Endocrinology Drugs

Front 1

How do you treat Type I DM generally? Type 2 DM?

Back 1

I - low sugar diet, insulin replacement
II - dietary modification & exercise for wt loss, oral hypoglycemics, insulin replacement

Front 2

Orlistat?
- Mechanism?
- Clinical use?
- Toxicity?

Back 2

M - alters fat metabolism by inhibiting pancreatic lipases (ORLISTAT GETS RID OF FAT)
C - long term obesity management (with a modified diet)
T - steatorrhea, GI discomfort, reduced absorption of fat soluble vitamins, headache

Front 3

Sibutramine?
- Mechanism?
- Clinical Use?
- Toxicity?

Back 3

M - sympathomimetic serotonin and norepinephrine reuptake inhibitor
C - short and long term obesity management
T - hypertension and tachycardia

Front 4

Propylthiouracil, Methimazole?
- Mechanism?
- Clinical Use?
- Toxicity?

Back 4

M - inhibits organification of iodide and coupling of thyroid hormone synthesis, Propylthiouracil also decreases peripheral conversion of T4 to T3
C - hyperthyroidism
T - skin rash, agranulocytosis, aplastic anemia

Front 5

Levothyroxine, Triiodothyronine?
- Mechanism?
- Clinical Use?
- Toxicity?

Back 5

M - thyroxine replacement
C - hypothyroidism, myxedema
T - tachycardia, heat intolerance, tremors, arrythmia

Front 6

Hypothalmic & Pituitary Drugs Clinical Use?
- GH?
- Somatostatin (Octreotide)?
- Oxytocin?
- ADH (Desmopressin)?

Back 6

GH - GH Def, Turner's Syndrome
Som - acromegaly, carcinoid, gastrinoma, glucagonoma
O - stimulates labor, uterine contractions, milk let-down, controls uterine hemmorhage
ADH - Central Diabetes Insipidus

Front 7

Demeclocyline?
- Mechanism?
- Clinical Use?
- Toxicity?

Back 7

* In the tetracycline family
M - ADH antagonist
C - SIADH
T - Nephrogenic Diabetes Insipidus, photosensitivity, abnormalities of bone & teeth

Front 8

Glucocorticoids?
- Mechanism?
- Clinical Use?
- Toxicity?

Back 8

Hydrocortisone, Prednisone, Triamcinolone, dexamethasone, beclomethasone
M - decreased production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of Cox-2
C - Addison's disease, inflammation, immune suppression, asthma
T - Iatrogenic Cushing's syndrome

Front 9

Symptoms of Iatrogenic Cushing's Syndrome?

Back 9

Buffalo Hump, Moon Facies, Truncal Obesity, Muscle Wasting, Thin Skin, Easily Brusiability, Osteoporosis, Adenocortical Atrophy, Peptic Ulcers, Diabetes (if chronic)

Front 10

Insulin - Lispro? Aspart? Regular? NPH? Glargine? Detemir?
Mechanism? Liver? Muscle? Fat?
Clinical Use?
Toxicity?

Back 10

Lispro, Aspart, Regular - short-acting, NPH - intermediate, Glargine, Detemir - long-acting
M - binds insulin receptors (tyrosine kinase)
Liver - increases glucose storage as glycogen
Muscle - increased glycogen & protein synthesis, K+ uptake
Fat - aids TG storage
C - Type I DM, type 2 DM, life-threatening hyperkalemia & stress-induced hyperglycemia
T - hypoglycemia, hypersensitivity rxn (rare)

Front 11

Sulfonylureas? Used in what kind of DM?
- First Generation - Tolbutamide? Chlorpropamide?
- Second Generation - Glyburide? Glimepride? Glipizide?
- Mechanism?
- Clinical Use?
- Toxicity? First Gen? Second Gen?

Back 11

M - close K+ channel in B-cell membrane, so cell depolarizes - triggers insulin release via Ca++ influx
C - stimulate insulin release in Type II DM (needs islet function so not helpful in Type I DM)
T - First - dilsufram-like effects, Second - hypoglycemia

Front 12

Biguanides? (Metformin)
- Mechanism?
- Clinical Use?
- Toxicity?

Back 12

M - exact mechanism unknown, decreases gluconeogenesis, increased glycolysis, decreased serum glucose (INSULIN SENSITIZATION)
C - oral hypoglycemic (can be used in patients WITHOUT islet function)
T - lactic acidosis (contraindicated in renal failure)

Front 13

Glitazones/Thiazolidinediones (Pigolitazone, Rosiglitazone)
- Mechanism?
- Clinical Use?
- Toxicity?

Back 13

M - increased insulin sensitivity in peripheral tissue
C - used as monotherapy in type 2 DM (or combined with other agents
T - weight gain, edema, hepatotoxicity, CV toxicity

Front 14

Alpha-Glucosidase Inhibitors (Acarbose, Miglitol)?
- Mechanism?
- Clinical Use?
- Toxicity?

Back 14

M - inhibits intestineal brush-border alpha-glucosidases, delayed sugar hyrdolysis and glucose absorption lead to decreased postprandial hyperglycemia
C - used in monotherapy in type 2 DM or with other agents
T - GI disturbances

Front 15

Mimetics (Pramlintide)?
- Mechanism?
- Clinical Use?
- Toxicity?

Back 15

M - decreased glucagon
C - Type 2 DM
T - hypoglycemia, nausea, diarrhea

Front 16

GLP-1 mimetics (Exenatide)?
- Mechanism?
- Clinical Use?
- Toxicity?

Back 16

M - increased insulin, decreased glucagon release
C - Type 2 DM
T - nausea, vomitting, pancreatitis