PHARMACOLOGY

PHARMACOLOGY PHARMACODYNAMICS
→ Study of biological effects of chemicals → How the drug affects the body
→ All drugs are chemicals and are introduced into the → Action of drug:
body via different routes of the body wherein some sort • Replace a missing substance
of change is expected o E.g., insulin, levothyroxine, corticosteroids
(addison’s), mineralocorticoids
DRUG NAMES • Increase cellular activities
→ CHEMICAL NAMES o E.g., epinephrine when HR stops, inotropes
• Atomic or chemical structure • Depress cellular activities
• o Anatomic structure of a drug o E.g., beta blockers (-olols), calcium channel
• E.g., propionic acid blockers
→ GENERIC NAMES • Interfere with the growth of a foreign cell
• Name approved by the medical association of o E.g., antibiotics (destroy microorganisms),
pharmaceutical in the original country of anticancer drugs/antineoplastic drugs
manufacture → Drug Actions Maybe Through:
• Adopted by all countries 1. Receptors
• When prescribing drugs to patients generic names 2. Enzymes
should be given because of the RA 6675 Generics 3. Pumps
act of 1988 4. Chemical Interactions (E.G., Antacids)
• E.g., Ibuprofen 5. Altering Metabolic Process
→ BRAND NAME
• Name given by the manufacturer of the drug I. DRUG-RECEPTOR INTERACTIONS
• E.g., Advil, Medicol → Agonists - binds to a receptor &
stimulate action
RIGHTS OF DRUG ADMINISTRATION • A drug that stimulates
1. Right Medication receptor site
• Should be checked at least three times • E.g., digoxin, epinephrine,
2. Right Dose dobutamine
• Right amount → Antagonists - block action
3. Right Patient • Competitive Antagonist
• Two identifiers: Name and birthday o Binds to a SAME receptor site
4. Right Time o The potency of an agonist is
5. Right Route BLOCKED
6. Right Documentation o E.g., morphine and naloxone
7. Right Client Education • Non-Competitive Antagonist
8. Right to Refuse o Binds to DIFFERENT
9. Right Assessment RECEPTOR
10. Right Evaluation o The potency of an
agonist is REDUCED
BASIC CONCEPTS OF PHARMACOLOGY o E.g., cefuroxime and
→ Receptors- receives the drugs omeprazole (it will
→ Pharmacodynamics: Mode of action reduce the effect of
→ Pharmacokinetics : response of the body towards the cefuroxime)
drug
• Kinetics means movement ANS Drugs
• Liberation
• Absorption
• Distribution
• Metabolism
• Excretion → Adrenergic - SNS
→ 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
 a. Intravenous (IV)
❖ 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
III. INHIBITING PUMPS ❖ Muscles are very vascular, therefore,
→ Example: Reuptake inhibitors aspirate to determine if a BV is hit
• 5HT (5 hydroxytryptamine): serotonin ❖ Next fastest absorption
• Effector cell - nerve d. Intradermal (ID)
• SSRI: selective serotonin reuptake inhibitor 3. Transmucosal - SL, Inhalational, topical
o Antidepressant 3. Distribution - reaches target cell/tissue
▪ To increase the level of norepinephrine, • The drug is already in the target tissue/cell → bind
dopamine and serotonin to receptor → distribution
▪ MOA: Blocks the reuptake of serotonin, • Only the unbound molecule will cause the effect
serotonin stays in the synaptic cleft,
increasing the serotonin relieving the
symptoms of depression
o Biogenic Amine Theory
▪ There’s an imbalance in norepinephrine,
dopamine and 5HT → depression
4. Metabolism – liver
• 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/
• 5HT will not be reabsorbed→ ↑ in number→ relief breakdown)→ result into a
of depression new drug (reduced to 350-
400 mg) that is less active
IV. CHEMICAL INTERACTION (first pass effect)→ the
→ Example: Antacids reduced drug will be
• Neutralizing the gastric acid returned to the blood for
distribution
V. INTERRUPTING METABOLIC PROCESSES • The liver reduces the dose
→ Example: Insulin, Cortisol, Growth hormone to reduce toxicity→
detoxification
PHARMACOKINETICS o Everything that goes
→ This is how the body reacts to the drug through the liver is
1. Liberation - release of the active ingredient being detoxified
• For IV drugs, if 500 mg will be given, 500 mg will be
used by the body because of the bypassing of the
Stomach 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
2. Absorption - drug reached the blood (sweating)
• Routes of drug administration → DOSE
1. Enteral route (GIT) • Amount of drug to be administered to the patient
a. Oral route → SCHEDULE
b. Nasogastric route • TIME, frequency, how many dose/s per day
c. Rectal route (fastest route) → RECOMMENDED DOSE
❖ (+) fastest absorption d/t high • The amount of drug administered to reach the
vascularity of the rectum critical concentration
2. Parenteral • RIGHT amount + RIGHT schedule
→ CRITICAL CONCENTRATION
• Level of drug in the blood which produces a
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 → Overdose - toxicity; give antidotes (competitive
usually given in emergency situations antagonism)
→ HALF LIFE
• Time it takes for a drug to become half of its For diarrhea, determine the cause of the diarrhea first before
previously peaked level giving antidiarrheal medications
• Also written as: T ½ → If because of bacteria→ allow the body to expel the
• E.g., cefuroxime 500 mg T1/2 = 8 hours bacteria then rehydrate the patient, replace lost fluids
o If this is given at 6 am, after 8 hours, at 2 pm it → If (x) cause by bacteria, give loperamide/ diatabs
will become 250 mg
o Day 1: Example
▪ 6:00 am → 500 mg Remdesivir 100 mg IV, OD for 5-10 days
1st dose- 200 mg
▪ 2:00 pm → 250 mg + 500 mg
→ Succeeding doses- 100 mg OD
▪ 10:00 pm → 125 mg + 250 mg + 500 mg
o Day 2:
▪ 6:00 am → 62.5 mg PHARMACOLOGY TIPS
▪ 2:00 pm → 31.25 mg → Remembering medications and the body system
▪ 10:00 pm → 15.6 mg affected
o Day 3: → Review the sympathetic and parasympathetic nervous
▪ 6:00 am → 7.8 mg system since many medications have actions that affect
▪ 2:00 pm → 3.9 mg these systems
▪ 10:00 pm → 1.9 mg
o Day 4: NERVOUS SYSTEM
▪ 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 the doctor, the physician will have to delay the
surgery
→ The nurse will tell the patient to discontinue ASA for
about 5 days to lower risk of bleeding → Neurons (functional unit of the nervous system)
→ Rationale: to remove remaining half lives, if all of the half- → The electrical impulses cannot cross the synapse→
lives are removed then bleeding tendencies will be impulse will be passing the information to the chemicals
decreased
in the axon terminals→ chemicals will cross the
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”
→ RD: ceftriaxone 500 mg → Produced by the nerves and are stored in the axon
→ Schedule: q8 for 7 days terminals of the nerves
→ T ½- 8 hours (the half life will tell the time of → Acetylcholine (ACh)
administration) • “Muscle contraction” and “Memory”
→ Start of the cure will only occur once critical • Cholinergic nerves
concentration is reached and it should be sustained to o A nerve that is producing, storing, releasing
reach the cure acetylcholine
• When a drug reaches the CRITICAL • LOW = AZ
CONCENTRATION, that is the time it will have a • HIGH = BPD
THERAPEUTIC EFFECT (CURE) → Norepinephrine and Epinephrine (NE / E)
→ RD: ceftriaxone 250 mg • AKA adrenalines/ catecholamines
• Underdosing - critical concentration will not be • Chemicals released during SNS stimulation
reached therapeutic effect will not be reached → • Fight or flight
(x) cure • Affects behavior as well
→ If a dose is misplaced take it immediately but if it is too o HIGH: Schizophrenia, Mania
close to the next does continue to the next dose o LOW: Depression, Parkinson’s, ADHD
→ Right dose, wrong time→ (x) critical concentration and • Norepinephrine
therapeutic effect o Released in adrenal medulla → Adrenaline
• NOT Taking on the prescribed SCHEDULE will • Adrenergic nerves
prevent reaching THERAPEUTIC LEVELS. DO not o A nerve that is producing, storing, releasing
DOUBLE DOSE norepinephrine
→ Once the loading dose is given, recommended dose → Dopamine (Dopa)
should be continued • Coordination of impulses & responses
• A LOADING DOSE may be used in certain drugs • Motor movement and cognition (thinking, learning
(for EMERGENCY) to reach THERAPEUTIC and reasoning)
EFFECT immediately followed by RECOMMENDED • HIGH: Schizophrenia, Mania
DOSE • LOW: Depression, Parkinson’s, ADHD
 o Parkinson's disease → decreased dopamine Effects to the body
(degeneration of the dopaminergic nerves) Eye (pupils) Dilation (mydriasis) Constriction
• Dopaminergic nerves - Produce dopamine • Accommod (miosis)
→ Serotonin (5HT) ate more
light
• It involves arousal and sleep
Nasal mucosa Mucus reduction Mucus increased
• Preventing depression
Salivary gland Saliva reduction Saliva increased
• Motivation Heart Rate increased and Rate decreased,
• Eat Chocolates & banana increased decreased
• “Happy Hormone/Chemical” contractility contractility
• HIGH: Schizophrenia Blood vessels Constriction Dilation
• LACK: Depression (smooth
• Serotonergic nerves - Produce serotonin muscles)
→ Gamma Amino Butyric Acid (GABA) Lung Bronchial muscle Bronchial muscle
relaxation contraction
• An inhibitory neurotransmitter used in
(bronchodilation) (bronchoconstricti
anticonvulsants and ↑ RR on)
• prevents overexcitability or stimulation such as • To allow
seizure activity more air
• HIGH: Treats seizures exchange
• Gabaminergic nerves - Produce GABA Gastrointestina Blood flow, motility, Increased
l tract and secretions will motility→ diarrhea
AUTONOMIC NERVOUS SYSTEM decrease→
constipation
• Decreased
because
this is not
needed in
stressful
situations,
blood is
directed
towards the
muscles
(more
needed)
Liver Conversion of Glycogen
glycogen to glucose synthesis
increased
→ Includes two neurotransmitters: Norepinephrine and Kidney Decreased urine Increased urine
acetylcholine formation d/t formation
decreased blood
flow
Two branches:
Bladder Sphincter→ Relaxation of
→ Sympathetic FIGHT OR FLIGHT contracted sphincter
• Adrenergic nervous system Detrusor muscle→ Contraction of the
• Uses Norepinephrine / Adrenalines relaxed detrusor muscle→
o Decrease secretion emptying of the
• Neurotransmitter: bladder
o Preganglionic nerve: acetylcholine (ach) Sweat glands ↑ sweating No change
o Postganglionic nerve: norepinephrine (ne) Adrenergic Cholinergic
Agonist- stimulate Antagonist- block
→ Parasympathetic REST AND DIGEST
Mimetic- copy, Lytic- block,
○ Cholinergic nervous system
mimic destroy dissolve
○ Uses Acetylcholine Sympathomimetic→ SNS
■ Increase secretion Sympatholytic→ block SNS
○ Neurotransmitter: Adrenergic agonist, cholinergic antagonist→ SNS
■ Preganglionic nerve: acetylcholine Anticholinergic→ SNS
(ach) Cholinergic→ PNS
■ Postganglionic nerve: acetylcholine
(ach) Sympathetic = adrenergic Parasympathetic =
cholinergic
Sympathetic and Parasympathetic Effects
Structure Sympathetic Parasympathetic Agonist - stimulate Antagonist - block
(adrenergic) (cholinergic)
General Fight or flight Rest and digest Mimetic - mimic, copy Lytic - block, destroy
response → Sympathomimetic to dissolve (anxiolytic,
Origin Thoracolumbar Craniosacral heart → increase HR mucolytic thrombolytic,
Thoracic to L1-L3 Cranial nerves → Sympathomimetic to GIT hemolytic, tocolytic)
1,3,7,9 and the → constipation → Sympatholytic to
sacral → Sympathomimetic to bladder → emptying
Preganglionic Short Long pupils → mydriasis → Sympatholytic to GIT →
nerve → Sympathomimetic to diarrhea
Neurotransmitt ACh ACh blood vessels→ → Sympatholytic to
er vasoconstriction bronchus →
Post Long Short → Sympathomimetic to bronchoconstriction
ganglionic bronchus → → Sympatholytic to pupils
nerve bronchodilation → mydriasis
Neurotransmitt NE ACh → Parasympathomimetic → Parasympatholytic to
er to kidney bf → increase blood vessel →
Termination of Monoamine oxidase Cholinesterase → Parasympathomimetic vasoconstriction
impulse and catechol-ortho to bladder → emptying → Sympatholytic to
methyl transferase → Parasympathomimetic bladder → emptying
(COMT)
 to GIT → diarrhea
→ Sympathomimetic to
blood vessels -
vasoconstriction
→ Parasympathomimetic
to GIT → diarrhea
→ Sympathomimetic to
blood vessels→
vasoconstriction

→ Adrenergic agonist to the heart → increase HR

→ Cholinergic antagonist to GIT → constipation
→ Anticholinergic to pupils → mydriasis
→ Atropine (anticholinergic)→ given to decrease
secretions to decrease risk of aspiration
→ Schizophrenia→ antipsychotics/ neuroleptics will be
given
• Neuroleptics SIDE EFFECT:
o NMS – neuroleptic malignant syndrome
o Tardive dyskinesia
o Pseudo-parkinsonism
o Akathisia
• Anticholinergic SE: **additional: Beta 2 receptors also has an effect to the blood
o Constipation vessels→ vasodilation
▪ NI: increase fluids and fiber
o Decreased emptying of bladder (retention)
Alpha 1 Receptors
▪ NI: bladder training (specific bladder time),
void first before taking the antipsychotic, → Found in the:
low salt • Urinary bladder sphincter→ retention
o Dryness of the mouth • Blood vessels→ vasoconstriction
▪ Increase OFI • Iris→ mydriasis
▪ Ice chips → Phenylephrine: Neozep (decongestant)
▪ Oral care to prevent ulcers • EFFECT: decreased blood flow to the nasal area,
▪ Sugarless candies to increase salivation reduced O2 and nutrients to cells→ cell shrinks→
nose decongestion
→ Ganglion → NI: be careful in giving to HTN pts
• Clusters of nerve bodies that is outside the CNS • SIDE EFFECT: increase total peripheral resistance
• All nerves that go out of the CNS and end in the (d/t vasoconstriction): directly proportional to BP→
ganglion are preganglionic nerves HTN
• Preganglionic nerves of the SNS are shorter in → EFFECT: vasoconstriction = ↑ TPR = ↑BP
comparison to the preganglionic nerves of the PNS BP= HR x SV x TPR / SVR (systemic vascular resistance)
because it only connects near the spinal cord → TPR- pressure inside the blood vessels
• Preganglionic nerves of the PNS are longer since If ↑ HR = ↑ BP
its origins are from the cranial and sacral areas If bleeding ↓ BV, ↓ SV, ↓SVR
which are distal to the organs
→ SINUPRET is used instead for HTN patients
• All nerves that go out of the ganglions are the
• Given three times a day
postganglionic nerves and ends in the organs
• Not a sympathomimetic drug
→ Not also given in patients with hyperthyroidism
(everything is increased→ HR, BP)
→ Also given as vasopressors
→ Used before eye procedures to cause mydriasis and
allow better visualization of the internal parts of the eyes

Side Effects
AUTONOMIC NERVOUS SYSTEM DRUGS: → Reflex bradycardia→ a compensatory mechanism of
Sympathomimetics the body
• baroreceptors of the aorta and the carotid artery
Adrenergic Agonists will detect increase in the blood pressure→ the
→ Epinephrine - CPR, shock hypothalamus will order decrease in heart rate to
→ Dobutamine - CHF decrease blood pressure→ reflex bradycardia
→ Dopamine - CHF, cardiogenic shock • Does not occur immediately
→ Norepinephrine - cardiac arrest → Hypertension d/t palpitation
Basta ito baliktad ang effect
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
• Decreases BP
• EFFECT: SNS effect
is decreased and
PNS dominates=
 ↓HR, ↓BP, less insulin release= hyperglycemia pheochromocytoma (tumor of the adrenal
• Methyldopa- given for PIH, given orally medulla→ ↑ release of NE/ E→ ↑ BP and HR)
• Will cause vasodilation→ ↓ TPR→ ↓BP
Alpha Adrenergic Agonists → Prazosin– binds to blood vessels = vasodilation = ↓ TPR
→ Nonspecific, will have an effect on both alpha 1 and = ↓BP
alpha 2 → Doxazosin and Terazosin
→ E.g., midodrine (vasopressor) • Binds to blood vessel: vasodilation = ↓ TPR = ↓ BP
• Midodrine • Binds to urinary bladder: Emptying of bladder
o DOC for orthostatic hypotension (SNS o INDICATION: Benign Prostatic Hypertrophy
agonist→ ↑ HR→ ↑ TPR → ↑BP) (urine stasis, dribbling, blood-streaked semen
d/t compression of prostate) and HTN
Beta 1 Adrenergic Agonists o Not reduce the size, it will only empty the
→ B1 (in the heart) bladder d/t retention because of the
• ↑ HR, ↑ contractility obstruction, ↑ risk for UTI
• Dobutamine (Inotropic) → Alfuzosin– binds to only the bladder and cause
o Synthetic dopamine emptying of bladder
(sympathomimetic drug) • INDICATION: BPH
o EFFECT: DOC for HF, helps → Tamsulosin– for BPH as it only binds to the urinary
heart contract, anti- bladder also
arrhythmic,
o SIDE EFFECT: palpitations, Beta 1 Adrenergic Antagonists
tachycardia→ ↑ BP → Propranolol
• Potassium will enter the cells once • DOC for palpitations d/t hyperthyroidism
beta cells are stimulated • Prophylaxis for migraine
→ Affects the kidneys→ ↑ renin release→ → Timolol
↑ BP (d/t sodium and water retention) • For open angle glaucoma (to promote miosis and
keep the angle open)
Beta 2 Adrenergic Agonists • SE- miosis
→ Found in the: • Prophylaxis for migraines (eye drops)
• Lungs, uterus, BV, → Nadolol
heart, liver • DOC for angina and hypertension
→ Bronchodilation → Labetalol
• Albuterol/Salbutamol • Most used in PIH (pregnancy- induced
[bronchodilator] hypertension)
o INDICATION: • Has an alpha receptor effect→ ↑in placental
asthma and COPD perfusion (PNS stimulation)
o SE: palpitation and
tremors (as Indications
albuterol beta 2 but 1. HTN: Negative chronotropic effect = ↓HR
also binds with b1 2. CAD (coronary artery diseases)- angina pectoris and
especially in high MI
doses→ SNS • Causes ↓O2 supply, ↑ O2 demand
activation) 3. Anxiety
o Also causes • ↓Tremors & palpitation = ↓ HR
arteriolar • ↓HR = ↓ O2 demand d/t ↓ workload, ↑ O2 supply
vasodilation in 4. Open Angle Glaucoma
skeletal muscles→ faster and increased blood • Decrease production of the aqueous humor
flow 5. Supraventricular Arrythmia, AFib– regulate and control
o SABA (short-acting beta agonist) rhythm of heart
• Isoproterenol 6. CHF – be cautious as heart is exhausted. – to ↓ cardiac
o INDICATION: Tx for bradycardia, heart block, workload = ↑ inotropic (force of contraction)
asthma 7. Migraine- prophylaxis as it can cause cerebral
• Terbutaline (tocolytic)– muscle tone relaxation vasoconstriction
(blocks the tone of the muscle)
o INDICATION: asthma, COPD, premature labor Side Effects Contraindications
o EFFECTS: Blood vessels of heart, lung & Bradycardia Hold if HR <60 bpm
skeletal muscle: vasodilation Hypotension Hold if BP <90/60
o Liver: Glycogenolysis→ hyperglycemia Bronchoconstriction** Avoid for asthma and
o LABA- long- acting beta agonist COPD patients
• Isoxsuprine HCl (duvadilan vasodilan)- also a Hypoglycemia Caution in patients with
tocolytic DM, can mask
hypoglycemia
o Peripheral vascular dilation, tx of preterm labor
Impotence**, erectile
dysfunction
Nursing Considerations
→ Avoid sudden withdrawal of the drug
→ Monitor vital signs Example
→ Provide comfort measures A 65 y/o male, smoking 10 packs years, non-alcoholic
→ Maintenance- beta blocker
→ Diagnosis- HTN and asthma
ANTAGONISTS
→ Only a beta 1 specific blockers should be given to
prevent bronchoconstriction as it only has an effect in the
Alpha Adrenergic Antagonists heart (BEAM BA)
→ Located in the blood vessels and urinary bladder • Bisoprolol
→ Phentolamine • Esmolol
• A nonspecific • Acebutolol
• Used for HTN crisis d/t MAOIs (decreases • Metoprolol
breakdown of NEs→ SNS stimulation→ ↑BP) and • Betaxolol
 crisis fast results ptosis and
• Atenolol
are needed) weakness)
Positive tensilon Negative tensilon
MYASTHENIA GRAVIS test test
→ Cholinergic receptors are destroyed by the antibodies
→ Number of acetylcholine is normal but there are no FAQs
receptors 1. You are a nurse assisting the doctor during a Tensilon
test, what should you prepare bedside?
→ Muscles have no contraction→ paralysis
• Always prepare atropine sulfate (anticholinergic,
• (+) weakness of the eyelids- ptosis (initial sign of an antidote)
myasthenia gravis) 2. If (+) atropine toxicity, give pyridostigmine (mestinon)
• Descending paralysis- MG (mata galing) 3. What is a negative tensilon test? Cholinergic crisis
o Ascending paralysis- GBS (galing baba siya) → Slow down the administration of cholinergic drugs to
→ Common in 20-40 years old women avoid severe cholinergic effects (PNS effects)

Signs and Symptoms ALZHEIMER’S DISEASE

→ Ptosis → (+) degeneration of the
• Check palpebral fissures cholinergic nerves→ atrophy of
→ Diplopia brain tissue due to its deficiency
→ Mask-like facial expression → No impulses and ACh production
→ Dysphagia- risk for aspiration
→ Weaking of laryngeal muscles Manifestations
• Airway is always the priority → A – amnesia, loss of memory
→ Respiratory muscle weakness → A - agnosia– unable to identify the
• Consequence- function and purpose of familiar
• Nursing consideration objects
→ Extreme muscle weakness → A – apraxia– unable to perform
→ Anticholinesterase will be given to prevent breakdown learned movements
of ACh→ increase the tone of muscles → A – aphasia- inability to
• Cholinergic drugs as it preserves acetylcholine communicate (write/understand)
→ Neostigmine- treatment • Expressive- Broca’s aphasia
→ Pyridostigmine- treatment (frontal lobe)
→ Physostigmine- treatment o Unable to speak
→ Edrophonium (Tensilon) is only used for diagnostic test • Receptive- Wernicke’s
• Short acting (10 minutes) aphasia (temporal lobe)
o Unable to understand
Nursing Management o More common in Alzheimer’s disease
→ Pharmacotherapeutics • Global/ mixed
→ Cholinergics or anticholinesterase agents o Both inabilities to speak and understand

Pharmacotherapy
→ Prevent breakdown of ACh to
increase memory
→ Anticholinesterase
→ Rivastigmine (Exelon)
→ Donepezil (Aricept)
→ Tacrine
→ Not used for myasthenia gravis
because target tissues (distribution) are
different
• MG→ muscles
→ Pyridostigmine (Mestinon)
• AD→ nerves
• First line drug for MG
→ These drugs won’t cure but will only delay the
• DOC for atropine toxicity
progression of the disease
→ Neostigmine (prostigmin)
• For long term use
Pharmacodynamics
• Increase the bonding of ACh and the receptors
→ Cholinergic drugs (anticholinesterase)
→ Corticosteroids
• Anti-inflammatory, therefore, blocks the immune CHOLINERGIC ANTAGONISTS (PARASYMPATHOLYTIC)
response 1. Atropine
• Decadron (dexamethasone) • Anticholinergic, prevent secretions
→ Cholinergic agonists for MG are to be taken 30 minutes
2. Dicyclomine
AC to give tone to muscles of mastication and swallowing
to prevent aspiration
• Antispasmodic and antimuscarinic
→ Monitor two types of crises • For hyperactive bowel in adults
Myasthenic Cholinergic 3. Scopolamine (HNBB)
Crisis Crisis • For motion sickness
Signs and Weakness and paralysis • For pupil dilation
symptoms • Post-op nausea and vomiting
Cause Underdosing of Overdosing of
cholinergic drugs cholinergic drugs DRUGS OF THE CENTRAL NERVOUS SYSTEM
Treatment Cholinergic Anticholinergic
(neostigmine, (atropine sulfate) Parkinson’s Disease
physostigmine,
→ Degeneration of the dopaminergic nerves
pyridostigmine)
→ There should be a balance of ACh and dopamine in the
Tensilon Increased muscle Worsening of
(edrophonium)- tone symptoms substantia nigra
via IV for fast (improvement of
results (already a
→ Acetylcholine→ contraction o Destroys of breakdown NE, E, serotonin, and
Fine motor movements
→ Dopamine→ inhibitory effect, relax dopamine
→ Dopamine production has o Isocarboxazid (Marplan)
degenerated→ dominate o Phenelzine (Nardil)
ACh o Selegiline (Emsam)
→ Goal: • Catechol-O-methyltransferase inhibitors (COMT)–
• Increase dopamine or “CAPONES”
inhibit acetylcholine o Destroy the catecholamines (NE/ E/ dopamine)
o Comtan® (entacapone)
Manifestations o Tasmar® (tolcapone)- not anymore used
→ Tremors d/t higher ACh, ↑ contractions that is not because of too many side effects
inhibited by dopamine o Ongentys® (opicapone)
• Others (not dopaminergic)
Management o Amantadine (antiviral) but can lessen the
→ Dopaminergic drugs (↑ dopamine) tremors in Parkinson’s
→ Anticholinergic drugs (inhibit ACh)
ANXIOLYTICS
Classes of Anti-Parkinson Agents → Blocks anxiety
→ Anticholinergic drugs– block stimulating effects of ACh → Beta blockers
to bring activity balance → Antipsychotics
• Biperiden (Akineton)- antimuscarinic → Benzodiazepines
• Trihexyphenidyl (Artane)- antimuscarinic → Antidepressants- SSRIs
• Diphenhydramine (Benadryl)- antihistamine (also • First line treatment for anxiety because it is
anticholinergic) nonaddictive
• Benztropine (Cogentin)- antimuscarinic • Disadvantage- full therapeutic effect is 4-6 weeks,
→ Dopaminergic drugs not good for acute attacks
• Dopamine precursors (Levodopa, Carbidopa)
o Levodopa + carbidopa is the mainstay Benzodiazepines (BZD)
treatment for Parkinson’s even if it has many ▪ for acute attacks
side effects → Pharmacodynamics- enhances the GABA effect
o Levodopa- improves bradykinesia, rigidity, and (inhibitory)→ block impulse transmission
tremors → Causes CNS depression
o NC: avoid vitamin B6 (pyridoxine) because it → Most commonly prescribed
reverses or blocks the effect of levodopa *but → Other indications:
is taken with isoniazid to prevent peripheral • Muscle relaxant (1) centrally acting- muscle
neuritis/ neuropathy relaxants (2) direct- acting muscle relaxants
o Precursor- not a dopamine but will give • BZD is a centrally acting MR, baclofen
dopamine • Direct-acting- dantrolene (DOC for malignant
▪ Dopamine cannot cross the BBB, hyperthermia d/t anesthesia), botulinum toxin A
therefore, a precursor is given (botox), botulinum toxin B (myoblock)
o Sinemet- carbidopa is combined→ decreases Malignant hyperthermia
the dose of levodopa needed to reach the Muscles are contracting too much→ ↑ heat
critical concentration by preventing • BZDs are also antiepileptics, DOC for status
decarboxylase from breaking it down epilepticus
o Carbidopa will block or destroy decarboxylase • Sleep disorders- insomnia as it causes sedation
to prevent breakdown of levodopa in the • Alcohol withdrawal (if withdrawal symptoms
periphery because it does not cross the BBB manifests)
o Ratio of carbidopa to levodopa 1:4 • Used in anesthesia induction
→ Diazepam (valium)
→ Lorazepam
→ 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)
• Dopamine receptor agonists
• Used as a short-term treatment for insomnia
o Bromocriptine
• Selectively bind to the BZD sites on the GABA
o Pergolide
receptors
• MAO- B Inhibitors
• Advantages:
 o No withdrawal effects Status Epilepticus
o Minimal rebound insomnia → Emergency
o Little or no tolerance on prolonged use → Crazy seizures in <5 minutes but can extend >5 minutes
→ Diphenhydramine • The brain needs 250 x the normal need
→ Buspirone
• Alternative to BZD Nursing Considerations
• Slower onset of action → ABC, establish IV access
• 5HT receptor agonist → DOC is BZD
• Useful in alcoholics→ has no potential CNS effect → Phenytoin
• Low potential for abuse • If status continues
• SE- priapism- painful erection → Intubate if seizures do not stop, phenobarbital 20 mg/
→ Propranolol kg IV
• A beta blocker • If status continues
• Anti-anxiety → Induce coma to prevent further hypoxia
• Allow the brain to rest and recuperate for the
ANTICONVULSANTS/ ANTISEIZURES oxygen needs
→ Seizure- burst of uncontrolled electrical activity → Bedside EEG monitoring
between the neurons → Treatment of choice- BZD
→ Epilepsy- two or more unprovoked seizures → Prophylactic of choice- phenytoin
→ Goal: to stop the seizure with minimal side effects
→ As much as possible monotherapy should be done d/t RESPIRATORY DRUGS
↑ risk of side effects
→ Never stop abruptly d/t rebound seizures INFLAMMATORY RESPONSE
→ normal response of a vascularized tissue to injury
Generalized Seizure → destroys pathogen, promotes healing
→ Spreads to the other lobe (spreads in hemispheres)
→ Tonic clonic (gran mal seizure)- extension and
contraction of muscles
• DOC BZD, phenobarbital, carbamazepine
(Tegretol), valproic acid (valproate), and phenytoin
(dilatin)
• Valproic acid is hepatotoxic (x) given to children
Phenytoin can cause the following:
→ Gingival hyperplasia
→ Can also result to fetal hydantoin syndrome (x) given to
pregnant women
• Microcephaly and low set ears
→ Part of the HIPP- drugs that induce SLE UPPER RESPIRATORY TRACT DRUGS (URT)
• H- hydralazine (vasodilator)
• I- INH (isoniazid)
ANTIHISTAMINE: Anticholinergic Drugs
• P- procainamide (antiarrhythmic)
→ Pharmacodynamics: selectively blocks H1 (present in
• P- phenytoin
→ Should be given using the sandwich method (NSS- the tissues, responsible for the inflammation) receptor
phenytoin- NSS) sites
→ Use only NSS when administering → First Generation:
→ Monitor serum levels • CNS depressant:
→ Absence/ petit mal (blank stare) o EFFECT: drowsiness, sedation
• Ethosuximide o NC:
→ Myoclonic- sporadic spasms ▪ Increase OFI to liquify phlegm
• Valproic acid ▪ Avoid driving and operating big machines
→ Febrile- d/t hyperthermia ▪ Sugarless gums; to increase salivation d/t
• Phenobarbital dryness of the mouth (effect of
→ Status epilepticus- emergency sympathetic response)
• Diazepam ▪ Humidifier; to add up moist in the air
▪ Avoid alcohol; also a CNS depressant
• Diphenhydramine (Benadryl): Anticholinergic drug
• Chlorpheniramine - part of Neozep
o This is removed in non-drowse Neozep
• Hydroxyzine
→ Second Generation
• No sedative effect; does not cause drowsiness
• Cetirizine (zyrtec)
o Take at bedtime, once a day
o Takes effect for 24 hours
• Loratadine (Alerta)
• Desloratadine

DECONGESTANTS
Partial Seizure → Pharmacodynamics: sympathomimetic drugs; alpha 1
→ Localized in one lobe receptor agonist → causing vasoconstriction
→ Simple • Caution in CV px:
→ Complex o Causes ↑HR → ↑workload of the heart
→ Carbamazepine (Tegretol) is the only drug used o Vasoconstriction → ↑TPR → ↑BP → ↑workload
• DOC for trigeminal neuralgia of the heart
→ ❗NOTE❗: Take only for 5 days
• >5 days can lead to rhinitis medicamentosa
(rebound effect; further congestion); reversible
→ Nasal Decongestants o Also used for COPD and allergic rhinitis
• Tetrahydrozoline → Methylxanthines (antiasthmatics) - CAT
• Phenylephrine • Pharmacodynamics: directly relax the bronchial
→ Oral Decongestants smooth muscles → ↑vital capacity
• Pseudoephedrine (Sudafed) • Caffeine
o Ingredient in crystal meth • Aminophylline
o Addictive • Theophylline
• Nursing Considerations:
EXPECTORANTS o Administer oral drug with food or milk to
→ Pharmacodynamics: reduces the adhesiveness and increase absorption
surface tension of URT fluids (loosen up phlegm) that o Monitor for side effects:
will facilitate the removal of viscous mucous ▪ Palpitation and tremors
• Take a lot of fluids to aid in loosening the phlegm o Dietary control of caffeine (palpitations)
→ Guaifenesin (Robitussin Expectorant) - for productive o Monitor the serum theophylline &
cough aminophylline level (can be toxic)
▪ Normal: 10-20 mcg/ml
MUCOLYTIC ❖ >20 mcg/ml: nausea (first sign of
→ Pharmacodynamics: Decrease the viscosity of toxicity)
secretions ❖ >35 mcg/ml: tremors (later sign of
→ INDICATION: productive cough toxicity)
→ Acetylcysteine (Fluimucil) → Nursing Considerations: Bronchodilators - BREATHE
• Protects the liver cells (hepatocytes) from • Breathing & coughing techniques
acetaminophen toxicity (antidote) o To remove the secretions and optimize oxygen
• NAC exchange
o 100 mg- sachet • Relaxation techniques
o 200 mg sachet - TID o Music, etc.
o 600 mg effervescent - OD/BID • Evaluate HR and BP (possible side effects)
→ Ambroxol • Appropriate positioning
→ S-Carboxymethyl Carbocisteine o High fowler’s - increase the AP diameter of the
→ Dornase Alfa chest and allow lung expansion
• Tremors (common side effect)
ANTITUSSIVE • Have 8 or more glasses of fluids
→ Pharmacodynamics: Suppress the cough reflex in the o Loosen phlegm
CNS • Emphasize no smoking
→ 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

→ Asthma, COPD (chronic bronchitis & emphysema)
→ PGE1 stimulates gastric acid secretion
• Obstruction s/t smoking (irreversible)
→ PGE2 will stimulate the hypothalamus→ stimulation of
the thermoregulation center→ fever
BRONCHODILATORS: (antiasthmatics)
→ If a process of the pathway is blocked, all the following
→ Pharmacodynamics: dilate the airways to facilitate
manifestations will be reversed (or the opposite will
respiration
manifest)
→ Sympathomimetics
→ Chemotaxis- inflammatory marker that causes the
• SNS Effect: causes bronchodilation
WBCs to move towards the injured site
• Epinephrine - act on alpha and beta receptor sites
in the SNS (adrenergic)
DRUGS AFFECTING INFLAMMATION
• Albuterol - beta 2 adrenergic agonist; SABA (short-
→ Inhaled Steroids
acting beta agonist)
• Corticosteroids will block arachidonic acid →
o Onset - <20 minutes
bronchodilation
o Duration - 4-6 hours
• Pharmacodynamics: blocks the immune response
• Terbutaline - beta 2 adrenergic agonist; LABA
(antibody production); anti-inflammatory
(long-acting beta agonist)
• INDICATION:
o Onset - <20 minutes
o Asthma: blocks arachidonic → (X) leukotriene
o Duration - 12 hours
→ (X) bronchoconstriction → bronchodilation
• Ephedrine - alpha and beta agonist
▪ Status asthmaticus: steroids via IV for
• Side Effects:
faster effect
o Tachycardia/palpitation
o Arthritis (inflammation/pain): blocks
▪ PNS drugs can be given if cannot be
arachidonic → (X) leukotriene → (X)
tolerated
prostaglandin, → (X) dolor
o Hypertension d/t ↑HR and vasoconstriction
o Allergy: blocks arachidonic → (X) histamine →
o Dryness of the mouth
↑vasoconstriction → ↓blood flow → (X)
→ Anticholinergics/Parasympatholytics (blocking PNS,
capillary permeability → (X) swelling
still SNS - bronchodilation)
o Pharmacodynamics: block vagally mediated Prostaglandin E2 → hypothalamus → stimulate
reflexes thermoregulation center → fever
▪ Vagus (X - vagal): PSNS effect (craniosacral) • -one
❖ 1973: CN3, 7, 9, 10 • Budesonide
o Ipratropium - for those who cannot tolerate the side • Fluticasone
effects of sympathomimetics • Triamcinolone
 • Nursing Considerations • For the ventricle to do that, the ventricles have to
o Given after meals stretch larger before contracting→ too much
▪ If before meals, the prostaglandin E1 in the stretching→ hypertrophy/ left ventricular
stomach will also be blocked → ↓mucous hypertrophy/ cardiomegaly (irreversible)
→ ↑HCL → gastric irritation • Branches: aorta (artery), arterioles, capillaries
o Not used during acute attacks (unless SABA • ↑Afterload → ↑Cardiac workload
can no longer manage the attack) • Chronic - hypertrophy, cardiomegaly
o Use bronchodilators before corticosteroid
aerosol ANGINA
o Teach clients how to use inhalers
▪ Puff and inhale at the same time
▪ Hold the inhaled drug for a few seconds
before exhaling
▪ Allow 1-3 minutes to elapse between each
inhalation
▪ Rinse mouth with water after → AKA Chest pain
❖ Block immune response → destroy • Pain d/t ↓oxygen → accumulation of lactic acid
the normal flora → stomatitis (singaw)
→ Reversible: still no damage to tissues
→ PROBLEM: ↓O2 supply, ↑O2 demand
→ CAUSES: Atheroma (plaques) - fatty tumors
• Narrowing d/t deposits of atheroma → ↓blood flow
→ ↓oxygen → ↑oxygen demand
→ GOAL: Increase O2 supply & decrease O2 demand
(need)
→ Cardiac enzymes are present only when there is tissue
damage
oNotify doctor or nurse if sore throat or sore
• Troponin I (-)
mouth occurs (superinfection)
o Do not stop abruptly (can lead to Addisonian
DRUGS FOR ANGINA
crisis)
o Taper off gradually under supervision
→ Leukotriene Receptor Antagonists
• Montelukast
o Given to patients with COVID for
bronchodilation
o Prophylaxis for asthma
o Taken for months, years for the asthma not to
be triggered
• Zafirlukast
• Zileuton
→ Surfactants
• Beractant
→ Vasodilators
CARDIOVASCULAR DRUGS
• improve blood flow
• GOALS: Increase oxygen supply
• Nitroglycerin
→ Cardiac depressants
• GOALS: Decrease the oxygen demand

Nitrates
→ Pharmacodynamics:
• Direct acting vasodilators
• Acts primarily on the veins
→ DOC for stable angina, unstable angina
→ Nitroglycerine
The Heart & Blood Pressure → Isosorbide Mononitrate
→ Preload → Isosorbide Dinitrate
• Initial stretching of the cardiac myocytes (muscle → Nursing considerations:
cells) prior to contraction • NTG Tablet
• Related to ventricular filling o Route: SL (fast absorption d/t
• Venous return presence of blood vessels)
• Venous pooling, thus decreases preload o No first pass effect
If vasodilators are given, lesser blood will return to the heart o Dose: 1 tab, q5 mins for 3 doses
d/t venous pooling before it can go back to the heart→ ↓ ▪ q5 mins: T1/2 is 3 mins
preload and afterload will decrease because of
▪ If within 15 mins the pain is still not relieve:
vasodilation→ ↓ workload
Myocardial Infarction
→ Afterload
o Shelf life: 3 months
• Is the force or load against which the heart has to
o Storage: in a dry, amber-colored container
contract to eject the blood
(photosensitive)
• Pressure in the left ventricle needed to push the o Encourage the patient to carry 3 tablets only
blood out of the circulation
• NTG Patch
• o N: 120 mmHg
o Sustained slow release d/t body heat →
• o E.g., If pressure in the peripheries is 180 absorbed to the blood
mmHg, the pressure in the ventricles should be o Effects in 30-60 minutes
higher (190 mmHg) to push the blood towards the o Apply over dry, hairless area (to allow the patch
extremities properly place to the skin)
 ▪ Do not shave, trim only if hair is present to MYOCARDIAL INFARCTION
prevent abrasion → Tissue death
▪ Abrasion → (X) barrier → fast absorption
→ hypotension DRUGS AFFECTING BLOOD COAGULATION
o Rotate sites to prevent skin irritation → Antiplatelets
o To prevent tolerance - nitrate-free hours (at • Aspirin
least 8 hours HS) • Clopidogrel
▪ Not worn 24/7 as it can result to tolerance → Anticoagulants
(needs higher dose for the same effect) • Warfarin
▪ Has a ceiling effect - limitation of effects • Heparin
despite higher doses → Thrombolytics
• Side Effects: • Alteplase
o Headache d/t vasodilation (administer • Streptokinase
paracetamol) • Reteplase
▪ Paracetamol may be given as prophylaxis • Urokinase
▪ Do not discontinue d/t headache. Tell the → Antifibrinolytic
patient that it will taper down after some • Aminocaproic Acid
time • Tranexamic Acid
o Orthostatic hypotension → Others
o Blurry vision • Low-molecular weight
o Tachycardia (compensatory mechanism) • Heparins
▪ Hypotension → baroreceptors in the brain • Deakteoarub
→ ↑HR → ↑BP • Enoxaparin
▪ Late manifestation → Anticoagulant adjunctive therapy
o Dry mouth • Vitamin k
• Contraindications: alcohol • Lepirudin
• Protamine sulfate
Calcium Channel Blockers (Very Nice And Friendly Drugs)
→ Calcium is for muscle contraction, coagulation/blood DRUGS USED IN MYOCARDIAL INFARCTION (MONA)
clotting
→ Morphine
• The calcium goes inside the cell for the muscle to
• Priority is pain
contract
• opioid/ narcotic agonist
• Pharmacodynamics: stimulate the opioid receptors
found in the CNS and GIT
• Uses:
o Mild to moderate pain (opioid analgesic)
o Generally safer than NSAIDs in older adults
▪ NSAIDS - gastric irritating effect
o Vasodilator → venous pooling → ↓preload →
↓workload of the heart → ↓O2 demand →
↑oxygen supply
• Contraindications:
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
→ -dipine: Acts on the blood vessels → Nitrates
→ Verapamil - antiarrhythmic → Drugs Affecting Coagulation:
→ Nifedipine / Nicardipine • Antiplatelets
→ Amlodipine • Anticoagulants
→ Felodipine • Thrombolytics
→ Diltiazem - antiarrhythmic • Antifibrinolytic

BETA BLOCKERS Increased Myocardial Interaction Of Antianginal

→ sympathomimetic drugs → ↓HR, ↓cardiac workload → Consumption Agents Affecting
↓O2 demand → ↑O2 supply Myocardial O2 Demand
→ cause vasodilation → ↓TPR total peripheral resistance ↑ Hr BBs, CCBs
→ ↓AFTERLOAD → ↓O2 demand → ↑O2 supply ↑ Preload
↑ Afterload BBs, CCBs, nitrates
→ Metoprolol
↑ L – ventricular muscle size
→ Nadolol - angina & HTN
↑ Muscle contractility BBs, CCBs
→ Propranolol

RANOLAZINE
→ A newer drug with limited indications
→ Now approved as first line therapy for chest pain but
nitrates are still used for acute pains
→ Can be combined with other drugs
 o WOF salicylate poisoning/salicylism
▪ Fatal dose: 150 mg/kg BW
▪ Tinnitus - most important sign in acute
poisoning
▪ Hyperventilation → respiratory alkalosis
▪ Severe toxicity → metabolic acidosis →
seizure

→ Extrinsic pathway is outside the BV

→ Clot will be dissolved by the body because it may → Clopidogrel (Plavix)
become dislodged and cause embolism, therefore, → Ticlopidine (Ticlid)
fibrinolysis will occur → Dipyridamole

Coagulation Cascade ANTICOAGULANT

→ Process of formation of a clot Warfarin
→ 2 pathways: → Pharmacodynamic: Blocks the vitamin K dependent
• Formation of platelet plug > intrinsic pathway clotting factors → no more clots
• Formation of platelet plug > extrinsic pathway
→ Will activate prothrombin clotting factor #2 (produced
in the liver with the help of Vit K) to become thrombin >
activates fibrinogen > fibrin = clot / emboli
→ FIBRINOLYSIS
→ Liver: creates Plasminogen – plasmin – block fibrin

ANTIPLATELETS
→ Aka Blood Thinners
→ Pharmacodynamics: blocks the formation of platelet
plug
• Hypertensive crisis → can activate the local
→ Route: Oral (Home)
coagulation cascade → forming clots →
• not absorbed in parenteral route
obstruction → decreased blood flow → decreased
→ Therapeutic test: Prothrombin time (PT)
oxygen supply → ischemia
• Time it takes for the prothrombin to form clots
→ Aspirin
o If this is prolonged→ ↑ risk for bleeding
• Indications:
o N: 8-12 seconds
o Anti-platelet - blocks thromboxane A2 → (X)
o Higher than 12 is expected when warfarin is
clotting
given
o Analgesic - blocks prostaglandin → (X) dolor
o INR (better test used, choose this in the test)-
o Antipyretic blocks prostaglandin E2 → (X)
international normalized ratio
fever
▪ N: 1
o Anti-Inflammatory - block inflammatory
▪ More preferred because it only has one
response
normal value unlike PT
• Side Effects: Bleeding
• Therapeutic margin- 1.5-2.0 x normal
• Nursing Considerations:
→ Therapeutic margin: 1.5-2.0 x normal
o Give PC (post cibum)/after meals to avoid
• Should know the BASELINE
gastric irritation
• Case: patient was prescribed with warfarin
o Give with glass of water/milk to lessen gastric
irritation o Dx: PT request = 12 secs (Normal: 8 - 12 secs)
o Educate the patient to WOF toxicity ▪ Nursing action: Give warfarin
▪ Bleeding gums ▪ The higher the PT, the higher the chance
of hemorrhage
▪ Tinnitus
▪ 12 x 1.5 = 18 secs
▪ Black tarry stool
o Increase risk of toxicity in elderlies and ▪ 12 x 2.0 = 24 secs
children o Dx: PT = 24 secs
o Avoid in children with a viral infection (e.g., ▪ Nursing action: Give warfarin (still within
the therapeutic range)
chickenpox, measles)
▪ Can cause reye syndrome o Initial: 10 secs so,
▪ 10 x 1.5 = 15 secs
▪ 10 x 2.0 = 20 secs
▪ Therapeutic range = 15-20 secs
o Initial: 8 secs
▪ Administer the warfarin (Normal: 8 - 12
secs)
▪ PT = 16 secs = GIVE (8 is the baseline, we
can give if 12-16)
▪ 8 x 1.5 = 12
▪ 8 x 2.0 = 16
 ▪ PT = 20 secs = HOLD (not anymore within → Recombinant Tissue Plasminogen Activator (RTPA)
the range of therapeutic level) → Side effects: bleeding
→ Side effect: Bleeding → Antidote: Antifibrinolytics
→ Antidote: Vitamin K • Because if there is fibrin there are clots
• Aminocaproic acid (Amicar)
• Tranexamic acid (Hemostan)
o Take home medications: Tooth extraction
o OB: Abnormal Uterine Bleeding (AUB)
→ Nursing Considerations:
• Monitor vital signs
• Monitor for signs of bleeding
o Petechiae
o Purpura
o Bruising
o Bleeding gums
o Black tarry stool
• Use soft bristled toothbrush
→ Nursing considerations: • Use electric shaver
• Monitor PT and INR
o If both PT and INR is in the exam, choose INR SUMMARY: Drugs Affecting Coagulation
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
o Petechiae
o Bruises
• Decrease intake of green leafy vegetables
o It contains vitamin K
• Avoid 3 Gs (garlic, ginger, ginseng)
o Blocks warfarin

Heparin
→ Pharmacodynamics: Blocks the formation of thrombin
→ no clots
→ Route: IV or SQ (Hospital)
ANTIHYPERTENSIVE DRUGS
→ Therapeutic test: Activated Partial Thromboplastin Time
(aPTT)
→ Therapeutic margin: 1.5 - 2.5 x normal
→ Side effect: bleeding
→ Antidote: Protamine Sulfate

When the patient is still in the hospital heparin will be

given→ IV/ SC (faster effect)
→ Not given orally, because it will only be destroyed by
the gastric acids and enzymes (same reason why
insulin cannot be given orally)
At home→ warfarin, oral
→ Not absorbed parenterally

THROMBOLYTICS Definition of Terms

→ Pharmacodynamics: activate the conversion of → BP = resistance exerted by the blood against the
plasminogen to plasmin smooth muscle wall
• Plasmin → (X) fibrin → (X) clot • ↑ CBV→ ↑ BP
→ SV = amount of blood ejected per beat
→ CO = amount of blood ejected per minute
→ SVR = pressure exerted by the smooth muscle wall
against the blood
→ TPR = Total Peripheral Resistance
• If vessels vasoconstrict, ↑ TPR

Mean Arterial Pressure (MAP)

→ Average pressure throughout each cycle of the
heartbeat
→ Clinical significance: tissue perfusion
→ GOAL: Dissolve the clot in order to restore the blood
flow
→ Golden hour: 3 hours; 1 hr (the soonest the diagnosis,
the soonest administration of thrombolytics, the
BETTER) → Normal: 70-100 mmHg - the cells are getting sufficient
→ Urokinase oxygen
→ Streptokinase • <70 mmHg - the cells are not getting sufficient
→ Alteplase oxygen
→ The thrombolytics will activate the plasminogen which o Hypoxia
will be plasmin and dissolve the clot o Tissue death
 • >100 mmHg - afterload is high • Stopping abruptly and taking it again
o Increased workload of the heart
o Damage to the heart ANGIOTENSIN 2 RECEPTOR BLOCKER (ARB) “ sartan ”
o Blood clots → Pharmacodynamics: Blocks the A2 receptors →
vasodilation → TPR decreases
Regulators of Blood Pressure → Losartan
→ Baroreceptors found in carotid artery and aorta → Valsartan
• Send signals to the brain→ ↑ or ↓ heart rate and → Telmisartan
blood pressure → Side effects:
→ Vascular Autoregulation • Angioedema
• Vasoconstriction → ↑TPR → ↑BP • Hyperkalemia - d/t no aldosterone, no Na
• Vasodilation → ↓TPR → ↓BP
→ Regulation of Body Fluid Volume DIRECT RENIN INHIBITORS
• ↑body fluid volume → ↑blood volume → ↑BP → Site of action: kidneys
• ↓body fluid volume→ ↓blood volume→ ↓BP → (x) renin→ RAAS will not start (x) ↑ BP
→ Renin Angiotensin Aldosterone System (RAAS) → Aliskiren

SELECTIVE ALDOSTERONE ANTAGONISTS

→ Blocks aldosterone
→ Epelrone
→ Adverse effect- hyperkalemia

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
→ TARGET CELLS: iris, blood vessels,
→ MECHANISM: Cholinergic
→ SIDE EFFECT: Abrupt drop in BP, orthostatic
hypotension
→ 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 effect→
↓ BP
→ EFFECT: decrease BP by decreasing HR
→ Clonidine
→ Methyldopa
ANTIHYPERTENSIVE DRUGS ACTING ON RAAS → NURSING INTERVENTION: Given SL can cause
→ Drug Acting on Renin rebound HTN
→ Drug Acting on ACE Receptor
→ Drug Acting on The Angiotensin 2 Receptors BETA ADRENERGIC BLOCKERS
→ Drug Acting on Aldosterone → “olol”
→ Propranolol
ACE INHIBITORS (“-pril”) → BETA SPECIFIC ADRENERGIC BLOCKERS “ olol ”
→ Pharmacodynamics: Blocks angiotensin converting • Betaxolol Bisoprolol
enzyme in the lungs → (X) conversion of angiotensin 2 • Esmolol
→ (X) bind in blood vessels → (X) enter in receptor → • Acebutolol Atenolol
blood vessels → dilates → TPR decreases → BP • Metoprolol
decreases → no osmolarity → no retention of sodium
→ At the same time, (X) angiotensin 2 → (X) bind in blood VASODILATOR ANTIHYPERTENSIVE DRUGS
vessels → (X) stimulation of adrenal cortex → no → Indirect Acting Vasodilators
retention of sodium → no osmolarity →(X) stimulation • Calcium Channel Blockers - Action is in the heart
of hypothalamus → (X) ADH → decrease TPR → and BVs
decrease BP o Verapamil
→ Captopril o Nifedipine
→ Enalapril o Nicardipine
→ Lisinopril o Amlodipine
→ Side effects: o Felodipine
• Angioedema o Diltiazem
• Cough (lung action) - most common o Common SE (-dipine): peripheral edema
o Can take with antitussive except for patients ▪ NC: elevate the legs and use one pillow
with asthma and COPD only to increase preload and prevent
• Elevated K d/t retention (x) Na retention venous stasis
→ Paradoxical effect:
 o Used for prinzmetal angina - obstruction d/t o >10 ng/ml
vasospasm of the coronary artery o Signs:
→ Direct Acting Vasodilators ▪ Nausea and vomiting
• Vasodilators ▪ Malaise
o Hydralazine (Apresoline) ▪ Depression
▪ DOC for PIH ▪ Arrhythmia
o Nitrates o Antidote: Digitalis Immune Fab (Digibind)
▪ Nitroglycerine– most commonly used • Monitor the levels of potassium
▪ Isosorbide Dinitrate or Mononitrate
o Nitroprusside → Phosphodiesterase Inhibitors
▪ DOC for hypertensive crisis • Milrinone
▪ Route: IV o Pharmacodynamics: blocks the enzyme
▪ Fast onset phosphodiesterase→ ↑ cyclic cAMP (energy in
▪ Short duration: given for 72 hours the cells) and ↑ calcium levels→ (+) inotropic
❖ It can cause cyanide poisoning effect
o Minoxidil
▪ SE: hair growth OTHER DRUG THERAPIES:
o SE: headache → Vasodilators:
• Used for hypertensive crisis • ACE Inhibitors: (x) ace→ (x) A2→ vasodilation→ ↓
preload→ ↓ workload→ (+) improved cardiac
DIURETICS function
→ Increases urine output → ↓CBV → decreases TPR → • Nitrates
decreases BP → Beta Adrenergic Agonists: Sympathomimetics - (+)
→ Thiazide Inotropic effect
• Hydrochlorothiazide • Dobutamine
• Side effects → Diuretics: Increases urine output → decrease preload
o Hypokalemia → decrease workload → improved cardiac function
o Hyperglycemia • Furosemide
o Hyperuricemia → Human B-type Natriuretic Peptide: Compensatory
• Most commonly used for HTN - gives mild diuresis response → produced myocardial cells → decrease
→ Loop Diuretic workload of the heart
• Furosemide (Lasix) • Nesiritide (Natrecor)
→ Potassium-Sparing
• Spironolactone ANTIARRHYTHMIC AGENTS
• Amiloride → ACTION POTENTIAL: electrical current occurring in
• Triamterene nerves and muscles
• Side effects: Hyperkalemia
→ Osmotic Diuretics
• Mannitol
→ Carbonic Anhydrase Inhibitors (CAH Inhibitors)
• Acetazolamide (Diamox)
o For increased intraocular pressure (↓
production of humor), lithium toxicity
o Idiopathic intracranial HPN, altitude sickness,
CHF, and epilepsy

DRUGS USED FOR HEART FAILURE ▪ Repolarization- relaxation

→ Pharmacodynamics: increases intracellular calcium ▪ Depolarization- contraction
levels in the heart inc contractility + INOTROPY ▪ RMP (resting membrane potential)→ heart is at
→ The heart is not pumping effectively rest, electrolytes are also in place (PISO, calcium
→ GOAL: help the heart pump also outside)
• Inotropic effect→ increased contractility ▪ When in the RMP, muscle can be stimulated
• Chronotropic effect→ decrease heart rate ▪ Phase 0: Stimulus→ sodium channel will open and
→ PD- increases intracellular calcium levels in the heart→ sodium gets inside the cells
↑ contractility→ (+) inotropy o Sodium will enter until sodium inside= sodium
outside
CARDIOTONIC DRUGS: ▪ Phase 1: Early repolarization- when some sodium
→ Cardiac Glycosides starts to go out
• Pharmacodynamics: increase the calcium in ▪ Phase 2: plateau because calcium comes in
myocardial cells ▪ Phase 3: once potassium goes out→ rapid
• Digoxin ( Lanoxin ) repolarization
• Most commonly used in ▪ Phase 4: RMP, when electrolytes have come back
o Heart failure to their original places
o Atrial fibrillation
• Normal level = 0.5-2.0 ng/ml → Arrhythmia
• Effects: • Change in the automaticity or conductivity of heart
o (+) Inotropic effect cells
o (-) Chronotropic effect • It can be tachycardia, bradycardia, atrial fibrillation,
▪ Increase CO, increase renal perfusion atrial flutter, ventricular fibrillation, ventricular
• Side effects: tachycardia, blocks
o Bradycardia d/t (-) chronotropic effect • Arrhythmia results from:
o Visual disturbance “halo” o Electrolyte imbalances: Na+, K+, Ca+
▪ Hallmark sign of digitalis toxicity o Decreased O2 delivery: Angina, Myocardial
• Digitalis toxicity Infarction
o Serious o Acidosis → alters AP
o Increase risk of toxicity: hypokalemia o Structural damage
▪ Valvular diseases
 o Drugs • Famotidine
▪ Epinephrine • Nizatidine
▪ Atropine → Proton Pump Inhibitors (PPI)
CLASS I: • Pharmacodynamics: blocks the proton pump →
→ Block the sodium channel: Phase 0 suppressing HCl secretions
→ Class 1a • Dose: 1 tab OD for 2 weeks
• Procainamide - HIPP (drugs induced SLE) • Most effective and cost effective
• Quinidine • Omeprazole
→ Class 1b • Lansoprazole
• Lidocaine - local anesthetic → GI Protectives
→ Class 1c • Sucralfate
• Propafenone → Prostaglandin
• Misoprostol
CLASS II:
→ Blocks the beta receptor: Phase 4 CYTOPROTECTIVE - PROTECT STOMACH LINING
→ Propranolol
→ Esmolol Sucralfate Misoprostol - Cytotec
(prostaglandin agonist)
CLASS III:
→ Blocks the potassium channel: Phase 3 → Sticky gel coating the → Acts as replacement for
→ Amiodarone - emergency ulcer endogenous
→ Given AC prostaglandin
→ Sotalol
→ Protective barrier • Prostaglandin
against pepsin and increases mucus and
CLASS IV: bicarbonate
gastric acid
→ Blocks the calcium channel: Phase 2 → Contraindication in
→ Small risk of
→ Diltiazem constipation pregnancy
→ Verapamil • Causes cervical
dilation →
FOR HEART BLOCKS: Abortifacient
→ Anticholinergic → May cause diarrhea
→ Action: prostaglandin
• Atropine
agonist

GASTROINTESTINAL DRUGS
Prostaglandin Agonist
How does the stomach protect itself?
→ MUCUS - coats the entire stomach
→ BICARBONATE - neutralizes the gastric acid
→ ADEQUATE BLOOD FLOW - nourishes the mucosa
• That is why people who smoke are prone to ulcers
• Smoke→ vasoconstriction→ ↓perfusion to the
stomach
→ PROSTAGLANDIN - stimulate mucus and bicarbonate
secretion
→ Ulcer - an erosion in the mucosal lining

DRUGS AFFECTING GASTRIC SECRETIONS

Drugs for PUD, GERD and Gastritis
→ Antacids
• Neutralize the acid
• Inactivate the pepsin LAXATIVES
• Enhance the mucosal protection → Chemical Stimulants
• Dose: 1 tab, 1-2 hours AC/PC HS for 6 months, 4x • Irritates the colon muscles → inducing bowel
a day (after lunch, breakfast, dinner, and at movement (BM)
bedtime) • Senna
• Note: • Bisacodyl ( Dulcolax )
o Prolonged use can lead to rebound acidity • Castor oil
o Liquid is better for liberation is faster → Bulk Forming / Osmotic Laxatives
• Aluminum Hydroxide • Absorbs water → adding volume to the stool
o SE: constipation (safest)
• Magnesium Hydroxide • Psyllium (sachet)
o SE: diarrhea o Mix in a glass of water → drink immediately
• Magaldrate (Maalox, Kremil-S) (because it forms like jelly ace)
o Combination of magnesium + aluminum → Stool Softener / Emollient Laxatives
hydroxide • Helps to wet and soften the stool
→ H2 Receptor Blockers • Lactulose
• Pharmacodynamics: blocks H2 receptors in the o DOC for hepatic encephalopathy
stomach lining (parietal cells) → suppression of Proteins→ amino acids→ ammonium and ammonia (toxic)→
HCl- secretions body has to remove ammonia via liver→ converted to urea
by the liver (water soluble)→ can mix with blood→ excreted
• OTC medication
through urine (smelly due to bacteria present)
• “Tidine”
• Dose: 2x a day for 2 months Hepatic Encephalopathy
• Cimetidine • Diet- low protein
o Causes gynecomastia (binds to androgen)
o Impotence ↑ ammonia because of liver damage→ pass the BBB→
o Decreased libido damage brain cells→ hepatic encephalopathy→ hepatic
• Ranitidine coma
 Neomycin- will kill the bacteria in the colon the converts
protein into ammonia → diarrhea
→ rare:
metabolic
HEPATIC ENCEPHALOPATHY acidosis
Diet: low protein (prevents ammonia buildup) (renal
impairment
LACTULOSE NEOMYCIN )

→ Binds with → Wastes in the colon contains Second → Stimulate Hypoglycemia

ammonia CHO, CHON and fats → colon Generation release of
has bacteria that would act on Sulfonylureas insulin from
protein → bacteria would break Glipizide, pancreas
down protein into ammonia → Glimepiride, → May increase
reabsorbed by the blood → Glyburide cellular
crosses BBB causing hepatic sensitivity to
encephalopathy First-Generation insulin
→ Neomycin kills bacteria that Sulfonylureas
converts protein to ammonia Chlorpropamide,
Tolazamide,
Tolbutamide
ANTI-DIARRHEAL DRUGS (Orinase)
→ Loperamide (Diatabs/Imodium)
• Effect: Meglitinides Promotes insulin Hypoglycemia
o Anticholinergic action → SNS → constipation (Glinides) secretion by the
Nateglinide, pancreas
o Also causes urinary retention
Repaglinide
o Decrease body secretions
→ Opiate Related Diphenoxylate with Atropine Thiazolidinedione → ↑ insulin Water retention
• Opioid narcotic s (Glitazones) sensitivity in (weight gain &
• *codeine can also cause constipation Pioglitazone NIDDM edema)
→ ↑ uptake by
ENDOCRINE DRUGS muscles
→ ↓ glucose
DRUGS TO CONTROL GLUCOSE production by
→ OHAs are given for T2DM; teratogenic the liver
→ GOAL: decrease blood glucose levels
Alpha- Inhibits CHO GI: flatulence,
• Increase use of glc by the muscles
Glucosidase digestion/absorptio cramps,
• Insulin is increased to carry more glc inhibitors n, ↓ post prandial distention,
• Absorption of glucose is decreased Acarbose, Miglitol blood glucose rise borborygmus
• Liver (T-B) - produces glucose Delay absorption of
o OHA decreases production of glucose ingested CHO
o Thiozolidinediones
o Biguanides DPP-4 inhibitors ↑ activity of incretins
• Muscle (T-B) - uptake/use of glucose (Gliptins) (inhibits their
o OHA increases the use of glucose by the Nesinal, Linagliptin breakdown)
↑ insulin release
muscles
↓ glucagon release
o Thiozolidinediones ↓ hepatic glucose
o Biguanides production
• Pancreas (S-M) - produce insulin → to bring
glucose into the cell Dopamine agonist
o OHA should be increased to enhance Bromocriptine
production of insulin
o Sulfonylureas GLP-1 and DPP-4 Inhibitors
o Meglitinides
→ DDP 4 enzyme will remove incretin reversing the
• Intestine (AGI) - absorption of glucose effects
o OHA is decreased to lessen absorption of
glucose
o Alpha Glucosidase Inhibitors

INSULIN
→ ACTION: liver, muscle & adipose to facilitate passage
of glucose, K+, and Mg
• Also used in hyperkalemia (d50 + insulin)
→ INDICATIONS : DM type 1, DM type 2, GDM
→ Dose: based on onset, peak & duration
ORAL HYPOGLYCEMIC AGENTS (OHA) → Syringe: Gauge: 27-29 (½ inch long
→ Nursing considerations:
DRUG MOA SIDE EFFECTS • Mix the ingredients well:
o Swirl vial gently
Biguanides ↓glucose production → GI o Rotate between palms
→ Metformin by the liver & disturbanc • Inject air into the insulin bottle
→ DOC for Type increase glucose e • Mixing insulins: draw up regular (clear first) then
2 DM uptake by muscle → ↓appetite cloudy
→ Nausea • May be mixed with NPH or Lente
 The only insulin that can't be mixed with other
o DRUGS AFFECTING THE THYROID GLAND
insulin → GLARGINE/LANTUS (long acting)
• Once mixed, administer within 5-15 minutes Thyroid Hormones: Functions
• Aspiration is NOT RECOMMENDED with self- → Control metabolic rate of tissues
injections of insulin → Accelerate heat production
→ Route: → Accelerate oxygen consumption
• SQ - 45 - 90 degrees on normal SQ mass → Development of secondary sexual characteristics
o 45-60 degrees on thin person → Brain development
o 90 degrees on fat patients
• IM - absorption would be too fast; can lead to Hypothyroidism (everything is low, slow and dry)
hypoglycemia → Bradycardia
• IV - can be given → Decreased appetite
o Only insulin can be given via IV - REGULAR → Weight gain
INSULIN → Constipation
→ STORAGE: → Intolerant to cold temperature
• Avoid extremes of temperature. → Males: impotence and incompetent penis
• Before injection : should be room temp → Females: amenorrhea
• if vial will be used in 1 month: room temp → Mental retardation
• Otherwise: refrigerate
Hypothyroidism is part of the newborn screening→
metabolism is decreased→ ↓appetite but (+) weight gain,
TYPE EXAMPLE ONSET PEAK DURATION
bradycardia, constipation, intolerant to cold, impotence,
amenorrhea, mental retardation
Very short Aspert, 12 30-60 2-4 hours
Lispro minutes minutes
Process of T3 and T4 production
Short Regular 30-60 2-4 4-6 hours → Diet: Iodine → Trapped in thyroid gland → Binding
minutes hours iodine + tyrosine → monoIodoTyrosine (MIT) → MIT +
MIT = DIT → MIT + DIT = T3 → DIT + DIT = T4
Intermediate NPH 2-4 6-8 16-20
hours hours hours THYROID DRUGS: THYROID REPLACEMENTS
→ INDICATIONS: Hypothyroidism
Long acting Ultralente 6-8 12-16 20-30
hour hours hours
→ Levothyroxine (Synthroid) - T4
→ Liothyronine (Triostat) - T3
Very long Glargine, 1 hour No peak 24 hours → Liotrix - T3 + T4
acting Lantus → Thyroid Hormone
→ Side effect:
• Hyperthyroidism effects (everything is high, fast
and wet):
→ Nursing Interventions
• Should be given at least 4 hours apart from; so as
not to decrease absorption
o Multivitamins
o Almg (Oh)
o Simethicone
o Calcium Carbonate
o Iron
o Sucralfate
• Instruct to avoid foods: Inhibit thyroid secretions
o Strawberries
o Peaches
o Pears
o Cabbage
HYPOGLYCEMIA o Turnips
→ Glucose-Elevating Agents o Cauliflower
• Diazoxide o Radishes
• DOC: Glucagon o Pea
o Used when patient is already unconscious
o D50 can also be used ANTI THYROID DRUGS
• Conscious and still at home, do 15 / 15 rule: → INDICATIONS: Hyperthyroidism
o 15 grams of FAC (fast acting carbohydrates, → Methimazole (Tapazole)
juice, soda, chocolates) → Propylthiouracil (PTU)
o Assess after 15 minutes, if still lethargic, repeat • Commonly used in pregnancy
until the patient becomes conscious or normal → Lugol’s Solution
• Strong iodine solution
• Action: block the synthesis of thyroid hormones
→ Iodide I 131
→ Side effect: Hypothyroidism effects
→ Nursing Interventions:
• Monitor VS (decrease in BP and HR)
• Monitor T3, T4, TSH
• Monitor weight for weight gain
• Take with meals
• Instruct how to measure PR
• Instruct re importance of medication compliance
• Abruptly stopping meds because this might lead to
thyroid storm:
 o Fever oProbenecid (uricosuric drug)
o Flushed skin ▪ Decrease the excretion of penicillin →
o Confusion increase blood levels of penicillin
o Tachycardia • Adverse effects:
o Dysrhythmia o Most common cause of medication allergic
o Signs of heart failure reactions
• Monitor sx of iodism: o Can occur with any of the PCN
o Complaints of nausea and vomiting o Symptoms:
o Metallic taste ▪ Hives
o Skin rash ▪ Rash
o Sore gums ▪ Itching
o Hypersalivation ▪ Angioedema
o Halitosis/Bad breath ▪ Anaphylaxis
• Consult MD before eating iodized salt and iodine o When the patient shows signs of an allergic
rich foods reaction, immediately STOP
• Avoid aspirin & meds w/ iodine because it can block • Common side effects:
the production of thyroid hormones o Nausea and vomiting
• PTU causes agranulocytosis o Diarrhea
o Advise the patient to contact healthcare o Abdominal pain
provider if fever or sore throat develops • Allergic Reactions
o If the patient is allergic to one PCN, avoid all of
ANTIMICROBIALS them
→ Bactericidal = kill o Very small chance of cross allergy to
→ Bacteriostatic = prevents growth of bacteria cephalosporins
→ Narrow spectrum = limited coverage • Alternatives
→ Broad spectrum = covers a wide range of bacteria o Vancomycin
→ Aerobic = kills bacteria who loves air o Erythromycin
→ Anaerobic = kills bacteria who thrives even without o Clindamycin
presence of air → Cephalosporins
• 1st Generation: Cephalexin, Cefazolin
BACTERIAL CELL WALL o Has gram positive coverage with a weak
→ Overall strength of the cell negative coverage
→ Growth • 2nd Generation: Cefuroxime, Cefaclor
→ Reproduction o Has gram positive coverage with some
→ Obtaining nutrition negative coverage
→ Protection • 3rd Generation: Ceftriaxone, Ceftazidime
o Has gram positive coverage and gram
BACTERIAL CELL WALL SYNTHESIS INHIBITORS negative coverage
o Effective concentration in CSF thus can enter
Beta Lactams: has beta lactam rings BBB
o DOC for Meningitis caused by gram negative
bacteria
• 4th Generation: Cefepime, Ceftaroline
o Has gram positive coverage and gram
negative coverage
→ Penicillins: “Cillins” • 5th Generation: Ceftobiprole
• Penicillins - G (+): narrow spectrum o Has gram positive coverage and gram
o Penicillin V - Given orally negative coverage
o Penicillin G Benzathine - Given IV o Newest and the only cephalosporin that can be
o Penicillin G Potassium - Given IV used for methicillin-resistant staphylococcus
o Penicillin G Procaine - Given IV aureus (MRSA)
• Extended-Spectrum Penicillins: gram (+) and gram → Carbapenems: Meropenem
(-) • Broad spectrum
o Amoxicillin - Given oral • Bactericidal
o Ampicillin - Given IV → Monobactam: Aztreonam
• Penicillinase-Resistant PCN • Narrow spectrum
o Penicillinase • Good for UTI, skin infections
▪ Enzyme produced by bacteria
▪ Destroys the structure of penicillin Glycopeptide - no beta rings
o Nafcillin → Vancomycin
o Oxacillin • DOC for MRSA
• Beta-Lactamase Inhibitors • Alternative drug for penicillin allergy
o Beta Lactamase • Adverse effects: hypersensitivity reaction
▪ Enzyme produced by the bacteria (sanay o Possible allergic reaction/anaphylaxis
na kay penicillin lmao) o Red man syndrome
▪ Breaks open the beta lactam ring → ▪ Occurs with fast infusion
inactivate the beta lactam ▪ Manifestations:
o Clavulanic Acid ❖ Flushed skin and neck
o Sulbactam ❖ Itchy
o coAmoXiClav (Augmentin) ▪ Prevention:
• Nursing Considerations: ❖ Slow IV infusion (30 minutes) / infusion
o Risk for hypersensitivity pump
▪ NI: skin testing
o Cross allergy with cephalosporins
▪ NI: If patient is allergic to penicillin, do not
give cephalosporin and vice versa
o Give 1 -2 hours AC or 2-3 hours PC
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
CLASSIFICATION OF ANTIMICROBIALS BASED ON SITE • Sulfasalazine
OF ACTION • Sulfamethoxazole
• Trimethoprim
Blocks Protein Synthesis • Adverse Effect: Steven Johnson’s disease
→ Macrolides
• Azithromycin
o Has a sustained release but the duration of
action is 10 days
o Dose: OD for 3 days (it is already effective for
3 days, and still lasts for 10 days)
▪ For COVID, OD for 5 days (also covers
gram negative bacteria)
• Clarithromycin
• Erythromycin
o Alternative drug for penicillin allergy
Nucleic Acid Synthesis Inhibitor
→ Chloramphenicol
→ Fluoroquinolones (-oxacin)
• Can cause gray baby syndrome
• Broad Spectrum
o Manifestations:
• Bactericidal Against G (-) And Some G (+)
▪ Cardiovascular collapse
• Ciprofloxacin
▪ Cyanotic
o For UTI, STDs
• Avoid in children <2 years old
• Ofloxacin
→ Lincosamines
• Clindamycin (Dalacin C - mixed in eskinol; for acne)
• Things To Remember: Rifampicin - anti-TB drug
o Allows clostridium difficile to infect colon, → SE: red-orange discoloration of body fluids
colitis, pseudomembranous (foul smelling
feces) 2 cuties (QTs) say no to OB
▪ Antibiotic-induced colitis → Quinolones
o Treatment: vancomycin → Tetracycline
→ Aminoglycosides - “mycin”/”cin”
• Streptomycin ANALGESICS AND ANTI INFLAMMATORY DRUGS
o Anti-TB drug → Corticosteroids
o SE: ototoxic • Acts on arachidonic acid and histamine
• Kanamycin → NSAIDS (ibuprofen, mefenamic acid)
• Neomycin • Acts on prostaglandin
o Used in hepatic encephalopathy • COX-2 inhibitors - acts on COX-2 (celecoxib,
• Gentamicin valdecoxib)
o Nephrotoxic → ASA
• Adverse Effects: nephrotoxic & ototoxic • Acts on prostaglandin, dolor
→ Antihistamine
→ Paracetamol
• Weak anti-inflammatory
• Action in the hypothalamus
→ NOTE: Given after meals to prevent gastric irritation

→ Tetracyclines
• Tetracyclines
o Indicated for:
▪ H. pylori (peptic ulcer disease)
▪ Acne vulgaris (oral/topical)
▪ Chlamydial infections
o Adverse Effects:
 • Example: Order: Tempra 250 mg q4 for fever PRN
WHO ANALGESIC LADDER 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
𝑚𝑔 𝑥 𝑘𝑔 𝑥 ℎ𝑟 𝑜𝑟 min 𝑜𝑟 𝑑𝑜𝑠𝑒
𝐴= 𝑄
𝑆
• Example:
o Order: Acetaminophen 15 mg/kg/dose q4h for
fever
▪ Recommended dose: 15 mg
o Weight: 12 kg
o Supply: acetaminophen 100 mg/ml
▪ Desired dose = 15 mg/kg/dose x 12 kg
(cancel kg, leave mg/dose) = 180 mg/dose
▪ 180 mg/dose / 100 mg x 1 ml (cancel mg,
→ Pain scale
leave ml/dose) = 1.8 ml/dose
• Mild pain: 1-3
• Moderate pain: 4-6
FORMULA IN COMPUTING FOR THE FLUID FLOW RATE
• Severe pain: 7-9; 10 is worst 𝐴𝑚𝑜𝑢𝑛𝑡 𝑡𝑜 𝑏𝑒 𝑖𝑛𝑓𝑢𝑠𝑒𝑑 (𝑚𝐿) 𝐷𝑟𝑜𝑝 𝑓𝑎𝑐𝑡𝑜𝑟
→ Mild pain: Non-opioid (PAN) 𝑥 = 𝑅𝑎𝑡𝑒
• Paracetamol 𝐻𝑜𝑢𝑟 𝑜𝑓 𝑖𝑛𝑓𝑢𝑠𝑖𝑜𝑛 (ℎ𝑟) 60 𝑚𝑖𝑛𝑠 𝑝𝑒𝑟 ℎ𝑜𝑢𝑟
• ASA
→ Microset for pediatrics = 60 ugtts/ml
• NSAIDs
→ Macroset = 10 gtts/ml or 15 gtts/ml or 20 gtts/ml
→ Moderate pain: opioid + non-opioid
→ Examples
→ Codeine
• Infuse 1.5 liters of D5W solution to be administered
→ Tramadol
over a 24 hour period. The IV set is calibrated to
→ Severe pain: opioid (strong)
deliver 15 gtts/ml
→ Morphine
o 1500/24 x 0.25 = 15.6 or 16 gtts/min
→ Fentanyl
• Infuse 0.1 L of D5NM to a severely dehydrated
infant for 30 mins. What is the rate of infusion?
DRUG CALCULATION
o 100 ml/.5 x 1 = 200 ugtts/min
• Infuse 1 L of IVF to the patient for 8 hours using a
ESTIMATING CHILD DOSAGES BASED ON ADULT DOSE
macroset. Rate?
→ Clark’s Rule:
o 1000/8 x 15/60 = 31.25 gtts/min / 31-32
𝐴𝑑𝑢𝑙𝑡 𝑑𝑜𝑠𝑒 𝑥 𝑤𝑒𝑖𝑔ℎ𝑡 (𝑙𝑏𝑠)
𝐶ℎ𝑖𝑙𝑑 ′ 𝑠 𝑑𝑜𝑠𝑒 = gtts/min
150 • Infuse 200 ml of IVF to a patient for 45 minutes. IV
• Example:
set is labeled at 10 gtts/mL. Rate?
o The adult dose of Cephalexin is 500 mg per
o 200ml/45 min x 10 = 44 to 45 gtts/min
dose. How much should be prescribed to a 3-
• For how long should the nurse infuse a 1000 ml of
year old child weighing 14 kg.
D5 0.9% NaCl running at a rate of 32 gtts/min. IV
▪ Conversion: 1 kg = 2.2 lbs
set is labeled at 15 gtts/min.
▪ 14 kg x 2.2 lbs/1kg = 30.8 lbs
o 1000 ml/32 gtts/min x 0.25 = 8 hr
▪ 500 mg x 30.8/150 = 103 mg
→ Young’s Rule: Shortcut
𝐴𝑑𝑢𝑙𝑡 𝑑𝑜𝑠𝑒 𝑥 𝑎𝑔𝑒 (𝑦𝑒𝑎𝑟𝑠) If the given is in minutes, conversion may not be done so
𝐶ℎ𝑖𝑙𝑑 ′ 𝑠 𝑑𝑜𝑠𝑒 =
𝑎𝑔𝑒 (𝑦𝑒𝑎𝑟𝑠) + 12 long as the 60 mins/ hr value (constant) is cancelled out.
• Example:
o The adult dose of Cephalexin is 500 mg per E.g.,
dose. How much should be prescribed to a 3- Infuse 200 ml of IVF to a patient for 45 minutes. IV set is
year old child weighing 14 kg. labeled at 10 gtts/mL. Rate?
▪ 500 mg x 3/15 = 100 mg 200 𝑚𝐿 10 𝑔𝑡𝑡𝑠
→ Fried’s Rule: up to 2 years old only 𝑥 = 44 − 45 𝑔𝑡𝑡𝑠/𝑚𝑖𝑛
45 𝑚𝑖𝑛𝑠 60 𝑚𝑖𝑛𝑠 𝑝𝑒𝑟 ℎ𝑜𝑢𝑟
𝐴𝑑𝑢𝑙𝑡 𝑑𝑜𝑠𝑒 𝑥 𝑎𝑔𝑒 (𝑚𝑜𝑛𝑡ℎ𝑠)
𝐶ℎ𝑖𝑙𝑑 ′ 𝑠 𝑑𝑜𝑠𝑒 =
150
• Example:
o The adult dose of Cephalexin is 500 mg per
dose. How much should be prescribed to a 1
and a half child weighing 14 kg.
▪ 500 mg x 18/150 = 60 mg

FORMULA IN COMPUTING FOR DRUG DOSAGES

𝐷
𝐴= 𝑄
𝑆
→ A = Amount
→ D = Desired Dose
→ S = Stock
→ Q = Quantity