Endocrine Flashcards
What is the Pathophysiology of Diabetes type 1
Type 1 DM is the destruction of insulin-secreting beta cells of the islets of Langerhans in the pancreas. As beta-cell mass declines, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels. After 80-90% of the beta cells are destroyed, hyperglycemia develops and diabetes may be diagnosed. Patients need exogenous insulin to reverse this catabolic condition, prevent ketosis, decrease hyperglucagonemia, and normalize lipid and protein metabolism. Currently, autoimmunity is considered the major factor in the pathophysiology of type 1 DM. In a genetically susceptible individual, viral infection may stimulate the production of antibodies against a viral protein that trigger an autoimmune response against antigenically similar beta cell molecules. Approximately 85% of type 1 DM patients have circulating islet cell antibodies, and the majority also have detectable anti-insulin antibodies before receiving insulin therapy. The most commonly found islet cell antibodies are those directed against glutamic acid decarboxylase (GAD), an enzyme found within pancreatic beta cells.
What is the Pathophysiology of type 2 Diabetes
Type 2 Diabetes Mellitus (T2DM) - one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin. Because insulin release and activity are essential processes for glucose homeostasis, the molecular mechanisms involved in the synthesis and release of insulin, as well as in its detection are tightly regulated.
What is the Pathophysiology of DKA
DKA – Increase in blood glucose and no insulin to uptake into cells. Body in response releases counter regulatory hormones such as cortisol, glucagon, adrenaline and growth hormone. This converts glycogen to glucose and proteins/lipids in glucose. This results in higher blood sugar levels. When this level exceeds the renal threshold excess glucose is excreted in urine which takes water and electrolytes with it (osmotic diuresis = polyuria, polydipsia). Also causes a shift of fluid from intracellular to extrasellar causing dehydration. Lipolysis occurs, fat into fatty acids (in the liver) for energy which produces ketone bodies (acetone = sweet smells) but are acidic which results in metabolic acidosis = Kusmal breathing (to blow it off). Hyperkalaemia in blood but once insulin is given, potassium is depleted.
What is the Pathophysiology of HHS
HHS- Develops slower then DKA (days). Absences of ketones as the amount of insulin present is higher enough to surpass lipolysis ( that’s why it happens in type 2 more often) Higher Blood glucose levels. Severe dehydration results in increased concentration of solutes in the blood. Raising osmolarity, hyper osmotic blood plasma drives water out of tissues and into blood causing cellular dysfunction. =altered conscious state.
What Does Insulin and Glucagon do
Insulin is produced in the islets of Langerhans (pancreatic islets), which are small isolated clumps of special cells in the pancreas. Insulin works alongside glucagon, another hormone produced by the pancreas, to manage the levels of glucose in your blood. Both insulin and glucagon are secreted directly into your bloodstream, and work together to regulate your blood glucose levels. Insulin should stop your blood sugar from rising too high and glucagon should prevent it from becoming too low. Insulin - is produced by the beta cells of the pancreatic islets. Insulin is released when you have just eaten a meal and the level of glucose in your bloodstream is high. It works by stimulating the uptake of glucose into cells, lowering your blood sugar level. Your liver and muscles can take up glucose either for immediate energy or to be stored as glycogen until it’s needed. Glucagon - is produced by the alpha cells of the pancreatic islets. It is released when your blood sugar levels are low (for example overnight, or if you have been fasting or exercising). Glucagon stimulates cells in the liver and muscles to convert stored glycogen to glucose. The glucose is then released into the bloodstream, raising your blood sugar level.
Pathophysiology of Hypoglycemia and Hyperglycemia.
Hyperglycemia
Hyperglycemia in a patient with type 1 diabetes is a result of genetic, environmental, and immunologic factors. These lead to the destruction of pancreatic beta cells and insulin deficiency. In a patient with type 2 diabetes, insulin resistance and abnormal insulin secretion lead to hyperglycemia.
Hypoglycemia
