Diabetes and Endocrine Flashcards
(31 cards)
Aspart, Glulisine, Lispro are all examples of:
What is their Clincal use?
What is are some (-) side effects?
Aspart, Glulisine and Lispro are all rapid acting insulin preparations
Use: Type 1 or Type 2 DM for RIGHT after meansl
Sides: hypoglyema
What is the MOA for all insulin drugs?
Binds insulin receptor (tyrosine kinase activity).
Liver: INCREASE ?glucose stored as glycogen.
Muscle:? INCREASE glycogen, protein synthesis;?
INCREASE K+ uptake.
Fat:?TG storage.
What insulin drugs are intermediate (12 hr) acting?
Which provide Long acting 24 hour coverage?
NPH is Intermediate coverage
Detemir and Glargine are Long Acting
Oral drug that is first-line therapy in type 2 DM, causes modest weight loss.
**Can be used in patients without islet function.
Metformin : oral hypoglycemic drug
What is the Mechanism of Metformin?
What is a toxicity of metformin?
Exact mechanism unknown.
? Decrease gluconeogenesis, ? Increase glycolysis, ?Increase peripheral glucose uptake (?INCREASES insulin sensitivity).
Metformin sensitivity: GI upset; most serious adverse effect is
lactic acidosis (contraindicated in renal insufficiency )
This drug has a risk for causing Lactic acidosis thus contraindicated in pts with renal fail
It’s first line with Type 2 DM and can be used in pts that don’t have islet cell function.
Metformin
These drugs are used to treat T 2 DM and require islet cell fuction to stimulate release of endogenous insluin.
(Thus useless in Type 2 DM)
Sulfonylureas
First generation:Chlorpropamide, Tolbuta mide
Second generation:
Glimepiride, Glipizide, Glyburide
What is the mechanism of action of the following drugs?
Glimepiride, Glipizide, Glyburide
What is their risk of toxicity?
Glimepiride, Glipizide, Glyburide are all sulfonylureas
Mech: Close K+ channel in B cell membrane–> cell depolarizes–> insulin release via Increase Ca++ influx:
thus stimulate release of endogenous insulin in type 2 DM
Sides = Hypoglycemia
What types of drugs are Pioglitazone, Rosiglitazone?
What is the Mechansim of action?
Glitazones/ thiazolidinediones:
?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.
?Increase insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator and activated by PPAR-γ regulate fatty acid storage and glucose metabolism. Activation of PPAR-γ will Increase ?insulin sensitivity and levels of adiponectin.
Pioglitazone, Rosiglitazone
What side effect are we worried about with Pioglitazone or Rosigliotazone?
It’s causes weight gain, edema
Hepatotoxicity, HF and Increase risk of fractures
MOA of Exenatide, Liraglutide
GLP-1 analogs : ?Increase insulin,? Decrease glucagon release.
For T2DM
Sides: Nausea, vomitting and pancreatitis
Linagliptin, Saxagliptin, Sitagliptin
MOA?
Use?
Toxicities
DPP-4 inhibitors
Increase ?insulin,? Decrease glucagon release.
Type 2 DM.
Mild urinary or respiratory infections.
MOA of Pramlintide
Uses?
?Side Effects?
Decrease gastric emptying,? Increase glucagon.
Uses: Type 1 DM, type 2 DM.
Sides; Hypoglycemia, nausea, diarrhea
Decrease gastric emptying,? Increase glucagon.
Uses: Type 1 DM, type 2 DM.
Sides; Hypoglycemia, nausea, diarrhea
Pramlintide
Block reabsorption of glucose in PCT.
Uses: Type 2 DM.
Sides: Glucosuria, UTIs, vaginal yeast infections
SGLT-2 inhibitors
Canagliflozin
Inhibit intestinal brush-border α-glucosidases.
delayed carbohydrate hydrolysis and glucose absorption –> Increased postprandial hyperglycemia.
α-glucosidase inhibitors
Acarbose, Miglitol
What is the mechanism of Propylthiouracil, methimazole
Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine?–> inhibition of thyroid hormone synthesis. Propylthiouracil also blocks 5′-deiodinase–> DECREASE??peripheral conversion of T4 to T3.
When would we prescribe Propylthiouracil, methimazole?
What is the toxicity seen with these drugs?
Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy (Methimazole isn’t safe).
Side: Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil).
Methimazole is a possible teratogen (can cause aplasia cutis).
When would we presrcibe Levothyroxine (T4), triiodothyronine (T3)
What’s it’s use?
What sides do we see?
Thyroid hormone replacement.
Uses: Hypothyroidism, myxedema. Used off-label as weight loss supplements.
Sides: Tachycardia, heat intolerance, tremors, arrhythmias.
What drug can we prescribe to a pt with SIADH?
What’s it’s mechanism?
ADH antagonists (conivaptan, tolvaptan)
SIADH, block action of ADH at V2-receptor.
When would we prescribe GH to a pt?
When would we prescribe Oxytocin to a pt?
GH: GH deficiency, Turner syndrome.
Oxytocin: Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage.
