Diabetes Flashcards
What is diabetes?
A chronic disease characterized by elevated blood glucose levels.
How is glucose normally handled in the kidneys?
It is reabsorbed in the proximal tubule and not found in urine.
Why is glucose found in urine in untreated diabetes?
Transporters are saturated due to high blood glucose, leading to glucose excretion.
What are classic symptoms of diabetes?
Polyuria, polydipsia, polyphagia, and weight loss.
What hormone regulates blood glucose?
Insulin, produced by the pancreas.
What causes diabetes?
Low insulin levels or resistance to insulin.
What is insulin and Where is insulin synthesized?
Insulin is a peptide hormone and produced By β cells in the islets of Langerhans in the pancreas.
What triggers insulin release?
Increased blood glucose.
What does insulin do in liver, muscle, and fat cells?
Promotes glycogen synthesis (liver), protein synthesis (muscle), triglyceride synthesis (fat).
What ion is important for insulin action?
Extracellular potassium.
What are the three types of diabetes?
Type I, Type II, and Gestational diabetes.
What causes Type I diabetes?
Autoimmune destruction of β cells, leading to little or no insulin production.
What causes Type II diabetes?
Insulin resistance and eventual decline in insulin synthesis.
What are risk factors for Type II diabetes?
Age, family history, obesity, lack of exercise, heart disease, ethnicity.
What is gestational diabetes?
Diabetes that begins during pregnancy, usually midway.
What is diabetic retinopathy?
Damage to retinal capillaries due to hyperglycemia, leading cause of blindness most common cause of blindness in people under the age of 65.
What is diabetic nephropathy?
Characterized by proteinuria, decreased GFR, increased BP.
What drugs help prevent diabetic nephropathy?
ACE inhibitors and ARBs.
What is the major cause of death in Type II diabetes?
Cardiovascular disease (CVD). Heart attack and stroke resulting from a combination of hyperglycemia and altered lipid metabolism * Statins reduce cardiovascular events in patients with diabetes, regardless of their LDL cholesterol levels.
What causes diabetic foot ulcers?
Poor circulation and nerve damage, leading to infection and risk of amputation. common cause of hospitalization.
What are the 4 tests for diagnosing diabetes?
- Fasting plasma glucose, 2. casual plasma glucose, 3.OGTT, 4. glycosylated hemoglobin.
What is a diagnostic level for fasting plasma glucose?
Blood is drawn after fasting for at least 8 hours. > 7.0 mmol/L- then diabetes is diagnosed.
When is casual plasma glucose diagnostic?
> 11.1 mmol/L with classic symptoms. * Blood can be drawn at any time.
How is OGTT performed?
75g glucose dose, plasma glucose measured after 2 hours.
What is the target HbA1C for diabetes management?
< 7% of total hemoglobin.
What is the goal of diabetes therapy?
Maintain tight control of plasma glucose.
What are the target glucose levels?
Pre-meal: 4.0-7.0 mmol/L, Post-meal: 5.0-10 mmol/L.
What are BP and lipid targets and * Urine albumin to creatinine ratio in diabetes?
BP: <130/80, LDL <2.6, Triglycerides <1.7, HDL (men >1.0, women >1.3), * Urine albumin to creatinine ratio <30 mg/g
Why is exercise important in Type I and II diabetes?
Increases insulin sensitivity and glucose tolerance
Who discovered insulin?
Sir Frederick Banting.
What are insulin’s anabolic effects?
Promotes glycogen(liver and muscle), triglyceride(adipose), and protein synthesis(muscle). Decreased hepatic gluconeogenesis (i.e. glucose synthesis).
What are effects of insulin deficiency?
Catabolic: glycogenolysis, gluconeogenesis, decreased glucose utilization.
What are the insulin types by duration?
Short-rapid, short-slow, intermediate, long.
Name 3 short duration rapid acting insulins.
Lispro, aspart, glulisine. “LAG before you eat!” SubQ or IV, clear
What is the only short duration slower acting insulin? When is slower-acting insulin used?How does it act slower
Unmodified human insulin.Before meals (for post-meal glucose control) Infused for basal (steady) control, By subcutaneous or rarely IM injection. It forms dimers (small clusters) after injection, which slows absorption. Clear
What are intermediate insulins? Why are the actions delayed?
Neutral Protamine Hormone (NPH) insulin, Insulin Detemir. Not for post meals, but injected once or twice daily to control blood glucose between meals and in the evening.
o NPH insulin – is insulin conjugated to protamine (a large protein). The protamine makes the molecule less soluble and decreases the absorption. Cloudy.
o Insulin Detemir – Insulin detemir molecules bind strongly to each other which delays absorption. (remember Module 2?) Clear.
What is the long acting insulin?
Insulin glargine. administered by subcutaneous injection once daily at bedtime. its low solubility at physiological pH. When it’s injected, it forms microprecipitates that slowly dissolve and therefore release insulin glargine in small amounts over an extended time.
Which insulin can be mixed with short acting?
Only NPH insulin.
What is the main complication of insulin therapy?
Hypoglycemia. Symptoms : Tachycardia, Palpitation, Sweat, Nervousness (if it is fast hypoglycemia) CNS symptoms (When blood sugar drops slowly, your brain runs low on fuel — and glucose is the brain’s main energy source.) Drowsiness, Headache(stress response) Confusion, Fatigue.
How is hypoglycemia treated?
Oral sugar if conscious, IV glucose or glucagon if unconscious.
What does glucagon do?
Converts glycogen to glucose.
When is glucagon ineffective?
In starving or malnourished patients due to no glycogen stores.
Name the 6 classes of oral antidiabetic drugs.
Biguanides, Sulfonylureas, Meglitinides, Glitazones, Alpha-glucosidase inhibitors, Gliptins.
Big Sulk Meg Glided Across Glassy Glacia
How do biguanides work?
Increase insulin sensitivity, decrease gluconeogenesis, reduce glucose absorption.
What is a major benefit of biguanides?
No risk of hypoglycemia.
Main side effects of biguanides?
Nausea, diarrhea, decreased B12/folic acid, rare lactic acidosis.
How do sulfonylureas work?
Stimulate insulin release, inhibit glycogenolysis.
Main risk with sulfonylureas?
Hypoglycemia and pancreatic burnout.
How are meglitinides different?
Shorter half-life, less hypoglycemia risk.
How do glitazones work?
Activate PPARγ to increase insulin sensitivity and decrease gluconeogenesis.
Main glitazone side effects?
Edema, headache, myalgia.
How do alpha-glucosidase inhibitors work?
Delay carb absorption by inhibiting alpha-glucosidase in intestine.
Side effects of alpha-glucosidase inhibitors?
GI: flatulence, cramps, distention, diarrhea.
How do gliptins work?
Inhibit DPP-4 to increase incretins, leading to more insulin and less glucagon.
Do gliptins have major adverse effects?
No known major adverse effects.
What do incretin mimetics do?
Mimic GLP-1 and GIP to increase insulin, decrease glucagon.
Side effects of incretin mimetics?
Hypoglycemia, pancreatitis.
Type 1 Diabetes Management/ Life Style Modification
Maintain weight, not lose it. Total calorie intake is split into meals 4-5 hours apart. Exercise but not strenuous because that may cause hyperglycemia. Insulin needed. BG lvl checks 3 or more per day.
Lifestyle Modifications – Type II Diabetes
Diet modification and lose weight. Excercise.
