PHARMACOLOGY Toxicology

Pharmacology Study of the adverse effects of drugs and other

chemicals on living systems
Study or science of drugs
Toxic effects are often an extension of a drug’s
therapeutic action

3 Basic Areas of Pharmacology Pharmacognosy

Pharmaceutics Study of natural (vs synthetic) drug sources (both

plants and animals)
Pharmacokinetics
PHARMACOKINETICS
Pharmacodynamics
Absorption
Pharmaceutics
Distribution
Study of how various dosage forms (e.g.,
injection, capsule, controlled release tablet) Metabolism (biotransformation)
influence the way in which the body metabolizes a
drug and the way in which the drug affects the Excretion
body
A. Absorption
Pharmacokinetics
Rate at which and extent to which a drug moves
Study of what the body does to the drug from its site of administration
molecules
Factors affecting the rate and efficacy of
Involves absorption, distribution, metabolism and absorption
excretion
Route of administration
Pharmacodynamics
Blood flow
Study of what the drug does to the body
Surface area available
Involves drug-receptor interactions
Solubility of the drug
Receptor Theory
Drug interactions
Pharmacotherapeutics
pH (acidity (>uncharged) and alkalinity affects
Focuses on the use of drugs and the clinical absorption)
indications for administering drugs to prevent and
Bioavailability
treat diseases
The fraction or biologic fluid of the administered
Defines the principles of drug actions (the cellular
drug that gains access to its site of action
processes that change in response to the
presence of drug molecules) IV injected blood – 100%
Empirical therapeutics – drug therapy that is NOT IV injected - < 100%
effective but for which the mechanism of action
(MOA) is unknown Factors affecting Bioavailability

Rational therapeutics – drug therapy in which First pass metabolism – biotransformation that
specific evidence has been obtained for the occurs before the drug reaches its site of action
mechanisms of drug action (MC site - liver)

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All of the factors affecting absorption: pH, blood Liquid for Injections
flow, drug interactions, route of administration
liquid with no particulate matter
Routes of Drug Administration
Epinephrine
Alimentary (Oral, Buccal, Sublingual,
Rectal/Suppository) Medication Forms

Parenteral (Intravenous, intramuscular, Gel

subcutaneous, intrathecal)
viscous substance that the patient swallows
Inhalation
Oral Glucose
Topical
Suspension
Subcutaneous
drug particles mixed in a solute
Routes of Administration
Activated Charcoal
Sublingual
Fine powder for Inhalation
Under the tongue
a crystalline solid mixed with liquid to form a
Nitroglycerin suspension

Oral Albuterol by hand-held metered-dose inhaler

The drug is swallowed and absorbed through the Gas

stomach and intestinal tract
Oxygen by mask
Oral Glucose
Spray
Aspirin
Nitroglycerin sub-lingual spray
Inhalation
Liquid/vaporized
a gas or aerosol inhaled by the patient
Albuterol by small-volume nebulizer
Oxygen by mask
B. Distribution
Albuterol by hand-held metered- dose inhaler or by
small-volume nebulizer Process by which a drug leaves the bloodstream
and enters the interstitium or the cells of the
Injection tissues

The drug is injected into a muscle mass Passive diffusion, transport o special carrier
proteins, active transport
Epinephrine by auto-injector
C. Metabolism/ Biotransformation
Medication Forms
Involves the biochemical alteration of a drug into
Tablets an inactive metabolite, a more soluble compound
or a more potent active metabolite
compressed powder shaped into a disk
Liver, (cytochrome P450 enzymes) skeletal
Aspirin muscle, kidneys, lungs, plasma and intestinal
mucosa
Nitroglycerin

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D. Excretion Theurapeutic index

Process by which a drug or metabolite is removed Ratio of a drug’s toxic level to the level that
from the body provides therapeutic benefits

Renal (MC), fecal, respiratory, breast milk, skin Drug interaction

Half life Alteration of the action of one drug by another

The time required for half of an administered dose Synergistic effects

of drug to be eliminated by the body
Occur when two drugs administered together
aka elimination half-life interact in such a way that their combined effects
are greater than the sum of the effects for each
Steady state drug given alone

Physiologic state in which the amount of drug Antagonistic effects

removed via elimination is equal to the amount of
drug absorbed with each dose Occur when the combination of two drugs results
in drug effects that are less than the sum of the
Onset of action effects for each drug given separately

Time required for the drug to elicit a therapeutic Rights of Medication Use
response
Right patient
Peak effect Right drug
Right time
Time required for a drug toto reach its maximum Right route
therapeutic response Right dose
Right documentation
Duration of action
Right assessment
Length of time that the drug concentration is Right education
sufficient (without more doses) to elicit a Right evaluation
therapeutic response Right to refuse

Peak level – highest blood level Effects

Trough level – lowest drug level The desired result of administration of a medication

Enzyme Side Effects

Substance that catalyzes biochemical reactions in Effects that are not desired and that occur in addition
a cell to the desired therapeutic effects

Agonist Medication error

A drug that binds to and stimulates the activity of
one or more biochemical receptor types in the
body
Antagonist
A drug that binds to and inhibits the activity of
one or more more biochemical receptor types in
the body
A preventable situation in which there is a
compromise in the five rights of medication use
Adverse Drug Reaction (ADR)
Any reaction to a drug that is unexpected and
undesirable and occurs at therapeutic drug
dosages

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Allergic Reaction Medication Names

Aka as hypersensitivity reaction Chemical Name

An immune response wherein various chemical
mediators (histamine, cytokines, other
inflammatory substances) are released
Immunoglobulins recognize the drug, its
metabolite or another ingredient in a drug
formulation as a dangerous foreign substance;
they bind to the substance in an attempt to
neutralize it
describes the drug’s chemical structure
Generic Name
reflects the chemical name, but in shorter form
Trade Name
the name the manufacturer uses to market the drug
Official Name
the name used in the U.S. Pharmocopoeia
Steps in Administering Medication

Can result in mild reactions (skin erythema or Obtain an Order

rashes) or to severe/ life threatening reactions Confirm Order
(constriction of bronchial airways and Steps in Administering Medication
tachycardia) Select Proper Medication
Avoid contamination
Idiosyncratic reaction Check Expiration Date
Check For Signs of Contamination
Not the result of a known pharmacologic property
Discoloration
of a drug or of a patient allergy but instead occurs
Cloudiness
unexpectedly in a particular patient
Particulate Matter
Genetically determined abnormal response to Verify Form & Route
normal dosages of a drug (ex, deficiency or Inform Patient of Order
excess of an enzyme) Inquire about allergies
Recheck Medication
Teratogenic effects – result in structural defects Expiration date
in the fetus Contamination
At least two more times after initial check
Mutagenic effects – permanent changes in the Assess Patient prior to administration of the drug
genetic composition of living organis; consist of Administer the correct dose by the correct route
alterations in chromosome structure, the number Dispose of Contaminated Equipment
of chromosomes, or the genetic code of the DNA Reassess After Administration

Carcinogenic effects – cancer-causing effects of

drugs, other chemicals, radiation and viruses COMMONLY USED ABBREVIATIONS

Indication a.c.
ante cibum
The reason for administering a medication or before meals
performing a treatment p.c.
post cibum
Contraindication after meals
ad. lib.
A factor that prevents the use of a medication or
ad libitum
treatment (eg. Allergies)
as desired
od
Dose
omni die
The amount of a drug to be administered at one time once a day
bid
Mechanism of Action bis in die
twice a day
How a drug works tid

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ter in die 1 dL = .1 L
three times a day 1 decaliter = 10 Liters
qid
quarter in die
Four times a day Units of weight (gram)
ADL 1 mcg = .000001 gm
Activities of daily living 1 mg = .001 gm
hs 1 cg = .01 gm
hora somni 1 dg = .1 gm
hours of sleep 1 kilogram = 1000 grams
OD Other units
oculus dexter 1 gm. = 15 gr.
right eye 1 gr = 60 mg
OS 1 mg = 1,000 mcg
oculus sinister 1 mL = 1 cc; 15 gtts; 1 gram
left eye 60 mcgtts
OU 1L = 1 qt; 1000 mL
oculus uterque 1 gal = 4 L; 4 qt., 4000 mL
both eyes 1 ounce = 30 gm., 30 cc
o.m. 1 kg = 2.2 lbs
omni mane 1 lb = 16 ounces
every morning
n.p.o. REVIEW OF THE AUTONOMIC
nulla per orem NERVOUS SYSTEM
nothing by mouth Nervous System
q.h.
quaque hora 1.Central Nervous System
every hour
p.r.n. 2. Peripheral Nervous System
pro re nata
as necessary Peripheral Nervous System
stat
1.Somatic Nervous System (innervates skeletal
statim
muscle)
immediately
Systems of Measurement 2.Autonomic Nervous System (ANS) – collection
Common Household Measurement of nuclei, cell bodies, nerves, ganglia, and
1 quart = 4 cups plexuses that provides afferent and efferent
1 pint = 2 cups innervation to smooth muscle and visceral organs
1 cup =8ounces of the body; regulates functions that are not
1 tbsp =3 tsp; 15 mlL under conscious control BP, HR and intestinal
1 tsp =60 gtts;5mL motility)

Apothecary Measurements Autonomic Nervous System (ANS)

60 minims = 1 fluidram
8 fluidrams = 1 fluid ounce 1.Sympathetic Nervous System- originates in the
thoracolumbar portion of the spinal cord
or 480 minims
2.Parasympathetic Nervous System – originates
16 fluid ounces = 1 pint
from the cranial nerve nuclei III, VII, IX, X as well
2 pints = 1 quart
as the 3rd and 4th sacral spinal roots
4 quarts = 1 gallon

Metric Measurements
Units of volume (liter)
1 mL = .001 L

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 Thrombolytic Drugs
Drugs Affecting the Renal System
Sympathetic Nervous System Diuretic Drugs

Flight or fight situations Endocrine Drugs

HR increases Thyroid and Antithyroid Drugs
BP rises Antidiabetic Drugs
Eyes dilate Adrenal Drugs
Blood sugar / glucoses rises
Bronchioles expand Drugs Affecting Reproductive Functions
Blood flow shifts from the skin to skeletal
muscles Respiratory Drugs
Antihistamines, Decongestants, Antitussives and
Sympathetic Nervous System Expectorants
Receptors: Bronchodilators and others
Adrenergic Receptors- alpha 1
alpha 2 Antiinfective Drugs
beta 1 Antibiotics
beta 2 Antiviral Drugs
Dopamine Receptors Antitubercular Drugs
Antifungal Drugs
Parasympathetic Nervous System Others
Rest and digest system
Slows HR Antiinflammatory and Antirheumatic Drugs
Lowers BP
Increases intestinal activity GIT Drugs
Constricts pupils Acid-controlling Drugs
Empties urinary bladder Antidiarrheals and laxatives
Antiemetics and Antinausea Drugs
Receptors: Vitamins and Minerals/ Nutrition Supplements
Cholinergic receptors – muscurinic
Drugs affecting the CNS
nicotinic Analgesic Drugs
General and Local Anesthetics
Neurotransmitters CNS Depressants and Muscle Relaxants
Major NT in the ANS Antiepileptic Drugs
Acetylcholine – cholinergic transmission Antiparkinsonian Drugs
Norepinephrine – adrenergic transmission Psychotherapeutic Drugs
ANS drugs achieve their effects by acting as CNS Stimulants and Related Drugs
either agonists or antagonists at cholinergic and
adrenegic receptors Drugs Affecting the Autonomic System
Adrenergic Drugs
DRUGS Adrenergic-Blocking Drugs
Cardiovascular Drugs Cholinergic Drugs
Positive Inotropic Drugs Cholinergic-Blocking Drugs
Antidysrhythmic Drugs
Antianginal Drugs Immunosuppressant and Antineoplastic Drugs
Antihypertensive Drugs
Antilipemic Drugs OTHERS: Hematologic, Dermatologic, Ophthalmic
and Otic Drugs
Coagulation Modifier Drugs
Anticoagulants Cardiovascular Drugs
Antiplatelet drugs Drugs used to improve CV function include:
Antifibrinolytic drugs Inotropic drugs

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Antiarrhtymic drugs 2. Take the apical pulse before giving this
Antianginal drugs meds
Antihypertensive drugs 3. Wihthold the drug and notify the
Diuretics prescriber if the pulse rate slows to 60
Antilipemic drugs bpm or less
Inotropic drugs 4. Infuse the IV form slowly over at least 5
minutes
Influence the contractility of muscular tissue
(increase the force of heart’s contarction) – PDE Inhibitors
POSITIVE INOTROPIC Typically used for short term-term management of
heart failure or long term management in patients
2 types: awaiting heart transplant surgery
1. cardiac glycosides Examples:
- slow the heart rate (negative chronotropic effect) Inamrinone
- slow electrical impulse conduction (negative Milrinone
dromotropic effect)
2. phosphodiesterase (PDE)
Warning:
- when giving PDE inhibitors (milrinone),
Cardiac Glycosides
remember that improvement of cardiac output
Group of drugs derived from digitalis ( foxglove
may result in enhanced UO. Expect a dosage
plants)
reduction in diuretic therapy as heart failure
Digoxin – most common prototype of cardiac
improves
glycosides
- potassium loss may predispose the patient to
Pharmacokinetics:
Digoxin toxicity
Capsules are absorbed most efficiently
Followed by elixir then tablets
Poorly bound to plasma proteins
Antianginal
Most of the drugs is excreted by the kidneys
Reducing myocardial oxygen demand (reducing
unchanged
the amount of oxygen the heart needs to do its
work)
Pharmacodynamics:
Or by increasing the supply of oxygen to the heart
It boosts intracellular clacium at the cell membrane
Enhance the movement of calcium into the
Three classes:
myocardial cells and stimulate the release, or block
Nitrates (acute angina)
the reuptake, of norepinephrine at the adrenergic
Beta-adrenergic blockers (long-term prevention of
nerve terminal
angina)
Acts on CNS
Calcium channel blockers (used when other drugs
fails)
Pharmacotherapeutics:
Heart failure, supraventricular arrhtymias, paroxysmal
Nitrates
atrial tachycardia
Commonly prescribed:
 Assessment:
Amyl nitrite
1. Obtain Hx
Isosorbide dinitrate
2. Monitor drug effectiveness – take apical
Isosorbide mononitrate
pulse for 1 minute before each dose
Nitroglycerin
3. Monitor digoxin levels (therapeutic blood
levels- 0.5 to 2 ng/ml)
Assessment:
4. Obtain blood for digoxin levels 8 hours
Monitor VS – IV nitroglycerin (monitor BP and PR q 5
after the last dose by mouth
to 15 minutes while adjusting the dose and every hour
5. Closely monitor K levels
thereafter)
 Intervention:
Monitor the effectiveness of prescribed drugs
1. Before giving a loading dose, obtain a
Observe for adverse reactions
baseline

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Interventions: Angiotensin II receptor blocking agents
Maybe given on empty stomach, either 30 minutes Lower BP by blocking the vasoconstrictive effects
before or 1 to 2 hours after meals (tell to swallow not of angiotension II
chew) Commonly used:
Have the patient sit or lie down when receiving the Losartan
first nitrate dose (take pulse/BP before giving the Valsartan
dose) Irbesartan
Don’t give beta-adrenergic blocker or calciul channel telmisartan
blocker to relieve angina Assessment:
Wihthold if heart rate < 60bpm Obtain baseline VS
Dilute IV nitro with D5W or NSS for injection (avoid IV Weight, fluid and electrolytes status
filters because it binds to plastic Compliance and treatment
Sublingual nitro can be repeated every 10 to 15 Tolerance and therapeutic effects
minutes up to 3 dose Dermatitis
Place topical ointments on paper as prescribed; place Adverse reactions
the paper on a nonhairy area and cover it with plastic Interventions:
Remove a transdermal patch before defibrillation If orally administer the drug with food or at bedtime
(aluminum back may be explode) If giving once daily, administer in the morning to
Be aware that the drug may initially cause headache prevent insomia
until tolerance develops or the dose is minimized
Beta-adrenergic blockers
Antihypertensive drugs Also used for long term prevention of angina
Used to treat hypertension Commonly used:
Classes: Atenolol
Angiotensin-converting enzyme (ACE) inhibitors Bisoprolol
Angiotensin-receptor blockers Carvedilol
Beta-adrenergic antagonist Nadolol
Calcium channel blocker Pindolol
Diuretics
Calcium channel blockers
ACE inhibitor Also used to treat arrhythmias and to prevent
Reduce BP by interrupting the renin-angiotensin angina
activating system (RAAS) Commonly used:
Commonly used: Amlodipine
Captopril Nifedipine
Enalapril verapamil
Lisinopril
Ramipril Sympatholytic drugs
Assessment: Reduce blood pressure by inhibiting or blocking
Obtain a baseline BP and pulse rate and rhythm the SNS
Monitor adverse reactions (headache, fatigue, dry Classified by their site or mechanism of action
non-productive cough, angioedema, tickling in the and include:
throat) Central-acting SNS inhibitors – clonidine Hcl,
Monitor monitor weight, fluid and electrolyte status methyldopa
Monitor a transdermal patch for dermatitis Alpha adrenergic blockers – prazosin, terazosin
Intervention: Mixed alpha and beta-adrenergic blockers –
If orally, administer before meals carvedilol, labetalol
Assist the patient to get up slowly to prevent Norepinephrine depletors – reserpine
orthostatic hypotension
Sodium restriction, calorie reduction, stress mngt, Direct vasodilators
exercise program should be maintain Decrease systolic and diastolic BP
Periodic eye examinations are recommended They act on arteries, veins or both

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Examples: 6. Trichlormethiazide
Diaxozide
Hydralazine Thiazide-like
Nitroprusside 1. Indapamide
2. Quinethazone
Renal Pharmacology 3. Metolazone
Drugs affecting the Kidney 4. Chlorthalidone
Outline of review
Recall the anatomy of the urinary system Thiazides
Recall the physiology of the urinary system Pharmacodynamics
Review- drugs of the following categories: These drugs BLOCK the chloride pump
1. Diuretics This will keep the Chloride and Sodium in the
2. Drug for BPH distal tubule to be excreted into the urine
Potassium is also flushed out!!
Diuretics
Agents that increase the amount of urine Special Pharmacodynamics: Side effects
produced by the kidneys Hypokalemia
DECREASED calcium excretionà hypercalcemia
Classes of Diuretics DECREASED uric acid secretionà hyperuricemia
Five major classes Hyperglycemia
1. Thiazides and thiazide-like
2. Loop diuretics Loop Diuretics
3. Potassium-sparing Prototype: Furosemide
4. Carbonic anhydrase inhibitors 1. Bumetanide
5. Osmotic diuretics 2. Ethacrynic acid
3. Torsemide
General indications for the use of the diuretics
Treatment of edema Pharmacodynamics
Urine output will increase and excess fluid is High-ceiling diuretics
flushed out of the body BLOCK the chloride pump in the ascending loop
of Henle
Treatment of CHF SODIUM and CHLORIDE reabsorption is
The sodium loss in the kidney is associated with prevented
water loss Potassium is also excreted together with Na and
Cl
Treatment of Hypertension
Diuretics will decrease the blood volume and Special Pharmacodynamics: side-effects
serum sodium Hypokalemia
Bicarbonate is lost in the urine
Treatment of Glaucoma INCREASED calcium excretionà Hypocalcemia
Diuretics will provide osmotic pull to remove Ototoxicity- due to the electrolyte imbalances
some of the fluid from the eye to decrease the IOP
Potassium sparing diuretics
time of administration of the diuretics Prototype: Spironolactone
Usually in the morning!! 1. Amiloride
2. Triamterene
Diuretics Comparison
Thiazides Potassium sparing diuretics
Prototype: Hydrochlorothiazide Pharmacodynamics
1. Bendroflumethiazide Spironolactone is an ALDOSTERONE antagonist
2. Benthiazide Triamterene and Amiloride BLOCK the potassium
3. Chlorothiazide (Diuril) secretion in the distal tubule
4. Hydroflumethiazide Diuretic effect is achieved by the sodium loss to
5. Methylclothiazide offset potassium retention

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 Allergy to sulfonamides may contraindicate the
use of thiazides
Potassium sparing diuretics Assess fluid and electrolyte balance
Pharmacokinetics: Side effects Assess other conditions like gout, diabetes,
HYPERkalemia! pregnancy and lactation
Avoid high potassium foods:
Bananas ASSESSMENT
Potatoes Physical assessment
Spinach Vital signs
Broccoli Special electrolyte and laboratory examination
Nuts Assess symptom of body weakness which may
Prunes indicate hypokalemia
Tomatoes
Oranges Nursing Diagnosis
Peaches Fluid volume deficit related to diuretic effect
Alteration in urinary pattern
Osmotic Diuretics Potential for injury (ototoxocity, hypotension)
Prototype: Mannitol Knowledge deficit
1. Glycerin
2. Isosorbide IMPLEMENTATION
3. Urea Administer IV drug slowly
Safety precaution for dizziness/hypotension
Osmotic Diuretics Provide potassium RICH foods for most diuretics,
Pharmacodynamics with the exception of spironolactone
Mannitol is a sugar not well absorbed in the Provide skin care, oral care and urinary care
nephronà osmotic pull of waterà diuresis
IMPLEMENTATION
Pharmacokinetics: side effects Monitor DAILY WEIGHT- to evaluate the
Sudden hypovolemia effectiveness of the therapy
Important for the nurse to warm the solution to Monitor urine output, cardiac rhythm. Serum
allow the crystals to DISSOLVE in the bottle! electrolytes
ADMINISTER in the MORNING!
Carbonic Anhydrase Inhibitors Administer with FOOD!
Prototype: Acetazolamide
1. Methazolamide EVALUATION: for effectiveness of therapy
Carbonic Anhydrase Inhibitors Weight loss
Pharmacodynamics Increased urine output
Carbonic Anhydrase forms sodium bicarbonate Resolution of edema
BLOCK of the enzyme results to slow movement Decreased congestion
of hydrogen and bicarbonate into the tubules Normal BP
plus sodium is lost in the urine
Pharmacokinetics: side effects Pharmacology of the Selected Endocrine Drugs
Metabolic ACIDOSIS happens when bicarbonate Endocrine Medications
is lost Thyroid Medications
Hypokalemia
Thyroid hormones
These products are used to treat the
The Nursing Process and the diuretics manifestations of hypothyroidism
ASSESSMENT Replace hormonal deficit in the treatment of
Assess the REASON why the drug is given:
ASSESSMENT HYPOTHYROIDSM
The nurse must elicit history of allergy to the Fatigue
drugs Weight gain
Cold intolerance

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Irregular Menses Endocrine Medications
Myxedema Anti-diuretic hormones
Enhance re-absorption of water in the kidneys
ANTI-THYROID medications Increases water permeability in the renal
1. Methimazole (Tapazole) collecting ducts
2. PTU (prophylthiouracil) Also stimulates VASOCONSTRICTION and
3. Iodine solution- SSKI and Lugol’s solution increases the blood pressure

ANTI-THYROID medications: Indications Therapeutic Indications

(hyperthyroidism) 1. Hormonal replacement
1. Grave’s disease 2. Used in diagnostic procedure
2. Thyrotoxicosis 3. Used to control the hemorrhage in
Hyperthyroidism variceal bleeding
Hypersensitivity to heat 4. Treatment of enuresis
Weight loss despite increased appetite
Nervousness (palpitation) Used in DI
Sweating 1. Desmopressin and Lypressin intranasally
2. Pitressin IntraMuscularly
ANTI-THYROID medications: Endocrine Medications
Absorption is good orally Anti-diuretic hormones

Side-effects of thionamides SIDE-effects

N/V, drowsiness, lethargy, bradycardia, skin rash Flushing and headache
GI complaints Water intoxication
Arthralgia, myalgia CVS: heart block, MI
AGRANULOCYTOSIS Renal: hyponatremia
Most important to monitor Gangrene due to vasoconstriction
DM Drug therapy
Side-effects of Iodine solutions Lugol’s
Most common adverse effects is DRUG THERAPY and MANAGEMENT
HYPOTHYROIDISM Usually, this type of management is employed if
Iodism= metallic taste, burning in the mouth, sore diet modification and exercise cannot control the
teeth and gums, diarrhea, stomach upset blood glucose level.

Nursing responsibilities These agents are employed to control the blood

1. Monitor VS, T3 and T4, weight
2. The medications WITH MEALS to avoid gastric
upset
3. Instruct to report SORE THROAT or
unexplained FEVER
4. Monitor for signs of hypothyroidism.
Instruct not to stop abrupt medication
Lugol’s Solution
Used to decrease the vascularity and size of the
thyroid (in preparation for thyroid surgery)
T3 and T4 production diminishes
Given per orem, can be diluted with juice,
administered WITH foods
Use straw to decrease staining
Monitor iodism
Thyroid Storm
Surgery, stress or illness
glucose level
They can be insulin and oral agents
These are given to replace the hormone in the
body
If hormone is still present BUT decreased, Oral
agents are given
Diabetes Mellitus
DRUG THERAPY and MANAGEMENT
Because the patient with TYPE 1 DM cannot
produce insulin, exogenous insulin must be
administered for life.
TYPE 2 DM may have decreased insulin
production, ORAL agents that stimulate insulin
production are usually employed.
PHARMACOLOGIC INSULIN

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This may be grouped into several categories REGULAR INSULIN
according to: ONSET- 30 minutes to 1 hour
1. Source- Human, pig, or cow PEAK- 2 to 4 hours
2. Onset of action- Rapid-acting, short- DURATION- 4 to 6 hours
acting, intermediate-acting, long-acting and very
long acting INTERMEDIATE ACTING INSULIN
Called “NPH” or “LENTE”
PHARMACOLOGIC INSULIN Appears white and cloudy
This may be grouped into several categories
according to: INTERMEDIATE ACTING INSULIN
3. Pure or mixed concentration ONSET- 2-4 hours
4. Manufacturer of drug PEAK- 4 to 6-12 hours
DURATION- 16-20 hours
Diabetes Mellitus
GENERALITIES LONG- ACTING INSULIN
1. Human insulin preparations have a shorter “UltraLENTE”
duration of action than animal source Referred to as “peakless” insulin
Diabetes Mellitus LONG- ACTING INSULIN
2. Animal sources of insulin have animal proteins ONSET- 6-8 hours
that may trigger allergic reaction and they may PEAK- 12-16 hours
stimulate antibody production that may bind the DURATION- 20-30 hours
insulin, slowing the action
3. ONLY Regular insulin can be used HEALTH TEACHING
INTRAVENOUSLY! Regarding Insulin SELF- Administration
Diabetes Mellitus 1. Insulin is administered at home
4. Insulin are measured in INTERNATIONAL subcutaneously
UNITS or “iu” Diabetes Mellitus
5. There is a specified insulin injection calibrated 2. Cloudy insulin should be thoroughly mixed by
in units gently inverting the vial or ROLLING between the
Mixed insulin are also available hands
The most common of which is the 70-30 insulin 3. Insulin NOT IN USE should be stored in the
Made up of :70% NPH and 30% regular insulin in refrigerator, BUT avoid freezing/extreme
the vial temperature
4. Insulin IN USE should be kept at room
Comparison of Insulin Peak action temperature to reduce local irritation at the
Diabetes Mellitus injection site
RAPID ACTING INSULIN 5. INSULIN may be kept at room temperature up to
Lispro (Humalog) and Insulin Aspart (Novolog) 1 month
Produces a more rapid effect and with a shorter 6. Select syringes that match the insulin
duration than any other insulin preparation concentration.
U-100 means 100 units per mL
RAPID ACTING INSULIN 7. Instruct the client to draw up the REGULAR
ONSET- 5-15 minutes (clear) Insulin FIRST before drawing the
PEAK- 1 hour intermediate acting (cloudy) insulin
DURATION- 3 hours 8. Pre-filled syringes can be prepared and should
Instruct patient to eat within 5 to 15 minutes after be kept in the refrigerator with the needle in the
injection UPRIGHT position to avoid clogging the needle
9. The four main areas for insulin injection are-
REGULAR INSULIN ABDOMEN, UPPER ARMS, THIGHS and HIPS
Also called Short-acting insulin Insulin is absorbed fastest in the abdomen and
“R” slowest in the hips
Usually Clear solution administered 30 minutes Instruct the client to rotate the areas of injection,
before a meal but exhaust all available sites in one area first
Diabetes Mellitus before moving into another area.

12
10. Alcohol may not be used to cleanse the skin
11. Utilize the subcutaneous injection technique-
commonly, a 45-90 degree angle.
12. No need to instruct for aspirating the needle
13. Properly discard the syringe after use.
T-I-E
Test bloodà Inject insulin à Eat food
ORAL HYPOGLYCEMIC AGENTS
These may be effective when used in TYPE 2 DM
that cannot be treated with diet and exercise
These are NEVER used in pregnancy!
ORAL HYPOGLYCEMIC AGENTS
There are several agents:
Sulfonylureas
Biguanides
Alpha-glucosidase inhibitors
Thiazolidinediones
Meglitinides
These drugs are given per orem and are effective
only in type 2 DM
Common adverse effects include:
Hypoglycemia
Diarrhea, jaundice, nausea and heartburn
Anemia , photosensitivity
General Nursing Consideration
1. Observe for manifestations of
hypoglycemia
2. Assess for allergic reaction
3. Instruct to take the medication at the
same time each day
4. Caution to avoid taking other drugs
without consultation with physician
5. THESE medications SHOULD NEVER be given
to pregnant women, so rule out pregnancy
6. Instruct to wear sunscreen
7. Advise to bring simple sugar to be taken when
hypoglycemic episodes occur
SULFONYLUREAS
MOA- stimulates the beta cells of the pancreas to
secrete insulin
Classified as to generations- first and second
generations
FIRST GENERATION- Acetoheximide,
Chlorpropamide, Tolazamide and Tolbutamide
SECOND GENERATION- Glipizide, Glyburide,
Glibenclamide, Glimepiride
Diabetes Mellitus: Sulfonylureas
The most common side –effects of these
medications are Gastro-intestinal upset and
dermatologic reactions.
HYPOGLYCEMIA is also a very important side-
effect
Given 30 minutes before meals- breakfast
Diabetes Mellitus: Sulfonylureas
Chlorpropamide has a very long duration of
action. This also produces a disulfiram-like
reaction when taken with alcohol
Second generation drugs have shorter duration
with metabolism in the kidney and liver and are
the choice for elderly patients
BIGUANIDES
MOA- Facilitate the action of insulin on the
peripheral receptors
These can only be used in the presence of insulin
BIGUANIDES= “formin”
They have no effect on the beta cells of the
pancreas
Metformin (Glucophage) and Phenformin are
examples
The most important side effect is LACTIC
ACIDOSIS!
These are not given to patient with renal
impairment
These drugs are usually given with a sulfonylurea
to enhance the glucose-lowering effect more than
the use of each drug individually
ALPHA-GLUCOSIDASE INHIBITORS
MOA- Delay the absorption of glucose in the GIT
Result is a lower post-prandial blood glucose
level
They do not affect insulin secretion or action!
Side-effect: DIARRHEA and FLATULENCE
Examples of AGI are Acarbose and Miglitol
They are not absorbed systemically and are very
safe
They can be used alone or in combination with
other OHA
Side-effect if used with other drug is
HYPOGLYCEMIA
Note that sucrose absorption is impaired and IV
glucose is the therapy for the hypoglycemia
THIAZOLIDINEDIONES
MOA- Enhance insulin action at the receptor site
They do not stimulate insulin secretion
Examples- Rosiglitazone, Pioglitazone
These drugs affect LIVER FUNCTION
13
Can cause resumption of OVULATION in peri- Methyltestosterone
menopausal anovulatory women Fluoxymesterone
Aqueous testosterone
MEGLITINIDES Reproductive Hormones
MOA- Stimulate the secretion of insulin by the Oral Contraceptive Pills
beta cells Two types are available: Combination estrogen
Examples- Repaglinide and Nateglinide and progesterone AND progestins only
Diabetes Mellitus Reproductive Hormones
MEGLITINIDES Oral Contraceptive Pills: DYNAMICS
They have a shorter duration and fast action Inhibits OVULATION by altering the hypothalamus
Should be taken BEFORE meals to stimulate the and gonadotropin axis
release of insulin from the pancreas Alters the MUCUS to prevent sperm entry
Diabetes Mellitus Alters the uterine endometrium to prevent
MEGLITINIDES implantation
Principal side-effect of meglitinides- Suppresses the ovaries
hypoglycemia Reproductive Hormones
Can be used alone or in combination Oral Contraceptive Pills: Indicators
Reproductive Hormones Suppression of ovulation for prevention of
Gonadal hormones include agents that affect the pregnancy
female and male reproductive cycle Regulation of menstrual cycle and management of
Female hormones include ESTROGENS, dysfunctional bleeding
PROGESTINS and ovarian hormones Treatment of endometriosis
Male hormones include ANDROGENS and Reproductive Hormones
anabolic steroids Oral Contraceptive Pills: Kinetics
Reproductive Hormones Easily absorbed orally
The GENERAL Mechanism of Action NORPLANT provides 5 years of contraception
These hormones interfere with the normal cycle of Provera provides 3 months of protection
hormone balance Metabolized and excreted in liver
Reproductive Hormones Reproductive Hormones
INDICATIONS Oral Contraceptive Pills:
1. FEMALE: Hormonal replacement therapy, Not to be used in patients with history of,
oral contraception, treatment of infertility hypertension, thromboemoblic or CVA disease
and management of some tumors Not given in certain cancers
2. MALE: replacement therapy, metabolic Contraindicated in pregnancy
stimulators and treatment of some SMOKING should be avoided when under therapy
tumors Reproductive Hormones
Reproductive Hormones Oral Contraceptive Pills: Drug Interaction
Estrogens Rifampicin, penicillin and tetracycline REDUCE
Conjugated estrogen effectiveness of contraception
Estradiol Benzodiazepines decrease the levels of OCP
Ethinyl estradiol Reproductive Hormones
Diethylstilbesterol (DES) Oral Contraceptive Pills:
Clomiphene Side effects
Reproductive Hormones CNS: headache
Progestins CV: Thromboembolic disease, MI, hypertension
Medroxyprogesterone acetate (Provera) and pulmonary edema
Megestrol NAUSEA and cholestatic JAUNDICE
Norethindrone Breast tenderness, weight gain, edema,
Levonorgestrel (Norplant) breakthrough bleeding, acne
Norgestrel Reproductive hormones
Norethindrone acetate Nursing Considerations
Reproductive Hormones 1. Assess for risk factors and the ability to
Androgens comply with medications
Testosterone cypionate 2. Determine the type of OCP used

14
Monophasic pills provide constant dosing of Antitussives- agents utilized to block the cough
BOTH estrogen and progestin reflex
Biphasic pills provide constant estrogen but Drugs for COPD (chronic obstructive pulmonary
varying progestin doses disease)- which includes the Bronchodilators,
Triphasic pills provide varying Estrogen and inhaled steroids, Leukotriene receptor blockers
Progesterone and other anti-asthma drugs
Reproductive hormones Decongestants- are utilized to decrease the blood
Nursing Considerations flow to the upper respiratory tract and decrease
3. Teach the common side-effects and re-assure the excessive production of secretions
that these will decrease in time Expectorants- are used to decrease the viscosity
4. Instruct to use other means of contraception if of sputum to effectively increase productive
antibiotics and anticonvulsants are also taken cough to clear the airways
5. WARN the client to avoid smoking because this The ANTIHISTAMINES
will increase the risk for embolic episodes Also called H1 blockers or H1 antagonists, these
Clomiphene are agents designed to relieve respiratory
A synthetic, non-steroidal estrogen symptoms and to treat allergic conditions.
Increases the secretion of gonadotropins and The ANTIHISTAMINES
initiates the secretion of FSH and LH The anti-histamines are group according to the
OVULATION will occur “generation”.
Used in the treatment of infertility The FIRST GENERATION agents have greater
Readily absorbed orally anticholinergic effects and can cause more
Clomiphene sedation and drowsiness! These agents cause
Side effects can be: drowsiness.
Risk for Multiple pregnancy The SECOND GENERATION agents have fewer
Nausea, breast discomfort, headache and GI anticholinergic effects that is why they cause less
disturbances sedation.
Visual disturbances The ANTIHISTAMINES
Enlargement of the ovaries The FIRST GENERATION ANTIHISTAMINES
Viagra (Sildenafil) 1. Azatadine 11.
A medication used for penile erectile dysfunction Dimenhydrinate
Selectively inhibits receptors and enzyme 2. Azelastine 12.
Phosphodiesterase E Diphenhydramine
This increases the nitrous oxide levels allowing 3. Brompheniramine 13. Hydroxyzine
blood flow into the corpus cavernosum 4. Buclizine 14.
Viagra (Sildenafil) Meclizine
Contraindicated in patients with bleeding 5. Cetirizine 15. Methdilazine
disorders and with penile implants 6. Chlorpheniramine 16.
Caution: Coronary Artery Disease and Promethazine
concomitant use of nitrates 7. Clemastine 17.
Side-effects: PRIAPISM, headache, flushing, Tripelenamine
dyspepsia, UTI, diarrhea and dizziness 8. Cyclizine 18.
Viagra (Sildenafil) Carbinoxamine
Nursing consideration 9. Cyproheptadine 19.
Assess for risk factors Trimeprazine
Instruct to take the drug ONE hour before sexual 10. Dexchlorpheniramine 20. Triprolidine
act The ANTIHISTAMINES
Drug is taken orally The SECOND GENERATION ANTIHISTAMINES
Pharmacology of Respiratory Drugs Fexofenadine
Drugs Affecting the Respiratory System Loratidine
Antihistamines- are used to block the release or Azelastine
action of histamine- a chemical mediator of Cetirizine
inflammation that increases secretions and Anti-Histamine
constricts the air passageway The Mechanism of Action

15
These agents SELECTIVELY block the effects of
histamine at the HISTAMINE-1 receptor sites in
the target tissue by competing with histamine for
receptor, decreasing the cellular responses
They also have antipruritic property.
Anti-Histamine
Clinical Indications for Use in respiratory system
1. rhinitis
2. allergic sinusitis
3. uncomplicated urticaria
Anti-Histamine
Contraindications and Precautions for the use of
the antihistamines
Pregnancy and lactation are contraindications,
and they agents are used cautiously in patient
with impaired liver and kidney functions.
Fatal arrhythmias
Anti-Histamine
Pharmacodynamics: Drug effects on the body
1. CNS- drowsiness and sedation, most
pronounced if first generation agents are
used
2. Fatigue, dizziness and disturbed
coordination.
3. Anticholinergic effects= drying of the
respiratory mucus membrane, GI upset
and nausea, arrhythmias, dysuria, urinary
retention
4. Skin dryness
Anti-Histamine
Implementation
The nurse should administer the drug on an
EMPTY stomach, or 1 hour before or 2 hours after
meals to increase the absorption.
Give with food if GI upset occurs
Offer sugarless lozenges or hard candy to
counteract dryness of the mouth. Give frequent
oral care
Provide safety measures if drowsiness may
occur. Side rails up, assist in ambulation, and
advise not to drive or operate dangerous
machineries or delicate tasks.
Anti-Histamine
Nursing implementation
Increase humidity in the room by utilizing
nebulizers and provide adequate hydration
Allow the patient to void first before administering
the drug.
Caution the patient against use of OTC drugs,
alcoholic beverages and sedatives because they
may cause extreme sedation.
Anti-Histamine
Evaluation
Monitor patient’s response to the drug, the
adverse effects and the effectiveness of comfort
measures employed
Decreased allergic symptoms
Decreased occurrence of rhinitis
Anti tussives
These are agents suppress the cough reflex on
the MEDULLA oblongata to suppress cough of
many respiratory conditions.
The anti-tussives are the following:
Benzonatate= narcotic anti-tussive
Butamirate citrate= non-narcotic
Codeine= narcotic
Dextromethorphan= non-narcotic
Hydrocodone= narcotic
Anti tussives
Pharmacodynamics: Therapeutic use of the
antitussives
The traditional antitussives act directly on the
MEDULLARY cough of the brain to depress the
cough reflex, but it does NOT suppress
respiration.
Dextromethorphan DOES not depress respiration.
Antitussives
Clinical Use of the antitussive:
utilized for the treatment of cough
Contraindications and Indications for use of
antitussives
These agents are NOT given to patients who have
undergone thoracic surgeries because they need
to cough to maintain airway patency. Precautions
are instituted when giving to patients with
asthma, emphysema or COPD because an
accumulation of secretions may occur.
Anti tussives
Pharmacodynamics: Drug Effects
Respiratory- dryness of mucosal membranes,
increased viscosity of secretions
CNS- drowsiness, dizziness and sedation
GIT- nausea, constipation and dry mouth, GIT
upset
Nursing Process and the antitussives
Anti tussives
Implementation
Emphasize that the drug should be taken only on
a specified time frame as ordered
16
Provide other measures to relieve cough like
provide humidified oxygen, cool temperatures,
fluids and use of lozenges
Provide health teaching as to drug name, dosage
and measures to handle side-effects
Caution that alcohol, narcotics, sedatives-
hypnotics can cause CNS depression when used
with antitussives.
Mucolytics
These are agents that breakdown mucous in order
to help respiratory patients in coughing up thick,
tenacious secretions.
The following are the mucolytics:
Acetylcysteine
Dornase alfa
Mucolytics
Pharmacodynamics: Mechanism of Action
These agents work in the following ways:
acetylcysteine affects the mucoproteins in the
respiratory secretions by splitting apart disulfide
bonds that are responsible for holding the mucus
materials together.
Mucolytics
Cautions should be used in cases of acute
bronchospasms, peptic ulcer and esophageal
varices.
The increased secretions can aggravate the
problem
Indications for use
COPD
Pneumonia
Tuberculosis
Atelectasis
Mucolytics
Pharmacodynamics: drug effects
GIT= GI upset, stomatitis, irritation of the
respiratory tract
others: Bronchospasm and rash
Mucolytics
Implementation
Instruct the patient to avoid combining with other
drugs in the nebulizer to avoid formation of
precipitates
The dug can be administered via nebulizers with
the drug diluted with sterile water.
Remind the patient that the drug may irritate the
respiratory mucosa
Provide through patient teaching including drug
name and prescribed dosage
Have suction machine available
Drugs for COPD
The agents used for COPD may be one of the
following:
Bronchodilators such as adrenergics and the
xanthines used to assist in opening the narrowed
airways
Steroids are used to decrease inflammation
Leukotriene modifiers reduce inflammation in the
lung tissue
Cromolyn sodium and nedocromil act as anti-
inflammatory agents by suppressing the release
of HISTAMINE from the mast cells
Expectorants are used to assist in loosening
secretions from the airways
Antibiotics are prescribed to prevent serious
complications from bacterial infections.
The BRONCHODILATORS
These are Bronchodilators medication used to
facilitate respiration by dilating the airways.
They are helpful in symptomatic relief or
prevention of bronchial asthma and
bronchospasm associated with COPD.
17
The BRONCHODILATORS Unlabeled uses include stimulation of respiration
in Cheyne – Stokes respiration and
The bronchodilators are:
the treatment of apnea and bradycardia in
Xanthines premature infants.

Sympathomimetics (beta-agonists) The XANTHINES

Anticholinergics Pharmacodynamics: drug effects

Inhaled steroids GI upset, anorexia, vomiting, gastric pain,

nausea, irritability, and tachycardia to seizures,
The XANTHINES brain damage, and even death.

Xanthines, including caffeine and theophylline,
come from a variety of naturally occurring
sources. These drugs were once main choice for
treatment of asthma and bronchospasm.
Theophylline toxicity occurs when concentration
is above 20 ug/mL.
Rapid IV administration of aminophylline can
cause dizziness, flushing, severe HYPOTENSION,
bradycardia and palpitations.

The Xanthines include: The XANTHINES

Aminophyline Implementation

Caffeine Monitor vital signs and note for the BP and HR

because there may be Hypotension and
Dyphilline tachycardia.

Oxytriphylline Administer oral drug with food to relieve GI

Pentoxyfilline
Theophylline
The XANTHINES
Pharmacodynamics: Drug action
The xanthines have a direct effect on the smooth
– muscles of the respiratory tract, both those on
the bronchi and the blood vessels.
The xanthines stimulate the CNS such that
respiration is stimulated, coronary arteries dilate
and pulmonary arteries dilate, with additional
effect of diuresis.
The XANTHINES
Clinical Use of the xanthines
Xanthines are indicated for the symptomatic relief
or prevention of bronchial asthma and reversal of
bronchospasm associated with COPD.
irritation, if GI upset is a problem.
Monitor patient response to the drug= relief of
respiratory difficulty and improved airflow, to
determine the effectiveness of the drug dosage
and to adjust dosage as needed.
The XANTHINES
Implementation
Provide comfort measures, including rest periods,
quiet environment, dietary control of caffeine, and
headache therapy as needed, to help the patient
cope with the effects of drug therapy.
Provide adequate hydration
Don’t crush enteric coated and sustained release
tablets
Encourage to stop smoking
The XANTHINES
Evaluation

18
Monitor patient response to the drug (improved
air flow, ease of respirations).
Monitor for adverse effects (CNS effects, cardiac
arrhythmias, GI upset, local irritation)
The SYMPATHOMIMETICS
These are drugs that mimic the effects of the
sympathetic nervous system.
One of the actions of the sympathetic nervous
system is dilation of the bronchi and increased
rate and depth of respiration.
This is the desired effect when selecting a
sympathomimetic as a bronchodilator.
The SYMPATHOMIMETICS
Sympathomimetics that are used as
bronchodilators include the following:
Albuterol
Bitolterol
Isoproterenol
Metaproterenol
Salbutamol
Terbutaline
Ephedrine
Epinephrine= the drug of choice for the treatment
of acute bronchospasm, including that which is
caused by anaphylaxis
The SYMPATHOMIMETICS
Clinical Use
Asthma and other Allergic conditions
bronchospasm in reversible obstructive airway
disease, such as acute and chronic asthma and
chronic bronchitis.
They have also been effective in preventing
exercise-induced bronchospasm.
Used also in Preterm labor
The SYMPATHOMIMETICS
CONTRAINDICATIONS/CAUTIONS
These drugs are contraindicated or should be
used with caution, depending on the severity of
the under- lying condition, in conditions that
would be aggravated by the sympathetic
stimulation.
Such conditions include cardiac disease,
vascular disease, arrhythmias, diabetes,
hyperthyroidism, pregnancy, and lactation.
The SYMPATHOMIMETICS
Pharmacodynamics: drug EFFECTS
Adverse effects of these drugs, which can be
attributed to sympathomimetic stimulation
include
CNS stimulation= tremors, headache,
nervousness
GI- GI upset
Cardio= cardiac arrhythmias, hypertension,
tachycardia and palpitations, vasoconstriction
Respi= bronchospasm, sweating, pallor, and
flushing.
Hyperglycemia, Urinary retention
The SYMPATHOMIMETICS
Implementation
Assure the patient that the drug of choice will
vary with each individual. These
sympathomimetics are slightly different
chemicals and are prepared in a variety of
delivery systems.
Advise patients to use the minimal amount
needed for the shortest period of time necessary,
to prevent adverse effects and accumulation of
drug levels.
The SYMPATHOMIMETICS
Implementation
Instruct the patient on how to use the inhalers.
Teach patients who use one of these drugs for
exercise-induced asthma to use it 30 to 60
minutes before exercising to ensure peak
therapeutic effects when they are needed.
19
Provide safety measures as needed if CNS effects
become a problem, to prevent patient injury.
The SYMPATHOMIMETICS
Implementation
Provide small, frequent meals and nutritional
consultation if GI effects interfere with eating to
ensure, proper nutrition.
Carefully teach the patient about the proper use of
the prescribed delivery system.
Review that procedure periodically as improper
use may result in ineffective therapy.
The SYMPATHOMIMETICS
Evaluation
Monitor patient response to the drug (improved
breathing).
Monitor for adverse effects (CNS effects,
increased pulse and blood pressure, GI upset)
INHALED STEROIDS
Inhaled steroids have been found to be a very
effective treatment for bronchospasm.
Agents include
Beclomethasone = given via MDI inhaler
Flunisolide
Triamcinolone
Dexamethasone= is given IV and orally, not
inhaled
Prednisone and prednisolone
INHALED STEROIDS
THERAPEUTIC ACTIONS AND INDICATIONS
Inhaled steroids are used to decrease the
inflammatory response in the airway.
In an airway swollen and narrowed by
inflammation and swelling, this action will
increase airflow and facilitate respiration.
Inhaling the steroid tends to decrease the
numerous systemic effects that are associated
with steroid use.
INHALED STEROIDS
THERAPEUTIC ACTIONS AND INDICATIONS
When administered into the lungs by inhalation,
steroids decrease the effectiveness of the
inflammatory cells.
This has two effects:
decreased swelling associated with inflammation
and promotion of beta adrenergic receptor
activity= which may promote smooth muscle
relaxation and inhibit broncho-constriction.
INHALED STEROIDS
CONTRAINDICATIONS/CAUTIONS
Inhaled corticosteroids are not for emergency use
and not for use during an acute asthma attack or
status asthmaticus.
They should not be used during pregnancy or
lactation.
INHALED STEROIDS
ADVERSE EFFECTS
Adverse effects are limited because of the route
of administration
Respiratory= Sore throat, hoarseness, coughing,
dry mouth, and pharyngeal and laryngeal fungal
infections are the most common side effects
encountered.
If a patient does not administer the drug
appropriately or develops lesions that allow
absorption of the drug, the systemic side effects
associated with steroids may occur.
INHALED STEROIDS
Implementation
Do not administer the drug to treat an acute
asthma attack or status asthmaticus, as these
drugs are not intended for treatment of acute
attack.
20
Taper systemic steroids carefully during the
transfer to inhaled steroids; deaths have occurred
from renal insufficiency with sudden withdrawal.
Have the patient use decongestant drops before
using the inhaled steroid to facilitate penetration
of the drug if nasal congestion is a problem.
INHALED STEROIDS
Implementation
Have the patient rinse the mouth after using the
inhaler, as this will help to decrease systemic
absorption and decrease GI upset and nausea
Monitor the patient for any sign of respiratory
infection; continued use of steroids during an
acute infection can lead to serious complications
related to the depression of the inflammatory and
immune responses.
INHALED STEROIDS
Evaluation
Monitor patient response to the drug (improved
breathing).
Monitor for adverse effects (nasal irritation, fever,
GI upset)
Cromolyn
Administered by INHALATION is a drug that is
frequently used in the treatment of asthma.
It does not have bronchodilating or
anticholinergic effects and does not fit into any
other pharmacological class.
Cromolyn
THERAPEUTIC ACTIONS AND INDICATIONS
Cromolyn is a mast cell stabilizer.
It works at the cellular level to inhibit the release
of histamine (released from mast cells in
response to inflammation or irritation).
It is inhaled from a capsule and may not reach its
peak effect for 1 week.
It is recommended for the treatment of chronic
bronchial asthma, exercise-induced asthma, and
allergic rhinitis.
Cromolyn
CONTRAINDICATION / CAUTIONS
Cromolyn cannot be used during an acute attack,
and patients need to be instructed in this
precaution.
Allergy to seafoods
It is not recommended for pregnant or nursing
women or children under the age of 6 years.
Cromolyn
ADVERSE EFFECTS
Few adverse effects have been reported with the
use of cromolyn
swollen eyes, headache, dry mucosa, and
nausea.
Cromolyn
Implementation
Review administration procedures with the patient
periodically; proper use of the delivery device is
important in maintaining the effectiveness of this
drug.
Caution the patient not to discontinue use
abruptly; cromolyn should be tapered slowly if
discontinuation is necessary to prevent rebound
adverse effects.
Caution the patient to continue taking this drug,
even in symptom-free periods, to ensure
therapeutic levels of the drug.
Cromolyn
Implementation
Administer oral drug one-half hour before meals
and at bedtime, which will promote continual drug
levels and relief of asthma.
Advise the patient not to wear soft contact lenses;
if cromolyn eye drops are used, lenses can be
stained.
Provide thorough patient teaching, including the
drug name and prescribed dosage, measures to
help avoid adverse effects, warning signs that
may indicate problems, and the need for periodic
21
monitoring and evaluation to enhance patient 8. monobactams
knowledge about drug therapy and to promote
compliance. 9. fluoroquinolones

Cromolyn 10. sulfonamides

Evaluation 11. nitrofurantoin

Monitor patient response to the drug (improved Aminoglycosides

breathing).
Are bactericidal (destroy bacteria)
Monitor for adverse effects (drowsiness,
headache, GI upset, local irritation). Effective against:

Evaluate the effectiveness of the teaching plan - gram-negative bacilli

(patient can name drug, dosage, adverse effects
- some aerobic gram-positive bacteria
to watch for, specific measures to avoid adverse
effects. - mycobacteria
Anti-infective drugs - some protozoa
Selecting an anti-infective drug Currently in use includes:
First, the microorganism must be isolated and - amikacin sulfate
identified generally through growing a culture
- gentamicin sulfate
Then its susceptibility to various drugs must be
determined - kanamycin sulfate

Location of the infection must be considered - neomycin sulfate

Cost of drugs as well as its potential adverse - streptomycin sulfate

effects and allergies
- tobramycin
Antibacterial drugs
 Pharmacokinetics:
Also known as antibiotics
- absorbed poorly form the GIT
Drugs that either kill or inhibit the growth of
bacteria - usually given parenterally

Mainly used to treat systemic bacterial infections - IV/IM absorption is rapid and complete

 Antibacterial drugs include: - distributed widely in extracellular fluid

1. aminoglycosides - readily crossess the placental barrier

but not BBB
2. cephalosporins
- arent metabolized
3. tetracyclines
- excreted primarily in the kidneys
4. lincomycin derivatives
Pharmacodynamics:
5. macrolides
- by binding to the bacteria’s 30S subunit,
6. vancomycin specific ribosomes thereby interrupting CHON
synthesis and causing the bacteria to die
7. carbapenems

22
Pharmacotherapeutics: - they bind reversibly to several enzymes
(penicillin-binding proteins) outside the bacterial
- infections caused by gram-negative cytoplasmic membrane
bacilli
Pharmacotherapeutics:
- serious nosocomial, gram-negative
bacteremia, peritonitis, pneumonia - wide spectrum

- UTI’s - they cover gram-positive, gram-

negative, and anaerobic organisms
- infections of the CNS
Cephalosporins
Penicillins
Are grouped into generations according to their
Remain the most important and useful effectiveness against different oraganisms,
antibacterial drugs characteristics and development

Divided into four groups: First generation

- natural penicillins ( penicillin G Cefadroxil

benzathine, penicillin G potassium, penicillin G
procaine, penicillin G sodium, penicillin V Cefasolin
potassium)
Cephalexin
- penicillinase-resistant penicillines
(dicloxacillin sodium, nafcillin sodium, oxacillin cephadrine
sodium)
Second generation
- aminopenicillins (amoxicillin, ampicillin)
Cefaclor
- extended-spectrum penicillins
(carbenicillin indanyl sodium, ticarcillin disodium) Cefotetan

Pharmacokinetics: Cefprozil

- absorption of oral penicillin varies and Ceftibuten

depends on such factors as:
cefuroxime
1. particular penicillin used
Third generation
2. pH of the stomach and intestine
Cefdinir
3. presence of food in the GIT
Cefoperazone
- most penicillins are given on an empty
Cefotaxime
stomach (1 before or 2 hours after meal)
Ceftazidime
- penicillins that can be given wihtout
regard to meals: amoxicillin, penicillin V and ceftriaxone
amoxicillin-clavulanate K
Fourth generation
- most penicillins are excreted 60%
unchanged by the kidneys (nafcillin and oxacillin Cefditoren
– bile)
cefepime
Pharmacodynamics:

23
Are administered parenterally (they are’nt - they penetrate the bacterial cell by an
absorbed from the GIT) energy-dependent process

Some are absorbed from the GIT but food usually - within the cell, they bind primarily to a
decreases their absorption rate subunit of the ribosome, inhibiting the CHON
synthesis required for maintaining the bacterial
Cefuroxime and cefpodoxime – increased cell
absorption when given with food
Pharmacotherapeutics:
Pharmacotherapeutics
- gram-positive/negative aerobic and
- 1st generation – gram positive anaerobic bacteria
organisms
- spirochettes
- used to treat
staph and strep infections - mycoplasma

- 2nd generation – gram – negative - rickettsiae

- 3rd generation – drug of choice for - chlamydia

enterobacter,P.
aeruginosa - some protozoa

- 4th generation – gram positive and - tetracyclines are used to treat:

1. rocky mountain spotted fever

negative
2. Q fever
Tetracyclines
3. lyme dse.
Broad-spectrum antibacterial
Macrolides
Classified as:
Includes erythromycin and derivatives such as:
- intermediate acting (demeclocycline
Hcl)
- estolate
- long acting (doxycycline and
- ethylsuccinate
minocycline)
- gluceptate
Pharmacokinetics:
- lactobionate
- absorbed from the duodenum when
taken orally - stearate

- distributed widely into body tissues and Other macrolides includes:

fluids concentrated in bile
- azithromycin
- excreted primarily by kidneys
- clarithromycin
- doxycycline – feces

- minocycline – enterohepatic
recirculation Pharmacokinetics:
Pharmacodynamics: - acid-sensitive (it must be buffered or
have an enteric coating to prevent destruction by
gastric acid)

24
 - erythromycin – absorbed in the Sulfadiazine
duodenum
sulfisoxazole
- metabolized in the liver
Sulfonamides
- excreted in bile in high concentrations,
small amounts are excreted in urine treat UTI

Pharmacodynamics: sulfamethazole(Gantanol)

- inhibit RNA-dependent CHON synthesis Sulfixazole(Gantrisin)

by acting on a small portion of the ribosome
sulfazaline( Azulfidine)
Pharmacotherapeutics:
sulfamethazole and trimethoprim(Bactrim and
- drug of choice for treating Mycoplasma Septra)
pneumoniae infections as well as pneumoniae
caused by Legionella pneumophila Sulfonamides

Carbapenems S/E;

Are a class of beta-lactam antibacterials that nausea and vomiting (gastric irritation) decreased
includes: absorption of folacin

- imipenem-cilastatin Na rash

- meropenem malaise

- ertapenem blood dyscrasias

Quinolones crystaluria(drug precipitation in acidic urine)

Structurally similar synthetic antibacterial drugs stomatitis , hypersensitivity and photosensitivity

Primarily administered to treat UTI’s, URTI, Sulfonamides

pneumonia, gonorrhea
I
Includes:
increase OFI
- ciprofloxacin
maintain alkaline urine
- gatifloxacin
monitor blood work – megaloblastic anemia(dec.
- levofloxacin folacin)

- moxifloxacin potentiates anticoagulant and oral hypoglycemic

effects
- norfloxacin
Antiviral drugs
- ofloxacin
Used to prevent or treat viral infections ranging
Sulfonamides from influenza to HIV

First effective systemic antibacterial drugs
Includes:
Co-trimoxazole (sulfamethoxazole and trimethoprim)
Major antiviral drug classes used to treat
systemic infections include:
Synthetic nucleosides

25
Nucleoside analog reverse transcriptase inhibitors PROVIDE PROPHYLAXIS WHEN EXPOSURE TO
(NRTIs) VIRAL INFECTION HAS OCCURRED

Non-nucleoside reverse transcriptase Acyclovir sodium (Zovirax)

inhibitors(NNRTIs)
Amantadine Hcl (Symmetrel)
Nucleotide analog reverse transcriptase inhibitors
Interferon(Roferon – A)
Protease inhibitors
AZT
ANTIVIRALS
Idoxuridine ( Stoxil)
PROVIDE PROPHYLAXIS WHEN EXPOSURE TO
VIRAL INFECTION HAS OCCURRED ANTIVIRALS

Acyclovir sodium (Zovirax) cns stimulation and orthostatic hypotension,

nephrotoxicity, dizziness and constipation
Amantadine Hcl (Symmetrel)
Nsg. Consideration:
Interferon(Roferon – A)
support natural defense
AZT
encourage high fiber foods
Idoxuridine ( Stoxil)
evaluate response
ANTIVIRALS
Anti Tuberculars
cns stimulation and orthostatic hypotension,
nephrotoxicity, dizziness and constipation administered in combination over a prolonged
time period to decrease the possibility of
Nsg. Consideration: mycobacterial drug resistance

support natural defense first line :

encourage high fiber foods ethambutol-mycobacterial RNA

evaluate response Isoniazid – mycobacterial cell wall

Synthetic nucleosides Paraaminosalicylic acid preparation(PAS)-

mycobacterial folic acid synthesis
Group of drugs used to treat various viral
syndromes that can occur in Rifampin-interferes with mycobacterial RNA
immunocompromised patients including HSV and
CMV Streptomycin sulfate – inhibits mycobacterial protein
synthesis
Drugs in this class includes:
second line:
Acyclovir
pyrazinamide
Famciclovir
ethionamide
Ganciclovir
capriomycin
Valacyclovir Hcl
Anti Tuberculars
Valgancyclovir Hcl
S/E:
ANTIVIRALS

26
GI irritation paresthesia( neurotoxicity)

suppressed absorption of fat and B complex , -spec. review proper method of application
folacin and B12, depletion of B6 by isoniazid
assess vital signs, throughout course of therapy
dizziness,CNS and liver disturbances
evaluate clients response
blod dyscrasias
Anti fungals
streptomycin : ototoxicity( direct auditory{eight cranial
nerve}toxicity) Amphotericin B

ethambutol: visual disturbances ( direct optic nerve use infusion control device and protect from light
toxicity)
monitor blood works-hypokalemia and
Anti Tuberculars hypomagnesemia

nursing care:  Griseofulvin – assess for

antagonism if patients are taking
support defense mechanisms anti coagulants. avoid sunlight

obtain sputum specimens for acid fast bacillus  topical prep- wash drug stained
clothing with soap and water.,
monitor blood work report signs of local irritation

enforce compliance , avoid alcohol Anti parasitics

instruct regarding nutriitonal deficits interfere with parasite metabolism and

reproduction, helminthic as well as protozoal
Rifampin – urine dark orange infestations respond to this class of drugs

Streptomycin: auditory exams Antihelmithic

Ethambutol – visual exams Mebendazole ( Vermox)

PZA – liver functions Piperazine ( Vermazine )

Anti fungals Pyrivinium Pamoate ( Povan)

used to treat sytemic and localized fungal Amebicides

infections
Chloroquine HCl ( Aralen)
Amphotericin ( Fungizone)
Emetine Hcl
Fluconazole (Diflucan )
Metronidazole ( Flagyl)
Griseofulvin ( Grisactin )
Antimalarials
Nystatin ( Mycostatin, Nilstat )
Chloroquine HCl ( Aralen)
Anti - fungals
Hydroxychloroquine SO4 ( Plaquenil)
nausea and vomiting( gastric irritation)
Pyrimethamine ( Darapime)
headache( neurotoxicity)
Primaquine PO4
fever and chills ( blood dyscrasias )
Anti parasitics

27
antihelminthics-GI irritation, CNS disturbance, Inflammation
skin rash
Characteristic Signs:
amebicides – GI iiritation, blood dyscrasias, skin
rash, headache, dizziness Pain (Dolor)

Antimalarials-nausea and vomiting, blood Swelling /Edema (Tumor)

dyscrasias, visual disturbances
Redness (Rubor)
Anti parasitics
Heat (calor)
administer drug with meals and assess VS
Impaired function of the part (severe injury)
monitor blood works and instruct client about Functio laesa
proper hygiene
Fig. 4.9
use safety precautions if CNS effects are
manifested ANTI-INFLAMMATORY AGENTS

antimalarials – frequent visual examinations
evaluate response to treatment and
understanding of therapy
Pharmacology of the anti-inflammatory agents
There are many different types of drugs utilized as
anti-inflammatory agents.
Steroids like cortisone, beclomethasone, etc,
systemically block inflammatory and immune
responses.

ANTI-INFLAMMATORY AGENTS Anti-histamines block the release of Histamine.

The anti-inflammatory response is designed to Another major class of drugs is termed Non-
protect the body from injury and pathogens. Steroidal Anti-inflammatory drug.

It employs a variety of potent chemical mediators Drugs

to produce the reaction that helps to destroy
pathogens and promote healing The Salicylates

Inflammatory Physiology These agents are some of the oldest anti-

inflammatory and pain reliever agents.
Inflammation: ETIOLOGY
Acetylsalicylic acid (aspirin)
Physical Agents
Choline magnesium trisalicylate
Mechanical objects causing trauma to objects
Choline salicylate
excessive heat & cold (burn & frostbite)
Mesalamine
radiation
Osalazine
Chemical Agents
Salsalate
external irritants – strong acids, alkalis, irritating
gasses Sodium thiosalicylate

internal irritants – substances manufactured Diflusinal (a derivative of salicylic acid)

within the body such as excessive HCL in the
Salicylates
stomach
Classification: Non-Steroidal Anti-inflammatory
Microorganisms – group of bacteria, viruses,
agents
fungi, protozoa, Rickettsia

28
Dynamics: Inhibit the enzyme that produces
prostaglandins
Kinetics: Administered orally and parenterally
Common side-effects Peptic ulceration, bleeding
NR: Administer with foods; bleeding precaution
Salicylates
Given for pain, fever and inflammation
Effectiveness is determined if manifestations of
pain, fever and inflammation resolve.
The Salicylates
Mechanism of Action of the Salicylates
Salicylates inhibit the synthesis of prostaglandin,
an important mediator of the inflammatory
reaction.
The Salicylates
Mechanism of Action of the Salicylates
The fever lowering property (antipyretic effect) of
salicylates is related to the blocking of a
prostaglandin mediator of pyrogens
Aspirin affects platelet aggregation by inhibiting
the synthesis of thromboxane A, a potent
vasoconstrictor normally increases platelet
aggregation
The Salicylates
Therapeutic Use of the Salicylates
Mild to moderate pain
Fever
Inflammatory conditions
Prevention of ischemic stroke
Aspirin is also given to patients with CAD, angina
or previous history of MI to reduce the risk of
myocardial infarction and death
The Salicylates
Pharmacokinetic profile of the Salicylates
Aspirin is well absorbed from the GIT.
Because of the GI effects, the Salicylates should
be taken with meals
The Salicylates
The Adverse Effects of Salicylate Use
GIT- gastric ulceration , nausea, dyspepsia,
heartburn and epigastric discomfort.
VASCULAR- bleeding abnormalities can be
expected. Patients can have occult blood loss and
spontaneous small hemorrhages.
The Salicylates
The Adverse Effects of Salicylate Use
SALICYLISM- this condition can occur with higher
levels of aspirin. Acute salicylate toxicity may
occur at 20 to 25 grams dosage intake in an adult,
or about 4 grams in children
The Salicylates
Acute MILD Salicylism early sings/symptoms-
Manifestations are ringing in the ear, dizziness,
mild bronchospasm, nausea, vomiting, mental
confusion and lassitude.
Acute SEVERE Salicylism late signs/symptoms-
Metabolic ACIDOSIS, tachypnea, respiratory
ALKALOSIS, hemorrhage, pulmonary edema,
pyrexia, coma convulsions, and shock, hypo
tension and multiple organ collapse (renal,
cardiovascular and respiratory)
The Salicylates
Contraindications and Cautions with Salicylate
Use
The use of Salicylates is contraindicated in the
presence of known allergy to Salicylates, NSAIDs,
and tartrazine. Impaired kidney function,
pregnant and lactating women should avoid
aspirin
A condition known as Reye’s syndrome can
possibly occur if children and adolescents are
given aspirin during a viral illness like chicken
pox and influenza.
The Salicylates
29
Nursing interventions for the Salicylates Para-Chlorobenzoic Acid (indoles)

Administer Salicylates WITH FOOD if GI upset is Indomethacin (chlorobenzoic acid)

likely. Provide small, frequent meals to alleviate
GI effects Nabumetone (chlorobenzoic acid)

Administer drug as indicated and monitor therapy Sulindac (chlorobenzoic acid)

to prevent toxicity
Monitor for severe drug effects= Tinnitus!!
Provide supportive care and comfort measures to
support the effects of Salicylates in relieving pain
and inflammation
The Salicylates
Nursing interventions for the Salicylates
For aspirin toxicity, the doctor orders sodium
bicarbonate to ALKALINIZE the urine for faster
drug excretion
The NSAIDS
Popularly called the NSAIDs, these agents are the
most commonly used drugs for inflammation and
pain.
The groups of NSAIDs are:
Salicylates
Propionic Acids and derivatives
Fenoprofen
Tolmetin (chlorobenzoic acid)
Fenamates- Anthranilic acids
Mefenamic acid
Meclofenamate
Diflusinal
Piroxicam
The NSAIDS
Mechanism of Action of the NSAIDs
The anti-inflammatory, analgesic, and antipyretic
effects are largely related to inhibition of
prostaglandin synthesis.
The NSAIDS
Mechanism of Action of the NSAIDs
The NSAIDs block two enzymes known as
cyclooxygenase-1 (COX-1) and cyclooxygenase-2
(COX-2) to stop turning arachidonic acid into
prostaglandin.

Flurbiprofen The NSAIDS

Ibuprofen Mechanism of Action of the NSAIDs

Ketoprofen By interfering with this part of the inflammatory

reaction, NSAIDs block inflammation before all of
Naproxen the signs and symptoms can develop

Oxaprozin The NSAIDS

The NSAIDS Therapeutic Use of NSAIDs

The groups of NSAIDs are: Moderate to severe pain

Acetic Acids Inflammatory conditions like rheumatoid arthritis,

osteoarthritis
Diclofenac (phenylacetic)
Primary dysmenorrhea
Etodolac (phenylacetic)
Sometimes, for fever reduction
Ketorolac (phenylacetic)

30
The NSAIDS The NSAIDS

Contraindication and Cautions with the use of IMPLEMENTATION

NSAIDs
Assure proper drug administration
Allergy to any NSAID or salicylate; with
cardiovascular dysfunction or hypertension due Administer with food if GI upset will occur
to the varying effects of prostaglandins;
Provide supportive and comfort measures to deal
With peptic ulcer or known GI bleeding because with adverse effects: small frequent meals, safety
of the potential exacerbation; and during measures if dizziness occurs, etc.
pregnancy and lactation because of potential
effects on the baby Provide patient teaching regarding drug, dosage,
side effects, precaution and warnings
The NSAIDS
The NSAIDS
The Adverse Effects of NSAIDs
IMPLEMENTATION
GIT- patients experience peptic Ulceration,
dyspepsia, GI pain, constipation or diarrhea, and Remind the patient that piroxicam can take up to 2
flatulence. The potential for GI bleeding should weeks before therapeutic effect can be seen
alert the nurse.
The NSAIDS
CNS- Patients may complain of dizziness,
EVALUATION
somnolence and fatigue.
Evaluate drug effects such as decreasing pain
VASCULAR- bleeding and bone marrow
and subsiding inflammatory response
depression have been reported in chronic users.
Monitor for adverse effects
The NSAIDS
Monitor for drug-drug interaction
The Selective COX-2 inhibitors- Second
generation NSAIDs NSAIDS
Because older NSAIDs inhibit both the COX-1 and N= o alcohol, aspirin
COX-2, they produce more side effects.
S= ide effects: “BIRTH”
By inhibiting COX-1, protection of stomach lining
is decreased and the clotting time is also B-one marrow depression, BLEEDING,
decreased.
I-ncreased GI distress, R- renal toxicity, T-
The selective COX-2 inhibitors only inhibit COX-2 tinnitus and H- hepatotoxicity
present in inflammatory cells; thereby the GI
effects are minimal. A= aspirin sensitivity= Don’t give NSAIDS

The NSAIDS I= Inhibits prostaglandin

The Selective COX-2 inhibitors- Second D= Do TAKE with food

generation NSAIDs
S= top 5-6 days before surgery
Examples are: The “COXIB”s
Paracetamol
CELECOXIB (Celebrex)
Acetaminophen is widely used to treat moderate
ROFECOXIB pain and fever when aspirin and NSAIDs cannot
be utilized
NIMESULIDE

31
Paracetamol
Acetaminophen lacks an anti-inflammatory
property that makes it ineffective for
inflammation.
Paracetamol
Mechanism of Action of Acetaminophen
Acetaminophen acts directly on the
thermoregulatory cells in the hypothalamus to
cause sweating and vasodilation; this in turn
causes the release of heat and lowers fever.
Analgesic action is still unclear
Paracetamol
Therapeutic use of Acetaminophen
Moderate pain
Fever
Prophylaxis of children receiving DPT
immunization
Paracetamol
Contraindications and Precaution with the use of
Acetaminophen
Acetaminophen is contraindicated in the presence
of allergy to the drug.
Hepatic dysfunction and chronic alcoholism are
important consideration.
Paracetamol
Adverse Effects of Acetaminophen
CNS- headache
Liver- hepatotoxicity is a potential adverse effect
that is usually fatal. This happens in drug
overdose. N-acetylcysteine is the antidote
Hemolytic anemia, renal dysfunction, skin rash
NARCOTIC AGONISTS
These are called agonists because they react with
the opiod receptors throughout the body to cause
analgesia, sedation and euphoria.
NARCOTIC AGONISTS
The following are examples of narcotic agonists
Morphine
Codeine
Meperidine
Methadone
Fentanyl
NARCOTIC AGONISTS
Therapeutic Use of Narcotic Agonists
Sedation
Analgesia
Antitussives
Adjunct to general anesthesia
Pain, acute and chronic pain
Pre-operative medication
NARCOTIC AGONISTS
Contraindications and Cautions: Use of Narcotics
The narcotic agonists are contraindicated in the
following conditions: allergy to narcotics,
pregnancy, labor and lactation because of
potential effects on the fetus/neonate including
respiratory depression, diarrhea caused by
poisons and following biliary surgery.
NARCOTIC AGONISTS
Adverse Effects of the Narcotic Agonist
CNS- respiratory depression, sedation,
lightheadedness, hallucinations, dizziness,
anxiety, psychoses, pupil CONSTRICTION
GIT- Nausea, vomiting (due to the stimulation of
the chemoreceptor trigger zone), constipation
(due to decreased GIT motility) and biliary spasm
(esp. morphine)
GU – ureteral spasms, urinary retention,
hesitancy, and loss of libido. These may be due to
the direct receptor stimulation or to CNS
activation of sympathetic pathways.
Triad of OPIOID toxicity
32
Respiratory depression
Coma
PIN POINT pupils
NARCOTIC AGONISTS
IMPLEMENTATION
Provide a narcotic antagonist and equipment for
ventilation on standby to support the patient in
case of severe reaction
Monitor timing of analgesic doses because
prompt administration may provide a more
acceptable level of analgesia leading to quicker
relief of pain.
Utilize additional measures to relieve pain such as
back rub, massage, stress reduction, hot/cold
packs to increase the effectiveness of narcotic
use and reduce pain.
NARCOTIC AGONISTS
IMPLEMENTATION
Assure patients that intake of medical doses of
narcotics will NOT lead to addiction
Advise to eat a high-fiber diet with liberal intake
of fluids to combat constipation
NARCOTIC AGONISTS
IMPLEMENTATION
Assure patients that intake of medical doses of
narcotics. Warn patients about orthostatic
hypotension and sedation so as to modify their
activities like driving , performing delicate tasks
and operating machineries
Take the drug with food may alleviate loss of
appetite and nausea.
Advise patient to avoid use of alcohol, anti-
histamine and other over-the counter drugs while
taking narcotics.
NARCOTIC AGONISTS
EVALUATION
Monitor the response of the patient to the drug
such as relief of pain, sedation and cough
suppression
The NARCOTIC AGONIST-ANTAGONIST
These drugs stimulate certain opiod receptors but
BLOCK other receptors
They have less abuse potential than pure narcotic
agonists but their analgesic properties may be
equal.
The NARCOTIC AGONIST-ANTAGONIST
The following are the narcotic agonists-
antagonist:
Buphenorphine
Butorphanol
Dezocine
Nalbuphine (Nubain)
Pentozacine
The NARCOTIC AGONIST-ANTAGONIST
Mechanism of Action of Narcotic Agonist-
Antagonist
The mixed narcotics act at specific opiod receptor
sites in the CNS to produce analgesia, sedation,
euphoria and hallucinations.
They also block opiod receptor that may be
stimulated by the pure agonists.
The NARCOTIC AGONIST-ANTAGONIST
Therapeutic Use of Mixed Narcotics
Relief of moderate to severe pain
Addition to general anesthesia
Relief of pain labor and delivery
The NARCOTIC AGONIST-ANTAGONIST
Adverse Effects of the Mixed Narcotics
Respiratory depression with apnea and
suppression of the cough reflex
33
Nausea and vomiting are due to the stimulation of
the CTZ
Constipation due to impaired GIT motility and
Biliary spasms due to stimulation of bile duct
contraction
CNS opiod receptor stimulation will cause:
hallucination, sedation, euphoria
lightheadedness, dizziness, psychoses, anxiety,
and impaired mental processes
GU effects are urinary hesitancy, retention, loss of
libido and ureteral spasms.
The NARCOTIC AGONIST-ANTAGONIST
IMPLEMENTATION
Provide a narcotic antagonist and equipment for
resuscitation in cases of very severe reactions to
provide supportive care
Institute comfort measures and safety
precautions such as side rails, assistance in
ambulation, bowel program and small frequent
meals
The NARCOTIC AGONIST-ANTAGONIST
IMPLEMENTATION
Provide additional pain relieving measures such
as hot/cold packs, stress reduction, massage and
back rubs
Assure patients that addiction is very minimal
Provide client teaching including drug name,
prescribed dosage, measures to handle adverse
effects, warning sings and the need for regular
evaluation
The NARCOTIC ANTAGONISTS
These are drugs that bind strongly to opiod
receptors but DO NOT activate them.
The following are the narcotic antagonists:
Nalmefene
Naloxone
Naltrexone
The NARCOTIC ANTAGONISTS
The Mechanism of Action of Narcotic Antagonist
The narcotic antagonists block opioid receptors
and reverse the effects of opoids, including
respiratory depression, sedation, and
psychomimetic effects.
The NARCOTIC ANTAGONISTS
Therapeutic Use of narcotic antagonists
Reversal of the effects of narcotics and over
dosage- naloxone and nalmefene are used to
manage these conditions.
Naloxone is used to diagnose narcotic overdose
using the naloxone challenge test
Narcotic dependence and alcoholic dependence-
naltrexone is used in the management of these
conditions.
The NARCOTIC ANTAGONISTS
The Adverse Effects of Narcotic Antagonists
The most common is acute narcotic abstinence
syndrome that is characterized by nausea,
vomiting, sweating, tachycardia, hypertension,
tremulousness, and anxiety.
CNS- excitement and reversal of analgesia
CV effects- tachycardia, blood pressure changes,
arrhythmias and pulmonary edema.
The NARCOTIC ANTAGONISTS
IMPLEMENTATION
Maintain open airway and provide artificial
ventilation and cardiac massage as needed in
severe reaction
Administer naloxone challenge before giving
naltrexone because of serious risk of acute
withdrawal
Monitor patient continually adjusting the dosage
as needed during treatment of acute overdose
The NARCOTIC ANTAGONISTS
IMPLEMENTATION
34
Ensure that patient is receiving naltrexone as part
of a comprehensive or alcohol withdrawal
program
Institute comfort measures such as side rails,
assistance with ambulation, bowel program,
environmental stimulation control and small
frequent feedings to relieve GI irritation.
ANTIGOUT
Gout is a metabolic disease characterized by
inflammation of the joints and deposition of uric
acid crystals in other parts of the body.
The joint most commonly affected is the
metatarsal joint of the big toe.
The etiologies of gout may be increased
accumulation of uric acid or ineffective clearance
of uric acid in the kidney.
Drugs for Gout
ANTIGOUT: Colchicine
ANTI-INFLAMMATORY Gout Drug
Cochicine is an anti-inflammatory drug that
inhibits the migration of leukocytes to the
inflamed site. Its action is attribute to the
inhibition of WBC microtubule assembly.
Indomethacin is also another drug used because
it can reduce WBC migration and phagocytosisà
decreased inflammation
ANTIGOUT: Colchicine
ANTI-INFLAMMATORY Gout Drug
It is effective in alleviating acute symptoms of
gout but not in other conditions. It does not
inhibit uric acid synthesis and does not promote
uric acid excretion.
It is not recommended for clients with severe
renal, cardiac or GI problems.
Gastric irritation is a common problem and it
should be taken with food. Other side effects are
Nausea, vomiting, diarrhea, abdominal pain.
ANTIGOUT
URIC ACID INHIBITOR: ALLOPURINOL
Allopurinol is the drug given to patients to reduce
the uric acid synthesis.
It is used frequently as prophylaxis to prevent
gouty attacks.
ANTIGOUT
URIC ACID INHIBITOR: ALLOPURINOL
Allopurinol
Increased fluid intake is recommended to promote
diuresis and prevent alkalinization of the urine.
Nurses must encourage at least 3 liters of fluid
per day.
ANTIGOUT
Pharmacodynamics: Action of Allopurinol
This drug inhibits the production of uric acid by
inhibiting the enzyme xanthine oxidase. This also
improves the solubility of the uric acid crystals.
Onset of action is 1 hour, and peak is 2-4 hours.
The effect of the drug may not be apparent for few
days to a few weeks.
Nurses must teach this to the patient to avoid
non-compliance.
ANTIGOUT
Pharmacokinetics
It is given orally in the management of gout.
Majority of the drug is absorbed from the GIT. The
half-life is 2-3 hours.
Most of the drugs and metabolites are excreted in
the feces and some in the urine. Its onset of
action is 1 hour and peak is 2-4 hours.
ANTIGOUT
Adverse Effects
GIT- anorexia, nausea, vomiting, diarrhea and
stomatitis.
35
CNS- dizziness, peripheral neuritis and vasculitis
Acute gouty attacks if allopurinol is given during
the acute stage of the disease.
Reportable manifestations are rashes and
swelling.
ANTIGOUT: Allopurinol
Patient should be warned not to drink alcoholic
beverages and to avoid foods that are rich in uric
acid- aged foods, legumes, beer, internal organ
meats.
Increase fluid intake to 3 liters per day
Report occurrence of rashes
Take with meals
Allopurinol and Gout
G= ulp 10-12 glasses of fluid/day. GI distress is
undesirable
O=utput and input should be monitored closely
U=ric acid production decreases and USE NO
ALCOHOL
T=ake AFTER meals when stomach is full
ANTIGOUT
URICOSURIC DRUGS: Probenecid
These agents are weak acids and can cause
increased excretion of uric acids in the kidney by
competing with uric acid, thus inhibiting its re-
absorption
They are effective in alleviating chronic gout but
they are not used in acute attacks.
ANTIGOUT
URICOSURIC DRUGS
Probenecid- is a uricosuric agent that blocks the
re-absorption of uric acid and promotes its
excretion.
It causes gastric irritation and should be
taken with meals.
ANTIGOUT
URICOSURIC DRUGS
Sulfinpyrazone- a metabolite of phenylbutazone is
more potent than probenecid.
It should also be taken with meals
because of gastric irritation.
Severe blood dyscrasias can occur.
GOLD compounds
Chrysotherapy (heavy metal therapy) is the
treatment of these rheumatic conditions with the
use of gold compounds.
GOLD compounds
There are currently 3 gold compounds for use:
Auranofin- is an oral agent used for long-term
therapy
Aurothioglucose- parenteral gold IM preparation
given in early disease
Gold Sodium Thiomalate- also a parenteral IM
preparation of gold salts
GOLD compounds
The Mechanism of action of Gold Salts
Gold salts are ingested by macrophages and
inflammatory cells resulting in the inhibition of
phagocytosis.
It depresses the migration of leucocytes and
suppress prostaglandin activity
GOLD compounds
It is important for the nurse to remember that the
therapeutic effect of these agents can take up to 8
weeks or 2 months (if given parenterally) or 3-6
months (if given orally)
GOLD compounds
The Adverse Effects of Gold Compounds
36
Tissue/local effects- these are associated with the Side-effects
deposition of the gold metal in the tissues.
Stomatitis, dermatitis, glossitis, pharyngitis, HYPERglycemia
laryngitis, colitis, diarrhea and GIT inflammation.
Increased susceptibility to infection
Other effects- Hypersensitivity, BONE MARROW (immunosuppression)
DEPRESSION , RENAL INSUFFICIENCY and
anaphylaxis Hypokalemia

Nurses must instruct the patient to report metallic Edema

taste in the mouth as it signals toxicity.
Peptic ulceration
GOLD compounds
STEROIDS
Nursing Responsibilities
Side-effects
Monitor CBC, urinalysis and liver enzymes
If high doses- osteoporosis, growth retardation,
Teach the client to avoid strong lights to prevent peptic ulcer, hypertension, cataract, mood
dermatitis changes, hirsutism, and fragile skin

Proper oral care to manage stomatitis STEROIDS

Explain to patients that therapeutic effect can be Nursing responsibilities

expected after several months of intake and
1. Monitor VS, electrolytes, glucose
administration
2. Monitor weight edema and I/O
STEROIDS
STEROIDS
Replaces the steroids in the body
Nursing responsibilities
Cortisol, cortisone, betamethasone, and
hydrocortisone 3. Protect patient from infection
STEROIDS 4. Handle patient gently
These drugs enter the cells and bind to receptors 5. Instruct to take meds WITH MEALS to
prevent gastric ulcer formation
They inhibit the enzyme phospholipase
STEROIDS
STEROIDS
Nursing responsibilities
Corticosteroids are used topically and locally to
achieve the desired anti-inflammatory effects at a 6. Caution the patient NOT to abruptly
particular site stop the drug
Examples: 7. Drug is tapered to allow the adrenal gland to
secrete endogenous hormones
Prednisone
STEROIDS
Bethamethasone
Evaluation:
Prednisolone
The drugs are effective if there is:
Fludrocortisone
1. Relief of signs and symptoms of
STEROIDS
inflammation

37
 2. Return of adrenal function to normal
Pharmacology of the GIT system
LECTURE Outline
REVIEW the Anatomy of the GIT
REVIEW the Physiology of the GIT
These drugs BLOCK the release of hydrochloric
acid in the stomach in response to gastrin
Drugs affecting GI secretions
Antacids
These drugs interact with the gastric acids at the
chemical level to neutralize them

Review common GI drugs in the following Drugs affecting GI secretions

categories:
Proton pump inhibitors
1. Drugs affecting GI secretions
These drugs suppress the secretion of
2. Laxatives hydrochloric acid into the lumen of the stomach

3. Anti-diarrheals Drugs affecting GI secretions

4. Emetics and anti-emetics Mucosal protectants

Drugs affecting GI secretions These are agents that coat any injured area in the
stomach to prevent further injury from acid
There are five types of drugs that affect gastric
acid secretions and are useful for the treatment of Drugs affecting GI secretions
peptic ulcer.
Prostaglandin analogs
1. Histamine (H2) receptor
antagonist/blockers These are agents that inhibit the secretion of
gastrin and
2. Antacids
increase the secretion of mucus lining of the
3. Proton pump inhibitors stomach, providing a buffer.

4. Mucosal protectants The H2 Blockers- “tidines”

5. Prostaglandin analogs Prototype: Cimetidine

Drugs affecting secretions: 1. Ranitidine

anti ulcer
2. Famotidine
General indication of the drugs affecting gastric
acid secretion 3. Nizatidine

Peptic ulcer The H2 Blockers- “tidines”

Gastritis Pharmacodynamics: Drug Action

Patient on NPO to prevent stress ulcer
General time of administration of the drugs
affecting gastric acid secretion
Pharmacodynamics
Histamine (H2) receptor blockers
The H2 blockers are antagonists at the receptors
in the parietal cells of the stomach.
The blockage results to inhibition of the hormone
gastrin.
There will be decreased production of gastric acid
from the parietal cells.

Also, the chief cells will secrete less pepsinogen.

38
The H2 Blockers- “tidines”
Therapeutic use of the H2 blockers
Short-term treatment of active duodenal ulcer or
benign gastric ulcer
Treatment of hypersecretory conditions like the
Zollinger-Ellison syndrome
Prevention of stress-induced ulcers and acute GI
bleeding
Treatment of erosive GERD (reflux disease)
Relief of Symptoms of heart burn and acid
indigestion
The H2 Blockers- “tidines”
Precautions and Contraindications
Any known allergy is a clear contraindication to
the use of the agents.
Conditions such as pregnancy, lactation, renal
dysfunction and hepatic dysfunction should
warrant cautious use.
Nizatidine can be used in hepatic dysfunction.
The H2 Blockers- “tidines”
Dynamics- Side effects/adverse effects
GIT= diarrhea or constipation
CNS= Dizziness, headache, drowsiness,
confusion and hallucinations
Cardio= arrhythmias, HYPOTENSION (related to
H2 receptor blockage in the heart)
Cimetidine= Gynecomastia and impotence in
males
The H2 Blockers- “tidines”
Drug-drug Interactions
Cimetidine, Famotidine, Ranitidine are
metabolized in the liver- they can cause slowing
of excretion of other drugs leading to their
increased concentration.
The H2 Blockers- “tidines”
Drug-drug Interactions
These drugs can interact with CIMETIDINE
Anticoagulants
Phenytoin,
Alcohol
Antidepressants.
The H2 Blockers- “tidines”
Nursing considerations:
Administer the drug WITH meals at BEDTIME to
ensure therapeutic level
One hour after Antacids
Stress the importance of the continued use for the
length of time prescribed
The H2 Blockers- “tidines”
Nursing considerations
Monitor the cardiovascular status especially if the
drugs are given IV
Warn patient of the potential problems of
increased drug concentration if the H2 blockers
are used with other drugs or OTC drugs. Advise
consultation first!
The H2 Blockers- “tidines”
Nursing considerations:
Provide comfort measures like analgesics for
headache, assistance with ambulation and safety
measures because of confusion
Warn the patients taking cimetidine that
drowsiness may pose a hazard if driving or
operating delicate machines.
The H2 Blockers- “tidines”
Nursing considerations:
Provide health teaching as to the dose, frequency,
comfort measures to initiate when side-effects are
intolerable
Evaluate the effectiveness
Relief of symptoms of ulcer, heart burn and GERD
39
The Antacids
These are drugs or inorganic chemicals
that have been used for years to neutralize acid in
the stomach
The Antacids
The following are the common antacids that can
be bought OTC:
Aluminum salts (hydroxide)
Calcium salts (carbonate)
Magnesium salts (milk of magnesia)
Sodium bicarbonate
Magaldrate (aluminum and magnesium
combination)
The Antacids
Pharmacodynamics: drug action
These agents act to neutralize the acidic pH in the
stomach.
They do not affect the rate of gastric acid
secretion.
The Antacids
Pharmacodynamics: drug action
The administration of antacid may cause an acid
rebound.
Neutralizing the stomach content to an alkaline
level stimulates gastrin production to cause an
increase in acid production and return the
stomach to its normal acidic state.
The Antacids
Therapeutic Indications
Symptomatic relief of upset stomach associated
with hyperacidity
Hyperacidic conditions like peptic ulcer, gastritis,
esophagitis and hiatal hernia
Special use of AMPHOGEL (aluminum hydroxide):
to BIND phosphate
The Antacids
Precautions of Antacid Use
Known allergy is a clear contraindication
Caution should be instituted if used in electrolyte
imbalances, GI obstruction and renal dysfunction.
Sodium bicarbonate is rarely used because of
potential systemic absorptionà metabolic
alkalosis!!!
The Antacids
Pharmacokinetics
These agents are taken orally and act locally in
the stomach
The Antacids
Pharmacodynamics: Effects of drugs
1. GIT= rebound acidity; alkalosis may
occur.
Calcium salts may lead to hypercalcemia
Magnesium salts can cause DIARRHEA
Aluminum salts may cause CONSTIPATION and
Hypophosphatemia by binding with phosphates in
the GIT.
2. Fluid retention due to the high sodium content
of the antacids.
The Antacids
Nursing Considerations:
Administer the antacids apart from any other
medications by ONE hour before or TWO hours
after- to ensure adequate absorption of the other
medications
Tell the patient to CHEW the tablet thoroughly
before swallowing.
Follow it with one glass of water
Regularly monitor for manifestations of acid-base
imbalances as well as electrolyte imbalances
The Antacids
Nursing Considerations:
40
Provide comfort measures to alleviate
constipation associated with aluminum and
diarrhea associated with magnesium salts.
Monitor for the side-effects, effectiveness of the
comfort measures, patient’s response to the
medication and the effectiveness of the health
teachings
The Antacids
Nursing Considerations
Evaluate for effectiveness:
Decreased symptoms of ulcer
Decreased Phosphate level (Amphogel) in
patients with chronic renal failure
The PPI
These are the newer agents for ulcer treatment
The “prazoles”
Prototype: Omeprazole
Lansoprazole
Esomeprazole
Pantoprazole
The PPI
Pharmacodynamics: drug action
They act at specific secretory surface receptors to
prevent the final step of acid production and thus
decrease the level of acid in the stomach.
The “pump” in the parietal cell is the H-K ATPase
enzyme system on the secretory surface of the
gastric parietal cells
The PPI
Clinical use of the PPIs
Short-term treatment of active duodenal ulcers,
GERD, erosive esophagitis and benign gastric
ulcer
Long-term- maintenance therapy for healing of
erosive disorders.
The PPI
Precautions with the use of the PPIs
Known allergy is a clear contraindication
Caution if patient is pregnant
The PPI
Pharmacodynamics: Adverse effects
CNS- dizziness, headache, asthenia (loss of
strength), vertigo, insomnia, apathy
GIT- diarrhea, abdominal pain, nausea, vomiting,
dry mouth and tongue atrophy
Respi- cough, stuffy nose, hoarseness and
epistaxis.
The PPI
Nursing considerations:
Administer the drug BEFORE meals. Ensure that
patient does not open, chew or crush the drug.
Provide safety measures if CNS dysfunction
happens.
Arrange for a medical follow-up if symptoms are
NOT resolved after 4-8 weeks of therapy.
The PPI
Nursing considerations:
Provide health teaching as to drug name, dosages
and frequency, safety measures to handle
common problems.
Monitor patient response to the drug, the
effectiveness of the teaching plan and the
measures to employ
The PPI
Nursing considerations:
Evaluate for effectiveness of the drug
Healing of peptic ulcer
Decreased symptoms of ulcer
The Mucosal Protectant
Sucralfate (Caralfate/ Iselpin)
41
This is given to protect the eroded ulcer sites in
the GIT from further damage by acid and digestive
enzymes
Sucralfate
Pharmacodynamics: Action of drug
It forms an ulcer-adherent complex at duodenal
ulcer sites, protecting the sites against acid,
pepsin and bile.
This action prevents further breakdown of
proteins in the area and promotes healing.
If used with aluminum salts= high risk of
accumulation of aluminum and toxicity.
If used with phenytoin, fluoroquinolones and
penicillamines- decreased levels of these drugs
when taken with sucralfate
The Mucosal Protectant
Nursing Considerations
Administer drug ON AN EMPTY stomach, 1 hour
before meals , or 2 hour after meals and at
BEDTIME

Sucralfate Monitor for side-effects like constipation and GI

upset
Clinical use of sucralfate
Encourage intake of high-fiber foods and
Short and long term management of duodenal increased fluid intake
ulcer.
Administer antacids BETWEEN doses of
NSAIDs induced gastritis sucralfate, NOT WITHIN 30 minutes of sucralfate
dose
Prevention of stress ulcer
The Mucosal Protectant
Treatment of oral and esophageal ulcers due to
radiation, chemotherapy or sclerotherapy. Nursing Considerations

Sucralfate Provide comfort measures if CNS effects occur

Precautions on the use of Sucralfate
This agent should NOT be given to any person
with known allergy to the drug, and to those
patients with renal failure/dialysis because of
build-up of aluminum may occur if used with
aluminum containing products.
Provide health teaching as to drug name, dosages
and frequency, safety measures to handle
common problems.
Monitor patient response to the drug, the
effectiveness of the teaching plan and the
measures employed

The Mucosal Protectant

The Mucosal Protectant Nursing Considerations

Pharmacodynamics: Side-effects & adverse Evaluate effectiveness of therapy

reactions
Healing of ulcer
Primarily GIT= CONSTIPATION, occasionally
diarrhea, nausea, indigestion, gastric discomfort, No formation of ulcer
and dry mouth may also occur
Prostaglandin analogue
CNS= dizziness, drowsiness, vertigo
Misoprostol
Others= rash and back pain
This agent is a synthetic prostaglandin E1 analog
The Mucosal Protectant that is employed to protect the lining of the
mucosa of the stomach
Drug-drug interactions

42
Prostaglandin analogue
Misoprostol: Pharmacodynamics
Being a prostaglandin analog, it inhibits gastric
acid secretion to some degree
It INCREASES mucus production in the stomach
lining.
Prostaglandin analogue
Misoprostol: Clinical use
NSAIDs-induced gastric ulcers
Duodenal ulcers unresponsive to H2 antagonists
Prostaglandin analogue
Precautions of Misoprostol Use
This drug is CONTRAINDICATED during
pregnancy because it is an abortifacient.
Women should be advised to have a negative
pregnancy test within 2 weeks of beginning
therapy and should begin the drug on the second
or third day of the next menstrual cycle.
They should be instructed in the use of
contraceptives during therapy.
Prostaglandin analogue
Pharmacodynamic effects: drug reactions
GIT= Nausea, diarrhea, abdominal pain, flatulence,
vomiting, dyspepsia
GU effects= miscarriages, excessive uterine
CRAMPING and bleeding, spotting, hyper-
menorrhea and menstrual disorders.
Prostaglandin analogue
Nursing Considerations
Administer to patients at risk for NSAIDs-induced
ulcers during the full course of NSAIDs therapy
Administer four times daily with meals and at
bedtime
Obtain pregnancy test within 2 weeks of
beginning therapy.
Begin the therapy on second or third day of
menstrual period to ensure that the woman is not
pregnant
Prostaglandin analogue
Nursing Considerations
Provide patient with both written and oral
information regarding the associated risks of
pregnancy
Provide health teaching as to drug name, dosages
and frequency, safety measures to handle
common problems.
Monitor patient response to the drug, the
effectiveness of the teaching plan and the
measures to employ
Laxatives
Generally used to INCREASE the passage of the
colonic contents
The general classifications is as follows:
1. Chemical stimulants- irritants
2. Mechanical stimulants- hyperosmotic
agents and saline cathartics
3. Lubricants and stool softeners
Laxatives
They promote bowel evacuation for various
purposes
They are classified into their mode of action
Laxatives
Therapeutic Indications of the Laxatives
SHORT term relief of Constipation
Prevention of straining in conditions like CHF,
post-MI, post partum, post-op
Preparation for diagnostic examination
Removal of poison or toxins
Adjunct in anti-helminthic therapy
43
To remove AMMONIA by use of lactulose Stimulating the local stretch receptors

Contraindications in Laxative use Activating local defecation reflex

ACUTE abdominal disorders Lubricants-Stool softener

Appendicitis Prototype: Docusate

Diverticulitis 1. Glycerin

Ulcerative colitis 2. Mineral oil

Chemical Stimulant Cathartics Lubricants-stool softeners

Prototype: Bisacodyl Pharmacodynamics

Irritant laxatives: Docusate increases the admixture of fat and water

producing a softer stool
1. Castor oil
Glycerin and Mineral oil form a slippery coat on
2. Senna the colonic contents

3. Cascara Pharmacokinetics:
Common Side-effects of the Laxatives
4. Phenolphthalein
Diarrhea
Chemical Stimulant Cathartics
Abdominal cramping
Pharmacodynamics
Nausea
These agents DIRECTLY stimulate the nerve
plexus in the intestinal wall Fluid and electrolyte imbalance

The result is INCREASED movement or motility of Sympathetic reactions- sweating, palpitations,

the colon flushing and fainting

Mechanical Stimulant Cathartics CATHARTIC dependence

Prototype: LACTULOSE (Cephulac) The Nursing Process and Laxative

Bulk-forming laxatives ASSESSMENT

1. Magnesium (citrate, hydroxide, sulfate)- saline Nursing History- elicit allergy to any laxatives,
cathartic elicit history of conditions like diverticulitis and
ulcerative colitis
2. Psyllium
Physical Examination- abdominal assessment
3. Polycarbophil
Laboratory Test: fecalysis, electrolyte levels
Mechanical Stimulant Cathartics
The Nursing Process and Laxative
Pharmacodynamics
NURSING DIAGNOSIS
These agents are rapid-acting laxatives that
INCREASE the GI motility by Alteration in bowel pattern

Increasing the fluids in the colonic material Alteration in comfort: pain

44
Knowledge deficit General Classifications

The Nursing Process and Laxative 1. Local anti-motility

IMPLEMENTATION 2. Local reflex inhibition

1. Emphasize that it is use on a SHORT term 3. Central action on the CNS

basis
The Anti-diarrheals
2. Provide comfort and safety measures like
ready access to the bathroom, side-rails Clinical Indications of drug use

3. Administer with a full glass of water Relief of symptoms of acute and chronic diarrhea

The Nursing Process and Laxative Reduction of fecal volume discharges from
ileostomies
IMPLEMENTATION
Prevention and treatment of traveler's diarrhea
4. Encourage fluid intake, high fiber diet and daily
exercise Contraindications of anti-diarrheal Use

5. DO NOT administer if acute abdominal Poisoning

condition like appendicitis is present
Drug allergy
6. Advise to change position slowly and avoid
hazardous activities because of potential GI obstruction
dizziness
Acute abdominal conditions
The Nursing Process and Laxative
Pharmacokinetics: Side effects
IMPLEMENTATION
Constipation
7. Record intake and output to assess fluid
Nausea, vomiting
alteration
Abdominal distention and discomfort
8. If possible, observe the character of stools
TOXIC MEGACOLON
9. Caution the patient that chronic use may
promote dependence and use during pregnancy Nursing process and anti-diarrheals
may cause uterine cramping and Vitamin
deficiency ASSESSMENT

The Nursing Process and Laxative
EVALUATION of drug effectiveness
1. Evaluate relief of GI symptoms, absence
of staining and increased evacuation of
GI tract
Nursing History – Elicit history of drug allergy,
conditions like poisoning, GI obstruction and
acute abdominal conditions
Physical Examination- Abdominal examination
Laboratory test- electrolyte levels

2. For Lactulose: decreased ammonia Nursing process and anti-diarrheals

3. Normal bowel function is restored NURSING DIAGNOSIS

The Anti-diarrheals Alteration in bowel pattern

These are agents used to calm the irritation of the Alteration in comfort: pain
GIT for the symptomatic relief of diarrhea

45
Nursing process and anti-diarrheals
IMPLEMENTATION
1. Monitor patient response within 48 hours.
Discontinue drug use if no effect
To induce vomiting as a treatment for drug
overdose and certain poisonings
EMETIC
Contraindications of Ipecac use

2. Provide comfort measures for pain Ingestion of CORROSIVE chemicals

3. Provide teaching regarding its short term Ingestion of petroleum products

use only
Unconscious and convulsing patient
Nursing process and anti-diarrheals
EMETIC
EVALUATION
Pharmacokinetics: side effects of Ipecac
1. Monitor effectiveness of drug- RELIEF of
diarrhea Nausea

2. Monitor adverse effects, effectiveness of Diarrhea

pain measures and effectiveness of
teaching plan GI upset

Emetics and Anti-emetics Mild CNS depression

Emetic Agent CARDIOTOXICITY if large amounts are absorbed

in the body
Syrup of Ipecac
Nursing process and the EMETIC
Anti-emetics
ASSESSMENT
1. Phenothiazines
Nursing History- elicit the exact nature of
2. Non-phenothiazines poisoning

3. Anticholinergics/Antihistamines Physical Examination- CNS status and abdominal

exam
4. Serotonin receptor Blockers
Nursing process and the EMETIC
5. Miscellaneous
IMPLEMENTATION
EMETIC
1. Administer to conscious patient only
Prototype: Ipecac Syrup
2. Administer ipecac as soon as possible
EMETIC
3. Administer with a large amount of water
Pharmacodynamics
4. Vomiting should occur within 20 minutes
Ipecac syrup irritates the GI mucosa locally, of the first dose. Repeat the dose and
resulting to stimulation of the vomiting center expect vomiting to occur within 20
minutes
It acts within 20 minutes
Nursing process and the EMETIC
EMETIC
IMPLEMENTATION
Clinical Use of ipecac

46
5. Provide comfort measures like ready access to Most drugs are metabolized in the liver excreted
bathroom, assistance with ambulation in the kidneys

6. Offer support ANTIEMETICS

Nursing process and the EMETIC Pharmacokinetics: Side-effects

EVALUATION 1. PHOTHOSENSITIVITY

1. Evaluate patient response within 20 2. Drowsiness, dizziness, weakness and tremors

minutes of drug ingestion and DEHYDRATON

2. Monitor for adverse effects 3. Phenothiazines= autonomic anti-cholinergic

effects like dry mouth, nasal congestion and
3. Evaluate effectiveness of comfort urinary retention
measures and teaching plan
Metoclopramide= EPS due to dopamine receptor
ANTI-EMETICS blockage

These are agents used to manage nausea and Nursing Process and the ANTIEMETICS
vomiting
ASSESSMENT
They act either locally or centrally
Nursing History- elicit allergy, impaired hepatic
In general, they may inhibit the chemoreceptor function and CNS depression
trigger zone in the medulla by blocking
DOPAMINE receptor Physical Examination- CNS status and abdominal
examination
ANTIEMETICS
Laboratory test- Liver function studies
ANTIEMETICS
Nursing Process and the ANTIEMETICS
ANTIEMETICS
NURSING DIAGNOSIS
ANTIEMETICS
1. Alteration in comfort: pain
Indications
2. High risk for injury
1. Prevention and treatment of vomiting
3. Knowledge deficit
2. Motion sickness
Nursing Process and the ANTIEMETICS
ANTIEMETICS
IMPLEMENTATION
Contraindications
1. Assess patient’s intake of other drugs
1. Severe CNS depression that may cause dangerous drug
interaction
2. Severe liver dysfunction
2. Emphasize that this is given on a short
ANTIEMETICS term basis

Pharmacokinetics: Nursing Process and the ANTIEMETICS

Oral absorption is good if vomiting is not present IMPLEMENTATION

IV drugs can be given if vomiting is active 3. Provide comfort and safety measures

47
Advise to change position slowly - treatment of Narcolepsy

Avoid hazardous activities - treatment of attention deficit disorder

Provide mouth care and ice chips
Monitor for dehydration and offer fluids if it
occurs
with hyperactivity in children
- exogenous obesity
D. Overview of nursing interventions

Nursing Process and the ANTIEMETICS
IMPLEMENTATION
4. Protect from sun exposure
- be aware that nursing interventions will
vary depending on the intended effect
- provide client teaching based on the
indication for using the drug

Sunscreens - note that the least amount possible of

the drug should be prescribed at one time to
Protective covering minimize the possibility of overdosage

5. Provide health teaching

Nursing Process and the ANTIEMETICS

CNS STIMULANTS
EVALUATION
CNS stimulants tend to produce an effect that
1. Monitor for the drug effectiveness increases energy or reduces fatique and
associated symptoms
• Relief of nausea and vomiting
PHARMACODYNAMICS/ACTION
2. Monitor for adverse effects

3. Evaluate effectiveness of comfort measures

and teaching plan 1. cause release of norepinephrine from
its storage sites in adrenergic nerve terminals
CENTRAL NERVOUS SYSTEM DRUGS
2. effects of these agents may be similar
CNS STIMULANTS: Overview to those of ephedrine

A. Description PHARMACOTHERAPEUTICS

- an effect that may be noted with use of - varies according to indications

many drugs
PHARMACOKINETICS
- actual indications for using CNS is
limited 1. most CNS stimulants are absorbed
through the GI system
- includes amphetamines and
amphetamine-like agents 2. duration of action is variable

B. Action 3. excretion occurs through the kidney

- stimulants enhance neurotransmitter CONTRAINDICATIONS

activity in the CNS, particularly the cerebral cortex
- produces peripheral effects on BP, GI
motility, vasoconstriction and pupillary dilation
C. Indications
1. in clients with symptomatic CV
disease, hyperthyroidism, nephritis, angina
pectoris, moderate to severe hypertension, types
of glaucoma, and history of drug abuse

48
 2. used caution in clients with DM or - ammonium chloride, ascorbic acid
seizure disorders, in elderly, hyperexcitable
clients - antacids, sodium bicarbonate,
acetazolamide
DRUG INTERACTIONS
- antihypertensives
- vary among specific drugs
- caffeine
NURSING MANAGEMENT:
- haloperidol, phenothiazine, tricyclic
ASSESSMENT antidepressants

a. assess client hx of drug abuse - insulin, oral antidiabetic

b. review the complete history and - ammonium chloride

physical examination
PLANNING AND IMPLEMENTATION
a. Monitor height and weight in children
b. Monitor for s/sx of Tourettes syndrome in
children
c. When used as “anorectic “ in obese,
make sure client is on a weight reduction
program. Give 30 to 60 minutes before
meals
d. Explain to client the reason, what to
expect, and dangers of this drugs
e. Tell the client to avoid caffeine containing
drinks
f. Warn the client to avoid activities that require
alertness
h. Instruct client to take 6 hours before bedtime to
avoid sleep interference
- bicarbonate
NURSING MANAGEMENT:
a. be aware that high doses can result in
acute psychotic picture
b. know that amphetamines are subject to
abuse, that leads to compulsive behavior,
paranoia, hallucinations and suicidal tendencies
c. be aware for the street names ( black
beauties, lid poppers, pep pills and speed)
d. note that amphetamines should only
be used in weight reduction programs for clients
in whom alternate therapy has been ineffective
II. DEXTROAMPHETAMINE (DEXEDRINE)
- related both chemical and
pharmacologic to norepinephrine
- peak occurs within 4 to 6 hours

i. Inform client that as drug wears off, fatigue may - elimination half-life is about 5 hours
result
- metabolized in the liver and excreted in
COMMON CNS stimulants: the urine

I. AMPHETAMINE SULFATE - drug interations: same as for

amphetamine
ACTION – in children with hyperkinesia
- side/adverse effects: same as for
CONTRAINDICATIONS amphetamine

a. In clients with parkinsonism III. METHAMPHETAMINE HYDROCHLORIDE

( DESOXYN)
b. Contraindicated within 14 days of MAO
inhibitors - like dextroamphetamine related to
norepinephrine. It is often referred to as “speed”
DRUG INTERACTIONS:

49
 - pharmacokinetics: same as for - causes anorexia
dextroamphetamine
NURSING CONSIDERATIONS:
- used with caution in clients with
hypertension 1. assess pain for type, intensity and
location
IV. DIETHYLPROPION HYDROCHLORIDE
(TENUATE) 2. assess VS especially the RR (<12 bpm
withhold)
- an anorexiant
3. assess for CNS changes including LOC
- half-life 4 to 6 hrs; effects of regular-
release tablets persist for 4 hours; effects of 4. assess client for allergic reaction
extended-release tablets and capsules can last for
12 hours 5. assess older adults frequently

- short term adjunct in exogenous obesity CLIENT EDUCATION:

- suppressing the appetite 1. avoid alcohol and other CNS

V. PHENTERMINE (IONAMINE)
- used along with Fenfluramine as diet
aid; known as the “phen/fen diet”
- less potent action in the CNS than most
amphetamines, with little stimulation of the CV
system
depressants
2. not over the counter
3. avoid ambulation, smoking, driving and
other activities without assistance
4. report any changes such as allergic
reactions or shortness of breath

- duration of action is prolonged and may 5. long-term use can lead to withdrawal
last up to 20 hours. symptoms with termination of use

ANALGESICS COMMON OPIOID ANALGESICS:

A. OPIODS Pure agonist – Codeine (Paveral)

- symptomatic relief of severe acute and - IM and PO

chronic pain
- Meperidine (Demerol)
- most commonly used in the
- PO, IM, IV,
postoperative setting and to treat pain caused by
SubQ
malignancy
- Morphine Sulfate
- produce effects by binding to opioid
receptors throughout the CNS and peripheral - PO, IV
tissues
- sevre pain,
- onset of action is immediate if given by short acting
IV and rapid if given by IM or by mouth
Mixed agonists-antagonist
- peak action is from 1 to 2 hours and
duration up to 7 hours - Nalbuphine hydrochloride (Nubain)

- these agents cross the BBB and - IM, IV, SubQ, IV

placental barriers and also into breast milk
- limited use for severe and
- may increase intracranial pressure chronic pain

50
b. OPIOID ANTAGONIST
- include Naloxone (Narcan) and
Naltrexone (ReVia)
- used to reverse respiratory depression
induced by overdose of opioids
- onset of effect 1-2 minutes, duration 45
minutes
NURSING CONSIDERATIONS:
1. assess VS q 3-5 minutes
2. assess ABG
3. assess cardiac status
4. assess RR and LOC
5. administer only with resuscitative
device nearby
c. NON-OPIOIDS
1. ACETYLSALICYLIC ACID (ASPIRIN)
- inhibits prostaglandin involved in the
production of inflammation, pain and fever
- blocks pain impulses in CNS
- antipyretic action results from
vasodilatation of peripheral vessels
- inhibits platelet aggregation
- dosage varies depending on age of
client
- gastric irritation may be decreased by
administering with full glass of water, milk, food
or antacid
- pills can be crushed or chewed but do
not crush enteric-coated preparations
- give 30 minutes prior to or 2 hours
following meals
- contraindicated in children < 12 y/o
because of risk of Reye’s syndrome, children w/
chicken pox or flu-like symptoms, pregnacy 3rd
trimester, lactation
- contraindicated with Vitamin K
deficiency, PUD, anemia, renal and hepatic
dysfunction
NURSING CONSIDERATIONS:
1. assess for allergy to salicylates
2. assess liver functions tests, renal
function tests (BUN,Crea) and blood studies
(CBC, Hct, Hgb, PT)
3. assess for hepatotoxicity
( dark urine, clay-colored stool,
jaundice, itching)
4. note for abdominal pain, fever, diarrhea
5. evaluate for therapeutic responses
6. assess for aspirin toxicity when
administered with ammonium chloride
CLIENT TEACHING:
1. report any symptoms of hepatotoxicity
or renal toxicity
2. report visual changes, tinnitus, allergic
reactions, and bleeding
3. take medication with 8 oz water, milk or
food
4. do no exceed recommended dose
5. do not combine with other OTC
medications containing ASA
6. therapeutic response can take up to 2
weeks
7. avoid alcohol ingestion to decrease
chance of GI bleeding
8. should not be given to children or
teens with flu-like symptoms or chicken pox
2. ACETAMINOPHEN (TYLENOL)
- inhibition to prostaglandin synthesis
- possess weak anti-inflammatory
properties
- more on anti-pyretic action
51
 - used to mild to moderate pain or fever,
especially when ASA or NSAIDs are not tolerated
- usual dose is 325 to 600 mg q4-6h PO or
PR, maximum dose is 4 grams per day
- oral forms may crushed or given as
whole or chewable tablets
- may give with food or milk to increase
gastric tolerance
- co-administration with high-
carbohydrate meal with significantly retard
absorption rate
CLIENT EDUCATION:
1. report blurred vision, ringing, roaring
in ears which may indicate toxicity
2. avoid driving or other hazardous
activities
3. report changes in urine pattern,
increased weight, edema, increased pain in joints,
fever, blood in urine indicating nephrotoxicity
COMMON NSAIDs AGENTS:

- hepatotoxicity 1. Celecoxib (Celebrex)

- cyanosis, anemia, neutropenia, - PO

jaundice, pancytopenia, CNS stimulation, delirium
- decreases effect of ASA, ACE
NURSING CONSIDERATIONS: inhibitors, diuretics

1. assess client for chronic poisoning 2. Diclofenac sodium (Voltaren)

(rapid, weak pulse, dyspnea, cold, clammy
extremities) - PO

2. assess for hepatotoxicity 3. Ibuprofen (Advil)

3. be prepared to administer - PO
ACETYLCYSTEINE (MUCOMYST) as antidote for
acetaminophen poisoning 4. Ketorolac (Toradol)

3. NONSTEROIDAL - IV, IM, PO

ANTIINFLAMMATORY DRUGS (NSAIDs)
5. Mefenamic Acid (Ponstan)
- inhibit cyclooxygenase and decrease
- PO
prostaglandins and thromboxane
6. Naproxen (Naprosyn)
- used to treat mild to moderate pain,
osteoarthritis and dysmenorrhea
- PO
- gastric irritants
7. Piroxicam (Feldene)
- crushed or chewed (Pills only)
- PO
- give 30 minutes prior to or 2 hours
ANTICONVULSANTS AGENT
following meals for best absorption
- These agents include hydantoins,
NURSING CONSIDERATIONS:
iminostillbenes, succinimides, valproic
acid
1. assess for renal and hepatic function
- Suppress seizure activity by altering ionic
2. audiometric, ophthalmic exam before,
during, and after treatment conductance, neuronal membrane
potentials and the level of certain
3. assess for ear and eye problems neurotransmitters

52
 - Management and control of partial and
generalized seizures that are idiopathic or
unresponsive to other interventions
- There are no contraindications to anti-
epileptic use
- teratogenecity: Fetal hydantoin
syndrome has been associated with antiepileptic
use in pregnancy (specifically phenytoin or other
hydantoin drugs)
HYDANTOINS
- suppress sodium influx across neuronal
cell membranes
- inhibit the spread of seizure activity in
the motor cortex
- used in general toni-clonic (grand mal),
status epilepticus, pyschomotor seizures
(complex focal seizures)
- do not interchange chewable phenytoin
products with capsules
- phenytoin readily binds with protein
- give ethosuximide, diazepam, and
carbamazepine with food or milk to reduce GI
symptoms
- significant food interactions: Phenytoin
absorption is decreased by enteral nutrition
products
- paresthesias, nystagmus, diplopia,
gingival hyperplasia
- Steven-Johnson syndrome
NURSING CONSIDERATIONS:
1. assess for seizure activity including
type, location, duration, and character
2. assess mental status, mood,
sensorium, affect and memory
3. assess for respiratory depression, rate,
depth and character
4. administer dose with food to reduce
risk of GI upset
CLIENT EDUCATION:
1. medication regimen (name, dose,
schedule, SE, and possible adverse effects)
2. urine may turn pink
3. do not discontinue abruptly or without
consulting physician
4. brush teeth with soft toothbrush and
do proper flossing to prevent gingival hyperplasia
5. avoid heavy used of alcohol
BARBITURATES
- decrease impulse transmission to the
cerebral cortex
- used in all forms of epilepsy
- give oral dose on empty stomach
- administer IM injection into large muscle
mass to prevent tissue sloughing
SUCCINIMIDES
- suppress Calcium influx into neurons,
inceasing the electrical threshold and decreasing
ability to generate an action potential
- used in absence seizures, partial and tonic-
clonic
NURSING CONSIDERATIONS:
1. Monitor renal studies including UA,
BUN and creatinine
2. Assess for eye problems
3. Monitor weight weekly
BENZODIAZEPINES
- enhance the inhibitory neurotransmitter
GABA to decrease anxiety and as an adjunct for
seizure activity
- give with food or milk
- IV injection should be given into large
vein
- contraindicated in acute narrow angle
glaucoma
53
 - contraindicated in children younger
than 6 months
- do not give to clients w/ liver disease
(clonazepam) or during lactation ( diazepam)
NURSING CONSIDERATIONS:
1. assess BP, pulse if systolic BP drops
20mmHg withhold then notify physician
2. assess hepatic and renal function
3. advice to use barrier contraceptives
while taking this drugs
Other antiepileptics:
1. CARBAMAZEPINE (TEGRETOL)
- inhibits nerve impulse by limiting influx
of sodium ions across cell membrane in motor
cortex
- used in tonic-clonic, complex partial and
mixed seizures
- give oral forms with food and milk
- contraindicated with bone marrow
depression
2. VALPROATES
- increases levels of GABA in brain,
which decreases seizure activity
- given by the oral or enteral (GI tube)
route
ANTIPYSCHOTICS
A. PHENOTHIAZINES
- neuroleptics
- also known as typical antipsychotic
agents
- predominantly dopamine antagonists
thus they block postsynaptic dopamine2
receptors in several DA in the brain
- typical antipsychotics are most effective
in treating the “positive” symptoms but are less
effective in the “negative” symptoms
- tolerance to antipsychotic medications
is very uncommon
- most toxic drugs used in psychiatry
a. CHLORPROMAZINE (THORAZINE)
- used primarily to treat psychotic
disorders
- 3 goals:
1. suppression of acute episodes
2. prevention of acute
exacerbations
3. maintenance of the highest
possible level of functioning
- effects can usually be seen in 1-2 days
but substantial improvement usually takes 2-4
weeks and full effects into months
AUTONOMIC NERVOUS SYSTEM
CHOLINERGIC DRUGS
These drugs promote the action of
neurotransmitter acetylcholine
Also called parasympathomimetic drugs
( because they produce effects that imitate
parasympathetic nerve stimulation
Two major classes of cholinergic drugs:
a. cholinergic agonist – mimic the action
of the neurotransmitter acetylcholine
b. anticholinesterase drugs – work by
inhibiting the destruction of acetylcholine at
cholinergic receptor sites
How cholinergic drugs work..
Cholinergic agonist
 When a neuron in the PNS is stimulated,
the neurotransmitter Ach is released. Ach
crosses the synapse and interacts with
receptors in the adjacent neuron.
Cholinergic agonist drugs work by
stimulating cholinergic receptors,
mimicking the action of Ach.
Anticholinesterase drugs
54
  After Ach stimulates the cholinergic
receptor, it’s destroyed by the enzyme
acetylcholinesterase. Anticholinesterase
drugs produce their effects by inhibiting
acetylcholinesterase. As a result, Ach
isn’t broken down and begins to
accumulate; therefore, the effects of Ach
are prolonged.
CHOLINERGIC AGONIST
Directly stimulating cholinergic receptors,
cholinergic agonists mimic the action of the
neurotransmitter acetylcholine
Example:
Acetylcholine Cevimeline
Pilocarpine Pilocarpine
Betanechol
Carbachol
Pharmacokinetics
- Depend on the affinity of the individual
drug for muscarinic or nicotinic receptors
- For example, the drug acetylcholine
poorly penetrates the CNS
- Usually administered: topically, with eye
drops
orally
subcutaneous injection
( more
rapidly than oral)
- Rarely administered by IM or IV
( because they’re almost immediately
broken down by cholinesterase in the interstitial
spaces between tissues and inside the blood
vessels)
( begin to work rapidly and can cause
cholinergic crisis)
- Cholinergic agonist are absorbed rapidly
and reach peak levels within 2 hours
- Food decreases their absorption
- Less than 20% is protein bound
Summed up:
- All cholinergic agonist are metabolize by
cholinesterase:
1. at the muscarinic and nicotinic
receptor sites
2. in the plasma ( the liquid portion of the
blood)
3. in the liver
- Excreted by the kidneys
Pharmacodynamics
- Works by mimicking the action of
acetylcholine on the neurons in certain
organs of the body called the target
organs
- They stimulate the muscle and produce:
salivation
bradycardia
dilation of BV constriction of
pulmonary
increase GI tract increased tone &
contraction
of the bladder
constriction of the pupils
Pharmacotherapeutics
- Treat atonic (weak) bladder conditions
and postoperative and postpartum urine
retention
- Treat GI disorders, such as postoperative
abdominal distention and GI atony
55
 - Reduce eye pressure in patients with
glaucoma and during eye surgery
- Treat salivary gland hypofunction
Drug interactions
- Other cholinergic drugs, especially
anticholinesterase drugs (ambenopium,
edrophonium, neostigmine) boost the
effects of cholinergic agonist and
increase the risk of toxicity
- Anticholinergic drugs
- Quinidine reduces the effectiveness of
cholinergic agomist
Assessment:
1. Assess for disorders in which cholinergic
agonist are used such as Myasthenia
gravis
2. Assess for urine retention and bladder
distention; determine the patients fluid
intake , time and amount of last urination
3. Assess for possible paralytic ileus
( check for bowel sounds, abdominal
distention and determine the patients
elimination pattern)
4. Assess for disorders that may be
aggravated by cholinergic agonist
(Alzheimers dse.)
Implementation:
1. Administer cholinergic drugs as
prescribed
2. Be aware that some drugs, such as
Bethanechol should be given before
meals
3. Monitor for effects of cholinergic drugs
and report adverse reactions( nausea,
vomiting, cramps, diarrhea, blurring of
vision)
4. Assess for respiratory adequacy
5. Assess for urinary adequacy and signs of
urine retention
Health teachings:
1. Take the drug as directed on a regular
schedule to maintain consistent blood
levels of the drug and symptom control
2. Don’t chew or crush sustained-release
tablets or capsules
3. Take oral cholinergics on an empty
stomach
4. If diarrhea or vomiting occurs, ensure
adequate fluid intake
5. Cholinergic drugs act within 60 minutes.
Make sure bathroom facilities are
available.
6. If taking in long term mode, wear or carry
medical alert identification
7. For those with MG, plan rest periods between
activities and space activities throughout the day
8. Report increased muscle weakness, difficulty
breathing, recurrence of MG symptoms
Anticholinesterase drugs
Block the action of the enzyme
acetylcholinesterase at cholinergic receptor site
Preventing the breakdown of the neurotransmitter
acetylcholine
As Ach builds up, it continues to stimulate the
cholinergic receptors
Divided into 2 categories: Reversible and
Irreversible
Reversible (short acting)
Ambenonium
Donepezil
Edrophonium
Neostigmine
Physostigmine
Rivastigmine
Tacrine
Irreversible (long acting)
56
Used primarily as toxic insecticides and
pesticides or as nerve gas agents in chemical
warfare
Echothiopate
Pharmacokinetics
- Readily absorbed from the GI tract,
subcutaneaous tissue and mucous
membrane
- Because neostigmine is poorly absorbed
from the GI tract, the patient needs a
higher dose when taking this drug orally
- When a rapid effect is needed, the drug
should be given in IM or IV route
- Distribution varies
- example: Physostigmine – cross the BBB
Donepezil – highly
bound to plasma
CHON
Tacrine – about 55%
bound
Rivastigmine – 40%
bound
Galantamine – 18%
bound
- Metabolized in the body by enzymes in
the plasma and excreted in the urine
- Donepezil, Galantamine, Rivastigmine,
and Tacrine are metabolized in the liver
but still excreted in urine
Pharmacodynamics
- Promote the action of acetylcholine
receptor sites
- They can produce a stimulant or
depressant effect on cholinergic
receptors
- Reversible – block the breakdown of
acetylcholine for minutes to hours
- Irreversible – can last for days or weeks
Pharmacotherapeutics
1. To reduce eye pressure
2. To increase bladder tone
3. To improve tone and peristalsis through
the GI tract in patients with reduced
motility and paralytic ileus
4. To promote muscular contraction in
patients with MG
5. To diagnosed MG
6. As antidotes to anticholenergic drugs,
tricyclic antidepressants
7. To treat mild to moderate dementia and
enhance cognition in patients with Alzheimers
dse.
Drug Interactions
- Other cholinergic agonist, particularly
cholinergic agonist ( bethanechol,
carbachol, pilocarpine)
- Carbamazepine, dexamethasone,
rifampicin, phenytoin and phenobarbital
- Aminoglycosides antibiotics, anesthetics
and anticholinergic drugs
- Inhibitors of cytochrome P450
( cimetidine and erythromycin)
- Cigarette used
Adverse Reactions
- Increased action of Ach at receptor sites
- Cardiac arrhythmias, nausea and
vomiting, diarrhea, SOB, wheezing,
seizures, headache, anorexia, insomnia,
pruritus, urinary frequency and nocturia
Assessment:
1. Assess for disorders in which
anticholinesterase drugs are used, such as MG,
alzheimers, glaucoma and altered bladder
function
2. Assess for urine retention and bladder
distention, determine the patient’s fluid intake,
57
and find out the time and amount of his last
urination
3. Assess for possible paralytic ileus by checking
for BS and abdominal distention and determining
the patients elimination pattern
Anticholinergic drugs
- Interrupt parasympathetic nerve impulses
in the CNS and ANS
- Prevent Ach from stimulating cholinergic
receptors
- Don’t block all cholinergic receptors, just
the muscarinic receptors sites
Belladonna Alkaloids
- Atropine
- Belladona
- Homatropine
- Hyocyamine
- Scopolamine
Synthetic derivatives of belladonna alkaloids
(quarternary ammonium drugs)
- Glycopyrrolate
- Methscopolamine
- Propantheline
Tertiary amines – newer synthetic drugs
- Centrally acting and more selective
- Fewer side effects
- Benztropine, Dicyclomine, Oxybutynin,
Tolterodine, Trihexyphenidyl
Pharmacokinetics
- Belladonna alkaloids are absorbed from
the eyes, GI tract, mucous membranes,
and skin
- Quarternary ammonium drugs and
tertiary amines are absorbed primarily
through the GIT
- Belladona class are distributed more
widely throughout the body
- Alkaloids readily cross the BBB
- Belladonna metabolized in the liver and
excreted in the kidneys
- Metabolism of tertiary amines is
unknown, but excretion is usually
through the kidneys and feces
- Quarternary ammonium drugs are bit
more complicated, hydrolysis occurs in
the GIT and liver, excretion is n feces and
urine
Pharmacodynamics
- Produces paradoxical effect (depending
on the dosage, condition being treated
and target oragn)
- Example: in the brain they can produce a
stimulating and depressing effect
- Example: Parkinson’s dse, characterized
by low dopamine levels that intensify the
stimulating effects of Ach, cholinergic
blcokers depress this effect
Pharmacotherapeutics
- anticholinergic drugs are used in various
GI situations
1. all anticholinergic drugs are used to
treat spastic or hyperactive conditions of the GI
and urinary tracts
- for bladder relaxation and urinary
incontinence, quarternary ammonium compounds
(propantheline) drug of choice because of fewer
adverse effects
2. the belladonna alkaloids are used with
morphine to treat biliary colic
3. given by injection before some
diagnostic procedures to relax the GI smooth
muscles
Drug Interactions
- Drugs that increase the effects of
anticholinergic drugs include:
58
 1. antidyskinetics ( amantadine)
2. antiemetics and antivertigo drugs
( meclizine)
3. antipsychotics (haloperidol)
4. cyclobenzaprine
5. tricyclic and tetracyclic
antidepressants
Adverse Reactions
- Dry mouth, reduced bronchial secretions,
increased heart rate, blurred vision, decreased
sweating
Assessment
- Assess for conditions in which
anticholinergic drugs would be used,
such as bradycardia, heart block,
diarrhea and PUD
- Assess for conditions in which
anticholinergic drugs would be
contraindicated ( glaucoma, MG, prostatic
hyperplasia, reflux esophagitis, GI
obstructive dse)
Implementation
1. Follow dosage recommendations, some
drugs should be given with meal
2. Monitor VS, cardiac rhythm, UO, and
vision for potential drug toxicity
3. Monitor for adverse reactions (dry mouth,
inc heart rate and blurred vision)
Adrenergic drugs
- Also called sympathomimetic drugs
- Classified into two groups based on their
chemical structure: cathecolamines and
noncatecholamines
- Also divided by action:
1. direct acting – acts directly on the
organ or tissue innervated by SNS
2. indirect acting – in which the drug
triggers the release of neurotransmitters
(norepinephrine)
3. dual acting - both
Catecholamines
- They stimulate the nervous system,
constrict peripheral blood vessels,
increase heart rate and dilate the bronchi
- Common examples:
dobutamine dopamine
epinephrine
norepinephrine
isoproterenol Hcl/sulfate
Pharmacokinetics
- can’t be take orally (destroyed by
digestive enzymes)
- In contrast, when these drugs are given
sublingually, rapidly absorbed though the
mucous membrane
- SC absorption is slowed ( cause the BV
around the injection site to constrict)
- IM faster because of less constriction
- Metabolized and inactivated
predominantly in the liver ( GIT, lungs,
kidneys, plasma, tissues)
- Excreted primarily in the urine ( isoproterenol –
feces, epinephrine – breast milk)
Pharmacodynamics
- Primarily direct acting
- Combine with alpha-adrenergic or beta-
adrenergic receptors
- Cause either excitatory and inhibitory
- Alpha-adrenergic – excitatory response
except for intestinal relaxation
- Beta-adrenergic – inhibitory except in the
cells of the heart
59
Pharmacotherapeutics
- Most adrenergics produce their effects by
stimulating alpha and beta adrenergic
receptors
- Norepinephrine has the most nearly pure
alpha activity
- Dobutamine and isoproterenol have only
beta therapeutic use
- Epinephrine stimulates alpha and beta
- Dopamine primarily exhibits
dopaminergic activity
- Cathecholamines that stimulate alpha-
adrenergic are used to treat hypotension
( loss of vasomotor tone, blood loss
- Cathecolamines that stimulate beta1-
adrenergic are used to treat bradycardia,
heart block, low cardiac output,
ventricular fibrillation, asystole, cardiac
arrest
- Cathecolamines that exert beta2-
adrenergic activity are used to: acute and
chronic bronchial asthma, emphysema,
bronchitis, acute hypersensitivity
- Dopamine is used in low doses to improve blood
flow to the kidneys (it dilates the renal blood
vessels)
Drug Interactions:
Alpha-adrenergic blockers (phentolamine) – can
produce hypotension
Epinephrine – may cause hyperglycemia
Beta-adrenergic blockers (propanolol) – can lead
to brochial constriction
Tricyclic antidepressants – can lead to
hypertension
Adverse reactions:
- Palpitations
- Cardiac arrhtyhmias
- Hypotension
- Hypertension and hypertensive crisis
- Increased glucose levels
- Tissue necrosis and sloughing
Assessment:
1. Assess the pt.’s condition before tx
2. Continuously monitor ECG, BP, PAWP,
cardiac condition, UO
3. Monitor electrolyte levels
4. After dopamine is stopped, watch closely
for a sudden drop in BP
Implementation:
1. Before starting catecholamines, correct
hypovolemia with plasma volume
expanders
2. Give cardiac glycosides before
cathecolamines; cardiac glycosides
increase AV node conductions and
patients with AF may develop rapid
ventricular rate
3. Administer drug using central venous
catheter or large peripheral vein
4. Dilute the concentrate for injection before
administration
5. Watch for irritation and infiltration;
extravasation can cause an inflammatory
response
6. Don’t give cathecolamines in the same IV line
as other drugs (beware of incompatibilities)
ex. Dobutamine – heparin,
hydrocortisone sodium
succinate, cefasolin, penicillin
7. Don’t mix dobutamine or dopamine with
sodium bicarbonate injection or phenytoin
( incompatible with alkaline solutions)
8. Change IV sites regularly to avoid phlebitis
60
9. Provide patient teaching
Noncathecolamines
- Many therapeutic uses because of the
various effects these drugs can have on
the body including:
1. local and systemic constriction of
blood vessels (phenylephrine)
2. nasal and eye decongestion and
dilation of the bronchioles ( albuterol, bitolterol,
ephedrine, formoterol, isoetharine Hcl,
terbutaline)
3. smooth muscle relaxation (terbutaline)
Pharmacokinetics:
- Depends on the route of administration
1. inhaled drugs (albuterol) – gradually
absorbed from the bronchi thus resulting in lower
drug levels in the body
2. oral drugs – absorbed well from the GI
tract and are distributed widely in the body fluids
and tissues
3. some crosses the BBB (ephedrine)
- Metabolism and inactivation of
noncathecolamines occur primarily in the liver but
also in the lungs, GIT and other tissues
- Excreted primarily in the urine
- Inhaled albuterol are excreted within 24
hours
- Oral albuterol – within 3 days
- Acidic urine increases excretion of many
noncathecolamines, alkaline urine slows
excretion
Pharmacodynamics:
- Noncathecolamines can be direct-acting,
indirect or dual ( unlike cathecolamines,
primarily direct-acting)
1. direct-acting noncathecolamines –
stimulate alpha activity receptors including
phenylephrine. Those that selectively stimulate
beta2 activity receptors (albuterol, isoetharine,
metaproterenol, terbutaline)
2. indirect-acting noncathecolamines –
exert their effect by indirect action on adrenergic
receptors
3. dual acting – ephedrine and
mephentermine
Pharmacotherapeutics:
- Stimulate SNS and produce various
effects on the body
1. mephentermine – causes
vasoconstriction and is used to treat hypotension
in severe shock
2. terbutaline – used to stop in preterm
labor
Drug interactions:
- Anesthetics – can cause arrthymias and
hypotension
- Monoamine oxidase inhibitors – severe
hypertension
- Tricyclic antidepressants – cause
hypertension and arrthymias
- Urine alkalizers ( acetazolamide and Na
bicarb) – can cause slow excretion
Assessment:
- Obtain a baseline assessment of the pt’s
respiratoty status, and assess it
frequently throughtout therapy
- Assess for adverse reactions and drug
interactions
- Assess the pt’s and family’s knowledge
of the drug therapy
Adrenergic blocking drugs
- Also called sympatholytic drugs
- Used to disrupt SNS
- Their action at these sites can be exerted
by:
61
 1. interrupting the action of adrenergic 3. Don’t give sublingual tablets with food or
drugs drink

2. reducing available NE 4. Provide patient teaching

3. preventing the action of cholinergic Beta-adrenergic blockers

drugs
- Most widely used adrenergic blockers
- Classified according to their site of action
as: - Prevent stimulation of the SNS by
inhibiting the action of cathecolamines at
1. alpha-adrenergic blockers (alpha beta adrenergic receptors
blockers)
- Beta-adrenergic blockers are selective or
2. beta-adrenergic blockers ( beta nonselective beta-adrenergic blockers
blockers) affect:

Alpha-adrenergic blockers 1. beta1 receptors site (heart)

- Work by interrupting the actions of the 2. beta2 receptor site (bronchi, BV and
cathecolamines ( E and NE) at alpha uterus)
receptors
Nonselective:
- This results in:
*Carvedilol
1. relaxation of the smooth muscle in the
blood vessels *Labetalol

2. decreased blood pressure - Levobunolol

- Drugs in this class includes: - Penbutolol

ergoloid mesylates ergotamine - Pindolol

- Propanolol
phenoxybenzamine phentolamine
* Also block alpha1 receptors
terazosin
Selective:
doxazosin
- Acebutolol
prazosin
- Atenolol
Pharmacotherapeutics:
- Betaxolol
- Hypertension
- Bisoprolol
- Peripheral vascular disorder
- Esmolol
- Pheochromocytoma
- metoprolol
- Vascular headache
Pharmacokinetics:
Implementation:
- Usually absorbed rapidly from the GIT
1. Give drugs at bedtime
- Protein bound to some extent
2. Begin tx with small dose to avoid
syncope

62
 - Distributed widely in body tissues, with Retching- Nausea and Vomiting
the highest concentrations found in the
heart, liver, lungs and saliva Fear and Anxiety

- Nadolol and atenolol – urine, feces and Stomatitis

breastmilk
General Guidelines for Anti-Neoplastic Agents
- Metabolized in the liver
CBC and Platelets monitoring
Pharmacotherapeutics:
Anti-emetics are given BEFORE drug
- Can be prescribed after a heart attack to
prevent another heart attack or to treat: NEPHROTOXICITY is an important Side effect

1. angina Counseling regarding reproductive issues

2. hypertension Encourage hand washing and avoidance of

crowds
3. hypertrophic cardiomyopathy
Recommend wig for alopecia
4. SV arrhythmias
General guidelines
Assessment:
General Types
- Assess respiratory status (COPD or
asthma because of potential vasospasm) ALKYLATING agents

- Check apical pulse rate ( alert the ANTI METABOLITES

prescriber if pulse rate is below 60bpm)
ANTIBIOTICS
- Monitor BP, ECG, HRR ( be alert for
MITOTIC INHIBITORS
progression of AV block or bradycardia)
HORMONAL agents
Nursing Pharmacology
IMMUNOSUPPRESANTS
Anti- Neoplastic
Alkylating Agents
Chemotherapeutic Drugs
DYNAMICS: cause cell death or mutation
General Description
INDICATIONS: Palliative treatment of chronic
These agents kill or inhibit the reproduction of
lymphocytic leukemia, malignant lymphomas,
neoplastic cells
Hodgkin’s disease, cancers of the breast, lungs
They may be cycle specific or non specific and ovaries

They are used in combination, or with other ADVERSE EFFECTS: Bone marrow depression,
treatment modalities anorexia, alopecia, N/V

Usull given IV Alkylating Agents

Undesirable effects Busulfan

“BARFS” Carboplatin

Bone Marrow Depression Carmustine

Alopecia Chlorambucil

63
Cisplatin Anti-metabolites

Cyclophosphamide Capecitabine

Ifosphamide Cytarabine

Mecholethamine Fluouracil

Alkylating Agents Methotrexate

Nursing Interventions Mercaptopurine

Monitor CBC weekly Thioguanine

Hydrate patient well Floxuridine

Pre-medicate with anti-emetics Anti-Metabolites

Monitor IV site Nursing Interventions

Prepare epi, steroids and antiH1 Evaluate complete blood count

Drug Specific Side effects Pre-medicate with anti-emetics

ANTI-METABOLITE Safety measures for dizziness

DYNAMICS: interferes with the building block of Instruct to report fever, sore throat, rash and
DNA synthesis bleeding

INDICATIONS: Myelocytic leukemia, acute Provide small, frequent feedings

lymphocytic leukemia, cancers of breast, cervix,
colon, liver, ovaries Suncreens for photosensitivity

ADVERSE EFFECTS: GI disturbance, oral and Anti-Metabolites

anal inflammation, bone marrow depression,
alopecia, renal dysfunction and thrombocytopenia Nursing Interventions

General Guidelines for anti-metabolites When administering methotrexate, prepare to

administer leucovorin (folinic acid or citrovorum
Monitor CBC and Platelets weekly factor) to prevent toxicity

Evaluate renal functions Anti-Neoplastic Antibiotics

Take temperature Q 4 hours DYNAMICS: these kill cancer cells by disrupting

the DNA synthesis and breaking up the DNA
Aseptic techniques linkages

Bleeding, anemia, infection and nausea INDICATIONS: Leukemia, carcinomas,

adenocarcinoma
Oral hygiene
ADVERSE EFFECTS: bone marrow suppression,
Lots of fluids (2-3 liters/day) alopecia, NAVD, renal toxcity

Intake and output, nutrition Anti-Neoplastic Antibiotics

The protocols for handling- follow them Bleomycin

Emphasize protective isolation Dactinomycin

64
Daunorubicin Vinorelbine

Doxorubicin MITOTIC INHIBITORS

Idarubicin Vincristine (Oncovin)

Mitocycin Can cause NEUROTOXICITY

Plicamycin Cause severe bone depressionà check CBC

Anti-Neoplastic Antibiotics MITOTIC INHIBITORS

Daunorubicinà CHF and Dysrhythmia NURSING INTERVENTIONS

Doxorubicinà Cardiotoxicity Arrange for blood tests

Bleomycinà pulmonary toxicity Avoid direct skin and eye contact with drugs

Plicamycinà excessive bleeding Ensure hydration

Anti-Neoplastic Antibiotics Small, frequent meals

NURSING INTERVENTIONS Wig

Monitor blood tests, cardiac functions Anti-emetics

Ensure that the patient is well-hydrated Hormone and Immunomodulators

Provide small, frequent feedings DYNAMICS: receptor-site specific drugs that

block the specific hormones in the cancer
Advise wig for alopecia
INDICATIONS: Breast cancer, prostate cancer
Instruct to maintain oral hygiene
ADVERSE EFFECTS: menopause associated
Assess the ECG frequently effects like hot flashes, vaginal dryness. Bone
marrow depression and HYPERCALCEMIA
MITOTIC INHIBITORS
Hormone and Immunomodulators
DYNAMICS: kill the cells as the process of Mitosis
begins by blocking the mitotic spindles causing Tamoxifen à anti-estrogen
cell death
Anastrazole
INDICATIONS: Combination therapy for
reproductive cancer, cancers of the lungs, Estramustine
Lymphomas
Letrozole
ADVERSE EFFECTS: bone marrow suppression,
NAVD, renal and hepatic toxicity , alopecia Testolactone

MITOTIC INHIBITORS Toremifene

Etoposide Goserelinà GnRH analogue

Teniposide Flutamide

Vinblastine Fluoxymesteroneà an ANDROGEN

Vincristine (Oncovin) Diethylstilbestrol (DES)à estrogen preparation

65
Hormone and Immunomodulators In Summary

NURSING INTERVENTIONS Anti-neoplastic agents affects both the normal

cells and the cancers cells
Arrange for blood tests to monitor bone marrow
depression They act by disrupting cell function and division

Provide small, frequent meals Most cancer drugs are MOST effective against
cancer cells that multiply RAPIDLY
Advise comfort measures for menopausal
symptoms In Summary

Utilize BARRIER methods of contraception The ULTIMATE GOAL of cancer therapy is to

decrease the size of the cancer so that the body’s
Miscellaneous immune system can eliminate the cancer

L-Asparaginase Anti-cancer drugs are BEST given in combination

so as to affect the cancer cells in various stages
Enzyme that destroys ASPARAGINE needed by
malignant cells for protein synthesis In Summary

Indicated for acute lymphocytic leukemia ADVERSE effects commonly encountered with
cancer therapy are related to damage to RAPIDLY
Adverse effects: PANCREATITIS, bone marrow multiplying cells like the BONE MARROW, hair
depression, fatal hyperthermia, hypersensitivity follicle and Gastro-intestinal lining

Miscellaneous In Summary

Azathioprine In general, these drugs SHOULD NOT be used

during pregnancy or lactation because they may
Used as adjunct to cyclosporine and steroids to
cause serious adverse effects on the FETUS
suppress immune system
Hematologic Drugs
CAN CAUSE bone marrow suppression and
increase incidence of cancers Hematologic drugs

Taken with meals There are numerous agents utilized to maintain,

preserve and restore circulation. The three
Avoid crowds, maintain hygeine
important dysfunction of blood are thrombosis,
Anti-emetics bleeding and anemia are commonly treated with
various agents. The common ones that nurses
Metoclopromide must REVIEW are the:

Odansetron Anticoagulants

Dronabinol Antilipemics

In Summary Antiplatelets (antithombotics)

Cancers arise from a single abnormal cell that Thrombolytics

multiplies and grows
Anti-anemics or Hematinics
Cancers can come from epithelia cells-
CARCINOMA or mesenchymal cells- SARCOMA Drugs to treat bleeding

Cancer cells lose their normal functions and they The Anti-Coagulants
grow uninhibited

66
The anticoagulants interfere with the coagulation
process by interfering with the clotting cascade
and thrombin formation. These agents are used
to inhibit clot formation, but they do NOT dissolve
existing clots.
The Anticoagulants commonly used are:
Heparin
Warfarin (Coumadin)
Dicumarol
Anisindione (Miradon)
Heparins
These are anticoagulants given orally or
parenterally- SQ and IV.
Heparin is naturally found in the human liver that
normally prevents clot formation.
Heparin is strongly acidic because of the
presence of sulfate and carboxylic acid groups in
the heparin chain.
Heparin
The mechanism of action of Heparin
Heparin (Liquamen Sodium) acts prophylactically
to prevent the formation of blood clots in the
vasculature.
It combines with ANTITHROMBIN III, a substance
in our blood sometimes called heparin factor that
inactivates THROMBIN.
By inhibiting the action of thrombin, conversion
of fibrinogen to fibrin does not occur and the
formation of a fibrin clot is prevented.
Heparins
Clinical Indications of Heparins
deep vein thrombosis
pulmonary embolism
coronary thrombosis,
patients with artificial heart valves and stroke
patients
Heparins
Contraindications of heparin
Anticoagulants are not given to patients with
bleeding disorders, peptic ulcers and patients
who underwent recent eye/brain/spinal surgery.
It is NOT given to patients with severe liver and
renal disease, hemophilia, and CVA.
Heparin is a large protein molecule that cannot
pass through the placenta easily and can be given
to pregnant women.
Heparins
Pharmacokinetics: the Adverse Effects of Heparin
INCREASES the clotting time and also
DECREASES the platelet count. In this regard,
monitoring of the aPTT/PTT (N= 20-30 seconds)
and platelet count is required.
Hematologic effects: increased bleeding,
thrombocytopenia
Skin-itching and burning
Hypersensitivity reactions like chills, fever,
urticaria or anaphylaxis can occur since heparin
is obtained from animal sources.
Life threatening adverse effect is Hemorrhage
Heparins
The Nursing process and Heparin
Assessment
Patient history
Physical examination- the nurse obtains baseline
vital signs and physical assessment.
She must obtain laboratory results of the
complete blood count, platelet count and
activated partial thromboplastin time (aPTT), and
clotting time.
Heparins
IMPLEMENTATION:
67
Monitor the aPTT closely (it should be 1.5-2.5
times normal value)
Monitor vital signs and hematological status
regularly.
Monitor signs of bleeding- hematuria, epistaxis,
ecchymoses, Hypotension and occult blood in
stool
Have available ANTIDOTE for heparin-
PROTAMIME SULFATE
Heparins
IMPLEMENTATION:
Instruct the client not to use any over the counter
drug without notifying the physician
Administer heparin subcutaneously in the
abdominal region, using a 25-28-gauge needle at a
90-degree angle. DO NOT MASSAGE OR RUB THE
AREA as this may cause bruising.
Advise patient not to smoke, use electric razors to
shave, use soft toothbrush and control sudden
hemorrhage by direct pressure for 5-10 minutes.
Provide gently skin and oral care.
Heparins
Evaluation
Monitor the effectiveness of the medication:
Decreased formation of clot
PTT is 2x the normal
The Oral Anticoagulants
There are three commonly used oral
anticoagulant agents in the hospital
Warfarin- most commonly used, synthesized from
dicumarol
Dicumarol
Anisindone
The Oral Anticoagulants
Pharmacodynamics: the mechanism of Action of
the Oral agents
These agents INHIBIT the liver synthesis of the
Vitamin K clotting factors – factors II, VII, IX, and
X.
The Oral Anticoagulants
Clinical indications of oral anticoagulants
These drugs are used to prevent blood clotting in
patients with thrombophlebitis
pulmonary embolism and embolism from atrial
fibrillation.
Because Warfarin crosses the placental barrier, it
is NOT given to pregnant mothers.
The Oral Anticoagulants
Contraindications and precautions
Oral anti-coagulants are NOT given to patients
with bleeding disorders, peptic ulcers, severe
renal/liver diseases, hemophilia, CVA blood
dyscrasias and eclampsia.
It is NOT given to pregnant mothers because it is
teratogenic and can cause abortion
The Oral Anticoagulants
Pharmacokinetics:
Oral anticoagulants prolong the clotting time and
are monitored by the Prothrombine Time (PT-
average of 9-12 seconds). This is usually
performed before administering the next dose.
The PT level should be 1.5-2 times the reference
value to be therapeutic.
The normal INR is 1-2. If the patient is on oral
anticoagulant therapy, the INR is maintained at an
INR of 2.0-3.0. If the INR is below the
recommended range, warfarin is increased. If it is
above the recommended range, warfarin should
be reduced.
The Oral Anticoagulants
Pharmacokinetics: the Adverse Effects of
Warfarin
Hematologic effects: increased bleeding,
thrombocytopenia
Anorexia, nausea, vomiting, diarrhea, abdominal
cramps, rash and fever.
68
Alopecia, bone marrow depression, and dermatitis. Should be 2x the normal

Life threatening adverse effect is Hemorrhage Anti-platelets

The Oral Anticoagulants These are agents decrease the formation of the
platelet plug by decreasing the responsiveness of
The Nursing process and Warfarin the platelets to various stimuli that would cause
them to stick and combine together on a vessel
Assessment wall

Patient history-. The nurse determines the current Aspirin

medications taken, PREGNANCY, and history of
recent surgery. Dipyridamole

Physical examination- the nurse obtains baseline Sulfinpyrazone

vital signs and physical assessment.
Ticlopidine
laboratory results of the complete blood count,
platelet count and Prothrombin time, INR and Clopidogrel
clotting time.
Glycoprotein receptor antagonists

Abciximab
The Oral Anticoagulants
Eptifibatide
Implementation
Tirofiban
Monitor vital signs and hematological status
Anti-platelets
Monitor signs of bleeding- hematuria, epistaxis,
The mechanism of action of platelet inhibitors
black tarry stools, echymoses, Hypotension and
occult blood in stool
These agents INHIBIT the aggregation of platelets
in the clotting process by blocking receptor sites
Have available ANTIDOTE for warfarin- VITAMIN K
on the platelet membrane, preventing platelet-to-
or phytonadione.
platelet interaction, thereby prolonging the
The Oral Anticoagulants bleeding time.

Implementation Anti-platelets

Advise patient not to smoke, use electric razors to Clinical indications

shave, use soft toothbrush and control sudden
Prevention of myocardial infarction and stroke
hemorrhage by direct pressure for 5-10 minutes.
Provide gently skin and oral care.
Prevention of a repeat myocardial infarction
Instruct the patient to avoid foods high in vitamin
Prevention of stroke for those with transient
K like spinach, nuts
ischemic attack
The Oral Anticoagulants
In patients with graft to maintain its patency.
Evaluation
Anti-platelets
Monitor the effectiveness of the medication
Pharmacodynamics: the adverse effects of
Antiplatelets
Decreased formation of blood clots
Bleeding is the most common side effect
Check the PT and INR

69
GIT- gum bleeding, gastric bleeding, tarry stools
CNS- headache, dizziness and weakness
Skin- petechiae, bruising, allergy
ASPIRIN toxicity: tinnitus
Anti-platelets
Nursing considerations
Determine if the patient is allergic or sensitive to
the medications
Monitor closely the vital signs and bleeding areas
Instruct the patient to take drug with food
Monitor the bleeding time, clotting time and
platelet count
Anti-platelets
Nursing considerations
Suggest safety measures including the use of an
electric razor and avoidance of contact sports.
Provide increased precautions against bleeding
during invasive procedures.
Use pressure dressings and ice to decrease
excessive blood loss.
Monitor for tinnitus
The Thrombolytics
These thrombolytic agents are used to activate
the natural anticlotting fibrinolytic mechanism to
convert plasminogen to plasmin, which destroys
and breaks down the fibrin threads in the blood
clot (FIBRINOLYSIS). The result is clot
disintegration.
The commonly used thrombolytics “---ase”
Streptokinase
Urokinase
Tissue plasminogen activator (t-PA) or alteplase
Anistreplase
Reteplase
The Thrombolytics
The mechanisms of actions of each agent
Streptokinase and urokinase are ENZYMES that
act SYSTEMICALLY to dissolve the blood clots by
activating plasminogen to plasmin.
The Thrombolytics
Clinical indications of thrombolytics
Myocardial infarction
Pulmonary embolism
Thromboemboilic stroke
Peripheral arterial thrombosis and
to open clotted IV catheters.
The Thrombolytics
Pharmacokinetics: The adverse effects of
Streptokinase
CVS- Hypotension and dysrhythmias (usually
upon reperfusion of the heart)
Hematological: increased bleeding- the most
common effect.
Headache, nausea, flush, rash and fever
Allergic reaction- especially steptokinase and
urokinase
Major adverse effect- hemorrhage.
The Thrombolytics
Implementation.
Monitor signs of active bleeding from mouth and
rectum bleeding- hematuria, epistaxis, echymoses
Have available ANTIDOTE for thrombolytics:
AMINOCAPROIC ACID!
Have available blood for emergency use.
Advise patient not to smoke, use electric razors to
shave, use soft toothbrush and control sudden
hemorrhage by direct pressure for 5-10 minutes.
Provide gently skin and oral care. As much as
possible, avoid frequent venipuncture.
70
The Thrombolytics HMG CoA reductase inhibitors= “statins”

Evaluation Atorvastatin

Monitor the effectiveness of the medication Cerivastatin

Clot lysis Fluvastatin

The Agents to treat bleeding Lovastatin

Aminocaproic acid and tranexamic acid Pravastatin

These are fibrin stabilizers that maintain or stabilize Simvastatin

the clot in the bleeding vessels
Nicotinic acid
The Agents to treat bleeding
Probucol
Protamine sulfate
statins
This agent antagonizes the anticoagulant effects of
heparin. It is derived from fish testis and is high in Pharmacodynamics: The mechanism of action of
arginine content. the Statins

The positive charge interacts with the negative charge These agents INHIBIT the enzyme HMG CoA
of heparin to forma stable inactive complex. reductase in the synthesis of cholesterol.

The Agents to treat bleeding By inhibiting the important enzyme in cholesterol

production in the liver, the statins decrease the
Vitamin K plasma concentration of cholesterol and lower the
LDL level with slight increase in the HDL level.
Vitamin K is given to antagonize the effects of the oral
anticoagulants. statins

The response to Vitamin K is slow, requiring about 24 Therapeutic indications

hours
These agents are given to patients with
thus, if immediate hemostasis or bleeding control is CORONAY ARTERY DISEASE and hyperlipidemia,
required, fresh frozen plasma should be ordered by hypercholesterolemia
the physician.
These statins are very effective in all types of
Antihyperlipidemics hyperlipidemias.

These drugs target the problem of elevated serum The antianemics: Iron preparations and Epoetin
lipids
Iron preparations
Resins and bile acid sequestrants
Iron is important for hemoglobin formation.
Cholestyramine
The iron preparations are:
Colestipol
Ferrous sulfate
Fibric Acid Derivatives
Ferrous fumarate
Clofibrate
Ferrous gluconate
Gemfibrozil
The antianemics: Iron preparations and Epoetin
Fenofibrate

71
Side-effects:
GIT- constipation (usually), diarrhea, vomiting,
epigastric pain, gastric ulceration and darkening
of stools.
Liquid preparation can stain the teeth, and
injectable iron can cause tissue discoloration
Other- dizziness
The antianemics: Iron preparations and Epoetin
Drug-Drug interaction
Tetracyclines and penicillamine- combine with
iron preparations and render the iron
unabsorbable.
Antacids and cimetidine- decrease iron
absorption and effects
Foods can impair iron absorption but they should
be taken with iron to reduce GI discomfort.
Milk containing foods, coffee, tea and eggs are
NOT given with iron because they delay iron
absorption.
The antianemics: Iron preparations and Epoetin
Implementation
Encourage the patient to eat iron-rich foods like
liver, lean meat, egg yolk, dried beans, green leafy
vegetables.
Administer iron preparations orally with foods to
decrease GI discomfort.
If increased absorption is necessary, administer
IN BETWEEN meals with full glass of water or
juice.
It is best to offer citrus juices because the vitamin
C content can increase iron absorption.
Instruct the patient to swallow the whole tablet
and remain upright for 30 minutes to prevent
esophageal corrosion from reflux.
DO NOT administer iron together with or within 1
hour of ingesting tetracyclines, antacids, milk and
milk-containing products.
Advise clients to increase fluid intake and
consume fiber rich foods if constipation becomes
a problem.
The antianemics: Iron preparations and Epoetin
Implementation
Warn the patient of possible iron poisoning if
tablets are left within child’s reach. Emphasize
that the therapeutic effect of iron therapy may not
be apparent until several weeks.
If injecting a parenteral iron preparation, inject
DEEP IM utilizing the Z-track method to avoid
leakage into the subcutaneous tissues and skin.
Offer straw if giving liquid iron preparation to
avoid staining the teeth.
To prevent undue alarm, instruct the patient that
the stools may turn black or dark green. This is a
harmless occurrence.
The antianemics: Iron preparations and Epoetin
Evaluation
The nurse evaluates the effectiveness of the drug
therapy by determining that the client is not
fatigued, with absence of pallor, and with
hemoglobin results within desired range.
Erythropoietin
The mechanism of action of epoetin alfa
(Epogen)
This drug acts like the natural glycoprotein
erythropoietin to stimulate the production of RBC
in the bone marrow.
Erythropoietin
Clinical indications
It is given SUBCUTANEOUSLY or
INTRAVENOUSLY for the treatment of anemia
associated with renal failure or for patients on
dialysis.
It is also used in patients for blood transfusion to
decrease the need for blood in surgical patients.
72
Erythropoietin Topical therapy

Pharmacodynamics: the adverse effects of Use of active drugs in an inactive vehicle like oil
epoetin alfa
Employs the use of topical preparations
CNS- headache, fatigue, asthenia, dizziness and
seizures- these are due to the cellular response to Topical preparations
the glycoprotein.
SOAKS
GIT- nausea, vomiting and diarrhea
LOTIONS
CVS- hypertension, edema and chest pain due to
increase RBC number SOLUTIONS

Erythropoietin PASTE

Implementation CREAM

Administer the drug SC or IV usually 3 times per OINTMENT

week.
POWDER
Monitor the IV access line if given IV. Do not mix
Commonly used topical agents
with other solutions
Caustics
Determine periodically the level of hematocrit and
iron stores during therapy. If patient does not Silver nitrate, Zinc chloride and Ferric subsulfate
respond to the drug, reevaluate the cause of
anemia. Used for granulation tissues, epitheliomas and
granulomas (benign skin tumors)
Maintain seizure precaution on stand by as
seizure can occur. Applied directly over the lesions

Provide comfort measures like small frequent Keratolytics

feedings and pain medications for headache.
Lactic acid, Glycolic acids, Urea, Salicylic acids
Provide thorough health teaching: need for
lifetime injection Causes desquamation of skin and denaturation of
skin proteins
Erythropoietin
Destroys the skin keratin
Evaluation
Applied over the skin lesions like acne, calluses,
Monitor patient response to the drug= increased warts and tinea versicolor
hemoglobin
Cytostatic agents
Nursing Pharmacology
Anthralin, Tars, Liquid carbonic detergents
Dermatological Agents
Suppresses the DNA synthesis of skin cells
Dermatological Agents
Used for psoriasis, eczema, seborrheic dermatitis
Agents which are applied and exert their effects
where they are administered Applied over the skin lesions

Dermatological Agents Cytotoxic agents

The target tissue for most agents is the SKIN Cantharadin, Podophylin, Fluouracil

73
Kill the cell by either binding to DNA Side-effects: skin peeling, erythema, burning and
microtubules, destroys mitochondria or inhibiting stinging sensation
DNA synthesis
Retinoids
Used for warts (condyloma), basal cell carcinoma
Isotretinoin (ACCUTANE)
Demelanizing agents - whitening
Normalizes the keratinization process of cell
Hydroquinone- bleaching agent that inhibits
TYROSINASE activity in the melanocytesà Taken ORALLY
decreased melanin
Adverse effect: TERATOGENIC
Monobenzone- bleaching agent that is MORE
potent than hydroquinone causing irreversible Pharmacology
and permanent whitening à used in extensive
Migrane/ Ophthalmic and ENT DRUGS
vitiligo
Migraine Drugs
Melanizing agents- darkening
The underlying cause of migraine is believed to
Psoralens- promotes melanin production in the
be ARTERIAL DILATATION
kin, used for psoriasis and mild vitiligo to darken
the skin May be due to release of bradykinin, serotonin
and other chemicals
Methoxalen- photosensitizer that makes the skin
sensitive to UV rays, used for psoriasis Migraine Drugs
Anti-infectives The ERGOT derivatives are the most frequently
used drug to treat migraine previuosly
Antibacterial drugs like bacitracin, terramycin
Recently the TRIPTANs have been introduced
Antifungal agents like clotrimazole, ketoconazole,
nystatin, tolnaftate ERGOT derivatives
Antiviral agents like zovirax These agents cause CONSTRICTION of the blood
vessels in the cranium and decrease the pulsation
Scabicides and pediculocides
of the arteries
Gamma Benzene Hexachloride, Crotamiton,
ERGOT derivatives
Benzoyl benzoate, Permethrin
Dihydroergotamine
Applied to body or hair to kill the parasites
Ergotamine
Retinoids
Methysergide
Include natural compounds and synthetic
derivatives of vitamin A ERGOT derivatives
Effects on the skinà reduction of keratinization Adverse effects
that leads to acne formation ; reduction of SEBUM
production and removal of Propionebacterium Numbness
acne
Muscle pain
Retinoids
Chest pain
Tretinoin (Retin-A)- reduces acne formation
Arrhythmias
Applied topically at night before bedtime

74
ERGOTISM- nausea, vomiting, hypoperfusion, Measures for safety
chest pain, confusion
Give with food to decrease GI effects
ERGOT derivatives
Glaucoma
NURSING RESPONSIBILITIES
Increased intra-ocular pressure
Avoid prolonged use and over-use
Glaucoma
Assess for presence of decubitus ulcer and
gangrene Two types

Give the medication BEFORE the pain occurs 1. Open angle

Provide supportive measures 2. Closed angle

Teach about ergotism Glaucoma

The TRIPTANs Glaucoma

These agents BIND to serotonin receptors in the MEDICAL MANAGEMENT

cranial blood vessels causing
VASOCONSTRICTION 1. Laser surgery

The TRIPTANs 2. Drug therapy to lower Increased IOP

Sumatriptan MiOtics to cause cOnstriction

Zolmitriptan Adrenergics, beta-blockers and CAI to cause

reduced production
Naratriptan
Miotics
Rizatriptan
These are also called parasympathomimetic
The TRIPTANs agents

Can be given orally, nasally, and SC Their action mimics the parasympathetic nervous
system
The TRIPTANs
The Cholinergic Agonists
ADVERSE Effects
DIRECTLY acts by occupying the receptor in the
Numbness, tingling sensation,coldness eyes

Dizziness Pilocarpine

GI discomfort Direct acting cholinergic agonists

Chest pain Pharmacodynamics

The TRIPTANs Similar to acetylcholine and directly act on the

acetylcholine receptors
NURSING RESPONSIBILITIES

Administer the drugs before the pain worsens Pilocarpine

Monitor blood pressure Parasympathetic stimulation will cause:

75
 DUMBELS scopolamine

urination The ANTI-cholinergics

miosis (pupil constriction) Anticholinergics: pharmacodynamics

Pilocarpine These agents work by BLOCKING or

COMPETING with acetylcholine for the
Clinical use acetylcholine receptors

1. Relief of increased intraocular pressure BEST taken BEFORE MEALS

of glaucoma by inducing miosis
Atropine
Pilocarpine
Depresses salivation
Direct acting cholinergic agonists: Adverse
effects (DUMBELS) Decreases bronchial secretions

CVS- bradycardia, heart block, hypotension Mydriasis

GIT- nausea, vomiting, diarrhea, increased Cyclopedia

salivation, lacrimation
Inhibits vagal response in the heart
GUT- sense of urgency, sphincter relaxation
Reverses cholinergic toxicity
Others- increased sweating, headache, miosis,
photophobia, blurred vision Atropine

Pilocarpine Scopolamine

Nursing considerations Decreases nausea and vomiting associated with

motion sickness
1. Assure proper administration of
ophthalmic preparations Anticholinergic

2. Provide safety precautions- because of Contraindications of anticholinergic

poor visual acuity and blurred vision
1. Known allergy
3. Promote cool environment, maintain
access to the bathroom (urination) 2. Glaucoma

Other Drugs for Glacoma 3. Bladder obstruction (like PBH)

CAI- acerazolamide Anticholinergic

Adrenergic agent- epineprhine Adverse effects: anticholinergic effects

The ANTI-cholinergics CNS- blurred vision, pupil DILATION,

photophobia, cycloplegia and increased
Anticholinergics: Intraocular pressure

Prototype: Atropine GI- dry mouth, constipation, bloatedness

dicyclomine CVS- tachycardia, palpitations

glycopyrrolate GU- urinary retention

propantheline Others- decreased sweating, flushing

76
Anticholinergic 3. Brompheniramine 13. Hydroxyzine

Nursing considerations 4. Buclizine 14.

Meclizine
Provide comfort measures
5. Cetirizine 15.
Frequent mouth care Methdilazine

Provide increased fluids 6. Chlorpheniramine 16.

Promethazine
Protect eyes fro lights
7. Clemastine 17.
Advise to avoid hazardous activities Tripelenamine

Provide high-fiber diet and laxative 8. Cyclizine 18.

Carbinoxamine
Avoid extremes of temperature
9. Cyproheptadine 19.
Instruct to void before administering the drug
Trimeprazine
Anticholinergic
10. Dexchlorpheniramine 20 Triprolidine
Nursing considerations
The ANTIHISTAMINES
2. Monitor for toxicity:
The SECOND GENERATION ANTIHISTAMINES
3. Ensure adequate hydration to prevent
Fexofenadine
hyperpyrexia
Loratidine
The ANTIHISTAMINES
Azelastine
Also called H1 blockers or H1 antagonists, these
are agents designed to relieve respiratory Cetirizine
symptoms and to treat allergic conditions.
Anti-Histamine
The ANTIHISTAMINES
These agents SELECTIVELY block the effects of
The anti-histamines are group according to the histamine at the HISTAMINE-1 receptor sites in
“generation”. the target tissue by competing with histamine for
receptor, decreasing the cellular responses
The FIRST GENERATION agents have greater
anticholinergic effects and can cause more They also have anticholinergic and antipruritic
sedation and drowsiness! These agents cause properties.
drowsiness.
Anti-Histamine
The SECOND GENERATION agents have fewer
anticholinergic effects that is why they cause less Clinical Indications for Use in respiratory system
sedation.
1. rhinitis
The ANTIHISTAMINES
2. allergic sinusitis
The FIRST GENERATION ANTIHISTAMINES
3. uncomplicated urticaria and angioedema.
1. Azatadine 11.
Dimenhydrinate 4. Motion sickness

2. Azelastine 12. Anti-Histamine

Diphenhydramine

77
 1. CNS- drowsiness and sedation, most Decreased occurrence of rhinitis
pronounced if first generation agents are
used The Topical Nasal Decongestants

2. Fatigue, dizziness and disturbed These include:

coordination.
Ephedrine
3. Anticholinergic effects= drying of the
respiratory mucus membrane, GI upset Oxymetazoline
and nausea, arrhythmias, dysuria, urinary
Phenylephrine
retention
Tetrahydrozoline
4. Skin dryness
Xylometazoline
Anti-Histamine
The Topical Nasal Decongestants
Implementation
Pharmacodynamics: action
The nurse should administer the drug on an
EMPTY stomach, or 1 hour before or 2 hours after These agents imitate the effects of the
meals to increase the absorption. sympathetic nervous system to cause
vasoconstriction, leading to decreased edema
Give with food if GI upset occurs
and decreased inflammation of the nasal
Anti-Histamine membranes.

Implementation The Topical Nasal Decongestants

Offer sugarless lozenges or hard candy to Pharmacokinetics: administration and

counteract dryness of the mouth. Give frequent preparations
oral care
These agents are available as nasal
Provide safety measures if drowsiness may sprays or drops used to relieve the discomfort of
occur. Side rails up, assist in ambulation, and nasal congestion
advise not to drive or operate dangerous
Topical Decongestants
machineries or delicate tasks.
Clinical use of the agents
Anti-Histamine
symptoms of nasal congestion in colds, rhinitis,
Nursing implementation
and sinusitis.
Increase humidity in the room by utilizing
These can be used when dilation of the nares is
nebulizers and provide adequate hydration
desired to facilitate medical examination and to
Allow the patient to void first before administering relieve the pain and congestion of otitis media.
the drug.
Topical Decongestants
Anti-Histamine
Contraindication and precautions
Evaluation
erosions of the nasal mucosa.
Monitor patient’s response to the drug, the
These following conditions need precautions-
adverse effects and the effectiveness of comfort
narrow angle glaucoma, hypertension, diabetes,
measures employed
thyroid diseases, and CAD because these
Decreased allergic symptoms conditions may be aggravated by the sympathetic
activity.

78
Topical Decongestants
Pharmacodynamics: the drug effects
Local effects- local stinging and burning, erosions
and ulceration if used for prolonged time.
If used for more than 5 to 10 days, rebound
congestion can occur, also called rhinitis
medicamentosa. The reflex reaction to
vasoconstriction is a rebound vasodilatation as
the drug effect wears off.
Sympathomimetic effects= tachycardia,
hypertension, urinary retention.
Topical Decongestants
Nursing Responsibilities
Teach the patient the proper administration of the
drug to ensure therapeutic effect.
The patients must clear the nasal passages first
before use; tilt the head back when applying and
keep tilted for a few seconds after administration
Emphasize that the drugs should NOT be used for
more than 5 to 10 days and to seek medical
attention if symptoms persist.
Topical Decongestants
Provide safety measures if dizziness or sedation
occur to prevent injury
Institute other measures to help relieve
discomfort of congestion like humidity, increased
fluid intake, cool environment and avoidance of
smoking
Anesthetics
Pharmacology in Nursing
Anesthetics
Anesthetics are drugs that are used to cause
complete or partial loss of sensation.
The numerous anesthetics can be broadly
classified as :
General
Local anesthetics
Anesthetics
General anesthetics
are central nervous system depressants used to
produce loss of pain sensation and
consciousness.
Anesthetics
Local anesthetics
are drugs used to cause loss of pain sensation
and feeling in a designated area of the body
without the systemic effects associated with
severe CNS depression
General Anesthetics
Produce the following effects:
analgesia (loss of pain sensation),
unconsciousness and
amnesia
General Anesthetics
Blockage of autonomic reflexes prevents
response of involuntary reflexes to injury to the
body that might compromise a patient’s cardiac,
respiratory, gastrointestinal and immune status.
Blockage of muscle reflexes prevents jerking
movements that might interfere with the success
of the surgical procedure.
Stages of Anesthesia Depth
Usually trained individuals with the special
equipments ready for life support administer the
agents
The patient undergoes through a predictable
stages known as STAGES of ANESTHESIA: 1 to 4
Stages of Anesthesia
STAGE 1
Referred to as the Analgesia Stage is loss of pain
sensation
with the patient still conscious and able to
communicate
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Stages of Anesthesia
STAGE 2- the Excitement Stage,
A period of excitement and often combative
behaviors are present such as restlessness, with
signs of sympathetic stimulation (tachycardia,
increased respiration and blood pressure
changes)
Stages of Anesthesia
STAGE 3
Surgical Anesthesia stage, involves relaxation of
skeletal muscles, return of regular respiration,
and progressive loss of eye reflexes and pupil
dilatation.
This is the best stage for surgical procedure.
Stages of Anesthesia
STAGE 4
Medullary Paralysis stage is a very deep CNS
depression with loss of respiratory and
vasomotor center stimuli in which death can
occur rapidly.
General Anesthesia
INHALATIONAL (gas and volatile liquid)
Halothane
Enflurane
Nitrous oxide
INTRAVENOUS
Barbiturates (Thiopenthal and Methohexital)
Ketamine
Profofol
General Anesthetics
Action of General Anesthetics
The mechanism is not clear. It is known that
depression of the reticular activating system and
the cerebral cortex occurs.
Therapeutic use of General Anesthetics
Sedation and anesthesia for surgical procedures
General Anesthetics
The anesthetics are administered by trained
personnel
Maintain equipment on standby to provide airway
and mechanical ventilation in cases of severe
drug reaction
Monitor temperature regularly, monitor pulse, BP
and respiration
Carefully monitor patient in the recovery room
until he regains consciousness and able to
communicate
Provide safety and comfort measures.
Pre-operative teaching must be provided and
information about the anesthetics should be
incorporated in the teaching plan.
Local Anesthesia
Local anesthetics are drugs that cause a loss of
sensation in limited areas of the body to abolish
pain.
They are powerful nerve blockers injected locally.
Systemic absorption of the anesthetics can
produce numerous side effects.
Local Anesthesia
Administering Local Anesthetics
There are five types of local anesthetic
administration- topical, infiltration, field block,
nerve block, and IV regional anesthesia.
Topical Administration- anesthetic agents are
incorporated in vehicles such as creams,
ointments, gels, lotions, drops and sprays.
Infiltration- this involves injecting the anesthetic
directly into the tissues to be treated.
Local Anesthesia
Field block – involves injecting the anesthetic
agents al around the area that will be affected by
the surgical operation.
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Nerve Block- involves injecting the anesthetic
agents at some point along the nerve that runs to
and from the region of operation. One example is
epidural anesthesia.
Intravenous regional Anesthesia involves
carefully draining all of the blood from an arm or
leg, securing a tourniquet to prevent the aesthetic
from entering the
Local Anesthesia
Examples of Local anesthetics: The “CAINES”
Lidocaine
Dibucaine
Procaine
Tetracaine
Local Anesthesia
Local anesthetics work by causing a temporary
interruption in the production and conduction of
nerve impulses.
They affect the permeability of sodium
(preventing it from entering the cell) and chloride
(by entering the cell).
The nerve cells become more negative, with
resultant decrease in depolarizationà no
transmission of pain
Local Anesthesia
These agents are used for infiltration anesthesia,
peripheral nerve block, spinal anesthesia and
relief of local pain.
Local Anesthesia
The side effects of local anesthetics
Local effects- local irritation and skin breakdown
CNS effects if systemic absorption occurs-
headache, restlessness, anxiety, dizziness,
tremors and blurred vision.
GI system- nausea, vomiting
Cardio- arrhythmias, peripheral vasodilation,
myocardial depression, and rarely, cardiac arrest
Local Anesthesia
Nursing Responsibilities
Maintain emergency equipment on standby to
provide life-support in cases of severe reactions
Ensure that drugs are available for managing
hypotension, cardiac arrest and CNS alterations.
Provide adequate hydration to patients receiving
spinal anesthesia. Position the client supine for
up to 12 hours after spinal anesthesia to minimize
spinal headache
Local Anesthesia
Nursing Responsibilities
Provide safety and comfort measures such as
side-rails up, frequent skin care and supportive
care
Give health teaching to explain things the patient
needs to know to allay fears.
Muscle Relaxants
Pharmacology in Nursing
Overview
Skeletal muscle relaxants are drugs that decrease
muscle tone and movements by reducing skeletal
muscle activities
Types of Relaxants
Central acting: Baclofen, Chlorphenesin,
Chlorzoxazone
Peripheral Acting: “Curium” and “curare”
Direct acting: Dantrolene
Central Acting Relaxants
These agents DEPRESS the CNS or BLOCK the
transmission of nerve impulses from the spinal
cord to the skeletal muscles
The result is muscle relaxation
Peripheral Acting Relaxants
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These agents interfere with nerve transmission
between the motor end plate and the skeletal
muscle receptors
These agents block the DEPOLARIZATON and
REPOLARIZATION activity of the skeletal muscles
leading to PARALYSIS
BACLOFEN (Lioresal)
Pharmacodynamics: inhibits the synaptic reflexes
at the SPINAL cord
The action does not reduce consciousness
This is prescribed for the treatment of spasticity
and muscle sprain; also as adjunct to physical
therapy
BACLOFEN (Lioresal)
Kinetics: absorbed orally, excreted in the feces
and kidney.
Thus drug is very lipophilic that can pass the
brain barrierà drowsiness
BACLOFEN (Lioresal)
Side-effects:
CNS: Drowsiness, dizziness and confusion
CVS: Hypotension, bradycardia
GU: Urinary frequency and impotence
BACLOFEN (Lioresal)
Nursing Responsibilities:
Avoid the use together with alcohol
Perform a baseline mental status examination
Supervise any ambulation and transfers to ensure
safety
Monitor blood pressure
Check deep tendon reflexes for any symptom of
toxicity
BACLOFEN (Lioresal)
Evaluate for effectiveness of the drug
The client displays evidence of increased range of
motion exercise
Decreased spasticity
Dantrolene
Pharmacodynamics: this agent acts DIRECTLY on
skeletal muscle to interfere with CALCIUM release
from the sarcoplasmic reticulum
This is useful in conditions like: MALIGNANT
hyperthermia and spastic conditions like multiple
sclerosis, spinal cord injury and CVA
Dantrolene
Kinetics: absorbed orally, can be given IV,
excreted in kidney
Dantrolene
Side-effects:
CNS: muscle weakness, drowsiness and dizziness
CVS: tachycardia an phlebitis
GIT: HEPATITIS
GU; Urinary frequency, hematuria and retention
Dantrolene
Nursing Responsibility
Note that this drug is not used if patient has liver
dysfunction as hepatitis can occur
Peripheral Acting Relaxants
Usually group into: NON-DEPOLARIZING and
DEPOLARIZING agents
NON-DEPOLARIZING are COMPETITIVE agents
that BLOCK acetylcholine receptors
DEPOLARIZING agent excites the muscle initially
then prevents the muscle from contracting
Peripheral Acting Relaxants
Non DEPOLARIZING Agents:
Atracurium besylate
Pancuronium
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Rocuromium Administered IV, relaxation occurs in 1 minute
and lasts for 6 minutes
Vecuronium
COMPUTATIONS
Tubocurarine
Oral Medications: Solids
DEPOLARIZING
Quantity of Drug =
Succinylcholine
Desired dose/Stock dose
Peripheral Acting Relaxants
(D/S = Q)
General indications:

Adjunct to general anesthesia

Oral/Parenteral: Liquids
Muscle relaxation during surgery, mechanical
ventilation and orthopedic manipulation Quantity of Drug =

Peripheral Acting Relaxants Desired dose

Side effects --------------------- X Dilution

Respiratory depression Stock dose x

Muscle weakness (D/S x dilution = Q)

Cardiac arrhythmias

Hypotension
IV Fluid Flow Rate
Peripheral Acting Relaxants
gtts/min
Nursing Responsibilities
Vol. in cc x gtt factor
Note that paralysis occurs from head to toe and
----------------------------
recovery starts from toe to head
no. of hours x 60 mins.
Monitor the BP and respiratory status frequently
IV Fluid Flow Rate
Note that consciousness in NOT affected
cc/hr
Peripheral Acting Relaxants
Vol. in cc
Evaluate for drug usefulness
-------------------------
The client will maintain skeletal relaxation without
respiratory depression
no. of hours
Peripheral Acting Relaxants
IV Fluid Flow Rate
Succinylcholine
Duration in hours
A depolarizing agent that prolongs the
Vol. in cc
depolarization of the muscle end plate
-------------------------
Used as muscle relaxant during surgery,
intubation and short procedures cc/hr

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Conversion of Temp

o
C to oF

(oC x 1.8) + 32

o
F to oC

(oF – 32) (.55)

THANK YOU.

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