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Dasar Farmakologi
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Ns. Shila Wisnasari, S.Kep., M.Biomed

Basic Nursing Compartment,
Nursing Department, Universitas Brawijaya
Introduction

Farmakologi
Studi yang mempelajari interaksi bahan kimia (obat)
dengan sistim biologi pada organisme hidup sehingga
menimbulkan efek  khasiat obat

Obat
diberikan pada organisme hidup untuk mempengaruhi
proses di dalam tubuh dan digunakan untuk diagnostik,
pencegahan, dan terapi
 Prinsip Kerja Obat
Efek obat ditentukan oleh interaksinya
dengan proses biologi di dalam tubuh
Pharmacology

 Pharmacokinetics
 Pharmaco (medicine) dan kinetics (movement)
 study of drug movement throughout the body
 what the body does to the drug (nasib obat)
 ADME (absorpsi, distribusi, metabolisme, ekskresi)

 Pharmacodynamics
 what the drug does to the body (efek obat)
 drug action/effect
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Pharmacokinetics

 Knowledge of pharmacokinetic data about a drug

tells us:
 What dose to give
 How often to give it
 How to change the dose / route in certain medical
conditions
 How some drug interactions occur
Pharmacokinetics
Process

• Pharmacokine
tics process
Pharmacokinetics Absorption

 primary pharmacokinetic factor determining the length of time

it takes a drug to produce its effect

 perpindahan obat dari tempat pemberian menuju sirkulasi

darah

 Mekanisme absorpsi obat

 Difusi pasif
 Transport aktif
 Filtrasi  Small water-soluble agents (urea, alcohol, water)
Pharmacokinetics Absorption

Mekanisme absorpsi obat

Diffusion: random movement of
particles from an area of high
concentration to an area of low
concentration

small, nonionized, and lipid

soluble drugs
Pharmacokinetics Absorption

Mekanisme absorpsi obat

Active Transport 
Protein Pumps -
transport proteins that
require energy to do
work
Large molecules,
ionized drugs, and
water-soluble agents Protein changes shape to move
molecules: this requires energy!
Pharmacokinetics Absorption

Drugs may not need to enter the cell

Receptors located on the plasma membrane 

drug-receptor binding  activate second
messenger within the cell  physiological change
Pharmacokinetics Absorption

 Main factor  route of administration

 Other factors controlling the rate and reliability of drug

absorption:
 Physiological factors
 Physico-chemical factors
Route of Administration Absorption
Faktor yang
Mempengaruhi
Absorpsi Obat
Faktor yang
Mempengaruhi
Absorpsi Obat
Bioavailability Absorption

 The fraction of the administered dose of the unchanged drug

that reaches the systemic circulation available to have an
effect
 Affected by:
 Dosage form
 Dissolution  how quickly the drug disintegrates and disperses into
simpler forms
 Route of administration
 Stability of the drug in the GI tract (if oral route)
 Presence of food/drugs in GI tract
 Extent of drug metabolism before reaching systemic circulation e.g.
First Pass metabolism
Rute Oral Rute IV
Physiological factors Absorption

 Blood flow to absorbing site

 The better the blood supply to the area the greater the rate of
absorption
 Good circulation  the better ability to absorb the drug

 Total surface area for absorption

 The greater the surface area the greater the rate of absorption
 The intestine has a very large surface area  ideal target for
drug absorption  most drugs are given orally where possible
Physiological factors Absorption

 Time of arrival and contact time at absorption site

 The longer the drug is in contact with the absorbing
surface the greater the rate of absorption
 If a person is suffering from diarrhea the chances of a drug
given orally being absorbed completely are lowered and
other means of administration must be considered
Physico-chemical factors Absorption

 Solubility  seberapa larut obat dalam cairan tubuh

 Beberapa obat tidak larut menjadi partikel yang kecil  absorpsi
cepat

 Chemical stability  apakah obat mudah terdegradasi?

 Lipid to water partition coefficient  lebih mudah larut dalam

lemak atau air?
 Pertimbangan penting
 Sel  phospho-lipid bilayer  semua obat yang larut dalam
lemak dapat melewati jaringan dengan lebih cepat
Physico-chemical factors Absorption

 Degree of ionization
 banyaknya obat yang terionisasi (menjadi bermuatan) ketika
dilarutkan dalam air
 semakin bermuatan  molekul makin sulit menembus membran
 semakin kurang bermuatan  molekul semakin lebih mudah
menembus membran
 Faktor penentu:
• Obat  asam lemah atau basa lemah
• pH larutan (asam atau basa)
– obat yang bersifat asam lemah akan lebih terionisasi pada
suasana basa
– obat yang bersifat basa lemah akan terionisasi pada suasana asam
Physico-chemical factors Absorption
Pharmacokinetics Absorption

Life Span Consideration

 Neonate and Pediatric
 the acid-producing cells of the stomach are immature (until 1-2 y.o)
 gastric emptying may be ↓ because of slowed or irregular peristalsis
 As the liver continues to mature  first-pass elimination ↓  higher
drug levels in the bloodstream
 Older adults
 ↓ blood flow to tissues within the GI tract
 changes in the gastric pH  alter the absorption of certain medications
 variations in available plasma proteins impact drug levels of
medications that are highly protein-bound
Pharmacokinetics Distribution
Pharmacokinetics Distribution

 For some drugs that the site is known and such drugs are available to give
locally or topically
 All other drugs need to be distributed throughout the body

 Only that fraction of drug which is non-protein-bound can bind to

cellular receptors and pass across tissue membranes  being
distributed to other body tissues, metabolized, and excreted

¨ The actual pattern of drug distribution reflects various

physiological factors (blood perfusing organ, capillary
permeability ) and physicochemical properties (protein plasma
binding, lipid solubility) of the drug
Pharmacokinetics Distribution

Four main elements

Distribution into body fluid

Uptake into body tissues/organs

The Extent of plasma protein binding

Passage through barriers

Pharmacokinetics Distribution

 Distribution into body fluids

 Mainly plasma, interstitial fluid and intracellular fluid
 Molecular targets for drugs are found in these areas

 Uptake into body tissues/organs

 Specific tissues take up some drugs – for example, iodine
and thyroid gland
Pharmacokinetics Distribution

 The Extent of plasma protein binding

 Plasma proteins (e.g. albumin) can bind drug molecules
 varies widely among drugs
 Drugs bound to plasma proteins are pharmacologically inert 
only free drugs are active
 Some drugs do not bind (e.g. caffeine) and some are highly
bound (e.g. warfarin which is 99% bound to plasma proteins)
 Some drugs can displace others from their binding sites on the
plasma proteins – e.g. phenylbutazone can displace warfarin
from plasma proteins  an important consideration for drugs
which have this effect
Pharmacokinetics Distribution

 Passage through barriers

 The two main examples are the placenta and the blood brain
barrier (BBB)
 Drugs must be highly lipid soluble to pass across these barriers
 If not, they may not be able to reach their site of action
The Placenta
 Almost all drugs will eventually cross the placenta to reach the fetus
 may be beneficial, drugs may be deliberately administered to the
mother in order to treat specific fetal conditions
 steroids may be given to the mother to promote fetal lung maturation and cardiac
drugs may be given to control fetal arrhythmias
 may have detrimental effects on the fetus  teratogenicity or
impairment of fetal growth and development
 The greatest risk of adverse drug effects on the fetus is probably during
organogenesis (the first trimester)
 The effects on the fetus  either direct or mediated via the alteration of
uteroplacental blood flow
Blood Brain Barrier
 Sistem pelindung aktivitas selular yang menjaga agar berbagai hal
(benda asing, toksin) tidak masuk ke dalam SSP

 Obat yang dapat melewati BBB  bermuatan rendah, ukuran kecil,

larut dalam lemak
 Arti klinis dalam pengobatan infeksi otak  hampir semua antibiotik
tidak larut dalam lemak  tidak dapat menembus BBB  terapi
kurang efektif
Pharmacokinetics Distribution

Factors affecting drug distribution

 Blood flow
 Reduced blood flow e.g. diabetics
 Which organ?
 Capillary permeability
 Capillary structure
 Binding of drugs to plasma tissues & proteins
 Volume of Distribution
Pharmacokinetics Distribution

 Binding of drugs to plasma tissues & proteins

 Many drugs bound to circulating plasma proteins such as
albumin
 Only free drug can act at receptor site
Pharmacokinetics Distribution
Pharmacokinetics Distribution

 Volume of Distribution
 ‘Measurement of the extent to which a drug is dissolved
throughout the body’s compartments’
 Drugs are distributed unevenly between various body
fluids and tissues according to their physical and chemical
properties
 For example, gentamicin
• Very good water solubility
• Very poor lipid solubility
• stays mainly in plasma and body water
Pharmacokinetics Distribution

 Volume of Distribution
Once a drug enters the body (any route), distributes to:
 Plasma Compartment (4L)  Total Body Water (42L)
• Very large molecular weight  Low molecular weight
• Protein bound  Hydrophobic (Lipophilic)
• 6% of body weight

 Extracellular Fluid (14L)

• Low molecular weight
• Hydrophilic (Lipophobic)
Pharmacokinetics Distribution

 Volume of Distribution (Vd)

 A low Vd  the drug is mainly confined to blood and body
water  very little has ‘overflowed’ into the tissues
 A high Vd  the drug is widely distributed to the tissues 
A lot has ‘overflowed’ into the tissues
 Vd will vary between different drugs according to:
• Lipid and water solubility  High lipid solubility lets the drug cross
membranes
• Plasma or tissue protein binding properties  High protein binding
leaves less drug circulating in the plasma
Pharmacokinetics Distribution

Life Span Consideration

 Neonate and Pediatric
 Fat content ↓ because of greater total body water
 the liver is still forming, ↓ protein binding capacity
 the developing blood-brain barrier  more drugs to enter the brain
 Older adults
 Body fat may increase  longer duration of action for many
medications
 ↓ Serum albumin  more active free drug within the body  older
adult patients require lower levels of medication
Pharmacokinetics Metabolism

 Biotransformation
 the process of metabolizing the parent drug compound to
different compounds called metabolites
 occurs mainly in the liver (hepatic metabolism)
Pharmacokinetics Metabolism

 Struktur intraseluler sel-sel hepatic dilapisi enzim  sistem

microsomal hepatic

 Obat oral  biotransformasi fase 1 (1st pass metabolism) 

menetralisasi sebagian besar obat yang masuk
 Oksidasi, reduksi, dan hidrolisis
 Oleh sitokrom p450 (enzim yang ditemukan paling banyak di hepar)

 Biotansformasi fase 2  reaksi konjugasi  obat kurang polar

 mudah diekskresi oleh ginjal
First pass metabolism Metabolism

Extent of
metabolism occurring
before drug enters
systemic circulation
First pass metabolism Metabolism
Pharmacokinetics Metabolism

 Drug metabolism can influence dose and frequency of

dosing

 quickly metabolized  have a short duration of action

and need to be administered more often (two, three or
four times daily)

 slowly metabolized  have a longer duration of action

and may only need to be given on a once-daily basis
Pharmacokinetics Metabolism

 The drug metabolite may have decreased, increased

or undergone no change in pharmacological activity
compared to the parent drug

 May also have a different activity

 Some drugs are what are termed pro-drugs  the drug
itself is pharmacologically inactive until it is metabolized by
the liver to its active form
 codeine, which is metabolized to morphine by the body
Pharmacokinetics Metabolism

Factors affecting drug metabolism

 Hepatic blood flow
 Liver disease
Pharmacokinetics Metabolism

Life Span Consideration

 Neonate and Pediatric
 The developing liver  ↓ levels of microsomal enzymes  ↓ ability to
metabolize medications
 Older children  hepatic enzymes are fully produced  increased
metabolism and require higher doses of medications
 Older adults
 Significant decline of Hepatic metabolism  dosages should be
adjusted according to the liver function and anticipated metabolic rate
 First-pass metabolism ↓ with aging  higher “free” circulating drug
concentrations  higher risk for side effects and toxicities
Pharmacokinetics Excretion

 Once drugs have had their desired effect they need to be

excreted by the body

 Principles  renal elimination and clearance, secretion

into bile for faecal elimination and enterohepatic
circulation

 Some drug metabolites can also have pharmacological

effects  were not eliminated  accumulate in the
bloodstream  cause toxic and unwanted effects
Pharmacokinetics Excretion

 Renal drug elimination depends on:

 Blood flow to kidney (normal 1500ml/min)
 Glomerular filtration rate (normal 120ml/min)
 Urine flow rate and pH which indirectly alter
• Passive reabsorption
• Active tubular secretion

Patients with poor renal function will not

eliminate renally excreted drugs very well
Pharmacokinetics Excretion

Life Span Consideration

 Neonate and Pediatric
 immature kidneys with ↓ GFR, resorption, and tubular secretion  do
not clear medications as efficiently from the body
 Dosing for most medications  based on weight in kg, smaller dose
 Higher levels of free circulating medication and may become toxic
quickly  frequent assessment of infants and children is vital
 Older adults
 Kidney and liver function ↓ with age  ↓ excretion of medications 
prolonged half-life with a greater potential for toxicity
 Smaller doses of medications are often recommended
Drug Plasma Concentration
and Therapeutic Response
 therapeutic response  directly related to drug
plasma level
 concentration of the medication at its target tissue 
more predictive of drug action, BUT the quantity is
impossible to measure in most cases
 Nurses often have to monitor the plasma levels of
certain drugs
Patient with headache:

½ tablet of aspirin 
plasma level will remain
below the MEC  pain
persist

2 or 3 tablets  plasma
level ↑  therapeutic
range  pain relief

6 or more tablet 
adverse effect, such as GI
bleeding, tinnitus
Minimum Effective
Concentration (MEC)

minimum concentration
of drug in plasma
required to produce the
therapeutic effect

a range of doses that

produces therapeutic
response without
causing any significant
adverse effect in
patients
Onset, Peak Level, Duration
of Action
 Onset of drug action  the amount of time to produce
therapeutic effect after drug administration

 Peak plasma level  the medication has reached highest

concentration in the bloodstream
 Not associated with therapeutic effect
 Multiple doses may be necessary to reach therapeutic drug levels

 Duration of drug action  the amount of time for a drug to

maintain its desired effect until termination of action
 Factors  drug concentration, dosage, route of administration, drug-
food interaction, drug-drug interaction, drug-supplement interaction,
drug-herbal interaction
Onset, Peak Level, Duration
Half Life
of Action
 most common description of a drug’s duration of action
 the time required to reduce the plasma concentration of a
drug to half of its original value
 Dipengaruhi oleh
keseimbangan
ADME
Onset, Peak Level, Duration
Half Life
of Action

• pedoman yang penting untuk menentukan interval dosis obat

• Semakin lama obat diekskresi  semakin besar waktu paruh
• Obat- obat dengan waktu paruh pendek, seperti aspirin (t ½
15-20 menit), diberikan beberapa kali sehari
• obat-obat dengan waktu paruh panjang, seperti digoksin (t ½
36 jam), diberikan sekali sehari  jika lebih  penimbunan
obat di dalam tubuh, toksisitas obat
• gangguan hati atau ginjal  waktu paruh obat ↑  diberikan
dosis tinggi atau sering  toksisitas obat
Loading Dose and
Maintenance Dose

• Some drugs is administered as a single dose

• Repeated dose  accumulation of drug in the bloodstream
• Plateau  level of drug in the plasma is maintained within the
therapeutic range (with the amount of drug being eliminated 
the distribution of a continuous therapeutic level of drug to body
tissues); 4-5 half life
• Loading dose  higher amount of drug, often given only once or
twice to “prime” the bloodstream with a sufficient level of drug
• Maintenance dose  to keep the plasma drug concentration in
the therapeutic range
Loading Dose and
Maintenance Dose
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Pharmacodynamics

 what the drug does to the

body (efek obat)

 Studi yang mempelajari

bagaimana bahan
kimia/obat mempengaruhi
tubuh untuk menimbulkan
efek biologis  tempat
kerjanya, mekanisme kerja,
efek obat pada sistem
biologi
Pharmacodynamics

 intuitive experience  practical method for determining

which doses of medications will be effective in a patient
 knowledge about therapeutic indexes, dose–response
relationships, and drug–receptor interactions  safe and
effective treatment
Interpatient Variability

 Same dose but different effects on some patients

 best understood by examining a frequency distribution
curve
 frequency distribution curve  a graphical representation
of the number of patients responding to a drug action at
different doses
Interpatient Variability

response to an antihypertensive
drug as being a reduction of 20
mmHg in SBP
 A few patients experienced the
desired 20-mm reduction at a
dose of only 10 mg of drug
 A 50-mg dose gave the largest
number of patients a 20-mmHg
reduction
 a few patients needed as much as
median effective dose (ED50)  dose 90 mg of drug to produce the
required to produce a specific therapeutic same 20-mmHg reduction
response in 50% of a group of patients
Interpatient Variability

 average dose predicts a satisfactory therapeutic response

for only half the population
 More or less dose may be required
 Nurses’ role  determine whether the average dose is
effective
• observing the patient
• taking vital signs
• monitoring associated laboratory data
Pharmacodynamics Therapeutic Index

 median lethal dose (LD50)  dose of drug that will be lethal in 50%
of a group of animals  determined in clinical trials
 larger the difference between LD50 and ED50  greater the
therapeutic index
 a measure of a drug’s safety margin
 offers the practical information on the safety of a drug
Pharmacodynamics Therapeutic Index

approximately 4 times the average the drug has a narrow

dose to be lethal to a patient safety margin
Pharmacodynamics Therapeutic Index

 LD50 cannot be experimentally determined in humans

 median toxicity dose (TD50)  dose that will produce a given toxicity
in 50% of a group of patients
 TD50 value may be extrapolated from animal data or based on
adverse effects recorded in patient clinical trials
 Graded Dose-Response
Pharmacodynamics Relationship

Increasing the
 describes a drug effect drug dose
produces no
which increases in additional
proportion to therapeutic
increasing drug dose response

 Graded dose-
response graphs plot
the most desirable
the response to a drug few target range of doses for
against its cells have pharmacotherapeutics
concentration been affected
by the drug
Pharmacodynamics Potency and Efficacy

 more potent drug will produce a therapeutic effect at a lower

dose, compared with another drug in the same class
Pharmacodynamics Potency and Efficacy

 the magnitude of maximal response that can be produced from a

particular drug
Pharmacodynamics Potency and Efficacy

 From a pharmacotherapeutic perspective, efficacy is almost

always more important than potency
 Patient with cancer is much more concerned about how many
cancer cells have been killed (efficacy) than what dose the nurse
administered (potency)
Pharmacodynamics Kerja Obat

 Mengganti zat kimia yang hilang

 Meningkatkan atau menstimulasi aktivitas seluler tertentu
 Menekan atau menghambat aktivitas seluler
 Mengganggu fungsi sel asing, seperti mikroorganisme atau
neoplasma
Pharmacodynamics Receptors

 cellular macromolecule to which a medication binds in order to

initiate its effects
 normal function  to bind endogenous molecules (hormones,
neurotransmitters, and growth factors)
 a drug receptor can be any type of macromolecule
 the vast majority  proteins
 some receptors are intracellular molecules (DNA or enzymes)
in the cytoplasm
Pharmacodynamics Receptors
Pharmacodynamics Receptor Sites

 specific areas on cell membranes

 react with certain chemicals to cause an effect within the cell
 nearby enzymes break down the reacting chemicals and open
the receptor site for further stimulation
 Drug-receptor
Pharmacodynamics
interaction
 primary way drugs produce an action
Interaksi obat dengan reseptor
 Agonis  senyawa yg bila berinteraksi dg reseptor
menimbulkan efek
 Antagonis  Senyawa yg bila berinteraksi dg reseptor
tidak menimbulkan efek
Interaksi obat dengan reseptor
Interaksi obat dengan reseptor

insulin reacts with specific insulin-receptor sites to change cell

membrane permeability, thus promoting the movement of
glucose into the cell
Interaksi obat dengan reseptor

Curare (a drug used on the tips of spears by inhabitants of the Amazon

basin to paralyze prey and cause death) occupies receptor sites for
acetylcholine, which is necessary for muscle contraction and movement.
Curare prevents muscle stimulation, causing paralysis

Curare is a competitive antagonist of acetylcholine

Interaksi obat dengan reseptor
Interaksi obat dengan reseptor
Pharmacodynamics

 some drugs act independently of cellular receptors

 associated with other mechanisms  non-specific cellular
response
 changing the permeability of cellular membranes,
 depressing membrane excitability, or
 altering the activity of cellular pump
 e.g., Ethyl alcohol, general anesthetics, and osmotic diuretics
 Drug-enzyme
Pharmacodynamics
interaction

 Obat juga dapat mempengaruhi sistem enzim yang

bertindak sebagai katalis berbagai reaksi kimia
 Acetazolamide (Diamox), a diuretic that blocks the
enzyme carbonic anhydrase  alterations in the
hydrogen ion and water exchange system in the
kidney, as well as in the eye
Drug Effects

 Tidak ada obat yang mempunyai efek tunggal

(therapeutic effects dan adverse effects/reaction)

 Adverse drug effects

 Adverse drug reaction
Drug Effects

 The definition of an adverse drug reaction (ADR) is often

confused with that of an adverse drug event (ADE)
 ADE  “any untoward medical occurrence that may present
during treatment with a pharmaceutical product but which
does not necessarily have a causal relationship with this
treatment” (WHO 2005)
 ADR  an unwanted, undesirable effect of a medication that
occurs during usual clinical use
 ADR occur despite appropriate prescribing and dosing
 ADR occur almost daily in health care institutions and can
adversely affect a patient’s quality of life, often causing
considerable morbidity and mortality
ADVERSE DRUG EFFECTS

TOXIC EFFECTS

Increased sensitivity of
the respiratory center to morphine
is found in patients with chronic
lung disease, in neonates, or during
concurrent exposure to other
respiratory depressant agents

LACKING ORGAN SELECTIVITY /

RECEPTOR SPECIFITY
ADVERSE DRUG EFFECTS

CONGENITAL EFFECTS
Drug Effects

Kerusakan Jaringan dan Organ Akibat Obat

 Reaksi dermatologis  ruam sampai dermatitis eksfoliatif
 Stomatitis  inflamasi membran mukosa (karena reaksi toksik
langsung atau akumulasi obat pada ujung kapiler membran
mukosa)
 Superinfeksi  infeksi yang disebabkan organisme yang
biasanya terkendali
 Diskrasia darah  supresi sumsum tulang yang disebabkan
efek obat, terjadi jika konsumsi obat yg menimbulkan
kematian sel (misal: antineoplastic, antibiotik)
Drug Effects

Kerusakan Jaringan dan Organ Akibat Obat

 Toksisitas
 Cedera hati (metabolisme obat di hepar  metabolit yang bersifat
toksik mempengaruhi integritas hepar)
 Cedera ginjal  beberapa molekul obat dapat menyumbat jaringan
kapiler  inflamasi akut  kerusakan ginjal
 Keracunan  dosis obat berlebih
 Perubahan metabolisme glukosa
 Hipoglikemia
 Hiperglikemia  stimulasi pemecahan glikogen  kadar glukosa darah
meningkat (contoh: Efedrin)
Drug Effects

Kerusakan Jaringan dan Organ Akibat Obat

 Ketidakseimbangan elektrolit
 Hipokalemia  obat yang mengubah sistem pertukaran kalium dan air
pada ginjal
 Hiperkalemia  retensi kalium, obat yg dapat kematian atau cedera sel
 pelepasan kalium oleh sel
 Efek sensorik
 Toksisitas okuler  beberapa obat terkumpul pada arteri2 kecil 
inflamasi dan kerusakan jaringan (kloroquin: rheumatoid)
 Kerusakan auditorius  iritasi atau kerusakan pembuluh darah kecil
dan saraf kranial VIII (Aspirin  telinga berdenging dan kerusakan saraf
kranial VIII)
Drug Effects

Kerusakan Jaringan dan Organ Akibat Obat

 Efek neurologis
 Efek pada SSP secara umum  mempengaruhi fungsi neurologis secara
langsung atau mengubah kadar elektrolit atau glukosa (beta blockers)
 Efek kolinergik  menyerupai efek sistem saraf parasimpatis (obat flu,
antihistamin)
 Sindrom seperti Parkinson’s Disease  mempengaruhi kadar
dopamine (antipsikotik)
 Teratogenisitas  obat yang mencapai janin atau embrio yang
berkembang dapat menyebabkan kematian atau defek
kongenital
Drug Interaction
Interaksi Obat

Tipe Interaksi Obat

1. Drug-Drug Pharmacokinetics
2. Drug-Drug Pharmacodynamics
3. Drug-Food/Nutrient
4. Drug-Disease
Interaksi obat-penyakit

 drugs that are helpful in one disease are harmful in another

disorder
 For example, some beta-blockers taken for heart disease or
high blood pressure can worsen asthma and make it hard for
people with diabetes to tell when their blood sugar is too low
 Diabetes, high or low blood pressure, an ulcer, glaucoma, an
enlarged prostate, poor bladder control, and insomnia 
more likely to have a drug-disease interaction
 common among older people
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