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Class: Immuno Block > Antibiotics_WalworthPilch > Flashcards

Antibiotics_WalworthPilch Flashcards

1
Q

MBC (minimal bacteriacidal concentration) - YES within therapeutic range of drug

A

Bacteriacidal (cell-wall active agent) - Rifampin, quinolones

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2
Q

Toxic Dose/Effective Dose

A

Therapeutic Index

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3
Q

Therapeutic Index >1 __

Therapeutic Index

A

Susceptibility

Resistance

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4
Q

Timeline of Antibiotic Drug Therapy

A
  1. Prophylactic (no infection) -> Pre-emptive
  2. Empiric (after infection, cultures of blood/infection site + lab techniques [gram stain/strep test]) - single, broad spectrum agent [causative microorganism NOT yet defined]
  3. Definitive - Specific and narrow-spectrum agent
    [causative microorganism YES defined]
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5
Q

Type of empiric therapy used to:
INCREASE antimicrobial activity for specific infection
DECREASE resistance + host toxicity

A

Combination Therapy

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6
Q

Combination Therapy Criteria

A

Usually use two agents that differ in mechanism (SIGNIFICANTLY lowered frequency of resistance)

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7
Q

What disease do you especially use combination therapy?

A

Tuberculosis

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8
Q

COMBINATION THERAPY: Relationship between bacteriostatic and bacteriacidal drugs

A

Bacteriostatic (Tetracyclins) ANTAGONIZE bacteriocidal (beta-lactams, rifampin, quinolones, aminoglycoside)

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9
Q

COMBINATION THERAPY: Relationship between combined usage of bacteriacidal drugs

A

Synergistic (one drug potentiates the inhibitory effect of the other)
Additive (one drug independent of action of other drug)

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10
Q

MIC (minimal inhibitory concentration) - YES, within therapeutic range of drug
MBC (minimal bacteriacidal concentration) - NO within therapeutic range of drug

A

Bacteriostatic agent (protein synthesis inhibitors)

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11
Q

MDR

A

Multi-drug resistant bacteria

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12
Q

4 Genetic Mechanisms of Developing Antibiotic Resistance

A
  1. Transformation - uptake of DNA from environment
  2. Transduction - uptake of DNA from bacteriophage (viral vector)
  3. Conjugation - transfer of plasmid from one bacterial cell to another by direct contact and pilus formation
  4. Transposition - for the antibiotic resistance gene to be phenotypically expressed by the bacteria, the gene has to be transferred from the plasmid to the bacterial chromosome (via insertion sequences)
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13
Q

beta-lactam antibiotics

A

penicillin (subclass: amoxicillin), methicillin, oxacillin, nafcillin, ampicillin + cephalosporins

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14
Q

AMINOGLYCOSIDE Antibiotics

A 
Gentamicin
Neomycin
Amikacin
Tobramycin
Streptomycin
Kanamycin
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15
Q

beta-lactamase inhibitor

A
  • beta-lactamase: bacteria evolved and acquired mutation in beta-lactamase that cleaves/renders inactive beta-lactams (penicillin/cephalosporin)
  • CLAVULANIC ACID
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16
Q

Combination Therapy: Amoxicillin (beta-lactam) + Clavulanic acid (beta-lactamase inhibitor)

A

Augmentin

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17
Q

Most common anti-fungal agent and its action

A

5-flucytosine
Action: Inhibits formation of dTMP -> Decreases fungal DNA synthesis
Caveat: Requires 3 metabolic enzymes to work - cytosine deaminase, UMP pyrophosphorylase, ribonucleotide reductase

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18
Q

Resistance to 5-flucytosine (anti-fungal agent) is most likely due to __

A

Downregulation of UMP PYROPHOSPHORYLASE - Enz required for the conversion of 5-flucytosine to a more active compound and its effect of decreasing fungal dTMP (DNA) synthesis

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19
Q

Combination Therapy: Sulfonamide + Trimethoprim (Synergistic Relationship)
Block 2 steps within the same pathway

A

Bactrim

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20
Q

Only time that bactrim will not work:

Mechanism of bacteria developing bactrim resistance

A

Overproduction of p-aminobenzoic acid (PABA): Increased flux of reacting metabolite to overcome competitive, antagonistic drug sulfonamide (part of bactrim)

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21
Q

LARGEST GROUP of ANTIBIOTICS = cell wall inhibitors

[ALL BACTERIACIDAL by weakening cell wall -> bacteria rupture by osmotic lysis]

A

beta-lactams (penicillin/amoxicillin + cephalosporins)
NOT beta-lactams (vancomycin)
carbapenems
monobactams

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22
Q

Mechanism in which bacteria acquired VRE (mostly enterocci and moderately in staphylococci)

A 
Bacteria acquired DNA to produce a mutational proteoglycan matrix of the cell wall: 
3 genes (VanHAX operon) that encoded for D-Ala-D-lactate (instead of D-Ala-D-Ala, target of vancomycin) -> Vancomycin can NO LONGER BIND
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23
Q

Resistances of S. aureus

A

1) PENICILLINASE - Resistant to penicillin
MRSA - methicillin resistant S. aureus (methicillin = “penicillinase-resistant” anti-staphylococcal beta-lacftams
2) VISA / VRSA - vancomycin intermediate/resistant S. aureus

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24
Q

beta-lactamase resistant penicillins (beta-lactam)

A

Nafcillin

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25
Q

Macrolide used to treat Chlamydia AND also gonorrhea or neonatal conjunctivitis (N. gonorrheae infections)
We have to assume Chlamydia co-infection whenever patient has gonorrhea

A

Azithromycin
Erythromycin
Clarithromycin
Telithromycin

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26
Q

N. gonorrheae is resistant to which antibiotics

A

Penicillin
Tetracycline
Quinolones
Reason: 20-30% of new gonorrhea cases are PPNG (penillinase-producing)/ TRNG (tetracycline resistant)/ QRNG (quinolone resistant)

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27
Q

2 IV aminoglycoside antibiotics used to treat SERIOUS infections

A

Gentamicin

Tobramycin

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28
Q

2nd line agent used to treat tuberculosis = __

What drug is this antibiotic combined with __

A

Streptomycin

Combined with INH or Rifampin - To prevent emergence of drug resistance

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29
Q

Aminoglycoside drug used when bacteria develops inactivating enzymes against tobramycin and gentamycin

A

Amikacin

30
Q

Topical aminoglycoside antibiotics used to treat skin/eye

A

Neomycin

Kanamycin

31
Q

Most NEPHROTOXIC aminoglycoside inhibitors when administered >5 days, elderly, renal insufficency

A

Gentomicin
Neomycin
Tobramycin

32
Q

Most OTOTOXIC (inner ear) aminoglycoside antibiotics with
AUDITORY manifestation
* Tinnitus + high-frequency hearing loss

A

Kanomycin
Amikacin
Neomycin

33
Q

Most OTOTOXIC (inner ear) toxic aminoglycoside - with
VESTIBULAR manifestation
* Vertigo/ataxia

A

Streptomycin

Gentomicin

34
Q

Bacteriostatic drug used to treat Gm+ Gm- aerobic anaerobic, non Gm+/Gm- [chlamydia, rickettsia, mycoplasma], protozoa [ameba]

A

Aminoglycosides

Doxycycline - most common

35
Q

Fluoroquinolones block ___ in Gm- bacteria

Fluoroquinolones block ___ in Gm+ bacteria

A

Gm-: DNA gyrase (Topo II)

Gm+: Topo IV

36
Q

When all other tetracyclines fail due to antibiotic resistance, the tetracycline of choice in the hospital setting is ___
* Not resistant to bacteria - VRE/MRSA

A

Tigecycline (IV)

37
Q

Reason for preference of doxycycline over tetracycline

A

1) Longer half-life: doxycycline [BID] versus tetracycline [TID]
2) Higher absorption: 100% for doxycycline + minocycline versus lower percentage for tetracycline

38
Q

Contraindications of doxycycline usage

A

1) Younger children Bound deposits in teeth and bones -> Interferes with growth (stature) + Teeth discoloration
2) Avoid dairy products + supplements + antacid tablets - Contain multivalent cations that doxycycline can bind to

39
Q

Treatment of choice for Lyme Disease

A

Doxycycline

40
Q

SECOND LARGEST GROUP of ANTIBIOTICS = PROTEIN SYNTHESIS INHIBITORS (bacterial protein synthesis via 30S or 50S subunit)

A

30S inhibitors - Aminoglycosides (BACTERIACIDAL) + Tetracyclines (BACFTERIOSTATIC)
50S inhibitors - Macrolides + Clindamycin + Streptogramins + Linezolid

41
Q

THIRD LARGEST GROUP of Antibiotics Part 1 = anti-DNA REPLICATION (DNA gyrase [Topo II] + Topo IV inhibitors)
[BACTERIACIDAL]

A

Fluoroquinolones (Ciprilfloxacin -oxacins)

42
Q

THIRD LARGEST GROUP of ANTIBIOTICS Part 2= anti-METABOLITES [anti-DNA biosynthesis]
Anti-biosynthetic drugs used to block folate metabolism

A

SULFONAMIDES + TRIMETHOPRIM - Both work synergistically (in the same pathway) in inhibiting enzymes required for the biosynthesis of purines (A/G)

43
Q

MINOR GROUP of Antibiotics = anti-CELL MEMBRANE (inner membrane)

A

Polymyxins + Daptomycin
* Cell membrane inhibitors are seldom used bec of high toxicity* - Difficult to get specificity for bacterial cell membrane (very similar to human membrane)

44
Q

TETRACYCLINES Antibiotics (30S inhibitor)

A 
Tetracycline
Oxytetraycline
Doxycycline
Tigecycline
Minocycline 
Demeclocycline
45
Q

MACROLIDE Antibiotics (50S Inhibitor)

A

Erythromycin
Azithromycin
Telithromycin
Clarithromycin

46
Q

Most common clinically used lincosamide and oxazolidinone (both 50S inhibitors)

A

Clindamycin

Linezolid

47
Q

STREPTOGRAMIN Antibiotics (50S inhibitor)

A

Quinupristin

Dalfopristin

48
Q

2 Possible antibiotics used to treat community-acquired PNEUMONIA (both have equal efficacy)

A

Tetracycline [Doxycyline]

Macrolide [Azithromycin, Clarithromycin]

49
Q

2 Drugs that can be used to treat Chlamydia infections

A

Tetracycline [Doxycycline]

Macrolides [Azithromycin/Clarithromycin]

50
Q

Only condition that TELITHROMYCIN (macrolide) is approved for __. Why is it not approved for other conditions?

A

Community-acquired pneumonia

Scare of cholestatic hepatitis (hepatotoxicity) with telithromycin usage

51
Q

Most common bacterial infection in skin/soft-tissue

A

Staphylococcus

52
Q

MOST effective antibiotic for acne

A

Clindamycin (Gm+)

53
Q

MOST effective antibiotic administered ONLY by IV for VRE E. faecium + skin infections caused by methicillin-sensitive S. aureus (MSSA)

A

STREPTOGRAMINS - Quinupristin/Dalfopristin

54
Q

Preferred antibiotic for any MDR Gm+ bacterial infection
#1 antibiotic used to treat MRSA systemic infections
VRE, penicillin-resistant streptococci

A

Linezolid

55
Q

Is bactrim bacteriostatic or bacteriacidal?

A

BacteriaCIDAL although its components (trimethoprim and sulfonamide individually are bacteriaSTATIC)

56
Q

Sulfasalazine is primarily used to treat ___

A

ulcerative colitis + enteritis

57
Q

UTIs can be treated by ___

Which is the most effective?

A

All DNA-synthesis inhibitor antibiotics:
Sulfonamides, Trimethoprime, TMP-SMX[bactrim/septra], Fluoroquinolones

Bactrim = most effective

58
Q

What is the course of treatment for bactrim? (How long do you administer bactrim?)

A
59
Q

Toxicity of bactrim if administered >5 days

A

Bactrim starts to act on the human THF synthesis and thus human DNA synthesis (purines) -> Hematologic effects
MEGALOBLASTIC ANEMIA + LEUKOPENIA

60
Q

Toxicity of Sulfa Drugs

A

1) #1 HYPERALLERGENIC - immune response that results in rash, fever, photosensitivity
2) LOW SOLUBILITY causing crystalluria and possibly hematuria

61
Q

Front-line antibiotic treatment for anthrax

A

Fluoroquinolone - Ciprofloxacin

62
Q

3 Respiratory FQs mainly used and is effective for treatment of upper and lower respiratory tract infections (Pseudonomonal infections for cystic fibrosis patients)

A

Levofloxacin
Gemifloxacin
Moxifloxacin

63
Q

2 Flouroquinolone Drugs that are PARTICULARLY effective against Gm+ bacteria (although it is also bacteriacidal against Gm- as well)

A

GEMifloxacin

MOXifloxacin

64
Q

4 REMAINING fluoroquinolone drugs that are PARTICULARLY effective against Gm- bacteria and mildly against Gm+ bacfteria

A

LEVofloxacin
LOMefloxacin
OFlofloxacin
CIPROfloxacin

65
Q

Treatment for ALL stages of syphilis

A

Penicillin

66
Q

Treatment option for Chlamydia infection manifestation of Trachoma (leading cause of blindness) + STI

A

Macrolides (azithromycin) OR tetracyclines (doxycycline) WITH
Ceftriazone (cephalosporin) - SINCE YOU ALWAYS ASSUME CO-INFECTION WITH GONORRHEA

67
Q

Which antibiotic can you NOT administer to neonates with neonatal conjunctivitis due to a Chlamydia trachomitis infection?
Which form do you give then?

A

TOPICAL macrolide - NO

ORAL macrolide - YES

68
Q

Bacterial infection that produces maculopapular rash (prominent in soles of hand and feet)

A

Syphilis - Treponema Pallidum

69
Q

Bacterial infection that produces a rash that SPARES the hands/feet and spreads centrally outwards

A

Rickettsia prowazekki

70
Q

Bacterial Infection that causes a rash that begins in the extremities and spreads centrally with fever/headache/myalgia

A

Rickettsia rickettsii

Class: Immuno Block (13 decks)

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