NURSING ▪ Phase II

• Testing the drug to

PHARMACOLOGY
volunteered patients
o Free
o They are willing
By Dra. Elenita Arreglo (Mommy Doc) to take down
the effects of
PHARMACOLOGY drug injected
• Study of biological effects of chemicals o Matagal at
magastos
Nursing Pharmacology gawin
• Refers to PHARMACOTHERAPEUTICS ▪ Phase III
o We only study those drugs that we used • Mass clinical trial
to: o Pag nakapasa
▪ Curative → Market
▪ Diagnose • Thousands of patients
▪ Prevent Diseases ▪ Phase IV
• Post marketing
Sources: evaluation
• Natural Sources o Pag labas sa
o Includes: market → 3
▪ Plants – ONE OF BEST names given
SOURCE ▪ Chemical
▪ Animals ▪ Generic
▪ Microorganisms / Microbes = ▪ Brand
Wherein the vaccines are made Thalidomide
▪ Minerals – Iron, aluminum, o 1950s – 1960s
silver, gold o Morning sickness
• Synthetic Sources ▪ Women developed phocomelia
• Biosynthetic • Putol ang kamay, paa
o Combination of Natural and Synthetic o Tanggal sa Market = ORPHAN DRUG
▪ Tinanggal sa market para pag
aralan ulit → no longer an
Drug Evaluation orphan drug → become an
• Clinical Trials ANTI-CANCER DRUG
o Pre-Clinical Trial – Test the drug to an
living being = rabbits, rats Drug Names
o Highly toxic – bad results / namatay • Chemical Name
yung animal = REJECTED o L Thyroxine
o Teratogenic – Adverse effect = ▪ Thyroid hormone replacement
REJECTED • Generic Name
▪ Phase I o Levothyroxine
• Test to normal volunteer • Brand Name
young healthy men o Eltroxin
• Normal human beings
• Women is not allowed –
women have limited egg
cells
o Men – have Over the Counter (OTC) – Have adverse effects
lifetime sperm
cells
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Deduque, Mick Angelo
Prescribed drugs • Substances in this schedule have a high
• Yellow prescription – Controlled drugs potential for abuse which may lead to severe
o Narcotics psychological or physical dependence
• White prescription – Antibacterial drugs • License S2 – Control drugs
o Steroids • Examples of Schedule II narcotics include:
o hydromorphone (Dilaudid®),
ROUTES OF DRUG ADMINISTRATION o methadone (Dolophine®),
• Enteral o meperidine (Demerol®),
o Through GIT o oxycodone (OxyContin®, Percocet®),
▪ Oral and
▪ Sublingual o fentanyl (Sublimaze®, Duragesic®).
▪ Rectal • Other Schedule II narcotics include:
o Be specific not only Enteral o morphine,
• Parenteral o opium,
o Outside the GI Tract o codeine, and
o Injections o hydrocodone.
▪ IM • Examples of Schedule IIN stimulants include:
▪ IV o amphetamine (Dexedrine®, Adderall®),
▪ SQ o methamphetamine (Desoxyn®), and
▪ ID o methylphenidate (Ritalin®)
▪ Intrathecal – SPINE • Other Schedule II substances include:
▪ Intraarterial – through ARTERY o amobarbital,
that is supplying the tumor o glutethimide, and
▪ Intratracheal o pentobarbital
• Local
o Topical - SKIN Schedule III/IIIN Controlled Substances (3/3N)
o Inhalation • Substances in this schedule have a potential for
o Drops - EYES abuse less than substances in Schedules I or II
o Vaginal suppositories and abuse may lead to moderate or low physical
dependence or high psychological dependence.
US CONTROLLED SUBSTANCE SCHEDULES • Examples of Schedule III narcotics include:
Schedule I Controlled Substances products containing not more than 90 milligrams
• Substances in this schedule have no currently of codeine per dosage unit
accepted medical use in the United States, a o (Tylenol with Codeine®), and
lack of accepted safety for use under medical ▪ Combination of narcotic and
supervision, and a high potential for abuse non-narcotic
• Some examples of substances listed in Schedule o buprenorphine (Suboxone®)
I are: • Examples of Schedule IIIN non-narcotics include:
o heroin, lysergic acid diethylamide (LSD), o benzphetamine (Didrex®),
o marijuana (cannabis) o phendimetrazine,
o peyote, o ketamine, and
o methaqualone, and o anabolic steroids such as Depo®-
o 3, 4-methylenedioxymethamphetamine Testosterone.
(“Ecstacy”) ▪ For muscle gaining

Schedule IV Controlled Substances

• Substances in this schedule have a low
potential for abuse relative to substances in
Schedule III.
Schedule II/IIN Controlled Substance (2/2N) • Examples of Schedule IV substances include:
Anxiolytic Drugs
o alprazolam (Xanax®),
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Deduque, Mick Angelo
 o carisoprodol (Soma®), ▪ Absorption – Activated
o clonazepam (Klonopin®), Charcoal in poisoning
o clorazepate (Tranxene®), • Charcoal attract the
o diazepam (Valium®), poison
o lorazepam (Ativan®), ▪ Mass of the Drug – Bulk
o midazolam (Versed®), laxatives like psyllium
o temazepam (Restoril®), and • For constipation →
o triazolam (Halcion®). initiates peristalsis
• Obstipation – Severe
Schedule V Controlled Substances constipation
• Substances in this schedule have a low potential ▪ Osmotic Property
for abuse relative to substances listed in • Osmotic Diuretics –
Schedule IV and consist primarily of preparations Mannitol → They attract
containing limited quantities of certain narcotics. water → actions to
• Examples of Schedule V substances include: kidneys
cough preparations containing not more than 200 • Osmotic Purgatives –
milligrams of codeine per 100 milliliters or per Magnesium Sulphate →
100 grams will attract water
o Robitussin AC®, o By chemical interaction
▪ Need prescription ▪ Antacids
o Phenergan with Codeine®), and • BEST EXAMPLE
▪ Best anti coughing effect • Neutralize acidity
o Ezogabine o HCl → activates
protein enzymes
PHARMACODYNAMICS → protect our
• Basic actions / effects of drugs in the body stomach from the
o To replace a missing substance entry of H. Pylori
▪ Thyroid Hormone Replacement • DO NOT TREAT GERD,
o To increase cellular activities and etc
▪ Increases HR • LIQUID FORM- Best type
o To depress cellular activities of antacid
▪ Decreases HR • TABLET FORM – must
o To interfere with the growth of foreign be chewed with 1 full
cells glass of water
▪ Chemotherapeutic Drugs – Kill
• 1-3 hours after meals
foreign cells
o 30 mins – 1 hour =
• Microbes considered
• cancer cells • 3x a day
• Virus • Many drug absorption if
• Drug actions maybe affected by antacid
o Through ion channels o Tetracycline
▪ Examples: o NSAIDs
• Calcium channels o Steroids
o If calcium cannot ✓ Hindi sila pwedeng
enter the cell → sabay → it should be
make it a channel 2 hours apart
• Sodium channels o By altering metabolic process
• Gaba Gated Chloride ▪ Chemotherapeutic Drugs
channels • Antimicrobial Drugs
• Antineoplastic Drugs
o By physical action
3|P a g e
Deduque, Mick Angelo
 1. Interfere with DNA / RNA synthesis
in the foreign cell
2. They interfere with the protein
synthesis of the foreign cell
3. They both interfere with the use of
folic acid for their growth
Anticancer drug = Methotrexate
Antibacterial drug = Cotrimoxazole
o Through receptors – exclusive for
Acetylcholine
▪ Agonists
o Mimic the action of
acetylcholine to
stimulate contraction
o Stimulate cholinergic
recptor
▪ Antagonists
o Competitive Antagonist
o Non Competitive
Antagonist
▪ They do not
compete to same
receptor site
▪ This chemical
have its own
receptor that
blocks the
neurotransmitter
o Blockers
▪ Block the
cholinergic
receptor
▪ Relaxes muscle
o Anticholinergic drug
Neuromuscular Junction → transmit
impulses (chemical in nature) →
neurotransmitter (acetylcholine) nasa
loob ng nerve → release acetylcholine
→ binds with the receptor → impulse
transmitted → stimulate muscle to
contract → acetylcholine removed by an
enzyme (acetylcholinesterase) →
muscles relaxed → acetylcholine
released → contract → removed →
relaxed.
Deduque, Mick Angelo
Lock and Key theory
• Configuration of acetylcholine and its receptor
compliment to each other like a lock and a key
Cholinergic receptor
• Acetylcholine
o Through enzymes and pump
AUTONOMIC DRUGS
❖ Parasympathetic
o Acetylcholine – ONLY CHEMICAL IN
PNS = Cholinergic receptor
▪ Cholinergic agonist =
PARASYMPATHOMIMETIC
DRUGS
• Stimulate PNS effects
▪ Cholinergic antagonist =
PARASYMPATHOLYTIC
DRUGS
• Blocks PNS effects
❖ Sympathetic
o Acetyl, epi, norepi = Adrenergic receptor
▪ Adrenergic agonist =
SYMPATHOMIMETIC DRUGS
• Stimulates SNS
o Same effect with
Parasympatholytic
▪ Adrenergic Antagonist =
SYMPATHOLITYC DRUGS
• Blocks SNS effect
o Same effect with
Parasympathomim
etic
4|P a g e
CHOLINERGIC RECEPTOR • Antagonist →
2 types: decreased HR
1. Nicotinic Receptors – nmj, cns, ans and contractility
2. Muscarinic Receptors – ans ▪ Located at Kidneys
• Agonist →
Examples: release of renin
1. Cholinergic agonists – Para-mimetic o Beta 2
o Pilocarpine eye drops -miotic ▪ Located at lungs
▪ Pupil constrict → open angle → • Agonists →
flow aqueous humor → bronchodilate
decrease IOP • Antagonist →
2. Anticholinergic – Para-lytic bronchoconstrict
o Atropine Sulfate ▪ Located at smooth
▪ Antidote for Cholinergic crisis muscles of the uterus
▪ Eyedrops → mydriatic → preop ▪ Liver → increase
anesthesia → severe glucogenesis
bradycardia → antidote for o Beta 3
cholinergic crisis ▪ Located at the adipose
tissues = Responsible
ADRENERGIC RECEPTORS for thermogenesis
2 types:
1. Alpha ADRENERGIC DRUGS
• 2 subtypes 1. Adrenergic Agonist - Sympa-mimetic
o Alpha 1 • Epinephrine,
▪ is located in the blood vessel • Norepinephrine
• agonist = vasoconstrict; • Dobutamine
vasodilate (antagonist) • Dopamine
▪ Also located at urinary bladder 2. Alpha 1 agonist → Blood vessels →
• urinary retention vasoconstriction of normal BV
(agonist); urinary • Phenylephrine
emptying (antagonist) • Pseudoephedrine
▪ Also located at the iris o Decongestants
• mydriasis (agonists); ▪ Gamot sa sipon
miosis (antagonist) ▪ Bawal sa HTN
o Alpha 2 3. Alpha 2 agonist – decrease SNS → Decrease
▪ Located in the CNS BP
• Agonist → decrease • Clonidine (catapres)
norepinephrine flow (ito o Centrally acting to HTN drugs
lang ang agonist ang 4. Beta agonists
nagdedecrease ng • Isoproterenol
Sympha)
• Salbutamol
• Antagonist → increase o Short-Acting Beta Agonist
norepi flow (SABA)
2. Beta o Best route: INHALATION
• 3 subtypes • Terbutaline
o Beta 1 o Long-Acting Beta Agonist
▪ Located at the heart (LABA)
• Agonist → 5. Beta-Blockers
Increase HR and a. Beta1 / 2
contractility • Propranolol

5|P a g e
Deduque, Mick Angelo
 b. B1 Blockers o Mono-amine Oxidase
• Metoprolol ▪ Enzyme inhibits 4
• Atenolol neurotransmitters
• Nebivolol o Mono-amine Oxidase Inhibitor
▪ Inhibits MAO
DRUG – ENXYMES INTERACTION ▪ Antidepressant drug
NMJ → Acetylcholine → Muscle contraction →
Actylecholine removed by Acetylcholinesterase Depression – extreme feeling of sadness
• Prolonged
Acetylcholinesterase – Chemical • S / sx
• Drug = inhibit the enzymes → retain • Explained by Biogenic Amine Theory
anticholinesterase → Myasthenia gravis → o Decreased:
destroy receptors ▪ Norepi
o Diagnostic: Tensilon (Brand name) ▪ Dopa
anticholinesterase → retain → improve ▪ Sero
muscle function → Positive: temporary o Management
improvement muscle function a. should increase NT →
▪ Short-acting administer MAOI → retain NT
• Cholinesterase inhibitors (anticholinesterase) ▪ Avoid: tyramine food →
• Long Acting anticholinesterase: onset 20- will extremely increase NT
30mins and last for 4-6 hours → develop Hypertensive
o Neostigmine Crisis
o Physostigmine b. Inhibit reuptake
o Pyridostigmine 1. Tricyclic Antidepressant
(TCA) → inhibits reuptake
Compliance: of Norepi, dopa, sero
• Overdose: increase acetylcholine → • Impramine
increase pns response → diarrhea → Adverse Effects:
incontinence “CASH”
o Cholinergic Crisis → tensilon • Cardiovascular
→ temporary worsening effects
• Underdose → decrease acetyl → • Anticholinergic
decrease pns response effects
o Both not have therapeutic effect • Sedation
o Both have muscle weakness o
Acetylcholine in CNS • Hypotension –
• Synapse → Hippocamus Orthostatic
o Alzheimer’s disease Hypotension
▪ Anticholinesterase 2. Selective Serotonin
▪ Drugs = retain acetylcholine Reuptake Inhibitor (SSRI)
• Rivastigmine → Increase Serotonin
• Donepezil • Fluoxetine
• Tacrine (Prozac)
• Setraline (Zoloft)
Neurotransmitters Adverse effects:
• Epi • Mild CNS
• Norepi Amine
symptoms
• Dopamine Neurotransmitter like
• Serotonin headache,
lethargy,
insomnia

6|P a g e
Deduque, Mick Angelo
 POTENCY

Amine neurotransmitter → removed by

MAO → reuptake (babalik sa neuron)

PUMP INHIBITORS AND REUPTAKE INHIBITORS

Parietal cells → produces HCl by releasing through
pump → when the histamine 2 bind with the parietal cells
to release HCl
• Seen when you compare the diff drugs
• We attain 50% response
Histamine 1 – Allergies
Histamine 2 – releasing HCl → bind with the parietal • Drug with the lesser dosage but similar effect
cells • The lower the dosage, the lesser side effects
• H2 receptor antagonist (3-4 months)
o Ranitidine
o Cimetidine EFFICACY
o Famotidine
o PPI – DOC for Peptic Ulcer Disease (4-6
weeks)
▪ Omeprazole
▪ Esomeprazole
▪ Pantoprazole
Histamine 3 - vertigo

• Attaining the maximum response

DOSE RESPONSE CURVE
• Lower dosage but attaining the maximum
response
• Lower dosage but similar effects

DOSE – RESPONSE RELATIONSHIP

• Therapeutic Index
o Ratio between toxic dose of 50% and
Effective dose
• The higher the concentration dosage of the drug, ▪ The wider the therapeutic index,
the higher the response up to the maximum the safest
effect ▪ The narrow the T.I, the narrow
margin of safety / dangerous

7|P a g e
Deduque, Mick Angelo
PHARMACOKINETICS • Potent drugs – New generation drug than can
pass to first pass metabolism but have the
same response

• Bioavailability
o The fraction of the drug that reaches the
systemic circulation following
administration by any route
• Movement of drugs in the body ▪ Kahit pareho sila ng generic
name, magkaiba sila ng
FACTORS AFFECTING ABSORPTION bioavailability
• From the site to blood ▪ Branded drugs is more high
o From GIT to the blood bioavailability than cheaper
o From skin to the blood drugs
• If no absorption, the faster the effect
1. Disintegration and Dissolution Time DISTRIBUTION
• Capsule gel – more faster absorption • Transfer of drug from the blood the drug moves
than tablets to different tissues / storage / site of action
2. Formulation
• The many formulas, the heavy molecular Factors Affecting Drug Distribution
weight → the less absorption 1. Blood flow
3. Particle Size o The slower the blood flow, the slower the
• The bigger particles, the less absorption distribution
4. Lipid Solubility 2. Protein Binding
• The more lipid solubility, the more o Albumin – main protein in the body
absorption 3. Lipid solubility
5. PH and Ionization 4. Blood brain barrier
• Ionization 5. Placenta & Breast Milk
o Combination of drug with an ion o Pregnancy and lactation are not absolute
o Unbound = free contraindication to drug therapy, just
• pH relative
o Acid to acid environment ▪ Allergy – is the ONLY ABSOLUTE
o Alkaline to alkaline environment CONTRAINDICATION
6. Area & Vascularity of the absorbing surface o Gestational DM – DM during
• Men are more better absorption through pregnancy
IM due to move muscles developed than o Diabetic Pregnant – DM before
Women pregnancy
7. Gastrointestinal Motility ▪ Insulin – BEST DRUG FOR DM
8. Presence of Food • Cannot pass to placenta and
• Ferrous sulfate will not have effect to fetus
• Erythromycin • Route: SQ → to prevent
lipodystrophy → erratic
• Anti TB drugs
absorption
o Before meals with one full glass
of water due to toxicity • Afreeza = INHALATION
INSULIN
FIRST PASS METABOLISM / FIRST PASS EFFECT • Oral Insulin = will destroy in
• The drug metabolized first before distributed in GIT
site of action ▪ Lactating DM
• Seen those drugs taken through GI tract • Insulin: DOC
o Can pass the
• GIT → Portal vein → Liver → Hepatic vein →
breastmilk → the
Inferior Vena Cava → Heart → Liver
baby will suck /
8|P a g e
Deduque, Mick Angelo
 breastfeed → the HALF LIFE
baby will destroy • The time it takes for the drug to reduce to half
insulin in his GIT from the peak level it previously achieved
o 100 mg after 6 hrs → 50 mg after 6 hrs
BIOTRANSFORMATION → 25mg → 12.5mg → 6.25mg
• Biochemical alterations of drugs in the body o Phenobarbital = 79 hours
o Antidepressant – 2-3 weeks
• Therapeutic Level
o The concentration of the drug to
achieved its therapeutic effect
o Critical concentration
▪ Binibigay ang medication ng
• Cytochrome P450 Enzymes tamang oras para mamaintain
o Responsible for biotransformation / ang critical concentration dahil
metabolism of drugs bumababa ito due to half life
• Transfer the drug to another chemical o Loading dose – Higher dose given
• Metabolism in LIVER initially
• The drug is converted to another form o Underdose – Below critical
o Active drug → ,Active metabolite → concentration
Exert action → Need to inactive o Overdose – Beyond critical
concentration
Factors affecting Biotransformation
1. Genetic variations TOXICOLOGY
o G6PD Deficiency = Kulang sa enzymes • Harmful effects of drugs
o Glucose 6 Phosphate • Paracelsus
Dehydrogenase o The father of modern pharmacology
▪ Responsible for o “All drugs are potentially risky”
metabolizing food • Adverse Drug Reaction
▪ Responsible for RBC o Any response to drug that is noxious an
membrane stability unintended and that occurs at doses use
• Magpuputukan = in man for prophylaxis, diagnosis, and
HEMOLYTIC therapy.
ANEMIA → • Pharmacovigilance
Manifestation: o Branch of Pharmacology that continuous
JAUNDICE study of drugs
2. Environmental Pollutants 1. Side Effect
o Chronic smoking – increase metabolism • Effect other than the therapeutic
of drug effect
3. Age • Not really harmful
4. Diseases of the Liver o Drowsiness
o Nausea and Vomiting
EXCRETION 2. Toxic Effect
Removal of drugs to the body • Harmful effect of drugs
= KIDNEYS – MAIN ORGAN OF EXCRETION DISCONTI
• Renal Excretion 3. Intolerance
• Fecal and biliary excretion • Inability of the patient to tolerate
• Pulmonary excretion adverse effects of drugs
• Sweat and Saliva 4. Iatrogenic
• Treatment induce
o Phlebitis
5. Drug Dependence
• Addiction
9|P a g e
Deduque, Mick Angelo
 • Idiosyncrasy TYPE I HYPERSENSITIVITY
o Rare and Bizarre adv effect of drug
• Hypersensitivity
o Allergy – absolute contraindication of
drug therapy
▪ Immune system is the problem
• Sees the drug as
antigen – protein that
stimulates antibody
formation
• Primary Adverse Effect
o Is the effect when you overdose the drug
▪ Hypotension • Most common type of Hypersensitivity
▪ Hypoglycemia • Basophil – Only WBC that not capable to
• Secondary Adverse Effect phagocytosis
o Side effect • Mast Cells – Release Histamine and Heparin
o Toxic effect o Histamine – Promotes ALLERGIC
o “Other effect” REACTION
• Hypersensitivity
o Allergy
TYPE II CYTOLYTIC REACTION
Example of Adverse effect:
1. Antibacterial drugs
a. GIT Toxicity
b. Superinfection
2. Anticancer drugs – labile cells – rapidly
regenerating (mabilis dumami)
a. Alopecia
b. Bone marrow suppression
i. RBC – 120 days
ii. Platelets – 10 days • Antibodies are in the WBC
iii. WBC – 2-3 days
c. Nausea and vomiting TYPE III ARTHUS REACTION

Example of Nephrotoxicity
1. Gentamycin (aminoglycoside)
2. NSAIDs
3. Amphotericin B (antifungal IV)
Management:
• Assess
o Oliguria
o Increase BUN and Creatinine (azotemia)

Example of Hepatotoxicity
1. Paracetamol
2. Anti TB drugs • Antibodies are in the blood vessels
Management: • Cause severe inflammatory response
• Assess
o Jaundice
o Increase ALT, AST

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Deduque, Mick Angelo
TYPE IV HYPERSENSIVITY FDA Pregnancy Categories
CATEGORY RISK EXAMPLES
A Adequate and well- Doxylamine
controlled studies Folic Acid
have failed to Levothyroxine
demonstrate a risk
to the fetus in the
first trimester of
pregnancy (and
there is no evidence
of risk in later
trimesters)
• Delayed type of hypersensitivity
o Antibody → will go to lymph node → will Both animals and
present first → before human have no side
effect
STEVEN JOHNSON SYNDROME B Animal reproduction Amoxicillin
studies have failed to Loratadine
demonstrate a risk to Ondansetron
the fetus and there
are no adequate and
well-controlled
studies in pregnant
women

Animals have no
adverse effect, but
TOXIC EPIDERMAL NECROLYSIS no test in pregnant

Relatively safe
C Animal reproduction Fluconazole
studies have shown Metropolol
an adverse effect on Sertraline
the fetus and there
are no adequate
and well-controlled
studies in humans,
but potential
benefits may
warrant use of the
drug in pregnant
TERATOGENICITY women despite
• Effects of drugs to the developing fetus potential risks
• Example:
o Thalidomide Chloramphenicol Adverse effect in
▪ Gray baby syndrome animals but no
o Tetracycline studies in human
▪ Bone and teeth abnormality
Benefits are higher
than risk
D There is positive Lisinopril – ACE
evidence of human inhibitor
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Deduque, Mick Angelo
 fetal risk based on Lithium Age in years = Young’s rule
adverse reaction Phenytoin o Pedia dose = age in years x ave adult dose
data from Age in years +12
investigational or Weight in pounds = Clark’s rule
marketing o Pedia dose = wt in pounds x ave adult dose
experience or 150 pounds
studies in humas, Dosage Formula
but potential o D/S x V = A
benefits may o Desired Dose
warrant use of the o Stock dose
drug in pregnant o Volume
women despite o Amount given per dose
potential risks
Flow rate
Ibibigay mo yan kasi a. Ml/hr
the benefits higher o Volume in ml / no. of hours
than the risk kahit b. Ml/minute
may positive o Volume in ml x drop factor
evidence Hours x 60 minute

We don’t treat 1. What is the pediatric dose of a 7 year old child if

cancer in pregnancy the average adult dose is 130 mg? = 48mg
X Studies in animals Methotrexate 2. What is the pediatric dose of a 20 pound child if
or humans have Simvastatin the average adult dose is 200 mg? = 26mg
demonstrated fetal Warfarin 3. What is the pediatric dose of a 9 month old child
abnormalities and/or if the average adult dose is 100mg? = 6mg
there is positive 4. Doctor’s order: Ampicillin1 gram IV ANST to be
evidence of human given initially then 500 mg IV every 6 hours.
fetal risk based on Available Ampicillin is 500 mg powder to be
adverse reaction dissolved in 2ml of distilled water. What is the
data from amount to be given initially? = 4ml
investigational or 5. Doctor’s order: Amoxicillin to be given at
marketing 30mg/kg/day TID. Weight of the patient is 22
experience, and the pounds. If the available Amoxicillin is 125mg/5ml.
risks involved in What is the amount of Amoxicillin to be given per
use of the drug in dose? = 4ml
pregnant women 6. Doctor’s order: Cefepime 30mg/kg/dose BID.
clearly outweigh Weight of the patient is 10 kg. If the available
potential benefits. Cefepime is 125mg/5ml. What is the amount of
Cefepime to be given per dose? = 12ml/dose
Ekis talaga 7. Prepare a 45% of 250 ml feeding solution. How
much feeding solution and water be mixed?
Both animals and ( All feeding solution has 100% strength)
humans have 8. 1.5 liters of IVF to be given for 12 hours. What is
adverse effect the flow rate in ml/hr? = 125ml/hr
9. 2 liters of IVF to be given for 20 hours. At the end
COMPUTATION of the second shift, how much fluid is left? =
Formula: 400ml
• Pediatric dose calculations 10. 500 ML of IVF to be given to a pediatric client for
Age of child in months = FRIED’s RULE 8 hours. If the drop factor is 60ugtts/ml. What is
o Pedia dose = age in months x ave adult dose the flow rate of IVF in ugtt/min? = 62 – 63
150 months ugtt/ml

12 | P a g e
Deduque, Mick Angelo
 11. 1.5 L of IVF to run at a rate of 20 gtts/min, If the
drop factor is 15 gtts/ml, how long do you infuse a. Thiopental (Pentothal)
the IVF?.= 18 – 19 hrs b. Methohexital (Brevital)
2. Non-Barbiturate Anesthetics – More potent
and efficacious
NEUROPHARMACOLOGY a. Midazolam
• Anesthetics b. Droperidol
• Muscle Relaxants c. Ketamine
d. Propofol – controversial drug = ginamit kay
Michael Jackson
GENERAL ANESTHESIA 3. Anesthetic Gases – Laughing gas
a. Nitrous Oxide (Blue Cylinder)
Balance Anesthesia b. Cycloppropane (orange)
• Goals in administering general anesthesia c. Ethylene (Red cylinder)
o Analgesia 4. Volatile Liquids
o Unconsciousness a. Halothane (Fluothane)
o Muscle relaxation b. Desflurane (Suprane)
o Amnesia c. Enflurane (Ethrane)
• Given by Anesthesiologists d. Isoflurane

Stages of Anesthesia LOCAL ANETHESIA

• Stage 1 • Lahat ng local anesthetic drug have the same
o The analgesia stage, Patient still MOA = CLOSE ALL SODIUM CHANNELS IN
conscious THE NERVES
▪ Numb 1. Topical Administration
• Stage 2 2. Infiltration
o The excitement stage, sympathetic 3. Field Block
stimulation o Cataract extraction
• Stage 3 4. Nerve Block
o Surgical Stage o Regional
▪ Kailangan mamaintain ng o Spinal
anesth an surgical stage
▪ Hanggang Surgical stage lang = Bakit bawal magpabunot ang may HTN?
COMA Lahat ng anesthetic drug may kasamang epinephrine →
• Stage 4 vasoconstriction → local anesthetic will stay in the
o Medullary Paralysis area and enhance its effectiveness

Administration of General Anesthesia Antiseizure Drugs

1. Induction • CNS depressants
• Giving IV meds • MOA: Close all sodium channels in the brain
2. Maintenance impulses
• Gases / Volatile 1. Electrical in nature
o Mabilis ang effect and mabilis 2. Chemical in Nature = Neurotransmitters
mawala a. Excitatory = Promotes impulse
3. Recovery transmission
i. Acetylcholine
• Side-lying position – Prevent aspiration
ii. Epinephrine
iii. Norepinephrine
Types of General Anesthesia
iv. Glutamate
1. Barbiturate Anesthetics – Increase GABA
b. Inhibitory = Blocks impulse
effect
transmission
Adverse Effect: CNS Depression
13 | P a g e
Deduque, Mick Angelo
 i. GABA ▪ Muscle Spasm → Injury of the
ii. Serotonin muscle → inflammation → pain
iii. glycine → will go the lower motor
neuron → reflexes occurs →
Examples of Local Anesthesia muscle spasm →
1. Benzocaine vasoconstriction → muscle
2. Procaine ischemia → Injury → cycle /
3. Bupivacaine paulit ulit
4. Lidocaine • Indication: To relieve
5. Ropivacaine the pain; to stop the
6. Dyclonine cycle; prevent further
injury to the muscle
NMJ BLOCKING AGENTS o Corticospinal tract
• Muscle Relaxant o Pyramidal tract
• Non Depolarizing ▪ Extrapyramidal Tract –
o No impulses → No Muscle Contraction Movement disorders →
• Use for general Anesthesia Extrapyramidal Symptoms
• Use for patients “Who fights” in mechanical (EPS)
ventilation o Basal Ganglia
o Humihinga ang pt and humihinga ang ▪ Responsible for:
mech vent → Naglalaban → we need to • Fine motor
paralyze the respiratory • Coordination
• “Curare” - plant • Muscle control
1. Atracurium o Cerebellum - Balance
2. Pancuronium
3. Tubocurarine
4. Vecuronium 1. Centrally Acting Muscle Relaxants
• Depolarizing NMJ Blockers o Suppress the motor neurons → no
o Succinylcholine impulse transmission → Muscle relax
▪ Prior to Electroconvulsant o CNS depressants
Therapy (ECT) → to prevent o Pag ang problema ay sa
fracture during convulsions muscle, CNS ang problem and
o May impulse transmission vice versa
o Muscle contraction → tetany → fatigue o preferably used to pts with muscle
→ relaxation spasm
o Bedtime – best time to give
MUSCLE RELAXANTS a. Baclofen (Lioresal)
• Spasmolytic Drug b. Orphenadrine (Banflex)
o Spasticity and Muscle Spasm c. Tizanidine (Zanaflex)
▪ Spasticity – Problem in d. Diazepam (Valium)
Pyramidal tract → Paralysis;
Matigas ang Muscle (e.g. Stroke 2. Direct Acting Skeletal Muscle Relaxants
patients) o Directly relax the Skeletal Muscle →
• Cause: Damage of the decrease calcium release → no calcium
upper motor neuron for contraction → muscle relax
• Indication of Muscle o Spasticity
Relaxant: a. Dantrolene (Dantrium)
To help in ROM exercises b. Botulinum Toxin A (Botox Cosmetic)
▪ Flaccidity → damaged the c. Botolinum Toxin B (Myobloc)
lower motor neuron →
malambot ang muscle

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Deduque, Mick Angelo
 3. Fixed Combination Skeletal Muscle Relaxants
o Muscle Relaxant + Pain Reliever Analgesic
a. Orphenadrine + Aspirin + Caffeine = • Narcotic
Norgesic o Action – CNS
b. Carisoprodol + Aspirin + Codeine = Soma o 3 types of Opioid Receptors ( all
Compound With Codeine located at the brain)
▪ Mu – causing analgesia
PAIN ▪ Delta
• Pain – unpleasant sensation that is both ▪ Kappa – central analgesia
PHYSICAL and EMOTIONAL due to injury o Adverse effects
o Only pain ▪ Respiratory depression
o Parietal lobe ▪ Mood alterations
✓ AT THE BEGINNING OF PAIN – Best time to ▪ Addiction / dependence
give pain medication ▪ Constipation
✓ PRN – you will give UPON YOUR ▪ Pupillary constriction
ASSESSMENT ▪ Cough Suppression
• Nociceptive o Indication: For severe pain
o Caused by tissue injury and ▪ Myocardial Infarction
inflammation ▪ Acute Pancreatitis
• Neuropathic Pain ▪ Cancer pain
o Caused by nerve damage ▪ Post op pain
o Classical pain due to trigeminal ▪ Post partum
neuralgia • Non Narcotic
• Cancer pain o Acetaminophen
• Non Malignant pain o Anti Inflammatory
• Acute pain
o Nadapa ka → inflammation Narcotics
o Naipit kamay mo sa pinto • Narcotic Agonists
• Chronic Pain o Tolerance – there is need to increase
o Rheumatoid arthritis the dose of drugs to be able to achieve
the same effect
Physiology of Pain o MI, Cancer pain
• Nociceptors – Free nerve endings o Goal: For terminally ill – no pain death
o Stimulated → parietal lobe → brain will o Don’t Give: Post op, post partum due to
release endorphins (enkephalins, many adverse effect
dynorphins, dynomorphins) → bind with a. Morphine
their receptors (analgesia) → PAIN ▪ Strong narcotic
RELIEF b. Codeine
▪ Opioid Receptor – receptor of ▪ Mild narcotic
endorphin c. Fentanyl
• Narcotics / Opiates – ▪ Strong narcotic
counteract with the d. Hydrocodone
opioid receptor ▪ Mild narcotic
▪ The more endorphins → e. Oxycodone
threshold of pain → minimum ▪ Strong narcotic
adaptation of pain f. Meperidine
▪ Tolerance → maximum amount ▪ Strong narcotic
of pain that a person can • Narcotic Agonist / Antagonist
tolerate o You stimulate other receptor for
• Sensory Nerve Fibers analgesic but you block some receptor
• Spinal Cord for adverse effects
o Good for: Post op, post partum
• Brain
15 | P a g e
Deduque, Mick Angelo
 a. Nalbuphine (nubain) ▪ Leukocytosis → releases more
b. Butorphanol (stadol) chemical mediators =
c. Pentazocine Interleukins → increase body
d. Buprenorphine temp = FEVER – sign of
e. Deocine systemic inflammation
• Narcotic Antagonist • Fever = Strong Immune
o NO ANALAGESIC EFFECT system pt → WBC
o ANTIDOTE for narcotic overdosed Activation
a. Naloxone (Narcan) • No fever =
b. Nalmefene immunocompromised
c. Naltrexone (common in elderly)

ACETAMINOPHEN
• Paracetamol → antipyretic effect → induce
sweating → releases heat → decrease fever ANTI INFLAMMATORY DRUGS
• Analgesic effect → decrease the sensitivity of 1. Aspirin – Inhibits prostaglandin synthesis
cells to pain sensation a. Analgesic
o For headache, dysmenorrhea, fever b. Antipyretic
• Has no anti-inflammatory effect c. Anti inflammation
o Rheumatoid arthritis • 300 – 600 mg / dose
o Osteoarthritis • Prostaglandin in the stomach – Barrier
▪ For acute osteoarthritis against corrosive effect of HCl
o To prevent ulcer
• Prostaglandin in kidneys – increase renal
INFLAMMATION blood flow
• Normal response of vascularized tissues to injury • Adverse effect
• Tissues with blood supply o Nephrotoxicity effect
o Naipit ka sa pinto → namaga → namula o Ototoxicity effect
= NORMAL RESPONSE
o Keratitis – Inflammation of cornea → 2. NSAIDs
namumuti ang cornea → risk for • Cox inhibitors
blindness o Cyclooxygenase → arachidonic
• Initial , transient and inconstant response acid → inhibits Prostaglandin
o Blood vessel = VASOCONSTRICTION a. Cox 1 Inhibitors
▪ Butas ang blood vessel → o Inhibit prostaglandin in ALL
lalabas ang blood → SITES (stomach, kidneys, etc)
vasoconstriction occur to stop o Aspirin like but more potent
bleeding and efficacious = BETTER
• Generalized Response DRUG than aspirin
o Tissues get injured: ▪ Mefenamic acid 250mg
▪ Vasodilation → Increase blood ▪ Ibuprofen 200mg
flow → redness = RUBOR; ▪ Naproxen 200mg
Increase heat = CALOR ▪ Diclofenac 25mg
▪ Increase capillary permeability o AFTER MEALS – Best time to
→ leak out fluid → edema, give
swelling = TUMOR b. Cox 2 inhibitors
▪ WBC activation → phagocytosis o Inhibit prostaglandin ONLY IN
= dead cells and injured tissues INFLAMMATION
→ inflammation chemical ▪ “coxib” drugs
mediators = PROSTAGLANDIN • Celecoxib -
→ pain = DOLOR celebrex

16 | P a g e
Deduque, Mick Angelo
 •Etoricoxib –
arcoxia
o For CHRONIC INFLAMMATION
▪ Rheumatoid arthritis
o Adverse effect
▪ Mild GI problems
▪ Discomfort
▪ Cardiotoxicity effect
o Valdecoxib
▪ Tinanggal sa market →
more people developed • Non Opioid
M.I because of o Mild to moderate pain
cardiotoxicity • Weak opioid
o Moderate to severe
3. Steroids – anti-inflammatory effect • Strong Opioid
• Glucocorticosteroid / Cortisol like steroids o Severe
a. Prednisone
b. Dexamethasone
c. Hydrocortisone
• Anti-inflam → suppress WBC function →
immunocompromised
• Increase glucose level
• Cause water retention
• Increase HCl acid secretion
o After meals – best time to give
• Risk for Cushing’s Syndrome
• Osteoporosis
• Not only for cancer patients but for CHRONIC
4. Gold Salts PAIN
• Use to pts with RHEUMATOID
ARTHRITIS only
o DMARDs – Disease Modifying
Antirheumatic drugs
• ADJUNT drug – relieving s/sx
o Methotrexate – also DMARD
• MOA: trapping macrophages → prevent
phagocytosis → decrease s/sx
o Auranofin
o Aurathioglucose
• Side effects:
o Metallic taste sensation
o Hepatotoxicity
o Bone Marrow Supression

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Deduque, Mick Angelo
 3. Paraldehyde (Paral)
o Old generation
SYSTEM PHARMA 4. Meprobamate (Miltown)
o Old generation
NEUROPHARMACOLOGY 5. Chloral Hydrate (Aquachoral)
• Sedative = hypnotic o Old generation
o Loss of awareness and reaction to 6. Antihistamines
environmental stimuli o Will increase drowsiness
o Hypnosis – extreme sedation results in ▪ Benadryl
further CNS depression 7. Buspirone (Buspar)
• Anxiolytic and Hypnotic Agents ( Minor o Promising Drug
Tranquilizers) o Less CNS depression effects
• Anxiety – feeling of tension, nervousness, o Anxiolytic drug
apprehension or fear that usually involves o No antiseizure effect
unpleasant reactions to a stimulus whether o No muscle relaxant
actual or unknown 8. Zolpidem (Stilnox)
• Reticular Action System o Hypnotic Drug
o Sleep and wake pattern o Causing psychological dependence
▪ Insomnia in anxiety – the
person with moderate to severe • Beta blockers
anxiety cannot create a sleep o Propanolol
▪ Insomnia in o To prevent tachycardia
o Limbic system – overall emotions and o For physical symptoms for pt with
behavior anxiety
1. Enhance GABA
2. Close the sodium channel = no impulses Antidepressant Drugs

Anxiolytic agents
1. Benzodiazepine – enhance GABA sa limbic
system and RAS
a. Diazepam (Valium)
b. Lorazepam (Ativan)
c. Flurazepam (Dalmane)
d. Triazolam (Halcion)
e. Chlordiazepoxide (Librium)
• Benzodiazipine Antidote
o Flumazenil (Romazicon) IV use only
used for:
a. Overdose of benzodiazepine
b. To reverse sedation in general
anesthesia
c. To reverse sedation in medical
procedures / Diagnostic tests
2. Barbituates – enhance GABA effects in entire
CNS
o Antiseizure drug
a. Phenobarbital (Luminal)
b. Pentobarbital (Nembutal)
c. Amobarbital (Amytal sodium)
d. Secobarbital (Seconal)
Deduque, Mick Angelo
Psychotherapeutic Drugs
Use for treatment of:
1. Schizophrenia – Increased Dopamine
• Antipsychotic drug = decreases dopamine
o Dopamine blockers
2. Mania
• Lithium
3. Narcolepsy
• Stimulants Methylphenidate (Ritalin)
4. Attention Deficit Disorders
• Stimulants Methylphenidate (Ritalin)
Antipsychotic / Neuroleptic Agents (MAJOR
TRANQUILIZERS)
1. Typical Antipsychotics (Phenothiazine)
• ALL Dopamine blockers
• Cheaper
• “-azine”
• More potent and efficacious
a. Chlorpromazine (Thorazine)
b. Thioridazine (Mellaril)
c. Fluphenazine (Moditen / Prolixin)
d. Perphenazine (Trilafan)
e. Haloperidol (Haldol)
18 | P a g e
 • Non phenothyzine • Dopa Decarboxylase
• TCA effects b. Levodopa & Carbidopa (Sinemet)
o Anticholinergic ▪ Carbidopa – is not levodopa
o Sedation • Destroy Dopa
o Hypotension - orthostatic Decarboxylase → It
o Extrapyramidal symptoms enhances Levodopa
2. Atypical Antipsychotics c. Amantadine (Symmetrel)
• Dopamine and serotonin blockers ▪ Increase release of dopamine
o Block only dopa and sero Substantial Nigra
responsible for s/sx of psychosis ▪ Antiviral
• Less adverse effects d. Bromocriptine (Parlodel)
• Expensive ▪ Dopamine Agonist
a. Clozapine (Clozaril) • Stimulate
b. Olanzapine (Zyprexa) • Enhance dopamine
c. Quetiapine (Seroquel) effects
d. Aripiprazole (abilify) e. Pergolide (Permax)
e. Ziprasidone (Geodon) ▪ Dopamine Agonist
f. Risperidone (Risperdal • Stimulate
Neuroleptic Malignant Syndrome • Enhance dopamine
• Worst adverse effect of antipsychotic drugs: effects
“FEVER” → WITHHOLD MEDICATION DOSE f. Selegilline
o Fever: Initial sign ▪ MAO – B Inhibitors
o Encephalopathy • Increase dopamine
o VS unstable ONLY
o ECG changes ▪ Together with levodopa for mngt
o Rigidity of parkinson’s disease
▪ Should Not combined with
Extrapyramidal Symptoms vitamin B6 → it will decrease
1. Dystonia the amount of levodopa
2. Akathesia 2. Anticholinergic Antiparkinsonism Drugs
o Restlessness a. Biperiden (Akineton)
3. Tardive Dyskinesia b. Benztropine (Cogentin)
o Nakalabas ang dila c. Diphenhydramine (Benadryl)
4. Pseudoparkinsonism or Parkinson’s like d. Trihexyphenidyl (Artane)
syndrome
o Medication: ANTICHOLINERGIC
ANTIPARKINSONISM DRUG not Antimanic Drugs
dopaminergic • Mania – Overstimulation of certain neurons in the
brain
Antiparkinsonism Drugs o Stabilized impulse transmission
1. Dopaminergic Agents • Drug of choice:
o For Parkinson’s Disease – Both o Lithium salts (Lithane/Lithotabs)
Dopaminergic and Anticholinergic ▪ 0.6 – 1.2 meq/L
▪ Degenerative disease = o Lamotrigine, Olanzapine, Aripiprazole,
Substantia nigra → Excretion of Ziprasidone, Quetiapine
dopamine ▪ Antiseizure
• Tremors Antiepileptic Drugs / Anticonvulsant Drugs
• Rigidity • Seizure – Characterize by abnormal and
• Bradykenesia excessive transmission in the brain
i. Dopamine precursor – o Primary – unknown cause
Levodopa – Blood Brain Barrier o Secondary – Known causes
→ Dopamine • Fever
19 | P a g e
Deduque, Mick Angelo
 ▪ Stroke 2. Alpha 2 Agonists
• Convulsant – Motor seizure • CNS
o Tonic – clonic • Decrease norepi flow → decrease SNS
1. Hydantoins • Centrally Acting Antihypertensive drugs
• enhance GABA effects a. Clonidine
• Closes Sodium Channels b. Methyldopa
• CNS depressants 3. Beta Antagonists
• Will most likely cause: Gingival Hyperplasia • Decrease HR → Decrease BP
o Nsg Mng: Oral Care • Renin Angiotensin Aldosterone System
• Convulsion: Hallmark in the mngt of seizure (RAAS)
a. Phenytoin (Dilantin) o Renin → angiotensinogen →
b. Fosphenytoin (Cerebyx) Angiotensin 1 → Angiotensin
c. Mephenytoin (Mesantoin) converting enzyme → Angiotensin
d. Ethotoin (Peganone) 2 → binding together →
2. Barbiturates Vasoconstriction → Increased BP
• Enhance GABA o Angiotensin2 → Aldosterone →
a. Phenobarbital - children Increase Na and water retention
b. Amobarbital – most sedating → Hypervolemia
c. Secobarbital a. Propanolol
3. Benzodiazepine b. Metoprolol
• NOT for long-term treatment c. Bisoprolol
• Emergency Status 4. ACE inhibitors
• Epilepticus • Vasodilators
a. Diazepam (Valium) • Adverse Effect: Hypotension
b. Clonazepam (Klonopin) • Side Effects: Cough
• Action in Enzyme
Antiepileptic Drug a. Captopril
1. Valpoic Acid – For Psychosis b. Cilazapril
2. Lamotrigine – For Mania c. Ramipril
3. Topiramate – Prophylaxis for migraine d. Enalapril
4. Carbamazepine – Neuropathic pain 5. Angiotensin II Receptor Antagonists
• -sartan
• Adverse: Hypotension
CARDIOVASCULAR PHARMACOLOGY • S/e: GI toxicity
• Hypertension → Increase BP → Normal → • Action in Receptor
Hypotension a. Losartan
• Primary – Idiopathic b. Candesartan
• Secondary – Known causes c. Telmisartan
o DM d. Valsartan
o Renal disease 6. Diuretics
o Pheochromocytoma – epi/norepi → a. Thiazide Diuretic – Hydrochlorthiazide
Increase SNS → Increase BP • Diuretic of choice
• Maintenance diuretic
Antihypertensive Drug • Distal convulated tubule → konti
1. Alpha 1 Antagonists lang angg fluid na nailalabas
• Located at the Blood vessels → 7. Vasodilators
Vasodilation → Decrease BP a. Direct – Acting Vasodilators
• Vasodilators b. Indirect – Acting Vasodilators
a. Prazosin
b. Terazosin
c. Doxazosin

20 | P a g e
Deduque, Mick Angelo
Vasodilators Trendelenburg → Apply Oxygen
• Action in Blood Vessel itself → Refer
• Adverse: Hypotension b. Isosorbide Di Nitrate
• Side effect: Headache c. Isosorbide Mononitrate
1. Direct – Acting Vasodilators 2. Beta Blockers
• Relax the smooth muscles of the blood • Decrease HR → Decrease BP → Decrease
vessels Cardiac Workload
a. Hydralazine (Apresoline) a. Metoprolol
b. Nitrates b. Propanolol
o Sensitive in light 3. Calcium Channel Blockers
o Sensitive to heat • Vasodilate → decrease BP → Decrease cardiac
o Easily to expired workload
i. Nitroprusside a. Amlodipine
ii. Nitroglycerine b. Diltiazem
iii. Isosorbide mono / Di nitrate c. Verapamil
2. Indirect Acting Vasodilators
• Decrease calcium release in the smooth Antiarrhythmic Drug
muscles of blood vessels = Calcium 1. Class I – Acts on Phase 0
Channel Blockers • Inhibits depolarization / Closes Na Channels
a. Calcium Channel Blockers a. Lidocaine - IV
i. Nifedipine 2. Class II – Acts on Phase 4
ii. Felodipine • Prolonged resting → decrease HR
iii. Amlodipine • Beta-Blockers
▪ 10mg → causing • Fibrillation
edema a. Propanolol
iv. Diltiazem 3. Class II – Acts on Phase 3
▪ Long acting calcium • Prolonged repolarization → Decrease HR
channel blocker a. Amniodarone – Slow down HR
v. Verapamil 4. Class IV – Acts on Phase 2
▪ Long acting calcium • Plateu
channel blocker • Calcium channel blockers
• Blocks abnormal rhythm
a. Diltiazem
Drugs for Coronary Artery Disease b. Verapamil
1. Drugs for MI Phase 0
a. Pain reliever • Depolarization
b. Thrombolytic Drug Phase 1
o Dissolve Thrombolysis • End of depolarization
2. Anti-Anginal Drugs Phase 2
a. To increase O2 supply
• Plateu
b. To decrease cardiac workload
Phase 3
• Repolarization
Antianginal Drugs
Phase 4
1. Nitrates
• Resting
• Coronary vasodilators → increase O2
• Peripheral vasodilators → decrease BP
Myocardial Infarction
→ decrease cardiac workload
• Dysrhythmia: Premature Ventricular Complex /
a. Nitroglycerine
Contraction 9PVC)
• Acute attack – ntg sublingual,
3-5 mins
• Unstable angina → BP: 80/40
→ position in Modified
21 | P a g e
Deduque, Mick Angelo
 • Visual
Drugs for Heart Failure Disturbances
• Inability of the heart to pump effectively • N/V
1. Diuretics – Congestive Heart Failure = Edema • lack of Appetite
a. Loop Diuretic (Furosemide) • ECG changes
o 40mg IV STAT ▪ Withhold medication
o Oral → decrease potassium dose then refer
b. K-Sparing Diuretic (Spironolactone) ▪ Anticipate antidote
o Increase potassium • Digibind
2. Sympathomimetic Drug • Monitor for s/sx
• Adrenergic Agonist → Increase HR of heart failure
• Cardiotonic drug
• (+) Inotropic effect
• (+) Chronotropic effect → Increase HR Drugs affecting blood coagulation
• IV thru infusion pump • Problem: BLEEDING
a. Dopamine • Damage blood vessel → Bleeding →
b. Dobutamine Hemostasis (arrest or stop bleeding)
3. Cardiac Glycosides o Processes:
a. Digoxin ▪ Vasoconstriction
o Drug of choice • Trying to stop the
o (+) inotropic effect --. Increase bleeding
Ca release in the cardiac cells ▪ Platelet Plug formation
o (-) Chronotropic effect → • Pag may injury →
Prolonged cardiac repolarization inflammation → release
→ Slow down HR chemical mediators →
▪ Cannot combine with: thromboxane A2 →
• Amiodarone Platelet plug formation
• Beta blocker ▪ Clot formation
o Cannot combine with Calcium • Much stronger clot
channel blocker • Coagulation
o Therapeutic Level: o Clotting factors –
▪ 0.5 – 2ng/ml Produced by
o Antidote: LIVER →
▪ DIGOCIN IMMUNE activating clotting
FAB (DIGIBIND) factors → CLOT
o Nursing Considerations: o Pag magaling na ang blood vessel →
▪ Monitor HR prior to clot dissolves
administration o Pag di pa rin gumaling → clot not
▪ Monitor K level dissolved → THROMBUS FORMATION
• Hypokalemia o Liver → needs vit K for production of
increases clotting factors X, IX, VII, II (1972 –
digoxin toxicity Martial Law)
▪ Monitor ECG • Source: 50% from food,
▪ Maintain Therapeutic 50% e.choli
level level ▪ I – Fibrinogen
▪ Do not combine with ▪ II – Prothrombin
Calcium Channel ▪ Active X → Activate II
Blocker, Beta Blocker, (Prothombin) → Unactive II =
Amiodarone. Thrombin
▪ Monitor for s/sx of ▪ Active I → Fibrinogen →
toxicity Fribrin → Clot
• Bradycardia
22 | P a g e
Deduque, Mick Angelo
 ▪ Thrombin → plasminogen → Globin - protein
plasmin → dissolve clot 2. Iron Preparations
1. Antiplatelet a. Ferrous Sulfate
• Thrombolytics b. Ferrous Fumarate
• Patient with hx Thrombus formation c. Iron Dextran
• Prevent Thrombus 3. Folic Acid Derivatives
• Inhibit thromboxane A1 a. Folic Acid
• Adverse: BLEEDING b. Leucovorin
a. Aspirin 4. Vitamin B12
• 30 – 100mg / dose • Route: Oral / Parental
b. Clopidogrel a. Cyanocobalamin
c. Ticlopidine b. Hydroxocobalamin
d. Dipyridamole
2. Anticoagulant How can you distinguish if drugs for anemia is
• Prevents Thrombus Effective?
• Antithrombotic • HEMOGLOBIN
a. Heparin
b. Warfarin
• Inhibit production of Vitamin K
dependent Clotting factors RESPIRATORY DRUGS
(1972)
c. Antithrombin Drugs Affecting UPPER RESPIRATORY TRACT
1. Decongestants
• Stop the thrombin formation
o Alpha 1 Agonist in Blood vessels
3. Thrombolytic Agents
o Vasoconstriction
• Tissue plasminogen activator
a. Ephedrine
a. Streptokinase
b. Pseudoephedrine
b. Urokinase
2. Antitussive
c. Alteplase
o For Dry Cough → to stop coughing
o Suppress the cough center of the brain
Anti-Anemic Drugs
a. Codeine
• Decrease O2 carrying capacity of the blood ▪ Direct suppress the cough
• Bone marrow – erythropoiesis center
1. Erythropoietin b. Dextromethorphan
• Kidneys: main organ ▪ Sinecod
a. Epoetin Alfa ▪ Levopront
b. Epogen 3. Expectorant
c. Epocinon o Liquify secretions
• For replacement a. Guiafenesin
• Given to pts with renal failure 4. Mucolytics
Stem cells → Proerythroblast → erythroblast (no o Dissolve the thick mucus
nucleus, immature cells) → normoblast (big cells, have o Water – Best dissolve thick mucusx
nucleus, staying in the bone marrow) → lumalabas na a. Acetylcysteine (fluimucil)
ang nucleus → reticulocyte → Mature RBC (with the b. Carbocisteine (Solmux)
help of Vitamin B12 and Folic Acid)
Matured RBC Causes:
a. anuclear • Viral infection
b. Biconcave • Allergy
Heme – pigment 5. Antihistamine
• Hfe-Hfe-Hfe-Hfe a. Diphenhydramine – Old
o Contains Iron carrying oxygen

23 | P a g e
Deduque, Mick Angelo
 b. Loratadine – new → Cetirizine = No
drowsiness
c. Promethazine – old
d. Chlorpheniramine – old

Drug for OBSTRUCTIVE PULMONARY

• Used for pt with:
o Asthma
o COPD
o Pneumonia
• Improve ventilation
• Directly relax the smooth muscles of the
bronchioles
• Adverse Effects: Increase HR, Palpitation,
Tremors

1. Bronchodilators
a. Xanthine – Caffeine containing
i. Aminophylline
ii. Theophylline
2. Sympathomimetic
a. Epinephrine
b. Albuterol
c. Terbutaline
d. Salbutamol

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Deduque, Mick Angelo