PHARMACOLOGY -​ Host (men) will list everything happen to them after drug

Comprehensive Phase administration

Pharmacology - study of biological effects of chemicals ●​ Phase II

(drugs/medicines) -​ Drugs will be tested to patients to whom the drugs are
intended for use
Pharmacotherapeutics -​ Double blinded experiment (1 group: placebo; 1 group:
-​ Drugs we refer as medicines that are used to cure and prevent drug experiment)
diseases -​ If both groups had positive effect = Discontinue

SOURCES OF DRUGS ●​ Phase III

●​ Natural -​ Vast clinical trial with thousands of patients
○​ Plants -​ FDA
○​ Animals -​ Must include 3 names: Chemical, Generic, Brand
​ Innovator drug
⭐
○​ Microbes (vaccines)
Alexander Fleming
-​ Discovered Penicillin at 1920
-​ Are those who discovered the drug first
-​ No price change, always expensive
-​ Mold from his culture is called Penicillium -​ FDA decides how long they will remain in the market
○​ Minerals without duplication

●​ Synthetic ●​ Phase IV
-​ Most of drugs come from synthetic sources -​ Post marketing evaluation
-​ Amoxicillin is combination of natural and synthetic -​ Already released in the market but still evaluated for any
sources severe adverse effect it may cause
-​ Might be retained or removed in the public market
DRUG EVALUATION Ex: Thalidomide were used 50’s-60’s for morning sickness during
-​ Drugs are considered drugs only if they undergo complete drug pregnancy but discovered adverse effect is phocomelia/amelia
evaluation (no limb)
-​ If no drug evaluation, it is only considered food supplement -​ If a drug is removed in the market it is called Orphan
drug but it can be used again but for another reason
CLINICAL TRIALS ​ Ex: Thalidomide is used for cancer instead for morning sickness
●​ Pre-clinical trials
-​ Test experimental drugs to living cells (animals: rats, DRUGS
rabbits) ●​ OTC
-​ Highly toxic: Host (animal) died after giving the drug -​ Drugs with no prescription needed
-​ Has side effect but relatively safe
●​ Phase I ●​ Prescribed
-​ Drugs are tested to human that are young healthy men -​ Drugs requiring physician’s prescription
-​ Not applicable to women as it may affect the reproductive ●​ Controlled/Regulated
system because women have limited number of egg cell -​ Drugs that requires prescription from physician with S2
only license and yellow prescription
ROUTES OF DRUG ADMINISTRATION
Airah B. Bolinbough, RN
 ●​ Enteral -​ Microbes and cancer cells are foreign cells →
○​ Oral chemotherapeutic drugs
○​ Sublingual -​ Important characteristic of chemotherapeutic drugs:
○​ Rectal Selective toxicity - harmful only to the foreign cells
●​ Parenteral
○​ Injectables
○​ Intraarterial
⭐ To know the action of the drug you must know the problem of the
disease/disorder
-​ Usually used for chemotherapy
-​ Subject artery is the artery that supplies the tumor DRUGS ACTIONS
○​ Intrathecal ●​ Through Ion channels
-​ Route: Spine -​ Cell membrane is semipermeable because it is made of
●​ Local - localized effect thus less systemic effects lipid layer in between proteins
○​ Topical -​ If the drug is not permitted to enter in the cell
○​ Inhalation membrane, they uses ions as their channel
○​ Drops 1.​ Calcium Channel
2.​ Sodium Channel
14 RIGHTS OF ADMINISTRATION OF DRUGS 3.​ Gabba-gated chloride channels
●​ Right Drug/Medication
●​ Right Client/Patient ●​ By physical action
●​ Right Route 1.​ Absorption - activated charcoal in poisoning
●​ Right Dose 2.​ Mass of the drug - bulk laxatives like psyllium
●​ Right Frequency/Time 3.​ Osmotic property
●​ Right Assessment -​ Osmotic diuretics (mannitol)
●​ Right Approach -​ Osmotic purgatives (magnesium sulphate)
●​ Right Education
●​ Right Evaluation ●​ By chemical interaction
●​ Right Documentation ​ Antacids
●​ Right to Refuse -​ Palliative not curative
●​ Right Principle of Care
●​ Right Prescriptions ●​ 💊
-​ Only decreases s/sx as as it only neutralizes the acidity

💊MgOH – causes diarrhea

●​ Right Nurse Clinician ●​
●​ 💊AlOH – causes constipation ​
MgAlOH (Maalox) – no side effect; liquid form
PHARMACODYNAMICS
-​ Actions/effects of drugs in the body ●​ 💊
(best form)
Calcium carbonate, 💊Sodium carbonate

BASIC ACTIONS OF DRUGS ⭐ (Gaviscon)

Tablets are supposed to be chewed + 1 full glass of
●​ To replace a missing substance
●​ To increase cellular activities ⭐
water after

❌
Antacids are given 30 minutes to 1 hour after meal
Antacids + Tetracyclines, NSAIDs, Aspirin, Steroids as
●​ To address cellular activities
●​ To interfere with the growth of foreign cells
⭐
MOA might be affected
If not sure if 2 drugs has adverse reaction if given
together, give 2 hours gap before taking the other
Airah B. Bolinbough, RN
 ●​ By altering metabolic process
💊Pantoprazole
-​ Given OD, before breakfast
Chemotherapeutic Drugs -​ Cure ulcer for 2-4 weeks
-​ Interfere with the DNA/RNA and protein (ribosome)
synthesis of the foreign cells ●​ Cytoprotective
-​ Only protects but does not cure
a.​ Antimicrobial drugs
i.​ Penicillin - interfere with biosynthesis of
bacterial cell wall
💊
○​ Antipeptic drug
Sucralfate - “coat”

b.​ Antineoplastic drugs 💊

○​ Prostaglandin
Misoprostol (Cytotec) - not usually
i.​
💊
Hormone modulators
Tamoxifen (Antiestrogen): Breast cancer
patient still has estrogen receptor that
used as it has abortifacient
content

causes spread of cancer cells → administer ●​ Through Receptors

tamoxifen to block the estrogen receptor -​ Surface receptors or nuclear receptors
●​ Agonist - mimic or stimulate the function
●​ Through pump Acetylcholine → drug bind → mimic or stimulate receptors
Disease: GERD, Gastritis, Peptic Ulcer Disease → contraction → impulse transmission = Cholinergic
Cause Agonist
●​ H. Pylori
-​ Gram negative bacteria ●​ Antagonist - blocker

●​ ⬆️
-​ Detected thru endoscopy

(prostaglandin) → ⬇️
corrosive effect of HCL due to
HCL and ⬆️⬇️
protective barrier
mucus
Acetylcholine → Block receptors → no muscle contraction
→ no impulse transmission = Cholinergic Antagonist

a.​ Competitive antagonist

Binding of Histamine 2 and its receptor will cause release of HCL -​ Antagonist drug binds and blocks the receptor thus
acid of the parietal cells prevents the agonist drug from binding with its
receptor

💊
●​ Histamine 2 Receptor Blocker

💊Cimetidine
-​ Reversible

b.​ Non-competitive antagonist

💊Ranitidine
Famotidine
-​ Cure ulcer for 2-4 months taken before meals, OD
-​ Antagonist drug has its own receptor → bind →
binded receptor and antagonist blocks the agonist
or BID drug to bind to its own receptor
○​ Histamine I - causes allergy -​ Irreversible
○​ Histamine II - release of HCL acid
○​ Histamine III - causes vertigo or dizziness ACETYLCHOLINE: CHOLINERGIC RECEPTORS
●​ Nicotinic Receptor
●​ Proton Pump Inhibitor ●​ Muscarinic Receptor

💊
💊
-​ Most effective and most cost effective
Omeprazole
Esomeprazole
EPINEPHRINE AND NOREPINEPHRINE: ADRENERGIC RECEPTORS
●​ Alpha Receptor
Airah B. Bolinbough, RN
 ○​ Alpha
-​
-​
I
Located in blood vessel and iris
Act as decongestant
●​ Agonist: Stimulate →
●​ Antagonist: Block → ⬇️⬆️HRHRand
and contractility
contractility

-​ Inflammation is due to vasodilation → administer ○​ Beta II - Found in the lungs

alpha I → vasoconstriction ●​ Agonist: Stimulate → Bronchodilate

​ ​
-​
further ⬆️
High BP with colds cannot take decongestant →
BP → advise only to take water
●​ Antagonist: Block → Bronchoconstriction

○​ Beta III

●​
●​
💊
Alpha I Agonist: Fight

💊 Phenylephrine
Phenylpropanolamine
-​ Found in adipose tissue
-​ Responsible for thermogenesis and lipogenesis

●​ 💊Prazosin
Alpha I Antagonist: Flight 💊
Beta Agonist
Salbutamol

●​ 💊Doxazosin
●​ 💊Terazosin
Beta Blockers

💊
a.​ Non selective B1 B2 Blocker

💊
Propranolol
Blood vessel

⬆️
●​ Agonist: Stimulate blood vessel → 💊
Pindolol
Timolol

b.​ Selective Beta blocker – ⬇️HR

vasoconstriction → BP

Vasodilate → ⬇️
●​ Antagonist: Blocked blood vessel →
BP 💊
💊 Metoprolol

Iris
●​ Agonist: Stimulate iris → Mydriasis
💊Atenolol
Nebivolol

●​ Antagonist: Block iris → Miosis AUTONOMIC DRUGS

●​ Cholinergic Agonist (Parasympathomimetic drug)
Urinary Bladder ●​ Cholinergic Antagonist (Parasympatholytic drug)
●​ Agonist: Stimulated urinary bladder → ●​ Adrenergic Agonist (Sympathomimetic drug)
Urinary retention
●​ Antagonist: Blocked urinary bladder →
Bladder emptying
⭐
⭐
●​ Adrenergic Antagonist (Sympatholytic drug)
Cholinergic Agonist and Adrenergic antagonist has the same effect
Cholinergic Antagonist and Adrenergic agonist has the same effect

○​ Alpha II
-​ Located in CNS ●​ 💊
Cholinergic Agonist: Parasympathomimetic drugs
Pilocarpine
-​ Higher than ANS
●​ Agonist: Stimulate CNS → ⬇️
⬇️SNS → ⬇️BP
Norepinephrine flow
-​ Available in eyedrops
-​ Used for glaucoma
⬇️
​ ​ ​
●​ Beta receptor
💊
●​ Antagonist: Block CNS →
Clonidine (Catapres) ⬇️
MOA: Miosis → open iridocorneal angle →
IOP
aqueous humor →

○​ Beta I - Found in the heart Cholinergic Antagonist: Parasymphatolytic drugs

(Anticholinergic drug)
Airah B. Bolinbough, RN
 ●​ 💊 Atropine Sulfate
MOA:
○​ Eye drops → mydriasis → used as pre-op drug before eye
Overdose: Cholinergic Crisis
-​ Signs and symptoms of ⬆️Acetylcholine = ⬆️PNS
⬇️⬆️
surgery Antidote: Atropine
○​ Severe bradycardia → HR
○​ General anesthesia → gastric secretion and saliva
○​ Antidote for cholinergic crisis
Underdose: Myasthenic Crisis
-​ Signs and symptoms of
Add: Anticholinesterase
⬇️
Acetylcholine = ⬇️PNS
Adrenergic Agonist: Sympathomimetic drugs
●​ Epinephrine In Alzheimer’s disease patient need anticholinesterase to retain
●​ Norepinephrine acetylcholine (enzyme) but long-acting anticholinesterase cannot cross
●​ Dobutamine the BBB
●​ Dopamine

Adrenergic Antagonist (blocker): Sympatholytic drugs

💊
DOC for Alzheimer’s Disease

💊 Rivastigmine
Donepezil
-​ For pheochromocytoma, a tumor that increases epinephrine -​ These cannot be given to Myasthenia Gravis as it can pass
●​ Guanethidine through BBB
●​ Labetalol
●​ Through Reuptake Inhibitors
●​ Through enzymes Junction between 2 nerves is called synapse → Epinephrine is
DRUG ENZYME INTERACTION released by nerve and is received by the receptor from another
Release of acetylcholine in nerve at neuromuscular nerve → removed by:
junction → binds with receptor in muscle → muscle ●​ Reuptake - epinephrine goes back to nerve
contraction → acetylcholine removed by ●​ Monoamine oxidase (MAO)
acetylcholinesterase (drug that inhibits the enzyme) -​ Enzyme that removes the epinephrine
-​ MAOI - inhibit the MAO
●​ Anticholinesterase/Cholinesterase Inhibitor ​ ​
-​ Inhibits enzyme → retains acetylcholine →
improve muscle transmission ​ ​ ​ 💊
Amine Neurotransmitters

💊 Epinephrine

​
​
​
​ ​
-​ Used for Myasthenia Gravis

Types of Anticholinesterase
💊
💊
Norepinephrine
Dopamine
Serotonin

💊
●​ Short-acting
Tensilon - used as diagnostic
●​ Long-acting
DEPRESSION
Biogenic Amine Theory
-​ Onset is 20-30 mins but can last for -​ Decrease in norepinephrine, dopamine and serotonin due to:

💊
4-6 hours
-​ Does not cross the BBB ●​ ⬆️
●​ Used up neurotransmitters
MAO activity → MAOI → ⬆️
Norepinephrine, Dopamine

💊
💊
Neostigmine
Physostigmine
Pyridostigmine
●​ ⬆️
and Serotonin
Reuptake
a.​ TCA

Airah B. Bolinbough, RN
 -​ Inhibit reuptake of norepinephrine and ●​ Disease
serotonin

💊 -​ Not the DOC due to its side effects

Imipramine
FIRST PASS EFFECT

⬇️
-​ Oral meds passes through the stomach → absorb in the
blood → goes to liver for biotransformation → effect →
b.​ SSRI systemic circulation
-​ Drug of choice as it carries less adverse -​ Oral meds are different from IM or IV medication →

💊
effect
-​ Increases serotonin ⬆️
straight to the blood (systemic circulation) → faster and
effect
​
​
​
​
​
​ 💊 Escitalopram
Fluoxetine POTENCY VS. EFFICACY
●​ Potency - lower dosage reaches the similar response
PHARMACOKINETICS ●​ Efficacy - lower dosage reaches the maximal response
-​ Movement of drugs in the body ​ = Less adverse effect
1.​ Liberation
-​ Release of drug from its original form 3.​ Distribution/Transport
ex: Dissolved film of capsule medication -​ Transport from tissue store to site of action

2.​ Absorption Factors Affecting Distribution

-​ What happens from the site of administration as it enters ●​ Blood flow
the blood Ex: DM → Viscous blood → slower distribution
-​ IV is the only drug without absorption
●​ Protein binding
Factors Affecting Absorption -​ Albumin is the most potent protein
●​ Disintegration and dissolution time -​ For better distribution the drug must be free and
-​ Slow liberation = slow absorption unbound
●​ Particle size Ex: Albumin binds with drug → heavier transport →
-​ Large molecule = slow absorption slower distribution
●​ Lipid solubility
-​ More lipid soluble = Faster absorption ●​ Lipid solubility
●​ Food -​ More lipid soluble = Faster distribution
-​ Some drug absorption may be affected by food -​ No need for ion channels to pass through the lipid
intake layer of cell membrane
-​ If so, take the drug before meals + 1 full glass of
water ●​ Blood Brain Barrier
-​ Enteric drugs may be given to avoid gastric -​ Only highly lipid soluble drug can pass the BBB
irritation as it is being absorbed in the small -​ BBB is the protective layer of the brain
intestines
●​ Area and vascularity of absorbing surface ●​ Placenta and Breast milk
-​ IM is best route for men as they have more muscle -​ Pregnancy and lactation is not contraindication,
-​ SQ is best route for women as they have more only allergy is considered a contraindication
subcutaneous fats ​
Airah B. Bolinbough, RN
 Gestational DM ●​ Sweat and saliva
-​ Not diabetic before pregnancy
-​ If diabetic before pregnancy it is called Diabetic HALF LIFE AND THERAPEUTIC LEVEL (critical concentration)
pregnant -​ Half life is the time it takes for the drug to reduce to half from

​
-​ Insulin is given SQ in rotating site
-​ Insulin cannot pass the placenta
Lactating DM
💊
the peak level it previously achieved
Phenobarbital half life = 79 hours
●​ Loading dose - higher dose is initially given to reach
-​ Insulin can pass through breast milk but it is destroyed critical concentration immediately followed by a lower
once it pass through the newborn’s GIT dose
​ ●​ Underdose - increased risk of resistance

●​ 💊
Teratogenic Drugs

💊
Thalidomide → phocomelia, amelia ●​ Narrow therapeutic index: Increased risk of toxicity →
●​
●​ 💊
Tetracycline → affects the teeth and bone
Chloramphenicol → Gray baby syndrome 💊
close monitoring
Digoxin
●​ Widened therapeutic index: Lesser risk
4.​ Biotransformation
-​ Changing of drug to another chemical (metabolite) by TOXICOLOGY
metabolism -​ Study of harmful effects of drugs in the body
-​ Metabolite can be active or inactive ingredient of the drug -​ All drugs are potentially harmful according to Paracelsus so he
​ MOA: introduced the use of single drug instead
●​ Active drug → inactivation → excretion
●​ Inactive drug → active metabolite → inactivation ●​ Primary Adverse Effect
-​ Pharmacodynamic effect, the effect when overdose
Factors Affecting Biotransformation
●​ Genetic variation
○​ Glucose 6PO4 Dehydrogenase → exposure to
Ex: ⬆️happens
BP → antihypertensive drug → decrease BP → overdose →
hypotension
contraindicated foods or medications → Hemolytic
anemia → jaundice ●​ Secondary Adverse Effect
●​ Environmental pollutant -​ Pharmacodynamic effects
-​ Chronic smoking increases the metabolism of drug -​ Adverse drug reactions
→ faster inactivation of drug → lesser effect -​ Effects that are noxious but unintended
duration -​ Meds given at right dose for cure, diagnostic or
●​ Age prevention yet it still cause adverse drug reaction
●​ Diseases of the liver
-​ Majority of medications transform in the liver a.​ Side effect - expected other effect of drug
-​ In liver cirrhosis patient, DOC are those that does b.​ Toxic effect - effect to other organ system
not need to undergo biotransformation in the liver ●​ GI toxicity - give after or with meals
●​ Nephrotoxicity → oliguria + high crea and BUN
5.​ Excretion ●​ Hepatotoxicity → jaundice + high ALT and AST
●​ Renal excretion - through kidneys or dialysis
●​ Fecal and biliary excretion
●​ Pulmonary Excretion
⭐ ●​ Ototoxic → tinnitus (early sign)
RN cannot discontinue medication but can withhold
c.​ Dependence
Airah B. Bolinbough, RN
 d.​ Iatrogenic - treatment induced ⭐ Skin test is not usually performed to newborn because they do not
e.​ Idiosyncrasy - bizarre or rare effect that is not usually
seen, can be due to genetic variation ⭐
have exposure to anything yet
Body might form an antigen at first drug administration → allergic
reaction on the following dosage
Medication Adverse Effect
TYPE II CYTOLYTIC REACTION
-​ Immediate reaction
Antibacterial Drugs ●​ GI toxicity
-​ Previously formed IgG or IgM antibodies binds to antigen on cell
●​ Superinfection - happen
surface → binded antibody kills the cell by phagocytosis or will
when there is distraction
just interfere with the cells’ normal function without killing them
of normal flora
-​ Common in autoimmune diseases where body produces
Anti-cancer drugs ●​ Alopecia antibodies to destroy its own cells
Ex: Hemolytic disease of newborn: Maternal antibody binds to D-antigen
-​ labile cells (rapid dividing)
- ⬇️
●​ Bone marrow suppression
RBC, WBC, Platelet
●​ Nausea and vomiting
on the surface of fetal RBC and destroy them

TYPE III ARTHUS REACTION

NSAIDs ●​ GI toxicity -​ Immediate reaction
●​ Nephrotoxicity -​ IgG and IgM antibody binds with free floating antigens →
forming antibody-antigen complexes (immune complex) →
Aspirin ●​ Ototoxicity immune complex activation → inflammation → damage to
affected tissue
Gentamicin ●​ Nephrotoxic Ex: Serum sickness due to large amount of antigens in the blood →
immune complex are deposited in the walls of blood vessel → triggers
Diuretics ●​ Fluid and electrolyte inflammation or vasculitis
imbalance
TYPE IV HYPERSENSITIVITY
Metabolic hormone ●​ Allergy -​ Delayed reaction mediated by T-cells
-​ Pre-sensitized T-cells are produced during the previous contact
with the antigen → re-exposure to same antigen → T-helper cells
Hypersensitivity
release inflammatory cytokines + T-killer release cytotoxic
-​ Pharmacokinetics effect
reactions
-​ Immune system attack the drug as it thought its an antigen (a
-​ No antibody → T cells activates the type IV hypersensitivity
protein that stimulates antibody formation)
ANALGESIC DRUGS
TYPE I HYPERSENSITIVITY
-​ Given at the beginning of pain unless the patient is post op
-​ Immediate reaction
-​ In post op patients, medications are given before the pain may
-​ Common reaction to medications
occur or before the anesthesia wear off
-​ 1st exposure to antigen → produce IgE antibodies → IgE binds
-​ Pain is an unpleasant sensation, both physical and emotional
to IgE receptor located in the surface of mast cells/basophils →
re-exposure to same or similar antigen → antigen binds to
Types of pain
adjacent IgE molecule → brings 2 IgE receptors together →
triggers release of histamine → Anaphylaxis (allergic reaction) Feature Nociceptive Pain Neuropathic Pain
Airah B. Bolinbough, RN
 Cause Tissue damage or Nervous system Pathophysiology Damaged/injured Caused by nerve
potential damage damage or tissue → send signal damage (central or
dysfunction through spinal cord to peripheral) randomly
parietal lobe → transmitting pain
Mechanism Activation of pain Abnormal processing endorphin release signals to the brain
receptors of pain signals by the (Enkephalins, without any trigger or
(nociceptors) nervous system Dynorphins, warning
Dynomorphine) →
Example ●​ Sprain ●​ Diabetic bind with opioid
●​ Burn neuropathy receptors → analgesia
●​ Cuts ●​ Shingles effect
●​ Carpal tunnel

Characteristic Sore, throbbing, dull, Electric shock,

⬆️
⬆️ Endorphins →
threshold and
tender, aching, stabbing, tingling, tolerance
cramping prickling pins and ●​ Threshold -
needles minimum pain
an individual
Purpose Protection - alerting Often can feel
the body to potential lacks protective ●​ Tolerance -
or actual damage function maximum pain
an individual
can hold

1.​ Narcotic drugs

-​ Interacts with opioid receptors (AKA opiates/opioids)
-​ Can cause physical and psychological dependence
​
Receptors Clinical Effects Location

MU ●​ Analgesia ●​ Mesenteric
●​ Changes plexus
smooth ●​ Brain
muscle tone ●​ Spinal cord
●​ Sedation ●​ Submucosal
●​ Mood plexus
alteration
●​ Nausea/
vomiting

Airah B. Bolinbough, RN
 -​ MU opioid agonist — has analgesia effects
DELTA ●​ Decreased ●​ Mesenteric
-​ Used for mild to moderate pain
colonic transit plexus
-​ Contains serotonin reuptake inhibitor and
time ●​ Brain
norepinephrine reuptake inhibitor
-​ Does not require S2 license
KAPPA ●​ Central ●​ Mesenteric
analgesia plexus
US CONTROLLED SUBSTANCE SCHEDULES
●​ Decreased ●​ Brain
colonic transit ●​ Spinal cord Schedule I Controlled Substances

💊
time -​ No currently accepted medical use

💊
●​ Visceral Heroine

💊
nociception Lysergic acid Diethylamide (LSD)

💊
antagonist Marijuana (cannabis)

Classifications of Narcotic Drugs

💊
💊
Peyote
Methaqualone
3,4-methylenedioxymethamphetamine (ecstasy)
A.​ Narcotic Agonist
-​ Stimulates analgesic effect but can also stimulate
Schedule II/IIN Controlled Substances (2/2N)
other receptors and cause adverse effects
-​ Have a high potential for abuse which may lead to severe
psychological or physical dependence
Adverse effects:
●​ Respiratory center depression
●​ Addiction/Dependence
●​ Mood swings
💊
Schedule II narcotics:

💊 Hydromorphone (Dilaudid®)
●​ Hallucination
●​ Constipation
💊
💊
Methadone (Dolophine®)
Meperidine (Demero/®)
●​ Pupillary constriction
●​ Cough suppression - especially codeine
💊
💊
Oxycodone (OxyContin®, Percocet®)
Fentanyl (Sublimaze®, Duragesic®)
​
Drugs under Narcotic Agonist
💊
💊
Morphine,
Opium
●​ Morphine
●​ Meperidine
💊 Codeine
Hydrocodone

⭐
●​ Fentanyl
These 3 narcotics are strong narcotics used for
💊
Schedule IIN stimulants:
severe pain (MI, cancer, acute pancreatitis)
●​ Codeine
💊 Amphetamine (Dexedrine®, Adderall®)

💊Methamphetamine (Desoxyn®)
Methylphenidate (Ritalin®).
⭐
●​ Oxycodone
These 2 narcotics are mild narcotics and can
cause cough suppression (antitussive)
💊
Schedule II substances:

💊 Amobarbital
‼️These medications cannot be prescribed without S2
license and yellow prescription
💊Glutethimide
Pentobarbital
●​ Tramadol
Airah B. Bolinbough, RN
 B.​ Narcotic agonist-antagonist
Schedule III/IIIN Controlled Substances (3/3N)
-​ Stimulate and blocks
-​ Have a potential for abuse less than substances in
Schedules I or II and abuse may lead to moderate or low
physical dependence or high psychological dependence
●​ 💊
-​ For post-op and post partum

💊 Nalbuphine (Nubain)

Schedule III narcotics: Products containing not more than 90

●​
●​ 💊 Buprenorphine
Butorphanol (Stadol) - common for postpartum

💊
milligrams of codeine per dosage unit

💊 Tylenol with Codeine®

Buprenorphine (Suboxone®)
C.​ Narcotic antagonist
-​ No analgesic effect but will serve as an antidote

●​ 💊
for overdose of narcotics
Naloxone
💊
Schedule IIIN non-narcotics include

💊 Benzphetamine (Didrex®)
-​ Used for babies whose mother received
narcotics during labor and delivery, it can
💊 Phendimetrazine

💊Ketamine,
Anabolic steroids such as Depo®- Testosterone
pass through the placenta causing
respiratory center depression

Schedule IV Controlled Substances

●​
●​
💊
💊
-​ Fast acting narcotic
Naltrexone
Nalmefene
-​ Have a low potential for abuse relative to substances in
Schedule III -​ Used to those who have narcotic addiction
during their withdrawal
-​ Slow onset
💊
Schedule IV substances:

💊 Alprazolam (Xanax®)
2. Non-narcotic Drugs
💊
💊
Carisoprodol (Soma®)
Clonazepam (Klonopin®) A.​ Acetaminophen
-​ Contains very little to no anti-inflammatory effect
💊
💊
Clorazepate (Tranxene®)
Diazepam (Valium®) -​ Cannot be a substitute to anti-inflammatory drug
●​ Antipyretic effect - induces sweating
💊
💊
Lorazepam (Ativan®)
Midazolam (Versed®) ●​ Analgesic effect - possible actions:
○​ Inhibit COX-2 with slight anti-inflammatory effect
💊 Temazepam (Restori|®)
Triazolam (Halcion®) ○​ Producing metabolite causing central analgesic
effect (inhibit endocannabinoid in the brain)
Schedule V Controlled Substances
-​ Have a low potential for abuse relative to substances listed B.​ Anti-inflammatory drug
in Schedule IV and consist primarily of preparations containing -​ An inflammation is a normal response of vascularized
limited quantities of certain narcotics. tissues to injury
-​ Blood vessels response: Vasoconstriction
Schedule V substances: Cough preparations containing not more

⬆️
●​ Vasodilation → ⬆️
-​ General response: Signs of inflammation
blood flow → Redness (rubor) +
💊
than 200 milligrams of codeine per 100 milliliters or per 100 grams

💊 Robitussin AC®
●​ ⬆️ heat (calor)
capillary permeability - fluid is leaking in the
💊 Phenergan with Codeine®
Ezogabine. interstitial space → edema (tumor)

Airah B. Bolinbough, RN
 ●​ WBC is activated (specially if cause is ‼️Valdecoxib
microorganism) → phagocytosis → dead cells + -​ Cardiotoxicity → MI
injured tissues release inflammatory mediators → -​ Used for chronic inflammatory infection (RA, gouty arthritis)
prostaglandins will cause pain (dolor) -​ Contraindicated to patients with cardiac disease or chest pain
●​ Rubor + calor + tumor + dolor = inflammation
STEROIDS
Systemic Inflammation
-​ Injury worsens → ⬆️ ⬆️
WBC → leukocytosis →
mediators → interleukins will
⬆️
chemical
body temperature → fever → ⬆️
-​ Hormone like drug
-​ Secretes adrenal cortex

WBC Adrenal cortex hormones

-​ Fever is a good sign of active immune system but is should be ●​ Mineralocorticoids - aldosterone
managed to prevent dehydration and seizure ●​ Sex hormone - androgens
●​ Glucocorticoids - cortisol
ASPIRIN -​ Has anti-inflammatory effect
-​ Inhibits prostaglandin inhibitor in all sites of prostaglandin
synthesis including GIT Addison’s disease - adrenal insufficiency
-​ Prostaglandin in GIT serve as protection of stomach from -​ Replace aldosterone with Fludrocortisone
corrosive effect of HCL → removed → GI toxicity -​ Replace androgen with Testosterone but only for patients
-​ Kidneys → nephrotoxicity suffering from severe muscle wasting
-​ Ears → ototoxicity -​ Replace cortisol with Prednisone, Dexamethasone,
Amount: 300-600 mg/dose Hydrocortisone
●​ Analgesic
●​ Antipyretic Diurnal pattern: High stress in AM and low stress level in PM
●​ Anti-inflammatory Dosage of cortisol:
-​ Cortisol is anti-stress hormone
COX INHIBITORS: NSAID -​ Stress level is higher in the morning thus high level of cortisol is
-​ Cyclooxygenase → Arachidonic acid → prostaglandin given in the morning
●​ ⅔ cortisol at AM
Nonselective COX inhibitor ●​ ⅓ cortisol at PM
-​ Inhibits prostaglandin in all site of prostaglandin synthesis -​ Cortisol has anti-inflammatory effect → WBC suppression →
-​ Higher potency and efficacy decrease s/sx
-​ Usually given for 3-5 days TID

●​ 💊
💊
-​ Nephrotoxic
Mefenamic acid: 250mg/500mg
Long term use of cortisol may lead to:

⬆️
●​ Immunosuppression
●​
●​ 💊Ibuprofen: 200mg
Naproxen: 200mg
●​
●​
●​
⬆️
blood glucose level

⬆️
HCL acid → GI toxicity
osteoclast activity → osteoporosis
COX2 selective inhibitors ●​ Water retention → Edema → buffalo hump + truncal obesity →
-​ Inhibit prostaglandin receptor in specific area Cushing’s disease

●​
●​
💊
-​ Less GI toxicity and nephrotoxicity

💊Celecoxib
Etoricoxib
-​ Sudden withdrawal to cortisol may lead to addisonian crisis

Airah B. Bolinbough, RN
Pathophysiology -​ K+ channel open → K+ goes out of the cell → outside of

gland → ⬇️
Overdosage of cortisol → send negative feedback to pituitary
acetylcholine → adrenal cortex will no longer produce
cortisol → adrenal cortex atrophy → sudden withdrawal from
the cell become more positive and inside of the cell is
negative
Ex: Lidocaine
cortisol intake → sudden in need of adrenal cortex production → -​ Closes all the Na+ channel in the cells → no
no cortisol d/t atrophy of adrenal cortex → Addisonian crisis depolarization → no impulse transmission → no pain
sensation
GOLD SALTS
-​ Used for rheumatoid arthritis only ●​ Hyperepolarization - inability to stimulate → no impulse

💊
💊
-​ Not DOC, only an adjunct drug
Auranofin
transmission

Aurothioglucose
MOA: Trap macrophages (inflammatory cells) →
Adverse effect:
⬇️inflammation Pump with the use of ATP (energy) will stimulate the Na+ and K+ to
return from where they should be to maintain homeostasis

●​ Metallic taste 2 types of neurotransmitter in the CNS

●​ Hepatotoxicity ●​ Excitatory neurotransmitter
●​ Bone marrow suppression Action potential is reached → calcium channel receptor in the
nerve opens → calcium enters → pushes the excitatory

💊
Disease Modifying Anti Rheumatic Drug (DMARD)
Methotrexate
-​ DOC for rheumatoid arthritis
neurotransmitter to the synapse → impulse transmission
○​ Acetylcholine
○​ Epinephrine
○​ Norepinephrine
NEUROPHYSIOLOGY ○​ Glutamate
Neurons ○​ Aspartate
-​ Functional unit of the brain
-​ Important function is conductivity, it is the ability of the cells to ●​ Inhibitory neurotransmitter
transmit impulses through action potential Action potential is reached → calcium channel receptor in the
-​ Action potential is the rapid change in membrane potential nerve opens → calcium enters → pushes the inhibitory to the
-​ Membrane potential synapse → bind with inhibitory receptor from another nerve →
- Cells have electrical charge (-60 to -90 millivolt) called K+ channel opens → K+ goes outside and Ca+ enters the cell →
cell membrane potential Hyperpolarization
- (+) cations and (-) anions ○​ GABA
●​ Na+ is outside cation ○​ Serotonin
●​ K+ is inside cation ○​ Glycine

●​ Resting membrane potential - electrical charge at rest CNS DRUGS

●​ Depolarization Anti-seizure drugs
-​ Na+ channel open → Na+ enters the cell → inside of the -​ Seizure is characterized with abnormal and excessive impulse
cell become more positive transmission
●​ Repolarization
Type of seizures
●​ Primary - unknown cause; epilepsy
Airah B. Bolinbough, RN
 ●​ Secondary - known cause; secondary to disease/disorder
Lamotrigine
Signs of seizure -​ Used for patient with partial seizure
●​ Motor symptoms: Convulsion -​ Has antimanic property
●​ Blank seizure - petit mal seizure
●​ Atonic seizure - fainting Topiramate
●​ Psychomotor seizure -​ Used for partial seizure
-​ Anti-seizure drug is CNS depressant -​ Used as prophylaxis for migraine
MOA: Decreases impulse transmission in the brain
-​ Best time to administer is at bedtime Valproic Acid
Adverse effect: CNS depression -​ Used for myoclonic seizure (clonic seizure only, no tonic)
‼️Anti-seizure drug + alcohol = severe CNS depression -​ Has antipsychotic effect

Ethosuximide
Action on Ion Enhance GABA Inhibit EAA
-​ For absent/petit mal seizure
channels transmission transmission
Benzodiazepine “-zepam”
Na - close or inhib ●​ Benzodiazepines ●​ Felbamate
-​ For acute management of seizure
depolarization (Diazepam, ●​ Topiramate
-​ For status epilepticus
●​ Phenytoin clonazepam)
-​ Not for long term treatment
●​ Carbamazepine ●​ Barbiturates
Antidote: Flumazenil
●​ Lamotrigine (phenobarbital)
●​ Topiramate ●​ Valproic acid
Barbiturates (Phenobarbital)
●​ Valproic Acid ●​ Gabapentin
-​ Most sedative
●​ Vigabatrin
-​ Can cause too much CNS depression
Ca - block ●​ Topiramate
-​ For children with tonic-clonic seizure (generalized)
●​ Ethosuximide ●​ Felbamate
●​ Valproic acid
Gabapentin
-​ For neuropathic pain (sciatica and disk herniation) and partial
Phenytoin (Dilantin) seizure
Classification: Hydantoin
-​ For generalized tonic clonic seizure Vigabatrin
-​ Given to adult seizure patients -​ For severe seizure
-​ Phenytoin is usually compared to benzodiazepines and Rare adverse effect: Blindness
barbiturates
-​ Phenytoin is least sedative Felbamate
Side effect: Gingival hyperplasia -​ For partial seizure

Carbamazepine ANTIPARKINSON’S DRUG

-​ Used to patients with partial seizure PARKINSON’S DISEASE
-​ Also used for neuropathic pain -​ Degenerative disorder
-​ DOC for trigeminal neuralgia causing neuropathic pain -​ Loss of cells in the substantia nigra located on the midbrain
Airah B. Bolinbough, RN
 -​ Substantia nigra is a dopamine producing neuron that is used by -​Occurs due to antipsychotic drug intake — common medication
basal ganglia for schizophrenia
-​ Basal ganglia is responsible for fine motor, control, and -​ Schizophrenia patients has high dopamine level → antipsychotic

-​
coordinated motor function
Basal ganglia function better when neurotransmitters (dopamine → ⬇️
drugs blocks ALL dopamine (including dopamine in basal ganglia)
s/sx of schizophrenia + movement disorder
and acetylcholine) are balanced

💊Dopaminergic - ⬆️dopamine
DOC: 💊
-​ Antipsychotic drugs may lead to Extrapyramidal symptoms
Anticholinergic → blocks acetylcholine

●​ Levodopa with carbidopa - dopamine precursor CARDIO DRUGS

-​ Dopadecarboxylase is an enzyme that destroys the Phase 4: Resting membrane potential
Levodopa before it enters the brain → less dopamine Phase 0: Depolarization
enters the brain → less effect -​ Sodium channel open → sodium enter
-​ Carbidopa is needed to protect the Levodopa so it can Phase 2: Plateau
enter the BBB — no need for increased dose of levodopa -​ Calcium channel opens → calcium enters
-​ If patient is taking levodopa, avoid vitamin B6‼️ Phase 3: Repolarization
-​ Potassium channel opens → potassium goes out
●​ Amantadine Phase 1: End of depolarization early rapid repolarization
-​ Increases the dopamine release in the substantia nigra
-​ Has antiviral property ANTIHYPERTENSIVE DRUGS

●​ Bromocriptine BP SYSTOLIC DIASTOLIC

-​ Dopamine agonist CLASSIFICATION PRESSURE PRESSURE
-​ Can only be used at early stage
Normal <120 <80
●​ MAO B inhibitors (Selegiline)
-​ Increases dopamine Prehypertension <120 - 139 80 - 89

‼️These drugs should still be continued with Levodopa and carbidopa Stage 1 140 - 159 90 - 99

💊Anticholinergic - ⬇️ acetylcholine effect = ⬇️ parasympathetic

●​ Diphenhydramine
Stage 2 =/> 160 =/> 100

●​ Benztropine
●​ Biperiden
●​ Trihexyphenidyl
-​ Can cause urinary retention, constipation, drying of the mouth
Nursing Dx: Risk for aspiration related to drying of the
mouth

placed in the mouth ⬆️

Nursing intervention: Offer sugarless gum — anything
salivation

PSEUDOPARKINSONISM DISEASE

Airah B. Bolinbough, RN
 💊
●​ Beta blockers ⬇️ ⬇️
HR → BP
○​
○​ 💊
Propranolol - non-selective B1 B2
Metoprolol - selective beta blockers

○​ 💊Captopril
●​ ACE inhibitors - vasodilators

○​ 💊Quinapril
○​ 💊Enalapril
​ Side effects
●​ Angioedema
●​ Cough
●​ Elevated potassium

●​ Angiotensin II Receptor Blocker (ARBS) - vasodilators

ARBS MOA:

Etiology
●​ Primary - unknown cause; HTN is the disease itself
●​ Secondary - known causes; sign of a disease
○​ Renal disease
○​ Diabetes mellitus
○​ Pheochromocytoma

Dependent Intervention
1. Drug therapy - antihypertensive drugs

💊
Vasodilation → ⬇️
●​ Alpha 1 antagonist (blood vessel)
BP

💊
💊
○​
○​
Prazosin
Doxazosin

❌ ○​ Terazosin
○​ 💊
ARBS inhibitor acts in

💊Losartan
​
​ ❌ Avoid warm shower
Avoid prolonged standing
○​
○​ 💊Valsartan
Telmisartan
​ Side effects: GI toxicity - take with meals
●​ Alpha 2 agonist (CNS)
⬇️ ⬇️
💊 ⬆️
Stimulate CNS → Norepinephrine flow → SNS
●​ Diuretics - urination; given AM
-​ Centrally acting antihypertensive drugs → drowsiness →
○​ Loop diuretic (Furosemide)
○​
○​
💊
bedtime administration

💊
Clonidine (Catapres)
Methyldopa (Caldomet)
-​ Effect on loop of Henle
-​ Cannot be used as maintenance drug because it

○​ 💊 can lead to tremendous loss of electrolytes

Thiazide diuretic (Hydrochlorothiazide)
Airah B. Bolinbough, RN
 -​ Effect on distal convoluted tubule -​ Diet: High fiber – morphine can cause constipation, may
lead to valsalva maneuver which is contraindicated to MI
ANGINA patients
-​ Chest pain due to ischemia

Angina Pectoris 💊
●​ Thrombolytic drugs

💊
Urokinase
-​ Imbalance between oxygen and cardiac workload
-​ Reversible
-​ Less than 15 minutes
💊
Streptokinase
Alteplase
-​ Dissolve the thrombus
-​ Relieving factor: Rest and NTG Primary adverse effect: Bleeding

💊
ANTIANGINAL DRUGS
💊
●​ Anti platelet drug

⬇️ ⬆️ ⬇️ 💊
●​ Nitroglycerine Aspirin

●​ 💊
-​ Coronary vasodilation →
Peripheral vasodilator → BP →
oxygen
Cardiac workload
‼️Acute attack: Give NTG sublingual (fast onset) every 5
Clopidogrel
-​ Prevent thrombus formation
-​ Contraindicated if with presence of bleeding or
minutes, call 911 after giving first NTG abnormality in bleeding laboratory tests

●​ Isosorbide nitrate
-​ Slow onset of action; not for acute attack
-​ For maintenance use only
💊
●​ Anticoagulant

💊
Heparin
Warfarin

-​ ⬇️ ⬇️
●​ Beta blocker (selective)
HR → Cardiac workload
●​
💊Sodium
Stool softener
decussate
-​ Valsalva maneuver is contraindicated as it can increase

-​ ⬇️BP → ⬇️Cardiac workload

●​ Calcium Channel blockers - vasodilators IAP

​
​
💊
💊Verapamil
Diltiazem
-​

●​ Sedatives
Can be classified as laxative

These medication will not cause sudden decrease of BP as -​ To promote rest

sudden decrease in BP will cause the heart to compensate
Dyrhythmia - most common complication of MI
MYOCARDIAL INFARCTION ●​ Premature Ventricular Complex
-​ Ischemia and necrosis of cardiac cells -​ Seen after acute attack
-​ Irreversible -​ 6 or more PVC/min
-​ More than 30 minutes chest pain Primary adverse effect:
-​ Given during acute attack

●​ Morphine
●​ Slow dysrhythmia
-​ Heart block →
-​ Atropine sulfate -
HR ⬇️ ⬆️
HR
-​ Pain reliever
-​ Several adverse effect

Airah B. Bolinbough, RN
-​ ⬇️
●​ Fast dysrhythmia
HR → remove abnormal rhythm
​ 💊
💊Digoxin - narrow therapeutic index → monitor closely

-​ (+) Inotropic → ⬆️Calcium in the cardiac cells

ANTIARRHYTHMIC DRUG Digitalis

-​ (-) Chronotropic → ⬇️HR

Class I: Phase 0 - inhibit depolarization of abnormal rhythm

💊 -​ Normal rhythm may also be affected → heart monitoring

Lidocaine IV -​ Prolong cardiac repolarization

Class II: Phase 4 - prolong resting → ⬇️HR → removes abnormal NURSING CONSIDERATION

💊
rhythms
Propranolol (Beta blocker)
1.​ Monitor HR prior to administration
2.​ Monitor potassium level – hypokalemia increases digoxin toxicity

Class III: Phase 3 - prolong repolarization → ⬇️HR → remove 3.​ Monitor ECG - action of drug is to prolong repolarization thus it
can affect the rhythm of the heart

💊
abnormal rhythm
Amiodarone
4.​ ‼️Do not combine with CCB – because they have opposite effect
5.​ ‼️Do not combine with beta blocker – both can decrease HR
6.​ ‼️Do not combine with amiodarone – both can decrease HR
Class IV: Phase 2 - blocks abnormal rhythm but can also block the 7.​ Maintain the therapeutic level: 0.5 - 2.0 ng/mL

💊
normal rhythm

💊 Diltiazem (CCB)
Verapamil (CCB)
8.​ Monitor for s/sx of toxicity
●​ Bradycardia
●​ GI toxicity: Nausea and vomiting, lack of appetite
‼️Vomiting after taking digoxin is an indication of toxicity,
HEART FAILURE DRUGS do not take another dose‼️
-​ Inability of the heart to pump effectively 9.​ Withhold and refer if with presence of toxicity
-​ Cardiac decompensation - heart can no longer compensate 10.​Antidote: Digibind
-​ DOC are drugs that can increase contractility or drugs with (+)
inotropic effect DRUGS AFFECTING BLOOD COAGULATION
Hemostasis - process by which we arrest or stop bleeding

​
​
💊
●​ Phosphodiesterase Inhibitor

💊 Milrinone
Amrinone
1.​ Vasoconstriction happens to stop the bleeding
2.​ Thromboxane A2
-​ Makes platelet very adhesive → aggregate to one another
-​ Commonly used → formation of platelet plug
-​ Route: IV via infusion pump 3.​ Coagulation
-​ Action similar to digoxin -​ Formation of clot with the use of clotting factors produced
-​ MOA: Increases calcium in the cardiac cells → stronger by liver
contraction → peripheral vasodilation → monitor BP -​ Liver needs vitamin K for some clotting factor to be
produced — Vitamin K dependent clotting factor: X, IX,

​ 💊
●​ Sympathomimetic drug

💊 Dobutamine
VII, II
-​ Clot is produced when clotting factor is activated
​ Dopamine

⬆️
-​ Has (+) inotropic (+) chronotropic effect →
and HR
⬆️contractility MOA: Liver produce clotting factors in inactive form → activation
of clotting factors by activating each other → clot → bleeding
stops → blood vessels turns to normal → clot is dissolved →
-​ Given IV via infusion pump homeostasis
●​ Clotting factor I: Fibrinogen
●​ Cardiac glycoside: DOC ●​ Clotting factor II: Prothrombin
Airah B. Bolinbough, RN
 Formation of clot: Coagulation -​Slow action
Dissolved clot: Fibrinolysis -​Inhibit production of vitamin K dependent clotting factors
If not dissolved: Thrombus as it cannot inhibit those clotting factors that are already
present

💊
●​ Antiplatelet

💊 Aspirin 30-100mg/dose
Clopidogrel - cannot be given to patient with bleeding; it is for ​
Antidote: Vitamin K

💊Thrombolytic
patient with history of MI, Ischemic stroke, and DVT ●​ Urokinase
-​ Inhibit thromboxane A2 → no platelet plug or thrombus ●​ Streptokinase
-​ AKA anti thrombotic ●​ Alteplase
-​ Dissolve the clot
-​ Tissue plasminogen activator → plasmin →
●​ Coagulation dissolve clot
-​ Given during hemodialysis -​ Not for patient with bleeding problem, only given
a)​ Extrinsic pathway to MI, Ischemic stroke, and DVT patients
-​ Faster clot formation
-​ Tissue trauma → activate clotting factor VII →
active VII → activate clotting factor X → active X
💊
Antidote: Antifibrinolytic drugs
Tranexamic Acid/Aminocaproic acid
-​ Will inhibit plasminogen activation → no
‼️These happen with the help of clotting factor IV, V, VIII plasmin → no dissolving of clot

b)​ Intrinsic pathway UPPER RESPIRATORY TRACT DRUGS

-​ Stimulus is when blood touches the surface → 1. Common colds
activate clotting factor XII → active XII → active
clotting factor XI → activated XI → activated
clotting factor IX → active IX → activate clotting
vessel) = vasoconstriction → BP⬆️
-​ Colds → inflammation → vasodilation → alpha I agonist (blood

factor X → active X
‼️These happen with the help of clotting factor IV, V, VIII 💊
●​ Decongestant

💊
Phenylephrine
Phenylpropanolamine

activate I → fibrin → clot​ ​ ​ ⬇️

Active X activates clotting factor II → thrombin → thrombin will

⬇️ 2. Allergy - antihistamine
​
​
​
​
​
​
​
​
​
​
​
​
​ ​
Thrombin will activate plasminogen
→ plasmin → dissolve clot
💊
First generation

💊 Diphenhydramine
Chlorphenamine

💊
●​ Anticoagulant
Heparin
-​ Parenteral route for faster absorption as it inhibits
💊
Second generation

💊Loratadine (10mg)
Cetirizine (10mg)
prothrombin activation → no thrombin and fibrin → no -​ More potent and highly efficacy
clot
Antidote: Protamine sulfate (heparin antagonist) 3. Cough (dry and productive)

​ 💊Warfarin
Airah B. Bolinbough, RN
-​ Protective reflex
-​ Dry cough is due to irritant
Dry cough drug 💊
●​ Sympathomimetic bronchodilator/Beta agonist
Salbutamol (SABA)

💊
●​ Antitussive - stop the cough

💊 Codeine (Narcotic)
Dextromethorphan and Butamirate (Non-narcotic)
-​ Available as oral and parenteral
-​ For patient with recurrent asthma, it is not advisable to
take SABA alone, it should be taken with steroids as it can
-​ Suppress the stimulation from respiratory tract

Productive cough drug

​ 💊 increase risk for attack
Terbutaline (LABA)

💊
●​ Expectorant
Guaifenesin
-​ Helps to remove phlegm through liquifying the secretion
●​ Anticholinergic bronchodilator
-​ Only available in inhalation form → lesser systemic
-​ Does not stop the cough
​ 💊
💊
adverse effect
Ipratropium (atrovent)

💊
●​ Mucolytic

💊
Carbocisteine
​
💊
Tiotropium
Combivent/duavent - Salbutamol + Ipratropium

💊
Acetylcisteine
Ambroxol
-​ Dissolve the mucus
●​ Steroid
-​ Anti-inflammatory

LOWER RESPIRATORY TRACT

Obstructive lung diseases: COPD, Bronchial asthma
💊
Inhalation form

💊 ⭐
Budesonide
Beclomethasone
Common cause of asthma: Allergy Advice to rinse mouth with water after steroid
Pathophysiology inhalation
-​ Allergen → antibody-antigen complex → inflammation of
bronchioles → release of histamine → swelling of bronchioles → 💊
Parenteral form
Hydrocortisone

expiration: wheezing + dyspnea → goblet cells swell →

production → productive cough
⬆️
leukotrienes causing bronchospasm → airway obstruction during
mucus
​
​
●​
💊Montelukast
Leukotriene-receptor antagonist

DOC -​ Given at bedtime as asthma attack usually happen in the

●​ Bronchodilators to relieve bronchospasm
●​ Steroids to decrease inflammation 💊 morning

💊Mast-cell stabilizer - prophylaxis

Cetirizine + Montelukast = Zykast

BRONCHODILATORS ●​ Nedocromil

💊
●​ Methylxanthines/Xanthine derivatives

💊
Aminophylline
Theophylline
​
●​ Cromolyn sodium
Mast cell release histamine → if stabilized → no histamine

-​ Relax the smooth muscle of bronchioles → bronchiole ENDOCRINE DRUGS

dilation Thyroid Hormones:

-​ ❌
papidilation, ⬆️
-​ Contains caffeine thus causing adverse effect such as
HR, tremor
No to caffeine containing foods
●​ T3 (Triiodothyronine)
●​ T4 (Tetraiodothyronine)
-​ These hormones control the rate at which glucose is used by the
cells as a source of energy
Airah B. Bolinbough, RN
 -​ Goiter is caused by iodine deficiency -​Human Placental Lactogen (HPL) make cells insensitive to
insulin
Radioactive Iodine ●​ Pre diabetic
-​ Destroys thyroid tissues ​ - Obesity + history of DM
●​ DM associated with
HYPOTHYROIDISM ○​ Chronic pancreatitis
-​ Common cause is Hashimoto’s disease ○​ Cushing's syndrome
-​ Levothyroxine and Liothyroxine are used as replacements, given
best in the morning DRUG THERAPY
●​ Replaces insulin
HYPERTHYROIDISM ●​ Increase sensitivity of cells to insulin
-​ Common cause is Grave’s Disease ●​ Increase entry of glucose into the cells
-​ Grave’s disease is reversible but exophthalmos is irreversible ●​ Decrease absorption of glucose in the GIT
-​ Antithyroid drugs are used to decrease excessive levels of ●​ Increase urinary excretion of glucose
thyroid hormones

a.​
​
💊
-​ The following drugs decreases the synthesis of T3 and T4
Propylthiouracil (PTU)
Primary adverse effect: Hypothyroidism
INSULIN
-​ Given to all types of D
Route: SQ + rotating sites

b.​
c.​
​
💊
💊
WOF: Agranulocytosis
Methimazole
Carbimazole
Route of Regular Insulin: SQ and IV
-​ To prevent lipodystrophy and erratic absorption
Insulin inhalation: Afreeza
-​ Patient must be seeing only 1 endocrinologist -​ Rapid acting, non invasive, less systemic adverse or side effect
Schedule: Morning before meals
DIABETES MELLITUS -​ Except the Glargine and Lantus (very long acting insulin)
-​ Most common endocrine disorder Primary adverse effect: Hypoglycemia
-​ A non-communicable disease but most common cause of death Best management for DM: Good glucose control
worldwide
-​ Metabolic disorder characterized by hyperglycemia due to insulin
Type Example Onset Peak Duration
problem
Very short Aspart 15 mins 30-60 mins 2-4 hours
Beta cells: Pancreas produces insulin to decrease glucose in the blood
Lipro
-​ Insulin binds with its receptor located in the liver and muscle
cells to enter the cell Short Regular 30-60 mins 2-4 hours 4-6 hours
Alpha cells: Produces glucagon to increase glucose in the blood
Intermediate NPH 2-4 hours 6-12 hours 16-20 hours
Types of Diabetes Mellitus
●​ Type 1 DM Long Acting Ultralente 6-8 hours 12-16 hours 20-30 hours
-​ (-) Insulin
●​ Type 2 DM Very long Glargine 1 hour No peak 24 hours
-​ (+) Insulin but slow production/ineffective/cells are acting Lantus
insensitive to insulin
●​ Gestational DM
Airah B. Bolinbough, RN
 -​ Aspirate regular insulin first because it is clear and will prevent
contamination
●​ 💊Empagliflozin (OHA)
-​ Increases urinary excretion of glucose = (+) Glycosuria
-​ Activities is possible but advise to always have snacks with them
-​ Illness and surgery can further increase glucose level thus
continuing insulin is necessary ○​ 💉
●​ Injectables

💉Semaglutide (Ozempic)
Classification Example MOA
○​
○​ 💉Tirzepatide (Mounjaro)
Liraglutide (Victoza)
-​ Increase insulin release
First generation Chlorpropamide Potentiate insulin
-​ Decrease glucose production by the liver
sulfonylurea 100mg action
-​ Reduce appetite thus causing weight loss
Second generation Glipizide Potentiate insulin -​ Only given to DM patients that are unresponsive to OHA
sulfonylurea Glyburide action
Glimeperide ANTIMICROBIAL

Non sulfonylurease Metformin Biguanides decrease

Biguanides Alpha Acarbose hepatic production of
glucosidase Inhibitors glucose and
decreases glucose
absorption in the
small intestine.

Acarbose also
decreases absorption
of glucose in the
small intestines

Thiazolidinedones Pioglitazone Insulin enhancing

agents
-​ Beta lactam ring inhibit cell wall synthesis → bacterial death
Meglinitinides Repaglinide Stimulate beta cells -​ Vancomycin is given slowly as it can cause severe vasodilation →
to release insulin red man’s disease
-​ Polymyxin is good for ear infection
DD4 Inhibitors Sitagliptin Increase the level of -​ Doxycycline as prophylaxis for leptospirosis
(Dipeptidyl-peptidase Linagliptin incretin hormones, -​ Teratogenic - can affect teeth and bones
4) increase insulin -​ Not for 8 years old and below
secretion and -​ Gentamicin and streptomycin are amino glycosides
decrease glucagon -​ Erythromycin (causes pseudomembranous colitis - bloody
secretion to reduce diarrhea) and azithromycin, Clindamycin (broad spectrum)
glucose production inhibits protein synthesis
-​ If DNA and RNA is inhibited, bacteria dies
Sodium-glucose Co-transporter 2 (SGLT2) Inhibitors -​ Quinolones: Ciprofloxacin

Airah B. Bolinbough, RN
 ●​ Fried's rule
MUST KNOW age in months
1. Goal of management is to decrease the number of microorganism Pedia dose = ----------------- x average adult dose
and let the immune system finish them 150 months

2. Empiric treatment are given by MD according to their professional ​ 4 mos

judgement that are evidence-based practice Pedia dose = ---------- x 250mg = 6.6 or 7 mg/dose
-​ Broad spectrum are usually used as empiric treatment 150 mos
-​ If patient’s condition worsen after broad-spectrum antibiotics →
culture and sensitivity to identify specific causative agent → ●​ Clark’s Rule
Definitive treatment is advised/prescribed weight in lbs
-​ If both narrow and broad bacteria occurs in culture and Pedia dose = ----------------- x average adult dose
sensitivity, give narrow spectrum antibiotics instead of broad to 150 lbs
prevent resistance

infection = Penicillin💊
-​ Gram (+) bacteria usually cause respiratory tract and skin ​ ​
Pedia dose =
10 lbs
----------- x 250 mg = 16.6 or 17 mg/dose

generation cephalosporin 💊
-​ Gram (-) bacteria usually cause GIT/GUT infection = 3rd

-​ Broad spectrum: Tetracycline

​ ​

●​ Young’s rule
150 lbs

-​ Narrow spectrum: Penicillin and amoxicillin age in years

Pedia dose = —-------------------- x average adult dose
3. Bacteria may produce resistance strains thru: age in years + 12
a.​ Bacteria produces an enzyme that inactivates the drug
-​ Penicillinase are enzyme that will inactivate the drug 6 years old
-​ Penicillinase resistant penicillin is made to counteract the Pedia dose = —-------------------- x 250 mg = 83.3 mg or 83 mg
penicillinase (Cloxacillin, nafcillin, coamoxiclav (amoxicillin 18 years old
+ clavulanic acid)
-​ If amoxicillin alone, it is narrow spectrum antibiotics but
broad spectrum if paired with clavulanic acid
b.​ Bacteria produces antagonist
⭐
DOSAGE FORMULA
Always follow the unit of stock dose
Desire
c.​ Change the cellular permeability ----------- x Volume = Amount to be given/dose
d.​ By changing receptor site of the medication so binding will not be Stock
possible
#1
4. Prevent resistance strain Desire: 1.5 g of drug A
MD: Give definitive treatment (C/S is required) Stock: 500 mg/ml drug A
RN: Give the drug on time
-​ Combination therapy 1,500 mg
------------- x 1mL = 3mL/dose
PEDIATRIC DOSE FORMULA 500 mg
-​ Used if the drug has no pediatric dose

Airah B. Bolinbough, RN
#2 Gtts/minute = -----------
Desire: 15mg/kg/dose ​ ​ 1,200
Stock: 120mg/5mL
Weight: 20 lbs Gtts/minute = 20-21 gtts/min
If given weight is lbs, divide it by 2.2

Weight: 20lbs / 2.2 = 9kg

Desire: 15mg/kg/dose x 9kg = 135mg/dose
135mg
—---------- x 5mL = 5.6 mL/dose
120mg

#3
Desire: 30mg/kg/day TID
Stock: 250mg/5mL
Weight: 15 kg

Desire: 30mg/kg/day TID x 15kg = 450 divided by TID = 150 mg/day

150mg
—---------- x 5mL = 3mL/dose TID
250mg

FLOW RATE
#1
Given: 2L for 16 hours
2,000 mL
-------------- = 125mL/hour
16 hours

#2
Given: 2.5L for 20 hours with drop factor 10 gtts/mL

​ ​ volume in mL x gtts/mL
Gtts/minute = ------------------------------
​ ​ hours x 60 minutes

​ ​ 2,500 mL x 10 gtts/mL
Gtts/minute = ------------------------------
​ ​ 20 hours x 60 minutes

​ ​ 25,000
Airah B. Bolinbough, RN