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41 Cards in this Set

  • Front
  • Back
5 important insulins and duration of actions:
-Lispro (short-acting)
-Insulin (short-acting)
-NPH (intermediate)
-Lente (long-acting)
Physiologic actions of insulins?
-Binds insulin receptor: tyrosine kinase activity
-Liver: ↑ glucose stored as glycogen
-Muscle: ↑ glycogen and protein synthesis, K+ uptake
-Fat: aids TG storage
Clinical use of insulins?
-Type I DM
-Type II DM
-life-threatening hyperkalemia
-stress-induced hyperglycemia
Toxicities of insulins?
-hypersensitivity reaction (very rare)
What drugs are 1st generation sulfonylureas?
What drugs are 2nd generation sulfonylureas?
MOA of Sulfonylureas?
-they close the K+ channel in Beta-cell membrane --> cell depolarizes --> triggers insulin release via ↑ Ca2+ influx
Uses of Sulfonylureas?
-stimulate the release of endogenous insulin in type 2 DM
-require some islet function, so they are useless in Type I DM
Toxicity of Sulfonylureas?
-1st gen: disulfiram-like effects
-2nd gen: hypoglycemia
What drug is a biguanide?
MOA of Metformin?
-exact MOA is unknown
-Possibly ↓ gluconeogenesis, ↑ glycolysis, ↓ serum glucose levels
Use of Biguanides?
-used as oral hypoglycemic
-can be used in patients w/o islet function
What's the worst adverse effect of Metformin?
lactic acidosis
What drugs are Glitazones?
MOA of Glitazones?
↑ target cell response to insulin (i.e. they increase insulin sensitivity)
How are the Glitazones used?
Used as monotherapy in Type 2 DM or combined with other agents already mentioned.
What are the toxicities associated with the Glitazones?
-weight gain
-hepatotoxicity (troglitazone no longer used)
What drugs are α-glucosidase inhibitors?
MOA of α-glucosidase inhibitors?
MOA = inhibit intestinal brush border α-glucosidases.

-delayed sugar hydrolysis and glucose absorption lead to ↓ postprandial hyperglycemia
For what are α-glucosidase inhibitors used?
used as monotherapy in type 2 DM in combination with other agents
Major toxicity with α-glucosidase inhibitors?
GI disturbances
MOA of Orlistat?
MOA = Alters fat metabolism by inhibiting pancreatic lipases
Clinical Use of Orlistat?
Long-term obesity management (in conjunction with modified diet).
Toxicities due to Orlistat?
-GI discomfort
-Reduced absorption of fat-soluble vitamins
MOA of Sibutramine?
MOA = Sympathomimetic serotonin and norepinephrine reuptake inhibitor
Clinical use of Sibutramine?
Short-term and long-term obesity management.
Toxicity of Sibutramine?
Hypertension and tachycardia
MOA of Propylthiouracil and Methimazole?
-Inhibit organification and coupling of thyroid hormone synthesis.

-PTU ↓ peripheral conversion of T4 to T3.
Clinical use of Propylthiouracil and Methimazole?
Toxicity of Propylthiouracil and Methimazole?
-skin rash
-agrunolocytosis (rare)
-aplastic anemia
Clinical use of GH (somatostatin)?
-GH deficiency
-Turner's syndrome
Clinical use of Octreotide?
Clinical use of Oxytocin?
-stimulates labor
-uterine contractions
-milk let-down
-controls uterine hemorrhage
Clinical use of Desmopressin (ADH)?
-pituitary (central, not nephrogenic) DI
MOA of Levothyroxine and triiodothyronine?
thyroxine replacement
Clinical use of Levothyroxine and triiodothyronine?
Toxicity of Levothyroxine and triiodothyronine?
-heat intolerance
What drugs are Glucocorticoids?
MOA of Glucocorticoids?
↓ the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2
Clinical uses of Glucocorticoids?
-Addison’s disease
-Immune suppression
Toxicities of Glucocorticoids?
Iatrogenic Cushing’s syndrome = buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic