Pharm: CV Infections Flashcards
1
Q
- What is the empiric treatment for ARF?
A
- PCN G + Gentamicin
2
Q
- Describe the synergy between PCN G, and gentamicin
A
- PCN G disrupts the cell wall of the target allowing gentamicin (aminoglycoside) to come in and act as a protein synthesis inhibitor at the 30S subunit
3
Q
- If patient has a PCN allergry or hypersensitivity to beta lactams, what would you give someone for ARF?
A
- Macrolides such as:
- erythromycin
- azithromycin
- clarithromycin
- Clindamycin
4
Q
- What is the most worrisome side effect of giving a hospitalized patient clindamycin?
A
- cdiff induced colitis
- clindamycin clean sweep of your gi
5
Q
- If you have a concern for recurrent acute RF in a patient hypersensitive to beta lactams what drugs should you use?
- which drug is contraindicated for prophylaxis of recurrent RF?
A
- Macrolides:
- Erythromycin
- Azithromycin
- Clarithromycin
- Clindamycin is NOT used for prophylaxis of recurrent RF due to chance of clindamycin induced cdiff colitis
6
Q
- To treat the joint pain and stiffness (migratory polyarthritis) associated with ARF, what should you prescribe along with the Abx?
A
-
NSAIDS like aspirin or naproxen
- Tylenol (acetaminophen) is not an NSAID so don’t pick that on the test.
7
Q
- What are the MOAs of macrolides?
- 3
A
- Causes tRNA to get stuck at a-site, prevent elongation of protein
- induce conformational change in 50S subunit, preventing elongation of protein
- can bind to 50S subunit and prevent it from binding to the other subunits–> cause a breakage of the ribosome
8
Q
- What are the mechanisms of resistance against macrolides?
- there are four
A
- Active drug efflux
- macrolides enter bacteria, the bacteria upregulate efflux pumps (green in pic), macrolide pumped out
- Methylase enzymes modify binding site
- “shield” (enzyme) prevents macrolide from binding
- Degraded by esterases from enterobacteriaceae
- hints why you don’t use them for enterobacter
- Mutation of binding site itself
9
Q
- What are the adverse effects of macrolides?
A
- Gi distress including N/V and anorexia
- particularly **erythromycin**
- __Hepatotoxicity… Cholestatic Hepatitis
- prolonged use of **erythromycin**
-
Hypersensitivity
- manifests as eosinophilia, fever
10
Q
- What are some drugs in the aminoglycoside family?
- don’t need to know them all just have general idea
- What is meant by the “side to the burger”
A
- streptomycin
- gentamicin
- tobramycin
- amikacin
- neomycin
- paromomycin
- kanamycin
- netilmicin
11
Q
- What are the three MOAs of aminoglycosides?
- why do aminoglycosides pair well with cell wall active agents?
A
- Fixate the 50S and 30S subunits to the start codon on the mRNA
- inhibit the 70S particle formation–> inhibit 50S and 30S from binding each other, which inhibits protein synthesis
- binding induced errors in reading mRNA leading to production of nonfunctional proteins
- *aminoglycosides are bacteriacidal*****, so they pair well with other bacteriacidal agents, like cell wall active agents
12
Q
- What are some adverse effects of aminoglycosides?
A
- A Mean Guy approaches you on the street
- punches you in the kidney- Nephrotoxic
- punches you in the ear- CNVIII Toxicity
- knocks you out- NM blockade
- all these effects are after more than 5 days of high dose in a likely elderly renal insufficient patient
13
Q
- Infective endocarditis originating in the following areas are likely to be caused by which bacteria?
- oral cavity
- skin
- URT
A
- Oral cavity
- Viridans streptococci
- Skin
- Staphylococci
- URT
- HACEK
14
Q
- What is the empiric treatment for IE?
A
- Vancomycin (IV) + ceftriaxone
15
Q
- What type of bacteria does Vancomyin work on?
A
Gram + only, Including MRSA