I. OBJECTIVES:

General Objectives: This study primarily aims to determine and assess the prevalence of previously diagnosed Type 2 Diabetes and its risk factors to (name of the patient) as well as providing the said patient with sufficient information on proper management to the disorders.

Specific Objectives:

After completing the case study, the student nurses should be able to:

Define Diabetes Mellitus Discuss the incidence and prevalence of Diabetes

Mellitus; Understand Type 2 Diabetes in to the relation to the

clinical presentation, patient characteristics and pathogenesis;

Describe the role of generic and environmental factors and immunology in the development of Type 2 Diabetes;

Identify the laboratory investigations used to diagnose Diabetes;

Discuss the appropriate nursing and medical management;

Identify appropriate treatment options for Type 2 Diabetes;

And discuss the dos and don’ts for patient’s education.

II. INTRODUCTION

Name: RTSAddress: Nibaliw Sur, Bautista Pangasinan

Age: 68 years old

Birthdate: May 23, 1940

Gender: Male

Civil Status: Married

Religion: Roman Catholic

Nationality: Filipino

Date of Admission: July 12, 2008Time: 12:30 pm

Attending Physician: Dr. EstradaDiagnosis: Type 2 diabetes mellitus

1

DISEASE PROPER

Type II diabetes is associated with obesity and with aging. It is a lifestyle-dependent disease, and has a strong genetic component (concordance in twins is 80-90%). The problem seems not so much in insulin production, but that when the insulin reaches its target cells, it doesn't work correctly. Most Type II diabetes patients initially have high insulin levels along with high blood sugar. However, since sugar signals the pancreas to release insulin, Type II diabetics eventually become resistant to that signal and the endocrine-pancreas soon will not make enough insulin. These people end up managing the disease with insulin and they need much higher doses because they are resistant to it.

When a person takes in a high load of sugar, the sugar stimulates the pancreas to release insulin. The targets for insulin are muscle, fat, and liver cells. These cells have insulin receptor sites on the outside of the cell membrane. For most people, when insulin has bound to the receptors, a cascade of events begins, which leads to sugar being transported from the blood into the interior of the cell. In Type II diabetics, even when insulin is present on the cell membrane, the process doesn't work. The glucose is never taken up into the cell and remains in the bloodstream.

The liver is responsible for glucose production and insulin is the regulatory agent of production. High blood sugar content causes the pancreas to release insulin, and the insulin should signal the liver to stop making sugars. But, in diabetics, there's resistance to that signal and the liver keeps producing glucose. Hyperglycemia leads to glucose toxicity.

It is not high blood sugar that is the disease process of diabetes, but complications from the high blood sugar. Standard complications for many diabetics are: retinopathy (blindness); neuropathy (nerve damage) which leads to foot ulcers, gangrene, and amputations; kidney damage, which leads to dialysis; and cardiovascular disease. A major problem faced by doctors is that some people with high blood sugar feel fine; it's hard to treat diseases that are asymptomatic since most people don't want to take a pill for something that they don't feel bad about.

III. SIGNIFICANCE OF THE STUDY

2IV. PATIENT’S PROFILE

Past historyThe patient was diagnosed with hypertension last December 2007. He was never been

hospitalized in the past because their family doctor, Dr. Castillo was attending the patient in their house regularly. Medications prescribe for his maintenance was NIFEDIPINE.

DEVELOPMENTAL DATE: (Base on Erik Erickson, Jean Piaget and Harry Stack Sullivan)

Developmental Stage by Erik Erickson

Developmental tasks by Erik Erickson stage of late adulthood: Integrity versus Despair perception of life as a culmination of positive and negative events, acceptance of one’s own life as it is: ultimately a positive sense of self intact.

This is the final phase of development of Erickson’s “late adulthood or maturity” in which the tasks is to accomplished integrity opposed to despair.

Individual review their experiences considering those objects they have successfully completed and those they have not. Persons who can accept their lives for what they have achieved undergo renewed sense of ego integrity. Life has meaning for them in both, in positive and negative events. They do not despair for what might have been. The end of life is perceived as a culmination of their many experiences rather than as something to be feared. The older person has thought a good deal about death and has usually had many experiences with it. Death is phase of development that one must pass through, which the ultimate goal being achievement of a positive sense in this final.

Behaviorally:

According to psychosocial theory by Erick Erickson the patient is in the stage of developmental in the late adulthood in which a person integrity. The patient is said to be that he has fulfilled his obligation to his children by providing them proper education. In which his children in return give him full financial and moral support.

V. PRESENT ILLNESS

3VI. ANATOMY AND PHYSIOLOGY

Pancreas is both an endocrine gland and an exocrine gland. A flattened organ that measures about 12.5 – 15 cm in (4.5 – 6 in) in length, the pancreas is located in the curve of the duodenum, the first part of the small intestinal and consist of the head, body, and a tail. Roughing 99% of the cells of the pancreas are arranged in the clusters called acini. The acini produce digestive enzymes, which flow into gastro intestinal tract trough a network of ducts. Scattered among the exocrine acini are 1-2 million tiny clusters of endocrine tissue called pancreatic islets of Langerhans. Abundant capillaries serve both the exocrine and endocrine portions of the pancreas.

Cell Types in the Pancreatic IsletsEach pancreatic islets includes four types of hormone – secreting cells;

1. Alpha or A cells continue about 17% of pancreatic islet cells and secrete glucagons.2. Beta or B cells constitute about 70% of pancreatic islet cells and secrete insulin.3. Delta cells or D cells constitute about 7% of the pancreatic islet cells and secrete

sematostatin (identical to the growth hormone inhibiting hormone secreted by the hypothalamus.

4. F cells constitute the remainder of pancreatic islets cells and secrete pancreatic polypeptide.

The interaction of the four pancreatic hormones is complex and not completely understood. We do know that glucagons raises blood glucose level, and insulin lowers it. Somatostatine acts in a paracrine manner to inhibit both insulin and glucagons to release from neighboring beta and alpha cells. It may also act as a circulating hormone to slow absorption of nutrients from the gastrointestinal tract. Pancreatic polypeptide inhibits somatostatine secretion, gallbladder contraction and secretion of digestive enzymes by the pancreas.

Regulation of Glucagon and Insulin Secretion The principal action of glucagons is to increase blood glucose level when it falls below

normal. Insulin, on the other hand, helps lower blood glucose level when it is too high. The level of blood glucose controls secretion of glucagons and insulin via negative feedback:

1. Low blood glucose level (hypoglycemia) stimulates secretion of glucagons from the alpha cells of the pancreatic islets.

2. Glucagon acts on hepatocytes (liver cells) to accelerate the coversion of glucagons (glycogenolysis) and to promote formation of glucose from lactic acid and certain amino acids (glyconeogenesis).

3. As a result, hypocytes release glucose into the blood more rapidly, and blood glucose level rises.

4. If blood glucose continues to rise, high blood glucose level (hyperglycemia) inhibits release of glucagons (negative feedback).

5. High blood glucose (hyperglycemia) stimulates secretions of insulin by beta cells of the pancreatic islets.

6. Insulin acts on various cells in the body to accelerate facilitated diffusion of glucose into cells especially skeletal muscle fibers; to speed conversion of glucose into glycogen (glycogenesis) to increase uptake of amino acids by cells and to increase protein synthesis of fatty acids (lipogenesis); to show the conversion of glycogen to glucose (glycogenolysis); and to show the formation of glucose from lactic acid and amino acids (gluconeogenesis).

7. As a result, blood glucose level falls.8. I f blood glucose level drops below normal, low blood glucose inhibits release of insulin

(negative feedback) and stimulates release of glucagons.

4

ANATOMY AND PHYSIOLOGY OF THE PANCREASES

5

ANATOMY OF THE KIDNEY

Kidney (ME, kinere), one of bean-shaped urinary organs in the dorsal part of the abdomen, one of the vertebral column. The cranial extremities of the kidneys are on a level with the third lumbar vertebra. In most individuals, the caudal extremities are on a level with the third lumbar vertebra. In most individuals, the right kidney s slightly more caudal (lower) than the left. Each kidney is about 11 cm long, 6 cm wide and 2.5 cm thick. In men, each kidney weights from 125-170 g; in women, each kidney weighs from 115-155g.

In the newborn, the kidneys are about three times as large in proportion to the body weight as in the adult. The kidneys produce and eliminate urine through a complex filtration composed of glomeruli and renal tubules that filter blood under high pressure , removing urea, salts, and other soluble wastes from blood plasma and returning the purified filtrate to the blood.

More than 2500 pints of blood pass through the kidneys every day, entering the kidneys through the renal arteries and leaving through the renal veins. All the blood in the body passes through the kidneys about 20 times every hour but only about one fifth of the plasma is filtered by the nephrons during the period. The kidneys remove water as urine and return water that has been filtered to the blood plasma, thus helping to maintain the water balance of the body. Hormones, especially the antidiuretic hormone (ADH), produced by the pituitary gland, control the function of the kidneys in regulating the water content of the body. ADH reaches the renal tubules in the blood and stimulates the reabsorption of water from filtrate into the blood.

\If the water intakes is inadequate to compensate for the water lost in perspiration in respiration, the change in concentration in the blood is detected by the brain and pituitary gland releases more ADH, thus reducing the loss of water in urine. If the blood is too dilute, the pituitary gland reduces the secretion of ADH, producing a large flow of dilute urine to restore the water balance.

6VII. PATHOPHISIOLOGY

Diabetes Mellitus Type 2 has modifiable factor such as lifestyle and non-modifiable factors like genetics, race and those people who are 45 years and above. These factors result in insulin deficiency that leads to inability to breakdown glucose causing increase glucose level in the blood. Increase glucose level in the blood attracts water thus, making the person urinate frequently. Polyuria leads to excessive loss of water in the body resulting to increase intake of liquids. The stored fats protein and carbohydrates are forced to be broken down when the glucose is not converted to energy. When this happens, signs such as weight loss, body malaise and polyphagia will be visible. The end product of forced breakdown of fats, CHON and CHO is fatty acids. This then leads to the formation of plaques that causes the blockage of the blood vessels. When this happens, the resulting disorders are macrovascular disease, CVA, myocardial infarction and kidney failure. Eye retinopathy may also arise when there is forced. Breakdown of protein since 90% of this stored in the eyes. If there is increased glucose level in the blood, the myelin and axon of the neurons are affected thus altering the transmission of impulse. This alteration cause’s deficient oxygen supply in the periphery of the body which then results to poor wound healing.

Insulin resistance means that body cells do not respond appropriately when insulin is present. Other important contributing factors are (a) increased hepatic glucose production (e.g. from glycogen degradation), especially at in appropriate times; (b) decreased insulin mediated glucose transport in (primarily) muscle and adipose tissues (receptor and post-receptor defects); (c) impaired beta-cell function loss of early phase of insulin release in response to hyperglycemic stimuli, (d) cancer survivors who received allogenic hematopoeitic cell transplant are 3.65 times more likely to report type 2 diabetes than their siblings; and (e) total body irradiation is also associated with a higher risk of developing diabetes. Type 2 Diabetes mellitus is often associated with obesity and hypertension and elevated cholesterol (combined hyperlipidemia), and with the condition Metabolic syndrome (also known as syndrome x, Reavan’s syndrome, or CHAOS). It is also associated with acromegaly, cushing syndrome and a number of other endocrinological disorders, additional factors found to increase risk of type 2 diabetes include aging, high-fat diets and a less active lifestyle.

7

PARADIGA

Modified factors Non-modified factor Lifestyle genetic race Obesity Age over 45 ________________________________________________________

Insulin Deficiency

Glucose Breakdown failure

Increased glucose level in blood

_________________________________________________________

Increased glucose Body unable to use glucose Myelin and axon are attracts water for energy effect

Polyuria Force breakdown of fats, Transmission of impulse CHO, CHON is altered

Excessive loss Of water

__________________________________________

Weight loss End product of Body malaise breakdown is Polyphagia fatty acids

Plaque formation protein breakdown

Clogged in the blood eye retinopathy Vessels (90% of CHON are in eye)

Macrovascular disease CVAMyocardial infarction kidney

failure

8

VIII. DIAGNOSTIC TEST

TEST EXPECTED VALUES RESULTGlucose substance conc.

(FBS)3.85 – 5.78 mmol/L 6.2 mmol/L

(RBS)

Up to 8.0 mmol/L 9.7 mmol/L

Cholesterol 3.09 – 7.30 mmol/L 5.7 mmol/L2.99 – 7.41 mmol/L mmol/L

Triglycerides 0.396 – 1.8 mmol/L 0.56 mmol/L

Various blood tests can be used to screen for diabetes, including:

Random blood sugar test. A blood sample will be taken at a random time. Regardless of when you last ate, a random blood sugar level of 200 milligrams per deciliter (mg/dL) or higher suggests diabetes.

Fasting blood sugar test. A blood sample will be taken after an overnight fast. A fasting blood sugar level between 70 and 100 mg/dL is normal. A fasting blood sugar level from 100 to 125 mg/dL is considered prediabetes, which indicates a high risk of developing diabetes. If it's 126 mg/dL or higher on two separate tests, you'll be diagnosed with diabetes.

IX. MEDICAL MANAGEMENT

The main goal of treatment is to normalize insulin activity and blood glucose levels to reduce the development of vascular and neurophatic complications. The therapeutic goal within each type of diabetes is to achieve normal blood glucose levels (euglycemia ) without hypoglycemia and without seriously disrupting the patient’s usual activities. There are five components of management for diabetes: nutrition, exercise, monitoring, pharmacologic therapy and education.

Primary treatment for type 2 diabetes is weight loss. Exercise is important in enhancing the effectiveness of insulin. Use oral hypoglycemic agents if diet and exercise are not successful in controlling blood

glucose levels. Because treatment varies throughout course because of changes in lifestyle and physical and

emotional status as well as advances in therapy, continuously assess and modify treatment plan as well as daily adjustments in therapy. Education is needed for both patient and family.

9X. NURSING MANAGEMENT

Nursing management of the patient with Diabetes can involve treatment of a wide variety of physiologic disorders, depending on the patient’s status & whether the patient is newly diagnosed or seeks care for an unrelated health problem. Because all diabetic patient’s must master the concepts & skills necessary for long-term management of diabetes & its potential complications, a solid educational foundation is necessary for competent self-care & is an ongoing focus of nursing care.

Nursing Care Plan

17XI. DISCHARGE PLANNING

Medications: Advice the patient to continue his medications according to the doctor’s order. He should take it at right dosage and time. Informed him of the possible side effects of the medication he may encounter. Also, make sure that he understands the correct use of his medications and how often he should take it to avoid overdose.

Exercise: Regular exercise can help reduce the risk of developing diabetes. Activity can also reduce the risk of developing complications of diabetes such as heart, stroke, kidney failure, blindness and leg ulcers. As little as 20 minutes of walking 3xa week has proven beneficial effect.

Treatment: The patient visits his physician for his check-up on the scheduled date and takes his prescribed medicines on the time.

Health Teaching:1. Advised the patient not to engage in strenuous exercise and have relaxation techniques.2. Instructed the patient to eat small meals rather than large ones.3. Emphasized proper hygiene to avoid infection.4. Advised the patient to avoid environmental irritants.5. Advised the patient to have enough sleep at night.6. Avoid sweet foods. 7. Advised the patient to maintain his nails short and that to cut it safely.8. Advised the patient to avoid using shoes made of plastic or rubber.9. Instructed the patient not to soak his foot on warm water.10. Emphasized regular check-up.

OPD appointment: We have advised the patient to consult health care professionals whenever he has concerns about his condition.

DIET:

23XII. DEFINATION OF TERMS

Diabetic ketoacidosis (DKA) – A condition in which the excess ketones are not removed adequately in the urine.

Diabetes mellitus – is a serious metabolic disorder related to the use of carbohydrate and its end product, glucose.

Diabetic retinopathy – an eye disease found in persons with long-standing diabetes; usually prevented through good diabetes management.

Glucagon – A counter regulatory hormone that is given by injection during severe bouts of hypoglycemia in an unconscious diabetic person.

Glucosuria – presence of glucose in the urine.

Glycogen – the storage form of carbohydrate found the liver and muscle tissues; released in the form of sugar as needed for energy or during times of physiologic stress.

Glycogenolysis – the breakdown of stored carbohydrate in the liver from glycogen to glucose.

Hyperglycemia – an elevation of glucose in the blood

Hyperlipidemia – an elevation of specific lipoproteins, cholesterol and triglycerides.

Hypoglycemia – a condition of low blood glucose, defined as blood glucose less than 70 mg/Dl

Nephropathy – the inability of the kidney to properly filter body toxins.

Neuropathy – a condition characterized by functional disturbances and pathologic changes outside the central region of the nervous system.

Non-insulin dependent dm –a form of diabetes that is typically overweight adults, it is a mild, asymptomatic form of DM with onset after 40; pancreatic insulin reserve is diminished but is rarely always sufficient to prevent ketoacidosis and dietary control is usually effective.

Oral hypoglycaemic agents – medications in pill form used to control glucose levels in type 2 dm.

Pancreas – a gland behind the stomach that releases insulin, glucagons, and some enzymes of digestion for fats and proteins.

Polydipsia – a condition of excess thirst.

Polyphagia – a condition of excess appetite.

Polyuria – a condition of excessive excretion of urine.

24XIII. BIBLIOGRAPHY

Johnson, Joyce Young Medical- Surgical Nursing 10th Edition

Kluwer, Wolters Nursing 2008 Drug Handbook. Philippines: Lippincott Williams and Wilkins

Peckenpaugh, Nancy J. Nutrition Essentials and Diet Therapy. Singapore: W.b Sauders Company, 2007

Doenges, Marilynn E, et al. Nurse’s Pocket Guide. Philadelphia: F.A Davis Company

www. wikipedia. com

www.medlineplus.com

25

University of PangasinanDagupan City

College of Nursing

Case study on

DIABETES MELLITUS(Type II)

Submitted to:

Mr. Avril B. JunioClinical Instructor

Submitted by:

Padilla, Ma. Cristina A.Padilla, Jordan Paner C.

Padilla, Jackieline N. Padilla, Sarah Jane J.

Padilla, Zendy Mae Stephanie G.Padua, Rachele R.

Pagarigan, Jacquelene I.

Palad, Karen R. Palaganas, Rose Ann D.

Palaje, Sandra B. Panilo, Darren Jay C.

Panganiban, Mark Paul V.

August 2008

Acknowledgement

ii

TABLE OF CONTENTS

Front Page

----------------------------------------- i

Acknowledgement

----------------------------------------- ii

Table of Contents

----------------------------------------- iii

I. Objectives

General -----------------------------------------

1

Specific -----------------------------------------

1

II. Introduction

Patient Profile -----------------------------------------

1

Disease Proper

----------------------------------------- 2

III. Significance of the Study

Nursing Education ------------------------------------------ 2

Practice research ------------------------------------------ 2

IV. Patient’s Profile

Past History ------------------------------------------ 3

Developmental Data

------------------------------------------ 3

V. Present Illness ------------------------------------------ 3

VI. Anatomy and Physiology

------------------------------------------ 4-6

VII. Pathophysiology

Paragraph ------------------------------------------ 7

Paradiga

------------------------------------------ 8

VIII. Diagnostic Test ------------------------------------------

9

IX. Medical Management

------------------------------------------ 9

Drug study ------------------------------------------ 9-

16

X. Nursing Management

------------------------------------------ 17

3 Actual NCP

------------------------------------------ 18-20

1 Potential NCP

------------------------------------------ 21

1 Risk NCP

------------------------------------------ 22

XI. Discharge Planning ------------------------------------------

24

XII. Definition of Terms ------------------------------------------

25

XIII. Bibliography ------------------------------------------ 26

iii