Republic of the Philippines Southern Luzon State University College of Allied Medicine Lucban, Quezon A.

Y 2012-2013

CASE STUDY DIABETES MELLITUS TYPE II UNCONTROLLED Nephrolithiasis

Submitted to: Mr. Marc Oneel Alvarez (Clinical Instructor)

In Partial Fulfillment Of the Requirements for the Subject Related Learning Experience

Submitted by: Ara Q. Maceda

(BSN IV- Group 2) September 2012

CHAPTER I OBJECTIVES

1. General objective

The objective of this study is to broaden the knowledge of the students about diabetes mellitus and its complications, and further evaluate the students learning experience in the previous clinical exposure.

2. Specific objectives After this study, the students will: a. State well the learnt information about the disease such as its definition, signs and symptoms, prevention, cure, and its pathophysiology.
b. Be able to give point of views about their handling experience with this kind of case.

c. Be able to connect the patients present history to his past and family history. d. Be able to assess if they have used the physical assessment for the patients properly. e. Explain the appropriate nursing interventions to be implemented to patients having diabetes mellitus f. Evaluate the effectiveness of the nursing care plans that were implemented during the clinical exposure. g. State the different actions of the drugs being administered to the patient.
h. Interpret the different laboratory tests whether it is normal or there are abnormal

interpretation

CHAPTER II INTRODUCTION OF THE DISEASE

.

The term "diabetes mellitus" refers to a group of diseases that affect how your body uses blood glucose, commonly called blood sugar. Glucose is vital to your health because it's an important source of energy for the cells that make up your muscles and tissues. It's your brain's main source of fuel. If patient have diabetes, no matter what type, it means that they have too much glucose in their blood, although the reasons may differ. Too much glucose can lead to serious health problems. Chronic diabetes conditions include type 1 diabetes (insulin dependent) and type 2 diabetes (non-insulin dependent). Potentially reversible diabetes conditions include prediabetes when your blood sugar levels are higher than normal, but not high enough to be classified as diabetes and gestational diabetes, which occurs during pregnancy.

CHAPTER III ANATOMY AND PHYSIOLOGY

Endocrine system includes cells, tissues, and organs collectively called endocrine glands, that secrete hormones into the internal environment. Hormones are substances that are secreted by the endocrine gland which transported into the blood, and regulates body mechanisms. Pancreas is an elongated, somewhat flattened organ posterior to the stomach and behind the parietal peritoneum. It consists of two major types of secretory tissues. This organization reflects the pancreas dual function as an exocrine gland that secretes digestive juice and an endocrine gland that release hormones. Islet of Langerhans (pancreatic islets) include two distinct type of cells the alpha cells, which secrete the hormone glucagon, and beta cells, which secrete the hormone insulin. Glucagon stimulates the liver to breakdown glycogen and converts certain noncarbohydrates, such as amino acids, into glucose, raising blood sugar concentration. It elevates blood glucose effectively. Insulin stimulates the liver to form glycogen from glucose and inhibits conversion of noncarbohydrates into glucose. It also has the special effect of promoting facilitated diffusion of glucose across cell membranes that have insulin receptors, such as those of cardiac muscles, adipose tissues, and resting skeletal muscles. Glyconeogenesis is the formation of glucose from fats and proteins.

Glycogenolysis is the breakdown of liver glycogen.

Normal Function of Glucagon and Insulin Control Center Beta cells secrete insulin

Receptors Beta cells detect rise in blood Glucose

Effectors Insulin: promotes movements of glucose into certain cells and stimulates formation of glycogen from glucose

Stimulus Rise in blood glucose level

Response Blood glucose drops toward normal

Too high blood glucose level

Normal Blood Glucose Concentration

Response Blood glucose level rises towards normal

Too low blood glucose level

Stimulus Drop in blood glucose level

Effectors Glucagon stimulates cells to Breakdown glycogen into Glucose

Receptors Alpha cells detect a drop in blood glucose

Control Center Alpha cells secrete glucagon

CHAPTER IV OVERVIEW OF THE DISEASE a. REVIEW OF RELATED LITERATURE 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 (as it will be in this article) 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. Diabetes is a chronic medical condition, meaning that although it can be controlled, it lasts a lifetime. What is the impact of diabetes? 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 microvascular 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 macrovascular disease. Diabetes affects approximately 17 million people (about 8% of the population) in the United States. In addition, an estimated additional 12 million people in the United States have diabetes and don't even know it. Causes 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 I 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 develops. Types of Diabetes There are two major types of diabetes, called type 1 and type 2. Type 1 diabetes was also called insulin dependent diabetes mellitus (IDDM), or juvenile onset diabetes mellitus. In type 1 diabetes, the pancreas undergoes an autoimmune attack by the body itself, and is rendered incapable of making insulin. Abnormal antibodies have been found in the majority of patients with type 1 diabetes. Antibodies are proteins in the blood that are part of the body's immune system. The patient with type 1 diabetes must rely on insulin medication for survival. In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type I diabetes is, in part, genetically inherited, though the details are not fully understood. Type 2 diabetes was also referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in

the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells). In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised. Diabetes can occur temporarily during pregnancy. Significant hormonal changes during pregnancy can lead to blood sugar elevation in genetically predisposed individuals. Blood sugar elevation during pregnancy is called gestational diabetes. Gestational diabetes usually resolves once the baby is born. However, 25%-50% of women with gestational diabetes will eventually develop type 2 diabetes later in life, especially in those who require insulin during pregnancy and those who remain overweight after their delivery. Patients with gestational diabetes are usually asked to undergo an oral glucose tolerance test about six weeks after giving birth to determine if their diabetes has persisted beyond the pregnancy, or if any evidence (such as impaired glucose tolerance) is present that may be a clue to the patient's future risk for developing diabetes. Manifestations The early symptoms of untreated diabetes are related to elevated blood sugar levels, and loss of glucose in the urine. High amounts of glucose in the urine can cause increased urine output and lead to dehydration. Dehydration causes increased thirst and water consumption. The inability of insulin to perform normally has effects on protein, fat and carbohydrate metabolism. Insulin is an anabolic hormone, that is, one that encourages storage of fat and protein. A relative or absolute insulin deficiency eventually leads to weight loss despite an increase in appetite. Some untreated diabetes patients also complain of fatigue, nausea and vomiting.

Patients with diabetes are prone to developing infections of the bladder, skin, and vaginal areas. Fluctuations in blood glucose levels can lead to blurred vision. Extremely elevated glucose levels can lead to lethargy and coma.

Diagnosis The fasting blood glucose (sugar) test is the preferred way to diagnose diabetes. It is easy to perform and convenient. After the person has fasted overnight (at least 8 hours), a single sample of blood is drawn and sent to the laboratory for analysis. This can also be done accurately in a doctor's office using a glucose meter. 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 100126mg/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. Oral Glucose Tolerance Test Though not routinely used anymore, the oral glucose tolerance test (OGTT) is a gold standard for making the diagnosis of type 2 diabetes. It is still commonly used for diagnosing gestational diabetes and in conditions of pre-diabetes, such as polycystic ovary syndrome. With an oral glucose tolerance test, the person fasts overnight (at least eight but not more than 16 hours). Then first, the fasting plasma glucose is tested. After this test, the person receives 75 grams of glucose (100 grams for pregnant women). There are several methods employed by obstetricians to do this test, but the one described here is standard. Usually, the glucose is in a sweet-tasting liquid that the

person drinks. Blood samples are taken at specific intervals to measure the blood glucose. Glucose tolerance tests may lead to one of the following diagnoses:

Normal response: A person is said to have a normal response when the

2-hour glucose level is less than 140 mg/dl, and all values between 0 and 2 hours are less than 200 mg/dl.

Impaired glucose tolerance: A person is said to have impaired glucose

tolerance when the fasting plasma glucose is less than 126 mg/dl and the 2-hour glucose level is between 140 and 199 mg/dl.

Diabetes: A person has diabetes when two diagnostic tests done on

different days show that the blood glucose level is high.

Gestational diabetes: A woman has gestational diabetes when she has

any two of the following: a 100g OGTT, a fasting plasma glucose of more than 95 mg/dl, a 1-hour glucose level of more than 180 mg/dl, a 2-hour glucose level of more than 155 mg/dl, or a 3-hour glucose level of more than 140 mg/dl. Hemoglobin A1c (A1c) To explain what an hemoglobin A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these cells, it gives us an idea of how much sugar is around for the preceding three months. In most labs, the normal range is 4%-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is <6.5%). The benefits of measuring A1c is that is gives a more reasonable and stable view of what's happening over the course of time (three months), and the value does not bounce as much as finger stick blood sugar measurements. There is a direct correlation between A1c levels and average blood sugar levels as follows. A1c(%) 6 7 8 Mean blood sugar (mg/dl) 135 170 205

9 10

240 275

Medications a. Insulin Secretagogs 2nd generation sulfonylureas Glipizide, Glyburide, Glicazide, Glimepiride (Glucotrol, Glynase,Amaryl)
o o o

Stimulate insulin secretion For lean elderly person Causes hypoglycemia

b. Meglitinides

Repaglinide (Prandin), Nateglinide (Starlix)

o o o o

Stimulate insulin secretion for a short interval Rapid onset and offset of action Used as preprandial agents No effect upon fasting glucose

c. Insulin sensitizers

Thiazolidinediones Pioglitazone (Actos), Rosiglitazone (Avandia)

o o o o

Improve insulin sensitivity primarily at muscle and adipose tissue Liver function should be monitored q 2 months Can cause weight gain & edema Contraindicated for CHF

d. Biguanide

Metformin
o o o

Improves insulin sensitivity primarily at the liver Generally preferred for obese patients Often aides weight loss

o o o o

Diarrhea, dyspepsia, nausea are common Lactic acidosis is rare Contraindicated in renal disease (CR CL <20ml.min) Not recommended in 80 years or older (usually with decline in renal function)

e. Others

Alpha glucosidase inhibitors Acarbose (Precose), Miglitol (Glyset)

o o o o

Inhibit absorption of carbohydrates in the small intestines Used only as preprandial agent Causes flatulence With insulin induced hypoglycemia, oral feeding will NOT be effective w/in 2 hours

f. Inhaled Insulin (Exubera)

Insulin Human (rDNA) inhalation powder (INH Inhaled Human Insulin) Reduced HbA1c equal to SC insulin Works synergistic with Oral agents Cough is the most common SE Long term pulmonary safety are small Well tolerated , cough in about 27% but transient & long term FEV1 no change High patient satisfaction

g. Exenatide (Byetta)

Incretin mimetic improves glycemic control

o o o o

Via glucoregulatory mechanism Insulinotropism Suppression of glucagon Delays gastric emptying (reduce food intake)

Complications Diabetic ketoacidosis can be caused by infections, stress, or trauma all which may increase insulin requirements. In addition, missing doses of insulin is also an obvious risk factor for developing diabetic ketoacidosis. Urgent treatment of diabetic ketoacidosis involves the intravenous administration of fluid, electrolytes, and insulin, usually in a

hospital intensive care unit. Dehydration can be very severe, and it is not unusual to need to replace 6-7 liters of fluid when a person presents in diabetic ketoacidosis. Antibiotics are given for infections. With treatment, abnormal blood sugar levels, ketone production, acidosis, and dehydration can be reversed rapidly, and patients can recover remarkably well. Hypoglycemia means abnormally low blood sugar (glucose). In patients with diabetes, the most common cause of low blood sugar is excessive use of insulin or other glucose-lowering medications, to lower the blood sugar level in diabetic patients in the presence of a delayed or absent meal. When low blood sugar levels occur because of too much insulin, it is called an insulin reaction. Sometimes, low blood sugar can be the result of an insufficient caloric intake or sudden excessive physical exertion. The major eye complication of diabetes is called diabetic retinopathy. Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina. Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms), and new but brittle blood vessels (neovascularization). Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision. Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered. Nerve damage from diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia). Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them. Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal. Sometimes, minor

foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts. Gangrene Gangrene is a term that describes dead or dying body tissue(s) that occur because the local blood supply to the tissue is either lost or is inadequate to keep the tissue alive. Gangrene has been recognized as a localized area of tissue death since ancient times. The Greeks used the term gangraina to describe putrefaction (death) of tissue. Although many laypeople associate the term gangrene with a bacterial infection, the medical use of the term includes any cause that compromises the blood supply that results in tissue death. Consequently, a person can be diagnosed with gangrene but does not have to be "infected." There are two major types of gangrene referred to as dry and wet. Many cases of dry gangrene are not infected. All cases of wet gangrene are considered to be infected, almost always by bacteria. The most common sites for both wet and dry gangrene to occur are the digits (fingers and toes) and other extremities (hands, arms, feet, and legs).

CHAPTER V CASE STUDY PROPER a. Patients Profile Case No. 20114643 Name: Patient X Address: Golden Meadows Subd. Brgy. Bucal Pagbilao, Quezon Age: 44 years old Sex: male Civil Status: Married Religion: Catholic Nationality: Filipino Place of birth: Pagbilao, Quezon

Date of birth: August 5, 1969 Name of Father: Ferrarin Musa Name of Mother: Yolanda Musa Name of Spouse: Lyn Musa Chief Complaint: Loss of consciousness and vomiting Admission Date: August 9,2012 Admission Time: 3:30 pm Admitting Physician: Dr. Lacerna Final Diagnosis: Diabetes Mellitus type II uncontrolled Nephrolithiasis

b. Physical assessment General Condition

Conscious and coherent Afebrile; T=36.0C With guarding behavior With episodes of vomiting

Head Eyes

With hair equally distributed on the scalp With good hair texture

With whitish sclera With pale conjunctiva With conjugate eye movements With pupil equally round and reactive to light accommodation

Ears Nose

No ear discharges noted Easily recoil when folded

Without nasal discharges; No nasal flaring

Mouth and Teeth Neck Without palpable mass noted With palpable carotid pulse Without distended vein noted upon palpation With pale and dry lips With good dentition

Chest and Lungs

With normal chest expansion upon breathing With clear breath sounds heard on both lung fields upon auscultation

Cardiovascular Without papitatons noted With fluctuating blood pressure With normal cardiac rate and rhythm upon auscultation

Abdomen With soft and non-tender abdomen upon palpation With normoactive bowel sounds of 19 BS/min.

Genitourinary Dysuria

Voids freely With increase in frequency of urination With yellowish urine; moderate in amount With non-healing scrotal wound with abscess noted

Extremities Skin With fair skin turgor With poor skin turgor pallor With IV inserted at right metacarpal vein Without redness or swelling on the IV insertion site With muscle wasting With Thin and flaccid muscle tone Limited range of motion With pale nailbeds

Vital signs: Day 1 Temperature Respiration rate Pulse rate BP (mmHg) 36.0C 23bpm 79bpm 130/80 Day 2 36.0C 18bpm 80bpm 110/80 Day 3 36.4C 25bpm 73bpm 120/80

b. History of Present Illness The patient was admitted at QMC on September 8,2012 at around 3:30 in the afternoon. The patient was sent to the hospital due to a episodes of vomiting and flaccidity of extremities The patient then was brought to the room of choice and

underwent such procedures. He is continuously taking insulin for the management of her diabetes. Also, he took medications for treatment of hyperlipidemia.

c. Past Medical History The patient was a known diabetic. He is taking antidiabetic medications for several years. He has no known other diseases except from her diabetes. He only experienced symptoms like fever, cough, colds, etc but they were managed at home.

d. Family Health History The family has a history of diabetes mellitus and hypertension. Other than that they have no family history of other chronic diseases like tuberculosis, cancer, etc.

e. Personal and Social History The patient is a food lover ever since. He loves to eat foods that He wanted. He also drinks alcoholic beverages occasionally. He is a smoker. He loves to hang out with her family. He also has a good relationship to her neighbors according to his significant other.

CHAPTER VIII COURSE IN THE WARD

At around 3:30 in the afternoon last August 8,2012, a 44 year old, married man was admitted at Quezon Memorial Center with the chief complaint of loss of consciousness and vomiting and flaccidity of extremities. He had been examined by Dr. Lacerna and then decided to be confined for medical management. DOCTORS ORDER: At the ER, the doctors order was with the patient which was as follows: Please admit to Medicine ward, diabetic diet, PNSS 1 L x 6 hours ,RBS q 2 ,for stat Na, K and urine ketone ABS, crea, HgbA1c CBC, urinalysis, chest xray, ECG. Included on the doctors order were medications such as fast drip of 300 cc IVF, metroclopramide 1 amp IV now then q 8, Omeprazole 40 mg IVP now, then refer accordingly. NURSING ACTIONS: Upon receiving the orders, the nurse at the ER made the requests for the laboratories and secured consent for hospitalization. Chest xray,ECG,CBC was done PATIENTS RESPONSE: The wife signed the consent while the patient cooperated during the blood extraction of the medical technologist on duty. After being sent to the room RBS was taken with the reading of 406mg/dl and had distended bladder with painful urination DOCTORS ORDER: Give regular insulin 5 units IVP now then RBS after an hour. Insert foley catheter NURSING ACTIONS:. The NOD secured consent for catheriization and the patients relative was instructed to facilitate the impending stat order for Na,K , hgba1C,crea with corresponding requests.The SNOD carried out the previous order and an hour after the administration of the drug, the blood sugar became 213mg/dl. August 9,2012 The patient was still in unstable condition of glucose tolerance and RBS at around 6 am is read as Hi DOCTORS ORDER: continue RBS monitoring IVF to flow is PNSS 1 L x 6 hours for 4 doses and fast drip of 300 cc to resent IVF NURSING ACTIONS:. The at around 11am the result of CBC and urinalysis had been referred with corresponding results hemoglobin 8.5, WBC 14 000 cumm, RBC in urine is 4-6 (0-2) WBC over 100 ( ) DOCTORS ORDER: for blood transfusion of 2 u of PRBC with proper blood typing and crossmatch and administer ciprofloxacin 500 mg 1 tab BID

NURSING ACTION: The NOD give proper instruction regarding the facilitation of blood and administered the prescribed dosage and medication The RBS increased to 490mg/dl at 1pm DOCTORS ORDER: Regular insulin 5 units SC now NURSING ACTION: The drug was administered August 10,2012 RBS result as of 6 am is read as Hi and the result of Na and K has been released with results of Na- 126.8(135-145) K 3.74 (3.5-5) DOCTORS ORDER: NaCl 1 tab TID and give Lantus 8 u SC now NURSING ACTION: The Nod administered the prescribed dosage of meds August 11,2012 At around 6 am RBS is 353 mg/dl with no alteration in vomiting DOCTORS ORDER: New orders made were as follows: Start bladder training and give Regular insulin SC injection 10 units now and decrease the RBS to 6 hours and discontinue metroclopramide NURSING ACTION: The NOD carried out the orders and explained to the patient what the doctor said. PATIENTS RESPONSE: The patient cooperated while administering the drug subcutaneously and started to have bladder training At 8:30 pm RBS taken the result was 502mg/dl. The result was then relayed to MROD DOCTORS ORDER: The doctor prescribed to start Lantus 10 units SC OD 9pm, Apidra 6 units SC TID premeals and decrease RBS to TID NURSING ACTION: The NOD administered the drug ordered and started give Lantus at night August 12,2012 At around 6am RBS reading is High DOCTORS ORDER: Regular insulin 10 units IVP now and repeat Na,K NURSING ACTION: The NOD administered it immediately after carrying out.

August 13,2012 RBS reading as of 6am is Hi and HgbA1C result is 7.4% (4.2-6.2%) DOCTORS ORDER: increased Apidra 8 units SC TID premeals Increase Lantus to 12 units SC OD PNSS 1 L x 8 3 doses August 14,2012 DOCTORS ORDER: Regular insulin 10 u SC for repeat Na, K now PNSS 1 L x 6 for 4 doses NURSING ACTION: The NOD gave request for Na,K and administered the prescribed dosage of meds August 15,2012 The results of Na is 137.0 (135-145) and K 2.95 (3.5-5) DOCTORS ORDER: Give ketosteril 600 mg 2 tabs TID and for UTZ KUB NURSING ACTION: The NOD gave request and proper instruction for the examination to be done and administered the prescribed dosage of meds. At around 12 nn RBS 131 mg/dl DOCTORS ORDER: decrease Apidra to 5 units SC

August 16,2012 Potassium result is 2.95 and hemoglobin result of 9.2 (12-15)

DOCTORS ORDER: Give Kalium Durule 1 tab TID and for BT of 2 units of PRBC NURSING ACTION: The NOD facilitate the transfusion of blood August 17,2012 Patient develops poor skin tugor August 19,2012 Patient appears pale and weak and depletion of hemoglobin takes place hemoglobin 8 mg/dl so the NOD facilitate blood transfusion of 1 u of PRBC

August 20,2012 At around 6 am RBS reading is 367 mg/dl DOCTORS ORDER: Give Humulin R 6 units Sc now August 21,2012 RBS taken with result of 378 gm/dl even though apidra was given MROD ordered Regular insulin 5 units SC now August 22,2012 Patient develops a loose bowel movement and 5 consecutive passage drooling stool the MROD ordered diatabs 2 tabs as stat order August 24,2012 The patient develops swelling and abscess on the scrotal area and refered according to SROD with order of wound care should be provided and Coamoxiclav 620mg 1 tab August 25,2012 RBS taken 320 mg/dl regular insulin 6 u SC was given and the last unit of PRBC was transfused August 26,2012 RBS 192 mg/dl regular insulin 6 u SC was given

August 27,2012 The result of KUB has an impression of Nephrolithiases, bilateral and the patient develops the sore on scrotal area DOCTORS ORDER: for H and H stat and for repeat na, K and give Acalka 1 tab TID and sambong I tab TID and refer to SROD for scrotal abscess NURSING ACTION: The NOD administered the prescribed meds and refer accordingly to SROD August 28,2012

The SROD seen the client with scrotal abscess and swelling and tenderness in the area and prescribed tramadol 50 mg I cap TID for reevaluation.

August 31,2012 The physician maintain the client on NPO for CP clearance and for incision and drainage/ debridement BT 1 u PRBC prior to OR 1 u standby for OR use NURSING ACTION: The NOD secured consent from the patient after giving explanations about the procedure. The NOD also referred MROD the patient for CP evaluation. PATIENTS RESPONSE: The patient signed the informed consent and understood the procedure. RBS 252 mg/dl DOCTORS ORDER: regular insulin 16 units SC todays pre dinner only. NURSING ACTION: The drug was administered subcutaneously. PATIENTS RESPONSE: The patient participated effectively during drug administration. September 1, 2012 Patients appears sluggish and with pallor still on the process of facilitating BT due to unavailability

CHAPTER VII PATHOPHYSIOLOGY Modifiable Risk Factors: *Loves eating sweets and fatty foods *engaged in alcohol drinking Occasionally Non-modifiable Risk Factors *Age: 44 years old *Family history of DM: both sides

*Laceration on the left foot Destruction of beta cells of islets of Langerhans that secretes insulin Decrease insulin production Insulin insufficiency Glucose cannot go to the cells Glucose stays at the systemic blood circulation Hyperglycemia RBS=406mg/dl Increase blood Osmolarity Intracellular fluid Dehydration glucose level exceeds renal threshold glucose exerts high osmotic pressure within the renal tubules osmotic dieresis occurs increase blood viscosity sluggish circulation and proliferation of microorganisms cell starvation polyphagia increase peripheral vascular resistance decrease oxygen & blood supply to distal extremities

infection muscle wasting WBC=14 000/cumm Polyuria increase decrease wound healing scrotal area Capillary permeability Extracellular fluid fever Dehydration glucose in the Urine; urinalysis: Stimulates thirst Glucose =3+ Center of the brain Polydipsia; increase thirst