Endocrine Drugs Flashcards
denosumab
RANK-L monoclonal ab used for osteoporosis
mechanism of -dronate drugs
bisphosphonates - pyrophosphate analogues that bind hydroxyapatite in bone and inhibit osteoclast activity and bone resorption by blocking apical GTPase that is used to induce bone hydrolysis
clinical use of -dronate drugs
- osteoporosis
- hypercalcemia
- Paget’s dz
- corticosteroid-induced osteoporosis
SEs of -dronate drugs
- corrosive esophagitis
- jaw osteonecrosis
mechanism of teriparatide
recombinant PTH analogue which, if given intermittently, actually stimulates osteoblasts to lay down new bone more than it stimulates osteoclasts to resorb bone
clinical use of teriparatide
severe osteoporosis with poor BMD or multiple fractures
SEs of teriparatide
- transient hypercalcemia
- do not use for longer than 2 yrs due to osteosarcoma risk
thionamides include:
methimazole, propylthiouracil
mechanism of methimazole, propylthiouracil (thionamides)
- block thyroid peroxidase to prevent oxidation of I an the organification of I –> inh of thyroid hormone synth
- propylthiouracil blocks 5’-deiodinase and thus peripheral conversion of T4 –> T3
clinical use of methimazole, propylthiouracil (thionamides)
- hyperthyroidism
- use PTU in pregnancy
SEs of methimazole, propylthiouracil (thionamides)
- itchy skin rash
- agranulocytosis
- aplastic anemia
- hepatotoxicity (PTU)
- teratogen (methimazole)
mechanism of levothyroxine
synthetic free T4 replacement
clinical use of levothyroxine
hypothyroidism, myxedema
SEs of levothyroxine
tachycardia, heat intolerance, tremors, arrythmias (so start low and titrate up esp in older pts)
Why do we give levothyroxine but not triiodothyronine?
b/c 85% of T3 comes from conversion of T4 by 5’-deiodinase
mechanism and use of -vaptan drugs
ADH antagonists - SIADH
mechanism and use of demeclocycline
ADH antagonist - SIADH
mechanism and use of cinacalcet
sensitizes CaSR to circulating Ca 2+, so less PTH secretion by PT glands - hypercalcemia due to primary or secondary hyperPTism
Lupron Depo-Ped
synthetic LHRH –> causes constant high level of LH that causes the body to stop the LH pulses involved with going through puberty
used to treat precocious puberty - just give this drug until the child is old enough to go through puberty normally
mechanism of sulfonylureas and -glinide drugs
closure of B cell K+ channel –> depolarization –> opening of VG Ca 2+ channels –> insulin secretion
clinical use of sulfonylureas and -glinide drugs
DM II - require functioning B cells (less and less effective w/ progressive B cell loss)
SEs of sulfonylureas and -glinide drugs
hypoglycemia (prevented by taking with food and eating often)
mechanism of biguanides (metformin)
- decreases gluconeogenesis
- increases glycolysis
- increases peripheral glucose uptake by muscles
- decreases hepatic steatosis
- increases liver’s insulin sensitivity
clinical use of biguanides (metformin)
first-line for DM II
SEs of biguanides (metformin)
- diarrhea, nausea
- lactic acidosis (rare)
mechanism of acarbose, miglitol
- inhibition of intestinal brush border a-glucosidases
- delayed carbohydrate hydrolysis and glucose absorption
- decrease in post-prandial hyperglycemia
clinical use of acarbose, miglitol
DM II (monotherapy or in combo)
SEs of acarbose, miglitol
GI disturbances like flatulence (causes a malabsorption!)
mechanism of thiazolidinediones (-glitazone)
increase insulin sensitivity in peripheral tissues by binding to PPAR-y nuclear transcription factor
clinical use of thiazolidinediones (-glitazone)
DM II (monotherapy or in combo)
SEs of thiazolidinediones (-glitazone)
CHF, weight gain, edema, anemia, hepatotoxicity, risk of fractures, risk of MI
mechanism of exenatide, liraglutide
GLP-1 analogues that stimulate insulin secretion and suppress glucagon secretion/gluconeogenesis, contribute significantly to post-prandial glucose control
clinical use of exenatide, liraglutide, -gliptin drugs
DM II (usually used with sulfonylurea or metformin in refractory cases)
SEs of exenatide, liraglutide
nausea, vomiting, pancreatitis
mechanism of -gliptin drugs
DPP4 inh –> prevents breakdown of GLP-1/GIP
SEs of -gliptin drugs
urinary or resp. infections
mechanism of canagliflozin
SGLT2 inh –> blocks reabsorption of glucose in PCT
clinical use of canagliflozin
DM II
SEs of canagliflozin
glucosuria –> UTIs, vaginal yeast infxns
mechanism of pramlintide
amylin analogue packaged with glucose that delays gastric emptying and decreases glucagon secretion, resembles amylin which is a molecule packaged in granules with natural insulin
clinical use of pramlintide
given with insulin in DM I or II, promotes weight loss by delaying gastric emptying and triggering satiety
SEs of pramlintide
hypoglycemia, diarrhea, nausea
mechanism and duration of action of aspart, glulisine, lispro
- rapid acting insulin (4-6 hrs)
- monomers (active already)
mechanism and duration of action of regular insulin
- short acting insulin (6-8 hrs)
- hexamers w/ central Zn 2+
- must be broken down into dimers and then monomers to be active
mechanism and duration of action of NPH insulin
- intermediate acting insulin (12-20 hrs)
- smaller crystals in protamine, Zn 2+ buffer
mechanism and duration of action of detemir, glargine, ultralente
- long acting insulin (18-24 hrs)
- larger crystals in acetate, Zn 2+ buffer
