Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

116 Cards in this Set

  • Front
  • Back
Acarbose & Miglitol MOA
Mechanism of Action: inhibits the activity of enzymes required to break carbohydrates down into simple sugars within the intestine.
Oral hypoglycemic drug not very efficacious at lowering A1c levels when used as monotherapy.
Acarbose & miglitol
oral hypoglycemic, alpha-glucosidase inhibitor
oral hypoglycemic, alpha-glucosidase inhibitor
side effects of alpha-glucosidase inhibitors
Side Effects: feelings of bloating, gas, abdominal discomfort, diarrhea.
Drug interactions alpha-glucosidase inhibitors
Major drug interactions: MAO inhibitors.
First generation sulfonylurea
First generation sulfonylurea
Sulfonylurea MOA
Mechanism of Action: Stimulates the release of insulin from pancreatic beta-cells.
Sulfonylurea SE
Side Effects: hypoglycemia (true for all sulfonylureas)
Second generation sulfonylurea
Second generation sulfonylurea
Second generation sulfonylurea
Mechanism of Action: stimulates the release of insulin from pancreatic beta-cells
sulfonylureas, Rapaglinide, Nateglinide
Glimepiride (Amaryl ®), Glipizide (Glucotrol ®, Glucotrol XL ®) ,Glyburide
sulfonylurea, second generation
What's the difference between first and second generation sulfonylureas?
Second generation (fewer drug interactions, & side effects, more commonly prescribed)

second generation sulfonylureas are contraindicated in patients with hepatic impairment
“euglycemic” oral hypoglycemics
- which ones? what does it mean?
Biguanide: Metformin

Thiazolidinediones (glitazones): Pioglitazone, Rosiglitazone
Metformin MOA
Mechanism of Action: decreases the liver's production of glucose, inhibits the breakdown of fatty acids used to produce glucose, and increases the removal of glucose from muscle, the liver, and other body tissues where it is stored.
Metformin Contraindications
Contraindications:severe infection; congestive heart failure or emphysema; metabolic acidosis; a history of alcohol abuse; or kidney or liver disease.
Notes: in rare cases, ------ may lead to lactic acidosis (it can impair the hepatic metabolism of lactic acid)
name a Biguanide:
Thiazolidinediones (glitazones):
Pioglitazone & Rosiglitazone
Drug Class: oral hypoglycemic, thiazolidinedione derivatives
Drug Class: oral hypoglycemic, thiazolidinedione derivatives
Thiazolidinediones (glitazones):
Drug: Pioglitazone (Actos ®) & Rosiglitazone (Avandia ®)
Mechanism of Action: increases the body's sensitivity to insulin. Their primary action is the nuclear regulation of genes involved in glucose & lipid metabolism and adipocyte differentiation. Glitazones are ligands of the peroxisome peroliferator-activated receptor gamma (PPAR-gamma) part of the steriod and thyroid superfamily of nuclear receptors. PPAR receptors are found in muscle, liver and fat.
Pharmacokinetics: Pioglitazone & Rosiglitazone
Pharmacokinetics: metabolized through the hepatic cytochrome P450 system
Drug Class: oral hypoglycemics, insulin secretagogue
Mechanism of Action: regulates potassium efflux from pancreatic beta-cells
Meglitinides: Rapaglinide
Phenylalanine Derivative: Nateglinide
Drug: Rapaglinide MOA
regulates potassium efflux from pancreatic beta-cells
Rapaglinide indications
Indications: used as a supplemental therapy to dietary measures and exercise to help control blood sugar levels in patients with type II diabetes mellitus
Ingest just prior to meals. oral hypoglycemic drugs
Meglitinides: Rapaglinide

Phenylalanine: Nateglinide
Pharmacokinetic: Rapaglinide
rapid onset and very short acting.
insulin secretagogue
Phenylalanine Derivative: Nateglinide
Meglitinides: Rapaglinide
Contraindications:severe infection; congestive heart failure or emphysema; metabolic acidosis; a history of alcohol abuse; or kidney or liver disease.
A1C Reduction (%) approx between 2 - 3 % (strong)
A1C Reduction (%)approx less than 1 % (weak)
Phenylalanine Derivatives
Glucosidase Inhibitors
A1C Reduction (%) approximately less than 1 -2% (medium)
major SE oral hypoglycemic drugs
Risk for hypoglycemia
Insulin Secretagogues
major SE oral hypoglycemic drug
kidney, liver, heart failure
major SE oral hypoglycemic drug
liver, heart failure
major SE oral hypoglycemic drug
Digestive problems
Glucosidase Inhibitors
hypoglycemic drugs, increase weight
glitazones, Secretagogues
hypoglycemic drugs, decrease weight
hypoglycemic drugs, decrease lipids
hypoglycemic drugs, decrease blood pressure
Estradiol MOA
Mechanism of Action: estrogens regulate the transcription of a limited number of genes. Estrogens diffuse through cell membranes, distribute themselves throughout the cell, and bind to and activate the nuclear estrogen receptor, a DNA-binding protein which is found in estrogen-responsive tissues. The activated estrogen receptor binds to specific DNA sequences, or estrogen-response elements, which enhance the transcription of adjacent genes and in turn lead to the observed effects. Estrogen receptors have been identified in tissues of the reproductive tract, breast, pituitary, hypothalamus, liver, and bone of women. Estrogens are important in the development and maintenance of the female reproductive system and secondary sex characteristics.
Indications for Estrogens as a class:
* primary hypogonadism
* intractable dysmenorrhea
* Carcinoma of the prostrate
* oral contraceptives
* morning after pill
* endometriosis
* postmenopausal hormonal
estrogen used for prostate cancer
DES is used
Morning after pill estrogen
(DES or ethinyl estradiol)
Contraindications for estrogen therapy
* known or suspected pregnancy.
* undiagnosed abnormal genital bleeding.
* known or suspected cancer of the breast except in appropriately selected patients being treated for metastatic disease.
* known or suspected estrogen-dependent neoplasia.
* active thrombophlebitis or thromboembolic disorders
* heavy smoking
estrogen metabolsm
glucuronidation by hepatic enzymes
estrogen SE
Side Effects: increased incidence of breast cancer (w/ or w/o a progestin) & endometrial carcinoma (if estrogen is taken w/o a progestin), nausea & vomiting, breast tenderness & enlargement, edema, hypertension, vaginal bleeding, headache, dizziness, increased risk of deep vein thrombosis w/ high doses, hyperpigemtation.
estrogen major drug interactions
Major drug interactions: phenytoin, barbiturates & rifampin induce hepatic enzymes that increase the metabolism of estrogens. They will decrease the effectiveness of oral contraceptives. Antimicrobial drugs can also reduce the bioavailability of estrogens due to their effect on GI flora & alterations in enterohepatic cycling of estrogens.
naturally occuring estrogens
Estradiol (E2) is the major secretory product of the ovary. Other naturally occurring estrogens include estrone (E1) and estriol (E3).
Estrogen therapy for treatment of postmenopausal women
Conjugated Estrogens (Premarin ®, contrains estrone and equilin sulfate from pregnant mare urine
Name Synthetic Estrogens
Ethinyl Estradiol
estrogens used in postcoital contraceptives.
Ethinyl Estradiol
estrogens in Oral Contraceptive
Ethinyl Estradiol
Indications: Treatment of prostatic carcinoma & as a postcoital contraceptive.
Drug Class: Oral Contraceptive & Postcoital Contraceptive
Ethinyl Estradiol
estrogen of the "morning after pill"
Ethinyl Estradiol
most common estrogen found in oral contraceptives.
Ethinyl estradiol
a prodrug that must be converted to ethinyl estradiol before it is active
Advantage of Mestranol over other estrogens
t has prolonged action and potency. Fat soluble & stored in fat tissue, from which it is slowly released.
name Anti-estrogens (SERMs)
Tamoxifen citrate
Raloxifene (partial agonist/antagonist)
Clomiphene MOA
Mechanism of Action: a competitive inhibitor (partial agonist) at estrogen nuclear receptors. An example of a SERM (Selective Estrogen Receptor Modulator). It interferes with the negative feedback of estrogens on the hypothalamus by binding to estrogen receptors and thereby causes an increase in the secretion of GnRH and gonadotropins.
Anti-estrogens (SERMs)used to treatment of infertility & anovulatory cycles. It is an ovulation-inducing agent.
Clomiphene SE
Side Effects: it can lead to ovarian hyper-stimulation, with formation of multiple cysts and a 6-8% incidence of multiple births. Other side effects: hot flashes, nausea, vomiting, nervousness (estrogenic effects).
Tamoxifen MOA
Mechanism of Action: two mechanisms - 1) decreases estrogen-induced mitogen production by antagonizing estrogen receptors; 2) it can directly induces growth factor inhibitors.
Indications: pallative (does not cure) treatment for carcinoma of the breast. It is indicated in estrogen receptor-positive, postmenopausal, soft-tissue metastases of mammary carcinoma.
----- will not work in estrogen-negative cancer, or cancer from bony metastases.
Estrogen partial agonist / antagonist
Raloxifene MOA
Mechanism of Action: has effects on bone, but does not stimulate the endometrium or breast.
Indications: prevention of post-menotpausal osteoporosis
Progesterone MOA
Mechanism of Action: Similar to estrogens, but binds to different receptors in the cytoplasm or nucleus which then interact with preogesterone-response elements to activate gene transcription.
Progesterone physiologic effects
Physiolgocial Effects:

* promotes secretory activity of endometrium "primed" by estrogen
* negative feedback on anterio pituitary FSH and LH
* Important (along with estrogen) in breast development & lactation
* the cause of midcycle increase in body temperature at ovulation
Progesterone indications
# contraception
# Control of functional uterine bleeding.
# management of endometriosis
How is Progesterone used for contraception?
# contraception - most commonly used in combination with estrogens. Progestin only "mini pills" are not as effective as combination pills. Progestins work as contraceptives via effects on cervical mucus, the uterine endometrium & uterine motility, all of which decrease the likelihood of conception & implantation. High dose formulations (e.g. depot medroxyprogesterone) also inhibit GnRH release & are therefore more effective contraceptives.
Progesterone SE
Side Effects:

* weight gain
* edema
* depression
* thrombophlebitis
* pulmonary embolism
* the more potent progestins, if used for a long period of time, will decrease HDL levels and lead to atherosclerosis.
(generic, Depo-Provera ®)
progesterone only contraceptives
Mini pill
Pharmacokinetics of Medroxyprogesterone
Pharmacokinetics: Injection is effective for 3 months. There is an optional implants formulation
Drug Class: Contraceptive Injection
Medroxyprogesterone SE
Side Effects: Menstrual irregularities (bleeding or amenorrhea, or both), weight changes, headache, nervousness, abdominal pain or discomfort, dizziness,
asthenia (weakness or fatigue). Reversible reduction of glucose tolerance.
Medroxyprogesterone return of fertility
Return of Fertility:
Depo-Provera contraceptive injection has a prolonged contraceptive effect. Clinical trials indicate that following the last injection, 68% of women who do become pregnant may conceive within 12 months, 83% may conceive within 15 months, and 93% may conceive within 18 months from the last injection.
the most common form of progestin used in oral contraceptives
: Norethindrone
The progestin component in these triphasic combination tablet formulations (which also contains ethinyl estradiol).
contained in the Mirena IUD, which continuously releases ----.
Why used Levonorgesterl in IUDs?
This lessens menstrual bleeding & contributes to contraception by this IUD.
Hormonal Contraceptives
What's does estrogen do?
Contraceptive Mechanisms:
* Estrogen: 1) it exerts a negative feedback control on the release of FSH & LH from the pituitary; 2) it causes a thickening of cervical mucus, which decreases sperm penetration; 3) endometrial alterations that impair implantation; & 4) changes in the motility & secretion in the uterine tubes.
Hormonal contraceptives, what does the progesterone do?
* Progestin: Low dose – changes to cervical mucus, endometrial & uterine changes similar to estrogen. High dose: inhibitory feedback on GnRH release from the hypothalamus.
Drug Class: Termination of Pregnancy
medical termination of intrauterine pregnancy through the first 49 days of gestation. 96% effective during the first 49 days, and 96-98% effective in the first 42 days.
Mifeprex, RU426 ®)
Mifepristone MOA
Mechanism of Action: inhibition of progesterone receptor results in a termination of pregnancy.
sed to treat tamoxifen-resistant breast cancers (breast cancer cells can have both estrogen & progesterone receptors.)
Used for termination of pregnancies and for tamoxifen-resistant breast cancers
Mifepristone contraindications
Contraindications: confirmed or suspected ectopic pregnancy, undiagnosed adnexal mass, an IUD in place, current long-term systemic corticosteroid therapy, chronic adrenal failure, severe anemia, known coagulopathy, anticoagulant therapy and drug allergy.
Finasteride MOA
Mechanism of Action: a specific inhibitor of steroid 5 alpha-reductase, an intracellular enzyme that converts the androgen testosterone into 5 -dihydrotestosterone (DHT). Finasteride has no affinity for the androgen receptor. By inhibiting 5-alpha reductase, it significantly lowers DHT levels in the plasma and prostatic tissue.
Drug Class: Inhibitor of DHT synthesis
# Treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to: a) Improve symptoms; b) Reduce the risk of acute urinary retention; c) Reduce the risk of the need for surgery including transurethral resection of the prostate (TURP) and prostatectomy.
treatment of male pattern baldness
------- is also is indicated to reduce the risk of symptomatic progression of BPH when administered in combination with the alpha-blocker doxazosin
The development and enlargement of the prostate gland is dependent on
on the potent androgen, 5 -dihydrotestosterone (DHT). 5 -alpha reductase metabolizes testosterone to DHT in the prostate gland, liver and skin. DHT induces androgenic effects by binding to androgen receptors in the cell nuclei of these organs.
----- metabolizes testosterone to DHT in the prostate gland, liver and skin.
5 -alpha reductase
Testosterone analogs
Testosterone cypionate
Testosterone cypionate MOA
Mechanism of Action: similar to testosterone. Testosterone is converted to dihydroxytestosterone (DHT) in many tissues, where DHT is the dominant androgen. Both hormones bind to intacellular androgen receptors, initiating events similar to those for estradiol and progesterone, leading to growth, differentiation, and the synthesis of a variety of enzymes & other functional proteins.
Indications: hypogonadism in males
Testosterone cypionate
Testosterone cypionate side effects
Side Effects:
increases LDL, decreases HDL,
increased aggression,
closure of epiphyses, edema, cholestatic jaundice,
priapism & decreased sperm count.
masculanization w/ acne,
danazol MOA
Mechanism of Action: a synthetic steroid derived from 17-alpha ethinyltestosterone. Danazol binds to androgen, progesterone, and glucocorticoid receptors. Danazol suppresses the pituitary-ovarian axis. This suppression is probably a combination of depressed hypothalamic-pituitary response to lowered estrogen production, the alteration of sex steroid metabolism, and interaction of danazol with sex hormone receptors.
treatment of fibrocystic breast disease & endometriosis in women.
Anabolic Steroid, Synthetic Testosterone Analog
Indications: Hereditary Angioedema. (Abused by atheletes).

* palliation of androgen responsive recurrent mammary cancer in postmenopausal women
* replacement therapy in conditions associated with symptoms of deficiency or absence of endogenous testosterone in men (e.g. hypogonadism or delayed puberty).
Contraceptive Mechanisms: Estrogen
Estrogen: maintained levels exert a negative feedback control on the release FSH & LH from the pituitary.
Contraceptive Mechanisms: progesterone
Low dose – causes a thickening of cervical mucus, makes the endometrial surface not receptive to implantation & decreases fallopian movement of eggs. High dose: decrease frequency of GnRH release