Revision pharm notes for medical students

2. Module content
 Introduction to
pharmacology-definition
of terms,stock control,
principle administration,
calculating
dosages,commonly used
drugs.
 Antimicrobial
agents/antibiotics,
 Sulphonamides
 Anti-tuberculosis
 Antifungal
 Antiviral
 narcotics
 Histamines and
antihistamines
 Brochodilators
 Antihypertensives
 Cytotoxic druds
 drugs used in
hyperthyroidism

3.  Analgesics narcotics,
 antihelminthics
 Antiprotozoa
 anti malarials
 anti spasmodics
purgatives
 cardiac glycosides
antihypertensives,
 Coagulants
anticoagulants,
 Steroids
 ,
 Drugs used in diabetes-
insulin and oral
agentsHematimics
 Diuretics
 Anesthetics drugs –local
and general anaesthesia
 Drugs used in PUD

4. Terminologies
1. Pharmacology: Science that deals with
origin, chemistry, uses and effects of
drugs.
2. Pharmacodynamics: Study of
mechanism of action of drugs and their
other biological and physiological
effects i.e. what the drug does to the
body

5. Terminologies cont’d
3. Pharmacokinetics: What the body
does to the administered drug.
Includes absorption, metabolism &
distribution and elimination.
4. Toxicology: branch of pharmacology
which deals with the undesirable
effects of chemicals on living
systems, from individual cells to
complex body systems.

6.  Drug Interactions: The effect produced when some drugs
are given together and in the course of their action they alter
each other’s duration and magnitude of pharmacological
action
 Intolerance: Low threshold to normal pharmacological
action of a drug
 Tolerance: Decreased response to a drug as a result of
continuous exposure at the same dose or need to increase the
dose of a drug to achieve the same effect


7. types of drugs dependence
 Dependence: State arising from repeated periodic or continuous
administration of a drug that results in harm to the individual and
sometimes society
 Persons feel a desire or a compulsion to continue using the drug and
feel ill if abruptly withdrawn or an antidote is used. Substances that
cause dependence are taken to induce good feelings, or avoid
discomfort of their absence
Psychological dependence: Usually first to appear, where individual
has a craving for the effect or response that the drug produces.
Emotional distress like fear, anxiety, and irritability occur when the
drug is withdrawn.
Physical dependence: This dependence is usually defined in terms of
withdrawal/ abstinence syndrome that are physical in nature i.e. there is
physical illness that accompanies withdrawal.

8.  Iatrogenic Responses: These are responses produced
unintentionally during the treatment of client e.g.
Penicillins may cause hepatic toxicity; steroids may
cause Cushing’s syndrome which is characterized by
moon face, hirsutism, high blood pressure overweight
among other effects
 Pharmacognosy: Study of drugs that come from
natural sources e.g. plants, animals and minerals

9.  Antagonist (blockers): These are substances/drugs
that are sufficiently similar to the natural substance to
be recognized by the receptors and to occupy them
without activation thereby preventing (blocking) the
natural substance from exerting its effect. The
antagonists that have completely no activating effect
are called pure antagonist. Others exert low degree
activation and are called partial agonist

10.  Therapeutic efficacy: Therapeutic efficacy is the
capacity of a drug to produce an effect and it refers to
the maximum effect e.g. if a drug A can produce a
therapeutic effect that cannot be obtained with drug B
no matter how much of drug B is given, then drug A
has the higher therapeutic efficacy

11.  Therapeutic index /window: When the dose of a
drug is increased progressively, the desired response
in the patient usually rises to maximum beyond which
further increases in dose elicit no further benefit but
induce unwanted effects. Therefore, therapeutic index
is the maximum tolerated dose divided by minimum
therapeutic dose. In man, a drug causing maximum
wanted effects with little or no unwanted effects has
wide/large therapeutic ratio.

12.  Placebo: Any component of therapy that is without specific
biological activity for the condition being treated e.g. inactive
substance such as saline or distilled water, usually used in
clinical trials research and for psychological treatments
 Agonists: These are drugs that bind and activate receptors
because they resemble the natural chemicals and produce the
same effects as the natural chemicals

13.  Therapeutic efficacy: Therapeutic efficacy is the capacity
of a drug to produce an effect and it refers to the maximum
effect e.g. if a drug A can produce a therapeutic effect that
cannot be obtained with drug B no matter how much of
drug B is given, then drug A has the higher therapeutic
efficacy.
 Contra- indication: A health condition/state that would
preclude the administration of a drug e.g. aspirin is
contraindicated in peptic ulcers
 Indication: An illness or disorder for the treatment of
which a specific drug has a documented usefulness

14.  Half-life or Half time (t½): Time taken for plasma
concentration of a drug to fall by half or 50%
following its elimination from the body. It enables one
to maintain a steady state/critical plasma
concentrations of a drug in which there is maximum
therapeutic effects and minimum adverse effects. It
determines the frequency of drug administration
 Half-life is determined by rate of biotransformation
and excretion of a drug hence any disease of the liver
and kidney requires the dose to be reduced since the
half life is prolonged which might lead to possible
toxicity
 Pharmacogenetics: The study of the effects that
genetics have on an individual’s response to a drug

15. Others.
 Drugs.-substances that act on biologic systems at
chemical level to produce an effect or alter their fxns.
 Drug receptors- the molecular components of the
body with which drugs interact to bring about their
effects.
 Elimination phase-the phase of drug inactivation or
removal from the body by excretion or metabolism.
 Distribution phase –movement of drug from
administration site in to the tissue.
 Transporter-a specialized molecule usually a protein
that carries a drug ,transmitter or other molecule
across a membrane in which its not permeable eg
Na/K ATPase,serotonin reuptake transporter etc.

16. Sources of drugs and their uses.
 a) Plants sources -Any part of the plant; including
leaves, roots and back can be used.
examples of active ingredients from plants .
 Alkaloids taste bitter and are poorly absorbed in water
but become soluble if dissolved in acids. Examples of
drugs derived from alkaloids include: Atropine,
cocaine quinine, codeine and morphine.
 (ii) Glycosides: These are Digitalis products e.g.
digoxin, digitoxin which are gotten from Digitalis
Purpurea or foxglove plant.

17.  (iii) Gums: These are polysaccharides exudates that
can be used for bulk laxatives and dental adhesives.
 (iv) Resins: the most common resin is benzoin which
is used as an antiseptic.
 (v) Oils: These can be volatile oils like peppermint,
spearmint, menthol, cinnamon, lemon camphor. These
have pleasant fragrance and evaporate easily. The
other type of oil is fixed oils which include castor oil-
used as laxative; olive oil for cooking; emollients used
in cosmetics; solvents for injections

18. b) Animal sources
 These are used to replace human chemicals that are not
produced adequately due to disease or genetic problems e.g.
insulin from pancreases of cows and pigs.
 However, genetic engineering permits scientists to produce
human insulin by altering Escherichia coli bacteria, making
insulin a better product without some impurities that come
with animal products. Other substances gotten from animals
include thyroid drugs (from animal thyroid) and growth
hormone preparation from animal hypothalamus. Despite
these animal sources most of these products are currently
produced synthetically which provides purer and safer
products than animal sources.

19. c) Inorganic sources
 Salts of various elements can have therapeutic effects
in the human body e.g. Aluminum (used as antacids),
Fluoride (used to prevent dental cavities and
osteoporosis), Gold (used for rheumatoid arthritis),
iron (used for Anemia) and potassium (used in K+
supplements).
d)Synthetic Sources
Many drugs are developed synthetically after chemicals
in plants, animals or other environment have been
screened for signs of therapeutic activity .Genetic
engineering are used to produce chemicals that have
therapeutic effects.

20.  Other technological advances are used to alter a
chemical with a proven therapeutic activity to make it
better. Sometimes a small change in a chemical
structure can make that chemical more useful as a
drug i.e. more potent, less toxic or more stable. These
alterations change the pharmacokinetic properties
which makes that chemical more useful as a drug in
different situations

21. Naming of drugs
 Chemical name –Is the name that shows the chemical
formulae of the drug.
 Generic name – Is the name assigned to the drug by
the company that first made it. It’s also called
nonproprietary name or approved name. Ensure that
you differentiate between generic name and generic
drug as the two terms do not mean the same thing.
 Trade name/proprietary name-Is the name that
identifies the different manufacturer of a particular
drug

22. Uses of drugs/medications
 Curative purpose- This could be primary therapy e.g. in
treating infections or auxillary therapy e.g. application of
anaesthetic medication.
 ii. Suppress, signs and symptoms, hence improve quality of
life without attaining cure e.g. anti diabetics.
 iii. Preventive/ prophylaxis- This could be primary e.g. use
of vaccines to prevent one from getting a disease or
secondary to stop progression of an already existing disease.
 iv. Diagnosis of disease- For instance the use of tuberculin
test to diagnose PTB.

23. Forms and preparation of drugs
 Solids e.g. Tablets, Caplets, Capsules, Troches
(lozenge) pastilles;
 Liquids e.g. Solutions, Syrups, Elixirs, Tinctures,
Suspensions, Emulsions ;
 Aerosols, Baths, Creams, Foams, Gels, Liniments,
Lotions,
Nebulizers, Ointments, Pastes, Patches, Powders,
Soaks, Sprays,
 Suppositories, Tinctures, Ampoules, Vials,
Cartridges, Intravenous infusions fluids;
 Implants e.g. Capsules, Pellets

24. Role of the nurse in drug
therapy.
 Patient education
 Ensure compliance
 Note side effects
 Report any change in patients clinical state
 Administration of medication
 Use safe and recommended drugs by ensuring safe
administration and correct drugs.

25. Patient education.
 Explain reason for drug therapy
 Explain dosage
 Instruct how to administer
 Report side effects
 Advice on danger of sudden withdrawal
 Advice on drug interaction
 Not to share drugs
 Keep drugs safely away from children

26. Route of administration
 Enteral-oral
 Parenteral
 Topical
 Inhalation
 Rectal

27. Enteral
27
 Drug administration by mouth, may involve it
swallowing, or it may be placement under the tongue
(sublingual)
 Simplest and most common means of drug
administration.

28. Oral route/enteral.
28
Advantages
 Convenient ;ease of administration, drug can be self
administered
 Reduces systemic infections which can complicate
treatment
 Toxicities can easily be countered using antidotes e.g.
activated charcoal,
 Cheap; no need for drug sterilization,

29. Ct orals.
29
 A variety of drugs can be administered e.g. tablets,
capsules, suspensions etc
Disadvantages
 Unsuitable for unconscious patients
 Harsh GIT environment may affect drug absorption
,limiting bioavailability
Drug absorption can be influenced by presence of food and
gastric motility.e.g the the absorption of tetracyclines can
be reduced by milk and milk products ,griseofulvin’s
absorption is enhanced by fatty meal.
 Some drugs may cause gastric irritation
 Effect is slow in emergencies
 Drugs may undergo first-pass metabolism hence limiting
their efficacy .

30. First-pass metabolism
30
 Refers to hepatic metabolism of a pharmacological
agent when orally administered before reaching
systemic circulation.
 Most drugs absorbed from the GI tract are transported
through the portal circulation and liver, where they
may undergo extensive metabolism before reaching
the systemic circulation. This reduces drug availability
at the target site.

31. Sublingual route
31
 Drugs placed under the tongue to diffuse into the
capillary network and, therefore enter the systemic
circulation directly. e.g. nitroglycerine
Advantages
 rapid absorption,
 convenience of administration,
 low incidence of infection,
 avoidance of the harsh GI environment, and first-pass
metabolism

32. 32
 Disadvantage
 Inconvenience in holding the drug in the mouth
 Only small doses can be administered at any given
time.
 Unfavorable for unpalatable /bitter drugs
 Irritation of the oral mucosa

33. Rectal route
33
 By suppositories or enemas
Advantages
 Mostly used in children
 Little or no first pass effect
 Higher concentrations rapidly achieved
 Useful for drugs that can induce vomiting/unpleasant
taste.


34. 34
Disadvantages
 Slow and erratic absorption
 Inconvenient
 Irritation /inflammation of rectal mucosa may occur

35. Parenteral
35
direct introduction of drug into the systemic
circulation, or other vascular tissue bypassing the
body's barrier defenses .
 Useful for poorly absorbed drugs e.g. heparin and
agents unstable in the GI tract e.g. Insulin
 unconscious patients and circumstances that require
rapid onset of action.

36. Parenteral
36
 highest bioavailability
 Drugs avoid first-pass metabolism or harsh GI
environments.
 provides the most control over the actual dose of drug

37. intravascular
37
 Maybe intravenous/intra-arterial
Advantages
 100% bioavailability
 Immediate onset of action
 Precise and accurate

38. 38
Disadvantages
 Drugs injected cannot be easily recalled
 Risk of infection through contamination
 Rapid infusion of drug may cause hemolysis or other
adverse effects.

39. Intramuscular
39
 Provides for administration of aqueous solutions or
specialized depot. Absorption is fast for aqueous
solution and slow for depot preparation.
Advantages
 Suitable for sustained release preparations
 Faster and more complete-higher bioavailability than
oral adm.
 Fast pass metabolism is avoided.
Disadvantages
 Pain at site of injection for certain drugs

40. subcutaneous route
40
 Slower than IV route.
 Minimizes risks associated with intravascular
injection.
 E.g administration of lidocaine and epinephrine ,some
contraceptives.

41. subcutaneous route
41
 Slower than IV route.
 Minimizes risks associated with intravascular
injection.
 E.g administration of lidocaine and epinephrine ,some
contraceptives.
 First pass metabolism is avoided.

42. Intrathecal:
In this route the drug is injected into the spinal
subarachnoid space, it by-passes the blood- brain barrier
which cannot be passed or is passed slowly by many
compounds. Hence, this route is appropriate when rapid
effects are required e.g. in treatment of an infection or
during administration of anaesthesia. The lumbar
puncture needle is used for this purpose.
 Epidural: Injection is given via a small catheter into
the epidural space used especially for opioids in pain
management

43. Epidural
 Injection is given via a small catheter into the
epidural space used especially for opioids in pain
management

44. Topical route
44
 Application of drug directly to the skin surface
 Drugs can be administered on mucous membranes e.g.
eyes,ear,nose,throat,airway,vagina and urethra.
 Topical dosage forms include;
 Lotions,creams,ointments for the skin
 Solutions,suspensions,ointments for the ears.
 Sprays and powders for nose and lungs
 Use to achieve local effect.

45. Advantages
45
 Local therapeutic effects
 Avoidance of first pass metabolism.
 Convenient and easy to apply.
 Achievement of efficacy with lower total daily dosage
of drug by continuous drug input.
 Ability to easily terminate the medications, when
needed.

46. Advantages
46
 A relatively large area of application in comparison
with buccal or nasal cavity
 Ability to deliver drug more selectively to a specific
site.
 Avoidance of gastro-intestinal incompatibility.

47. Disadvantages
47
 Skin irritation of contact dermatitis may occur due to
the drug and/or excipients.
 Poor permeability of some drugs through the skin.
 Possibility of allergenic reactions.
 Can be used only for drugs which require very small
plasma concentration for action
 Enzyme in epidermis may denature the drugs
 Drugs of larger particle size not easy
to absorb through the skin

48. Others
48
Inhalation route
 provides rapid delivery drugs across the large surface
area of the mucous membranes of the respiratory tract
and pulmonary epithelium, producing an effect almost
as rapidly as with IV injection.
 used for drugs that are gases e.g. anesthetics, anti-
asthmatics etc.

49. Transdermal
 Application to skin for systemic effect.
 Absorption occurs very slowly because of skin
thickness
 First pass effect is avoided.

50. Factors determining the route of
absorption
50
 Accuracy of dosage
 The condition of the patient
 Physical characteristics of the drug
 Need to bypass first pass metabolism to achieve high
concentration at particular sites
 Speed of drug absorption/release

51. principles of drugs
prescription.
51
Medicines have the potential to enhance health and also
cause harm when used inappropriately.
Rational prescribing is therefore essential in prevention and
treatment.
 Clarity of reasons for prescribing( why? benefits?)
 Accurate history before prescribing eg drug allergies
 Account for factors that may alter the benefits and risks of
treatment.
 Account for patient’s concerns, ideas and expectations
 Select safe, cost effective and individualized treatment .
 Adherence to national guidelines and formulation where
appropriate

52. 52
 Monitor the beneficial and adverse effects of
medicines
 Communicate and document prescribing decisions
with patients, care givers etc
 Prescribe within the limitations of your knowledge
,skills and experience.

53. Five drug rights.
 The nurse should observe the following rights when
administering drugs:
 Right patient- checking their identification tags
(babies, unconscious patients), calling out their
names
 Right drug: confirm using treatment sheet
 Right time: check time. Is it possible for 100 patients?
 Right route: confirm using treatment sheet
 Right dose: confirm using treatment sheet, read
pharmacology

54. Classification of drugs
Drugs can be classified according to
1. System
 respiratory medications
 cardiac medications
 nervous system medications, etc.
2. Function or use. For example,
 nonsteroidal anti-inflammatory medications
 narcotic analgesics
 antidepressants, etc.

55. Classification of drugs contd’
3. Chemical makeup. Examples include:
 aminoglycosides
 estrogens
 opioids, etc.
Classification systems enable us to readily identify
the similarities and differences among a large
number of medications within and outside of a
particular classification.

56. PHARMACOKINETICS AND
PHARMACODYNAMICS OF DRUGS
 pharmacokinetics as the process by which the body,
sick or well, handles and affects the drugs.
 it deals with the rate at which drug molecules cross
cell membranes to enter the body, distribute within it,
structural changes which they are subjected and
finally how they leave the body .
 pharmacokinetics is characterized by four processes:
absorption, distribution, metabolism
(biotransformation) and excretion (elimination)

57. Absorption
 This is the movement of drug molecules from site of
administration into the body. It’s essential for
subsequent steps of pharmacokinetics. The rate of
absorption is vital because it determines when the
drug is available to exert its action. The duration and
intensity of drug action is influenced by absorption
hence, the route of drug administration, dose and the
dosage form are vital considerations during
absorption.

58. Factors influencing drug
administration
 The nature of the absorbing surface i.e. cell membrane
through which the drug must traverse, e.g. the ileum is
large with surface area of 4560 m2 (1/2 football pitch) and a
single layer of epithelium. In the colon and the stomach
there is little absorption. In the buccal mucosa there is good
absorption.
 2) Blood flow to the site of administration. Increased blood
flow e.g. in sublingual route, facilitates drug absorption.
The Pulmonary epithelium also has good blood flow and
surface area and this facilitates speedy absorption of
anaesthetic medication

59.  The health status of the person taking the drug
influences the rate of drug absorption and
transportation, e.g. congestive heart failure or
circulatory shock delay the rate of drug transport to
the active sites. During the management of shock,
intramuscularly administered drugs produce poor
response while intravenously administered drugs
produce good response because they are directly
introduced into circulation. The intravenous route
achieves immediate action. During inflammation e.g.

60.  The lipid solubility of the drugs. The higher the
solubility the more a drug is absorbed. Lipid solubility
ensures high absorption especially in some areas e.g.
the GIT. When in solution drugs form a mixture of
ionized & non ionized forms. The Ionized drug is lipid
insoluble & polar hence non-diffusible. The non-
ionized portion is lipid soluble non-polar & diffuse
rapidly through cell membranes.

61.  The PH of the drugs: Acidic drugs are relatively less
ionized in acidic environment e.g. stomach hence
diffuse easily across membranes due to their lipid
solubility. Basic drugs: Ionize in acidic environment
hence they are not well absorbed through gastric
membrane since they are lipid insoluble and non-
diffusible. Since drugs exist as weak acids or weak
bases the environment of administration is vital

62.  Drug Concentration. Highly concentrated drugs get
absorbed better as the rate of absorption is guided by
the law of mass action. Drugs may be administered in
large doses that exceed the body’s capacity to excrete
(priming or loading doses). For some drugs that take
prolonged periods to reach a critical concentration if
their effect is needed urgently, a loading dose is
recommended e.g. digoxin and aminophyline.
Thereafter, smaller doses (maintenance doses) are
administered to replace the excreted amount. This is

63.  Critical concentration is determined by drug
evaluation studies. The recommended dosage is based
on the amount that must be given to reach critical
concentration. Too much of a drug produce toxic
effects & too little will not produce the desired effects

64.  The dosage form i.e. Tablets, patches, capsules,
suppositories. Drug concentrations can be
manipulated in pharmaceutical processing e.g.
combining an active drug with a resin slows its
release. Other substances are made to resists digestive
action (enteric coated tablets).

65. Distribution
 Distribution is transport of a drug in body fluids from
bloodstream to various tissues of the body and
ultimately its site of action. The rate of distribution
depends on:

66.  The permeability of the capillaries to the drug.
 ii. Lipid solubility and ionization of the drug. Lipid-soluble
drugs are more rapidly absorbed and distributed than lipid
insoluble drugs. As we saw earlier ionized drugs are more
readily absorbed compared to the unionized.
 iii. Cardiac function e.g. cardiac output and regional blood
also influence distribution. Drugs are first distributed to
areas with the richest blood flow e.g. heart, liver, kidney,
brain and later to those with poor blood supply e.g. muscle,
fat tissue.
 iv. The plasma protein and tissue binding

67. The human body has some biological membranes
which limit the distribution of drugs. These
membranes are
Blood brain barrier: Allows distribution of only lipid
soluble drugs e.g. general anesthetics, barbiturates into
the brain and CSF. Blood brain barrier is made of a row
of capillary endothelial cells joined continuously by
tight intercellular junctions. Capillaries are covered by a
fatty sheath of glial cells. Drugs that don’t or slowly
cross blood brain barrier cannot be used to treat
infections in the brain. The use of intrathecal
administration avoids this barrier. Inflammation of the
meninges however, increases permeability of ionized
drugs.

68.  b. Placental barrier: These are Membranous layers
that separate blood vessels of the mother from those
of the fetus. Lipid soluble and some lipid insoluble
substances can
 diffuse through it hence, some drugs meant for the
mother may pass through the barrier to harm fetus.
Examples of such drugs include: steroids, narcotics
and, anesthetics.
 c. Blood – testis barrier: This may limit the
effectiveness of some chemotherapeutic agents used
for treating testicular neoplasm

69. Metabolism/Biotransformation
 Metabolism.Many drugs are inactivated by the liver
(e.g.lignocaine).Such drugs may accumulate in liver
disease.
 Renal excretion.Other drugs are mainly excreted into the
urine (e.g.digoxin,gentamicin).These drugs will accumulate
in renal failure.
 Some drugs are inactivated both by renal excretion and
metabolism(e.g.oxprenolol).
 Plasma half-life is the time taken for plasma drug
concentrations to reduce by half.

70.  Age
 Drug elimination is often reduced in the elderly ,who
are also more sensitive to drug effects.
.

71.  ADVERSE DRUG REACTIONS
 These may be due to:
 Unwanted pharmacological effects (e.g.vomiting with
digoxin).
 Idiosyncrasy,reactions only occuring in certain
individuals(e.g.aspirin-induced asthma).
 Hypersensitivity,due to immunological reactions,the
most important being anaphylaxis(asthma and
hypotension) which may be fatal within minutes ,and
blood dyscrasias(e.g.aplastic anaemia).
 Liver damage and skin rashes also occur by these

72.  Age
 Drug elimination is often reduced in the elderly ,who are
also more sensitive to drug effects.
VARIATION OF DOSAGE
 Dosage in children should be related to the size of the
child.
 The elderly usually only tolerant smaller doses.
 Owing to incomplete absorption,or metabolism,larger
doses are often required when given by mouth,rather than
parenterally.
 Maximal effects only occur after several doses,unless a
higher initial dose is given(loading dose).
 Dosage may be adjusted if the drug effect can be measured
(e.g.heart rate for digoxin in atrial fibrillation;prothrombin

73. VARIATION OF DOSAGE
 Dosage in children should be related to the ageand
weight of the child.
 The elderly usually only tolerant smaller doses.
 Owing to incomplete absorption,or metabolism,larger
doses are often required when given by mouth,rather
than parenterally.
 Maximal effects only occur after several doses,unless a
higher initial dose is given(loading dose).

74.  Dosage may be adjusted if the drug effect can be
measured (e.g.heart rate for digoxin in atrial
fibrillation;prothrombin time for warfarin).
 Measurements of plasma drug concentrations are
occasionally helpful(e.g.anticonvulsants).

75. ROLE OF A NURSE IN DRUG TREATMENT

76. function

77. Antihypertensive drugs
 Definition of hypertension: a chronic medical
condition in which the blood pressure in the arteries is
elevated. Normal systolic pressure is 100-130mmHg
and normal diastolic pressure is 60-90mmHg.
 Classification
 Primary HTN (90-95%) is HTN without obvious
underlying cause. Occurs from > 40yrs
 Secondary HTN (5-10%) caused by other conditions
that affect the kidneys (kidney failure), arteries
(stiff/fat deposits), or heart (failure).

78. Risk factors for HTN
Smoking
Obesity or being overweight
Sedentary lifestyle
Lack of physical activity
Increased intake of sodium
Stress
Aging
Chronic kidney disease (ESRD)

79. Blood pressure
Arterial blood pressure
Peripheral resistance
Cardiac output
Affected by sodium content
in blood and in turn affects
amount of fluid in blood
vessels.
Affected by:
-Blood viscosity
-Hormones
norepinephine/epineph
rine
- vasocnstriction

80. Antihypertensive drugs
 They prevent or control high blood pressure.
 This classification is further divided into:
 Angiotensin-converting enzyme (ACE)
inhibitors e.g. captopril
 b-adrenergic blockers e.g. atenolol (lols)
 Calcium channel blockers e.g. nifedipine
 Centrally acting adrenergics e.g.
methyldopa
 Diuretics e.g. lasix
 Vasodilators e.g. hydralazine

81. Renin-angiotensin system
From the kidneys
From the liver
From the
lungs
Low blood pressure
From
adrenal
cortex
affects
P. R
Affects
C.O
Pressure increases
Pressure
increases

82. Renin Aldosterone System
 When blood volume is low, juxtaglomerular cells
in the kidneys secrete renin directly into
circulation. Plasma renin then carries out the
conversion of angiotensinogen released by the liver
to angiotensin I. Angiotensin I is subsequently
converted to angiotensin II by the enzyme ACE
found in the lungs.
 Angiotensin II is a potent vaso-active peptide that
causes blood vessels to constrict, resulting in
increased blood pressure. Angiotensin II also
stimulates the secretion of the hormone
aldosterone from the adrenal cortex.

83. Renin Aldosterone System
Aldosterone causes the tubules of the
kidneys to increase the reabsorption of
sodium and water into the blood. This
increases the volume of fluid in the
body, which also increases blood
pressure.

84. Mode of Action
 Angiotensin-converting
enzyme inhibitors- dilatation of
the arterial and venous systems
occur through the suppression of
renin-angiotensin I to angiotensin
II conversion
 e.g. captopril, Enalapril

85. Captopril
 Capoten
 Dose : 25mg bd/tds up to 50mg bd/tds
 Indications: hypertension, CCF
 Side effects: cough , metallic taste, hyperkalemia,
protenuria, dizziness/lightheadedness, Fatigue,
Hypotension, Diarrhea, Nausea.
 Contraindications: hypersensitivity, cross
sensitivity among ACE inhibitors, Pregnancy

86. Captopril
 The nurse should keep in mind that Captopril may
cause false-positive result for urine acetone.
 The drug should be administered 1 hour before or 2
hours after meals. It may be crushed if the patient has
difficulty swallowing.
 Keep this medication in the container it came in,
tightly closed, and out of reach of children.
 Store it at room temperature and away from excess
heat and moisture (not in the bathroom).
 Inform the patient that Captopril tablets may have a
slight sulfur odor (like rotten eggs).

87. Captopril
 Instruct the patient to notify the physician
immediately when the following
manifestations are experienced:
 chest pain
 swelling of the face, eyes, lips, tongue, arms,
or legs
 difficulty breathing or swallowing
 fainting
 rash

88. Centrally acting adrenergics
The sympathetic adrenergic nervous
system plays a major role in the
regulation of arterial pressure.
Activation of these nerves to the heart
increases the heart rate, contractility
and velocity of electrical impulse
conduction. sympathetic adrenergic
nerves cause the release of
norepinephrine.

89. Centrally acting adrenergics
 M.O.A : inhibit impulses in the CNS and the
sympathetic nervous system, decreases cardiac
output, blood pressure and pulse rate e.g.
methydopa (aldomet)
 Dose: Initial dose: 250-500mg PO bid-tid or 250mg-1g
IV
 S.E: Discolors urine, initial transient sedation,
edema, hemolytic anemia, hepatic disorders,
fevers, dizziness
 C.I: Liver disease, bisulfate allergy

91. Methyldopa
Nursing Management
 Monitor hepatic function, especially in
the first 6---12 wk of therapy or if
unexplained fever appears. Discontinue
drug if fever or jaundice occur..
Discontinue if edema progresses or
signs of CHF occur.

92. Vasodilators
Vasodilators- reduce blood pressure,
cardiac rate and cardiac output by
relaxing and dilating the smooth
muscle of the arteries. This lowers
blood pressure and allows blood to
flow more easily through the veins and
arteries. e.g. hydralazine (Apresoline)

94. Hydralazine
 Dosage: initial dose: 10 mg po qid first 2 to 4 days.
to 25 mg po qid a day for the balance of the first
week.
 Indications:
 Moderate to severe hypertension (with a diuretic).
Lowering high blood pressure helps prevent
strokes, heart attacks, and kidney problems.
 CHF unresponsive to conventional therapy with
Digoxin and diuretics

95. Hydralazine
Side effects: Dizziness, Drowsiness,
Headache, edema, N, V, D, Sodium
retention, arthritis, peripheral
neuropathy, drug induced lupus
syndrome
Contraindications:
Hypersensitivity, Severe
tachycardia

96. Hydralazine
 Nursing Management
 Monitor the client’s blood pressure and pulse
frequently during initial dosage adjustment and
periodically throughout therapy.
 Report significant changes to the physician.
 Monitor frequency of prescription refills to determine
adherence.
 IM or IV route should be used only when the drug
cannot be given orally.

97. Uses of antihypertensive drugs
 Hypertension-the blood pressure in the
arteries is elevated
 Heart failure-heart is unable to provide
sufficient pump action to distribute blood
flow to meet the needs of the body
 Angina-chest pain due to ischemia of the
heart muscle, generally due to obstruction
or spasm of the coronary arteries

98. Side effects
Hypotension
Tachycardia (HR>100beats/min)
 bradycardia (HR <60 beats/min)
Nausea
vomiting
 headache.

99. Nursing responsibilities
Check for edema especially lower
limbs
Monitor renal function- fluid intake
and urine output
Monitor blood pressure, pulse rate
Check for symptoms of congestive
heart failure e.g. difficulty in breathing
Monitor side effects e.g. hypotension

100. Antianginal drugs
Angina-chest pain due to
ischemia of the heart muscle,
generally due to obstruction
or spasm of the coronary
arteries

104. Antianginals
This classification is further
divided into:
Calcium channel blockers e.g.
nifedipine (adalat)
b-adrenergic blockers e.g.
atenolol

105. Calcium channel blockers
Increased calcium
Increased muscle contraction
Increased pumping action of the heart
Increased blood pressure

106. Nifedipine
 C.I: Contraindicated with allergy to nifedipine, Use
cautiously with lactation, pregnancy.
 Dosage: 10 mg tid PO. Maintenance range, 10–20 mg
tid
 S.E: Dizziness, light-headedness, headache, fatigue,
nervousness, sleep disturbances, blurred vision,
Peripheral edema, hypotension, arrhythmias,
dermatitis, pruritus, urticaria
 N.R: Monitor patient carefully (BP, cardiac rhythm,
input and output), Protect drug from light and
moisture.

107. Nifedipine
Patient teaching :
 Change position slowly to prevent orthostatic
events.
 May cause dizziness or fatigue(use caution when
driving or engaging in tasks that require
alertness).
 Drug may cause inflamed gums.
 Concomitant administration with strong P450
inducers, such as rifampin, are contraindicated
since the efficacy of nifedipine tablets could be
significantly reduced. Hypersensitivity

108. B adrenargic blockers
 M.O.A: Blocks beta-adrenergic receptors of the
sympathetic nervous system in the heart and
juxtaglomerular apparatus (kidney), thus
decreasing the excitability of the heart,
decreasing cardiac output and oxygen
consumption, decreasing the release of renin
from the kidney, and lowering blood pressure.
e.g. atenolol
Dosage:50 mg PO daily

109. Atenolol
Contraindications: bradycardia, may
cause broncho-constriction,
allergy/hypersensitivity, symptomatic
hypotension (blood pressure of less
than 90/60 mm Hg)
 dizziness, vertigo.
NB: masks hypoglycemia

110. Uses
Angina
hypertension

111. Side effects
Postural/orthostatic hypotension
fatigue
headache
edema
dizziness

112. Nursing responsibilities
Monitor for side effects like fatigue
Monitor B/P
Continue to assess angina pain-
pressure or squeezing in the chest,
shoulders, arms, neck, jaw, or back

114. Cardiac Glycosides
 Actions
 1. they increase the strength or force of the
contraction of the heart muscle (myocardium)
 2. they slow the heart rate
 inhibits the Na-K-ATPase membrane pump,
resulting in an increase in intracellular
sodium.
 The sodium calcium exchanger in turn tries
to extrude the sodium and in so doing,
pumps in more calcium.

115. Digoxin
This increases intracellular calcium
and allows more calcium to enter
the myocardial cell: this increases
force of contraction, increases renal
perfusion, decreases heart rate.

117. digoxin
 Uses: Chronic Heart Failure, atria fibrillations
(abnormal heart rhythm characterized by
palpitations, chest pain, fainting.) on ECG P wave
is absent.
 Side effects
 CNS: Headache, weakness, drowsiness, visual
disturbances, mental status change
 GI: GI upset, anorexia

119. Digoxin
Metabolism: Some hepatic
 Distribution: May cross placenta; enters
breast milk
 Excretion: Largely unchanged in the urine
 Contraindications:
 Hypersensitivity
 Caution among patients with imbalances of
calcium, acute MI, severe respiratory
disease, renal or liver disease, pregnancy,
the elderly.

120. digoxin
 Drug-drug interactions
 Therapeutic and toxic effects of D with
erythromycin, quinine
 Incidence of cardiac arrythmias with loop &
thiazide diuretics
 Decreased therapeutic effects with thyroid
hormones, metoclopramide
Increased or decreased effects of oral digoxin
with oral aminoglycosides

121. Cardiac Glycosides
 dosage: 0.125–0.25 mg/day PO
 Nursing considerations:
 Assess vital signs
 check pulse rate for one full minute prior
to administration (if less than 60,
withhold the dose and notify the MD),
 Renal (Monitor I & O) and hepatic
function.
 Avoid giving with meals; this will delay
absorption

124. Antidiarrheals
 MOA: prevents or relieves diarrhea;
inhibits peristalsis and reduces fecal
volume
 E.g. loperamide (slows the passage of
stools through the intestines. This allows
more time for water and salts in the stools to
be absorbed back into the body)
 S.Es: drowsiness, tiredness, or constipation
may occur.

125. Loperamide
 Tablets, capsules, and liquid:
Initial: 4 mg orally after the first loose stool, then
Maintenance: 2 mg after each loose stool, not to
exceed 16 mg in any 24-hour period. Clinical
improvement is usually observed within 48 hours.
 Chewable tablets:
Initial: 4 mg after the first loose stool, then
Maintenance: 2 mg after each subsequent loose stool,
but not exceeding 8 mg in 24 hours.

126. Loperamide
 Monitor fluid and electrolyte balance.
 Patient & Family Education
 Notify physician if diarrhea does not stop in a few days
or if abdominal pain, distension, or fever develops.
 Record number and consistency of stools.
 Do not drive or engage in other potentially hazardous
activities until response to drug is known.
 Do not take alcohol and other CNS depressants
concomitantly unless otherwise advised by physician;
may enhance drowsiness.

128. Bismuth subsalicylate
MOA: Hydrolyzed in GI tract to salicylate, which
inhibits synthesis of prostaglandins responsible for GI
hypermotility and inflammation.
 Dosage: 262 mg tablets prn not more than 8 doses/day
Child: 131mg
 S.E: Temporary darkening of stool and tongue,
metallic taste, bluish gum line; bleeding tendencies.
With high doses: fecal impaction. Encephalopathy
(disorientation, muscle twitching). Hematologic:
Bleeding tendency. Special Senses: Tinnitus, hearing
loss. Urogenital: Incontinence.

130. Nursing Responsibilities
Monitor bowel function; note
that stools may darken and
tongue may appear black. These
are temporary effects and will
disappear without treatment.

132. Laxatives
 This group is also subdivided as below:
 bulk products,
 lubricants,
 osmotics,
 saline laxative stimulants, and
 stool softeners
E.g. magnesium hydroxide, mineral oil,
bisacodyl

133. MOA
 Bulk laxatives - absorb water thus adding bulk to
the stool
 Lubricants- increase water retention in the stool
 Stimulants- speed up peristalsis
 Saline laxatives- pull water into the intestines
 Osmotics- enhance peristalsis and increase
distention
 Stool softeners- reduce the surface tension of
liquids within the bowel

135. Laxatives
 Uses: Constipation
 Adverse Reactions and Side Effects:
abdominal Cramping, diarrhea, and nausea
 Contraindications: abdominal pain, nausea,
vomiting, impaction, GI obstruction or
perforation, gastric retention and colitis.
Caution with large hemorrhoids and rectal
bleeding

136. Laxatives
Nursing considerations:
Monitor blood, I & O, and urine
electrolytes.
Administer only with water to
enhance absorption.

139. Antifungal drugs
 They are divided into;
1. Systemic antifungal drugs for
systemic infections e.g. amphotericin
B
2. Oral drugs for mucocutaneous
infections e.g. ketoconazole
3. Topical drugs for mucocutaneous
infections e.g. clotrimazole

140. Antifungal drugs
 Actions: Decreases sodium, potassium and
nutrients in the cell and increases cell permeability
therefore causing fungus cell death.
 Uses: Fungal infections such as cryptococcosis,
aspergillosis, and candidiasis
 Adverse Reactions and Side Effects: Renal and liver
damage and failure, gastroenteritis, hypokalemia,
anorexia, nausea and vomiting.

142. Nursing responsibilities
 For IV administration, check for
extravasation
 Protect drug from light (cover with foil).
WHY?
 Monitor vital signs, I & O, blood, weight,
renal and hepatic function, hypokalemia
and ototoxicity

143. Amphotericin B

144. Reconstitution of ampho.
 1. Aseptically add 12 mL of Sterile Water for Injection,
to each AmBisome vial to yield a preparation
containing 4 mg amphotericin B/mL.
 DO NOT RECONSTITUTE WITH SALINE OR ADD
SALINE TO THE RECONSTITUTED
CONCENTRATION, OR MIX WITH OTHER DRUGS.
The use of any solution other than those
recommended, may cause precipitation of AmBisome.

145. Reconstitution
Immediately after the addition of
water, SHAKE THE VIAL
VIGOROUSLY for 30 seconds to
completely disperse the AmBisome.
AmBisome forms a yellow, translucent
suspension. Visually inspect the vial for
particulate matter and continue
shaking until completely dispersed.

146. Amphotericin B
 MOA: alters the permeability of the cell by forming
pores in the cell membrane.
 Antifungal activity: has the broadest spectrum of
action against Candida albicans, cryptococcus
neoformans, Aspergillus fumigatus.
 Indications: immunosuppressed pt with severe
fungal pneumonia, cryptococcal meningitis or fungal
sepsis.
 SE: fever, chills, muscle spasms, hypotension, renal
damage, dizziness, nausea, fever, or if you have a slow
heartbeat, chest tightness, or trouble breathing.

147. Dosage
 I.V should be administered by slow intravenous
infusion. IV infusion should be given over a period of
approximately 2 to 6 hours. concn for I.V infusion is 0.1
mg/mL (1 mg/10 mL)
 patients having severe and rapidly progressive
fungal infection, therapy may be initiated with a
daily dose of 0.3 mg/kg of body weight.
 CAUTION: Under no circumstances should a total
daily dose of 1.5 mg/kg be exceeded.
Amphotericin B overdoses can result in
potentially fatal cardiac or cardiorespiratory
arrest

148. Clotrimazole

149. Candidiasis

150. Clotrimazole pessaries

151. Nursing responsibilities
Inform patient to use
them at night
Position for proper
insertion

152. Read more on:
Azoles
- Ketoconazole
- Itraconazole
- Fluconazole
- Voriconazole
- Miconazole
Systemic antifungal drugs for mucocutaneous infections:
Griseofulvin
Terbinafine

153. Read
 Topical antifungal therapy
 - nystatin

154. Sample questions
List four indications of fluconazole
(2mks)
Outline four (4) nursing considerations
for a patient on corticosteriod therapy
(4mks)

155. RESPIRATORY DRUGS

156. ASTHMA.
 Asthma is believed to be an autoimmune disease that
is characterized by wheezes due to narrowing of
bronchi, bronchospasm and inflammation of the
bronchial mucosa. It is a common disorder causing
considerable morbidity and mortality

157.  Pathogenesis of asthma:
 The bronchi become hyperactive as a result of a
number of stimuli that include allergens, viruses and
environmental chemicals.
 Inflammatory mediators are liberated from mast cells,
eosinophils, neutrophils, monocytes and
macrophages.
 Some mediators such as histamine are preformed and
their release causes an immediate bronchial reaction.
 Others such as prostaglandins are formed after
activation of cells and produce more sustained
bronchoconstriction

158. Sympathomimetic
 These drugs mimic the effect of sympathetic nervous
system.
 The sympathetic nervous system has a brochodilating
effect on the bronchioles through the effect on the beta
2-adrenergic receptors found on the bronchioles.
 short-acting beta2-adrenergic
 drugs to bronchodilate: albuterol, pirbuterol,
metaproterenol, terbutaline, levalbuterol
 Non selective sympathomimetics
Epinephrine,isoproterenol
 long-acting beta2-adrenergic
keep airways open, not for acute symptoms:salmeterol,
formoterol,indacaterol.

159. Administer leukotriene modulators
 reduce local inflammatory response in lungs
 does not have immediate effect on symptoms
 Inhibit synthesis of leukotriene
Examples -zafirlukast, zileuton, montelukast
Administer mast cell stabilizer
 reduces release of inflammatory and
bronchoconstrictor mediators from sensitized mast
cells
 Examples- cromolyn, nedocromil

160. • Administer steroids
• to decrease inflammation, which will help open
airways;
• • hydrocortisone, methylprednisolone
beclomethasone, triamcinolone, fluticasone,
budesonide, flunisolide, mometasone inhalers•
prednisolone, prednisone orally
 Antibodies –binds IgE antibodies on mast cell
reduces reaction to inhaled antigen.

161. methyxanthines
• Administer methylxanthines
to assist with bronchodilationoften used when other
medications not effective:• aminophylline, theophylline
 side effect
GI disturbances such as epigastric pain/ nausea
Headache, dizziness, nervousness Mild diuresis, dilation
of blood vessels. Inceased hydrochloric acid secretion
Contraindications and cautions
 These drugs are contraindicated or used cautiously in
cardiac disease, vascular disease, arrhythmias,
diabetes, pregnancy, lactation and hyperthyroidism

162. anticholinergic
Administer anticholinergic drugs (Antimuscarinic
 Mechanism of action
 When given by aerosol, ipratropium competitively
blocks muscarinic receptors in the airways and
effectively prevents bronchoconstriction mediated by
vagal discharge
examples ipratropium inhaler, tiotropium inhaler.
 The most important agent in this group is ipratropium

163. Summary of drugs
SHORT-ACTING β -AGONISTS
a. Albuterol /salbutamol
b. Metaproterenol
c. Terbutaline
LONG ACTING β AGONIST
a. Salmeterl
b. Formoteral
NON-SELECTIVE SYMPATHOMIMETICS
a. Epinephrine
b. Isoproterenol
INDIRECT ACTING SYMPATHOMIMETICS
a. Ephedrine
CORTICOSTEROIDS
a. Inhaled Eg. Beclomethasone
b. Systemic Eg. Prednisone
MAST CELL STABILIZERS
a. Cromolyn
b. Nedocromil

164. METHYLXANTHINES
a. Aminophylline
b. Theophylline
c. Caffeine
ANTIMUSCARINIC
AGENTS
a. Ipratropium
b. Tiotropium
LEUKOTRENE antagonist
a) Montelukast
a. Zafirlukast
b. Zoleuton
Antibodies.-omalizumab.

165. Antihistamines
They block the effect of histamine and
bring relief to patients suffering from
itchy eyes, swelling, congestion, and
drippy nose
Antagonists of histamine (Histamine
triggers the inflammatory response)

166. Uses: Allergies, pruritus and rhinitis
Adverse Reactions and Side Effects:
Most cause drowsiness, headache,
urinary retention, blood dyscrasias,
thickened bronchial secretions and GI
effects
Contraindications: Sensitivity, asthma

167. Antihistamines
Nursing considerations: Monitor
urinary, respiratory and cardiac status.
Examples of Medications in This
Classification:
cetrizine
chlorpheniramine maleate (piriton)

168. Cetrizine
 MOA: Potent histamine (H1) receptor antagonist;
inhibits histamine release during inflammation,
leading to reduced swelling and decreased
inflammatory response
 Indications: allergic rhinitis, urticaria
 S.Es: sedation, Palpitation, edema, Nausea,
diarrhea, abdominal pain, constipation,
Bronchospasm, pharyngitis, Fever,
photosensitivity, rash.

169. N.R Cetrizine
 Take this drug without regard to meals.
 You may experience these side effects:
Dizziness, sedation, drowsiness (use caution
if driving or performing tasks that require
alertness); thickening of bronchial
secretions, dryness of nasal mucosa
(humidifier may help).
 Report difficulty breathing, hallucinations,
tremors, loss of coordination, irregular
heartbeat.

170. Cetrizine
 Adults
 5–10 mg daily PO; maximum dose 20 mg/day (BD)
 Pediatrics
 6 mnths–5 yr: 2.5 mg (one-half teaspoon) PO once
daily. In children 1 yr and older, may increase to
maximum 5 mg daily given as one-half teaspoon q
12 hr; 2–5 yr—one 5 mg chewable tablet per day.
 6–11 yr: 5 or 10 mg daily PO.
 > 12 yr: Use adult dosage.

171. Piriton
MOA: Competes with histamine for H1
receptor sites and reduces allergic
response by blocking histamine.
 Indications: Relief of allergy symptoms such
as urticaria.
 S.E s: Drowsiness, Headache, Urinary
retention, Dry mouth, Blurred vision.
 NB: Sedation increased by alcohol.

172. Piriton
 Ensure patients are warned that this medication
may cause drowsiness and that if they are
affected they should not drive or operate
machinery.
 - Advise patients to avoid alcohol as this may
increase the medication's sedative effects.
 - Drowsiness may improve after a few days of
treatment.
 - In allergy management patients should also be
advised to limit exposure to the allergen.

173. DRUGS USED IN GIT.

174. Drugs acting on symptoms manifested in the
GASTROINTESTINAL SYSTEM
PEPTIC ULCERS AND GERD
Physiology - participating cell-types
1. Parietal cells – secrete HCL and intrinsic factor.
2. Peptic cells (chief cells) –secretes pepsinogen
3. Neuroendocrine cells- secretes histamine
4. Mucous and bicarbonate secreting cells
5. Prostaglandin-secreting cells
174

175. HCL secretion stimulated by
 ACh
 Gastrin hormone
 Histamine
HCL secretion inhibited by prostaglandins
Histamine
175

176. PEPTIC ULCERS
A breach in the mucosa
Location: Duodenum, stomach etc
♦ Basis:
Imbalance between damaging factors
and mucosal defense mechanisms
176

177. Pathophysiology PUD
 A peptic ulcer is an excavation that form in the mucosal
wall of the stomach, duodenum or in the esophagus.
 Peptic ulcer mainly occur in the gastroduodenal mucosa.
The erosion is caused by the increased concentration or
activity of acid-pepsin or decreased resistance of the
mucosa.
 Damage of the mucosa decreases resistance to bacteria
predisposing to infection with H.pylori

178. CAUSES & DEFENSE MXN
AGAINST PEPTIC ULCER
Normal state
DAMAGING FORCES
1. Acid – gastric
2. Peptic enzymes
Normal state
DEFENSIVE FORCES
1. Surface mucus
2. Bicarbonate
3. Blood flow
4. Prostaglandins
5. Epithelial Regeneration
Mucus layer
178

179. DRUGS FOR PEPTIC ULCERS
Principle/Mxn:
♦ Reduction of gastric acid secretion
1. H2-histamine receptor blockers
2. Proton-pump inhibitors
3. Anticholinergic agents(antimuscarinic)
♦ Neutralization of secreted acid
- Antacids
♦ Promoting mucosal protection (cytoprotectants)
- Prostaglandins
- Bismuth cpds
- Sucralfate
♦ Eradication of H. pylori infection
179

180. 1. H2-HISTAMINE RECEPTOR ANTAGONISTS
♦ Moa: competitively bind and block Histamine H2 receptors
 reduce all phases of gastric acid secretion
 No effect on gastric emptying
►E.g. cimetidine, famotidine, ranitidine, nizatidine,
roxatidine(CRAFARON)
P’kinetics
♦ Rapid oral absorption, Parenteral
♦ Distribution – wide- breast milk, placenta
♦ Elimination – urine
180

181.  N/B-if drug receptor binding site results in
activation of the receptor the drug is termed as an
agonist
 If inhibition results the drug is considered an
antagonist

182. Uses of H2-HISTAMINE RECEPTOR
BLOCKERS
1. Duodenal ulcer
2. Gastric ulcer
3. GERD
4. Prophylaxis
5. As pre-anesthetic agent
6. Zollinger-Ellison syndrome
7. with oral enzyme supplements
182

183. Adverse effects of H2-HISTAMINE RECEPTOR
ANTAGONISTS
 Hypergastrinemia
 CNS effects headache and confusion
 Muscular pains
 Skin rashes
 Cimetidine (only) is a weak anti-androgen –
 Nizatidine – urticaria, somnolence, sweating
 rapid infusion – release of histamine, bradykinin
183

184. Ranitidine (zantac)
 Is a histamine H2 receptor agonist that helps lower
the production of stomach acid.
 Indications :
 Short-term treatment of active duodenal ulcer
 Short-term treatment of active, benign gastric
ulcer
 Contraindicated with allergy to ranitidine,
lactation.
 Use cautiously with impaired renal or hepatic
function, pregnancy.

185. Ranitidine
 S.E: Headache, malaise, dizziness,
somnolence (drowsiness), insomnia,
vertigo, Tachycardia, bradycardia,
 Rash, alopecia
 Adult: Active duodenal ulcer: 150 mg bid PO
for 4–8 wk
 Paediatrics: Safety and efficacy not
established.
 Crosses placenta; enters breast milk

186. Ranitidine
 Decrease doses in renal and liver failure.
 Provide concurrent antacid therapy to
relieve pain.
 · Arrange for regular follow-up,
including blood tests, to evaluate effects.
 Teaching: Take drug with meals and at
bedtime. Therapy may continue for 4–6 wk
or longer.

187. cimetidine
Cimetidine is associated with more side effects
which include:
 Granulocytopenia
 Gynecomastia
 Diarrhea
 Fatigue
 Dizziness
 Rash
 Mental confusion

188. 2. PROTON PUMP INHIBITORS
MOA
► Block H+ /K + ATPase
 acid production reduced by ~95%
DRUGS
 Omeprazole
 Esomeprazole
 Iansoprazole
 Rabeprazole
P’kinetics
 Abs: Rapid, enteric coated, swallow whole;
can be reduced by some drugs e.g. sucralfate
 Metabolized (1st pass)- rapid
188

189. 2. PROTON PUMP INHIBITORS
Uses of
Zollinger-Ellison syndrome - DOC
-GERD –2nd line
-Peptic ulcers –1st line
Gastritis
-Dyspepsia
-Prevention of stress related mucosal bleeding
Adverse effects
Dry mouth,
 Hypergastrinemia
 CNS effects
 Skin Rashes
 Mild liver damage
 GIT disturbance - diarrhea can be severe
189

190. 3. ANTIMUSCARINIC AGENTS
MOA: block muscarinic receptor
E.g. Pirenzepine, telezepine more selective for receptors in
stomach mucosal cells
Potency: telezepine more potent than pirezepine
♦ Other antimuscarinicis – mepenzolate, hyoscamine
P’kinetics
Abs:
Poor CNS entry
Largely biliary & renal elimination
Uses
Duodenal and gastric ulcers
190

191. Cytoprotectants
4. PROSTAGLANDIN ANALOGUES E.g. Misoprostol
Effects of PGE2 & PGE1 -
● stimulate secretion of mucus and HCO3
● Increase blood flow
● *Inhibit gastric acid secretion
Uses
1. Prevention/ prophylactic & NSAID
2. Peptic ulcers
Adverse effects
Commonest -Diarrhea, abdominal pain
Uterus -, spotting, dysmenorrhoea, arbotifacient (to be taken
after day 1 of menses)
C/I in pregnancy
191

192. 5. SUCRALFATE (a cytoprotectant)is a prodrug
MOA : form a viscous, sticky gel in the acidic environment &
coats the mucosa
S/E
Constipation
D/I –
Chelates some drugs ∟↓absorption e.g. phenytoin, digoxin
Uses
 Peptic ulcers – long term maintenance
 Prophylaxis – stress ulcers
192

193. 6. BISMUTH COMPOUNDS
MOA: Chelates w/ proteins of ulcer base thus coats it
 active against H. plylori
S/E
 Encephalopathy w/ ↓renal function
 Blackening of tongue, teeth, stool
Uses:
Peptic ulcers
H. pylori
193

194. 7. ANTACIDS
Mxn: neutralize HCL
 may inactivate Pepsin (pH 5)
E.g. Are AL3+, Mg2+ or Na+ hydroxides, carbonates or
bicarbonates, Mg-trisilicates
 Comparison of properties: differ in their capacities, rates,
duration and adverse effects – Often prepared as mixtures
 Na+ salts – most rapid, most potent, most absorbed,
 Mg2+ & Al3+ – slower, more sustained action
 Additive with presence of food
 Ca2+ can cause rebound hyperacidity
 Cations absorbed eliminated by kidney
Uses
 Symptomatic relief of dyspepsia(heartburn)
194

195. S/E of ANTACIDS
 On GIT – abdominal distension, belching, flatulence
 Diarrhea (Mg)
 Kidney stones (silica)
 Constipation (Al)
 Encephalopathy, osteoporosis, myopathy (Al)
 Hypophosphotemia (Al)
 Systemic alkalosis (Na)
 Hypercalcemia & milk-alkali syndrome (Ca)
 Bismuth salts - encephalopathy and arthropathy.
D/I
 Change urine pH
 Alter gastric pH
 Chelate or adsorb drug
195

196. H. PYLORI ERADICATION(PMTCB)
1. Penicillins – Amoxycillin
2. Metronidazole, tinidazole
3. Clarithromycin
4. Tetracycline
5. Bismuth compounds
E.g. Regimens used
 Amoxicillin, metronidazole + omeprozole
 Omeprozole + either amoxycillin or clarithromycin
 Bismuth + two antibiotics (metronidazole or
tinidazole with amoxicillin or tetracycline)
196

198. Review of Kidney Structure

199. The renal system functions
 control of blood pressure
 secretion of erythropoietin,
 regulation of vitamin D activation,
 maintenance of acid-base balance and electrolyte
levels and
 maintenance of volume and composition of body
fluids.
 Diuretics increase urine flow by acting on the
kidney.

200. Classification
 thiazides diuretics
 loop diuretics
 potassium-sparing diuretics
 osmotic diuretics
carbonic anhydrase inhibitors

201. Nephron sites of action of diuretics

203. Types of diuretics and therapeutic uses and
mechanism of action
 Carbonic anhydrase inhibitors (work in proximal
tubule)
 Cystinuria (increase alkalinity of tubular urine)
 Glaucoma (decrease occular pressure)
 Acute mountain sickness
 Metabolic alkalosis
MOA
 Inhibits carbonic anhydrase in PT,
 Blocks reabsorption of bicarbonate and NA is excreted
with HCO.
DRUGS-acetazolamide,dorzolamide,brinzolamide

204. Osmotic diuretics (proximal tubule,
loop of Henle)
 INDICATIONS
 Acute or chronic renal failure
 Reduce preoperative intraocular or intracranial pressure
 Acute glaucoma
 Brain edema
 MOA
 Osmotically retains water in tubule by reducing
reabsorption in PT Descending limb of henles loop and
collecting ducts
 Extract water from cells
DRUGS; mannitol.
 s/e H/A N&V,hypernatremia

205.  Loop diuretics (ascending limb of loop)
 Hypertension, in patients with impaired renal function
 Congestive heart failure (moderate to severe)
 Acute pulmonary edema
 Chronic or acute renal failure
 Nephrotic syndrome
 Hyperkalemia
 Chemical intoxication (to increase urine flow)
MOA
• inhibit the reabsorption of sodium and chloride in the thick
ascending limb of the loop of Henle.
• Causes powerful diuresis and increased ca excretion
 Side effects
 hypotension , ototoxicity
 Drugs.frusemide,bumetanide,torsemide

206. Furosemide (Lasix)
 Uses: Pulmonary edema, acute renal failure,
Chronic heart failure.
 CI: sensitivity to sulfonamides, overzealous
use is dangerous in liver cirrhosis, renal
failure with anuria and heart failure.
 S.Es: Hyponatraemia, hypokalaemia,
Hypotension, Nausea, Dizziness.
 Dosage: 20-80mg. As a single dose or in two
divided doses

207. Furosemide
Furosemide is often given in conjunction
with a potassium supplement or a
potassium-sparing diuretic to counteract
potassium loss.
The medication has a rapid onset of effect
of about one hour when taken orally and
five minutes by injection.
Duration of action is about six hours so it
is possible to use a twice daily dose if
necessary.

208. Nursing considerations
 The drug causes increased urination..
 Give daily doses early so that increased urination does
not interfere with sleep.
 Measure and record regular weight to monitor
mobilization of edema fluid.
 Give food rich in potassium e.g. bananas, fruit juices
 Arrange for regular evaluation of serum electrolytes
 Input /output chart

209. Thiazide diuretics (distal convoluted tubule
 Hypertension
 Congestive heart failure (mild)
 Renal calculi
 Nephrogenic diabetes insipidus
 Chronic renal failure (as an adjunct to loop diuretic)
 Osteoporosis
 MOA
• slow resorption in the distal convoluted tubule, thus
increasing the excretion of sodium and water.
Hydrochlorothiazide
• Reduced excretion of calcium causes moderate diuresis
• DRUGS-hydrochlorothiazide

210. Potassium-sparing diuretics (collecting
tubule
Indication
 Chronic liver failure
 Congestive heart failure, when hypokalemia is a problem
 Aldosterolism
 They are usually combined with thiazides & loop diuretics so that
K+ is conserved in oedema associated with Heart failure, hepatic
cirrhosis and ascites
MOA These diuretics cause retention and sodium loss by
inhibiting Na+ retaining action of Aldosterone.
DRUGS- Amiloride, Triamterene, and Spironolactone.
SIDE EFFECTS- Gynaecomastia, impotence, reduced libido

211. Sprinolactone (Aldactone)
 Uses : edema associated with CHF, nephrotic
syndrome, hepatic cirrhosis when other therapies
are inadequate or inappropriate
 Treatment of hypokalemia or prevention of
hypokalemia in patients who would be at high risk
if hypokalemia occurred.
 CI: allergy to spironolactone, hyperkalemia, renal
disease, anuria.
 Use cautiously with pregnancy, lactation.

212. Sprinolactone
 DOSE: 25mg 1-4 times daily
 N.R: Give daily doses early so that increased
urination does not interfere with sleep.
 Measure and record regular weight to
monitor mobilization of edema fluid.
 Avoid giving food rich in potassium.
 Arrange for regular evaluation of serum
electrolytes
 Input /output chart

214. Anti-diabetic drugs
 Diabetes - Disease resulting from a
breakdown in the body’s ability to produce
or utilize insulin (Causes liver, muscle and
fat cells to absorb glucose).
 Types:
 Type I: results from autoimmune
destruction of insulin-producing beta
cells of the pancreas.
 Type II: results from insulin resistance

215. Glycogen

216. Insulin
Insulin is a hormone produced by beta
cells in the pancreas. It regulates the
metabolism of carbohydrates and fats
by promoting the absorption of glucose
from the blood to skeletal muscles and
fat tissue and by causing fat to be
stored rather than used for energy.

217. Antidiabetic drugs
Anti-diabetics are also subdivided into
the following groups:
Insulin
oral hypoglycemic agents

218. Insulin
Insulin: Lowers the blood glucose by
facilitating the uptake and utilization
of glucose by muscle and fat cells and
by decreasing the release of glucose
from the liver.

219. Insulin
 Sources: beef or pork pancreases or can be produced
semi-synthetically
 Types:
 Rapid acting insulin e.g. Humalog (insulin Lispro)
Onset: 10-30min; duration of action: 3-5hrs
Time: injected 10mins before a meal. Used with longer-
acting insulin.
• Short acting insulin e.g. actrapid (soluble insulin)
Onset: 30min-1hr; duration of action: 5-8hrs
Time: injected 30-60 minutes before meals

220. Types of insulin
 Intermediate acting e.g. Isophane insulin also
known as Humulin N, Novolin N
Onset: 1-2½hrs; duration of action: 18-24hrs
Time: injected 1hr before meals. It is often combined
with rapid- or short-acting insulin.
 Long acting e.g. Ultralente
Onset: 30mins-3hrs; duration: 20-36hrs
Action: Covers insulin needs for about one full day. This
type of insulin is often combined, when needed, with
rapid- or short-acting insulin.

221. Cont’d
 Premixed: a combination of specific proportions of
intermediate-acting and short-acting insulin in one
bottle. E.g. Mixtard (dose -0.3 and 1.0 IU/kg/day)
Time: depending on combination given 30-45mins
before meals
Administered twice in a day.

222. MIXTARD
 2 formulations of Mixtard
 Mixtard® 30
Containing 30% short-acting insulin and 70%
intermediate acting
 Mixtard® 50
Containing 50% short-acting insulin and 50%
intermediate-acting insulin

223. insulin
General guidelines, 0.5–1 unit/kg/day.
The number and size of daily doses,
times of administration, and type of
insulin preparation are determined
after close medical scrutiny of the
patient's blood and urine glucose, diet,
exercise, and intercurrent infections
and other stresses

224. Sites of insulin injection

225. Administration of insulin

226. Uses
Diabetes
ketoacidosis

227. Side effects
Hypoglycemia
hepatotoxicity
allergic responses

228. Contraindications
Sensitivity
hypoglycemia

229. Oral hypoglycemic drugs
Include:
Sulfonylureas e.g. glibenclamide
Biguanide e.g. Metformin
Thiazolidinediones e.g. pioglitazone
(bladder cancer)
Alpha-glucosidase inhibitors e.g.
acarbose (Precose)

230. sulfonylureas

231. Oral hypoglycemic drugs
1. Sulfonylureas
 e.g. glibenclamide/ glybride (1.25
mg),chlorpropamide / diabinese (100-500mg)
 MOA: stimulate insulin secretion
 S.E: Hypoglycemia
2. Biguanide: e.g. Metformin (250mg)
MOA: increases insulin action i.e. by suppression
of glucose output from the liver.

232. Cont’d
 Metformin (glucophage) is often used in patients with
type 2 diabetes who are obese, because it promotes
weight reduction.
 Given in combination with a sulfonylurea lowers blood
glucose concentrations more than either drug alone.
 Advantages:
 less likely to cause hypoglycemia.
 It has prominent lipid-lowering activity
S.E: GIT-metallic taste in the mouth, mild anorexia,
nausea, abdominal discomfort, and diarrhea.

233. Cont’d
4. Thiazolidinediones – e.g. Actos (Pioglitazone)
increase glucose up take of glucose in muscle.
Inhibits the breakdown of fat to FFA.
5. Alpha-glucosidase inhibitors – e.g. acarbose
(Precose) & Miglitol (Glycet), available in the US. They
inhibit the upper GIT enzymes that converts dietary
starch and other complex carbohydrates into simple
sugars which can be absorbed. The result is to slow the
absorption of glucose after meals.

234. sulfonylureas

235. Nursing considerations
Monitor blood glucose i.e. FBS and
RBS
assess for hypoglycemia –lethargy,
sweating
rotate insulin injection sites,
and use human insulin with pork
or beef sensitivity.

237.  Examples of classes of antibiotics includes:
 Beta-lactam antibiotics
 tetracycline,
 aminoglycosides,
 macrolides,
 quinolones,
 Azoles,
 Antimycobacterial agents,.

238.  Sulphonamides
 lincosamides
 other unclassified antibiotics like chloramphenical,
Spectinomycin and vancomycin

239. Inhibits

240.  They all posses the beta - lactam ring as a basic
chemical structure and are further subdivided into:
 Penicillin
 Cephalosporin
 Others e.g. carbapenenerns and monobactams

241. Beta lactams
 Beta-lactams prevent bacteria from constructing a cell
wall, by binding to PBP (Penicillin-binding proteins)
which are enzymes inside bacterial cells involved in
the final stage in the synthesis of peptidoglycan, which
is the major component of bacterial cell walls.
 Contain a beta-lactam 'ring' which attaches to the
active site of the bacterial enzymes.
 Sub-categories: penicillins, cephalosporins
monobactams, carbapenems

242. Penicillins can be classified into
 1. Narrow spectrum (natural penicillins) Examples: benzyl
penicillin, phenoxymethyl penicillin, phenethicillin.
 2. Antistaphylloccoccal penicillins: these are also called
beta-lactamase resistant penicillins or penicillinase-
resistant penicillins): e.g.nafcillin, Cloxacillin,
flucloxacillin, Methicillin.
 3. Broad spectrum penicillins: e.g. Ampicilin, amoxicillin,
baccampicilin, pivampicillin, talampicilin and mezlocillin.
 4. Antipseudomonal (Extended spectrum penicillin) e.g.
Carbecillin, Carfecillin, Ticarcillin, Temocillin, Aziocillin
and Piperacillin.

243. Penicillins
• Gonorrhea- 2-3.5g is administered as a
single dose with probenecid.
 Urinary tract infections:
iii. Meningitis 500mg 4-6 hourly is given
Active against Staphylococci,
Streptococci, Haemophilus influenzae,
Salmonella, and Group A streptococci

244.  First generations e.g. cephalothin, cephapirin, cephalexin,
cefadroxil, Cephradine, cefazolin.
 These are generally active against gram positive bacteria.
They have moderate activity against gram negative
organisms.
 ii. Second generations e.g.: Cefactor, Cefuroxime,
Cephamandole/Cefamandole, Cefotetan, Cefonicid,
cefprozil, ceforanide, carbacephem.
 They are generally active against gram negative e.g.
Haemophilus influenza and Neisseria gonorrhea, E. coli,
Shigella.
 also to some extent gram positive organisms e.g.
clostridium, staphylococcus, streptococcus, pneumococcal

245.  Third generation: e.g. Cefotaxime, ceftazidine,
cefodizime, ceftriaxone, cefixime, ceftizone,
moxalactam, cefperazone. They are generally active
against gram positive and gram negative bacteria.
They are especially better than 2nd generation or first
generation against gram negative bacteria.
 iv. Fourth generation: e.g. cefepime and cefditoren
and loracarbef. These are very good against both gram
positive and gram negative bacteria

246. Pharmacokinetics
 They are metabolized in the liver with half life of 1-4
hours. They excreted unchanged in urine especially by
tubular secretion. Dosage reduced for patients with
renal impairment. Active secretion in the kidney can is
blocked by probenecid.
 Indications: Resistance is occurring due to
chromosomal beta lactamase (especially gram –v

247.  Indications: septicemia, pneumonia, meningitis,
biliary tract infections, peritonitis, urinary tract
infections, and sinusitis.
 Unwanted effects: Most common is hypersensitivity
Hemorrhage due to interference with blood clotting
factors. Use of cephalosporin for more than two
weeks causes thrombocytopenia, neutropenia, and
interstitial nephritis and abnormal liver function tests

248.  Drug interactions
 Cephalosporins interact with alcohol to produce
disulfiram- like effects. Therefore, you will need to
counsel the client to avoid taking alcohol when taking
cephalosporins.
 High ceiling diuretics like frusemide and torsemide
when administered together with cephalosporins are
likely to cause nephrotoxicity. This same effect may
be caused when used with aminoglycosides.
 Oral anticoagulants like warfarin when administered
together with cephalosporin may cause bleeding. This

249. ceftriaxone
 It is indicated for such conditions as serious infections
e.g. septicemia, pneumonia, meningitis, UTI, RTI,
skin and soft tissue infections. Also used for surgical
prophylaxis. It’s contraindicated in penicillin
sensitivity and should be administered with caution in
renal impairment. Calcium ceftriaxone may appear as
precipitate in urine or as gall stones. Ceftriaxone is
also contra-indicated in infants under 6 weeks

250. Monobactams
 E.g. aztreonam (azactam)
 Dose: 1-2g tid
 Active against gram-negative bacteria Citrobacter,
Enterobacter, E. coli, Haemophilus, Klebsiella, Proteus,
pseudomonasand Serratia species
 They have no activity against gram positive bacteria
and anaerobes
 S.e: Rashes

251. Carbapenem
 E.g. Meropenem
Imipenem + Cilastin
 Dose: 250mg-500mg tds or qid
 active against both Gram-positive and Gram-negative
bacteria (pseudomonas aeruginosa)
 Carbapenem antibiotic resistance is a recent scare
story originating from Asia

252. Macrolides
Macrolides act as bacterial protein
synthesis inhibitors
used for people who have an allergy to
penicillins
Streptococcus pneumoniae species have
developed resistance to macrolides.
Erythromycin, clarithromycin,
azithromycin

253. unwanted effects
The common ones include GIT effects like abdominal
cramping, anorexia, antibiotic associated colitis,
vomiting and diarrhea.
They may also cause some neurological effects like
confusion, abnormal thinking, and uncontrollable
emotions

254. Indication:
 They are indicated for gram positive and gram negative
cocci like H. Influenzae, N. gonorrhea,
 Mycoplasma pneumoniae and Streptococcal
pneumoniae,
 some legionella species.
 They can be used to treat infections like acne
vulgaries,
 mycoplasma pneumonia,
 legionnaire’s disease, ocular infections and Diphtheria
among other indications

255. Tetracyclines
 Tetracyclines are broad spectrum bacteriostatic
antibiotics that inhibit protein synthesis.
 Food reduces the absorption of tetracycline, so it
should be taken at least two hours before or after
meals
 Originally quite a wide antimicrobial spectrum but
resistance is now a problem
 Doxycycline, minocycline
 Uses : urinary tract infections, acne

256. Tetracyclines
Do not use tetracycline if you are
pregnant causes permanent
discoloration of the teeth later in
life. Tetracycline can make birth
control pills less effective

257. Quinolones
Quinolones interfere with DNA
replication and transcription in
bacteria therefore inhibit bacteria
multiplication.
Numerous pathogens now exhibit
resistance worldwide.

258. Quinolones
 These are broad spectrum antibiotics though some like
nalidixic acid and cinoxacin have a relatively narrow
antibacterial spectrum.
 Other newer quinolones include: norfloxacin,
ciprofloxacin, ofloxacin, levofloxacin, Acrosoxacin and
pefloxacin

259.  Adverse effects
 These antibiotics cause GIT effects like nausea,
vomiting and diarrhea; they also cause CNS effects
like dizziness, headache, confusion, convulsions
among others. Allergic reactions in form of skin
rashes; they are reported to cause arthropathy in
immature animals hence not recommended for
children and adolescents unless the benefits outweigh
the risk. Other unwanted effects include
photosensitivity and bone marrow suppression.

260.  Contraindication or caution: History of epilepsy or seizures,
glucose-7-phosphate dehydrogenase deficiency, myasthenia
gravis, pregnancy and breast feeding
 Indications
 urinary tract
 invasive external otitis, salmonella typhi infection,
Gonorrhea bacteria prostatitis and cervicitis.
 They are also indicated for anthrax which has been
used as a biological warfare e.g. in 2001 Gulf war. So
the soldiers can take quinolones just before they go to
war in case they are at a risk of exposure to anthrax

261.  Drug interactions
 i. These antibiotics are enzyme (cytochrome P-450)
inhibitors hence interact with other drugs at
metabolism e.g. theophylline, warfarin and caffeine.
 ii. NSAIDS and quinolones causes and increase in the
risk of convulsions. NSAIDS tend to potentiate the
effects

262. Aminoglycosides
Aminoglycosides are bactericidal
antibiotics that inhibit protein
synthesis
Side effects e.g. ototoxicity ,
nephrotoxicity
Examples: Gentamicin, Streptomycin ,
Neomycin, amikacin

263. Amino glycosides are
contraindicated in:
 Patients with hearing deficit because they damage the
8th cranial nerve (vestibulo- cochlear /auditory
nerve).
 Myasthenia gravis since they cause neuromuscular
blockade
 Patients with severe renal disease as they are
nephrotoxic, and those with hypersensitivity.
 Neonates, geriatrics, infant botulism and in patients
with Parkinsonism.

264. Nursing considerations:
 Aminoglycosides require monitoring of drug plasma
concentration especially in the infants, elderly, obese,
in renal impairment states, when administering high
doses and if treatment exceeds 7 days
 Aminoglycosides have a synergistic therapeutic effect
when given with beta lactam antibiotics

265. Azoles
 These include several classes of drugs e.g.
Metronidazole and tinidazole which have anti
bacterial and anti protozoal activity. Others are
fluconazole, itraconazole, clotrimazole, econazole,
ketoconazole, and miconazole which are anti fungal
drugs.
 mebendazole, thiabendazole which are anti
helminthic drugs. Our interest for now is those drugs
with antibacterial activity i.e. metronidazole and
tinidazole. The other classes of drug will be discussed
under their respective classes later. The most
important of the two antibacterial agents is
metronidazole which we are going to discuss here

266.  Metronidazole
 It’s very active against anaerobic bacteria and also
protozoa
 Metronidazole is active against anaerobic bacteria and
protozoa. It is used for treatment of sepsis caused by
organisms like Bacteroids species and anaerobic cocci,
intra-abdominal infections and septicemia, wounds
and pelvic infections, osteomylits, and infections of
the brain /lungs

267.  . Also used in prevention of postoperative infections
especially after bowel surgery, antibiotic- related colitis
e.g. pseudomembraneous colitis, amoebiasis
(entamoeba histolytica) whether in symptomless
carriers and cysts or intestinal and extra-intestinal
infections. Other indications include Giardias, acute
ulcers, gingivitis and dental infections, and Aerobic
vaginosis

268.  Unwanted effects:
 Vomiting and nausea, diarrhea, furred tongue,
unpleasant metallic taste in the mouth, Headache,
dizziness and ataxic,-Rashes, urticaria, angiodema,
peripheral neuropathy is treated prolonged.
Epileptiform seizure if the dose is high, Disulfiram-like
effect occurs with alcohol metronidazole inhibits
aldehyde dehydrogenate which metabolism alcohol.
These effects can be lethal-e.g. tachycardia,
diaphoresis, vomiting, nausea and arrhythmias

269. Sulphonamides
 They inhibit bacteria growth by inhibiting folic
acid synthesis. They are bacteriostatic.
 Bacteria require folate for the synthesis of
precursors (purines and pyrimidines) of DNA
and RNA which are necessary for replication
 Possible side effects include hypersensitivity
(allergic reactions), liver and kidney damage
 E.g. Sulfamethoxazole used in combination with
trimethoprim (the combination is bactericidal)

271. Anticoagulants
E.g. warfarin, heparin
Actions : Prevent clot formation.
Uses:
Myocardial Infarction (MI)
pulmonary embolus
deep vein thrombosis (DVT)
It is also used with dialysis
Primary polycythemia

273. Warfarin
 Oral anticoagulant (Coumadin)
 MOA: Interferes with the hepatic synthesis of vitamin
K-dependent clotting factors (factors II-
prothrombin, VII, IX, and X), resulting in their
eventual depletion and prolongation of clotting times.
 Indications: pulmonary embolism, Venous thrombosis
 C.I.s: hypersensitivity, Peptic ulcer, Severe
hypertension, Pregnancy
 Dosage: adult- initial 2–5 mg/day PO, maintenance 2-
10mg PO

274. Warfarin
 Note: Crosses placenta; enters breast milk
 S.E s: Alopecia, urticaria, dermatitis,
Nausea, vomiting, anorexia, abdominal
cramping, diarrhea, hepatitis, jaundice,
mouth ulcers, nephropathy, red-orange
urine, hemorrhage
 NR: Do not use drug if patient is pregnant
(heparin is anticoagulant of choice); advise
patient to use contraceptives.

275. Warfarin patient teaching
 Carry or wear a medical ID tag to alert emergency
medical personnel that you are taking this drug.
 · Avoid situations in which you could be easily
injured (contact sports, shaving with a straight
razor).
 · Use contraception; do not become pregnant
while taking this drug.
 · You may experience these side effects:
Stomach bloating, cramps (transient); loss of hair,
rash;

276. Patient teaching
 orange-red discoloration to the urine (if
upsetting, add vinegar to your urine and the
color should disappear).
 Report unusual bleeding (from brushing
your teeth, excessive bleeding from injuries,
excessive bruising), black or bloody stools,
cloudy or dark urine, sore throat, fever,
chills, severe headaches, dizziness,
suspected pregnancy.

277. Heparin
 MOA: inhibits thrombus and clot formation
by blocking the conversion of prothrombin
to thrombin and fibrinogen to fibrin, the
final steps in the clotting process.
 Contraindications: Hypersensitivity to
heparin; severe thrombocytopenia;
uncontrolled bleeding; labor and immediate
postpartum period; women older than 60 yr
are at high risk for hemorrhaging.
 Use cautiously with pregnancy; recent
surgery or injury.

280. Heparin contd’
Adult: 5,000 units by deep
subcutaneous injection 24 hr before
surgery and 8–12 hr thereafter for 7
days or until patient is fully
ambulatory.
Pediatric dose: Initial IV bolus of
50 units/kg and then 100 units/kg IV q
4–6 hr.

281. Heparin
Route: Subcutaneous (deep
subcutaneous injection)
Adverse effects: Loss of hair,
Hemorrhage; bruising;
thrombocytopenia; Hypersensitivity:
Chills, fever, urticaria, asthma Others:
suppression of renal function (long-
term, high-dose therapy)

283. Heparin contd’
 Nursing considerations: Do not give IM
injections to patients on heparin therapy
(heparin predisposes to hematoma
formation).
 Apply pressure to all injection sites after
needle is withdrawn; inspect injection sites
for signs of hematoma; do not massage
injection sites.
 Mix well when adding heparin to IV
infusion.
 Check for signs of bleeding; monitor blood
tests.

284. Heparin
 Alert all health care providers of heparin use.
 Have protamine sulfate (heparin antidote)
readily available in case of overdose; it binds to
heparin.
 For treatment of overdose, give protamine sulfate
(1% solution). Each mg of protamine neutralizes
100 USP heparin units. Give very slowly IV over 10
min, not to exceed 50 mg.

285. All anticoagulants
C.I s
Bleeding disorders, such as hemophilia
and leukemia
Ulcers
Nephritis
Endocarditis
Thrombocytopenia purpura.

286. NCK AUGUST 2010 P1
 SAQ
 State four (4) health messages a nurse would share
with a patient on oral anticoagulants. (4mks)

288. Depression

289. Pathophysiology
 Causes: Stressful life events, genetics, personality, and
sex may also play a role.
 Neurotransmitters attach themselves to the end of
brain receptors as a means of communication.
 In depressed individuals, the neurotransmitters do not
stay with the receptors long enough which upsets the
balance of communication.

290. Neurotransmitters involved
 Serotonin: inadequate levels lead to low mood
 Dopamine: responsible for positive effects and
perceptions in the mind such as pleasure and desire ,
regulates memory.
 Evidence suggests that in depression, abnormalities in
dopamine may be related to impaired motivation and
concentration, low levels of noradrenaline and
dopamine may play a role in the fatigue and hypersomnia,
and impaired noradrenaline and serotonergic
regulation may contribute to physical symptoms

291. Antidepressants
Divided into:
 TCAs (Tricyclic Antidepressants) e.g.
amitriptyline, clomipramine
 Heterocyclics e.g. amoxapine, trazadone and
bupropion
 SSRIs (Selective serotonin reuptake inhibitors)
e.g. fluoxetine (Prozac)
 Monoamine oxidase(MAO) inhibitors e.g.
Phenelzine (Nardil)

292. MOA (Monoamine Oxidase)
inhbitors
 MAOs- inhibit MAO (enzyme that breaks down
serotonin, noradrenaline) and thus they increase
epinephrine, norepinephrine, serotonin, and
dopamine.
 MAO is one of the enzymes that break down biogenic
amines (Norepinephrine, epinephrine & serotonin).
 These drugs prevents this process therefore amines
accumulate in the presynaptic granules , increase the
concentration of neurotransmitters causing nerve
stimulation antidepressant effect

293. . Tricyclics/Heterocyclics- block the reuptake of serotonin
and norepinephrine in the nerve endings, thus increasing
their actions of both in the nerve cells.
 Indications: Major depressive disorders, anxiety disorders

295. cont’d
 SSRIs (Selective serotonin reuptake inhibitors) : increase
the extracellular level of serotonin by inhibiting its
reuptake into the pre synaptic cell, therefore
increasing the level of serotonin in the synaptic cleft
available to bind to the post synaptic nerve.

297. Uses
 Depression.
 Nocturnal enuresis in children.

298.  Orthostatic hypotension,
 mouth dryness,
 dizziness,
 drowsiness,
 urinary retention,
 hypertension,
 renal failure
 paralytic ileus.
Side effects

299. contraindications
 Hypertrophy of the prostate,
 seizure disorders,
 renal, hepatic and cardiac disease.

300. Nursing considerations
 Monitor standing and lying BP, orthostatic hypotension
 blood, mental status, hepatic function.
 Observe for urinary retention.
 Withdrawal symptoms occur with abrupt cessation.
 Teach patient on MAO inhibitors to avoid food containing
tyramine (dairy products, meat, fish, liver, some fruits
(such as avocado, fig, and banana), chocolate, and yeast
extracts. Coz tyramine breaks down in the GI tract (in the
presence of MAO inhibitors) and release vasopressors will
lead to hypertensive crisis (severe elevation in blood
pressure).
 Teach patient to avoid alcohol and other sleep inducing
drugs.

302. ANTIPSYCHOTIC
 The groups are:
 Phenothiazines e.g. chlorpromazine
 Thioxanthenes e.g. thiothixene
 Butyrophenones e.g. haloperidol
 Dibenzoxazepines e.g. loxapine succinate (Loxapac)
 Dibenzodiazepines e.g. clozapine

303. Antipsychotics cond’
 Actions: All of these pharmacological agents block
the dopamine receptors in the brain, the area that
involves psychotic behavior
 Uses: Schizophrenia, mania, paranoia, and anxiety.
They are also sometimes used for unrelieved
hiccups, nausea, vomiting, and pediatric
behavioral problems as well as pre-operative
relaxation.
 Adverse Reactions and Side Effects: dry mouth,
photosensitivity, hypotension

304. Antipsychotics contd’
 Contraindications: severe hypertension, severe
depression, parkinsonism
 Nursing considerations: Monitor liver function, I
& O, blood pressure lying and standing
(orthostatic hypotension). Observe for dizziness,
palpations, tachycardia, changes in affect, level of
consciousness, gait and sleep patterns.
 E.g. :Haloperidol, chlorpromazine

305. Artane
 Indicated for control of extrapyramidal disorders
caused by antipsychotic drugs
 S.Es: dry mouth, nausea

307. ANTITUSSIVES and
EXPECTORANTS
 Actions:
Antitussives (e.g. codeine)- suppression of the
cough reflex
Expectorants- decrease the viscosity of thick,
tenacious secretions
 Uses: The expectorants are used with a cough
associated with bronchitis, TB, pneumonia and
COPD. Antitussives are used for nonproductive
coughs.
 Adverse Reactions and Side Effects: Dizziness,
drowsiness and nausea

308. ANTITUSSIVES and
EXPECTORANTS contd’
 Contraindications: pregnancy, lactation .
Caution with the elderly and those with
asthma
 Nursing considerations: Monitor the cough
and the sputum. Increase fluid intake and
humidification to thin secretions

310. CHOLINERGIC BLOCKERS
 E.g. atropine, scopolamine
 Actions: Blocks the autonomic nervous system's acetylcholine
 Uses: Prevention of surgical secretions, to decrease the motility
of the urinary, biliary and GI tracts, reverses neuromuscular
blockade.
 Adverse Reactions and Side Effects: Constipation and dryness of
the mouth.

311. CHOLINERGIC BLOCKERS
 Contraindications: GI obstruction, and
hypersensitivity.
 Nursing considerations: Monitor urinary status
and I & O with particular attention to any dysuria,
frequency or retention.
 Observe mental status and for constipation.
 Administer oral doses with milk or food and
administer parenteral doses slowly with the person
in a recumbent position to prevent postural
hypotension

312. (NSAIDS)

313.  An inflammatory response involves production of
potent chemical mediators that are meant to
destroy pathogens and promote healing.
 As the body reacts to these chemicals it produces
some signs and symptoms of disease, such as
swelling, pain, fever and redness.
 Anti-inflammatory agents block or alter the
chemical reactions associated with the
inflammatory response to stop one or more of the
signs and symtopms of inflammation
 Several drugs are used as anti-inflammatory
agents: corticosteroids, antihistamines and non-
steroidal anti-inflammatory drugs (NSAIDs).

314. Classification
a. Propionic Acid derivatives such as fenbufen, ibuprofen,
ketoprofen, naproxen and fenoprofen.
b. Salicylates and their related substances such as aspirin,
diflunisal
c. Indoleacetic acid derivatives such as indomethacin,
sulindac, etodolac, tolmetin, diclofenac, ketorolac
d. Anthranilic acid/Fenamic acid derivatives such as
mefenamic acid, flufenamic acid/meclofenamate
e. Oxicams such as piroxicam,tenoxicam,meloxicam
f. Pyrozolones such as azapropazone,
phenylbutazone,oxyphenbutazone

315. INDICATIONS
Anti-inflammatory effect-
 NSAIDS decrease prostaglandins E2 and prostacyclin
decreases Vasodilation and indirectly, Oedema.
Analgesic effect-
 They inhibit Prostaglandins synthesis which decreases
sensitization of nociceptive nerve endings to inflammatory
mediators. Prostaglandins sensitize nociceptors to
inflammatory mediators e.g. bradykinin, serotonin by
lowering their threshold of response to pain. Headache
relieve is due to decreased prostaglandin- mediated
vasodilation.
Antipyretic effect-
 Bacterial endotoxins cause release of pyrogenic interleukin
1 which stimulate hypothalamus to produce prostaglandin
E2 which cause increase in temperature. NSAIDS such as
piroxicam, naproxen, and ibuprofen prevent this by
inhibiting prostaglandin synthesis

316.  Other conditions.
 Prevention of premature labor. They inhibit
prostaglandins E2 which are involved in the physiology
of labor (uterine contraction).
 Cardiovascular conditions- The NSAIDS are used in
the treatment of CVS conditions eg transient
ischaemic attacks, angina pectoris and coronary artery
bypass graft. Due to their antiplatelet aggregation
effect as thomboxane A2 is inhibited for instance by
use of aspirin.
 Dysmenorrhea- They inihibit prostaglandins involved
in uterine contractions hence reduce dysmenorrhoea.
 Rheumatoid arthritis and juvenile arthritis- NSAIDS
reduce pain and inflammation in these conditions

317. The adverse effects
Gastrointestinal effects
 dyspepsia
 diarrhoea,
 nausea,
 constipation,
 gastric bleeding/ ulceration due to inhibition of
gastric COX1 which is responsible for synthesis of
prostaglandind that normally inhibit acid production
and protect the mucosa.
 Prostaglandin analogue, misoprostol reduce this
damage.
 Selective COX-2 inhibitors have minimal GI effects. EG
celecoxib

318. Skin eruptions –
rashes,
urticaria,
photosensitivity reactions.
Adverse renal effects.
These are due to inhibition of biosynthesis of
prostanoids which are involved in maintenance of renal
blood flow. –nephrotoxicity
-hepatoxicity
-
Others - - bronchospasms,
- bone marrow depression

319. NSAIDS.
 Contraindications: Asthma, severe liver and/or renal
disease, hypersensitivity. Cautious use with the elderly,
children, lactation, pregnancy and for patients with
GI, cardiac and/or bleeding disorders.
 Nursing considerations: Monitor blood, renal and
hepatic function. Baseline hearing and eye exams are
recommended so that changes can be identified.
Toxicity may be signaled with tinnitus and/or blurred
vision.

321. Salicylates
 E.g. aspirin
 Actions: Antipyretic (inhibits the heat
regulation center in the hypothalamus),
anti-inflammatory (inhibits
prostaglandin), analgesic (inhibits
prostaglandin).
 Has an antiplatelet effect by inhibiting the
production of thromboxane which binds
platelets together to create a patch over
damaged walls of blood vessels.

322. Cont’d
 Uses: Mild to moderate pain, inflammation (arthritis),
fever, used long term at low doses to prevent heart
attacks, strokes and blood clot formation in patients at
high risk of developing blood clots.
 SEs: GIT ulcers, stomach bleeding, tinnitus $vertigo in
high doses
 CI: allergy, hemophilia and other bleeding disorders
 Caution in people with peptic ulcers
 Toxicity-metabolic
acidosis,dehydration,hyperthermia,collapse coma and
death in high doses
 NO SPECIFIC ANTIDOTE

323. Aspirin dosage
 Action low dose aspirin (75-81mg) to prevent heart
attack- junior or baby asprin
 High dose aspirin 325mg-650mg 4-6 hrly max
4000mg/day
 Aspirin 325mg tablet
 Aspirin child 80mg tablet