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Pharmacology II > Endocrine Pharmacology > Flashcards

Endocrine Pharmacology Flashcards

1
Q

Describe the chemistry of levothyroxine (T4).

A

Affects DNA transcription and stimulates protein synthesis

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2
Q

List the important effects of Synthroid.

A

a. Promotes gluconeogenesis
b. Mobilizes glycogen stores
c. Increases basal metabolic rate

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3
Q

List three drugs used to treat hyperthyroidism.

A

a. Propylthiouracil
b. Iodides
c. Methimazol (Tapazole)

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4
Q

Describe the dental considerations of patients with thyroid disease.

A

a. Hypothyroid: cold, tired fatigued. More sensitive to CNS depressants so need lower dose sedatives and opiates.
b. Hyperthyroid: nervous, increased BP, may be sensitive to epinephrine (if active disease = absolute contraindication to epinephrine), palpitations and tachycardia, can perceive more pain, less sensitive to CNS depressants = may require higher dose pain meds

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5
Q

Name the drug used to treat Type I diabetes.

A

Insulin is the only effective drug to treat type 1

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6
Q

Describe how various preparations of insulin are characterized.

A

a. Classified 3 ways: onset, peak, duration of action

b. Short acting, rapid acting, intermediate acting, intermediate to long acting, long acting.

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7
Q

Identify several classes of oral drugs used to treat Type II diabetes.

A

a. Sulfonylureas – traditional
b. Biguanides (metaformin)
c. Alpha-glucosidase inhibitors
d. Thiazolidinediones (TZDs)
e. Incretins – GLP agonists, DDP-4 Inhibitors

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8
Q

Describe the mechanisms of action of sulfonylureas (oral hypoglycemic drugs) used to manage Type II diabetes.

A

Sulfonylureas: Promote insulin release from pancreatic beta cells, enhances effect of insulin to stimulate glucose uptake in muscle and fat cells.

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9
Q

Describe the mechanisms of action of biguanides (oral hypoglycemic) drugs used to manage Type II diabetes.

A

Biguanides: inhibits absorption of glucose from the gut, decreases liver glucose production, increases insulin sensitivity at the receptor sites and increases peripheral glucose uptake and utilization.

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10
Q

Describe the mechanisms of action of alpha-glucosidase inhibitors (oral hypoglycemic drugs) used to manage Type II diabetes.

A

Alpha-glucosidase inhibitors: inhibits the enzyme responsible for degrading complex carbohydrates in the gut. So no monosaccharides are made available for absorption after a meal. There is delay in blood glucose concentrations after a meal when on this drug.

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11
Q

Describe the mechanisms of action of thiazolidinediones (oral hypoglycemic drugs) used to manage Type II diabetes.

A

Thiazolidinediones: improves target cell response to insulin without increasing pancreatic insulin secretion. Resets insulin receptors = reduces insulin resistance. Depends on presence of insulin for activity. Decreases hepatic glucose output. Increases insulin stimulated glucose uptake in skeletal muscle and decreases lipolysis in adipocytes.

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12
Q

Describe the mechanisms of action of incretins (oral hypoglycemic drugs) used to manage Type II diabetes.

A

Incretins: mimic hormones produced by the body to stimulate release of insulin.

i. GLP-1 Receptor agonists: boosts insulin production by pancreas, slows absorption of food. Injectable!
ii. DPP-4 inhibitors: blocks enzyme DPP-4 that breaks down GLP-1 peptide in gut.
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13
Q

Discuss the serious drug interaction associated with sulfonylurea drugs.

A

a. Administration of aspirin and sulfonylureas can enchance the hypoglycemic response. Aspirin displaces the sulfonylurea from plasma proteins causing increased blood levels of the sulfonylurea and can cause hypoglycemia.
b. Aspirin can also inhibit prostaglandin E synthesis. PGE inhibits glucose induced insulin secretion, so inhibition increases the insulin response and enhances the sulfonylureas = hypoglycemia

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14
Q

Discuss the A1C test and how it is used to assess glycemic control in patients with diabetes.

A

Glycated hemoglobin (HbA1c)= gold standard. Measures glycemic control for 6-12 weeks. Normal value 6.5%

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15
Q

Discuss common cardiovascular risks that occur in patients with diabetes.

A

a. Obsesity in diabetes increases the cardiovascular risks. b. Sulfonylureas are a drug used to treat diabetes, promote insulin release= increase cardiovascular mortality.

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16
Q

Describe the forms of estrogen in Premarin, Estratab, and Estraderm transdermal patch.

A

Premarin= conjugated equine estrogens, Estrab= esterfied estrogens, Estraderm transdermal patch= estradiol preps

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17
Q

Describe the rationale for use of Prempro.

A

Relieve symptoms of menopause, prevention of osteoporosis

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18
Q

Describe the results of the HERS study and the impact of the results on HRT use.

A

When on HRT saw cholesterol levels go down but they suffered increases in blood clots and no reduction of heart disease.

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19
Q

Describe the results of the Nurses Health Study study and the impact of the results on HRT use.

A

found that estrogen in combination with progestin may increase risk of stroke, this outwieghs long term use to prevent osteoporosis

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20
Q

Describe the results of the WHI study and the impact of the results on HRT use.

A

Didn’t see this in the notes.

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21
Q

Describe the most recent recommendations for use of HRT in terms of indications for use and duration of therapy.

A

short term use only= less than 5 years. Used to treat symptoms of menopause

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22
Q

Describe the mechanism of raloxifene (Evista)

A

activates estrogen receptors in bone

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23
Q

Describe the use for raloxifene (Evista)

A

prevention of osteoporosis in post menopausal women and breast cancer prevention

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24
Q

Describe the common side effects of raloxifene (Evista)

A

hot flashes, leg cramps

25
Q

Describe the mechanism of action of bisphosphonate medications, including alendronate (Fosamax), risedronate (Actonel) and ibandronate (Boniva).

A

inhibits osteoclastic activity= inhibits bone resorption. Inhibits formation, growth and dissolution of bone hydroxyapatite

26
Q

Discuss the relationship between use of bisphosphonates and oral osteonecrosis.

A

oral complication of bisphosphonate= osteonecrosis of the jaw. Associated with extractions. Most cases of jaw osteonecrosis are in pts undergoing chemo with these drugs who also recieved steroids.

27
Q

Describe how calcium is used for the prevention and treatment of osteopororis.

A

Parathyroid Hormone (1-34); Recombinant Human Parathyroid Hormone (1-34); rhPTH(1-34)

28
Q

Describe how Vitamin D is used for the prevention and treatment of osteopororis.

A

Vit D increases bone mass, potentially increases bone formation, decreases PTH which decreases resorption, decreases fracture rates

29
Q

Describe how denosumab is used for the prevention and treatment of osteopororis.

A

Denosumab is a bone-modifying agent that promotes release of bone-derived growth factors, increases serum calcium levels, prevents osteoclast formation, leading to decreased bone resorption and increased bone mass in osteoporosis.

30
Q

Describe how Teriparatide is used for the prevention and treatment of osteopororis.

A

Teriparatide (recombinant human PTH) helps in stimulating osteoblast function, increasing gastrointestinal calcium absorption, and increasing renal tubular reabsorption of calcium. Treatment with teriparatide results in increased bone mineral density, bone mass, and strength.

31
Q

Describe how calcitonin is used for the prevention and treatment of osteopororis.

A

calcitonin reverses action of PTH, inhibits bone resorption, blocks removal of calcium from bone and decreases plasma calcium and phosphate levels.

32
Q

Compare and contrast anabolic and androgenic effects of testosterone.

A

androgenic effect: male secondary sex characteristics

anabolic effect: muscular bulk

33
Q

Discuss why anabolic steroids enhance athletic performance.

A

they exhibit more anabolic effects and can increase muscle mass by 30% (probably allowing for formation of more striated muscle cells)

34
Q

Describe the mechanism of action of estrogen and progesterone as ovulatory inhibitors

A

Estrogen inhibits FSH thus inhibiting ovulatory stimulation and progresterone inhibits LH thus inhibiting follicular growth

35
Q

Describe the clinical implications of inadequate Vitamin D.

A

increased likelihood for bone fractures, greater risk for prostate, breast and ovarian cancer, type I diabetes, hypertension

36
Q

Who may be candidates for Vitamin D supplementation?

A

Institutionalized populations, those living far from equator and those avoiding sun exposure.

37
Q

Describe the differences between the following oral contraceptive preparations: combination, sequential and single entity.

A

combination (contains estrogen and progestin), sequential (contain different amounts of progestin w/same amount of estrogen), single entity (progestin only “minipills”, estogen alone “Plan B, ella”, DES for rape or incest)

38
Q

List the adverse effects associated with oral contraceptive use.

A

increased risk for MI & stroke, N/V, headache, breast pain, weight gain, breakthrough menstrual bleeding, mental depression, fatigue, ocular conditions, etc.

39
Q

Describe some adverse oral effects associated with oral contraceptive use.

A

OCs may mimic effects of pregnancy on gingiva causing mild inflammation, hyperemia, spontaneous gingival bleeding. Loss of tissue tone and tenderness/ulceration may result and OCs may decrease defense to plaque bacteria resulting in irritation or progression of perio disease

40
Q

Describe the dental considerations associated with oral contraceptive use.

A

Though antimicrobial-induced OC failure is very low, patients may consider additional non-homronal contraception at initiation and duration of antimicrobial therapy. Tetracycline, doxycycline, ampicillin, metroniazole, fluconazole and fluoroquinolones do not affect OC steroid levels in women taking combination OC.

41
Q

Explain the primary mechanism of action of the drug interaction associated with oral contraceptives and antibiotics.

A

OC are inactive (prodrugs) that are activated by the normal flora in the intestines. If antibiotics wipe out the normal flora there is a greater likelihood that ovulation and pregnancy may occur.

42
Q

What are the four therapeutic uses of hormones?

A

Replace, diagnose, stimulate, inhibit

43
Q

Describe the use for men of the hypothalamic hormone GnRH in medicine.

A

In men, GnRH is used for the treatment of idiopathic hypogonadotropic hypogonadism. GnRH replacement therapy results in achieving mature spermatogenesis.

44
Q

Name some hormones used therapeutically for diagnosis.

A

ACTH (apparent adrenal dysfunction), TSH (to differentiate between pituitary and primary hypothyroidism), HCG (pregnancy)

45
Q

Name some hormones used therapeutically for stimulating normal body functions.

A

TSH stimulates production of thyroid hormone, GnRH stimulates release of LH and FSH, ACTH stimulates release of glucocorticoids from adrenal gland, etc.

46
Q

Name some hormones used therapeutically for inhibiting normal body functions.

A

progesterone and estrogen (inhibit FSH and LH secretion), thyrocalcitonin (calcitonin) inhibits bone resorption

47
Q

Name some hormones used therapeutically for replacement.

A

progesterone (for menstrual disorders, endometriosis), GnRH (to treat hypognoadism in males), estrogen, insulin (in the treatment of Type 1 diabetes), T4 (Synthroid) hypothyroidism, vasopressin (diabetes insipidus)

48
Q

Describe the use for women of the hypothalamic hormone GnRH in medicine.

A

Of the hypothalamic releasing hormones, only GnRH is used as a drug. It is used for ovulation induction in women with primary hypothalamic amenorrhea. Clomiphene (Clomid) is an analog used as an ovulatory stimulant.

49
Q

Describe the pharmacology of ACTH (an anterior pituitary hormone) and its uses in medicine

A

ACTH stimulates the release of glucocorticoids from adrenal gland. Cotisone feedback to shut down ACTH output from pituitary.

50
Q

Describe the uses of ACTH (an anterior pituitary hormone) and in medicine.

A

ACTH is used as a diagnostic tool (to diagnose apparent adrenal dysfunction) and serves as an alternative to corticosteroids in inflammatory conditions.

51
Q

Describe the pharmacology of FSH (an anterior pituitary hormone) and its uses in medicine

A

Promotes development of ovarian follicles and maintains spermatogenesis. It is a glycoprotein effective only if given IM. Deficiencies in FSH cause sterility in males and menstrual abnormalities in females.

52
Q

Describe the pharmacology of GH (an anterior pituitary hormone) and its uses in medicine

A

Growth homrone is the most abundant hormone in the anterior pituitary and is now made from recombinant DNA techniques. It is officially used to treat pituitary dwarfism though it is subject to wide abuse.

53
Q

Describe the pharmacology of TSH (an anterior pituitary hormone) and its uses in medicine

A

Thyrotropic hormone (thyroid stimulating hormone) is used as a diagnostic tool ot differentiate between pituitary and primary hypothyroidism. Preparation: glycoprotein from bovine pituitaries. Lack of iodine in diet causes excessive secretion of TSH and may result in a goiter.

54
Q

Describe the pharmacology of LH (an anterior pituitary hormone) and its uses in medicine

A

LH is a glycoprotein that induces ovulation and regulates progesterone secretion in women, testosterone in men. It can be administered effectively via IM injections.

55
Q

Describe vasopressin (a posterior pituitary hormone) and its clinical applications in medicine.

A

Vasopressin (ADH; arginine vasopressin: AVP) is a vasoconstrictor and antidiuretic hormone; used for replacement in diabetes insipidus. High levels of vasopressin can trigger uterine contractions.

56
Q

Describe oxytocin (a posterior pituitary hormone) and its clinical applications in medicine.

A

Oxytocin has slight antidiuretic function and serves primarily to contract uterine smooth muscle at term, induce labor, and control postpartum bleeding or hemorrhage.

57
Q

Describe the action of parathyroid hormone in the regulation of plasma calcium levels.

A

increases plama calcium (mobilization of calcium from bone to plasma and increases calcium resoprtion in renal tubules)

58
Q

Describe the action of Vitamin D-3 (cholecalciferol) in the regulation of plasma calcium levels.

A

promotes gut absorption of calcium by stimulating formation of calcium-binding protein within intestinal epithelial cells and stimulates osteoclast proliferation and bone resorption (acts synergistically with PTH, though much slower).

59
Q

Describe the action of thryocalcitonin (calcitonin) hormone in the regulation of plasma calcium levels.

A

Decreases plasma calcium and phosphate levels and is used in medicine to treat hypercalcemia. It reverses the action of parathyroid hormone and lowers blood calcium by inhibiting bone resoprtion.

Pharmacology II (13 decks)

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