CASE REPORT: TYPE 2 DIABETES MELLITUS

Case Report
Presented to
Arthur Christian B. Mangio
The Nursing Department
Of Manila Adventist College

In Partial
Fulfillment of the
Requirements for the
Anatomy and Physiology Laboratory

By
Gynesis Roquero
Athina Villaruz Campul
Brynne Rhen Fortaleza
Rune Abraham Balagtas
December 2019
 INTRODUCTION

Diabetes Mellitus is a group of metabolic disorders that leads to high blood

glucose level, resulting in excessive urination, increased thirst, blurred vision,

tingling, sweating and many other symptoms. Acute conditions include diabetic

ketoacidosis and nonketotic hyper osmolar coma while long term condition results

in stroke, kidney failure, and cardiovascular disease. Blood glucose increases due

to lack of insulin production less insulin action (resistance) commonly detected

after the age of 40. (Morgan M, 2006).

 CHAPTER II

EPIDEMIOLOGY

Type 2 diabetes is a lifelong disease that keeps your body from

using insulin the way it should. People with type 2 diabetes are said to have insulin

resistance. People who are middle-aged or older are most likely to get this kind of

diabetes, so it used to be called adult-onset diabetes. But type 2 diabetes also

affects kids and teens, mainly because of childhood obesity. Patient suffering from

diabetes due to many reasons included less production of the insulin by beta cells

of the Pancreas or resistance of body against insulin, a major reason of diabetes is

genetics, majority of diabetic patient suffering from type 2 diabetes due to their

genetics and family history. (Plotnick L, 2008).

If this condition is not properly treated or is for long term it results in

cardiovascular disease, shock, permanent damage to eye and chronic kidney

disease. Diabetic patient should properly manage his/her daily dietary intake

because if patient is taking oral hypoglycemic agents as medication and not taking

diet according to body need then he/she may suffer from hypoglycemic state that

can be more dangerous than the hyperglycemia. Small meals should be taken 4 to 5

time in a day instead of eating a lot at single time.

 Insulin or other hypoglycemic agents should always be taken before 10

minutes of taking meal, because medicine or external source of insulin will trigger

the beta cells of the body to produce insulin inside the body according to need of

body. Diabetic condition can also be treated by non - pharmacological method as

by doing exercise, by stopping intake of high sugar content food. Type 2 diabetes,

long considered a relatively uncommon and low-profile disease, is now a major

international public health problem and one of the major health challenges of the

21st century. It may yet be, along with obesity, the greatest chronic disease

epidemic in the history of human existence. (Gill JM, 2003)

CHAPTER III

ETIOLOGY

Type 2 diabetes is caused by a combination of genetic factors related

to impaired insulin secretion and insulin resistance and environmental factors such

as obesity, overeating, lack of exercise, and stress, as well as aging. It is typically a

multifactorial disease involving multiple genes and environmental factors to

varying extents. A fact considered important in pathogenesis is that Japanese show

lower insulin secretory capacity after sugar loading, suggesting smaller potential

for pancreatic cell function than Western people. It has also been pointed out that

Japanese individuals may have many diabetes-sensitive genes including thrifty

genes. The number of diabetic patients is increasing rapidly reflecting the changes

in lifestyle. Aging, obesity, insufficient energy consumption, alcohol drinking,

smoking, etc. are independent risk factors of pathogenesis. Obesity (particularly

visceral fat obesity) due to a lack of exercise is accompanied by a decrease in

muscle mass, induces insulin resistance, and is closely associated with the rapid

increase in the number of middle- and high-aged patients. (Gulliford MC, 2006)

The changes in dietary energy sources, particularly the increase in fat intake,

the decrease in starch intake, the increase in the consumption of simple sugars, and

the decrease in dietary fiber intake, contribute to obesity and cause deterioration of

glucose tolerance. Even mild obesity (BMI 25) causes a 4- to 5-fold increase in the

risk of developing diabetes, if accompanied by the increase in visceral fat mass.

The Japanese are prone to visceral fat accumulation due to hyper alimentation, and

risk factors for diabetes are linked to the accumulation of visceral fat. (National

Diabetes Statistics , 2011)

 CHAPTER IV

PATHOPHYSIOLOGY

Impaired insulin secretion and insulin resistance contribute more or

less jointly to the development of pathophysiological conditions. Impaired insulin

secretion Impaired insulin secretion is a decrease in glucose responsiveness, which

is observed before the clinical onset of disease. More specifically, impaired

glucose tolerance (IGT) is induced by a decrease in glucose-responsive early-phase

insulin secretion, and a decrease in additional insulin secretion after meals causes

postprandial hyperglycemia. An oral glucose tolerance test (OGTT) in IGT cases

generally indicates an over-response in Western and Hispanic individuals, who

have markedly high insulin resistance. On the other hand, Japanese patients often

respond to this test with decreased insulin secretion. Even when an over-response

is seen in persons with obesity or other factors, they show a decrease in early-phase

secretory response. The decrease in early-phase secretion is an essential part of this

disease, and is extremely important as a basic pathophysiological change during

the onset of disease in all ethnic groups.3 Impaired insulin secretion is generally

progressive, and its progression involves glucose toxicity and lipo-toxicity.

Shoback D (2011)
 When untreated, these are known to cause a decrease in pancreatic cell mass

in animal experiments. The progression of the impairment of pancreatic cell

function greatly affects the long-term control of blood glucose. While patients in

early stages after disease onset chiefly show an increase in postprandial blood

glucose as a result of increased insulin resistance and decreased early-phase

secretion, the progression of the deterioration of pancreatic cell function

subsequently causes permanent elevation of blood glucose. Insulin resistance

Insulin resistance is a condition in which insulin in the body does not exert

sufficient action proportional to its blood concentration. The impairment of insulin

action in major target organs such as liver and muscles is a common

pathophysiological feature of type 2 diabetes. Insulin resistance develops and

expands prior to disease onset. (Cappola AR, 2012)

The investigation into the molecular mechanism for insulin action has

clarified how insulin resistance is related to genetic factors and environmental

factors (hyperglycemia, free fatty acids, inflammatory mechanism, etc.). Known

genetic factors, include not only insulin receptor and insulin receptor substrate

(IRS)-1 gene polymorphisms that directly affect insulin signals but also

polymorphisms of thrifty genes such as the 3 adrenergic receptor gene and the

uncoupling protein (UCP) gene, associated with visceral obesity and promote

insulin resistance. Glucolipotoxicity and inflammatory mediators are also

important as the mechanisms for impaired insulin secretion and insulin signaling

impairment. Recent attention has focused on the involvement of adipocyte-derived

bioactive substances (adipokines) in insulin resistance. While TNF-, leptin,

resistin, and free fatty acids act to increase resistance, adiponectin improves

resistance. Clinical tests to assess the extent of insulin resistance include

homeostasis model assessment for insulin resistance (HOMA-IR), insulin

sensitivity test (loading test), steady-state plasma glucose (SSPG), minimal model

analysis, and insulin clamp technique. The Matsuda index 4 is now gaining

recognition as a relatively simple procedure that can simultaneously evaluate

insulin resistance in the liver and muscles. After performing OGTT, this index is

calculated by the formula: Matsuda Index10,000/(FPGFPI)(mean PGmean PI),

where FPG is fasting plasma glucose and FPI is fasting plasma insulin. A more

convenient way to estimate the degree of resistance is to check for the presence of

high fasting blood insulin, visceral obesity, hypertriglyceridemia, etc. (Diamond JJ,

2003).
 CHAPTER V
SIGNS AND SYMPTOMS

The symptoms of type 2 diabetes can be so mild that you don't notice them.

About 8 million people who have it don't know it. Symptoms include: Being very

thirsty, Peeing a lot, Blurry vision, Being cranky, Tingling or numbness in your

hands or feet, Fatigue/feeling worn out, Wounds that don't heal, Yeast

infections that keep coming back, Hunger, Weight loss without trying, Getting

more infections, Dark rashes around your neck or armpits (called acanthosis

nigricans) that are often a sign of insulin resistance. Causes of Type 2 Diabetes

your pancreas makes a hormone called insulin. It helps your cells turn glucose, a

type of sugar, from the food you eat into energy. (Bailey CJ ,2005)

People with type 2 diabetes make insulin, but their cells don't use it as well

as they should. At first, your pancreas makes more insulin to try to get glucose into

your cells. But eventually, it can't keep up, and the glucose builds up in your blood

instead. Usually, a combination of things causes type 2 diabetes. They might

include: Genes. Scientists have found different bits of DNA that affect how your

body makes insulin extra weight.  Being overweight or obese can cause insulin

resistance, especially if you carry your extra pounds around your middle.

Metabolic syndrome. People with insulin resistance often have a group of

conditions including high blood sugar, extra fat around the waist, high blood

pressure, and high cholesterol and triglycerides. Too much glucose from

your  liver . When your blood sugar is low, your liver makes and sends out

glucose. After you eat, your blood sugar goes up, and your liver will usually slow

down and store its glucose for later. But some people's livers don't. They keep

cranking out sugar, bad communication between cells. Sometimes, cells send the

wrong signals or don't pick up messages correctly. (Gardner DG ,2015).

When these problems affect how your cells make and use insulin or glucose,

a chain reaction can lead to diabetes broken beta cells. If the cells that make insulin

send out the wrong amount of insulin at the wrong time, your blood sugar gets

thrown off. High blood sugar can damage these cells, too. More thirst: When sugar

builds up in your blood, your kidneys work overtime to get rid of it. This pulls

fluids from your tissues and makes you dehydrated, so you feel thirsty.

More hunger: Diabetes can stop glucose from getting to your cells, so you feel

hungry, even after you’ve eaten. Dry mouth: Dehydration and peeing a lot can

drain moisture from your mouth as well. Frequent urination: You’ll pee more

because your kidneys are working to get rid of extra sugar in your system, and

you’re drinking more to keep up with your thirst this causes. Unexplained weight

loss: When you lose sugar from peeing a lot, you lose calories, too. You might lose

weight even though you’re eating and feel hungry. Fatigue: 

 When your body can’t use energy from food, you could feel weak and tired. 

Dehydration can do it, too. Blurred vision: High blood sugar pulls fluids from

your eyes, so they have trouble focusing. Headaches: High blood sugar levels can

cause your head to hurt. Loss of consciousness: It’s rare, but when your blood

sugar goes too low, you could pass out. It can happen from too much medication,

after you exercise, or if you skip a meal. Infections or sores that don’t heal: High

blood sugar can slow blood flow and make it harder for your body to heal.

Tingling hands and feet: Type 2 diabetes can affect nerves in your hands and feet.

Red, swollen, tender gums: You might be more likely to get infections in your

gums and the bones that hold your teeth in place. Your gums may get infected or

pull away from your teeth. Your teeth might get loose.

Type 2 diabetes is usually not diagnosed until there are health complications.

Most often, there are no diabetes symptoms or a very gradual development of the

above symptoms of type 2 diabetes. In fact, about one out of every four people

with type 2 diabetes don't know they have it.

 CHAPTER VI
DIAGNOSTIC PROCEDURES

Type 2 diabetes is usually diagnosed using the:

Jeppesen KM, Coyle JD, Miser WF.(2009). Glycated hemoglobin (A1C)

test. This blood test indicates your average blood sugar level for the past two to

three months. Normal levels are below 5.7 percent, and a result between 5.7 and

6.4 percent is considered prediabetes. An A1C level of 6.5 percent or higher on

two separate tests means you have diabetes. If the A1C test isn't available, or if you

have certain conditions — such as an uncommon form of hemoglobin (known as a

hemoglobin variant) — that interfere with A1C test, your doctor may use the

following tests to diagnose diabetes:

Random blood sugar test. Blood sugar values are expressed in milligrams per

deciliter (mg/dL) or millimoles per liter (mmol/L). Regardless of when you last

ate, a blood sample showing that your blood sugar level is 200 mg/dL (11.1

mmol/L) or higher suggests diabetes, especially if you also have signs and

symptoms of diabetes, such as frequent urination and extreme thirst.

Fasting blood sugar test. A blood sample is taken after an overnight fast. A

reading of less than 100 mg/dL (5.6 mmol/L) is normal. A level from 100 to 125
mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes. If your fasting blood sugar is

126 mg/dL (7 mmol/L) or higher on two separate tests, you have diabetes.

Oral glucose tolerance test. This test is less commonly used than the others,

except during pregnancy. You'll need to fast overnight and then drink a sugary

liquid at the doctor's office. Blood sugar levels are tested periodically for the next

two hours.

A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal. A reading

between 140 and 199 mg/dL (7.8 mmol/L and 11.0 mmol/L) indicates prediabetes.

A reading of 200 mg/dL (11.1 mmol/L) or higher after two hours suggests

diabetes.

The American Diabetes Association recommends routine screening for type 2

diabetes beginning at age 45, especially if you're overweight. If the results are

normal, repeat the test every three years. If the results are borderline, ask your

doctor when to come back for another test.

Screening is also recommended for people who are under 45 and overweight

if there are other heart disease or diabetes risk factors present, such as a sedentary

lifestyle, a family history of type 2 diabetes, a personal history of gestational

diabetes or blood pressure above 140/90 millimeters of mercury (mm Hg).

 If you're diagnosed with diabetes, the doctor may do other tests to distinguish

between type 1 and type 2 diabetes — since the two conditions often require

different treatments. After the diagnosis A1C levels need to be checked between

two and four times a year. Discuss your target A1C goal with your doctor, as it

may vary depending on your age and other factors. For most people, the American

Diabetes Association recommends an A1C level below 7 percent.

An elevated A1C level may signal the need for a change in your medication,

meal plan or activity level. In addition to the A1C test, your doctor will measure

your blood pressure and take blood and urine samples periodically to check your

cholesterol levels, thyroid function, liver function and kidney function. Regular eye

and foot exams also are important.

 CHAPTER VII

TREATMENT

Drugs

The goal of diabetes treatment is to secure a quality of life (QOL) and

lifespan comparable to those of healthy people, and a prerequisite for attaining this

goal is the prevention of onset and progression of vascular complications. The risk

of macrovascular disease such as cardiovascular disorders (atherosclerotic lesions)

is increased already in individuals with marginal blood glucose levels,

underscoring the need for early intervention. Effective treatment to control

vascular complications Reports on the interventions to prevent the onset of

diabetes, control complications, and improve prognosis have demonstrated the

following facts: (1) lifestyle improvement and anti-diabetic drugs (-glucosidase

inhibitor, metformin, thiazolidine) to treat IGT suppress the risk of developing type

2 diabetes,5–7 (2) SU drugs, metformin, and insulin are effective in controlling

both microvascular disease and macrovascular disease, and earlier intervention is

essential to the control of macrovascular disease,8–11 (3) comprehensive

intervention including blood pressure and lipid management is extremely effective

in controlling vascular complications and reducing mortality rate,12,13 and (4)

pioglitazone suppresses the recurrence of cardiovascular disorders.14 Earlier and

more comprehensive (including blood glucose, blood pressure, and lipid)

intervention is more effective in controlling vascular complications and improving

prognosis.( Lenhard MJ , 2003).

SU drugs and insulin therapy. On the other hand, the common practice in

Japan is to select appropriate oral hypoglycemic agents when the patient has failed

to achieve the blood glucose control target despite sufficient patient education on

the nature of diabetes and dietary therapy and exercise therapy for 2 to 3 months.

There are five groups of oral agents currently in use: SU drugs, fast-acting insulin

secretion stimulators (glinides), biguanides, thiazolidines, and -glucosidase

inhibitors—some of these are the drugs developed after UKPDS. In view of the

difference between Japanese and Western populations in the pathophysiological

features of diabetes, and considering our own stance on the blood glucose control

target and treatment paradigm, it is logical that we need treatment guidelines that

are different from those in Western countries. (Cooke DW, 2005).

Surgery

 Metabolic surgery perspective, this epidemiological reality is important for

decision making. This applies not only in the countries of origin of ethnic peoples,

but also to their Diaspora communities where there has been large-scale migration

of Chinese and Indian peoples to Western nations like the U.S. and U.K. The
diabetes epidemic in Asia has spurred an increasing interest in the relationship of

obesity as a risk determinant of type 2 diabetes and other co morbidities in Asians.

This has important implications for decisions on the criteria for bariatric surgery

interventions. Type 2 diabetes develops in Asian people at a lower BMI compared

with people of European origin. At any given level of BMI, type 2 diabetes is more

likely to develop in an Asian person. This means that criteria based on obesity for a

decision on metabolic surgery will be lower. Cappola AR.(2012).

Are there determinants of the ethnic differences in diabetes or cardiovascular risk

other than the suggested genetic contribution? Whincup et al. Have made the

intriguing suggestion that factors operating in utero or at birth, including maternal

nutrition and maternal glucose control, and body composition at birth, could be

important contributors, and help to explain ethnic differences in type 2 diabetes

and cardiovascular risk. Early-life events and the intrauterine environment can

have an impact on the risk of many chronic diseases later in life, including obesity

and type 2 diabetes. (Naithani S, Morgan M, 2006).

Developed nations are failing badly in their attempts to control the obesity

epidemic, a prime driver of type 2 diabetes. This also applies to developing nations

with even more limited resources, so we can expect even less success as they

tackle alarming increases in obesity and type 2 diabetes. We have suggested that

this failure results in part from the focus on adult lifestyles, the traditional
“scapegoat.” However, this ignores the mounting evidence that biological and

cultural factors operating early in life affect adult health status. To stem the rising

obesity burden in both developing and developed countries, scientists and policy

makers must address obesity-promoting factors from early childhood to adulthood.

Exercises

Early initiation of intervention is also important for curbing the progression

of pathophysiological conditions. Early efforts to remove the effect of glucose

toxicity as much as possible and to preserve pancreatic cell function are essential

prerequisites for long-term management of diabetes. Ideally, the aim should be to

prevent the onset of diabetes among individuals with (primary prevention). In

addition to proactive intervention for lifestyle improvement management of type 2

diabetes includes: Weight loss, Healthy eating, Regular exercise, possibly diabetes

medication or insulin therapy, Blood sugar monitoring these steps will help keep

your blood sugar level closer to normal, which can delay or prevent complications.
 REFERENCES

Bogner HR, Morales KH, De Vries HF, Cappola AR.(2012). Integrated

management of type 2 diabetes mellitus and depression treatment to

improve medication adherence: randomized controlled trial.

Cooke DW, Plotnick L (2008) Type 1 diabetes mellitus in pediatrics. Pediatr

Gill JM, Mainous 3rd. AG, Diamond JJ, Lenhard MJ (2003).

Impact of provider continuity on quality of care for persons with

diabetes l mellitus.

Gulliford MC, Naithani S, Morgan M.(2006).

Measuring continuity of care in diabetes mellitus: An experience-based ;

measure.

Gardner DG, Shoback D (2011) Greenspan's Basic & Clinical Endocrinology 9th ;

(Edn.), Yale J Biol Med.

Koopman RJ, Mainous 3rd AG, Diaz VA, Geesey ME.( 1988 to 2000)

Changes in age at diagnosis of type 2 diabetes mellitus in the United States

Krentz AJ, Bailey CJ (2005) Oral antidiabetic agents: current role intype 2 diabetes

mellitus. Drugs 65(3): 385-411.

National Diabetes Clearinghouse (NDIC): National Diabetes Statistics (2011)

US Department of Health and Human Services.