FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION

PHARMA B - ANTIMICROBIALS PART 2

King of Wakanda, O.D. 2020
SULFONAMIDES (Antifolate Drugs)
Chemistry Resistance Pharmacokinetics Clinical Uses Adverse Reactions
Basic formulas and structure Sulfonamides are resistant to: Absorption: A. Oral, absorbable agents * Cross-allergenic
- similar to p-aminobenzoic acid (PABA) • organisms that lack the enzymes needed - stomach UTI: Sulfisoxazole and
for folate synthesis from PABA (like - small intestines sulfamethoxazole * Cross-reactivity is uncommon; even if
Differentiating properties are produced by mammals) allergic to nonantibiotic sulfonamides =
attaching substituents to the: • organisms with mutations that: Widely distributed: Acute Toxoplasmosis: may safely receive antibiotic sulfonamides
- amido group (-SO2-NH-R); OR o cause overproduction of PABA - to tissues and Sulfadiazine + Pyrimethamine
- amino group (-NH2) of the sulfanilamide o cause production of folic acid body fluids (synergistic) * Most common adverse effects:
nucleus synthesizing enzyme with low (including the CNS • fever, skin rashes, exfoliative
affinity for sulfonamides and CSF) Folinic acid: must be dermatitis, photosensitivity,
pH: MORE SOLUBLE at alkaline than acid o impair permeability to - placenta administered to minimize bone urticaria
sulfonamide - fetus marrow suppression • nausea, vomiting, diarrhea and
Sodium salts urinary tract symptoms
- form of most preparations; used for IV Sulfonamide-resistant dihydropteroate synthase Protein binding: Malaria: Sulfadoxine + (sulfadiazine precipitate in urine
administration mutants also can emerge under selective pressure - varies from 20%- Pyrimethamine in neutral pH)
90% (2nd line tx)
Mechanism of Action & Antimicrobial Activity Pharmacokinetics * Steven Johnson Syndrome: uncommon;
Sulfonamide-susceptible organisms Divided into 3 major groups: Therapeutic B. Oral, nonabsorbable agents fatal type of skin and mucus membrane
- cannot use exogenous folate but must synthesize • Oral, absorbable concentrations: eruption assoc with sulfonamide use
it from PABA (w/c makes it the target of • Oral, nonabsorbable - in the range of 40- Ulcerative colitis, enteritis, and
sulfonamides) • Topical 100 mcg/mL of other inflamm bowel disease: * Other unwanted effects:
The oral, absorbable sulfonamides can be blood Sulfadoxine • stomatitis, conjunctivitis, arthritis,
MOA: inhibition of the dihydropteroate synthase classified as: (salicylazosulfapyridine) hepatitis and rarely, polyarteritis
and folate production Peak of blood nodosa and psychosis
levels: C. Topical agents
Coverage: - 2-6 hours after oral Bacterial conjunctivitis and A. Urinary Tract Disturbances
- G (+) and G (-) administration adjunctive therapy for trachoma: * May precipitate in urine at neutral or acid
- Nocardia sp., C. trachomatis, some protozoa Na Sulfacetamide pH = crystalluria, hematuria, or even
- enteric bacteria such as: E. coli, K. pneumoniae, In the liver… obstruction
Salmonella, Shigella and Enterobacter sp. - portion of the Burn sites: Mafenide Acetate * Sulfadiazine - crystalluria (large doses
absorbed drug is (but may cause metabolic particularly when fluid intake is poor; give
Rickettsiae acetylated or acidosis due to its primary Na HCO3 alkalinize urine)
- NOT INHIBITED but instead are stimulated to glucuronidated metabolite that inhibit carbonic * Nephrosis and allergic nephritis
grow anhydrase
Excretion: B. Hematopoietic Disturbances
Poor activity vs: anaerobes - mainly by Silver sulfadiazine - less toxic * Hemolytic or aplastic anemia
GLOMERULAR and preferred over mafenide for * Granulocytopenia, thrombocytopenia,
P. aeruginosa FILTRATION prevention of burn wound leukemoid reactions
- intrinsically resistant infections * Provoke hemolytic rxns in pxs with G6PD
In case of renal * Sulfonamides near the end of pregnancy:
failure: kernicterus in newborns
- REDUCE dosage

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This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!
 FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020
TRIMETHOPRIM & TRIMETHOPRIM-SULFAMETHOXAZOLE MIXTURES (Antifolate Drugs)
Mechanism of Action Pharmacokinetics Clinical Uses Adverse Effects
TMP A. Oral TMP Mimics the effects in the body of a
- usually given ORALLY - alone in acute UTI person with FOLATE DEFICIENCY!
TMP - a trimethoxybenzylpyrimidine - alone or in combination with - many community-acquired orgs are
SULFAMETHOXAZOLE (similar HL) susceptible to the high concentration found in - megaloblastic anemia
MOA: selective inhibition of the bacterial the urine - leukopenia
dihydrofolic acid reductase, which converts TMP + Sulfamethoxazole - granulocytopenia
dihydrofolic acid to tetrachydrofolic acid (a step leading - may also be given through IV B. Oral TMP-SMZ
thesynthesis of purines and ultimately to DNA) - effective and active vs: TMP + SMZ
Well-absorbed: • P. jiroveci, pneumonia, shigellosis, - may cause untoward effects
Pyrimethamie - also a benzylpyrimidine - in the gut systemic salmonella infections, UTI, associated with sulfonamides
prostatitis, nontuberculous
MOA: selective inhibition of dihydrofolic acid Distribution: mycobacterial infections The ff may also occasionally occur:
reductase of protozoa compared with that of - wide in body fluids and tissues including • MSSA and MRSA - nausea and vomiting
mammalian cells CSF • Respiratory tract pathogens - drug fever
(pneumococcus, Haemophilus sp, M. - vasculitis
* In combination with a sulfonamide: Lipid Solubility: catarrhalis, K. pneumoniae BUT - renal damage
- marked enhancement of the activity of both drugs - TMP > Sulfamethoxazole (TMP then has NOT Mycoplasma pneumoniae) - CNS disturbances
DUE to SYNERGISM a larger volume of distribution so 1 part - can be used as PROPHYLAXIS in
TMP: 5 parts sulfamethoxazole; peak RECURRENT UTI In patients with AIDS and
* Sulfonamide alone = BACTERIOSTATIC plasma conc: 1:20) pneumocytosis:
* Sulfonamide + TMP or PMT = BACTERICIDAL C. Intravenous TMP-SMZ TMP+SMZ may produce:
Excretion in the urine within 24 hours: - IV infusion as AGENT OF CHOICE for: - fever
Resistance - sulfonamide - 30-50% • moderately severe to severe - rashes
Results from: - TMP - 50-60% pneumocytis pneumonia - leukopenia
- reduced cell permeability - may be also used for - diarrhea
- overproduction of dihydrofolate reductase If creatinine clearance of 15-30 mL/min: • G (-) sepsis (those caused by MDR - elevations of hepatic
- production of an altered reductase with reduced drug - reduce dose to HALF Enterobacter and Serratia) aminotransferases
binding • shigellosis - hyperkalemia
TMP: concentrates in more acidic pH • typhoid fever - hyponatremia
Resistance can emerge by: since it is a weak base; hence more antibac • UTI caused by a susceptible
- mutation activity in PROSTATIC and VAGINAL organism when the patient is unable
- more commonly due to: plasmid-encoded TMP- fluids than other antimicrobials to take drug by MOUTH
resistant dihydrofolate reductases (coded within
transposons on conjugative plasmids) D. Oral Pyrimethamine with Sulfonamide
- for treatment of toxoplasmosis (PMT +
sulfadiazine)
- has been used for falciparum malaria (PMT
+ sulfadoxine)

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First Generation
- Nalidixic Acid
- Oxolinic Acid
- Cinoxacin
* Better activity vs G (-) aerobes but limited vs G (+)
- Synthetic fluorinated analogs of nalidixic acid
- Earlier quinolones: Nalidixic acid, oxolinic acid, cinoxacin - low systemic level; useful only for treatment of lower UTI
Mechanism of Action Antibacterial Activity
MOA: Blockage of bacterial DNA
synthesis by inhibition of bacterial
topoisomerase II (DNA gyrase) and
topoisomerase IV
Inhibition of DNA gyrase would lead to:
- prevention of the relaxation of
positively supercoiled DNA that is
required for normal transcription and
replication
Inhibition of topoisomerase IV:
- interferes with separation of replicated
chromosomal DNA into the respective
daughter cells during cell division
Resistance
Due to:
- one or more point mutations in the
quinolone binding region of the target
enzyme; OR
- change in the permeability of the
organism
Two types of plasmid-mediated
resistance:
- Type I: utilizes Qnr proteins which
protect DNA gyrase from FQs
- Type II; variant of aminoglycoside
acetyltransferase capable of modifying
ciprofloxacin
Remember:
Resistance to one FQ (particularly if it is
of high level) - generally confers cross-
resistance to all other members of this
class
This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!
FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020
DNA GYRASE INHIBITORS
Second Generation Third Generation
- Norfloxacin - Ofloxacin - Enoxacin - Gatifloxacin
- Ciprofloxacin - Pefloxacin - Levofloxacin - Gemifloxacin
- Lomefloxacin - Moxifloxacin
* Excellent G (-) and moderate to good G (+) activity * Improved G (+) activity esp vs S. pneumoniae and Staph
FLUOROQUINOLONES (DNA Gyrase Inhibitors)
Pharmacokinetics Clinical Uses Adverse Effects
2nd Gen (See above for 1st gen) Absorption: Effective vs: Most common:
Norfloxacin - well-absorbed after oral administration - UTI infections caused by many orgs - nausea, vomiting, diarrhea
- least active of the FQs vs G (-) (bioavailabity of 80-95%) including P. aeruginosa (EXCEPT Moxi Occasionally:
& G (+) which achieves low urinary levels) - HA, dizziness, insomnia, skin
- MICs are 2-8x higher than Oral absorption is impaired by divalent and - bacterial diarrhea caused by Shigella, rash, or abnormal liver fxn tests
ciprofloxacin trivalent cations (Katzung inc trivalent) Salmonella, ETEC, and Campylobacter
including those in antacids - Infections of soft tissue, bones, and Lome and peflo:
Ciproflox, enox, lomeflox, - Oral FQs must be taken 2 hours before or 4 joints and in intra-abdominal and - photosensitivity
levoflox, oflox, peflox hours after any products containing these respiratory tract infections including
- Excellent G (-) and mod to cations! those caused by MDR orgs like Respiratory FQs:
good activity vs G (+) Pseudomonas and Enterobacter - prolongation of the QT interval
Distribution: (EXCEPT Norflo which doesn’t achieve - caution in patients with:
MSSA - generally susceptible to - widely distributed in tissues and body fluids adequate systemic concentrations) • hx of QT prolongation
FQs (prostate, stool, bile, lung, neutrophils, urine & • uncorrected hypoK+
MRSA - often resistant to FQs kidneys) Ciprofloxacin: • receiving Class 1A or
- DOC for prophylaxis and treatment of Class 3 antiarrhythmics
Efficacy vs strep and Metabolism anthrax • receiving agents known
enterococci Serum-half lives: to prolong QT interval
- limited compared to staph - range from 3-10 hours Cipro and Levo: such as erythromycin
- Levo, gati, gemi, moxi - long half-lives that - effective for chlamydial urethritis or and TCAs
Ciprofloxacin permit once a day dosing cervicitis
- most active agent vs G (-) Gatifloxacin:
particularly vs P. aeruginosa Serum concentrations of IV-administered FQs are Cipro, Levo, or Moxi: - assoc with:
the same with orally-administered. - occasionally used vs TB and atypical • hyperglycemia in
3rd Gen pneumonia diabetics
Gemifloxacin Elimination: - eradication of meningococci from • hypoglycemia taking
- effective vs. ciprofloxacin- - most are eliminated by renal mechanisms carriers OHAs
resistant strains of S. either by GF or TS - prophylaxis of infection in neutropenic
pneumoniae - also excreted via boobies (breastmilk) cancer patients FQs
If crea clearance = <50 mL/minute: dosage -may cause damage to growing
Moxifloxacin adjustment needed depending on the degree of Levo, Gati, Gemi, Moxi: cartilages and cause arthropathy
- modest activity vs anaerobic impairment and specific FQ used - enhanced G (+) activity and activity (not recommended for pxs < 18)
bacteria against atypical pneumonia agents - tendon rupture in adults
Nonrenally cleared FQs - aka respiratory FQs - peripheral neuropathy either
* These 3rd gen FQs are not as - relatively contraindicated in patients with - effective in treatment of URTI and LRTI orally or IV
active as ciprofloxacin vs G (-) hepatic failure - avoided in pregnancy
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MISCELLANEOUS ANTIMICROBIAL AGENTS & URINARY ANTISEPTICS
METRONIDAZOLE
- nitroimidazole antiprotozoal drug
- potent antibac act vs anaerobes inc. Bacteroides and Clostridium
- selectively absorbed by anaerobes and protozoa
MOA: Inhibits nucleic acid synthesis by disrupting DNA of microbial
cells when it is enzymatically reduced by reacting with reduced
ferredoxin inside anaerobes
- well absorbed orally
- reaches 4-6mcg/mL after 250mg oral dose
- penetrates CF and brain reaching levels similar to those in serum
- metabolized in the liver (may accumulate in hepatic insufficiency
Clinical Use: (IV, oral, suppository, vaginal gel)
- anaerobic or mixed intra-abdominal infections
(combined with agents covering aerobes)
- vaginitis (trichomonas, bacte vaginosis)
- C difficile infection
- brain abscess
Adverse Effects:
- Stomatitis, anorexia, nausea, diarrhea and vomiting
- Peripheral neuropathy, seizure, tea-colored urine
- Disulfiram-like effect (avoid alcohol)
MUPIROCIN
- natural substance produced by Pseudomonas fluorescens
- rapidly inactivated after absorption, systemic levels are undetectable
- active vs G (+) cocci including MSSA and MRSA
MOA: Inhibition of the staphylococcal isoleucyl tRNA synthase
- Low-level resistance observed after prolonged use (however, with
topical application, MIC is well above 100mcg/mL so it doesn’t lead to
clinical failure)
- High-level resistance - MICs exceeding 1000mg/mL - due to the
presence of a second isoleucyl tRNA synthase gene which is plasmid-
encoded; complete loss of activity is observed
Indicated for: minor skin infections
Impt factor leading to resistant strains: topical application over large
infected areas such as decubitus ulcers or open surgical wounds
This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!
FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020
POLYMIXIN B NITROFURANTOIN (Urinary Antiseptic)
- Included under the polymyxin group of basic peptides active - BACTERICIDAL for many G (+) and G (-) bacteria
against G (-) bacteria (group also includes Polymixin E also - P. aeruginosa and Proteus are inherently resistant
known as colistin)
MOA: Correlates with rapid intracellular conversion into highly
MOA: Acts as cationic detergent that attach to and disrupt reactive intermediates by bacterial reductases which then react
bacterial cell membrane. Also binds and inactivates endotoxin. nonspecifically with many ribosomal proteins and disrupt the
synthesis of proteins, RNA, DNA, and metabolic processes
- Resistant to:
• G (+) organisms - No cross-resistance with other antimicrobials; resistance
• Proteus sp. emerges slowly
• Neisseria sp. - Important alternative oral agent for: uncomplicated UTI
- Well-absorbed after ingestion; metabolized and excreted so
- BACTERICIDAL rapidly (hence no systemic antibac action)
- Excretion is through urine by both GF and TS
- toxic with systemic administration: especially nephrotoxic - Contraindicated in pxs with renal insufficiency
- also with neurologic toxicity - Can be given for months for the suppression of recurrent UTI
- NOT USED in URTI; Antagonizes NALIDIXIC ACID
- treatment of serious enteric infections: EPEC, Shigella,
Enterobacter, Klebsiella, Pseudomonas, BUT NOT PROTEUS!!! Adverse Effects: anorexia, nausea, vomiting (principal)
- Neuropathies and hemolytic anemia in G6PD patients
- topical ointments: in mixtures with bacitracin or neomycin or - Rashes, pulmonary infiltration and fibrosis and other
both: for infected superficial skin infections hypersensitivity actions have been reported
FIDAXOMICIN METHENAMINE MANDELATE & METHENAMINE HIPPURATE (Urinary
Antiseptic)
- Narrow-spectrum, macrocyclic antibiotic Methenamine mandelate
- Active vs: - salt of both mandelic acid and methenamine
• G (+) aerobes
• G (+) anaerobes Methemnamine Hippurate
- Lacks activity vs: - salt of hippuric acid and methenamine
• G (-) bacteria
- Below pH of 5.5, methenamine releases formaldehyde, which is
MOA: Inhibition of bacterial protein synthesis by binding to the antibacterial
sigma subunit of RNA polymerase.
Mandelate and Hippurate
- When orally administered: - taken orally - excreted unchanged in the urine in which these
• systemic absorption is negligible drugs are BACTERICIDAL for some G (-) bacteria when pH is <5.5
• fecal concentrations are high
- Urinary antiseptic only to suppress and NOT treat UTI (Manual)
- Approved by FDA for: C. difficile infection in adults
- NOT given together with sulfonamides as they may form an
- Effective as oral vancomycin insoluble compound with formaldehyde
- May be assoc with lower rates of relapsing disease
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 FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020

CLINICAL USE OF ANTIMICROBIAL AGENTS

Empiric Therapy (Presumptive Therapy) Monitoring Therapeutic Response
- use of antimicrobial agents before the pathogen responsible for a Tarticular illness or the susceptibility
to a particular antimicrobial agent is known • Microbiologically - culture of specimens
- goal is to improve the outcome with early intervention • Clinically - systemic manifestations
• Duration of therapy depends on: pathogen, site of infection and host factors
Definitive Therapy • Failure of treatment: systemic investigation should be done; drug dosing and absorption
- narrower in coverage should be scrutinized and tested directly using serum measurements, pill counting or
- given for an appropriate duration based on the results of clinical trials or experience when clinical trial observed therapy
data are not available
Antimicrobial Pharmacodynamics
Approach to Empiric Therapy
1.) Formulate a Clinical Diagnosis of Microbial Infection * The time course of drug concentration = closely related to the antimicrobial effect at the site of
2.) Obtain Specimens for Laboratory Examination infection and to any toxic effects
3.) Formulate a Microbiologic Diagnosis * Factors include:
4.) Determine the Necessity for Empiric Therapy • pathogen susceptibility testing
5.) Institute Treatment • drug bactericidal vs bacteriostatic activity
o Bacteriostatic - MIC is much lower than MBC
Considerations Critical for the Selection of Antimicrobials o Bactericidal - divided into 2 groups:
1.) Type of bacteria inhibited by each drug ▪ concentration-dependent killing (quinolones and aminoglycosides)
2.) Bacteria most commonly associated with infections at a particular anatomic site - rate and extent of killing is directly proportional to drug concentration
3.) Antibiotics that attain high enough concentration at the specific site of infection ▪ time-dependent killing (beta-lactams and vancomycin)
4.) Antibiotic resistance - activity continues as long as serum concentrations are greater than
MBC
Host Factors that affect Selection of Antimicrobials • drug synergism, antagonism, and post-antibiotic effects
1.) concomitant disease states (AIDS, neutropenia, organ transplant, severe chronic liver/kidney disease) * Post-antibiotic effect (PAE) - persistent suppression of bacterial growth after limited exposure to an
or use of immunosuppressive meds antimicrobial agent; reflects the time required for bacteria to return to logarithmic growth
2.) prior adverse drug effects
3.) impaired elimination or detox of the drug (may be genetically predetermined but more frequently Antimicrobial Pharmacokinetic Considerations
associated with impaired renal or hepatic function due to underlying disease)
4.) age of the patient * Route of administration: Oral vs. IV
5.) pregnancy status • IV is preferred for: (1) critically ill patients; (2) pxs with bacterial meningitis or endocarditis;
6.) epidemiologic exposure (3) pxs with nausea, vomiting, gastrectomy, ileus, or diseases that alter oral absorption; and
(4) when giving antimicrobials poorly absorbed ff oral administration
Pharmacologic Factors that affect Selection of Antimicrobials
1.) kinetics of absorption, distribution, and elimination * Conditions that alter antimicrobial pharmacokinetics
2.) ability of the drug to be delivered to the site of infection
3.) potential toxicity of an agent • (1) impairment of renal and hepatic function; (2) patients with burns, CF, or trauma; (3)
4.) pharmacokinetic or pharmacodynamic interactions with other drugs elderly; (4) neonates; (5) trauma

Guiding Antimicrobial Therapy of Established Infections * Drug Concentrations in Body Fluids

* Susceptibility Testing: MIC (min inhibitory concentration) and MBC (min bactericidal concentration) • Most agents are well distributed to most body tissues and fluids except penetration into the
* Specialized Assay Method: CSF.
• Beta-lactamase assay - chromogenic beta-lactam substrate (nitrocephin disk)
• Synergy studies - in vitro to measure synergistic, additive, indifferent or antagonistic
drug interactions

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This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!
 FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020
Management of Antimicrobial Toxicity Antimicrobial Prophylaxis
1.) Skin Test * General Principles
2.) Desensitization
3.) Dosage Adjustment 1.) The antibiotic should be active against common surgical wound pathogens; unnecessarily broad
4.) Antihistamine coverage should be avoided
5.) Corticosteroids 2.) The antibiotic should have provided efficacy in clinical trials
3.) The antibiotic must achieve concentrations greater than the MIC of suspected pathogens, and these
Antimicrobial Drug Combinations concentrations must be present at the time of incisions
Rationale for combination antimicrobial therapy 4.) The shortest possible course - ideally a single dose - of the most effective and least toxic antibiotic
1.) To provide broad spectrum empiric therapy in seriously ill patients should be used
2.) To treat polymicrobial infections (such as intra-abdominal abscesses); chosen combination should 5.) The newer broad-spectrum antibiotics should be reserved for therapy of resistant infections
cover the most common known or suspected pathogens 6.) If all other factors are equal, the least expensive agent should be used
3.) To decrease the emergence of resistant strains
4.) To decrease dose-related toxicity by using reduced doses of one or more components of the drug Nonsurgical Prophylaxis
regimen
5.) To obtain enhanced inhibition or killing * Administration of antibiotic to prevent colonization or asymptomatic infection as well as the
administration of rugs following colonization by or inoculation of pathogens before development of the
Synergism & Antagonism disease
* Synergism - marked by 4-fold or greater reduction in the MIC or MBC of each drug
• Blockade of the sequential steps in a metabolic sequence * Indicated in individuals who are at high risk, for temporary exposure to selected virulent pathogens
• Inhibition of enzymatic inactivation and in immunocompromised patients
• Enhancement of antimicrobial uptake
* Antagonism - occurs when the combined inhibitory or killing effects of 2 or more antimicrobials are (PLEASE CHECK OUT THE FOLLOWING PAGES FOR TABLES DERIVED FROM THE MANUAL which
significantly less than expected when the drugs are used individually were copied from Katzung)
• Inhibition of -cidal activity by static agents
• Induction of enzymatic inactivation

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 FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020

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This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!
 FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020

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This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!
 FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020

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This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!
 FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020

10 | P a g e
This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!
 FAR EASTERN UNIVERSITY - NICANOR REYES MEDICAL FOUNDATION
PHARMA B - ANTIMICROBIALS PART 2
King of Wakanda, O.D. 2020

11 | P a g e
This is a book outline of Basic and Clinical Pharmacology by Katzung and Trevor 13 th Edition with the Pharma 2B Workbook as guide. Let this outline sho u de we!