EXAM

FINAL EXAM: Wednesday, May 6th, 2009. St Albert's Hall. B75. 8-10 AM. wait outside until you are called into the room.

EXAM REVIEW: Friday, May 8th, 2009. St. Albert's Hall. Room 164 (in the back). 12.30 - 2.30 PM. This will be the last day to discuss the outcome of the exam. Final grades will be posted on UIS that afternoon.

GOOD LUCK!

BREAST CANCER- Part 2

From the chalkboard lecture:

SWINE FLU UPDATE

1. As of today, how many cases of swine flu have been reported in the USA? How many deaths?

BREAST CANCER:

1. What is the difference between sporadic breast cancer and hereditary breast cancer?

2. What is the difference between an oncogene and a tumor suppressor gene?

3. Is BRCA1 a tumor suppressor gene? Why is it important? What happens if a woman inherits a mutated BRCA1 gene? What does that do to her risk of developing breast cancer? of developing ovarian cancer? What are the patient's drug options? surgical options? What does having a baby due to the risk of breast cancer in a woman with an inactivating BRCA1 mutation?

4. What is DCIS? LCIS? IDC? ILC? Which of them has the poorest prognosis? (PLEASE NOTE THAT sporadic breast cancers and hereditary breast cancers both surface as either: DCIS, LCIS, IDC or ILC. The only way to know if you have an inactivating mutation in BRCA1 is to have a DNA test performed.)

BREAST CANCER- part 1

From the chalkboard lecture:

SWINE FLU UPDATE
1. As of today, how many cases of swine flu have been reported in Mexico? How many deaths?

2. As of today, how many cases of swine flu have been reported in the USA? How many deaths? What is the endemic rate of flu deaths each year in the USA?

BREAST CANCER:

1. What is the difference between sporadic breast cancer and hereditary breast cancer?

2. What is the suspected role of estrogen in breast cancer? Is there a drug, used in the treatment of sporadic breast cancer, that works by inhibiting the activity of estrogen in the breast? What is the name of that drug?

3. What is BRCA1? Why is it important? What happens if a woman inherits a mutated BRCA1 gene? What does that do to her risk of developing breast cancer?

4. Can you list other chronic diseases which affect the public health?

5. About how many women get breast cancer each year in the USA?

6. What two things can a woman do to decrease her risk of getting breast cancer?

Antimicrobial Resistance- Part 4

From the chalkboard lecture:

1. As of today, how many cases of swine flu have been reported in Mexico? How many deaths?

2. As of today, how many cases of swine flu have been reported in the USA? How many deaths?

3. What two drugs can be used to treat those infected with swine flu? (both brand name and generic name of each)

4. What has NYC done to try to prepare for a swine flu pandemic?

PROTECT YOURSELF
http://www.youtube.com/watch?v=ZlDqcmY_EV8&eurl=http%3A%2F%2Fwww.pandemicflu.gov%2F&feature=player_embedded

KNOW THE SYMPTOMS
http://www.youtube.com/watch?v=0wK1127fHQ4&feature=channel

---FUNGI---

What gene is upregulated in yeasts which are resistant to fluconazole? In addition to upregulation of lanosterol 14 alpha-demethylase (ERG11), how else can the yeast cells decrease the effects of a drug? Why do we worry about fluconazole-resistance anyway?

What is a fungistatic compound? Can you name one? What is a fungicidal compound? Can you name one? What kind of drug is fluconazole? Why do fungistatic drugs eventually stop working in immunocompromised people? Are immunocompromised people prone to fungal infections? What kinds of fungal infections? What happens when a fungal infection gains access to the systemic circulation? Is that a dangerous infection or one which you should not worry about?

What is the Pma1p? What does it do in yeast? Why might it be a good target for the develpment of novel antifungals? Can you name one compound used by Dr. Billack's lab which inhibits Pma1p?

Antimicrobial Resistance- Part 3

From the chalkboard lecture:

1. Why is the pig (swine) a potential threat to the development of flu viruses capable of infecting humans?

2. As of today, how many cases of swine flu have been reported in Mexico? How many deaths?

3. As of today, how many cases of swine flu have been reported in the USA? How many deaths?

4. What has NYC done to try to prepare for a swine flu pandemic?

---FUNGI---

List at three three types of fungal pathogens that can causes disease in humans.

What types of infections can be caused by Candida albicans?

What is the mechanism of action of terbinafine? What is the mechanism of action of fluconazole? voriconazole? ketoconazole?

What is the mechanism of action of amphotericin B? Why is ergosterol important to the fungi? Do humans have ergosterol in their cell membranes?

What gene is upregulated in yeasts which are resistant to fluconazole? Why do we worry about fluconazole-resistance anyway?

Lecture 33- Antimicrobial Resistance- Part 2

After today's lecture, you should be able to answer the following questions:

Questions 1-3 are from today's Powerpoint slides..
1. What is NARMS? Which three governmental Public Health agencies are involved with NARMS? How many NARMS sites are there? How many such sites are in New York?

2. Describe at least one pro and one con of antibiotic use in livestock.

3. Unnecessary antibiotic prescriptions increase the likelihood of antibiotic resistance. Why? About how many unnecessary prescriptions for antibiotics are filled each year in the U.S.? What did the Finnish study show concerning erythromycin resistance?

Questions 4-11 are from the chalkboard lecture or the article entitled, "The Bacteria Fight Back." This article was posted on the professor's drive in the folder named: april_24_2009_antimicrobial_resistance_continued.

4. According to the data from the CDC, how many deaths occurred in the US in 2002 as a result of bacterial infections? Of those deaths, how many were caused by drug-resistant strains of bacteria?

5. Why is the hospital environment particularly conducive to the acquisition and spread of drug-resistant bugs?

6. Who is Alexandar Tomasz and what did he have to say about penicillin? (What is penicillinase? What is a plasmid epidemic?)

7. What is MRSA? Why is MRSA a threat to public health? What is the name of the gene which confers the resistance to methicillin? According to data from 2002, what is the estimated number of hospital-acquired MRSA infections per year?

8. What is vancomycin? When was it discovered? What is VRSA?

9. When was linezolid approved by the FDA? When were linezolid-resistant bacteria first observed?

10. Describe the trend in new antibiotics approved by the FDA over the past 10-15 years. What might such a 'paltry pipeline' mean to the public health?

11. Is there an effective vaccine to prevent infection by S. aureus? What limits the usefulness of this vaccine?

Lecture 32: Antibiotic Resistance- Part 1

After today's lecture, you should be able to answer the following types of questions (Note that today I gave an "all-chalkboard" lecture).

1. Describe the role of antibiotics in their natural environments. Why are they there? How do the bacteria that make them survive their toxicity?

2. From what natural source were the first antibiotics harvested? What antibiotic is produced by members of the bacterial species known as Streptomyces? At which university was streptomycin discovered?

3. What are three ways of getting drug resistance in bacteria?

4. How do antimicrobial resistance genes move from one bacteria into another?

5. What is the significance of gene mutation with respect to antimicrobial drug resistance?

6. What is the significance of drug efflux pumps on the surface of bacteria? Why is Pharma interested in developing new drugs to block these types of pumps?

7. What were the names of the genes discussed in class which confer resistance of Mycobacterium tuberculosis to some of the anti-TB drugs? Are these genes mutated in all strains of TB? For example, which gene is mutated in drug-sensitive TB strains? Which gene is mutated in isoniazid-resistant strains of TB? in rifampin-resistant strains of TB? etc...

8. What is the mechanism of antibacterial action for each of these compounds: isoniazid, rifampin, pyrazinamide, ethambutol, streptomycin, fluoroquinolones, and linezolid?

Make sure to also do the assigned readings and the reading questions for today.

Lecture 31: Tuberculosis

After this lecture, you should be able to answer the following:

1. You want to identify a pathogen that causes a specific disease. Using Robert Koch's four postulates, how would you do that? Which pathogens did Koch identify using these postulates?

2. What is the infectious agent that causes tuberculosis (TB)? Is it a spirochete? a bacilli? a cocci?

3. What is streptomycin? How was this discovery important to patients with tuberculosis?

4. Why is tuberculosis sometimes called "consumption?" In the 18th and 19th centuries, what percentage of recorded adult deaths in the U.S. could be attributed to TB? Is TB still a leading killer in the U.S.? How many people die each year in the U.S. from active TB? How many people worldwide die each year from active TB? Why the discrepancy?

5. Is TB contagious? If so, how is TB spread? What two types of TB infection occur in people? Is it true that people with latent TB do not feel sick? Is it true that people who have latent TB will test positive in a Mantoux Tuberculin Skin Test?

6. Which organ of the body is the preferred site of TB infection?

7. Describe the symptoms of a patient with latent TB.

8. Describe the symptoms of a patient with active TB. How are chest X-rays and sputum cultures used to confirm active cases of the disease? What are acid-fact bacilli?

9. True or False? The rate of MDR-TB cases in the United States is lower now than in 1953.

10. Describe the Mantoux Tuberculin Skin Test. What is it? Why does it work? What kinds of factors can hinder interpretation of the result?

11. Who is at risk for exposure or infection with TB?

12. Is there a vaccine for TB? Does it protect adults against the disease? What is the name of the vaccine? What type of mycobacterium is used in the vaccine? Is that the same pathogen that causes human TB? HMMM... might that be a problem? Are not the immune memory cells being formed against mycobacterium bovis? Might that be why the vaccine "wears-off" in adulthood? Is the BCG vaccine on the list of vaccines administered to children by the U.S. National Immunization Program?

13. Discuss chest X-rays. How do they work? What do they show? What do they look like for people with active TB?

14. How can training and education help to control the spread of TB?

15. Is TB a reportable (notifiable) disease?

16. What are the two primary pharmacological agents used to treat TB? How are people infected with latent TB treated (what drugs and how long?) What is the mechanism of action of each of these drugs? What is the chemical structure of isoniazid? What other drugs are used to treat TB?

17. What is drug-resistant Tuberculosis? Describe the different types of drug-resistant strains? What is multidrug-resistant TB? What drug has had some success against MDR-TB? What is a major side effect of this drug?

18. Please make sure to read all the assigned homework material and carefully answer all the homework questions.For additional reading on the pharmacological aspects of TB , please see the links below. Note: They are not required, but are quite interesting:Streptomycin

Info:http://acswebcontent.acs.org/landmarks/antibiotics/trials.htmlMDR-TB

Info:http://www.cdc.gov/ncidod/eid/vol4no2/rattan.htm

Good Luck!!