What is polyuria?
What is polydipsia?
What is polyphagia?
What is Ketonuria?
production of abnormally large volumes of dilute urine.
abnormally great thirst as a symptom of disease (such as diabetes) or psychological disturbance.
A medical sign meaning excessive hunger and abnormally large intake of solids by mouth.
the excretion of abnormally large amounts of ketone bodies in the urine, characteristic of diabetes mellitus, starvation, or other medical conditions.
What are the 2 hormones secreted by the pancreas? and what do they do?
Insulin and glucagon.
Insulin: It helps control blood glucose levels by signaling the liver and muscle and fat to take in glucose form the blood to be used as energy. - if the body has sufficient energy, insulin signals the liver to take up glucose and store it as glycogen.
Glucagon: It is produced by alpha cells in the pancreas. It signals the liver to release stored glucose from its cells into the blood, when there is low glucose. When blood glucose is high, glycogen is not produced.
What are the most important aspects of endogenous insulin? How much is secreted in adults?
It facilitates the passage of glucose into cells for energy.
Protein hormone secreted by the beta cells in the pancreas.
pancreas secrets 1-2 units/hr AND additional of 4-6 units/hr after meals. (average daily of 40-60 units/day)
Insulin is secreted into the portal circulation and transported into the liver.
Insulin binds and activates receptors on the cell membrane to become permeable for glucose.
Insuline is cleared from the blood in about 15 mins.
What are the main differences b/t type I and type II diabetes? alternative names? age of onset? speed of onset? family history? Prevalence? Etiology? Primary defect?
TYPE I: insulin-dependend/juvenile-onset/ketosis-prone diabetes mellitus,
TYPE II: Non-insulin-dependent/adult-onset diabetes mellitus.
TYPE 1: Usually childhood or adolescence.
TYPE 2: usually over 40.
TYPE I: abrupt
TYPE II: Gradual.
TYPE 1: Usually negative.
TYPE 2: frequently positive.
TYPE I : 5 to 10 % of diabetics have type 1.
TYPE II: 90 to 95% of diabetics have type 2 diabetes.
TYPE 1: autoimmune process.
TYPE 2: Unknown- but there is a strong familial association, suggesting heredity is a risk factor.
TYPE I: loss of pancreatic beta cells.
TYPE II: Insuline resitance and inappropriate insulin secretion.
What are the main differences b/t type I and type II diabetes? Insulin levels? treatment? blood glucose? symptoms? body composition? ketosis?
TYPE I: reduced early in the disease and completely absent later.
TYPE II: levels maybe low (indicating deficiency), normal, or high (indicating resistance)
TYPE 1: Insulin replacement is mandatory, along with strict dietary control; oral hypoglycemic drugs are not effective.
TYPE 2: Exercise and reduce calorie diet may be sufficient; if not an oral hypoglycemic agent and/or insulin is required.
TYPE I: Levels fluctuate widely in response to infection, exercise, and changes in caloric intake and insulin dose.
TYPE II: levels are more stable than in type 1.
TYPE 1: polyuria, polydipsia, polyphagia, weight loss.
TYPE 2: may be asymptomatic.
TYPE I: Usually thin and undernourished.
TYPE II: Frequently obese.
TYPE 1: Common, especially if insulin dosage is insufficient.
TYPE 2: uncommon.
What is diabetic Ketoacidosis? Symptoms? Treatment?
It is an acute condition that occurs primarily in type I diabetes.
It occurs as a result of altered energy metabolism (fats) in the cell from the lack of insulin.
High potassium and low sodium level (acidosis - pH is less than 7) - Insulin could diffuse this problem and bring potassium to the right level.
Common symptoms polyuria, gastrointestinal upset, and abdominal pain.
What drug is in the biguanides group? MA? PK? TU? SE? and Toxicity?
Merformin is the drug in this group.
MA: It lowers blood glucose and improves glucose tolerance in 3 ways. 1) inhibits glucose production in the liver 2) reduces glucose absorption in the gut (slightly) 3) it sensitizes insulin receptors (increase glucose uptake).
* it does not stimulates insulin release from pancreas, therefore, no hypoglycemia risk.
PK: absorbed in the small intestine, it is not metabolized, hence in the case of renal impairment, it could be toxic.
TU: Used for type II diabetes, ppl who skip meals, gestational diabetes, and PCOS (polycystic overian syndrome)- works better in combination.
SE: Decrease appetite, nausea, diarrhea. Decreased absorption of B12 and Folic acid. Pts loose average of 7-8 pounds.
Toxicity: Lactic acidosis (renal insufficiency pts), increased lactic acid production (heavy alcohol consumers, liver disease pts), iodinated radio contrast media may intensify acidosis (contrast CAT scans)
Sulfonylureas? how are they classified? examples? MA? TU? AE?
First oral hypoglycemics: Stimulates the pancreas to increase insulin secretion, increase glucose utilization in tissue, and decrease hepatic gluconeogenesis. - ide suffix.
First generation: controversy bc they cause cardiovascular toxicity (not used as much anymore) - T,A,C - mide
1st gen ex: Tolbutamide, Acetohexamide, Tolazamide, chlorpropamide.
Second generation agents: better. G-ide
2nd gen EX: Glipizide (glucotrol), glyburide (DiaBeta), Glimepiride (amaryl).
MA: promote insulin release from the pancreatic islets. increased glucose utilization in tissue, and decreases hepatic gluconeogenesis in liver.
TU: type II diabetes only. No effect in type I.
AE: the main adverse effect is hypoglycemia.
What are the most common combinations of hypoglycemics?
Metformin and second generation sulfonylureas.
SGLT2 inhibitors? MOA? examples? AE?
Sodium glucose co-transporter 2. -ozin suffix.
MOA: block the reabsorption of glucose in kidney, increase glucose excretion, and lower blood glucose levels.