Diabetes drugs
- 2. -GLUT-5 is also the main transporter of FRUCTOSE
- 3. Starch/Saccharides In diet Decreases gastric emptying Alpha glucosidase Release of Insulin Increases Ca entry Depolarisation ATP formed from glucose inhibits ATP-K+ channels Stimulates GLUT-2 receptors On Beta islet cells Glucose enters circulation Releases Insulin & amylin Stimulates Pancreas Increases release of Incretin or GLP-1 Enters intestinal epithelial cells Glucose Increases GLUT-4 on surface of cells Metabolised by DPP-4 Enzyme - Gliptins -Acarbose voglibose + Exenatide Liraglutide - Meglitinides Sulfonylureas Amylin analogue: Pramlinitide
- 4. -This drugs inhibits conversion of starch into glucose accumulation of starch S/E:Flatulence>Diarrhoea Prevents rise in glucose levels During both prandial and post- Prandial levels (But not pre- Prandial) Acarbose reduces fibrinogen levels but also several other markers of inflammation are reduced.
- 5. -Acarbose -Voglibose -Miglitol Used as an add on drug in Type-2 DM Absorbed in systemic circulation,hence dose is reduced In Renal Failure.
- 7. ULTRA-SHORT Short Intermediate Ultra long Glulisine Regular NPH Glargine Lispro Semi-lente Lente Detemir Aspart Onset=20min Duration=4min Onset= 1hr Duration=6-8hrs Duration=16hrs
- 9. Smooth and peakless effect is caused by : Glargine & Detemir Insulin increases K+ and Glucose uptake by cells and thus leads To Hypokalemia
- 11. Glargine has a acidic pH. So not mixed with other insulins Other all Insulins are Neutral Insulins.
- 16. 1st Generation 2nd Generation Chlorpropamide Glybenclamide Tolbutamide Gliclizide Acetohexamide Glyburide Causes Hepatotoxicity ( Mnemonic; T for tolbutamide and there are 3Ts in hepatotoxicity) Causes SIADH and Disulfiram like reaction
- 18. -Insulin Secretagogues i.e they stimulate Insulin Release. -Max. potency among sulfonylureas = Glyburide -C.I. in = Liver disease Renal Disease Pregnancy/Lactation -S/E: Hypoglycemia Weight Gain -Causes maximum decrease in HbA1C levels ( 2nd : Biguanides) and increases C-peptide values -Long acting(Max.; Chlorpropamide) and hence increases insulin for long time whereas meglitinides are short acting.
- 19. -Short acting Insulin secretagogues. -Hence used for Post-prandial Hyperglucemia -Metabolised in liver and excreted in Kidney. Hence, dose to be reduced in both liver and renal failure. -Rapeglinide -Nateglinide
- 22. -Metformin = S/E: Vit. B12 deficiency -Phenformin = S/E : Lactic acidosis -Reduces gluconeogenesis -Decreases hepatic glucose production -Decreases insulin resistance -Increases lipid oxidation = Decreases LDL levels -Decreases gastric emptying -Contra-Indication : Renal Failure MC side effect of Metformin : Dyspepsia
- 23. 1) Causes weight loss 2) PCOD 3) Metabolic Sx in HIV 4) Non alcoholic fatty Liver disease
- 24. Q. Only anti-daiabetic group which causes weight loss ??
- 25. Ans. Biguanides
- 27. Stimulates PPAR-@ Increase transcription factors for GLUT-4 Production Increase GLUT-4 receptors on tissue cells But still requires Insulin to bring glucose to cells so that glucose can be taken up by cells. - They decreases Insulin Resistance -Metabolised in Liver -Safe in Renal Failure
- 29. 1) Weight gain 2) Sodium and water retention 3) Macular edema 4) Increase risk of bone fracture in childrens.
- 30. -This inhibitors prevent glucose reabsorption and thus eliminates excess glucose in Urine
- 31. -Canagliflozin -Dapagliflozin -Empagliflozin Decreases sodium and glucose reabsorption Increase Glucose In Urine UTI & Vaginal Infection Glucose is a good media for bacterial growth MC Side Effect
- 32. 1) Bromocriptine 2) Colesevelam 3) Pramlintide : Amylin Analogue Can be given in both Type1 and Type 2 DM
- 33. Qn. Anti-diabetic drug which can be given Sub-cutaneous
- 34. Ans. Pramlintide
- 35. Group Main Side Effect Alpha glucosidase Inhibitor Flatulence/Dyspepsia SGLT-2 Inhibitors UTI & Vaginal infections Gliptins Steven Johnson Sx Thiazolidinediones Water retention/Macular edema Insulin Hypoglycemia/ Lipodystrophy Chlorpropamide SIADH/Disulfiram like reaction Tolbutamide Hepatotoxicity Metformin Vit. B12 deficiency Phenformin Lactic acidosis Meglitinides Hypoglycemia
- 36. 1)Q. A 45-year-old woman presents to your office with a serum glucose of 250 mg/dL and you diagnose diabetes mellitus type II. You intend to prescribe the patient metformin, but you decide to order laboratory tests before proceeding. Which of the following basic metabolic panel values would serve as a contraindication to the use of metformin? A. K+ > 4.0 B. Na+ > 140 C. HCO3- > 30 D. Creatinine > 2.0
- 37. Metformin is absolutely contraindicated in patients with renal failure due to the risk of lactic acidosis. An elevated serum creatinine suggests a decrease in GFR and the presence of renal failure. Metformin is a drug in the biguanide class used to treat diabetes mellitus type II. Metformin treats hyperglycemia by inhibiting gluconeogenesis. Metformin carries no risk of hypoglycemia, but is known to occasionally cause lactic acidosis in patients with renal failure, liver dysfunction, CHF, alcoholism, and sepsis. D. Creatinine > 2.0
- 38. 2.Q.A 45-year-old African-American male presents to the family medicine physician to assess the status of his diabetes. After reviewing the laboratory tests, the physician decides to write the patient a prescription for miglitol and states that it must be taken with the first bite of the meal. Which of the following bonds will be most likely affected by taking miglitol? 1. Phosphodiester bonds 2. Glycosidic bonds 3. Peptide bonds 4. Cystine bonds 5. Hydrogen bonds
- 39. The bonds that will be most likely affected by taking miglitol are glycosidic bonds. Miglitol is an alpha-glucosidase inhibitor that prevents the breakdown of disaccharides/polysaccharides into monomers by alpha-glucosidases located along the intestinal brush border. Miglitol prevents these bonds from being hydrolyzed. This delays sugar hydrolysis, resulting in a delayed glucose absorption. This is advantageous for patients with type II diabetes mellitus as it decreases postprandial hyperglycemia, thereby reducing insulin demand. Common side effects of these inhibitors are upset stomach, diarrhea, and flatulence. 2. Glycosidic bonds
- 40. 3.Q. A 60-year-old African-American female presents to your office complaining of dysuria, paresthesias, and blurry vision. Her body mass index is 37.2 kg/m2. Which of the following drugs would most significantly increase the levels of C-peptide in the blood when administered to this patient? 1. Metformin 2. Insulin 3. Glipizide 4. Acarbose
- 41. Glipizide is a second generation sulfonylurea that triggers release of insulin from pancreatic beta cells. Increased release of endogenous insulin results in elevated levels of C-peptide in the blood. This patient's presentation is consistent with type II diabetes mellitus. Dysuria due to a urinary tract infection (the presence of glucosuria creates a good growth media for bacteria with subsequent increased risk of UTI), paresthesia due to diabetic neuropathy, blurry vision due to osmotic damage of the lens of the eye, and obesity are all associated with diabetes. Glipizide is used in the treatment of diabetes type II only. 3. Glipizide
- 42. 4.Q. A patient presents to the emergency room in an obtunded state. The patient is a known nurse within the hospital system and has no history of any medical problems. A finger stick blood glucose is drawn showing a blood glucose of 25 mg/dL. The patient's daughter immediately arrives at the hospital stating that her mother has been depressed recently and that she found empty syringes in the bathroom at the mother's home. Which of the following is the test that will likely reveal the diagnosis? A. C-peptide level B. 24 hr cortisol C. Fasting blood glucose D. Urine metanephrines
- 43. This patient is presenting with severe hypoglycemia likely secondary to exogenous administration of insulin. C-peptide is the portion of pro-insulin that is cleaved away within the pancreatic beta cell. In normal physiology, c-peptide is present within the circulation in equimolar concentrations with insulin. With the exogenous use of insulin, additional c-peptide is not present within the circulation. This scenario of hypoglycemia often occurs in individuals failing to administer insulin correctly or in healthcare workers wishing to harm themselves. An insulin producing tumor should also be on the differential diagnosis for these patients. A. C-peptide level
- 44. 5.Q. A simple experiment is performed to measure the breakdown of sucrose into glucose and fructose by a gut enzyme that catalyzes this reaction. A glucose meter is used to follow the breakdown of sucrose into glucose. When no enzyme is added to the sucrose solution, the glucose meter will have a reading of 0 mg/dL; but when the enzyme is added, the glucose meter will start to show readings indicative of glucose being formed. Which of the following diabetic pharmacological agents, when added before the addition of the gut enzyme to the sucrose solution, will maintain a reading of 0 mg/dL? 1. Insulin 2. Glyburide 3. Metformin 4. Acarbose
- 45. The gut enzyme that is added to the solution is most likely alpha-glucosidase. The only agent that will inhibit the enzyme from breaking down sucrose into glucose and fructose thus showing a 0 mg/dL reading on the glucose meter is acarbose. Acarbose and miglitol are alpha-glucosidase inhibitors that prevent the breakdown of disaccharides and polysaccharides into monomers by alpha-glucosidase located along the intestinal brush border. This delays sugar hydrolysis resulting in a delayed glucose absorption. This is advantageous for patients with type II diabetes mellitus as it decreases postprandial hyperglycemia, thereby reducing insulin demand. Common side effects of these inhibitors are upset stomach, diarrhea, and flatulence. 4. Acarbose
- 46. 6.Q. A 55-year-old male is hospitalized for acute heart failure. The patient has a 20-year history of alcoholism and was diagnosed with diabetes mellitus type 2 (DM2) 5 years ago. Physical examination reveals ascites and engorged paraumbilical veins as well as 3+ pitting edema around both ankles. Liver function tests show elevations in gamma glutamyl transferase and aspartate transaminase (AST). Of the following medication, which most likely contributed to this patient's presentation? 1. Glargine 2. Glipizide 3. Metformin 4. Pioglitazone 5. Pramlintide
- 47. Weight gain, edema (fluid retention), hepatotoxicity, and heart failure are toxicities associated with pioglitazone. The drug should not be administered to patients with heart failure or liver disease. Pioglitazone and rosiglitazone are thiazolidinedione derivatives that reduce insulin resistance in patients with DM2. They are occasionally used as monotherapy for DM2 but are most often combined with other hypoglycemics. The drugs are also used to treat polycystic ovarian syndrome. 4. Pioglitazone
- 48. 7.Q. A 53-year-old male presents to your office for a regularly scheduled check-up. The patient was diagnosed with type II diabetes mellitus two years ago. To date, diet, exercise, and metformin have failed to control his elevated blood glucose. Past medical history is also significant for hypertension. The patient does not smoke or use cigarettes. Laboratory values show a hemoglobin A1c (HbA1c) of 8.5%. You decide to add sitagliptin to the patient’s medication regimen. Which of the following is the mechanism of action of sitagliptin? 1. Inhibits degradation of endogenous incretins 2. Inhibits alpha-glucosidases at the intestinal brush border 3. Activates transcription of PPARs to increase peripheral sensitivity to insulin 4. Depolarizes potassium channels in pancreatic beta cells 5. Increases secretion of insulin in response to oral glucose loads and delays gastric emptying
- 49. Sitagliptin is a dipeptidyl peptidase 4 (DPP-4) inhibitor. This class of drugs acts to inhibit degradation of the endogenous incretins GLP-1 and GIP. Incretins are a group of gastrointestinal hormones that increase the amount of insulin released from the beta cells of the islets of Langerhans after eating. They begin to act before blood glucose levels become elevated. Incretins also inhibit glucagon release from alpha cells of the islets of Langerhans. DPP-4 inhibitors block degradation of incretins and promote enhanced insulin secretion. 1. Inhibits degradation of endogenous incretins