ENDOCRINE Flashcards
Levothyroxine
Synthetic T4–Pro hormone for T3
USES: replacement therapy for hypothyroidism
SIDE EFFECTS: tachycardia, heat intolerance, tremors, arrhythmias
Propylthiouricil
Anti-thyroid drug
MOA: inhibits thyroid peroxidase, inhibiting the oxidation of iodide and organification (coupling) of iodine–>inhibition of thyroid hormone synthesis. Also blocks 5’-deiodinase, which decreases peripheral conversion of T4 to T3
USES: hyperthyroidism. Used in pregnancy
SIDE EFFECTS: skin rash, agranulocytosis (can present with infection since decreased neutrophils), aplastic anemia, hepatotoxicity, vasculitis, hypoprothrombinemia, rash
Cortisone
Glucocorticoid
MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB
USES: Addison’s disease, inflammation, immune suppression, asthma
TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use
Prednisone
Intermediate acting glucocorticoid
Converted to prednisolone in liver
Moe potent as glucocorticoid than mineralocorticoid
USES: to prevent rejection; anti-inflammatory effect is 4X more potent than cortisol
Avoid in patients with liver disease
Triamcinolone
Glucocorticoid
MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB
USES: Addison’s disease, inflammation, immune suppression, asthma
TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use
Dexamethasone
Glucocorticoid
MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB
USES: Addison’s disease, inflammation, immune suppression, asthma
TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use
Betamethasone
Long acting glucocorticoid–similar to dexamethasone
Not metabolized by placenta–can be used to induce lung surfactant production in preterm fetuses
Beclomethasone
Glucocorticoid
MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB
USES: Addison’s disease, inflammation, immune suppression, asthma
TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use
Fludrocortisone
mineralocorticoid and glucocorticoid activity
MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB
USES: Addison’s disease, inflammation, immune suppression, asthma
TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use
Mifepristone
Progesterone receptor antagonist used as abortion pill and at higher doses an antagonist of the glucocorticoid receptor
Used for Cushing’s syndrome
Cholecalciferol
Vitamin D3–decreases transcription of PTH gene and increases calcium absorption
USES: osteoporosis, osteomalacia, rickets, hypoparathyroidism, secondary hypoparathyroidism (chronic kidney disease)
SIDE EFFECTS: hypercalcemia, renal calculi, hyperphosphatemia
Ergocalciferol
Vitamin D2–decreases transcription of PTH gene and increases calcium absorption
USES: osteoporosis, osteomalacia, rickets, hypoparathyroidism, secondary hypoparathyroidism (chronic kidney disease)
SIDE EFFECTS: hypercalcemia, renal calculi, hyperphosphatemia
Calcitriol
ACTIVE form of vitamin D–decreases transcription of PTH gene and increases calcium absorption
USES: osteoporosis, osteomalacia, rickets, hypoparathyroidism, secondary hypoparathyroidism (chronic kidney disease)
SIDE EFFECTS: hypercalcemia, renal calculi, hyperphosphatemia
Cinacalcet
MOA: sensitized ca++ sensing receptor (CaSR) in parathyroid gland to circulating ca++ leading to decreased PTH
USES: hypercalcemia due to primary or secondary hyperparathyroidism
TOXICITY: hypocalcemia
Alendronate
Bisphosphonate
MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption
USES: osteoporosis, Paget’s disease
SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures
EFFICACY: decrease incidence of vertebral AND hip fractures
Risedronate
Bisphosphonate
MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption
USES: osteoporosis, Paget’s disease
SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures
EFFICACY: decrease incidence of vertebral AND hip fractures
Ibandronate
Bisphosphonate
MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption
USES: osteoporosis, Paget’s disease
SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures
EFFICACY: decrease incidence of vertebral AND hip fractures
Pamidronate
Bisphosphonate–IV only
MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption
USES: Paget’s disease, hypercalcemia of malignancy
SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures
EFFICACY: decrease incidence of vertebral AND hip fractures
Zoledronic acid
Bisphosphonate-IV only
MOA: Synthetic analog of pyrophosphate–bind to hydroxyapatite in bone and selectively localize to areas of bone turnover and inhibit resorption
USES: Paget’s disease, hypercalcemia of malignancy
SIDE EFFECTS: esophageal erosion, jaw osteonecrosis, acid reflux, headache, atypical femur fractures
EFFICACY: decrease incidence of vertebral AND hip fractures
Raloxifene
Selective estrogen receptor modulator–acts at estrogen receptor selectively in bone (does not increase risk for breast or uterine cancer)
USES: osteoporosis
SIDE EFFECTS: hot flashes, venous thromboembolism
EFFICACY: decreases vertebral but NOT hip fractures
Calcitonin nasal spray
MOA: binds to and activates the calcitonin receptor on osteoclasts and decreases resorptive activity
USES: post menopausal osteoporosis treatment NOT prevention
SIDE EFFECTS: rhinitis, nasal symptoms
Calcitonin injection
MOA: binds to and activates the calcitonin receptor on osteoclasts and decreases resorptive activity
USES: post menopausal osteoporosis treatment NOT prevention, Paget’s disease,
SIDE EFFECTS: nausea, flushing, diarrhea
Denosumab
Humanize monoclonal antibody to RANKL–prevents bone resorption
USES: osteoporosis
SIDE EFFECTS: hypocalcemia, infections, dermatitis, eczema, rash, jaw osteonecrosis, musculoskeletal pain
PTH in pulses
Briefly stimulates osteoclasts, increases blood calcium, decreases blood phosphorus, and activates 1,25-vitamin D–> results in brief period of bone turnover followed by osteoblast recruitment of the BFUs
PTH analogs
Blocks osteoblasts from undergoing apoptosis–cerastes trabecular connections, increases cortex thickness, makes bones stronger
USES: good for osteoporosis
Regular insulin
Rapid-acting to be administered 30-45 minutes prior to meals; Duration of action 3-6h (increases with increasing doses)
USES: DM1/2, GDM, DKA (IV), hyperkalemia (+ glucose), stress hyperglycemia
NPH
Intermediate-acting insulin analog
USES: DM1, DM2, GDM
Glargine
Long acting insulin
USES: DM1/2, GDM
Detemir
Long acting insulin
USES: DM1/2, GDM
Pramlinitide
Amylin analog
MOA: decreases emptying and glucagon
USES: type 1/2 diabetes
TOXICITY: hypoglycemia, nausea, diarrhea
Metformin
Biguanide diabetes drug
MOA: exact mechanism unknown–increases insulin sensitivity, decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake
USES: drug of choice for T2DM. Can be used with patients without islet function
TOXICITY: GI upset; most serious adverse effect is lactic acidosis via anaerobic glycolysis (thus contraindicated in renal failure)
Rosiglitazone
Glitazone/Thiazolidinedione
MOA: increases insulin sensitivity in peripheral tissues–binds PPARgamma nuclear transcription regulator and enhances glucose uptake into fat and muscle
USES: mono therapy in T2DM or combined
SIDE EFFECTS: edema, weight gain, CHF, hepatotoxicity. Takes days-weeks to see effects
Pioglitazone
Glitazone/Thiazolidinedione
MOA: increases insulin sensitivity in peripheral tissues–binds PPARgamma nuclear transcription regulator and enhances glucose uptake into fat and muscle
USES: mono therapy in T2DM or combined
SIDE EFFECTS: edema, weight gain, CHF, hepatotoxicity. Takes days-weeks to see effects
Acarbose
Alpha glucosidase inhibitor
MOA: inhibit intestinal brush border alpha glucosidase–>delayed sugar hydrolysis and glucose absorption–>decreases postprandial hyperglycemia
USES: Monotherapy in T2DM or in combination
TOXICITY: GI disturbances
Miglitol
Alpha glucosidase inhibitor
MOA: inhibit intestinal brush border alpha glucosidase–>delayed sugar hydrolysis and glucose absorption–>decreases postprandial hyperglycemia
USES: Monotherapy in T2DM or in combination
TOXICITY: GI disturbances
Exenatide
GLP-1 receptor agonist
MOA: slows gastric emptying, stimulates glucose-induced insulin secretion, and suppresses glucagon release
USES: T2DM
SIDE EFFECTS: nausea, vomiting, pancreatitis
Liraglutide
GLP-1 receptor agonist
MOA: slows gastric emptying, stimulates glucose-induced insulin secretion, and suppresses glucagon release
USES: T2DM
SIDE EFFECTS: nausea, vomiting, pancreatitis
Somatostatin
USES: acromegaly, carcinoid, gastronomy, glucagonoma, esophageal varices
Oxytocin
USES: stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage
ADH
USES: pituitary (central, not nephrogenic) DI
Demeclocycline
MOA: ADH antagonist (member of the tetracycline family)
USES: SIADH
TOXICITY: nephrogenic DI, photosensitivity, abnormalities of bone and teeth
Canagliflozin
Sodium-glucose co transporter (SGLT2) inhibitor
Hydrocortisone
Glucocorticoid
MOA: metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB
USES: Addison’s disease, inflammation, immune suppression, asthma
TOXICITY: iatrogenic Cushing’s syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes. Adrenal insufficiency when drug stopped abruptly after chronic use
Growth hormone
USES: GH deficiency, turners syndrome
Triiodothyronine
MOA: thyroxine replacement
USES: hypothyroidism, myxedema
TOXICITY: tachycardia, heat intolerance, tremors, arrhythmia
Sitagliptin
DPP-4 inhibitor
MOA: increases insulin, decreases glucagon release
USES: T2DM
TOXICITY: mild urinary or respiratory infections
Saxagliptin
DPP-4 inhibitor
MOA: increases insulin, decreases glucagon release
USES: T2DM
TOXICITY: mild urinary or respiratory infections
Linagliptin
DPP-4 inhibitor
MOA: increases insulin, decreases glucagon release
USES: T2DM
TOXICITY: mild urinary or respiratory infections
Glipizide
Second generation Sulfonylurea
MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx
USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM
TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia
Glimepiride
Second generation Sulfonylurea
MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx
USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM
TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia
Glyburide
Second generation Sulfonylurea
MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx
USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM
TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia
Chlorpropamide
First generation Sulfonylurea
MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx
USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM
TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia
Tolbutamide
First generation Sulfonylurea
MOA: closes K+ channel in B cell membrane, so cell depolarizes–>triggering of insulin release via increased calcium influx
USES: stimulate release of endogenous insulin on type 2 DM. Require some islet function, so useless in T1DM
TOXICITY: risk of hypoglycemia increased in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia
Methimazole
Anti-thyroid drug
MOA: thyroid peroxidase inhibitor–prevents incorporation of iodide ion onto tyrosyl residues of thyroglobulin, resulting in decreased production of T3/T4
USES: hyperthyroidism (action takes time due to large stores of thyroid hormone that must be exhausted)
SIDE EFFECTS: agranulocytosis, hepatotoxicity, vasculitis, hypoprothrombinemia, rash, associated with birth defects
Tesamorelin
GHRH analog used to treat HIV-associated lipodystrophy
Octreotide
Somatostatin analog used to treat GH excess.
Pegvisomant
Growth hormone receptor antagonist used to treat GH excess
