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Flashcards in Endocrine Pharmacology Deck (31)
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Name the 3 rapid acting insulins, and their peak time.



What is the MOA of insulin in Liver, Muscle, Fat, and Cell Membranes.

Bind insulin receptor (tyrosine kinase activity).
Liver: Increase glucose stored as glycogen.
Muscle: increase glycogen, protein synthesis.
Fat: increase triglyceride storage.
Cell membrane: increase K+ uptake


Name the short acting insulin, and its peak time.

Regular - peak time 2-3hrs


Name the intermediate acting insulin, and it’s peak time.

NPH - 4-10hrs peak time


Name the 3 long acting insulins, and their peak times.

Detemir (Levemir) - 24hrs
Glargine (Lantis/Toujeo) - 20-24hrs
Degludec (Tresiba) - 42hrs


MOA: Normally secreted with insulin (made also in beta cells)- Decrease glucagon release, decrease gastric emptying, and increase satiety. Used in Px taking insulin but either type 1 or type 2. What class of drug is at hand, and what is its name?

Amylin analogs - Pramlintide


MOA: Decrease glucagon release, decrease gastric emptying, and increase glucose dependent insulin release, with increased satiety. What class of drugs are at hand, and what are their names. Side effects are nausea, vomiting, pancreatitis, and promotion of weight loss.

GLP-1 analogs: Exenatide, Liraglutide, Dulaglutide


MOA: Inhibit mGPD —> inhibition of hepatic gluconeogenesis and the action of glucagon. Increase glycolysis, peripheral glucose uptake (increase insulin sensitivity). SE: GI upset, B12 deficiency. Promotes weight loss. Name the class and medication.

Biguanides - Metformin


MOA: close K+ channel in pancreatic beta cell membrane —> cell depolarizes —> insulin release via increased Ca2+ influx. SE: Hypoglycemia (increased risk with renal failure), weight gain. Name the class of drug, and the first generation and second generations + their SEs.

1st Gen: Clorpropamide, Tolbutamide. SE: Disulfiram-like reactions/effects.
2nd Gen: Glimepiride, Glipizide, Glybiride. SE: hypoglycemia


MOA: close K+ channel in pancreatic beta cell membrane —> cell depolarizes —> insulin release via increased Ca2+ influx. SE: Hypoglycemia (increased risk with renal insufficiency), weight gain. Name the drug class plus medications.

Meglitinides - Nateglinide, Repaglinide

*Differs from Sulfonylureas because occurs at different binding site).


MOA: inhibits DPP-4 enzyme that deactivates GLP-1. Decrease glucagon release, gastric emptying. Increase glucose-dependent insulin release, satiety. SE: mild urinary or respiratory infections, weight neutral. Name the drug category and the 3 associated drugs.

DPP-4 Inhibitors.
Names: Linagliptin, saxagliptin, sitagliptin.


MOA: This drug binds to PPAR-gamma nuclear transcription regulator —> increasing insulin sensitivity and levels of adiponectin (in peripheral tissue of adipose and skeletal tissue)—> regulation of glucose metabolism and fatty acid storage. SE: weight gain, edema, HF, increased risk of fractures and hepatically excreted (CI in liver failure). Delayed onset of action (several weeks). Name the drug class and it’s associated drugs.

Glitazones/ Thiazolidinediones:
Pioglitazone (risk of bladder CA and osteoporosis) and Rosiglotazone (incr. MI and cardiovascular death)


MOA: Block the re absorption of glucose in proximal convoluted tubule. What is the drug class and associated drug?

Sodium-glucose-cotransporter 2 (SGLT2): Canagliflozin, dapagliflozin, empagliflozin


MOA: Inhibit intestinal brush-border alpha-glucosidases —> delayed carbohydrate hydrolysis and glucose absorption—> decreased postprandial hyperglycemia. SE: osmotic diarrhea, and CI in patients with impaired kidney function. What is the drug class and drug?

Alpha-glucosidase inhibitors: Acarbose and miglitol.


What if the MOA of Propylthioiracil and Methimazole.

Block conversion of T4 to T3.


What is the MoA of Sevelamer?

Nonabsorbable phosphate binder that prevents phosphate absorption from the GI tract. Used in Px with hyperphosphatemia in chronic kidney disease.


What is the MOA of Cinacelet?

Sensitizes Ca2+ -sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ —> decreasing PTH. Used in Px with refractory hypercalcemia in primary/secondary hyper parathyroidism or parathyroid carcinoma.


What is Fludrocortisone and what is it’s MoA?

Synthetic analog of Aldosterone with little glucocorticoid effects. Clinical use: Mineralocorticoid replacement in Px with primary adrenal insufficiency.


What is Demeclocycline and what is its MOA?

It’s an antibiotic that is an ADH antagonist (member of tetracycline family). It is used for SIADH.


Most common SE is hypoglycemia...



This drug is not safe in settings of hepatic dysfunction or CHF. What drug is it?



This drug is metabolized in the liver, so a good choice in patients with renal disease. What drug is it?



Exenatide, Liraglutide, Dulaglutide are part of what family of medications???

GLP-1 analogs


This medication is a synthetic analog of aldosterone with little glucocorticoid effects. Used in the treatment of primary adrenal insufficiency. SE include: edema, exacerbation of heart failure, hyperpigmentation.



These medications are aromatase inhibitors... name them.

Anastrazol, Exemestrane


This substance blocks the conversion of Cortisol into Cortisone. What is it?

Glycyrrhetinic Acid


This drug interferes with ADH signaling, a tetracycline. What is the drug and clinical use?

Demeclocycline —> SIADH


This drug is used to treat von Willebrand disease, sleep enuresis, hemophilia A, and Central DI. What is this drug?



These drugs are ADH antagonists and used for SIADH (block action of ADH at V2-receptor). Name the possible drugs:

Conivaptan or tolvaptan


This drug is used to treat esophageal varices, glucagonoma, gastrinoma, carcinoid syndrome, and acromegaly. Name the drug:

Octreotide (a Somatostatin analog)


These medications bind K+ in colon in exchange for other cations (eg Na+, Ca2+) —> K+ excreted in feces. What are they, and their clinical use:

Hyperkalemia- cation exchange resins:
Partiromer, Sodium polystyrene sulfonate (Kayexalate), zirconium cyclosilicate