a. Aetiology:Predisposing Factors

Factors Presence Mechanism/JustificationGenetic Initial decrease in beta cell mass

related to genetic factors responsible for beta cell differentiation or presence of diabetogenic gene.

Age >40 Pancreas, similar to several other components of the body, does not function well due to old age.

Precipitating FactorsFactors Presence Mechanism/JustificationOver weight/Obesity Obese people have increased

resistance to the action of insulin and impaired suppression of glucose by liver, resulting both hyperglycemia and hyperinsulinemia. 85% of all people with diabetes are obese.

Environment(intrapartal stage) Initial decrease in beta cell mass related to presence of Maternal Diabetes Mellitus during pregnancy or in uterine factors such as intrauterine growth restriction.

Virus Infection Mumps, coxsackeivirusPresence of Toxin Nitrosamines that are found in

smoked and cured meats, are related to streptozoin that is used to induce DM in experimental animals, rat poison named Vacor that induces DM when ingested by Human

Decrease serum potassium level Low potassium level impairs release of insulin

b. Symptomatology

Symptoms Presence Mechanism/JustificationPolyuria (excessive urination) Glucose exceeds the amount

that can be reabsorbed by renal tubules this results glycosuria.

Polydipsia (excessive thirst) Excess glucose in the blood pulls

Pathophysiology Diabetes Mellitus

water out of the cell causing intracellular dehydration, including those in thirst center.

Polyphagia (excessive hunger) Results from depleation of cellular reserves of carbohydrates, fats and proteins.

Blurred Vision Lens and retina are exposed to hyperosmolar fluids

Weakness and fatigue Lowered plasma volumeParesthesias Temporary dysfunction of

peripheral sensory nervesPruritus, vaginitis, chronic skin infections

Hypergycemia and glycosuria favors growth of yeast organisms.

Weight loss Initial loss due to depleation of water, glycogen, and triglyceride store; chronic loss secondary to decrease muscle mass as amino acid are diverted to form glucose and ketone bodies.

Often Asymptomatic The body is able to adopt ta a slow rise of blood glucose level to a greater extent than it can to a rapid rise.

c. Schematic Tracing

Gastroparesis

Impotence Dry, cracked skin

Neurogenic bladderCharcot changes in joints

Diabetic foot ulceration

Wasting of intrinsic muscles

Autonomic neuropathy

Symmetrical loss of sensation

End-stage renal failure

Loss of vision

Diabetic nephropathy

Diabetic retinopathy

Small vessel disease

Diabetic neuropathy

Coronary artery disease

Hypertension

Increase LDL levels

Accelerated atherosclerosis

Delayed wound healing

Infection

Impaired immune function

Chronic elevation of Serum Glucose

Weight loss

PolyphagiaPolyuriaPolydipsia

Increased Osmolarity due to Glucose

Elevated Serum Glucose

Precipitating Environment(intrapartal) Toxin/Virus Obesity Decrease Serum

Potasium

Predisposing Factors Genetics Age >40

Decrease insulin production/sensitivity

Numbness and paresthesia

d. Narrative

Type two Diabetes Mellitus is a heterogeneous condition that describes the presence of excess serum glucose level in association with relative insulin deficiency. Type 2 Diabetes is associated with high, normal, low insulin levels. However there is a presence of insulin resistance thus the insulin cannot function effectively and hyperglycemia will occur. Most people with this type of diabetes are older and obese, but type 2 Diabetes is becoming a more common occurrence in obese adolescent. The metabolic abnormalities that contribute in hyperglycemia in people with type 2 diabetes are impaired beta cell function and insulin production, peripheral insulin resistance, and increase hepatic glucose production.

Insulin is a anabolic hormone. Without insulin three major metabolic problem occur: decrease glucose uptake and utilization, increase fat and lipid mobilization and increased protein and amino acid utilization.

Beta cells chronically exposed to high blood levels of glucose become progressively less efficient when responding to further glucose elevation. Insulin resistance initially produces an increase beta cell secretion of insulin as body attempt to maintain normoglycemic state. In time, however the insulin response declines because of increasing beta cell dysfunction. This results to postprandial hyperglycemia. Eventually fasting blood glucose level also rise until frank type 2 Diabetes occurs.

Cells that require insulin as carrier of glucose can take only 25% of glucose they require for fuel, but nerve tissues, erythrocytes, and cells of intestine, liver, kidney tubules do not require insulin for glucose transport. However, adipose tissue, along with skeletal and cardiac muscle requires insulin for glucose transport.

During severe stress such as hospitalization, the body of a type 2 diabetes patient will turn fat reserves into glucose for energy production when glucose is not available. Fat and lipid metabolism cause breakdown products called ketones to form. Ketones accumulate in the blood and excreted through kidneys and lungs. Ketones interfere with the body’s acid base balance by producing Hydrogen ions. The pH can decrease, and metabolic acidosis can result. In addition when ketone is excreted in urine, sodium is also eliminated, causing sodium depletion and further acidosis. The excretion of ketone also increases osmotic pressure, leading to increase fluid loss.

In this type of Diabetes Mellitus the onset of clinical manifestation may develop gradually that clients may notice a few or no clinical manifestations for a number of year. Some of the manifestations are frequency in urination, increase thirst or fluid intake, and as the disease progresses, weight loss despite hunger and increased food intake.

Clients with diabetes mellitus are living longer, with an increased risk for development of chronic complications. Chronic complication are the major cause of morbidity and mortality in client with diabetes mellitus. Diabetes mellitus-related complications are classified into two types: macrovascular, including coronary artery diseases, cerebrovascular disease, hypertension, peripheral vascular disease and infection; and microvascular, including retinopathy, nephropathy, and neuropathy.

The very-low density lipoprotein and low density lipoprotein level are increased and high density lipoproteins are decreased, and the most characteristic of lipid abnormality in diabetes mellitus is an increase triglyceride level. Therefore the influence of diabetes in these disease are not additive, it is multiplicative. Macrovascular disease tends to occur year before the onset of clinical diabetes mellitus.

Clients with DM are two to four times more likely to have coronary artery disease than those who do not have DM. In many clients with DM, often presents atypical or silent CAD, that often presents as indgestion, or unexplained heart failure, dyspnea or excretions, or epigastric pain. CAD is common in clients younger than 40 years old, of diabetes mellitus is of long duration. DM patients with history of myocardial infarction have higher chance of having second infarct than the patient who does not have DM. The incidence of cerebrovascular disease is two to three times greater in diabetic client, and is

more severe. Atherothromboembolic infarction manifested by transient ischemic attracts and cerebrovascular accidents are the most commont incidence of CVD that are the complication of DM.

Hypertension has increased of 40% occurrence in diabetic population. Hypertension is a major risk factor for stroke and nephropathy.

Diabetis mellitus augments the process of atherosclerosclerosis by variety of mechanism thus causing peripheral vascular disease. Hyperglycemia and insulin resistance contribute to endothelial dysfunction by decreasing available nitric oxide bioavailability and altering the function of various cell mediators.

Clients with diabetes are susceptible to different type of infection. Three factors may contribute to the development of infection are impaired polymorphonuclear-leukocyte function, diabetic nephropathies and vascular insufficiencies. Damaged area heals slowly because the damaged vascular system cannot carry sufficient amount of oxygen, white blood cells, nutrients and antibodies to the injured site. Infection increases the need for insulin and enhances the possibility of ketoacidosis. Urinary tract infection is the most common infection especially in women. Factors that impairs the polymorphonuclear-leukocyte is the presence of glycosuria and the development of neurogenic bladder, which results in incomplete emptying and or urinary stasis.

About 80% of clients with DM have some form of retinopathy, the exact cause of retinopathy is not understood but it is probably a multifactorial and associated with protein glycosylation, ischemia, and hemodynamics mechanism that increases the permeability and decreases the elasticity of capillaries.

About 20% of diagnosed DM type 2 patients have nephropathy 5 to 10 years after diagnosis. A consequence of microangiopathy, nephropathy involves damage to and eventual obliteration of the capillaries that supply the glomeruli of the kidney. This damage leads to complex pathologic changes and manifestations such as intercapillary glomerolonecrosis, nephrosis, gross albuminuria and hypertension. Unsuccessful treatment of nephropathy will lead to stage 5 chronic kidney disease. Like retinopathy, diabetic nephropathy is irreversible.

Neuropathy, the most common chronic complication of diabetes mellitus. Nearly 60% of diabetic patients experience it. Because nerve fibers do not have their own blood supply, they depend on diffusion of nutriens, and oxygen across membrane. When axon and dendrites do not receive nourishment their transmission of impulses becomes slow. Both temporary and permanent neurologic problem may develop. The neuropathy might be mild that causing minor inconveniences or severe that quality of life is affected. Clients might present mononeuropathy or polyneuropathy and may have motor or sensory impairment, depending on which nerve that are involved. Mononeuropathy usually involves single or group nerves. It produces sharp, stabbing pain and is usually caused by an infarction of blood supply. Polyneuropathy also known as diffuse neuropathy, which involves both sensory and autonomic nerves. Sensory neuropathy is most common type. It is commonly assed as bilateral, symmetrical and is affecting the lower extremity. Client may describe tingling, numbness, burning, and mild to severe sensory loss, a major factor in injuries to the legs.Autonomic neuropathy affects the nerves that regulate vital functions, including the heart muscle and smooth muscles. Autonomic neuropathy involves damage to the nerves that run through a part of the peripheral nervous system. The peripheral nervous system includes the nerves used for communication to and from the brain and spinal cord (central nervous system) and all other parts of the body, including the internal organs, muscles, skin, and blood vessels. Damage to the autonomic nerves affects the function of areas connected to the problem nerve. Some of the autonomic neuropathy are: autonomic neuropathy of the pupil which interferes with pupils ability to adapt to dark because pupils dilation is inadequate; autonomic neuropathy of the cardiovascular system is evidence by abnormal response to exercise, fixed heart maybe noted; autonomic neuropathy of gastrointestinal, client may have dysphagia, abdominal pain, nausea, vomiting, diarrhea malabsorption, post prandial hypoglycemia, constipation, or fecal incontinence and gastroparesis. Bladder hypotonisity of neurogenic bladder is

common manifestation of autonomic neuropathy of genitourinary organs. In male client it can contribute to erectile dysfunction and retrograde ejaculation. Women may experience painful coitus.

All of these complication can be prevented by good control of blood sugar level, exercise and diet modification.