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Flashcards in Endocrine Drugs Deck (57):
0

Treatment strategy for type 1 DM

Low sugar diet, insulin replacement

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Treatment strategy for type 2 DM

Dietary modification and exercise for weight loss; oral hypoglycemics and insulin replacement

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Rapid Acting Insulin

Lispro, Aspart, Glulisine

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Short acting insulin

Regular insulin

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Intermediate Insulin

NPH

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Long acting insulin

Glargine, Detemir

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Insulin: Action

Bind insulin receptor (tyrosine kinase activity)
Liver: increase glucose stored as glycogen
Muscle: *increase glycogen and protein synthesis*
Fat: aids TG storage

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Insulin: Clinical Use

Type 1 DM, type 2 DM
Gestational Diabetes
Life-threatening hyperkalemia
Stress-induced hyperglycemia

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Insulin : Toxicity

Hypoglycemia
Hypersensitivity Reactions (very rarely)

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Biguanides

Metformin

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Metformin: Action

Exact mechanism is unknown
*decrease* gluconeogenesis
*increase* glycolysis, peripheral glucose uptake (insulin sensitivity)

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Metformin: Clinical Use

Oral: 1st line therapy in type 2 DM

Can be used in patients without islet function

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Metformin: Toxicity

GI upset; most serious adverse effect is lactic acidosis (thus contradicted in renal failure)

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1st generation: Sulfonylureas

Tolbutamide
Chlorpropramide

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2nd generation: Sulfonylureas

Glyburide
Glimepiride
Glipizide

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Sulfonylureas

Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release via increase of Ca+ influx
(JUST LIKE INSULIN)

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Sulfonylureas: Clinical Use

Stimulate release of endogenous insulin in type 2 DM.
Require some islet function, so useless in type 1 DM

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Sulfonylureas: Toxicity

1st generation: disulfiram-like effect.
2nd generation: hypoglycemia (avoid use with EtOH)

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Glitazones/ thiazolidinediones

Pioglitazone
Rosiglitazone

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Glitazones/thiazolidinediones (Pioglitazone, Riosiglitazone): Action

Increase insulin sensitivity in peripheral tissue. Binds to PPAR-gamma nuclear transcription regulator.

*PPAR-gamma regulate FA storage and glucose metabolism. Activation of PPAR-gamma increases insulin sensitivity and levels of adiponectin.

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Glitazones/ Thiazolidinediones: Clinical Use

Used as monotherapy in type 2 DM or combined with above agents

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Glitazones/ Thiazolidinediones: Toxicity

Weight gain, edema, hepatotoxicity, heart failure

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Alpha Glucosidase inhibitors

Acarbose
Miglitol

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Alpha-Glucosidase Inhibitors: Action

Inhibit intestional brush border alpha glucosidases
Delayed sugar hydrolysis and glucose absorption --> DECREASED postprandial hyperglycemia

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Alpha-glucosidase inhibitors: Clinical Use

Used as monotherapy or in combination with other diabetic drugs

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Alpha-glucosidase: Toxicity

GI disturbances

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Amylin analogs

Pramlintide

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Pramlintide: Action

Decrease glucagon

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Pramlintide: Clinical Use

Type 1 and type 2 DM

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Pramlintide: Toxicity

Hypoglycemia, Nausea, Diarrhea

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GLP-1 analogs:

Exenatide
Liraglutide

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GLP-1: Action:

Increase insulin
Decrease glucagon release

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GLP-1 analog (Exenatide, Liraglutide): Clinical Use

Type 2 DM

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GLP-1 analog (Exenatide, Liraglutide): Toxicity

Nausea, vomiting, pancreatitis

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DPP-4 inhibitors:

Linagliptin, Saxagliptin, Sitagliptin

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DPP-4 inhibitors: Linagliptin, Saxagliptin, Sitagliptin: Mechanism

Increase insulin, Decrease Glucagon release

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DPP-4 inhibitors (Litaglipton, Saxagliptin, Sitagliptin): Clinical Use

Type 2 DM

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DPP-4 inhibitors (Litagliptin, Saxagliptin, Sitagliptin): Toxicity

Mild urinary or respiratory infections

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Thioamides

Propylthiouracil, Methimazole

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Thioamides (Propylthiouracil, Methimazole): Mechanism

Block peroxidase, thereby inhibiting organification of iodine and coupling of thyroid hormone synthesis.

*Propylthiouracil also blocks 5'-deiodinase which decrease peripheral converseion of T4 to T3.

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Thioamides (Propylthiouracil, Methimazole): Clinical Use

Hyperthyroidism

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Thioamies (Propylthiouracil, Methimazole): Toxicity

Skin rash, agranulocytosis (rare), aplastic anemia
Propylthiouracil: hepatotoxicity, safer during pregnancy
Methimazole: possible teratogen

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Levothyroxine, Triiodothyronine: Mechanism

Thyroxine replacement

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Levothyrozine, Triiodothyronine: Clinical Use

Hypothyroidism, Myxedema

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Levothyroxine, Triiodothyronine: Toxicity

Tachycardia, Heat intolerance, Tremors, Arrhythmias (signs of hyperthyroidism)

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Growth Hormone: Clinical Use

GH deficiency, Turner Syndrome

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Somatostatin (Octeotride): Clinical Use

Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices

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Oxytocin: Clinical use

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

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ADH (desmopressin): Clinical Use

Pituitary (central NOT nephrogenic) DI

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Demeclocycline: Mechanism

ADH antagonist (member of tetracycline family)

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Demeclocycline: Clinical Use

SIADH

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Demeclocycline: Toxicity

Nephrogenic DI, photosensitivity, abnormalities of bone and teeth

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Glucocorticoids

Hydrocortisone, Prednisone, Triamcinolone, Dexamethasone, Beclamethasone

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Glucocorticoids (-asone/ - isone): Mechanism

Decrease the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2

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Glucocorticoids: Clinical Use

Addison's disease, inflammation, immune suppression, asthma

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Glucocorticoids (-asone/-isone: Toxicity

Iatrogenic Cushing's syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic)

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Risk of stopping glucocorticoids abruptly

Adrenal insufficiency -- must taper the glucocorticoids to prevent this.