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Infectious Diseases Module > EXAM TWO COVERAGE > Flashcards

EXAM TWO COVERAGE Flashcards

1
Q

Macrolides

A

Extended G+ Spectrum
MOA: Bind to MLSb site on subunit 50S, inhibit protein synthesis
AE: GI intolerance and QT Prolongation
Resistance Mechanism: Mutation in MLS and Efflux Pumps

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2
Q

Erythromycin

A

Macrolide
Extended G+
PO or IV
Half Life: 1.4 hr
Metabolized in Liver, CYP430 3A4
Mainly excreted through bile/feces

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3
Q

Clarithromycin

A

Macrolide
Extended G+, some activity against SOME anaerobes
PO ONLY
Half-Life: 3.7 hr
Metabolized in Liver, CYP450 3A4
60% excreted through bile/feces, 40% KIDNEY – consider renal adjustments
AE: metallic taste

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4
Q

Azithromycin

A

Macrolide
Extended G+
PO or IV
Half Life: 68 hr
NOT METABOLIZED - lowest DDIs
Mainly excreted through bile/feces
15-Membered Ring = AZOLIDES

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5
Q

Ketolide - Telithromycin

A

Substituting cladinose sugar with KETO GROUP and attaching a CYCLIC Carbamate making it EFFECTIVE against macrolide resistant bacteria due to their ability to bind at 2 SITES (Domain 5 &2)

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6
Q

Fidaxomicin/Dificid

A

Macrolide
Inhibits the bacterial enzyme RNA polymerase by binding and preventing movement of the SWITCH REGIONS resulting in the death of C.Diff
Narrow Spectrum

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7
Q

Rifamycins

A

Broad Spectrum
MOA: Inhibit bacterial RNA polymerase, inhibit RNA synthesis
Resistance Mechanism: single amino acid change in the bacterial RNA polymerase
Primarily used for tuberculosis

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8
Q

Rifampin

A

Rifamycin
Broad Spectrum
Used in combo with Isoniazid for chemo, unreliable alone
PO, Take on empty stomach
Powerful inducer of CYP3A4, increases metabolism of other drugs
AE: body fluids are red/orange, GI intolerance, hepatotoxicity
MOA: bind B-subunit of RNA Polymerase specifically in mycobacteria
Resistance: mutations in B-subunit

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9
Q

Rifabutin

A

Rifamycin
Broad Spectrum
Used in combo with Isoniazid for chemo, unreliable alone
PO, Take on empty stomach
Does not induce CYP3A4 as much, preferred for HIV positive patients
Preferred in TB because: longer half life, less CYP3A4, effect against some rifampin resistant strains
AE: same as Rifampin
Prophylaxis agent against mycobacterium in HIV Positive patients

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10
Q

Rifaximin

A

Rifamycin
Broad Spectrum
For Travelers Diarrhea caused by E.coli
PO, short term treatment, without regard to food
AE: Peripheral edema
1st MOA: interferes with transcription by binding to B-subunit of bacterial RNA Polymerase blocking translocation
NON SYSTEMIC, GI SPECIFIC, poor absorption
2nd MOA: activates the pregnane X receptor inhibits pro inflammatory transcription factor NF-kappa-B making it effective for IBD

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11
Q

Quinolones/Fluoroquinolones

A

Broad Spectrum BEST oral drugs for P.Aeruginosa
Concentration Dependent
1st-4th Generation
MOA: inhibit DNA replication by irreversibly binding to bacterial enzymes - DNA gyros and Topoisomerase IV, which uncoil DNA
Resistance Mechanism: modification of target enzyme, modification of porins, and efflux pumps
AE: tendons, cartilage rupture, CNS excitation and seizures

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12
Q

Ozenoxacin

A

NON-FLUORINATED
Effective against some resistant gram + s.aureus and s.pyrogenes that cause IMPETIGO

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13
Q

Ciprofloxacin

A

Second Gen Fluoroquinolone
(better gram - than +)
AE: QT Prolongation
PO and IV, food decreases absorption
Short half life 4 hr
Metabolized in liver, excreted in urine = dose adjust in renal insufficiency

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14
Q

Levofloxacin

A

Third Gen Fluoroquinolone
Best Activity against ANAEROBEs (better gram+ activity)
AE: QT Prolongation
PO and IV, food decreases absorption
Long half life 6-12 hr
Metabolized in liver, excreted in urine = dose adjust in renal insufficiency

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15
Q

Moxifloxacin

A

Third Gen Fluoroquinolone
Best Activity against ANAEROBEs (better gram+ activity)
AE: QT Prolongation
PO and IV, food decreases absorption
Long half life 6-12 hr
EXCRETED IN BILE = Decreased DDIs

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16
Q

Delafloxacin

A

Fourth Gen Fluoroquinolone
ACTIVE AGAINST MRSA
NO qt prolongation
PO and IV, food decreases absorption
Long half life 6-12 hr
Metabolized in liver, excreted in urine = dose adjust in renal insufficiency

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17
Q

For patients with what disease states should fluoroquinolone be reserved unless there are no alternative treatments options as recommended by the FDA?

A
  1. Acute sinusitis
  2. Acute bronchitis
  3. Uncomplicated UTI
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18
Q

Fluoroquinolone are Concentration Dependent meaning what?

A

Higher the Peak = Better the Killing
Ratio of peak drug concentration and MIC determine rate of killing
Kill even after plasma levels drop below MIC aka post-antibiotic effect
ADMIN ONCE DAILY

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19
Q

Tetracyclines

A

Broad
MOA: bind to 30s ribosomal subunit, inhibit protein synthesis
Resistance Mechanism: mutation of binding site, efflux pump, and production of ribosomal protective protein
NOT ACTIVE against P.Aeruginosa
AE: photosensitivity, teeth discoloration (avoid in pregnancy and children younger than 8yrs)

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20
Q

Tetracycline

A

Broad, NOT Active against MRSA
PO, decreased by food
Half Life 6-8 hrs
NOT metabolized
Eliminated in URINE = DDIs and dose adjust renal
Esophageal Irritation

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21
Q

Doxycycline

A

Broad, active against SOME MRSA
PO and IV
Half Life: LONG 18-20 hr
PARTLY Metabolized
60% bile/feces 40% urine = DDIs and dose adjust renal
Esophageal Irritation

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22
Q

Minocycline

A

Broad, active on SOME MRSA
PO and IV
Half life LONG: 18-20 hrs
FULLY metabolized by liver
Mostly bile/feces
Esophageal Irritation

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23
Q

Tigecycline

A

Broad, ACTIVE Against MRSA and Tetracycline Resist
IV ONLY
Half Life LONG: 36 hr
PARTLY metabolized
Mostly bile/feces
Slight increased risk of death
MOA: inhibits protein translocation by binding to the 30s ribosomal unit and blocking entry of amino-acyl tRNA molecules into the A site of the ribosome

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24
Q

Omadacycline

A

Broad, ACTIVE Against MRSA and Tetracycline Resist
PO and IV, only new gen with ORAL option!!
Half Life LONG: 36 hr
NOT metabolized
Mostly bile/feces
Pneumonia and Skin Infections

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25
Q

Eravacycline

A

Broad, ACTIVE Against MRSA and Tetracycline Resist
IV ONLY
Half Life LONG: 36 hr
Metabolized in the liver
Mostly bile/feces
Halogenated/Fluorinated
For complicated intra-abdominal infections

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26
Q

Aminoglycosides

A

Extended G-, INACTIVE against Anaerobes
Concentration Dependent
MOA: penetrate bacteria using oxygen dependent influx pumps w/ irreversible binding to 30S and 50S or membrane disruption
Resistance Mechanism: production of AG modifying enzyme, mutation of binding site, mutation of influx pump, and efflux pump
Aminoglycoside + Beta Lactam = BROAD, not active against MRSA but active against P. Aeruginosa
Excreted in Urine = UTI = dose adjust
AE: renal toxicity, neuromuscular junction blockade, ototoxicity

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27
Q

Gentamicin

A

Aminoglycoside
Extended G-

28
Q

Amikacin

A

Aminoglycoside
Extended G-

29
Q

Tobramycin

A

Aminoglycoside
Extended G-

30
Q

Plazomicin

A

Aminoglycoside
Extended G-, ACTIVE against aminoglycoside resistant G-
Complicated UTI

31
Q

Polypeptide Antibiotics

A

Narrow G-
Amphipathic
MOA: cationic moiety interacts with neg charged LPS on gram neg outer membrane and hydrophobic moiety inserts in membrane forming pores
Resistant Mechanism: decrease of neg charge on outer membrane (rare)
Last therapeutic option for multi drug resistant G-
IV ONLY
Excreted in urine = renal dose adjust
ACTIVE AGAINST: P.aeruginosa, A. baumannii, and Klebsiella pneumoniae

32
Q

Colistin

A

Polypeptide
Narrow G-
Both hydrophilic and lipophilic with interact with cytoplasmic membrane like a detergent, solubilizing the membrane in an aqueous environment = bactericidal

33
Q

Polymixin B

A

Polypeptide
Narrow G-
Binds and neutralizes endotoxin

34
Q

Nitroimidazoles

A

Gram +/- ANAEROBES ONLY
MOA: reactive intermediates bind DNA causing DNA fragmentation
Food does not affect oral absorption
Excreted in urine but NO renal dose adjustments

35
Q

Metronidazole/Flagyl

A

Nitroimidazole
Gram +/- ANAEROBES
PO, IV, and topical
Half Life 6-8 hr
Prodrug, reduction of 5 nitro group leads to 2-OH active metabolite

36
Q

Secnidazole/Solosec

A

Nitroimidazole
Gram +/- ANAEROBES
PO ONLY
Half Life 17-29 hr
Single Dose ORAL treatment for bacterial vaginosis

37
Q

UTI Agent Considerations

A

Drug should reach high concentration in the urine (excreted in the urine) and be active at a low pH
E.Coli is the most common cause, gram - activity is desired

38
Q

Agents used in UTIs

A

Cefiderocol for complicated
Bactrim
Plazomicin for complication
Fluoroquinolone, avoid is possible
AEs = GI irritation
PO, rapidly excreted in the urine

39
Q

Nitrofurantoin/Macrobid

A

UNCOMPLICATED UTIs
MOA: bacteria reduces it to a reactive metabolize that damages their DNA, similar to nitroimidazoles but the reduction can be performed in AEROBIC cells
Resistance NOT common
GI distress common
Take with food
Microcrystalline form better tolerated
RENALLY DOSE ADJUSTED

40
Q

Fosfomycin/Moniril

A

BLADDER INFECTIONS
Broad Spectrum
MOA: inhibit pyruvyl transferase, required for cell wall biosynthesis, inactivates MurA aka one of the first steps of peptidoglycan biosynthesis
Resistance development is rapid
Given as single large dose

41
Q

Methenamine/Hiprex

A

Prodrug
Depends on the liberation of formaldehyde to become active
Used in UTIs
Resistance: bacteria that creates UREASE prevents the activation of methenamine
Combat by giving Methenamine with salt to decrease resistance

42
Q

Pleuromutilins

A

Fused 5,6, and 8 membered rings MUTILIN core
Gram +/-
Bind to bacteria 50s ribosome at the PEPTIDYL Transferase Center both at the A and P sites

43
Q

Lefamulin

A

Pleuromutilins

44
Q

Retapamulin

A

Pleuromutilins

45
Q

Empiric Dosing

A

NON SERIOUS MRSA Infections
Weight Based mg/kg
Pre-Dose Trough at steady state
Goal = 10-15 mg/L

46
Q

No Monitoring Dosing

A

NON SERIOUS Infections and SHORT TERM Therapy <5 days
Weight Based mg/kg
No serum concentration monitoring

47
Q

Individualized Dosing/Peak Trough Monitoring Dosing

A

ALTERED VANC CLEARANCE (ex. AKI)
Dosing selected to achieve target peak and trough Cp
CP MIN GOAL = 10-15 mg/L non-serious or 15-20 mg/L serious
Pre-Dose Trough and Post-Dose Peak

48
Q

AUC Based Dosing

A

SERIOUS MRSA Infections
Desired AUC 400-600 mg-hr/L
Post Dose Peak and Trough preferred at steady state

49
Q

Vancomycin Dosing Strategy

A

Determined by severity of infection, renal function, and duration of treatment
Method of Sampling = impacts PK parameter accuracy
Dosing of Vanc can be determined prior to steady state acheived

50
Q

Mechanisms of Resistance: Alterd Penetration

A
  1. Altered Porin Channels
  2. Efflux pumps
51
Q

Mechanisms of Resistance: Inactivation

A
  1. B-Lactamase
  2. Aminoglycoside modifying enzyme
52
Q

Mechanisms of Resistance: Altered Binding/Target Mods

A
  1. Altered penicillin binding proteins
  2. Altered ribosomes
  3. Topoisomerase II/IV mutations
  4. Altered D-Ala
53
Q

Gram Positive Resistance

A

Thick cell wall - PBP maintains integrity
Cytoplasmic Membrane with efflux pumps
NO barrier
Create a cloud of beta lactamase on the outside of the cell wall aka drugs are inactivated outside the cell

54
Q

Gram Negative Resistance

A

Thin cell wall
Outer Membrane w/ Polysaccharide Capsule that repels hydrophilic drugs
Plumbing System - water filled channels based on osmotic gradient
BARRIER
Beta Lactamase in the periplasmic space aka drugs are inactivated inside the cell

55
Q

Porin Channels

A

Common in GRAM NEG
Hydrophilic antibiotic use this to gain entry to site of action
Outer membrane, water filled that exchange nutrients and waste products

56
Q

Efflux Pumps

A

GRAM POS/NEG
Energy Dependent, expel toxic substances
Largely responsible for intrinsic resistance of P. Aeruginosa
Cytoplasmic Membrane, Outer Membrane

57
Q

Tetracycline Efflux Pump Against

A

Enteric Gram Neg
Gram Pos

58
Q

Macrolides Efflux Pump Against

A

S. Pneumoniae
Enterococci

59
Q

Macrolides Streptogramin B Efflux Pump Against

A

S. Aureus

60
Q

Fluoroquinolone Efflux Pump Against

A

S. Aureus
S. Pneumoniae

61
Q

Gram Positive B-Lactamase

A

Hydrolyze Penicillins -beta lactamase
Primarily Produced in Staphylococci
NOT all gram pos produce beta lactamases, strep does not and enterococcus has low production

62
Q

Gram Negative B-Lactamase

A

Hydrolyze BOTH cephalosporins and penicillins
Found in ALL gram neg organisms
Extended Spectrum B-Lactamases ESBLs: should be considered resistant to all penicillins, cephalosporins, and monobactams –> found in E.Coli and Klebsiella
Carbapenamases: found in Klebsiella Pneumoniae should be considered resistant to all penicillins, cephalosporins, monobactams, and +/- carbapenems (can cause resistance to carbapen) susceptibility may only exist to polymyxin or tigecycline

63
Q

Aminoglycoside Modifying Enzyme

A

GRAM POS/NEG
Add functional groups into amino glycoside to decrease binding affinity
1. Acetylation AAC: gentamicin, tobramycin
2. Adenylation ANT: gentamicin, tobramycin
3. Phosphorylation APH: amikacin

64
Q

Altered Binding Site PBP

A

Altered or Loss of PBP
Staph Aureus MRSA = altered PBP, resistance to all B-Lactams
Neisseria Gonorrhoaeae = altered PBP, resistance to THIRD gen cephalosporins
Strep Pneumoniae = mosaic PBP, resistance to penicillin and +/- cephalosporins

65
Q

Altered Binding Site Ribosomes

A

Altered Ribosomes- decrease affinity
Tetracyclines, Macrolides, Streptogramins, Lincosamides, Linzeolid
MLS Resistance Macrolide/Lincosamide/Streptogramin = principal resistance to macrolides/clinda in gram positive organisms

66
Q

Altered Binding Site Topoisomerase

A

DNA Gyrase (gyr A) = fluoroquinolone in gram neg organisms
Topoisomerase IV (par C,E) = fluoroquinolone in gram pos organisms

67
Q

Factors Associated with INCREASED Resistance

A

Infection Control Practices
1. Poor Handwashing
2. Poor infection control
3. Use of antibiotics in food industry
Patient Factors
-Prior exposure to IV antibiotics (within past 90 days)

Infectious Diseases Module (5 decks)

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