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Weaknes S/ Fatigue Polyphag Ia
Weaknes S/ Fatigue Polyphag Ia
Weaknes S/ Fatigue Polyphag Ia
o Race: African, Hispanics Destruction of Beta-Cells in the Pancreas Precipitating Factors Obesity Lifestyle Diet Environmental Stress
Hyperglycemia
Hyperosmolarity of Serum
Renal Threshold of Glucose Reabsorption Decrease d Energy Productio n Satiety Center responds by Increasing Appetite
Excess Glucose Secreted in the Urine Excess Glucose Secreted in the Urine
Weaknes s/ Fatigue
Polyphag ia
Glucose acts Osmotic Leakage of Protein onto the Macula Dec. Blood Blindnes Nerve Increased Neuropathy Polydips Blindne Decreased Blood Supply in the Kidneys Decreased Ecretion of Metabolic Waste Blurring of
Diabetic
Autonomicneurop
-Symmetrical loss of protective sensation -Numbness and tingling sensation of lower extremities -Wasting of Intrinsic Muscles -Changes in the Joints
Acidosi s
Kidney Impairment
Nausea/ Vomitting
Dec. Production of
Pale
Diabetes Mellitus
Diabetes Mellitus Type 2 is the most common form of Diabetes. Formerly known as adult-onset diabetes, it usually affects people aged over 40 and progresses gradually. In this type the
pancreas has not ceased to produce insulin, but the quantity is insufficient, or the hormone is not stimulating the glucose uptake in muscles and tissues required for energy. The result is a build-up of glucose in blood and urine. Although the cause of this malfunctioning is unclear, non-insulin dependent diabetes mellitus tends to run in families. Other risk factors, such as increasing age, obesity, and a sedentary lifestyle, probably contribute to its increased incidence in developed countries. Non-insulin dependent diabetes mellitus can often be controlled initially by diet alone, or in combination with tablets that reduce the amount of blood glucose. There are two main types of blood glucose-reducing drugs: sulphonylureas work mainly by stimulating the pancreass islet cells (known as the Islets of Langerhans) to produce more insulin and biguanides increase the effectiveness of insulin on cells. Eventually, however, patients may need insulin injections.
Predisposing Factors
Age - Type 2 DM usually occurs at the age 40 years old and above. Type 2 DM occurs most commonly in people older than 30 years who are obese. Family history of DM - Type 2 DM has a strong genetic component. Although the major gene that places the patient at risk is not yet identified, it is clear that the disease is polygenic and multifactorial. Individuals with a parent with type 2 DM have an increased risk for diabetes. Genetic factors are thought to play a role in insulin rsistance and impaired insulin secretion in type 2 DM.
Race (African-Americans, Hispanic-Americans) - The risk for type 2 diabetes varies among population groups. Diabetes also seems to pose higher or lower risks for specific complications among racial groups.
Precipitating Factors
Obesity Elevated levels of free fatty acids, a common feature of obesity, may contribute to the pathogenesis of type 2 DM. It can impair glucose utilization in skeletal muscles, promote glucose production by the liver and impair beta cell function. Environmental Factors/Stress An increase in stress hormone triggers the release of epinephrine and norepinephrine which will promote the secretion of glucose leading to hyperglycemia. Inactive Lifestyle A risk factor that had contributed in the occurrence of DM due to the fact that lack of muscle activities decreases the need for the body to utilize glucose as a form of energy. Diet Foods rich in carbohydrates can easily promote the increasing level of glucose along the bloodstream.
POLYDIPSIA
Increased thirst and fluid intake. This may be due to the activation of the thirst center in the hypothalamus resulting form the intracellular dehydration or volume depletion. POLYPHAGIA Increased hunger and food intake. This may be due to the decrease glucose uptake by the cells leading the stimulation of the satiety center in the hypothalamus resulting to the hunger sensation. WEAKNESS/ FATIGUE This is due to the decreased glucose uptake by the cells leading to decreased energy production. GLYCOSURIA The kidney filters the blood, making it to its normal state. Glucose was filtered out and excreted in the urine. Due to the excess glucose ad compared to the kidney threshold, which results to the excretion of glucose in the urine. GASTROPARESIS (Stomach fullness) ,CONSTIPATION and BLOATING This is due to changes in nerves and damages the blood vessels that carry oxygen and nutrients to the nerves. Over time, high blood glucose can damage the vagus nerve. The stomach fails to empty properly and is likely due to the generalized neuropathy. NAUSEA/ VOMITING Due to stomach fullness, there will be an involuntary emptying of stomach contents that are forcefully expelled by the mouth. A compensatory mechanism due to acidity of body because of decrease excretion of metabolic waste. PALE Due to decreased production of erythropoietin.