Reproduction Flashcards
Which of the following adverse reactions of oral contraceptives is the most common and the most serious?
- Hypotension
- Hepatotoxicity
- Uterine neoplasia
- Thromboembolic disorder
- Decrease resistance to infection
Thromboembolic disorder
Methyltestosterone
Class: Androgens
Schedule III drug
Mechanism of action:
- Intracellular conversion of testosterone to dihydrotestosterone
- Testosterone diffuses into target cells
- 5α-reductase converts testosterone to dihydrotestosterone
- Dihydrotestosterone bonds to its receptor and is transported to the nucleus
- Initiates transcription of androgen dependent genes
Indication:
- Delayed puberty in males
- Breast cancer
- Therapy after testicular cancer
- Controversial indications:
- Enhancement of athletic performance
- Female hypo-gonadism
- Male contraception
- Catabolic and wasting states (cancer, AIDS)
- Blood dyscrasias
Pharmacological effects:
How this drug might effect dental treatment of patient oAdverse effects you have to consider: -Hair growth, acne, baldness, virilization, gynecomastia -Dyslipidemia -Prostate hypertrophy, cancer -Jaundice -Osteoporosis -Behavioral effects "roid rage"
oContraindicated drugs:
oContraindications:
oWhich analgesic can the patient take:
Finasteride (Proscar, Propecia)
Class: Anti-Androgen
Mechanism of action: -5 α-reductase: enzyme testosterone to dihydroxytestosterone -Mediator of the actions of the hormone -Testosterone can be aromatized to estrogen, DHT cannot -Competitive inhibitor of 5-α reductase
Indication:
- Benign prostatic hypertrophy (Proscar)
- Alopecia (Propecia)
Pharmacological effects:
How this drug might effect dental treatment of patient
oAdverse effects you have to consider:
-Erectile dysfunction (verbatim)
-Cancer (verbatim)
oContraindicated drugs:
oContraindications:
oWhich analgesic can the patient take:
Estrogen/Progesterone
Class:
Mechanism of action:
-Mechanisms of oral contraceptives
Monophasic: Fixed dose of hormones throughout month
Biphasic: Fixed dose of estrogen, progesterone dose increases during month
Triphasic: Varying amounts of hormones during the month
-Progesterone is present to protect the endometrium from estrogen effects (endometrial cancer)
-Basically, estradiol and progesterone go to the pituitary and they are a negative feedback loop; leutinizing hormone and follicle stimulating hormone are not released and the ovary does not produce any eggs
Indication: Pre-menopausal women -Birth control -Adolescents when puberty is absent Post-menopausal women -Prevention of osteoporosis related fractures -Vasomotor symptoms (hot flashes) -Controversial in women over 60:CVD, breast cancer, stroke, DVT
Pharmacological effects:
How this drug might effect dental treatment of patient
oAdverse effects you have to consider:
oContraindicated drugs:
- Do antibiotics reduce the effectiveness of oral contraceptives?
- Rifampin: (Tuberculosis) Yes because it induces enzymes in liver that metabolize the hormones
- Others ? Changes in intestinal flora lead to enhanced excretion
- Have pt use an alternative method for birth control while she’s on antibiotics for the whole month
oContraindications:
oWhich analgesic can the patient take:
Daily whole-body calcium balance
In a state of whole-body calcium balance, the fluxes of calcium include net uptake of 200 mg per day from the GI tract and excretion of 200 mg per day by the kidneys. Calcitriol [1,25(OH)2D3] enhances absorption of Ca2+ from the GI tract. Continuous secretion of parathyroid hormone (PTH) increases bone formation and (even more) bone resorption, and stimulates renal tubular reabsorption of calcium; both effects raise plasma Ca2+. Continuous secretion of PTH also enhances renal clearance of inorganic phosphate (PO4). In contrast, once-daily injection of PTH stimulates new bone formation (accretion) more than it stimulates bone resorption and has only transient (and consequently minor) effects on renal clearance of Ca2+ and PO4. Exogenous calcitonin (CT) inhibits bone resorption
Interaction of osteoblasts and osteoclasts in bone remodeling
Bone resorption and bone formation are coupled by the interactions between osteoblasts and osteoclasts: (1) Factors such as parathyroid hormone (PTH), shear stress, and transforming growth factor β (TGF-β) cause osteoblast precursors to express the osteoclast differentiation factor RANK-ligand (RANKL). (2) RANKL binds to RANK, a receptor expressed on osteoclast precursors. (3) The RANKL–RANK binding interaction, together with macrophage colony-stimulating factor (M-CSF), causes osteoclast precursors to differentiate into mature osteoclasts. (4) As mature osteoclasts resorb bone, matrix-bound factors such as TGF-β, insulin-like growth factor 1 (IGF-1), other growth factors, and cytokines are released. (5) These liberated factors stimulate osteoblast precursors to develop into mature osteoblasts, which begin to refill the resorption cavities excavated by the osteoclasts.
Bone mass as a function of age
In both men and women, bone mass increases with age until a peak is reached in young adulthood; the growth spurt begins earlier and peaks earlier in women compared to men (not shown). After the peak, bone mass gradually declines by approximately 0.7% per year. In women, the reduction in the frequency of menses coincides with a sharp decline in bone mass, as the decrease in estrogen production leads to increased bone resorption. As bone mass decreases with age, the skeleton may become sufficiently fragile that minor trauma can cause fractures. The goal of antiresorptive agents is to arrest or slow the loss of bone. In contrast, bone anabolic agents can be used to reverse bone loss that has already occurred and restore bone mass and bone structure.
Pathophysiologic basis of osteoporosis
Several interrelated factors contribute to the development of osteoporosis. Many of these factors are activated by the decline in estrogen levels in perimenopausal women. Disinhibited production of cytokines and other regulatory molecules leads to the activation of osteoclasts. Decreased estrogen allows these osteoclasts to have a longer functional lifespan; conversely, the lack of estrogen promotes apoptosis in osteoblasts and osteocytes. The resulting imbalance between osteoclast and osteoblast activity leads to the formation of deep and large resorption cavities, which make the bone fragile and prone to fracture. The relative paucity of osteocytes impairs the mechanosensory network on which repair of microdamage in bone depends. Increased microdamage also predisposes to bone fragility and eventual fracture. Estrogen and raloxifene reverse this pathophysiologic sequence of events by suppressing cytokine production, promoting osteoclast apoptosis, and inhibiting osteoblast and osteocyte apoptosis.
Osteoporosis treatments
- Calcium and Vitamin D:facilitates absorption of calcium and phosphate from the small intestine
- Evista: Selective Estrogen Receptor Modulator
- Forteo (teriparatide) human parathyroid hormone: regulation of bone metabolism, renal tubular reabsorption of calcium and phosphate, and intestinal calcium absorption; 2 years during a patient’s lifetime due to risk of osteosarcoma
- Bisphosphonates
Raloxifene (Evista)
Class: Selective Estrogen Receptor Modulator (SERM)
Mechanism of action:
-Partial agonist: stimulates estrogen receptors in bone but inhibits in other tissues (this is good because it won’t cause breast cancer or endometrium)
Indication:
Pharmacological effects:
- Effects on bone similar to estrogen:
- Decrease resorption of bone
- Decrease bone turnover
- Increase bone mineral density
How this drug might effect dental treatment of patient
oAdverse effects you have to consider:
-Increase risk of deep vein thrombosis (DVT)
oContraindicated drugs:
oContraindications:
- Pre-menopausal
- Pregnancy
- Concurrent estrogen therapy
- History of breast cancer
oWhich analgesic can the patient take:
Alendronate (Fosamax)
Others: Zoledronate (Zometa) Ibandronate (Boniva) once a month Risedronate (Actonel) Pamidronate (Aredia) Etidronate (Didronel) Zoledronic Acid (Reclast) once a year 15 min infusion Tiludronate (Skelid)
Class: Bisphosphonates
Mechanism of action: -Inhibition of farnesyl diphosphate synthase -Reduction of geranylgeranyl diphosphate -Decrease of GTPase prenylation Osteoclast inactivation Osteoclast apoptosis Inhibition of osteoclast formation
Indication: -Osteoporosis Decrease the incidence of fractures -Paget's disease Reduce bone turnover rate Slow disease progression
Pharmacological effects:
How this drug might effect dental treatment of patient
oAdverse effects you have to consider:
oContraindicated drugs:
oContraindications:
oWhich analgesic can the patient take:
