Usmle Step 1 Fa Endo-Pharmacology

Front 1

Somatropin/Somatrem
(a) mechanism
(b) indications

Back 1

(a) recombinant forms of GH; stimulates linear/skeletal growth for pediatric patients
(b) growth failure, Turner's, cachexia, somatotropin deficiency

Front 2

Octreotide
(a) mechanism
(b) indications

Back 2

(a) long acting octapeptide that mimics somatostatin; inhibits release of GH, glucagon, gastrin, thyrotropin, insulin
(b) acromegaly, carcinoid, glucagonoma, gastrinoma, other endocrine tumors

Front 3

Thioamides
(a) examples
(b) indications
(c) mechanism
(d) side effects

Back 3

(a) PTU, methimazole
(b) long term hyperthyroid tx
(c) inhibit synth against thyroid hormones (do NOT inactivate existing T4, T3); PTU can inhibit peripheral conversion of T4 to T3
(d) skin rash (common); hematologic effects (rare)

Front 4

Iodides
(a) examples
(b) indications
(c) mechanism

Back 4

(a) Lugol's solution, potassium iodide alone
(b) prep for thyroid surgery; treat thyrotoxic crisis and thyroid blocking in radiation emergency
(c) inhibit release of T4 and T4 (primary); also inhibit biosynth of T4, T3 and decrease size and vascularity of thyroid gland

Front 5

Beta blockers in thyroid treatment
(a) examples
(b) indication

Back 5

(a) nadolol, propranolol
(b) nonselective beta blockers used for palpitation, anxiety, tremor and heat intolerance; partially inhibit conversion of T4

Front 6

Radioactive iodine
(a) indications
(b) mechanism

Back 6

(a) 1st line therapy for Grave's; treatment of choice for thyrotoxicosis in adults/elderly
(b) ablation of thyroid gland

Front 7

Glucocorticoids
(a) example
(b) indications
(c) mechanism

Back 7

(a) hydrocortisone
(b) adrenocortical insufficiency (Addison disease, acute adrenal insufficiency from other causes)
(c) replacement therapy

Front 8

Mineralcorticoids
(a) example
(b) indications
(c) mechanism

Back 8

(a) gludrocortisone
(b) chronic treatment of Addison's disease in patients requiring mineralcorticoids
(c) replacement therapy

Front 9

Glucocorticoid synthesis inhibitors
(a) examples
(b) indications

Back 9

(a) aminoglutethimide, metyrapone, ketoconazole
(b) suppress adrenocortical steroid roduction (Cushing's, Cushingoid states, congenital adrenal hyperplasia)

Front 10

Bisphosphonates
(a) examples
(b) indications
(c) mechanism
(d) side effects

Back 10

(a) alendronate, etidronate, pamidronate, risedronate
(b) osteoporosis, Paget disease
(c) decr bone resorption
(d) esophageal ulceration may occur

Front 11

Give examples
(a) short acting
(b) rapid acting
(c) intermediate acting
(d long acting
(e) ultralong acting

Back 11

(a) short acting: lispro, aspart
(b) rapid acting: regular
(c) intermediate acting: NPH, Lente
(d long acting: ultralente
(e) ultralong acting: glargine, detemir

Front 12

Insulin
(a) action
(b) clinical use
(c) toxicity

Back 12

(a) Bind insulin receptor (tyrosine kinase activity)
Liver: incr glucose (stored as glycogen)
Muscle: incr glycogen and protein synth; K+ uptake
Fat: aids TG storage
(b) TI and TIIDM; also life threatening hyperkalemia and stress induced hyperglycemia
(c) hypoglycemia, hypersensitivity (rare)

Front 13

Name 1st generation sulfonylureas

Back 13

Tolbutamide
Chlopropamide

Front 14

Name 2nd generation sulfonylyreas

Back 14

Glyburide
Glimepiride
Glipizide

Front 15

Sulfonylureas
(a) action
(b) clinical use
(c) toxicities

Back 15

(a) close K+ channel in beta cell membrane so cell depolarizes, triggerig insulin release via increased Ca++ influx
(b) stimulates release of endogenous insulin in type II DM. Require some islet fct so not used in TIDM
(c) first generation: disulfiram like effects
Second gen: hypoglycemia

Front 16

Biguanides
(a) examples
(b) mechanism of action
(c) clinical use
(d) toxicities

Back 16

(a) metformin
(b) possibly decr gluconeogenesis, incr glycolysis, decr serum glucose levels (acts as an insulin sensitizer)
(c) oral hypoglycemic; used in patients without islet fct
(d) can cause lactic acidosis

Front 17

Glitazones/Thiazolidinediones
(a) examples
(b) mechanism of action
(c) clinical use
(d) toxicities

Back 17

(a)rosiglitazone, pioglitazone
(b) bind PPARgamma receptor to incr target tissue sensitivity to insulin, inhibits hepatic glucose output, incr glucose uptake
(c) used as monotherapy in TIIDM or combined with other agents
(d) wt gain, edema, hepatotoxicity, CV toxicity

Front 18

Alpha glucosidase inhibitors
(a) examples
(b) mechanism of action
(c) clinical use
(d) toxicities

Back 18

(a) acarbose, miglitol
(b) inhibit intestinal brush border alpha glucosidase to delay sugar hydrolysis, glucose absorption (leads to decreased posprandial hyperglycemia)
(c) used as monotherapy in TIIDM or in combo with other agnets
(d) Gi disturbances (flatulence and diarrhea)

Front 19

Pramlintide
(a) mechanism of action
(b) clinical use
(c) toxicity

Back 19

(a) mimetic; decreases glucagon
(b) type IIDM
(c) hypoglycemia, nausea, diarrhea

Front 20

GLP-1 mimics
(a) examples
(b) mechanism of action
(c) toxicity

Back 20

(a) exenatide
(b) increase insulin, decrease glucagon release
(c) type IIDM
(d) nausea, vomiting;

Front 21

Orlistat
(a) mechanism
(b) clinical use
(c) toxicity

Back 21

(a) inhibits pancreatic lipase
(b) long term obesity management (in conjunction w/diet)
(c) steatorrhea, GI discomfort, reduced absorption of fat soluble vits, HA

Front 22

Sibutramine
(a) mechanism
(b) clinical use
(c) toxicity

Back 22

(a) sympathomimetic serotonin and norep reuptake inhibitor
(b) short and long term obesity management
(c) HTn and tachycardia

Front 23

PTU, methimazole
(a) mechanism
(b) clinical use
(c) toxicity

Back 23

(a) inhibit organification and coupling of TH synthesis; PTU also decr converstin of T4 to T3
(b) hyperthyroidism
(c) skin rash, agranulocytosis (rare), aplastic anemia

Front 24

Hypothalamic/pituitary drugs clinical uses
(a) GH
(b) somatostatin (octreotide)
(c) oxytocin
(d) ADH (desmopressin)

Back 24

(a) GH: GH deficiency, Turner's
(b) somatostatin (octreotide): acromegaly, carcinoid, gastrinoma, glucagonoma
(c) oxytocin: stimulates labor, uterine contractions, mil let down; controls uterine hemorrhage
(d) ADH (desmopressin): pituitary diabetes insipidus

Front 25

Levothyroxine, triidiothyronine
(a) mechanism
(b) clinical use
(c) toxicity

Back 25

(a) thyroxine replacement
(b) hypothyroidism, myxedema
(c) tachycardia, heat intolerance, tremors, arrhythmias

Front 26

Glucocorticoids
(a) examples
(b) mechanism
(c) clinical use
(d) toxicity

Back 26

(a) hydrocortisone, prednisone, triamcinolone, dexamethasone, becomethasone
(b) decr the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2
(c) addison's disease, inflammation, immune suppression, asthma
(d) Iatrogenic cushings;osteoporosis, adrenocorticocal atrophy, peptic ulcers, diabetes (if chronic)

Front 27

Demeclocycline
(a) mechanism
(b) clinical use
(c) toxicity

Back 27

(a) ADH antagonist (member of tetracycline family)
(b) Diabetes Insipidus, SIADH
(c) photosensitivity, abnormalities of bone/teeth