Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ozenoxacin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Eravacycline
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
26
Aminoglycosides
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
27
Gentamicin
Aminoglycoside Extended G-
28
Amikacin
Aminoglycoside Extended G-
29
Tobramycin
Aminoglycoside Extended G-
30
Plazomicin
Aminoglycoside Extended G-, ACTIVE against aminoglycoside resistant G- Complicated UTI
31
Polypeptide Antibiotics
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
Colistin
Polypeptide Narrow G- Both hydrophilic and lipophilic with interact with cytoplasmic membrane like a detergent, solubilizing the membrane in an aqueous environment = bactericidal
33
Polymixin B
Polypeptide Narrow G- Binds and neutralizes endotoxin
34
Nitroimidazoles
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
Metronidazole/Flagyl
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
Secnidazole/Solosec
Nitroimidazole Gram +/- ANAEROBES PO ONLY Half Life 17-29 hr Single Dose ORAL treatment for bacterial vaginosis
37
UTI Agent Considerations
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
Agents used in UTIs
Cefiderocol for complicated Bactrim Plazomicin for complication Fluoroquinolone, avoid is possible AEs = GI irritation PO, rapidly excreted in the urine
39
Nitrofurantoin/Macrobid
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
Fosfomycin/Moniril
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
Methenamine/Hiprex
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
Pleuromutilins
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
Lefamulin
Pleuromutilins
44
Retapamulin
Pleuromutilins
45
Empiric Dosing
NON SERIOUS MRSA Infections Weight Based mg/kg Pre-Dose Trough at steady state Goal = 10-15 mg/L
46
No Monitoring Dosing
NON SERIOUS Infections and SHORT TERM Therapy <5 days Weight Based mg/kg No serum concentration monitoring
47
Individualized Dosing/Peak Trough Monitoring Dosing
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
AUC Based Dosing
SERIOUS MRSA Infections Desired AUC 400-600 mg-hr/L Post Dose Peak and Trough preferred at steady state
49
Vancomycin Dosing Strategy
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
Mechanisms of Resistance: Alterd Penetration
1. Altered Porin Channels 2. Efflux pumps
51
Mechanisms of Resistance: Inactivation
1. B-Lactamase 2. Aminoglycoside modifying enzyme
52
Mechanisms of Resistance: Altered Binding/Target Mods
1. Altered penicillin binding proteins 2. Altered ribosomes 3. Topoisomerase II/IV mutations 4. Altered D-Ala
53
Gram Positive Resistance
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
Gram Negative Resistance
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
Porin Channels
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
Efflux Pumps
GRAM POS/NEG Energy Dependent, expel toxic substances Largely responsible for intrinsic resistance of P. Aeruginosa Cytoplasmic Membrane, Outer Membrane
57
Tetracycline Efflux Pump Against
Enteric Gram Neg Gram Pos
58
Macrolides Efflux Pump Against
S. Pneumoniae Enterococci
59
Macrolides Streptogramin B Efflux Pump Against
S. Aureus
60
Fluoroquinolone Efflux Pump Against
S. Aureus S. Pneumoniae
61
Gram Positive B-Lactamase
Hydrolyze Penicillins -beta lactamase Primarily Produced in Staphylococci NOT all gram pos produce beta lactamases, strep does not and enterococcus has low production
62
Gram Negative B-Lactamase
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
Aminoglycoside Modifying Enzyme
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
Altered Binding Site PBP
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
Altered Binding Site Ribosomes
Altered Ribosomes- decrease affinity Tetracyclines, Macrolides, Streptogramins, Lincosamides, Linzeolid MLS Resistance Macrolide/Lincosamide/Streptogramin = principal resistance to macrolides/clinda in gram positive organisms
66
Altered Binding Site Topoisomerase
DNA Gyrase (gyr A) = fluoroquinolone in gram neg organisms Topoisomerase IV (par C,E) = fluoroquinolone in gram pos organisms
67
Factors Associated with INCREASED Resistance
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions