Endo Flashcards
(23 cards)
Rapid-acting Insulin (Lispro, Aspart, Glulisine)
[MOA, clinical use]
Binds insulin receptor.
For DM 1, 2, GDM – postprandial control
Short-acting Insulin (Regular)
Clinical use
DM 1, 2, GDM
DKA, Hyperkalemia (+ glucose)
Stress hyperglycemia
Intermediate-acting Insulin
[Name, use]
NPH (Neutral Protamine Hagedorn; Humulin N, Novocain N).
DM 1, 2, GDM.
Long-acting Insulin (Detemir, Glargine)
[Clinical use]
DM 1, 2, GDM – basal glucose control.
Biguanides (Metformin)
[Clinical use, Toxicity]
Suppresses hepatic gluconeogenesis.
First-line for DM2; can be used for DM1.
>Toxicity: lactic acidosis (lactate produced in intestine is normally converted to glucose in hepatic gluconeogenesis; CI in renal insufficiency).
Sulfonylureas
[Names (1st gen, 2nd gen), MOA, use]
> 1st gen: Chlorpropamide, Tolbutamide.
2nd gen: Glimepiride, Glyburide, Glipizide.
Closes K channel in B-islet cells – depol – opens voltage-gated Ca channels – inc. intracellular Ca – release insulin.
For DM2.
*Needs islet cell function – can’t be used in DM1
Glitazones/Thiazolidinediones (Pioglitazone, Rosiglitazone)
[MOA, Use, Toxicity]
> Inc. insulin sensitivity in peripheral tissues (adipose, skeletal muscle) – upregulates GLUT4 and adiponectin by binding to PPAR-gamma transcription regulator.
For DM2; monotherapy or combined w/ sulfonylureas, biguanides.
SE: wt. gain, edema; hepatoxicity, HF
GLP-1 analogs (Exenatide, Liraglutide)
[MOA, use, SE]
> Inc. insulin, Dec. glucagon.
For DM2.
SE: pancreatitis
*Glucose-like peptide: inc. glucose-dependent insulin secretion.
DPP-4 inhibitors (Linagliptin, Saxagliptin, Sitagliptin)
[MOA, use, SE]
> Inc. endogenous GLP-1 – inc. insulin, dec. glucagon.
For DM2.
SE: urinary/respi infections (nasopharyngitis)
*DPP-4 inhibits endogenous GLP-1 secretion
Pramlintide (Amylin analog)
[MOA, use]
> Dec. gastric emptying, dec. glucagon.
For DM1, 2
*Amylin: peptide co-secreted w/ insulin from pancreatic beta cells (satiety agent)
Canagliflozin (SGLT-2 inhibitor)
[MOA, use, SE]
> Blocks glucose reabsorption in PCT.
For DM2.
SE: glycosuria, vaginal yeast infxn.
*Assess renal impairment
alpha-glucosidase inhibitors (Acarbose, Miglitol)
[MOA, use]
> Inhibit intestinal brush border alpha-glucosidases – delayed carb hydrolysis and glucose absorption – dec. postprandial hyperglycemia.
Can be monotherapy or combination for DM2.
Propylthiouracil, Methimazole
[MOA, use, toxicity]
> Block thyroid peroxidase – inhibits oxidation and coupling of iodine – inhibits TH synthesis.
PTU also inhibits 5’-deiodinase – no peripheral conversion of T4 into T3.
For Hyperthyroidism.
SE: Agranulocytosis (rare), aplastic anemia; hepatotoxicity (PTU); teratogen (methimazole).
Levothyroxine (T4), Triiodothyronine (T3)
[use]
Thyroid hormone replacement.
For hypothyroidism, myxedema.
Off-label weight loss supplements.
Conivaptan, Tolvaptan (ADH antagonists)
[use, MOA]
For SIADH
Blocks ADH at V2 receptor
Desmopressin acetate
[use]
For central DI
Somatostatin (octreotide)
[use]
For acromegaly, carcinoid syndrome, gastronoma, glucagonoma, esophageal varices
Demeclocycline (ADH antagonist)
[Use, toxicity]
> Member of tetracycline family.
For SIADH.
Toxicity: nephrogenic DI, abnormalities w/ bone and teeth.
Cinacalcet
[MOA, use]
> Sensitizes Ca-sensing receptor in parathyroid gland to circulating Ca – dec. PTH.
For Hypercalcemia (due to hyperparathyroidism).
*Sense the Calcium
Glucocorticoids (-one)
Names
Beclomethasone, Dexamethasone, Hydrocortisone, Methylprednisolone, Prednisone, Triamcinolone,
Fludrocortisone (mineralocorticoid and glucocorticoid activity)
Glucocorticoids
[MOA, Use]
Metabolic, Catabolic, Anti-inflammatory, immunosuppressive.
>Inhibits phospholipase A2 – no leukotrienes, PGs.
>Inhibits NFkB transcription factor – blocks DNA and cytokine production.
>For Addison dse, inflammation, immunosuppression, asthma.
Glucocorticoid
Toxicity
> Iatrogenic Cushing syndrome (HTN, wt. gain, obesity, buffalo hump, striae, hyperglycemia, etc).
Adrenal insufficiency when abruptly stopped after chronic use.
Immunosuppression.
Why should you beware of chronic glucocorticoid use?
CRH, ACTH, and cortisol will no longer rise in stressful situations. There will be relative glucocorticoid deficiency even if baseline is maintained w/ therapy. This may lead to hypotension and shock.
>Higher stress dose needed to compensate and prevent adrenal crisis.
