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Flashcards in Endocrine Drugs Deck (46):
1

denosumab

RANK-L monoclonal ab used for osteoporosis

2

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

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clinical use of -dronate drugs

- osteoporosis
- hypercalcemia
- Paget's dz
- corticosteroid-induced osteoporosis

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SEs of -dronate drugs

- corrosive esophagitis
- jaw osteonecrosis

5

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

6

clinical use of teriparatide

severe osteoporosis with poor BMD or multiple fractures

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SEs of teriparatide

- transient hypercalcemia
- do not use for longer than 2 yrs due to osteosarcoma risk

8

thionamides include:

methimazole, propylthiouracil

9

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

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clinical use of methimazole, propylthiouracil (thionamides)

- hyperthyroidism
- use PTU in pregnancy

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SEs of methimazole, propylthiouracil (thionamides)

- itchy skin rash
- agranulocytosis
- aplastic anemia
- hepatotoxicity (PTU)
- teratogen (methimazole)

12

mechanism of levothyroxine

synthetic free T4 replacement

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clinical use of levothyroxine

hypothyroidism, myxedema

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SEs of levothyroxine

tachycardia, heat intolerance, tremors, arrythmias (so start low and titrate up esp in older pts)

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Why do we give levothyroxine but not triiodothyronine?

b/c 85% of T3 comes from conversion of T4 by 5'-deiodinase

16

mechanism and use of -vaptan drugs

ADH antagonists - SIADH

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mechanism and use of demeclocycline

ADH antagonist - SIADH

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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

19

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

20

mechanism of sulfonylureas and -glinide drugs

closure of B cell K+ channel --> depolarization --> opening of VG Ca 2+ channels --> insulin secretion

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clinical use of sulfonylureas and -glinide drugs

DM II - require functioning B cells (less and less effective w/ progressive B cell loss)

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SEs of sulfonylureas and -glinide drugs

hypoglycemia (prevented by taking with food and eating often)

23

mechanism of biguanides (metformin)

- decreases gluconeogenesis
- increases glycolysis
- increases peripheral glucose uptake by muscles
- decreases hepatic steatosis
- increases liver's insulin sensitivity

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clinical use of biguanides (metformin)

first-line for DM II

25

SEs of biguanides (metformin)

- diarrhea, nausea
- lactic acidosis (rare)

26

mechanism of acarbose, miglitol

- inhibition of intestinal brush border a-glucosidases
- delayed carbohydrate hydrolysis and glucose absorption
- decrease in post-prandial hyperglycemia

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clinical use of acarbose, miglitol

DM II (monotherapy or in combo)

28

SEs of acarbose, miglitol

GI disturbances like flatulence (causes a malabsorption!)

29

mechanism of thiazolidinediones (-glitazone)

increase insulin sensitivity in peripheral tissues by binding to PPAR-y nuclear transcription factor

30

clinical use of thiazolidinediones (-glitazone)

DM II (monotherapy or in combo)

31

SEs of thiazolidinediones (-glitazone)

CHF, weight gain, edema, anemia, hepatotoxicity, risk of fractures, risk of MI

32

mechanism of exenatide, liraglutide

GLP-1 analogues that stimulate insulin secretion and suppress glucagon secretion/gluconeogenesis, contribute significantly to post-prandial glucose control

33

clinical use of exenatide, liraglutide, -gliptin drugs

DM II (usually used with sulfonylurea or metformin in refractory cases)

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SEs of exenatide, liraglutide

nausea, vomiting, pancreatitis

35

mechanism of -gliptin drugs

DPP4 inh --> prevents breakdown of GLP-1/GIP

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SEs of -gliptin drugs

urinary or resp. infections

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mechanism of canagliflozin

SGLT2 inh --> blocks reabsorption of glucose in PCT

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clinical use of canagliflozin

DM II

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SEs of canagliflozin

glucosuria --> UTIs, vaginal yeast infxns

40

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

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clinical use of pramlintide

given with insulin in DM I or II, promotes weight loss by delaying gastric emptying and triggering satiety

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SEs of pramlintide

hypoglycemia, diarrhea, nausea

43

mechanism and duration of action of aspart, glulisine, lispro

- rapid acting insulin (4-6 hrs)
- monomers (active already)

44

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

45

mechanism and duration of action of NPH insulin

- intermediate acting insulin (12-20 hrs)
- smaller crystals in protamine, Zn 2+ buffer

46

mechanism and duration of action of detemir, glargine, ultralente

- long acting insulin (18-24 hrs)
- larger crystals in acetate, Zn 2+ buffer