Endocrine Pharm 3Rd Test

Front 1

Overview of the Endocrine System

Back 1

Endocrine glans - releases hormones into bloodstream and has homeostasis.
Hypothalamus and anterior pituitary are the primary controllers.
Steriods are derived from adrenal cortex and sex hormones.
Amino acid is derived from peptides/proteins.
Posterior pituitary hormones

Front 2

What does the hypothalamus release in the CNS negative feedback mechanism?

Back 2

Hormones: CRH (Corticotropin Releasing Hormone), GnRH (Gonadotropin Releasing Hormone), TRH (Thyrotropin Releasing Hormone)

Front 3

What does the anterio pituitary release in the CNS negative feedback mechanism?

Back 3

Pituitary hormones: ACTH (Adrenocorticotropic Hormones (Corticotropin)), FSH (Follicle Stimulating Hormone), LH (Lutenizing Hormone), TSH (Thyrotropin Releasing Hormone).

Front 4

What does the endocrine/Target Gland release in the CNS negative feedback mechanism?

Back 4

Endocrine Hormones.
Cortisol, sex hormones, T3, and T4.

Front 5

What are the axes for the endocrine system?

Back 5

Hypothalamus --> Anterior Pituitary --> Endocrine/Target gland.

Front 6

What are pathological implications for the Feedback control mechanisms and endocrine function?

Back 6

Primary hypothyroidism and replacement therapy.
The hypo is due to decreased T3 and T4, feedback inhibition, increased TSH, and a goiter.
Replacement is when T3 and T4 go to normal and the goiter shrinks.

Front 7

What are the indications for the endocrine glands drugs?

Back 7

Estrogens and analogs inhibit FSH and LH release.
Also they are used as oral contraceptives and antithryoid drugs.

Front 8

What is the progression for the axis at CRH?

Back 8

Hypothalamus/CRH (+) --> Anterior Pituitary/ACTH--> Adrenal Cortex--> Glucocorticoids/Mineralcorticoids. Gluco cause stress (cortisol). Mineral cause electrolytes

Front 9

What is the progression for the axis at LH and FSH?

Back 9

Hypothalamus/GnRH--> Anterior Pituitary/LH+FSH--> Gonads--> Sex hormones (egg/sperm).

Front 10

Control of synthesis and secretion of Glucocorticoids(Dexamthasone (Decadron); Hydrocortisone (Cortef); Triamcinolone (Aristocort))

Back 10

ACTH stimulates cortisol synthesis in the adrenal coretx.
Negative feedback leads to plasma cortisol inhibition of CRH and ACTH release.
A cyclic release leads to circadian rhythm.
Stress Release that act on a hypothalamic level.

Front 11

Indications for Glucocorticoids (Dexamthasone (Decadron); Hydrocortisone (Cortef); Triamcinolone (Aristocort))

Back 11

Stimulates the adrenocorticotropic hormone (ACTH) release from the anteiror pituitary.

Front 12

What are the primary hormones?

Back 12

Glucocorticoids, Mineralcorticoids, and Small amounts of androgens and estrogens.

Front 13

Therapeutic uses of steroid hormones

Back 13

Replacement therapy and antiinflammatory/immunosuppressant.

Front 14

Sythesis of Steroid Hormones

Back 14

Done as a cholesterl precursor and have three families of related compounds.
The mineral structural changes, synthetic modification enhance gluco and reduce mineral. There is also cross over in actions.
Also has ver little intracellular storage.

Front 15

Mechanism of Action for Glucocorticoids(Dexamthasone (Decadron); Hydrocortisone (Cortef); Triamcinolone (Aristocort))

Back 15

Alter protein synthesis. Bind to a receptor in the cytoplasm. Binds to specific DNA sequence. Causes direct protein synthesis. Can also more immediate actions via cell membrane receptors.

Front 16

Physiologic effects of Glucocorticoids(Dexamthasone (Decadron); Hydrocortisone (Cortef); Triamcinolone (Aristocort))

Back 16

Glucose, protein, and lipid metabolism. Leads to an increase in glucose production and glycogen storage.
Has antiinflammatory effects that inhibit cytokines (Interleukin-1). Inhibits inflammatory cells (macrophages/T lymphocytes). Inhibit adhesion molecules that attract leukocytes.
Immunosuppression. Done at many antiinflam effect that inhibit migration of leukocytes and macrophages.
Have a mineral corticoid action that enhance sodium and water absorption.
Have enhanced vascular reactivity to NE and EPI.
Have altered CNS activity.

Front 17

Therapeutic Glucocorticoids (Dexamthasone (Decadron); Hydrocortisone (Cortef); Triamcinolone (Aristocort)) drugs

Back 17

Have analogs of cortisol.
Administered in systemic and specificly in the nasal/inhalation/topical

Front 18

Replacement therapy of Glucocorticoids (Dexamthasone (Decadron); Hydrocortisone (Cortef); Triamcinolone (Aristocort))

Back 18

Used primarily for Addison's and adrenal sufficiency. Also used following adrenalectomy.

Front 19

Glucocorticoids (Dexamthasone (Decadron); Hydrocortisone (Cortef); Triamcinolone (Aristocort)) used for Nonendocrine conditions

Back 19

Used to control inflammation and the immune respone for relatively short periods of time.
Usd for inflammatory disorders.
Used for immunosuppression.
Used for anti organ rejection for transplants

Front 20

Adverse effects of Glucocorticoids (Dexamthasone (Decadron); Hydrocortisone (Cortef); Triamcinolone (Aristocort))

Back 20

Adrenocortical suppresison due to a systemic administration. This leads to a decreased ACTH and produces adrenal atrophy.
Can lead to drug-induced Cushing syndrome.
Can have breakdown of supporting tissues.
Ulcers, infections, cataracts, mood changes, sodium and water retention.

Front 21

Decribe the GNRH

Back 21

It is called the Gonadotropin releasing hormone which comes from the hypothalamus and stimulates the FSH (follicle stimulating hormone) and LH (lutenizing hormone from the anterior pituitary.

Front 22

What are androgens?

Back 22

Testosterone is synthesis by LH.
T is produced constantly leading to high blood levels which can inhibit GnRH, FSH, and LH release.
Lead to spermatogenesis, maturation of genitalia.
Increaes skeletal muscle and bone mass (anabolic effects).
Stimulation of protein synthesis

Front 23

What does a FSH increase?

Back 23

Androgen binding protein (ABP). Also sperm production.

Front 24

What does ABP faciliatates?

Back 24

Testosterone transport

Front 25

Indications for replacement therapy

Back 25

Delayed puberty, following orchiectomy (cancer), male menopause

Front 26

Adverse effects of clinical androgen

Back 26

Masculinizing effects, irregular menstruation in women. Premature clsoing of epiphyseal plates in children.
Liver damage and tumors.
HTN and water retention.
Increased risk of prostate cancer.
Severity related to dose and duration of therapy.
Testicular atrophy, decreased T production due to feedback inhibiton of FSH and LH.

Front 27

Estrogen (estradiol) and progestins (progesterone) physiologic effects

Back 27

Growth and development of reproductive organs (uterus, vagina, oviducts).

Front 28

Estrogen (estradiol) and progestins (progesterone) cyclic production

Back 28

Follicular phase due to FSH stimulates maturation of follicle which secretes hormones. Have a proliferation and thickening of endometrium.
Ovulation (burst in LH) due to follicle increase.
Luteal phase is a corpus luteum secretes hormones. Further endometrial development.
Pregnancy or menstruation.

Front 29

Pharmacological use of Estrogen (estradiol) and progestins (progesterone)

Back 29

Have a replacement therapy in menopause (HRT). Prevention and treatment of osteoporsis. Have a different increase in bone mineral density, a reduction, and used in combination with calcium/physical activity.
Used for hypogonadism or failure.
Endometriosis which tries to mimick pregnancy.
Used for cancer and contraception.

Front 30

Adverse effects of Estrogen (estradiol)

Back 30

Nausea, swelling of feet and ankles.
Cancer risks especially in postmenopausal women. Risk of coronary event, stroke, gall bladder, and invasive breast cancer.
Premenopausal women can get endometrial cancer risk may decrease, and breast and liver cancers risks may increase.
Can lead to thromboembolism such as MI, stroke.

Front 31

Adverse effects of progesterone

Back 31

Adronergic side effects (acne), menstrual abnormalities, abnormal blood clotting.

Front 32

Selective estrogen receptor modulators (SERMs) Tamoxifen (Novadex) and Raloxifene (Evista)

Back 32

Have both agonist and antagonist actions.
Have estrogen receptor agonists in bone and vasculature.
Anatagonists of receptors in breast and uterus.
Indicated for treatment of breast cancer.
Evista is a full agonist only at bone, osteoporosis use. It has no benefit demonstrated in the prevention of cardiovascular disease.

Front 33

Mechanism of action of Oral Contraceptives: estrogen and progestin combination

Back 33

Inhibit ovulation and impair endometrium development. There are high levels in blood inhibit LH and FSH release. There is a lack of midcycle LH spike and ovulation. Ovarian function is depressed.
Excess mucus secretions in cervix impede sperm penetration.

Front 34

Alternative os Oral Contraceptives: estrogen and progestin combination

Back 34

Transdermal patches and vaginal rings.
Progestin only "minipills" implants and depot injections.
Postcoital intervention (morning-after pill) is a traditional combination that is a high dose of estrogen and progestin and it interferes with implantation.
RU 486 mifepreisone (Mifeprex) is a progestin receptor antagonist. Mifeprex is approved for termination of pregnancy of 49 days or less.

Front 35

Adverse effects of Oral Contraceptives: estrogen and progestin combination

Back 35

Venous thromboembolic disease-PE.
MI.
Stroke.
Cancer.
N/V, weight gain, HA, increased skin pigmentation, GI problems