Pharm: CV Infections Flashcards
(36 cards)
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
16
Q
- For a highly penicillin suceptible strep viridans infection, what would you use?
A
- PCN G
- or another beta lactam–> Ceftriaxone
17
Q
- If your patient has a Strep Viridans IE infection, and doesn’t have any renal disease, how can you speed up the process of treating their infection?
A
- Gentamicin + PCN G
- Gentamicin + Ceftriaxone
PCN G, Ceftriaxone punch holes in cell wall, allow fries on the side to get in (aminoglycosides)
18
Q
- If patient has a Strep Viridans IE infection, but has a mild pcn allergy, how would you treat it?
A
- Ceftriaxone
- Gentamicin + Ceftriaxone
- mild: itchiness, upset stomach etc, no life-threatening rxn
19
Q
- If your patient has a Strep Viridans IE infection, but has a severe pcn allergy, how would you treat it?
A
- Penicillin desensitization (first) only because strep viridans is subacute IE
- IF that doesn’t work–> Vancomycin
20
Q
- What mediates an allergic reaction to pcn?
- what must be present to maintain desensitization?
A
- IgE mediated
- Drug must be physically present to maintain desensitization
21
Q
- If your patient has Staph Aureus IE, that is methicillin-susceptible, how would you treat it?
A
- By a Penicillinase-resistant penicillin such as
- nafcillin
- oxacillin
22
Q
- If your patient has a Staph Aureus IE that is methicillin resistant (MRSA), how would you treat it?
A
- Vancomycin
- Alternatively, Daptomycin
23
Q
- If your patient has a Staph Aureus IE, but has a mild pcn allergy, how yould you treat it?
A
- Give a beta lactam like Cefazolin
24
Q
- If your patient has a Staph Aureus IE, but has a severe pcn allergy, how would you treat?
A
- Go straight to either
- Vancomycin or
- Daptomycin (still alternative)
25
* Which penicillinase-resistant penicillin is used to treat Staph aureus IE that has been complicated by the development of a **brain abscess?**
* Nafcillin
* penetrates BBB well
26
* What bacteria is Daptomycin effective against?
* gram + including MRSA
27
* What is the MOA of Daptomycin?
* Not completely understood
* what we know is
* binds to cell membrane via calcium-dependent insertion of its lipid tail leading to depolarization, potassium efflux, and rapid cell death.
28
* How would you treat S. epidermidis and other coagulase-negative staphylococci?
* Vancomycin
29
* How do you treat HACEK group IE?
* Ceftriaxone
30
* How would you treat Enterococci IE (mostly E. faecalis)?
* [PCN G **or** ampicillin **or** _vancomycin_] **+** gentamicin
* vanc if there is a severe pcn allergy
31
* Vancomycin is what type of drug?
glycopeptide
32
* What generation is cefazolin?
1st
33
* How do you treat pericarditis in _immunocompetent_ patients?
* what test should you order to track tx?
* what drug should only be used in severe or refractory cases? what is the risk of doing this?
* NSAID (asprin or naproxen) + colchicine
* CRP to track, measures inflammation
* corticosteroids (prednisone) are used in severe or refractory cases, but there is a _risk to prolong illness or to increase the chance of relapse_
34
* The anti-inflammatory action of colchicine is mediated by binding to?
* what is the end result of colchicine therapy?
* tubulin
* prevents tubulin polymerization into microtubules, which leads to _inhibition of leukocyte migration and phagocytosis_
35
* What are the adverse effects associated with Colchicine?
* when are the severe effects likely to be seen?
* Diarrhea, and occasional N/V, and abdominal pain
* Hair loss, bone marrow depression, peripheral neuritis, myopathy
* \*\*more likely to be seen w/ IV colchicine versus oral\*\*
36
* What is the moa of Vancomycin?
* **binds D-ala-D** terminus of cell wall precursors w/ high affinity
* leads to **inhibition of transglycosylase** thus **prevents extension and cross-linking of the peptidoglycan**. (cell wall synthesis inhibition)
* this process also damages the cell wall, which contributes to the antibacterial activity.
