Académique Documents
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PRESENTED BY:
GROUP 16th
FACULTY OF MEDICINE
AIRLANGGA UNIVERSITY
Scenario Creator
Prof. Dr. Suhartati, dr., MS
Edhi Rianto, dr., MS
Leader :
Shaleh Muhammad D 010911171
Members:
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
CONTENTS
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
EIGHTH MODULE
HUMAN FUNCTION MODULE
PROBLEM BASED LEARNING
INSTRUCTIONAL OBJECTIVES
CHAPTER I
FIRST TUTORIAL
1.1 Scenario
1.2. Main Problem
1.3.1. Female
1.3.2. Numbness in both lower extremities
1.3.3. Outpatient treatment
1.3.4. Sleepy
• Diabetes Mellitus
• Malnutrition deficiency
• Anemia
• Neuron disorders
• Cardio-vascular disorders
• Lipid metabolism disorders
• Hypoxia
FINANCIAL
METABOLISM AND NUTRITION MODULE
CONDITION
16th Group
9
Female; 41 y.o
Physical
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:
DM
Malnutrition Deficiency
Neuron Disorders
CHAPTER II
SECOND TUTORIAL
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.
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.
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
adolescents.
2. Increased prevalence in some ethnic groups, e.g., African Americans,
Hispanic/Latino, Native Americans, Asian Americans, and Pacific
Islanders.
3. Strong genetic predisposition.
4. Frequently obese.
5. Not prone to ketoacidosis until late in course or with prolonged
hyperglycemia.
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.
C. Treatment
1. Diet/weight management
2. Exercise/increase physical activity
3. Oral hypoglycemic/antihyperglycemic agents, insulin sensitizers, or
insulin
4. Education
5. Monitoring
6. Treatment of co morbid conditions (e.g., hypertension, lipid abnormalities)
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
postprandial.
2. Ketones: test for ketones using first morning urine sample. Presence of
ketones may indicate starvation rather than hyperglycemic ketosis.
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
people, these early changes do not cause vision problems. However, if these
changes progress undetected, they can lead to vision loss and blindness.
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
work.
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
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.
SI Units
pH
Adults 7.35–7.45 7.35–7.45
Panic values ≤7.2 and >7.6 ≤7.2 and >7.6
Children
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
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.
Increased PaCO2.
Increased PaO2.
Increased HCO3-.
Increased O2 Saturation.
Decreased pH.
Decreased PaCO2.
Decreased PaO2.
Decreased HCO3-.
Decreased O2 Saturation.
See diagram.
Shift to Left.
Shift to Right.
Description.
The arterial blood gas test measures the dissolved oxygen and carbon dioxide in
the arterial blood and reveals the acid-base state and how well the oxygen is being
carried to the body. 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:
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.
Increased pCO2.
Increased pO2.
Increased HCO3-.
Increased O2 Saturation.
Decreased pH.
Decreased pCO2.
Decreased pO2.
Decreased HCO3-.
Decreased O2 Saturation.
Description.
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.)
SI Units
pH
Adults 7.35–7.45 7.35–7.45
Panic values <7.2 or >7.6 <7.2 or >7.6
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.
Increased pCO2.
Increased pO2.
Increased HCO3-.
Increased O2 Saturation.
Decreased pH.
Decreased pCO2.
Decreased pO2.
Decreased HCO3-.
Decreased O2 Saturation.
Description.
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)
Glucose—Blood
Norm.
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
Children
Cord blood 38–82 mg/dL 2.1–4.6 mmol/L
Premature infant 17–51 mg/dL 0.9–2.8 mmol/L
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
Serum
Adults 65–100 mg/dL 3.6–5.5 mmol/L
>60 years 80–115 mg/dL 4.4–6.4 mmol/L
Children
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
Increased.
Decreased.
Description.
Usage.
Increased.
Decreased.
Description.
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)
Triglycerides—Blood
Norm.
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
Increased.
Decreased.
Description.
Increased.
Decreased.
Description.
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.
Other clinical guides should also be used in deciding on the presence and
severity of a metabolic acidosis. Significant lactic acidosis may be associated with
an anion gap which remains in the reference range. Lactate levels of 5 to 10
mmols/litre are associated with a high mortality if associated with sepsis, but the
AG may be reported as within the reference range in as many as 50% of these
cases! (Dorwart & Chalmers 1975).
The anion gap is useful especially if very elevated or used to confirm other
findings. Causes of a high anion gap acidosis can be sorted out more specifically
by using other investigations in addition to the history and examination of the
patient. Investigations which may be very useful are:
• Lactate
• Creatinine
• Plasma glucose
• Urine ketone test
brittleness and dryness: later there is flattening and thinning and finally concavity
(spoon-shaped nails).
CHAPTER III
THIRD TUTORIAL
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,
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.
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,
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)
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.
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.
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 /
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).
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.
Intravenous
Second
glucose
Phase
stimulation
IGT
First-Phase Normal
Insulin Secretion
Type 2DM
Basal
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
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.
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
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
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.
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)
Free insulin: fasting ≤25 IU/mL (<172.5 pmol/L, SI units). (Norms and
standardization of the test method vary widely by laboratory.)
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.
Increased Insulin.
Decreased Insulin.
Description.
Hematocrit (Hct)—Blood
Norm.
SI Units
Females
Adult 37%–47% 0.37–0.47
SI Units
Pregnant 30%–46% 0.30–0.46
Adult Males 40%–54% 0.40–0.54
Children
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
history.
Increased.
Decreased.
Description.
Creatinine—Serum
Norm.
SI Units
Jaffe, Manual Method 0.6–1.6 mg/dL 52–142 μmol/day
Jaffe, Kinetic or Enzymatic Method
Adults
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
Children
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
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
Increased.
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,
Decreased.
Description.
Lipid Profile—Blood
Norm.
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
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
Description.
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
components of the lipid profile, as well as levels for which lifestyle changes and
therapeutic drug regimens are recommended. (Chernecky & Berger, 2008)
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.
3.2 ANALYSIS
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
Anamnesis
• Age : 41 years
• Job : Housewife
• She has tingling since 1 month ago, all the time and progressive.
• Diabetes : unknown
• Hypertension : disputed
• Family history :
• Her eldest sister dead in 40th years old with a wound in her leg which
cannot be healed and nasty smell
Physical Examination
• General condition : good
• Weight : 89 kg
• Height : 157 cm
• Waist Circumference : 93 cm
Inspection :
• Cyanosis, Anemia, Icterus = Negative (-)
Palpation:
• Hepar and Lien cannot be felt
Percussion :
Thorax :
• Heart and Lungs = Normal
Laboratory Result
• Fasting Glucose : 199 mg/dL
• Hemoglobin : 12 g/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.
• Fasting plasma glucose levels of more than 126 mg/dl on two or more tests
on different days indicate 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.
We try to compare the patient’s blood glucose level with the standard
itself.
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)
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
Anamnesis:
Tingling all time since a
month ago
Wake up at night for A Female, 41 years old
micturing
vital sign examination:
Often feel sleepy Pulse : 80/min
3 kgs weight losses Examination
RR : 20/min
Inspections:
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
3.4 FINAL MIND MAPPING
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
Obese
Others factor
High lypotoxic
Sensivity of insulin
receptor decreased polydypsea polyuria
Polyphagya
Chardiovascula
r disease
CASE MAPPING
Complication of diabetes Neuropaty
melitus
Blood glucose increase
Other
complication
Compensated by pancreas to
increase the insulin Type 2 diabetes
production mellitus
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
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.
3.6 OBSTACLES
References
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http://www.nlm.nih.gov/medlineplus/ency/article/003208.htm (Accessed
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1. PAPER COMPLETION :
Item Existence (with page)
Acknowledgement No
2. RESEARCH VALIDITY
Objective: To determine the long-term risk of diabetic polyneuropathy and the
factors affecting that risk.
Hierarchy of Evidence 5
Intervention -
3. IMPORTANCE
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).