PHARMACOLOGY LECTURE pg1 *mast cell from Basophils color blue

granules
Acetaminophen- blocks cox1 and cox2
primarily in proximal or center HISTAMINE
-similar to paracetamol  Directly stimulate pain receptor
 Stores in mass cell
 Key chemical mediator
INFLAMMATION inflammation
 Natural, nonspecific defense  Release of histamine produces
mechanism vasodilatation.
 Occurs in response to an injury or  Capillaries become leaky
antigen.  Causes tissue swelling
 Limit spread of injury or antigen.  Responsible for symptoms of
Controls injury anaphylaxis.
Destroy microorganism.
 Acute – 8-10 days HISTAMINE RECEPTORS
 Chronic- months or years. Histamine can produce effects by
interacting with two diff. receptors:
Sign:  H1 receptors- found in smooth
 Swelling muscle of vascular system,
 Pain bronchial tree and digestive system
 Redness and on sensory nerve. Benadril
 Warmth -stimulation results in itching, pain,
 Rabor- redness edema, vasodilatation,
 Dolor- swelling bronchoconstriction.
 Calor- warmth -characteristic symptoms of
inflammation and allergy.
CHEMICAL MEDIATORS  H2 receptor-located in stomach
Alert surrounding tissue of injury -stimulation results in secretion of large
 Histamine amount of hydrochloric acid.
 Leukotrienes Santax- Ranitidine
 Bradykinin
 Complement NONSTERIODAL ANTI-INFLAMMATORY
 Prostaglandin DRUGS
 Primary drugs for treatment of mild
ACUTE INFLAMMATION to moderate inflammation.
Occurs after cellular injury causes release of  Include Aspirin, Ibuprofen, and cox2
chemical mediators. inhibitors.
Five basic steps:  All have above same efficacy
 Vasodilation  All have analgesics ,anti-pyretic and
 Vascular anti-inflammatory
impermeability(edema)  Side effects vary
 Cellular infiltration(pus)  Acetaminophen has no anti-
 Thrombosis(clots) inflammatory reaction and is not
 Stimulation of nerve endings classified as an NSAID.
CYCLOOXYGENASE
Two forms of Cyclooxygenase:
 Cyclooxygenase-1 (cox1)
-present in all tissue
pg.2
-reduces gastric acid secretion, promotes
renal blood flow to the kidney, regulating
smooth muscle tone in blood vessels and
the bronchial tree.
 Cycloooxygenase-2 (cox2)
-eg. Cerebrex
-present only after tissue injury and
serves to promote inflammation.
-promotes inflammation, sensitizes
pain, mediates fever in brain.
-results in suppression
inflammation.
ASPIRIN
 Treats inflammation by
inhibiting both c0x1 and cox2.
 Ready available, inexpensive,
effective
 Large doses needed to relieve
severe inflammation.
Adverse effect:
 Irritate digestive system
 May cause bleeding
 Salicylism may occur in toxicity
 Tinnitus, dizziness, headache,
excessive perspiration.
IBUPROFEN
 Alternative to aspirin
 Inhibits cox1 and cox2
 Common side effect are nausea and
vomiting
 Causes less gastric irritation and
bleeding like aspirin.
COX INHIBATORS
 Newest and most controversial class
 No inhibition of cox1
 Do not affect blood coagulation
 Do not irritate digestive system
 Treatment of choice for moderate
to severe inflammation.
 Eg. Rofecoxib (vioxx) found to
double risk of heart attack and
stroke; removed from the market
since 2004.
 Eg. Valdecoxib (Bextra) removed in
the market in 2005.
 Colecoxib-still in the market.
SYSTEMIC GLUCOCORTICOIDS
 Effective in treating severe
inflammation.
 Naturally released by adrenal
cortex.
of  Suppress histamine and
Prostaglandin.
 Can inhibit immune system to
reduce inflammation.
 Toxicity can lead to Cushing’s
syndrome.
Serious adverse effect:
 Suppression at adrenal gland
function; hyperglycemia
 Mood changes, cataract, peptic
ulcer
 Electrolyte imbalance,
osteoporosis.
*sodium retention and potassium
excreted.
*steroids will be given less than 7
yrs. old coz it can cause growth
retardation.
 Can mask infection
-creates potential for existing
infection to grow rapidly and
undetected.
-contraindicated in active
infection.
*treatment with
Glucocorticoids
-used for shot-term treatment
of acute inflammation.
- Long term- treatment = keep
dose as low as possible; use
alternative- day dosing.
Pg.3
ANTI-INFLAMMATORY DRUGS (NSAIDS)
 Obtain baseline kidney and
liver function test, CBC
 Monitor bleeding time with
long term administration.
 Assess for changes in pain ,
reduce in temperature and
inflammation.
 Assess for Gastrointestinal
bleeding, Hepatitis,
Nephrotoxicity, Hemolytic
anemia. Salicylate toxicity.
 Use cautiously in elderly
clients; potential for
increase bleeding.
 Aspirin is contraindicated
for pediatric client;
possibility of Reye’s
Syndrome
 Assess for infection.
 For long term use, consider
alternate day therapy plan.
 Monitor client for serum
glucose level, body weight,
BP, CBC.
*FOU-fever of unknown origin.
ANTI-PYRETIC DRUG
 Assess development status, origin
of fever, associated symptoms
 Determine appropriate formulation
or route.
 Clients who are vomiting:
antipyretic can be given in a form of
suppository.
 Young children: flavored elixirs
 Baseline lab data necessary to
assess kidney and liver status.
ACETAMINOPHEN
 Contraindicated in the client with
significant liver disease.
 Inhibit warfarin metabolism, may
result in bleeding.
NSAID
PROTOTYPE DRUG: IBUPROFEN (ADVIL..)
 Mechanism of action: to inhibit of
Prostaglandin synthesis
 Primary use: musculoskeletal
disorders such as rheumatoid
arthritis and osteoarthritis, mild to
moderate pain
ANTIPYRETIC/ ANALGESIC
 PROTOTYPE DRUG:
ACETAMINOPHEN (TYLENOL)
 Mechanism of action: reduce fever
by direct action at level of
Hypothalamus and dilatation of
peripheral blood vessels.
ANTI-INFLAMMATION/ GLUCOCORTICOID
PROTOTYPE DRUG: PREDNISON
(METICORTEN, OTHERS)
 Action: the result of being
metabolized to an active form,
which is also available as a drug
called nisolone
 Use: occasionally used to terminate
acute bronchospasm in client with
asthma; antineoplastic agent for
client with certain cancers such as
Hodgkin’s dse. acute leukemia and
lymphomas.
 Adverse effect: result in cushing’s
syndrome, a condition includes
hyperglycemia, fat redistribution to
the shoulder and face, muscle
weakness, bruising, and bones that
easily fractures; gastric ulcer.
Pg.1 TETRACYCLINE
PHARMACOLOGY LECTURE Given for more than 7 yrs. old
Binds with Calcium
PENICILLIN PROTOTYPE DRUG: TETRACYCLINE HCL
 Considered bacteriocidal antibiotic (ACHROMYCIN, OTHERS)
 PBP- penicillin binding proteins  Mechanism of action; effective
creates leakage forming LPS cell against broad range of gram + and –
wall to destroy cell wall of the organisms.
bacteria and it will disintegrate.  Use: Chlamydia, rickettsiae, and
 Copies and destroy cell wall to mycoplasma
disintegrate the bacteria.  Adverse effect: superinfection,
nausea and vomiting, epigastric
PROTOTYPE DRUG: PENICILLIN G burning, diarrhea, discoloration of
(PEPTIDS) teeth, photosensitivity.
 Mechanism of action: to kill  *cephalosporin= safest antibiotic
bacteria by disrupting their cell wall. can be given to a pregnant woman
 Primary use: drug of choice against esp. with UTI.
Streptococci, pnuemococci, and
taphylococci organisms that do not MACROLIDE
produce penicillinase. DNA synthesis
 Also medication of choice for Eg. Ilozone
gonorrhea and syphilis PROTOTYPE DRUG: ERYTHROMYCIN (E-
 Adverse effect: diarrhea, nausea, MYCIN, ERYTHROCIN)
vomiting, superinfections,  mechanism of action: to act as
anaphylaxis. spectrum similar to that penicillin
*superinfection- kills both good or  also to be effective against gram+
normal flora and bad bacteria that bacteria.
caused by prolong used of antibiotic  Primary: for bordetella pertusis
that can result for grow and (whooping cough) and
multiplication of bad bacteria. corynebacterium diphtheriae, most
gram + bacteria.
CEPHALOSPORIN  Adverse effect: nausea, abdominal
Derived from penicillin cramping and vomiting.
PROTOTYPE DRUG: CEFOTAMINE  Most severe is hepatoxicity
(CLAFORAN)
 Mechanism of action; to act with AMINOGLYCOSIDE
broad spectrum activity against PROTOTYPE DRUG: GENAMIN
gram – organisms. (GERAMYCIN)
 Use: serious infection of lower  Mechanism of action: is a broad
respiratory tract, central nervous spectrum; bactericidal antibiotic.
system, genitourinary system,  Used: for serious urinary,
bones, blood, and joints. respiratory, nervous or GI infection.
 Adverse effect: hypersensitivity,  Often used in combination with
anaphylaxis, diarrhea, vomiting, other antibiotics.
nausea, pain at injection site.  Used parenterally or a drop
 Eg. Rosepin for gonorrhea and (Genoptic) for eye infections
syphilis. Pg.2
  Adverse effect: toxicity and nephro -anaerobic= without oxygen eg.
Clostridium Tetanus

FLUOROQUINOLONE
Bacteriostatic  Staining characteristics
PROTOTYPE DRUG: CIPROFLOXACIN (CIPRO) -gram+ (crystal violet, iodine, alcohol,
 Mechanism of action: to inhibit secondary color sapranine)
bacterial DNA girace -gram- ( LPS; red)
 Effects bacterial replication and
repair ANTI- INFECTIVE DRUGS
 Primary used: for respiratory  Known as antibacterial,
infection, bone and joint infections, antimicrobial, antibiotic
sinusitis and prostatitis.  Classified by
 Adverse effect; nausea, vomiting, -chemical structures (eg.
diarrhea, phototoxicity, headache, Aminoglycoside, fluoroquinolone
dizziness, hindi makatulog. -mechanism of action (cell wall
inhibitor, folic-acid inhibitor
PATHOGENS  Affects target organisms structure,
 Organism that can cause disease. metabolism, or life cycle.
 Must bypass the body’s defenses  Goal is to eliminate pathogen
-bacteria, viruses -bactericidal
-fungi, intracellular organisms -bacteriostatic
-multi cellular animals
 Cause dse. in two ways: ACQUIRED RESISTANCE
-divide rapidly to overcome body  Occurs when pathogen acquires
defenses. gene for bacterial resistance
-disrupt normal cell function -through mutation
 Secrete toxins  Antibiotics destroy sensitive
- disrupt animal cell function bacteria
 Insensitive (mutated) bacteria
PATHOGENICITY AND VIRULENCE remains
 Pathogens- ability of organism to  Mutations ramdom, ocuur during
cause infection. cell division
 Virulence- measure of disease-  Resistance not cause by but is
producing potential. worsened by over prescription of
 Highly virulent pathogen can cause antibiotics
dse. when present in small number. -results in loss antibiotive effectiveness
 Nosocomial infection often resistant
METHODS OF DESCRIBING BACTERIA  Prophylactic use sometimes
 Basic shape appropriate.
-bacilli= rod shape  Nurse should instruct client to take
-cocci= spherical shape full dose.
-spirilla= spiral shape

 Ability to use oxygen ROLE OF THE NURSE

-aerobic= with oxygen  Monitor client’s condition
 Provide client education
 Pg.3 -effect on linear skeletal growth of fetus
 Obtain medical, surgical and drug and child
hx.  Contraindicated in children has less
 Assess lifestyle and dietary habits than 8 yrs. of age.
 Obtain description of -permanent mottling and discoloration of
symptomology and current teeth.
therapies  Tetracyclines decrease effectiveness
 Obtain specimen for culture and of oral contraceptives
sensitivity prior to start of therapy. -alternate birth-control method should
 Monitor for indications of response be used while taking medication
to therapy.  Used with caution in client with
-reduce fever impaired kidney and liver function.
-normal white blood count  Photosensitivity may result
-improved appetite  Don not takes with milk products,
-absence of symptoms such as cough iron supplement, magnesium-
 After parenteral administration, containing laxatives or antacids.
observe closely for possible allergic
reactions MACROLIDES THERAPY
 Monitor for superinfection  Assess for presence of respiratory
-replace natural colon flora with infection.
probiotics supplements or cultured  Examine client with hx of cardiac
dairy products disorder.
 Teach client to
-wear medic-alert bracelets if allergic to
antibiotics AMNIOGLYCOSIDE THERAPY
-report symptoms of allergic reaction  Monitor for ototoxicity and
-not stop taking drug until complete nephrotoxicity.
prescription has been taken  Hearing loss after therapy has been
 Assess previous drug reaction to completed.
penicillin  Neuromuscular function may also
be impaired.
CEPHALOSPORIN THERAPY  IFO, unless otherwise
 Avoid cephalosporins if client has contraindicated to promote
the hx of severe penicillin allergy excretion.
 Monitor for hypercalemia and
hypernatremia FLUOROQUILONE THERAPY
 Monitor cardiac status, including  Monitor WBC
ECG changes  Monitor client with liver and renal
 Assess for presence or hx of dysfunction.
bleeding disorders  Teach that drugs may cause
-cephalosporin may reduce dizziness and light headedness
prothrombin level -advice against driving or performing
hazardous tasks during drug therapy.
 Nefloxacin (Neroxin may cause
TETRACYCLIN THERAPY photophobia0
 Contraindicated for clients who are  Teach that drug may affect tendons,
pregnant or lactating esp. in children
 Pg.4  Immune system status
SULFONAMIDE THERAPY  Local conditions at infection site
 Assess renal failure, crystauria  Allergic reaction
 Contraindicated with hx of  Age
hypersensitivity to sulfonamides.  Pregnancy status
-can induce skin abnormality called  Genetics
Stevens Johnson Syndrome
 Teach client hoe to decrease effects
of photosensitivity.

ANTITUBERCULOSIS THERPAY
 Contraindicated for client with hx of
alcohol abuse, AIDS, liver dse. or
kidney ds.
 Use caution for certain clients
-with renal dysfunction
-pregnant or lactating
-hx of convulsive disorder
 Assess for gouty arthritis
 Some antituberculosis drugs
interact with contraceptives
-use alternate form of birth control
 If taking isoniazid (taking b4
breakfast), avoid foods containing
tyramine

SELECTION OF AN ANTIBIOTIC
 Careful selection of correct
antibiotic essential
-use of culture and sensitivity testing
-for effective pharmacotherapy to limit
adverse effects

MULTIDRUG THERAPY
 Affect by antagonism-combining
two drugs may decrease efficacy of
each.
 Use of multiple antibiotic increases
risk of resistance.
 Multidrug therapy can be used
-when multi-organism cause infection
-for treatment of TB
-for treatment of HIV PHARMACOLOGY LECTURE pg1

FACTORS INFLUENCE CHOICE OF INFLAMMATION

ANTIBIOTICS
  Occurs in response to many diff.
stimuli including physical injury,
exposure to toxic chemicals,
extreme heat, invading
microorganism or death of cells.
CHEMICAL MEDIATORS OF INFECTION
(BCHLP)
 Bradykinin-present in inactive
form in plasma and mast cell;
vasodilators that causes pain;
effects are similar to those of
histamine.
 Complement- series of at least
20 proteins that combine in a
cascade fashion to neutralize
and destroy antigen.
 Histamine- stored and release
by mast cell; causes dilation of
blood vessels; smooth muscle
constriction; tissue swelling and
itching.
 Leukotrienes- stored and
release by mast cell; effect are
similar to those of histamine
 Prostaglandins- present in most
tissue and release by mast cell;
increase capillary permeability;
attract WBC to site of
inflammation, and cause pain.
FF. ARE SOME COMMON DSES. THAT HAVE
AN INFLAMMATORY COMPONENT THAT
MAY BENEFIT FROM ANTI-INFLAMMATORY
PHARMACOTHERAPY:
 Allergic rhinitis
 Anaphylaxis
 Ankylosing spondylitis
 Contact dermatitis
 Crohn’s dse.
 Glomerulonephrititis
 Hashimoto’s arthritis
 Peptic ulcer
 Rheumatoid arthritis
 Systemic lupus erythematosus
 Ulcerative arthritis
HISTAMINE
 Key chemical mediator of
inflammation
 Located in tissue spaces under
epithelial membranes such as the
skin, bronchial tree, digestive
system and along blood vessels.
 Mat cell detect foreign agents or
injury and respond by releasing
histamine which initiates the
inflammatory response within
seconds
 Histamine also directly stimulates
pain receptors and primary agent
responsible for the symptoms of
seasonal allergy.
STEPS IN ACUTE INFLAMMATION
 Cellular injury
 Mast cell release of chemical
mediators such as bradykinin,
complement, histamine,
leukotrienes, prostaglandin
 Vasodilation (redness, heat)
 Vascular impermeability
 Cellular infiltration
 Thrombosis
 Stimulation of nerve endings
ANAPHYLAXIS
 Caused by rapid release of chemical
mediators of inflammation on a
large scale throughout the body; it
is a life-threatening allergic
response that may result in shock
and death.
FORMS OF CYCLOOXYGENASE
 COX1
Location: present in all cell
Function: protects gastric mucosa,
support kidney function, promotes
platelets aggression
Inhibition by medication: undedirable:
increases risk for gastric bleeding and
kidney failure
 COX2
 Location: present at site of tissue injury
Function: mediates inflammation,
sensitizes pain receptor, mediates fever
in the brain
Inhibition by medication: desirable:
results in suppression of inflammation
SALICYLISM
 Caused by high dose of aspirin that
may produce symptoms such as
tinnitus, headache, dizziness and
excessive sweating
REYE’S SYNDROME
 Is a rare, though serious, disorder
characterized by an acute increase
in intracranial pressure and massive
accumulation of lipids in the liver.
ANTI-INFECTIVE-is general term for any
medication that is effective against
pathogens.
ACTIONS OF ANTI- INFECTIVE DRUGS:
 Bactericidal- killing bacteria
 Bacteriostatic- growth slowing
drugs.
ANTIMETABOLITES
 sulfonamides
BROAD SPECTRUM ANITBIOTICS
 These are antibacterial effective
against many different species of
pathogens.
NARROW-SPECTRUM ANTIBIOTICS
 Effective against only one or
restricted group of microorganism.
CULTURE AND SENSITIVITY TESTING
 Process of growing the pathogen
and identifying the most effective
antibiotic.
SUPERINFECTION
 One common side effect of anti-
infective therapy is the appearance
of secondary infection which occur
when microorganism normally
present in the body are destroyed.
Removal of host flora by an
antibiotic gives the remaining
microorganisms an opportunity to
grow, allowing for overgrowth of
pathogenic microbes.

MECHANISM OF ACTION ANTAGONIST- drugs that blocks cell activity

RNA SYNTHESIS INHIBATORS AGONIST- drug enhances cell activity
 Rifampicin
DNA SYNTHESIS INHIBATOR
 Fluoroquinolones
PROTEIN SYNTHESIS INHIBATORS
 aminoglycosides
 chloramphenicol
 clindamycin
 linezolid
 macrolides
 streptogramins
 tetracyclines
CELL WALL SYNTHESIS INHIBATORS
 carbapenums
 cephalosporins PHARMACOLOGY LECTURE Pg.1
 isoniazid Pg.506 on pharmacology book
 penicillins
 vancomycin TUBERCULOSIS
  Caused by Mycobacterium
Tuberculosis
 Cell wall resistant to anti-infective
 Body’s immune response attempts
to isolate pathogens by walling it off
 Tuberculosis may remain dormant
in walled-off areas called tubercles.
 Decrease immune system can give
tuberculosis opportunity to become
active.
LONG TERM THERAPY
 6-12 months of drug-therapy
needed to reach isolated pathogens
it tubercles
 Therapy must be continued even if
no systems.
 Client with multi drug-resistant
infections require therapy for 24
months.
MULTI DRUG THERAPY
 2-4 Antibiotics administered
concurrently
 Different combinations used during
coursed of therapy.
 Necessary bec. Mycobacterium
grows slowly and is commonly
resistant
 Therapy initiated with first –choice
drugs.
 When resistance develops, second-
choice drugs.
CHEMOPROPHYLAXIS
 Anti tuberculosis drugs used to
prevent disease in a high risk
population.
 Close contacts and family members
of recently infected tuberculosis
client.
 Clients with aids
 Clients who are HIV positive or are
receiving immunosuppressant drug.
CLIENT RECEIVING ANTI BACTERIAL
THERAPY
 Assessment
-obtain complete health history,
allergies, drugs, drug interactions
-obtain specimen for culture and
sensitivity before initiating therapy.
-perform infection-focused physical
examination=vital signs, WBC count,
sedimentation rate.
*15,000 higher of WBC count signals
infection.
*erythrocyte sedimentation rate
*erythrocyte-settling of RBC
=Determining fast decrease of RBC
meaning increase in protein in blood
that signals infection. Eg. Rheumatic
heart disease.
NURSING DIAGNOSIS
 Infection risk for injury
 Deficient knowledge r/t therapeutic
regimen
PLANNING- CLIENT WILL
 Report reduction in symptoms r/t
diagnosis
 State – results for laboratory and
diagnostic test.
 Demonstrate understanding of drug
action
 Report side effects
-rash, SOB, swelling
-fever, stomatitis, loose stools
-vaginal discharge, cough
 Complete full course of antibiotic
therapy and follow-up care.
IMPLEMENTATION
 Monitor for superinfection
 Administer drug around the clock.
 Monitor intake of OTC products.
 Monitor for photosensitivity.
 Determine food and beverages
interactions.
 Monitor IV site for signs.
EVALUTION
  Report decrease in symptoms; has
improved laboratory results.
 Accurately state drug action
See pg507 TB DRUGS
*color blindedness if the ethambutol is
given to a child less than 8 yrs. old
*hemaptytis- blood from stomach.
*TB meningitis- TB in brain
*Pott’s disease Tb in bones or spinal cord
*hematuria- TB in kidney
*there is also TB of digestive system.
Pg.514 chapter 35 in pharmacology books
DRUGS FOR FUNGAL, PROTOZOAL, AND
HELMINTH INFECTIONS
CHARACTERISTICS OF FUNGI
 Single-celled or multi-cellular
organisms
 More complex than bacteria
 Include mushrooms, yeast, molds.
 Purpose is to decomposed dead
organisms
 Human is exposed by handling
contaminated soils or inhaling
spores.
*mycosis Fungosis- once inhaled it
affects or eat CNS.
*dominancy of the brain happens in 7
yrs. old thus, removal of the brain as a
remedy for mycosis fungosis happens
before 7 yrs. old.
 Superficial
-affect hair, skin, nails, mucus
membranes.
-treated with topical agents.
 Systemic
-affect internal organs
-are less common
-can be fatal in immunosuppressed.
-treated with oral or parenteral agents.
 Fungi unaffected by most antibiotics
CLIENT OF RISK FOR FUNGAL INFECTION
 Human body quite resistant to
fungi.
 Most serious
 Community-acquired infections
-can affect those with intact immune
systems.
 Opportunistic infections
-nosocomial infections that occurs in
immunosuppressed.
PROTOZOAN INFECTION
 single-celled animals
 Caused disease in Africa, South
America and Asia.
 Thrive in areas of poor sanitation.
 Travelers may transmit organisms.
 Drugs used to treat bacterial and
fungal infections are ineffective.
 Most common protozoal disease
Malaria.
 2nd most fatal infections disease in
world.
 Caused by protozoan plasmodium.
 Transmitted by bite of female
Anopheles mosquito (female) night
biting mosquito.
 Requires multi-drug therapy due to
complicated life cycle of parasite.
 Drugs administered for prophylaxis,
as therapy for acute attacks and to
prevent relapses.
Pg.524 see life cycle of plasmodium on
pharmacology book.
*during the height of the fever is the
best time to obtain blood specimen to
determine if there are present of
merozoites (malaria) in the blood.
*aedes mosquito- bites during 6-8 am
and 4-6 pm
GOALS OF ANTIMALARIAL THERAPY
 PREVENTION
-Center for disease control recommends
prophylactic antimalarias.
-use prior to, during and for 1 week
after visiting affected areas.
  Prevention of relapse
 Elimination latent forms
plasmodium residing in liver.
NONMALRIAL PROTOZOAN
 Thrive in unsanitary conditions
 Amebiasis , toxoplasmosis (from
dog and cat), giardiasis (from feces
of pig), crystosporidosis (from
spores coming from cats, birds and
other pets), trichomoniasis,
trypanosomiasis (sleeping sickness
disease) and leishmaniasis.
 Treatment of nonplasmodium
protozoan disease requires different
set of medications from those used
of malaria.
HELMINTH INFECTION (WORM)
 Parasitic worms that
significant dse. in certain regions of
world.
 Ringworms (nematodes)
 Flukes (trematodes)
 Tapeworms (cestodes)
 Enteriobiasis (pinworm)
-most common hewlminth infection in
US.
 Most helminthes enter body
through skin or gastrointestinal
tract.
GOALS OF PHARMACOLOGY
 Kills parasites locally.
 Disrupt life cycle.
 Prevention
-CDC recommends
role of the nurse
 Obtaining description
SYSTEMIC ANTIFUNGAL THERAPY
 Use cautiously with
impairment, sever
marrow suppression and
of pregnancy.
 Amphotericin B (Fungizone) can
cause kidney damage.
-closely monitor fluid and
electrolyte status
 can also cause ototoxicity
-assess for hearing loss, vertigo,
unsteady gait, and tinnitus.
AZOLE THERAPY (NIZORAL)
 contraindicated with chronic
alcoholism
 toxic to liver
 assess for nausea, vomiting,
abdominal pain, diarrhea.
 Monitor for signs and symptoms of
hepatoxicity.
 May affect glycemic control in
cause diabetic client: monitor blood sugar.
 Monitor for alcohol use.
SUPERFICIAL ANTIFUNGAL THERAPY
 Assess for signs of contact
dermatitis; if present withhold drug
and notify primary health-care
provider.
 Do not use superficial (suppository
form administer at night) antifungal
intravaginally during pregnancy to
treat infections caused by
Gardnerella Vaginalis or Trichomas
species; used cautiously for
lactating client.
 Medications may be “swished and
swallowed” or “swished and spit” to
treat candidiasis.
 Monitor for nausea, vomiting,
diarrhea with high doses.
*amoeba= metronidazole IV or IM
ANTIPROTOZOAN DRUG
 Contraindicated with hamatologic
disorders, severe skin disorders and
renal pregnancy
bone
  Use cautiously with preexisting PROTOTYPE DRUG: AMPHOTERICIN B
cardiovascular disease and lactating (FUNGIZONE)
client. Mechanism of action: act by binding to
 Test foe G6PD ergosterol in fungi cell membranes, causing
 Obtain baseline ECG coz of potential them to become permeable or leaky.
cardiac complications. Use:
 Monitor GI side effect such as Adverse effect: fever, chills, vomiting, and
vomiting, diarrhea, abdominal pain. headache at the beginning of therapy,
 Take with food in stomach. phlebitis, electrolyte imbalance, cardiac
 Monitor for signs and symptoms arrest, hypotension and dysrhythmias.
 Contraindicated in client with blood
discrasias, AZOLE ANTIFUNGAL
 Contraindicated in alcoholics PROTOTYPE DRUG: FLUCONAZOLE
 Monitor for GI distress. (DIFLUCAN)
 Metronidazole (flagyl) may cause Action: act by interfering with the synthesis
dry mouth and metallic taste. of ergosterol.
 Monitor foe CNS toxicity. Use: penetrate most body membranes to
reach infection in the CNS, bone, eye,
ANTIHELMINTHIC DRUG urinary tract, and respiratory tract. Effective
 Use cautiously in client who are against Candida albicans, may not be
pregnant or lactating, have effective against not Candida albicans
preexisting liver disease or younger species.
than age 2. Adverse effect: nausea, vomiting, diarrhea.
 Identify specific worm before
initiating treatment. SYSUPERFICIAL ANTIFUNGAL
 Monitor lab result; Leukopenia PROTOTYPE DRUG: NYSTATIN
(decrease RBC), thrombocytosis (MYCOSTATIN)
(decrease platelets count), Action: binds to sterols in the fungi cell
agranulocytosis (increase monocyte membranes, causing leakage in the
and increase lymphocyte), intracellular contents
associated with Albendazole Use: Candida infections of the vagina, skin
(Albenza) and mouth; to treat candidiasis of intestine
 Educate client on nature of worm and GI tract.
infection; some type of worm will Adverse effect: minor skin irritation, nausea
be expelled in stool; take showers and vomiting.
rather than baths, change
undergarment, linens and towels ANTIMALARIAL
daily. PROTOTYPE DRUG: CHLOROQUINOLONE
*example of drug foe superficial infection- (ARALEN)
nystatin and Griseofulvin (Fulvicin) Action: concentrate in the food vacuoles of
Plasmodium residing in RBC; prevent the
metabolism of heme, which then builds to
toxic levels within the parasite.
ANTIFUNGAL DRUG Use:prototype medication for treating
malaria for 6 yrs. old.
SYSTEMIC ANTIFUNGAL Adverse effect: CNS and cardiovascular
toxicity, confusion, convulsions, reduced
reflexes, hypotension and dysrhythmias.
 *The most common helminth dse.
ANTIPARASITIC/AMEBICIDE worldwide is Ascariasis, which is caused
PROTOTYPE DRUG: METRONIDAZOLE by the roundworm Ascaris
(FLAGYL) lumbriciodes.
Action: antiprotozoal drugs in that it also *Enteriobiasis an infection by the
has antibiotic activity against anaerobic pinworm.
bacteria. *Enterobius vermicularis is the most
Use: treat most form amebiasis. common helminth infection in the US.
Adverse effect: anorexia, nausea, diarrhea,
dizziness, and headache, dryness of the
mouth and unpleasant metallic taste.

ANTIHELMINTHIC
PROTOTYPE DRUG: MEBENDAZOLE
(VERMOX)
Action: broad-spectrum drug.
Use: treat wide range of helminthes
infection
Adverse effect: as the worms die, some
abdominal pain, distention, and diarrhea.

LIFE CYCLE OF PLASMODIUM

1. Infected mosquito bites person.
2. Plasmodium travels to liver.
3. Merozoites divide inside
hepatocytes.
4. Meroziotes are release to
bloodstream causing fever and
chills.
5. Meroziotes enter RBC.
6. Mosquito bites persona and
become infected to restart cycle.

VOCABULARY:
DERMATOPHYLIC- they are the
superficial infections.
AZOLES- drug consist of two different
chemical classes, the imidazoles and the
triazoles.
MALARIA- cused by 4 species of the
protozoan Plasmodium, Anopheles
mosquito- carrier for the parasite.
MEROZOITES- Plasmodium multiplies to
the liver and transforms into progeny.
ERYTHROCYTIC STAGE- stage in which PHAEMACOLOGY LECTURE pg.1
Meroziotes infect RBC, which eventually
rupture, releasing more meroziotes and CHARACTERISTICS OF VIRUSES
causing sever fever and chills.
  Non-living agents that infect
bacteria, plants, animals.
 In a cellular parasite; must be in
host cell to replicate and caused
infection; many viruses infect
specific host cell
 Eg. HIV= has Reverse transcriptase;
it has RNA and can convert into
DNA to invade cell to replicate. This
virus hide at the T Helper Cell and
later on disrupt or it will go to
explode and then to infect other T
helper cell.
PRIMITIVE STRUCTURE OF VIRUSES
 Surrounded by Capsid (protein
coat)
 Contain a few dozen genes, either
RNA or DNA.
*window period= period when there is
no sign and symptoms disease.
*pneumostatic scorine=US
*tuberculosis in the Philippines.
*Glycoprotein= can be found on the test
on the client with HIV.
Parts of virus: glycoprotein; capsule,
core.
THERAPY FOR VIRAL INFECTIONS
 Most self-limiting require no
pharmacotherapy. eg Rhinovirus
that causes common colds.
 Some viruses cause serious dse. and
require aggressive therapy; eg. HIV
is fatal if left untreated; herpes virus
can caused significant pain and
disability if left untreated.
*HPV virus vaccine to prevent cervical
cancer best given at 9 yrs. old.
CHALLEGES OF ANTIVIRAL THERAPY
 Viruses mutate rapidly and drugs
become ineffective.
 Difficult for drug to find virus
without injuring normal cells.
 Each antiviral drug specific to one
particular virus.
REPLICATION OF HIV
 HIV targets CD4 receptor on T4
lymphocyte; using reverse
transcriptase, makes viral DNA from
RNA.
 Virus bud from host cell; enzyme
protease enables virus to infect
other T4 lymphocytes.
 Result is gradual destruction of
immune system.
 HIV called “retrovirus” coz of
reverse synthesis process.
HIV PHARMACOLOGY
 No cure yet, but many new drugs
developed.
 Some therapeutic successes; people
live symptom-free longer; rates of
transmission from mother to
newborn reduced; 70% decline in
death rate in US.; incidence of
infections still very high in African
nations.
PHASES OF HIV THERAPY
 LATENT PHASE-virus lies dormant;
people often unaware they have
HIV.
 Once dx. Confirmed, decision made
about starting or delaying
treatment.
 Current protocols: defer treatment
in asymptomatic adult who have
CO4 counts above 350 cells/mcL.
 Therapy is initiated when CD4 is
under 200 cells/mcL or symptoms
appear.
TREATMENT FAILURES
 Common with antiretroviral
therapy; client non-tolerance of
adverse effects; client
nonadherence to complex regimen
(5 tablets a day);e emergence of
resistant strains; generic variability
(eg. Allergy, idiosyncratic effect)
  Therapy always changing- stay  Vaccination is best approach;
current with latest treatment antiviral available to prevent
influenza; most useful when
ROLE OF THE NURSE combined with vaccines
 Monitor client’s condition.  Neuraminidase inhibitors; shorten
 Provide client education. discomfort period for influenza
 Obtain medical and surgical, drug symptoms; have limited efficacy.
history.
 Assess lifestyle and dietary habits DRUGS FOR HEPATITIS
 Obtain description of  viral hepatitis caused by HAV and
symptomology and current HBV; best prevented through
therapies… vaccination; only a few medications
available for post exposure
treatment
NRTI-NNRTI AND PI THERAPY  Immunoglobulin sometimes used to
 Nursing care similar for NRTI’s, confer passive community.
NNRTI’s and PI’s.  Antiviral such as interferon alpha-
 Establish trusting, non judgmental 2a or lamivudine are available for
relationship with client. HAV.
 Assess client’s understanding of HIV  Interferon alpha-2b (intron a) with
disease process. riviran is available for HCV.
 Assess for symptoms of HIV and any
opportunistic virus. DRUG THERAPY FOR VIRAL INFECTIONS
  Assess for presence or history of
 Assess for bone marrow HIV infection.
suppression, liver toxicity and  Obtain..
Steven Johnson syndrome.
 Client should not drive or perform NURSING DIAGNOSIS
hazardous activities until  Risk for infection r/t compromised
medication reactions are known. immune system
 Be aware of conditions and drug  Decisional conflict r/t therapeutic
that are problematic with regimen.
antiretroviral therapy.  Fear r/t HIV diagnosis
 Teach client how to practice blood
etc for with precaution?
PLANNING
ANTIVIRAL THERAPY  Exhibit decrease in viral load and
 Use drug with extreme caution with increase CD4 count.
pre-existing renal or hepatic  Demonstrate knowledge of dse.
disease. process
 Judicious as is warranted during
pregnancy.
 Emphasize compliance with antiviral IMPLEMENTATION
drug.  Monitor foe hypersensitivity
reactions
 Monitor v/s and for symptoms of
DRUGS FOR INFLUENZA interferon.
  Monitor WBC count.
 Monitor client for stomatitis
 Determine potential drug-drug and
drug food interaction.
 Monitor foe symptoms of
pancreatitis.
 Provide resources for medical and
emotional support.
 Assess client knowledge regarding
use and effect of medication.
 Monitor blood glucose.
THERAPEUTIC GOALS FOR
PHARMACOLOGY OF HIV-AIDS:
 Reduction of HIV RNA load in the
blood to an undetectable level or
less than 50 copies/ml.
 Increased lifespan.
 Higher quality of life.
 Decreased transmission from
mother to child in HIV infected
pregnant client.
HIV-AIDS ANTIRETROVIRALS ARE
CLASSIFIED INTO THE FF. GROUPS, BASED
ON THEIR MECHANISM OF ACTION:
 Nucleoside reverse transcriptase
inhibitor (NRTI).
 Nonnucleoside reverse
transcriptase inhibitor (NNRTI)
 Protease inhibitor (PI)
 Nucleotide reverse transcriptase
inhibitor (NtRTI)
 Fusion (entry) inhibitor.
REPLICATION OF HIV
1. Virus attaches to receptor on host’s
plasma membrane. Its core
disintegrates and viral RNA enters the
cytoplasm.
2. Viral reverse transcriptase produces
DNA, using viral RNA as template.
3. Viral DNA enters the nucleus and is
corporate into host chromosomes. It is
transcribed into mRNA and more viral
mRNA, which moves to the cytoplasm.
4. Viral proteins are synthesized, using
mRNA.
5. Viral proteins and RNA are
assembled.
6. Viruses bud from the plasma
membrane.
ANITRETROVIRAL-NRTI
PROTOTYPE DRUG: ZIDOVUDINE
(RETROVIR, AZT)
Mechanism of action: it mistakenly uses
zidovudine as nucleoside, thus creating
defective DNA strand.
Use: use in combination with other
antiretrovirals for both symptomatic and
asymptomatic HIV-infected clients.
-Also for post-exposure prophylaxis in HIV
positive mother to fetus; oral antiviral
therapy given 7-10 days.
Adverse effect: toxicity to blood cells at high
doses; anemia and neutropenia, anorexia,
nausea and diarrhea, fatigue and
generalized weakness.
ANITRETROVIRAL-NNRTI
PROTOTYPE DRUG: NEVIRAPINE
(VIRAMUNE)
Mechanism of action: binds directly to
reverse transcriptase, disrupting the
enzyme’s active site.
Use: use in combination with other antiviral
in treatment using HAART.
Adverse effect: GI related effect such as
nausea, diarrhea, and abdominal pain, fever
and fatigue, dyspepsia and general fatigue.
ANTIVIRAL
PROTOTYPE DRUG: ACYCLOVIR (ZOVIRAX)
Mechanism of action: limited to
Herpesviruses, for which it is a drug of
choice
Use: to prevent viral DNA synthesis.
Adverse effect: nephrotoxicity is possible
when the medication is given IV.
*INTRACELLULAR PARASITE- they must
inside the host cell to cause infection.
ANTITUBERCULOSIS DRUGS:
FIRST-LINE AGENTS
 Ethambutol
 Isoniazid
 Pyrazinamide
 Rifampin
 Rifapentine
 Rifater
 Streptomycin
SECOND –LINE AGENT
 Amikanin
 Capreomycin
 Ciprofloxacin
 Cycloserine
 Ethionamide
 Kanamycin
 ofloxacin