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26 Cards in this Set

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Insulin (Lispro, Aspart, Glulisine)

Binds insulin receptor (tk activity) RAPIDLY: DM 1, DM 2, GDM


liver- increase glycogen,


muscle- increase glycogen, protein synthesis, K+ uptake,


fat- increase TG storage

S/E: Hypoglycemia, lipodystrophy

Insulin

Binds insulin receptor (tk activity) REGULAR: DM 1, DM 2, GDM, DKA(IV), hyperkalemia(+glucose), stress hyperglycemia liver- increase glycogen, muscle- increase glycogen, protein synthesis, K+ uptake, fat- increase TG storage

S/E: Hypoglycemia, lipodystrophy

Insulin (NPH)

Binds insulin receptor (tk activity) INTERMEDIATE: DM 1, DM 2, GDMliver- increase glycogen, muscle- increase glycogen, protein synthesis, K+ uptake, fat- increase TG storage

S/E: Hypoglycemia, lipodystrophy

Insulin (Detemir, Glargine)

Binds insulin receptor (tk activity) LONG ACTING: DM 1, DM 2, GDM (basal)liver- increase glycogen, muscle- increase glycogen, protein synthesis, K+ uptake, fat- increase TG storage

S/E: Hypoglycemia, lipodystrophy

Metformin

BIGUANIDES: first line for DM2, weight loss, use in pts w.o islets


Decrease gluconeogenesis, increase glycolysis, increase INSULIN SENSITIVITY(peripheral glucose uptake)

S/E: GI upset, LACTIC ACIDOSIS (in Renal insufficiency)

Chlorpropamide, Tolbutamide

SULFONYLUREAS 1st GEN: Closes K+ channel in beta-cell membrane > cell depolarizes > insulin release via increase Ca2+ influx


Stimulates release of endogenous insulin in DM2

S/E: Hypoglycemia in RF patients, weight gain, Disulfiram-like effects

Glimepiride, Glipizide, Glyburide

SULFONYLUREAS 2nd GEN: Closes K+ channel in beta-cell membrane > cell depolarizes > insulin release via increase Ca2+ influxStimulates release of endogenous insulin in DM2

S/E: Hypoglycemia in RF patients, weight gain, Hypoglycemia and increase hepatic enzymes

Pioglitazone, Rosiglitazone

THIAZOLIDINEDIONES: monotherapy in DM2 or with others (safe in Renal)


Increase insulin sensitivity in peripheral tissue, Binds PPAR-gamma nuclear transcription regulator (regulate fatty acid storage and glucose metabolism, increase levels of adiponectin)

S/E: Weight gain, edema, hepatotoxicity, HF, increase risk of fractures

Nateglinide, Repaglinide

MEGLITINIDES: monotherapy in DM2 or w. Metformin


Stimulate postprandial insulin release by binding to K+ channels on beta cell membranes (different site from sulfonylureas)

S/E: hypoglycemia (increase risk with RF), weight gain

Exenatide, Liraglutide (sc injection)

GLP-1 ANALOGS: DM2


Increase glucose dependant insulin release, decrease glucagon release, decrease gastric emptying, increase satiety

S/E: Nausea, vomiting, pancreatitis, modest weight loss

Linagliptin, Saxagliptin, Sitagliptin

DPP-4 INHIBITORS: DM2


Inhibits DPP-4 enzyme that deactivates GLP-1, thereby increasing glucose dependant insulin release, decrease glucagon release, decrease gastric emptying, increase satiety

S/E: Mild urinary or respiratory infections, weight neutral

Pramlintide (sc injection)

AMYLIN ANALOGS: DM1, DM2


Decrease gastric emptying, decrease glucagon

S/E: Hypoglycemia (mistimed prandial insulin), nausea

Canagliflozin, dapagliflozin, empagliflozin

SODIUM-GLUCOSE-COTRANSPORTER 2 (SGLT-2) INHIBITORS: DM2


Block reabsorption of glucose in PCT

S/E: Glucosuria, UTIs, vaginal yeast infections, hyperkalemia, dehydration (orthostatic hypotension)

Acarbose, miglitol

ALPHA-GLUCOSIDASE INHIBITORS at intestinal brush-border: DM2


Delayed carbohydrate hydrolysis and glucose absorption leads to decrease postprandial hyperglycemia

S/E: GI disturbances

Methimazole

THIONAMIDES: Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine > inhibition of thyroid hormone synthesis


HYPERTHYROIDISM

S/E: Skin rash , AGRANULOCYTOSIS, APLASTIC ANEMIA, hepatotoxicity, TERATOGEN (causes aplasia cutis)

Propylthiouracil (PTU)

THIONAMIDES: Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine > inhibition of thyroid hormone synthesis; PTU blocks 5'-deiodinase > decrease peripheral conversion of T4 --> T3HYPERTHYROIDISM, block peripheral conversion of T4 to T3, PREGNANCY

S/E: Skin rash , AGRANULOCYTOSIS, APLASTIC ANEMIA, hepatotoxicity

Levothyroxine (T4), Triiodothyronine (T3)

Thyroid replacement therapy


HYPOTHYROIDISM, MYXEDEMA, off the label weight loss supplements

S/E: Tachycardia, heat intolerance, tremors, arrhythmias

Conivaptan, Tolvaptan

ADH ANTAGONISTS: Block ADH at V2-receptor


SIADH

Desmopressin acetate

CENTRAL DI

GH

GH deficiency, Turner syndrome

Oxytocin

Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

Octreotide

SOMATOSTATIN:


Acromegaly


Carcinoid Syndrome


Gastrinoma


Glucagonoma


Esophageal Varices

Demeclocycline

ADH ANTAGONIST: Member of tetracycline family


SIADH

S/E: Nephrogenic DI, photosensitivity, abnormalities of bone and teeth

Beclomethasone, Dexamethasone, Hydrocortisone, Methylprednisolone, Prednisone, Triamcinolone

GLUCOCORTICOIDS: metabolic, catabolic, anti-inflam, and immunosuppressive effects (inhibition of Phospholipase A2, inhibition of transcription factors such as NF-kB


Adrenal Insufficiency, Inflammation, Immunosuppression, Asthma

S/E: Iatrogenic Cushing syndrome (hypertension, weight gain, moon facies, truncal obesity, buffalo hump, thinning skin, striae, acne, osteoporosis, hyperglycemia, amenorrhea, immunosuppression) , adrenocortical atrophy, peptic ulcers, steroid diabetes, steroid psychosis, cataracts.


Adrenal Insufficiency when drug is stopped abruptly after long term use

Fludrocortisone

SYNTHETIC ANALOG OF ALDOSTERONE w little glucocorticoid effects


Primary Adrenal Insufficiency

S/E: similar to glucocorticoids; Edema, exacerbated HF, Hyperpigmentation

Cinacalcet

Sensitizes Ca2+-sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ --> decrease PTH


Primary and Secondary hyperparathyroidism

S/E: hypocalcemia