Microbiology - Antimicrobials

Front 1

The penicillin type drugs work by blocking ------ synthesis, specifically by inhibiting this molecule from cross-linking?

Back 1

blocks bacterial cell wall synthesis by inhibition of peptidoglycan synthesis.

Front 2

Which other drugs (aside from penicillin) have this same mechanism of action?

Back 2

cephalosporins

Front 3

Bacitracin, vancomycin block the synthesis of this molecule, preventing cell wall synthesis

Back 3

peptidoglycans

Front 4

These drugs block the 50s ribosomal subunit

Back 4

clindamycin, chloramphenicol, erythromycin

Front 5

These drugs block the 30s ribosomal subunit

Back 5

Aminoglycosides and tetracyclines

Front 6

These drugs block nucleotide synthesis by interfering with the folate pathway

Back 6

Sulfonamides (e.g. Bactrim)

Front 7

These drugs block DNA topoisomerases

Back 7

Quinolones (e.g. Cipro)

Front 8

Which drug blocks mRNA synthesis

Back 8

rifampin

Front 9

Which are the bacteriacidal Abx

Back 9

Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones, metronidazole

Front 10

These drugs disrupt the bacterial/fungal cell membranes

Back 10

polymyxins

Front 11

These specific disrupt fungal cell membranes

Back 11

amphotericin B, nystatin, fluconazole/azoles (FAN the fungal cell membranes)

Front 12

Penicillin: Which is the IV form and which is the oral form

Back 12

G = IV, V=oral

Front 13

Penicillin: Which of these is not a mechanism of penicillin action: (1) binds penicillin-binding protein, (2) blocks peptidoglycan synthesis, (3) blocks transpeptidase catalyzed cross-linking of cell wall and (4) activates autolytic enzymes

Back 13

Penicillin does not block peptioglycan synthesis, bacitracin, vancomycin and cycloserine do that

Front 14

Penicillin: T or F: penicillin is effective against gram pos and gram neg rods

Back 14

False: penicillin is used to treat common streptococci (but not staph), meningococci, gram pos bacilli and spirochetes (i.e. syphilis, treponema). Not used to treat gram neg rods.

Front 15

Penicillin: What should you watch out for when giving penicillin?

Back 15

Hypersensitivity rxn (urticaria,severe pruritus) and hemolytic anemia

Front 16

Methicillin, nafcillin, dicloxacillin: These drugs are used mainly for what type of infection

Back 16

Staphlococcal infection (hence very narrow spectrum)

Front 17

Methicillin, nafcillin, dicloxacillin: T or F: these drugs have the same mechanism of action as penicillin

Back 17

TRUE

Front 18

Methicillin, nafcillin, dicloxacillin: Are these drugs penicillinase resistant? If so why?

Back 18

Bulkier R group makes these drugs resistant to penicillinase

Front 19

Ampicillin and amoxicillin: T or F: these drugs have the same mechanism of action as penicillin

Back 19

TRUE

Front 20

Ampicillin and amoxicillin: Which has greater oral bioavailability?

Back 20

amOxicillin (O for Oral)

Front 21

Ampicillin and amoxicillin: Can penicillinase effect these drugs efficacy?

Back 21

Yes, they are penicillinase sensitive

Front 22

Cephalosporins: What is the mechanism of action of Cephalosporins?

Back 22

inhibit cell wall synthesis

Front 23

Cephalosporins: How are they similar/different from penicillin?

Back 23

both have a beta-lactam ring structure but cephalosporins are less susceptible to penicillinases

Front 24

Vancomycin: Is it bactericidal or bacteriastatic and why?

Back 24

Bactericidal because it blocks cross linkage and elongation of peptidoglycan by binding D-ala D-ala protion of cell wall.

Front 25

Vancomycin: How does resistance to Vanco occur?

Back 25

D-ala D-ala is replaced with D-ala D-lactate which vanco does not block

Front 26

Vancomycin: What is it used for?

Back 26

Used for serious infection that is resistant to other drugs (e.g. gram pos multi-drug resistant organisms like S. aureus and C. difficile, methicillin resistant staph (MRSA))

Front 27

Vancomycin: What are the important toxicities of vanco?

Back 27

generally NOT many problems except, Nephrotoxicity, Ototoxicity and Thrombophlebitis

Front 28

Vancomycin: What can happen with rapid infusion of vanco?

Back 28

Red man's syndrome. Diffuse flushing which can be controlled by pretreatment with anti-histamines and with slow infusion rate

Front 29

Protein Synthesis Inhibitors: Which drugs target bacterial protein synthesis by blocking the 30S unit vs 50S unit?

Back 29

Aminoglycosides, tetracyclines

Front 30

Aminoglycosides: Name some aminoglycosides?

Back 30

tobramycin and streptomycin

Front 31

Aminoglycosides: How do these drugs work?

Back 31

They inhibit formation of the initiation complex in mRNA translation

Front 32

Aminoglycosides: Why are they ineffective against anaerobes?

Back 32

They require oxygen for uptake into bacteria

Front 33

Aminoglycosides: When would you use aminoglycosides?

Back 33

against severe gram-negative rod infections

Front 34

Aminoglycosides: What drugs can you use aminoglycosides with for synergy?

Back 34

the drugs that inhibit cell wall synthesis (e.g. penicillin and cephalosporins -- the beta-lactam antibiotics). Presumably this allows the drug to get in with out reliance on oxygen transport

Front 35

Aminoglycosides: What are the two major toxicities?

Back 35

Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides

Front 36

Tetracyclines: Name some tetracylcines

Back 36

Tetracycline, doxycycline, minocycline

Front 37

Tetracyclines: How does it work?

Back 37

Blocks t-RNA attachment to 30S subunit

Front 38

Tetracyclines: Which tetracycline can you use in patients with renal failure and why?

Back 38

Can use doxycycline because its elimination is fecal

Front 39

Tetracyclines: What are tetracyclines used for?

Back 39

VACUUM your Bed Room -- Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi, Rickettsia, tularemia

Front 40

Tetracyclines: What are the common toxicities

Back 40

GI distress, teeth discoloration, inhibition of bone growth in children, liver damage in pregnant women

Front 41

Macrolides: Name some macrolides?

Back 41

Erythromycin, azithromycin, clarithromycin

Front 42

Macrolides: How do these drugs work?

Back 42

inhibit protein synthesis

Front 43

Macrolides: What are they used for?

Back 43

URIs, pneumonias, STDs -- gram pos cocci in patients that are allergic to PNC --- Mycoplasm, Legionella, Chlamydia, Neisseria.

Front 44

Macrolides: Pneumonic for macrolide use?

Back 44

Eryc's Niple is at his Mid Clavicular Line (Eryc is brand name for erythromycin). Mycoplasm, Legionella, Chlamydia, Neisseria.

Front 45

Macrolides: What are the major toxicities?

Back 45

GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes

Front 46

Macrolides: What is the most common cause for non-compliance to macrolides?

Back 46

GI discomfort

Front 47

Chloramphenicol: How does this drug work?

Back 47

inhibits 50S peptidyltransferase

Front 48

Chloramphenicol: Main use?

Back 48

Meningitis (H. influenzae, N. meningitides, S. pneumo). Used conservatively b/c of toxicity

Front 49

Chloramphenicol: What are the main toxicities?

Back 49

Anemia and aplastic anemia (both dose dependent), gray baby syndrome (in premes b/c they lack UDP-glucoronyl transferase)

Front 50

Clindamycin: How does it work?

Back 50

blocks peptide bond formation at 50S

Front 51

Clindamycin: When do you use it?

Back 51

Anaerobic infections (e.g. Bacteroides fragilis and C.perfringens)

Front 52

Clindamycin: Toxicities?

Back 52

Pseudomembranous colitis, fever, diarrhea

Front 53

Sulfonamides: Name some sulfonamides

Back 53

Sulfamethoxazole (SMX), sulfisoxazole, triple sulfa and sulfadiazine

Front 54

Sulfonamides: How does it work?

Back 54

Inhibits bacterial folic acid synthesis from PABA by blocking dihydropteroate synthase.

Front 55

Sulfonamides: What are its uses?

Back 55

Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas and SMX for simple UTIs

Front 56

Sulfonamides: Toxicities?

Back 56

hypersensitivity rxn, hemolysis if G6PD deficient, nephorotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (e.g. warfarin)

Front 57

Trimethoprim: How does it work?

Back 57

inhibits folic acid pathway by blocking dihydrofolate reductase which humans have as well

Front 58

Trimethoprim: What are its uses?

Back 58

used in combo with Sulfamethoxazole (TMP-SMX) causing a sequential block of folate synthesis. Used for recurrent UTIs, Shigella, Salmonella, and prophylaxis for PCP in AIDS patients

Front 59

Trimethoprim: Toxicities?

Back 59

Megaloblastic anemia, pancytopenia (may be alleviated with suplemental folinic acid)

penetrates the brain and CSF

Front 60

Fluoroquinolones: What the most famous floroquinolone?

Back 60

Ciprofloxacin (treatment for Anthrax)

Front 61

Fluoroquinolones: How does it work?

Back 61

inhibits DNA gyrase (topoisomerase II)

Front 62

Fluoroquinolones: What are its uses?

Back 62

Gram neg rods or urinary and GI tract (incl. pseudomonas), Neisseria, some gram pos sp

Front 63

Fluoroquinolones: What population is contraindicated for use?

Back 63

pregnancy and children

Front 64

Fluoroquinolones: What are its toxicities?

Back 64

GI upset, superinfection, skin rashes, headache, dizziness and tendonitis and tendon rupture in adults. FluoroquinoLONES hurt attachment to BONES.

Front 65

Metronidazole: How does it work?

Back 65

forms toxic metabolites in the bacteria. Bactericidal.

Front 66

Metronidazole: What are its uses?

Back 66

anti-protozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (bacteroides, clostridium)

Front 67

Metronidazole: What is the role of Metronidazole in H. pylori infection?

Back 67

Used as part of triple therapy: bismuth, amoxicillin and metronidazole

Front 68

Metronidazole: Main toxicity?

Back 68

disulfiram-like (antabuse) reaction to alcohol and headache

Front 69

Metronidazole: Which drug do you use to treat anaerobic infections above the diaphram and below the diaphram

Back 69

anaerobes above diaphram: Clindamycin, and anaerobes below diaphram: metronidazole

Front 70

Polymyxins: How does it work?

Back 70

attaches to phospholipids and causes disruption

Front 71

Polymyxins: What is it used for?

Back 71

resistant gram negative infections

Front 72

Polymyxins: Toxicities?

Back 72

neurotoxicity, ATN

Front 73

Isoniazid: How does it work?

Back 73

decreases synthesis of mycolic acid

Front 74

Isoniazid: What is it used for?

Back 74

MTB (mycobacterium tuberculosis). The only agent used as solo prophylaxis against TB

Front 75

Rifampin: How does it work?

Back 75

inhibits DNA-dependent RNA polymerase

Front 76

Rifampin: What is it used for?

Back 76

Mycobacterium tuberculosis (also used with isoniazid and ethambutol)

Front 77

Rifampin: Toxicities?

Back 77

Minor hepatotoxicity and increases P-450

Front 78

Rifampin: How can it be used for leprosy?

Back 78

rifampin delays resistance to dapsone when used for leprosy

Front 79

Rifampin: What would happen if you used rifampin alone?

Back 79

get rapid resistance

Front 80

Rifampin: What does it do to bodily fluids?

Back 80

makes them red/orange in color

Front 81

Rifampin: What are the 4 R's of Rifampin

Back 81

RNA polymerase inhibitor, Revs up microsomal p-450, Red/Orange body fluids, Resistance is rapid

Front 82

Anti-TB Drugs: What are the anti-TB drugs?

Back 82

Rifampin, Ethambutol, Streptomycin, Isoniazid

Front 83

Anti-TB Drugs: What toxicity is common to all?

Back 83

hepatotoxicity

Front 84

Most common resistance mechanism for penicillins / cephalosporins.

Back 84

Beta-lactamase cleavage of beta-lactam ring.

Front 85

Most common resistance mechanism for vancomycin.

Back 85

Terminal D-ala of cell wall component replaced with D-lac; decrease affinity.

Front 86

Nonsurgical antimicrobial prophylaxis: Drug of choice for meningococcal infection.

Back 86

Rifampin (drug of choice), minocycline.

Front 87

Nonsurgical antimicrobial prophylaxis: Drug of choice for Pneumocystis carinii pneumonia.

Back 87

TMP-SMX (drug of choice)

Front 88

Amphotericin B: Clinical uses of Amphotericin B.

Back 88

Used for a wide spectrum of sytemic mycoses.

Front 89

Amphotericin B: Symptoms of Amphotericin B toxicity.

Back 89

Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible").

Front 90

Mechanism of action for fluconazole, ketoconazole, clotrimazole, miconazole

Back 90

These are azoles

Inhibits fungal steroid (ergosterol) synthesis.

Front 91

Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole

Back 91

Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.

Front 92

Antiviral chemotherapy: Viral nuclei acid synthesis is blocked by --------.

Back 92

Purine, pyrimidine analogs; reverse transcriptase inhibitors.

Front 93

Mechanism of aciton of Acyclovir and gancyclovir.

Back 93

Blocks transcription of DNA, mimics deoxyguanosine

Front 94

Acyclovir: Clinical use of Acyclovir.

Back 94

Used to treat herpes simplex

Front 95

HIV therapy: Zidovudine, Azidothymidine (AZT), examples of --------- reverse transcriptase inhibitors.

Back 95

Nucleoside.

Front 96

HIV therapy: Mechanism of action of reverse transcriptase inhibitors.

Back 96

Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of viral genome into host DNA.

Front 97

HIV therapy: Symptoms of reverse transcriptase inhibitor toxicity.

Back 97

Bone marrow supression (neutropenia, anemia), periphral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).

Front 98

HIV therapy: Highly active antiretroviral therapy (HAART) generally entails combination therapy with ---------- and -----------.

Back 98

Protease inhibitors, reverse transcriptase inhibitors.

Front 99

HIV therapy: -------- is used during pregnancy to reduce risk of fetal transmission.

Back 99

AZT.

Front 100

Interferons: Mechanism of action of Interferons.

Back 100

Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis.

Front 101

Interferons: Clinical use of Interferons.

Back 101

Chronic hepatitis B and C, Kaposi's sarcoma.

Front 102

Interferons: Symptoms of Interferon toxicity.

Back 102

Neutropenia.

Front 103

Clinical uses of Mebendazole

Back 103

Nematode/roundworm (e.g., pinworm, whipworm) infections.

Front 104

Clinical us of Niclosamide

Back 104

Cestode/tapeworm

first choice for tapeworm acquired from sushi

Front 105

Bateriostatic

Back 105

"Were ECSTaTiC about bacteriostatics"

Erythromycin

Clindamycin

Sulfamethoxazole

Trimethoprim

Tetracyclines

Chloramphenicol

Front 106

Bacteriocidal

Back 106

"Very Finely Proficienct At Cell Murder"

Vancomycin

Flouroquinolones

Penicilin

Aminoglycosides

Cephalosporins

Metronidazole