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
Describe the feedback regulation effects of GC?
Suppression of the HPA axis which suppresses ACTH release
26
How are the GCs excreted?
Via the kidney
27
Side effects of MC receptor activation?
Hypernatremia, hypokalemia, edema, hypertension
28
What is the rate limiting step in TH synthesis?
The conversion of iodide to iodine via perioxidase
29
Long duration of action of levothyroxine (T4) is due to which factor?
highly protein bound
30
Slow onset of levothyroxine is due to what?
Conversion to T3 in the body
31
Why is liothyroine rapid onset?
less protein-bound and more potent
32
When should liothyroine be considered?
prior and following radioiodine treatment, TSH suppression
33
Why is there a slow onset with thyroid drugs?
it takes time to empty the plasma binding sites since the effects are mediated by protein synthesis and resetting metabolism
34
What drug interactions are present with thyroid drugs?
degradation of vitamin K dependent clotting factors (interfere with warfarin); Increase cardiac responsiveness to catecholamines
35
What drug is used to treat the sympathetic stimulation of hyperthryoidism?
propranolol
36
Methimazole and Propylthiouracil belong to which drug class?
Thioamides
37
What enzyme is inhibited by the thioamides?
Perioxidase
38
How do PTU and methimazole work to control TH?
decrease the synthesis by interfering with iodination and the coupling steps
39
What is a major adverse effects of the hyperthyroid drugs?
Agranulocytosis
40
Which is the more potent of the thioamides?
Methimazole
41
Why is methimazole preferred over PTU?
longer plasma half life and duration and no liver toxicity
42
When is PTU used over methamazole?
First trimester of pregnancy and thyroid storms
43
How does potassium iodide differ from PTU and methimazole in controlling TH?
Inhibits synthesis and release of TH
44
What is PTU mechanism of action in regards to T4 and T3?
Inhibition of T4 conversion to T3
45
When is potassium iodide used most often?
decrease size and vascularity of the thyroid gland prior to a thyroidectomy
46
When shouldn't potassium iodide be used?
prior to radio-iodine therapy
47
When is radioactive iodine contraindicated?
pregnancy, breast-feeding, young children, salivary adenitis, radiation thyroiditis
48
Explain why thioamides are used with radioactive iodine.
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
In treating a thyroid storm, what drugs are used and why?
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
Sex hormones bind to which kind of receptor?
Nuclear transcription factor receptor
51
What effect does estrogen have on cholesterol?
Increase HDL and decrease LDL
52
What effect does estrogen have on the CV system?
Increased clotting factors, decreased fibrinogen, antithrombin, and protein S, plasminogen activator type I
53
What effect does estrogen have on the bones?
Increased bone mineral density, bone maturation, closure of the epiphyseal plates
54
What are the therapeutic uses of estrogen?
Replacement therapy, post menopause or after oophorectomy, suppressive therapy
55
What are the three types of estrogens used in drugs?
Estradiol, Conjugated estrogens, Ethinyl Estradiol
56
When are progestins used?
Replacement therapy and suppressive therapy
57
Which progestin have little to no androgen effects?
Medroxyprogesterone acetate
58
Which progestin is structurally related to testosterone?
Norethindrone
59
What side effects are strictly related to norethindrone?
Acne, weight gain, masculinization, altered libido
60
What symptoms are relieved in HRT for post menopausal women?
vasomotor, urogenital atrophy, psychological
61
What are the risks of long-term HRT?
increased risk of heart disease, strokes, PE, breast cancer, endometrial cancer (E only)
62
How do SERMs work?
Agonist and antagonist effects at estrogen receptors depending on the receptor conformation which will active different response elements
63
What are the two SERM drugs?
Raloxifene and Tamoxifen
64
How do the SERM drugs differ in their effects?
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
In the combo contraceptives, what is the estrogen component?
Ethinyl estradiol
66
What is the progestin component in COC?
norethinadrone
67
How do COC work to disrupt the cycle?
increase estrogen levels which negatively inhibit the hypothalamus and anterior pituitary to release less FSH and LH = no follicular development
68
What is the primary way that COC work to stop pregnancy from occurring?
Prevent ovulation
69
What are the secondary ways that COC work to inhibit pregnancy?
thickening of the cervical mucus
70
Which progestin components avoid the masculinizing effects?
Norethynodrel, norgestimate, drospirenone
71
Which progestin is anti-androgenic?
drospirenone
72
Which progestins have androgenic side effects?
Norethindrone, levonorgesterol
73
When would you need to consider back up contraceptives when using COCs?
Missed 2 or more consecutive doses
74
When will menses and fertility return after discontinuation of COCs?
30 days and 90 days
75
What lifestyle factors increase risk of thromboembolism in patients using COCs?
over the age of 35 and smoking history
76
Why do COCs have many drug interactions?
they are metabolized by the liver
77
What are absolute contraindications of using COCs?
Pregnancy, estrogen-responsive tumors, tobacco smoking over the age of 35
78
What are the progestin only slow release drugs used?
Levonorgestral, etonogestral, medroxyprogesterone acetate
79
What are the progestin only oral drugs?
Norethindrone, drosperinone
80
When would an progestin only oral drug be used?
when estrogen is contraindicated and greater chance of pregnancy is acceptable
81
How does norethindrone stop pregnancy?
inhibition of fertilization and implantation
82
How does drosperinone stop pregnancy?
inhibition of ovulation
83
What is the MOA of the emergency contraceptive drugs?
inhibition or delay of ovulation; inhibition of fertilization but not implantation (DOESN'T AFFECT AN ESTABLISHED PREGNANCY)
84
What are the two options of emergency contraceptive drugs?
Levonorgestral, ulipristal
85
What is the MOA of ulipristal?
Mixed agonist/antagonist actions at progestin receptors to delay ovulation
86
Which emergency contraceptive is sold over the counter?
Levonorgestral
87
How long after unprotected sex can ulipristal be used to impede ovulation?
up to 5 days