Diabetes Mellitus:casepre


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Diabetes Mellitus:casepre

  1. 1. POLYTECHNIC COLLEGE OF DAVAO DEL SUR MacArthur Highway, Digos City A CASE STUDY OF Diabetes Mellitus Type 1: uncontrolled IN PARTIAL FULFILLMENT OF THE REQUIREMENTS IN RLE/NCM 102 Presented to Ms. Christella Dae J. Tenepre, RN Presented by Radee King R. Corpuz March, 2009
  2. 2. INTRODUCTION Type 1 diabetes mellitus is a chronic medical condition that occurs when the pancreas, an organ in the abdomen, produces very little or no insulin (show figure 1). Insulin is a hormone that helps the body to absorb and use glucose and other nutrients from food, store fat, and build up protein. Without insulin, blood glucose (sugar) levels become elevated. Elevated blood glucose levels (called hyperglycemia) cause a person to urinate more frequently, causing loss of body water and dehydration. A person can also feel tired and lose weight. In addition, a serious and potentially life- threatening complication known as diabetic ketoacidosis can develop. Long term complications associated with hyperglycemia can affect the eyes, nerves, kidneys, and cardiovascular system, leading to blindness, loss of sensation in the feet, the need for amputation of toes or a foot, kidney failure, and an increased risk of heart attack and stroke. Type 1 diabetes requires regular blood glucose monitoring and treatment with insulin. Treatment, lifestyle adjustments, and self-care can effectively control blood glucose levels and minimize a person's risk of ketoacidosis and other disease-related complications. Type 1 diabetes usually begins in childhood or young adulthood, but can develop at any age. In the United States, Canada, and Europe, type 1 diabetes accounts for 5 to 10 percent of all cases of diabetes. It is relatively more common in people who are white compared to people of African or Asian descent. Data on diabetes prevalence by age and sex from a limited number of countries were extrapolated to all 191 World Health Organization member states and to United Nations’ population estimates for 2000 and 2030. Urban and rural populations were considered separately for developing countries. As the result — The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% in 2000 and 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030.
  3. 3. The prevalence of diabetes is higher in men than women, but there are more women with diabetes than men. The urban population in developing countries is projected to double between 2000 and 2030. The most important demographic change to diabetes prevalence across the world appears to be the increase in the proportion of people 65 years of age. As they conclude to the findings, indicate that the “diabetes epidemic” will continue even if levels of obesity remain constant. Given the increasing prevalence of obesity, it is likely that these figures provide an underestimate of future diabetes prevalence There are an estimated 177 million diabetics worldwide. Of the eight million patients in North America, one million have Type 1 diabetes and another eight million are believed to be undiagnosed. About 30,000 new Type 1 cases are diagnosed each year in North America and the incidence is rising annually. According to the Diabetic Resources Network, there are an estimated 1.5 million diabetics in Canada and this number is expected to double by 2010. It is the leading cause of death by disease and is also the number one cause of adult blindness..(Surgical Medical Research Institute Department of Surgery,Mohammadreza Mirbolooki, MD, PhD) Our patient Ms. A, was 18 years old, living at Sinawilan, Badiang Digos City, she was admitted at Davao Medical Center last February 4, 2009, at 2:20pm, with chief complain of persistent vomiting. But before she was admitted at Davao Medical Center, she was admitted to Davao Sur Provincial Hospital, with the chief complain of vomiting and weight loss. The father of the patient was fluent in vernacular language, according to him, 3 months ago, the patient, Ms. A, manifested spotted bruises and vomiting. But they don’t mind it, because their economic status was low, and that affects the health of Ms. A according to him, they can’t eat 3 times a day. But as months passed by, the vomiting symptoms continuous, the father decided to consult to a “kwak doctor” because they believe it was being witchcraft, because of unexplainable weight loss But weeks further after, until the family decide to get to hospital at Digos City then, as being diagnosed it was procedd to Davao Medical Center, as Diabetes Mellitus Type 1.
  4. 4. IDENTIFICATION OF THE CASE A. PERSONAL PROFILE Name : Ms. A Address : Badiang, Sinawilan Digos City Age : 18y/o Gender : Female Civil status : Single Occupation : student Admitting Doctor : Dr. Guillermo Admitting Diagnosis : T/C Diabetes Mellitus type 1-uncontrolled, Electrolyte Imbalanced 2o to vomiting Religion : Islam Nationality : Muslim Educational Attainment: High School: Post Graduate Spouse name : Mr. T Occupation : fish vendor Date of admission : February 04, 2009; 2:20am B. Background/History DM HPN CA ASTHMA Maternal Paternal In there family background, in the maternal side had a positive of Diabetes Mellitus but not specified as what type. In this background, we can conclude that there’s a percent of the patient acquired the disease of the maternal.
  5. 5. C. Medical History In the medical history of the patient, Ms A, had no other disease than Diabetes Mellitus, but before, patient experienced headache due to lack of meals, fever and cough due to their environmental factor. Ms A. was hospitalized due to vomiting 3 months ago. D. History of Present Illness 1 week prior to admission, again experience sudden onset of (vomiting) post-prandial vomiting, and had episodal vomiting with 4-5 times/day. With no associated symptoms, abdominal pain. With palpable auscultation in the abdominal region. E. Socio-economic background Patient A, had a low-economic status, wherein the family cannot support or buy the necessary medication for the patient, which needed to the patient. The father is a fish vendor at their baranggay, which had an income of Php 200.00-400.00 depending on the sales per day
  6. 6. DEFINITION OF TERMS Glucose – The simple sugar (monosaccharide) that serves as the chief source of energy in the body. Glucose is the principal sugar the body makes. The body makes glucose from proteins, fats and, in largest part, carbohydrates. Glucose is carried to each cell through the bloodstream. Cells, however, cannot use glucose without the help of insulin. Glucose is also known as dextrose. Insulin – A natural hormone made by the pancreas that controls the level of the sugar glucose in the blood. Insulin permits cells to use glucose for energy. Cells cannot utilize glucose without insulin Islets of Langerhans – known as the insulin-producing tissue, the islets of Langerhans do more than that. They are groups of specialized cells in the pancreas that make and secrete hormones. There are five types of cells in an islet: alpha cells that make glucagon, which raises the level of glucose (sugar) in the blood; beta cells that make insulin; delta cells that make somatostatin which inhibits the release of numerous other hormones in the body; and PP cells and D1 cells, about which little is known. Degeneration of the insulin-producing beta cells is the main cause of type I (insulin-dependent) diabetes mellitus. Polyuria – The excessive passage of urine (at least 2.5 liters per day for an adult) resulting in profuse urination and urinary frequency (the need to urinate frequently). Polyuria is a classic sign of diabetes mellitus that is under poor control or is not yet under treatment. Polydipsia – Excessive thirst all the time. Polydipsia occurs, for example, in untreated or poorly controlled diabetes mellitus. Polyphagia – A person with polyphagia eats excessive amounts of food. In uncontrolled diabetes, some of the excess sugar that builds up in the blood passes out of the body in the urine. The calories (energy) that the sugar contains are also lost from the body when this happens. This causes the person to get very hungry and eat large amounts of food to make up for the lost calories.
  7. 7. ANATOMY AND PHYSIOLOGY Endocrine System Although we rarely think about them, the glands of the endocrine system and the hormones they release influence almost every cell, organ, and function of our bodies. The endocrine system is instrumental in regulating mood, growth and development, tissue function, and metabolism, as well as sexual function and reproductive processes. In general, the endocrine system is in charge of body processes that happen slowly, such as cell growth. Faster processes like breathing and body movement are controlled by the nervous system. But even though the nervous system and endocrine system are separate systems, they often work together to help the body function properly.
  8. 8. The foundations of the endocrine system are the hormones and glands. As the body's chemical messengers, hormones transfer information and instructions from one set of cells to another. Although many different hormones circulate throughout the bloodstream, each one affects only the cells that are genetically programmed to receive and respond to its message. Hormone levels can be influenced by factors such as stress, infection, and changes in the balance of fluid and minerals in blood. A gland is a group of cells that produces and secretes, or gives off, chemicals. A gland selects and removes materials from the blood, processes them, and secretes the finished chemical product for use somewhere in the body. Some types of glands release their secretions in specific areas. For instance, exocrine glands, such as the sweat and salivary glands, release secretions in the skin or inside of the mouth. Endocrine glands, on the other hand, release more than 20 major hormones directly into the bloodstream where they can be transported to cells in other parts of the body. The major glands that make up the human endocrine system are the hypothalamus, pituitary, thyroid, parathyroids, adrenals, pineal body, and the reproductive glands, which include the ovaries and testes. The pancreas is also part of this hormone-secreting system, even though it is also associated with the digestive system because it also produces and secretes digestive enzymes. Although the endocrine glands are the body's main hormone producers, some non-endocrine organs — such as the brain, heart, lungs, kidneys, liver, thymus, skin, and placenta — also produce and release hormones.
  9. 9. Pancreas: A fish-shaped spongy grayish-pink organ about 6 inches (15 cm) long that stretches across the back of the abdomen, behind the stomach. The head of the pancreas is on the right side of the abdomen and is connected to the duodenum (the first section of the small intestine). The narrow end of the pancreas, called the tail, extends to the left side of the body. The pancreas makes pancreatic juices and hormones, including insulin. The pancreatic juices are enzymes that help digest food in the small intestine. Insulin controls the amount of sugar in the blood. As pancreatic juices are made, they flow into the main pancreatic duct. This duct joins the common bile duct, which connects the pancreas to the liver and the gallbladder. The common bile duct, which carries bile (a fluid that helps digest fat), connects to the small intestine near the stomach. The pancreas is thus a compound gland. It is quot;compoundquot; in the sense that it is composed of both exocrine and endocrine tissues. The exocrine function of the pancreas involves the synthesis and secretion of pancreatic juices. The endocrine function resides in the million or so cellular islands (the Islets of Langerhans) embedded between the exocrine units of the pancreas. Beta cells of the islands secrete insulin, which helps control carbohydrate metabolism. Alpha cells of the islets secrete glucagon that counters the action of insulin.
  10. 10. Gluconeogenesis pathway with key molecules and enzymes. Many steps are the opposite of those found in the glycolysis. Gluconeogenesis (abreviated GNG) is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids. The vast majority of gluconeogenesis takes place in the liver and, to a smaller extent, in the cortex of kidneys. This process occurs during periods of fasting, starvation, or intense exercise and is highly endergonic. Gluconeogenesis is often associated with ketosis. Gluconeogenesis is also a target of therapy for type II diabetes, such as metformin, which inhibit glucose formation and stimulate glucose uptake by cells. Entering the pathway Several non-carbohydrate carbon substrates can enter the gluconeogenesis pathway. One common substrate is lactic acid, formed during anaerobic respiration in skeletal muscle. Lactate may also come from red blood cells, which obtain energy solely from glycolysis as they have no membrane- bound organelles for aerobic respiration. Lactate is transported back to the liver where it is converted into pyruvate by the Cori cycle using the enzyme lactate dehydrogenase. Pyruvate, the first designated substrate of the gluconeogenic pathway, can then be used to generate glucose.[2] All citric acid cycle intermediates, through conversion to oxaloacetate, amino acids other than lysine or leucine, and glycerol can also function as substrates for gluconeogenesis.[3] Amino acids must have their amino group removed by transamination or deamination before entering the cycle directly (as pyruvate or oxaloacetate), or indirectly via the citric acid cycle. The brain and liver can absolutely take the glucose uptake regardless of Insulin or Gluconeogenesis. Fatty acids cannot be converted into glucose in animals, the exception being odd-chain fatty acids which yield propionyl CoA, a precursor for succinyl CoA. In plants, specifically in seedlings, the glyoxylate cycle can be used to convert fatty acids (acetate) into the primary carbon source of the organism. The glyoxylate cycle produces four-carbon dicarboxylic acids that can enter gluconeogenesis.[4] Glycerol, which is a part of all triacylglycerols, can also be used in gluconeogenesis. In organisms in which glycerol is derived from glucose (e.g., humans and other mammals), glycerol is sometimes not considered a true gluconeogenic substrate, as it cannot be used to generate new glucose.
  11. 11. Regulation While most steps in gluconeogenesis are the reverse of those found in glycolysis, three regulated and strongly exergonic reactions are replaced with more kinetically favorable reactions. Hexokinase/glucokinase, phosphofructokinase, and pyruvate kinase enzymes of glycolysis are replaced with glucose-6-phosphatase, fructose-1,6-bisphosphatase, and PEP carboxykinase. This system of reciprocal control allow glycolysis and gluconeogenesis to inhibit each other and prevent the formation of a futile cycle. The majority of the enzymes responsible for gluconeogenesis are found in the cytoplasm; the exceptions are mitochondrial pyruvate carboxylase, and, in animals, phosphoenolpyruvate carboxykinase. The latter exists as an isozyme located in both the mitochondrion and the cytosol.[5] As there is no known mechanism to transport phosphoenolpyruvate from the mitochondrion into the cytosol, the cytosolic enzyme is believed to be the isozyme important for gluconeogenesis. The rate of gluconeogenesis is ultimately controlled by the action of a key enzyme, fructose-1,6-bisphosphatase, which is also regulated through signal tranduction by cAMP and its phosphorylation. Most factors that regulate the activity of the gluconeogenesis pathway do so by inhibiting the activity or expression of key enzymes. However, both acetyl CoA and citrate activate gluconeogenesis enzymes (pyruvate carboxylase and fructose-1,6-bisphosphatase, respectively). Due to the reciprocal control of the cycle, acetyl-CoA and citrate also have inhibitory roles in the activity of pyruvate kinase. Glycogenolysis (also known as quot;Glycogenlysisquot;) is the catabolism of glycogen by removal of a glucose monomer through cleavage with inorganic phosphate to produce glucose-1-phosphate. This derivative of glucose is then converted to glucose-6-phosphate, an intermediate in glycolysis. The hormones glucagon and epinephrine stimulate glycogenolysis Function Glycogenolysis transpires in the muscle and liver tissue, where glycogen is stored, as a hormonal response to epinephrine (e.g., adrenergic stimulation) and/ or glucagon, a pancreatic peptide triggered by low blood glucose concentrations produced in the Alpha cells of the Islets of Langerhans. • Liver (hepatic) cells can consume the glucose-6-phosphate in glycolysis, or remove the phosphate group using the enzyme glucose-6-phosphatase and release the free glucose into the bloodstream for uptake by other cells. • Muscle cells in humans do not possess glucose-6-phosphatase and hence will not release glucose, but instead use the glucose-6-phosphate in glycolysis
  12. 12. How are carbohydrates broken down into glucose? For example, excess glucose (a cause of hyperglycemia) is converted in the liver to glycogen (glycogenolysis) in response to the hormone insulin, and stored. Likewise, if blood sugar levels fall, (eg. between meals), the glycogen is re-converted to glucose (glycogenolysis) in response to messages conveyed by the hormone glucagon, to prevent hypoglycemia. If glycogen levels are exhausted, glucagon can trigger the formation of glucose from some amino acids (protein) or glycerol (fats) - a process called gluconeogenesis. How We quot;Digest Carbohydratesquot; In simple terms, the digestive system from the mouth to the small intestine (carbohydrates digested in digestive system) is designed to break down disaccharides and polysaccharides into monosaccharides. This metabolism of carbohydrates is achieved through the secretion of a number of digestive enzymes into the gastrointestinal tract quot;intestinal digestionquot; (especially in the duodenum) where they attack carbohydrates and gradually convert them into simple sugars like glucose so they can be absorbed into the blood. Digestive enzymes are involved in digesting carbohydrates Digestive enzymes are like biological scissors - they chop long starch molecules into simpler ones. Sometimes our bodies require the help of quot;digestive aidsquot; What Determines Speed of quot;Digesting Carbohydratesquot;? Generally speaking, the speed of carbohydrate digestion is determined by the chemical nature of the carbohydrate itself, and thus how quot;resistantquot; it is to the activity of the enzymes.
  13. 13. ETIOLOGY AND SYMPTOMATOLOGY Etiology Ideal Actual Justification Predisposing Factor DM type 1 occurs in childhood and young adulthood and may occurs also in person has one or more genes that make Genetic them susceptible to the disease. (+) susceptibility Our patient had a genetic disease in Diabetes Mellitus, in the maternal side, it means that the patient acquired a percent of the disease. In the stomach, where the metabolism process occurs, improper breakdown can cause toxin in the body related to diabetes. Toxins (+) Because our patient don’t eat enough meal, that why the patient’s body produce toxins which can irritate the gastrointestinal area Precipitating Factors Results in destruction of insulin- producing beta cells of the pancreas, in Autoimmune which the body's immune system mistakenly response (+) attacks healthy tissue. It because the patient had not enough insulin to produce, in order to compensate the percent of glucose of the body. Such as exposure to certain viruses and foods early in life, may trigger the Unidentified autoimmune response. viruses, and environmental (+) The environment of our patient is poor, factors because they’ve live in a semi-squatters area, which many bacteria living, that can affect the patient’s condition. Low socio-economic, can affect the health status of an individual, improper meals or Economic Status skipping of meals can cause irritation in the (+) gastrointestinal, and effect of abnormal production of the insulin, that produces gastric acid.
  14. 14. Symptomatology Ideal Actual Justification Insufficient fluid distribution in the body, due to increasing blood sugar Excessive thirst This was manifested by (+) the patient because she always need to drink a water even though she’s lying flat on bed. And poor skin turgor. Sudden vision Increase blood sugar in the changes body, that may cause (-) blurred vision and can be blindness. Tingling or numbness Nerve damage can lead to in the hands or feet numbness or pain. The (+) patient was so sensitive in touching, she felt pain. Impaired tissue perfusion, Very dry skin because of fluid imbalance (+) in the body. The patient manifested scaly skin. Unexplained weight Abnormal breakdown of the nutrients in the body can loss (+) cause weight loss. The patient was endomorphic at size, Damage proliferation of the kidney due to increase blood sugar in the body, Frequent urination that can’t filter by the (+) kidney. The had this symptom as evidenced by her diaper, 800cc at 3 diapers. Extreme hunger Abnormal metabolism , (+) causes improper absorption of the nutrients
  15. 15. COMPLICATION Diabetic ketoacidosis Diabetic ketoacidosis (DKA) is an acute and dangerous complication that is always a medical emergency. Low insulin levels cause the liver to turn to fat for fuel (ie, ketosis); ketone bodies are intermediate substrates in that metabolic sequence. This is normal when periodic, but can become a serious problem if sustained. Elevated levels of ketone bodies in the blood decrease the blood's pH, leading to DKA. On presentation at hospital, the patient in DKA is typically dehydrated, and breathing rapidly and deeply. Abdominal pain is common and may be severe. The level of consciousness is typically normal until late in the process, when lethargy may progress to coma. Ketoacidosis can easily become severe enough to cause hypotension, shock, and death. Urine analysis will reveal significant levels of ketone bodies (which have exceeded their renal threshold blood levels to appear in the urine, often before other overt symptoms). Prompt, proper treatment usually results in full recovery, though death can result from inadequate or delayed treatment, or from complications (eg, brain edema). DKA is always a medical emergency and requires medical attention. Ketoacidosis is much more common in type 1 diabetes than type 2. Hypoglycemia Hypoglycemia, or abnormally low blood glucose, is an acute complication of several diabetes treatments. It is rare otherwise, either in diabetic or non- diabetic patients. The patient may become agitated, sweaty, and have many symptoms of sympathetic activation of the autonomic nervous system resulting in feelings akin to dread and immobilized panic. Consciousness can be altered or even lost in extreme cases, leading to coma, seizures, or even brain damage and death. In patients with diabetes, this may be caused by several factors, such as
  16. 16. too much or incorrectly timed insulin, too much or incorrectly timed exercise (exercise decreases insulin requirements) or not enough food (specifically glucose containing carbohydrates). The variety of interactions makes cause identification difficult in many instances. It is more accurate to note that iatrogenic hypoglycemia is typically the result of the interplay of absolute (or relative) insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes. Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine are the primary glucose counterregulatory factors that normally prevent or (more or less rapidly) correct hypoglycemia. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses causes defective glucose counterregulation. In most cases, hypoglycemia is treated with sugary drinks or food. In severe cases, an injection of glucagon (a hormone with effects largely opposite to those of insulin) or an intravenous infusion of dextrose is used for treatment, but usually only if the person is unconscious. In any given incident, glucogon will only work once as it uses stored liver glycogen as a glucose source; in the absence of such stores, glucagon is largely ineffective. In hospitals, intravenous dextrose is often used. Retinopathy An eye disease, associated with Diabetes Mellitus is the major cause of blindness in the U.S. It is the result of microvascular changes associated with hyperglycemia. Two distinct patterns develop in DM retinopathy: (1) non- proliferative or background retinopathy and (2) proliferative retinopathy. Non proliferative retinopathy represents the earliest type of eye involvement. The changes associated with non-proliferative retinopathy include microaneurysms, exudates, and retinal edema. The microaneurysm appear as red dots on the retina. Increased vascular permeability leads to leakage of fats and fluids. The
  17. 17. fats appear as shiny yellow spots with distinct borders or hard exudates. Retinal ischemia is visible as hazy yellow areas with indistinct borders or cotton wool spots. Proliferative retinopathy includes neovascularization with the growth of new capillaries. Since these capillaries can exert an abnormal traction on the retina, there is an increased risk of retinal detachment. Nephropathy Is the result of an alteration in glomerular function. It is characterized by proteinuria, hypertension, and progressive insufficiency. There is thickening of the basement membranes of the glomerular capillaries, leading to the development of glomerular sclerosis. These changes in the glomeruli are accomplanied by a small urinary loss of albumin. However, over time this can progress to proteinuria. Hypertension develops as the renal diseases progresses. However, hypertension can also increase the progression of diabetic nephropathy; thus, the control of hypertension becomes an important part of treatment for diabetic nephropathy. Neuroapathy The proposed mechanism for the alteration in neuropathy appears to be a combination of altered metabolism and vascular insufficiency. As mentioned previously, hyperglycemia enhances the activity of the sorbitol pathway, promoting sorbitol excess. This changes the cellular osmolarity, ultimately imparing cellular physiologic activity. The activity of Na+/K+ ATPAse is decreased, compromising neuronal function. The injured cells are unable to remove free radicals, so that additional tissue damage occurs. Impaired blood flow reduces oxygen delivery to the nerves, further compromising them. There is also atrophy of the nerve axon with loss of myelin. Thus, the neuronal damage seen in diabetic neuropathy is most probably due to a combination of factors. The alterations associated with diabetic neuropathy, either alone or in combination with the other previously mentioned complications, lead to the
  18. 18. development of a variety of problems. The accompanying sensory loss seen in both hands and feet (glove and stocking syndromes) not only alter the life style of individuals with DM but also contribute to chronic problems such as foot ulcers. Autoimmune neuropathy is associated with tachycardia, orthostatic hypotension, impotence, and incontinence. Impairment of specific cranial nerves causes headaches, ptosis and impaired eye movement
  19. 19. PATHOPHYSIOLOGY Predisposing factors Precipitating factors Age Lifestyle Gender (adolescent) Environment Hx of Diabetes Mellitus Economic Status (maternal) Diet Pathological impairment of Beta cells Insufficient insulin production Increase glucose in the Blood stream Hyperglycemia S/Sx: Diabetes Mellitus Excessive Thirst Type 1 Sudden vision changes Tingling or numbness in the Hands or feet Very dry skin Unexplained weight loss Excessive hunger Hypokalemia Hyponatremia If disorder is not treated, Complication occurs If disorder is Treated Diabetic ketoacidosis Normalized glucose and Hypoglycemia insulin production related to: Retinopathy •Insulin therapy Nephropathy Neuroapathy •Diet (prescribed diet) •Exercise •Proper Education about the disease Bad Prognosis
  20. 20. Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus. Most of the carbohydrates in food are converted within a few hours to the monosaccharide glucose, the principal carbohydrate found in blood and used by the body as fuel. The most significant exceptions are fructose, most disaccharides (except sucrose and in some people lactose), and all more complex polysaccharides, with the outstanding exception of starch. Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism. Higher insulin levels increase some anabolic (quot;building upquot;) processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).
  21. 21. If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.
  22. 22. MEDICAL MANAGEMENT Referred to Dr. Guillermo  Admit pt to Med IMCU under blue level II  Diabetic Diet o Carbohydrate – 180g/day o Protein – 120g/day o Fat – 80g/day  V/S every 4hrs  Labs: o CBC, PC o RBC, Crea, Na+, P+ o CXR-PA o X-ray abdomen U/S, U/A ketones o Stool exam and ABG  IVF PNSS 1L fast drip now, then regulate 140cc/hr  Medication: o Metoclopramide 1 amp IVTT now o Ranitidine 150mg, OD  CBG monitor q6hrs refer for <90 or >200  Secure 1 pack RBC and transfuse and cross-matching  Watch for unusualities  Monitor I/O  KCl drip: KCl 80mEqs + 1L PNSS sidedrip x 2 cycles, please label tubings as do not fastdrip at 120 cc/hr  K+ citriate 1tab TID 02/26/09  For U/A; urine ketones  For request serum, K+, Cl+, stat ABG  Hgt analysis and refer result to MROD  IVF PNSS1L at 200cc as fast drip and regulated 140cc/hr for 8hrs  Shift ranitidine 1g IVTT q12 (ANST)  Con’t KCl drip  CBG monitor q6
  23. 23. 02/28/09  May d/c RI  Decrease CBG monitor q12  Still for electrolyte test  Please give metachlopramide 1 amp IVTT (+) vomiting 3x episode 03/01/09  Still for repeat K+ for U/A  d/c O2  for possible discharge 03/02/09  Diagnotics  CBC, Plt  HgB A, C  Na+, K+  Ff up U/A, F/A  Hold RI  Please give KCl syrup 15ml q6 x 4doses  CBG monitoring q12  FeSO4 + FA 1tab, OD  Ff up official CXR 03/03/09  Please comply with KCl syringe c/o nurse station  Hold CBG monitoring  Ff up lab tables yesterday  Ff up official CXR result 03/04/09  Hold giving milk  Please ff up F/A  Please con’t KCl syrup as ordered  IVF at KVO  Increase OFI  Doxycyclene 100g 1tab BID 8:30pm – Fast drip with 300cc the reguate to 200cc 03/05/09 Discharge at 8:30pm, HAMA with signature.
  24. 24. Laboratory Hematology Normal Clinical Test Result Remarks Values Significance CBC+Plt Hemoglobin – L 115-155 Decreased in -decresed- 70 various anemias, pregnancy, severe or prolonged hemorrhage, and with execessive fluid intake Hematocrit – L 0.30-0.4 Severe anemias, -decreased- 0.22 8 anemia of pregnancy, acute massive blood loss RBC – L 2.59 4.20-6.1 Adequate number of -decreased- 0 Red Blood Cell primarily to ferry oxygen in blood to all cells of the body WBC – 5.0-10.0 -normal range- 9.52 Neutrophil – H 87 55-75 -increased- Lymphocytes – 0.2-0.4 Aplastic anemia, -decreased- L .11 SLE, immunodeficiency including AIDS Monocytes – 2 2-10 -normal range- Eosinophil – 0 1-8 -decrease- Basophil – 0 0-1 -normal range- Platelet count – -normal range- 214,000/cu mm
  25. 25. Laboratory Chemistry Test Result Normal Values Clinical significance Remarks Na+ H 150 135-145mEq/L hemoconcentration -increased- K+ L 2.5 3.5-5 mEq/L Vit. D deficiency -decreased- Creatinine L 37.90 F: 75-115mL/min Kidney dse -decreased- Glucose- H 21.3 3.3-6.05mmol/L Diabetes Mellitus -increased- fasting Laboratory Clinical Microscopy Chemical PE Exam Pus cells: Light yellow Albumin (-) 0-2/hpf Clear Sugar (-) RBC: 0-1/hpt Rrn 6.0 Bacteria (+) Specific gravity – 1.075 Laboratory ABG Clinical Test Result Normal Values Remarks significance pH 7.352 7.35-7.45 -normal range- pCO2 41.6 35-45 -normal range- HCO3 22.6 22.0-27.0 -normal range- O2 Sat 95% 80-100% -normal range- Cf CO2 23.9 23.0-30.0 -normal range- PO2 77.9 80-100 -decreased- MEDICAL MANAGEMENT Ideal Management
  26. 26. The main goal of treatment is to normalize insulin therapy and blood glucose levels to reduce the development of vascular and neuropathic 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 of type 1 diabetes is insulin  Primary treatment of type 2 diabetes is weight loss  Exercise is important in enhancing the effectiveness of insulin  Use oral hypoglycemia agents if diet and exercise are not successful in controlling blood glucose levels. Insulin injections may be used in acute situations  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 adjustment in therapy.  Education is needed for both patient and family Nutritional Management  Meal plan should be based on patient’s usual eating habits and lifestyle and should provide all essential food  Goals are to achieve and maintain ideal weight, meet energy needs, prevent wide daily fluctuations in blood glucose levels (keeps as close to normal as is safe and practical), and decrease blood lipid levels, if elevated  For patients who require insulin to help control blood glucose levels, consistency is required in maintaining calories and carbohydrates consumed at different meals.  Consult dietitian for diabetes management planning to gradually increase or add fiber in meal plan (grains, vegetables)
  27. 27. Calorie Requirement  Determine basic caloric requirements, taking into consideration age, gender, body, weight, and height and factoring in degree of activity  Long-term weight reduction can be achieved (1-2 pound loss per week) by reducing basic caloric requirements NURSING ASSESSMENT Physical Assessment Neurological
  28. 28. The patient had a GCS score of 13, she can able to express self and understand, the patient is oriented in time and place, +1 reflexes response. And can determine hot and cold. Eye/Vision Our patient, doesn’t have manifested burring of vision, she can see person and recognized them, the pupils’ size are in 3mm, symmetrical and no discharges, poor conjuctiva appearance Ears/Hearing Our patient doesn’t have hearing problem, but have discharges due to lack of self-care or hygiene, symmetrical, no swelling and tenderness. Can response or awake in normal voice tone Nose Our patient doesn’t have nasal problem, no discharges, no swelling and tenderness, uniform in color. Discharges are observed due to lack of self-care or hygiene. Mouth/Tongue/Teeth/ Speech The patient’s had a crack and pallor lips, reddened gums, with distant teeth. And the patient had a slurred speech, aside from being a Muslim. Tongue is slightly pale. Throat/Neck Symmetrical with head, can turned head from right to left gradually, but with resistance, no palpable lymph nodes Respiratory System Patient use accessory muscle in order to breathe normally, patient had a breath sounds of bronchial (tubular) Circulatory/Cardiovascular
  29. 29. Patient pulse rate was 65bpm, and the heart rate of 85bpm, and O2 Sat of 97% and blood pressure reading of 80/60-90/70. Irregular palpatory pulse point. No edema, swelling. Gastrointestinal Palpable abdominal area, localized areas of increased tension Genitourinary Patient had excessive urination, with minimum of 800cc per diaper Muscoloskeletal The patient was atrophic, decreased muscle tone at both upper and lower extremeties, and endomorphic in physical appearance Integumentary The patient was skin warm to touch, with spotted bruises in both extremeties, afebrile, poor skin turgor NURSING MANAGEMENT NURSING ASSESSMENT AND DIAGNOSIS
  30. 30. • Focus on signs and symptoms of prolonged hyperglycemia and physical, social, and emotional factors that affect ability to learn and perform diabetes self-care activities. • Ask for a description of symptoms that preceded the diagnosis: polyuria, polydipsia, polyphagia, skin dryness, blurred vision, weight loss, vaginal itching and nonhealing ulcers. • Assess for signs of DKA, including ketonuria, Kussmaul respirations, orthostatic hypotension, and lethargy. • Monitor laboratory signs for metabolic acidosis (decreased pH, decreased bicarbonate) and electrolyte imbalance • Assess physical factors that impair ability to learn or perform self-care skills: visual defects, motor coordination defects, neurologic defects • Improving Nutritional Intake o Plan the diet with glucose control as the primary goal. o Take into consideration patient” lifestyle, cultural background, activity level, and food preferences. o Encourage patient to eat full meals and snacks as per diabetic diet o Make arrangements for extra snacks before increased physical activity o Ensure that insulin orders are altered as needed for delays in eating due to diagnostic and other procedures. • Reducing Anxiety o Provide emotional support; set aside time to talk with patient o Clear up misconceptions patient or family may have regarding diabetes o Assist patient and family to focus on learning self-care behaviors o Encourage patient to perform the skills feared most: self-injection for finger stick for glucose monitoring o Give positive reinforcement for self-care behaviors attempt • Administering Insulin Therapy
  31. 31. o Insulin preparations vary according to four main characteristics: time course of action, concentration, species (source), and manufacturer. NURSING THEORIES Florence Nightingale Her Notes on Nursing emphasized that a clean environment, warmth, ventilation, sunlight, and a quiet environment lead to good health.
  32. 32. Reaction: a non-stimulating environment is essential especially for our patient, in a way that it promotes faster recovery on our patient through minimizing external and stressful stimuli such as limiting visitors during resting periods that may worsen the situation of our client. Virginia Henderson Virginia Henderson defined nursing as quot;assisting individuals to gain independence in relation to the performance of activities contributing to health or its recoveryquot; Hildegard Peplau Hildegard Peplau used the term, psychodynamic nursing, to describe the dynamic relationship between a nurse and a patient. She identified nursing roles of the nurse and in our case this three roles fitted us for our client: • Counseling Role - working with the patient on current problems • Teaching Role - offering information and helping the patient learn Reaction: As a nursing student, we had many roles to perform to our patient. One of these roles is being a councilor. As a councilor, it is our duty to lessen if not alleviate the client’s problem. HEALTH TEACHINGS PRIMARY 1. Instruct the patient to have a maintenance of insulin injection/fluid at home for continuous medication 2. Instruct the patient to have a proper diet that she can tolerate, such as fruits, to help promote wellness.
  33. 33. 3. Instruct the patient to have deep breathing exercise, to promote non- pharmacological treatment 4. Advice the patient to have fluid intake or adequate hydration, to help her body re-hydrate to prevent fluid imbalance. 5. Assist patient to perform self-care activities she cannot tolerate, to help her maintain her activities of daily living. 6. Encourage patient to perform self care activities within her level of own ability. 7. Initiate and encourage patient to perform bed exercises to improve circulation ( ROM to arms, hands and fingers, feet and legs; leg flexion and leg lifting; abdominal and gluteal contraction) 8. Ask patient to perform as much as possible and then to call for assistance. Collaborate with patient for progressive activity before and after schedule activity. SECONDARY 1. Administer medications as ordered by the physician 2. Advice patient to have proper nutrition to enhance immune system TERTIARY 1. Instruct patient to comply for medication regimen 2. Discuss the importance of having a regular check-up with his physician DISCHARGE PLAN When the doctor noted that the patient is for discharge it is very important to continue the medication depending on the duration the doctor ordered for the total recovery of the patient. Patient with Diabetes Mellitus Type 1 - uncontrolled
  34. 34. needs to have a light exercise such as motor development in both arms and feet, clear verbalization and spontaneous with the duration of 10-15 minutes and must get enough rest. It is also important to maintain proper hygiene to prevent further infection that may happen to the. She also needs to have a regular insulin injection She must have to relax in order to recover her present condition and minimal exposure to a pressure and positive atmosphere can be a high risk factor that may cause severity of her condition. The diet of the patient is also a factor for fast recovery. She is encouraged to eat nutritious foods intended for diabetic patient the family of the patient plays a big role for the fast recovery. Regular consultation to the physician can be factor for recovery to assess and monitor her condition M- advice patient not to skip the meds that the doctor ordered E- encourage patient to have exercise early in the morning at lease twice a day T- regular insulin injection, for maintenance H- separate utensils for the patient and other personal things that will be use for the whole family O- provide information about how to control or prevent the spread of the disease D- encourage patient to eat nutritious food such as vegetable and fruits especially those that contains vitamin C S- provide emotional support and provide care for the mother PROGNOSIS Good Fair Poor Justification Duration of Duration of illness is Illness poor since the condition - occur and she was given ample treatment.
  35. 35. Onset of The onset is since right Illness after the she was - diagnosed, she was automatically brought to DMC hospital Compliance Patient can’t afford to to sustain the needed Medication - laboratory exams and the feasibility of having the condition Family The family members Support supported the patient - both financially and emotionally. Environment The hospital setting is not well ventilated and - may promote for further infection of the patient’s current situation. Age Patient is 18 years old therefore she has a goodr chance of - recovering for her immune system is still generating in the process of development. Precipitating The patient manifested Factors all the factors that may lead to Diabetes Mellitus - type 1 which urged the family and the health provider to set-up the proper action Percentage Poor: 5/7x100= 71% Fair: 1/7x100=14% Good: 2/7x100=29% Overall Prognosis
  36. 36. The prognosis is poor, because the precipitating factors, environment, compliance to the medication, duration of illness and the onset of illness are the factors that contributes to have poor prognosis, and patient also had HAMA with signature, which denotes also a bad prognosis EVALUATION Through our hardship in preparing for this research, tried to interact and communicate our patient in good manner for us to gather the specific and
  37. 37. accurate data that we need that could help us in studying the disease which could lead us into successful research. The patient’s condition is in recovery period as she had already undergone medication for certain, which thereby prevented occurrence of complications. They are financially capable in sustaining such pregnancy condition and the medications after. Her husband is the one taking good care of her in throughout her hospitalization, giving emotional and moral support. IMPLICATION Nursing Practice
  38. 38. - this can be used as a guide for practice by other nurses. They may get many relevant ideas in giving proper care and interventions to patients with related illness or those who have the same illness (Diabetes Mellitus Type - uncontrolled) Nursing Education - this study may serve as a helpful learning tool for student nurses. They may utilize this complied study as their reference for research; this will also give them good examples on nursing managements, and nursing diagnoses, which will be a very useful guide when they will be making their own Nursing Care Plans. Nursing Research - students may use this compilation as their guide for research. This will hand them good views and factual ideas which will be very essential for their added learning on knowledge for Diabetes Mellitus Type 1 – uncontrolled condition REFERENCES
  39. 39. • Surgical Medical Research Institute Department of Surgery, Mohammadreza Mirbolooki, MD, PhD • http://www.springerpub.com/prod.aspx?prod_id=72628 • wikipedia.org/wiki/Diabetes • www.medicinenet.com/diabetes_mellitus/article.htm • www.who.int/topics/diabetes_mellitus • www.vetmed.wsu.edu/ClientEd/diabetes • Medical-Surgical, Brunner and Suddart 11th Ed, Diagnostic Test and Results, pp 2148-2152 • Handbook for Medical-Surgical Nursing, 11th Ed, Management for Diabetes Mellitus, pp. 302-307