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Flashcards in Endocrine - Pharmacology Deck (17):
1

Diabetes drugs:
Treatment strategies

  • DM1
  • DM2
  • Gestational DM (GDM)

  • DM1
    • Low-sugar diet
    • Insulin replacement
  • DM2
    • Dietary modification and exercise for weight loss
    • Oral agents, non-insulin injectables, insulin replacement
  • Gestational DM (GDM)
    • Dietary modifications, exercise
    • Insulin replacement if lifestyle modification fails

2

Insulin, rapid acting

  • Example(s)
  • Action
  • Clinical use
  • Toxicities

  • Example(s)
    • Lispro
    • Aspart
    • Glulisine
  • Action
    • Bind insulin receptor (tyrosine kinase activity).
    • Liver: increase glucose stored as glycogen.
    • Muscle: increase glycogen, protein synthesis; increase K+ uptake.
    • Fat: increase TG storage.
  • Clinical use
    • DM1, DM2, GDM (postprandial glucose control).
  • Toxicities
    • Hypoglycemia
    • Rare hypersensitivity reactions.

3

Insulin, short acting

  • Example(s)
  • Clinical use

  • Example(s)
    • Regular
  • Clinical use
    • DM1, DM2, GDM
    • DKA (IV)
    • Hyperkalemia (+ glucose)
    • Stress hyperglycemia.

4

Insulin, intermediate acting

  • Example(s)
  • Clinical use

  • Example(s)
    • NPH
  • Clinical use
    • DM1, DM2, GDM.

5

Insulin, long acting

  • Example(s)
  • Clinical use

  • Example(s)
    • Glargine
    • Detemir
  • Clinical use
    • DM1, DM2, GDM (basal glucose control).

6

Biguanides

  • Example(s)
  • Action
  • Clinical use
  • Toxicities

  • Example(s)
    • Metformin
  • Action
    • Exact mechanism is unknown.
    • Decrease gluconeogenesis, increase glycolysis, increase peripheral glucose uptake (insulin sensitivity).
  • Clinical use
    • Oral.
    • First-line therapy in type 2 DM.
    • Can be used in patients without islet function.
  • Toxicities
    • GI upset
    • Most serious adverse effect is lactic acidosis (thus contraindicated in renal failure).

7

Sulfonylureas

  • Example(s)
  • Action
  • Clinical use
  • Toxicities

  • Example(s)
    • First generation:
      • Tolbutamide
      • Chlorpropamide
    • Second generation:
      • Glyburide
      • Glimepiride
      • Glipizide
  • Action
    • Close K+ channel in β-cell membrane, so cell depolarizes -->Ž triggering of insulin release via increased Ca2+ influx.
  • Clinical use
    • Stimulate release of endogenous insulin in type 2 DM.
    • Require some islet function, so useless in type 1 DM.
  • Toxicities
    • Risk of hypoglycemia increased in renal failure.
    • First generation: disulfiramlike effects.
    • Second generation: hypoglycemia.

8

Glitazones / thiazolidinediones

  • Example(s)
  • Action
  • Clinical use
  • Toxicities

  • Example(s)
    • Pioglitazone
    • Rosiglitazone
  • Action
    • Increased insulin sensitivity in peripheral tissue.
    • Binds to PPAR-γ nuclear transcription regulator.
      • Genes activated by PPAR-γ regulate fatty acid storage and glucose metabolism.
      • Activation of PPAR-γ increases insulin sensitivity and levels of adiponectin
  • Clinical use
    • Used as monotherapy in type 2 DM or combined with above agents.
  • Toxicities
    • Weight gain, edema.
    • Hepatotoxicity, heart failure.

9

α-glucosidase inhibitors

  • Example(s)
  • Action
  • Clinical use
  • Toxicities

  • Example(s)
    • Acarbose
    • Miglitol
  • Action
    • Inhibit intestinal brush-border α-glucosidases.
    • Delayed sugar hydrolysis and glucose absorption --> decreased postprandial hyperglycemia.
  • Clinical use
    • Used as monotherapy in type 2 DM or in combination with above agents.
  • Toxicities
    • GI disturbances.

10

Amylin analogs

  • Example(s)
  • Action
  • Clinical use
  • Toxicities

  • Example(s)
    • Pramlintide
  • Action
    • Decreased gastric emptying
    • Decreased glucagon.
  • Clinical use
    • Type 1 and type 2 DM.
  • Toxicities
    • Hypoglycemia, nausea, diarrhea.

11

GLP-1 analogs

  • Example(s)
  • Action
  • Clinical use
  • Toxicities

  • Example(s)
    • Exenatide
    • Liraglutide
  • Action
    • Increased insulin
    • Decreased glucagon release.
  • Clinical use
    • Type 2 DM.
  • Toxicities
    • Nausea, vomiting
    • Pancreatitis.

12

DPP-4 inhibitors

  • Example(s)
  • Action
  • Clinical use
  • Toxicities

  • Example(s)
    • Linagliptin
    • Saxagliptin
    • Sitagliptin
  • Action
    • Increased insulin
    • Decreased glucagon release.
  • Clinical use
    • Type 2 DM.
  • Toxicities
    • Mild urinary or respiratory infections.

13

Propylthiouracil, methimazole

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine -->Ž inhibition of thyroid hormone synthesis.
    • Propylthiouracil also blocks 5′-deiodinase, which decreases peripheral conversion of T4 to T3.
  • Clinical use
    • Hyperthyroidism.
    • PTU blocks Peripheral conversion, used in Pregnancy.
  • Toxicity
    • Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil).
    • Methimazole is a possible teratogen (can cause aplasia cutis).

14

Levothyroxine, triiodothyronine

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • Thyroxine replacement.
  • Clinical use
    • Hypothyroidism, myxedema.
  • Toxicity
    • Tachycardia, heat intolerance, tremors, arrhythmias.

15

Clinical use of these hypothalamic / pituitary drugs

  • GH
  • Somatostatin (octreotide)
  • Oxytocin
  • ADH (DDAVP)

  • GH
    • GH deficiency, Turner syndrome.
  • Somatostatin (octreotide)
    • Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices.
  • Oxytocin
    • Stimulates labor, uterine contractions, milk let-down
    • Controls uterine hemorrhage.
  • ADH (DDAVP)
    • Pituitary (central, not nephrogenic) DI.

16

Demeclocycline

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • ADH antagonist (member of the tetracycline family).
  • Clinical use
    • SIADH.
  • Toxicity
    • Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.

17

Glucocorticoids

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity

  • Examples
    • Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone, fludrocortisone (mineralocorticoid and glucocorticoid activity).
  • Mechanism
    • Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects
    • Mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB.
  • Clinical use
    • Addison disease, inflammation, immune suppression, asthma.
  • Toxicity
    • Iatrogenic Cushing syndrome—buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis (treat with bisphosphonates), adrenocortical atrophy, peptic ulcers, diabetes (if chronic).
    • Adrenal insufficiency when drug stopped abruptly after chronic use.

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