Subject : PHARMACOLOGY

Date

❖ BRANCHES OF PHARMACOLOGY

THERAPEUTIC METHODS ➢ PHARMACOGNOSY

- dealing with economic, biological and
1. Drug therapy chemical aspects of natural drugs and their
- txt with drugs constituents
- proper administration of drugs to treat - study of the sources of drugs and physical
disease characteristics of crude or unrefined drugs
2. Diet therapy - drugs derived from herbal and other
- tx by diet natural sources and how the body reacts
- low salt diet for cardio diseases to them
3. Physiotherapy - study of natural drug sources (plant and
- identification of stressors and methods to animal)
reduce or eliminate stress/use of drugs
● Animals Products
PHARMACOLOGY > insulin ( for treating diabetes) = cow and pig
- greek = pharmakon = “drugs” - used to replace human chemicals that fail to be
- scientific study of origin, nature, chemistry, effects, produced because of disease and genetic
and use of drugs problems
- how drugs interact with biological systems to affects >thyroid drug & growth hormones
function - animal thyroid hypothalamus tissues
- branch of knowledge that deals with chemicals that
have biological effect ● Plants
- Digitalis - for cardiac disorders
- Opiates - for sedation or pampatulog
PHARMACOLOGIST
- scientist
- specializes in the study of pharmacodynamics, MARIJUANA legal sa states kase for
employing all kinds of biochemical, physiological, medications daw
and other techniques
good eka for asthma

PHARMACY prevents nausea (ex.

- medical science concerned with safe and effective marinol) vomiting, cancer
use of medicines
MINERAL/INORGANIC salts, fluoride, iron and
- study of techniques involved in the preparation, PRODUCTS gold(ex. ferrous sulfate)
compounding, dispensing, preservation and storage
of the drugs for medical use mineral drugs are tx for
IDA and rheumatoid

PHARMACIST SYNTHETIC PRODUCTS artificially produced.

- qualified and licensed duplicates substance used
- functions: to be found in plants/
● to prepare and dispense drugs animals/environment
● manufacture of the dosage from drugs benefits:
(tablets, capsules, etc) ● eliminate side
effects
DRUG ● increase potency
of drug
- a.k.a medications (ex. barbiturates,
- any chemical substances which affects living amphetamines,
systems sulfonamides, aspirin)
- dutch word “droog” = dry
- used for treatment of disease, for the prevention of MICROBIAL PRODUCTS genetic engineering
(altering of DNA)
illness of pathologic states and fro diagnosing
disease condition permits production of
human insulin by altering
E.coli = less impurities than
CLINICAL PHARMACOLOGY
animal products
- study of drugs in humans (Patients and volunteers)
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➔ PHARMACOKINETICS
- what body does to drug:
ABSORPTION
DISTRIBUTION
METABOLISM/
BIOTRANSFORMATION
EXCRETION
➔ PHARMACOTHE
RAPEUTICS
➔ PHARMACOGEN
ETICS
➔ TOXICOLOGY
● MECHANISM OF ACTION
- pharmacodynamics
● INDICATIONS
- use of drug to treat particular disease
● SIDE EFFECT
- all drugs have potential to affect more than
1 body system simultaneously
● ADVERSE EFFECT
movement of drug from GI
tract to body fluids by
passive absorption, active
absorption
site to blood stream
blood to tissues
inactivated by liver
enzymes
converted by hepatic
enzyme to inactive
metabolites ( excretion)
process of energy
liver = major site of drug
metabolism
elimination of drugs
thru:
bile, feces, saliva, sweat,
breast milk
kidney= organ responsible
for excretion
how drugs may be used in
treatment of disease
which drugs will be
effective
use of drugs to prevent and
treat disease
e=genetically determined
reactions of drugs in
human body
poisonous effects of drugs
- undesired effect maybe dangerous
may occur as:
1. have other effects on body besides therapeutic
effect
2. Pt is sensitive to drug
3. dru’s action cause response that are unpleasant
4. pt taking too much/little of drug
● TOLERANCE
- begins require higher doses to produce
same effects sa lower doses
ex. heroin addiction= body metabolize drug more rapidly
than before
● DEPENDENCE
- A.K.A addiction / habituation
- unable to control ingestion of drugs
- common on scheduled/ controlled meds. such as
opiates and benzodiazepines
may be:
physical= withdrawal symptoms
physiologic= emotionally attached sa drugs
● CUMULATIVE EFFECT
- drug may accumulate on body of next doses are
administered before nametabolized yung previously
med na na ininom
- may lead to drug toxicity
● OTC (OVER-THE-COUNTER)
- non prescription drugs sold w/o prescription in a
pharmacy
● PLACEBO
- drug dosage na walang pharmacologic act
- dosage form = no active ingredients
● HALF - LIFE
- time it takes for the half of original amount of drug in
the body to b removed
- determine how often drug needs to be given to
remain in a therapeutic range
● FIRST- PASS EFFECT
- absorbed in mesenteric blood system -> liver
(biotransformation) before traveling on to general
systemic circulation
- some drug are inactivated not all will be used
BRIEF HISTORY OF PHARMACOLOGY
❖ PRIMITIVE PERIOD
- drugs: mystical or magic rather than
physiologic effect
- evil spirits caused diseases
- alcohol & opium = first medicinal plants
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❖ ANCIENT PERIOD
- Egypt = coral=dle of civilization (oldest
phase of med)
- Ebers papyrus = written 3000 years ago;
medical source
= 700 remedies
may prayers in driving away diseases and
may recipes (aloe, oil, opium, peppermint,
vinegar)
- Greece = pharmaceutical history begins w/ legends
and goddesses
● Aesculapius = god of healing
● Hippocrates = father of medicine
● Dioscorides = wrote Materia Medica; described 60
plants and classified them by substance rather
disease; main source of pharmaceutical knowledge
up tp 16th cent
- Rome = after roman conquest of greece greek ,
med migrates to rome
● Galen = greek physician establishes
system of med and pharma
= 1st to prepare cold cream and rose
water ointment
❖ MEDIEVAL PERIOD
● Arabian Influence
- establishment of schools and hospitals and
discovery of new drugs
- originator of : syrups. alcohol, , and aromatic water
- 1st pharmaceutical formula (apothecary system)
● Geber
- 1st great Mohammedan and reputed discoverer of
nitric ais, sulfuric acid, and nitrohydrochloric acid
- Father of Arab Chemistry
❖ 16TH CENTURY
● Paracelsus = Father of Pharmacology
- swiss scientist that 1st advocate use of single drug
rather than mixtures and potions
- advantage: dosage of 1 single dose regulatts more
precisely than that of complex mixtures
- improves pharmacy and therapeutics, new
remedies and compounds and reduce overdose
❖ 17TH CENTURY
- interest in chemistry and pharmacy and many
preparations are in use
ex. Cinchona bark - discovered by indians; used in
treating and preventing diseases
Syrup of ipecac - natives of brazil; amoebic
dysentery
● William Harvey
- explained how drugs exert beneficial or
harmful effects
- demonstrated circulation of blood in and
introduced new way of administering = IV
❖ 18 TH CENTURY
● Edward Jenner = english physician who
made 1 st public inoculation of smallpox
vaccine in 1756
● William Withering = introduced infusion
digitalis of treatment in heart disease
❖ 19TH CENTURY
● Friedrich Serturner = german pharmacist
discovered alkaloid morphine substance
● Francois Magendie & Claude Bernard =
use of purified drug, demonstrated certain
drugs works at specific sites of action
within the body
● French Codex = 1st important
pharmacology book produced in 1818
● Ether and Chloroform = 1st used as
general anesthesia 1840’s
❖ 20TH CENTURY
- important legislation was instituted to
control the manufacture and sales of drugs
- Food and Drug Act of 1906 ^1938
- Harrison Narcotic Drug Act of 1914
- Controlled Substance Act of 1970
- Lister & Semmelweis
= introduced use of antiseptics to prevent infection during
surgery
- landmarks:
● Ehrlich = introduces salvarsan for treating syphilis
and responsible for the introduction of antibiotics
● Banting & Best’s discovery of insulin in treating
diabetes
PHARMACOLOGY: ANTI-INFECTIVE
● ANTIBIOTICS= bacteria
● ANTI VIRAL= virus
● ANTI FUNGAL
❖ ANTIBIOTICS
- kills bacteria by preventing them to reproduce
- “against life”
- Antibiotics are agents made from living microorganisms,
synthetic manufacturing, and genetic engineering that are
used to inhibit specific bacteria.
- They can be bacteriostatic, bactericidal, or both.
● Broad spectrum Antibiotic
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- Wide range of disease causing bacteria lethargy ( panlalata)begin to show up.

- The goal: decrease the population of invading bacteria to a

● Narrrow spectrum antibiotic point at which the human immune system can effectively
- Few types lang kinikill deal with the invader.

2 CLASSIFICATIONS

- indicated for infections

Prevents growth caused by gram-negative=
BACTERICIDAL bacteria (may shape na rod and
spherical ), aerobic bacilli
= ( mabuhay ng may
oxygen)
-Stop bacteria from AMINOGLYCOSIDES
bacteria - replaced by newer,
-Bacteria is a cell kaya less-toxic drugs in treating
BACTERIOSTATIC nagrereproduce thats less serious infections
-have potentially serious
why bacteriostatic adverse effects
prevents that

Exert bactericidal effect

➢ KIRBY- BAUER TEST (GCS- gram staining and through inhibition of protein
culture sensitivity) synthesis ( sa ribosomes)
- Test to determine what choice of antibiotics should in susceptible strains of
be used THERAPEUTIC ACTION gram-negative bacteria.

-They bind to a unit of the

MAJOR CLASSES OF ANTIBIOTICS bacteria ribosomes and
cause misreading of the
➔ Aminoglycosides genetic code leading to cell
➔ Carbapenems death
➔ Cephalosporins
● First generation INDICATIONS Infections caused by
● 2nd gen *if allergic sa penicillin susceptible strains:
● 3rd gen gamit ng aminogly
● 4th gen * Pseudomonas
aeruginosa,
➔ Fluoroquinolone *Escherichia coli*
➔ Penicillins and penicillinase - resistant antibiotics Proteu sspp.,
➔ Sulfonamides *Klebsiella-Enterobacter-S
➔ Tetracyclines erratia group
*Citrobacter spp.,
➔ Antimycobacterials - med for tuberculosis
*Staphylococcus spp.
- First line second line
➔ Leprostatic - leprosy Serious infections
susceptible to penicillin
Other: when penicillin is
contraindicated.
➔ Ketolide
➔ Lincosamides
➔ Lipoglycopeptides
➔ Macrolides
➔ Monobactam important aspects to remember for indication of
antibiotics in different age groups:
BACTERIA AND ANTIBIOTICS
- Bacteria are microorganisms that invade the human body
through many routes like respiratory, gastrointestinal( ecoli), - very sensitive to GI and
and skin(pores). CNS adverse effects of
antibiotics.
- Human immune response is activated once bacteria
- important to monitor their
invade the body. As the body tries to rid itself of bacteria, nutritional and hydration
classic signs of inflammation (e.g. swelling, heat, redness, status while on therapy.
and pain), fever, and
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-fluid sa bata: 60-80%
comprised their body
weight. (nagsuka= bilis
papayat) full stomach
pagtake ng antibiotic
- Oral candidiasis(oral
trush) = a superinfection is
CHILDREN common in this age group
which makes eating and
drinking difficult.
- Fluoroquinolones= are
associated with
damage to developing
cartilage and are not
recommended for growing
children.
- pediatric dosages should
be double-checked to
decrease the risk for
adverse effects.
-Most of all, parent
education is important in
cutting down
the unnecessary use of
antibiotics in children.
- tendency to cure simple
manifestations with
antibiotics.
- antibiotics are effective
ADULT only for certain bacteria
and not for simple
manifestations like
common colds, which may
be viral. (self limiting)
- Storage of unused pills for
future infections and
sharing antibiotics with
symptomatic friends should
be avoided and
emphasized in health
teachings.
- Assessing the problem
OLDER ADULTS and obtaining appropriate
specimens for culture is
especially important with
this population. Older
patients may be more
susceptible
to adverse effects of
antibiotic therapy.
➢ PHARMACOKINETICS
*characteristic interactions of aminoglycosides and the body
in terms of absorption, distribution, metabolism, and
excretion:
ROUTE ONSET PEAK (of DURATION
effect)
IM, IV Rapid 30-90 mins N/A
T1/2: 2-3 h
(half time,
naubos
kalahating
dose ng
gamot)
Metabolism:
liver
Excretion:
kidney (urine)
➢ CONTRAINDICATIONS AND CAUTIONS
● Known allergy to aminoglycosides. ( need health
history)
● Renal (excretion) or hepatic disease. Can be
exacerbated by aminoglycosides and may interfere
with metabolism and excretion of these drugs.
★ rationale: pag sira ang renal hindi
maeexcrete and excess med, tendency
maiipon lang
● Preexisting hearing loss. Can be intensified by toxic
drug effects on the auditory nerve.
★ cause hearing loss
★ if bibigyan pa, di mo malalaman if may
effect or toxicity
● Active infection with herpes or mycobacterial
infections( causes tb). Can be worsened by the
effects of an aminoglycoside on normal defense
mechanisms.
★ di pwede sabayan ng aminogly ang patient
na may herpes or tb
● Myasthenia gravis(paralysis) or parkinsonism. Can
be exacerbated by the effects of a particular
aminoglycosides on the nervous system.
● Lactation. Aminoglycosides are excreted in the
breast milk and can potentially cause serious
effects in the infant.
★ baka mapasa sa baby sinece excreted to
● Amikacin( type of aminogly)should not be used for
longer than 7-10 days because it is particularly toxic
to the bone marrow(produce blood cells), kidneys,
and GI.
★ babagsak immune system
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● Streptomycin is only for special situations because
● P.mirabilis
it is very toxic to the 8th cranial nerve(vestibular) ● P.aeruginosa
and kidney. ● P.bivia.

➢ ADVERSE EFFECT
● CNS: ototoxicity, irreversible deafness, ➢ PHARMACOKINETICS
vestibular paralysis, confusion, depression, characteristic interactions of carbapenems and the
disorientation, numbness, tingling, body in terms of absorption, distribution,
weakness metabolism, and excretion:
● Renal: renal failure
● Hematology: bone marrow depression,
leading to immunosuppression and
resultant superinfections ROUTE ONSET PEAK (of DURATION
effect)
● GI: nausea, vomiting, diarrhea, weight
loss, stomatitis, hepatotoxicity IM, IV Rapid 30-120 mins N/A
● CV: palpitations, hypotension,
hypertension T1/2: 2-4 h
● Hypersensitivity reactions: purpura, rash, (half time,
naubos
urticaria, exfoliative dermatitis
kalahating
dose ng
➢ INTERACTIONS gamot)
● Penicillins, cephalosporins, ticarcillin:
synergistic bactericidal effect
Metabolism:
● Diuretics: increased incidence of
pwede
ototoxicity, nephrotoxicity, and magbigay
neurotoxicity gamot sa
● Anesthetics, nondepolarizing NM blockers, may renal
succinylcholine, citrate anticoagulated failure, kase
metabolism
blood: increased NM blockade with niya direct na
paralysis sa inefctions

CARBAPENEMS -relatively new class of
broad-spectrum
antibiotics effective against
gram-positive and
gram-negative
bacteria
THERAPEUTIC Exert bactericidal effect by
ACTIONS inhibiting cell membrane
synthesis in susceptible
bacteria, leading to cell death
-binubutas cell memebrane
INDICATIONS - Serious intra-abdominal,
urinary tract, skin and skin
structure, bone and joint, and
gynecological infections
-Infections caused by
susceptible strains:
Excretion:
kidney (urine)
/ unchanged
➢ CONTRAINDICATIONS AND CAUTIONS
● Known allergy to carbapenems or beta-lactams.
● Seizure disorders. Exacerbated by drugs.
● Meningitis. Safety is not established.
★ meninges = protects brain
● Lactation. Not known whether drug can cross into
breast milk or not.
● Ertapenem is not recommended for use in patients
younger than 18 years of age.
★ di kaya ng younger
● Meropenem is associated with development of
pseudomembranous colitis and should be used in
caution in patients with inflammatory bowel disease(
affected colon)
★ can cause colitis (pamamaga)
pseudomonas colitis

● S.pneumoniae,
● H.influenzae
➢ ADVERSE EFFECT
● E.coli ● GI: pseudomembranous colitis, C.difficile
● K.pneumoniae diarrhea, nausea, vomiting, dehydration
● B.fragilis and electrolyte imbalance
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★ potassium, sodium, chloride
-less effective against
(electrolytes, help body & muscle gram-positive bacteria.
to contract)
● CNS: headache, dizziness, altered mental ● Third-generation
state Superinfections -effective against:

*all of the previously

➢ INTERACTIONS mentioned strains
● Valproic acid (prevents seizure): *relatively weak against
Carbapenems reduce serum valproic acid gram- positive bacteria but
and this can increase risk of seizures. are more potent against
gram-negative bacilli
★ pag bumaba ang VA possible na
*S.marcescens
magkaseizure (di pwede ihalo
ang carbapenems sa VA) ● Fourth-generation
● Imipenem and ganciclovir can cause - active against:
seizures.
*gram-negative
★ lahat ng may vir sa dulo ay anti *gram-positive organisms:
viral meds; nem ay carbapenem >cephalosporin-resistant
● Meropenem and probenecid can lead to staphylococci
toxic levels of meropenem. > P.aeruginosa.

➢ PHARMACOKINETICS
CEPHALOSPORINS -first introduced in the
1960s. characteristic interactions of cephalosporins and the
body in terms of absorption, distribution, metabolism,
-There are and excretion:
currently four generations of
cephalosporins, each with a
specific spectrum of activity. ROUTE ONSET PEAK (of DURATION
effect)
- These drugs are similar to
penicillins in structure and ORAL N/A 30-60 mins 8-10HR
activity.
T1/2: 30-60
THERAPEUTIC -Exert bactericidal and min
ACTIONS bacteriostatic effects by (half time,
interfering with the naubos
cell-wall building ability of kalahating
bacteria during cell division. dose ng
gamot)
-prevent the bacteria from
bio synthesizing the
framework of Metabolism:
their cell walls N/A

● First-generation
- effective against: Excretion:
kidney (urine)
*same gram-positive / unchanged
bacteria affected by
penicillin G
*gram- negative bacteria
*P.mirabilis ➢ CONTRAINDICATIONS AND CAUTIONS
*K.pneumoniae* ● Known allergy to cephalosporins and bea-lacams.
E.coli.
Cross reacions are common.
● Second-generatio ● Hepatic or renal impairment. These drugs are toxic
n to the kidneys and could interfere with the
- effective against: metabolism and excretion of the drugs.
● Pregnancy and lactation. Potential effects on the
*previously mentioned fetus and infant are not known; use only if benefits
strains clearly outweigh the potential risk of toxicity to the
*H.influenzae fetus or infant.
INDICATIONS *E.aerogenes ● Reserve cephalosporins for appropriate situations
*Neisseria spp. because cephalosporin-resisant bacteria are
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appearing in increasing numbers. Perform culture
● S.epidermidis
and sensitivity test before start of therapy. ● N.gonorrhoea
e
● group D
streptococci

Ciprofloxacin= was
approved in 2001 for
➢ ADVERSE EFFECT prevention of anthrax
● GI: nausea, vomiting, diarrhea, anorexia, infection in areas that
abdominal pain, flatulence, might be exposed to
germ warfare. It is also
pseudomembranous colitis effective against
● CNS: headache, dizziness, lethargy, typhoid fever.
paresthesias
● Nephrotoxicity in patients who have
predisposing renal insufficiency ➢ PHARMACOKINETICS
● Superinfections characteristic interactions of fluoroquinolones and the
● Phlebitis and local abscess at the site of body in terms of absorption, distribution, metabolism,
IM injection and/or IV administration. and excretion:

➢ INTERACTIONS
● Aminoglycosides: increased risk for ROUTE ONSET PEAK (of DURATION
effect)
nephrotoxicity
● Oral anticoagulants: increased bleeding ORAL VARIES 60-90mins 4-5HR
● Alcohol: avoided for 72 hours after
discontinuation of the drug to IV 10 MIN 30 MIN 4-5 HR
prevent disulfiram-like reaction (e.g. flushing,
throbbing headache, nausea and vomiting, chest T1/2: 3.5-4H
(half time,
pain, palpitations, dyspnea, syncope, vertigo, naubos
convulsions, etc.) kalahating
dose ng
gamot)

new synthetic class of

FLUOROQUINOLONES antibiotics with a broad Metabolism:
spectrum of activity. liver

Interfere with the action Excretion:

of DNA enzymes liver (bile),
necessary for growth kidney (urine)
and
reproduction of the
THERAPEUTIC bacteria.
ACTIONS
Has little ➢ CONTRAINDICATIONS AND CAUTIONS
cross-resistance but ● Known allergy to fluoroquinolones.
misuse of this drug for
● Pregnancy and lactation. Potential effects on the
a short time will
lead to the existence of fetus and infant are not known; use only if benefits
resistant strains. clearly outweigh the potential risk of toxicity to the
fetus or infant.
● Seizures. Can be exacerbated by the drugs’ effects
Treating infections
on cell membrane channels
(respiratory, urinary
tract, and skin) caused
by susceptible strains: ➢ ADVERSE EFFECT
● E.coli ● GI: nausea, vomiting, diarrhea, dry mouth
● P.mirabilis ● CNS: headache, dizziness, insomnia,
● K.pneumoniae
● P.vulgaris, depression
● M.morganii ● Immunological: bone marrow depression
● P.aeruginosa ● Risk for tendinitis and tendon rupture in
● H.influenzae, patients over age 60, on concurrent
INDICATIONS ● S.aureus,
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Date
steroids, and those with renal, heart, or
lung transplants
● Photosensitivity and severe skin reactions
so advise patient to avoid sun and
ultraviolet light exposure and to use
protective clothing and sunscreens.
➢ PHARMACOKINETICS
➢ INTERACTIONS
● Iron salts, sucralfate, mineral supplements,
antacids: increased therapeutic effects of
ROUTE ONSET PEAK (of DURATION
fluoroquinolones. Administration should be effect)
separated by at least 4 hours.
● Quinidine, procainamide, pentamidine, ORAL VARIES 1HR 6-8H
tricyclics, phenothiazines: severe-to-fatal
cardiac reactions due to increased QT c T1/2: 1-2.4H
(half time,
interval and/or torsades de pointes naubos
● Theophylline: increased theophylline levels kalahating
because these two drugs have the same dose ng
metabolic pathway gamot)
● Steroids: increased CNS stimulation
Metabolism:
PENICILLINS AND -first antibiotic introduced N/A
PENCILLINASE for clinical use.
RESIISTANT
ANTIBIOTICS -Various Excretion:
modifications were kidney (urine)
subsequently made to
address resistant strains
and to decrease drug
➢ CONTRAINDICATIONS AND CAUTIONS
adverse effects.
Penicillinase-resistant ● Known allergy to penicillins and cephalosporins.
antibiotics were developed ● Renal disease. Drug excretion is reduced.
to address ● Pregnancy and lactation. No adequate studies on
penicillin-resistant bacteria. the effect on fetus but these drugs can cause
diarrhea and superinfections may occur in the
THERAPEUTIC ACTION Exert bactericidal effect by infant.
interfering with the ability of
susceptible bacteria to ➢ ADVERSE EFFECTS
build their cell walls when ● GI: nausea, vomiting, diarrhea, abdominal
they are dividing.
pain, glossitis, stomatitis, gastritis, sore
These drugs mouth, furry tongue
prevent the bacteria from ● Pain and inflammation at the injection site
bio synthesizing the can occur with injectable forms of the
framework of the cell drugs.
wall, and the bacteria with
weakened cell walls swell ● Hypersensitivity reactions: rash, fever,
and then burst from wheezing, anaphylaxis with repeated
osmotic pressure within the exposures
● Superinfections, e.g. yeast infections.

INDICATIONS Treatment of:

● streptococcal ➢ INTERACTIONS
infections (e.g. ● Tetracyclines: decrease in effectiveness of
pharyngitis, penicillins
tonsillitis, ● Parenteral aminoglycosides: inactivation of
scarlet fever, endocarditis).
aminoglycosides
● meningococcal
meningitis if given
at high doses
drugs that inhibit folic acid
SULFONAMIDES synthesis
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Inhibit folic acid synthesis Excretion:
required as precursors of kidney (urine)
RNA and DNA.

They competitively block

paraaminobenzoic acid to
THERAPEUTIC ACTION prevent synthesis of folic
acid in susceptible bacteria
that synthesize their
own folates for the
production of RNA and
DNA.
➢ CONTRAINDICATIONS AND CAUTIONS
● Known allergy to sulfonamides, sulfonylureas, or
thiazide diuretics. Cross-sensitivity can occur.
● Renal disease. Increased toxic effects of the drug.
● Pregnancy. Can cause birth defects.
● Lactation. Increased risk for kernicterus, diarrhea,
and rash in infants.

*Treatment of infections ➢ ADVERSE EFFECTS

caused by susceptible
strains: ● GI: nausea, vomiting, diarrhea, abdominal
pain, anorexia, stomatitis, and hepatic
● C.trachomatis injury
● Nocardia, ● Renal: crystalluria, hematuria, proteinuria,
some strains of:
toxic nephrosis
● H.influenzae, ● CNS: headache, dizziness, vertigo, ataxia,
E.coli convulsions, depression
● P.mirabilis. ● Bone marrow depression
INDICATIONS ● Dermatological: photosensitivity, rash,
No longer used much but
they remain an inexpensive hypersensitivity reactions
and effective
treatment for: ➢ INTERACTIONS
● Tolbutamide, tolazamide, glyburide,
● UTIs and glipizide, chlorpropamide: increased risk of
trachoma,
especially in hypoglycemia
developing ● Cyclosporine: increased risk of
countries nephrotoxicity
where cost is an issue.

Can also be used in: semisynthetic antibiotics

● treatment of based on the structure
sexually TETRACYCLINES of a common soil mold.
transmitted
diseases.
Inhibit protein synthesis
Sulfasalazine is used in leading to inability of the
treatment of ulcerative bacteria to multiply.
colitis and rheumatoid The affected protein is
arthritis. THERAPEUTIC ACTION similar to protein found in
human cells so
these drugs can be toxic to
➢ PHARMACOKINETICS humans at high
concentrations.
ROUTE ONSET PEAK (of DURATION
effect) Treatment of infections
caused by susceptible
ORAL rapid 1-4h N/a strains:
T1/2: 8-10H ● Ricketssiae
(half time, ● M.pneumoniae
naubos ● B.recurrentis,
kalahating INDICATIONS ● H.influenzae
dose ng ● H.ducreyi
gamot) ● Bacteroides spp.,
● V.comma
● Shigella spp.
Metabolism: ● D.pneumoniae
N/A ● S.aureus.
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● Hematologic: hemolytic anemia, bone
Adjunct in treatment of
protozoal infections. marrow depression
● Hypersensitivity reactions:

➢ INTERACTIONS
● Penicillin G: decreased
effectiveness of penicillin G
● Oral contraceptives: decreased
effectiveness of oral
contraceptives and additional
➢ PHARMACOKINETICS
form of birth control is needed
● Digoxin: increased digoxin toxicity
ROUTE ONSET PEAK (of DURATION ● Calcium salts, magnesium slats,
effect) zinc salts, aluminum salts,
bismuth salts, iron, urinary
ORAL Varies 2-4h N/a
alkalinizers, and charcoal:
Topical Minimal N/A N/A decreased absorption of
absorption tetracyclines
occurs

T1/2: 6-12H -antibiotics used in the

(half time, treatment of
naubos infections caused by
kalahating pathogens responsible
dose ng for tuberculosis and
gamot) leprosy.

-Mycobacterium
Metabolism: tuberculosis causes
N/A tuberculosis, the leading
cause of death from
infectious disease in the
Excretion: ANTIMYCOBACTERIALS world.
kidney (urine)
-Mycobacterium leprae
causes leprosy or
Hansen’s disease,
characterized by disfiguring
➢ CONTRAINDICATIONS AND CAUTIONS skin lesions and destructive
● Known allergies to tetracyclines or to tartrazine effects on
the respiratory tract.
● Pregnancy and lactation. Effect on developing
bones and teeth
● Fungal, mycobacterial, or viral ocular infections. THERAPEUTIC ACTION Act on the DNA and/or
Ophthalmic preparations can kill both undesired RNA of the bacteria,
bacteria and normal flora leading to lack of growth
and eventually to bacterial
● Use in caution in children below age of 8. Can death.
potentially damage developing bones and teeth.
● Hepatic or renal dysfunction. Drugs are
concentrated in the bile and are excreted in urine. INDICATIONS Tetracyclines are indicated
for the following medical
conditions:
➢ ADVERSE EFFECTS
● GI: nausea, vomiting, diarrhea, abdominal ● Treatment of
pain, glossitis, dysphagia, fatal tuberculosis and
hepatotoxicity leprosy.
● Skeletal and bones: weakening the
structure and causing staining and pitting ➢ PHARMACOKINETICS
of teeth and bones
● Dermatological: photosensitivity and rash
ROUTE ONSET PEAK (of DURATION
● Superinfection
effect)
● Local: pain and stinging with topical or
ocular applications ORAL Varies 2-4h N/a
 Subject : PHARMACOLOGY
Date
T1/2: 1-4H They are used to treat
(half time, severe infections when
naubos penicillin or other less
kalahating toxic antibiotics cannot
dose ng be used.
gamot)
LIPOGLYCOPEPTIDE antibiotics introduced
S in 2010.
Metabolism:
liver They are used to treat
complicated skin and
skin-structure
Excretion: infections caused by
kidney (urine) susceptible strains of
gram-positive
organisms.

➢ CONTRAINDICATIONS AND CAUTIONS MACROLIDES are antibiotics that

● Known allergies to antimycobacterials. interfere with protein
● Pregnancy. Adverse effects on fetus. Safest synthesis in
antituberculosis regimen in pregnancy isoniazid, susceptible bacteria.
ethambutol, and rifampin. They are used to treat
● Severe CNS dysfunction. Exacerbated by the respiratory infections
effects of the drug and in adults and and
● Hepatic or renal dysfunction. Interfere with the pharyngitis/in children.
metabolism and excretion of drugs.
Erythromycin is the
drug of choice for
➢ ADVERSE EFFECTS Legionnaires disease
● CNS: neuritis, dizziness, headache, and infections caused
malaise, drowsiness, and hallucinations by C.diphtheriae,
Ureaplasma spp.,
● GI: nausea, vomiting, anorexia, stomach mycoplasma , and
upset, abdominal pain chlamydial infections.
● Rifampin, rifabutin, and rifapentine can
cause discoloraion of body fluids from
● KETOLIDES
urine to sweat and tears. They may stain
orange- ROUTE ONSET PEAK (of DURATION
● tinged and may permanently stain contact effect)
lenses.
ORAL Rapid 0.5-4 N/a
➢ INTERACTIONS
● Rifampin and INH in combination: T1/2: 10H
increased toxic liver reactions (half time,
● Rifampin and rifabutin with beta blockers, naubos
corticosteroids, OCPs, ora; anticoagulants, kalahating
dose ng
methadone, phenytoin, verapamil, gamot)
ketoconazole, and cyclosporine: increased
metabolism and decreased drug
effectiveness Metabolism:
N/A

KETOLIDES a class of antibiotics Excretion:

introduced in 2004. It kidney (urine)
is indicated for colon (feces)
treatment of mild to
moderate
community-acquired ● LINCOSAMIDES
caused by susceptible
bacteria
ROUTE ONSET PEAK (of DURATION
LINCOSAMIDES are similar to effect)
macrolides but they
are more toxic. ORAL VARIES 1-2H 8-12 H
 Subject : PHARMACOLOGY
Date
IM 20-30 MIN 2-3 H 8-12 H

IV IMMEDIAT MINUTES 8-12 H Metabolism:

E liver

TOPICAL MINIMAL N/A N/A

ABSORPTI Excretion:
ON kidney (urine)
liver (urine)
T1/2: 2-3H
(half time,
naubos
kalahating
dose ng
ROUTE ONSET PEAK (of DURATION
gamot)
effect)

ORAL Varies 2-4h N/a

Metabolism:
N/A
T1/2: 1-4H
(half time,
naubos
Excretion:
kalahating
kidney (urine)
dose ng
colon (feces)
gamot)

● LIPOGLYCOPEPTIDES Metabolism:
liver

ROUTE ONSET PEAK (of DURATION

effect) Excretion:
kidney
IV RAPID END OF N/a (urine)
INFUSION

T1/2: 8-9.5H
(half time,
naubos MONOBACTAM indicated for treatment of
kalahating ANTIBIOTICS gram-
dose ng negative enterobacterial
gamot) infections.

Metabolism: THERAPEUTIC ACTIONS ● Ketolides and

UNKNOWN lincosamides
-block protein synthesis
leading to cell
Excretion: death.
kidney (urine)
● Ketolamides
are structurally the same
with macrolides.
● MACROLIDES
● Lipoglycopeptid
es
ROUTE ONSET PEAK (of DURATION -inhibit bacterial cell wall
effect) synthesis by interfering
with polymerization and
ORAL 1-2 H 1-4h N/a cross-linking of
peptidoglycans.
IV RAPID 1H N/A
They bind to
T1/2: 3-5H the bacterial membrane
(half time, and disrupt the membrane
naubos barrier function
kalahating causing bacterial cell
dose ng death.
gamot)
 Subject : PHARMACOLOGY
Date
● Ketolides: loss of therapeutic effects if
● Macrolides
- bind to the bacterial cell combined with rifampin, phenytoin,
membrane and change carbamazepine, phenobarbital; increased
protein function. This serum levels of digoxin and metoprolol;
prevents bacteria from increased GI toxicity with theophylline
dividing and cause their
● Lipoglycopeptides: increased risk for
cell death.
prolonged QT interval if combined with
● Monobactam drugs known to cause prolonged QT
-disrupts bacterial cell wall interval
synthesis ● Macrolides: food in the stomach decreases
absorption of oral macrolifes. Antibiotic
should be taken on an empty stomach with
➢ PHARMACOKINETICS a full, 8-oz glass of water 1 hour before or
at least 2-3 hours after meals.
ROUTE ONSET PEAK (of DURATION ● Monobactams: incompatible in solution
effect) with nafcillin, cephradine, and
metronidazole.
ORAL Varies 60-90 MINS 6-8 H

IV IMMEDIATE 30 MIN 6-8H

❖ Nursing Considerations foR Antibiotics
T1/2:
1.5-2H
(half time,
naubos Nursing Assessment Assess for the mentioned
kalahating cautions and
dose ng contraindications (e.g. drug
gamot) allergies, CNS depression,
CV disorders, etc.) to
prevent any untoward
Metabolism: complications.
N/A
Perform a thorough
physical assessment (other
Excretion: medications taken,
kidney CNS, skin, respirations,
(urine) and laboratory tests like
renal functions tests
and complete blood count
or CBC) to establish
baseline data before
drug therapy begins, to
determine effectiveness of
➢ CONTRAINDICATIONS AND CAUTIONS therapy, and to
● Ketolides: telithromycin with antiarrhythmics and evaluate for occurrence of
antilipidemics can cause serious adverse effects. It any adverse effects
might also cause potentially fatal respiratory failure associated with drug
therapy.
in patients with myasthenia gravis.
● Lincosamides: use in caution in patients with Perform culture and
hepatorenal insufficiency. Usage in pregnancy and sensitivity tests at the site
lactation is only indicated if benefit clearly of infection to ensure
outweighs the risk to the fetus or neonate. The appropriate use of the
drug.
same is true with lipoglycopeptides, macrolides, and
monobactams. Conduct orientation and
reflex assessment, as well
➢ ADVERSE EFFECTS as auditory testing to
● GI: nausea, vomiting, potential for evaluate any CNS effects
of the drug
pseudomembranous colitis, (aminoglycosides).
superinfections, taste alterations, risk for
C.difficile diarrhea
Nursing Diagnoses Acute pain related to GI or
➢ INTERACTIONS CNS drug effects

Deficient fluid volume and

 Subject : PHARMACOLOGY
Date
imbalanced nutrition: less
than body requirements
related to diarrhea
Disturbed sensory
perception (auditory)
related to CNS drug effects
Risk for infection related to
bone marrow suppression
(aminoglycosides) and
repeated injections
(cephalosporins).
Monitor for adverse effects
(e.g. orientation and affect,
hearing
changes, bone marrow
suppression, renal toxicity,
hepatic dysfunction, etc).
Evaluate patient
understanding on drug
therapy by asking patient to
name the drug, its
indication, and adverse
effects to watch for.

Monitor patient compliance

Implementation with Check culture and to drug therapy.
Rationale sensitivity reports to ensure
that this is the drug of
choice for this patient.

Ensure that patient

receives full course of
aminoglycosides as
prescribed, divided around
the clock to increase
effectiveness and
decrease the risk for
development of resistant
strains of bacteria.

Monitor infection site and

presenting signs and
sympoms throughout
course of drug therapy
because failure of these
manifestations to
resolve may indicate the
need to reculture the site.

Provide safety measures to

protect the patient if CNS
effects (e.g.
confusion, disorientation,
numbness) occur.
Educate client on drug
therapy to promote
understanding and
compliance.

Provide the following

patient teaching: safety
precautions (e.g.
changing positions,
avoiding hazardous tasks,
ec.), drinking lots of
fluids and to maintain
nutrition even though
nausea and vomiting
may occur, report difficulty
breathing, severe
headache, fever,
diarrhea, and signs of
infection.

Evaluation Monitor patient response to

therapy (decrease in signs
and symptoms of infection).