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Pharmacology > Endocrine Drugs > Flashcards

Endocrine Drugs Flashcards

1
Q

denosumab

A

RANK-L monoclonal ab used for osteoporosis

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2
Q

mechanism of -dronate drugs

A

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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3
Q

clinical use of -dronate drugs

A
  • osteoporosis
  • hypercalcemia
  • Paget’s dz
  • corticosteroid-induced osteoporosis
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4
Q

SEs of -dronate drugs

A
  • corrosive esophagitis

- jaw osteonecrosis

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5
Q

mechanism of teriparatide

A

recombinant PTH analogue which, if given intermittently, actually stimulates osteoblasts to lay down new bone more than it stimulates osteoclasts to resorb bone

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6
Q

clinical use of teriparatide

A

severe osteoporosis with poor BMD or multiple fractures

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7
Q

SEs of teriparatide

A
  • transient hypercalcemia

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

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8
Q

thionamides include:

A

methimazole, propylthiouracil

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9
Q

mechanism of methimazole, propylthiouracil (thionamides)

A
  • 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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10
Q

clinical use of methimazole, propylthiouracil (thionamides)

A
  • hyperthyroidism

- use PTU in pregnancy

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11
Q

SEs of methimazole, propylthiouracil (thionamides)

A
  • itchy skin rash
  • agranulocytosis
  • aplastic anemia
  • hepatotoxicity (PTU)
  • teratogen (methimazole)
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12
Q

mechanism of levothyroxine

A

synthetic free T4 replacement

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13
Q

clinical use of levothyroxine

A

hypothyroidism, myxedema

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14
Q

SEs of levothyroxine

A

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

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15
Q

Why do we give levothyroxine but not triiodothyronine?

A

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

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16
Q

mechanism and use of -vaptan drugs

A

ADH antagonists - SIADH

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17
Q

mechanism and use of demeclocycline

A

ADH antagonist - SIADH

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18
Q

mechanism and use of cinacalcet

A

sensitizes CaSR to circulating Ca 2+, so less PTH secretion by PT glands - hypercalcemia due to primary or secondary hyperPTism

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19
Q

Lupron Depo-Ped

A

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
Q

mechanism of sulfonylureas and -glinide drugs

A

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

21
Q

clinical use of sulfonylureas and -glinide drugs

A

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

22
Q

SEs of sulfonylureas and -glinide drugs

A

hypoglycemia (prevented by taking with food and eating often)

23
Q

mechanism of biguanides (metformin)

A
  • decreases gluconeogenesis
  • increases glycolysis
  • increases peripheral glucose uptake by muscles
  • decreases hepatic steatosis
  • increases liver’s insulin sensitivity
24
Q

clinical use of biguanides (metformin)

A

first-line for DM II

25
Q

SEs of biguanides (metformin)

A
  • diarrhea, nausea

- lactic acidosis (rare)

26
Q

mechanism of acarbose, miglitol

A
  • inhibition of intestinal brush border a-glucosidases
  • delayed carbohydrate hydrolysis and glucose absorption
  • decrease in post-prandial hyperglycemia
27
Q

clinical use of acarbose, miglitol

A

DM II (monotherapy or in combo)

28
Q

SEs of acarbose, miglitol

A

GI disturbances like flatulence (causes a malabsorption!)

29
Q

mechanism of thiazolidinediones (-glitazone)

A

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

30
Q

clinical use of thiazolidinediones (-glitazone)

A

DM II (monotherapy or in combo)

31
Q

SEs of thiazolidinediones (-glitazone)

A

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

32
Q

mechanism of exenatide, liraglutide

A

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

33
Q

clinical use of exenatide, liraglutide, -gliptin drugs

A

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

34
Q

SEs of exenatide, liraglutide

A

nausea, vomiting, pancreatitis

35
Q

mechanism of -gliptin drugs

A

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

36
Q

SEs of -gliptin drugs

A

urinary or resp. infections

37
Q

mechanism of canagliflozin

A

SGLT2 inh –> blocks reabsorption of glucose in PCT

38
Q

clinical use of canagliflozin

A

DM II

39
Q

SEs of canagliflozin

A

glucosuria –> UTIs, vaginal yeast infxns

40
Q

mechanism of pramlintide

A

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

41
Q

clinical use of pramlintide

A

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

42
Q

SEs of pramlintide

A

hypoglycemia, diarrhea, nausea

43
Q

mechanism and duration of action of aspart, glulisine, lispro

A
  • rapid acting insulin (4-6 hrs)

- monomers (active already)

44
Q

mechanism and duration of action of regular insulin

A
  • short acting insulin (6-8 hrs)
  • hexamers w/ central Zn 2+
  • must be broken down into dimers and then monomers to be active
45
Q

mechanism and duration of action of NPH insulin

A
  • intermediate acting insulin (12-20 hrs)

- smaller crystals in protamine, Zn 2+ buffer

46
Q

mechanism and duration of action of detemir, glargine, ultralente

A
  • long acting insulin (18-24 hrs)

- larger crystals in acetate, Zn 2+ buffer

Pharmacology (22 decks)

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