Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Endocrine
Exam 2: Diabetes: Dr. Yendapally Material
| Question | Answer |
|---|---|
| Which drugs fall into the GLP-1 agonist class? | Exenatide, Liraglutide, Dulaglutide, Semaglutide |
| Which drugs belong to the GIP/GLP-1 drug class? | Tirzepatide |
| Which drugs belong to the amylin agonist drug class? | Pramlintide |
| Which SUs are 1st gen? | Chlorpropamide, Tolbutamide, Tolazamide |
| Which drugs fall into the meglitinide class? | Repaglinide and Nateglinide |
| Which drugs fall into the a-glucosidase inhibitor class? | Acarbose and Miglitol |
| Where is insulin secretion from? | B cells of iselt of Langerhans |
| What hormone promotes the storage of glucose? Where does this occur? | Insulin promotes storage of glucose as glycogen, in the liver and muscle |
| Composition of insulins stucture? | 51 amino acid peptide |
| Onset of short acting insulin? Duration? | 0.5-1 hour, lasts 6-8 hours |
| How is insulin lispro created from regular insulin? | Changes the B28 Pro to Lys, and B29 Lys to Pro, swaps proline and lysine at B28-29 |
| Onset of action and duration of rapid acting insulins? | Onset 15 min, lasts 4 hours |
| Duration of action of inhaled insulin? | 90-270 minutes |
| CI for inhaled insulin (afrezza)? | Chronic lung disease or bronchospasms |
| What does NPH stand for? | Neutral protamine Hagedorn |
| Onset and duration of NPH insulin? | Onset of 2 hours, duration of 12-18 hours |
| Which insulin has a cloudy appearance? | NPH |
| Which insulin is positively charged? | NPH |
| How is aspart made from regular insulin? | Pro swapped for Asp |
| How is Glulusine made from regular insulin?? | Lys swapped for Glu |
| Onset and duration of Glargine? | Onset of 2 hr, lasts 20-24 hours |
| How is Glrgine made from regular insulin? | Change Asn to Gly, *add Arg to B31-32 |
| Aside from the added structures, what gives glargine its long acting properties? | Its acidic nature allows it to precipitate at body pH, allowing for slow dissolution of the formed micro-crystals |
| How is insulin detemir made from regular insulin? | Removes Thr, adds C14 fatty acid chain (myristic acid) |
| What allows for the long duration of Detemir? | Fatty acid chain that is added binds to plasma albumin to produce longer action |
| Onset and duration of Detemir? | Onset of 2 hr, lasts 12-24 hour |
| Which insulin product is the longest acting and is considered ultra-long acting? | Degludec (Tresiba) |
| How is Deglucdec made from regular insulin? | Removes Thr, adds glutamic acid and a hexacanedioic fatty acid |
| Onset and duration of degludec's action? | Onset of 1 hour, lasts > 24 hours |
| Which insulin has an Arg added to it? | Glargine |
| Which insulin has a 14 Carbon fatty acid chain (myristic acid)? | Detemir |
| Which insulin product swaps Lys and Pro? | Lispro |
| Which insulin product has a Hexa-decanedioic fatty acid added to it? | Degludec |
| Which meds can have hyperglycemic activity? | Glucocorticoids, Niacin, Diuretics (thiazides), Phenytoin (Hydantoins), Atypical antipsycotics (2nd gen APs) |
| Which meds can have hypoglycemic activity? | Oral diabetes meds, ACEi Salicylates |
| Where does GLP (incretin) act in the body? | Pancreas (B-cells), GI tract, brain (causes satiety) |
| Incretin is short for? | Intestinal secretion insulin |
| Structure of incretin? | 37 amino acid peptide |
| Effects of incretin on physiology? | Increases insulin secretion Decreases glucagon secretion Delays gastric emptying Decreases food intake |
| Why do we give GLP-1 agonists instead of just giving GLP-1 itself? | GLP-1 is rapidly hydrolyzed by DPP-4 and giving GLP to a DM patient would have little/no clinical effect. Using GLP-1 receptor agonists or DPP-4 inhibitors are far more effective |
| Where does DPP-4 bind on the GLP-1 structure? | Between Ala-8 and Glu-9 |
| Brand name of Exenatide? | Byetta |
| DDIs of GLP-1 agonists? | Can delay absorption of oral medications (since they slow gastric emptying) |
| BBW for GLP-1 agonists? | Risk of thyroid tumors |
| Half life of exenatide IR vs ER? | IR: 3-4 hours (BID dosing) ER: 2 weeks (QW dosing) |
| Which drug utilized microspheres? | Exenatide ER (bydureon) |
| Which GLP-1 agonist has the lowest homology to human GLP-1? | Exenatide with 53% homology, other GLP-1 agonists range between 90-100% homology |
| How is liraglutide different from human GLP-1? | It has a 16C fatty acid side chain added to Lys-26 |
| Half life of Liraglutide (victoza) ? | 13 hours, given QD |
| Which GLP-1 drug has a Modified IgG4 Fc Domain? | Dulaglutide (trulicity) |
| Half life and dosing freq of dulaglutide (Trulicity)? | Half life of 5 days, given QW |
| Which GLP-1 agonist has a alpha-aminoisobutyric acid and a C18 fatty di-acid side chain? | Semaglutide |
| Dosing Freq of SQ and oral semaglutide? | Oral: QD SQ: QW dosing |
| Which GLP-1 agonist is the newest? | Tirzepatide (Mounjaro or Zepbound) |
| How is tirzepatide different vs human GLP-1? | Has an added C20 fatty di-acid moiety |
| What is the function of amylin? Where is it released? | Amylin works alongside insulin to control blood sugar, it slows gastric emptying, promotes satiety, and suppresses glucagon. It is secreted by the B-cells, like insulin |
| Why is Amylin itself NOT used as a drug? | It self-aggregates and it is insoluble in solution, using an Amylin agonist is more practical and effective |
| Which drug(s) are Amylin agonists? | Pramlintide |
| How is pramlintide different from human amylin? Why is this important? | It is substituted with Proline, which decreases self-aggregation and increases water solubility |
| Metabolism of pramlintide? | Des-lys1 pramlintide is the active form |
| Which DM medications are non-peptides? | SUs, meglitinides, biguanides, TZDs, DPP-4s, a-glucosidase inh, SGLT-2 |
| What is the base structure of a SU? | Benzene ring with a sulfonylurea, with an R group at both ends of the molecule |
| MOA of SU? | Stimulate insulin release |
| How do SUs stimulate insulin release? | Binding to SUR of ATP-K channel on B-cells |
| Structurally speaking, how can we differentiate 1st and 2nd gen SUs? | First gen: small substitution with cyclic AND not cyclic groups 2nd gen: bulky substituion with ONLY cyclic R groups |
| Which SU has the shortest Half-life? | Glipizide, 2-4 hour half-life |
| Why do we heavily prefer 2nd gen over 1st gen SUs? | 2nd gen SUs are more potent and half less DDIs |
| ADRs and warnings for SUs? | Can cause hypoglycemia and increase CV risk |
| Meglitinide structure? | Core structure has a benzene ring with Cl and OCH3 groups |
| MOA of meglitinides? | Stimulates insulin release |
| Which drugs are meglitinides? | Repaglinide and Nateglinide |
| Which meglitinide is selective to the SUR1 receptor? | Nateglinide |
| MOA of metformin? | Lowers hepatic glucose production Increases glucose utilization |
| Advantages of metformin? | Improves lipid profile (lower free FA concentrations) Weight neutral No hypoglycemia |
| DDIs of metformin? | Cimetidine can increase metformin con Contrast agents (may increase metformin ADRs) |
| CIs of metformin? Why? | Renal disease, since metformin is eliminated by active tubular secretion in kidneys |
| MOA of TZDs? | Stimulates PPARy |
| What is the effect of stimulating PPARy? | Increases insulin sensitivity Increases glucose uptake |
| DDIs of TZDs? | DDIs with 2C8 inhibitors (gemfibrozil) or inducers (rifampin) |
| ADRs of pioglitazone? | CHF (rapid weight gain and edema), increased bone fractures in women |
| What is the effect of inhibiting DPP-4? | Increases beta-cell sensitivity to glucose (increases insulin secretion) Delayed gastric emptying Suppresses glucagon |
| Which DPP-4 has a piperazine ring + pyrazole ring? | Sitagliptan |
| Which drug has multiple fluorine groups? | Sitagliptin |
| Which DPP-4 has a nitrile group? | Saxagliptin |
| Which DPP-4 is most potent? | Saxaliptin |
| What is the function of a nitrile group in a DPP-4 (specifically saxagliptin)? | Forms covalent bond with Ser630, making it irreversible |
| Unlike all the other DPP-4s, which drug is eliminated mostly via feces | Linagliptin |
| MOA of a-glucosidase inh? | Prevent hydrolysis of carbs, lowers the rate of absorption |
| Which drugs are a-glucosidase inhibitors? | Acarbose and Miglitol |
| Absorption profile of a-glucosidase drugs? | Acarbose: minimal absorption Miglitol: Complete absorption |
| Which drugs (aside from metformin) may lead to ketoacidosis? | SLGT-2 |
| Core structure of SLGT-2 drugs? | 6 member ring with an O with multiple OH groups on it |
| Which drug is a dual SGLT inhibitor (inhibits SGLT 1 and 2)? | Sotagliflozin |
Created by:
cdaughtry