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pharmacology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

The adrenal medulla is responsible for secreting ____ and ____.

A

Epinephrine and Norepinephrine

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2
Q

The adrenal cortex secretes ______ and _____.

A

Corticosteroids and androgens

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3
Q

What effect does cortisol have on glucose levels?

A

Increases glucose levels

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4
Q

What are the cardiovascular effects of cortisol?

A

Increased CO and vasoconstriction

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5
Q

What is the effect that cortisol has on the fetus?

A

Induced fetal lung surfactant secretion

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6
Q

What are some of the physical findings of excess cortisol?

A

Buffalo hump, muscle wasting, moon face, striae, poor wound healing

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7
Q

What are some of the physical findings of too little cortisol?

A

Bronze pigmentation of the skin, changes in body hair distribution, GI disturbances, weakness, weight loss

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8
Q

What type of receptor is activated via glucticocorticoids?

A

intracellular nuclear transcription factor receptors

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9
Q

What is the response of glucocorticoid receptor activation?

A

Up or down regulation of specific genes

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10
Q

How is the metabolism of glucocorticoids slowed down?

A

Increasing oral effectiveness, increase the potency, increase the duration of action

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11
Q

What drug is used in endocrine replacement therapy?

A

Hydrocortisone

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12
Q

What receptors does hydrocortisone active?

A

GC and MC

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13
Q

What is the duration of hydrocortisone?

A

8-12 hrs (short acting)

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14
Q

How is prednisone different than hydrocortisone?

A

Intermediate acting (18-36 hrs), partially GC selective, slower metabolism

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15
Q

Which glucocorticoid is the longest acting?

A

Dexamethasone

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16
Q

Which GC drug is MC selective?

A

Fludrocortisone

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17
Q

What properties make dexamethasone long acting (36-54 hrs)?

A

Low protein binding (higher free drug concentration); slower metabolism

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18
Q

When would fludrocortisone be used?

A

adrenal failure, 21-hydroxylase deficiency

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19
Q

Which drug is a MC antagonist?

A

Spironolactone

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20
Q

What is the MOA for decreasing redness and swelling of GC?

A

Vasoconstriction, decrease vascular permeability, decrease histamine release

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21
Q

What is the MOA of how GC decrease fever and pain?

A

Inhibition of arachidonic acid metabolism which decreases prostaglandins and leukotrienes

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22
Q

What is the cause of the poor wound healing of excess GCs?

A

Decreased fibrin and collagen formation

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23
Q

Why is risk of infection a side effect of GC use?

A

suppression of the immune system via decreased leukocytes and inhibition of the neutrophils

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24
Q

Describe the proper ways to dose GCs?

A

Short term –> high dose or Long term–> low dose

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25
Q

Describe the feedback regulation effects of GC?

A

Suppression of the HPA axis which suppresses ACTH release

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26
Q

How are the GCs excreted?

A

Via the kidney

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27
Q

Side effects of MC receptor activation?

A

Hypernatremia, hypokalemia, edema, hypertension

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28
Q

What is the rate limiting step in TH synthesis?

A

The conversion of iodide to iodine via perioxidase

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29
Q

Long duration of action of levothyroxine (T4) is due to which factor?

A

highly protein bound

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30
Q

Slow onset of levothyroxine is due to what?

A

Conversion to T3 in the body

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31
Q

Why is liothyroine rapid onset?

A

less protein-bound and more potent

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32
Q

When should liothyroine be considered?

A

prior and following radioiodine treatment, TSH suppression

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33
Q

Why is there a slow onset with thyroid drugs?

A

it takes time to empty the plasma binding sites since the effects are mediated by protein synthesis and resetting metabolism

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34
Q

What drug interactions are present with thyroid drugs?

A

degradation of vitamin K dependent clotting factors (interfere with warfarin); Increase cardiac responsiveness to catecholamines

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35
Q

What drug is used to treat the sympathetic stimulation of hyperthryoidism?

A

propranolol

36
Q

Methimazole and Propylthiouracil belong to which drug class?

A

Thioamides

37
Q

What enzyme is inhibited by the thioamides?

A

Perioxidase

38
Q

How do PTU and methimazole work to control TH?

A

decrease the synthesis by interfering with iodination and the coupling steps

39
Q

What is a major adverse effects of the hyperthyroid drugs?

A

Agranulocytosis

40
Q

Which is the more potent of the thioamides?

A

Methimazole

41
Q

Why is methimazole preferred over PTU?

A

longer plasma half life and duration and no liver toxicity

42
Q

When is PTU used over methamazole?

A

First trimester of pregnancy and thyroid storms

43
Q

How does potassium iodide differ from PTU and methimazole in controlling TH?

A

Inhibits synthesis and release of TH

44
Q

What is PTU mechanism of action in regards to T4 and T3?

A

Inhibition of T4 conversion to T3

45
Q

When is potassium iodide used most often?

A

decrease size and vascularity of the thyroid gland prior to a thyroidectomy

46
Q

When shouldn’t potassium iodide be used?

A

prior to radio-iodine therapy

47
Q

When is radioactive iodine contraindicated?

A

pregnancy, breast-feeding, young children, salivary adenitis, radiation thyroiditis

48
Q

Explain why thioamides are used with radioactive iodine.

A

Decreases in TH will cause an increase in TSH which will lead to more thyroid activity so more of the radio-active iodine will be taken up into the thyroid

49
Q

In treating a thyroid storm, what drugs are used and why?

A

Iodides–decrease release of preformed TH; PTU–decrease synthesis and conversion of T3 from T4; Glucocorticoids–prevent shock and slow conversion; Propanolol–symptomatic relief of sympathetic effects

50
Q

Sex hormones bind to which kind of receptor?

A

Nuclear transcription factor receptor

51
Q

What effect does estrogen have on cholesterol?

A

Increase HDL and decrease LDL

52
Q

What effect does estrogen have on the CV system?

A

Increased clotting factors, decreased fibrinogen, antithrombin, and protein S, plasminogen activator type I

53
Q

What effect does estrogen have on the bones?

A

Increased bone mineral density, bone maturation, closure of the epiphyseal plates

54
Q

What are the therapeutic uses of estrogen?

A

Replacement therapy, post menopause or after oophorectomy, suppressive therapy

55
Q

What are the three types of estrogens used in drugs?

A

Estradiol, Conjugated estrogens, Ethinyl Estradiol

56
Q

When are progestins used?

A

Replacement therapy and suppressive therapy

57
Q

Which progestin have little to no androgen effects?

A

Medroxyprogesterone acetate

58
Q

Which progestin is structurally related to testosterone?

A

Norethindrone

59
Q

What side effects are strictly related to norethindrone?

A

Acne, weight gain, masculinization, altered libido

60
Q

What symptoms are relieved in HRT for post menopausal women?

A

vasomotor, urogenital atrophy, psychological

61
Q

What are the risks of long-term HRT?

A

increased risk of heart disease, strokes, PE, breast cancer, endometrial cancer (E only)

62
Q

How do SERMs work?

A

Agonist and antagonist effects at estrogen receptors depending on the receptor conformation which will active different response elements

63
Q

What are the two SERM drugs?

A

Raloxifene and Tamoxifen

64
Q

How do the SERM drugs differ in their effects?

A

Raloxifene is an antagonist in both the breast and uterus (reducing risk) and Tamoxifen is only antagonizing in breast tissue and agonizing in the endometrial tissues

65
Q

In the combo contraceptives, what is the estrogen component?

A

Ethinyl estradiol

66
Q

What is the progestin component in COC?

A

norethinadrone

67
Q

How do COC work to disrupt the cycle?

A

increase estrogen levels which negatively inhibit the hypothalamus and anterior pituitary to release less FSH and LH = no follicular development

68
Q

What is the primary way that COC work to stop pregnancy from occurring?

A

Prevent ovulation

69
Q

What are the secondary ways that COC work to inhibit pregnancy?

A

thickening of the cervical mucus

70
Q

Which progestin components avoid the masculinizing effects?

A

Norethynodrel, norgestimate, drospirenone

71
Q

Which progestin is anti-androgenic?

A

drospirenone

72
Q

Which progestins have androgenic side effects?

A

Norethindrone, levonorgesterol

73
Q

When would you need to consider back up contraceptives when using COCs?

A

Missed 2 or more consecutive doses

74
Q

When will menses and fertility return after discontinuation of COCs?

A

30 days and 90 days

75
Q

What lifestyle factors increase risk of thromboembolism in patients using COCs?

A

over the age of 35 and smoking history

76
Q

Why do COCs have many drug interactions?

A

they are metabolized by the liver

77
Q

What are absolute contraindications of using COCs?

A

Pregnancy, estrogen-responsive tumors, tobacco smoking over the age of 35

78
Q

What are the progestin only slow release drugs used?

A

Levonorgestral, etonogestral, medroxyprogesterone acetate

79
Q

What are the progestin only oral drugs?

A

Norethindrone, drosperinone

80
Q

When would an progestin only oral drug be used?

A

when estrogen is contraindicated and greater chance of pregnancy is acceptable

81
Q

How does norethindrone stop pregnancy?

A

inhibition of fertilization and implantation

82
Q

How does drosperinone stop pregnancy?

A

inhibition of ovulation

83
Q

What is the MOA of the emergency contraceptive drugs?

A

inhibition or delay of ovulation; inhibition of fertilization but not implantation (DOESN’T AFFECT AN ESTABLISHED PREGNANCY)

84
Q

What are the two options of emergency contraceptive drugs?

A

Levonorgestral, ulipristal

85
Q

What is the MOA of ulipristal?

A

Mixed agonist/antagonist actions at progestin receptors to delay ovulation

86
Q

Which emergency contraceptive is sold over the counter?

A

Levonorgestral

87
Q

How long after unprotected sex can ulipristal be used to impede ovulation?

A

up to 5 days

pharmacology (4 decks)

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