5-Antibiotics & Antivirals

Front 1

What is selective toxicity? Why is it important?

Back 1

Injuring a target cell or organism without injuring other cells or organisms in intimate contact with the target. Makes antibiotics safer.

Front 2

What is the difference between bactericidal and bacteriostatic?

Back 2

Bactericidal – kills bacteria
Bacteriostatic – slows growth, phagocytes eliminate bacteria

Front 3

What are ranges and chances of drug resistance with narrow-spectrum and broad-spectrum antibiotics?

Back 3

Narrow: smaller range
less resistance
Broad: larger range
more resistance

Front 4

What is acquired resistance? What are four ways bacteria become resistant to antibiotics? How do we lessen the chance for resistance?

Back 4

Bacteria become less susceptible or lose sensitivity to drug.
1) Reduce drug concentration at sites, 2) Alter drug receptors, 3) Synthesize an antagonist, & 4) Produce drug-metabolizing enzymes.
Treat infection, not colonization, and use correct drug in correct concentration for entire course of therapy.

Front 5

What is the difference between the MIC and MBC?

Back 5

MIC – amount of drug required to halt growth
MBC – amount of drug required to kill 99.9%

Front 6

Explain the importance of conjugation. What bacteria are most affected?

Back 6

Conjugation allows the DNA code for drug resistance to be passed to other bacteria. Gram negative bacteria.

Front 7

What are two examples of suprainfections?

Back 7

Candidiasis (yeast infection), Clostridium difficile infection (CDI) – 3 or more unformed stools in 24 hours with C. difficile or toxin from C. difficile in stools.

Front 8

What is the difference between an additive and potentiative effect?

Back 8

Additive – sum of the effect
Potentiative – greater than the sum of the effects

Front 9

How do penicillins kill bacteria?

Back 9

Disrupts cell wall (inhibits cross-linkages between peptidoglycan strands and lyses cell wall bonds)

Front 10

What is the major adverse effect of penicillins?

Back 10

Allergic reactions

Front 11

What are some common signs and symptoms of anaphylaxis and serum sickness to penicillins?

Back 11

Laryngeal edema, bronchoconstriction, severe hypotension, nausea and vomiting, tachycardia
Rash, hives, pruritis, arthralgias, fever

Front 12

Which three penicillins can be taken with food?

Back 12

Penicillin V, Amoxicillin, Augmentin

Front 13

Why is Penicillin G given IM?

Back 13

Destroyed by gastric acid

Front 14

What lab abnormality can occur with Penicillin G or V when administered with potassium supplements?

Back 14

Hyperkalemia

Front 15

What types of enzymes can destroy the penicillin molecule?

Back 15

General beta-lactamases and penicillinases. Cephalosporinases deactivate cephalosporins.

Front 16

What is the advantage of Nafcillin over other penicillins?

Back 16

Penicilinase-resistant

Front 17

Amoxicillin has what kind of bacterial spectrum?

Back 17

Broad-spectrum

Front 18

How does clavulanic acid prevent amoxicillin from being deactivated?

Back 18

Clavulanic acid inhibits beta-lactamase

Front 19

What are other beta-lactam antibiotic groups other than the penicillins?

Back 19

Cephalosporins, carbapenems

Front 20

How do cephalosporins kill bacteria?

Back 20

Inhibits cell wall synthesis

Front 21

Each subsequent generation of cephalosporins show more activity against what type of bacteria? How does each subsequent generation penetrate into the cerebral spinal fluid?

Back 21

Gram negative bacteria and anaerobes, more resistant to beta-lactamases.
Each subsequent generation is more likely to reach the cerebral spinal fluid.

Front 22

What percentage of penicillin-allergic patients will have an allergic reaction to a cephalosporin?

Back 22

1%

Front 23

What is the adverse effect seen with some cephalosporins and alcohol?

Back 23

Antabuse-like effects: weakness, pulsating headache, chest pain, abdominal cramps

Front 24

What is the drug interaction is seen between IV calcium and IV cephalosporins?

Back 24

Lung and renal precipitates

Front 25

How does vancomycin kill bacteria? What bacteria does it kill?

Back 25

Inhibits cell wall synthesis. Gram-positive bacteria.

Front 26

For what types of infection is vancomycin reserved? How is it given for CDI?

Back 26

Severe C. difficile infections (CDIs), MRSA, & Staph. Epidermidis. Must be given PO for CDI, because cannot cross between GI tract and bloodstream.

Front 27

What are the signs and symptoms of Red Man Syndrome seen with the rapid infusion of vancomycin?

Back 27

Red rash, hives, flushing, and pruritis on face & upper body. Hypotension, tachycardia. From histamine release, NOT an allergic reaction.

Front 28

Creatinine (Cr) is monitored with vancomycin therapy to avoid what? What is an indication for stopping vancomycin?

Back 28

Renal failure. Stop if Cr rises 50%.

Front 29

Aztreonam is used to treat what type of infection? Why?

Back 29

Gram-negative aerobic bacteria. Only attaches to PBPs on gram-negative aerobic bacteria.

Front 30

1. How to tetracyclines inhibit the replication of bacteria?

Back 30

Inhibits protein synthesis at ribosomes

Front 31

How long should a patient wait after taking tetracycline before he has a glass of milk?

Back 31

2 hours

Front 32

Why are tetracyclines avoided in children younger than 8 years of age?

Back 32

Discoloration and hypoplasia of teeth

Front 33

What precautions should patients take with tetracycline?

Back 33

Sun protection for photosensitivity. Take with a full glass of water to prevent esophageal ulcerations.

Front 34

How does erythromycin increase the chance of drug interactions?

Back 34

Inhibits hepatic drug metabolism by P450 system.

Front 35

What is the major risk of drug interactions with erythromycin?

Back 35

QT prolongation, which places person at risk for Torsades de Pointes,

Front 36

How does erythromycin inhibit the replication of bacteria?

Back 36

Inhibits protein synthesis at ribosomes

Front 37

What are common adverse effects of erythromycin? How can this be mitigated?

Back 37

Nausea, vomiting, diarrhea, epigastric pain. Give ethylsuccinate or enteric-coated tablets with food.

Front 38

How does clarithromycin (Biaxin) inhibit the replication of bacteria?

Back 38

Inhibits protein synthesis at ribosomes

Front 39

Which macrolide does not inhibit hepatic enzymes? What drug interaction is still significant with this drug?

Back 39

Azithromycin (Zithromax). Raises warfarin (Coumadin) levels.

Front 40

Why is telethromycin (Ketek) only used for multidrug-resistant Streptococcus pneumonia?

Back 40

Hepatoxicity.

Front 41

How do sulfonamides inhibit replication of bacteria?

Back 41

Competes with PABA in synthesizing folic acid and inhibits enzyme (dihydrofolate reductase) used to synthesize folic acid

Front 42

Why are sulfonamides contraindicated for infants less than 2 months old?

Back 42

Kernicterus

Front 43

Which antibiotic drug class is avoided in patients with G6PD deficiency? Why?

Back 43

Sulfonamides may cause hemolytic anemia.

Front 44

What drugs should be used with caution if the person in allergic to sulfonamides? Should a person with anaphylaxis try these drugs?

Back 44

Sulfonylureas (oral antidiabetic drugs), loop diuretics, thiazide diuretics, and Celebrex (COX-2 inhibitor). Absolutely not due to a higher risk of hypersensitivity.

Front 45

Why should a patient stop using a sulfonamide with a blistering, sunburn-like rash? What other skin reaction may occur

Back 45

Risk for Stevens-Johnson Syndrome. Photosensitivity.

Front 46

How do fluoroquinolones kill bacteria?

Back 46

Inhibit synthesis of nucleic acids

Front 47

Why should fluoroquinolones not be used in patients under the age of 18?

Back 47

Tendon injury

Front 48

For what type of bacteria are aminoglycosides given?

Back 48

Aerobic gram negative bacilli

Front 49

Fluoroquinolones are ordered to be given in the morning with a multivitamin with minerals. Why is this contraindicated?

Back 49

Calcium, aluminum, magnesium, iron, zinc may combine with the fluoroquinolone and prevent its absorption. Give fluoroquinolones on an empty stomach.

Front 50

Ciprofloxacin (Cipro) is given for what common disease processes?

Back 50

UTIs, enteric organisms.

Front 51

What are the two mechanisms of action for aminoglycosides?

Back 51

Inhibit protein synthesis at ribosomes and insert abnormal proteins into the cell wall.

Front 52

Instead of keeping the serum drug levels above the MIC (minimum inhibitory concentration), how do aminoglycosides kill bacteria?

Back 52

Concentration-dependent kill with post-antibiotic effect.

Front 53

Discuss the distribution of aminoglycosides.

Back 53

Unable to cross cell membranes. Not absorbed orally and does not cross blood-brain barrier.

Front 54

What two organs can be damaged by aminoglycosides?

Back 54

ears and kidneys

Front 55

When are gentamicin peak and trough levels drawn?

Back 55

Multiple doses: Peak level 30 min after IM or after 30-min IV infusion. Trough level immediately before next dose.
Daily dose: Trough level 1 hr before next dose. No need for peak level.

Front 56

What two antibiotics are reserved mainly for anaerobic bacteria?

Back 56

Clindamycin (Cleocin) and metronizadole (Flagyl).

Front 57

What viruses does acyclovir (Zorivax) treat? Does it cure the disease?

Back 57

Herpes simplex viruses (HSVs) – cold sores and genital infections, varicella-zoster virus (VZV) – chickenpox and shingles. The drug manages the symptoms, but does not cure or prevent transmission.