Endocrine - Pharmacology Flashcards
1
Q
Diabetes drugs:
Treatment strategies
- DM1
- DM2
- Gestational DM (GDM)
A
- 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
Q
Insulin, rapid acting
- Example(s)
- Action
- Clinical use
- Toxicities
A
- 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
Q
Insulin, short acting
- Example(s)
- Clinical use
A
- Example(s)
- Regular
- Clinical use
- DM1, DM2, GDM
- DKA (IV)
- Hyperkalemia (+ glucose)
- Stress hyperglycemia.
4
Q
Insulin, intermediate acting
- Example(s)
- Clinical use
A
- Example(s)
- NPH
- Clinical use
- DM1, DM2, GDM.
5
Q
Insulin, long acting
- Example(s)
- Clinical use
A
- Example(s)
- Glargine
- Detemir
- Clinical use
- DM1, DM2, GDM (basal glucose control).
6
Q
Biguanides
- Example(s)
- Action
- Clinical use
- Toxicities
A
- 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
Q
Sulfonylureas
- Example(s)
- Action
- Clinical use
- Toxicities
A
- Example(s)
- First generation:
- Tolbutamide
- Chlorpropamide
- Second generation:
- Glyburide
- Glimepiride
- Glipizide
- First generation:
- Action
- Close K+ channel in β-cell membrane, so cell depolarizes –> 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
Q
Glitazones / thiazolidinediones
- Example(s)
- Action
- Clinical use
- Toxicities
A
- 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
Q
α-glucosidase inhibitors
- Example(s)
- Action
- Clinical use
- Toxicities
A
- 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
Q
Amylin analogs
- Example(s)
- Action
- Clinical use
- Toxicities
A
- Example(s)
- Pramlintide
- Action
- Decreased gastric emptying
- Decreased glucagon.
- Clinical use
- Type 1 and type 2 DM.
- Toxicities
- Hypoglycemia, nausea, diarrhea.
11
Q
GLP-1 analogs
- Example(s)
- Action
- Clinical use
- Toxicities
A
- Example(s)
- Exenatide
- Liraglutide
- Action
- Increased insulin
- Decreased glucagon release.
- Clinical use
- Type 2 DM.
- Toxicities
- Nausea, vomiting
- Pancreatitis.
12
Q
DPP-4 inhibitors
- Example(s)
- Action
- Clinical use
- Toxicities
A
- Example(s)
- Linagliptin
- Saxagliptin
- Sitagliptin
- Action
- Increased insulin
- Decreased glucagon release.
- Clinical use
- Type 2 DM.
- Toxicities
- Mild urinary or respiratory infections.
13
Q
Propylthiouracil, methimazole
- Mechanism
- Clinical use
- Toxicity
A
- Mechanism
- Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine –> 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
Q
Levothyroxine, triiodothyronine
- Mechanism
- Clinical use
- Toxicity
A
- Mechanism
- Thyroxine replacement.
- Clinical use
- Hypothyroidism, myxedema.
- Toxicity
- Tachycardia, heat intolerance, tremors, arrhythmias.
15
Q
Clinical use of these hypothalamic / pituitary drugs
- GH
- Somatostatin (octreotide)
- Oxytocin
- ADH (DDAVP)
A
- 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.
