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GROUP 16th



16th Group

3rd SEMESTER – 2010


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


16th Group

16th Group Members

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

Tutor :
dr. Subagio


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Cover ......................................................................................................................1
Scenario Creator....................................................................................................2
Group Members ....................................................................................................3
Contents .................................................................................................................4
Instructional Objectives .......................................................................................5
Chapter I : 1st Tutorial ..........................................................................................6
1.1 Scenario.............................................................................................................6
1.2 Main Problem ........................................................................................6
1.3 Keywords ..............................................................................................6
1.4 Additional Information..........................................................................7
1.5 Early Hypothesis ...................................................................................8
1.6 Early Mind Mapping .............................................................................9
1.7 Learning Issue 1...................................................................................10
Chapter II : 2nd Tutorial .....................................................................................11
2.1 Methods and Steps to Find the Information.........................................11
2.2 The Answer of Learning Issue 1..........................................................11
2.3 Learning Issue II .................................................................................41
Chapter III : 3rd Tutorial ....................................................................................42
3.1 The Answer of Learning Issue 1I.........................................................42
3.2 Analysis ...............................................................................................69
3.3 Final Hypothesis .................................................................................76
3.4 Final Mind Mapping............................................................................77
3.5 Group Opinion.....................................................................................79
3.6 Obstacles..............................................................................................79
References ............................................................................................................80
EBL & Critical Appraisal ..................................................................................83
Appendix (Journal Appraisal) ...........................................................................91
Journal ................................................................................................................97


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After finishing this module, students of Airlangga university- School of

Medicine in third semester can explain the patophysiology of health problem
through understanding the intermediate metabolism.


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1.1 Scenario
1.2. Main Problem

A woman, came to the outpatient polyclinic with complaints often

sleepy, sometimes feel tingling in both feet.

• Often feels sleepy

• Often feels sleepy and numbness

1.3 Key Words

1.3.1. Female
1.3.2. Numbness in both lower extremities
1.3.3. Outpatient treatment
1.3.4. Sleepy


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1.4 Additional Information

1.4.1. Woman, age: 41 years old

1.4.2. Status: Married with 1 child
1.4.3. Occupation: Housewive
1.4.4. Address: Kupang Indah; Surabaya
1.4.5. She has been feeling numbness for 1 month
1.4.6. Almost every night wakes up to go to the toilet
1.4.7. Medical Record: No hypertension
Body weight has decreased 3 kg recently
1.4.8. 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
1.4.9. Husband’s occupation: Private Company Officer
1.4.10. Physical Examination: Body weight: 89 kg
Height: 157 cm
Blood Pressure:120/80 mmHg
Pulse: 80 times per minute
RR: 20 times per minute
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


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1.5 Early Hypothesis

• Diabetes Mellitus
• Malnutrition deficiency
• Anemia
• Neuron disorders
• Cardio-vascular disorders
• Lipid metabolism disorders
• Hypoxia

1.6 Early Mind Mapping

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Female; 41 y.o

Examination: Supporting Exam:
Anamnesis: Weight 89 kg Hepar & Spleen normal
Tingling Height 157cm Heart & Lung normal
Sleepy BP 120/80 mmHg
No anemic, cyanotic,
Weight Loss PP 80 tpm
RR 20 tpm icterus
Temperature 37 ºC

Early hypothesis:
Malnutrition Deficiency
Neuron Disorders

1.7 Learning Issue 1

1.7.1. What are the causes of drowsiness?


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1.7.2 How is the mechanism of numbness/tingling?

1.7.3 How is the patophysiology of Diabetes Mellitus?
1.7.4 What are the symptoms of Diabetes Mellitus?
1.7.5 What is normal stomach circumference of human?
1.7.6 What are the risk factors of Diabetes Mellitus?
1.7.7 What are the complications of Diabetes Mellitus?
1.7.8 What is blood gas analysis?
1.7.9 How is the normal blood glucose measurement?
1.7.10 How is the normal rate of TG?
1.7.11 How is the normal rate of Haemoglobin?
1.7.12 What is anion gap?
1.7.13 What are the symptoms of anemia?


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To get the information we need, we use some sources, such as:

1. Text Books
We used text books from library, our relative’s books. We also
bought some books to get more information.
2. Internet
We got information from internet in the form of scientific journals
and articles. By typing the keywords in the search engine, we got
much information both in English and in Indonesian.
Sources in English are cited directly into this report but sources in
Indonesian are translated into English first.


2.2.1 What are the causes of drowsiness?

• Having to work long hours or different shifts (nights, weekends)

• Medications (tranquilizers, sleeping pills, antihistamines)
• Medical conditions (such as hypothyroidism, hypercalcemia, and
hyponatremia /hypernatremia)
• Not sleeping for long enough
• Sleep disorders (such as sleep apnea syndrome and narcolepsy)


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2.2.2 How is the mechanism of numbness/tingling?

Any time you remain still for a long period, particularly if you're leaning
on your arm or sitting cross-legged, you are bound to develop a pins-and-needles
sensation in one or more limbs. This feeling results from temporary nerve
compression and diminished blood flow, and it passes as soon as you move
around a bit.
Many medical conditions, however, cause a persistent tingling sensation
— usually in the hands, arms, feet, or legs — that is unrelated to posture and
unrelieved by movement. While several of these conditions originate in the
peripheral nervous system (the network of nerves branching out from the spinal
cord to the extremities), others are based primarily in different parts of the body.
In general, persistent tingling is a troubling symptom that requires a thorough
medical workup.

2.2.3 What are the patophysiologies of Diabetes Melitus?

Diabetes is a chronic metabolic disorder in which the body cannot

metabolize carbohydrates, fats, and proteins because of a lack of, or ineffective
use of, the hormone insulin. Diabetes is classified into three primary types that are
different disease entities but share the symptoms and complications of
hyperglycemia (high blood glucose). Impaired glucose tolerance, formerly known
as "borderline diabetes" is a degree of hyperglycemia that may precede type 2

The pathophysiology of diabetes mellitus in all forms is related to the

insulin hormone. Insulin is secreted by cells in the pancreas and is responsible for
regulating the level of glucose in the bloodstream. It also aids the body in
breaking down the glucose to be used as energy. When someone suffers from
diabetes, however, the body does not break down the glucose in the blood as a
result of abnormal insulin metabolism. This results in elevated levels of glucose in


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the blood, which is known as hyperglycemia. When glucose levels remain high
over an extended period of time, severe complications including cardiovascular
disease, kidney damage, eye disorders, and nerve problems can occur. Diabetes
mellitus occurs in three different forms - type 1, type 2, and gestational.

I. Type 1 (previously called insulin dependent diabetes mellitus (IDDM) or

juvenile onset diabetes)
A. Causes
1. Genetic predisposition.
2. Environmental exposure: virus, toxin, stress.
3. Autoimmune reaction: beta-cells that produce insulin in the pancreas are
destroyed. When 80-90% of the beta-cells are destroyed, overt symptoms
B. Characteristics
1. Usually occurs before 30 years of age, but can occur at any age. Peak
incidence occurs during puberty, around 10-12 years of age in girls and
12-14 years in boys.*
2. Abrupt onset of signs and symptoms of hyperglycemia: increased thirst
and hunger, frequent urination, weight loss, and fatigue.
3. Ketosis prone.

* Source: American Diabetes Association. Diabetes Facts. November, 2003.

C. Treatment
1. Insulin by injection with syringes or pumps
2. Diet
3. Exercise
4. Education
5. Monitoring

II. Type 2 (previously called non-insulin-dependent diabetes mellitus,

NIDDM, or adult onset diabetes)
A. Causes


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1. Insulin resistance: unable to utilize insulin that the body makes because of
cell-receptor defect; glucose is unable to be absorbed into cells for fuel.
2. Decreased insulin secretion: pancreas does not secrete enough insulin in
response to glucose levels.
3. Excess production of glucose from the liver: result of defective insulin
secretor response; dawn phenomenon (see glossary) is an example.
B. Characteristics
1. Usually occurs after 30 years of age, but is now occurring in children and
2. Increased prevalence in some ethnic groups, e.g., African Americans,
Hispanic/Latino, Native Americans, Asian Americans, and Pacific
3. Strong genetic predisposition.
4. Frequently obese.
5. Not prone to ketoacidosis until late in course or with prolonged
6. May or may not have symptoms of hyperglycemia.
7. May also have extreme tiredness, blurred vision, delayed healing,
numbness and tingling of hands and feet, recurring yeast infection.
8. 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.2.
• Overweight
• Sedentary lifestyle

• Pre-puberty.

• Signs of insulin resistance or conditions associated with insulin

resistance (acanthosis nigricans [dirty-neck syndrome],
hypertension [high blood pressure], dyslipidemia [lipoproteins
inbalance], polycystic ovarian syndrome [PCOS]).


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C. Treatment
1. Diet/weight management
2. Exercise/increase physical activity
3. Oral hypoglycemic/antihyperglycemic agents, insulin sensitizers, or
4. Education
5. Monitoring
6. Treatment of co morbid conditions (e.g., hypertension, lipid abnormalities)

III. Gestational Diabetes Mellitus (GDM)

A. Causes
1. Insulin resistance due to pregnancy
2. Genetic predisposition
B. Characteristics
1. 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). If the 1-hour screen for glucose is
>140 mg/dl (>7.8 mmol/l), a full diagnostic 100-g, 3-hour oral glucose
tolerance test (OGTT) is indicated.
C. Treatment
1. Diet: provide adequate calories without hyperglycemia or ketonemia
2. Exercise: program that does not cause fetal distress, contractions, or
hypertension (>140/90 mmHg).

3. Insulin: if unable to consistently maintain blood glucose <95 mg/dl fasting

(<5.3 mmol/ l) and <140 mg/dl (<7.8 mmol/l) 1 hour postprandial and
<120 mg/dl (<6.7 mmol/l) 2 hours postprandial.


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D. Monitoring
1. Blood glucose: required to determine effectiveness of treatment and
possible need for insulin. Glucose should be checked fasting and 1-2 hours
2. Ketones: test for ketones using first morning urine sample. Presence of
ketones may indicate starvation rather than hyperglycemic ketosis.

2.2.4 What are the symptoms of Diabetes Mellitus?

Excessive thirst and increased urination
Excessive thirst and increased urination are classic diabetes signs and
symptoms. When you have diabetes, excess sugar (glucose) builds up in your
blood. Your kidneys are forced to work overtime to filter and absorb the excess
sugar. If your kidneys can't keep up, the excess sugar is excreted into your urine
along with fluids drawn from your tissues. This triggers more frequent urination,
which may leave you dehydrated. As you drink more fluids to quench your thirst,
you'll urinate even more.
You may feel fatigued. Many factors can contribute to this. They include
dehydration from increased urination and your body's inability to function
properly, since it's less able to use sugar for energy needs.
Weight loss
Weight fluctuations also fall under the umbrella of possible diabetes signs
and symptoms. When you lose sugar through frequent urination, you also lose
calories. At the same time, diabetes may keep the sugar from your food from
reaching your cells — leading to constant hunger. The combined effect is
potentially rapid weight loss, especially if you have type 1 diabetes.

Blurred vision
Diabetes symptoms sometimes involve your vision. High levels of blood
sugar pull fluid from your tissues, including the lenses of your eyes. This affects
your ability to focus.
Left untreated, diabetes can cause new blood vessels to form in your retina
— the back part of your eye — as well as damage established vessels. For most


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people, these early changes do not cause vision problems. However, if these
changes progress undetected, they can lead to vision loss and blindness.

Slow-healing sores or frequent infections

Doctors and people with diabetes have observed that infections seem more
common if you have diabetes. Research in this area, however, has not proved
whether this is entirely true, nor why. It may be that high levels of blood sugar
impair your body's natural healing process and your ability to fight infections. For
women, bladder and vaginal infections are especially common.

Tingling hands and feet

Excess sugar in your blood can lead to nerve damage. You may notice
tingling and loss of sensation in your hands and feet, as well as burning pain in
your arms, hands, legs and feet.

Red, swollen, tender gums

Diabetes may weaken your ability to fight germs, which increases the risk
of infection in your gums and in the bones that hold your teeth in place. Your
gums may pull away from your teeth, your teeth may become loose, or you may
develop sores or pockets of pus in your gums — especially if you have a gum
infection before diabetes develops.

2.2.5 What is normal stomach circumference of human?

To determine whether suffering abdominal obesity or not, the people of

Indonesia have the ideal waist size. Usually, women's waist size 90 inches biggest
meter and men's 80 inch meter. If more than that, they sign congested hormone
bad fats in the stomach. This will trigger the spread of various diseases metabolic
If someone has abdominal circumference more than the normal number,
then it could be said he was experiencing abdominal obesity. What causes
obesity? It is said that there are two factors causing the genetic and lifestyle
factors. However, more cases of abdominal fat due to diet and an increasingly
unbalanced motion.
In fact, unhealthy lifestyle diseases (metabolic syndrome), stage 1 has
been ongoing since early 1990, particularly in urban areas. Since then the
Indonesian people begin to experience obesity. Especially since the fast-food


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restaurants to grow and increasingly giving kemudahkan for people to eat all the
time. Meanwhile, the pattern of motion (sports) in the stomach the less. 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.
Also explained that the fat can not be removed through liposuction,
because the fat inside the abdomen, rather than under a layer of skin. The
hormone estrogen source of fat in the thighs, the center of power, and bearing, on
the contrary in the stomach, the hormone is more dangerous, and in abdominal fat,
there are a lot of the mobility of free fatty acids to the liver and
muscles. Furthermore, it will affect the fatty acid metabolism and pancreatic

2.2.6 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, a type of fat molecule (250
mg/dL or more)
• 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
A condition called acanthosis nigricans, which causes dark, thickened skin
around the neck or armpits


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Persons from certain ethnic groups, including African Americans,

Hispanic Americans, Asian Americans, and Native Americans, have a higher risk
for diabetes.
Everyone over 45 should have a blood sugar (glucose) test at least every 3
years. Regular testing of blood sugar levels should begin at a younger age, and be
performed more often if you are at higher risk for diabetes. (MedlinePlus, 2010)

2.2.7 What are the complications of Diabetes Mellitus?

Without proper management it can lead to various complications such as
cardiovascular disease, kidney failure, blindness and nerve damage. Short-term
• 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 exercised more than anticipated or have not eaten
enough). Hypoglycaemia can be corrected rapidly by eating some sugar. If
it is not corrected it can lead to the person losing consciousness.
It is important that the person with diabetes recognises the signs of
• Ketoacidosis
When the body breaks down fats, acidic waste products called ketones are
produced. The body cannot tolerate large amounts of ketones and will try
to get rid of them through the urine. However, the body cannot release all
the ketones and they build up in your blood, causing ketoacidosis.
Ketoacidosis is a severe condition caused by lack of insulin. It mainly
affects people with type 1 diabetes.
• Lactic acidosis
Lactic acidosis is the build up of lactic acid in the body. Cells make lactic
acid when they use glucose for energy. If too much lactic acid stays in the


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body, the balance tips and the person begins to feel ill. Lactic acidosis is
rare and mainly affects people with type 2 diabetes.
• Bacterial/fungal infections
People with diabetes are more prone to bacterial and fungal infections.
Bacterial infections include sties and boils. Fungal infections include
athlete’s foot, ringworm and vaginal infections.
Long-term complications:
• Eye disease (retinopathy)
Eye disease, or retinopathy, is the leading cause of blindness and visual
impairment in adults in developed societies. About 2% of all people who
have had diabetes for 15 years become blind, while about 10% develop a
severe visual impairment.

IDF fact sheet on diabetes and eye disease

• Kidney disease (nephropathy)
Diabetes is the leading cause of kidney disease (nephropathy). About one
third of all people with diabetes develop kidney disease and approximately
20% of people with type 1 diabetes develop kidney failure.

IDF fact sheet on diabetes and kidney disease

• Nerve disease (neuropathy)
Diabetic nerve disease, or neuropathy affects at least half of all people
with diabetes. There are different types of nerve disease which can result
in a loss of sensation in the feet or in some cases the hands, pain in the foot
and problems with the functioning of different parts of the body including
the heart, the eye, the stomach, the bladder and the penis. A lack of
sensation in the feet can lead to people with diabetes injuring their feet
without realising it. These injuries can lead to ulcers and possibly
• Diseases of the circulatory system


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Disease of the circulatory system, or cardiovascular disease, accounts for

75% of all deaths among people with diabetes of European origin. In the
USA, corony heart disease is present in between 8% and 20% of people
with diabetes over 45 years of age. Their risk of heart disease is 2-4 times
higher than those who do not have diabetes. It is the main cause of
disability and death for people with type 2 diabetes in industrialized

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. People with diabetes are 15 to 40 times more likely to require
lower-limb amputation compared to the general population. (International
Diabetes Federation, 2010)

2.2.8 What is the blood gas analysis?

Blood Gases, Arterial (ABG)—Blood


Must be corrected for body temperature.

SI Units
Adults 7.35–7.45 7.35–7.45
Panic values ≤7.2 and >7.6 ≤7.2 and >7.6
Birth to 2 months 7.32–7.49 7.32–7.49
2 months to 2 years 7.34–7.46 7.34–7.46
>2 years 7.35–7.45 7.35–7.45
PaCO2 35–40 mm Hg 4.7–5.3 kPa
Panic values <20 mm Hg <2.7 kPa


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SI Units
>70 mm Hg >9.4 kPa
PaO2 80–100 mm Hg 10.7–13.3 kPa
Panic values <40 mm Hg <5.3 kPa
HCO3- 22–31 mEq/L 22–31 mmol/L
Panic values <10 mEq/L <10 mmol/L
>40 mEq/L >40 mmol/L
O2 Saturation 96%–100% 0.96–1.00
Panic value <60% <0.60
Oxyhemoglobin Dissociation Curve No shift

Increased pH.

Alkali ingestion, Cushing's disease, diarrhea, fever, high altitude,

hyperventilation, hysteria, intestinal obstruction (pyloric, duodenal), metabolic
alkalosis, peptic ulcer therapy, renal disease, respiratory alkalosis, salicylate
intoxication, and vomiting (excessive). Drugs include sodium bicarbonate.

Increased PaCO2.

Acute intermittent porphyria, aminoglycoside toxicity, asthma (late stage), brain

death, coarctation of the aorta, congestive heart failure, electrolyte disturbance
(severe), emphysema, empyema, hyaline membrane disease, hyperemesis,
hypothyroidism (severe), hypoventilation (alveolar), metabolic alkalosis, near
drowning, pleural effusion, pleurisy, pneumonia, pneumothorax, poisoning,
pulmonary edema, pulmonary infection, renal disorders, respiratory acidosis,
respiratory failure, shock, tetralogy of Fallot, transposition of the great vessels,
and vomiting. Drugs include aldosterone, ethacrynic acid, metolazone,
prednisone, sodium bicarbonate, and thiazides.

Increased PaO2.

Hyperbaric oxygenation and hyperventilation.


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Increased HCO3-.

Anoxia, metabolic alkalosis, and respiratory acidosis.

Increased O2 Saturation.

High altitudes, hypocapnia, hypothermia, increased cardiac output, hyperbaric

oxygenation, increased oxygen affinity for hemoglobin, oxygen therapy, positive
end-expiratory pressure (PEEP) added to mechanical ventilation, respiratory

Decreased pH.

Addison's disease, asthma, cardiac disease, diabetic ketoacidosis, diarrhea,

emphysema, dysrhythmias, hepatic disease, hypercapnia, hypoventilation,
malignant hyperthermia, metabolic acidosis, myocardial infarction, nephritis,
nephrosis, pneumonia, pulmonary edema, pulmonary embolism, pulmonary
infection, pulmonary malignancy, pulmonary obstructive disease, renal disease,
respiratory acidosis (also caused by large volumes of lactated Ringer's),
respiratory failure, sepsis, and shock.

Decreased PaCO2.

Dysrhythmias, asthma (early stage), diabetic ketoacidosis, diabetes mellitus,

fever, high altitude, hyperventilation, metabolic acidosis, respiratory alkalosis,
and salicylate intoxication. Drugs include acetazolamide, dimercaprol, methicillin
sodium, nitrofurantoin, nitrofurantoin sodium, tetracycline, and triamterene.

Decreased PaO2.

Acute respiratory distress syndrome, anoxia, anesthesia, aortic valve stenosis,

arteriovenous shunt, asthma, atelectasis, atrial septal defect, berylliosis, carbon
monoxide poisoning, cerebrovascular accident, coarctation of the aorta,
emphysema, flail chest, Hamman-Rich syndrome, head injury, hyaline membrane
disease, hypercapnia, hypoventilation, lung resection, lymphangitic
carcinomatosis, near drowning, phrenic nerve paralysis, pickwickian syndrome,


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pain causing restricted diaphragmatic breathing, pleural effusion, pneumonia,

pneumothorax, poisoning, poliomyelitis (acute), pulmonary adenomatosis,
pulmonary embolism, pulmonary infection, pulmonary hemangioma, pulmonic
stenosis, respiratory failure, sarcoidosis, shock, smoke inhalation, status
epilepticus, tetanus, transposition of the great vessels, tricuspid atresia, and
ventricular septal defect.

Decreased HCO3-.

Hypocapnia, metabolic acidosis, and respiratory alkalosis.

Decreased O2 Saturation.

Acute respiratory distress syndrome, anesthesia, anoxia, anorexia, aortic valve

stenosis, arteriovenous shunt, asthma, atelectasis, atrial septal defect, berylliosis,
carbon monoxide poisoning, cerebrovascular accident, coarctation of the aorta,
congenital heart defects, decreased cardiac output, decreased oxygen affinity for
hemoglobin, emphysema, fever, flail chest, Hamman-Rich syndrome, head injury,
hyaline membrane disease, hypercapnia, hypoventilation, hypoxia, lung resection,
lymphangitic carcinomatosis, near drowning, phrenic nerve paralysis, pickwickian
syndrome, pain causing restricted diaphragmatic breathing, pleural effusion,
pneumonia, pneumothorax, poisoning, poliomyelitis (acute), pulmonary
adenomatosis, pulmonary embolism, pulmonary infection, pulmonary
hemangioma, pulmonic stenosis, respiratory acidosis, respiratory failure,
sarcoidosis, shock, smoke inhalation, status epilepticus, tetanus, transposition of
the great vessels, tricuspid atresia, and ventricular septal defect.

Oxyhemoglobin Dissociation Curve.

See diagram.

Shift to Left.

2,3-DPG deficiency, high altitude, hypocapnia, hypothermia, and respiratory



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Shift to Right.

Cluster headaches, emphysema, fever, hypercapnia, increased production of 2,3-

DPG, and respiratory acidosis.


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. The pH is the measurement of free H+ ion concentration in
circulating blood. Intracellular metabolism results in the continuous production of
hydrogen ions, which are buffered as either an acid (HCO3-) or a base (H2CO3).
The body demands that pH remain constant. The kidneys and lungs regulate pH
by preserving the ratio of acid to base. Any alteration in the ratio between
bicarbonate and carbonic acid will cause a reciprocal change in release or uptake
of free H+, thereby altering pH value. Significant deviations in pH can be life
threatening. Both bicarbonate (HCO3-) and carbonic acid (H2CO3) are components
of the body's acid-base system that influence pH. The partial pressure of carbon
dioxide (pCO2, 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. When pH decreases, more CO2 dissociates from carbonic
acid and is exhaled through the lungs, counteracting the pH reduction and
increasing the breathing rate. The partial pressure of oxygen (pO 2, PaO2) is the
amount of oxygen dissolved in plasma and represents the status of alveolar gas
exchange with inspired air. 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. 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,
SaO2) of hemoglobin at varying partial pressures of oxygen. P-50 is the partial
pressure of oxygen at which the given hemoglobin sample is 50% saturated. The


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Hem-O-Scan machine analyzes and plots the hemoglobin-oxygen dissociation on

a curve. When the curve is shifted to the left, more oxygen is delivered to the
tissues for a given partial pressure of oxygen; when the shift is to the right, less
oxygen is delivered to the tissues. Generally, decreased oxygen saturation to less
than 90%–92% must be addressed by thorough assessment of the client and
clinical status.

Blood Gases, Venous—Blood


Must be corrected for body temperature.

SI Units
pH 7.32–7.43 7.32–7.43
Panic value <7.2 or >7.6 <7.2 or >7.6
pCO2 35–45 mm Hg 4.6–6.0 kPa
pO2 20–49 mm Hg 2.6–6.5 kPa
HCO3- 17–23 mEq/L 17–23 mmol/L
Panic values <10 mEq/L <10 mmol/L
>40 mEq/L >40 mEq/L
O2 Saturation 60%–80% 0.60–0.80

Increased pH.

See Blood gases, Arterial—Blood .

Increased pCO2.

See Blood gases, Arterial—Blood .

Increased pO2.

Interpretation of oxygen levels is not appropriate on venous blood specimens.

Increased HCO3-.


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See Blood gases, Arterial—Blood .

Increased O2 Saturation.

Interpretation of oxygen saturation is not appropriate on venous blood specimens.

Decreased pH.

See Blood gases, Arterial—Blood .

Decreased pCO2.

See Blood gases, Arterial—Blood .

Decreased pO2.

Interpretation of oxygen levels is not appropriate on venous blood specimens.

Decreased HCO3-.

See Blood gases, Arterial—Blood .

Decreased O2 Saturation.

Interpretation of oxygen saturation is not appropriate on venous blood specimens.


A method for assessing acid-base status and for cellular hypoxia without
performing an arterial puncture. Venous blood gases may be used in situations
where assessment of oxygenation is unnecessary. (See Blood gases, Arterial—
Blood for complete descriptions of the test components.)

Blood Gases, Capillary—Blood


Must be corrected for body temperature.

SI Units
Adults 7.35–7.45 7.35–7.45
Panic values <7.2 or >7.6 <7.2 or >7.6


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SI Units
Children (arterialized capillary sample)
Birth to 2 months 7.32–7.49 7.32–7.49
2 months to 2 years 7.34–7.46 7.34–7.46
>2 years 7.35–7.45 7.35–7.45
pCO2 26.4–41.2 mm Hg 3.5–5.4 kPa
Panic values <20 mm Hg <2.7 kPa
>70 mm Hg >9.4 kPa
pO2 75–100 mm Hg 10.0–13.3 kPa
Panic values <40 mm Hg <5.3 kPa
HCO3- 22–26 mEq/L 22–26 mmol/L
Panic values <10 mEq/L <10 mmol/L
>40 mEq/L >40 mmol/L
O2 Saturation 96%–100% 0.96–1.00
Panic value <60% <0.60

Increased pH.

See Blood gases, Arterial—Blood .

Increased pCO2.

See Blood gases, Arterial—Blood .

Increased pO2.

See Blood gases, Arterial—Blood .

Increased HCO3-.

See Blood gases, Arterial—Blood .

Increased O2 Saturation.

See Blood gases, Arterial—Blood .

Decreased pH.


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See Blood gases, Arterial—Blood .

Decreased pCO2.

See Blood gases, Arterial—Blood .

Decreased pO2.

Capillary pO2 interpretation is limited to assessment for hypoxia.

Decreased HCO3-.

See Blood gases, Arterial—Blood .

Decreased O2 Saturation.

See Blood gases, Arterial—Blood .


A method for determining acid-base status from a heel stick for capillary blood.
Used mostly in infants to assess pH and pCO2. (See Blood gases, Arterial , for
complete description of the test components.) (Chernecky & Berger, 2008)

2.2.9 How is the normal blood glucose measurement?


Dependent on time and content of last meal. In normal clients, glucose levels
return to the fasting level (given in these norms) within 2 hours after the last meal.

SI Units
Whole Blood
Adults 60–89 mg/dL 3.3–4.9 mmol/L
>60 years 68–98 mg/dL 3.8–5.4 mmol/L
Cord blood 38–82 mg/dL 2.1–4.6 mmol/L
Premature infant 17–51 mg/dL 0.9–2.8 mmol/L


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SI Units
Neonate 25–51 mg/dL 1.4–2.8 mmol/L
Newborn to 24 hours 34–51 mg/dL 1.9–2.8 mmol/L
Newborn >24 hours 42–68 mg/dL 2.3–3.8 mmol/L
Child 51–85 mg/dL 2.8–4.7 mmol/L
Adults 65–100 mg/dL 3.6–5.5 mmol/L
>60 years 80–115 mg/dL 4.4–6.4 mmol/L
Cord blood 45–96 mg/dL 2.5–5.3 mmol/L
Premature infants 20–60 mg/dL 1.1–3.3 mmol/L
Neonates 30–60 mg/dL 1.7–3.3 mmol/L
Newborn to 24 hours 40–60 mg/dL 2.2–3.3 mmol/L
Newborn >24 hours 50–80 mg/dL 2.8–4.4 mmol/L
Child 60–100 mg/dL 3.3–5.5 mmol/L
NOTE: Whole-blood glucose values are about 15% less than serum glucose values
because of greater dilution.
Panic Levels
Adults <40 mg/dL or >700 mg/dL <2.2 mmol/L or >38.6 mmol/L
Neonates <30 mg/dL or >300 mg/dL <1.6 mmol/L >16.0 mmol/L


Acromegaly, anesthesia, burns, carbon monoxide poisoning, cerebrovascular

accident, convulsions, Cushing's disease, Cushing's syndrome, cystic fibrosis,
diabetes mellitus, eclampsia, encephalitis, erectile dysfunction, gigantism,
hemochromatosis, hemorrhage, hyperosmolar hyperglycemic nonketotic coma
(HHNK), hyperthyroidism, hyperpituitarism, hyperadrenalism, hypertension,
hypervitaminosis A (chronic), infections, injury, malnutrition (chronic),
meningitis, myocardial infarction, obesity, pancreatic carcinoma, pancreatic


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insufficiency, pancreatitis (chronic), pheochromocytoma, pituitary adenoma,

pregnancy, shock, subarachnoid hemorrhage, stress, trauma, and Wernicke's
encephalopathy. Drugs include anabolic steroids, androgens, arginine, ascorbic
acid, asparaginase, aspirin, atenolol, baclofen, benzodiazepines, bisacodyl
(prolonged use), chlorpromazine, chlorthalidone, cimetidine, clonidine,
corticosteroids, corticotropin, dextran, dextrothyroxine, diazoxide, disopyramide
phosphate, epinephrine, epinephrine bitartrate, epinephrine borate, epinephrine
hydrochloride, estrogens, ethacrynic acid, furosemide, glucose infusions,
haloperidol, imipramine, isoproterenol hydrochloride, heparin calcium, heparin
sodium, hydralazine hydrochloride, hydrochlorothiazide, indomethacin, isoniazid,
levodopa, levothyroxine sodium/T4, lithium carbonate, magnesium hydroxide
(prolonged high doses), meperidine, mercaptopurine, methimazole, methyldopa,
methyldopate (hydrochloride), metronidazole, nalidixic acid, niacin, nicotine,
nicotinic acid, oral contraceptives, oxazepam, p-aminosalicyclic acid,
phenolphthalein, phenytoin, phenytoin sodium, progestins, promethazine
hydrochloride, propranolol (in diabetic clients), propylthiouracil, protease
inhibitors, reserpine, rifampin, risperidone, ritodrine hydrochloride, sildenafil,
terbutaline sulfate, tetracyclines, thiazides/thiazide diuretics, thyroglobulin,
thyroid medications, tolbutamide (SMA methodology), and triamterene.


Addison's disease, adrenal medulla unresponsiveness, alcoholism, carcinoma

(adrenal gland, stomach, fibrosarcoma), cirrhosis, cretinism, diabetes mellitus
(early), dumping syndrome, exercise, fever, Forbes' disease (type III glycogen
deposition disease), fructose intolerance, galactosemia, glucagon deficiency,
hepatic phosphorylase deficiency (type VI glycogen storage disease), hepatitis,
hyperinsulinemia, hypopituitarism, hypothermia, hypothyroidism, infant of
diabetic mother, insulin overdose (factitious hypoglycemia), insulinoma,
kwashiorkor, leucine sensitivity, malnutrition, maple syrup urine disease, muscle
phosphofructokinase deficiency (type VII glycogen storage disease), myxedema,
pancreatic islet cell tumor, pancreatitis, postoperatively (after gastrectomy or


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gastroenterostomy), postprandial hypoglycemia, Reye's syndrome, Simmonds'

disease, vomiting, von Gierke's disease (type I glycogen storage disease),
Waterhouse-Friderichsen syndrome, and Zetterstrom syndrome. Drugs include
acetaminophen, allopurinol, amphetamines, aspirin, atenolol, beta-adrenergic
blockers, caffeine, cerivastatin, chlorpropamide, clofibrate, edetate disodium,
ethyl alcohol (ethanol), gatifloxacin, guanethidine sulfate, isoniazid, insulin,
isocarboxazid, marijuana, nitrazepam, oral hypoglycemic agents, p-aminosalicylic
acid, pargyline hydrochloride, phenacetin, phenazopyridine, phenelzine sulfate,
phenformin, propranolol (in diabetics), tetracyclines, theophylline, and
tranylcypromine sulfate. Herbs or natural remedies include zhi mu (‘know-
mother,' Anemarrhena asphodeloides, an herb) and shi gao (‘stone-plaster,'
calcium sulfate, gypsum) taken in combination; xuan shen (‘black ginseng,'
Scrophularia ningpoensis, figwort) and cang zhu (‘green-shu/zhu herb,'
Atractylodes lancea, var. ovata) taken in combination; shan yao (‘mountain-
medicine,' Dioscorea batatas, potato yam) and huang qi (‘yellow-old 60,'
Astragalus reflexistipulus, or A. hoantchy, yellow vetch) taken in combination;
and karela (Momordica charantia, balsam apple) taken in combination with
chlorpropamide. Herbs or natural remedies include teas (decoctions, infusions)
containing chromium, karela, ginseng, guar gum, meshasringi (Gymnema
sylvestre, mesha shringi, Indian milkweed vine), methi (fenugreek leaves),
syzigium cumini (jamun), tundika (Coccinia indica).


Glucose is a monosaccharide found naturally occurring in fruits. 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. Glucose is essential for brain and
erythrocyte function. Excess glucose is stored as glycogen in the liver and muscle
cells. Hormones influencing glucose metabolism include insulin, glucagon,
thyroxine, somatostatin, cortisol, and epinephrine. Fasting glucose levels are used
to help diagnose diabetes mellitus and hypoglycemia. A randomly timed test for
glucose is usually performed for routine screening and nonspecific evaluation of


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carbohydrate metabolism. The American Diabetes Association criteria for

diagnosis of diabetes mellitus include a fasting plasma glucose level of >126
mg/dL (7 mmol/L).

Glucose, 2-Hour Postprandial—Serum

SI Units
Newborn to 50 years 65–140 3.6–7.7
mg/dL mmol/L
50–60 years 65–150 3.6–8.3
mg/dL mmol/L
>60 years 65–160 3.6–8.8
mg/dL mmol/L
American Diabetes Association diagnosis of diabetes >200 mg/dL >11 mmol/L
(after 75-g glucose load)


Screening for diabetes mellitus and assessing control of hyperglycemia.


Acromegaly, anoxia, anxiety, brain tumor, cirrhosis, convulsive disorders,

Cushing's disease, Cushing's syndromea, diabetes mellitus, dumping syndrome
(after gastrectomy), hepatic disease (chronic), hyperlipoproteinemia,
hyperthyroidism, infarction (myocardial, cerebral), lipoproteinemias,
malnutrition, malignancy, nephrotic syndrome, pancreatitis, pheochromocytoma,
preeclampsia, pregnancy, sepsis, and stress (physical, emotional). Drugs include
those discussed under Glucose—Blood.



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Addison's disease, adrenal insufficiency, anterior pituitary insufficiency,

congenital adrenal hyperplasia, hepatic insufficiency, hyperinsulinism,
hypoglycemia, hypopituitarism, hypothyroidism, insulinoma, islet cell adenoma,
malabsorption syndrome, myxedema, steatorrhea, and von Gierke's disease. Drugs
include those discussed under Glucose—Blood.


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.
In normal clients, glucose should return to fasting levels within 2 hours after the
ingestion of the test meal. (Chernecky & Berger, 2008)

2.2.10 How is the normal rate of TG?

Serum Values SI Units
Adult Females
20–29 years 10–100 mg/dL 0.11–1.13 mmol/L
30–39 years 10–110 mg/dL 0.11–1.24 mmol/L
40–49 years 10–122 mg/dL 0.11–1.38 mmol/L
50–59 years 10–134 mg/dL 0.11–1.51 mmol/L
>59 years 10–147 mg/dL 0.11–1.66 mmol/L
Adult Males
20–29 years 10–157 mg/dL 0.11–1.77 mmol/L
30–39 years 10–182 mg/dL 0.11–2.05 mmol/L
40–49 years 10–193 mg/dL 0.11–2.18 mmol/L
50–59 years 10–197 mg/dL 0.11–2.22 mmol/L
>59 years 10–199 mg/dL 0.11–2.24 mmol/L


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Serum Values SI Units

Female: 1–19 years 10–121 mg/dL 0.11–1.36 mmol/L
Male: 1–19 years 10–103 mg/dL 0.11–1.16 mmol/L
NOTE: Plasma values are lower by about 3%.

Classification of Triglyceride Levels

Borderline high 200–400 mg/dL 2.3–4.5 mmol/L
High 400–1000 mg/dL 4.5–11.3 mmol/L
Very high >1000 mg/dL >11.3 mmol/L


Alcoholism, aortic aneurysm, aortitis, arteriosclerosis, diabetes mellitus, diet

(recent high-carbohydrate, prolonged high-fat), familial hypertriglyceridemia, fat
embolism, glycogen storage diseases, gout, hepatic cholesterol ester storage
disease, hypercholesterolemia, hyperlipoproteinemia, hypothyroidism, metabolic
syndrome (>150 mg/dL), myocardial infarction (for up to 1 year), myxedema,
nephrotic syndrome, obesity, pancreatitis, pregnancy, renal insufficiency
(chronic), starvation (early), stress, Tangier disease, and von Gierke's disease.
Tobacco use. Drugs include cholestyramine, corticosteroids, estrogens, ethyl
alcohol (ethanol), miconazole (intravenous), oral contraceptives, and


Abetalipoproteinemia, acanthocytosis, cirrhosis (portal), chronic obstructive

pulmonary disease, hyperalimentation, hyperthyroidism, malabsorption, and
malnutrition. Drugs include ascorbic acid, asparaginase, clofibrate,
dextrothyroxine, gemfibrozil, heparin, lovastatin, metformin, niacin, phenformin,
pravastatin, and sulfonylureas. Herbal or natural remedies include Cordyceps
sinensis, garlic (aged extract taken over time), and soy.


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Also known as “fat,” 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. Dietary triglycerides are carried as part of chylomicrons
through the lymphatic system and bloodstream to adipose tissue, 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. They may be later retrieved and formed into glucose through
gluconeogenesis when needed by the body. Triglyceride levels are taken into
consideration with total cholesterol, high-density lipoprotein cholesterol, and
chylomicron levels when categorizing a client's serum into lipoprotein phenotypes
that represent genetic lipoprotein abnormal-ities. Treatments differ for the
different phenotypes. (Chernecky & Berger, 2008)

2.2.11 How is the normal rate of Haemoglobin?

Hemoglobin (Hb, Hgb)

SI Units
Females 12–16 g/dL 7.45–9.90 mmol/L
Pregnant 10–15 g/dL 6.3–9.9 mmol/L
Males 13.6–18.0 g/dL 8.44–11.17 mmol/L
Neonates 14–27 g/dL 8.69–16.76 mmol/L
3 months 10–17 g/dL 6.21–10.55 mmol/L
1–2 years 9–15 g/dL 5.58–9.31 mmol/L
6–10 years 11–16 g/dL 6.82–9.92 mmol/L
Panic Levels <5 g/dL <3.10 mmol/L
>20 g/dL >12.41 mmol/L


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Burns (severe), congestive heart failure, chronic obstructive pulmonary disease

(COPD), dehydration, diarrhea, erythrocytosis, hemorrhage, hemoconcentration,
high altitudes, intestinal obstruction (late), polycythemia vera, snorers, and
thrombotic thrombocytopenic purpura. Also conditions that increase red blood
cells (RBCs). Drugs include gentamicin, methyldopa, and pentoxifylline.


Andersen's disease, anemia (iron deficiency), carcinomatosis, cirrhosis, cystic

fibrosis, fat emboli, fatty liver, fluid retention, hemorrhage, hemolysis, hemolytic
reaction to chemicals or drugs or prosthetics, Hodgkin's disease, hydremia of
pregnancy, hyperthyroidism, hypervitaminosis A, hypothyroidism, idiopathic
steatorrhea, intravenous overload, leukemia, lymphoma, platelet apheresis,
pregnancy, renal cortical necrosis, sarcoidosis, severe hemorrhage, systemic lupus
erythematosus, tetralogy of Fallot, and transfusion of incompatible blood. Also,
conditions that decrease RBCs. Drugs include antibiotics, antineoplastic agents,
Apresoline (hydralazine HCl with hydrochlorothiazide), aspirin, hydantoin
derivatives, indomethacin, monoamine oxidase inhibitors, primaquine, rifampin,
sulfonamides, tridione, and zidovudine (AZT); vegetarian diet.


Hemoglobin is the oxygen-carrying pigment of the RBCs. It is composed

of amino acids that form a single protein called “globin” and a compound called
“heme.” Heme contains iron atoms and the red pigment porphyrin. Each
erythrocyte contains approximately 300 million molecules of hemoglobin.
(Chernecky & Berger, 2008)

2.2.12 What is anion gap?


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Definition & Clinical Use

The term anion gap (AG) represents the concentration of all the
unmeasured anions in the plasma. 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. The acid anions (eg
lactate, acetoacetate, sulphate) produced during a metabolic acidosis are not
measured as part of the usual laboratory biochemical profile. The H+ produced
reacts with bicarbonate anions (buffering) and the CO2 produced is excreted via
the lungs (respiratory compensation). 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.

AG is calculated from the following formula:

Anion gap = [Na+] - [Cl-] - [HCO3-]

Reference range is 8 to 16 mmol/l. An alternative formula which includes

K+ is sometimes used particularly by Nephrologists. In Renal Units, K+ can vary
over a wider range and have more effect on the measured Anion Gap.

This alternative formula is:

AG = [Na+] + [K+] - [Cl-] - [HCO3-]

The reference range is slightly higher with this alternative formula. 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.

Major Clinical Uses of the Anion Gap

• To signal the presence of a metabolic acidosis and confirm other findings


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• 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:


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• 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


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


2.3.1 What is the connection between Diabetes Mellitus and drowsiness?

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


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3.1.1 What is the connection between Diabetes Mellitus and drowsiness?

Two possible causes are often sleepy at this woman is atherosclerosis and
sleep apnea.
With time, the fatty streaks grow larger and coalesce, and the surrounding
fibrous and smooth muscle tissues proliferate to form larger and larger plaques.
Also, the macrophages release substances that cause inflammation and further
proliferation of smooth muscle and fibrous tissue on the inside surfaces of the
arterial wall. 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,
sometimes completely occluding the vessel. Even without occlusion, the
fibroblasts of the plaque eventually deposit extensive amounts of dense
connective tissue; sclerosis (fibrosis) becomes so great that the arteries become
stiff and unyielding. Still later, calcium salts often precipitate with the cholesterol
and other lipids of the plaques, leading to bony-hard calcifications that can make
the arteries rigid tubes. Atherosclerotic arteries lose most of their dispensability,


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and because of the degenerative areas in their walls, they are easily ruptured.
Also, where the plaques protrude into the flowing blood, their rough surfaces can
cause blood clots to develop, with resultant thrombusor embolus formation,
leading to a sudden blockage of all blood flow in the artery. With the obstructive
on the artery, it can also decrease blood flow to the brain; it is this which is the
reason why women are often sleepy.
Besides atherosclerosis, other thing that easily allows the woman drowsy
is sleep apnea. Most patients develop diabetes after age 40 years, and, although
much progress has been made in therapy, the majority of diabetic patients
continue to die from macrovascular complications (i.e., cardiovascular disease).
Recently it has become clear that sleep disturbances (e.g., chronic insomnia, sleep
apnea) have an impact on health and quality of life. Neuropathy may also
contribute to the significant reduction in quality of life for patients. These
problems are frequently overlooked on routine medical interviews; furthermore, in
some cases, short-term disturbances of sleep may evolve into chronic conditions.
The indiscriminate use of sleeping pills may further disrupt the sleep-wake cycle
and contribute to stress in patients with sleep disorders. In type 2 diabetes, sleep
disturbances are believed to be common and have been attributed to impaired
glucose metabolism and general physical distress. So because this woman's
quality of sleep less, and even when sleep is enough, then it cause of this woman
is easy sleepy during the day.

3.1.2 How is the pathogenesys of Neuropathy?

The most common form of neuropathy associated with diabetes mellitus is distal
symmetric sensorimotor polyneuropathy, often accompanied by autonomic
neuropathy. This disorder is characterized by striking atrophy and loss of
myelinated and unmyelinated fibers accompanied by Wallerian degeneration,
segmental, and paranodal demyelination and blunted nerve fiber regeneration. All
values for nerve conduction velocity in sensory and motor nerves were slower,


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and the sensory amplitude of the radial nerve and the motor amplitude of the
median nerve were lower. (Partanen et al., 1995) In both humans and laboratory
animals, this progressive nerve fiber damage and loss parallels the degree and/or
duration of hyperglycemia. Several metabolic mechanisms have been proposed to
explain the relationship between the extent and severity of hyperglycemia and the
development of diabetic neuropathy. One mechanism, activation of the polyol
pathway by glucose via AR, is a prominent metabolic feature of diabetic rat
peripheral nerve, where it promotes sorbitol and fructose accumulation, myo-
inositol depletion, and slowing of nerve conduction by alteration of neural Na(+)-
K(+)-ATPase activity or perturbation of normal physiological osmoregulatory
mechanisms. ARIs, which normalize nerve myo-inositol and nerve conduction
slowing, are currently the focus of clinical trials. Other specific metabolic
abnormalities that may play a role in the pathogenesis of diabetic neuropathy
include abnormal lipid or amino acid metabolism, superoxide radical formation,
protein glycation, or potential blunting of normal neurotrophic responses.
Metabolic dysfunction in diabetic nerve is accompanied by vascular insufficiency
and nerve hypoxia that may contribute to nerve fiber loss and damage. (Greene, et
al, 1992)

3.1.3 What is the connection between Diabetes Mellitus and polydipsi,

polyuria, and polyfagia??

Excessive thirst (polydipsia): A person with diabetes develops high blood

sugar levels, which overwhelms the kidney's ability to reabsorb the sugar as the
blood is filtered to make urine. Excessive urine is made as the kidney spills the
excess sugar. The body tries to counteract this by sending a signal to the brain to
dilute the blood, which translates into thirst. 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.


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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. This can also lead to
dehydration because excreting the sugar carries a large amount of water out of the
body along with it.
Excessive eating (polyphagia): If the body is able, it will secrete more
insulin in order to try to deal with the excessive blood sugar levels. Moreover, the
body is resistant to the action of insulin in type 2 diabetes. One of the functions of
insulin is to stimulate hunger. Therefore, higher insulin levels lead to increased
hunger and eating. Despite increased caloric intake, the person may gain very
little weight and may even lose weight.

3.1.4 What is the connection between Diabetes Mellitus and body


Obesity can increase risk factor to type 2 diabetes mellitus.

In type 2 DM, insulin resistance is often associated with abdominal
obesity (as opposed to hip and thigh obesity) and hypertriglyceridemia (Kasper,
Type 2 DM is characterized by three pathophysiologic abnormalities:
impaired insulin secretion, peripheral insulin resistance, and excessive hepatic
glucose production. Obesity, particularly visceral or central (as evidenced by the
hip-waist ratio), is very common in type 2 DM. Adipocytes secrete a number of
biologic products (leptin, TNF-α, free fatty acids, resistin, and adiponectin) that
modulate insulin secretion, insulin action, and body weight and may contribute to
the insulin resistance. In the early stages of the disorder, glucose tolerance


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remains normal, despite insulin resistance, because the pancreatic β cells

compensate by increasing insulin output. As insulin resistance and compensatory
hyperinsulinemia progress, the pancreatic islets in certain individuals are unable
to sustain the hyperinsulinemic state. IGT, characterized by elevations in
postprandial glucose, then develops. A further decline in insulin secretion and an
increase in hepatic glucose production lead to overt diabetes with fasting
hyperglycemia. Ultimately, β cell failure may ensue. Markers of inflammation
such as IL-6 and C-reactive protein are often elevated in type 2 diabetes (Kasper,
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, 2005).
Another emerging theory proposes that elevated levels of free fatty acids, a
common feature of obesity, may contribute to the pathogenesis of type 2 DM.
Free fatty acids can impair glucose utilization in skeletal muscle, promote glucose
production by the liver, and impair β cell function (Kasper, 2005).

Diabetes mellitus can reduce body weight.

Body weight is dynamic due to fat accumulation (triacylglicerol) in
adipocytes cells. Fat is dynamic because the amount of fat follow the energy
situation in one's body. If someone is having excess energy, the food material will
be deflected into the path of formation triacylglicerol. However, if someone
experienced hunger, triacylglicerol stored will be split into 3 fatty acids and 1
glycerol. Fatty acids will be distributed and to enter into the lane on the
mitochondrial oxidation β cells that would produce, acetyl CoA. Acetyl-CoA will
enter the Krebs cycle which produces nucleoside phosphate compounds-energy
high (Murray, 2003).


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In solving triacylglycerol (lipolysis) is required enzyme hormone-sensitive

lipase enzyme which is sensitive to insulin levels. The enzyme is inhibited by
insulin. However, if insulin levels are decreased (as in diabetes), the inhibition of

lipolysis is greatly reduced. Thus, the rate of formation of fatty acids will increase.
Fatty acid that increases will shift the use of glucose as energy to the use of fatty
acids for energy. Swift fatty acids will result in the number of acetyl-CoA
resulting in β oxidation. Acetyl-CoA which many will be deflected towards the
formation of ketone compounds which, if too many will lead to many
complications associated blood acidosis (Murray, 2003).
Thus, low levels of insulin will lead to lower the barriers for hormone-
sensitive lipase, so that the process of lipolysis will go well. The number of
reserves will result in triacylglycerol lipolysis in adipocytes cells is reduced, so
that the weight will decrease.


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3.1.5 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. This disease affects not only individually, but
the health system a country. Although no national survey, in line with changes
lifestyle, including eating patterns of Indonesian society is estimated patient. DM
is increasing, especially in adults and older age groups in all socio-economic
status. Currently, efforts to control disease DM has not occupied the main
priorities in health care, although the known negative impact thereof large enough
between, other chronic complications in chronic heart disease, hypertension,
brain, system nerve, liver, eyes and kidneys. DM is a degenerative disease, where
an interruption occurs metabolism of carbohydrates, fats and proteins and is
characterized by high blood sugar levels (hyperglycemia) and in urine.

Clinically, this disease is progressive travel and tend to involve too fat or
protein metabolism disorders. Increased blood glucose levels because of
utilization that are not going perfectly in turn often led to the clinical
abnormalities of blood lipid levels. 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, in addition to
efficacious drugs that reduce insulin resistance (insulin sensitizers).
Inadequate phase 1, which is then followed by performance improvement
phase 2 insulin secretion, in the early stages will not cause disruption to the blood
glucose levels. Clinically, then at the stage of decompensation, can be detected
condition called impaired glucose tolerance which is also called as a prediabetic
state. At this stage of compensatory mechanisms have started no longer adequate,
the body that may be deficient in relative terms, an increase in postprandial blood
glucose levels. In impaired glucose tolerance (IGT) was found postprandial blood
glucose levels, or after being fed a solution of 75 g glucose load with Oral
Glucose Tolerance Test (oral glucose tolerance), ranged between 140-200 mg /


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dl. Also known as prediabetes, when fasting blood glucose levels between 100-
126 mg / dl, which is also known as Fasting Blood Glucose Disturbed (GDPT).

State of hyperglycemia that occurs, both at the stage of chronic diabetes,

or acute postprandial hyperglycemia that occurred were ulangkali every day since
the stage of IGT, has negative long-term tissue complications of chronic
diabetes.Tingginya blood glucose levels (glucotoxicity) which followed by
dyslipidemia (lipotoxicity) is responsible for tissue damage both directly through
oxidative stress, and widespread process of glycosylation.

Insulin resistance from prominent role since the change or conversion into
DMT2 TGT phase. 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. This
is evident from the fact that in the early stages DMT2, although the serum insulin
levels are high enough, but hyperglycemia can still occur. Tissue damage occurs,
particularly microvascular, increased dramatically at this stage of diabetes,
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. Accordingly, at the higher levels of hepatic insulin
resistance, the lower the ability of inhibition to the process of glycogenolysis and
gluconeogenesis, causing the higher the level of hepatic glucose production.

We have to know that, Secreation of phase (Acute insulin secretion

responce = AIR) is the secretion of insulin that occurs immediately after
stimulation of beta cells, arise quickly and ended too quickly. Secretion of phase 1
(AIR) usually have a relatively high peak, because it is necessary to anticipate the
blood glucose levels typically rise sharply, immediately after eating. Performance
of a rapid and adequate water is essential for normal glucose regulation because
pasa turn contribute significantly in controlling postprandial blood glucose
levels. Thus, the presence of normal water needed to sustain the process of
physiological glucose metabolism. WATER normal lasting, beneficial in


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preventing the occurrence of acute hyperglycemia after a meal or postprandial

blood glucose spikes (postprandial spike) with all consequences thereof including
compensed inemia.

Furthermore, after the secretion phase 1 ended, appear secretion phase 2

(sustained phase, latent phase), where insulin secretion increased again slowly and
survive in a relatively longer time. After the end of phase 1, the task of blood
glucose regulation subsequently taken over by the secretion phase 2. Insulin
secretion phase 2, which lasted relatively long, how high the peak (quantitative)
will be determined by how much the blood glucose level at the end of phase 1, in
addition to insulin resistance factor. So, a kind of adjustment mechanism of
secretion of phase 2 to phase 1 previous performance. If the phase 1 secretion is
inadequate, there was a mechanism of compensation in the form of increased
secretion of insulin in Phase 2.Increased insulin production is essentially aimed at
meeting the needs of the body for blood glucose levels (postprandial) remained
within normal limits. In the prospective course of the disease, insulin secretion
phase 2 will be heavily influenced by phase 1.In the figure below (Fig. 2)
demonstrated the dynamics of insulin secretion in normal circumstances,
Disturbed Glucose Tolerance (IGT = Impaired Glucose Tolerance), and Type 2
Diabetes Mellitus.

Usually, with a normal phase 1 performance, accompanied also by the

action of insulin which is also normal in the network (without insulin resistance),
the secretion of phase 2 will also be normal. Thus no additional need (extra)
synthesis and secretion of insulin in Phase 2 above normal in order to maintain the
state of normoglycaemia.This is a physiological condition which is ideal for
without raising blood glucose levels that may impact glucotoxicity, also without
hyperinsulinemia with various negative impacts.


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First-Phase Normal
Insulin Secretion

Type 2DM


So, it can be concluded trip DMT2 disease, initially determined by the

performance of Phase 1 which then gives a negative impact on the performance of
phase 2, and a direct result of elevated levels of blood glucose
(hyperglycemia). Hyperglycemia occurs not only due to impaired insulin secretion
(insulin deficiency), but at the same time also by the low response of body tissues
to insulin (insulin resistance).Disruption or environmental influences such as
lifestyle or obesity will accelerate progression of the disease. Impaired glucose
metabolism will continue in fat and protein metabolism disorders and the damage
to various body tissues. The series of disorders that are motivated by insulin
resistance, other than intolerance to glucose and its various consequences, often
leading to a collection of symptoms called metabolic syndrome.


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3.1.6 What is the connection between Diabetes Mellitus Type 2 and

Carbohydrate Metabolism?

With type 2 diabetes, the impairment of glucose metabolism arises as a

result of a decreased sensitivity to insulin by the body’s cells. This means that the
cells do not respond to insulin to take up glucose from the bloodstream and utilize
it. This is known as insulin resistance. This causes glucose in human blood cannot
be converted into glycogen by hepar’s cells (glycogenesys doesn’t work). 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.
Compensatory mechanism:
The insulin levels in the blood are elevated, above the norm
(hyperinsulinemia) as the pancreas secretes higher amounts of glucose in an
attempt to overcome this resistance (compensatory mechanism). This
mechanism causes hyperinsulinemia until bile is overworked and
malfunctioned as well, leading to inappropriate amount of insulin in human
Overlap point with lipogenesys:
Upon consuming foods, particularly carbohydrates, the digestive system along
with the liver, break down the food into simple sugars like glucose. Glucose
then enters the blood stream where it is transported to cells throughout the
body. Excess glucose is converted to glycogen and stored in the liver and
muscles. Any remaining glucose may be converted for fat storage. This blood
glucose regulating mechanism is primarily controlled by the hormone, insulin,
which is secreted by the pancreas (beta cells in the islets of Langerhan’s).

Insulin triggers cells to take up glucose from the blood so that individual
cells can burn this glucose for energy. Alternatively, excess glucose is converted
into glycogen and stored in the liver due to the action of insulin. In insulin
resistance, seen in impaired glucose tolerance (or pre-diabetes), the body’s cells
and liver do not respond to insulin. Excess glucose builds up in the blood stream


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and the pancreas attempts to secrete more insulin. This excess insulin secretion
may not always trigger the desired effect resulting higher than normal blood
glucose levels. Over time, insulin resistance and pre-diabetes will lead to type 2
diabetes, also known as adult-onset diabetes or non-insulin dependent diabetes.

3.1.7 What is the connection between Diabetes Mellitys Type 2 with

lipid metabolism?

After a normal meal there is an ample supply of carbohydrate, and the fuel
for most tissues is glucose. In the starving state, 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). Other tissues can utilize
alternative fuels such as fatty acids and ketone bodies. As glycogen reserves
become depleted, so amino acids arising from protein turnover and glycerol
arising from lipolysis are used for gluconeogenesis. These events are largely
controlled by the hormones insulin and glucagon. 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), leading
to severe metabolic derangement.
The nutritional state of the organism is the main factor regulating the rate
of lipogenesis. Thus, the rate is high in the well-fed animal whose diet contains a
high proportion of carbohydrate. It is depressed under conditions of restricted
caloric intake, on a fat diet, or when there is a deficiency of insulin, as in diabetes
mellitus. These latter conditions are associated with increased concentrations of
plasma free fatty acids, and an inverse relationship has been demonstrated
between hepatic lipogenesis and the concentration of serum-free fatty acids.
Insulin stimulates lipogenesis by several other mechanisms as well as by
increasing acetyl-CoA carboxylase activity. It increases the transport of glucose
into the cell (eg, in adipose tissue), increasing the availability of both pyruvate
for fatty acid synthesis and glycerol 3-phosphate for esterification of the newly


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


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defects, some of which cause hypercholesterolemia, and premature

atherosclerosis. (Murray, 2003)

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


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5. In the liver, insulin depresses the rate of gluconeogenesis. It does this

by decreasing the activity of the enzymes that promote
gluconeogenesis. Because the substrates most used for synthesis of
glucose by gluconeogenesis are the plasma amino acids, this
suppression of gluconeogenesis conserves the amino acids in the
protein stores of the body.
In summary, insulin promotes protein formation and prevents the
degradation of proteins.

Insulin Lack Causes Protein Depletion and Increased Plasma Amino Acids.
Virtually all protein storage comes to a halt when insulin is not available.
The catabolism of proteins increases, protein synthesis stops, and large quantities
of amino acids are dumped into the plasma. The plasma amino acid concentration
rises considerably, and most of the excess amino acids are used either directly for
energy or as substrates for gluconeogenesis. This degradation of the amino acids
also leads to enhanced urea excretion in the urine. The resulting protein wasting is
one of the most serious of all the effects of severe diabetes mellitus. It can lead to
extreme weakness as well as many deranged functions of the organs. (Guyton and
Hall, 2006)

3.1.9 What is the normal rate of Insulin, Haematocrit, and Creatinin?

Insulin and Insulin Antibodies—Blood


Free insulin: fasting ≤25 IU/mL (<172.5 pmol/L, SI units). (Norms and
standardization of the test method vary widely by laboratory.)

Insulin Level via Radioimmunoassay:

SI Units
Adult, fasting level <17 μIU/mL or 1.00 mg/L <117 pmol/L
Newborn 3–20 μIU/mL 21–139 pmol/L


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SI Units
Infant <13 μIU/mL ≤89 pmol/L
Prepubertal child <13 μIU/mL ≤89 pmol/L
Panic levels >30 μIU/mL >207 pmol/L
Last trimester, amniotic fluid 11.3 μIU/mL 78 pmol/L

Insulin Antibodies.

Undetectable to less than 4% when using either bovine or porcine insulin as a

reagent. Insulin antibodies have been shown to occur more frequently with aging
and more in females than in males.

Increased Insulin.

Acromegaly, Beckwith-Wiedemann syndrome, beta-cell adenoma, Cushing's

syndrome, dystrophia myotonica, familial fructose and galactose intolerance,
hyperinsulinism, hypoglycemia, insulin-resistance syndromes, insulinoma, liver
disease, non–insulin-dependent diabetes mellitus, metabolic syndrome,
nesidioblastosis, obesity, overdose of insulin, pancreatic islet cell lesion, and
pheochromocytoma. Drugs include albuterol, calcium gluconate in the newborn,
estrogen, fructose, glucagon, glucose, insulin, levodopa, medroxyprogesterone,
oral contraceptives, prednisolone, quinine, quinidine, spironolactone, sucrose,
terbutaline, tolazamide, and tolbutamide.

Decreased Insulin.

Diabetes mellitus, hyperglycemia, hypopituitarism, and pancreatectomy-induced

diabetes. Drugs include beta-adrenergic blockers, asparaginase, calcitonin,
cimetidine, diazoxide, ethacrynic acid, ethyl alcohol (ethanol), ether, furosemide,
metformin, nifedipine, phenformin, phenobarbital, phenytoin, and thiazide

Positive Insulin Antibodies.


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Factitious hypoglycemia, autoimmune insulin syndrome (AIS).

Negative Insulin Antibodies.

Normal finding. Also negative in insulinoma.


Insulin is a hormone that regulates carbohydrate metabolism. It is produced in the

pancreas by the beta cells of the islets of Langerhans, and its rate of secretion is
determined primarily by the level of blood glucose. The radioimmunoassay test
measures endogenous insulin by using a series of tubes containing a fixed amount
of antibody label and an aliquot of standard, control, or unknown. The client's
unlabeled antigen in the blood competes with labeled antigen for antibody-binding
sites. The percentage of antigen bound to antibody is related to the total antigen
present and is reflected by the distribution of a radioactive label. Low
immunoreactive insulin levels have been associated with a higher risk of
developing degenerative diseases such as atherosclerosis, hypertension, and
dyslipidemia. Insulin antibodies, also referred to as anti–insulin-Ab, may be
present in diabetic clients treated for several weeks or more with conventional
insulin. These antibodies may also be present in persons who have never received
insulin but have autoimmune insulin syndrome (AIS), a rare condition
characterized by hyperinsulinemia and hypoglycemia. For diabetic clients, this
test may be used with C-peptide to determine whether hypoglycemia is caused by
insulin abuse. Insulin antibodies are transferred through the placenta and are
present in 30%–50% of children at the time of diagnosis before beginning insulin

Hematocrit (Hct)—Blood
SI Units
Adult 37%–47% 0.37–0.47


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SI Units
Pregnant 30%–46% 0.30–0.46
Adult Males 40%–54% 0.40–0.54
Neonates 40%–68% 0.40–0.68
3 months 29%–54% 0.29–0.54
1–2 years 35%–44% 0.35–0.44
6–10 years 31%–45% 0.31–0.45
Panic Levels <15% or >60% <0.15 or >0.60
Panic Level Symptoms and Treatment—Increased

NOTE: Treatment choice(s) depend(s) on client's history and condition and episode

Cause Symptoms Possible Treatments

Hemoconcentration Decreased pulse pressure and Administer IV fluids.
volume, decreased skin turgor, monitor hematocrit.
decreased venous filling, dry mucous Stop or reduce dose of
membranes, low central venous diuretics if they are
pressure, orthostatic hypotension, contributors to
tachycardia, thirst and weakness condition.
True polycythemia Extremity pain and redness, facial Administer IV fluids.
overtransfusion flushing, irritability, anasarca Monitor hematocrit.
decreasing QRS voltage with severe Observe for signs of
fluid overload thrombosis.
Perform bloodletting
by venipuncture

Panic Level Symptoms and Treatment—Decreased

Cause Symptoms Possible Treatments
Hemodilution Rales, anxiety, edema, Administer diuretics.
hypertension, jugular venous Restrict sodium.
distention, restlessness, and Restrict fluids.
shortness of breath Monitor hematocrit and intake
and output.
Administer oxygen.


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Cause Symptoms Possible Treatments

Blood loss Hypotension, bleeding, hypoxia Identify and treat cause of
Give isotonic fluids.
Perform blood transfusion.
Administer omeprazole (if
blood loss is caused by
bleeding esophageal varices).
Protect airways; administer
oxygen as needed.


Addison's disease, blood doping (autologous transfusion to improve athletic

performance), burns (severe), dehydration (severe), diabetes mellitus, diarrhea,
eclampsia, erythrocytosis, hemorrhage, hemoconcentration, pancreatitis (acute),
polycythemia, shock, and tetralogy of Fallot. Any condition that increases red
blood cells (RBCs).


Anemia, bone marrow hyperplasia, burns (severe), cardiac decompensation,

cirrhosis, congestive heart failure, cystic fibrosis, fatty liver, fluid overload,
hemolytic reactions to chemicals or drugs or prosthetics, hemorrhage, hydremia of
pregnancy, hyperthyroidism, hypothyroidism, idiopathic steatorrhea, intestinal
obstruction (late), leukemia, overhydration, pancreatitis (hemorrhagic),
pneumonia, and pregnancy. Also, conditions that decrease RBCs. Drugs include
acetaminophen, acetohexamide, aminosalicylic acid, amphotericin, antimony
potassium tartrate, antineoplastic agents, antibiotics, atabrine hydrochloride,
chloramphenicol, chloroquine hydrochloride or phosphate, doxapram
hydrochloride, ethosuximide, ethotoin, furazolidone, haloperidol, hydralazine
hydrochloride, indomethacin, isocarboxazid, isoniazid, mefenamic acid,
mephenytoin, mercurial diuretics, metaxalone, methaqualone, methsuximide,
methyldopa, methyldopate hydrochloride, nitrates, nitrofurantoin, novobiocin
sodium, oleandomycin, oxyphenbutazone, paramethadione, pargyline


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hydrochloride, penicillins, phenacemide, phenelzine sulfate, phenobarbital,

phensuximide, phenylbutazone, phenytoin sodium, phytonadione, primidone,
radioactive agents, rifampin, spectinomycin hydrochloride, sulfonamides,
tetracyclines, thiazide diuretics, thiocyanates, thiosemicarbazones, tolazamide,
tolbutamide, tranylcypromine sulfate, trimethadione, tripelennamine
hydrochloride, troleandomycin, valproic acid, vegetarian diet, vitamin A, and
zidovudine (AZT).


Hematocrit is the percentage of red blood cells in a volume of whole blood.

SI Units
Jaffe, Manual Method 0.6–1.6 mg/dL 52–142 μmol/day
Jaffe, Kinetic or Enzymatic Method
Females 0.5–1.1 mg/dL 44–97 μmol/L
Males 0.6–1.2 mg/dL 53–105 μmol/L
Elderly May be lower May be lower
Cord blood 0.6–1.2 mg/dL 53–105 μmol/L
Newborn 0.8–1.4 mg/dL 71–124 μmol/L
Infant 0.7–1.7 mg/dL 62–150 μmol/L
1 year, female ≤0.5 mg/dL ≤44 μmol/L
1 year, male ≤0.6 mg/dL ≤53 μmol/L
2–3 years, female ≤0.6 mg/dL ≤53 μmol/L
2–3 years, male ≤0.7 mg/dL ≤62 μmol/L
4–7 years, female ≤0.7 mg/dL ≤62 μmol/L
4–7 years, male ≤0.8 mg/dL ≤71 μmol/L
8–10 years, female ≤0.8 mg/dL ≤71 μmol/L


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SI Units
8–10 years, male ≤0.9 mg/dL ≤80 μmol/L
11–12 years, female ≤0.9 mg/dL ≤80 μmol/L
11–12 years, male ≤1.0 mg/dL ≤88 μmol/L
13–17 years, female ≤1.1 mg/dL ≤97 μmol/L
13–17 years, male ≤1.2 mg/dL ≤106 μmol/L
18–20 years, female ≤1.2 mg/dL ≤106 μmol/L
18–20 years, male ≤1.3 mg/dL ≤115 μmol/L


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


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meclofenamate sodium, methicillin sodium, metoprolol tartrate, minoxidil,

mithramycin, nitrofurantoin, nitrogen oxide (inhaled), propranolol, protein,
pyruvate, sulfobromophthalein, sulfonamides, streptokinase, testosterone,
testosterone cypionate, testosterone enanthate, testosterone propionate,
triamterene, and viomycin. Herbal or natural remedies include products
containing aristolochic acids (Akebia spp., Aristolochia spp., Asarum spp.,
birthwort, Bragantia spp., Clematis spp., Cocculus spp., Diploclisia spp.,
Dutchman's pipe, Fang chi, Fang ji, Guang Kan-Mokutsu, Menispernum spp.,
Mokutsu, Mu tong, Sinomenium spp., and Stephania spp.).


Diabetic ketoacidosis (artifactual decrease) and muscular dystrophy. Drugs

include cefoxitin sodium, cimetidine, chlorpromazine, chlorprothixene, marijuana,
thiazide diuretics, and vancomycin. Herbal or natural remedies include Cordyceps


Creatinine is produced continuously as a nonprotein end product of anaerobic

energy-producing creatine phosphate metabolism in skeletal muscle. Because it is
continually and easily excreted by the renal system, increased levels indicate a
slowing of the glomerular filtration rate. Creatinine is thus a very specific
indicator of renal function, revealing the balance between creatinine formation
and excretion. A diurnal variation in creatinine may be related to meals, with
troughs occurring around 0700 (7 AM) and peaks occurring around 1900 (7 PM).

Lipid Profile—Blood

See individual test listings for age-specific norms, including norms for children.

SI Units
Lipids, total 400–800 mg/dL 4.0–8.0 g/L


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SI Units
Triglycerides 10–190 mg/dL 0.2–4.8 mmol/L
HDL cholesterol
Females 35–85 mg/dL 0.9–2.2 mmol/L
Males 30–65 mg/dL 0.8–1.7 mmol/L
LDL cholesterol 80–190 mg/dL 2.0–4.9 mmol/L
VLDL cholesterol (calculated) ≤30 mg/dL <0.78 mmol/L
Total-to-HDL cholesterol ratio Median = 5

Condition Triglycerides Total Cholesterol HDL LDL

Alcoholism Increase Increase Increase Increase
Aortic aneurysm Increase Increase Increase Increase
Aortitis Increase Increase Increase Increase
Arteriosclerosis Increase Increase Decrease Increase
Diabetes mellitus Increase Increase Increase Increase
Glycogen storage Increase — — Increase
Hyperalimentation Decrease Decrease Decrease Decrease
Hypercholesterolemia Increase Increase — Increase
Hyperlipoproteinemia Increase Increase Increase Increase
Hypothyroid Increase — Decrease —
Malabsorption Decrease Decrease Decrease Decrease
Myxedema Increase Increase Increase Increase
Nephrotic syndrome Increase Increase Increase Increase
Pancreatitis Increase Increase Increase Increase


Lipid profile is a battery of laboratory studies to help determine the risk factors in
coronary artery disease. Blood lipids comprise cholesterol, triglycerides, and
phospholipids. Fasting lipid profiles are recommended every 5 years in clients
older than age 19. See individual test sections for further descriptions of the


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components of the lipid profile, as well as levels for which lifestyle changes and
therapeutic drug regimens are recommended. (Chernecky & Berger, 2008)

Total Cholesterol—Coronary Heart Disease Risk

Desirable Borderline High Risk High Risk
Norm SI Units mg/dL SI Units mg/dL SI Units
mg/dL mmol/L mmol/L mmol/L
Adult <200 <5.18 200– 5.18–6.19 ≥240 ≥6.22
Child <170 <4.40 170– 4.40–5.15 ≥200 ≥25.18

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 >1.554 45–59 1.16–1.53 35–45 0.91–1.16 <35 <0.91

Total to HDL Ratio

Coronary Heart Disease Average Risk 2 × Average 3 × Average Risk
Risk Risk
Male 5.0 9.6 23.4
Female 4.4 7.1 11.0

LDL Cholesterol—Coronary Heart Disease Risk

Low Risk Moderate Risk High Risk
Optima Near Optimal Borderline High High Very High
mg/dL SI Units mg/dL SI Units mg/dL SI Units mg/dL SI Units mg/dL SI Units
<100 <2.59 100–129 2.59– 130–159 3.37– 160–189 4.14– >190 >4.92
3.34 4.12 4.89


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3.1.10 What is the solution of this problem?

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


16th Group

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


16th Group

• Fluid: nonkelotik hiperglikemik hyperosmolar coma treated by giving

fluids in bulk and slow correction of potassium deficit. This incident can
be prevented by good diet control.
• Pharmacological interventions that can be considered to be given to
patients with diabetes are antihypertensive medications. Anti-hypertensive
medications have been proven to reduce hypertension in patients with
diabetes and kidney disease awitan slow.
• 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. Treatment in this manner gives hope for diabetes cure in
the future.
• Insertion of genes for insulin: is currently also being carried out
preliminary experiments designed to allow insertion of the insulin gene to
type 1 diabetes. In future, this procedure is to provide hope for healing
diabetes, compared with drug therapy.


16th Group


A woman came with problems of her drowsiness and her tingling. In order
to get the diagnosis and the possible patophysiology of her problems, series of
anamnestic question, physical examination, and laboratory test should be done
• Age : 41 years

• Marital status : Married, have 1 child

• Address : Kupang Indah Surabaya

• Job : Housewife

• She has tingling since 1 month ago, all the time and progressive.

• She often fell sleepy.

• She often wakes up at night for micturing.

• She losses 3 kg of her weight.

• Diabetes : unknown

• Hypertension : disputed

• Family history :

• Her father dead from complication


16th Group

• 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.

• She often feels thirsty and drinks much.

• She often feel hungry too.

• She rarely, practically never, 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, Anemia, Icterus = Negative (-)

• Ascites = negative (-)

• Hepar and Lien cannot be felt


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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 : 0,7 mg/dL

• HDL : 38 mg/dL ; LDL : 94 mg/dL; Total Cholesterol : 171 mg/dl

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


16th Group

First, the patient has an increase frequency in urination, especially at night

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


16th Group

Insufficient production of insulin (either absolutely or relative to the

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


16th Group

midst of plenty". The abundant, unutilized glucose is wastefully excreted in the

Insulin is a hormone that is produced by specialized cells (beta cells) of
the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind
the stomach.) In addition to helping glucose enter the cells, insulin is also
important in tightly regulating the level of glucose in the blood. After a meal, the
blood glucose level rises. 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. When the blood glucose levels are
lowered, the insulin release from the pancreas is turned down. 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. In
normal individuals, such a regulatory system helps to keep blood glucose levels in
a tightly controlled range. As outlined above, in patients with diabetes, the insulin
is either absent, relatively insufficient for the body's needs, or not used properly
by the body. All of these factors cause elevated levels of blood glucose
The fasting blood glucose (sugar) test is the preferred way to diagnose
• Normal fasting plasma glucose levels are less than 100 milligrams per
deciliter (mg/dl).

• Fasting plasma glucose levels of more than 126 mg/dl on two or more tests
on different days indicate diabetes.

• A random blood glucose test can also be used to diagnose diabetes. A

blood glucose level of 200 mg/dl or higher indicates diabetes.

When fasting blood glucose stays above 100mg/dl, but in the range of
100-126mg/dl, this is known as impaired fasting glucose (IFG). While patients
with IFG do not have the diagnosis of diabetes, this condition carries with it its
own risks and concerns, and is addressed elsewhere.


16th Group

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

So we should analyze more from other data.

We got a data about the risk factors for type 2 Diabetes Mellitus from Harrison's
Principles Of Internal Medicine, 16th Edition,2005 by Kasper.


16th Group

In this patient, we find some risk factors for type 2 Diabetes Mellitus in
this patient. The first factor is she is obese (the BMI is about 36,1). Second, she is
habitual physical inactivity. Third, triglyceride level is > 250 mg/dL (278
mg/dL). There is one more risk factor that maybe she have but we aren’t sure
about that. That is she have family history of diabetes. From anamneses we know
that her father dead from complication and her eldest brother dead in 40 th years
old with a wound in her leg which cannot be healed and nasty smell. We think
that her father and her brother had suffered from diabetes, because uncontrolled
diabetes can make complication problem and diabetic patient often have wound
that hard to be healed (ulcer).


Miss X , 41 years old, has the symptoms of Diabetes Mellitus Type 2 with
hyperglycemia, dysllipidemia due to the decreasing of sensitivity of insulin
receptor in cells caused by her obesity


16th Group

Tingling all time since a
month ago
Wake up at night for A Female, 41 years old
vital sign examination:
Often feel sleepy Pulse : 80/min
3 kgs weight losses Examination
RR : 20/min
Family sick: father dead from Temp: 37 oC Cyanosis, Anemia,
complication and eldest
Icterus (-)
sister dead in 40 years old Blood pressure :
with a wound in her leg 120/80 mmHg Ascites (-)
which can’t be healed and
nasty smell Weight: 89 kgs Extremity
deformities (-)
Often feels thirsty and drinks Height: 157 cms
much Waist
Often feel hungry too circumference: 93 Laboratory results:
cms Fasting Glucose: 199 mg/dL
Hasn’t received any Obese
treatments before 2-h PP Glucose: 317 mg/dL

rarely, practically never, does High lipotoxic from Triachilglicerol 278 mg/dL
any sports adipocyte
Hemoglobin: 12 g/dL
Sensitivity of insulin Palpation, percussion, & Creatinin Level: 0,7 mg/dL
receptor is decreased auscultation :
Ascites (-) HDL: 38 mg/dL ; LDL: 94
Hepar & Lien normal mg/dL; Total Cholesterol:
171 mg/dl
Compensated by pancreas to
produce more insulin

Decompensation of β cell of pancreas

High level of blood glucose

Other complications:
Polyuria, polydipsia,
sleepy, and other 16th Group Type 2 Diabetes Mellitus
progressive complication
like atherosclerosis,


Large amount of adipocytes

Others factor

High lypotoxic

Sensivity of insulin
receptor decreased polydypsea polyuria
r disease

Glucose can not enter

into cells with GLUT-4 Renal disease

Complication of diabetes Neuropaty
Blood glucose increase

Compensated by pancreas to
increase the insulin Type 2 diabetes
production mellitus

Sensivity of insulin High level of

receptor decrease blood glucose


16th Group
Decompensation of beta
cell of pancreas Low level of insulin


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


16th Group

insulin, so it can help the insulin’s receptor activity to fulfill the cell needs for
glucose. And the most important, this woman should have diet. She must be
decrease carbohydrate intake, she should has a struggle to restrain her apatite,
because if she is not change her diet, her glucose level will always be high that
have many risk for her health.


1. 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.
2. Difficult for gathering the members of our group because of our
3. Since all of us are involved in medical science held by the students of
Airlangga University Medical Faculty, we do not have enough time
to gather and discuss

U.S. National Library of Medicine, 2010. Drowsiness. Department of Health and
Human Services. Available at:
http://www.nlm.nih.gov/medlineplus/ency/article/003208.htm (Accessed
on November 6th 2010)
National Institute of Neurological Disorders and Stroke, 2010, Peripheral
Neuropathy Fact Sheet, National Institute of Neurological Disorders and
Stroke. Available at:


16th Group

neuropathy.htm (Accessed on November 11th 2010)
Pathophysiology Of Diabetes Mellitus, unknown year. Pathophysiology Of
Diabetes Mellitus. [Online] (unknown updated date). Available at:
http://www.pathophysiologyofdiabetesmellitus.com/index.html (Accessed
November 7th 2010)
Unknown author, 2009. Phatophysiology of Diabetes. [internet] Diabetes
Manegement in School Setting. Available at:
http://www.dhss.mo.gov/diabetes/DMOverview.pdf (Accessed on
November 7th 2010)
Mayo Clinic, 2010. Diabetes symptoms: When diabetes symptoms are a concern.
[online] (Updated 12 Oct 2010). Available at:
(Accessed 7 November 2010)
Mayo Clinic, 2010. Diabetes symptoms: When diabetes symptoms are a concern.
[online] (Updated 12 Oct 2010). Available at:
symptoms/DA00125/NSECTIONGROUP=2 (Accessed 7 November
Hani L. .2010. Lingkar Perut Membesar dan Kegemukan. Available at
dan-kegemukan (Accesed on November 17th 2010)
MedlinePlus. 2010. Type 2 Diabetes – risk factors. A service of the U.S. National
Library of Medicine
National Institutes of Health (Online). Available at:
http://www.nlm.nih.gov/medlineplus/ency/article/002072.htm (Accessed
on Nopember 10th 2010)
International Diabetes Federation. 2010. Complications of diabetes. International
Diabetes Federation (Online). Available at:


16th Group

http://www.idf.org/complications-diabetes, (Accessed on November 10th

Chernecky & Berger, 2008, Laboratory Tests and Diagnostic Procedures, 5th
Edition, Missouri: Saunders Elvesier
Brandis, Kerry. 2007. Acid-base Physiology. Availablet at
http://www.anaesthesiamcq.com/AcidBaseBook/ab3_2.php (Accessed on
November 8th 2010)
Davidson, S, et al., 1973. Human Nutritions and Dietetics. Edinburgh: English
Language Book Society.
Robert et al., 2003, Harper’s Illustrated Biochemistry, twenty six edition.USA:
Lange Medical
Lopes et al, 2005. Restless Legs Syndrome and Quality of Sleep in Type 2
Greene et al., 1992, Complications: neuropathy, pathogenetic considerations,
Diabetes Care December 1992 Vol. 15 no. 12. Avalable at:
http://care.diabetesjournals.org/content/15/12/1902 (Accessed on
November 11th 2010)

eMedicineHealth, 2010, Diabetes Symptoms. Available at

http://www.emedicinehealth.com/diabetes/page3_em.htm (Accessed
November 17th 2010)
Kasper, Dennis L. et al. eds. 2005. Harrison’s Principles of Internal Medicine
16th ed. New York: McGraw-Hill Companies
Murray, Robert K. et al. 2003. Harper’s Illustrated Biochemistry 26th ed. New
York: Lange Medical Books
at http://www.google.co.id/url?


16th Group

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


16th Group

EBL and Critical Apraissal

For Answering Searching Information Validity Importance Applicability
Question Method Type Foundation Result Foundation Result Foundation Result
Internet Content of Is it
/003208.htm 1 Digital Article Yes Yes Yes
Browsing information applicable?
(Accessed on
November 6th
Internet Content of Is it
peripheralneuro 2 Digital Article Yes Yes Yes
Browsing information applicable?
(Accessed on
November 11th
Internet Content of Is it
om/index.html 3 Digital Idea No Yes Yes
Browsing information applicable?
November 7th
http://www.dhss 3 Internet Digital Article Yes Content of Yes Is it Yes
.mo.gov/diabete Browsing information applicable?
pdf (Accessed
on November


16th Group

7th 2010)

Internet Content of Is it
symptoms/DA0 4 Digital Idea No Yes Yes
Browsing information applicable?
0125 (Accessed
November 7th
Internet Content of Is it
0125/NSECTIO 4 Digital Idea No Yes Yes
Browsing information applicable?
November 7th
cle&id=1145:lin Internet Content of Is it
5 Digital Idea No Yes Yes
gkar-perut- Browsing information applicable?
(Accesed on
November 17th
http://www.nlm. 6 Internet Digital Article Yes Content of Yes Is it Yes


16th Group

Browsing information applicable?
(Accessed on
Nopember 10th

-diabetes, Internet Content of Is it
7 Digital Article Yes Yes Yes
(Accessed on Browsing information applicable?
November 10th

Tests and
Content of Is it
Diagnostic 8,9,10,11 eBook Digital Textbook Yes Yes Yes
information applicable?
Procedures, 5th
Internet Content of Is it
b3_2.php 12 Digital Idea No Yes Yes
Browsing information applicable?
(Accessed on
November 8th
Human Borrowed
Content of Is it
Nutritions and 13 from the Textbook Article Yes Yes Yes
information applicable?
Dietetics library


16th Group

Personal Content of Is it
Biochemistry, 1,4,7 Textbook Textbook Yes Yes Yes
Inventory information applicable?
twenty six

Restless Legs
Syndrome and Borrowing
Content of Is it
Quality of Sleep 1 from the Textbook Article Yes Yes Yes
information applicable?
in Type 2 library
ontent/15/12/19 Internet Digital Content of Is it
2 Journal Yes Yes Yes
02 (Accessed on Browsing (PDF) information applicable?
November 11th
Partanen, et al. 2 Internet Digital Journal Yes Content of Yes Is it Yes
Browsing (PDF) information applicable?
1995. Natural
History of
Neuropathy in
Patients with


16th Group

Mellitus. The
(Online), Vol.
333 No. 2.
Available at:
(Accessed on
November 20th

Internet Content of Is it
3_em.htm 3 Digital Idea No Yes Yes
Browsing information applicable?
November 17th


16th Group

Principles of
Using Content of Is it
Internal 4 Text Textbook Yes Yes Yes
Textbook information applicable?
Medicine 16th
Internet Digital Content of Is it
EKRESI_DAN_ 5 Article Yes Yes Yes
Browsing (Word) information applicable?
(Accesed at
November 17th
http://www.gizi. 5 Internet Digital Article Yes Content of Yes Is it Yes
net/makalah/Ma Browsing (PDF) information applicable?
(Accesed on


16th Group

November 17th

12/7425.full.pdf Internet Digital Content of Is it
6 Article Yes Yes Yes
(Accessed at Browsing (PDF) information applicable?
November 11th

Personal Content of Is it
Biochemistry, 7 Textbook Text Yes Yes Yes
inventory information applicable?
Textbook of
Physiology 11th Personal Content of Is it
8 Textbook Text Yes Yes Yes
Ed. Missisipi : inventory information applicable?
Elsevier Inc.
p.966 - 967

Tests and
Content of Is it
Diagnostic 9 eBook Digital Article Yes Yes Yes
information applicable?
Procedures, 5th

Pathophysiolog Content of Is it
10 from the Text Report Yes Yes Yes
y information applicable?


16th Group


16th Group

Group : 16th group

Title : Natural History of Peripheral Neuropathy in Patients with Non-
Insulin-Dependent Diabetes Mellitus

Item Existence (with page)

 Title Yes (page 89)

 Abstract and or Summary Yes (page 89)

 Introduction, Background Yes (page 89)

 Method Yes (page 89)

 Result Yes (page 89)

 Discussion Yes (page 93)

 Acknowledgement No

 Reference Yes (page 93-94)

Conclusion : the format is not complete

Objective: To determine the long-term risk of diabetic polyneuropathy and the
factors affecting that risk.

PBL Group 1st Medical Faculty of Airlangga University

Medical Ethic and Law Module
Method: Cross-sectional Study
Item Items found (with page)

Design Cross-sectional study (Page 89)

Hierarchy of Evidence 5

Sample 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
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)
Sample Size 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

PBL Group 1st Medical Faculty of Airlangga University

Medical Ethic and Law Module
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)
Eligibility Criteria 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
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 Total Sampling

Collecting Data Method The diagnosis of diabetes4 was

confirmed by an oral glucose-
tolerance 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)
Measurement and or assessment 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

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Medical Ethic and Law Module
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 base-
line study, albumin was measured
by immunodiffusion in 24-hour
urine samples (Behringswerke,
Mahrburg Lahn, Germany).
(Page 89-90)
Instrument The differences in mean values
between the groups were
analyzed by Student's t-test (two-
tailed), 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. Time-
related 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

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Medical Ethic and Law Module
trapezoidal rule. The Spearman
correlation coefficient was
calculated for the relation
between nerve function and the
metabolic variables (glycemic
control and serum insulin values).
All the data were analyzed with
SPSS software (SPSS, Chicago).
(Page 91)
Randomization -

Intervention -

Analysis Method Statistical Method (Page 91)

Coherence between design and objective: coherent

Coherence between measurement and instrument used: coherent


CI : There is no CI.
P : 0.083
If this research were done repeatedly (100x), 8.3 researches will show the same
result as the previous result (by chance).

Conclusion : Because there is no CI, the importance can’t be


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Medical Ethic and Law Module