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  • Scenario Creator
  • Group Members
  • 1.3 Key Words
  • 1.2. Main Problem
  • 1.5 Early Hypothesis
  • 3.2 ANALYSIS
  • References








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



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


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

METABOLISM AND NUTRITION MODULE 16th Group . students of Airlangga university.5 EIGHTH MODULE HUMAN FUNCTION MODULE PROBLEM BASED LEARNING INSTRUCTIONAL OBJECTIVES After finishing this module.School of Medicine in third semester can explain the patophysiology of health problem through understanding the intermediate metabolism. Main Problem A woman. Female 1. Numbness in both lower extremities 1.3.6 CHAPTER I FIRST TUTORIAL 1. Outpatient treatment 1.2. sometimes feel tingling in both feet.1 Scenario 1.1.4. Sleepy METABOLISM AND NUTRITION MODULE 16th Group .3 Key Words 1. • • Often feels sleepy Often feels sleepy and numbness 1.2. came to the outpatient polyclinic with complaints often sleepy.

4.4. Address: Kupang Indah.4. Almost every night wakes up to go to the toilet 1. She has been feeling numbness for 1 month Woman. Surabaya 1. Status: Married with 1 child 1.7 Husband’s occupation: Private Company Officer 1.6.10. Occupation: Housewive Additional Information 1.4.3. 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. age: 41 years old 1. Medical Record: No hypertension Body weight has decreased 3 kg recently 1.8.4. 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 .

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

7 Learning Issue 1 1.1. What are the causes of drowsiness? METABOLISM AND NUTRITION MODULE 16th Group . cyanotic.9 Female. icterus Early hypothesis: DM Malnutrition Deficiency Neuron Disorders 1. 41 y.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.

8 1.6 1.7.11 1.2 1.10 1.7.7 1.10 1.12 1.4 1.7.13 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 . 1.7.7.

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

arms. Diabetes is classified into three primary types that are different disease entities but share the symptoms and complications of hyperglycemia (high blood glucose). and it passes as soon as you move around a bit. Many medical conditions. the hormone insulin. particularly if you're leaning on your arm or sitting cross-legged. It also aids the body in breaking down the glucose to be used as energy. feet.12 2. Impaired glucose tolerance. The pathophysiology of diabetes mellitus in all forms is related to the insulin hormone. or ineffective use of.3 What are the patophysiologies of Diabetes Melitus? Diabetes is a chronic metabolic disorder in which the body cannot metabolize carbohydrates. you are bound to develop a pins-and-needles sensation in one or more limbs. others are based primarily in different parts of the body. however. formerly known as "borderline diabetes" is a degree of hyperglycemia that may precede type 2 diabetes. cause a persistent tingling sensation — usually in the hands. and proteins because of a lack of. persistent tingling is a troubling symptom that requires a thorough medical workup.2. or legs — that is unrelated to posture and unrelieved by movement. the body does not break down the glucose in the blood as a result of abnormal insulin metabolism. In general. While several of these conditions originate in the peripheral nervous system (the network of nerves branching out from the spinal cord to the extremities). This feeling results from temporary nerve compression and diminished blood flow. 2.2 How is the mechanism of numbness/tingling? Any time you remain still for a long period. This results in elevated levels of glucose in METABOLISM AND NUTRITION MODULE 16th Group . When someone suffers from diabetes. Insulin is secreted by cells in the pancreas and is responsible for regulating the level of glucose in the bloodstream. fats. however.2.

Insulin by injection with syringes or pumps 2. Type 2 (previously called non-insulin-dependent diabetes mellitus. C. stress. Diabetes mellitus occurs in three different forms . Causes METABOLISM AND NUTRITION MODULE 16th Group . Education 5. overt symptoms occur. Peak incidence occurs during puberty. * Source: American Diabetes Association. and fatigue. 3. around 10-12 years of age in girls and 12-14 years in boys. severe complications including cardiovascular disease. Treatment 1. Environmental exposure: virus. Usually occurs before 30 years of age. 2. Characteristics 1. Type 1 (previously called insulin dependent diabetes mellitus (IDDM) or juvenile onset diabetes) A. kidney damage. and gestational. but can occur at any age. When glucose levels remain high over an extended period of time. 2003. eye disorders.type 1. type 2. weight loss. or adult onset diabetes) A. Autoimmune reaction: beta-cells that produce insulin in the pancreas are destroyed. and nerve problems can occur. B. 3. NIDDM. toxin.* 2. Ketosis prone. Abrupt onset of signs and symptoms of hyperglycemia: increased thirst and hunger. Causes 1. Exercise 4. Diet 3. which is known as hyperglycemia. Genetic predisposition. November. Diabetes Facts. I. frequent urination. When 80-90% of the beta-cells are destroyed. Monitoring II.13 the blood.

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

Diet/weight management 2. contractions. If the 1-hour screen for glucose is >140 mg/dl (>7. Causes 1. Exercise: program that does not cause fetal distress.8 mmol/l). Oral hypoglycemic/antihyperglycemic agents. 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). lipid abnormalities) III. a full diagnostic 100-g. Insulin resistance due to pregnancy 2. hypertension.. Treatment of co morbid conditions (e. Diet: provide adequate calories without hyperglycemia or ketonemia 2. Genetic predisposition B. C.g. Education 5. Gestational Diabetes Mellitus (GDM) A. insulin sensitizers. 3.8 mmol/l) 1 hour postprandial and <120 mg/dl (<6. Exercise/increase physical activity 3. Treatment 1. Characteristics 1. 3-hour oral glucose tolerance test (OGTT) is indicated. or insulin 4. or hypertension (>140/90 mmHg). METABOLISM AND NUTRITION MODULE 16th Group . Monitoring 6. Treatment 1.15 C.7 mmol/l) 2 hours postprandial. Insulin: if unable to consistently maintain blood glucose <95 mg/dl fasting (<5.3 mmol/ l) and <140 mg/dl (<7.

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

then it could be said he was experiencing abdominal obesity. swollen. Since then the Indonesian people begin to experience obesity.5 What is normal stomach circumference of human? To determine whether suffering abdominal obesity or not. Especially since the fast-food METABOLISM AND NUTRITION MODULE 16th Group . has not proved whether this is entirely true. particularly in urban areas. Slow-healing sores or frequent infections Doctors and people with diabetes have observed that infections seem more common if you have diabetes. unhealthy lifestyle diseases (metabolic syndrome). What causes obesity? It is said that there are two factors causing the genetic and lifestyle factors. as well as burning pain in your arms. 2. hands. Red. more cases of abdominal fat due to diet and an increasingly unbalanced motion. If someone has abdominal circumference more than the normal number.2. It may be that high levels of blood sugar impair your body's natural healing process and your ability to fight infections. However. For women. In fact. the people of Indonesia have the ideal waist size. Research in this area. However. If more than that. tender gums Diabetes may weaken your ability to fight germs. bladder and vaginal infections are especially common. which increases the risk of infection in your gums and in the bones that hold your teeth in place. legs and feet. Your gums may pull away from your teeth. these early changes do not cause vision problems. however. if these changes progress undetected. Usually. they sign congested hormone bad fats in the stomach. your teeth may become loose. You may notice tingling and loss of sensation in your hands and feet. This will trigger the spread of various diseases metabolic disorders. women's waist size 90 inches biggest meter and men's 80 inch meter. Tingling hands and feet Excess sugar in your blood can lead to nerve damage. or you may develop sores or pockets of pus in your gums — especially if you have a gum infection before diabetes develops. they can lead to vision loss and blindness. stage 1 has been ongoing since early 1990.17 people. nor why.

there are a lot of the mobility of free fatty acids to the liver and muscles. 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 is more dangerous. the center of power. Also explained that the fat can not be removed through liposuction. because the fat inside the abdomen. the pattern of motion (sports) in the stomach the less. rather than under a layer of skin. 2.6 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. The hormone estrogen source of fat in the thighs. on the contrary in the stomach. thickened skin around the neck or armpits METABOLISM AND NUTRITION MODULE 16th Group .18 restaurants to grow and increasingly giving kemudahkan for people to eat all the time. Meanwhile. 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.2. which causes dark. and bearing. and in abdominal fat. it will affect the fatty acid metabolism and pancreatic work. Furthermore.

If it is not corrected it can lead to the person losing consciousness. causing ketoacidosis. The body cannot tolerate large amounts of ketones and will try to get rid of them through the urine. 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. and Native Americans. However. Ketoacidosis is a severe condition caused by lack of insulin. Hispanic Americans. the body cannot release all the ketones and they build up in your blood. • Ketoacidosis When the body breaks down fats. Asian Americans. and be performed more often if you are at higher risk for diabetes. have exercised more than anticipated or have not eaten enough).19 Persons from certain ethnic groups. 2010) 2.7 What are the complications of Diabetes Mellitus? Without proper management it can lead to various complications such as cardiovascular disease. It mainly affects people with type 1 diabetes. It is important that the person with diabetes recognises the signs of hypoglycaemia.2. • Lactic acidosis Lactic acidosis is the build up of lactic acid in the body. Everyone over 45 should have a blood sugar (glucose) test at least every 3 years. kidney failure. (MedlinePlus. acidic waste products called ketones are produced. Regular testing of blood sugar levels should begin at a younger age. blindness and nerve damage. If too much lactic acid stays in the METABOLISM AND NUTRITION MODULE 16th Group . Hypoglycaemia can be corrected rapidly by eating some sugar. including African Americans. Cells make lactic acid when they use glucose for energy.

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

46 7.21 Disease of the circulatory system. corony heart disease is present in between 8% and 20% of people with diabetes over 45 years of age.35–7.49 7. or cardiovascular disease.3 kPa <2.45 35–40 mm Hg <20 mm Hg 7. People with diabetes are 15 to 40 times more likely to require lower-limb amputation compared to the general population.45 ≤7. accounts for 75% of all deaths among people with diabetes of European origin.35–7.35–7.8 What is the blood gas analysis? Blood Gases. 2010) 2.46 7.2.35–7.32–7. It is the main cause of disability and death for people with type 2 diabetes in industrialized countries. Arterial (ABG)—Blood Norm.32–7.49 7.34–7.2 and >7.6 7. In the USA.7–5.45 ≤7. Must be corrected for body temperature.45 4.2 and >7. (International Diabetes Federation. Their risk of heart disease is 2-4 times higher than those who do not have diabetes.6 METABOLISM AND NUTRITION MODULE 16th Group .7 kPa 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.34–7. SI Units pH Adults Panic values Children Birth to 2 months 2 months to 2 years >2 years PaCO2 Panic values 7.

pulmonary infection. prednisone. renal disorders. transposition of the great vessels. renal disease.3 kPa 22–31 mmol/L <10 mmol/L >40 mmol/L 0. poisoning. emphysema. and thiazides. respiratory alkalosis. brain death.4 kPa <5.96–1. respiratory acidosis. duodenal). pleurisy.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. diarrhea. congestive heart failure. METABOLISM AND NUTRITION MODULE 16th Group . tetralogy of Fallot. near drowning.7–13. coarctation of the aorta. and vomiting (excessive). high altitude. Drugs include aldosterone.00 <0. and vomiting. hyperemesis. pulmonary edema. respiratory failure. Hyperbaric oxygenation and hyperventilation. Increased PaCO2. metabolic alkalosis.3 kPa Oxyhemoglobin Dissociation Curve No shift Increased pH. pneumonia. intestinal obstruction (pyloric. pleural effusion. fever.60 80–100 mm Hg 10. Acute intermittent porphyria. pneumothorax. peptic ulcer therapy. aminoglycoside toxicity. sodium bicarbonate. empyema. hysteria. electrolyte disturbance (severe). hyaline membrane disease. ethacrynic acid. metabolic alkalosis. Increased PaO2. Cushing's disease. Alkali ingestion. hypothyroidism (severe). salicylate intoxication. metolazone. shock. Drugs include sodium bicarbonate. asthma (late stage). hypoventilation (alveolar). hyperventilation.

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

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

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. counteracting the pH reduction and increasing the breathing rate. The METABOLISM AND NUTRITION MODULE 16th Group . The body demands that pH remain constant. When pH decreases. and respiratory acidosis. thereby altering pH value.3DPG. 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. Significant deviations in pH can be life threatening. emphysema. Cluster headaches. The kidneys and lungs regulate pH by preserving the ratio of acid to base. Description. The partial pressure of carbon dioxide (pCO2. fever. increased production of 2. PaO2) is the amount of oxygen dissolved in plasma and represents the status of alveolar gas exchange with inspired air. hypercapnia. Both bicarbonate (HCO3-) and carbonic acid (H2CO3) are components of the body's acid-base system that influence pH. 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. SaO2) of hemoglobin at varying partial pressures of oxygen. Any alteration in the ratio between bicarbonate and carbonic acid will cause a reciprocal change in release or uptake of free H+. more CO2 dissociates from carbonic acid and is exhaled through the lungs. The partial pressure of oxygen (pO 2. 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.25 Shift to Right. The pH is the measurement of free H+ ion concentration in circulating blood. which are buffered as either an acid (HCO3-) or a base (H2CO3). 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 pO2.43 <7. when the shift is to the right. less oxygen is delivered to the tissues.0 kPa 20–49 mm Hg 2. Generally. See Blood gases.2 or >7.6 7.6–6.80 O2 Saturation 60%–80% Increased pH. When the curve is shifted to the left.26 Hem-O-Scan machine analyzes and plots the hemoglobin-oxygen dissociation on a curve. Blood Gases. Arterial—Blood . more oxygen is delivered to the tissues for a given partial pressure of oxygen. Interpretation of oxygen levels is not appropriate on venous blood specimens. Increased HCO3-.43 <7. SI Units pH Panic value pCO2 pO2 HCO3Panic values 7.5 kPa 17–23 mEq/L 17–23 mmol/L <10 mEq/L >40 mEq/L <10 mmol/L >40 mEq/L 0.2 or >7.6–6. METABOLISM AND NUTRITION MODULE 16th Group .60–0. decreased oxygen saturation to less than 90%–92% must be addressed by thorough assessment of the client and clinical status. Venous—Blood Norm.32–7. Increased pCO2.32–7. See Blood gases. Arterial—Blood .6 35–45 mm Hg 4. Must be corrected for body temperature.

See Blood gases.27 See Blood gases.2 or >7.35–7. Increased O2 Saturation. Decreased pCO2.6 7.6 METABOLISM AND NUTRITION MODULE 16th Group . Arterial—Blood .45 <7. Decreased pO2. Interpretation of oxygen levels is not appropriate on venous blood specimens. Must be corrected for body temperature. Arterial— Blood for complete descriptions of the test components.2 or >7.45 <7. Arterial—Blood . (See Blood gases. Arterial—Blood .) Blood Gases. See Blood gases. Venous blood gases may be used in situations where assessment of oxygenation is unnecessary. Capillary—Blood Norm. See Blood gases. Decreased O2 Saturation. Decreased HCO3-. Description. Interpretation of oxygen saturation is not appropriate on venous blood specimens. Arterial—Blood . SI Units pH Adults Panic values 7. Decreased pH. Interpretation of oxygen saturation is not appropriate on venous blood specimens.35–7. A method for assessing acid-base status and for cellular hypoxia without performing an arterial puncture.

46 7. Arterial—Blood .46 26. Decreased pH. Arterial—Blood . See Blood gases. Increased pCO2.49 7. See Blood gases.00 <0. Arterial—Blood .34–7. Increased pO2.49 7.34–7. See Blood gases.32–7.60 2 months to 2 years 7.5–5.4 kPa Increased pH.32–7. See Blood gases. Arterial—Blood . Increased HCO3-.3 kPa <5.45 <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% 7.45 <2.2 mm Hg 3.28 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. Increased O2 Saturation. See Blood gases.7 kPa >9.35–7.3 kPa 22–26 mmol/L <10 mmol/L >40 mmol/L 0. Arterial—Blood .4 kPa 10.35–7.96–1.0–13. METABOLISM AND NUTRITION MODULE 16th Group .4–41.

Capillary pO2 interpretation is limited to assessment for hypoxia.6 mmol/L 0.29 See Blood gases.) (Chernecky & Berger. Arterial—Blood . for complete description of the test components. Decreased HCO3-. Decreased O2 Saturation.9 How is the normal blood glucose measurement? Glucose—Blood Norm. See Blood gases. Description.1–4.9–2. SI Units Whole Blood Adults >60 years Children Cord blood Premature infant 38–82 mg/dL 17–51 mg/dL 2. See Blood gases. Dependent on time and content of last meal.2.3–4.9 mmol/L 3. 2008) 2. (See Blood gases. A method for determining acid-base status from a heel stick for capillary blood. Decreased pO2. Used mostly in infants to assess pH and pCO2.4 mmol/L METABOLISM AND NUTRITION MODULE 16th Group . Arterial—Blood .8 mmol/L 60–89 mg/dL 68–98 mg/dL 3. Arterial—Blood . In normal clients. See Blood gases.8–5. Arterial . Arterial—Blood . glucose levels return to the fasting level (given in these norms) within 2 hours after the last meal. Decreased pCO2.

6 mmol/L >16. hyperadrenalism. pancreatic carcinoma. hyperosmolar hyperglycemic nonketotic coma (HHNK).2–3.7–3. cystic fibrosis. hypervitaminosis A (chronic).4–2. carbon monoxide poisoning. injury. hyperthyroidism. hypertension.3 mmol/L 1.3 mmol/L 1.2 mmol/L or >38.6 mmol/L <30 mg/dL or >300 mg/dL <1. hemochromatosis.8 mmol/L 2.30 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 2.4 mmol/L 25–51 mg/dL 34–51 mg/dL 42–68 mg/dL 51–85 mg/dL 1. eclampsia. pancreatic METABOLISM AND NUTRITION MODULE 16th Group . Acromegaly.4 mmol/L 3. myocardial infarction. Panic Levels Adults Neonates <40 mg/dL or >700 mg/dL <2. cerebrovascular accident. encephalitis. meningitis.3–5.5 mmol/L 4. anesthesia.4–6.8 mmol/L 2.3 mmol/L 2. infections.8 mmol/L 1. diabetes mellitus.9–2.8–4. malnutrition (chronic).3 mmol/L 2.8–4.6–5.5–5.3–3. gigantism.0 mmol/L Increased.1–3. obesity.5 mmol/L 65–100 mg/dL 80–115 mg/dL 3. burns. convulsions. hemorrhage.7 mmol/L NOTE: Whole-blood glucose values are about 15% less than serum glucose values because of greater dilution. Cushing's disease. hyperpituitarism. erectile dysfunction. Cushing's syndrome.

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

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

6–8. hyperthyroidism. convulsive disorders. Glucose.6–7.8 mmol/L American Diabetes Association diagnosis of diabetes >200 mg/dL >11 mmol/L (after 75-g glucose load) Usage. The American Diabetes Association criteria for diagnosis of diabetes mellitus include a fasting plasma glucose level of >126 mg/dL (7 mmol/L). infarction (myocardial. Cushing's disease. malignancy. 2-Hour Postprandial—Serum Norm. cirrhosis.3 mmol/L 3. METABOLISM AND NUTRITION MODULE 16th Group . pregnancy. hyperlipoproteinemia. nephrotic syndrome. emotional). Increased. malnutrition. Screening for diabetes mellitus and assessing control of hyperglycemia. and stress (physical. pancreatitis. preeclampsia. Decreased.6–8. diabetes mellitus.33 carbohydrate metabolism. Cushing's syndromea. pheochromocytoma. lipoproteinemias. anoxia. hepatic disease (chronic). SI Units Newborn to 50 years 50–60 years >60 years 65–140 mg/dL 65–150 mg/dL 65–160 mg/dL 3. dumping syndrome (after gastrectomy). sepsis. Drugs include those discussed under Glucose—Blood. cerebral). anxiety.7 mmol/L 3. Acromegaly. brain tumor.

11–1. hyperinsulinism.11–1.66 mmol/L SI Units METABOLISM AND NUTRITION MODULE 16th Group . hepatic insufficiency. and von Gierke's disease.51 mmol/L 0.11–1. 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. islet cell adenoma.11–2.11–1. 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. insulinoma.34 Addison's disease.38 mmol/L 0. myxedema.10 How is the normal rate of TG? Triglycerides—Blood Norm.2. Description.11–2. 2008) 2.22 mmol/L 0. hypoglycemia. steatorrhea. In normal clients. malabsorption syndrome. Drugs include those discussed under Glucose—Blood.11–1. congenital adrenal hyperplasia.05 mmol/L 0. hypothyroidism. anterior pituitary insufficiency.11–2.13 mmol/L 0. hypopituitarism. (Chernecky & Berger.24 mmol/L 10–100 mg/dL 10–110 mg/dL 10–122 mg/dL 10–134 mg/dL 10–147 mg/dL 0.11–1.77 mmol/L 0.24 mmol/L 0. adrenal insufficiency.11–2. glucose should return to fasting levels within 2 hours after the ingestion of the test meal.

3 mmol/L 400–1000 mg/dL 4. diabetes mellitus.36 mmol/L 0.11–1. starvation (early). hypothyroidism. gemfibrozil. miconazole (intravenous). Herbal or natural remedies include Cordyceps sinensis.35 Serum Values Children Female: 1–19 years Male: 1–19 years 10–121 mg/dL 10–103 mg/dL SI Units 0. stress. hyperlipoproteinemia. pancreatitis. lovastatin. Alcoholism. hypercholesterolemia. obesity. ethyl alcohol (ethanol). metabolic syndrome (>150 mg/dL). heparin. glycogen storage diseases. aortitis.5 mmol/L >11. acanthocytosis.3–4. garlic (aged extract taken over time). METABOLISM AND NUTRITION MODULE 16th Group 2. phenformin. hyperalimentation. hyperthyroidism. and soy. estrogens. niacin. familial hypertriglyceridemia. Tobacco use. dextrothyroxine. asparaginase. and spironolactone. Drugs include cholestyramine. gout. and malnutrition. and von Gierke's disease. myocardial infarction (for up to 1 year).5–11. aortic aneurysm. Abetalipoproteinemia. metformin. Classification of Triglyceride Levels Borderline high 200–400 mg/dL High Very high Increased. arteriosclerosis. prolonged high-fat). Tangier disease. renal insufficiency (chronic). malabsorption. chronic obstructive pulmonary disease. nephrotic syndrome.3 mmol/L >1000 mg/dL . oral contraceptives. pravastatin. hepatic cholesterol ester storage disease. diet (recent high-carbohydrate. cirrhosis (portal). pregnancy. corticosteroids.11–1. clofibrate. myxedema. and sulfonylureas. fat embolism. Decreased. Drugs include ascorbic acid.16 mmol/L NOTE: Plasma values are lower by about 3%.

6–18. 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 8.58–9. Dietary triglycerides are carried as part of chylomicrons through the lymphatic system and bloodstream to adipose tissue.92 mmol/L <3.3–9.76 mmol/L 6.2. high-density lipoprotein cholesterol.45–9.90 mmol/L 6.69–16.36 Description.0 g/dL 8. Also known as “fat.44–11.21–10.10 mmol/L >12.41 mmol/L 12–16 g/dL 10–15 g/dL 7.82–9.31 mmol/L 6. Hgb) Norm. Triglyceride levels are taken into consideration with total cholesterol.55 mmol/L 5. (Chernecky & Berger. and chylomicron levels when categorizing a client's serum into lipoprotein phenotypes that represent genetic lipoprotein abnormal-ities.” 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. They may be later retrieved and formed into glucose through gluconeogenesis when needed by the body.9 mmol/L 13. where they are released for storage. 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. Treatments differ for the different phenotypes.11 How is the normal rate of Haemoglobin? Hemoglobin (Hb. 2008) 2.17 mmol/L Panic Levels <5 g/dL METABOLISM AND NUTRITION MODULE 16th Group .

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

sulphate) produced during a metabolic acidosis are not measured as part of the usual laboratory biochemical profile. 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 . This alternative formula is: AG = [Na+] + [K+] . K+ can vary over a wider range and have more effect on the measured Anion Gap. In Renal Units.[Cl-] .[HCO3-] Reference range is 8 to 16 mmol/l. 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.38 Definition & Clinical Use The term anion gap (AG) represents the concentration of all the unmeasured anions in the plasma. The H+ produced reacts with bicarbonate anions (buffering) and the CO2 produced is excreted via the lungs (respiratory compensation). An alternative formula which includes K+ is sometimes used particularly by Nephrologists. acetoacetate.[Cl-] . 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.[HCO3-] The reference range is slightly higher with this alternative formula. AG is calculated from the following formula: Anion gap = [Na+] . 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. The acid anions (eg lactate.


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:



• • • •

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



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,


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

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

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

higher insulin levels lead to increased hunger and eating. 3. insulin action. and adiponectin) that modulate insulin secretion. insulin resistance is often associated with abdominal obesity (as opposed to hip and thigh obesity) and hypertriglyceridemia (Kasper. Obesity. TNF-α. Adipocytes secrete a number of biologic products (leptin.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. and body weight and may contribute to the insulin resistance. Type 2 DM is characterized by three pathophysiologic abnormalities: impaired insulin secretion. In the early stages of the disorder. free fatty acids. it will secrete more insulin in order to try to deal with the excessive blood sugar levels.1. the body is resistant to the action of insulin in type 2 diabetes. glucose tolerance METABOLISM AND NUTRITION MODULE 16th Group . particularly visceral or central (as evidenced by the hip-waist ratio). This can also lead to dehydration because excreting the sugar carries a large amount of water out of the body along with it. Despite increased caloric intake.4 What is the connection between Diabetes Mellitus and body weight? Obesity can increase risk factor to type 2 diabetes mellitus. peripheral insulin resistance. Moreover. the person may gain very little weight and may even lose weight. In type 2 DM. Excessive eating (polyphagia): If the body is able. Therefore. and excessive hepatic glucose production. resistin. is very common in type 2 DM. 2005). One of the functions of insulin is to stimulate hunger.

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

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

including eating patterns of Indonesian society is estimated patient. in the early stages will not cause disruption to the blood glucose levels. other chronic complications in chronic heart disease.1.5 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. Clinically. where an interruption occurs metabolism of carbohydrates. fats and proteins and is characterized by high blood sugar levels (hyperglycemia) and in urine.48 3. Currently. brain. Clinically. in line with changes lifestyle. the body that may be deficient in relative terms. eyes and kidneys. then at the stage of decompensation. this disease is progressive travel and tend to involve too fat or protein metabolism disorders. DM is a degenerative disease. but the health system a country. 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. or after being fed a solution of 75 g glucose load with Oral Glucose Tolerance Test (oral glucose tolerance). In impaired glucose tolerance (IGT) was found postprandial blood glucose levels. liver. Inadequate phase 1. 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. hypertension. DM is increasing. especially in adults and older age groups in all socio-economic status. an increase in postprandial blood glucose levels. although the known negative impact thereof large enough between. system nerve. ranged between 140-200 mg / METABOLISM AND NUTRITION MODULE 16th Group . efforts to control disease DM has not occupied the main priorities in health care. in addition to efficacious drugs that reduce insulin resistance (insulin sensitizers). This disease affects not only individually. which is then followed by performance improvement phase 2 insulin secretion. At this stage of compensatory mechanisms have started no longer adequate. Although no national survey.

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

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

METABOLISM AND NUTRITION MODULE 16th Group . and a direct result of elevated levels of blood glucose (hyperglycemia).51 Intravenous glucose stimulation First-Phase Second Phase IGT Normal Type 2DM Insulin Secretion Basal So. Impaired glucose metabolism will continue in fat and protein metabolism disorders and the damage to various body tissues. it can be concluded trip DMT2 disease.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). often leading to a collection of symptoms called metabolic syndrome. but at the same time also by the low response of body tissues to insulin (insulin resistance). initially determined by the performance of Phase 1 which then gives a negative impact on the performance of phase 2. The series of disorders that are motivated by insulin resistance.

excess glucose is converted into glycogen and stored in the liver due to the action of insulin. Excess glucose is converted to glycogen and stored in the liver and muscles. This causes glucose in human blood cannot be converted into glycogen by hepar’s cells (glycogenesys doesn’t work). This is known as insulin resistance. particularly carbohydrates. seen in impaired glucose tolerance (or pre-diabetes). the digestive system along with the liver. the impairment of glucose metabolism arises as a result of a decreased sensitivity to insulin by the body’s cells. Compensatory mechanism: The insulin levels in the blood are elevated.52 3. insulin. In insulin resistance. 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. above the norm (hyperinsulinemia) as the pancreas secretes higher amounts of glucose in an attempt to overcome this resistance (compensatory mechanism). This blood glucose regulating mechanism is primarily controlled by the hormone. leading to inappropriate amount of insulin in human METABOLISM AND NUTRITION MODULE 16th Group .1. the body’s cells and liver do not respond to insulin. This means that the cells do not respond to insulin to take up glucose from the bloodstream and utilize it. Alternatively. Any remaining glucose may be converted for fat storage. Insulin triggers cells to take up glucose from the blood so that individual cells can burn this glucose for energy. which is secreted by the pancreas (beta cells in the islets of Langerhan’s). Glucose then enters the blood stream where it is transported to cells throughout the body. Overlap point with lipogenesys: Upon consuming foods. This mechanism body. break down the food into simple sugars like glucose. Excess glucose builds up in the blood stream causes hyperinsulinemia until bile is overworked and malfunctioned as well.6 What is the connection between Diabetes Mellitus Type 2 and Carbohydrate Metabolism? With type 2 diabetes.

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

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

Insulin increases the translation of messenger RNA. and premature atherosclerosis. fats. 2003) 3. insulin also increases the rate of transcription of selected DNA genetic sequences in the cell nuclei. In the absence of insulin. Thus. 2. Insulin stimulates transport of many of the amino acids into the cells. Over a longer period of time. The manner in which insulin causes protein storage is not as well understood as the mechanisms for both glucose and fat storage. insulin “turns on” the ribosomal machinery. Some of the facts follow. However. METABOLISM AND NUTRITION MODULE 16th Group . almost as if insulin operates an “on-off” mechanism.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. leucine. not only carbohydrates and fats but proteins as well are stored in the tissues. In some unexplained way. the ribosomes simply stop working. thus forming increased quantities of RNA and still more protein synthesis— especially promoting a vast array of enzymes for storage of carbohydrates. tyrosine. thus forming new proteins. (Murray. insulin is required for this to occur. and phenylalanine. thus decreasing the rate of amino acid release from the cells. Insulin inhibits the catabolism of proteins. Among the amino acids most strongly transported are valine. isoleucine. 1. insulin shares with growth hormone the capability of increasing the uptake of amino acids into cells.1. and proteins. especially from the muscle cells. 3.55 defects. Presumably this results from the ability of insulin to diminish he normal degradation of proteins by the cellular lysosomes. the amino acids affected are not necessarily the same ones. 4. some of which cause hypercholesterolemia.

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

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

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

tachycardia. Monitor hematocrit and intake and output. monitor hematocrit. Administer oxygen.35–0.44 0.45 30%–46% 0.54 Adult Males 40%–54% Panic Levels <15% or >60% <0.59 SI Units Pregnant Children Neonates 3 months 1–2 years 6–10 years 40%–68% 29%–54% 35%–44% 31%–45% 0.29–0. Stop or reduce dose of diuretics if they are contributors to condition. edema. decreased skin turgor.40–0.60 Panic Level Symptoms and Treatment—Increased NOTE: Treatment choice(s) depend(s) on client's history and condition and episode history.31–0.15 or >0. dry mucous membranes. jugular venous distention.40–0. facial flushing. Restrict fluids. METABOLISM AND NUTRITION MODULE 16th Group . Cause Hemoconcentration Symptoms Decreased pulse pressure and volume. anxiety. decreased venous filling.46 0. Restrict sodium. and shortness of breath Administer diuretics. thirst and weakness Extremity pain and redness.54 0. restlessness. Perform bloodletting by venipuncture (phlebotomy). low central venous pressure. irritability. anasarca decreasing QRS voltage with severe fluid overload Possible Treatments Administer IV fluids. True polycythemia overtransfusion Panic Level Symptoms and Treatment—Decreased Cause Symptoms Possible Treatments Hemodilution Rales. orthostatic hypotension. hypertension. Observe for signs of thrombosis.30–0. Monitor hematocrit.68 0. Administer IV fluids.

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

thiocyanates. rifampin. vitamin A.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. phenytoin sodium. tolazamide. trimethadione. Creatinine—Serum Norm. female 4–7 years. sulfonamides. tranylcypromine sulfate.5 mg/dL ≤0. spectinomycin hydrochloride.61 hydrochloride. Hematocrit is the percentage of red blood cells in a volume of whole blood. Manual Method Jaffe. primidone. female 0.4 mg/dL 71–124 μmol/L 0. Description.8 mg/dL ≤0.7 mg/dL ≤0. vegetarian diet. penicillins. and zidovudine (AZT).6 mg/dL ≤0.6 mg/dL 52–142 μmol/day METABOLISM AND NUTRITION MODULE 16th Group . troleandomycin.2 mg/dL 53–105 μmol/L May be lower May be lower 0.6–1. thiosemicarbazones.6–1. Kinetic or Enzymatic Method Adults Females Males Elderly Children Cord blood Newborn Infant 1 year. valproic acid.7 mg/dL ≤0. radioactive agents. phenacemide. thiazide diuretics. phenylbutazone.2 mg/dL 53–105 μmol/L 0. female 2–3 years.7–1. female 1 year. SI Units Jaffe.7 mg/dL 62–150 μmol/L ≤0. tripelennamine hydrochloride. male 2–3 years. phensuximide.8–1. male 4–7 years. phenobarbital.6–1.6 mg/dL ≤0.5–1. male 8–10 years.1 mg/dL 44–97 μmol/L 0. phenelzine sulfate. tetracyclines. tolbutamide. phytonadione.

hypovolemic shock. allergic purpura. Values are 20–40% higher in the late afternoon than in the morning. diuretics. pancreatitis (necrotizing). subacute bacterial endocarditis. high dietary intake. cephalexin).0 mg/dL ≤1. sickle cell anemia. azotemia (prerenal. muscle destruction. gigantism. gout.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. cephalosporins (Cefoxitin. male ≤0. female 18–20 years. toxic shock syndrome. renal failure. congestive heart failure. male 13–17 years. Acromegaly.62 SI Units 8–10 years. scleroderma. glucose. renal tuberculosis. disopyramide phosphate.9 mg/dL ≤1. arginine. uremia. preeclampsia. glomerulonephritis (chronic). diabetes mellitus. micro albuminemia. pyelonephritis. testosterone therapy. hypothyroidism. KimmelstielWilson syndrome. fenofibrate. bleomycin-induced pulmonary toxicity. amphotericin B. ammonia (inhaled). urinary obstruction. captopril. nephrosclerosis. dopamine. androgens. cimetidine.2 mg/dL ≤1. polyarteritis nodosa. nephritis. Goodpasture's syndrome. corticosteroids. Drugs include acetohexamide. renal cortical necrosis. acyclovir. analgesic abuse. congenital hypoplastic kidneys. gentamicin sulfate. clofibrate. diet (high meat content). nephropathy (hypercalcemic. metal poisoning. infants (first 2 weeks of life). amyloidosis. female 11–12 years. fosinopril. hydroxyurea. systemic lupus erythematosus. and vomiting.9 mg/dL ≤0.1 mg/dL ≤1. male 11–12 years. METABOLISM AND NUTRITION MODULE 16th Group . lithium carbonate. mannitol. Lipomul. hydralazine hydrochloride.2 mg/dL ≤1. Bromsulphalein. losartan. polycystic disease. male 18–20 years. fructose. hypokalemic). hemoglobinuria. intestinal obstruction. female 13–17 years. renal artery stenosis or thrombosis. rheumatoid arthritis (active). cinchophen. multiple myeloma. renal vein thrombosis. diacetic acid. postrenal).

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

2–4. and phospholipids.2 mmol/L 0. Blood lipids comprise cholesterol. triglycerides. See individual test sections for further descriptions of the METABOLISM AND NUTRITION MODULE 16th Group .78 mmol/L 10–190 mg/dL 0.9–2.7 mmol/L 2.8 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.8–1.0–4.9 mmol/L <0.64 SI Units Triglycerides HDL cholesterol Females Males LDL cholesterol 35–85 mg/dL 30–65 mg/dL 80–190 mg/dL 0. Fasting lipid profiles are recommended every 5 years in clients older than age 19. Increase Decrease Increase Increase Increase Lipid profile is a battery of laboratory studies to help determine the risk factors in coronary artery disease.

14– 4.18 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 >1.15 High Risk mg/dL SI Units mmol/L ≥240 ≥200 ≥6.91–1.4 11.37– 4.19 4. (Chernecky & Berger.89 SI Units mg/dL SI Units mg/dL High Risk Very High >190 >4.59 Near Optimal 100–129 2.12 High 160–189 4.92 SI Units mg/dL SI Units METABOLISM AND NUTRITION MODULE 16th Group .40–5.91 Total to HDL Ratio Coronary Heart Disease Risk Male Female Average Risk 2 × Average Risk 5.0 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. as well as levels for which lifestyle changes and therapeutic drug regimens are recommended.18 <4.16 <35 <0.0 4.4 9.53 35–45 0.554 45–59 1.59– 3.6 7.22 ≥25.65 components of the lipid profile.34 mg/dL SI Units mg/dL Moderate Risk Borderline High 130–159 3.40 Borderline High Risk mg/dL SI Units mmol/L 200– 239 170– 199 5.16–1.18–6.1 3 × Average Risk 23.

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

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

METABOLISM AND NUTRITION MODULE 16th Group . • 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. In future. This incident can be prevented by good diet control. this procedure is to provide hope for healing diabetes. Treatment in this manner gives hope for diabetes cure in the future. • Pharmacological interventions that can be considered to be given to patients with diabetes are antihypertensive medications. • 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. compared with drug therapy.68 • Fluid: nonkelotik hiperglikemik hyperosmolar coma treated by giving fluids in bulk and slow correction of potassium deficit. Anti-hypertensive medications have been proven to reduce hypertension in patients with diabetes and kidney disease awitan slow.

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

Icterus = Negative (-) Ascites = negative (-) Palpation: • Hepar and Lien cannot be felt METABOLISM AND NUTRITION MODULE 16th Group .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. 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. She often feel hungry too. She rarely. She often feels thirsty and drinks much. practically never. Anemia.

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

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

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

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

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

1). triglyceride level is > 250 mg/dL (278 mg/dL). because uncontrolled diabetes can make complication problem and diabetic patient often have wound that hard to be healed (ulcer). 41 years old. dysllipidemia due to the decreasing of sensitivity of insulin receptor in cells caused by her obesity METABOLISM AND NUTRITION MODULE 16th Group . That is she have family history of diabetes. we find some risk factors for type 2 Diabetes Mellitus in this patient. Second. The first factor is she is obese (the BMI is about 36. 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. There is one more risk factor that maybe she have but we aren’t sure about that.76 In this patient. Third. has the symptoms of Diabetes Mellitus Type 2 with hyperglycemia. We think that her father and her brother had suffered from diabetes.3 FINAL HYPOTHESIS Miss X . 3. she is habitual physical inactivity.

LDL: 94 mg/dL. practically never. percussion. polydipsia.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. tingling. 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. & 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. Anemia. Mellitus .7 mg/dL HDL: 38 mg/dL . polyphagia. Total Cholesterol: 171 mg/dl High lipotoxic from rarely. 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.4 FINAL MIND MAPPING Sensitivity of insulin receptor is decreased Palpation. and other progressive complication like atherosclerosis. METABOLISM AND NUTRITION MODULE 16th Group Type 2 Diabetes sleepy. does adipocyte any sports 3.

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 .

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

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

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

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

Departemen Kesehatan RI.org/content/77/12/7425. p. Available at: http://www. PERAN DIIT DALAM PENANGGULANGAN DIABETES.83 METABOLISME. Twenty-Sixth Edition.doc&ei=cPDjTOrFKYi3cIm6ra0M&usg=AFQjCNGSQ oXZMYjqnExky-cWrgX8Al_FyQ (Accesed at November 17th 2010) Direktur Gizi Masyarakat. Hall. Direktorat Jenderal Bina Kesehatan Masyarakat. and glucose intolerance.12. Insulin release.PDF (Accesed on November 17th 2010) Efendic. Elizabeth (2001). Jakarta. Textbook of Medical Physiology 11th Ed.2003. 77.Harper’s Illustrated Biochemistry. Lange Medical Books/McGraw-Hill Medical Publishing Division. (Online). 1980. et al. EGC Penerbit Buku METABOLISM AND NUTRITION MODULE 16th Group .gizi. Guyton. insulin sensitivity. Kedokteran Pathophysiology. Available at http://www. Proceedings of the National Academy of Sciences.967 Corwin.pnas.966 . Robert K.net/makalah/Makalah%20Pekan%20DM.pdf (Accessed at November 11th 2010) Murray. Missisipi : Elsevier Inc. Vol. 2003. 2006. No.full.

nih.dhss .htm (Accessed on November 6th 2010) http://www.c om/index.gov/disord ers/peripheralne uropathy/detail_ peripheralneuro pathy. 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 .path ophysiologyofdi abetesmellitus.nih.nind s.html (Accessed November 7th 2010) http://www.htm (Accessed on November 11th 2010) http://www.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.gov/medline plus/ency/article /003208.nlm.gov/diabete s/DMOverview.mo.

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 .com/heal th/diabetessymptoms/DA0 0125 (Accessed November 7th 2010) http://www.may oclinic.nlm.com/heal th/diabetessymptoms/DA0 0125/NSECTIO NGROUP=2 (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.id /index.co.85 7th 2010) http://www.may oclinic.indo nesiapower.

5th Edition http://www.htm (Accessed on Nopember 10th 2010) http://www.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. (Accessed on November 10th 2010) Laboratory Tests and Diagnostic Procedures.9.anae sthesiamcq.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 .com/ AcidBaseBook/a b3_2.o rg/complications -diabetes.86 nih.gov/medline plus/ency/article /002072.10.idf.

87 Harper’s Illustrated Biochemistry.4. 1995. et al.org/c ontent/15/12/19 02 (Accessed on November 11th 2010) Partanen.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 .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. twenty six edition 1.

2.eme dicinehealth.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 .1056/NEJM19 9507133330203 (Accessed 2010) on November 20th http://www. Available Vol.co m/diabetes/page 3_em.nej m. (Online).88 Diabetes Mellitus. 333 No.org/doi/pdf/1 0. NEW ENGLAND JOURNAL MEDICINE. at: of The http://www.

co.u nand.doc &ei=cPDjTOrF KYi3cIm6ra0M &usg=AFQjCN GSQoXZMYjqn ExkycWrgX8Al_FyQ (Accesed at November 17th 2010) http://www.id %2F96%2F1%2 FINSULIN__M EKANISME_S EKRESI_DAN_ ASPEK_META BOLISME.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.ac.goo gle. http://www.gizi. net/makalah/Ma kalah%20Pekan %20DM.id/url? sa=t&source=w eb&cd=2&ved= 0CBkQFjAB&u rl=http%3A%2F %2Frepository.

Textbook of Medical Physiology 11th Ed. p. Twenty-Sixth Edition. Missisipi : Elsevier Inc. 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.full.967 Laboratory Tests and Diagnostic Procedures.966 .


SCIENTIFIC PAPER APPRAISAL Group : Title : 16th group Natural History of Peripheral Neuropathy in Patients with NonInsulin-Dependent Diabetes Mellitus 1. 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. PBL Group 1st Medical Faculty of Airlangga University Medical Ethic and Law Module 2009 . PAPER COMPLETION : Item  Title  Abstract and or Summary  Introduction. RESEARCH VALIDITY Objective: To determine the long-term risk of diabetic polyneuropathy and the factors affecting that risk.

000 inhabitants of the county of Kuopio in eastern Finland.4 The control subjects were recruited from among 180. (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.). Of these. and December 31. after 10 years. respectively. 1979.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. 1981.2 Both groups were evaluated between May 1. At base line. 132 patients with NIDDM and 142 control subjects underwent clinical evaluation and measurement of nerve conduction velocity. 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). 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 .

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

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


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

3 researches will show the same result as the previous result (by chance). (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) 3.083 If this research were done repeatedly (100x). 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. IMPORTANCE CI P : : There is no CI. Chicago). All the data were analyzed with SPSS software (SPSS. 8. the importance can’t be measured PBL Group 1st Medical Faculty of Airlangga University Medical Ethic and Law Module 2009 .Randomization Intervention Analysis Method trapezoidal rule.

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