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Endocrine 2 pharm > Thyroid > Flashcards

Thyroid Flashcards

1
Q

what is the drug of choice for hypothyroidism

A

levothyroxin

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2
Q

what is the chemical structure of levothyroxin

A

L-isomer of t4

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3
Q

what is the drug with the chemical structure of T3 and what is its indication

A

liothyronine, used for myxedema coma

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4
Q

Which drug has the longer half-life, levothyroxin or liothyronine

A

levothyroxin (t4) gives it a prodrug buffer concentration in blood good for different metabolic situations

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5
Q

why give liothyronine for myxedema coma

A

quick onset for life threatening situations

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6
Q

when do you give radioactive iodide 131

A

hyperthyroidism and thyrotoxicosis

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7
Q

what is the MOA of radioactive iodide 131

A

emits beta particles causing local destruction of the thyroid gland

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8
Q

What is the concern regarding radioactive iodide 131

A

may cause hypothyroidism after too much destruction

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9
Q

what role does the na/I symporter play in the uptake of radioactive iodide 131?

A

it cannot distinguish between the radioactive form and the endogenous form of 127.

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10
Q

what is the wolf chaikoff effect

A

increase in iodide inhibits thyroid hormone synthesis and release because the NA/ I- symporter is down regulated

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11
Q

what is the use of potassium iodide/inorganic iodide

A

given before thyroid gland surgery because iodide reduces valcularization and size of the gland making excision easier

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12
Q

why can’t potassium iodide be given chronically to hyperthyroid patients

A

only causes a transient suppression of hormone release, after a while the hormones are back to normal

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13
Q

what are the 2 thioamines

A

propylthiouracil and methimazole

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14
Q

what is the MOA of thioamines

A

compete with thyroglobulin for oxidized iodide inhibiting organification and coupling INHIBITS THYROID PEROXIDASE

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15
Q

When do you see the effects of thioamines

A

2 weeks later because of preformed hormone, affects synthesis not secretion

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16
Q

what drugs cause goiter formation?

A

thioamines

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17
Q

Why does thioamines cause goiter?

A

the increase in TSH due to the decrease in hormone causes thyroid hypertrophy.

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18
Q

what thioamine is the drug of choice in clinical practice?

A

methimazole because it only requires 1 dose a day (longer half life ) and has a less adverse profile

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19
Q

what are the 2 indications of propothiouracil?

A

thyroid storm, and first trimester of pregnancy

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20
Q

why is propothiouracil used in thyroid storm

A

block thyroid peroxidase but also inhibits the conversion of t4 to t3 in peripheral cells

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21
Q

what side effect can methomixazole cause in pregnancy?

A

aplasia cutis

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22
Q

What is the regimen of thyroid drugs given for pregnancy?

A

propothiouracil for first trimester (upto 13 weeks) and then give methimazole for the rest.

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23
Q

What class of drugs can be used to stop symptoms of hyperthyroidism?

A

beta blockers

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24
Q

What two beta blockers are used?

A

propanolol (nonspecific) and esmolol

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25
Q

What is the specific use of esmolol dealing with hyperthyroidism?

A

used in thyroid storm because of rapid onset and short elimination 1/2 life.

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26
Q

what is amiodarone?

A

antiarrythmic drug

27
Q

how can amiodarone cause hypothyroidism

A

has a lot of iodide creating a wolf chaskoff like effect

28
Q

how can amiodarone cause hyperthyroidism

A

Type 1 thyrotoxicosis –> increased iodide leads to increased thyroid synthesis and release
Type 2 Throiditis –> autoimmune thyroiditis is induced that leads to release of excess thyroid hormone from the colloid.

29
Q

how does amiodarone effect thyroid hormone in the peripherally?

A

inhibits type 1 deiodinase resulting in decrease conversion of T4 to T3 and increased rT3.

30
Q

When should you give IV insulin?

A

diabetic type 1 ketoacidosis

31
Q

what are the two alpha glucosidase inhibitors?

A

acarbose and miglitol

32
Q

what is the MOA of acarbose and miglitol

A

bind to alpha glucosidase enzmes and inhibit the cleavage of carbs to glucose and reside the postprandial peak in glucose.

33
Q

what are the 3 limitations of alpha glucosidase inhibitors?

A

only effective when taken with meals, cause diarrhea, flatulence , contraindicated with inflammatory bowel disease

34
Q

what are the 2 indications of acarbose and miglitol?

A

post prandial mild hyperglycemia, and new onset patients with mild hyperglycemia

35
Q

sulfonyl and meglitinide MOA

A

bind to the SUR 1 subunit inhibiting the K+/ATP channel causing depolarization and increased insulin release from the cell.

36
Q

what are the two first generation sulfonylureas

A

chlorpromide and tolbutamide

37
Q

What are the 3 second generation sulfonylureas

A

Glimepiride, gpizide, glyburide

38
Q

what are the 2 megliinides

A

Nateglinide and repaglinide

39
Q

what is the difference between sulfonylureas and meglitinides?

A

both bind to SUR 1 subunits causing depolarization and increasing insulin release, however they bind to different subunits.

40
Q

2 adverse effects of insulin secratogues are

A

hypoglycemia and weight gain

41
Q

when should you avoid sulfonryl ureas?

A

patient with a sulfa drug allergy

42
Q

what is the MOA of metformin?

A

biguanide that decreases glucose production in the liver by increasing AMPK.

43
Q

what else does metformin inhibit?

A

gluconeogenesis in the liver, cholesterol synthesis and fatty acid synthesis

44
Q

what are the benefits of metformin over insulin secratogues

A

lower lipid profiles and a decrease in weight

45
Q

what is the major adverse effect of metformin

A

lactic acidosis from shutting away metabolic acids through gluconeogenic pathways.

46
Q

what is the b-cell hormone that is co -secreted with insulin

A

amylin

47
Q

what is the name of an amylinin analogue

A

pramlintide

48
Q

what are the two GLP-1 analogues?

A

exenatide and liraglutide

49
Q

What is the main adverse effect of GLP-1 analogues?

A

acute pancreatitis

50
Q

what is the MOA of GLP-1 analogues?

A

increase secretion of insulin by pancreatic B-cells in a glucose dependent manner, suppresses glucagon, slows emptying, decreases appetite

51
Q

what is the MOA of DPP 4 inhibitors?

A

prolong GLP-1 by inhibiting DPP 4, promote insulin secretion and decrease glucagon.

52
Q

What is the respiratory infection caused by DPP 4 inhibitors?

A

respiratory infection

53
Q

what are the 3DPP inhibitors?

A

sitagliptin, saxagliptin, linagliptin

54
Q

what is the MOA of TMZs?

A

insulin sensitizers that enhance the function of insulin at target tissues and is a synthetic ligand which affects adipose cell differentiation and lipid metabolism

55
Q

where does TMZ cause fatty acids to go?

A

adipose tissue rather than skeletal, muscle or liver.

56
Q

what is one side effect of TMZ related to its MOA?

A

bone fractures and weight gain

57
Q

what is TMZ’s current contraindication

A

hepatotoxiciy

58
Q

what are the 2 TMZs?

A

rosiglitazone and pioglitazone

59
Q

what does rosiglitazone cause?

A

myocardial infarction (only give to those who couldnt be saved otherwise.)

60
Q

what is the MOA of sglt2 inhibitors?

A

inhibit SGLT in renal tubules to reduce glucose reabsorption

61
Q

current indication of SGLT2 inhibitors?

A

adjunct to diet and exercise in type 2 diabetic patients

62
Q

what is the MOA of diazoxide?

A

bind to sur1 subunit of k+/ATP and stabilizes open state so B- cells remain hpyerpolarized and less insulin is released.

63
Q

When is diazoxide used?

A

stabilize hypoglycemia preoperatively and decrease BP in hypertensive state

64
Q

when should you administer gluccagon?

A

treat hypoglycemia

Endocrine 2 pharm (1 decks)

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