Katzung, Chapter 41; 723-745
After reading the chapter and attending the lectures, you should be able to answer the following:
REVIEW QUESTIONS FOR DIABETES LECTURES
1. What are the differences between Type 1 and Type 2 diabetes mellitus? What are some of the complications of diabetes mellitus? What are pancreatic islets? What types of islet cells make insulin? Islet amyloid polypeptide (IAPP)? Glucagon? Note: Be very comfortable with the slide dealing with glucose homeostasis and the effects of insulin.
2. What is preproinsulin? Proinsulin? Insulin?
3. Describe the Insulin receptor and its signaling pathways… in your answer make sure to use terms such as, “signal transduction,” “phosphorylation,” “tyrosine kinase,” “IRS-1,” “Shc,” “GLUT4” etc…
4. What is ketoacidosis? Can you smell acetone on the breath of severe Type 1 diabetics? Good video describing this at: https://www.youtube.com/watch?v=jYF0Y0uBgVo I watched the video. It is accurate.
5. Describe glucose uptake into cells. Describe all GLUT transporters and comments as to where they are in the body
6. Understand the role of glucose uptake through GLUT2 in beta cells and how that affects the ATP-gated K+ channel and insulin release.
7. What happens to GLUT4 transporters when insulin levels rise? Where are they normally… where do they go? What happens to these transporters when insulin levels in blood decrease? Do GLUT4 transporters stay in the cell membrane? or do they return home.. back to the cytoplasm where they are contained in vesicles?
8. What are some of the metabolic effects of insulin on the liver? On the skeletal muscle? On fat cells?
9. What are the four major types of insulin preparations available? Is insulin administered orally? Why not? Does it have a long half-life? Which of the insulins are slowly absorbed and why?
10. Using these terms…. Hexamers… dimers… monomers…. Two amino acid change.. insulin…. Lispro…decreased hydrogen binding of insulin with itself… Explain to your study partner or a complete stranger who is willing to listen why insulin lispro, insulin aspart and insulin glulisine are rapid acting.
11. What effect(s) are caused as the result of having zinc and acetate in an insulin preparation?
12. Protamine can be combined with regular insulin to produce intermediate-acting insulin preparations. WHY does that work in slowing down absorption of regular insulin?
13. Please be very familiar with the tables listing the different types of insulin preparations. Focus on the type.. the time to peak effect.. and the duration of action.
14. Is hypoglycemia the most common side effect of insulin therapy? Are all type 1 diabetics treated with insulin replacement? Is type 1 the result of beta pancreatic cell destruction?
15. What are the clinical indications for pramlintide? What are its chief pharmacological actions? What are its most relevant ADME parameters? Is there a boxed warning associated with this drug? What’s that all about?
16. Would you use sulfonylureas in Type 1 or Type 2 patients?? Think about the role of the beta cell in the action of these drugs.
17. Where do the sulfonylureas act? (inhibit the ATP-dependent K+ channel of beta cells). Be able to identify sulfonylureas such as first generation and second generation: NOTE: These drugs can induce hypoglycemia…..nausea, diarrhea & vomiting.
The following link is interesting: http://www.mja.com.au/public/issues/180_02_190104/vei10508_fm.html
It provides some case studies and things to think about in patients using sulfonylureas.
Please read the article. It’s not required… but suggested.
18. Meglitinides cause insulin release from beta cells. Two major meglitinides- repaglinide & nateglinide. How do they work? adverse effects? Receptor binding sites? Which seems to be more efficacious in people and what is your decision based on?
19. What is lactic acidosis and is it related to metformin use, especially in patients with liver disease, renal impairment and cardiopulmonary insufficiency? Know the MOA of metformin and common adverse effects. Is B12 absorption affected?
20. Understand the relationship of rosiglitazone and the receptor for PPARgamma (peroxisome proliferator activated receptor- gamma). What are the shared adverse effects of rosiglitazone and pioglitazine? Increased risk of which cancer has been associated with pioglitazone? (Treating Type 2 Diabetes With Pioglitazone May Increase Risk of……. Go to: http://www.aafp.org/online/en/home/publications/news/news-now/health-of-the-public/20120611pioglitazone.html#.UFvpQz4HUsg.twitter … —which ends up to be something like an extra 16.9 cases per 100,000 person years.
21. How may chromium be related to diabetes? What affect does chromium deficiency have on the body?
22. Alpha-glucosidase inhibitors. HOW DO THEY WORK? Chief adverse effects? Any contraindications for this class of drugs?
23. Glucagon is the physiological antagonist to insulin made by alpha cells of the pancreatic islet. Is glucagon often elevated in patients with Type 2 diabetes? If so, why?
24. How does exenatide work? Adverse effects? Receptor binding sites? Compare and contrast exenatide with liraglutide.
25. Incretin mimetics. Adverse effects? Mechanism of action?
26. DPP-IV inhibitors. Adverse effects? Mechanism of action?
27. Describe the pharmacology of sodium glucose co-transporter 2 inhibitors in terms of mechanism of actions and adverse effects. How do these drugs differ in terms of anticipated adverse effects compared to sulfonylureas?
28. What does the following website have to say about dapagliflozin and its approval status by the FDA? http://www.drugs.com/newdrugs/fda-approves-farxiga-type-2-diabetes-4002.html
Friday, September 16, 2016
Thursday, September 15, 2016
THYROID AND ANTITHYROID DRUGS
REQUIRED READING: THYROID AND ANTITHYROID DRUGS
Katzung’s Basic and Clinical Pharmacology
13th edition
Chapter 38, pp. 663-677
After attending the lecture and reading the textbook, you should be able to answer these questions.
1. What is the chemical name for the three hormones secreted by the thyroid gland? Can you draw the structures of T3? T4? Where do the ‘iodides’ come from? Are they synthesized by the body? Are they derived from the diet? What is the RDA of iodide in the diet?
2. Describe the biosynthesis of thyroid hormones. Make sure to use terms like iodide trapping, thyroidal peroxidase, tyrosine, MIT, DIT, thyroglobulin, proteolysis of thyroglobulin. What is the ratio of T4 to T3 on thyroglobulin? Which of these is released to a higher degree from the thyroid gland? Which of the two is the more active hormone? How is T4 converted to T3 in the periphery?
3. What are the two chemical activities of thyroidal peroxidase? Compared to T4 and T3, what is the biological activity of rT3? What is the half life of T4? T3? Describe the possible metabolic fates of T4 after it is released from the thyroid gland. Describe the usual relationship among the thyroid gland, the hypothalamus, and the pituitary gland.
4. What are the relevant ADME pharmacokinetic parameters of T3 and T4? For example, which is better absorbed? Are there factors that can affect absorption? Which has the longer half-life?
5. What is the net effect of an ‘activating’ mutation of the TSH receptor? Provide an example of an abnormal thyroid stimulating agent.
6. What happens to T4 when it enters the cell? What is 5’deiodinase? What kind of receptors are thyroid hormone receptors? For example, are they transmembrane spanning receptors? What other types of receptors are related to thyroid receptors? Can T4 bind to T3 receptors?
7. What are the various physiological targets of thyroid hormones? What happens to these tissues in the hyperthyroid state? Remember to detail the effects of the hyperthyroid state on skin, eyes, cardiovascular system, GI, CNS, musculoskeletal and hematopoietic systems as well as on metabolism. (See also Table 38-4 in your text for help, p.670).
8. What are ‘antithyroid agents?’ What are ‘goitrogens?’ How do the thioamides work to reduce the production of thyroid hormones by the thyroid gland? Can you describe three different thioamides that do this? Be sure to include relevant PK differences in your answer. Aside from inhibiting thyroidal peroxidase, what other enzyme is blocked by these agents (hint: it’s in the periphery). Discuss the pertinent pharmacokinetic properties of these thioamides. Do these agents have a fast or a slow onset of pharmacologic effect? What is the most common adverse reaction caused by these agents? What is a rare but serious adverse effects associated with these agents? Carbimazole is a prodrug. How does it work as an anti-thyroid agent? What are its most significant adverse effects? Based on its PK, would you recommend carbimazole over propylthiouracil in pregnancy? Why or why not?
9. What is Grave’s Disease? Is Grave’s Disease frequently associated with exophthalmus and swelling of the periorbital tissues?
10. What is ipodate? What is it’s mechanism of action? What are its most significant adverse effects?
11. What is the antithyroid mechanism of action of I-131 (radioactive iodine)? What is its half-life? Should it be used in pregnant patients? Why or why not?
12. What is the antithyroid mechanism of action of propranolol?
13. List three anion inhibitors of the Na+/I- transporter? Why do such agents have antithyroid activity? What type of toxicity is associated with potassium perchlorate?
14. How do iodides work to block thyroid function? What is the proposed mechanism of iodide’s antithyroid actions? Why might iodides be helpful in preoperative preparation for surgery?
15. How does guanethidine work as a potential anti-thyroid agent? Does it have direct effects on the thyroid gland?
16. What are some of the clinical manifestations of hypothyroidism? What is Hashimoto’s thyroiditis? What is ‘cretinism?’ What is ‘myxedema?’
17. Describe the types of synthetic and animal-derived thyroid hormones available for replacement therapy. What is the preparation of choice for thyroid replacement therapy?
18. How might drugs like lithium or amiodarone affect levels of T4 in the body (Hint: see Table 38-3)? Your patient is hyperthyroid; how can that impact their warfarin dosing (Hint: see Table 38-3, p. 668)?
19. What is ‘thyroid storm?’ What is the presenting syndrome? Which pharmacological agents can be used to treat thyroid storm? What is the rationale behind using each of those reagents?
20. Describe the functional domains of the thyroid hormone receptor? What is the mechanism of thyroid hormone action? Can genes be both activated or inhibited by thyroid hormone?
Katzung’s Basic and Clinical Pharmacology
13th edition
Chapter 38, pp. 663-677
After attending the lecture and reading the textbook, you should be able to answer these questions.
1. What is the chemical name for the three hormones secreted by the thyroid gland? Can you draw the structures of T3? T4? Where do the ‘iodides’ come from? Are they synthesized by the body? Are they derived from the diet? What is the RDA of iodide in the diet?
2. Describe the biosynthesis of thyroid hormones. Make sure to use terms like iodide trapping, thyroidal peroxidase, tyrosine, MIT, DIT, thyroglobulin, proteolysis of thyroglobulin. What is the ratio of T4 to T3 on thyroglobulin? Which of these is released to a higher degree from the thyroid gland? Which of the two is the more active hormone? How is T4 converted to T3 in the periphery?
3. What are the two chemical activities of thyroidal peroxidase? Compared to T4 and T3, what is the biological activity of rT3? What is the half life of T4? T3? Describe the possible metabolic fates of T4 after it is released from the thyroid gland. Describe the usual relationship among the thyroid gland, the hypothalamus, and the pituitary gland.
4. What are the relevant ADME pharmacokinetic parameters of T3 and T4? For example, which is better absorbed? Are there factors that can affect absorption? Which has the longer half-life?
5. What is the net effect of an ‘activating’ mutation of the TSH receptor? Provide an example of an abnormal thyroid stimulating agent.
6. What happens to T4 when it enters the cell? What is 5’deiodinase? What kind of receptors are thyroid hormone receptors? For example, are they transmembrane spanning receptors? What other types of receptors are related to thyroid receptors? Can T4 bind to T3 receptors?
7. What are the various physiological targets of thyroid hormones? What happens to these tissues in the hyperthyroid state? Remember to detail the effects of the hyperthyroid state on skin, eyes, cardiovascular system, GI, CNS, musculoskeletal and hematopoietic systems as well as on metabolism. (See also Table 38-4 in your text for help, p.670).
8. What are ‘antithyroid agents?’ What are ‘goitrogens?’ How do the thioamides work to reduce the production of thyroid hormones by the thyroid gland? Can you describe three different thioamides that do this? Be sure to include relevant PK differences in your answer. Aside from inhibiting thyroidal peroxidase, what other enzyme is blocked by these agents (hint: it’s in the periphery). Discuss the pertinent pharmacokinetic properties of these thioamides. Do these agents have a fast or a slow onset of pharmacologic effect? What is the most common adverse reaction caused by these agents? What is a rare but serious adverse effects associated with these agents? Carbimazole is a prodrug. How does it work as an anti-thyroid agent? What are its most significant adverse effects? Based on its PK, would you recommend carbimazole over propylthiouracil in pregnancy? Why or why not?
9. What is Grave’s Disease? Is Grave’s Disease frequently associated with exophthalmus and swelling of the periorbital tissues?
10. What is ipodate? What is it’s mechanism of action? What are its most significant adverse effects?
11. What is the antithyroid mechanism of action of I-131 (radioactive iodine)? What is its half-life? Should it be used in pregnant patients? Why or why not?
12. What is the antithyroid mechanism of action of propranolol?
13. List three anion inhibitors of the Na+/I- transporter? Why do such agents have antithyroid activity? What type of toxicity is associated with potassium perchlorate?
14. How do iodides work to block thyroid function? What is the proposed mechanism of iodide’s antithyroid actions? Why might iodides be helpful in preoperative preparation for surgery?
15. How does guanethidine work as a potential anti-thyroid agent? Does it have direct effects on the thyroid gland?
16. What are some of the clinical manifestations of hypothyroidism? What is Hashimoto’s thyroiditis? What is ‘cretinism?’ What is ‘myxedema?’
17. Describe the types of synthetic and animal-derived thyroid hormones available for replacement therapy. What is the preparation of choice for thyroid replacement therapy?
18. How might drugs like lithium or amiodarone affect levels of T4 in the body (Hint: see Table 38-3)? Your patient is hyperthyroid; how can that impact their warfarin dosing (Hint: see Table 38-3, p. 668)?
19. What is ‘thyroid storm?’ What is the presenting syndrome? Which pharmacological agents can be used to treat thyroid storm? What is the rationale behind using each of those reagents?
20. Describe the functional domains of the thyroid hormone receptor? What is the mechanism of thyroid hormone action? Can genes be both activated or inhibited by thyroid hormone?
Friday, September 02, 2016
OSTEOPOROSIS DRUGS
REQUIRED READING: AGENTS THAT AFFECT BONE MINERAL HOMEOSTASIS
Katzung’s Basic and Clinical Pharmacology
13th edition
Chapter 42
After attending the lecture and reading the textbook, you should be able to answer these questions.
1. Is osteoporosis a condition that disturbs the structural support of the body? What are the three major body organs involved in calcium and phosphate homeostasis? What is the normal range of calcium in the blood?
2. What is parathyroid hormone (PTH)? Which glands of the body secrete PTH? What is the physiological effect of PTH? How many amino acids are in PTH? Is the secretion of PTH inversely related to plasma Ca++ levels? What hormone in the body has the opposite effect of PTH? What physiological effect is achieved with prolonged, chronic, exposure to PTH? How does that differ from intermittent exposures to PTH?
3. Describe the PTH receptor. Is it a nuclear receptor? What 2nd messenger accumulates within the cell following activation of the receptor? Does PTH stimulate the activity of many proteins? Does it inhibit the activity of other proteins? Pretty cool, eh? (PS. No need to memorize that list. But one should realize that PTH can both stimulate and inhibit the functions of unique gene products.)
4. What vitamin is required for PTH to exhibit its full spectrum of action? Describe the relevant steps in the conversion of 7-dehydrocholesterol to vitamin D3 and metabolism of D3 to 1,25(OH)2D3 (calcitriol). What do you suspect could happen to calcitriol biosynthesis in a patient with renal failure?
5. What is hypocalcemia? What are the pharmacotherapeutic options available to treat HYPOcalcemia?
6. What is osteoporosis? What pharmacologic options are available to treat this disease? Which of these agents are hormonal? Which of them are non hormonal?
7. Draw the general structure of the nitrogen-containing bisphosphonates. What is FPPS? What is the therapeutic mechanism of action of the bisphosphonates? Are these agents well-absorbed after oral administration? Are there dietary factors that can influence the absorption of these agents?
8. What are the FDA-labeled indications for alendronate? What is the mechanism of action of alendronate? Does the bioavailability of this drug? Describe the Phase I and Phase II metabolism of alendronate. What are the common adverse effects associated with this drug? What are some rare but serious adverse effects associated with this drug? Is alendronate given as an oral administration? As an intramuscular administration? As an inhalational administration?
9. What are the clinical indications for risedronate? Is it given orally? Intramuscularly? Intravenously? What are its chief adverse effects?
10. What are the clinical indications for ibandronate? Is it given orally? Intramuscularly? Intravenously? What are its chief adverse effects? Daily? Yearly? Monthly? Weekly?
11. What are some contraindications to the bisphosphonates?
12. Any relevant drug drug interactions with bisphosphonates?
13. What are the clinical indications for zoledronic acid? Is it given orally? Intramuscularly? Intravenously? What are its chief adverse effects? Why do you think that esophageal toxicity not on this list?
14. Why is salmon calcitonin the preferred agent to human calcitonin? How does the drug work? What is it used for? Is the preferred route of administration oral dosing? Why or why not? What are the common adverse effects of calcitonin?
15. Raloxifene is important in osteoporosis. Why? How does it work? In breast and uterus, how does raloxifene work? What about in the bone? Is it an agonist or an antagonist of estrogen receptors? Is it well absorbed after oral administration? What is its bioavailability? Why the big difference in absorption vs. bioavailabilty? What is the predominant Phase II conjugate of raloxifene? What is its elimination half-life? What are some precautions and adverse effects associated with this drug?
16. What are the clinical uses of calcitriol? What are some of its proposed mechanisms of action in the relief of osteoporosis? Is calcitriol absorbed well via oral administration? Compare and contrast the physiological actions of PTH and calcitriol.
17. What is teriparatide? What are its FDA-labeled indications? What is one of the rare but serious adverse effects associated with this drug? Will it be administered orally? Why or why not?
HRT and menopause
1. What is menopause? What are the symptoms associated with menopause that have found to be alleviated by estrogen?
2. Aside from increased chance of postmenopausal bleeding, what other adverse effects can occur in patients taking estrogen replacement therapy? How can adverse effects like nausea and breast tenderness be managed? Does E+P HRT increase the risk of certain adverse effects? What are those adverse effects? Do these adverse effects occur in all women taking estrogen? Is the endometrium particularly sensitive to unopposed estrogen toxicity? What happens to the risk of endometrial cancer in patients taking estrogen and progesterone combination therapy?
Katzung’s Basic and Clinical Pharmacology
13th edition
Chapter 42
After attending the lecture and reading the textbook, you should be able to answer these questions.
1. Is osteoporosis a condition that disturbs the structural support of the body? What are the three major body organs involved in calcium and phosphate homeostasis? What is the normal range of calcium in the blood?
2. What is parathyroid hormone (PTH)? Which glands of the body secrete PTH? What is the physiological effect of PTH? How many amino acids are in PTH? Is the secretion of PTH inversely related to plasma Ca++ levels? What hormone in the body has the opposite effect of PTH? What physiological effect is achieved with prolonged, chronic, exposure to PTH? How does that differ from intermittent exposures to PTH?
3. Describe the PTH receptor. Is it a nuclear receptor? What 2nd messenger accumulates within the cell following activation of the receptor? Does PTH stimulate the activity of many proteins? Does it inhibit the activity of other proteins? Pretty cool, eh? (PS. No need to memorize that list. But one should realize that PTH can both stimulate and inhibit the functions of unique gene products.)
4. What vitamin is required for PTH to exhibit its full spectrum of action? Describe the relevant steps in the conversion of 7-dehydrocholesterol to vitamin D3 and metabolism of D3 to 1,25(OH)2D3 (calcitriol). What do you suspect could happen to calcitriol biosynthesis in a patient with renal failure?
5. What is hypocalcemia? What are the pharmacotherapeutic options available to treat HYPOcalcemia?
6. What is osteoporosis? What pharmacologic options are available to treat this disease? Which of these agents are hormonal? Which of them are non hormonal?
7. Draw the general structure of the nitrogen-containing bisphosphonates. What is FPPS? What is the therapeutic mechanism of action of the bisphosphonates? Are these agents well-absorbed after oral administration? Are there dietary factors that can influence the absorption of these agents?
8. What are the FDA-labeled indications for alendronate? What is the mechanism of action of alendronate? Does the bioavailability of this drug? Describe the Phase I and Phase II metabolism of alendronate. What are the common adverse effects associated with this drug? What are some rare but serious adverse effects associated with this drug? Is alendronate given as an oral administration? As an intramuscular administration? As an inhalational administration?
9. What are the clinical indications for risedronate? Is it given orally? Intramuscularly? Intravenously? What are its chief adverse effects?
10. What are the clinical indications for ibandronate? Is it given orally? Intramuscularly? Intravenously? What are its chief adverse effects? Daily? Yearly? Monthly? Weekly?
11. What are some contraindications to the bisphosphonates?
12. Any relevant drug drug interactions with bisphosphonates?
13. What are the clinical indications for zoledronic acid? Is it given orally? Intramuscularly? Intravenously? What are its chief adverse effects? Why do you think that esophageal toxicity not on this list?
14. Why is salmon calcitonin the preferred agent to human calcitonin? How does the drug work? What is it used for? Is the preferred route of administration oral dosing? Why or why not? What are the common adverse effects of calcitonin?
15. Raloxifene is important in osteoporosis. Why? How does it work? In breast and uterus, how does raloxifene work? What about in the bone? Is it an agonist or an antagonist of estrogen receptors? Is it well absorbed after oral administration? What is its bioavailability? Why the big difference in absorption vs. bioavailabilty? What is the predominant Phase II conjugate of raloxifene? What is its elimination half-life? What are some precautions and adverse effects associated with this drug?
16. What are the clinical uses of calcitriol? What are some of its proposed mechanisms of action in the relief of osteoporosis? Is calcitriol absorbed well via oral administration? Compare and contrast the physiological actions of PTH and calcitriol.
17. What is teriparatide? What are its FDA-labeled indications? What is one of the rare but serious adverse effects associated with this drug? Will it be administered orally? Why or why not?
HRT and menopause
1. What is menopause? What are the symptoms associated with menopause that have found to be alleviated by estrogen?
2. Aside from increased chance of postmenopausal bleeding, what other adverse effects can occur in patients taking estrogen replacement therapy? How can adverse effects like nausea and breast tenderness be managed? Does E+P HRT increase the risk of certain adverse effects? What are those adverse effects? Do these adverse effects occur in all women taking estrogen? Is the endometrium particularly sensitive to unopposed estrogen toxicity? What happens to the risk of endometrial cancer in patients taking estrogen and progesterone combination therapy?
ESTROGENS SERMs PROGESTINS and ANDROGENS
REVIEW QUESTIONS: ESTROGENS SERMs PROGESTINS ANDROGENS
REQUIRED READING:
Katzung’s Basic and Clinical Pharmacology
13th edition
Chapter 40
Infertility- know the mechanism of action, route of administration, most common adverse effects, any rare but serious adverse effects, efficacy rates (in other words, are these drugs effective?), incidence of multiple gestation, risks to the developing baby (if any), risk of ovarian hyperstimulation syndrome, etc… pertaining to clomiphene, metformin and bromocriptine.
Hormonal Contraception (the answers are in your lecture notes, lecture slides, the narrations of slides not presented in class-- see DropBox-- or in the book chapter).
1. What happens to the release of LH and FSH by the pituitary when plasma levels of both estrogen and progesterone are high?
2. What two types of agents do combination oral contraceptives (OCs) contain? For most OCs, what is the standard dosing regimen? Of 28 tablets, how many are “active” and how many are “inert?” What happens during the seven days of “inert” tablets? Is the choice of combo OC universal? Or is it patient-specific? How should the doses be decided?
3. What are the proposed mechanisms of action for the combination oral contraceptives? How about for the progestin-only OCs? What types of products are available? What is emergency contraception? What types of emergency contraceptive products are available? What is extended regimen contraception?
4. Comment on some of the interesting adverse effects relating to transdermal administration or administration via vaginal ring (see narrated slides for best information).
5. Compared to estradiol, what are the chief pharmacokinetic parameters (half-life, bioavailability, protein binding) for ethinyl estradiol? How is the compound eliminated from the body?
6. What is the major metabolite of the synthetic progestins? Is that metabolite active or inactive? How are progestins eliminated from the body? Compared to progesterone, what are the chief pharmacokinetic parameters (half-life, bioavailability, protein binding) for norethindrone?
7. With respect to the combination OCs, does either drug alter the pharmacokinetics of the other?
8. What is the difference between monophasic, biphasic, and triphasic OCs? Why are withdrawal- bleeding periods, on average, shorter for products such as loestrin 24 Fe than with other combo OCs?
9. Long-duration contraception with progesterone-only agents can be achieved using parenteral routes of administration such as implantable or intramuscular preps. Which progestin is available as a subcutaneous implant? As an i.m. injection? Why are progestin-only contraceptive tablets a possible option for nursing mothers? Are menstrual irregularities commonly observed in women taking progesterone-only OCs? Do women on oral progestin-only tablets need to take them every day? Or do they take 21 active pills and 7 inactive pills each month?
10. Estrogens and clotting factors. Estrogens increase the synthesis by the liver of of clotting factors VII, VIII, IX and X and decrease the synthesis of antithrombin III. Why is that not good? (SEE slides) What are the pharmacological effects of the combination oral contraceptives on: the ovaries, the skin (chloasma, what is that?) and the cardiovascular system?
11. In which patients are the oral contraceptives contraindicated. Why? What are some of the common and rare but serious adverse effects associated with the OCs?
12. What possible drug-drug interactions can be predicted in patients taking oral contraceptives and certain antibiotics? In patients taking oral contraceptives and inducers of CYP450s (eg. Rifampin, griseofulvin)? How about gabapentin and OCs?
13. What is so unique about drospirenone? Does is have antiandrogenic activity? Does it have antimineralocorticoid activity? Should women with renal failure take an oral contraceptive that contains drospirenone?
14. You will need to look this up (beyond the slides)... is there a relationship between the use of depot leuprolide and depot medroxyprogesterone with regard to adverse effects on bone mineral density?
15. See slides on Androgens (not narrated, sorry).. List the pharmacological effects associated with testosterone replacement therapy in men.
16. What is gynecomastia and how is it related to testosterone replacement therapy?
17. Describe the androgen receptor in detail.
18. List the name and routes of administration for the most common androgens used in testosterone replacement therapy.
REQUIRED READING:
Katzung’s Basic and Clinical Pharmacology
13th edition
Chapter 40
Infertility- know the mechanism of action, route of administration, most common adverse effects, any rare but serious adverse effects, efficacy rates (in other words, are these drugs effective?), incidence of multiple gestation, risks to the developing baby (if any), risk of ovarian hyperstimulation syndrome, etc… pertaining to clomiphene, metformin and bromocriptine.
Hormonal Contraception (the answers are in your lecture notes, lecture slides, the narrations of slides not presented in class-- see DropBox-- or in the book chapter).
1. What happens to the release of LH and FSH by the pituitary when plasma levels of both estrogen and progesterone are high?
2. What two types of agents do combination oral contraceptives (OCs) contain? For most OCs, what is the standard dosing regimen? Of 28 tablets, how many are “active” and how many are “inert?” What happens during the seven days of “inert” tablets? Is the choice of combo OC universal? Or is it patient-specific? How should the doses be decided?
3. What are the proposed mechanisms of action for the combination oral contraceptives? How about for the progestin-only OCs? What types of products are available? What is emergency contraception? What types of emergency contraceptive products are available? What is extended regimen contraception?
4. Comment on some of the interesting adverse effects relating to transdermal administration or administration via vaginal ring (see narrated slides for best information).
5. Compared to estradiol, what are the chief pharmacokinetic parameters (half-life, bioavailability, protein binding) for ethinyl estradiol? How is the compound eliminated from the body?
6. What is the major metabolite of the synthetic progestins? Is that metabolite active or inactive? How are progestins eliminated from the body? Compared to progesterone, what are the chief pharmacokinetic parameters (half-life, bioavailability, protein binding) for norethindrone?
7. With respect to the combination OCs, does either drug alter the pharmacokinetics of the other?
8. What is the difference between monophasic, biphasic, and triphasic OCs? Why are withdrawal- bleeding periods, on average, shorter for products such as loestrin 24 Fe than with other combo OCs?
9. Long-duration contraception with progesterone-only agents can be achieved using parenteral routes of administration such as implantable or intramuscular preps. Which progestin is available as a subcutaneous implant? As an i.m. injection? Why are progestin-only contraceptive tablets a possible option for nursing mothers? Are menstrual irregularities commonly observed in women taking progesterone-only OCs? Do women on oral progestin-only tablets need to take them every day? Or do they take 21 active pills and 7 inactive pills each month?
10. Estrogens and clotting factors. Estrogens increase the synthesis by the liver of of clotting factors VII, VIII, IX and X and decrease the synthesis of antithrombin III. Why is that not good? (SEE slides) What are the pharmacological effects of the combination oral contraceptives on: the ovaries, the skin (chloasma, what is that?) and the cardiovascular system?
11. In which patients are the oral contraceptives contraindicated. Why? What are some of the common and rare but serious adverse effects associated with the OCs?
12. What possible drug-drug interactions can be predicted in patients taking oral contraceptives and certain antibiotics? In patients taking oral contraceptives and inducers of CYP450s (eg. Rifampin, griseofulvin)? How about gabapentin and OCs?
13. What is so unique about drospirenone? Does is have antiandrogenic activity? Does it have antimineralocorticoid activity? Should women with renal failure take an oral contraceptive that contains drospirenone?
14. You will need to look this up (beyond the slides)... is there a relationship between the use of depot leuprolide and depot medroxyprogesterone with regard to adverse effects on bone mineral density?
15. See slides on Androgens (not narrated, sorry).. List the pharmacological effects associated with testosterone replacement therapy in men.
16. What is gynecomastia and how is it related to testosterone replacement therapy?
17. Describe the androgen receptor in detail.
18. List the name and routes of administration for the most common androgens used in testosterone replacement therapy.
Monday, December 09, 2013
Monday, December 9, 2013
Today's lecture topics included:
Mycobacterium tuberculosis, M. leprae, and M. avium, properties, diseases caused and treatments
Hepatitis viruses, properties, diseases caused (acute/chronic) and treatments
Vaccines, the basics.
Be familiar with everything that was discussed today in class pertaining to these topics.
good luck.
Mycobacterium tuberculosis, M. leprae, and M. avium, properties, diseases caused and treatments
Hepatitis viruses, properties, diseases caused (acute/chronic) and treatments
Vaccines, the basics.
Be familiar with everything that was discussed today in class pertaining to these topics.
good luck.
Thursday, December 05, 2013
Thursday, December 5, 2013
PHS_3506- Instructor: Dr. Billack
December 5, 2013 :
Lecture Topic(s):
Chapter 18: Staphylococcus….. pp.174-187
Chapter 19: Streptococcus…. pp. 188-204
Chapter 20: Enterococcus.. pp. 204-208
Reading Assignments from:
Medical Microbiology, 7th edition
Patrick R. Murray, Ken S. Rosenthal, Michael A. Pfaller
Elsevier Saunders, Philadelphia, PA
Homework Assignment: (based upon the lectures and the reading assignment)
To assist your understanding of the assigned readings, please answer the following questions in the space below:
(Chapter 18-related)
1. Describe the different types of clinical syndromes caused by (a) S. aureus, (s) S. epidermidis and (c) S. saprophyticus.
2. Describe the pathogenesis of infection by S. aureus.
(Chapter 19-related)
1. What are some of the general characteristics of Streptococci?
2. Describe the important factors related to the pathogenicity of Group A Streptococcus (S. pyogenes). What kinds of diseases are caused by Group A Streptococcus? What is the primary drug treatment in these situations?
3. Describe the important factors related to the pathogenicity of Group B Streptococcus (S. agalactiae). What kinds of diseases are caused by Group B Streptococcus? What is the primary drug treatment in these situations?
4. Describe the important factors related to the pathogenicity of Viridans Streptococci (S. pneumoniae). What kinds of diseases are caused by S. pneumoniae ? What types of drug treatments are commonly used to combat S. pneumoniae? in these situations?
(Chapter 20-related)
5. What are some of the general characteristics of Enterococcus? What can we say about Enterococcus and drug resistance? Most common type of Enterococcus?
December 5, 2013 :
Lecture Topic(s):
Chapter 18: Staphylococcus….. pp.174-187
Chapter 19: Streptococcus…. pp. 188-204
Chapter 20: Enterococcus.. pp. 204-208
Reading Assignments from:
Medical Microbiology, 7th edition
Patrick R. Murray, Ken S. Rosenthal, Michael A. Pfaller
Elsevier Saunders, Philadelphia, PA
Homework Assignment: (based upon the lectures and the reading assignment)
To assist your understanding of the assigned readings, please answer the following questions in the space below:
(Chapter 18-related)
1. Describe the different types of clinical syndromes caused by (a) S. aureus, (s) S. epidermidis and (c) S. saprophyticus.
2. Describe the pathogenesis of infection by S. aureus.
(Chapter 19-related)
1. What are some of the general characteristics of Streptococci?
2. Describe the important factors related to the pathogenicity of Group A Streptococcus (S. pyogenes). What kinds of diseases are caused by Group A Streptococcus? What is the primary drug treatment in these situations?
3. Describe the important factors related to the pathogenicity of Group B Streptococcus (S. agalactiae). What kinds of diseases are caused by Group B Streptococcus? What is the primary drug treatment in these situations?
4. Describe the important factors related to the pathogenicity of Viridans Streptococci (S. pneumoniae). What kinds of diseases are caused by S. pneumoniae ? What types of drug treatments are commonly used to combat S. pneumoniae? in these situations?
(Chapter 20-related)
5. What are some of the general characteristics of Enterococcus? What can we say about Enterococcus and drug resistance? Most common type of Enterococcus?
Monday, December 02, 2013
Monday, December 2, 2013
PHS_3506- Instructor: Dr. Billack
December 2, 2013 :
Lecture Topic(s):
Chapter 14: Mechanisms of Bacterial Pathogenesis; p. 138-146
Chapter 18: Staphylococcus….. pp.174-187
Reading Assignments from:
Medical Microbiology, 7th edition
Patrick R. Murray, Ken S. Rosenthal, Michael A. Pfaller
Elsevier Saunders, Philadelphia, PA
Homework Assignment: (based upon the lectures and the reading assignment)
To assist your understanding of the assigned readings, please answer the following questions in the space below:
(Chapter 14-related)
1. What is the mucociliary escalator of the respiratory tract? How may viruses affect the mucociliary escalator?
2. In what way are alveolar macrophages involved in fighting respiratory infections? What may happen if a brochus becomes obstructed?
3. Why are the muscles of the chest wall and diaphragm important in fighting infections? What impact can trauma or surgery have on these muscles?
4. What bacterial products can exert tissue destruction? What is the difference between cytotoxins, neurotoxins, enterotoxins? Can you list one example, as mentioned in class, of each of the types?
5. What types of bacteria produce coagulase? What does coagulase do? What types of bacteria produce collagenase? What does collagenase do? What types of bacteria produce hemolysins? What does this enzyme do? What types of bacteria produce leukocidins? What do leukocidins do?
6. Describe what a, “superantigen” is. What is, “TSST-1?” and what is its relationship to S. aureus?
7. Explain the role of a capsule in bacterial virulence. Is it an immunogenic structure? Can you list several examples of bacteria with capsules, as mentioned in class?
(Chapter 18-related)
8. Describe the morphology and physiology of Staphylococcus spp.
9. Describe the different types of clinical syndromes caused by (a) S. aureus, (s) S. epidermidis and (c) S. saprophyticus.
10. Describe the pathogenesis of infection by S. aureus.
11. What is MRSA? MVRSA? What are natural penicillins? What are semi-synthetic penicillins? Examples? What is penicillinase and why is it a problem?
12. (from the slides) (a) What is Staphylococcus aureus? (b) What is MRSA (methicillin-resistant Staphylococcus aureus)? (c) Who gets staph or MRSA infections? (d) What is community-associated MRSA (CA-MRSA)? (e) Are certain people at increased risk for community-associated staph or MRSA infections? (f) What are the clinical features of CA-MRSA? (g) What are the criteria for distinguishing community-associated MRSA (CA-MRSA) from healthcare-associated MRSA (HA-MRSA)? (h) What is the main way that staph or MRSA is transmitted in the community? (i) How is a MRSA infection diagnosed? (j) How are CA-MRSA infections treated?
13. Common oral treatments for MRSA? Iv treatment? Why not penicillins, cephalosporins or carbapenems?
14. What is vancomycin resistance? What is vanA?
December 2, 2013 :
Lecture Topic(s):
Chapter 14: Mechanisms of Bacterial Pathogenesis; p. 138-146
Chapter 18: Staphylococcus….. pp.174-187
Reading Assignments from:
Medical Microbiology, 7th edition
Patrick R. Murray, Ken S. Rosenthal, Michael A. Pfaller
Elsevier Saunders, Philadelphia, PA
Homework Assignment: (based upon the lectures and the reading assignment)
To assist your understanding of the assigned readings, please answer the following questions in the space below:
(Chapter 14-related)
1. What is the mucociliary escalator of the respiratory tract? How may viruses affect the mucociliary escalator?
2. In what way are alveolar macrophages involved in fighting respiratory infections? What may happen if a brochus becomes obstructed?
3. Why are the muscles of the chest wall and diaphragm important in fighting infections? What impact can trauma or surgery have on these muscles?
4. What bacterial products can exert tissue destruction? What is the difference between cytotoxins, neurotoxins, enterotoxins? Can you list one example, as mentioned in class, of each of the types?
5. What types of bacteria produce coagulase? What does coagulase do? What types of bacteria produce collagenase? What does collagenase do? What types of bacteria produce hemolysins? What does this enzyme do? What types of bacteria produce leukocidins? What do leukocidins do?
6. Describe what a, “superantigen” is. What is, “TSST-1?” and what is its relationship to S. aureus?
7. Explain the role of a capsule in bacterial virulence. Is it an immunogenic structure? Can you list several examples of bacteria with capsules, as mentioned in class?
(Chapter 18-related)
8. Describe the morphology and physiology of Staphylococcus spp.
9. Describe the different types of clinical syndromes caused by (a) S. aureus, (s) S. epidermidis and (c) S. saprophyticus.
10. Describe the pathogenesis of infection by S. aureus.
11. What is MRSA? MVRSA? What are natural penicillins? What are semi-synthetic penicillins? Examples? What is penicillinase and why is it a problem?
12. (from the slides) (a) What is Staphylococcus aureus? (b) What is MRSA (methicillin-resistant Staphylococcus aureus)? (c) Who gets staph or MRSA infections? (d) What is community-associated MRSA (CA-MRSA)? (e) Are certain people at increased risk for community-associated staph or MRSA infections? (f) What are the clinical features of CA-MRSA? (g) What are the criteria for distinguishing community-associated MRSA (CA-MRSA) from healthcare-associated MRSA (HA-MRSA)? (h) What is the main way that staph or MRSA is transmitted in the community? (i) How is a MRSA infection diagnosed? (j) How are CA-MRSA infections treated?
13. Common oral treatments for MRSA? Iv treatment? Why not penicillins, cephalosporins or carbapenems?
14. What is vancomycin resistance? What is vanA?
Monday, November 25, 2013
Monday, November 25, 2013
PHS_3506- Instructor: Dr. Billack
November 25 :
Lecture Topic(s):
Chapter 2: Commensal and Pathogenic Microbial Flora in Humans, p. 6-15.
Chapter 14: Mechanisms of Bacterial Pathogenesis, p. 138-146
Reading Assignments from:
Medical Microbiology, 7th edition
Patrick R. Murray, Ken S. Rosenthal, Michael A. Pfaller
Elsevier Saunders, Philadelphia, PA
Homework Assignment: (based upon the lectures and the reading assignment)
To assist your understanding of the assigned readings, please answer the following questions in the space below:
(Chapter 2-related)
1. What is the role of commensal microbes, such as those that live in the microflora of the gut?
2. What are three outcomes of exposure of an individual to a microorganism? What is the difference between colonization and disease?
3. Define the term, “strict pathogens.” List 5 examples of strict pathogens.
4. Define the term, “opportunistic pathogens.” List 3 examples of opportunistic pathogens.
5. The upper respiratory tract (mouth, oropharynx and nasopharynx) is colonized by numerous bacteria. Which are the most common anaerobes? Aerobes? And potentially pathogenic organisms?
6. The ear is colonized by which strain of bacteria. Which are the most common bacterial pathogens of the ear?
7. The eye is usually colonized by which strains of bacteria? Bacterial pathogens of the eye are?
8. Which structures comprise the lower respiratory tract? Which strains normally colonize the lower respiratory tract? List some bacterial and fungal pathogens of the lower respiratory tract.
9. The esophagus is colonized by which strains of bacteria? Which species cause most cases of infective esophagitis?
10. Describe the microbial environment of the acidic stomach.
11. Describe the microbial environment of the small intestine. The large intestine?
12. Describe the microflora of the anterior urethra. Pathogens of this tissue?
13. Describe the microflora of the vagina. Pathogens of this tissue?
14. Describe the normal microflora of the cervix. Bacterial pathogens of this tissue?
15. Describe the normal microflora of the skin? Most common bacterial skin pathogens?
Chapter 14-Related
1. What are the processes involved in allowing a bacteria to “settle in” the host?
2. What are the processes by which bacteria “cause” disease?
3. Explain virulent bacteria vs. opportunistic bacteria
4. What are the main portals of entry into the body?
5. Explain adhesins. Can you name some?
6. What is a biofilm? What advantage does it provide to the organisms?
7. Name some enzymes that help bacteria gain entry to host cells/tissues.
8. What is a bacterial toxin? What’s the difference between an endotoxin and exotoxin? Describe the endotoxin response. What is an A-B exotoxin? Describe the mechanism of diphtheria toxin, cholera toxin, tetanus toxin, botulinum toxin (see Figure 14-2, p. 141).
9. What components of Gram+ organisms elicit an immune response in host cells? Same question for G- organisms.
10. What is a superantigen? List some examples of superantigens? What is the problem associated with superantigens?
11. How can bacteria evade host defenses?
November 25 :
Lecture Topic(s):
Chapter 2: Commensal and Pathogenic Microbial Flora in Humans, p. 6-15.
Chapter 14: Mechanisms of Bacterial Pathogenesis, p. 138-146
Reading Assignments from:
Medical Microbiology, 7th edition
Patrick R. Murray, Ken S. Rosenthal, Michael A. Pfaller
Elsevier Saunders, Philadelphia, PA
Homework Assignment: (based upon the lectures and the reading assignment)
To assist your understanding of the assigned readings, please answer the following questions in the space below:
(Chapter 2-related)
1. What is the role of commensal microbes, such as those that live in the microflora of the gut?
2. What are three outcomes of exposure of an individual to a microorganism? What is the difference between colonization and disease?
3. Define the term, “strict pathogens.” List 5 examples of strict pathogens.
4. Define the term, “opportunistic pathogens.” List 3 examples of opportunistic pathogens.
5. The upper respiratory tract (mouth, oropharynx and nasopharynx) is colonized by numerous bacteria. Which are the most common anaerobes? Aerobes? And potentially pathogenic organisms?
6. The ear is colonized by which strain of bacteria. Which are the most common bacterial pathogens of the ear?
7. The eye is usually colonized by which strains of bacteria? Bacterial pathogens of the eye are?
8. Which structures comprise the lower respiratory tract? Which strains normally colonize the lower respiratory tract? List some bacterial and fungal pathogens of the lower respiratory tract.
9. The esophagus is colonized by which strains of bacteria? Which species cause most cases of infective esophagitis?
10. Describe the microbial environment of the acidic stomach.
11. Describe the microbial environment of the small intestine. The large intestine?
12. Describe the microflora of the anterior urethra. Pathogens of this tissue?
13. Describe the microflora of the vagina. Pathogens of this tissue?
14. Describe the normal microflora of the cervix. Bacterial pathogens of this tissue?
15. Describe the normal microflora of the skin? Most common bacterial skin pathogens?
Chapter 14-Related
1. What are the processes involved in allowing a bacteria to “settle in” the host?
2. What are the processes by which bacteria “cause” disease?
3. Explain virulent bacteria vs. opportunistic bacteria
4. What are the main portals of entry into the body?
5. Explain adhesins. Can you name some?
6. What is a biofilm? What advantage does it provide to the organisms?
7. Name some enzymes that help bacteria gain entry to host cells/tissues.
8. What is a bacterial toxin? What’s the difference between an endotoxin and exotoxin? Describe the endotoxin response. What is an A-B exotoxin? Describe the mechanism of diphtheria toxin, cholera toxin, tetanus toxin, botulinum toxin (see Figure 14-2, p. 141).
9. What components of Gram+ organisms elicit an immune response in host cells? Same question for G- organisms.
10. What is a superantigen? List some examples of superantigens? What is the problem associated with superantigens?
11. How can bacteria evade host defenses?
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