Pharm: CV Infections Flashcards

1
Q
  • What is the empiric treatment for ARF?
A
  • PCN G + Gentamicin
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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
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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
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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
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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
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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.
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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
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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
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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
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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
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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
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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
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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
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14
Q
  • What is the empiric treatment for IE?
A
  • Vancomycin (IV) + ceftriaxone
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15
Q
  • What type of bacteria does Vancomyin work on?
A

Gram + only, Including MRSA

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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
Q
  • Which penicillinase-resistant penicillin is used to treat Staph aureus IE that has been complicated by the development of a brain abscess?
A
  • Nafcillin
    • penetrates BBB well
26
Q
  • What bacteria is Daptomycin effective against?
A
  • gram + including MRSA
27
Q
  • What is the MOA of Daptomycin?
A
  • 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
Q
  • How would you treat S. epidermidis and other coagulase-negative staphylococci?
A
  • Vancomycin
29
Q
  • How do you treat HACEK group IE?
A
  • Ceftriaxone
30
Q
  • How would you treat Enterococci IE (mostly E. faecalis)?
A
  • [PCN G or ampicillin or vancomycin] + gentamicin
    • vanc if there is a severe pcn allergy
31
Q
  • Vancomycin is what type of drug?
A

glycopeptide

32
Q
  • What generation is cefazolin?
A

1st

33
Q
  • 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?
A
  • 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
Q
  • The anti-inflammatory action of colchicine is mediated by binding to?
    • what is the end result of colchicine therapy?
A
  • tubulin
  • prevents tubulin polymerization into microtubules, which leads to inhibition of leukocyte migration and phagocytosis
35
Q
  • What are the adverse effects associated with Colchicine?
    • when are the severe effects likely to be seen?
A
  • 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
Q
  • What is the moa of Vancomycin?
A
  • 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.