PHARMACOLOGY

 How the drug affects the body

PHARMACOLOGY  Action of drug:
 Study of biological effects of chemicals  Replace a missing substance
 All drugs are chemicals and are introduced into the body o E.g., insulin, levothyroxine, corticosteroids
via different routes of the body wherein some sort of (addison’s), mineralocorticoids
change is expected  Increase cellular activities
o E.g., epinephrine when HR stops, inotropes
DRUG NAMES  Depress cellular activities
 CHEMICAL NAMES o E.g., beta blockers (-olols), calcium channel
 Atomic or chemical structure blockers
 o Anatomic structure of a drug  Interfere with the growth of a foreign cell
 E.g., propionic acid o E.g., antibiotics (destroy microorganisms),
 GENERIC NAMES anticancer drugs/antineoplastic drugs
 Name approved by the medical association of  Drug Actions Maybe Through:
pharmaceutical in the original country of 1. Receptors
manufacture 2. Enzymes
 Adopted by all countries 3. Pumps
 When prescribing drugs to patients generic names 4. Chemical Interactions (E.G., Antacids)
should be given because of the RA 6675 Generics act 5. Altering Metabolic Process
of 1988
 E.g., Ibuprofen I. DRUG-RECEPTOR INTERACTIONS
 BRAND NAME  Agonists - binds to a receptor &
 Name given by the manufacturer of the drug stimulate action
 E.g., Advil, Medicol  A drug that stimulates
receptor site
RIGHTS OF DRUG ADMINISTRATION  E.g., digoxin, epinephrine,
1. Right Medication dobutamine
 Should be checked at least three times  Antagonists - block action
2. Right Dose  Competitive Antagonist
 Right amount o Binds to a SAME receptor site
3. Right Patient o The potency of an agonist is
 Two identifiers: Name and birthday BLOCKED
4. Right Time o E.g., morphine and naloxone
5. Right Route  Non-Competitive Antagonist
6. Right Documentation o Binds to DIFFERENT
7. Right Client Education RECEPTOR
8. Right to Refuse o The potency of an
9. Right Assessment agonist is REDUCED
10. Right Evaluation o E.g., cefuroxime and
omeprazole (it will
BASIC CONCEPTS OF PHARMACOLOGY
reduce the effect of
 Receptors- receives the drugs cefuroxime)
 Pharmacodynamics: Mode of action
 Pharmacokinetics : response of the body towards the ANS Drugs
drug
 Kinetics means movement
 Liberation
 Absorption
 Distribution
 Metabolism  Adrenergic - SNS
 Excretion  SNS, receptors: ADRENERGIC RECEPTORS: alpha 1,
alpha 2, beta 1, beta 2
 PSNS, receptors: NICOTINIC & MUSCARINIC

II. DRUG ENZYME INTERACTIONS - breakdown

 Example: Cholinesterase inhibitors
 An enzyme which breaks down acetylcholine (ACh)
= relaxation
 -ase: enzyme
 Effector cells - muscle
 Cholinesterase is still important to prevent the muscle
of continuous contraction and allow relaxation
 Normal: Presynaptic Neuron – Axon – Impulse –
ACh binds Effector - Muscle = Muscle contraction
 Neostigmine for MG (S/SX: weakness, paralysis)
 GOAL: increase the tone of the muscle, relieve
weakness and paralysis (palliative care)
 MOA: blocks the cholinesterase from breaking down
ACh to promote better muscle contractions

PHARMACODYNAMICS
  Fastest absorption
b. Subcutaneous (SQ) - 45 degrees
 The drug will look for blood vessels,
going to the muscle as well to be
absorbed
 Insulin should be administered slowly
(slow absorption), to prevent
hypoglycemia
 Tuberculin syringe is used
c. Intramuscular (IM) - 90 degrees
 Muscles are very vascular, therefore,
aspirate to determine if a BV is hit
III. INHIBITING PUMPS
 Next fastest absorption
 Example: Reuptake inhibitors
d. Intradermal (ID)
 5HT (5 hydroxytryptamine): serotonin 3. Transmucosal - SL, Inhalational, topical
 Effector cell - nerve 3. Distribution - reaches target cell/tissue
 SSRI: selective serotonin reuptake inhibitor  The drug is already in the target tissue/cell → bind to
o Antidepressant receptor → distribution
 To increase the level of norepinephrine,  Only the unbound molecule will cause the effect
dopamine and serotonin
 MOA: Blocks the reuptake of serotonin,
serotonin stays in the synaptic cleft,
increasing the serotonin relieving the
symptoms of depression
o Biogenic Amine Theory
 There’s an imbalance in norepinephrine,
4. Metabolism – liver
dopamine and 5HT → depression
 Oral 500 mg→ stomach
(liberation)→ absorbed→
Before distribution the drug
will have to first pass the
liver (hepatic first pass)
 500 mg→ cytochrome p450
(enzyme in the liver) will act
on the drug→ metabolism
(biotransformation/
breakdown)→ result into a
new drug (reduced to 350-
400 mg) that is less active
 5HT will not be reabsorbed→ ↑ in number→ relief of (first pass effect)→ the
depression reduced drug will be
returned to the blood for
IV. CHEMICAL INTERACTION distribution
 Example: Antacids  The liver reduces the dose to
 Neutralizing the gastric acid reduce toxicity→
detoxification
V. INTERRUPTING METABOLIC PROCESSES o Everything that goes
 Example: Insulin, Cortisol, Growth hormone through the liver is
being detoxified
PHARMACOKINETICS  For IV drugs, if 500 mg will
 This is how the body reacts to the drug be given, 500 mg will be
1. Liberation - release of the active ingredient used by the body because of the bypassing of the
liver (no first pass effect). First pass only occurs in
oral medications
 For people with problems in the liver, lower doses
should be given to prevent hepatotoxicity
5. Excretion - outside the body
 Whatever is not used by the body will be eliminated
through the lungs, kidneys, feces, and skin (sweating)
 DOSE
 Amount of drug to be administered to the patient
2. Absorption - drug reached the blood  SCHEDULE
 Routes of drug administration  TIME, frequency, how many dose/s per day
1. Enteral route (GIT)  RECOMMENDED DOSE
a. Oral route  The amount of drug administered to reach the critical
b. Nasogastric route concentration
c. Rectal route (fastest route)  RIGHT amount + RIGHT schedule
 (+) fastest absorption d/t high  CRITICAL CONCENTRATION
vascularity of the rectum  Level of drug in the blood which produces a
2. Parenteral therapeutic effect (cure and healing)
 THERAPEUTIC EFFECT
 Favorable response after a treatment of any kind
 Cure
 LOADING DOSE
 Initial dose, immediate response, provides immediate
effect
 Usually higher than the recommended dose and is
usually given in emergency situations
 HALF LIFE
a. Intravenous (IV)
  Time it takes for a drug to become half of its then rehydrate the patient, replace lost fluids
previously peaked level  If (x) cause by bacteria, give loperamide/ diatabs
 Also written as: T ½
 E.g., cefuroxime 500 mg T1/2 = 8 hours Example
o If this is given at 6 am, after 8 hours, at 2 pm it Remdesivir 100 mg IV, OD for 5-10 days
will become 250 mg 1st dose- 200 mg
o Day 1:  Succeeding doses- 100 mg OD
 6:00 am → 500 mg
 2:00 pm → 250 mg + 500 mg PHARMACOLOGY TIPS
 10:00 pm → 125 mg + 250 mg + 500 mg  Remembering medications and the body system affected
o Day 2:  Review the sympathetic and parasympathetic nervous
 6:00 am → 62.5 mg system since many medications have actions that affect
 2:00 pm → 31.25 mg these systems
 10:00 pm → 15.6 mg
o Day 3: NERVOUS SYSTEM
 6:00 am → 7.8 mg
 2:00 pm → 3.9 mg
 10:00 pm → 1.9 mg
o Day 4:
 6:00 am → 0.9 mg
 2:00 pm → 0.45 mg
 10:00 pm → 0.2 mg
o Day 5:
 6:00 am → 0.1 mg
 2:00 pm → something
o Note: the drug accumulates in the body
Application
 Patient needs surgery but is taking ASA for 10 years, inform  Neurons (functional unit of the nervous system)
the doctor, the physician will have to delay the surgery  The electrical impulses cannot cross the synapse→
 The nurse will tell the patient to discontinue ASA for about 5 impulse will be passing the information to the chemicals
days to lower risk of bleeding
in the axon terminals→ chemicals will cross the
 Rationale: to remove remaining half lives, if all of the half-
lives are removed then bleeding tendencies will be decreased
synapse→ once in the dendrites electrical impulses will
be created again→ axon terminals→ information passes
through the neurotransmitters→ bind to the receptors of
effector cells
 If the effector cells are:
 Muscles→ contract
 Glands→ release hormones
 Nerves→ transmission of impulses

NEUROTRANSMITTERS
 Body’s chemical “messengers”
 Produced by the nerves and are stored in the axon
terminals of the nerves
 RD: ceftriaxone 500 mg  Acetylcholine (ACh)
 Schedule: q8 for 7 days  “Muscle contraction” and “Memory”
 T ½- 8 hours (the half life will tell the time of  Cholinergic nerves
administration) o A nerve that is producing, storing, releasing
 Start of the cure will only occur once critical acetylcholine
concentration is reached and it should be sustained to  LOW = AZ
reach the cure  HIGH = BPD
 When a drug reaches the CRITICAL  Norepinephrine and Epinephrine (NE / E)
CONCENTRATION, that is the time it will have a  AKA adrenalines/ catecholamines
THERAPEUTIC EFFECT (CURE)  Chemicals released during SNS stimulation
 RD: ceftriaxone 250 mg  Fight or flight
 Underdosing - critical concentration will not be  Affects behavior as well
reached therapeutic effect will not be reached → o HIGH: Schizophrenia, Mania
(x) cure o LOW: Depression, Parkinson’s, ADHD
 If a dose is misplaced take it immediately but if it is  Norepinephrine
too close to the next does continue to the next dose o Released in adrenal medulla → Adrenaline
 Right dose, wrong time→ (x) critical concentration  Adrenergic nerves
and therapeutic effect o A nerve that is producing, storing, releasing
 NOT Taking on the prescribed SCHEDULE will norepinephrine
prevent reaching THERAPEUTIC LEVELS. DO not  Dopamine (Dopa)
DOUBLE DOSE  Coordination of impulses & responses
 Once the loading dose is given, recommended dose  Motor movement and cognition (thinking, learning
should be continued and reasoning)
 A LOADING DOSE may be used in certain drugs  HIGH: Schizophrenia, Mania
(for EMERGENCY) to reach THERAPEUTIC  LOW: Depression, Parkinson’s, ADHD
EFFECT immediately followed by o Parkinson's disease → decreased dopamine
RECOMMENDED DOSE (degeneration of the dopaminergic nerves)
 Overdose - toxicity; give antidotes (competitive  Dopaminergic nerves - Produce dopamine
antagonism)  Serotonin (5HT)
 It involves arousal and sleep
For diarrhea, determine the cause of the diarrhea first before  Preventing depression
giving antidiarrheal medications  Motivation
 If because of bacteria→ allow the body to expel the bacteria  Eat Chocolates & banana
  “Happy Hormone/Chemical” relaxation contraction
 HIGH: Schizophrenia (bronchodilation) and (bronchoconstriction
↑ RR )
 LACK: Depression
 To allow
 Serotonergic nerves - Produce serotonin more air
 Gamma Amino Butyric Acid (GABA) exchange
 An inhibitory neurotransmitter used in Gastrointestinal Blood flow, motility, Increased motility→
anticonvulsants tract and secretions will diarrhea
 prevents overexcitability or stimulation such as decrease→
seizure activity constipation
 Decreased
 HIGH: Treats seizures
because this
 Gabaminergic nerves - Produce GABA is not
needed in
AUTONOMIC NERVOUS SYSTEM stressful
situations,
blood is
directed
towards the
muscles
(more
needed)
Liver Conversion of Glycogen synthesis
glycogen to glucose
increased
Kidney Decreased urine Increased urine
formation d/t formation
decreased blood flow
Bladder Sphincter→ contracted Relaxation of
Detrusor muscle→ sphincter
relaxed Contraction of the
detrusor muscle→
 Includes two neurotransmitters: Norepinephrine and emptying of the
acetylcholine bladder
Sweat glands ↑ sweating No change
Two branches: Adrenergic Cholinergic
 Sympathetic FIGHT OR FLIGHT Agonist- stimulate Antagonist- block
 Adrenergic nervous system Mimetic- copy, mimic Lytic- block, destroy
dissolve
 Uses Norepinephrine / Adrenalines
Sympathomimetic→ SNS
o Decrease secretion
Sympatholytic→ block SNS
 Neurotransmitter: Adrenergic agonist, cholinergic antagonist→ SNS
o Preganglionic nerve: acetylcholine (ach) Anticholinergic→ SNS
o Postganglionic nerve: norepinephrine (ne) Cholinergic→ PNS
 Parasympathetic REST AND DIGEST
○ Cholinergic nervous system Sympathetic = adrenergic Parasympathetic =
○ Uses Acetylcholine cholinergic
■ Increase secretion
○ Neurotransmitter: Agonist - stimulate Antagonist - block
■ Preganglionic nerve: acetylcholine (ach)
■ Postganglionic nerve: acetylcholine Mimetic - mimic, copy Lytic - block, destroy dissolve
(ach)  Sympathomimetic to heart (anxiolytic, mucolytic
→ increase HR thrombolytic, hemolytic,
 Sympathomimetic to GIT tocolytic)
Sympathetic and Parasympathetic Effects
→ constipation  Sympatholytic to bladder
Structure Sympathetic Parasympathetic
(adrenergic) (cholinergic)  Sympathomimetic to → emptying
General Fight or flight Rest and digest pupils → mydriasis  Sympatholytic to GIT →
response  Sympathomimetic to diarrhea
Origin Thoracolumbar Craniosacral blood vessels→  Sympatholytic to bronchus
Thoracic to L1-L3 Cranial nerves vasoconstriction → bronchoconstriction
1,3,7,9 and the  Sympathomimetic to  Sympatholytic to pupils →
sacral bronchus → mydriasis
Preganglionic Short Long bronchodilation  Parasympatholytic to
nerve  Parasympathomimetic to blood vessel →
Neurotransmitte ACh ACh kidney bf → increase vasoconstriction
r  Parasympathomimetic to  Sympatholytic to bladder
Post ganglionic Long Short bladder → emptying → emptying
nerve  Parasympathomimetic to
Neurotransmitte NE ACh GIT → diarrhea
r  Sympathomimetic to
Termination of Monoamine oxidase Cholinesterase blood vessels -
impulse and catechol-ortho vasoconstriction
methyl transferase  Parasympathomimetic to
(COMT) GIT → diarrhea
Effects to the body  Sympathomimetic to
Eye (pupils) Dilation (mydriasis) Constriction blood vessels→
 Accommoda (miosis) vasoconstriction
te more light
Nasal mucosa Mucus reduction Mucus increased
Salivary gland Saliva reduction Saliva increased  Adrenergic agonist to the heart → increase HR
Heart Rate increased and Rate decreased,  Cholinergic antagonist to GIT → constipation
increased contractility decreased  Anticholinergic to pupils → mydriasis
contractility  Atropine (anticholinergic)→ given to decrease secretions to
Blood vessels Constriction Dilation decrease risk of aspiration
(smooth  Schizophrenia→ antipsychotics/ neuroleptics will be given
muscles)  Neuroleptics SIDE EFFECT:
Lung Bronchial muscle Bronchial muscle
 o NMS – neuroleptic malignant syndrome SIDE EFFECT: increase total peripheral resistance
o Tardive dyskinesia (d/t vasoconstriction): directly proportional to BP→
o Pseudo-parkinsonism HTN
o Akathisia  EFFECT: vasoconstriction = ↑ TPR = ↑BP
 Anticholinergic SE: BP= HR x SV x TPR / SVR (systemic vascular resistance)
o Constipation  TPR- pressure inside the blood vessels
 NI: increase fluids and fiber If ↑ HR = ↑ BP
o Decreased emptying of bladder (retention) If bleeding ↓ BV, ↓ SV, ↓SVR
 NI: bladder training (specific bladder time),
void first before taking the antipsychotic, low  SINUPRET is used instead for HTN patients
salt  Given three times a day
o Dryness of the mouth  Not a sympathomimetic drug
 Increase OFI  Not also given in patients with hyperthyroidism
 Ice chips
(everything is increased→ HR, BP)
 Oral care to prevent ulcers
 Sugarless candies to increase salivation  Also given as vasopressors
 Used before eye procedures to cause mydriasis and allow
better visualization of the internal parts of the eyes
 Ganglion
 Clusters of nerve bodies that is outside the CNS Side Effects
 All nerves that go out of the CNS and end in the  Reflex bradycardia→ a compensatory mechanism of the
ganglion are preganglionic nerves body
 Preganglionic nerves of the SNS are shorter in  baroreceptors of the aorta and the carotid artery will
comparison to the preganglionic nerves of the PNS detect increase in the blood pressure→ the
because it only connects near the spinal cord hypothalamus will order decrease in heart rate to
 Preganglionic nerves of the PNS are longer since its decrease blood pressure→ reflex bradycardia
origins are from the cranial and sacral areas which  Does not occur immediately
are distal to the organs  Hypertension d/t palpitation
 All nerves that go out of the ganglions are the Basta ito baliktad ang effect
postganglionic nerves and ends in the organs Alpha 2 Adrenergic Agonists
 Located in the:
 CNS nerve
membranes
 Stimulation of the alpha 2
in the SNS is opposite
 E.g., clonidine (catapres)
 Given when (+)
HTN crisis, SL
AUTONOMIC NERVOUS SYSTEM DRUGS:  Decreases BP
Sympathomimetics  EFFECT: SNS effect
is decreased and
Adrenergic Agonists PNS dominates=
 Epinephrine - CPR, shock ↓HR, ↓BP, less
 Dobutamine - CHF insulin release=
 Dopamine - CHF, cardiogenic shock hyperglycemia
 Norepinephrine - cardiac arrest  Methyldopa- given
for PIH, given orally

Alpha Adrenergic Agonists

 Nonspecific, will have an effect on both alpha 1 and alpha
2
 E.g., midodrine (vasopressor)
 Midodrine
o DOC for orthostatic hypotension (SNS agonist→
↑ HR→ ↑ TPR → ↑BP)

Beta 1 Adrenergic Agonists

 B1 (in the heart)
 ↑ HR, ↑ contractility
 Dobutamine (Inotropic)
o Synthetic dopamine
(sympathomimetic drug)
o EFFECT: DOC for HF, helps
heart contract, anti-arrhythmic,
o SIDE EFFECT: palpitations,
tachycardia→ ↑ BP
 Potassium will enter the
cells once beta cells are
stimulated
Alpha 1 Receptors  Affects the kidneys→ ↑ renin
 Found in the: release→ ↑ BP (d/t sodium
 Urinary bladder sphincter→ retention and water retention)
 Blood vessels→ vasoconstriction
 Iris→ mydriasis Beta 2 Adrenergic Agonists
 Phenylephrine: Neozep (decongestant)  Found in the:
 EFFECT: decreased blood flow to the nasal area,  Lungs, uterus, BV, heart,
reduced O2 and nutrients to cells→ cell shrinks→ liver
nose decongestion  Bronchodilation
 NI: be careful in giving to HTN pts  Albuterol/Salbutamol
[bronchodilator]
 o INDICATION: asthma and COPD  Decrease production of the aqueous humor
o SE: palpitation and tremors (as albuterol beta 2 5. Supraventricular Arrythmia, AFib– regulate and control
but also binds with b1 especially in high doses→ rhythm of heart
SNS activation) 6. CHF – be cautious as heart is exhausted. – to ↓ cardiac
o Also causes arteriolar vasodilation in skeletal workload = ↑ inotropic (force of contraction)
muscles→ faster and increased blood flow 7. Migraine- prophylaxis as it can cause cerebral
o SABA (short-acting beta agonist) vasoconstriction
 Isoproterenol
o INDICATION: Tx for bradycardia, heart block, Side Effects Contraindications
Bradycardia Hold if HR <60 bpm
asthma
Hypotension Hold if BP <90/60
 Terbutaline (tocolytic)– muscle tone relaxation Bronchoconstriction** Avoid for asthma and COPD
(blocks the tone of the muscle) patients
o INDICATION: asthma, COPD, premature labor Hypoglycemia Caution in patients with DM,
o EFFECTS: Blood vessels of heart, lung & can mask hypoglycemia
skeletal muscle: vasodilation Impotence**, erectile
o Liver: Glycogenolysis→ hyperglycemia dysfunction
o LABA- long- acting beta agonist
 Isoxsuprine HCl (duvadilan vasodilan)- also a Example
tocolytic A 65 y/o male, smoking 10 packs years, non-alcoholic
o Peripheral vascular dilation, tx of preterm labor  Maintenance- beta blocker
 Diagnosis- HTN and asthma
Nursing Considerations  Only a beta 1 specific blockers should be given to prevent
bronchoconstriction as it only has an effect in the heart
 Avoid sudden withdrawal of the drug
(BEAM BA)
 Monitor vital signs  Bisoprolol
 Provide comfort measures  Esmolol
 Acebutolol
ANTAGONISTS  Metoprolol
 Betaxolol
Alpha Adrenergic Antagonists  Atenolol
 Located in the blood vessels and urinary bladder
 Phentolamine
MYASTHENIA GRAVIS
 A nonspecific
 Cholinergic receptors are destroyed by the antibodies
 Used for HTN crisis d/t MAOIs (decreases
 Number of acetylcholine is normal but there are no
breakdown of NEs→ SNS stimulation→ ↑BP) and
receptors
pheochromocytoma (tumor of the adrenal medulla→
 Muscles have no contraction→ paralysis
↑ release of NE/ E→ ↑ BP and HR)
 (+) weakness of the eyelids- ptosis (initial sign of
 Will cause vasodilation→ ↓ TPR→ ↓BP
myasthenia gravis)
 Prazosin– binds to blood vessels = vasodilation = ↓ TPR
 Descending paralysis- MG (mata galing)
= ↓BP
o Ascending paralysis- GBS (galing baba siya)
 Doxazosin and Terazosin
 Common in 20-40 years old women
 Binds to blood vessel: vasodilation = ↓ TPR = ↓ BP
 Binds to urinary bladder: Emptying of bladder
Signs and Symptoms
o INDICATION: Benign Prostatic Hypertrophy
 Ptosis
(urine stasis, dribbling, blood-streaked semen d/t
 Check palpebral fissures
compression of prostate) and HTN
o Not reduce the size, it will only empty the  Diplopia
bladder d/t retention because of the obstruction,  Mask-like facial expression
↑ risk for UTI  Dysphagia- risk for aspiration
 Alfuzosin– binds to only the bladder and cause emptying  Weaking of laryngeal muscles
of bladder  Airway is always the priority
 INDICATION: BPH  Respiratory muscle weakness
 Tamsulosin– for BPH as it only binds to the urinary  Consequence-
bladder also  Nursing consideration
 Extreme muscle weakness
Beta 1 Adrenergic Antagonists  Anticholinesterase will be given to prevent breakdown of
 Propranolol ACh→ increase the tone of muscles
 DOC for palpitations d/t hyperthyroidism  Cholinergic drugs as it preserves acetylcholine
 Prophylaxis for migraine  Neostigmine- treatment
 Timolol  Pyridostigmine- treatment
 For open angle glaucoma (to promote miosis and  Physostigmine- treatment
keep the angle open)  Edrophonium (Tensilon) is only used for diagnostic test
 SE- miosis  Short acting (10 minutes)
 Prophylaxis for migraines (eye drops)
 Nadolol Nursing Management
 DOC for angina and hypertension  Pharmacotherapeutics
 Labetalol  Cholinergics or anticholinesterase agents
 Most used in PIH (pregnancy- induced hypertension)
 Has an alpha receptor effect→ ↑in placental
perfusion (PNS stimulation)

Indications
1. HTN: Negative chronotropic effect = ↓HR
2. CAD (coronary artery diseases)- angina pectoris and MI
 Causes ↓O2 supply, ↑ O2 demand
3. Anxiety
 ↓Tremors & palpitation = ↓ HR
 ↓HR = ↓ O2 demand d/t ↓ workload, ↑ O2 supply
4. Open Angle Glaucoma
 Pyridostigmine (Mestinon) 2. Dicyclomine
 First line drug for MG  Antispasmodic and antimuscarinic
 DOC for atropine toxicity  For hyperactive bowel in adults
 Neostigmine (prostigmin) 3. Scopolamine (HNBB)
 For long term use  For motion sickness
 Increase the bonding of ACh and the receptors  For pupil dilation
 Corticosteroids  Post-op nausea and vomiting
 Anti-inflammatory, therefore, blocks the immune
response DRUGS OF THE CENTRAL NERVOUS SYSTEM
 Decadron (dexamethasone)
 Cholinergic agonists for MG are to be taken 30 minutes AC Parkinson’s Disease
to give tone to muscles of mastication and swallowing to  Degeneration of the dopaminergic nerves
prevent aspiration  There should be a balance of ACh and dopamine in the
 Monitor two types of crises substantia nigra
Myasthenic Crisis Cholinergic Crisis
Signs and Weakness and paralysis
symptoms  Acetylcholine→ contraction Fine motor movements
Cause Underdosing of Overdosing of  Dopamine→ inhibitory effect, relax
cholinergic drugs cholinergic drugs  Dopamine production has
Treatment Cholinergic Anticholinergic
degenerated→ dominate
(neostigmine, (atropine sulfate)
physostigmine,
ACh
pyridostigmine)  Goal:
Tensilon Increased muscle Worsening of  Increase dopamine or
(edrophonium)- via tone (improvement symptoms inhibit acetylcholine
IV for fast results of ptosis and
(already a crisis fast weakness) Manifestations
results are needed)  Tremors d/t higher ACh, ↑ contractions that is not
Positive tensilon Negative tensilon
inhibited by dopamine
test test
Management
FAQs
1. You are a nurse assisting the doctor during a Tensilon test,  Dopaminergic drugs (↑ dopamine)
what should you prepare bedside?  Anticholinergic drugs (inhibit ACh)
 Always prepare atropine sulfate (anticholinergic, an
antidote) Classes of Anti-Parkinson Agents
2. If (+) atropine toxicity, give pyridostigmine (mestinon)  Anticholinergic drugs– block stimulating effects of ACh
3. What is a negative tensilon test? Cholinergic crisis to bring activity balance
 Slow down the administration of cholinergic drugs to  Biperiden (Akineton)- antimuscarinic
avoid severe cholinergic effects (PNS effects)  Trihexyphenidyl (Artane)- antimuscarinic
 Diphenhydramine (Benadryl)- antihistamine (also
ALZHEIMER’S DISEASE anticholinergic)
 (+) degeneration of the cholinergic nerves→ atrophy of  Benztropine (Cogentin)- antimuscarinic
brain tissue due to its deficiency
 Dopaminergic drugs
 No impulses and ACh production
 Dopamine precursors (Levodopa, Carbidopa)
o Levodopa + carbidopa is the mainstay treatment
Manifestations
for Parkinson’s even if it has many side effects
 A – amnesia, loss of memory
o Levodopa- improves bradykinesia, rigidity, and
 A - agnosia– unable to identify the function and purpose
tremors
of familiar objects
o NC: avoid vitamin B6 (pyridoxine) because it
 A – apraxia– unable to perform learned movements
reverses or blocks the effect of levodopa *but is
 A – aphasia- inability to communicate (write/understand) taken with isoniazid to prevent peripheral
 Expressive- Broca’s aphasia (frontal lobe) neuritis/ neuropathy
o Unable to speak o Precursor- not a dopamine but will give
 Receptive- Wernicke’s aphasia (temporal lobe) dopamine
o Unable to understand  Dopamine cannot cross the BBB, therefore,
o More common in Alzheimer’s disease a precursor is given
 Global/ mixed o Sinemet- carbidopa is
o Both inabilities to speak and understand combined→ decreases the
dose of levodopa needed
Pharmacotherapy to reach the critical
 Prevent breakdown of ACh to increase memory concentration by
 Anticholinesterase preventing decarboxylase from
 Rivastigmine (Exelon) breaking it down
 Donepezil (Aricept) o Carbidopa will block or destroy
 Tacrine decarboxylase to prevent
 Not used for myasthenia gravis because target breakdown of levodopa
tissues (distribution) are different in the periphery because it
 MG→ muscles does not cross the BBB
 AD→ nerves o Ratio of carbidopa to
 These drugs won’t cure but will only delay the levodopa 1:4
progression of the disease

Pharmacodynamics
 Cholinergic drugs (anticholinesterase)

CHOLINERGIC ANTAGONISTS
(PARASYMPATHOLYTIC)
1. Atropine
 Anticholinergic, prevent secretions
  Clonazepam
 Antidote for BZD toxicity- flumazenil

Side Effects
 Sedation
 Drowsiness
 Impair intellectual function
 Respiratory depression

Barbiturates
 Seldomly used because it has many side effects
 More side effects and more addicting and does not
have an antidote
 Phenobarbital
 Secobarbital
 Amobarbital

Non- benzodiazepines, non-barbiturates

 Enhance the GABA effect
 Paraldehyde
 Chloral hydrate
 Zolpidem (ambien)
 Used as a short-term treatment for insomnia
 Selectively bind to the BZD sites on the GABA
 Dopamine receptor agonists receptors
o Bromocriptine  Advantages:
o Pergolide o No withdrawal effects
 MAO- B Inhibitors o Minimal rebound insomnia
o Destroys of breakdown NE, E, serotonin, and o Little or no tolerance on prolonged use
dopamine  Diphenhydramine
o Isocarboxazid (Marplan)  Buspirone
o Phenelzine (Nardil)  Alternative to BZD
o Selegiline (Emsam)  Slower onset of action
 Catechol-O-methyltransferase inhibitors (COMT)–  5HT receptor agonist
“CAPONES”  Useful in alcoholics→ has no potential CNS effect
o Destroy the catecholamines (NE/ E/ dopamine)  Low potential for abuse
o Comtan® (entacapone)  SE- priapism- painful erection
o Tasmar® (tolcapone)- not anymore used because  Propranolol
of too many side effects  A beta blocker
o Ongentys® (opicapone)  Anti-anxiety
 Others (not dopaminergic)
o Amantadine (antiviral) but can lessen the tremors ANTICONVULSANTS/ ANTISEIZURES
in Parkinson’s  Seizure- burst of uncontrolled electrical activity between
the neurons
ANXIOLYTICS  Epilepsy- two or more unprovoked seizures
 Blocks anxiety  Goal: to stop the seizure with minimal side effects
 Beta blockers  As much as possible monotherapy should be done d/t ↑
 Antipsychotics risk of side effects
 Benzodiazepines  Never stop abruptly d/t rebound seizures
 Antidepressants- SSRIs
 First line treatment for anxiety because it is Generalized Seizure
nonaddictive  Spreads to the other lobe (spreads in hemispheres)
 Disadvantage- full therapeutic effect is 4-6 weeks,  Tonic clonic (gran mal seizure)- extension and
not good for acute attacks contraction of muscles
 DOC BZD, phenobarbital, carbamazepine (Tegretol),
Benzodiazepines (BZD) valproic acid (valproate), and phenytoin (dilatin)
 for acute attacks  Valproic acid is hepatotoxic (x) given to children
 Pharmacodynamics- enhances the GABA effect Phenytoin can cause the following:
(inhibitory)→ block impulse transmission  Gingival hyperplasia
 Causes CNS depression  Can also result to fetal hydantoin syndrome (x) given to
 Most commonly prescribed pregnant women
 Other indications:  Microcephaly and low set ears
 Muscle relaxant (1) centrally acting- muscle relaxants  Part of the HIPP- drugs that induce SLE
 H- hydralazine (vasodilator)
(2) direct- acting muscle relaxants
 I- INH (isoniazid)
 BZD is a centrally acting MR, baclofen  P- procainamide (antiarrhythmic)
 Direct-acting- dantrolene (DOC for malignant  P- phenytoin
hyperthermia d/t anesthesia), botulinum toxin A  Should be given using the sandwich method (NSS-
(botox), botulinum toxin B (myoblock) phenytoin- NSS)
Malignant hyperthermia  Use only NSS when administering
Muscles are contracting too much→ ↑ heat  Monitor serum levels
 BZDs are also antiepileptics, DOC for status  Absence/ petit mal (blank stare)
epilepticus  Ethosuximide
 Sleep disorders- insomnia as it causes sedation  Myoclonic- sporadic spasms
 Alcohol withdrawal (if withdrawal symptoms  Valproic acid
manifests)  Febrile- d/t hyperthermia
 Used in anesthesia induction  Phenobarbital
 Diazepam (valium)  Status epilepticus- emergency
 Lorazepam
  Diazepam o This is removed in non-drowse Neozep
 Hydroxyzine 
 Second Generation
 No sedative effect; does not cause drowsiness 
 Cetirizine 
o Take at bedtime, once a day
o Takes effect for 24 hours
 Loratadine (Alerta) 
 Desloratadine

DECONGESTANTS 
 Pharmacodynamics: sympathomimetic drugs; alpha 1
receptor agonist → causing vasoconstriction
 Caution in CV px: 
o Causes ↑HR → ↑workload of the heart
Partial Seizure o Vasoconstriction → ↑TPR → ↑BP → ↑workload
 Localized in one lobe of the heart 
 Simple  ❗NOTE❗: Take only for 5 days
 Complex  >5 days can lead to rhinitis medicamentosa
 Carbamazepine (Tegretol) is the only drug used (rebound effect); reversible 
 DOC for trigeminal neuralgia  Nasal Decongestants 
 Tetrahydrozoline
 Phenylephrine
 Oral Decongestants 
Status Epilepticus
 Pseudoephedrine (Sudafed)
 Emergency o Ingredient in crystal meth
 Crazy seizures in <5 minutes but can extend >5 minutes o Addictive
 The brain needs 250 x the normal need
EXPECTORANTS 
Nursing Considerations
 Pharmacodynamics: reduces the adhesiveness and
 ABC, establish IV access surface tension of URT fluids (loosen up phlegm) that
 DOC is BZD will facilitate the removal of viscous mucous 
 Phenytoin  Guaifenesin (Robitussin Expectorant) - for productive
 If status continues cough
 Intubate if seizures do not stop, phenobarbital 20 mg/ kg
IV MUCOLYTIC
 If status continues  Pharmacodynamics: Decrease the viscosity of
 Induce coma to prevent further hypoxia secretions 
 Allow the brain to rest and recuperate for the oxygen  INDICATION: productive cough
needs  Acetylcysteine (Fluimucil)
 Bedside EEG monitoring  Protects the liver cells from acetaminophen toxicity
 Treatment of choice- BZD (antidote)
 Prophylactic of choice- phenytoin  NAC
o 200 mg sachet - TID
RESPIRATORY DRUGS o 600 mg effervescent - OD/BID
 Ambroxol 
INFLAMMATORY RESPONSE   S-Carboxymethyl Carbocisteine 
 normal response of a vascularized tissue to injury
 Dornase Alfa 
 destroys pathogen, promotes healing
ANTITUSSIVE
 Pharmacodynamics: Suppress the cough reflex in the
CNS 
 INDICATION: non-productive cough 
 ❗NOTE❗: not to be taken more than one week
 Dextromethorphan/DM (Robitussin DM) 
 Benzonatate
 Codeine
 Narcotic and antitussive 
 Addictive 

LOWER RESPIRATORY TRACT DRUGS

UPPER RESPIRATORY TRACT DRUGS (URT)
 Asthma, COPD (chronic bronchitis & emphysema)
ANTIHISTAMINE: Anticholinergic Drugs   Obstruction s/t smoking (irreversible)
 Pharmacodynamics: selectively blocks H1 receptor sites
BRONCHODILATORS: (antiasthmatics) 
 First Generation:
 Pharmacodynamics: dilate the airways to facilitate
 CNS depressant:
respiration
o EFFECT: drowsiness, sedation 
 Sympathomimetics 
o NC: 
 SNS Effect: causes bronchodilation
 Increase OFI to liquify phlegm
 Avoid driving and operating big machines  Epinephrine - act on alpha and beta receptor sites in
the SNS (adrenergic)
 Sugarless gums; to increase salivation d/t
dryness of the mouth (effect of sympathetic  Albuterol - beta 2 adrenergic agonist; SABA
response) (short-acting beta agonist)
 Humidifier; to add up moist in the air  o Onset - <20 minutes
 Avoid alcohol; also a CNS depressant  o Duration - 4-6 hours
 Diphenhydramine (Benadryl): Anticholinergic drug   Terbutaline - beta 2 adrenergic agonist; LABA
 Chlorpheniramine - part of Neozep (long-acting beta agonist)
 o Onset - <20 minutes  If before meals, the prostaglandin E1 in the
o Duration - 12 hours stomach will also be blocked → ↓mucous →
 Ephedrine - alpha and beta agonist ↑HCL → gastric irritation 
 Side Effects: o Not used during acute attacks; unless SABA is
o Tachycardia/palpitation  not effective anymore?
 PNS drugs can be given if cannot be o Use bronchodilators before corticosteroid aerosol
tolerated o Teach clients how to use inhalers 
o Hypertension d/t ↑HR and vasoconstriction  Hold the inhaled drug for a few seconds
o Dryness of the mouth  before exhaling
 Anticholinergics/Parasympatholytics (blocking PNS,  Allow 1-3 minutes to elapse between each
still SNS - bronchodilation) inhalation 
o Pharmacodynamics: block vagally mediated  Rinse mouth with water after 
reflexes   Block immune response → destroy the
 Vagus (X - vagal): PSNS effect (craniosacral)  normal flora → stomatitis (singaw)
 1973: CN3, 7, 9, 10 
o Ipratropium - for those who cannot tolerate the side
effects of sympathomimetics 
 Methylxanthines (antiasthmatics) - CAT
 Pharmacodynamics: directly relax the bronchial
smooth muscles → ↑vital capacity
 Caffeine
 Aminophylline 
 Theophylline  o Notify doctor or nurse if sore throat or sore
 Nursing Considerations: mouth occurs (superinfection)
o Administer oral drug with food or milk to o Do not stop abruptly (can lead to Addisonian
increase absorption crisis)
o Monitor for side effects: o Taper off gradually under supervision
 Palpitation and tremors  Leukotriene Receptor Antagonists
o Dietary control of caffeine (palpitations)  Montelukast 
o Monitor the serum theophylline & aminophylline o Given to patients with COVID for
level (can be toxic) bronchodilation
 Normal: 10-20 mcg/ml o Prophylaxis for asthma
 >20 mcg/ml: nausea (first sign of o Taken for months, years for the asthma not to be
toxicity) triggered
 >35 mcg/ml: tremors (later sign of  Zafirlukast 
toxicity)  Zileuton 
 Nursing Considerations: Bronchodilators -  Surfactants 
BREATHE   Beractant
 Breathing & coughing techniques 
o To remove the secretions and optimize oxygen CARDIOVASCULAR DRUGS
exchange
 Relaxation techniques
o Music, etc.
 Evaluate HR and BP (possible side effects)
 Appropriate positioning
o High fowler’s - increase the AP diameter of the
chest and allow lung expansion
 Tremors (common side effect)
 Have 8 or more glasses of fluids
o Loosen phlegm 
 Emphasize no smoking
The Heart & Blood Pressure 
DRUGS AFFECTING INFLAMMATION  Preload
 Inhaled Steroids  Initial stretching of the cardiac myocytes (muscle
 Corticosteroids will block arachidonic acid → cells) prior to contraction
bronchodilation  Related to ventricular filling 
 Pharmacodynamics: blocks the immune response  Venous return
(antibody production); anti-inflammatory   Venous pooling, thus decreases preload 
 INDICATION:  Afterload 
o Asthma: blocks arachidonic → (X) leukotriene
 Is the force or load against which the heart has to
→ (X) bronchoconstriction → bronchodilation  contract to eject the blood
 Status asthmaticus: steroids via IV for faster
 Pressure in the left ventricle needed to push the blood
effect
out of the circulation 
o Arthritis (inflammation/pain) : blocks
o Pressure in left ventricle: greater than the
arachidonic → (X) leukotriene → (X)
pressure outside (180); stretches too much leads
prostaglandin, →(X) dolor
to left ventricular hypertrophy/cardiomegaly
o Allergy: blocks arachidonic → (X) histamine →
(seen in CXR)
↑vasoconstriction → ↓blood flow → (X)  Branches: aorta (artery), arterioles, capillaries 
capillary permeability → (X) swelling
 If vasodilator is given → ↓afterload → ↓workload of
Prostaglandin E2 → hypothalamus → stimulate thermoregulation the heart (good for the heart) 
center → fever  ↑Afterload → ↑Cardiac workload 
 -one  Chronic - hypertrophy, cardiomegaly
 Budesonide 
 Fluticasone ANGINA 
 Triamcinolone 
 Nursing Considerations
o Given after meals
  Abrasion → (X) barrier → fast absorption
→ hypotension 
o Rotate sites to prevent skin irritation 
o To prevent tolerance - nitrate-free hours (at least
8 hours HS)
 Not worn 24/7 as it can result to tolerance
(needs higher dose for the same effect)
 Has a ceiling effect - limitation of effects
despite higher doses
 Side Effects:
o Headache d/t vasodilation (administer
paracetamol)
o Do not discontinue d/t headache. Tell the patient
that it will taper down after some time
 AKA Chest pain  o Orthostatic hypotension 
 Pain d/t ↓oxygen → accumulation of lactic acid o Tachycardia (compensatory mechanism)
 Reversible: still no damage to tissues  Hypotension → baroreceptors in the brain
 PROBLEM: ↓O2 supply, ↑O2 demand → ↑HR → ↑BP
 CAUSES: Atheroma (plaques) - fatty tumors   Late manifestation 
 Narrowing d/t deposits of atheroma → ↓blood flow
→ ↓oxygen → ↑oxygen demand Calcium Channel Blockers (Very Nice And Friendly Drugs)
 GOAL: Increase O2 supply & decrease O2 demand  Calcium is for muscle contraction, coagulation/blood
(need) clotting
 Cardiac enzymes are present only when there is tissue  The calcium goes inside the cell for the muscle to
damage contract
 Troponin I (-)

DRUGS FOR ANGINA 

 Vasodilators 
 improve blood flow
 GOALS: Increase oxygen supply
 Nitroglycerin 
 Cardiac depressants  -dipine: Acts on the blood vessels 
 GOALS: Decrease the oxygen demand   Verapamil - antiarrhythmic
 Nifedipine / Nicardipine
Nitrates  Amlodipine
 Pharmacodynamics:   Felodipine
 Direct acting vasodilators  Diltiazem - antiarrhythmic
 Acts primarily on the veins 
 DOC for stable angina, unstable angina BETA BLOCKERS
 Nitroglycerine  sympathomimetic drugs → ↓HR, ↓cardiac workload →
 Isosorbide Mononitrate ↓O2 demand → ↑O2 supply
 Isosorbide Dinitrate  cause vasodilation → ↓TPR total peripheral resistance →
 Nursing considerations: ↓AFTERLOAD → ↓O2 demand → ↑O2 supply
 NTG Tablet  Metoprolol 
o Route: SL (fast absorption d/t  Nadolol - angina & HTN
presence of blood vessels)  Propranolol 
o No first pass effect
o Dose: 1 tab, q5 mins for 3 doses RANOLAZINE 
 q5 mins: T1/2 is 3 mins  A newer drug with limited indications
 If within 15 mins the pain is still not relieve:  Approves as first line therapy for chest pain
Myocardial Infarction   Can be combined with other drugs
o Shelf life: 3 months
o Storage: in a dry, amber-colored container MYOCARDIAL INFARCTION
(photosensitive)  Tissue death
o Encourage the patient to carry 3 tablets only 
 NTG Patch DRUGS AFFECTING BLOOD COAGULATION
o Sustained slow release d/t body heat → absorbed  Antiplatelets
to the blood  Aspirin 
o Effects in 30-60 minutes   Clopidogrel
o Apply over dry, hairless area (to allow the patch  Anticoagulants
properly place to the skin)  Warfarin
 Do not shave, trim only if hair is present to  Heparin
prevent abrasion  Thrombolytics
  Alteplase  Aspirin
 Streptokinase  Indications:
 Reteplase o Anti-platelet - blocks thromboxane A2 → (X)
 Urokinase clotting
 Antifibrinolytic o Analgesic - blocks prostaglandin → (X) dolor
 Aminocaproic Acid o Antipyretic  blocks prostaglandin E2 → (X)
 Tranexamic Acid fever
o Anti-Inflammatory - block inflammatory
DRUGS USED IN MYOCARDIAL INFARCTION response
(MONA)  Side Effects: Bleeding
 Morphine  Nursing Considerations: 
 Priority is pain o Give PC (post cibum)/after meals to avoid
 opioid/ narcotic agonist gastric irritation 
 Pharmacodynamics: stimulate the opioid receptors o Give with glass of water/milk to lessen gastric
found in the CNS and GIT irritation
 Uses: o Educate the patient to WOF toxicity 
o Mild to moderate pain (opioid analgesic)  Bleeding gums
o Generally safer than NSAIDs in older adults  Tinnitus
 NSAIDS - gastric irritating effect  Black tarry stool
o Vasodilator → venous pooling → ↓preload → o Increase risk of toxicity in elderlies and children 
↓workload of the heart → ↓O2 demand → o Avoid in children with a viral infection (e.g.,
↑oxygen supply  chickenpox, measles) 
 Contraindications:  Can cause reye syndrome 
o Hypersensitivity 
o Increased ICP and suspected head injuries 
 Can mask headache 
 Side Effects:
o Euphoria
o Constipation 
o Bradycardia 
o Respiratory depression (CNS effect)
o Addiction 
 Morphine toxicity - pinpoint pupils 
 Nitrates
 Drugs Affecting Coagulation:
 Antiplatelets o WOF salicylate poisoning/salicylism 
 Anticoagulants  Fatal dose: 150 mg/kg BW
 Thrombolytics  Tinnitus - most important sign in acute
 Antifibrinolytic poisoning
 Hyperventilation → respiratory alkalosis 
COAGULATION CASCADE  Severe toxicity → metabolic acidosis →
seizure 
 Clopidogrel (Plavix) 
 Ticlopidine (Ticlid) 
 Dipyridamole

FIBRINOLYTIC CASCADE

ANTICOAGULANT
Warfarin 
 Pharmacodynamic: Blocks the vitamin K dependent
clotting factors → no more clots
 Route: Oral (Home) 
 not absorbed in parenteral route
 Therapeutic test: Prothrombin time (PT)
 Time it takes for the prothrombin to form clots 
ANTIPLATELETS  Problem: Laboratories have different normal values
 Aka Blood Thinners o Lab 1: 8-12 secs before liver produces
 Pharmacodynamics: blocks the formation of platelet prothrombin
plug  o If warfarin is given, the result should be higher
 Hypertensive crisis → can activate the local than 12 (delayed)
coagulation cascade → forming clots → obstruction  Better test: International Normalized Ratio (INR)
→ decreased blood flow → decreased oxygen supply o Normal: 1
→ ischemia  Therapeutic margin: 1.5-2.0 x normal 
  Should know the BASELINE   The thrombolytics will activate the plasminogen which
 Case: patient was prescribed with warfarin will be plasmin and dissolve the clot 
o Dx: PT request = 12 secs (Normal: 8 - 12 secs)  Recombinant Tissue Plasminogen Activator (RTPA)
 Nursing action: Give warfarin   Side effects: bleeding 
 The higher the PT, the higher the chance of  Antidote: Antifibrinolytics 
hemorrhage   Because if there is fibrin there are clots
 12 x 1.5 = 18 secs  Aminocaproic acid (Amicar)
 12 x 2.0 = 24 secs   Tranexamic acid (Hemostan)
o Dx: PT = 24 secs o Take home medications: Tooth extraction 
 Nursing action: Give warfarin (still within o OB: Abnormal Uterine Bleeding (AUB) 
the therapeutic range)  Nursing Considerations:
o Initial: 10 secs so,  Monitor vital signs
 10 x 1.5 = 15 secs  Monitor for signs of bleeding
 10 x 2.0 = 20 secs o Petechiae 
 Therapeutic range = 15-20 secs 
o Purpura 
o Initial: 8 secs
o Bruising 
 Administer the warfarin (Normal: 8 - 12
o Bleeding gums 
secs)
 PT = 16 secs = GIVE (8 is the baseline, we o Black tarry stool
can give if 12-16)  Use soft bristled toothbrush
 8 x 1.5 = 12  Use electric shaver
 8 x 2.0 = 16 
 PT = 20 secs = HOLD (not anymore within SUMMARY: Drugs Affecting Coagulation 
the range of therapeutic level)
 Side effect:
 Bleeding 
 Antidote: Vitamin K

ANTIHYPERTENSIVE DRUGS

 Nursing considerations:
 Monitor PT and INR
o If both PT and INR is in the exam, choose INR
o INR = 2-3
  Monitor I&O
o To check for signs of bleeding 
 Monitor vital signs
o If there’s bleeding patient will be hypotensive
 Monitor for signs of bleeding such as:
o Epistaxis Definition of Terms
o Petechiae   BP = resistance exerted by the blood against the smooth
o Bruises muscle wall
 Decrease intake of green leafy vegetables   SV = amount of blood ejected per beat
o It contains vitamin K   CO = amount of blood ejected per minute
 SVR = pressure exerted by the smooth muscle wall
Heparin against the blood
 Pharmacodynamics: Blocks the formation of thrombin  TPR = Total Peripheral Resistance
→ no clots
 Route: IV or SQ (Hospital) Mean Arterial Pressure (MAP) 
 Therapeutic test: Activated Partial Thromboplastin Time  Average pressure throughout each cycle of the heartbeat
(aPTT)  Clinical significance: tissue perfusion
 Therapeutic margin: 1.5 - 2.5 x normal
 Side effect: bleeding
 Antidote: Protamine Sulfate 
 Not given orally because this will only be destroyed by
 Normal: 70-100 mmHg - the cells are getting sufficient
gastric acids and enzymes
oxygen
THROMBOLYTICS  <70 mmHg - the cells are not getting sufficient
oxygen
 Pharmacodynamics: activate the conversion of
o Hypoxia 
plasminogen to plasmin
o Tissue death
 Plasmin → (X) fibrin → (X) clot
 GOAL: Dissolve the clot in order to restore the blood  >100 mmHg - afterload is high
flow o Increased workload of the heart
 Golden hour: 3 hours; 1 hr (the soonest the diagnosis, the o Damage to the heart
soonest administration of thrombolytics, the BETTER) o Blood clots
 Urokinase 
 Streptokinase  Regulators of Blood Pressure 
 Alteplase   Baroreceptors found in carotid artery and aorta
  Increase or decrease HR  Angioedema 
 Vascular Autoregulation   Hyperkalemia - d/t no aldosterone, no Na
 Vasoconstriction → ↑TPR → ↑BP
 Vasodilation → ↓TPR → ↓BP DIRECT RENIN INHIBITORS 
 Regulation of Body Fluid Volume  Site of action: kidneys 
 ↑body fluid volume → ↑blood volume → ↑BP  Aliskiren 
 Renin Angiotensin Aldosterone System (RAAS) SELECTIVE ALDOSTERONE ANTAGONISTS
 Blocks aldosterone
 Epelrone 

ANTIHYPERTENSIVE DRUGS ACTING ON ANS

RECEPTORS 
  Drugs Acting on Alpha 1 Adrenergic Receptors
  Drugs Acting on the CNS( Alpha 2 Receptors )
  Drugs Acting on Beta Adrenergic Receptors

ALPHA 1 ADRENERGIC ANTAGONISTS 

 “zosin”
 Prazosin
 Doxazosin
 Terazosin
 First dose effect:
 Orthostatic hypotension
o NC: Split the first dose (10 mg → 5 mg; give HS
to prevent feeling of hypotension)

ALPHA 2 ADRENERGIC AGONIST

 Has opposite effect 
 Decreased NE→ weakened SNS → PSNS
 Clonidine 
 Methyldopa

BETA ADRENERGIC BLOCKERS 

 “olol”
 Propranolol
 BETA SPECIFIC ADRENERGIC BLOCKERS “ olol
”
 Betaxolol Bisoprolol 
 Esmolol
 Acebutolol Atenolol
 Metoprolol
ANTIHYPERTENSIVE DRUGS ACTING ON RAAS 
 Drug Acting on Renin VASODILATOR ANTIHYPERTENSIVE DRUGS
 Drug Acting on ACE Receptor  Indirect Acting Vasodilators
 Drug Acting on The Angiotensin 2 Receptors  Calcium Channel Blockers
 Drug Acting on Aldosterone o Verapamil
o Nifedipine
ACE INHIBITORS (“-pril”)
o Nicardipine
 Pharmacodynamics: Blocks angiotensin converting
o Amlodipine
enzyme in the lungs → (X) conversion of angiotensin 2
o Felodipine
→ (X) bind in blood vessels → (X) enter in receptor →
blood vessels → dilates → TPR decreases → BP o Diltiazem
decreases → no osmolarity → no retention of sodium  o Common SE (-dipine): peripheral edema
 At the same time, (X) angiotensin 2 → (X) bind in blood  NC: Elevate the legs to increase venous
vessels → (X) stimulation of adrenal cortex → no preload 
retention of sodium → no osmolarity →(X) stimulation of o Used for prinzmetal angina - obstruction d/t
hypothalamus → (X) ADH → decrease TPR → decrease vasospasm of the coronary artery
BP  Direct Acting Vasodilators
 Captopril  Vasodilators
 Enalapril o Hydralazine (Apresoline)
 Lisinopril   DOC for PIH 
 Side effects: o Nitrates
 Angioedema   Nitroglycerine
 Cough (lung action) - most common  Isosorbide Dinitrate or Mononitrate 
o Can take with antitussive except for patients with o Nitroprusside
asthma and COPD  DOC for hypertensive crisis
 Elevated K   Route: IV
 Fast onset
 Paradoxical effect: 
 Short duration: given for 72 hours
 Stopping abruptly and taking it again
 It can cause cyanide poisoning
o Minoxidil
ANGIOTENSIN 2 RECEPTOR BLOCKER (ARB) “
 SE: hair growth 
sartan ”
o SE: headache
 Pharmacodynamics: Blocks the A2 receptors →
vasodilation → TPR decreases   Used for hypertensive crisis
 Losartan
DIURETICS
 Valsartan
 Increases urine output → decreases TPR → decreases BP
 Telmisartan 
 Thiazide 
 Side effects:
 Hydrochlorothiazide
  Side effects
o Hypokalemia
o Hyperglycemia
o Hyperuricemia   ANTIARRHYTHMIC AGENTS
 Most commonly used for HTN - gives mild diuresis  ACTION POTENTIAL: electrical current occurring in
 Loop Diuretic nerves and muscles
 Furosemide (Lasix)  Repolarization: relaxation
 Potassium-Sparing  Depolarization: contraction 
 Spironolactone  Process: 
 Amiloride o Resting membrane potential, all elec are in place,
 Triamterene  K in, Na out
o Stimulation of the muscle, Na channels open, so
 Side effects: Hyperkalemia 
it can get in = Phase 0 depolarization 
 Osmotic Diuretics
o Until there is normalization of sodium in and
 Mannitol
out, eventually some goes outside = Phase 1
 Carbonic Anhydrase Inhibitors (CAH Inhibitors)
repolarization
 Acetazolamide (Diamox)
o However Ca enters = Phase 2 Plateau
o For increased intraocular pressure, lithium
o K  channels open and k goes outside = Phase 3
toxicity 
rapid repolarization 
o Then K goes inside and Na goes outside (PISO)
DRUGS USED FOR HEART FAILURE
= Phase 4 resting potential 
 Pharmacodynamics: increases intracellular calcium
levels in the heart inc contractility  + INOTROPY
 The heart is not pumping effectively
 GOAL: help the heart pump
 (+) Inotropic effect - increase contractility
 (-) Chronotropic effect - rate of contraction

CARDIOTONIC DRUGS:
 Cardiac Glycosides
 Pharmacodynamics: increase the calcium in
myocardial cells
 Digoxin ( Lanoxin ) 
 Most commonly used in
o Heart failure
o Atrial fibrillation 
 Normal level = 0.5-2.0 ng/ml
 Effects: 
o (+) Inotropic effect
o (-) Chronotropic effect 
 Increase CO, increase renal perfusion
 Side effects:
o Bradycardia  Arrhythmia 
o Visual disturbance “halo”  Change in the automaticity or conductivity of heart
 Hallmark sign of digitalis toxicity  cells
 Digitalis toxicity   It can be tachycardia, bradycardia, atrial fibrillation,
o Serious sign atrial flutter, ventricular fibrillation, ventricular
o Increase risk of toxicity: hypokalemia  tachycardia, blocks 
o >10 ng/ml  Arrhythmia results from:
o Signs: o Electrolyte imbalances: Na+, K+, Ca+ 
 Nausea and vomiting  o Decreased O2 delivery: Angina, Myocardial
 Malaise Infarction 
 Depression  o Acidosis  → alters AP
 Arrhythmia  o Structural damage
o Antidote: Digitalis Immune Fab (Digibind)   Valvular diseases
 Phosphodiesterase Inhibitors o Drugs 
 Milrinone  Epinephrine
o Pharmacodynamics: blocks the enzyme  Atropine 
phosphodiesterase; increase cAMP (cyclic CLASS I: 
AMP); increase calcium levels  Block the sodium channel: Phase 0
o Effect: (+) Inotropic   Class 1a
 Procainamide - HIPP (drugs induced SLE)
OTHER DRUG THERAPIES:  Quinidine
 Vasodilators:  Class 1b 
 ACE Inhibitors: Blocks ACE → no A2 →  Lidocaine - local anesthetic 
vasodilation → decrease preload → decrease  Class 1c
workload of the heart → improved cardiac function   Propafenone 
 Nitrates
 Beta Adrenergic Agonists: Sympathomimetics - (+) CLASS II: 
Inotropic effect  Blocks the beta receptor: Phase 4
 Dobutamine  Propranolol
 Diuretics: Increases urine output → decrease preload →  Esmolol
decrease workload → improved cardiac function  
 Furosemide CLASS III: 
 Human B-type Natriuretic Peptide: Compensatory  Blocks the potassium channel: Phase 3
response → produced myocardial cells → decrease  Amiodarone - emergency
workload of the heart   Sotalol
 Nesiritide (Natrecor)
CLASS IV:   Chemical Stimulants
 Blocks the calcium channel: Phase 2  Irritates the colon muscles → inducing bowel
 Diltiazem movement (BM) 
 Verapamil  Senna
 Bisacodyl ( Dulcolax )
FOR HEART BLOCKS:  Castor oil
 Anticholinergic   Bulk Forming / Osmotic Laxatives
 Atropine   Absorbs water → adding volume to the stool (safest)
 Psyllium (sachet)
GASTROINTESTINAL DRUGS o Mix in a glass of water → drink immediately
 MUCUS - coats the lining (because it forms like jelly ace)
 BICARBONATE - neutralizes the gastric acid  Stool Softener / Emollient Laxatives
 ADEQUATE BLOOD FLOW - nourishes the mucosa   Helps to wet and soften the stool
 PROSTAGLANDIN - stimulate mucus and bicarbonate  Lactulose
secretion o DOC for hepatic encephalopathy 
 Ulcer - an erosion in the mucosal lining  Hepatic encephalopathy d/t increased
ammonia level d/t damaged liver 
DRUGS AFFECTING GASTRIC SECRETIONS  Ammonia (toxic) is from proteins (protein
Drugs for PUD, GERD and Gastritis → amino acids → ammonium + ammonia) 
 Antacids  Ammonia → metabolizes in the liver → to
 Neutralize the acid  be converted into urea (water soluble) →
 Inactivate the pepsin  excreted via urine (smelly due to bacteria
 Enhance the mucosal protection present)
 Dose: 1 tab, 1-2 hours AC/PC HS for 6 months, 4x a  Ammonia → build ups → enters to BBB →
day damaging brain cells → hepatic
 Note:  encephalopathy 
o Prolonged use can lead to rebound acidity 
o Liquid is better for liberation is faster HEPATIC ENCEPHALOPATHY
 Aluminum Hydroxide  Diet: low protein (prevents ammonia buildup)
o SE: constipation 
 Magnesium Hydroxide  LACTULOSE NEOMYCIN
o SE: diarrhea
 Magaldrate (Maalox, Kremil-S)  Binds with  Wastes in the colon contains
ammonia CHO, CHON and fats → colon
o Combination of magnesium + aluminum has bacteria that would act on
hydroxide  protein → bacteria would break
 H2 Receptor Blockers down protein into ammonia →
 Pharmacodynamics: blocks H2 receptors in the reabsorbed by the blood →
stomach lining (parietal cells) → suppression of HCl- crosses BBB causing hepatic
secretions encephalopathy
 OTC medication   Neomycin kills bacteria that
converts protein to ammonia
 “Tidine”
 Dose: 2x a day for 2 months 
 Cimetidine  ANTI-DIARRHEAL DRUGS 
o Causes gynecomastia (binds to androgen)  Loperamide (Diatabs/Imodium)
o Impotence   Effect: 
o Decreased libido  o Anticholinergic action → SNS → constipation 
 Ranitidine o Also causes urinary retention 
 Famotidine   o Decrease body secretions 
 Nizatidine   Opiate Related Diphenoxylate with Atropine
 Proton Pump Inhibitors (PPI)   Opioid narcotic
 Pharmacodynamics: blocks the proton pump →
suppressing HCl secretions  ENDOCRINE DRUGS
 Dose: 1 tab OD for 2 weeks
 Most effective and cost effective  DRUGS TO CONTROL GLUCOSE
 Omeprazole  OHA is teratogenic; GDM - insulin 
 Lansoprazole  GOAL: decrease blood glucose levels
 GI Protectives  Liver (T-B) - produces glucose
 Sucralfate o OHA decreases production of glucose
 Prostaglandin o Thiozolidinediones
 Misoprostol o Biguanides 
 Muscle (T-B) - uptake/use of glucose
PROTECT STOMACH LINING o OHA increases the use of glucose by the muscles
Sucralfate Misoprostol - Cytotec
o Thiozolidinediones
(prostaglandin agonist) o Biguanides 
 Pancreas (S-M) - produce insulin → to bring
 Sticky gel coating the  Acts as replacement for glucose into the cell
ulcer endogenous prostaglandin  o OHA should be increased to enhance production
 Given AC  Prostaglandin increases of insulin
 Protective barrier mucus and bicarbonate o Sulfonylureas
against pepsin and  Contraindication in
o Meglitinides 
gastric acid pregnancy
 Causes cervical dilation  Intestine (AGI) - absorption of glucose
 Small risk of o OHA is decreased to lessen absorption of
→ Abortifacient 
constipation
 May cause diarrhea glucose
 Action: prostaglandin o Alpha Glucosidase Inhibitors 
agonist 

ORAL HYPOGLYCEMIC AGENTS (OHA)

LAXATIVES
 DRUG MOA SIDE EFFECTS  Route: 
 SQ - 45 - 90 degrees on normal SQ mass; 45-60
Biguanides ↓glucose production  GI degrees on thin person; 90 degrees on fat patients 
 Metformin by the liver & disturbance  IM - absorption would be too fast; can lead to
 DOC for Type increase glucose  ↓appetite hypoglycemia 
2 DM uptake by muscle  IV - can be given
 Nausea
 diarrhea  o Only insulin can be given via IV - REGULAR
 rare: INSULIN
metabolic  STORAGE: 
acidosis 1. Avoid extremes of temperature.
(renal 2. Before injection : should be room temp
impairment) 3. if vial will be used in 1 month: room temp
4. Otherwise: refrigerate
Second Generation  Stimulate release Hypoglycemia 
Sulfonylureas of insulin from
Glipizide, pancreas  TYPE EXAMPLE ONSET PEAK DURATIO
Glimepiride, N
 May increase
Glyburide cellular
Very short Aspert, 12 30-60 2-4 hours
sensitivity to
First-Generation Lispro minutes minutes 
insulin 
Sulfonylureas
Chlorpropamide, Short  Regular  30-60 2-4 4-6 hours
Tolazamide, minutes hours 
Tolbutamide
(Orinase) Intermediate  NPH 2-4 6-8 hours 16-20
hours hours 
Meglitinides Promotes insulin Hypoglycemia
(Glinides) secretion by the Long acting Ultralente  6-8 hour 12-16 20-30
Nateglinide, pancreas hours hours
Repaglinide
Very long Glargine, 1 hour No peak 24 hours
Thiazolidinediones  ↑ insulin Water retention acting Lantus 
(Glitazones) sensitivity in (weight gain &
Pioglitazone NIDDM edema)
 ↑ uptake by
muscles
 ↓ glucose
production by
the liver

Alpha-Glucosidase Inhibits CHO GI: flatulence,

inhibitors digestion/absorption, cramps,
Acarbose, Miglitol ↓ post prandial blood distention,
glucose rise  borborygmus

DPP-4 inhibitors ↑ activity of incretins

(Gliptins) (inhibits their
Nesinal, Linagliptin breakdown) 
↑ insulin release
↓ glucagon release
↓ hepatic glucose
production HYPOGLYCEMIA
 Glucose-Elevating Agents
Dopamine agonist  Diazoxide
Bromocriptine
 DOC: Glucagon 
o Unconscious patient 
 Conscious and still at home, do 15 / 15 rule:
o 15 → grams of FAC (fast acting carbohydrates) -
soda, chocolates 
o 15 → minutes, assess again 
 If still lethargic, repeat the rule again, until
patient becomes normal 
INSULIN
 ACTION: liver, muscle & adipose to facilitate passage of
glucose, K+, and Mg
 Hyperkalemia → D50 + insulin 
 INDICATIONS : DM type 1, DM type 2, GDM
 Dose: based on onset, peak & duration
 Syringe: Gauge: 27-29 (½ inch long 
 Nursing considerations:
 Mix the ingredients well:
o Swirl vial gently
o Rotate between palms 
 Inject air into the insulin bottle
 Mixing insulins: draw up regular (clear first) then
cloudy DRUGS AFFECTING THE THYROID GLAND
 May be mixed with NPH or Lente 
o The only insulin that can't be mixed with other Thyroid Hormones: Functions
insulin → GLARGINE/LANTUS  Control metabolic rate of tissues
 Once mixed, administer within 5-15 minutes  Accelerate heat production
 Aspiration is NOT RECOMMENDED with self-  Accelerate oxygen consumption
injections of insulin  Development of secondary sexual characteristics
 Brain development o Halitosis/Bad breath
 Consult MD before eating iodized salt and iodine rich
Hypothyroidism (everything is low, slow and dry) foods
 Bradycardia  Avoid aspirin & meds w/ iodine because it can block
 Decreased appetite  the production of thyroid hormones
 Weight gain  PTU causes agranulocytosis
 Constipation o Advise the patient to contact healthcare provider
 Intolerant to cold temperature  if fever or sore throat develops 
 Males: impotence and incompetent penis 
 Females: amenorrhea ANTIMICROBIALS
 Mental retardation   Bactericidal = kill
 Bacteriostatic = prevents growth of bacteria
Process of T3 and T4 production  Narrow spectrum = limited coverage
 Diet: Iodine → Trapped in thyroid gland → Binding  Broad spectrum = covers a wide range of bacteria 
iodine + tyrosine → monoIodoTyrosine (MIT) → MIT +  Aerobic = kills bacteria who loves air
MIT = DIT → MIT + DIT = T3 → DIT + DIT = T4  Anaerobic = kills bacteria who thrives even without
presence of air
THYROID DRUGS: THYROID REPLACEMENTS
 INDICATIONS: Hypothyroidism  BACTERIAL CELL WALL
 Levothyroxine (Synthroid) - T4  Overall strength of the cell
 Liothyronine (Triostat) - T3  Growth
 Liotrix  - T3 + T4  Reproduction
 Thyroid Hormone  Obtaining nutrition
 Side effect:  Protection 
 Hyperthyroidism effects (everything is high, fast
and wet): BACTERIAL CELL WALL SYNTHESIS INHIBITORS
 Nursing Interventions
 Should be given at least 4 hours apart from; so as not Beta Lactams: has beta lactam rings 
to decrease absorption
o Multivitamins
o Almg (Oh) 
o Simethicone
o Calcium Carbonate  Penicillins: “Cillins” 
o Iron  Penicillins - G (+): narrow spectrum
o Sucralfate o  Penicillin V - Given orally
 Instruct to avoid foods: Inhibit thyroid secretions  o  Penicillin G Benzathine - Given IV
o Strawberries o  Penicillin G Potassium - Given IV
o Peaches o  Penicillin G Procaine - Given IV 
o Pears  Extended-Spectrum Penicillins: gram (+) and gram
o Cabbage (-)
o Turnips o Amoxicillin - Given oral
o Cauliflower o Ampicillin - Given IV
o Radishes  Penicillinase-Resistant PCN
o Pea o Penicillinase 
 Enzyme produced by bacteria 
ANTI THYROID DRUGS  Destroys the structure of penicillin 
o Nafcillin
 INDICATIONS: Hyperthyroidism 
o Oxacillin
 Methimazole (Tapazole)
 Propylthiouracil (PTU)   Beta-Lactamase Inhibitors
 Commonly used in pregnancy  o Beta Lactamase
 Lugol’s Solution  Enzyme produced by the bacteria (sanay na
kay penicillin lmao)
 Strong iodine solution
 Breaks open the beta lactam ring →
 Action: block the synthesis of thyroid hormones 
inactivate the beta lactam 
 Iodide I 131 o Clavulanic Acid
 Side effect: Hypothyroidism effects  o Sulbactam
 Nursing Interventions: o coAmoXiClav (Augmentin) 
 Monitor VS (decrease in BP and HR)
 Nursing Considerations:
 Monitor T3, T4, TSH o Risk for hypersensitivity 
 Monitor weight for weight gain  NI: skin testing
 Take with meals  o Cross allergy with cephalosporins 
 Instruct how to measure PR  NI: If patient is allergic to penicillin, do
 Instruct re importance of medication compliance not give cephalosporin and vice versa
 Abruptly stopping meds because this might lead to o Give 1 -2 hours AC or 2-3 hours PC
thyroid storm: o Probenecid (uricosuric drug)
o Fever  Decrease the excretion of penicillin →
o Flushed skin increase blood levels of penicillin
o Confusion  Adverse effects: 
o Tachycardia o Most common cause of medication allergic
o Dysrhythmia  reactions
o Signs of heart failure o Can occur with any of the PCN
 Monitor sx of iodism: o Symptoms:
o Complaints of nausea and vomiting  Hives
o Metallic taste  Rash
o Skin rash  Itching
o Sore gums  Angioedema
o Hypersalivation  Anaphylaxis
 oWhen the patient shows signs of an allergic CLASSIFICATION OF ANTIMICROBIALS BASED ON
reaction, immediately STOP SITE OF ACTION
 Common side effects:
o Nausea and vomiting Blocks Protein Synthesis
o Diarrhea  Macrolides
o Abdominal pain   Azithromycin
 Allergic Reactions o Has a sustained release but the duration of action
o If the patient is allergic to one PCN, avoid all of is 10 days 
them  o Dose: OD for 3 days (it is already effective for 3
o Very small chance of cross allergy to days, and still lasts for 10 days)
cephalosporins  For COVID, OD for 5 days (also covers
 Alternatives  gram negative bacteria)
o Vancomycin  Clarithromycin 
o Erythromycin  Erythromycin 
o Clindamycin   o Alternative drug for penicillin allergy 
 Cephalosporins   Chloramphenicol 
 1st Generation: Cephalexin, Cefazolin  Can cause gray baby syndrome 
o Has gram positive coverage with a weak o Manifestations:
negative coverage  Cardiovascular collapse 
 2nd Generation: Cefuroxime, Cefaclor   Cyanotic
o Has gram positive coverage with some negative  Avoid in children <2 years old
coverage  Lincosamines
 3rd Generation: Ceftriaxone, Ceftazidime   Clindamycin (Dalacin C - mixed in eskinol; for
o Has gram positive coverage and gram negative acne)
coverage  Things To Remember:
o Effective concentration in CSF thus can enter o Allows clostridium difficile to infect colon,
BBB colitis, pseudomembranous (foul smelling feces)
o DOC for Meningitis caused by gram negative  Antibiotic-induced colitis  
o Treatment: vancomycin 
bacteria
 4th Generation: Cefepime, Ceftaroline  Aminoglycosides - “mycin”/”cin”
o Has gram positive coverage and gram negative  Streptomycin
coverage o Anti-TB drug 
 5th Generation: Ceftobiprole o SE: ototoxic
o Has gram positive coverage and gram negative  Kanamycin
coverage  Neomycin
o Newest and the only cephalosporin that can be o Used in hepatic encephalopathy 
used for methicillin-resistant staphylococcus  Gentamicin
aureus (MRSA) o Nephrotoxic 
 Carbapenems: Meropenem  Adverse Effects: nephrotoxic & ototoxic
 Broad spectrum 
 Bactericidal 
 Monobactam: Aztreonam 
 Narrow spectrum
 Good for UTI, skin infections

Glycopeptide - no beta rings 

 Vancomycin
 DOC for MRSA
 Alternative drug for penicillin allergy
 Adverse effects: hypersensitivity reaction 
o Possible allergic reaction/anaphylaxis
o Red man syndrome 
 Occurs with fast infusion
 Manifestations:  Tetracyclines
 Flushed skin and neck   Tetracyclines
 Itchy o Indicated for:
 Prevention:   H. pylori (peptic ulcer disease)
 Slow IV infusion (30 minutes) /  Acne vulgaris (oral/topical)
infusion pump  Chlamydial infections 
o Adverse Effects:
PROTEIN IN A BACTERIAL CELL  Staining of the teeth (gray)
 Vital for bacterial cell replication → growth   GI irritation 
 If bacteria cannot synthesize protein → no growth →  Fetal exposure can lead to dental enamel
death  dysplasia 
 Not given to pregnant women
(teratogenic)
 Hepatotoxic  
 Doxycyclines 
o DOC for leptospirosis 🐀 
 For treatment and prophylaxis  
 Demeclocycline
o Used in SIADH - has a diuretic effect 

Folic Acid Synthesis Inhibitor 

 Folic acid- vital for maturation of RBC
 Sulfonamides 
 Sulfasalazine
  Sulfamethoxazole  Codeine
 Trimethoprim   Tramadol 
 Adverse Effect: Steven Johnson’s disease   Severe pain: opioid (strong)
 Morphine
 Fentanyl 

DRUG CALCULATION

ESTIMATING CHILD DOSAGES BASED ON ADULT

DOSE
 Clark’s Rule:

Nucleic Acid Synthesis Inhibitor 

Example:
 Fluoroquinolones (-oxacin) o The adult dose of Cephalexin is 500 mg per
 Broad Spectrum  dose. How much should be prescribed to a 3-
 Bactericidal Against G (-) And Some G (+) year old child weighing 14 kg.
 Ciprofloxacin   Conversion: 1 kg = 2.2 lbs
o For UTI, STDs   14 kg x 2.2 lbs/1kg = 30.8 lbs
 Ofloxacin  500 mg x 30.8/150 = 103 mg
 Young’s Rule: 
Rifampicin - anti-TB drug
 SE: red-orange discoloration of body fluids 

2 cuties (QTs) say no to OB

Example: 
 Quinolones
o The adult dose of Cephalexin is 500 mg per
 Tetracycline 
dose. How much should be prescribed to a 3-
year old child weighing 14 kg.
ANALGESICS AND ANTI INFLAMMATORY DRUGS  500 mg x 3/15 = 100 mg
 Corticosteroids   Fried’s Rule: up to 2 years old only
 Acts on arachidonic acid and histamine 
 NSAIDS (ibuprofen, mefenamic acid)
 Acts on prostaglandin 
 COX-2 inhibitors - acts on COX-2 (celecoxib,  Example: 
valdecoxib) o The adult dose of Cephalexin is 500 mg per
 ASA  dose. How much should be prescribed to a 1 and
 Acts on prostaglandin, dolor  a half child weighing 14 kg.
 Antihistamine   500 mg x 18/150 = 60 mg 
 Paracetamol
 Weak anti-inflammatory FORMULA IN COMPUTING FOR DRUG DOSAGES 
 Action in the hypothalamus
 NOTE: Given after meals to prevent gastric irritation  

WHO ANALGESIC LADDER 

 A = Amount
 D = Desired Dose 
 S = Stock
 Q = Quantity
 Example: Order: Tempra 250 mg q4 for fever PRN
o Supply/Quantity
 Tempra 100 mg / ml
 Tempra 125 mg / 5 ml
 Tempra 250 / 5 ml
 Tempra 250 mg cap
 Tempra 500 mg cap
o Supply: 125 mg/5ml
 250 mg/125 mg x 5 ml = 10 ml

COMPUTING DRUG DOSAGES BASED ON WEIGHT

Steps:
1. Convert
2. Desired dose = recommended dose x weight in kg

 Pain scale 3.
 Mild pain: 1-3  Example:
 Moderate pain: 4-6 o Order: Acetaminophen 15 mg/kg/dose q4h for
 Severe pain: 7-9; 10 is worst fever
 Mild pain: Non-opioid (PAN)  Recommended dose: 15 mg
 Paracetamol o Weight: 12 kg
 ASA o Supply: acetaminophen 100 mg/ml
 NSAIDs  Desired dose = 15 mg/kg/dose x 12 kg
 Moderate pain: opioid + non-opioid  (cancel kg, leave mg/dose) = 180 mg/dose
  180 mg/dose / 100 mg x 1 ml (cancel mg,
leave ml/dose) = 1.8 ml/dose  

FORMULA IN COMPUTING FOR THE FLUID FLOW

RATE

 Microset for pediatrics = 60 ugtts/ml

 Macroset = 10 gtts/ml or 15 gtts/ml or 20 gtts/ml
 Examples
 Infuse 1.5 liters of D5W solution to be administered
over a 24 hour period. The IV set is calibrated to
deliver 15 gtts/ml
o 1500/24 x 0.25 = 15.6 or 16 gtts/min
 Infuse 0.1 L of D5NM to a severely dehydrated
infant for 30 mins. What is the rate of infusion?
o 100 ml/.5 x 1 = 200 ugtts/min 
 Infuse 1 L of IVF to the patient for 8 hours using a
macroset. Rate?
o 1000/8 x 15/60 = 31.25 gtts/min / 31-32 gtts/min
 Infuse 200 ml of IVF to a patient for 45 minutes. IV
set is labeled at 10 gtts/mL. Rate?
o 200ml/45 min x 10 = 44 to 45 gtts/min
 For how long should the nurse infuse a 1000 ml of
D5 0.9% NaCl running at a rate of 32 gtts/min. IV set
is labeled at 15 gtts/min.
o 1000 ml/32 gtts/min x 0.25 = 8 hr