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Type 1 Diabetes Aetiology: Autoimmune destruction of the beta cells located in the pancreas, both genetic predisposition (Parent/s have type 1 Diabetes) and environment factors (virus: mumps, rubella and toxic chemicals.) upper respiratory infection triggers involved in type 2 Diabetes often referred to as childhood diabetes due to the age of patients diagnosed with this form.
Type 1 Diabetes Pathophysiology: Autoimmune- Anti islet antibodies attack through Lymphocyte infiltration and destruction of the insulin secreting beta cells of the langerhans within the pancreas.
Destruction of beta cells > Beta cells decline> insulin secretion decreases until insulin is no longer available to maintain normal blood glucose levels.>Beta cells
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Diabetic Ketoacidosis is a condition of Insulin deficiency and hyperglycaemia resulting in metabolic acidosis and severe osmotic diuresis. An inadequate amount of the hormone insulin that the body requires to enable the cells to use the glucose as energy triggers the breakdown of fatty acids for energy use by cells leading to increased formation of acids called ketones in blood and urine.
The kidney’s inability to excrete ketones and cells are unable to use ketones resulting in ketones building up in blood. Blood glucose levels increased as the liver produces glucose in an attempt to correct the body to homeostasis.
Acidosis occurs with a blood ph balance becomes less than 7.35 and cellular injury occurs in addition hyperglycaemia accompanies osmotic diuresis as the kidneys cannot absorb the glucose and its leaked into urine causing water to move by osmosis from blood to urine resulting in electrolyte loss of salt and water causing dehydration.
DKA develops from an increased demand of insulin during periods of stress, infection, severe illness, inadequate insulin production or administration.
In Joan’s case it could possibly be due to her type 2 Diabetes where her body is unable to make adequate insulin or insulin resistant as her doctor recently
The blood glucose level has very limited range for humans to survive and stay healthy. Generally, people are able to remove excess glucose rapidly from the body but this is not the case when they are diagnosed with diabetes and insulin resistant situations. The lack of insulin resistance can also lead to a decrease in glycogen synthesis and storage as it usually converts glucose to energy for cell’s use (Jensen & et al. 2011). When insulin is produced under insulin resistance, the cells are incapable of using them effectively which then leads to high blood sugar level as ketones and ketoacids are produced as an alternative energy source for the body. The rise of ketoacid causes the blood pH acidic and the patient may also be diagnosed with ketoacidosis (Newton & Raskin 2004). There would also be less intake of lipid and more of stored triglycerides as the lipids are effected by the insulin. As the glucose levels increase, the muscle glucose uptake will decrease while the liver glucose production and blood fatty acid concentration will also increase within the body (Lichtenstein & Schwab 2000). Excess glucose within the blood are converted to fat which can lead to Diabetic Dyslipidaemia and furthermore to obesity, hypertension and
DKA is presented with three major physiological disturbances which are hyperosmolality due to hyperglycemia, metabolic acidosis because of the buildup of ketoacids, and hypovalemia from osmotic diuresis. Diabetic ketoacidosis is caused by a profound deficiency of insulin, its most likely occur in people with type 1 diabetes, inadequate insulin dosage, poor self management, undiagnosed type 1 diabetes, illnesses and infections. In type 1
Ketosis is the metabolic state that most of the body's energy supply comes from ketone bodies in the blood, contrasting to the state of glycolysis in which blood glucose provides most of the energy (Taubes, 2011, 140-141). Ketosis might be better known as acetone breath, a common symptom of progressing diabetes mellitus type. It is characterized by serum concentrations of ketone bodies, with low and stable levels of insulin and blood glucose. It is commonly generalized with hyper-ketonemia, which is an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis as the liver glycogen stores are depleted (Taubes, 2011, p.155). The ketone bodies used for energy are acetoacetate and beta-hydroxybutyrate, with that, the levels of ketone bodies are regulated mainly by glucagon and insulin (p.156). Most cells can then be used by both glucose and ketone bodies for fuel, and during ketosis, free fatty acids and glucose synthesis fuel the rest.
Diabetic acidosis is due to an increased amount of ketones in the bodies of those suffering from uncontrolled diabetes. Diabetics rely upon insulin as fuel to “run” the body and when the body is unable to use glucose it uses fat. Ketones are the “waste” that is left after fat is broken down for fuel, they are acid and when they build up in a diabetic’s blood and eventually urine, their kidney’s are unable to dispel it as fast as it is being used (Wisse, 2013). Since ketones are acidic any impairment in removal of the ketones or continued uncontrollable diabetes will cause the sudden change that could cause life-threatening complications and severe illness.
Due to the lack of insulin patients with type I diabetes are unable to use glucose as their primary energy source, as a result their body switches to fat metabolism as its source of energy. As a result acidic ketones are produced as metabolic byproduct, this can be directly detected as a decrease in pH on ABG analysis. Patients with moderate to severe DKA have a blood pH ranging from 6.9-7.2, lowered bicarbonate levels and a carbon dioxide partial pressure in the rage of 15-20mmHg. The the cause of our patient her partial pressure of carbon dioxide was 15mmHg, bicarbonate was low and a blood pH of 7.14, these values suggest that the patient has metabolic acidosis and that the diagnosis of DKA is likely correct. While ABG analysis can be used to diagnose DKA several studies suggest that the ABG test results rarely effect a physicians diagnosis, treatment and management of the condition (3). In addition the same studies have shown that the pH venous of venous blood was precise enough to serve as a substitute to arterial pH analysis and is less painful for the patient
As we discuss acid and bases along with pH balance in blood a term that came to mind was Diabetic Ketoacidosis (DKA). This is a term that I have heard numerous times but didn’t not understand the meaning or cause. The term is commonly associated with diabetes but can also be associated with extreme exercise, low carbohydrate diets and eating disorders
Type 1 diabetes is also called insulin-dependent because the pancreas produce little to no insulin due to the destruction of beta cell in pancreas(Bardsley et al, 2004). Therefore, the insulin have to be injected manually for body to function normally. (Seewaldt et.al, 2000) states that in type 1 diabetes, the beta cell located in the islets of Langerhans have antigen that cause the immune system to produce antibodies and kill the insulin producing cells. The autoimmune response is thought to be caused by the autoreactive CD4 and CD8 effector cells that recognise islet self-antigens, as an outcome there is greater than 90% destruction on insulin producing cell BACH (1994). Similarly, (Nakayama et al,2005) and (Kent et al, 2005) supports that insulin in itself is a
Classic symptoms of diabetes usually presented with newly diagnosed diabetics are: hyperglycaemia, polyuria, polydipsia, polyphagia, fatigue, blurred vision, headaches, and unexplained weight loss. Ketone bodies are found in the urine, this abnormal finding occurs when fatty acid by-products (acetones) are excreted in the urine. The ketones are present from a lack of the insulin hormone used to metabolize fats and carbohydrates. Diabetic ketoacidosis (DKA) is a life-threatening complication which results from minimal useful insulin hormone in the body, hypoglycaemia, or insufficient food intake (American Diabetes Association, 2008).
Diabetic ketoacidosis is an event which occurs when there is not enough insulin in the body to utilize sufficient amount of glucose needed to provide cells with energy; body then starts to use fatty acids as a fuel, which are converted to ketones in the liver. In healthy people who do not have diabetes, ketone bodies are produced in normal quantities and then successfully used by tissues as energy supply. This state is known as dietary ketosis and it is completely normal and may even provide health benefits. But in those who have diabetes, ketones are produced in enormous quantities and aren't used in full by cells, so they start to build up in the blood. Acids 3-hydroxybutyric acid and acetoacetic acid are produced rapidly causing decrease in buffering capacity of the blood and eventually depleting buffering systems (Manninen, 2004).
Dehydration is induced by polyuria when the subject’s blood sugar is above 230mg/dL (hypoglycemic). The body’s loss of energy weakens the immune system and can cause easy limb loss if the skin is broken near the feat. Neuropathy (damage to the nerves) is due to the higher levels of sugar in the capillaries that feed the nerve endings. The sugar sticks to the sides of the capillaries and restricts the blood flow. The nerves in the eyes can also be damaged from the same process, leading to possible blindness. Polyuria can also damage the kidneys the same way alcohol can damage them. When the blood stream contains too much sugar or alcohol, the kidneys filter the excess out. When the kidneys are overused, the kidneys can shut down. The body needs glucose to function, and when the blood sugar drops below 20mg/dL, the brain makes the body go into a seizure. These seizures can be very dangerous and harmful to the body, leading to memory loss or personality changes; however, the body releases glucagon during the seizure causing the blood sugar to jump back to a tolerable
Counter regulatory hormones consist of cortisol, glucagon, growth hormone, and catecholamines. A rise in counter regulatory hormones cause insulin to not be utilize. This causes a rise in glucose, loss of fluids, loss of electrolytes, and ketosis (Kitabchi & Gosmanov, 2012). They worsen with the patient that has diabetic ketoacidosis because they increase glucose and ketone production in the liver when there is a severe decrease in insulin. This increases the ketone to even higher concentrations and the liver produces B-hydroxybutyrate. Ketones arise in the blood and may not
For unknown reasons, the body of a T1D attacks the insulin producing cells, called islets, that are formed in the pancreas and destroys them. This type of attack is known as an autoimmune disorder (Diabetes Research Institute Foundation [DRIF], n.d.). Insulin is the hormone that allows sugar to enter cells, and produce energy. The body now sees islet cells as foreign and eventually the pancreas yields little to no islet cells. Once there are no more islet cells to produce the insulin hormone the sugar levels in the blood become high, called hyperglycemia. This disturbance in homeostasis is not like type 2 diabetes (T2D), where the body becomes insulin resistant. In a T2D, the pancreas still produces islet cells and they are still
Diabetes type 2 is a condition in which blood sugar levels are too high. After eating foods that contain carbohydrates, chemicals in the small intestine break down the carbohydrates into simple sugar molecules called glucose. The cell lining in the small intestine absorb the glucose, which then passes into the bloodstream. When the blood reaches the pancreas, beta cells inside the pancreas detect the rising glucose levels. To reduce the glucose level, beta cells release insulin into the bloodstream. As the blood circulates through the body, the insulin and glucose exit the bloodstream into tissue to reach the body’s cells. Most cells of the body have certain receptors on their surface that bind to the circulating insulin. Insulin acts like a key in a lick to open up the cell so that the circulating glucose can get inside the cell. The cell can use the glucose to produce the energy it needs to function properly. If a person has insulin resistance, insulin cannot unlock the cells to let glucose in because the locks, called receptors, are abnormal and/or missing. As a result, glucose is locked out of the cells. The amount of glucose builds up in the bloodstream in a condition called hyperglycemia. To compensate for hyperglycemia, the pancreas produces more and more insulin. Overworked beta cells try to keep with the demand, but gradually lose their ability to produce enough insulin.
The disease of type two diabetes is largely due to the result of making consistently poor life style choices. It has been found that the disease of type two diabetes is largely caused by poor diet high in sugar, obesity, and also lack of exercise. It is possible that the disease of type two diabetes can also have a genetic factor, making the disease of type two diabetes hereditary. It has been found through research that there is a pre-condition that develops in people before the onset of the disease type two
Type 1 diabetes is an autoimmune disease that destroys beta cells, beta cells produce insulin in the the pancreas. When beta cells are destroyed It leads to lack of insulin, insulin lowers blood sugar (glucose). When immune system cells are seen it can also cause a viral infection.