Diabetes Flashcards
(34 cards)
Glucagon
- Synthesized in the Liver**
- Breaks down fats and muscles / not simple carbs
- Helps maintain steady blood glucose when you have used all simple carbohydrates
- GLUCAGON IS FOR WHEN GLUCOSE IS GONE
Risk Factors after Liver Biopsy
- Assess the lungs for: ** PRIORITIZE THE LUNG COLLAPSE
- NOTHING - collapsed lung - silent lung - Bleeding
- Clotting factors come from the liver so check for bleeding if there are liver issues
Diabetes Type 1
- Juvenile-onset diabetes
- Results from autoimmune process that destroys beta cells of the pancreas
- Leads to loss of insulin production
Diabetes Type II
-Pathophysiology
- Adult-onset diabetes
2. Insulin Resistance
Diabetes Type II
-Risk factors
- Age
- Obesity
- Family Hx
Diabetes Type II
-Process
- Increases insulin secretion to compensate for peripheral tissue resistance until system fails
- If pancreas “burns out” then the type II diabetic will need insulin replacement just like a Type I diabetic
Diabetes
-Definition
- Starvation in the midst of plenty
Hyperglycemia
-S/S
- Weight loss
- Polyphagia (excessive appetite)
- Elevated blood glucose
- Increase infections
- Polydypsia
- Polyuria
Normal Fasting Plasma Glucose
- < 126 mg/dL
Normal Random plasma Glucose
- <200 mg/dL
Normal 2 hr Post-Glucose Tolerance test
- Plasma glucose < 200 mg/dL
HBA1C
- Refers to the permanent attachment of glucose to hbg molecules and reflects the average plasma glucose exposure over the LIVE OF THE RBC
Process of Inulin Production
- Islets of langerhan (Beta cells) in the pancreas produce insulin in response to blood glucose levels.
- Insulin is the bus that drives glucose into the cell
Type 1 Diabetes
-Pathologic process
- Autoimmune disease that causes immune system to attack beta cells in the pancreas.
- Pt then loses insulin production capabilities
Type 2 Diabetes
-Pathologic process
- Insulin resistance
- Beta cells and islets of langerhans are capable of producing insulin
- Cells that are receiving the insulin are resistant
Type 2 Diabetes
-What happens over time
- Blood glucose increases because insulin cannot move it into the cell.
- The pancreas then goes into overdrive and produces large amounts of insulin
- After years, the pancreas and beta cells cannot compensate and insulin levels drop. Blood glucose levels then go well above normal
Type 1 Diabetes Complications
-Diabetic Ketoacidosis (DKA) Causes
- Caused by increase glucose demand from a stressor (infection)
or - Pt stops taking insulin administration
Type 1 Diabetes Complications
-Diabetic Ketoacidosis (DKA) Manifestations
- Blood Glucose becomes VERY high
- Cells shift to using proteins and lipids for energy because there is not enough insulin moving glucose into the cell
- Breakdown of proteins and lipids causes Kitone bodies
Insulin
-Na/K pump
- Insulin is the regular of the sodium/potassium pump. If insulin is not present there is hypokalemia inside of the cell.
- When insulin is restored, the serum potassium can drop very quickly to compensate for the intercellular hypokalemia
Diabetes
-Long-term Effects
- Due to hyperglycemia in the cell which causes damage to the endothelial and atherosclerosis
Glycolysis
- = ATP
2. Storage as: Glycogen (glycogenesis), fat and protein
Hyperglycemia
-S/S
- Weight loss
- Polyphagia (excessive appetite)
- Elevated Blood glucose
- Increased infections
- Polydypsia
- Polyuria
Hyperglycemia
-Diagnostics
- Fasting plasma glucose greater than 126 mg/dL
- Random plasma glucose greater than 200 mg/dL
- w/ polyuria & polydipsia - 2 hour post glucose tolerance test with BG level greater than 200mg/dL
Hyperglycemic Treatment
-For High Blood Sugar?
- Reduce pt’s sugar intake
2. Metformin (decreases hepatic gluconeogenesis