (Accessed at November 11th 2010) Murray.967 Corwin. Proceedings of the National Academy of Sciences. Available at: http://www. Elizabeth (2001). 77. Direktorat Jenderal Bina Kesehatan Masyarakat.doc&ei=cPDjTOrFKYi3cIm6ra0M&usg=AFQjCNGSQ oXZMYjqnExky-cWrgX8Al_FyQ (Accesed at November 17th 2010) Direktur Gizi Masyarakat.

path ophysiologyofdi abetesmellitus.htm (Accessed on November 11th 2010) http://www.nind s.CRITICAL APPRAISAL EBL and Critical Apraissal For Answering Question Searching Method Information Type Validity Foundation Result Importance Foundation Result 84 Applicability Foundation Result LEARNING ISSUES 1 http://www. nih.c om/index.gov/disord ers/peripheralne uropathy/detail_ peripheralneuro pathy.dhss . pdf (Accessed on November 1 Internet Browsing Digital Article Yes Content of information Yes Is it applicable? Yes 2 Internet Browsing Digital Article Yes Content of information Yes Is it applicable? Yes 3 Internet Browsing Digital Idea No Content of information Yes Is it applicable? Yes 3 Internet Browsing Digital Article Yes Content of information Yes Is it applicable? Yes METABOLISM AND NUTRITION MODULE 16th Group .html (Accessed November 7th 2010) http://www.gov/medline plus/ency/article /003208.mo.nlm.gov/diabete s/DMOverview.htm (Accessed on November 6th 2010) http://www.nih.

com/heal th/diabetessymptoms/DA0 0125/NSECTIO NGROUP=2 (Accessed November 7th 2010) http://www.may oclinic.85 7th 2010) http://www.com/heal th/diabetessymptoms/DA0 0125 (Accessed November 7th 2010) http://www.php? option=com_co ntent&view=arti cle&id=1145:lin gkar-perutmembesar-dankegemukan (Accesed on November 17th 2010) http://www.co.indo nesiapower. 4 Internet Browsing Digital Idea No Content of information Yes Is it applicable? Yes 4 Internet Browsing Digital Idea No Content of information Yes Is it applicable? Yes 5 Internet Browsing Digital Idea No Content of information Yes Is it applicable? Yes 6 Internet Digital Article Yes Content of Yes Is it Yes METABOLISM AND NUTRITION MODULE 16th Group .nlm.may oclinic.id /index.

10.php (Accessed on November 8th 2010) Human Nutritions and Dietetics Browsing information applicable? 7 Internet Browsing Digital Article Yes Content of information Yes Is it applicable? Yes 8.htm (Accessed on Nopember 10th 2010) http://www.idf.86 nih.com/ AcidBaseBook/a b3_2. (Accessed on November 10th 2010) Laboratory Tests and Diagnostic Procedures.9.gov/medline plus/ency/article /002072.o rg/complications -diabetes.11 eBook Digital Textbook Yes Content of information Yes Is it applicable? Yes 12 Internet Browsing Digital Idea No Content of information Yes Is it applicable? Yes 13 Borrowed from the library Textbook Article Yes Content of information Yes Is it applicable? Yes LEARNING ISSUES 2 METABOLISM AND NUTRITION MODULE 16th Group .anae sthesiamcq. 5th Edition http://www.

1995.7 Personal Inventory Textbook Textbook Yes Content of information Yes Is it applicable? Yes Restless Legs Syndrome and Quality of Sleep in Type 2 Diabetes http://care.87 Harper’s Illustrated Biochemistry. twenty six edition 1.4.org/c ontent/15/12/19 02 (Accessed on November 11th 2010) Partanen. et al.diabet esjournals. History Peripheral Neuropathy Patients Dependent Non-Insulinin with Natural of 1 Borrowing from the library Textbook Article Yes Content of information Yes Is it applicable? Yes 2 Internet Browsing Internet Browsing Digital (PDF) Digital (PDF) Journal Yes Content of information Content of information Yes Is it applicable? Is it applicable? Yes 2 Journal Yes Yes Yes METABOLISM AND NUTRITION MODULE 16th Group .

htm (Accessed November 17th 2010) 3 Internet Browsing Digital Idea No Content of information Yes Is it applicable? Yes METABOLISM AND NUTRITION MODULE 16th Group . 333 No.co m/diabetes/page 3_em. Available Vol.1056/NEJM19 9507133330203 (Accessed 2010) on November 20th http://www. NEW ENGLAND JOURNAL MEDICINE. (Online). 2.org/doi/pdf/1 0.nej m. at: of The http://www.88 Diabetes Mellitus.eme dicinehealth.

u nand.PDF (Accesed on 4 Using Textbook Text Textbook Yes Content of information Yes Is it applicable? Yes 5 Internet Browsing Digital (Word) Article Yes Content of information Yes Is it applicable? Yes 5 Internet Browsing Digital (PDF) Article Yes Content of information Yes Is it applicable? Yes METABOLISM AND NUTRITION MODULE 16th Group .89 Harrison’s Principles of Internal Medicine 16th ed.co.id %2F96%2F1%2 FINSULIN__M EKANISME_S EKRESI_DAN_ ASPEK_META BOLISME.doc &ei=cPDjTOrF KYi3cIm6ra0M &usg=AFQjCN GSQoXZMYjqn ExkycWrgX8Al_FyQ (Accesed at November 17th 2010) http://www.goo gle. net/makalah/Ma kalah%20Pekan %20DM. http://www.gizi.id/url? sa=t&source=w eb&cd=2&ved= 0CBkQFjAB&u rl=http%3A%2F %2Frepository.ac.

967 Laboratory Tests and Diagnostic Procedures. p. Textbook of Medical Physiology 11th Ed. Twenty-Sixth Edition. 5th Edition Pathophysiolog y 6 Internet Browsing Digital (PDF) Article Yes Content of information Yes Is it applicable? Yes 7 Personal inventory Textbook Text Yes Content of information Yes Is it applicable? Yes 8 Personal inventory Textbook Text Yes Content of information Yes Is it applicable? Yes 9 eBook Digital Article Yes Content of information Yes Is it applicable? Yes 10 Borrowing from the library Text Report Yes Content of information Yes Is it applicable? Yes METABOLISM AND NUTRITION MODULE 16th Group .pnas .org/content/77/ 12/7425.pdf (Accessed at November 11th 2010) Harper’s Illustrated Biochemistry.90 November 17th 2010) http://www.966 . Missisipi : Elsevier Inc.full.

91 METABOLISM AND NUTRITION MODULE 16th Group .

RESEARCH VALIDITY Objective: To determine the long-term risk of diabetic polyneuropathy and the factors affecting that risk. Background  Method  Result  Discussion  Acknowledgement  Reference Existence (with page) Yes (page 89) Yes (page 89) Yes (page 89) Yes (page 89) Yes (page 89) Yes (page 93) No Yes (page 93-94) Conclusion : the format is not complete 2. PAPER COMPLETION : Item  Title  Abstract and or Summary  Introduction.SCIENTIFIC PAPER APPRAISAL Group : Title : 16th group Natural History of Peripheral Neuropathy in Patients with NonInsulin-Dependent Diabetes Mellitus 1. PBL Group 1st Medical Faculty of Airlangga University Medical Ethic and Law Module 2009 .

132 patients with NIDDM and 142 control subjects underwent clinical evaluation and measurement of nerve conduction velocity.4 The control subjects were recruited from among 180.Method: Cross-sectional Study Item Items found (with page) Cross-sectional study (Page 89) 5 We recruited 133 patients with newly diagnosed NIDDM who were 45 to 64 years old at the time of Table 1 Characteristics of the Patients with NIDDM and the Control Subjects at Base Line. and 86 (65 percent) and 121 (85 percent). At base line.). 114 patients with NIDDM (86 percent) and 128 control subjects (90 percent) were evaluated after 5 years of follow-up. respectively. diagnosis and 144 randomly Design Hierarchy of Evidence Sample Sample Size PBL Group 1st Medical Faculty of Airlangga University Medical Ethic and Law Module 2009 .2 Both groups were evaluated between May 1. 1981. and December 31. (Page 89) We recruited 133 patients with newly diagnosed NIDDM who were 45 to 64 years old at the time of Table 1 Characteristics of the Patients with NIDDM and the Control Subjects at Base Line. Of these. diagnosis and 144 randomly selected nondiabetic control subjects in the same age group (Table 1Table 1 Characteristics of the Patients with NIDDM and the Control Subjects at Base Line. after 10 years. 1979.000 inhabitants of the county of Kuopio in eastern Finland.

Eligibility Criteria

selected nondiabetic control subjects in the same age group (Table 1Table 1 Characteristics of the Patients with NIDDM and the Control Subjects at Base Line.).2 Both groups were evaluated between May 1, 1979, and December 31, 1981.4 The control subjects were recruited from among 180,000 inhabitants of the county of Kuopio in eastern Finland. At base line, 132 patients with NIDDM and 142 control subjects underwent clinical evaluation and measurement of nerve conduction velocity. Of these, 114 patients with NIDDM (86 percent) and 128 control subjects (90 percent) were evaluated after 5 years of follow-up, and 86 (65 percent) and 121 (85 percent), respectively, after 10 years. (Page 89) We recruited 133 patients with newly diagnosed NIDDM who were 45 to 64 years old at the time of Table 1 Characteristics of the Patients with NIDDM and the Control Subjects at Base Line. diagnosis and 144 randomly selected nondiabetic control subjects in the same age group (Table 1Table 1 Characteristics of the Patients with NIDDM and the Control Subjects at Base Line.).2 Both groups were evaluated between May 1, 1979, and December 31, 1981.4 The control subjects were recruited from among 180,000 inhabitants of the county of Kuopio in eastern Finland. At base line, 132 patients with NIDDM and 142 control subjects underwent

PBL Group 1st Medical Faculty of Airlangga University Medical Ethic and Law Module 2009

clinical evaluation and measurement of nerve conduction velocity. Of these, 114 patients with NIDDM (86 percent) and 128 control subjects (90 percent) were evaluated after 5 years of follow-up, and 86 (65 percent) and 121 (85 percent), respectively, after 10 years. (Page 89) Exclusion Criteria Sampling Frame Collecting Data Method
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Total Sampling The diagnosis of diabetes4 was confirmed by an oral glucosetolerance test, in which subjects were given 75 g of glucose after a 12-hour overnight fast5; the test was performed in both the diabetic patients and the control subjects. Information about cigarette smoking and the use of alcohol was obtained by questionnaire. (Page 89) Glucose tolerance was assessed by measuring blood or plasma glucose concentrations (in blood at base line and in plasma at 5 and 10 years) and serum insulin and C-peptide concentrations before and one and two hours after the oral administration of 75 g of glucose. Glucose was measured by the glucose oxidase method (at base line and at the 10-year examination) or the glucose dehydrogenase method (at 5 years).7 Serum insulin was measured by a double-antibody radioimmunoassay (at base line: Novo Industries, Copenhagen, Denmark; at 5 and 10 years: Phasedeph, Pharmacia, Uppsala, Sweden). Serum C peptide was measured by radioimmunoassay (at 5 years: Novo-Nordisk, Copenhagen; at 10 years: 125-I, Incstar, Stillwater, Minn.).7

Measurement and or assessment

PBL Group 1st Medical Faculty of Airlangga University Medical Ethic and Law Module 2009

Instrument

At all examinations, serum lipid concentrations were determined in samples obtained after the subjects had fasted for 12 hours. Lipoproteins were analyzed enzymatically after ultracentrifugation and precipitation.6,8 Glycosylated hemoglobin was measured at the 5-year and 10-year examinations by liquid cation-exchange chromatography (normal range, 4.0 to 6.0 percent). In the baseline study, albumin was measured by immunodiffusion in 24-hour urine samples (Behringswerke, Mahrburg Lahn, Germany). (Page 89-90) The differences in mean values between the groups were analyzed by Student's t-test (twotailed), the Mann-Whitney U test, or analysis of covariance with control for confounding variables. The categorical variables were analyzed by the chi-square test, McNemar's test, or Fisher's exact test. Timerelated changes within a group were analyzed by paired t-tests or the Wilcoxon matched-pairs signed-rank test. Differences in the areas under the serum insulin curve (at base line, 5 years, and 10 years, with insulin-treated patients omitted) between the patients with and without neuropathy were analyzed by repeated-measures analysis of variance (for time of investigation, group, and fasting glucose value at base line and at 5 and 10 years). Serum insulin concentrations were analyzed after logarithmic transformation. The area under the serum insulin curve was calculated by the

PBL Group 1st Medical Faculty of Airlangga University Medical Ethic and Law Module 2009

083 If this research were done repeatedly (100x).3 researches will show the same result as the previous result (by chance). IMPORTANCE CI P : : There is no CI. 8. the importance can’t be measured PBL Group 1st Medical Faculty of Airlangga University Medical Ethic and Law Module 2009 . 0. The Spearman correlation coefficient was calculated for the relation between nerve function and the metabolic variables (glycemic control and serum insulin values). Conclusion : Because there is no CI. Chicago).Randomization Intervention Analysis Method trapezoidal rule. (Page 91) Statistical Method (Page 91) Coherence between design and objective: coherent Coherence between measurement and instrument used: coherent Conclusion: valid (ONLY BASED FROM TWO CONCLUSIONS ABOVE) 3. All the data were analyzed with SPSS software (SPSS.

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