Pharmacology

INTRODUCTION TO PHARMACOLOGY

OUTLINE
I Definitions o exogenous chemicals that alter normal
A Pharmacology biochemical function (basically how it is
B Drugs processed by the body and how it affects
C Pharmacodynamics
the body)
D Pharmacokinetics
E Pharmacotherapeutics Drug
F Pharmacognosy - substance (or mixture of substances) used in the:
G Toxicology o diagnosis
II Sources of Drugs o cure
I. Plants
o treatment
II. Animals
III. Synthetics o prevention of disease
IV. Inorganic compounds
III Drug Classifications Pharmacodynamics
I. Prescription - study of the biochemical and physiological effects
II. Non-Prescription
of drugs
III. Investigational
IV. Illicit/Street - drug’s mechanism of action
V. Orphan - what drug does to the body
IV Pregnancy Categories
V Drug Names Pharmacokinetics
A Chemical
B Generic - study of the absorption, distribution,
C Branded biotransformation (metabolism) and excretion of
VI Sources of Drug Information drugs
VII The Nursing Process in Pharmacology - Absorption, Digestion, Metabolism, Excretion
VIII Factors Influencing Drug Action
IX Drug Interactions
(ADME)
A Additive - What the body does to the drug
B Synergistic
C Antagonistic
D Interference
OTHER TERMS
E Incompatibility Pharmacotherapeutics
X Reaction to Drugs - Study of how drugs may best be used in the
A Photosensitivity
treatment of illnesses
B Hypersensitivity
C Idiosyncratic o Which drug would be most or least
XI Principles of Drug Actions appropriate to use for a specific disease
A Guiding principles o What does would be required
XII Phases of Clinical Trials
Pharmacognosy
- Study of drugs derived from herbal and other
natural sources
Toxicology
DEFINITIONS - Study of poisons and poisonings; deals with the
toxic effects of substances on the living organism
Pharmacology

- from Greek word, pharmakon, “drug”; and -logia,

“study” SOURCES OF DRUGS
- how drug interact within biological systems to 1. PLANTS
affect function ➢ Digitalis (purple foxglove) – antiarrhythmic for
- study of the interactions that occur: the heart; to treat dysrhythmias or irregular
o between a living organism rhythm
o ➢ Vincristine (periwinkle) – used in cancer
o ➢ Morphine (opium) - painkiller

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 B - Either animal studies have not
2. ANIMALS demonstrated fetal risk but no
➢ Insulin – from pigs and cows controlled studies in pregnant women
➢ Vaccine – killed/attenuated (weakened)
microorganisms from horses (ex. Mmr) - Animal reproduction studies show
3. SYNTHETICS adverse effect (other than decreased
- Uses genetic engineering to alter bacteria to fertility) but not confirmed in
produce chemicals that are therapeutic and controlled studies in women in the 1st
effective (man-made)
trimester (and no evidence of risk in
4. ORGANIC COMPOUNDS
later trimesters)
- Salts of various elements (have therapeutic effects
in the human body) C - Animal studies revealed adverse
- Used to treat various conditions effect on fetus (teratogenic or
o Aluminum (antacid for hyperacidity)
embryological) but no controlled
o Fluoride (prevention of dental carries and
studies in women (or not available)
osteoporosis)E
- Should be given only when potential
DRUG CLASSIFICATION
benefit justifies potential risk to the
1. Prescription fetus
- An order often in written form by a qualified
health care professional to a pharmacist or other D - Positive evidence of human fetal risk
therapist for a specific treatment to be provided to but benefits may be acceptable for
their patients use in pregnant women despite the
- Components: risk (if drug is needed in a life-
o Date and time the drug is written
threatening situation, or serious
o Drug name
disease which other drugs are not
o Drug dosage
o Route of administration effective)
o Frequency and duration of administration
X - Studies in animals or humans have
o Signature of the physician
demonstrated fetal abnormalities (or
2. Non-prescription
- Over the counter medications evidence of fetal risk based on human
3. Investigational experience of both)
- Subjected to clinical studies in order to evaluate
- Risk of drug use in pregnant women
the usefulness of the drug in treating the disease it
clearly outweighs any possible benefit
claims to affect
- Contraindicated in women who are or
PREGNANCY CATEGORIES may become pregnant
4. Illicit drugs or street drugs
- Distributed illegally; are used for non-medical
purposes, generally to alter mood or feeling
- E.g, Heroin, Nubain, Cytotec DRUG NAMES
5. Orphan 1. Chemical
- For a rare disease (affecting fewer than 200,000 in - Systematically derived name which identifies
the US) the chemical structure of the drug; shows the
- Study of these drugs often neglected because exact chemical constitution of the drug and
profits from sales may not be enough to cover exact placing of atoms
costs of development a. N – Acetyl – para – aminophenol
2. Generic
Category Description - Given before drug becomes official; reflects
A - Controlled studies in women fail to some important pharmacological or chemical
demonstrate risk to fetus in 1st characteristic of the drug
trimester (and no evidence of risk in a. Acetaminophen
later trimesters) 3. Brand
- Followed by the symbol ®
- Possible of fetal harm is remote

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 - Indicates the name is registered, that its use is
restricted to the owner of the drug (usually
the manufacturer of the product)
a. Tylenol
SOURCES OF DRUG INFORMATION
1. Pharmacopoeia
2. Formulary
3. Nursing textbook
4. Package inserts (inserts inside the drug packaging)
5. Reference books
a. PDR (Physician’s Directory Reference)
b. Drug facts & comparisons
c. Nursing drug guide / handbook
6. Journals
a. Medical letter
b. American Journal of Nursing
7. Internet
THE NURSING PROCESS IN PHARMACOLOGY
“Paano gamitin ADPIE for drug therapy? Do planning ano
pinaka maganda na gamot for patient but you need to wait
& confirm for doctor’s order, then implement and evaluate
effect of drug to patient ”
ASSESSMENT
• Forms basis on which the care is:
o Planned
o Implemented
o Evaluated
• Assess for
o Findings/Cues
▪ Subjective cues
▪ Objective cues
▪ Drug history - essential because old
medicine na gi take and new medicine na
binigay pag ma-mixed, it might cause
unwanted effect or nag bigay ka ng gamot
tapos di mo alam currently naga take na
pala ang patient nun so magkaroon ng
over dosed.
Drug History
• to evaluate the patient’s need for medication
• to obtain current and past use of medicines
(OTC medicines, prescribed medicines, herbal
products, illicit drugs)
• to identify problems related to drug therapy -
baka magkasakit dahil sa gamot niya
• to identify risk factors in drug therapy -
possible situations if you’re going through
another therapy, possible contraindications or
reactions of a drug to another drugs
DIAGNOSIS
• Based on analysis of the assessment data
• May be actual or potential
• Examples:
o knowledge deficit r/t lack of experience with
medication regimen and second grade reading
level as an adult as evidenced by inability to
perform a return demonstration and inability
to state adverse effects to report to the
prescriber - nalaman mo na deficient pala
yung knowledge ng patient kasi nung nag turo
ka sakanya at pina describe mo sakanya paano
inumin yung gamot kasi hindi nya kaya gawin
at hindi din mabilis mag basa
o risk for injury r/t forgetfulness - baka
makalimutin ang patient tapos hindi nya
maalala na naka inom na sya ng gamot tas
iinum sya ulit, mas deikado yun.
o ineffective therapeutic regimen management
r/t lack of finances - ineffective therapy kasi
hindi niya kaya bilhin ang gamot
PLANNING
o characterized by goal setting (or expected
outcomes) which represent effectiveness of nursing
care:
o patient goals
o state of desired patient behaviors or responses
• Include:
o identification of the therapeutic intent for
every medication
o side effects to be expected and reported
o identification of the recommended dosage and
route of administration
o scheduling of the administration of medication
o teaching the patient to keep written records of
his responses - for example, for people who are
getting their covid vaccine shots, sinasabihan
ano signs and symptoms maexperience then
tell them to take note and if di na kaya kasi call
the hotline
o additional teaching as needed
o techniques of administration, proper storage
of medication - example: puffs for asthma,
paano ba itake, ilang inhalation muna bago
mag puff, when ipuff, etc.
IMPLEMENTATION
• Nursing actions necessary to achieve
outcomes:
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 o Independent - actions that doesn’t need
order or assistance from other medical
personnel
o Dependent - Some nursing interventions
require instructions or input from a
doctor, such as prescribing new
medication
o Interdependent - actions that are
implemented in a collaboration or
consultation with other health care
professionals.
• Include:
o client teaching and education
o administration of drug
o assessment of drug effectiveness
o self-administration
o diet
o side effects
o cultural considerations
EVALUATION
• The on-going process that assesses for:
o effectiveness of the medication (as
prescribed)
o observation of signs and symptoms of
recurring illness
o development of the side/ adverse effects
o effectiveness of the health teaching or
client education
FACTORS INFLUENCING DRUG ACTION
➢ Age
- Extremes of age are most sensitive to dosage and
response
- Adjusted depending on the age of the patient
o Newborns
o Infants
o Elderly
➢ Body weight
- Dosage depends on the weight
- Obvious in pediatrics
o Overweight (increase)
o Underweight (decrease)
- Note: pediatrics always uses mg/kg
➢ Metabolism/ genetics
- Individual genetic susceptibilities metabolize
medications differently
- Person to person
o Lack of enzymes may prolong plasma
level (and increase risk of toxicity)
o Field of pharmacogenomics
▪ Study of the genetic
relationship of drugs and
genes
➢ Illnesses
- Pathologic conditions alter rate of absorption,
distribution, metabolism, and excretion
o Short gut syndrome (has decreased
absorption capacity compared to a
normal person)
o Billroth (surgery) – remove some
parts of stomach due to necrosis and
ulceration; size of stomach
decreases, thus there is changes in
the rate of pharmacokinetics
compared to a normal person
➢ Psychological
- Attitudes and expectations
- Willingness to take the medications as prescribed
(compliance)
➢ Dependence
- Known as addiction or habituation
- Body is dependent on the drugs, and once you stop
it will elicit:
o Withdrawal symptoms (physical)
▪ Fever and chills
o Emotionally attached to the drug
(emotional)
➢ Tolerance
- When higher doses are required to produce the
same effect that lower doses once provided
o May be caused by psychological
dependence
o Ex: smoking (contains chemicals that
has effect on the body)
▪ Fine with 1 stick a day then
eventually feels like it is
lacking so consumed 2 packs
a day until the person
becomes a chain smoker
o Ex. Illicit drugs – started with small
doses first until the body becomes
dependent on the drug, not achieving
the desired effect; thus, increasing
the dosage
➢ Cumulative effects
- If the next doses are administered before
previously dose was fully metabolized
o May result in drug toxicity (liver)
o Rate of consumption exceeds rate of
metabolism
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 - Ex: person took paracetamol after 2 hours even
though it should be taken every 4 hours
DRUG INTERACTIONS
- Interaction of one drug to another
➢ Additive
- 2 drugs with similar effects lead to a double effect
- 1+1=2
➢ Synergistic
- The combined effect of 2 drugs is greater than or
equal to the sum of the effect of each drug given
alone
- Ex: ampicillin + sulbactam = prolonged action of the
antibiotic
- Work well with each other producing prolonged
effect (more than double)
➢ Antagonistic
- 1 drug interferes with the action of another
- Ex: tetracycline + antacid = DECREASE absorption of
the tetracycline
➢ Interference
- 1 drug inhibits the metabolism or excretion of a 2nd
drug, causing INCREASE activity of the 2nd drug
- Interferes the process of excretion leading to the
other drug to stay in the body and prolong the
effect
- Ex: probenecid + spectinomycin = PROLONGED
antibacterial activity from spectinomycin due to
blocking renal excretion by probenecid
➢ Incompatibility
- should not be mixed or administered at the same
site
- signs of incompatibility: haziness, a precipitate, or a
change in color of solution when mixed
- ex: ampicillin + gentamicin = ampicillin inactivates
gentamicin
- if you want to give both drugs, wait the 1 drug to be
totally eliminated in the body before giving the
other drug
OTHER TERMINOLOGIES
➢ Desired action
- expected response
➢ Side effect
- effect other than what is intended (due to
pharmacological effects of the drug)
- occurs when medication is administered regardless
of the dose
- something you may expect; may or may not happen
➢ Adverse effect
- range of undesirable responses (unintended and at
normal doses) which can cause mild to severe
reactions
- an adverse event is an undesired occurrence that
results from taking a medication correctly
- undesirable effects
o ex. Hypersensitivity after giving a
medication
➢ Carcinogenicity
-ability to induce cells to mutate and become
malignant
- drugs that suppress the immune system
- drugs cause normal cells to mutate and becomes
cancer cells
- put the patient at risk for cancer
➢ Teratogenicity
- induces birth defects
REACTION TO DRUGS
➢ Photosensitivity
-sensitivity to light
o skin
o eyes
- ex. Gluta
- ex. vit C and retinol supplements have a dark
packaging (tinted) because once expose to light, it
deactivates the drug; not being effective
- patients who are taking photosensitive drugs would
be sensitive as well
➢ Hypersensitivity
- exaggerated immunologic response to a drug
(considered a foreign substance)
- allergy
- ex. Rash due to Tegretol, eruption reaction,
phenytoin-allergy
➢ Idiosyncratic
- occurs in first intake of drug (due to differences in
metabolism between individuals)
- case to case basis; depending on the person
PRINCIPLES OF DRUG ACTIONS
• Drugs do not create new cellular functions (but only
alter them)
o antibiotic slows the growth and/or
reproduction of microbial organisms
o drug action is relative to the physiological
state which existed when the drug was
administered
• drugs may interact with the body in several different
ways
o alter the chemical composition of a body
fluid
o accumulate in certain tissues because of
their affinity for a tissue component
(forming a chemical bond with specific
receptors within the body)
o drugs have different mechanism reaction.
Other drugs absorbed in the mouth or
stomach; others distribute well and work on
the different organs; other drugs will go to
the specific organ and will take effect; other
drugs need receptors
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 • drug response (or strength of the effect) depends on Keys to giving it safely. You should be able to
the drug molecule’s fit in the receptor site identify interventions to counteract the adverse
o precise fit -> strong effect effects of the drug.
o loose fit -> weak effect
o 1 drug (consider it as a car) tries to fit in the
receptor site (parking space); if it fits
perfectly, the drug is strong and
effective
• Agonist-antagonist drugs exert both agonist and
antagonist responses
o Agonist (produces a response)
o Antagonist (counter/depresses the
response)
▪ Used in antidote therapies;
whenever 1 drug is very toxic

PHASES OF CLINICAL TRIALS

PHASE SUBJECTS DESCRIPTION
I Normal • Determines dose-response
human relationship and
volunteers pharmacokinetics of the
new drug (exception is a
cancer drug)
• Effects of dosages are
observed (to determine
significant response or
toxic effect)
II Small number • Effect is compared with a
of sick placebo drug/agent (to
patients with determine if agent truly
target disease has desired effect)
(volunteers) **Placebo drug/agent –
pretend drug
III Many human • Same above except with
volunteers double-blind studies
sick with • Effect is compared to
target disease standard or previous
up to 6000 treatment
cases in some strategies/protocols/agents
centers
IV All patients • Post-marketing surveillance
sick with • Detects toxicities early to
target disease prevent major therapeutic
(as disorders
prescribed)

GUIDING PRINCIPLES
Check why the medication is given & know
the classification of the drug
How will you know if the medication is
effective? What are your assessment
parameters in monitoring the effects
of the drug?
Exactly what time should the medication be given?
Client teaching tips. What are the therapeutic and
side effects of the medication?

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Pharmacology 25
GELIANNE ALBA-LOQUEZ, RN 21 O2
▪ Excipients
PHASES OF DRUG THERAPY

OUTLINE ▪ Excepients
I Pharmaceutic • Fillers (inert substances/additives) to allow a
drug to take on a particular size and shape
A Disintegration • Enhances drug dissolution
B Dissolution • Increases absorbability of a drug
C Rate limiting • Partner of drug to be process effectively by
D Excipients the body
• Examples:
II Pharmacokinetics
o Potassium → Penicillin potassium
➢ ADME o Sodium → Penicillin G sodium
III Pharmacodynamics
PHARMACOKINETICS
IV Prescription
o Process of drug movement to achieve drug action
o What the body does to the drug we intake.
PHARMACEUTICS o Four (4) processes: (ADME)
▪ Absorption - Movement of drug particles from GI
o Disintegration - Breakdown of a tablet into smaller
tract to body fluids through passive or active
particle
absorption, or pinocytosis
• Passive - Drug molecule moves from a region
o Dissolution - Dissolving process of the smaller particles
of relatively higher to lover concentration
in the GIT fluid prior to absorption
without requiring energy
e.g. Nag-take ka ng medicine tablet
• Active - Process that uses energy to actively
tablet will breakdown into smaller particle
move a molecule across a cell membrane
(disintegration) then that smaller particle will be
o Pinocytosis (Cell Drinking) - Process by
dissolved
which cells carry the drug across the
• Dissolution will depend on the form of the
membranes through engulfing the drug
drug
particles
• Factors affecting absorption:
o Blood flow
o Pain
o Stress and food
o Exercise
o Nature of the absorbing surface
o Drug solubility
o pH
o Drug concentration
o Dosage form – e.g. tablets, syrups,
powder
o Hepatic first-pass effect
o Enterohepatic recycling
o Depends on: o Route of administration
▪ Rate limiting • Nature of absorbing surface
• Time it takes for the drug to disintegrate, o Absorption through a single layer of cells
dissolve, and be available for the body to is faster compared to the multi-layered
absorb skin
e.g. GI Tract (single layer cell): fast
• Each drug has diff rate of disintegrating
absorption
• The longer the drug takes to disintegrate then
Skin (multi-layered): slow absorption
the longer it takes effect to the body.
▪ Respiratory epithelium (steroids)
• Only talks about time
▪ Intestinal epithelium (carbohydrates)

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 • Hepatic First-Pass effect: Inactivation of drugs
by hepatic enzymes before the drug reaches
systemic circulation for distribution
o Past liver first before drug is absorb
by the body
o Liver will inactivate the drug first
then distribute the drug, that the
time it will take effect.
o Bioavailability → percentage of
administered drug dose that reaches
systemic circulation.
• Enterohepatic recycling: Absorption of drug
from bile into small bowel and then into
circulating system
• Route of Administration - Linked to the blood
supply (vascularity)
IM/IV – High rate of absorption than P.O
Route of Administration Factors Affecting Absorption
Intravenous (IV) Blood volume (vascularity)
Intramuscular (IM) and Perfusion, fat content, and
Subcutaneous (SQ) temperature
Acidity of the stomach, length
of time in stomach, blood flow
Oral
to GIT, presence of interacting
food or drug
Perfusion, integrity, presence
Mucus Membrane of food, smoking, length of
time in the area
▪ Distribution-Process by which drug becomes
available to body fluids and body tissues
• Factors influencing distribution:
o Blood flow
o Affinity to body tissues
o Protein-binding effect
• Manner of Distribution
o Protein-binding - Drugs that bind with
specific protein components such as:
Protein will regulate the drug
▪ Bound portion is inactive (does not
exert pharmacologic response)
Inactive: drug bound to protein
▪ Unbound portion is active (free drug)
Active: unbound drug
▪ Toxicity may occur:
• Too much of free-circulating
drug→When 2 highly-protein
bound drugs are given to a
patient with liver disease or low
albumin
o Blood-brain barrier (BBB)- Protective
system of cellular activity (keeps foreign
invaders/poisons away from CNS) It’s like
a coating of brain
▪ Highly lipid-soluble drugs most likely
to pass through blood-brain barrier
▪ Antibiotics cannot pass through
▪ CNS effects by medications result
from indirect processes and not by
the actual response of the CNS to the
drug
e.g. A drug causes hypoxia indirectly
it causes dizziness to CNS
o Placenta (and breastmilk)
▪ Drugs readily pass through (can affect
the developing fetus)
▪ Secreted into breastmilk
Category Description
A NO RISK evident
NO RISK evident in human or animal
B
studies
C RISK cannot be ruled out
D (+) evidence of risk exists
X CONTRAINDICATED in pregnancy
▪ Metabolism-Chemical changes a substance
undergoes in the body (such as through enzymatic
action)
• Drugs are metabolized in both GI tract and
liver
• Most drugs inactivated by liver enzymes and
converted into water-soluble substances (for
renal excretion)
• Half-life (t ½) -Time it takes for ½ of the drug
concentration to be eliminated
Decrease in ½ the drug concentration every
intake of the drug
o First order - Proportional rate of
elimination to concentration
Increase in concentration = increase in
rate metabolism & elimination
o Zero order - Constant rate of elimination
regardless of concentration
Will eliminate a constant amount no
matter how you change the
concentration.
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 Secondary – Whitening
Example of Half-Life
Time Dosage (at ▪ Example:
T1/2
Elapsed 20mg start)
Percentage left • Diphenhydramine HCL (1st generation
antihistamine)
1 2 hours 10 mg 50% o Treats allergies (primary)
o CNS depression – drowsiness (secondary)
2 4 hours 5 mg 25% o Receptor Theory:
▪ Drugs act through receptors by binding through a
3 6 hours 2.5 mg 12.5%
receptor to produce (initiate) a response or to
4 8 hours 1.25 mg 6.25% block (prevent) a response
o Drug Actions:
▪ Replace or act as substitutes for missing chemicals
▪ Excretion ▪ Increase or stimulate certain cellular activities
• Process of eliminating substances by body ▪ Depress or slow cellular activities
organs or tissues (as part of natural metabolic ▪ Interfere with the functioning of foreign cells (such
activity) as invading microorganisms) e.g.
• Kidneys (main route of elimination [free, antibacterial/antiviral
water-soluble, and unbound drugs]) o Onset of Action: Time it takes to reach the minimum
• Urine pH → influences drug excretion effective concentration (MEC) after a drug is
o Acidic → elimination of weak base drugs administered
o Alkaline → elimination of weak acid o Peak of Action: Condition that occurs when the drug
drugs reaches its highest blood or plasma concentration
• Others (bile, feces, lungs, saliva, sweat, o Duration of Action: Length of time the drug exerts a
breastmilk) pharmacological effect
o Agonists: Drugs that produce a response
SUMMARY OF PHARMACOKINETICS o Antagonists: Drugs that block a response e.g. antidotes
o Therapeutic Index: Measures margin of safety of a
drug
▪ Narrow margin of safety (low therapeutic index)
▪ Wide margin of safety (high therapeutic index)
• The closer the ratio is to “1”, the greater the
danger of toxicity
o Therapeutic Range (therapeutic window): Between
minimum effective concentration in the plasma and
minimum toxic concentration
The wider the therapeutic range the better
▪ e.g. Paracetamol (10 mg to 15 mg /kg)

o Peak Drug Level: Highest plasma concentration of a

drug at a specific time
Highest drug concentration in your body
o Trough Level: Lowest plasma concentration of a drug
and measures rate at which drug is eliminated
▪ Indicates rate of elimination of a drug

PHARMACODYNAMICS

o Study of drug concentration and its effects on the

body
o What the drug does to the body
o Drug response can cause a primary and secondary
physiologic effect
▪ Primary → desirable
▪ Secondary → may or may not be desirable
Glutathione:
Primary – Treat liver problems

3
 • Written on patient’s chart, brand name
enclosed in parenthesis shall be written
after generic name

PRESCRIPTIONS NOT ALLOWED:

PRESCRIPTION
- The written order and instruction of a validly
registered physician, dentist or veterinarian for
the use of a specific drug product for a specific
patient
- For the purpose of these rules and regulations,
doctor’s order on the patient’s chart for the use
of specific drugs shall be considered as a
prescription
- Basis: rules and regulations to implement
prescribing Requirements under the Generics Act
of 1088 (R.A No. 6675)
1. VIOLATIVE
- Generic name is not written
- Not legible and a brand name which is legible is
written
- Brand name indicated and instructions added
such as the phrase “no substitution which tend to
obstruct, hinder or prevent generic dispensing
-
2. ERRONEOUS
- Brand name precedes the generic name
- Generic name is the one in parenthesis
- Brand name is not in parenthesis
- More than one drug product is prescribed on one
prescription form
-
3. IMPOSSIBLE
- Only generic name is written but not legible
- Generic name does not correspond to the brand
name
- Both generic and brand name are not legible
- Drug product prescribed is not registered with the
BFAD

Legal basis

- In addition to the guidelines contained in section

2, the ff shall specifically guide prescribing under
the generic acts of 1988

GENERIC NAMES
- Shall be used in all prescriptions
• For drugs with a single active
ingredient, the generic name of that
active ingredient shall be used in
prescribing
• Drugs with 2 or more active
ingredients, the generic name as
determined by BFAD shall be used in
prescribing
- Must be written in full but the salt or chemical
form may be abbreviated
- Must be clearly written on the prescription
immediately after the Rx symbol, or on the order
chart
- Brand name may also be indicated in such cases
the ff shall be observed:
• If written on prescription pad, brand
name enclosed in parenthesis shall be
written below the generic name

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 09 L E C
Pharmacology 02
GELIANNE ALBA-LOQUEZ, RN 21O3
ANTIBACTERIALS 1 – AMINOGLYCOSIDES & SPECTINOMYCIN

OUTLINE
REFERENCES
I Antimicrobials and Antibacterial
• Pharmacokinetics
“PROF’S PPT ON QUIPPER AND LECTURE”
II Resistance to Antibacterials
• Inherent or Natural
• Acquired Mechanism Effect Drug
• To beat the problem INHIBITION BACTERICIDAL: Penicillin,
III Antibiotic Combinations OF CELL WALL enzyme cephalosporin,
• Additive effect SYNTHESIS breakdown of vancomycin
• Potentiative (synergistic) effect cell wall;
inhibition of the
• Antagonistic
enzyme in the
IV Spectrum synthesis of the
• NARROW SPECTRUM cell wall=loss of
• BROAD SPECTRUM structural
• General Adverse Reactions integrity of the
1. HYPERSENSITIVITY bacterial cell &
2. SUPERINFECTION death of the
3. ORGAN TOXICITY organism
V Nursing Considerations ALTERATION BOTH: amphoterin B,
in Membrane nystatin,
VI Aminoglycosides
MEMBRANE permeability is polymyxin
• Modes of Antibacterial Action PERMEABILITY increased; loss of
• Pharmacokinetics cellular
• Mechanism of Action substances
• Mechanism of Resistance causes lysis of
• Clinical Uses cell=permitting
VII Toxicity leakage of
intracellular
a. Ototoxicity
component=
b. Nephrotoxicity
BACTERICIDAL
c. Neuromuscular Blockade INHIBITION of BACTERIOSTATIC: Aminoglycosides,
d. Skin Reactions PROTEIN Interferes with tetracyclines,
VIII NURSING RESPONSIBILITIES (CHON) CHON synthesis erythromycin,
Antimicrobials and Antibacterial SYNTHESIS w/o affecting lincomycin
normal
cells=prevent
ANTIMICROBIALS – inhibit the growth of or kill normal growth &
bacteria/ microorganisms outright (e.g., bacteria, reproduction
fungi, parasites and some viruses) (host defenses
eradicate
organism)
Inhibition of BACTERIOSTATIC: fluoroquinolones
ANTIBACTERIAL/Antibiotics – chemicals that
SYNTHESIS of Inhibits synthesis
specifically kills bacteria; destructive or inhibiting the BACTERIAL of RNA & DNA;
growth of bacteria RNA & DNA binds to the
nucleic acid and
to the enzymes
needed for
nucleic acid
synthesis

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 INTERFERENCE BACTERIOSTATIC: Sulfonamides,
with cellular Interferes with INH, Rifampicin Antibiotic Combinations
metabolism steps of
metabolism of
the cell – • ADDITIVE EFFECT
essential for
normal function ✓ equal to the SUM of the effects of 2
and/or growth of antibiotics
bacterial cell • POTENTIATIVE (SYNERGISTIC) EFFECT
✓ one antibiotic potentiates the effect
PHARMACOKINETICS of the 2nd antibiotic

• Must only penetrate the bacterial cell wall in • ANTAGONISTIC

sufficient concentration; must have affinity to
the binding sites
• TIME drug remains at the binding site =
INCREASE EFFECT;
• Controlled by DISTRIBUTION, HALF-LIFE &
ELIMINATION
• Most are not highly CHON bound = longer
HALF-LIFE greater concentration at binding
sites; mostly eliminated from the body
through URINE after the 7th half-life
Resistance to Antibacterials
❖ INHERENT or NATURAL – occurs without
previous exposure to the antibacterial drug
❖ ACQUIRED - caused by PRIOR exposure to
antibacterial
• Responsible for causing Penicillin
resistance = PENICILLINASE (enzyme
that metabolizes PenG = drug is
ineffective)
• CAUSES:
o mutant bacteria- grown a thicker
cell wall
o transfer of genetic instruction to
another bacterial species
To beat the problem:
• New antibiotics are developed
• Development of ANTIBIOTIC RESISTANT
DISABLERS (disable antibiotic-resistant
mechanism in the bacteria)
• Bacterial Vaccines (e.g., DPT, Flu Vaccine, TT)
• Prevent antibiotic abuse
• COMPLIANCE and MULTI ANTIBIOTIC
THERAPY
✓ combination of a drug that is
BACTERICIDAL PENICILLIN + drug
that is BACTERIOSTATIC,
TETRACYCLINE = desired effect may
be reduced
SPECTRUM
• NARROW SPECTRUM
o against one type of organism
o Penicillin & Erythromycin – for gram
(+) bacteria
• BROAD SPECTRUM
o against both gram (+) & gram (-)
o Tetracycline & Cephalosporins
General Adverse Reactions
1. HYPERSENSITIVITY – rash, pruritus &
hives; severe anaphylactic shock
TX: antihistamine, epinephrine,
bronchodilators
2. SUPERINFECTION – secondary infection
due to disturbed normal flora; occur with
use of broad-spectrum antibiotics
3. ORGAN TOXICITY – damage to organs
that are involved in drugs metabolism &
excretion (liver & kidneys)
aminoglycosides = OTOTOXIC &
NEPHROTOXIC

2
 NURSING CONSIDERATIONS
• Monitor for superinfections
• Evaluate renal [BUN & creatinine] & liver
[AST, ALT] functions
• Diarrhea r/t superinfections (mgt: take
yogurt, more fluids)
• Inform physician before taking other meds
• Cultures- prior to 1st dose
• Alcohol is OUT! / Ask about allergies
• Take full course of meds
• Evaluate cultures, WBC, C&S
Aminoglycosides
Modes of Antibacterial Action
• Multiple daily dosage regimens are
traditionally used
o to maintain serum concentrations
above minimum inhibitory
concentration (MIC)
▪ Minimum inhibitory
concentrations (MICs) are
defined as the lowest
concentration of an
antimicrobial that will inhibit
the visible growth of a
microorganism after
overnight incubation
• As plasma levels increase, aminoglycosides kill
an increased proportion of bacteria at a more
rapid rate
• Same with penicillins and cephalosporins
• *Time-dependent killing (more bacteria are
killed the longer drugs are maintained above
the MIC → same moment it becomes
independent of concentration)
• Aminoglycosides are capable of post-
antibiotic effect
• Killing action continues even after plasma
levels have declined below measurable levels
• Aminoglycosides have greater efficacy if given
as a large single dose (compared to multiple
smaller doses)
o Toxicity depends on both actual
increased plasma concentration and
duration the level is exceeded
o Leads to: once daily dosing → more
advantageous
PHARMACOKINETICS
• Structurally related amino sugars attached by
glycosidic linkages
• Must be given thru IM or IV (for systemic
effect)
o Not absorbed well through oral
administration (and have limited
tissue penetration in CNS)
PHARMACOKINETICS
• Undergoes renal excretion (plasma levels are
greatly affected by renal function)
• Excretion is proportional to creatinine
clearance
• Dosage adjustments necessary in renal
dysfunction
Mechanism of Action
• Aminoglycosides are bactericidal inhibitors of
protein synthesis
• May be enhanced by bacterial cell wall
synthesis inhibitors
• Binds to 30s ribosomal subunit and interferes
with protein synthesis in at least three (3)
ways:
o Block formation of initiation complex
o Cause misreading of code in the
mRNA template
o Inhibit translocation
o May also disrupt polysomal structure,
resulting in non-functional
monosomes (possible 4th MOAas
proposed)
Mechanism of Resistance
• Streptococci (S pneumoniae) and Enterococci
→ relatively resistant (due to drug’s inability
to penetrate their cell walls)
Clinical Uses
• Main differences due to activities against
specific microorganisms: gram (-) rods
3
• Gentamicin, Tobramycin, and Amikacin →
serious infections of aerobic gram-negative
bacteria
o E. coli, Enterobacter, Klebsiella,
Proteus, Providencia, Pseudomonas,
and Serratia
o alternative medications for:
▪ H. influenzae, M. catarrhalis,
and Shigella spp
• not reliably effective against gram-positive
cocci (instead, combined with cell wall
inhibitors e.g., penicillins)
• Streptomycin → used in regimens against:
o Enterococcal carditis (Infective
endocarditis) - infection in the heart
valves or endocardium
o Plague - a contagious bacterial
disease characterized by fever and
delirium, typically with the formation
of buboes (bubonic plague) and
sometimes infection of the lungs
(pneumonic plague)
o Tularemia
o Pulmonary tuberculosis (if resistant
to streptomycin, use amikacin
instead)
• Spectinomycin → administered thru IM
o Single dose for treatment of
gonorrhea
o not an aminoglycoside (but a related
drug it is an aminocyclitol)
Toxicity
Ototoxicity
• Two (2) main possible conditions:
a. Auditory damage (amikacin and
kanamycin)
b. Vestibular damage (gentamicin and
tobramycin)
i. BOTH ARE IRREVERSIBLE
(may be decreased with use
of loop diuretics)
• Contraindicated in pregnancy (due to damage
to hearing of fetus after exposure)
• Unless potential benefits outweigh risks
cephalosporins, or
vancomycin)
o Most nephrotoxic:
gentamicin
tobramycin
Neuromuscular Blockade
o Rare, but may result in respiratory
paralysis
o Reversible: calcium and neostigmine
o May require a mechanical ventilator
Skin Reactions
o Most likely to cause these reactions
→ Neomycin
o Allergic skin reactions
o Contact dermatitis
NURSING RESPONSIBILITIES
• Monitor periodical audiograms,
BUN/creatinine & vestibule function studies
over 10 days therapy
• Adjust for renal insufficiency
• Monitor VS, peak and serum levels
• For IV admin., dilute and administer slowly to
prevent toxicity
• Monitor I & O, hydrate well before and during
therapy (flush in between)
• If anorexia or nausea occurs, SFF meals
• Establish plan for safely if vestibular nerve
effects occur.
• Administer other antibiotics 1 hour
before/after amino
• Recommend using sunblock & protective
clothing when exposed to the sun.

Nephrotoxicity
• Acute tubular necrosis → reversible but more
common in:
▪ Elderly
▪ Taking other medications
(amphotericin B,

4
 09 L E C
Pharmacology 22
GELIANNE ALBA-LOQUEZ, RN O3
21

TOPIC TITLE HERE

BETA-LACTAM ANTIBIOTICS
REFERENCES
I. Penicillin’s
II. Cephalosporins
“PROF’S PPT ON QUIPPER AND LECTURE”
III. Other Beta-Lactam Drugs
• Aztreonam
• Carbapenems
•Imipenem
•Meropenem Penicillin’s
•Ertapenem
• Beta-Lactamase Inhibitors
IV. OTHER CELL WALL OR MEMBRANE-ACTIVE • Derivatives of 6-aminopenicillanic acid
AGENTS
• Contains a beta-lactam ring essential for
antibacterial activity
• Have additional chemical substituents
BETA-LACTAM ANTIBIOTICS which confer differences (antimicrobial
activity, susceptibility to acid, enzymatic
hydrolysis, and biodisposition)
• Pharmacokinetics
• Vary in resistance to gastric acid (and
thus have variable bioavailability)
• Not metabolized extensively (in effect
excreted unchanged in the urine via
glomerular filtration and tubular
secretion)
• Tubular secretion is inhibited by
probenecid
• Nafcillin (excreted mainly in bile)
• Ampicillin (undergoes enterhepatic
recycling)
• half-lives of mostly 30 minutes to 1 hour

• Procaine and Benzathine have longer

half-lives (given IM active drug has
slow release into the bloodstream)
BETA-LACTAM ANTIBIOTICS
• Note: most penicillin’s are able to cross
Penicillin’s
the blood-brain barrier only when
Cephalosporins meninges are inflamed
Carbapenems - Not really a beta-lactam but retains its
ring structure

1
Mechanism of Action: bactericidal
-Inhibits cell wall synthesis by the following steps:
• Drug binds to specific enzymes (penicillin-
binding proteins [PBPs] located in the
bacterial cytoplasmic membrane
• Inhibition of the transpeptidation reaction
that crosslinks the linear peptidoglycan chain
constituents of the cell wall
• Activation of autolytic enzymes that cause
lesions in the bacterial cell wall
• Resistance:
• Enzymatic hydrolysis of the beta-lactam ring
results in the loss of antibacterial activity
• Formation of beta-lactamases (penicillinases)
by mostly staphylococci and many gram-
negative organisms is the major cause of
resistance
• To combat this development, inhibitors of
these bacterial enzymes are often used in
combination with penicillins to prevent their
inactivation
1.Clavulanic acid
2.Tazobactam
3.Sulbactam
• In the case of MRSA 🡪 structural changes in
the target PBPs (also in resistance to penicillin
G in pneumococci)
• In some gram-negative rods (pseudomonas),
changes in porin structures in the outer cell
wall may contribute resistance (it prevents
penicillins from accessing and binding to the
PBPs)
Clinical Uses
Narrow spectrum Penicillinase-susceptible agents
• Penicillin G
– Prototype of a subclass of penicillins with
limited spectrum of antibacterial activity (and
susceptible to beta-lactamases)
– Used against common streptococci,
meningococci, gram-positive bacilli, and
spirochetes
– Many strains of pneumococci are now
resistant to penicillins (PRSP)
– Most strains of S. aureus and N. gonorrhea
are resistant due to beta-lactamse
production
– No longer DOC for gonorrhea, but still for
syphilis
– enhanced by co-administration of
aminoglycosides
• Penicillin V
– Used for oropharyngeal infections (given
orally)
Very Narrow Spectrum Penicillinase-Resistant
• Subclass of penicillins which includes:
– Methicillin (prototype, but rarely used due to
its nephrotoxic potential)
– Nafcillin
– Oxacillin
• Primary use: staphylococcal infections
• Note: MRSA and MRSE (S. epidermidis) are
resistant to all penicillins, and often against
multiple antimicrobials
Wider Spectrum Penicillinase-Susceptible
• Ampicillin and Amoxicillin:
– Subgroup that has wider spectrum of
antibacterial activity compared to penicillin G
(but still susceptible to penicillinase)
– Clinical use similar to penicillin G, as well as
against:
• Enterococci, L. monocytogenes, E.
coli, P. mirabilis, H. influenzae, and
M. catarrhalis
(Some resistant strains have
developed)
– Activity is enhanced when used with
penicillinase inhibitors (e.g. clavulanic acid 🡪
Co-Amoxiclav)
– Synergistic with aminoglycosides in
enterococcal and listerial infections
(ampicillin)
• Piperacillin and Ticarcillin:
– Activity against some gram-negative rods,
including:
• Pseudomonas
• Enterobacter
• Klebsiella
– Often used with penicillinase inhibitors
(tazobactam and clavulanic acid) to enhance
their activity
Penicillins
• Toxicity:
– Allergic reactions
o Urticaria, severe pruritus, fever, joint
swelling, hemolytic anemia, nephritis,
and anaphylaxis
o Allergic response occurs if given
penicillin again (in 5-10% of persons)
o Maculopapular skin rash (but mimics an
allergic reaction) 🡪 ampicillin
– Gastrointestinal disturbances
o Nausea and diarrhea (oral penicillins)
o May be due to direct irritation or by
overgrowth of gram-positive organisms
or yeasts
o Pseudomembranous colitis (ampicillin)
2
 – Miscellaneous:
2nd GENERATION
o Neutropenia (nafcillin) • Lesser activity against gram-positive microbes versus
o Interstitial nephritis (methicillin) 1st generation drugs
– But have extended gram-negative coverage
– Marked differences between usefulness
Cephalosporins between drugs in the group
• Examples:
• Derivatives of 7-aminocephalosporanic acid
– Bacteroides fragilis (cefotetan and cefoxitin)
and contain the beta-lactam ring structure
Sinus, ear, and respiratory infections caused by H.
• Many members are in clinical use
influenzae or M. catarrhalis (cefamandole, cefuroxime, and
– Vary in antimicrobial activity and are
cefaclor)
designated according to their
generations (in order of their
introduction into clinical use) 3RD GENERATION
• Pharmacokinetics:
– Many are available for oral use (mostly
• Increased activity against gram-negative microbes
parenteral)
resistant to other beta-lactam medications
– Those with sidechains may undergo
– Plus, the ability the penetrate the blood-
heptaic metabolism but majority
brain barrier (except for cefoperazone and
undergo renal excretion via active
cefixime)
tubular secretion
• Most active against:
• Only Cefoperazone and Ceftriaxone
– Providencia, serratia marcescens, and beta-
are excreted mainly in the bile
lactamase-producing strains of H. influenzae
– Most cephalosporins do not enter the
and Neiserria
cerebrospinal fluid even when meninges
- If the bacteria produces penicillinase, beta-
are inflamed
lactamase can be used
• Mechanism of Action
• Less active against:
– Enterobacter strains that produce extended-
– Bind to penicillin-binding proteins to
spectrum beta-lactamases
inhibit bacterial cell wall synthesis (just
like penicillins) - extended-spectrum beta-lactamases is a
• bactericidal mutated version of beta-lactamase and it is
– Some structural differences make them much stronger
less susceptible to penicillinase • Most drugs in this class are reserved usually for
produced by staphylococci serious infections:
• Resistance – Pseudomonas → cefoperazone, ceftazidime
– Some bacteria are able to produce beta- – B. fragilis →cetizoxime
lactamases which can inactivate • Except for: ceftriaxone (parenteral) and
cephalosporins cefixime (oral) →for gonorrhea
– May occur from decreases in membrane
permeability to cephalosporins or from 4TH GENERATION
changes in PBPs • Cefepime →more resistant to beta-lactamases
– MRSA is resistant produced by gram-negative microorganisms:
• Cefepime is effective against beta lactamase
•
1st Generation
Cefazolin (parenteral) and Cephalexin (oral) producing gram negative microorganism
– Active against gram-positive cocci – Enterobacter, haemophilus, neisseria, and
(staphylococcus and common streptococci) some penicillinase-resistant pneumococci
– Effective against many strains of E. coli and K. – combines:
pneumoniae o Gram-positive activity of 1st
– Usually used as surgical prophylaxis generation
– Minimal activity against: o Wider gram-negative spectrum of 3rd
• Gram-negative cocci generation
• Enterococci
• MRSA
• most gram-negative rods

3
 5TH GENERATION
• Indicated for treating bacteria which are otherwise
resistant to commonly used antibiotics
• Ceftaroline – has broad spectrum activitiy against:
- Gram-positive bacteria including
- MRSA
- Extensively resistant strains such as VRSA
(Vancomycin – resistant s. aureus)
- Sulbactam, and Tazobactam)
• Ceftobiprole – this drug has been called a 5th gen
cephalosporin, but the terminology is not universally
accepted.
- has powerful antipseudomonal activity, and
binds strongly to PBP 2a
- has activity against MRS, S. pneumonia,
enterococci
- newer medication used for healthcare-
associated pneumonia (HCAP) or HAP
• Toxicity
- Allergies (skin rashes to anaphylactic shock)
-Between cephalosporins (100%)
-Between a cephalosporin and penicillin is
incomplete (5-10%)
• Cross Alergenicity
– If you are allergic to cephalosporin then you
have a 100% change to be allergic to another
generation of cephalosporin
– If you are allergic to Penicilin then you have
a 5-10% change to be allergic to
cephalosporin
• Other Adverse Effects:
– May cause pain at IM injections (as well as
phlebitis if given IV)
– May increase nephrotoxicity of
aminoglycosides (if given together)
– If aminoglycosides mix with cephalosporin it
may increase the nephrotoxicity of the
aminoglycosides
– Some may cause: hypoprothrombinemia and
disulfiram-like actions with ethanol
– The common are cefamandole,
cefoperazone, and cefotetan due to
their methylthiotetrazole group
– If undergoing antibiotic therapy do not
consume alcohol as it will cause :
hypoprothrombinemia and disulfiram-like
actions
• Disulfuram-like action:
- reaction to alcohol leading to
nausea, vomiting, flushing,
dizziness, throbbing headache,
chest and abdominal discomfort,
and general hangover-
like symptoms among others
OTHER BETA-LACTAM DRUGS
• Aztreonam
• Carbapenems (Imipenem, Meropenem, and
Ertapenem)
• Beta-Lactamase Inhibitors (Clavulanic acid,
AZTREONAM
• monobactam resistant to beta-lactamases produced
by some gram-negative rods (including Klebsiella,
pseudomonas, and serratia)
• No activity against gram-positive bacteria or
anaerobes
• Cell wall synthesis inhibitor (preferentially binds with
penicillin-binding protein (PBP3)
• Once Aztreonam is attached to PBP3 it will cause cell
wall synthesis
• Synergistic with aminoglycosides
• Given intravenously and is eliminated via renal
tubular secretion
• Half-life is prolonged in renal failure
• Adverse effects include GI upset with possible
superinfection, vertigo, headache, and rarely
hepatotoxicity
– Skin rash may occur but there is no cross-
allergenicity with penicillins
CARBAPENEMS
(Imipenem, Doripenem, Meropenem, Ertapenem)
• Chemically different from penicillins but retain the
beta-lactam ring structure
• Have low susceptibility to beta-lactamases which
makes them useful against:
– Gram-positive cocci
– Gram-negative rods
– anaerobes
• All are active against P. aeruginosa and acinetobacter
spp, except for ertapenem
– Often paired with an aminoglycoside if used
against pseudomonas
• Given parenterally, are useful against microbes
resistant to other antibiotics
- But is not effective against MRSA
• Co-drugs of choice for:
– Enterobacter, citrobacter, and serratia spp
Imipenem
• Cannot be administered alone
• Rapid inactivation by renal dehydropeptidase I
• Administered in fixed combination with cilastatin
(an inhibitor of the enzyme above)
4
 – Increases its half-life and inhibits the
formation of a metabolite toxic to the
kidneys
Note: other carbapenems are not significantly
degraded by the kidneys
Imipenem-Cilastatin
a. Partial cross-allergenicity with penicillins
b. Adverse effects:
– GI distress, and skin rash
– CNS toxicity 🡪 confusion, encephalopathy,
and seizures (at very high plasma levels)
Meropenem
• Similar to imipenem but not metabolized by renal
dehydropeptidases
• Less likely to cause seizures
• –
Ertapenem
• Long half-life but less active against enterococci and
pseudomonas
• Intramuscular route causes pain and irritation
BETA-LACTAMASE INHIBITORS
(Clavulanic acid, Sulbactam, Tazobactam)
• Used in fixed combinations with certain hydrolyzable
penicillins
• Most active against plasmid-encoded beta-
lactamases (produced by gonococci, streptococci, E.
coli, and H. influenzae)
• Not useful against enterobacter, pseudomonas, and
serratia
– Their type of beta-lactamase is chromosomal
(and not plasmid-encoded)
OTHER CELL WALL OR MEMBRANE-ACTIVE AGENTS
(Vancomycin, Fosfomycin, Bacitracin, Cycloserine,
Daptomycin)
Vancomycin
• Bactericidal glycoprotein which inhibits
transglycosylation
– Prevents elongation of the peptidoglycan
chain and interferes with cross-linking
– Resistance → due to decreased affinity for
the binding site
• Narrow spectrum of activity
– Used for serious infections caused by drug-
resistant gram-positive organisms
• Methicillin-resistant staphylococci
(MRSA)
• Penicillin-resistant pneumococi
(PRSP) 🡪 in combination with a 3rd
generation cephalosporin (usually
ceftriaxone)
– Used for serious infections caused by drug-
resistant gram-positive organisms
• Backup drug for Clostridium difficile
infection
• Not absorbed in the GI tract (and may be given orally
for bacterial enterocolitis)
• Given parenterally, it penetrates most tissues and is
eliminated unchanged in the urine
• Dosage modification is mandatory in renal failure
patients
• Toxicity:
– Chills, fever, phlebitis, ototoxicity, and
nephrotoxicity
– Rapid intravenous infusion 🡪 Red Man
Syndrome (due to histamine release)
Fosfomycin
• Antimetabolite inhibitor of cytosolic enolpyruvate
transferase
Prevents formation of N-acetylmuramic acid
(an essential precursor for peptidoglycan
chain formation)
– Resistance 🡪 decreased intracellular
accumulation of the drug
• Excreted by the kidney in urinary levels higher than
minimum inhibitory concentrations (MIC) →makes it
useful against UTIs
• In multiple dosing, diarrhea is common
• May be synergistic with beta-lactam and quinolone
antibiotics in some infections
Bacitracin
• Peptide antibiotic which interferes with a late stage
in cell wall synthesis in gram-positive organisms
• Limited to topical use because of its marked
nephrotoxicity
Cycloserine
• Antimetabolite that blocks incorporation of amino
acids into the side chain of the peptidoglycan
• Highly neurotoxic (tremors, seizures, and psychosis)
– Limited use to tuberculosis that is resistant to
first-line antituberculosis drugs
Daptomycin
• Novel cyclic lipopeptide with spectrum similar to
vancomycin (but active against vancomycin-resistant
strains of enterococci and staphylococci)
• Eliminated via the kidney
• Monitor creatinine since it causes myopathy