NMT 04209 - Basic Pharmacology-1

SESSION 1: INTRODUCTION TO PHARMACOLOGY
Total Session Time:120 minutes

Prerequisites: None
Learning Tasks
At the end of this session a learner is expected to be able to:
Define terms related to pharmacology
Identify the different sources of medicine
Explain the forms of medicine preparations
Explain the factors affecting bioavailability of medicine
Resources Needed:
 Flip charts, marker pens, and masking tape
 Black/white board and chalk/whiteboard markers
 LCD Projector and computer
 Note Book and Pen
Session Overview Box
Step Time (min) Activity/ Content
Method
1 05 Presentation Presentation of session title and learning
tasks
2 35 Brainstorming
/presentation Definition of terms
3 10 Lecture discussion Different sources of medicine
4 30 Buzzing/Lecture Forms of medicine preparations

discussion
5 30 Lecture discussion Factors affecting bioavailability of medicine
6 05 Presentation Key Points

7 05 Presentation Session Evaluation
SESSION CONTENTS
STEP 1: Presentation of Session Title and Learning Tasks (05 minutes)
READ or ASK participants to read the learning objectives
ASK participants if they have any questions before continuing
STEP 2: Definition of Terms Related to Pharmacology (35 minutes)
Activity: Brainstorming (10 minutes)

ASK students to brainstorm on the definition of the following terms
 Pharmacology
 Pharmacokinetics
 Pharmacodynamics
 Medicine
 Dose
ALLOW time for them to respond
WRITE their answers on a flip chart/board.
CLARIFY and provide summary using the content below
 Pharmacology
o Is the study of drugs and its interaction in the living cell, it include its origin,
chemical structure, preparations, administration, action, metabolism and
excretion
 Pharmacokinetics
o Is the study of drug movement, it includes the way the body handle the drugs
from administration to elimination.
 Pharmacodynamics
o Is the study of mechanism of action of drugs and other biochemical and
physiological effects.
 Medicine
o Is a drug or other preparation for the treatment or prevention of disease.
 Dose
o Is a quantity of medicine prescribed to be taken at one time
 Dosage
o Is the prescribed administration of a specific amount, number, and frequency of
doses over a specific period of time
 Tolerance
o This is decreased responses to drugs even in increasing dosage
 Agonist
o Is a drug that interact with a receptor to stimulate a response
 Antagonist
o Is the drug that attach to the receptor but does not stimulate a response
 Minimum dose
o Is the smallest dose giving effects
 Maximum dose
o Is the highest dose which can be used without causing side effects
 Therapeutic dose
o Is the dose between maximum and minimum dose
 Hypersensitivity
o is abnormal sensitivity to an allergen, drug, or other agent, where the body
reacts with an exaggeratedimmune response
 Habituation
o Is a desire of continue to take a drug in increasing dose, there is psychological
and physical dependence with no withdraw symptoms if the drugs are stopped
 Prescription
o Is an instruction written by a medical practitioner that authorizes a patient to be
issued with a medicine or treatment
 Therapeutic index
o A ratio that compares the blood concentration at which a drug becomes toxic
and the concentration at which the drug is effective.
 Bioavailability
o Refers to the degree and rate at which an administered drug is absorbed by the
body's circulatory system
 First pass effect
o Is a phenomenon of drug metabolism whereby the concentration of a drug is
greatly reduced before it reaches the systemic circulation.
 Half life
o This is the period of time required for the concentration or amount of drug in the
body to be reduced by one-half (50%)
STEP 3: Different Sources of Medicine (10 minutes)
There are different sources of medicine and these include:
 Plants sources
o All parts of plants are used as drugs example steam wood roots grasses
o Example of plant sources drug are quinine opium digital
 Animal sources
o The drug are derived from animal bodies fluids glands etc.
o Example insulin, epinephrine
o Animal and plant sources as organic sources
 Mineral salts
o These are derived from mineral
o Example iron sulphate, folic acids
 Synthetic sources
o These are drugs synthesized in pharmaceuticals laboratories, they are artificial
madethis is the most important group of modern therapeutic agents
o Example magnesium sulphate, hydrogen peroxide, aluminum hydroxide
STEP 4: Forms of Medicine Preparation (30 minutes)

Activity: Buzzing (10 minutes)
ASK students to buzz on the forms of medicine preparation
Forms of medicine preparation includes:
 Solid forms/tablets
o These are dry – compressed powder which can be on test with small doses.
o Some are coated and some are not coated example
 Bacall tablets – like panadol, aspirin, septrine
 Enteric coated tablets – start to dissolve while in the stomach
 Lozenges – kept in the moth until it dissolves, they usually contain water
sugarand mucilage
 Capsule – powder which is coated in special easily digested covers
 Pills – a solid spherical body containing medical agent in a base
 Suppositories – conical shaped bodies, made of gelatin or cacao butter
containingdrug for introduction into the rectum
 Pessaries – similar to suppository but larger for introduction into the vagina
 Semi- solid forms
o Liniment – used for external application only
o Ointments – it is a greasy form/base which containing petroleum jelly
o Creams – the same as above
 Liquid forms
o Emulsions – a suspension of two invisible liquid for example oil and water
o Mixture – a liquid preparation consist of more than one drugs dissolved in water or
other fluids
o Syrup – a concentrated solution of sugar and water
 Gases
o They are taken through inhalations, they most of the time act on the respiratory
mucosa.
o Example oxygen
STEP 5: Factors Affecting Bioavailability of Medicine (30 minutes)
The factors affecting bioavailability of medicine includes:
 Absorption
o Most of the drugs are absorbed in the gastrointestinal tract, by the process of
diffusion to the bloodstream, few drugs are absorption by active transport
process
o The rate of absorption depends on physical properties of the drugs which include
how is it will pass the wall of the gut
o Absorption also depends on presence or absence of food in the stomach or
interaction with other drugs
 First pass effects
o Most drugs after absorption are carried by portal circulation to the liver, some
may be metabolized and hence only proportional of absorbed drug reaches the
circulation and therefore there bioavailability is reduced
o Drug like lignocain shows a very larger first pass and thus they are not
administered by ingestion method
 Hepatic first pass elimination
o Drugs absorbed from the GIT are transported by portal circulation to the liver
o As a result the drug may be taken up by the liver cells and metabolized
o Metabolites has no therapeutic effects to most drugs but some the metabolites
is theone with therapeutic effect
o The concentration of a drug in the blood stream is a good index of whether the
correctdose is being given to produce a satisfactory therapeutic effects
Factors that Influence Drug Blood Concentration

 Dose the higher the dose the higher concentration
 Route of administration I/V has rapid raises in blood concentration
 The distribution of the drug which enter the tissue has low blood concentration
 The rate of elimination the faster the body breaks down or excrete the drug the more
rapid the blood level falls
STEP 8: Key Points (05 minutes)

 Pharmacology is the study of drugs and its interaction in the living cell, it include its
origin, chemical structure, preparations, administration, action, metabolism and
excretion
 Pharmacokinetics is the study of drug movement, it includes the way the body handle
the drugs from administration to elimination
 Pharmacodynamics is the study of mechanism, action of drugs and other by biochemical
and physiological effects
 Sources of medicine includes; animal source, plant source, mineral source and synthetic
source
STEP 9: Session Evaluation (05 minutes)
 What are the different forms of medicine?
 What are the factors affecting bioavailability of medicine?
References
Champe, P. C. (2008). Lippincott's illustrated reviews: Pharmacology.
Clayton, B. D., & Willihnganz, M. (2013). Basic Pharmacology for Nurses16: Basic Pharmacology for
Nurses. Elsevier Health Sciences.
Katzung, B. G., Masters, S. B., & Trevor, A. J. (Eds.). (2004). Basic & clinical pharmacology (Vol. 8). New
York: Lange Medical Books/McGraw-Hill.
SESSION 2: PRINCIPLES OF MEDICINE ADMINISTRATION
DURING MEDICATION
Total Session Time:120minutes
Prerequisites: NMT 04101 Human Anatomy and Physiology
NMT 04102 Professionalism in Nursing
Learning Tasks
Describe the roles of a nurse in drugs administration
Describe the routes of medicine administration
Explain factors considered in medicine administration
Outline principles of medicine administration
Resources Needed:
Method
1 05 Presentation Presentation of session title and learning tasks
2 10 Brainstorming /presentation Roles of a nurse in drugs administration
3 50 Lecture discussion Routes of medicine administration
4 10 Lecture discussion Factors considered in medicine administration

5 20 Buzzing/Lecture discussion Principles of medicine administration
7 05
Presentation Session Evaluation
SESSION CONTENTS
READ or ASK participants to read the learning tasks
STEP 2: Roles of a Nurse in Drug /Medicine Administration (05 minutes)

ASK students to brainstorm on the roles of a nurse in drug/medicine administration
The roles includes
 To ensure safe and reliable administration and to monitor side effects.

 To help patients understand the purpose of their treatment and promote compliance
with taking medication.
 To ensure the correct administration of drugs, this includes pharmacology, anatomy,
physiology and legal issues.
 To take a reliable drug history from the patient and if necessary, from relative or friends
which include previous exposure to drugs, drugs being taken at the time and, in
particular any adverse effects resulting from their use
STEP 4: Routes of Medicine Administration (35 Minutes)

 A route of drug administration is the path by which a drug or other substance is brought
into contact with the body.
 The choice of which route of drug administration to be used depends on two factors which
are:
o Depending of the drug
 The existing preparations
o Depend on the state of the patient
 Emergency or the impossibility of intake to some routes
 When administering a drug, the nurse should ensure that the pharmaceutical preparation is
appropriate for the route specified
 The routes which are used for drug administration are as follows:
Enteral route
In this route drugs are administered into the gastrointestinal tract either by oral, sublingual or rectal.
 Oral route
o The mouth is used for administering drugs
Advantage of oral route administration
o Most convenient
o Usually least expensive- cheaper to manufacture Safe, does not break skin
barrier
o Administration usually does not cause stress
o The gastrointestinal tract provides a huge surface area for absorption.
o The drug can be taken home and does not need the attendance of a medical
professional
o No pain, easy to take.
o Cheap, no need to sterilize (but must be hygienic of course.)
Disadvantage of oral route administration

o Absorption can be variable and depends on the chemical nature of the drug, e.g.
its ionization, solubility and stability
o Absorption can also depend on the stomach contents. For example the
absorption of tetracycline antibiotics is inhibited in the presence of milk.
o Drugs may affect gastric emptying and this may affect absorption.
o Inappropriate for patient with nausea and vomiting
o Drug may have unpleasant taste and odor
o Inappropriate when gastrointestinal tract has reduced motility
o Inappropriate if patient cannot swallow or is unconscious (limited uses)
o Drug may discolor teeth, harm teeth enamel. Example hydrochloric acid.
o Drug may irritate gastric mucosa
o Some of the drug may be partially absorbed or destroyed by the gastric juices
example insulin
 Sublingual route
o The medication is placed under the tongue, and allowed to dissolve slowly
o Because of the reach blood supply in this region it results into rapid onset of the
action
o The patient is instructed not to move the drug with the tongue nor to eat or
drink anything until the medication has completely dissolved
Advantage of sublingual route administration
o Same as oral route plus
o Drug can be administered for the local effects
o More potent than oral because the drug directly enter the circulation and by
passes the liver
Disadvantage of sublingual route administration
o If swallowed drug may be inactivated by gastric juice
o Drug must remain under the tongue until dissolved and absorbed
o Drug is rapidly absorbed into the blood stream
 Buccal route
o The tablet or capsule is placed in the oral cavity between the gum and the cheek.
o The client is instructed not to manipulate the medication with the tongue;
otherwise, it could get displaced to the lingual area where it will be more rapidly
absorbed, or to the back of the throat, where it could be swallowed
Advantage of buccal route administration
o Same as sublingual route
Disadvantage of buccal route administration
o Dose absorbed is unpredictable
o If swallowed drug may be inactivated by gastric juice
o Drug must remain under the tongue until dissolved and absorbed
o Drug is rapidly absorbed into the blood stream
 Rectal Route
o This means the drugs passed through the rectum
o Rectal drugs are normally in suppository form, although a few laxatives and
diagnostic agent are given via enema.
Advantage of rectal route
o Favor the drugs which has objectionable taste or odor, or when it can be
changed by digestive enzymes
o Drug released at slow steady rate
o It avoids irritation of the upper gastrointestinal tract
o Is reasonable convenient and safe method of giving drugs when the oral method
is unsuitable, as when the patient is unconscious
o Venous blood from the rectum doesn’t pass to the liver thus no first pass effects
Disadvantage of rectal route
o Absorption is slower than other routes
o It is irregularly and uncompleted absorption
o Causes irritation to the rectum
o Inconvenience to administer
 Inhalation route
o Inhalation is the breathing of air vapour or volatile drugs into the lungs
o The gaseous drugs are inhaled and absorbed through epithelium of the alveoli of
the lungs
o Drug administered through this route may be for the local or systemic effects
o Examples of the drug given by inhalation for systemic effects are volatile
anesthetics agents such as ether, and halothane
Advantage of inhalation route
o Acts very quickly because the lungs have a larger surface area for absorption and
they are reach supplied with blood
o Drug act at the site of action .e.g. pulmonary diseases
o Introduces drug throughout respiratory tract
o Can be used to unconscious client
Disadvantage of inhalation route
o Poor regulation of dosage
o Inconvenience
o Drug intended for localized effect can have systemic effects
o Is used only for respiratory system
 Topical Route
o This means application of drug locally at an intended site such as skin, eye, ear or
nose
o Smoothing and softening the dry and rough areas of the skin
o To provide antiseptic or bacteriostatic effects in order to inhibit the growth and
multiplication of micro organism
o To provide a cleansing effects for the removal of dirt demis or infected tissue
Advantage of topical applications
o Provide a local effect
o Few side effects
Disadvantage of topical route
o Drug can enter body through abrasions and cause systemic effects
 Parenteral route
o The term parenteral “refer to method of drug administration other than oral and
topical
o It is commonly used to indicate the administration of drugs by “Injections”
o The common types of injections includes, intradermal, subcutaneous,
intramuscular and intravenous
o Drugs given parenterally must be sterile, readily soluble, absorbable, and non
irritating.
o Sterile aseptic technique must be used to avoid infection
o Accurate drug dosage, proper rate of injection and proper site of injection are
essential to avoid harm such as tissue injuries.
o An injected drug is irretrievable, and an error in dosage or method or site of
injection is not easy corrected.
o
 Intradermal
o Injection is made in the upper layer of the skin to the dermis

o The amount of drug given is small and absorption is slow
o Common method used for allergy testing
o The injections are best made with a fine, short needle (26 gauge) and a small
barrel syringe
Advantage of intradermal route of administration
o Absorption is slow (this is an advantage in testing for allergies).
Disadvantage of intradermal route
o Amount of drug administered must be small
 Subcutaneous route
o Small amount of drug in solution are given subcutaneously (hypodermically)
o The needle is inserted through the skin with quick movement, but the injection is
made slowly and steadily
o The piston of the syringe should be withdrawn slightly before injecting the drug
to make sure that a blood vessel has not been entered
o The angle of insertion should be 45 to 60 degrees and should be made on the
outer surface of the upper arm or on the anterior surface of the thigh
o Movement of the part after administration tends to increase the rate of
absorption
o Injected drugs are limited (0.5 – 2ml)
o Irritating drugs can results into formation of sterile abscesses and necrotic tissue
Advantage of subcutaneous route
o Onset of drug action is faster than oral route
Disadvantage of subcutaneous route
o Involve sterile technique
o More expensive than oral
o Only small volume of drug can be administered
o Some drugs can irritate tissue and cause pain.
 Intramuscular route
o Injections are made through the skin and subcutaneous tissue into the muscular
tissue
o Muscle tissue has a rich blood supply, medication moves quickly into blood
vessels to produce more rapid onset of action than oral
o The anatomical structure of the muscle permits this tissue to receive a larger
volume of medication. e.g. deltoid and biceps muscle should receive a maximum
of 3ml
o Injection site must be located away from bone, larger blood vessels, and nerves
o The size and length of the needle are determined by body size and muscle mass,
the type of the drug to be administered, the amount of adipose tissue overlying
the muscle, and the age of the client
o Muscles into which injection can usually be made conveniently are those of the
buttock, the lateral side of the thigh, and the deltoid region of the arm
o The gluteal muscles are usually thick and well suited to the injection of the larger
intramuscular doses
o The drugs may be in aqueous solution, aqueous suspension, or a solution or
suspension of oil
Advantage of intramuscular injection
o Pain from irritating drug is minimized
o Can administer larger volume than subcutaneous
o This injection is technically easier than IV.
o The gastrointestinal tract and first pass metabolism are avoided
Disadvantage intramuscular injections
o Break skin barrier
o Injections can be painful.
o Self-administration is difficult.
o Rarely, abscesses can form at the site of injection.
o The needle may puncture a small blood vessel and cause bruising of the skin.
 Intravenous injections(IV)
o In this route medications and fluids are administered directly into the blood
stream and immediately available for use by the body
o The IV route is used when a very rapid onset of action is desired
o It requires skill and sterile asepsis, and the drug must be highly soluble and
capable of withstanding sterillization
o IV route is of great value in emergencies
o The dose and amount of absorption can b determined with accuracy
o The injection is usually made into the median basilic or median cephalic vein at
the bend of the elbow; however any accessible vein can be used
o Factors that determine the choice of a vein are related to the thickness of the
skin over the vein, the closeness of the vein to the surface, and the presence of
firm support (bone) under the vein
o A vein that normally is distended with blood is much easier to enter than a
partially collapsed vein
Advantage of IV route
o A rapid onset of action is achieved
o The entire injected dose is almost instantly available, since it bypasses the
gastrointestinal tract and first pass metabolism
o A lower dose is administered than if the drug is given orally
o Administration is useful for drugs that are irritant when administered
intramuscularly
Disadvantage of IV routes
o Break skin barrier
o Limited to highly soluble drugs
o Drug distribution inhibited by poor circulations
o The drug has to be administered by trained person
o Inadvertent injection into an artery can cause arterial spasm with resulting tissue
damage
o Accidental overdose can have serious consequences
STEP 5: Factors Considered in Medicine Administration (15 minutes)

ASK students to buzz on the factors considered in medicine administration
 Pharmacodynamics: how the drug works in the body

 Interactions this are possible effects of other medication or food on the ordered
medication
 Allergies- patient history of hypersensitivity to drug or drug class
 Contraindications: medical conditions that preclude the use of the ordered drug
 Side effects: potential adverse reactions to the drug
 Toxic effects: dangerous effects that often occur due to buildup of drug in body or
impaired metabolism
 Tolerance: certain drugs require increasing doses over time to achieve the same effect
 Physiological variables: sex, age, size, and physical condition may alter how a drug is
processed in the body
 Diet: certain foods, liquids, or nutritional states may alter the drug's effect on the body
STEP 8: Principles of Medicine Administration (5 minutes)

The principles of drug administration includes the “Five Rights” of Drug Administration
Traditional Rights
 Right client: Nurse must do the following
o Verify client
o Check ID bracelet & room number
o Have client state his/her name
o Distinguish between two clients with same last names
 Right drug: Medication order may be prescribed by
o Physician
o Dentist
o Advanced Practice Registered Nurse (APRN)
 Right dose: A nurse must:

o Calculate and check drug dose accurately
o Check PDR, drug package insert or drug handbook for recommended range of
specific drugs
o Check heparin, insulin and IV digitalis doses with another nurse
 Right time: A nurse must :
o Administer drugs at specified times
o Administer drugs that are affected by foods, before meals
o Administer drugs that can irritate stomach, with food
o Drug administration may be adjusted to fit schedule of client’s lifestyle, activities
and diagnostic procedures
o Check expiration date
 Right route:A nurse must :
o Assess ability to swallow before giving oral meds
o Do not crush or mix meds in other substances before consultation with physician
or pharmacist
o Use aseptic technique when administering drugs
o Administer drug at appropriate sites
o Stay with client until oral drugs have been swallowed
Additional Rights
 Right assessment
o Get baseline data before drug administration
 Right Documentation
o Immediately record appropriate information
o Name, dose, route, time and date, nurse’s initial or signature
o Client’s response
o Narcotics
o Analgesics
o Antiemetic
o Sedatives
o Unexpected reactions to medications
o Use correct abbreviations and symbols
 Right to Education:Client teaching on the following:
o Therapeutic purpose
o side-effects
o Diet restrictions or requirements
o skill of administration
o laboratory monitoring
 Right Evaluation
o Client’s response to medications
o Effectiveness
o Extent of side-effects or any adverse reactions.
 Right to Refuse:Nurse must:
o Determine when possible reason for refusal.
o Facilitate patient compliance.
o Explain risk for refusing medications and reinforce the reason for medication.
o Refusal should be documented immediately.
o Head nurse or health care provider should be informed when omission pose
threat to patient

 The routes of administration includes Enteral (Oral, Sublingual and Bucal), Parenteral
(Intravenous, Intrademal and Intramuscular), Topical and Inhalation
 A nurse should take a reliable drug history from the patient and if necessary, from
relative or friends which include previous exposure to drugs, drugs being taken at the
time and, in particular any adverse effects resulting from their use
 If the patient refuse to take the prescribed medicine it should be documented
immediately.
 Head nurse or health care provider should be informed when omission of the dose pose
threat to patient

 What are the principles of drug/medicine administration?
 What are the roles of a nurse during drug administration?
References
Rang, H. P. (1995). Pharmacology (3rd ed.). London: Churchill Livingstone.

Rang, H., & Dale, M. (2007). Pharmacology (6th ed.). Edinburgh: Livingstone Churchill
SESSION 3: DRUG PRESCRIPTION AND DOSAGE
CALCULATION
Total Session Time:60 minutes
Prerequisites: None
Learning Tasks
Define drug prescription and dose calculation
Identify the components of a drug prescription
Calculation of a drug/medicine dosage
Resources Needed:
Method
1 05 Presentation
Presentation of session title and learning tasks
2 05 Brainstorming
/presentation Definition of prescription and dose calculation
3 10 Lecture discussion Components of a drug prescription
4 30 Lecture discussion Calculation of a drug dosage
5 05
Presentation Key Points
6 05
SESSION CONTENTS
STEP 2: Definition of Drug Prescription and Dosage Calculation (05Minutes)

ASK students to brainstorm on anaesthetics
Drug prescription (drug order)

 Is an instruction written by a medical practitioner that authorizes a patient to be issued
with a medicine or treatment
Drug dosage calculation
 This is a method for calculating medication (drug dosages)
o The drug quantities of medicines are not always indicated on the prescription
STEP 3: Components of Drug Prescription (10 Minutes)

Components of a Drug Order (Prescription)
 Date & time the order is written
 Drug name (generic preferred)
 Drug dosage
 Frequency and duration of administration
 Any special instructions for withholding or adjusting dosage
 Physician or other health care provider’s signature or name
 Signature of licensed practitioner
Nurse must check the following in a prescription before dispensing medicine

 Check medication order is complete & legible
 know general purpose or action, dosage & route of drug
 Compare drug card with drug label three times
o At time of contact with drug bottle/ container
o Before pouring drug
o After pouring drug
Table 3.1: Abbreviations used in a prescription

English Latin abbreviation
Once daily o.d. or q.d.
Twice daily b.i.d
Three times daily t.d.s./t.i.d
Four times daily q.i.d
Night time Nocte
Orally p.o
Intramuscular i.m
Intravenous i.v
Subcutaneous s.c.
Rectally p.r
Before food a.c
After food p.c.
As required p.r.n.
STEP 4: Calculation of Drug Dosage (30 Minutes)

 It is the responsibility of the dispenser to calculate the required amount of the drug to
be dispensed
 The quantities are expressed in various ways and it often depends on the type of drug
that has been prescribed
 The quantities are expressed in various ways and it often depends on the type of drug
that has been prescribed including:
o As weight (e.g. 50mg, 5g) or volume (e.g. 5ml, 50ml or 300ml)
o As number of units of the dosage form (e.g. 40tablets or 20capsules)
o As number of original packs from the manufacturer e.g. 2 boxes
o Other drugs are being packed in unit packs which contain a full course of
treatment (e.g.for 1 week or 4 weeks, such as ARVs).
o The quantity of a drug to be calculated is often based on the duration of
treatment and daily dosage
 Duration of the treatment may be indicated:
o 5/7 = for 5 days (out of 7 days in a week)
o 2/52 = for 2 weeks (out of 52 weeks in a year = 14 days)
o 1/12 = for 1 month (out of 12 month in a year)
Tablet and capsule calculation

 To calculate the number of tablets or capsules or amount to be taken at each dose by
applying the following formula
 Desired dose (amount) = ordered Dose amount/amount on Hand x Quantity(D/H x Q =
x)
o D-dose ordered
o H- amount on hand
o Q- quantity
o X-desired dose(amount)
 To calculate how much of the drug should be supplied the following guide is useful:
o Number of tablets or capsules to be taken at each dose x Number of dose per
day x number of days to be taken = total number of tablets /capsules to be
supplied
o Ensure all measurements are in the same system of the measurement and the
same size unit measurement.
o If not convert before proceeding.
 Example 1: A prescription reads: Paracetamol tablets 1000mg t.i.d daily for 5/7
o Calculate the desired dose /amount of dose to give to a patient
o Calculate the total amount to be dispensed to the patient
 Paracetamol tablets 500mg are available in your in the pharmacy
 Solution
o Formula D/H x Q = x
o D=1000mg H=500mg Q=1 tablet or capsule
o 1000/500 x 1=2 tablets
o There for 2 tablets should be given t.i.d
o Total amount to be dispensed to the patient= Number of tablets or capsules to
be taken at each dose x Number of dose per day x number of days to be taken
 Number of tablets or capsules to be taken at each dose=2 tablets
 Number of dose per day=3
 Number of days to be taken=5
 Therefore 2x3x5=30 tablets should be dispensed
For liquid calculation
 Same formula Desired dose (amount) = ordered Dose amount/amount on Hand x
Quantity(D/H x Q = x)
o D-dose ordered
o H- amount on hand
o Q- quantity
X-desired dose (amount
 But here the volume is calculated
 A provider requests lorazepam 4 Mg IV Push for a patient in severe alcohol withdrawal.
The clinician has 2 mg/mL vials on hand. How many milliliters should he or she draw up
in a syringe to deliver the desired dose?
 Solution
o D/H x Q = x, or Desired dose (amount) = ordered Dose amount/amount on Hand
x Quantity
 Dose ordered=4mg
 Amount on hand=2mg
 Quantity=1 ml
o 4/2x1ml=2
 Units of measurement must match, for example, milliliters and milliliters, or one need to
convert to like units of measurement. In the example, above, the ordered dose was in
milligrams, and the have dose was in milligrams, both which cancel out leaving milliliters
(answer called for milliliters), so no further conversion is required

 Drug prescription (drug order)is an instruction written by a medical practitioner that
authorizes a patient to be issued with a medicine or treatment
 Drug dosage calculation is a method for calculating medication (drug dosages)
 It is the responsibility of the dispenser to calculate the required amount of the drug to
be dispensed
 The quantity of drug dosage is expressed in various ways and it often depends on the
type of drug that has been prescribed.

 What is the components of a drug prescription
 What does b.i.d mean?
References

SESSION 4: ANALGESICS AND STEROIDS
Total Session Time: 120 minutes
Prerequisites: None
Learning Tasks
Define of analgesics
List commonly used analgesics
Describe the indication ,mechanism of action and side effects of non-opioid
analgesics (non-steroidal anti-inflammatory drugs)
Describe the indication ,mechanism of action and side effects of opioid
analgesics
List commonly used steroids
Describe the indications, mechanism of action and side effects of steroids
Resources Needed:

Step Time Activity/ Content
(min) Method
2 05 Brainstorming /presentation
Definition of analgesics
3 10 Lecture discussion Commonly used analgesics
4 30 Lecture discussion Indication ,mechanism of action and side
effects of non opiod analgesics (non-steroidal
anti-inflammatory drugs)
5 30 Lecture discussion Indication ,mechanism of action and side effects
of opioids analgesics
6 10 Buzzing/Lecture discussion Commonly used steroids
7 20 Lecture discussion Indication ,mechanism of action and side effects
of steroids
8 05
9 05
SESSION CONTENTS
STEP 2: Definition of Analgesics (05 minutes)

ASK students to brainstorm on the definition of analgesics
Analgesics
 Are drugs that relieve pain due to multiple causes
o Analgesic drugs act in various ways on the peripheral and central nervous
systems
STEP 3: Commonly Used Analgesics (10Minutes)

 Narcotic (opioids) which act in the central nervous system and cause drowsiness,i.e
o Pethidine
o Morphine
o Fentanyl
o Codaine
 Non-narcotic non opioids which act chiefly peripherally
o The commonly used non opioid antipyretics agents are the Non-steroidal Anti-
inflammatory Drugs/medicines (NSAID) which have both antipyretic and anti-
inflammatory effect including:
 Aspirin(acetylsalicylic acid, ASA)
 Paracetamol (Acetaminophen)
 Indomethacin
 Diclofenac
 Ibuprofen
STEP 4: Indications, Mechanism of Action and Side Effects of Non Opioid analgesics [Non-
steroidal Anti-Inflammatory Drugs (NSAIDs)] (30 minutes)
Mechanism of actions of NSAIDs
 The mechanism of action of traditional NSAIDs involves blockade of the production of
prostaglandins
 This is by inhibition of the enzyme cyclooxygenase (COX) at the site of injury in the
periphery, thus decreasing the formation of mediators of pain in the peripheral nervous
system
Pharmacological effects of NSAIDs

 Has analgesia effects
o They reduce certain types of pain.
 Has anti-inflammatory effects:
o The drugs modify the inflammatory reactions.
 Antipyretic effect
o The drugs can lower raised body temperature
All these effects are related to their ability to inhibit the action of cyclooxygenase on
arachidonic acid.
Indications, mechanism of action and side effects of specific NSAIDS
Aspirin (Acetylsalicylic Acid)

 It is indicated for mild to moderate pain, pyrexia, rheumatoid arthritis and is also used
to reduce the risk of myocardial infarction and deep venous thrombosis
 To be given with cautions for a patient with
o Asthma; as it may induce bronchospasm
o Allergic disease
o Hepatic impairment or renal impairment
 Contra-indications
o It is not advised to give aspirin-containing preparations to children under 16
years and breast-feeding mothers unless specifically indicated (as it may
precipitate to Reye's syndrome)
o Asthma
o Peptic ulceration or gastritis and bleeding disorders like haemophilia
 Interaction
o NSAIDs cause salt retention and therefore reduce potency of diuretics
 Dose
o By mouth: 300–900 mg every 6 hours, when necessary
o Maximum dose is 4g daily
Side effects
o Acute renal insufficiency in susceptible patients but reversible on stopping the
drug.
o Chronic use of NSAIDs can cause “ analgesic nephropathy”:- chronic nephritis
and renal papillary necrosis
o Salicylism:
 Occurs after repeated ingestion of large doses:- tinnitus, vertigo ,
decreased hearing, nausea and vomiting
o Reyes’ syndrome – occurs in children
o Large doses alter the acid-base balance and the electrolyte balance
o Hyperpyrexia due to increased metabolic rate
o It is a combination of liver disorder and encephalopathy that can follow an acute
viral illness (mortality 20-40%).
o Generally mild and infrequent but high incidence of gastro-intestinal irritation
with slight asymptomatic blood loss
o Increased bleeding time, bronchospasm and skin reactions in hypersensitive
patients
Paracetamol (Acetaminophen)
 Is one of the most commonly used non-narcotic analgesic-antipyretic agents
 It has relatively weak anti-inflammatory activity
 Dose
o (500mg)by mouth: 0.5–1 g every 6 hours to a maximum 4g daily
 Children 2 months 60 mg for post immunization pyrexia, repeated once after 6 hours if
necessary
 Side effects
o Allergic skin reactions sometimes occur
o Regular intake of large doses over long periods may increase the risk of kidney
damage
Ibuprofen
 It has propionic derivates and is a therapeutically significant anti-inflammatory
 The drug is used also in rheumatoid arthritis (including juvenile arthritis) and post
operative analgesia
 Dosage:
o 400mg after every 8 hours and should be taken with food to avoid gastric
irritation
 Side effects
o Acute renal insufficiency in susceptible patients but reversible on stopping the
drug
Indomethacin
 Indicated in moderate pain and rheumatoid disease and dysmenorrhea
 Not recommended in children
 Dosage:
o 50mg every 8 hours with food
 Side effects
o Skin rashes
o Kidney problems
o Stomach or intestinal bleeding
Diclofenac
 Used in the relief of pain and suppression of inflammation in rheumatic disease, other
musculoskeletal disorders, acute gout, and postoperative pain
 Dosage:
o 50mg every 8 hours after meals.
o Formulations for deep intramuscular injections into the gluteal muscles are also
available.
STEP 5: Indications, Mode of Action and Side Effects of Opioid Analgesics (Narcotics)
(30Minutes)
Mechanism of action of opioid
 The central nervous system contain a series of receptors that controls pain .known as
opiates receptors
 The opioids work by mimicking the endogenous (meaning produced by the human
body) endorphins by stimulating opioid receptors in the central and peripheral nervous
systems which results in relief of pain
 The opioid receptors are subdivided into four types,mu (µ), delta (δ),kappa (κ) and
epsilon (ε)
Morphine
 It controls somatic pain following trauma or surgery.
 Morphine is given through I/V, followed by an anti-emetic to alleviate severe visceral pain.
 Morphine is also extremely valuable in the treatment of shock for relieving pain if present and for
calming the patient
 Dose:
o Given at a dose of 10-20mg by month or by subcutaneous, I/M or I/V injection, if necessary
the dose is repeated after 4 hours.
 Morphine is the opioid of choice for the oral treatment of severe pain in palliative care
 Side effects
o Decreased respiratory effort and low blood pressure
o Nausea and vomiting
o Constipation
o Morphine is addictive and prone to abuse
o If the dose is reduced after long-term use, opioid withdrawal symptoms may occur
including
 Agitation
 Anxiety
 Muscle pains
 Increased tearing
 Trouble sleeping
Pethidine
 Is a synthetic narcotic analgesic
 Commonly used for postoperative pain relief.
 Given at a dose of 50-100mg I/M or by slow I/V injection; if necessary the dose is
repeated after every 4-6 hours in severe pain (A dose of 150mg may be required).
 It is also particularly useful in the reduction of severity of labour pain without reducing
the force of contraction of the uterus.
 Dependence is likely to occur if taken without caution.
 Side effects
o Respiratory depression
o Hypotension
 Pethidine cause more severe hypotension than morphine
o Nausea
STEP 6: List of Commonly Used Steroids with Anti-inflammatory effects (10Minutes)

ASK students to buzz on the list of common used steroids
 These are mostly referred as corticosteroids

o Corticosteroids are man-made drugs that closely resemble cortisol, a hormone
that your adrenal glands produce naturally
 Corticosteroids are divided into two groups
o Glucocorticoid( Which are anti-inflammatory and ant-allergy)
 Hydrocortisone
 Prednisolone
o Mineralcorticoids
 Which are for maintaining fluids and electrolyte like aldosterone
STEP 7: Indications, Mode of Action and Side Effects of Steroids(Corticosteroids)

(20Minutes)
Mechanism of action of glucocorticoids
 Glucocorticoids affect cells by binding to the glucocorticoid receptor.
 The activated glucocorticoid receptor-glucocorticoid complex up-regulates the
expression of anti-inflammatory proteins in the nucleus (a process known
as transactivation)
 And represses the expression of proinflammatory proteins in the cytosol by preventing
the translocation of other transcription factors from the cytosol into the nucleus
(transrepression)
Hydrocortisone
 These reduce the inflammatory component in chronic asthma and are life-saving in
status asthmaticus (acute severe asthma)
 They do not prevent the immediate response to allergen or other challenges
 The mechanism of action involves decreased formation of mediators like cytokines and
other inflammatory cells
 They are given by inhalation (e.g. beclometasone), or intravenous hydrocortisone
 Side effects
o sleep problems (insomnia), mood changes
o acne, dry skin, thinning skin, bruising or discoloration
o slow wound healing
o increased sweating
o headache, dizziness, spinning sensation
o nausea, stomach pain, bloating
Prednisolone
 Indicated for suppression of inflammatory and allergic disorders
 Dose:
o 10-20mg orally daily up to 60mg daily. Acute asthma, 30-40mg daily for few days
gradually reduced when asthma has been reduced
 Precaution, avoid rapid withdraw
 Common side effects includes
o Acne.
o Dry or thinning skin.
o Bruising or discoloration of the skin.
o Mild nausea or stomach pain.
o Bloating.
o Sleep problems.
o Mild mood changes.
o Increased sweating

 Analgesics are drugs that relieve pain due to multiple causes
o Analgesic drugs act in various ways on the peripheral and central nervous
systems
 Analgesics are of two types narcotics (opioids) and Non narcotics(Non opioids )
 Steroids that are responsible for anti-inflammatory effects are the glucocorticoids

 What is the most common used glucocorticoids?
 What is the mode of action of NSAIDs?
References
SESSION 05: ANAESTHETICS
Learning Tasks
Define of anaesthetics
List commonly used anaesthetics
Describe the indication ,mechanism of action and side effects of local
anaesthetics
Describe the indication ,mechanism of action and side effects of general
anaesthetics
Resources Needed:
Method
1 05 Presentation
2 05 Brainstorming
/presentation Definition of anaesthetics
3 05 Lecture discussion Commonly used anaesthetics
4 15 Lecture discussion Indication ,mechanism of action and side effects of

local anaesthetics
5 20 Lecture discussion Indication ,mechanism of action and side effects of
general anaesthetics
SESSION CONTENTS
STEP 2: Definition of Anaesthetics (05 Minutes)

ASK students to brainstorm on anaesthetics
 These are agents that produce anaesthesia

o Anaesthesia is a state of controlled, temporary loss of sensation or awareness
that is induced for medical purposes.
o It may include analgesia, paralysis, amnesia, or unconsciousness. These are
group of opiods that affect the central nerve system.
STEP 3: Common Anaesthetics Used (05 Minutes)

 General anaesthetics
o Ether
o Halothane
o Nitrous oxide
o Ketamine
o Thiopental
 Local anaesthetics
o Esthers like procaine and cocaine
o Amides like lignocaine and prilocaine
STEP 4: Indications, Mechanism of Action and Side Effects of Local Anaesthetics (15
minutes)
Local anaesthetic
 Is a medication that causes absence of pain sensation.
 When it is used on specific nerve pathways, paralysis also can be achieved
 The local anaesthetics can be either ester (the aromatic part is linked by an ester bond
to a basic side chain) or amide (the aromatic part is linked by an amide bond)
Mode of action
 Local anaesthetic produces a localized reversible block to nerve conduction by reducing
the permeability of the membrane to sodium.
 Most useful local anaesthetics physically plug the transmembrane pore.
 Local anaesthetics block conduction in small – diameter nerve fibres more readily than
in larger fibres.
 Pain sensation is blocked more readily than other sensory modalities
Commonly used local anaesthetics includes:
 Lignocaine
o A widely used in injection for local application to mucous membranes effective in
concentration of 1%.
o Indication of lignocaine
 It is used to produces a local effect like loss of pain and other sensations,
vasodilatation and loss of motor power.
o It can be administered parenteral or topical
 Adverse effects is due to over dosing and includes
o Anxiety and excitement
o Which then progress to :
 Sedation
 Disorientation
 Angular and circumoral anaesthesia
 Restlessness
 Twitching
 Tremors
 Convulsions and unconsciousness.
 Coma may be accompanied by apnoea and cardiovascular collapse.
STEP 5: Indications, Mode of Action and Side Effects of General Anaesthetics (20 Minutes)
General anaesthetics
 These are the compounds which induces unconsciousness
 General anaesthetics can be administered through
o Intravenous
o Inhalational
o And intramuscular
Mode of action of general anaesthetics
 General anaesthetics act on the brain primarily on the mid brain reticular activity system
and the cortex.
 A principal site of action (of both general and local anaesthetics) seems to be along the
neuronal lipid bilayer membrane, which is altered by the drugs so that exchanges of Na+
and K+ is inhibited hence prevent transmission of nerve impulses
Commonly used general anaesthetics

Halothane
 The most widely used agent.

 Administered by inhalation
 It is potent, non explosive,non irritant, hypotensive, and has a sweet odour
 Depresses both cerebral function and sympathetic activity
 The recovery time is rapid with very minimal incidences of post operative nausea and
vomiting
 It is about 30% metabolised
 Hangover is likely due to high lipid solubility
 It has slow induction and recovery due to its high solubility in blood
 Risk of liver damage if used repeatedly
 Can be used during intrauterine manipulation.
Adverse Effects
 Halothane induces cardiac dysarrythmia
 Hepatic damage occurs in a small proportion of exposed patients, in some cases short
lived jaundice
 Halothane is contraindicated in a history of jaundice caused by repeated exposure to
halothane
Ether (Diethyl Ether)

 A colourless highly volatile and flammable liquid that depresses the cerebral activity
 A reliable potent anaesthetic, useful when elaborate apparatus is not available
 Induction is slow; it follows the classical stages of anaesthesia because it is highly
soluble in body tissues
 Premedication with atropine is necessary to reduce excessive bronchial and salivary
excretion.
Adverse Effects
 Laryngeal spasm often occurs during induction
 Severe nausea and vomiting may occur postoperatively
 Dependence may occur in some individuals after repeated exposure
 Ether is contraindicated in severe liver disease and in raised cerebrospinal fluid pressure
 Ether potentiates the action of non-depolarising neuromuscular blocking agents and
causes depression of myocardium in patients on beta adrenoceptor blocking agents like
Propranolol
Nitrous Oxide
 A colourless gas with a slightly sweet odour
 Depresses cerebral activity, producing light anaesthesia without depressing respiration
 Nitrous oxide is very useful in minor operations such as dental extractions
 Its major disadvantage when compared to Ethers and Halothane is that it is very
expensive
 Nausea and vomiting may occur and prolonged use may cause bone marrow depression

 Anaesthetics are agents that produce anaesthesia
 Anaesthesia is a state of controlled, temporary loss of sensation or awareness that is
induced for medical purposes: It may include analgesia, paralysis, amnesia, or
unconsciousness
 Anaesthetics can be either general or local anaesthetics

 What is the most common used general anaesthetics?
 What is the mode of action of local anaesthetics?
References
SESSION 6: COMMON ANTIBACTERIAL AND ANTIFUNGAL
Prerequisites: NMT 04101 Infection Prevention and Control
NMT 04103 Human Anatomy and Physiology
Learning Tasks
Define antibacterial and antifungal
Identify common antibacterial and antifungal
Explain mechanism of action of common antibacterial and antifungal
Explain side effects of common antibacterial and antifungal
Resources Needed:

Method
objectives
2 05 Brainstorming Definition of antibacterial
Presentation
3 50 Presentation Commonly used antibacterial
4 05 Brainstorming Definition of antifungals

Presentation
5 45 Presentation Commonly used antifungals

SESSION CONTENTS
STEP 2: Definition of Antibacterial (05 minutes)

ASK students to brainstorm on the definition of antibacterial
CLARIFY and provide summary using the content below:
Antibacterial
Antibacterial also called antibiotics are a drug that either destroys bacteria or suppresses their growth or
their ability to reproduce.
STEP 3: Commonly Used Antibacterial Drugs (50 minutes)

 Antibiotics which kill bacteria are known as bactericidal while antibiotics which inhibit
bacteria multiplications are known as bacteriostatic.
 Narrow spectrum antibiotics are antibiotics which has therapeutic effects in a narrow
range of bacteria example, antibiotics which kills only gram negative bacteria and not
otherwise.
 Broad spectrum antibiotics are antibiotics which has therapeutic effect against wide
range of bacteria i.e. gram negative as well as gram positive bacteria.
Common antibacterial drugs

 Most commonly used types of antibiotics are: Penicillins, Cephalosporin,
Aminoglycosides, Fluoroquinolones, Macrolides, and Tetracyclines.
 While each class is composed of multiple drugs, each drug is unique in some way.
Penicillins
 The penicillins share features of chemistry, mechanism of action, pharmacology, and
immunologic characteristics with cephalosporins, monobactams, carbapenems, and β-
lactamase inhibitors.
 All are β-lactam compounds, so named because of their four-membered lactam ring.
 They are divided into four groups which includes:
o Long acting penicillins e.g. Procaine Benzyl-penicillin (Crystalline penicillin =
crystapen), Fortified Procaine Penicillin (Procaine benzyl penicillin = PPF)
o Acid-resistant penicillins e.g. Phenoxy-methyl penicillin (Penicillin V)
o Penicillin resistance penicillase e.g. Cloxacillin (Orbenin)
o Broad spectrum penicillins e.g. Ampicillin (Penbritin), Cloxacillin
Mechanism of action
 Penicillins, like all β-lactam antibiotics, inhibit bacterial growth by interfering with the
transpeptidation reaction of bacterial cell wall synthesis.
 The cell wall is a rigid outer layer unique to bacterial species. It completely surrounds
the cytoplasmic membrane, maintains cell shape and integrity, and prevents cell lysis
from high osmotic pressure.
 The cell wall is composed of a complex, cross-linked polymer of polysaccharides and
polypeptides, peptidoglycan (also known as murein or mucopeptide).
 Penicillin binding protein (PBP, an enzyme) removes the terminal alanine in the process
of forming a cross-link with a nearby peptide. Crosslinks give the cell wall its structural
rigidity.
 Beta-lactam antibiotics, covalently bind to the active site of PBPs and this inhibits the
transpeptidation reaction, halting peptidoglycan synthesis, and the cell dies.
 The exact mechanism of cell death is not completely understood, but autolysins and
disruption of cell wall morphogenesis are involved.
 Beta-lactam antibiotics kill bacterial cells only when they are actively growing and
synthesizing cell wall.
Side effects
 The penicillins are generally well tolerated, and unfortunately, this encourages their
misuse and inappropriate use.
 Allergic reactions which include anaphylactic shock; urticaria, fever, joint swelling,
intense pruritus; and a variety of skin rashes.
 Oral lesions, fever, interstitial nephritis (an autoimmune reaction to a penicillin-protein
complex), eosinophilia, hemolytic anemia and other hematologic disturbances, and
vasculitis may also occur.
 In patients with renal failure, penicillin in high doses can cause seizures.
 Nafcillin is associated with neutropenia; oxacillin can cause hepatitis; and methicillin
causes interstitial nephritis (and is no longer used for this reason).
 Large doses of penicillins given orally may lead to gastrointestinal upset, particularly
nausea, vomiting, and diarrhea.
 Ampicillin has been associated with pseudomembranous colitis.
Cephalosporins
 Cephalosporins are similar to penicillins, but more stable to many bacterial β lactamases
and therefore have a broader spectrum of activity.
 Cephalosporins are not active against enterococci and L monocytogenes.
 Although they are efficient antibiotics they are rarely the drug of choice as for many
infections there are cheaper effective substitute.
 They can be divided into three groups:
o 1stgeneration include cephalexin
 1stgeneration cephalosporins have good activity against gram +VE
organism and moderate activity against gram –VE, including Escherichia
coli, Klebsiela pneumonia, Proteus mirabilis
 They are given orally
o 2ndgeneration e.g. cefamandole

 2ndgeneration cephalosporins have increased activity against gram –VE
organisms
o 3rdgeneration e.g. ceftriaxone and celfdimir

 3rdgeneration cepahlosporins are less active against gram +VE organisms
but more active against the Enterobacteriaceae with some activity
against pseudomonas aeruginosa.
Mechanism of action
 Cephalosporins inhibit cell wall synthesis or activate enzymes that disrupt the cell wall,
causing cell lysis and cell death.
 May be bactericidal or bacteriostatic
 Most effective against rapid dividing cells
Side effects
 Local irritation can produce pain after intramuscular injection and thrombophlebitis
after intravenous injection.
 Renal toxicity, including interstitial nephritis and tubular necrosis
 Seizures in high dose
 Diarrhoea, nausea and vomiting, abdominal cramps
 Hypersensitivity reactions including rashes, urticaria
 May increase bleeding tendency, haemolytic anaemia
Aminoglycosides
 This is the group of antibiotics which interferers with protein synthesis in the bacteria
i.e. bactericidal i.e. kills bacteria.
 Have fairly wide antibacterial range (broad spectrum)
 Aminoglycosides are not absorbed in the GIT and are most given by injection except
kanamycin and neomycin
 Aminoglycosides include gentamycin, neomycin streptomycin and kanamycin
 They are most active against gram +ve and many gram –ve organisms
 The common side effect of this group is dose related therefore care must be taken with
dosage and whenever possible Rx should not exceed 7 days
 Aminoglycosides have a number of common properties:
o All are poorly/not absorbed in GIT therefore given by injection except kanamycin
and neomycin
o All are excreted by kidney and accumulate occurs due to impaired renal function
o They are all, to greater or lesser degree ototoxic or nephrotoxic
 Streptomycin is active against Mycobacterium tuberculosis and is reserved for
tuberculosis
Mechanism of Action
 They are transported across bacterial cell membrane, irreversibly binds to specific
receptor proteins of bacterial ribosomes.
 It therefore interfere with protein synthesis, preventing cell reproduction and eventually
causing cell death
Side effects
 May result into hypersensitivity reactions
 High parenteral dose lead to muscle paralysis
 Ototoxicity and nephrotoxicity in high doses
 May affect fluid and electrolyte balance by causing hypomagnesia
Macrolides
 This act primarily against Gram – positive microorganism and gram – ve cocci
 Marcolides are used in the Rx of pharyngitis/ tonsillitis sinusitis, chronic bronchitis
pneumonia, uncomplicated skin and skin structure infractions
 Absorbed well after oral administration and diffuse widely but doesn’t enter CSF
 It is bacteriostatic and act against a wide range of organisms including Streptococcus
pyogenes, Staphylococcus aureus, not effective against Haemophilus influenza a
common cause of respiratory infection
 Marcolides include erythromycin, azithromycin and clarithromycin
Mechanism of action
 Reversibly binds to the P site of the 50s ribosomal subunit of susceptible organisms,
inhibiting RNA dependent protein synthesis, it suppress protein synthesis
 Useful in individual with penicillins resistance as a substitute
Side effects
 Hypersensitivity reactions such as rashes
 Ototoxicity
 Nausea, vomiting, abdominal pain cramping, diarrhea, hepatitis
Tetracyclines
 Following the discovery of penicillins and streptomycin a larger – scale investigation was
carried out into substances that were produced by various fungi.
 Three important antibiotics which were discovered are known as tetracyclines
 They are similar in chemical structure and toxic effects
 The 3 tetracycline are chlortetracycline, oxytetracyclines and tetracyclines
 Usually given orally and are quite absorbed from the GIT and 6 hourly dosage is
satisfactory
 Tetracycline hydrochloride may be given IV, however it is very irritating to the vein
Mechanism of Action
 Inhibit bacterial protein synthesis
Side effects
 Benign intracranial hypertension, increase in children, and dizziness
 Vestibular reactions
 Diarrhea, vomiting, nausea, esophagitis, pancreatitis
 Photosensitivity rashes, pigmentation of skin and mucous membrane
Fluoroquinolones/quinolones
 This group of antibacterial drugs is increasing important, several are available already
and more will be produced probably in a few years coming
 Quinolones act against a wide range of gram –VE and gram +VE organisms
 They are used primarily in the Rx of lower respiratory infections, skin and skin structure
infections, UTIs and STI
 Common ones are ciprofloxacin and ofloxacin
Mechanism of action
 Inhibit DNA gyrase in susceptible micro-organisms, interfere with bacterial DNA
replications and repair.
 It cause death of susceptible bacteria, therefore it is bactericidal
Side effects
 Dizziness, drowsiness, headache, insomnia, acute psychosis agitation, confusion,
hallucination and increase intracranial pressure
 arrhythmiasis vasodilatation
 Abdominal pain, darrhoea, nausea, altered taste
 interstial cystitis vaginitis
 Photosynthesis
 Hyperglycemia
Sulphonamides
 This is one of the oldest group of antibacterial agent
 It’s importance has decreased due to increase bacterial resistance and replaced by
antibiotics which are more active
 They differ in range of organisms (bacteria, plasmodia, cancer cells etc) which they
attack but most of their pharmacological properties are similar
 All sulphonamide are well absorbed in the GIT, circulate widely in the body fluids and
crosses the meningeal barrier to enter cerebrospinal fluid (CSF)
 It circulates in the body partially bind to the plasma protein and partially in free state.
Only the free state has therapeutic effects
 After absorption the liver start to acetylated the sulphonamides.
 The acetylated together with unaltered sulphonamide are excreted in the urine
 The acetylated are poorly soluble, and therefore they precipitate in the urine unless an
adequate flow is maintained by taking a lot of water
 The common sulphonamide in use are:
trimethoprim/sulphamethoxazole(cotimoxazole/septrine/batrium), sulfadiazine,
sulphadimidine, trimethroprim, sulphacetamide, sulphasalazine
Mechanism of action
 It affects the cell by interfering with their use of Para – aminobenzoic acid, which is a
precursor of Folic acid which is essential for cell division
 Trimethoprim which is common combined with sulphonamide, interfere with folic acid
metabolism and thus inhibit build up cell nucleus and thus cell dies
 The combination of sulphonamide with trimethoprin is partially effective in preventing
bacterial cells division and bactericidal
 Sulphonamide are similar to PABA and are taken by bacteria, however can’t be used and
bacteria ceases to multiply
Side effects
 Hypersensitivity reactions such as itching and rash
 Diarrhoea, nausea, vomiting, and stomach upset
 Loss of appetite
 Changes in taste
 Headache
STEP 4: Definition of Antifungal (5 minutes)

ASK students to brainstorm on the definition of antifungal
Antifungal
These are drugs that limit or prevent the growth of yeasts and other fungal organisms.
 Fungal infections can be divided into two quite different conditions depending on the
location of the infection.
 The antifungal drugs presently available fall into the following categories:
o Systemic drugs (oral or parenteral) for systemic infections
o Oral systemic drugs for mucocutaneous infections
o Topical drugs for mucocutaneous infections
STEP 5: Commonly Used Antifungal Drugs (45 minutes)

 The antifungal drugs are subdivided into the following groups
o Drugs that act by altering cell membrane permeability
 Polyenes ( e.g. Amphotericin)
 Azoles: such as Imidazoles (e.g. Ketaconazole, miconazole, and
clotrimazole) and Triazoles (e.g. fluconazole and itraconazole).
 Allylamine: Terbinafine.
o Drugs that block dioxynucleic acid (DNA) synthesis e.g. Flucytosine
o Drugs that disrupt microtubule function and inhibit mitosis e.g. Griseofluvin
SYSTEMIC ANTIFUNGAL DRUGS FOR SYSTEMIC INFECTIONS

Amphotericin B
 Amphotericin B is an antifungal antibiotics produced by Streptomyces nodosus.
 Amphotericin B is poorly absorbed from the gastrointestinal tract.
 Oral amphotericin B is thus effective only on fungi within the lumen of the tract and
cannot be used for treatment of systemic disease.
Mechanism of action
 Amphotericin B is selective in its fungicidal effect because it exploits the difference in
lipid composition of fungal and mammalian cell membranes.
 Ergosterol, a cell membrane sterol, is found in the cell membrane of fungi, whereas the
predominant sterol of bacteria and human cells is cholesterol.
 Amphotericin B binds to ergosterol and alters the permeability of the cell by forming
amphotericin B-associated pores in the cell membrane.
Side effects
 Infusion-related reactions consist of fever, chills, muscle spasms, vomiting, headache,
and hypotension.
o They can be ameliorated by slowing the infusion rate or decreasing the daily
dose.
o Premedication with antipyretics, antihistamines, meperidine, or corticosteroids
can be helpful.
 Renal damage is the most significant toxic reaction.
 Seizures and a chemical arachnoiditis may develop, after intrathecal therapy with
amphotericin often with serious neurologic sequelae.
Azoles
 Azoles are synthetic compounds that can be classified as either imidazoles or triazoles.
 The imidazoles consist of ketoconazole, miconazole, and clotrimazole. The latter two
drugs are now used only in topical therapy.
 The triazoles include itraconazole, fluconazole, voriconazole, and posaconazole.
Mechanism of action
 The antifungal activity of azole drugs results from the reduction of ergosterol synthesis
by inhibition of fungal cytochrome P450 enzymes.
 Imidazoles exhibit a lesser degree of selectivity than the triazoles, accounting for their
higher incidence of drug interactions and adverse effects.
Ketoconazole
 Has a narrow antifungal spectrum.
 For oesophageal candidiasis, give 200-400mg orally daily until remission is obtained.
 Oral dosages of ketaconazole with or immediately after meals.
Fluconazole
 The drug of choice in esophageal and oropharyngeal candidiasis
 A single oral dose usually eradicates vaginal candidiasis.
 Fluconazole is now the drug of choice for initial and secondary prophylaxis against
cryptococcal meningitis.
Side effects
 Adverse effects of the azoles include vomiting, diarrhoea, rash, and sometimes
hepatotoxicity (especially in patients with pre-existing liver dysfunction).
 Ketoconazole inhibits hepatic cytochrome P450 isozymes and may increase the plasma
levels of other drugs, including anticoagulants, cyclosporine, oral hypoglycemics, and
phenytoin.
 Ketoconazole interferes with the synthesis of adrenal and gonadal steroids and may lead
to gynecomastia, menstrual irregularities, and infertility.
ORAL SYSTEMIC ANTIFUNGAL DRUGS FOR MUCOCUTANEOUS INFECTIONS

Griseofulvin
 Griseofulvin is a very insoluble fungistatic drug derived from a species of penicillium.
 Its only use is in the systemic treatment of dermatophytosis.
 Absorption is improved when it is given with fatty foods.
 Because its action is to prevent infection of these new skin structures, griseofulvin must
be administered for 2-6 weeks for skin and hair infections to allow the replacement of
infected keratin by the resistant structures.
 Nail infections may require therapy for months to allow regrowth of the new protected
nail and is often followed by relapse.
 It potently induces cytochrome P450 enzymes and causes several clinically important
drug interactions.
Mechanism of action
 Griseofulvin interferes with microtubule function in dermatophytes and may also inhibit
the synthesis and polymerization of nucleic acids.
Side effects
 Headaches
 Mental confusion
 Gastrointestinal irritation
 Photosensitivity
 Changes in liver function
 A drug interaction may enhance coumarin metabolism, resulting in decreased
anticoagulant effect
TOPICAL ANTIFUNGAL THERAPY

Nystatin
 Nystatin is a polyene macrolide much like amphotericin B.
 It is too toxic for parenteral administration and is only used topically.
 Nystatin is currently available in creams, ointments, suppositories, and other forms for
application to skin and mucous membranes.
 It is not absorbed to a significant degree from skin, mucous membranes, or the
gastrointestinal tract.
 Nystatin is active against most Candida species and is most commonly used for
suppression of local candidal infections.
 Some common indications include oropharyngeal thrush, vaginal candidiasis, and
intertriginous candidal infections.
Topical azoles
 Other topical antifungal agents include the azole compounds miconazole and
clotrimazole.
 Miconazole and clotrimazole are both synthetic imidazoles which are active against
fungi (both dermatophytes and yeast) and gram positive (staphlylococcus and
streptococcus species).
 Miconazole and clotrimazole are used for the topical treatment of most common fungal
infection of the skin and vagina.
 Specific indication includes ringworm, diaper dermatitis, vaginal candidiasis, and fungal
infection of the outer ear.
 Miconazole is used in the treatment of and prevention of oral candidiasis and denture
stomatitis.

 Antibiotics have the power to kill or stop the growth of invading micro-organisms
without harming the host micro-organisms
 Fungal infection of deep tissues may be controlled by systemic administration of
amphotericin, flucytoscine, or azole derivatives.
 Candidiasis can be controlled by the topical administration of nystatin or by the use of
azole derivatives.
 Widespread ringworm infection may be controlled by oral griseofluvin or azole
derivatives.
 Localized ringworm infection may be controlled by topical administration of imidazole
(e.g. miconazole).

 What is the definition of antibacterial drugs?
 What are antifungal drugs?
 What are the side effects of tetracyclines?
References
Katzung, B. G., Masters, S. B., & Trevor, A. J. (2012). Basic and Clinical Pharmacology (LANGE Basic
Science). McGraw-Hill Education. Bennett, P. N. (2003). Clinical pharmacology. (9th ed.). London:
Churchill Livingstone.
Gould, D., Greenstein. B., & Trounce, J. (2004). Trounce’s clinical pharmacology for nurses (17th ed.).
London: Churchill Livingstone.
Greenstein, B. Gold, D. Trounce, J. (2009): Clinical pharmacology for nurses, (18 th Ed.) Livingstone China,
Churchill
Hopkins, S. J. Kelly, J.C. (2008): Drugs and Pharmacology for nurses, Livingstone China, Churchill
Laurence, D. R., Bennett, P. N., & Brown, M. J. (1997). Clinical pharmacology (8th ed.). Edinburgh:
Livingstone Churchill.
SESSION 7: COMMON ANTIHELMINTHIC AND ANTIMALARIAL
Learning Tasks
Define anti-helminthic and antimalarial
Identify common anti-helminthic and antimalarial
Explain mechanism of action of common anti-helminthic and antimalarial
Explain side effects of common anti-helminthic and antimalarial
Resources Needed:

Method
objectives
2 05 Brainstorming Definition of anti-helminthic
Presentation
3 35 Presentation Commonly used anti-helminthic
4 05 Brainstorming Definition of antimalarial

Presentation
5 60 Presentation Commonly used antimalarial

SESSION CONTENTS
STEP 1: Presentation of Session Title and Learning Objectives (5 minutes)
READ or ASK participants to read the learning objectives
STEP 2: Definition of Anthelminthic drugs (5 minutes)

Antiheminthics
 Anthelmintics are drugs that are used to treat infections with parasitic worms
(helminths) and other internal parasites from the body by either stunning or killing them
and without causing significant damage to the host.
STEP 3: Commonly Used Anthelminthic drugs (35 minutes)

 Among the most widespread of all chronic infections are those caused by various
species of parasitic helminthes (worms).
 Basic antihelminthics drugs includes;
o Mebendazole
o Albendazole
o Levamisole
o Niclosamide
o Thiabendazole
o Praziquantel
o Piperazine
 Drugs under this class of drugs act on worms by either killing or paralysing them.
 Helminthic infections are caused by one kind or another.
o They produce annoying symptoms.
o Prolonged infestations may cause risk to health and life.
o The worms may be classified into two main groups.
o Those which:-
 Infect the alimentary canal such as, tapeworms, roundworms,
threadworms, hookworms and whip worms.
 Live in the tissue of the patient; such as schistosoma filaria and others
(onchocerciasis, loiasis).
 Some of the specific drugs under this class of drugs are mebendazole and
piperazine.
Mebendazole
 Mebendazole is a synthetic benzimidazole that has a wide spectrum of antihelminthic
activity and a low incidence of adverse effects.
 Effective against hookworms, thread worms, round worms and whipworm infestations
by blocking the parasites’ glucose uptake.
 It can be taken before or after meals; the tablets should be chewed before swallowing.
 Less than 10% of mebendazole is absorbed after oral administration, but a fatty meal
increases absorption.
 Metabolized in the liver and only about 5 to 10 per cent of an oral dose is recovered in
urine.
 The plasma half-life ranges between 2 and 9 hours.
 Mebendazole is excreted in the faeces mainly in the unchanged forms.
 It is used for mass treatment in community (Chemoprophylaxis) in eradication programs
Mechanism of action
 Mebendazole acts by inhibiting microtubule synthesis; the parent drug appears to be
the active form.
Side effects
 Mostly tolerated and nearly free from side effects.
 Gastro-intestinal disturbances, headache, toxic effects include vomiting, nausea occurs
infrequently.
 Mebendazole is teratogenic in animals and therefore contraindicated in pregnancy.
 It should be used with caution in children younger than 2 years of age because of limited
experience and rare reports of convulsions in this age group.
Albendazole
 Albdendazole is a benzimidazole derivative with a blood-spectrum antihelminthic
activity.
 Albendazole, a broad-spectrum oral antihelminthic, is the drug of choice for treatment
of hydatid disease and cysticercosis.
 It is also used in the treatment of pinworm and hookworm infections, ascariasis,
trichuriasis, and strongyloidiasis.
 Albendazole is administered on an empty stomach when used against intraluminal
parasites but with a fatty meal when used against tissue parasites.
Mechanism of action
 Albendazole act against nematodes by inhibiting microtubule synthesis.
 Albendazole also has larvicidal effects in hydatid disease, cysticercosis, ascariasis, and
hookworm infection and ovicidal effects in ascariasis, ancylostomiasis, and trichuriasis.
Side effects
 When used for 1–3 days, albendazole is nearly free of significant adverse effects.
 Mild and transient epigastric distress, diarrhea, headache, nausea, dizziness, lassitude,
and insomnia can occur.
 In long-term use for hydatid disease, albendazole is well tolerated, but it can cause
abdominal distress, headaches, fever, fatigue, alopecia, increases in liver enzymes, and
pancytopenia.
STEP 4: Definition of Antimalarial drugs (5 minutes)

ASK students to brainstorm on the definition of antimalarial
Antimalarial
 Antimalarial are drugs designed to prevent or cure malaria.
 Such drugs may be used for some or all of the following: Treatment of malaria in
individuals with suspected or confirmed infection.
STEP 5: Commonly Used Antimalarial drugs (60 minutes)

 Drugs used to treat the acute attack of malaria act on the parasites in the blood (blood
schizonticides).
 They can cure infections with parasites (e.g. Plasmodium falciparum) that have no
exoerythrocytic stage.
 Drugs used for chemoprophylaxis (causal prophylactics) act on merozoites emerging
from liver cells
 Drugs used for radical cure are active against parasites in the liver
 Drugs that act on gametocytes prevent transmission by the mosquito
 WHO recommends Artemisinin-based combination therapies (ACTs) for the treatment
of uncomplicated malaria caused by P. falciparum.
TREATMENT OF UNCOMPLICATED MALARIA

Artemether Lumefantrine (ALu)
 The first line drug for treatment of a patient with uncomplicated malaria is Artemether-
Lumefantrine
 Table 7.1 shows dosage and administration of ALu-Coartem (Artemether 20mg –
Lumefantrine 120mg) for Uncomplicated Malaria.
 0* hours means the time of starting medication
 The first dose should be given at any time, but preferably in the morning so as enhance
compliance and timing of the 2nd dose.
 The second dose should be strictly given after 8 hours.
 Subsequent doses should be given twice daily in the 2nd and 3rd day of treatment ideally
starting 12 hours after the 2nd dose.
 For convenience and to make ALu administration simple, it is suggested to administer
3rd, 4th, 5th and 6th ALu doses in the morning and evening of the 2nd and 3rd day of
treatment.
Table 7.1 Dosage and Administration of ALu
Day 1 Day 2 Day 3
Dose 1st 2nd 3rd 4th 5th 6th
Hours 0* 8 24 36 48 60
Kg Age Tablets Tablets Tablets Tablets Tablets Tablets
5 to 15 kgs 3 months up to 3 1 1 1 1 1 1
years
15 to 25 kgs 3 years up to 8 2 2 2 2 2 2
years
25 to 35 kgs 8 years up to 12 3 3 3 3 3 3
years
35kgs and 12 years and 4 4 4 4 4 4

above above
Source: (MoHSW, 2006)
Dihydroartemisinin-Piperaquine (DPQ)
 An alternative artemisinin-based combination therapy (ACT) is Dihydroartemisinin-
Piperaquine (DPQ).
 Strength: Standard tablet, fixed formulation containing 40mg of Dihydroartemisinin
(DHA) and 320 mg Piperaquine (PPQ).
 Paediatric formulation contains a fixed combination of 20 mg of Dihydroartemisinin
(DHA) and 160 mg Piperaquine (PPQ).
SP (Sulfadoxine 500mg + Pyrimethamine 25mg)

 This drug is used for uncomplicated malaria.
 It is also used as a prophylaxis for malaria in pregnancy.
Side effects
 Skin reactions - Stephen Jonson syndrome
 Bone Marrow suppression
 Haemolysis in G6PD – Deficient
Table 7.2 Dosage of SP
Age (Years/Months Weight (Kg) # of SP tablets as single dose
2 up to 4 months 5 up to 7 ¼
4 up to 12 months 7 up to 11 ½
1 up to 5 11 up to 19 1
5 up to 9 19 up to 30 1½
9 up to 14 30 up to 45 2
14 and above Over 45 3
Source: (MoHSW, 2006)
 Malaria is quite uncommon in children one week up to 2 months.

 If such children are proved to have malaria parasites it is considered as severe malaria.
 It is managed with Parental Quinine.
 Dose 10mg/kg 8hrly for 7 days
 Lactating mothers whose children are below 2 months should be treated with
Artemether Lumefantrine (ALU) or Amodiaquine
Amodiaquine Tablet, 200mg
 Second line drug for treatment of malaria
 1st line drug for treatment of malaria in lactating mothers of children less than 2 months
 Drug of child for treatment of malaria of patient with allergy to sulfa drugs.
Side Effects
 Nausea
 Vomiting
 Abdominal pain
 Diarrhoea and vomiting
 Rare side effect:
o A granulocytosis
o Hepatic drysfunction
o Hypotension
TREATMENT OF SEVERE MALARIA
Artesunate
 This is currently the first line drug of choice for the treatment of severe malaria
Route
 Parenteral
Dosage
 2.4 mg/kg of body weight. IV or IM given on admission (time = 0 hour), then at 12 hours
and 24 hours for a minimum of 3 injections in 24 hours regardless of patient’s recovery
 For children weighing less than 20 kg the dosage is as follows:
o 3 mg/kg/dose (or higher).
o Same schedule as indicated above (0, 12, 24 hours)
o Complete artesunate injection treatment by giving a complete course (3 days) of
artemether-lumefantrine (AL) or other ACT
Administration and dosage (60 mg strength)

 Injectable artesunate has 2-steps dilutions.
o The powder for injection should be diluted with 1ml of 5% sodium bicarbonate
solution (provided in each box) and shaken vigorously 2–3 minutes for better
dissolving until the solution becomes clear
 For slow intravenous infusion (3–4 minutes), add 5 ml of 5% sodium
chloride or normal saline or dextrose to obtain Artesunate concentration
of 10 mg/ml.
 For deep intra–muscular injection, add 2 ml of 5% dextrose or normal
saline to obtain an Artesunate concentration of 20 mg/ml.
Injectable Artemether
 Artemether should be administered in a dose of 3.2mg/kg body weight loading dose IM
stat then 1.6mg/kg body weight (time= 0h then at 24 hrs and 48hrs).
Quinine
 Quinine and quinidine remain important therapies for falciparum malaria especially
severe disease, although toxicity may complicate therapy.
 Quinine is a rapid-acting, highly effective blood schizonticide against the four species of
human malaria parasites.
 The drug is gametocidal against P. vivax and P ovale but not P. falciparum.
 It is not active against liver stage parasites.
 The mechanism of action of quinine is unknown
Side effects
 Therapeutic dosages of quinine and quinidine commonly cause tinnitus, headache,
nausea, dizziness, flushing, and visual disturbances, a constellation of symptoms termed
cinchonism.
 Mild symptoms of cinchonism do not warrant the discontinuation of therapy.
 After prolonged therapy, side effects may include more marked visual and auditory
abnormalities, vomiting, diarrhoea, and abdominal pain.
 Hypersensitivity reactions include skin rashes, urticaria, angioedema, and
bronchospasm.
 Hematologic abnormalities include hemolysis (especially with G6PD deficiency),
leukopenia, agranulocytosis, and thrombocytopenia.
 Therapeutic doses may cause hypoglycemia through stimulation of insulin release; this is
a particular problem in severe infections and in pregnant patients, who have increased
sensitivity to insulin.
 Quinine can stimulate uterine contractions, especially in the third trimester.
 Intravenous infusions of the drugs may cause thrombophlebitis.
 Severe hypotension can follow too-rapid intravenous infusions of quinine or quinidine.
 Blackwater fever is a rare severe illness that includes marked hemolysis and
hemoglobinuria in the setting of quinine therapy for malaria. It appears to be due to a
hypersensitivity reaction to the drug, although its pathogenesis is uncertain.

 Mebendazole is teratogenic in animals and therefore contraindicated in pregnancy.
 It should be used with caution in children younger than 2 years of age because of limited
experience and rare reports of convulsions in this age group.
 WHO recommends Artemisinin-based combination therapies (ACTs) for the treatment
of uncomplicated malaria caused by P. falciparum.
 The first line drug for treatment of a patient with uncomplicated malaria is Artemether
Lumefantrine (ALu)
 Severe and complicated malaria or persons who are resistant to first line drugs for
malaria are treated with quinine.
 What are the common antimalarial drugs?
 What are the common antihelminthic drugs?
 What is the first line drug for the treatment of uncomplicated malaria?
References
Science). McGraw-Hill Education.
MOHSW. (2006). National guidelines for malaria diagnosis and treatment. Dar es Salaam, Tanzania:
Ministry of Health & Social Welfare.
SESSION 8: COMMON ANTIVIRAL
Learning Tasks
Define antiviral
Identify common antiviral
Explain mechanism of action of common antiviral
Explain side effects of common antiviral
Resources Needed:
Method
1 05 Presentation
Presentation of session title and learning objectives
2 05 Brainstorming Definition of antiviral
Presentation
3 35 Presentation Commonly used antiviral
4 05
5 05
SESSION CONTENTS
STEP 2: Definition of Antiviral drugs (5 minutes)

Antivirals
 Antivirals are drugs that kill a virus or that suppresses its ability to replicate and, hence,
inhibits its capability to multiply and reproduce.
STEP 3: Commonly Used Antiviral drugs (10 minutes)

 Viruses are obligate intracellular parasites; their replication depends primarily on
synthetic processes of the host cell.
 Therefore, to be effective, antiviral agents must either block viral entry into or exit from
the cell or be active inside the host cell.
 Antiviral drugs share the common property of being virustatic; they are active only
against replicating viruses and do not affect latent virus.
 Whereas some infections require monotherapy for brief periods of time (eg, acyclovir
for herpes simplex virus), others require dual therapy for prolonged periods of time
(interferon alfa/ribavirin for HCV), whereas still others require multiple drug therapy for
indefinite periods (HIV).
Acyclovir
 Acyclovir is an acyclic guanosine derivative with clinical activity against Herpes Simplex
Virus type 1 and 2, and Varicella Zoster Virus.
 Oral acyclovir has multiple uses. In first episodes of genital herpes, oral acyclovir
shortens the duration of symptoms by approximately 2 days, the time to lesion healing
by 4 days, and the duration of viral shedding by 7 days.
 In recurrent genital herpes, the time course is shortened by 1–2 days.
 Intravenous acyclovir is the treatment of choice for herpes simplex encephalitis,
neonatal HSV infection, and serious HSV or VZV infections.
 In immunocompromised patients with VZV infection, intravenous acyclovir reduces the
incidence of cutaneous and visceral dissemination.
Mechanism of action
 Acyclovir triphosphate inhibits viral DNA synthesis by two mechanisms: competition
with deoxyGTP for the viral DNA polymerase, resulting in binding to the DNA template
as an irreversible complex; and chain termination following incorporation into the viral
DNA.
 Acyclovir diffuses readily into most tissues and body fluids.
Side effects
 Acyclovir is generally well tolerated.
 Nausea, diarrhea, and headache have occasionally been reported.
 Intravenous infusion may be associated with reversible renal toxicity or neurologic
effects.
 Somnolence and lethargy may occur in patients receiving concomitant zidovudine and
acyclovir.
STEP 4: Commonly Used Antiretroviral Agents (90 minutes)
ASK students to pair up and buzz on commonly used antiretroviral agents
ALLOW few pairs to respond and let other pairs to add on points not mentioned
WRITE their response on the flip chart/board
CLARIFY and SUMMARIZE by using the content below
 Antiretroviral drugs are medications for the treatment of infection by retroviruses,

primarily HIV. Different classes of antiretroviral drugs act at different stages of the HIV
life cycle.
 Combination of several (typically three or four) antiretroviral drugs is known as Highly
Active Anti-Retroviral Therapy (HAART).
 Six classes of antiretroviral agents are currently available for use:
o nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)
o nonnucleoside reverse transcriptase inhibitors (NNRTIs)
o protease inhibitors (PIs)
o fusion inhibitors
o CCR5 receptor antagonists
o integrase inhibitors
NUCLEOSIDE & NUCLEOTIDE REVERSE TRANSCRIPTASE INHIBITORS
Abacavir
 Abacavir is a guanosine analog that is well absorbed following oral administration and is
unaffected by food.
 Abacavir is often co-administered with lamivudine, and a once daily, fixed-dose
combination formulation is available.
 Abacavir is also available in a fixed-dose combination with lamivudine and zidovudine.
Mechanism of action
 The NRTIs act by competitive inhibition of HIV-1 reverse transcriptase; incorporation
into the growing viral DNA chain causes premature chain termination due to inhibition
of binding with the incoming nucleotide.
Side effects
 Symptoms, which generally occur within the first 6 weeks of therapy, include fever,
fatigue, nausea, vomiting, diarrhea, and abdominal pain.
 Possible increase in myocardial infarction
 Respiratory symptoms such as dyspnea, pharyngitis, and cough may also be present.
 Other potential adverse events are rash, headache, and pancreatitis
Didanosine (ddI)
 Didanosine (ddI) is a synthetic analogy of deoxyadenosine.
Side effects
 Peripheral neuropathy
 Pancreatitis
 Diarrhea
 Nausea
 Hyperuricemia
 Possible increase in myocardial infarction
Lamivudine (3TC)
 Lamivudine (3TC) is a cytosine analog with in vitro activity against HIV-1 that is
synergistic with a variety of antiretroviral nucleoside analogs-including zidovudine and
stavudine-against both zidovudine-sensitive and zidovudine-resistant HIV-1 strains.
 Lamivudine is often co-administered with abacavir, and a once-daily, fixed-dose
combination formulation is available.
 Lamivudine is also available in a fixed-dose combination with zidovudine, either alone or
in combination with abacavir.
Side effects
 Potential adverse effects are headache, dizziness, insomnia, fatigue, dry mouth, and
gastrointestinal discomfort
Stavudine (d4T)
 The thymidine analog stavudine (d4T) has high oral bioavailability that is not food-
dependent.
 Because the co-administration of stavudine and didanosine may increase the incidence
of lactic acidosis and pancreatitis, concurrent use should be avoided. This combination
has been implicated in several deaths in HIV-infected pregnant women.
 There is no evidence of human teratogenicity in those taking stavudine.
Side effects
 Lipodystrophy
 Hyperlipidemia
 Rapidly progressive ascending neuromuscular weakness (rare)
 Pancreatitis
Zidovudine (AZT)
 Zidovudine (azidothymidine; AZT) is a deoxythymidine analog that is well absorbed and
distributed to most body tissues and fluids.
 Zidovudine is available in a fixed-dose combination formulation with lamivudine, either
alone or in combination with abacavir.
 Zidovudine was the first antiretroviral agent to be approved and has been well studied.
 The drug has been shown to decrease the rate of clinical disease progression and
prolong survival in HIV-infected individuals.
 Efficacy has also been demonstrated in the treatment of HIV-associated dementia and
thrombocytopenia.
Side effects
 The most common adverse effect of zidovudine is myelosuppression, resulting in
macrocytic anemia or neutropenia.
 Gastrointestinal intolerance, headaches, and insomnia may occur
 Lipoatrophy
 Less common toxicities include thrombocytopenia, hyperpigmentation of the nails, and
myopathy.
 High doses can cause anxiety, confusion, and tremulousness.
NONNUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS

 The NNRTIs bind directly to HIV-1 reverse transcriptase, resulting in allosteric inhibition
of RNA- and DNA dependent DNA polymerase activity.
 The binding site of NNRTIs is near to but distinct from that of NRTIs.
 Unlike the NRTI agents, NNRTIs neither compete with nucleoside triphosphates nor
require phosphorylation to be active.
 As a class, NNRTI agents tend to be associated with varying levels of gastrointestinal
intolerance and skin rash, the latter of which may infrequently be serious (e.g. Stevens-
Johnson syndrome).
Nevirapine
 The oral bioavailability of nevirapine is excellent and is not food-dependent.
 There is no evidence of human teratogenicity on the use of nevirapine during
pregnancy.
 Nevirapine therapy should be immediately discontinued in patients with severe rash and
in those with accompanying constitutional symptoms; since rash may accompany
hepatotoxicity, liver function tests should be assessed.
Side effects
 Rash, usually a maculopapular eruption that spares the palms and soles, usually in the
first 4–6 weeks of therapy.
 Severe and life-threatening skin rashes have been rarely reported, including Stevens-
Johnson syndrome and toxic epidermal necrolysis.
 Symptomatic liver toxicity may occur
 Other adverse effects include fever, nausea, headache, and somnolence.
Efavirenz
 Efavirenz can be given once daily because of its long half-life (40–55 hours).
 It is moderately well absorbed following oral administration.
 Since toxicity may increase owing to increased bioavailability after a high-fat meal,
efavirenz should be taken on an empty stomach.
 Efavirenz should be avoided in pregnant women, particularly in the first trimester as it
may cause congenital anomalies.
Side effects
 The principal adverse effects of efavirenz involve the central nervous system. These
include dizziness, drowsiness, insomnia, nightmares, and headache.
 Psychiatric symptoms such as depression, mania, and psychosis have been observed and
may necessitate discontinuation.
 Skin rash
 Other potential adverse reactions are nausea, vomiting, diarrhea, crystalluria, elevated
liver enzymes, and an increase in total serum cholesterol.

 Antiviral drugs share the common property of being virustatic; they are active only
against replicating viruses and do not affect latent virus.
 Whereas some infections require monotherapy for brief periods of time (eg, acyclovir
for herpes simplex virus), others require dual therapy for prolonged periods of time
(interferon alfa/ribavirin for HCV), whereas still others require multiple drug therapy for
indefinite periods (HIV).
 Nevirapine therapy should be immediately discontinued in patients with severe rash and
in those with accompanying constitutional symptoms; since rash may accompany
hepatotoxicity, liver function tests should be assessed.

 What are the common antiretroviral drugs?
 What are the side effects of lamivudine?
 What are the side effects of nevirapine?
References
SESSION 9: COMMON ANTIHYPERTENSIVE
Learning Tasks
Define antihypertensive
Identify common beta blockers, diuretics, vasodilators, medicine acting on heart
muscles
Explain mechanism of action and side effects of common beta blockers,
diuretics, vasodilators, medicine acting on heart muscles
Explain management of side effects of common beta blockers, diuretics,
vasodilators, medicine acting on heart muscles
Resources Needed:
(min) Method
1 05 Presentation of session Presentation title and learning tasks
2 05 Brainstorming
Presentation Definition of anti-hypertensive
3 30 Presentation Commonly used beta blockers, diuretics, vasodilators,
medicine acting on heart muscles
4 50 Lecture discussion mechanism of action and side effects of common beta
blockers, diuretics, vasodilators, medicine acting on heart
muscles
5 20 Lecture discussion Management of side effects of common beta blockers,
diuretics, vasodilators, medicine acting on heart muscles
6 05
7 05
SESSION CONTENTS
STEP 2: Definition of Anti-hypertensive (5 minutes)

ASK students to brainstorm on the definition of anti-hypertensive
 Anti-hypertensives are a class of drugs that are used to treat hypertension (high blood
pressure).
o Antihypertensive therapy seeks to prevent the complications of high blood
pressure, such as stroke and myocardial infarction.
o Evidence suggests that reduction of the blood pressure by 5 mmHg can decrease
the risk of stroke by 34%, of ischaemic heart disease by 21%, and reduce the
likelihood of dementia, heart failure, and mortality from cardiovascular disease
STEP 3: Common Used Beta Blockers, Diuretics, Vasodilators, Medicine Acting On Heart
Muscles (20 Minutes)
There are many classes of antihypertensives, which lower blood pressure by different means. Among the
most important and most widely used drugs are beta blockers, Diuretics, Vasodilators, Medicine acting on
heart muscles.
 Beta Blockers also written β-blockers are a class of medications that are predominantly
used to manage abnormal heart rhythms, and to protect the heart from a second heart
attack (myocardial infarction) after a first heart attack (secondary prevention). They are
also widely used to treat high blood pressure (hypertension).( Atenolol, Carvedilol,
Propanolol, Labetalol)
 Diuretics A diuretic is any substance that promotes diuresis, they increased production
of urine. ( loop diuretics-Furosemide, Bendofurothiazide, potassium sparing diuretics-
spironolactone, amiloride)
 Vasodilators examples are Nitropruside, Hydralazine and Captopril.
 Medicine acting on heart muscles examples are Hydralazine,Isosorbide dinitrate
(Isordil) sosorbide mononitrate (Imdur)
STEP 4: Mechanism of Action and Side Effects of Common Beta Blockers, Diuretics,
Vasodilators, Medicine Acting on Heart Muscles(50 Minutes)
Beta Blockers
 Class of medications that are predominantly used to manage abnormal heart rhythms,
and to protect the heart from a second heart attack (myocardial infarction) after a first
heart attack (secondary prevention), also widely used to treat high blood pressure
(hypertension) .( Atenolo, Carvedilol, Propanolol,Labetalol)
Mechanism of action and Pharmacodynamics

 Propranolol is classified as a non-cardioselective sympatholytic beta blocker that crosses
the blood–brain barrier.
o It is lipid soluble and also has sodium channel blocking effects.
o Propranolol is a non-selective beta blocker; it blocks the action
of epinephrine (adrenaline) and norepinephrine (noradrenaline) at both β1-
and β2-adrenergic receptors.
o It has little intrinsic sympathomimetic activity, but has strong membrane
stabilizing activity (only at high blood concentrations, e.g. overdose).
o Propranolol is able to cross the blood–brain barrier and exert effects in
the central nervous system in addition to its peripheral activity.
Side effects
The more common side effects of propranolol can include;
 slower heart rate, diarrhea,dry eyes ,hair loss ,nausea, weakness or tiredness
o If these effects are mild, they may go away within a few days or a couple of
weeks. If they’re more severe or don’t go away, talk to your doctor or
pharmacist.
 Seriously side effects ( though are rare but may be necessitate withdraw from
medication)
o Allergic reactions. Symptoms can include:
 skin rash
 itching
 hives
 swelling of your face, lips, or tongue
o Breathing problems, changes in blood sugar, cold hands or feet, nightmares or trouble
sleeping, Hallucinations, Muscle cramps or weakness, swelling of your legs or ankles,
sudden weight gain, vomiting.
 Carvedilol: Carvedilol is both a non-selective beta adrenergic receptor blocker (β1, β2) and
an alpha adrenergic receptor blocker (α1).
o Carvedilol reversibly binds to beta adrenergic receptors on cardiac myocytes. Inhibition of
these receptors prevents a response to the sympathetic nervous system, leading to
decreased heart rate and contractility. This action is beneficial in heart failure patients
where the sympathetic nervous system is activated as a compensatory mechanism.
o Carvedilol block also α1 receptors causes vasodilatation of blood vessels. This inhibition
leads to decreased peripheral vascular resistance and an antihypertensive effect. There is
no reflex tachycardia response due to carvedilol blockade of β1 receptors on the heart.
o The pharmacokinetics of carvedilol is about 25% to 35% bioavailable following oral
administration due to extensive first-pass metabolism.
 The compound is metabolized by liver enzymes. The three active metabolites
exhibit only one tenth of the vasodilating effect of the parent compound.
 Side effects
o The most common side effects (>10% incidence) include:
 Dizziness, fatigue, low blood pressure , diarrhea, weakness, slowed heart rate,
weight gain, erectile dysfunction
o Carvedilol is not recommended for people with uncontrolled bronchospastic
disease (e.g. current asthma symptoms) as it can block receptors that assist in
opening the airways.
o Carvedilol may mask symptoms of low blood sugar (hypoglycemia) resulting
in hypoglycemia unawareness. This is termed beta blocker induced hypoglycemia
unawareness.
Diuretics
A diuretic is any substance that promotes diuresis, they increased production of urine. (Loop diuretics-
Furosemide, Bendofurothiazide, potassium sparing diuretics- spironolactone, amiloride)
Mechanism of action and Pharmacodynamics

 Furosemide( Lasix)
o Furosemide works by blocking the absorption of sodium, chloride, and water
from the filtered fluid in the kidney tubules, causing a profound increase in the
output of urine (diuresis). The onset of action after oral administration is within
one hour, and the diuresis lasts about 6-8 hours
o The pharmacokinetics of furosemide are apparently not significantly altered by
food.No direct relationship has been found between furosemide concentration
in the plasma and furosemide efficacy. Efficacy depends upon the concentration
of furosemide in urine
Side effects
 Furosemide also can lead to gout caused by hyperuricemia.
 Hyperglycemia is also a common side effect.
 Tendency, as for all loop diuretics, to cause low serum potassium concentration
(hypokalemia) it is corrected by combination of products, either with potassium or with
the potassium-sparing diuretic amiloride (Co-amilofruse).
 Other electrolyte imbalance that can result from furosemide use include hyponatremia,
hypochloremia, hypomagnesemia, and hypocalcemia.
Mechanism of action and pharmacodynamic

 Potassium sparing diuretics- spironolactone
o Mechanism of action. aldactone (spironolactone) is a specific pharmacologic
antagonist of aldosterone, acting primarily through competitive binding of
receptors at the aldosterone-dependent sodium-potassium exchange site in the
distal convoluted renal tubule.
o Pharmacodynamics; the bioavailability of spironolactone when taken by mouth is 60 to
90%.The bioavailability of the medication improves significantly when it is taken with food.
Side effects
 The most common side effect of spironolactone is urinary frequency.
 Other general side effects include
o dehydration,
o hyponatremia (low sodium levels),
o mild hypotension (low blood pressure)
o ataxia (muscle incoordination),
o drowsiness, dizziness,
o dry skin, and rashes.
 Because of its antiandrogenic activity can in men, cause
o breast tenderness,
o gynecomastia (breast development),
o feminization in general,
o demasculinization,
o sexual dysfunction including loss of libido and erectile dysfunction,
NB:Although these side effects are usually confined to high doses of spironolactone.
Vasodilators
Mechanism of Action and pharmacodynamics

 Hydralazine: Although the precise mechanism of action of hydralazine is not fully
understood, the major effects are on the cardiovascular system.
o Hydralazine apparently lowers blood pressure by exerting a peripheral
vasodilating effect through a direct relaxation of vascular smooth muscle.
o It is a direct-acting smooth muscle relaxant and acts as a vasodilator primarily
in resistance arterioles; by relaxing vascular smooth muscle, vasodilators act to
decrease peripheral resistance, thereby lowering blood pressure and decreasing
after load
Side effects
 May cause a syndrome similar to lupus which can become fatal if the symptoms are not noticed
and drug treatment stopped on prolong use.
 Very common side effects include headache, high heart rate, and palpitations
 Other side effects include flushing, hypotension, anginal symptoms, aching or swelling joints,
muscle aches, positive tests for ANP, stomach upset, diarrhea, nausea, and vomiting,
and swelling ( due to sodium and water retention)
Mechanism of Action and pharmacodynamics
 Captopril: the mechanism of action of captopril has not yet been fully elucidated.
o Its beneficial effects in hypertension and heart failure appear to result primarily from
suppression of the renin-angiotensin-aldosterone system.
o However, there is no consistent correlation between renin levels and response to the drug
o Captopril, is an angiotensin-converting enzyme (ACE) inhibitor used for the treatment
of hypertension and some types of congestive heart failure.
o Its pharmacokinetics unlike the majority of ACE inhibitors, captopril is not administered as
a prodrug (the only other being lisinopril).
 About 70% of orally administered captopril is absorbed.
 Bioavailability is reduced by presence of food in stomach. It is partly metabolised
and partly excreted unchanged in urine.
Side effects
 Adverse effects of captopril include cough due to increase in the plasma levels of
bradykinin, angioedema, agranulocytosis, proteinuria, hyperkalemia, taste
alteration, teratogenicity, postural hypotension, acute renal failure, and leukopenia.
 Other side effects itching, headache, tachycardia, chest pain, palpitations, weakness.
Medicine acting on heart muscles

 Isosorbide dinitrate and sosorbidemononitrate
o Used for the prevention of angina pectoris due to coronary artery disease and the
treatment of acute and chronic angina pectoris, hypertension, and myocardial
infarction .
 Pharmacodynamics:
o Isosorbide-5-mononitrate, the long-acting metabolite of isosorbide dinitrate, is
used as a vasodilatory agent in the management of angina pectoris.
o By dilating the vessels, it lowers the blood pressure and reduces the left
ventricular preload and afterload, therefore, leads to a reduction of myocardial
oxygen requirement.
Mechanism of Action
 It activate the cGMP enzymes that leads to subsequent release of calcium ions results in
the relaxation of the smooth muscle cells and vasodilation.
Side effects
 Symptoms of overdose include
o vasodilatation,
o venous pooling, reduced cardiac output, and hypotension.
STEP 5: Management of side effects of common beta blockers, diuretics, vasodilators,

medicine acting on heart muscles(30 Minutes)
Coping with Antihypertensive Drug Side Effects
 In taking medication to control blood pressure, we may experience symptoms some of which may
be side effects from the medication.
o Many medication-related side effects diminish with time,
 but if they persist or are troublesome,
o a prescriber may be able to minimize them by lowering the dosage,
o switching to another drug,
o Prescribing medication to counteract the side effects.
 Alternatively, some side effects—particularly the less severe ones—can be managed with lifestyle
or self-care measures.
 The measures taken for some common side effects of antihypertensive drugs are described
below.(Always consult your doctor before taking any over-the-counter remedies or making changes
to your diet).
o Constipation (calcium channel blockers and central alpha agonists).
 Eat foods high in fiber (such as fruits, vegetables, whole grains) and
 Engage in moderate exercise on most days of the week.
 If these measures are not helpful laxatives may be prescribed.
o Dehydration (loop diuretics). Drink plenty of fluids each day.
o Dizziness, lightheadedness or fainting (all types of antihypertensive medications but
especially alpha blockers).
 When standing up from a seated position, rise slowly.
 When getting up from a recumbent position, sit on the edge of the bed with your
feet dangling for one to two minutes and then stand up slowly.
 Be especially careful about rising slowly when getting up in the middle of the night
to use the bathroom.
 Also, try to avoid standing for long periods of time and consuming large amounts
of alcohol.
o Drowsiness (alpha blockers, beta blockers and central alpha agonists).
 A patient can take medication once a day 30 minutes before bedtime.
 If multiple doses taken each day, ask if the last dose can be taken close to
bedtime.
 Also, try to avoid other medications that can lead to drowsiness, such as
antihistamines, sleeping pills, prescription pain relievers and muscle relaxants.
o Dry mouth (central alpha agonists). Try sucking on sugarless candy, chewing sugarless
gum or melting ice cubes in your mouth. If these measures do not provide relief, saliva
substitutes.
o Frequent urination at night (beta blockers and diuretics). Ask your doctor whether you can
take your medication in a single dose in the morning after breakfast. If you require more
than one dose daily, ask whether you can take the last dose before 6 p.m.
o Headaches (ACE inhibitors, alpha blockers, angiotensin II receptor blockers, calcium
channel blockers and direct vasodilators). Taking a hot shower or bath, pressing a cold
pack to the painful area, regular exercise and deep breathing may relieve headaches. If
these measures aren't helpful, ask your doctor to recommend a headache medication.
o Increased sensitivity to cold (alpha blockers, beta blockers and direct vasodilators). Dress
warmly and be sure to keep your ears, hands and feet covered in cold weather. Take extra
precautions when you anticipate prolonged exposure to cold.
o Tender, swollen or bleeding gums (calcium channel blockers). Practice good dental
hygiene by brushing and flossing teeth and massaging gums daily. Have your teeth
cleaned regularly by a dentist.
o Upset stomach (angiotensin II receptor blockers, beta blockers, direct vasodilators and
diuretics). Ask your doctor if you can take your medication with meals or with a glass of
milk.

 Antihypertensives are a class of drugs that are used to treat hypertension (high blood
pressure).
 Antihypertensive therapy seeks to prevent the complications of high blood pressure,
such as stroke and myocardial infarction.
 Evidence suggests that reduction of the blood pressure by 5 mmHg can decrease the risk
of stroke by 34%, of ischaemic heart disease by 21%, and reduce the likelihood
of dementia, heart failure, and mortality from cardiovascular disease
 There are many classes of anti-hypertensive, which lower blood pressure by different
means. Among the most important and most widely used drugs are beta blockers,
Diuretics, Vasodilators, Medicine acting on heart muscles.
 In taking medication to control blood pressure, we may experience symptoms some of which may
be side effects from the medication, however many medication-related side effects diminish with
time.

 What are anti-hypertensives drugs?
 What are the common beta blockers?
 What are the diuretics?
References
SESSION 10: COMMON ANTI-DIABETICS AND ANTICOAGULANTS
Learning Tasks
Define anti-diabetics and anticoagulants
Identify common anti-diabetics and anticoagulants
Explain mechanism of action and side effects of common anti-diabetics and
anticoagulants
Explain management of side effects of common anti-diabetics and
anticoagulants
Resources Needed:
(min) Method
1 05 Presentation
2 05 Brainstorming Definitions of anti-diabetics and anticoagulants
Presentation
3 30 Presentation Commonly anti-diabetics and anticoagulants
4 50 Lecture discussion mechanism of action and side effects of common

anti-diabetics and anticoagulants
5 20 Lecture discussion Management of side effects of common anti-

diabetics and anticoagulants
6 05
7 05
SESSION CONTENTS
STEP 2: Definition ofAnti-Diabetics And Anticoagulants (10 Minutes)

ASK students to brainstorm on the definitions of anti-diabetics and anticoagulants
 Anti-Diabetes these are drugs used to treat diabetes mellitus by lowering the glucose
level in the blood. With the exceptions of insulin, all are administered orally are
called oral hypoglycaemic agents or oral anti-hyperglycaemic agents
 An anticoagulant is a drug (blood thinner) that treats, prevents, and reduces the risk of
blood clots-breaking off and traveling to vital organs of the body, which can lead to life
threatening situations.
o They work by preventing blood from coagulating to form a clot in the vital organs
such as the heart, lungs and brain.
Step 3: Common Anti-Diabetics And Anticoagulants (20 Minutes)

Common Anti-Diabetes
 Diabetes is of two types Diabetes mellitus type 1 caused by the lack of insulin so Insulin
must be used in type 1, which must be injected.
 Diabetes mellitus type 2 is a disease of insulin resistance by cells, the most common
diabetes.
 Treatments include
o agents that increase the amount of insulin secreted by the pancreas,
o agents that increase the sensitivity of target organs to insulin,
o Agents that decrease the rate at which glucose is absorbed from the
gastrointestinal tract.
 The common drugs are;
o Insulin commonly used for type 1 diabetes
 Types of insulin and their mode of action
Rapid-acting insulinis taken just before or after meals, to control spikes in

blood sugar. It often works in 15 minutes, peaks between 30 and 90
minutes, and lasts 3 to 5 hours.
 Intermediate-acting insulincan control blood sugar levels for about 12
hours or longer, so it can be used overnight. It begins to work within one
to four hours.
 Long-acting insulinhas an onset of one hour, and lasts for 20 to 26 hours
with no peak.
o Common oral hypoglycemic agents (OHA)
 Acetohexamide (Dymelor)
 Metformin
 Chlorpropamide (Diabinese)
 Tolazamide (Tolinase)
 Tolbutamide (Orinase)
 Glibenclamide (sulfonylureas)
Common Anti-Coagulants
 The traditional ones which are commonly known as vitamin K anticoagulants/vitamin K antagonist
are:
o Heparins 5000units intravenous or subcutaneous injectable anticoagulant
o Warfarin(Coumadin )2,5, 10mg found in plants (tablet form)
STEP 4: Mechanism of Action and Side Effects of Common Anti-Diabetics And

Anticoagulants (50 Minutes)
Anti-Diabetes Drugs
 Diabetes is of two types Diabetes mellitus type 1 caused by the lack of insulin so Insulin
must be used in type 1, which must be injected and diabetes mellitus type 2 is a disease
of insulin resistance by cells, the most common diabetes so insulin or oral
hypoglycaemia are used.
Insulin
Mechanism of action of insulin
 Increases insulin in the body and these results in increase insulin receptor binding route
of administration for all types by subcutaneous injection.The
molecular mechanism of insulin actioninitiates its action by binding to a glycoprotein
receptor on the surface of the cell. Activation of this kinase is believed to generate a
signal that eventually results in insulin's action on glucose, lipid, and protein
metabolism.
Side Effects of Insulin

 The major side effects of taking insulin include:
o Low blood sugar
o Weight gain when first start using it
o Lumps or scars where too many insulin injections done
o Rash at the site of injection or, rarely, over the entire body
 Injection site reactions (such as pain, redness, irritation) may occur.
Common oral hypoglycemic agents (OHA

Used fortype II diabetes (non insulin dépendant diabetes mellitus, NIDDM).
Acetohexamide (Dymelor)
Mechanism of action
 Lowers blood sugar by stimulating the pancreas to secrete insulin and helping the body
use insulin efficiently.The pancreas must produce insulin for this medication to work
 Therapeutic effects are more potent and have longer action than Tolbutamide. It promotes and
increase effectiveness of endogenous insulin.
 It pharmacokinetics;
o Absorption: Rapidly absorbed from GI tract.
o Onset: 1 h. Peak: 2–4 h. Duration: 12–24 h.
Side effects
 Symptoms of severe hypoglycemia include extreme weakness, blurred vision, sweating,
trouble speaking, tremors, stomach pain, confusion, seizure (convulsions), or coma
Metformin (Glucophage, Glumetza).
• Generally, metformin is the first medication prescribed for type 2 diabetes.
Mechanism of action
• It works by improving the sensitivity of body tissues to insulin so that body uses insulin more
effectively. Metformin also lowers glucose production in the liver.
Side effects
• Nausea and diarrhea are common
Sulfonylureas.
 These medications help body secrete more insulin.
 Examples of medications in this class include glyburide (DiaBeta, Glynase), glipizide (Glucotrol)
and glimepiride (Amaryl).
Side effects
 Include low blood sugar and weight gain.
Diabinese (chlorpropamide)
 Indicated as an adjunct to diet and exercise to improve glycemic control in adults with
type 2 diabetes mellitus
 Initial therapy the mild to moderately severe, middle-aged, stable type 2 diabetes
patient should be started on 250 mg daily.
The most common side effects
• Nausea, vomiting, heartburn, diarrhea, headache
ANTICOUGULANTS
An anticoagulant medicine is used in patients to prevent blood clots from forming in veins, arteries, the
heart, and the brain of a patient.
Heparins and Warfarin/Coumadin

Mechanism of action
 Coumadin is an oral anticoagulant that inhibits Vitamin K epoxide reductase, an enzyme
that recycles oxidized vitamin K. Vitamin K is an activator of coagulating factors II, VII, IX
and X, so by decreasing the availability of Vitamin K synthesis of these factors are
decreased.
Side effects
 Bleeding,Abdominal pain, Flatulence (intestinal gas, Headache, Lethargy, Dizziness, Fever
Local injection site reactions, Nausea
Severe side effect
 Intraocular hemorrhage
 Tissue necrosis
 Hematuria
 Anemia
 Hepatitis
STEP 5: Management of Side Effects of Common Anti-Diabetics and Anticoagulants (30

Minutes)
Coping with anti-diabetes Drug Side Effects
 In taking medication to control blood sugar, may experience symptoms some of which may be side
effects from the medication.
o Many medication-related side effects diminish with time,
o Some side effects can make blood sugar levels go too high or too low. You may have to
check your blood sugars more often.
Management of side effects of Anticoagulants

Give protamine 1 g by slow IVinjection.
• Avoid Antiplatelet medicine such as aspirin and other non-steroid anti-inflammatory medications
(for example, ibuprofen
• Foods with high vitamin K content (for example, green leafy vegetables) should be reduced.
• Dress the wound with sterile gauze.
• The doctor should be informed
• Regular monitoring of INR should be performed on all treated patients; those at high risk of
bleeding may benefit from more frequent INR monitoring, careful dose adjustment to desired INR,
and a shorter duration of therapy
• Patients should be instructed about prevention measures to minimize the risk of bleeding and to
immediately report any signs or symptoms of bleeding to their physician

 Anti-Diabetes these are drugs used to treat diabetes mellitus by lowering the glucose
level in the blood.
 An anticoagulant is a drug (blood thinner) that treats, prevents, and reduces the risk of
blood clots-breaking off and traveling to vital organs of the body, which can lead to life
threatening situations.
 Many medication-related side effects diminish with time,
 Some side effects can make blood sugar levels go too high or too low. They may have to
check your blood sugars more often.

 What are anti-diabetes drugs?
 What are oral hypoglycaemic drugs?
 What are anti-coagulants?
References
Livingstone Churchill. Bennett, P. N. (2003). Clinical pharmacology. (9th ed.). London: Churchill
Livingstone.
Churchill
SESSION 11: COMMON EMETICS AND ANTI-EMETICS
Learning Tasks
Define emetics, anti-emetics
Identify common emetics and anti-emetics
Explain mechanism of action and side effects emetics and anti-emetics
Explain management of side effects of emetics and anti-emetics
Resources Needed:

Method
2 05 Brainstorming Definitions of emetics and anti-emetics
Presentation
3 10 Presentation Common emetics and anti-emetics
4 20 Lecture discussion mechanism of action and side effects of

common emetics and anti-emetics
5 10 Lecture discussion Management of side effects of common emetics

and anti-emetics
6 05
7 05
SESSION CONTENTS
STEP 2: Definition of Emetics and Anti-Emetics (05 Minutes)

ASK students to brainstorm on the definitions of emetics anti-emetics
 Emetic, any agent that produces nausea and vomiting. The use of emetics is limited to
the treatment of poisoning with certain toxins that have been swallowed. Although its
use is now discouraged.
 Anti-emetics:are drugs prescribed to help with nausea and vomiting that are side effects
of other drugs.
o This may include drugs for anaesthesia used during surgeries or chemotherapy
for cancer.
o Antiemetic drugs are also used for nausea and vomiting caused by
 motion sickness
 morning sickness during pregnancy
 severe cases of the stomach flu (gastroenteritis)
 other infections
Step 3: Common Emetics and Anti-Emetics (10 minutes)

Common Emetics
 There are two general classes of emetics,
o one acting on the chemoreceptor trigger zone (CTZ) of the medulla
o The second acting on the stomach itself.
o The prototypical central emetic is apomorphine, and the prototypical gastric
emetic is ipecac.
Common Anti-Emetics
 Some antiemetic drugs are taken orally; others are available as an injection or as a patch
placed on body. The type of antiemetic drugs depends on what is causing the
symptoms:
o Antiemetics for motion sickness they prevent nausea and vomiting e.g
dimenhydrinate (Dramamine, Gravol) and meclizine (Dramamine Less Drowsy
o Antiemetics for chemotherapy e.g
 serotonin 5-HT3 receptor antagonists: dolasetro, ondansetron
 dopamine antagonists: prochlorperazine ,domperidone and olanzapine
o Hyperemesis gravidarum
 antihistamines, such as dimenhydrinate
 vitamin B-6 (pyridoxine)
 dopamine antagonists, such as prochlorperazine, promethazine
(Pentazine, Phenergan)
 metoclopramide if other treatments don’t work
STEP 4: Mechanism of Action and Side Effects of Common emetics and anti-emetics (20
Minutes)
EMETICS DRUGS
 The prototypical central emetic is apomorphine, and the prototypical gastric emetic
is ipecac.
Mechanism of action of Emetics
 The precise mechanism of action of apomorphine as a treatment for Parkinson's
disease is unknown, although it is believed to be due to stimulation of post-synaptic
dopamine D2-type receptors within the brain.
 Apomorphine causes vomiting by acting on dopamine receptors in
the chemoreceptor trigger zone of the medulla; this activates the nearby vomiting
cente
 Pharmacokinetics of apomorphine it lower bioavailability when taken orally, due to
not being absorbed well in the GI tract and undergoing heavy first-pass metabolism.
It has a bioavailability of 100% when given subcutaneously. It reaches peak plasma
concentration in 10–60 minutes.
Side Effects of Emetics

Emetics are contraindicated in patients that are hypoxic, dyspneic, unable to swallow, hypovolemic
or comatose.
ANTI-EMETICS
Mechanism of action of Anti-emetics
(Domperidone, ondansetron, metochlopramide)
 Antiemetics including: 5-HT3 receptor antagonists block serotonin receptors in the
central nervous system and gastrointestinal tract.
 Dopamine antagonists act in the brain and are used to treat nausea and vomiting
associated with neoplastic disease, radiation sickness, opioids, cytotoxic drugs and
general anaesthetics.
 Ondansetron; block the serotonin receptors in the chemoreceptor trigger zone (CTZ)
within the medulla oblongata. The CTZ communicates with the vomiting center to
initiate vomiting. By blocking the serotonin receptors, there's less serotonin that enters
the CTZ, which decreases communication with the vomiting center. Ultimately, the
patient experiences reduced nausea and vomiting.
Side effects of Anti-Emetics

 The side effects depend on the type of antiemetic drug taken:
o antihistamines: drowsiness, dry mouth
o dopamine antagonists: dry mouth, fatigue, constipation, tinnitus, muscle
spasms, restlessness
o serotonin 5-HT3 receptor antagonists: constipation, dry mouth, fatigue
o corticosteroids: indigestion, acne, increased appetite and thirst
o cannabinoids: changes in perception, dizziness
 If you experience any of the following, consult your doctor:
o worsening of nausea or vomiting
o severe constipation
o muscle weakness
o convulsions
o loss of hearing
o rapid heartbeat
o severe drowsiness
o slurred speech
o psychological symptoms, like hallucinations or confusion
STEP 5: Management of Side Effects of Common Emetics and Anti-Emetics (30 minutes)
Coping with emetics and Anti-emetics Side Effects
 In taking medication to control nausea may experience symptoms some of which may be side
effects from the medication.
o Many medication-related side effects diminish with time.

 Anti-emetics:are drugs prescribed to help with nausea and vomiting.
 Dopamine antagonists act in the brain and are used to treat nausea and vomiting
associated with neoplastic disease, radiation sickness, opioids, cytotoxic drugs and
general anaesthetics.
 Ondansetron; block the serotonin receptors in the chemoreceptor trigger zone (CTZ)
within the medulla oblongatadrugs.
 The side effects of antiemetic drug depend on the type of drug taken: examples
antihistamines causing drowsiness and dry mouth,dopamine antagonists causing dry
mouth, fatigue, constipation, tinnitus, muscle spasms, restlessness and serotonin 5-HT3
receptor antagonists causing constipation, dry mouth, fatigue
 What are emetics?

 What are common anti-emetics drugs?
 What are side effects of anti-emetics?
References
Churchill
SESSION 12: COMMON ANTI-ACIDS AND ANTICHOLINERGIC
Learning Tasks
Define anti-acids and anticholinergic
Identify common anti-acids and anticholinergic
Explain mechanism of action and side effects anti-acids and anticholinergic
Explain management of side effects of anti-acids and anticholinergic
Resources Needed:

Method
2 05 Brainstorming
Definitions of anti-acids and anticholinergic
Presentation
3 05 Presentation Common anti-acids and anticholinergic
4 25 Lecture discussion mechanism of action and side effects of common anti-
acids and anticholinergic
5 10 Lecture discussion Management of side effects of common anti-acids and
anticholinergic
6 05
7 05
SESSION CONTENTS
STEP 2: Definition Of Anti-Acids And Anticholinergic (05 Minutes)

ASK students to brainstorm on the definitions of anti-acids and anticholinergic
 Anti-acid
o Is a substance which neutralizes stomach acidity and is used to relieve
heartburn, indigestion or an upset stomach.
 Anticholinergic
o Are drugs that block the action of acetylcholine.
o Acetylcholine is a neurotransmitter, or a chemical messenger.
Step 3: Common Anti-Acids And Anticholinergic (5 Minutes)

Common Acids
 Aluminium Hydroxide and Magnesium Trisilicate
 Magnesium hydroxide insoluble and forms magnesium chloride in the stomach
 Aluminium hydroxide gel forms aluminium chloride in the stomach
 Sodium Bicarbonate and Alginates
Common Anticholinergic
 Atropine
 Antipsychotic like clozapine
 Itratropium
STEP 4: Mechanism of Action and Side Effects of Common Anti-Acids and Anticholinergic
(25 Minutes)
Anti-Acids Drugs
 Antiacids are commonly used for heartburn ,excessive eating and for peptic ulcer disease
Mechanism of action
o These are weak alkalis and so they partly neutralize free acid in the stomach and
partly they stimulate mucosal repair mechanisms around the ulcers possibly by
stimulating local prostaglandin release
o This is by buffering the hydrochloric acid (Normal pH1 to 2) to a lower hydrogen
ion concentration with pH of 3 to 4 which is highly desired because the
proteolytic action of pepsin is reduced and the gastric loses its corrosive effect
 Aluminium Hydroxide and Magnesium Trisilicate

o It acts by raising the gastric pH, this also has the effect of inhibiting the activity of
pepticenzymes, which practically ceases at pH 5
o Given in sufficient quantity for long enough, they can produce healing of
duodenalulcers but are less effective for gastric ulcers
o They do not reduce the volume of hydrochloric acid secreted
o Therapeutic uses
 Antacids are used to relieve the pain of gastric and duodenal ulcers and
refluxoesophangitis by neutralising hydrochloric acid in gastric
 Magnesium hydroxide insoluble and forms magnesium chloride in the stomach

o It does not produce systemic alkalosis, because Mg2+ is poorly absorbed from
the gut
o Another salt, magnesium trisilicate, is also insoluble that it reacts slowly with the
gastric juice, forming magnesium chloride and colloidal silica
o This agent has a prolonged antacid effect, and it also adsorbs pepsin which is
believed to be a mediator for acid secretion.
 Sodium Bicarbonate and Alginates

o These are also used as antiacids and now mixed in some preparation
o Sodium bicarbonate is a very popular home remedy for dyspepsia and is taken
alone or in mixtures
o It reacts with hydrochloric acid and neutralizes it, therefore affording a speedy
relief
o Sodium bicarbonate is not recommended for use as an antacid because it is
absorbed and if ingested in large amounts can cause systemic alkalosis
 Aluminium hydroxide gel forms aluminium chloride in the stomach

o Aluminium hydroxide raises the pH of the gastric juice to about 4, and also
adsorbs pepsin
o Dosage
 When using aluminium hydroxide gel BP (mixture), give a dose of 7.5-15
ml and repeat according to the needs of the patient
 With aluminium hydroxide gel BP (powder), give 0.5-1 gram and repeat
according to the needs of the patient
 With magnesium trisilicate BP, give a dose of 0.5-2 grams and repeat
according to the patient's needs
Side Effects of Acids
 Antacids that contain aluminum hydroxide may cause

o Constipation
o Aluminum-intoxication
o Osteomalacia
o Hypophosphatemia
 Antacids that contain magnesium may cause
o Diarrhea
 This is because they have a laxative effect
o Increased magnesium level in blood
 In patients with renal failure they may cause increased magnesium levels in the
blood, because of the reduced ability of the kidneys to eliminate magnesium from
the body in the urine
 Chalky taste
Anticholinergic
 The ant cholinergic drugs are used clinically for treatment of the gastro intestinal and
opthalamic disorders
Mechanism of action
 These drugs act by occupying receptors sites at the parasympathetic nerve ending
 Which then prevent the action of acetylcholine
 The parasympathetic response is reduced ,depending on the amount of anti-cholinergic
drug activity
 The effect includes mydriasis of the pupil with increased intraocular pressure in patients
with glaucoma, dry tenacious secretions of the mouth , throat ,nose and bronchi and
increased heart rate and gastrointestinal tract motility
 Atropine
o Atropine is used as pre-operative medications
 The usual dosage is 0.5 to 1 mg IV push, may repeat every 3 to 5 minutes
up to a total dose of 3 mg (maximum 0.04 mg/kg)
 An action ison the parasympathetic nervous system inhibits salivary and
mucus glands hence reduce saliva and bronchial secretions during
surgery.
 Also for treatment of pylorospasm and spastic condition on the
gastrointestinal tract
o Also atropine is used in the examination of the eye to dilate the pupil
Side effects of Anticholinergic

 Sensory
o Blurred vision
 Gastrointestinal
o Constipation
o Dryness of the mucus of the mouth, nose and throat
 Genitourinary
o Urinary retention
 Psychological
o Confusion
o Depression
o Nightmares
o Hallucinations
 Cardiovascular
o Orthostatic hypotension
o Palpitation,dysrhythmias
STEP 5: Management of Side Effects of Common Anti-Acids and Anticholinergic (30

Minutes)
Coping with anti-acid drug Side Effects
 Encourage adequate fluids intake to alleviate constipation
 Stop the drug in case of toxicity
Management of side effects of Anticholinergic
 Encourage adequate fluids intake to alleviate constipation
 Give the patient stool softener
 Encourage sucking ice chips or hard candy for the dryness
 Reduce the dose in case of psychological effects
 Monitor the patient’s blood pressure daily in both supine and standing position

 Anti-acid is a substance which neutralizes stomach acidity and is used to relieve
heartburn, indigestion or an upset stomach
 Anticholinergic are drugs that block the action of acetylcholine
Acetylcholine is a neurotransmitter, or a chemical messenger

 What are the commonly used antacids?
 What are the effects of anti-cholinergic?
References

Nurses. Elsevier Health Sciences
Science). McGraw-Hill Education
SESSION 13:ANTI-ASTHMATICS AND COUGH REMEDIES
Learning Tasks
Define of ant-asthmatics
List commonly used ant-asthmatics
Describe the indication ,mechanism of action and side effects of anti-asthmatics
List the commonly used cough remedies
Describe the indication ,mechanism of action and side effects of cough remedies
Resources Needed:

Method
2 05 Brainstorming
/presentation Definition of anti-asthmatics
3 10 Lecture discussion Commonly used anti-asthmatics
4 35 Lecture discussion Indication ,mechanism of action and side effects of anti-

asthmatics
5 10 Lecture discussion Commonly used cough remedies
6 35 Lecture discussion Indication ,mechanism of action and side effects of cough
remedies
8 05
9 05
SESSION CONTENTS
STEP 2: Definition of Anti-Asthmatic (05 minutes)

ASK students to brainstorm on the definition of ant-asthmatics
Is defined as follows
 These are the drugs used to treat asthma

o Recurrent reversible airway obstruction, with attacks of wheeze, shortness of
breath and often nocturnal cough
STEP 3: Commonly Used Ant-Asthmatics (10minutes)

 Most common used ant-asthmatic drugs includes;
o Bronchodilators
 Theophylline
 Aminophyline (theophylline ethylenediamine)
 Beta adrenoreceptors agonists like salbutamol and terbuline
o Anti-inflammatory agents(Glucocorticoids)
 Main drugs used for their anti-inflammatory action in asthma
 are not bronchodilators rather they prevent the progression of chronic
asthma, but are also effective in acute severe asthma like beclometasone
and budesonide
STEP 4: Indications, Mechanism of Action and Side Effects of Ant-Asthmatic
drugs (35 Minutes)
Theophylline
 Tablets contain 125 mg or 250 mg intended for oral administration.

 Dosage
o Acute severe asthma adults orally 100-300mg 3- 4 times daily after food or by
slow intravenous injection over at least 20 minutes (with close monitoring), 250–
500 mg(5 mg/kg) and children 5 mg/kg
 Theophylline reverse airways obstruction and acute severe asthma
 It is a bronchodilator used for asthma and stable chronic obstructive pulmonary disease
 It may have an additive effect when used in conjunction with small doses of beta2
agonists; the combination may increase the risk of side-effects, including hypokalaemia
 Mechanism of action of drug
o The ways in which these drugs produce effect in asthma are still unclear.
o However relaxant effect on smooth muscle has been attributed to inhibition of
the phosphodiesterase (PDE) isoenzymes
Side effects
 Severe or continued vomiting
 Rapid or uneven heartbeats
 Seizure (convulsions)
 Confusion, tremors or shaking
 Severe headache
 Rapid heart rate
 Muscle weakness or limp feeling) due to lowering of potassium level
 High blood sugar (increased thirst, increased urination, hunger, dry mouth, fruity breath
odor, drowsiness, dry skin, blurred vision, weight loss)
Aminophylline
 A mixture of theophylline withethylenediamine, which is 20 times more soluble than

theophylline alone
 It is given by injection when needed rarely for severe attacks of asthma
 Formulations/Preparation Available Injections and tablets
 It must be given by very slow intravenous injection (over at least 20 minutes), it is
tooirritant for intramuscular use
 Dose
o Aminophylline Injection B.P. 250mg/10ml is for slow intravenous administration
for 10 minutes
Side effects
 May cause seizures, tremor, nausea, insomnia, or tachycardia at high drug
concentration.
 Allergy to ethylenediamine can cause urticaria, erythema, and exfoliative dermatitis
 and convulsion may also occur if given by rapid I/V injection
Management of side effects
 Anticonvulsant therapy should be administered in case of seizures like diazepam.
 The serum theophylline concentration should be measured immediately upon
presentation, 2-4 hours later
Salbutamol
 Is a beta2 agonist which acts by stimulating the beta 2 receptors in the smooth muscles
of the bronchi causing relaxation
 Preparations Available
o Tablets, syrup, and aerosol/ inhalation
 Dose 4mg tid daily
o Inhalation 200microgram -2 puff 3 to 4 times a day
 Cautions
o Non-steroidal anti-inflammatory drugs (NSAIDs), especially aspirin, can
precipitateasthma in sensitive individuals
 Mechanism of action
o The beta adrenergic agonists stimulate the beta receptors in the smooth muscles
of the tracheobronchial tree to relax
o Opening the airway passage to greater volume of air
STEP 5: Commonly used Cough Remedies (10 Minutes)

 Anti-cough Drug(cough remedy)
o Are drugs that play role of clearing irritants and infections from the airway
o Cough results from a powerful reflex initiated through irritation of receptors in
the mucosa of the upper respiratory tract
o The receptors are sensitive to stimulation by mediators of inflammation
associated with allergy or infection, by chemicals (sulphur dioxide, cigarette
smoke) or particles
 The anti-cough drugs includes
o Cough Suppressants
o Mucolytics
o Expectorant
o Demulcent
o Steam inhalation
STEP 6: Indications, Mode of Action and Side Effects of Cough Remedies (35Minutes)
Expectorants
 Is a medication that helps bring up mucus and other material from the lungs, bronchi,
and trachea
Mechanism of action
 Expectorants aid clearance by increasing bronchial secretions and the production of
mucus that is less viscous and therefore coughed up more easily.
 Thus the combination ciliary action and coughing expels the phlegm from the pulmonary
system
Guaifenesin
 Is one of the expectorant used
Side effects
 Nausea and vomiting
Steam
 Inhalation of steam aids expectoration
 The warm water vapour hydrates the bronchial tree and increases the secretion of
mucus that is less viscous which can easily be removed by coughing
 Addition of menthol, tincture of benzoin, eucalyptus encourages deep inhalation of the
steam
Mucolytic agents
 One of the mucolytic agent used is acetylcysteine

Mechanism of action
 Acetylcysteine acts by dissolving chemical bonds within the mucus itself ,causing it to
separate and liquefy, reducing viscosity
 It is used to dissolve abnormally viscous mucus that may occur in chronic
emphysema ,emphysema with bronchitis and asthmatic bronchitis
 The reduced viscosity allows easier removal of secretions by coughing ,percussion and
postural drainage
 Also used to treat acetaminophen toxicity
Side effects
 Nausea and vomiting
 Can cause bronchoconstriction and bronchiospasm
o Hence there may be a need for the use of bronchodilators
Cough Suppressants
 Codeine may be effective but it is constipating and can cause dependence

 Dextromethorphan and pholcodine have fewer side-effects than codeine
 The use of cough suppressants containing codeine or similar opioid analgesics is not
generally recommended in children and should be avoided altogether in those under 1
year of age
Side effects
 Dependence
 Sedation
Nasal Decongestants
 Aromatic Inhalations
o Inhalations containing volatile substances such as eucalyptus oil are traditionally
used and although the vapour may contain little of the additive, it encourages
deliberate inspiration of warm moist air which is often comforting in bronchitis
 Pseudoephedrine
o Pseudoephedrine is available over the counter
o Dose
 Adult 60 mg 3–4 times daily
 Child 2–6 years 15 mg 3–4 times daily, 6–12 years 30 mg 3–4 times daily
Side Effects
 Tachycardia, anxiety, restlessness, insomnia, rarely hallucinations, rash, and
urinaryretention also reported

 Anti-asthmatics are the drugs used to treat or prevent asthmatic attacks.Drugs used
includes bronchodilators and anti-inflammatory drugs
 Anti-cough are remedies used to treat coughing,including expectorants and mucolytic
agents
 What is the mechanism of action of salbutamol?
 What is an example of nasal decongestion drug?
References
SESSION 14:ANTI-TUBERCULOSIS DRUGS

Learning Tasks
Define anti-tuberculosis
Identify common anti-tuberculosis
Explain mechanism of action of common anti-tuberculosis
Explain side effects of common anti-tuberculosis
Resources Needed:
 Handout: Pyrazinamide, Streptomycin and Ethambutol
Method
1 05 Presentation
2 05 Brainstorming Definition of anti-tuberculosis
Presentation
3 40 Presentation Commonly used anti-tuberculosis
4 05
5 05
SESSION CONTENTS
STEP 2: Definition of Anti-tuberculosis (05 minutes)

ASK students to brainstorm on the definition of anticancer
Anti-tuberculosis
 These are drugs that are used to manage tuberculosis.
STEP 3: Commonly Used Anti-tuberculosis (40 minutes)

Basic Classification of Anti-Tuberculosis Drugs
Common Essential first line drugs
 Isoniazid (INH or H)
 Rifampicin (RIF or R)
 Pyrazinamide (PZA or Z)
 Streptomycin (SM or S)
 Ethambutol (EMB or E)
Common Second Line Anti-TB Drugs

If a patient is resistant to first line anti-TB drugs, can be initiated on second line drugs
 Ethionamide
 Cycloserine
 Capreomycin
 Kanamycin
 Streptomycin
 Fluoroquinolones (E.g. Ofloxacin, Moxifloxacin)
TB Treatment Regimens
 Tuberculosis is treated in two phases:
o Initial /intensive phase, which consists of: RHZE for 2 months for new case AND SRHZE
for 2 months then RHZE 1 month for re-treatment case.
o Continuation phase, which consists of: RH for 4 months for new patient AND RHE 5
months for re-treatment case.
Table Recommended Daily Doses of first-line anti-TB drugs for adults and children
New/Retreatment Initial phase Continuation phase
New Rifampicin + Isoniazid + Rifampicin + Isoniazid (RH) for 4

Pyrazinamide and Ethambutol in months
fixed dose (RHZE) for 2 months
Retreatments Streptomycin + Rifampicin + Rifampicin + Isoniazid + Ethambutol

Isoniazid + Pyrazinamide and (RHE) for 5 months
Ethambutol for 2 months then
RHZE for 1 month
Source: Standard Treatment Guidelines 2017
Table Daily Dosage of Anti-TB Drugs (FDCs) in new adult patients

Body weight Number of tablets in initial phase: 2 Number of tablets in continuation
months (R150/H75/Z400/E275) mg phase: 4 months (R150/H75) mg
21 – 30 kg 2 2
31 – 50 kg 3 3
51 – 74 kg 4 4
≥ 75 kg 5 5
Table Daily Dosages of anti-TB Drugs (FDCs) in new Pediatric Patients

Duration Drug Weight Bands (Number of Tablets)
4 – 7 kg 8 – 11 kg 12 – 15 kg 16 – 24 kg 25 kg +
2 months of RHZ 1 2 3 4 Go to adult

intensive (75/50/150) dosages and
phase, daily preparation
observed
treatment E (100)
1 2 3 4
4 months of RH (75/50) 1 2 3 4
continuation
phase, daily
observed
treatment
Rifampicin
 Rifampicin is the most important drug to be discovered for TB.
 It was discovered in the late 1950s but registered for use in TB treatment in 1963 (UK)
and 1964 (US).
 In Tanzania rifampicin is only available for management of TB.
Mechanism of action
 Bactericidal and affects RNA/protein synthesis
Administration
 Mainly oral but can be given intravenously
Absorption
 Well absorbed when given orally and reaches peak concentration in plasma 2-4 hours
after oral administration
 Absorption is improved when the oral dose is taken on an empty stomach.
Bioavailability
 90-95%, and undergoes wide distribution into most body tissues and fluids, including
penetration into the cerebrospinal fluid.
 This is an advantage in management of TB meningitis.
 Because of extensive body distribution, saliva, tears, sweat, urine, and faeces are
colored orange-red; this can frighten patients if they are not warned about that.
 And they should be informed that it is sign that the patient is taking the treatment.
Metabolism and elimination

 Rifampicin is metabolized in the liver and intestinal wall
 Rifampicin is an enzyme inducer and this is the basis for many drug interactions,
especially ARV’s (e.g. NVP and PIs).
 So before prescribing it, clinicians need to be aware of this and take the necessary
precautions.
 Patients with liver disease must either avoid use or use at a reduced doses
 Half-life 6-7 hours (can be given once a day)
 About 15-30% of the drug is excreted though urine while 60% to 65% is excreted
through the feces.
 Because most of the drug is excreted through stool, the drug can still be given at renal
failure without dosage adjustment.
Indications
 Rifampicin is the most effective (able to kill the TB bacilli) drug therefore backbone of TB
treatment.
 Used in initial and continuation phases of TB treatment
 Kills both rapidly multiplying and dormant TB organisms
Side effects
 Nausea, vomiting, diarrhoea
 Headache
 Fever
 skin rash and itching
 Thrombocytopaenia and acute haemolytic anaemia.
 Thrombocytopenia refers to reduced number of platelets.
 Patients with severe thrombocytopenia have problems with clotting.
 Rifampicin can also cause red blood cells to disintegrate or hemolyse and this can lead
to anemia and jaundice.
Isoniazid
 Isoniazid (INH) is one of the main drugs used in TB treatment during both the intensive
phase (first two months) and during the continuation phase (6 months)
Mechanism of action
 Bactericidal for rapidly dividing mycobacteria but bacteriostatic for slow growing
mycobacteria
 Inhibits the synthesis of mycolic acid in the mycobacterial cell wall.
 INH also disrupts DNA, lipid, carbohydrate, and interferes with other metabolic activities
of the TB organisms, thus making it difficult for them to live.
Administration
 Mainly oral (tablets or syrup) but can be given intravenously and intramuscularly
Absorption
 Food and antacids such as aluminium hydroxide interfere with absorption
 Metabolized in the liver so the dose must be reduced if liver function is impaired.
 Isoniazid causes hepatotoxicity and patients who develop jaundice should be referred
Excretion
 Isoniazid and its metabolites are excreted in the urine
Indications
 Kills 90% of the total population of bacilli during the first few days of treatment (hence
used in the initial phase).
 Most effective against the metabolically active, continuously growing bacilli.
 Isoniazid and rifampicin are most effective in preventing resistance to other drugs.
 Isoniazid can be used to prevent development of TB disease in a program referred to as
Isoniazid Preventive Therapy (IPT).
o PLHIV who have been exposed to TB with no “active” TB (no signs and
symptoms) are given INH to prevent them from developing active TB according
to the National TB & Leprosy guideline.
Dosage Forms
 Dosage forms: Available as fixed dose combination (FDC), single drug, syrup and
injection (but rarely used)
Side effects
 Unwanted effects depend on the dosage and occur in about 5% of individuals
 Liver problems (Hepatitis)
 It also causes a skin rash, fever, nausea and vomiting may cause haemolytic anaemia in
individuals with glucose 6-phosphate dehydrogenase deficiency deficiency
Drug interaction
 It decreases the metabolism of the antiepileptic agents; phenytoin, ethosuximide and
carbamazepine, resulting in an increase in the plasma concentration and toxicity of
these drugs.

 The aim of TB treatment is to cure patients, and to prevent: relapse, death, drug
resistant organisms, and further transmission
 TB treatment needs to be tailored based on the category of TB disease
 TB treatment must be monitored in order to:
o Assess adherence
o Identify side effects
o Prevent drug resistance
Step 5: Evaluation (5 minutes)

 What are the principle actions of first line Tuberculosis (TB) medication?
 What are the common side effects of first line anti-TB drugs?
 What are the main TB treatment regimens used in Tanzania?
References
MOHCDGEC, 2017. The United Republic of Tanzania Standard Treatment Guidelines and National
Essential Medicines List5th ed., Dar es Salaam.
Handout: Pyrazinamide, Streptomycin and Ethambutol

Pyrazinamide
 Pyrazinamide (PZA) is a relative of nicotinamide.
 The drug is taken up by macrophages and exerts its activity against mycobacteria
residing within the acidic environment of lysosomes.
Mechanism of Action
 Pyrazinamide is converted to pyrazinoic acid - the active form of the drug - by
mycobacterial pyrazinamidase.
 The specific drug target is unknown, but pyrazinoic acid disrupts mycobacterial cell
membrane metabolism and transport functions.
Indications
 Pyrazinamide is an important front-line drug used in conjunction with isoniazid and
rifampin in short-course (ie, 6-month) regimens as a “sterilizing” agent active against
residual intracellular organisms that may cause relapse.
 Tubercle bacilli develop resistance to pyrazinamide fairly readily, but there is no cross-
resistance with isoniazid or other antimycobacterial drugs.
Side effects
 Major adverse effects of pyrazinamide include hepatotoxicity (in 1–5% of patients)
 Nausea
 Vomiting
 drug fever
 hyperuricemia
Streptomycin
 Streptomycin was isolated from a strain of Streptomyces griseus.
Mechanism of action
 Irreversible inhibitor of protein synthesis, but the precise mechanism for bactericidal
activity is not known.
Indications
 Streptomycin is mainly used as a second-line agent for treatment of tuberculosis.
 Nontuberculous Infections: In plague, tularemia, and sometimes brucellosis
Dosage
 The dosage is 0.5–1 g/d (7.5–15 mg/kg/d for children), which is given intramuscularly or
intravenously.
 It should be used only in combination with other agents to prevent emergence of
resistance.
 The typical adult dose is 1 g/d (15 mg/kg/d).
Side effects
 Streptomycin is ototoxic and nephrotoxic.
 Vertigo and hearing loss are the most common adverse effects and may be permanent.
 Toxicity can be reduced by limiting therapy to no more than 6 months whenever
possible.
 Fever, skin rashes, and other allergic manifestations may result from hypersensitivity to
streptomycin.
 Pain at the injection site is common but usually not severe.
 Streptomycin given during pregnancy can cause deafness in the newborn and,
therefore, is relatively contraindicated.
Ethambutol
 Susceptible strains of Mycobacterium tuberculosis and other mycobacteria are inhibited
in vitro by ethambutol, 1–5 mcg/mL.
 Ethambutol is well absorbed from the gut.
 Ethambutol crosses the blood-brain barrier only when the meninges are inflamed.
 As with all anti-tuberculous drugs, resistance to ethambutol emerges rapidly when the
drug is used alone. Therefore, ethambutol is always given in combination with other
antituberculous drugs.
Mechanism of action
 Ethambutol inhibits mycobacterial arabinosyl transferases.
Dosage
 The higher dose is recommended for treatment of tuberculous meningitis.
 The dose of ethambutol is 50 mg/kg when a twice-weekly dosing schedule is used.
Side effects
 The most common serious adverse event is retro-bulbar neuritis, resulting in loss of
visual acuity and red-green colour blindness.
 This dose-related adverse effect is more likely to occur at dosages of 25 mg/kg/d
continued for several months.
Contraindications
Ethambutol is relatively contraindicated in children too young to permit assessment of visual acuity
SESSION 15: ANTIPSYCHOTIC AND ANTIDEPRESSANT DRUGS

Learning Tasks
Define antipsychotics and antidepressants
Identify common antipsychotics and antidepressants
Explain mechanism of action of common antipsychotics and antidepressants
Explain side effects of common antipsychotics and antidepressants
Resources Needed:

Method
tasks
2 05 Brainstorming Presentation Definition of antipsychotics
3 20 Presentation Commonly used antipsychotics
4 05 Brainstorming Presentation Definition of antidepressants
5 15 Presentation Commonly used antidepressants
SESSION CONTENTS
STEP 2: Definition of Antipsychotics (05 minutes)

ASK students to brainstorm on the definition of antipsychotic
Antipsychotics
 Antipsychotic drugs, sometimes called major tranquilizers or neuroleptics are drugs
which are effective in treatment of schizophrenia, although most have additional
indications.
 They are primarily used to manage psychosis (including delusions, hallucinations,
paranoia or disordered thought), principally in schizophrenia and bipolar disorder.
STEP 3: Commonly Used Antipsychotics (20 minutes)

Medications used to treat psychotic disorders are well known and include typical antipsychotics, such as
the phenothiazines (e.g. chlorpromazine) and the butyrophenones (e.g. haloperidol)
Chlorpromazine
Mechanism of Action
 Chlorpromazine is a narcoleptic drug (often known as a “major tranquillizer”) which
abolishes or reduces the thought disorder which characterizes schizophrenia.
 It is believed to act by blocking the D2 dopamine receptors in the limbic areas.
Indications
 Chlorpromazine is used in the treatment of schizophrenia and related disorders.
 For long-term treatment of schizophrenia the patient should be maintained on the
lowest possible dose that will prevent major exacerbation of symptoms of the disease
 Chlorpromazine is also used in the treatment of severe organic psychosis
 The dosage is to give 50-300mg orally every 8 hours depending on clinical requirements.
Side Effects
 Chlorpromazine may adversely affect movement, autonomic nervous functions and
hematopoiesis.
 These may occur after some years of antipsychotic therapy.
 There may be tardive dyskinesia, a movement disorder usually with involuntary
movement of the tongue, jaw and face.
 Postural hypotension, dryness of mouth, visual disturbances, retention of urine and
constipation may also occur.
 Jaundice, rashes and agranulocytosis are rare.
Contraindications
 Chlorpromazine is contraindicated in hypersensitivity, glaucoma, Parkinson’s disease
and impaired consciousness.
Drug Interactions
 Chlorpromazine and haloperidol interact with Reserpine, leading to increased risk of
extra pyramidal effects.
 Metoclopramide interacts in the phenothiazines and Haloperidol, also causing increased
risk of extra pyramidal effects.
Haloperidol
Mechanism of Action
 A selective depressant action on the CNS and reduces psychomotor activity
 Produces less sedation than chlorpromazine
 Marked antiemetic activity
 Long duration of up to 24 hours and therefore need not be given more frequently
thanonce or twice daily
 Readily absorbed from the GIT, concentrated in the liver and in part excreted in the bile
 Slowly excreted in the urine, with less than half of the dose taken being eliminated in
4days
Indications
 Haloperidol is used in the treatment of mania and schizophrenia to control
delusions,hallucinations and paranoia
 It is also used in tranquilizing and treatment of behavioral disturbances in adults
andchildren. It is used in short-term adjunctive treatment of severe anxiety
Dosage
 Treatment of psychoses in adults, given by mouth initially 2-5mg daily in divided
dosesgradually, increasing to 100mg daily in severely disturbed patients
 For treatment of psychoses in children, give 25-50 micrograms per kg body weight
dailyto a maximum of 10mg
 For adolescents, give up to 30mg daily in two divided doses
 In severe anxiety, give adults 500 micrograms orally twice daily
 For the treatment of psychoses, given by I/M injection 2-10mg (increasing to 30
foremergency control) and then 5mg every 4 to 6 hours or more frequently, as may
bedeemed necessary
Side Effects
 Adverse effects and contraindications are the same as with chlorpromazine
 It is less sedating than chlorpromazine and has fewer ant cholinergic and
hypotensivesymptoms
Drug Interactions
 Haloperidol and phenothiazines may increase risk of extra pyramidal effects
 Carbamazepine, phenothiazines and rifampicin interact with haloperidol causing
reduced plasma concentrations of haloperidol
STEP 4: Definition of Antidepressant (05 minutes)

ASK students to brainstorm on the definition of antidepresants
Antidepressant
 An antidepressant is a medication used primarily in the treatment of depression.
 The available antidepressant drugs include the (SSRIs) selective serotonin reuptake
inhibitors (SSRIs), MAOIs or monoamine oxidase inhibitors, tricyclic antidepressants,
tetracyclic antidepressants, and others.
STEP 5: Commonly Used Antidepressants (15 minutes)

 Antidepressant drugs are effective for treating moderate to severe depression
associated with psychomotor and physiological changes such as loss of appetite and
sleep disturbance, improvement in sleep is usually the first benefit of therapy.
 They are also effective for dysthymia (lower grade chronic depression).
 Drug treatment of mild depression may also be considered in patients with a history of
moderate or severe depression.
 There is little to choose between the different classes of antidepressants in terms of
efficacy, so choice should be based on the individual patient’s requirements, including
the presence of concomitant disease, existing therapy, suicide risk, and previous
response to antidepressant therapy.
 SSRIs are better tolerated and are safer in overdose than other classes of
antidepressants and should be considered first-line for treating depression.
 MAOIs have dangerous interactions with some foods and drugs, and should be reserved
for use by specialists.
 St John’s Wart (Hypericumperforatum) is a popular unlicensed herbal remedy for
treating mild depression.
TRICYCLIC ANTIDEPRESSANTS
 Imipramine and Amitriptyline are the most widely used in the treatment or depressive
episodes
 Imipramine is less sedative compared to Amitriptyline
Mechanism of action
 Inhibitors of the reuptake of nor adrenaline (nor epinephrine) and serotonin (5-HT)
incentral monoaminergic neurons
Imipramine
 Indicated for depressive illness; also used for nocturnal enuresis in children
 Cautions, Contraindications and Side Effects
 see under Amitriptyline Hydrochloride (but less sedating)
Dose
 Depression, initially up to 75 mg daily in divided doses increased gradually to 150–200
mg (up to 300 mg in hospital patients); up to 150 mg may be given as a singledose at
bedtime; in elderly initially 10 mg daily, increased gradually to 30–50 mg daily;in child
not recommended for depression.
 Nocturnal enuresis, child 7–8 years 25 mg, 8–11 years 25–50 mg, over 11 years 50–75
mg at bedtime; maximum period of treatment (including gradual withdrawal) 3 months-
full physical examination before further course.
Amitriptyline
Indications
 Depressive illness and as a prophylaxis of migraine.
Dose
 For depressive illness, initially 50-70mg in a single or divided dose, gradually increased
to 150mg.
 For prophylaxis of migraine, 25mg at night increased to 75mg
Precautions
 Avoid alcohol and driving as it causes drowsiness
Side Effect
 Dry mouth
 Constipation
 urinary retention
 impotence
 drowsiness
 anorexia

 Antidepressant drugs are effective for treating moderate to severe depression
associated with psychomotor and physiological changes such as loss of appetite and
sleep disturbance, improvement in sleep is usually the first benefit of therapy.
 Drug therapy should be used addition to behavioral therapy.
 Adherence counseling is of significant importance to psychotic patients.

What are the classes of antidepressants?
What drugs are used to treat schizophrenia?
References
Bennett, P. N. (2003). Clinical pharmacology. (9th ed.). London: Churchill Livingstone.
Churchill
SESSION 16: ANTICONVULSANTS AND HYPNOTICS AND ANXIOLYTICS
Learning Tasks
Define anticonvulsants, hypnotics and anxiolytics
Identify common anticonvulsants, hypnotics and anxiolytics
Explain mechanism of action of common anticonvulsants, hypnotics and
anxiolytics
Explain side effects of common anticonvulsants, hypnotics and anxiolytics
Resources Needed:

Method
tasks
2 05 Brainstorming Definition of anticonvulsant
Presentation
3 20 Presentation Commonly used anticonvulsants
4 15 Presentation Hypnotics and anxiolytics

SESSION CONTENTS
STEP 2: Definition of Anticonvulsants (05 minutes)

ASK students to brainstorm on the definition of anticonvulsant
Anticonvulsants
 Anticonvulsants (also commonly known as antiepileptic drugs or as anti-seizure drugs)
are a diverse group of pharmacological agents used in the treatment
of epileptic seizures.
STEP 3: Commonly Used Anticonvulsants (20 minutes)

Phenobarbitone
 The most common medicine and cheapest for use
Mechanism of Action
 Like the other barbiturates, phenorbabitone acts in a non-selective manner, at its
mainmechanism of action is that of potentiation, the effect of Gamma Amino Butyric
Acid(GABA) and reducing the action of glutamic acid at the receptor sites.
Indications
 It is used for temporal lobe epilepsy, tonic clonic seizures, status epilepticus
andprevention of febrile convulsions status epilepsy, except absence seizures
Dosage
 It should be given only once daily at night
 In children dosage is, by mouth 3 – 5 mg/kg body weight per day
 Adults, 60–180 mg at night
 For status epilepticus, by intravenous injection (dilute injection 1 in 10 with water
forinjections), 10 mg/kg at a rate of not more than 100 mg/minute, max 1 g
Contraindications
 Phenorbabitone is contraindicated in porphyria
Drug Interactions
 Phenorbabitone is a potent liver enzyme inducer and increases the clearance of
manymedicines including warfarin, carbamazepine, oral contraceptives steroids and
folicacid.
 It also has additive effect with other sedative or hypnotic medicines
Side Effects
 Hepatitis, hypotension;
 respiratory depression,
 behavioural disturbances, drowsiness,lethargy, depression, ataxia, hallucinations,
impaired memory and cognition,
 hyperactivity particularly in the elderly and in children;
 osteomalacia,
 megaloblasticanaemia (may be treated with folic acid)
Phenytoin
 It is one of the most effective drugs for the treatment of partial and
generalizedtonic/clonic seizures.
Mechanism of Action
 Phenytoin has a number of actions on neurons
 It acts on voltage-sensitive sodium channels thereby blocking the repetitive firing
ofneurons
 It reduces calcium entry into neurons which block neurotransmitter release, and
itenhances the action of the inhibitory neurotransmitter GABA
Indications
 It is used as a prophylaxis in partial seizures and as treatment in tonic/clonic seizures
 Phenytoin is not normally effective against other generalized seizure types.
 Phenytoin is the third choice after phenorbabitone and diazepam.
The Metabolism and Dosage

 A standard adult dose of 300 mg daily can be toxic or sub therapeutic in 50% ofpatients
 Doses start at 200-300 mg daily, usually given as a single dose and may go up to 500mg
daily (or even higher in exceptional cases) to reach the therapeutic range
Side Effects
 These are common in about 50% of patients, with 10% requiring withdrawal of
themedicine.
 Dose related adverse effect include ataxia, nystagmus, lethargy, slurred speech
andhaematological disturbances requiring regular blood counts during treatment.
Drug Interactions
 Phenytoin like phenorbabitone is an inducer of hepatic enzymes.
 It enhances the elimination of warfarin, carbamazepine, oral contraceptive steroidsand
theophylline.
 Hepatic enzyme inhibitors such as sulphonamides, sulphoneureas, cimetidine
andketoconazole may increase plasma concentration of phenytoin.
Diazepam
 It has several indications and one of them is the management of status epilepticus.
 Dose, mode of action, contraindication and side effects for this drug are discussed
below.
STEP 4: Hypnotics and Anxiolytics (15 minutes)

 These medicines can produce the following effects:
o Reduction of anxiety and aggression
o Sedation and induction of sleep
o Reduction of muscle tone and coordination
o Anticonvulsant effect
Benzodiazepines
 The most commonly used anxiolytics and hypnotics
 They act at benzodiazepine receptors which are associated with gamma-amino
butyricacid (GABA) receptors.
 They enhance the activity of the inhibitory neurotransmitter at the GABA receptor
whichis situated on chloride channel.
 The benzodiazepines act on another receptor on the chloride channel which is
distinctfrom the GABA receptor site.
 The commonly used benzodiazepine at the primary facility is Diazepam.
 Others includeLorazepam, Olanzepam and Clonazepam.
Diazepam
 This has a relatively selective action on components of the limbic, thereby
reducinganxiety at doses that have little effect on the reticular activating system (i.e.
little sedativeeffect). It has also the relaxant effect on skeletal muscle (mediated
centrally).
 Diazepam has an anticonvulsant activity and has long half-life and also it can also
causeamnesia; this is why is used in pre-anesthetic medication (e.g. in dental
procedures)
 It is indicated for short term use in anxiety or insomnia, recurrent seizures,
febrileconvulsions, adjunct in alcohol withdrawal and status epilepticus.
Dosage
 Anxiety: adult doses orally 2mg every 8 hours, increase if necessary to 15 – 30 mgdaily in
divided doses
 Insomnia associated with anxiety: orally 5-15 mg at night
 Night terrors and somnambulism in children: orally 1-5 mg at night
 Severe anxiety: control of acute panic attack by intramuscular injection or slow
IVinjection (rate not more than 5 mg /minute) 10 mg repeated if necessary after 4
hours.
 Status epilepticus: by I/V injection 10-20 mg at a rate of 5mg/minute, repeated
ifnecessary after 30-60 minutes, may followed by I/V infusion to the maximum
of3mg/kg body weight over 24 hours, children 200 – 300 μg/kg.
 Diazepam can be given intramuscularly, but I/V administration is most preferredbecause
absorption can be irregular and unpredictable.
Precautions
 Respiratory disease, alcohol, avoid prolonged use and abrupt withdrawal
 Avoid in patients with porphyria (liver disease) or renal impairment
 Other sedative drugs can produce addictive CNS depression when taken with Diazepam

Contraindications
 Respiratory depression
 Chronic psychosis phobic or obsession state
 Acute pulmonary insufficiencies
 Severe hepatic impairment and myasthenia gravis
Side Effects
 Drowsiness, confusion and ataxia (especially in the elderly)
 Dependency, amnesia, muscle weakness headache, gastro intestinal disturbances,
urinary retention blood disorders and jaundice
 Skin reaction, raised liver enzymes and vertigo

 Phenorbabitone is a potent liver enzyme inducer and increases the clearance of many
medicines including warfarin, carbamazepine, oral contraceptives steroids and folic acid.
 Diazepam has an anticonvulsant activity and has long half-life and also it can also cause
amnesia; this is why is used in pre-anesthetic medication (e.g. in dental procedures)
 It is one of the most effective drugs for the treatment of partial and generalized
tonic/clonic seizures.

 How do Benzodiazepines act?
 What are the side effects of phenobarbitone?
References

Churchill
SESSION 17: ANTICANCER DRUGS

Learning Tasks
Define anticancer
Identify common anticancer
Explain mechanism of action of common anticancer
Explain side effects of common anticancer
Resources Needed:

Method
objectives
2 05 Brainstorming Definition of anticancer
Presentation
3 40 Presentation Commonly used anticancer
4 05
5 05
SESSION CONTENTS
STEP 2: Definition of Anticancer (05 minutes)

ASK students to brainstorm on the definition of anticancer
Anticancer
 Anticancers are drugs used to destroy malignant cells with minimal damage to normal
cells, but few drugs are so selective.
 The majority of anticancer agents (with the exceptional of hormonal drugs) attack all
rapidly dividing cells which accounts for their severe side effect.
STEP 3: Commonly Used Anticancer Drugs (40 minutes)

Anti-cancers can be categorized into the following groups:
 Alkylating Agents
 Ant-metabolites
 Cytotoxic Antibiotics
 Vinca Alkaloids
 Hormones
Alkylating Agents
 Alkylating drugs kill cancer cells by directly attacking DNA, the genetic material of
thegenes.
 By attacking the DNA, the drug prevents the cell from forming new cells.
 Nitrogen mustards, which were the first nonhormonal chemicals with anticancer
abilities,are alkylating drugs. Cyclophosphamide and Mustargen are two alkylating
agents.
 Cyclophosphamide, the most common alkylating agent, is often used in combination
withother drugs to treat breast cancer, lymphomas, and other tumors in both children
andadults.
 Mustargen is part of the treatment for Hodgkin's disease.
Antimetabolites
 These drugs interfere with the production of DNA and keep cells from growing
andmultiplying.
 They are used to treat a variety of cancers including breast cancer, leukemia,
lymphoma,colorectal cancer, head and neck cancer, osteogenic sarcoma,
choriocarcinoma (a rareuterine cancer), and urothelial cancer.
 Examples of antimetabolites are 5-fluorouracil (5-FU), Tegafur, and Uracil.
Antitumor Antibiotics (cytotoxic drugs)

 These are made from natural substances such as fungi in the soil.
 They interfere with important cell functions, including production of DNA and
cellproteins.
 Examples of drugs in this group include, Doxorubicin, Daunorubicin,
Idarubicin,Epirubicin, Dactinomycin, and Bleomycin
Vinca Alkaloids (Antimicrotubule Agents)

 A microtubule is an important part of a cell, and is the target of a class of
anticancerdrugs.
 Vinca alkaloids, which attack the cell's microtubules, are found in very small amounts
inthe periwinkle plant.
 Three types of vinca alkaloids are vincristine, vinblastine andvinorelbine.
 Vincristine is used more frequently in treating childhood, rather than adult, cancers.
 It is used in combination chemotherapy for the treatment of acute lymphocytic
leukemiaand Hodgkin's and non-Hodgkin's lymphoma, as well as other cancers.
 Vinblastine is used in combination chemotherapy for Kaposi's sarcoma, as well as
cancersof the bladder, brain and breast.
 It is also used in the treatment of advanced cases of lymphoma and germ cell cancers.
 Vinorelbine is used mainly in non-small cells lung cancer and in relapsed or
resistantadvanced lung cancer
Hormones
 Steroid hormones slow the growth of some cancers that depend onhormones
 For example, drugs in this group include:
o Progestogens: They are alternative drugs used in breast cancer.
o Examples include:
 Tamoxifen: is used to treat breast cancers that depend on the hormone
estrogen for growth.
 It is given in dose of 10mg twice a day, subsequently increased as
required upto 20mg twice a day.
 Gestronol is used in endometrial cancer and benign prostate hypertrophy
in doses of200-400mg weekly by intramuscular injection
o Oestrogens: Inhibits the production of androgens, and on that account they have
beenused in the treatment of prostatic cancer.
o Examples of drugs in this group include:
 Ethinyloestradol which is given in a dose of 3mg daily.
Side effects of anticancer drugs

Common side effects of anticancer drugs are:
 Low blood counts causes an increased possibility of developing infection or anemia
 Tiredness
 Mouth soreness
 Nausea, vomiting
 Loss of appetite
 Constipation or diarrhea
 Hair loss (alopecia)
 Skin changes or reactions
 Pain or nerve changes
 Changes in fertility and sexuality

 The overall goal of cancer chemotherapy is to give a dose large enough to be lethal
(cytotoxic) to the cancer cells but small enough to be tolerable for normal cells.
 Combination therapy, using cell cycle-specific and cell cycle-nonspecific agents, is
superior in therapeutic effect than the use of single-agent chemotherapy.
 When a cancer is beyond control, the goal of treatment may be palliation (alleviation) of
symptoms.
 What are the common side effects of anticancer drugs?
 How do Alkylating drugs kill cancer cells?
References

Churchill

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SESSION 1: INTRODUCTION TO PHARMACOLOGY

Total Session Time:120 minutes

4 30 Buzzing/Lecture Forms of medicine preparations

6 05 Presentation Key Points

STEP 2: Definition of Terms Related to Pharmacology (35 minutes)

Activity: Brainstorming (10 minutes)

STEP 4: Forms of Medicine Preparation (30 minutes)

Forms of medicine preparation includes:

Factors that Influence Drug Blood Concentration

STEP 8: Key Points (05 minutes)

3 50 Lecture discussion Routes of medicine administration

4 10 Lecture discussion Factors considered in medicine administration

STEP 2: Roles of a Nurse in Drug /Medicine Administration (05 minutes)

Activity: Brainstorming (3 minutes)

The roles includes

 To ensure safe and reliable administration and to monitor side effects.

STEP 4: Routes of Medicine Administration (35 Minutes)

Advantage of oral route administration

Disadvantage of oral route administration

o Injection is made in the upper layer of the skin to the dermis

STEP 5: Factors Considered in Medicine Administration (15 minutes)

 Pharmacodynamics: how the drug works in the body

STEP 8: Principles of Medicine Administration (5 minutes)

 Right dose: A nurse must:

STEP 8: Key Points (05 minutes)

STEP 9: Session Evaluation (05 minutes)

Rang, H. P. (1995). Pharmacology (3rd ed.). London: Churchill Livingstone.

4 30 Lecture discussion Calculation of a drug dosage

STEP 2: Definition of Drug Prescription and Dosage Calculation (05Minutes)

Activity: Brainstorming (3 minutes)

Drug prescription (drug order)

STEP 3: Components of Drug Prescription (10 Minutes)

Nurse must check the following in a prescription before dispensing medicine

Table 3.1: Abbreviations used in a prescription

STEP 4: Calculation of Drug Dosage (30 Minutes)

Tablet and capsule calculation

STEP 5: Key Points (5 minutes)

STEP 6: Session Evaluation (5 minutes)

Rang, H. P. (1995). Pharmacology (3rd ed.). London: Churchill Livingstone.

Session Overview Box

STEP 2: Definition of Analgesics (05 minutes)

Activity: Brainstorming (3 minutes)

STEP 3: Commonly Used Analgesics (10Minutes)

Pharmacological effects of NSAIDs

Indications, mechanism of action and side effects of specific NSAIDS

Aspirin (Acetylsalicylic Acid)

STEP 6: List of Commonly Used Steroids with Anti-inflammatory effects (10Minutes)

Activity: Buzzing (3 minutes)

 These are mostly referred as corticosteroids

STEP 7: Indications, Mode of Action and Side Effects of Steroids(Corticosteroids)

STEP 8: Key Points (5 minutes)

STEP 9: Session Evaluation (5 minutes)

Rang, H. P. (1995). Pharmacology (3rd ed.). London: Churchill Livingstone.

4 15 Lecture discussion Indication ,mechanism of action and side effects of

STEP 2: Definition of Anaesthetics (05 Minutes)

Activity: Brainstorming (3 minutes)

 These are agents that produce anaesthesia

STEP 3: Common Anaesthetics Used (05 Minutes)

Commonly used general anaesthetics