Pharm Test 3 Goz 2

Front 1

In post-menapausal women, where is most of the estrogen coming from?

Back 1

Adrenal cortex

Front 2

What are the three synthetic pathways for steroid hormones?

Back 2

(1) Mineralocorticoid
(2) Glucocorticoid
(3) Androgen/Estrogen Pathway

Front 3

What is the mineralocorticoid pathway?

Back 3

In the liver...
Cholesterol --> Progesterone --> Aldosterone

Front 4

What is the glucocorticoid pathway?

Back 4

Cholesterol --> Cortisol or..
Progesterone --> Cortisol

Front 5

What is the androgen/estrogen pathway?

Back 5

Estradiol --> Testosterone

Front 6

Describe the mechanism of steroid hormones.

Back 6

Steroids diffuse into the cell cytoplasm where they combine with receptors specific for each of the steroids. The steroid-receptor complex translocates into the nucleus where it binds to specific promotor regions of DNA to activate or enhance transcription of mRNA from steroid-specific genes with subsequent translation into proteins.

Front 7

What are two possibilites when binding to promoter region?

Back 7

(1) Either increase production of a specific protein or
(2) Decrease the synthesis of a protein

Front 8

Explain what it means for glucocorticoids to have a permissive effect.

Back 8

Glucocorticoids allow for (1) greater effects of catecholamines on the vascular and bronchial smooth muscle
(2) lipolysis on fat cells which can increase the glucose levels (3) stimulate the breakdown of muscle to amino acds

Front 9

Define Addison's Disease and Cushing's disease.

Back 9

Addison's - deficiency in glucocorticoid production
Cushing's- overproduction of glucocorticoid production

Front 10

When do we use glucocorticoids the most?

Back 10

Conditions associated with inflammatory reactions and similarly autoimmune diseases.

Front 11

What is the mechanism of an inflammatory reaction?

Back 11

(1) Antigen present
(2) § The antigen is taken up by antigen presenting cells which break up the protein/antigen ad display on the surface of the antigen presenting cells.
(3) This then acts on T cells (CD4 Helper cells) and that causes formation of activated T cells.
(4) § The activated T cells produce cytokines - such as the IL, interferons. One of the effects of the cytokines is to take CD8 cells to activate them and these then will lyze such things as invading bacteria.
(5) Another important effect is that the cytokines act on B cells. B cells produce antibodies and bind to the mast cell and basophils.
(6) The antigen crosslinks the antibodies and causes the release of histamine and platelet activating factor - histamine, PAF, leukotriens.
(7) he cytokines also produce eosinophils --> histamines and luekotrienes
□ The histamine and leukotrienes and the histamine, PAF and leukotrienes will cause vasodilation and inflammation.

Front 12

Where do gluocorticoids fit in?

Back 12

Glucocorticoids block the activation of T cells which in effect blocks the release of CD8 cells, blocks the release of cytokines, blocks the release of inflammatory mediators from the mast cells and basophils, blocks the release of eosinophils. They also appear to have a direct action causing vasoconstriction at the site of inflammation.
Also, bind to phospholipase E2, which then prevents the arachidonic acid formation and thus the downstream products

Front 13

When are glucocorticoids contraindicated?

Back 13

For emergency situations - so not anaphylaxis (use epinephrine instead).

Front 14

What are some indications for glucocorticoids?

Back 14

(1) Leukemas and Lymphomas
(2) Premature Infants
(3) Asthma
(4)

Front 15

What are possible toxicities of glucocorticoids?

Back 15

(1) Must taper off of drug
(2) At high pharmacological doses, can get mineral imbalance.
(3) Diabeteic because glucocorticoids can induce gluconeogenesis.
(4) Long term use can deem cataracts
(5) Osteoporosis
(6) Mood changes - insomnia
(7) Moon face and hump back.

Front 16

What is the short-acting, intermediate-acting, and the long-acting luoccorticoid called?

Back 16

(1) short-acting Hydrocortison: 8-12 hours
(2) Intermeidate-acting: Prednisone: 12-36 hours
(3) Long-acting Flutacasone: 24-72 hours

Front 17

With regards to glucocorticoids, what is the duration related to?

Back 17

he duration of action is not related to the half life. The effect persists with the proteins being made and therefore has a lag time. The duration probably has something to do with the turnover of many proteins.

Front 18

What ae two mineralcorticoids? both physiological and synthetic?

Back 18

(1) Aldosterone - physiological
(2) Fludrocortisone - synthetic

Front 19

What is fludrocortisone used to treat?

Back 19

Orthostatic Hypotension.

Front 20

Where and what do aldosterone and fludrocortisone do?

Back 20

Both Aldosterone and fludrocortisone enhance the reabsorption of sodium from the distal convoluted and proximal collecting renal tubules through increasing the number of lumenal channels and the Na+ ATPase and thus promotes increased Na+ in the blood.

Front 21

What drug acts as an antagonist to fludrocortisone and aldosterone?

Back 21

Spironolactaone

Front 22

What are the two naturally occuring hormones produced by the ovaries?

Back 22

(1) Beta-estradiol
(2) Progesterone.

Front 23

What are the ovarian drugs, such as ethinyl estradiol and norethindrone used for?

Back 23

(1) Hypogonadism
(2) Orthostatic hypotension
(3) oral contraceptives.

Front 24

In order to make ethinyl estradiol effective oraly,what was added to it?

Back 24

an ethinyl group

Front 25

What are the synthetic derivatives of the ovarian hormones?

Back 25

(1) Ethinyl etradiol
(2) Norethindrone

Front 26

Why are oral contraceptives not effective when taking antibiotics or rifampin?

Back 26

(1) By inhibiting the bacterial glucoronidase in bacteria. When the drug is glucoronidated in the liver and made more polar will be reabsorbed back into the blood. If you kill the bacteria - you are decreasing this enzyme and making the drug less polar and less secreted.
(2) Since the steroids are metabolized by the cytocrome p450 enzyme, you have greater metabolism of the oral contraceptive and both of these cause a decrease concentration of the oral contraceptive.

Front 27

What is the mechanism of ethinyl-estradiol? Norethindrone?

Back 27

Ethinyl-estradiol will block the effect of FSH. Norethindrone will block the effect on the lutenizing hormone and the maturation of the oocyte. In addition, Norethindrone will make the cervical mucouse less hospitable. Both effect the endometrium to prevent pregnancy.

Front 28

What are some possible probems with ethinyl-estradiol and norethindrone?

Back 28

□ Increase risks for acquiring clots- this problem has diminished because lower doses of these can be used. A woman who smokes is at greater risks for developing clots.

Front 29

What are two antagonists of estrogen and pregesterone?

Back 29

(1) Tamoxifen
(2) Roloxafene
These are both antagonists of uterine and breast estrogen receptors.

Front 30

What are the uses of Tamoxifen?

Back 30

To prevent the relapse of breast cancer.

Front 31

What is raloxifene used for?

Back 31

To txt osteoporosis.

Front 32

Which estrogen antagonist has been used to abort early pregnancies?

Back 32

Mifepristone

Front 33

What is testosterone used for?

Back 33

For the txt of hypogonadism

Front 34

How is Finasteride used?

Back 34

Finasteride inhibits the alpha reductase and thus, inhibits the formation of dihydrotestosterone (active form of testosterone).Used in the txt benign prostatic hyperplasia - increased prostate size.