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DIT Microbiology > Micro 16 - Other Antibiotics > Flashcards

Micro 16 - Other Antibiotics Flashcards

1
Q

What antimicrobial prophylaxis can be used in Meningococcal meningitis?

A

Ciprofloxacin, Rifampin, Ceftriaxone.

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2
Q

What antimicrobial prophylaxis can be used in H. Influenzae meningitis?

A

Rifampin.

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3
Q

What antimicrobial prophylaxis can be used in Gonorrhea?

A

Ceftriaxone.

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4
Q

What antimicrobial prophylaxis can be used in Syphilis?

A

Benzathine Penicillin G.

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5
Q

What antimicrobial prophylaxis can be used in History of recurrent UTIs?

A

TMP-SMX, Nitrofurantoin, Amoxicillin, Cephalexin.

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6
Q

What antimicrobial prophylaxis can be used in Pneumocystis jiroveci?

A

TMP-SMX, if sulfa allergic, use aerosolized pentamidine, dapsone.

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7
Q

What antimicrobial prophylaxis can be used in endocarditis in patients which damaged valves or mechanical ones?

A

Penicillin, Amino-penicillins, Cephalexin.

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8
Q

What antimicrobial prophylaxis can be used in pregnant woman with GBS?

A

Ampicillin (during labor).

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9
Q

What antimicrobial prophylaxis can be used in gonococcal or chlamydial conjunctivitis in newborn?

A

Erythromycin ointment.

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10
Q

What are antibiotics to avoid in pregnancy?

A

Clarithromycin (embryotoxic), Sulfonamides (kernicterus), Aminoglycoside (Otoxicity), Fluoroquinolones (Cartilage damage), Metronidazole (Mutagenesis), Tetracylines (Discolored teeth, inhibition of bone growth), Ribavirin (Teratogenic), Griseofulvin (Teratogenic).

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11
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Sulfonamides?

A

MOA: Inhibit dihydropterate synthetase. CU: G(+/-). AE: UTIs, GI infections, PCP. AE: Hypersensitivity, Kernicterus (late pregnancy), hemolysis, Steven-Johnson syndrome.

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12
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Trimethoprim?

A

MOA: Inihibit dihydrofolate reductase. CU: UTIs, GIs. AE: Anemia.

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13
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Nitrofurantoin?

A

MOA: Bacterial ribosomes, vague. CU: UTIs (can be used in Preg). AE: GI symptoms.

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14
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Fluoroquinolones?

A

MOA: Topoisomerase II. CU: G(-/+). UTIs, GIs, URI. AE: GIs, Cartilage, tendon dmg.

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15
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Metronidazole?

A

MOA: Toxic free radicals. CU: [GeT GAP on the Metro] Giardia, Trich, Gard, Anaerobes, H.pylori. AE: Disulfiram.

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16
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Penicilin?

A

MOA: Bind PBP. CU: G(+), Syphilis. AE: Hypersen.

17
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Methicillin, Nafcillin, Oxacillin, Dicloxacillin?

A

MOA: Bind PBP. CU: Staph aureus. AE: Hypersen.

18
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Ampicillin, Amoxicilin.

A

MOA: Bind PBP. CU: G(+), [HEELPSS]: H.influenzae, E.coli,Enterococci,Listeria,Proteus mirabilis, Salmonella,Shigella. AE: Hypersens.

19
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Ticarcillin, Carbenicillin, Piperacillin?

A

MOA: Bind PBP, CU: G(+/-), Pseudomonas. AE: Hypersens.

20
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Polymyxins.

A

MOA: Cationic detergent, cell membranes. CU: G(-). AE: Nephro, Neuro.

21
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of 1st gen Cephalosporins?

A

MOA: Bind PBP. CU: G(+), [PEcK] Proteus mirabilis,E.coli,Klebsiella. AE: Hypersens, Nephrotox when used w/ aminoglycosides.

22
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of 2nd gen Cephalosporins?

A

MOA: Bind PBP. CU: Less G(-), [HEN PEcK]: H.influenzae,Enterobacter,Neiserria,Serratia marcens. AE: Hypersens, Nephrotox when used w/ aminoglyco.

23
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of 3rd gen cephalosporins?

A

MOA: Bind PBP. CU: Strep pneumo, Serious G(-), ceftazidime can be used for pseudomonas. AE: Hypersens, Nephrotox w/ aminoglyco.

24
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of 4th gen Cephalosporins (cefepime)?

A

MOA: Bind PBP. CU: Broad spec, Pseudomonas. AE: Hypersens, Nephrotox w/ aminoglyco.

25
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Aztreonam?

A

MOA: Bind PBP-3. CU: G(-) only. AE: Nontoxic.

26
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Carbopenems: Imipenem-cilastatin, Meropenem?

A

MOA: Bind PBP. CU: Broad spec, Pseudomonas. AE: GI, neurotox, Skin rash.

27
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Vancomycin.

A

MOA: Bind D-ala, D-ala. CU: MRSA, enterococci. AE: [NOT] Nephro Oto Tox, Thrombophlebitis.

28
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Linezolid?

A

MOA: Bind 23s portion of 50s. CU: MRSA, VRE. AE: GIs, thrombocyto.

29
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of tetracyclines?

A

MOA: Bind 30s. CU: [VACUUM The Bed Room] Vibrio cholera,Acne,Chlamydia,Ureoplasma Urolyticum,Mycoplasma pneumoniae,Tuleremia,H.pylori,Borrelia burgdorferi,Rickettsia. AE: GIs, Tooth discolor, Inhib bone growth, photosensitivity.

30
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of aminoglycosides?

A

MOA: Bind 30s. CU: Severe G(-). AE: [NOT] Nephro Oto tox, Teratogenic.

31
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of macrolides?

A

MOA: Bind 23s of 50s. CU: [PUS] Pneumonia, URIs, STDs. AE: Prolonging QT interval.

32
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Chloramphenicol?

A

MOA: Bind 50s. CU: meningitis. AE: Anemia, Gray baby.

33
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Clindamycin?

A

MOA: bind 50s. CU: Anaerobic infection, MRSA (skin). AE: Pseudomembranous Colitis.

34
Q

What is the Mechanism of action (MOA), Clinical use (CU), and adverse effect (AE) of Quinupristin-Dalfopristin?

A

MOA: Bind 23s of 50s. CU: MRSA, VRE. AE: Hepatotox, althralgia, myalgias.

35
Q

What is the drug of choice of anthrax infection?

A

Ciprofloxacin.

36
Q

What drugs are effective against Pseudomonas?

A

Fluoroquinolones, extended spectrum penicillins, 3rd gen cephalosporins, cefepim, Aztreonam, aminoglycosides, polymixins.

37
Q

What is the mechanism of action of Polymyxins and its applications?

A

They are cationic detergents. Given in IV, they are last resort for resistant G(-) infections. Topically, they are used in many OTC antibiotic ointments. Toxicity includes neuron and renal damage.

DIT Microbiology (33 decks)

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