Pharmacology (Intensive) ACTION OF DRUGS

Dr. Grageda ● Replace a missing substance

PHARMACOLOGY
- Study of biological effects of chemicals
- Drugs: introduced into the body and we expect some
sort of change
DRUG NAMES
● Chemical names: atomic or the chemical structure
○ Example: propionic acid
● Generic names: name approved by the medical
association of pharmaceutical in the original country
of manufacture
○ adopted by all countries
○ Inside a parenthesis
○ Example, the generic name of Propionic acid
is Ibuprofen; Propionic Acid (Ibuprofen)
● Brand name: name given by the manufacturer of
the drug
○ Like insulin, if pxn has DM1, administer
insulin
● Increase cellular activities
○ Epinephrine, this increases heart rate.
○ Digoxin, to help the heart pump.
● Decrease cellular activities
○ Beta blockers, CCB (Calcium Channel
Blockers), MAOIs, SSRIs
● Interfere with the growth of a foreign cell
○ Antibiotics, it will destroy microorganism
○ Anti cancer drugs
Drug actions may be through:
1. Receptors
2. Enzymes (cholinesterase inhibitors, MAOIs)
3. Pumps (Reuptakes)
4. Chemical interaction (antacids + gastric acids)
5. Altering metabolic process (Insulin, levothyroxine)

I. DRUG RECEPTOR INTERACTIONS

● Agonists: stimulates a receptor sites
- Like a key and a lock
- Ex: digoxin, dopamine, epinephrine

● Antagonists: blocks
○ Competitive antagonist:
- Bind to a same receptor site
10 RIGHTS OF DRUG ADMINISTRATION - Potency of agonist = BLOCKED
➔ Morphine and Naloxone
○ Noncompetitive antagonist:
- Binds to a different receptor sites
- potency of an agonist = REDUCED
➔ Cefuroxime (2nd gen
cephalosporin) and
Omeprazole (PPI)
Example:
Autonomic drugs
● Receptors
● Adrenergic Receptors
○ Alpha 1 & 2
○ Beta 1 & 2

II. DRUG ENZYME INTERACTION

BASIC CONCEPTS OF PHARMACOLOGY
PHARMACODYNAMICS
- Drugs to the body and it will find its way towards the
target cell (receptor) after they bind, there will be
change and that’s Pharmacodynamics.
- How drug affects the body = mode of action
● Cholinesterase inhibitors: an enzyme that
breaks down Acetylcholine (ACh)
ACh binds with muscle → result to contraction →
cholinesterase breaks down ACh → results to muscle
relaxation

➔ Neostigmine: drug that is administered to

Myasthenic Gravis’ patients to block the
cholinesterase, thus ACh is not break down and
remains in the receptor, so the muscle continuously
contracts thus increasing the tone of the muscle in
patients with Myasthenia gravis.
III. INHIBITING PUMPS
● Reuptake inhibitor
When 5HT (Serotonin) binds with the receptor cells, there will
then be action - impulse/transmission. After doing its job, the
5HT goes back.
- SSRIs an antidepressant that blocks the reuptake of
5HT (not allowing the serotonin to go back and will
stay on the synaptic cleft) → inc serotonin
○ If IV 500mg, the body/tissue will fully use the full
strength because there was NO FIRST PASS
EFFECT. (didn’t undergo metabolism)
Example:
Patient 65 yr old male, non smoker, but for 50 years he keeps
on drinking (alcohol) w/ cirrhosis.
➔ Lower down the dose of the drug like 400 mg to
prevent hepatotoxicity

BIOGENIC AMINE THEORY 5. Excretion - happens in the kidneys

● Norepinephrine - When the body no longer uses the drug, it is excreted
● Dopa to the outside world like urine, poop, sweat.
● 5HT
↓
● DOSE
DEPRESSION (their goal is to increase) – ANTIDEPRESSANT
○ amount of drug to be administered to the
patient
IV. CHEMICAL INTERACTION
● Antacids - neutralizing the gastric acid ● SCHEDULE “right time/frequency”
V. INTERRUPTING METABOLIC PROCESSES ○ frequency, how many dose/s per day

PHARMACOKINETICS ● RECOMMENDED DOSE

- this is the response of the body to the drug ○ the amount of drug administered to reach the
- Body to drug critical concentration
- LADME ○ RIGHT dose + RIGHT time = recommended
dose

1. Liberation - the drug is released

● CRITICAL CONCENTRATION
2. Absorption - drug has reached the blood
○ The level of drug in the blood which
Routes:
produces a therapeutic effect
○ Enteral route: git
○ If the recommended dose is given,
- Oral
therapeutic effect is reached.
- Rectal - fastest absorption d/t veins and
blood vessels that line the rectum
● THERAPEUTIC EFFECT
- Nasogastric
○ favorable response after a treatment of any
○ Parenteral
kind
- IV
○ “The effectiveness” of the drug → cure
- SC: no need to aspirate (fats); slower
- IM: vascular; massage for faster absorption
- Z-track: don’t massage ● LOADING DOSE
- ID ○ Initial dose, immediate response
○ Transmucosal ○ Usually higher than the recommended dose
- Sublingual ○ For emergency cases
- Inhalation
- Topical: intranasal and buccal ● HALF LIFE “t ½”
○ Time it takes for a drug to become half of its
➔ Overall - IV is the fastest route for absorption previously peaked level
○ Ex: RD Ceftriaxone 500 mg, q8h for 7 days
3. Distribution - from the blood to tissue, binds w/ the cells ■ T ½: 8hr
■ 6am: 500mg
4. Metabolism - detoxifies and “breakdown” the drug
■ 2pm: 250mg
● FIRST PASS EFFECT
■ 10pm: 125mg
○ If oral 500mg, it has to first pass the liver
○ Cytochrome p450 enzyme: acts on the drug
■ 6am: 62.5mg
and undergoes metabolism/breakdown →
■ 2pm:31.25mg
after, the oral 500mg becomes 350mg or
■ 10pm: 15.62mg
400mg
○ Hence, the 500 mg is active and is toxic and the new
■ 6am: 7.8mg
drug is less active and was detoxified and it's the
■ 2pm: 3.9mg
one that goes back to the blood for distribution
■ 10pm: 1.95mg
 NEUROTRANSMITTERS
■ 6am: 0.9mg - body’s chemical “messengers”
■ 2pm: 0.45mg - produced by the neurons and stored in the axon
■ 10pm: 0.2mg terminal

■ 6am: 0.2 mg ● Acetylcholine (Ach)

■ 2pm: something
➔ the 500mg is excreted mga 5 days
➔ The BP goes down because of half life, not because the
pxn is drug dependent
Example:
Patient is taking Aspirin which is a blood thinner that can cause
bleeding.
➔ Notify the physician first then the physician will
instruct client to discontinue ASA for 5-7 days (to
eliminate the half life of the drug)
➔ If clear na from aspirin patient can resume to have
surgery.
- muscle contraction and memory
- Nerve producing ACh: CHOLINERGIC NERVE
● Norepinephrine and Epinephrine (NE/E)
- produced in adrenal medulla
- released during SNS stimulation
- affects behavior = tells us if there’s depression
- Nerve is producing and storing NE/E:
ADRENERGIC NERVE
● Dopamine (Dopa)
- motor and coordination,
- cognition (thinking, learning, and reasoning)
- Nerve producing and storing is Dopa:
DOPAMINERGIC NERVE

● Serotonin (5HT)
- for arousal, sleep, motivation, and prevents
depression → happy hormones (milk, chocolates,
nuts, banana)
- Nerve is producing and storing is serotonin:
SEROTONERGIC NERVE

● Gamma Amino Butyric Acid (GABA)

- inhibitory neurotransmitter → used in seizure as an
anticonvulsant
- Nerve is producing and storing Gaba:
*Myasthenia Gravis: Myasthenic crisis happens if underdose GABAminergic NERVE
ang client
AUTONOMIC NERVOUS SYSTEM
Loading Dose - initial dose, immediate effect; usually higher
2 branches:
than RD
● Sympathetic (Adrenergic Nervous System)
Example ○ Neurotransmitter
RD: Remdesivir 100mg, IV for 5-10 days ■ Preganglionic Nerve: Acetylcholine ACh
■ 1st dose: 200 mg (Loading dose) ■ Postganglionic: Norepinephrine (NE)
■ Succeeding dose: 10mg ○
● Parasympathetic (Cholinergic Nervous System)
PHARMACOLOGY TIPS: ○ Neurotransmitters
■ Preganglionic nerve: Acetylcholine (Ach)
Sympathetic and Parasympathetic System
■ Preganglionic nerve: Acetylcholine (Ach)
● Neuron: functional unit of the nervous system
● Effector cells: they produces the effects
○ They can be a muscle, gland, nerve
→ Muscle = Contract
→ Glands = secretinghormones
→ Effector cell = transmits impulse
 ● Ganglion: clusters of nerve bodies outside of the CNS Sympathetic (SNS) = Adrenergic
➔ Preganglionic nerves: The nerve before the ● Agonist: stimulate
ganglion ● “-mimetic” to copy
➔ Postganglionic nerve
● Thoracolumbar: origin of sympathetic nerves Parasympathetic (PSNS) = cholinergic
● Cranial nerves (cranial nerves and sacral nerve) ● Antagonist: block
“craniosacral”: origin of parasympathetic ● “-lytic” to dissolve, block, destroy
○ Example, anxiolytic, mucolytic,
Autonomic Sympathetic Parasympathetic thrombolytic, tocolytic
Nervous System (emergency)
Drills:
General Response “Fight or flight” “Rest and digest”

Origin Thoracolumbar Craniosacral

CN 9, 10, 7, 3 (1973)

Preganglionic Nerve Short Long

Neurotransmitter ACh (cholinergic) ACh (cholinergic)

Postganglionic Long Short

Nerve

Neurotransmitter NE (adrenergic) ACh (cholinergic)

➔ Atropine (Anticholinergic drug during surgery so it blocks
Termination of MAO (MonoAmine Cholinesterase or the PSNS which produces a SNS effect) → decrease
impulse Oxidase): breaks Acetylcholinesterase secretions (dry mouth) → prevent risk of aspiration & during
down the sympathetic surgery, it promotes bronchodilation
COMT (Catechol-
Ortho ➢ Antipsychotics/Neuroleptics
Methyltransferase)
Side effects:
Response to: - Akathisia
↑ HR, increase ↓ HR, decrease
Heart contractility contractility
- EPS (Extrapyramidal Symptoms)
- NMS (Neuroleptic Malignant Syndrome)
Lungs, ↑ RR, causes ↓ RR, - Pseudoparkinsonism
Bronchus bronchodilation to bronchoconstriction - Tardive dyskinesia
allow more air - Anticholinergic side effects (sympathetic effect)
● Constipation - ↑ oral fluid intake, high
Pupils Dilation → Constriction
“Mydriasis” to “Miosis” fiber in the diet
accommodate more ● Urinary retention - bring pxn to toilet
light q2h (bladder training), void first before
taking meds
GIT ↓ blood flow, motility, Increased blood flow,
(blood flow, motility, motility, and ● Dryness of the mouth → increase oral
and secretions →
secretions) constipation secretions → fluid intake, offer ice chips, sugarless
diarrhea candy, oral care
● Mydriasis/ Photosensitivity
Kidney ↓ kidney blood flow → ↑ kidney blood flow
● Blood decrease urine formed → more urine formed
flow

Urinary Sphincter: contracts Sphincter: relaxed

bladder
● Sphincter Detrusor muscle: Detrusor muscle:
● Detrusor relaxed contracts
muscle
→ Leads to retention → results to
of the urine emptying of the
bladder

Blood Vessels VasoCONSTRICTION VasoDILATION

(smooth muscle)
 Nursing Considerations: ANS Drugs
- Avoid sudden withdrawal of drug = may cause
rebound effect (HPN, arrhythmias and flushing)
- Monitor vital signs (BP and HR)
- Provide comfort measures - to dec CNS irritation
- Provide adequate health teaching on the name of
drug, prescribed dosage, effects, and adverse effects.

ADRENERGIC DRUG RECEPTORS

1. Alpha
● Alpha 1 Receptors
AUTONOMIC NERVOUS SYSTEM DRUGS ○ Bladder sphincter
ANS DRUGS: SYMPATHOMIMETICS ■ It closes which leads to retention
1. Adrenergic Agonists ○ Blood vessels
○ Epinephrine ■ Vasoconstriction
○ Dobutamine ○ Iris
○ Dopamine: ■ Dilation: mydriasis
○ Norepinephrine: Example:
A. Alpha 1 Adrenergic Agonist
2. Alpha Adrenergic Agonist
○ Phenylephrine (Neozep, Bioflu)
○ Midodrine
■ Nasal decongestant
3. Alpha 2 Adrenergic Agonist ■ Vasopressor → causes vasoconstriction
○ Clonidine (catapres) → decrease blood flow which causes
the cells to shrink
4. Beta 1 Adrenergic Agonist ■ Can also cause mydriasis (dilation) →
○ Dobutamine used in eye procedures
■ S/E: reflex bradycardia (no effect on the
5. Beta 2 Adrenergic Agonist
heart)
○ Albuterol/Salbutamol
= heart has baroreceptors and it
○ Isoproterenol
can detect high blood pressure →
○ Terbutaline
signal to the brain → decrease HR
○ Isoxsuprine
Situation:
Pxn, 50 yr old female with cold + hypertension
ADRENERGIC ANTAGONISTS: SYMPATHOLYTIC
➔ Do not give neozep because it can cause
1. Alpha and Beta Adrenergic Antagonist
vasoconstriction that may lead to increase BP,
○ Carvediol
Total Parenteral Resistance (pressure inside the
○ Labetalol
blood vessels)
2. Alpha Adrenergic Antagonist
○ Phentolamine ● Alpha 2 Receptors
○ Found in the CNS Nerve Membrane
3. Alpha 1 Adrenergic Antagonist ■ DEC norepinephrine release (SNS
○ Prazosin effect) → weakens SNS → so
○ Doxazosin PSNS now dominates
○ Terazosin ○ Pancreas
○ Alfuzosin ■ DEC insulin release →
○ Tamsulosin hyperglycemia (d/t daghan pa sugar
4. Beta Adrenergic Antagonist “olol” mabilin sa blood since gamay ra
○ Propranolol nadeliver sa cell)
○ Pindolol Example:
○ Timolol B. Alpha 2 Adrenergic Agonist
- the sns effect is opposite due to the decreased NE
5. Beta 1 Specific Adrenergic Antagonist release
○ Betaxolol ○ Clonidine (Catapres)
○ Esmolol - Used for Hypertensive crisis
○ Atenolol - Decrease BP: due to the opposite
○ Metoprolol sns response
○ Bisoprolol
○ Acebutolo
 ○ Methyldopa
- Used for Pregnancy-induced ○ Terbutaline
hypertension (PIH) - Long Acting Bronchodilator Agonist (LABA)
S/E: - Also used in asthma and COPD
- Bradycardia - Also used in premature labor → tocolytic (blocks
- Reflex tachycardia the tone of the muscles/uterine contractions)
- Hypotension bc HR is decreased - S/E: palpitations

C. Alpha Adrenergic Agonist (1 & 2) ○ Isoxsuprine

○ Midodrine
- Used for orthostatic hypotension
- Vasoconstriction → inc TPR → inc
BP
2. Beta
● Beta 1 Receptors
○ Found in the heart
- Increase HR and contractility
- Potassium enters cell
(Antiarrhythmic drugs)
○ Kidneys
- Increase Renin Release → Renin
Angiotensin Aldosterone System
(RAAS) that causes an increased
BP
Example:
A. Beta 1 Adrenergic Agonists:
SYMPATHOMIMETICS
○ Dobutamine
- a synthetic dopamine that is used in
congestive heart failure
- S/E: Tachycardia, Increase BP
● Beta 2 Receptors
○ Found in the lungs/bronchus - bronchodilation
○ Uterus - relaxation
○ Blood vessels - vasodilation
○ Liver (Glycogenolysis, Hyperglycemia )
○ More on skeletal muscles
Example:
➢ Beta 2 Adrenergic Agonists
○ Albuterol/Salbutamol (Ventolin)
- bronchodilation → asthma and COPD
- Short Acting Bronchodilator Agonist
(SABA)
➔ Onset <20 mins
➔ Duration: 4-6hrs
- S/E: tremors and palpitation (because it
has affinity w/ beta 1 so it may also affect
the heart and causes palpitation if given
in high dosage)
Situation:
Acute attack of Asthma
➔ Give a loading dose and parenteral of Beta 2 agonist
- Tocolytic
Alpha Adrenergic Antagonist: SYMPATHOLYTIC
(PARASYMPATHETIC EFFECT)
○ Phentolamine
- Non-selective adrenergic blocker
- Used in hypertensive crisis due to; MAOI’s
(increases norepinephrine → hypertension)
and Pheochromocytoma (tumor in adrenal
medulla) so you will have an increased
Norepinephrine → SNS effect → increase
BP/Hypertension
- PD: vasodilation → decrease peripheral
resistance → decrease blood pressure
- S/E: hypotension, reflex tachycardia
Alpha 1 Adrenergic Antagonist (-zosin)
○ Prazosin
- Blood vessels → vasodilation → decrease
TPR → decrease BP
- Only used for hypertension
○ Doxazosin (the same w/ terazosin)
- Blood vessels (vasodilation) → decreased
TPR & BP
- Can be used for hypertension
- Urinary bladder → emptying of the bladder
- Can be used for Benign Prostatic
Hyperplasia (BPH)
○ Terazosin
- Blood vessels (vasodilation) → decreased
TPR & BP
- Can be used for hypertension
- Urinary bladder → emptying of the bladder
→ BPH → complains about
● Dribbling
● Blood- streaked semen
- used for Benign Prostatic Hyperplasia/
Hypertrophy (BPH)
○ Alfuzosin
- Urinary bladder so there’s emptying of the
bladder
- Used also in BPH
○ Tamsulosin
- Urinary bladder so there’s emptying of the
bladder
- Used also in BPH

Situation:
Patient with HPN and BPH
➔ Give Doxazosin or Terazosin.
Beta Adrenergic blockers CHOLINERGIC (Parasympathetic)
○ Propranolol ● Muscarinic Agonist
- DOC in palpitation due to hyperthyroidism, anxiety ○ Miosis to the pupils
and stage fright, prophylaxis for migraine ○ Diarrhea to the GIT
- Used in hypertension bc it can decreased BP and HR
- Coronary Artery Disease (Angina & MI) so there’s dec ● Nicotinic Agonist
O2 supply and inc O2 demand ○ Antinicotinic to git = constipation
➔ It will then decrease HR (parasympa effect) ○ To bladder = retention
thus decreasing workload, O2 demand, and
increases O2 supply MYASTHENIA GRAVIS
- Prophylaxis to migraine - Autoimmune disease (antibodies destroys the
➔ Pharmacodynamics: vasoconstriction receptor)
- Anxiolytic (Stage fright) - Descending muscle weakness
- Open Angle Glaucoma ○ ptosis : initial sign
➔ PD: dec the production of aqueous humor - Common in women 20-40 yrs
➔ Ascending muscle weakness: Guillain Barre
S/E Nursing Considerations Syndrome GBS (Galing Baba)

1. Bradycardia Hold if HR is less than 60 bpm Clinical Manifestations:

and monitor HR - Ptosis: drooping of upper lid
- Diplopia
2. Hypotension Hold if BP is less than 90/60 - Mask like facial expression
and monitor BP - Dysphagia → risk for aspiration
- Weakening of laryngeal muscle
3. Bronchoconstriction Don't give to pts with asthma ○ There is hoarseness of the voice = ask the pt
and COPD to say “eeee”
- Respiratory muscle weakness
4. Hypoglycemia Caution in pts with DM = may ○ Consequence: respiratory arrest
mask the hypoglycemia ○ Nursing consideration: prepare a
tracheostomy set
5. Impotence/ ED — - Extreme muscle weakness
○ Prepare activity in the morning
○ Timolol - Paralysis
- Used in open angle glaucoma by decreasing the
Nursing Priority:
aqueous humor
● Airway
- Prophylaxis for migraine (eye drops)
● Aspiration
- S/E: miosis (parasympathetic)
● Immobility

○ Nadolol Drugs: Cholinergic drugs (Anticholinesterase)

- Drug used in HTN + Angina NO CURE FOR MG; ONLY DRUGS TO SLOW DOWN
PROGRESSION
○ Labetalol ● Neostigmine
- Most used in pregnancy and HTN or PIH ● Pyridostigmine
- Has an alpha receptor effect which can cause an ● Physostigmine
increase in placental flow ● Edrophonium (Tensilon)
Situation: ○ For diagnostic because it is a short acting
65 year old, male, smoking 10 pack years, alcoholic (10 mins)
drinker ; ER: Dyspnea ; Nx: (+) wheezing
Nursing Management
➔ We can give patient a Beta 1-Selective Adrenergic Pharmacotherapeutics:
Blockers (no effect on the lungs)
Cholinergics or Anticholinesterase Agents
Beta 1 - Selective Adrenergic Blockers (sympatholytic) ● Pyridostigmine (Mestinon)
BEAM - 1st line drug for MG
○ Bisoprolol and Betaxolol - DOC for atropine toxicity → Atropine is an
○ Esmolol anticholinergic so give cholinergics
○ Acebutolol and Atenolol
○ Metoprolol ● Neostigmine (Prostigmin)
- For long term use
- Increases Ach-receptor binding
 ● Corticosteroids
- it suppresses immune response
- Blocks antibody production
- Immunocompromised pxns
➔ Avoid crowded places
➔ Avoid eating raw foods
- Ex: Decadron (Dexamethasone)
Side Effects of Anticholinesterase:
● Diarrhea
● Emptying of the bladder
● Increase salivation
● Miosis
Monitor for 2 Types of Crisis
1. Myasthenic crisis
2. Cholinergic crisis
Myasthenic Crisis
Signs and Symptoms: Alzheimers
● Amnesia: loss of memory
● Apraxia: unable to recognize the FUNCTION of
familiar objects
● Agnosia: unable to recognize familiar objects
● Aphasia: speech problem / language disorder
3 Types of Aphasia
1. Expressive: unable to speak
- the problem is the frontal lobe
namely the BROCA’S AREA
2. Receptive: unable to understand the spoken
words. Hence, no comprehension but CAN
SPEAK
- Temporal lobe in the
WERNICKE'S AREA
- More common in alzheimer’s
disease
3. Global / Mixed
- both
Cholinergic Crisis

Symptoms Weakness, paralysis Weakness, paralysis NO CURE FOR ALZHEIMER’S DISEASE; ONLY DRUGS TO
SLOW DOWN PROGRESSION
Cause Underdose of Overdose of
cholinergic drugs cholinergic drugs ● Anticholinesterase (Cholinergic Drugs)
- Rivastigmine (Exelon)
Treatment Cholinergic drugs like Anticholinergic Drugs - Donepezil (Aricept)
pyridostigmine, like atropine
- Tacrine
neostigmine

**You cannot interchange the drugs for MG and AD because

➔ In differentiating which is which, perform a TENSILON TEST
- Tensilon is a cholinergic drug - strengthen muscle
temporarily
- (+) Tensilon test: Myasthenic Crisis
➔ This should improve the weakness and
paralysis because you are using the
treatment for testing
- (-) Tensilon test: Cholinergic Crisis (worsen)
➔ Prepare the antidote @ bedside: ATROPINE
SULFATE
➔ Antidote for Atropine Toxicity:
PYRIDOSTIGMINE
➢ Slow IV administration
○ To avoid severe cholinergic effects
(parasympathetic)
■ Diarrhea
■ Hypersalivation
■ Emptying of the bladder
■ Bronchoconstriction
ALZHEIMER’S DISEASE
- Atrophy of brian tissue due to a deficiency of
cholinergic nerves
- Normally, if there’s electrical impulse, Ach will be
produced and enters the receptor, resulting to
contraction of the nerve cell that results to memory
- In Alzheimer’s disease, there’s a degeneration of
cholinergic nerves → so no Ach, no memory
they have different area affected
Pharmacodynamics
Cholinergic Antagonists: PARASYMPATHOLYTIC
● Atropine
- Non-selective muscarinic blocker
- Preop (dec salivation - dec risk of aspiration)
● Dicyclomine
- Antispasmodic drug
- Antimuscarinic
- Used for hyperactive bowel in adults
● Scopolamine (Hyoscine)
- Motion sickness
- Dec salivation
- Pupil dilation
- Post op NV (dec motility)
CENTRAL NERVOUS SYSTEM DRUGS
PARKINSON’S DISEASE
- Degeneration of dopaminergic neurons
- Normally, Ach (contract) and Dopa (inhibitory
effect/relax) should be balanced in substantia nigra in
midbrain = fine movements are created
- Dopamine is the problem here so there’s no problem
in Ach in terms of number or amount → tremors
because contract contract contract since dopamine
cannot inhibit or balance it → they can no longer
button their shirt or tie their shoelaces
 - Treatment: increase the dopamine or inhibit
acetylcholine
Classes of Drugs for Parkinson’s Disease
A. Dopaminergic drugs: drugs to increase the dopamine
➢ Dopamine precursors
● Levodopa
- Levodopa is NOT A DOPAMINE
- Dopamine can’t cross the BBB
- Mainstay in the treatment of PD
- improves symptoms of bradykinesia,
rigidity, and even the tremors
- has many side effects
- AVOID VIT. B6 (pyridoxine) bc this
reverses the action of Levodopa
● Carbidopa
- decrease the amount of levodopa
needed to reach the critical
concentration level in the brain
- reduce the adverse effects
- Give on an empty stomach
➢ Dopamine receptor agonists
➢ MonoAmine Oxidase-B inhibitors (MAOIs)
- breakdown amines (↑NE, Dopa & Serotonin/5HT)
● Selegiline
● MAO-B more on nerves in the periphery
● MAO-A: more on antipsychotic
➢ Catechol-O-Methyl transferase (COMT) Inhibitors:
- block or destroy catecholamine (↑ NE, E & Dopa)
● Entacapone
● Tolcapone (withdrawn)
➢ Others
● Amantadine: antiviral drug
B. Blood brain barrier (BBB): keeps substance away
from the brain
- Dopamine: cannot cross the BBB so we need
a chemical that can pass through the BBB
and converted in the brain as the Dopamine
→ Levodopa Drug
- Carbidopa aids the levodopa because this
blocks the decarboxylase mao na makasud
na ang tanan mg nga ge administer
- 1 carbidopa: 4 levodopa
C. Anticholinergic drugs: blocks the AcH
● Biperiden (Akineton): antimuscarinic drug
● Trihexyphenidyl (Artane): antimuscarinic
● Diphenhydramine (Benadryl): antihistamine
● Benztropine (Cogentine): antimuscarinic
***Antidote for overdose: Pyridostigmine
ANXIOLYTICS
● Antidepressant (SSRIs/SNRI)
- First line treatment for anxiety because
they are non-addictive
- Disadvantage: the full therapeutic effect is
4-6 weeks, therefore it is not good in acute
attacks
● Benzodiazepine
- For acute attacks
- PD: enhances the GABA effect → blocks
the impulse transmission
- Short acting and fast acting
■ Diazepam
■ Lorazepam
■ Clonazepam
- DIstribution: CNS depressant
- INDICATIONS:
● anxiety
● antiepileptic drugs - DOC for status
epilepticus
● sleep disorders
● alcohol withdrawal
● anesthesia induction
● Muscle relaxants (Centrally-Acting
MR and Direct-Acting MR)
Side Effects:
- Drowsiness
- Reduced motor control
- respiratory depression in overdose esp. with
alcohol and opioids
- Addiction
➔ Antidote for benzo toxicity/overdose: FLUMAZENIL
BARBITURATES
- More addicting than benzodiazepines
- Phenobarbital: anti epileptic drugs
➔ Drug of choice for febrile seizure
➔ SE: addiction, respiratory depression
○ Secobarbital
○ Amobarbital
NON-BENZODIAZEPINES, NON-BARBITURATES
- enhances the GABA
 ● Paraldehyde ○ Myoclonic: sporadic contractions, pa konti konti
● Chloral hydrate lang
● Zolpidem - DOC: Valproic acid/valproate
● Diphenhydramine (Benadryl) ➔ Avoid giving to children = hepatotoxic
- Antihistamine & Anticholinergic for PD
○ Febrile: due to high temperature
● Zolpidem (Ambien) - DOC: Phenobarbital
- short term tx for insomnia
○ Status epilepticus
- Selectively bind to BZD site on GABA
- emergency, this is an uncontrolled seizure
receptor
- Body requires 250x O2
Advantage:
- In < 5 mins crazy seizures
● No withdrawal effect
- DOC: Diazepam
● Minimal rebound insomnia
- Treatment of choice: BZD
● Little to no tolerance on prolonged use
- Prophylactic of Choice: Phenytoin
● Buspirone
- Alternative for BZD Nursing Considerations:
- Slower onset of action 1. ABC, establish IV access
- PD: 5HT receptor antagonist 2. DOC is BZD
- Useful in alcoholics → no potential CNS effect 3. Phenytoin if status continues
- Low potential for abuse 4. Intubate if not already, Phenobarbital 20 mg/kg IV if
status continues
● Propranolol 5. Induced coma
- Beta blocker & Anti anxiety 6. Bedside EEG monitoring
● Beta-blockers
● Antipsychotics II. Partial Seizure
- Localized in 1 lobe
SEIZURE - DOC for trigeminal neuralgia: Carbamazepine
- Burst of uncontrolled electrical activity between ■ Simple
neurons ■ Complex

Inflammatory response: normal response of a vascularized

EPILEPSY tissue to injury
- 2 or more unprovoked seizures - It destroys pathogen, promotes healing
- Prophylactic of choice: Phenytoin (Dilantin)
Antiepileptic Drugs
Goal:
UPPER RESPIRATORY TRACT DRUGS
1. Stop the seizure with minimal effects
- Nose, pharynx and larynx
2. Monotherapy
3. Treatment is indicated on the 2nd unprovoked seizure 1. Antihistamine
4. Meds should not be abruptly stopped unless needed - selectively blocks H1 receptor sites (for allergy)

I. Generalized Seizure: spreads to the other lobe ● First generation (CNS effect → can cause
○ Tonic clonic: extension and contraction, rolling of drowsiness and sedation)
eyeballs ○ Diphenhydramine (Benadryl)
- Diazepam, phenobarbital, phenytoin, valproic ○ Chlorpheniramine
acid, carbamazepine (Tegretol) ○ Hydroxyzine
- Phenytoin (Dilantin) S/E:
● gingival hyperplasia ● Second generation (non-sedating)
● fetal hydantoin syndrome to ○ Cetirizine
pregnant women (microcephaly, low ○ Loratadine
set ears) ○ Desloratadine
Nursing Care:
■ HIPP: drug-induced SLE - Encourage plenty of water
Hydralazine (vasodilator) - Administer on empty stomach
Isoniazid (anti TB) - Suggest sugarless gums – inc secretions =
Procainamide (antiarrythmia) anticholinergic effects
Phenytoin (Dilantin) - Avoid alcohol
- Use humidifier
○ Absence: “blank stare” or “petit mal”
- DOC: Ethosuximide 2. Decongestants
 - sympathomimetic → alpha 1 receptor agonist and
will cause vasoconstriction
- CAUTION: Cardio pxns esp hypertensive
- Wean slowly, do not abruptly stop. And use it only for
5 days. → this may cause RHINITIS
MEDICAMENTOSA (rebound congestion)
- Caution in cardiovascular patients → can cause
palpitations
- Increase oral fluid intake
● Nasal Decongestants
○ Tetrahydrozoline
○ Phenylephrine
● Oral Decongestants
○ Pseudoephedrine
- Ingredient in crystal meth
RESPIRATORY TRACT DRUGS
- COPD (chronic bronchitis and emphysema), asthma
➔ There is an obstruction and irreversible
1. Bronchodilators “Antiasthmatic” drugs
- dilates the airways and facilitates respiration
● Sympathomimetics
- reacts at alpha and beta receptors in SNS →
bronchodilation, inc HR, RR, BP
○ Epinephrine: both beta and alpha agonists
○ Albuterol: “SABA” because onset is less
than 20mins, duration 4-6 hrs, a beta 2
adrenergic agonist
○ Terbutaline: beta 2 adrenergic agonist:
LABA, can last for 12H
○ Ephedrine

3. Expectorants ● Anticholinergics / Parasympatholytic

- Reduces the adhesiveness and surface tension of
the upper respiratory tract fluid. Therefore,
facilitates the removal of the viscous mucus
- Used for productive cough
● Guaifenesin (Robitussin)
4. Mucolytic
- decrease the viscosity of the mucus secretions
- Used for productive cough
● Acetylcysteine (Fluimucil): protects the liver cells from
Acetaminophen toxicity
● Ambroxol
● S-Carxymethyl Carbocisteine
● Dornase Alfa
5. Antitussive
- binds to the receptors in the CNS and
suppresses the cough reflex
- Used for non-productive/dry cough
● Dextromethorphan/ DM (Robitussin DM): OTC and
opioid derivative without euphoria effect in a normal dose
● Benzonatate
● Codeine: a narcotic drug but is also used as an
antitussive; MOST EFFECTIVE for treating cough esp in
elderly. — COUGH SYRUP (maka high)
- blocks the vagally mediated reflexes by blocking
the ACh
- Uses: COPD, allergic rhinitis as a nasal spray
○ Ipratropium: used for pts who cant tolerate
the side effects of the sympathomimetics
● Methylxanthines
- directly relaxes the bronchial smooth muscle →
increases the vital capacity
○ Caffeine
○ Aminophylline
○ Theophylline
Nursing Considerations: METHYLXANTHINES
- Administer oral drug with food or milk
- Monitor common S/E: palpitations and tremors
- Dietary control of caffeine
- Monitor serum theophylline levels N: 10-20 mcg/mL
→ 20 mcg/mL = NAUSEA (1st sign)
→ 35 mcg/mL = TREMOR (Late sign)
Nursing Considerations: BRONCHODILATORS
- Breathing and coughing techniques: to remove
secretions and optimize O2 exchange
- Relaxation techniques: music
- Evaluate HR and BP
- Appropriate positioning: high fowler’s position
- Tremors
- Have 8 or more glasses of fluids to liquefy phlegm
- Emphasize no smoking

2. Drugs Affecting Inflammation

● Inhaled steroids
○ Budesonide
○ Fluticasone
○ Triamcinolone
● Leukotriene Receptor antagonists
○ Montelukast
○ Zafirlukast
LOWER ○ Zileuton
 ● Surfactants - Vasodilator can cause hypotension (give
○ Beractant PHENYLEPHRINE = alpha 1 agonist -
vasoconstrictor) → inc TPR = inc BP
Corticosteroids
- will block the histamine and the arachidonic acid *Venous Pooling?
- blocks the immune response, anti inflammatory ↓preload = ↓workload
- Used for asthma, arthritis, allergy
- Consideration: administer steroid drug after meals Angina
cause this can cause gastric irritation - Atheroma = fatty tumors → can cause obstruction →
dec blood flow → dec o2 supply → ischemia →
Nursing Considerations: CORTICOSTEROIDS anaerobic metabolism → lactic acid production →
- Not used in acute attacks PAIN
- Use bronchodilators before a corticosteroid aerosol - TX: ANGIOPLASTY / STENTING
- Hold the inhaled drug for a few seconds before - If di kaya gihapon sa stenting → CABG
exhaling PROBLEM GOAL
- Allow 1-3 mins to elapse between each inhalation
- Rinse mouth with water after because it will destroy ↓O2 SUPPLY ↑O2 SUPPLY
the normal flora that may cause stomatitis ↑O2 DEMAND ↓O2 DEMAND
- Notify provider if sore throat or sore mouth occurs
- Do not stop abruptly because this can lead to
Addisonian crisis
- Must taper off gradually under supervision and
increase oral fluid

Leukotriene inhibitor
● Montelukast:
- used for pts with asthma and as a
prophylaxis
- Used for a long time to prevent attacks

CARDIOVASCULAR DRUGS
● Antianginal drugs
DRUGS USED IN ANGINA
● Drugs affecting blood coagulation
● Antihypertensive drugs
I. Nitrates
● Drugs used in congestive heart failure
● Antiarrhythmic drugs
- Vasodilators
- Directly relax the smooth muscle of the blood vessels
- DOC: stable and unable angina
- Also used for HTN

Nursing Considerations: NITRATES

- If veins are dilated = decreased pressure
- There is decreased pressure in inferior cava na
mopush sa blood pasaka – kailangan motaas
pressure para mosaka
- Afterload = pressure in left ventricle
- Pressure when heart is contracting (SYSTOLIC)
N: 120mmHg
- Relax (DIASTOLIC): N: 80mmHg
- Uncontrolled HPN → Cardiomegaly or LV hypertrophy
1. Route: SL
1. Bypass the first pass effect
2. Dose: 1 tab q 5 mins; max of 3 tabs
➔ Given every 5 mins due to it’s half life which
is T ½: 3 mins
➔ If pain is still felt after 3 tabs = MI
3. Patient can carry only 3 tabs in pocket
4. Storage: Dry amber colored container
(photosensitive)
5. Shelf life: 3 months
6. Side Effect of Nitrates:
○ Headache d/t cerebral vasodilation
➔ Don’t d/c: Paracetamol (as days pass =
lessen headache)
○ Hypotension
➔ Dangling feet, slow getting up, inc OFI
○ Compensatory mechanism: reflex tachycardia –
inc HR – brain – baroreceptor
7. PATCH = prophylaxis (can cause vasodilation to inc
blood flow and O2 supply)
 ○ Use gloves when applying patch to pt Summary drugs for Angina:
○ Heat of body releases the nitrates 1. Nitrates - DOC for stable and unstable angina
○ Apply to non hairy areas (trim) 2. CCB - DOC for Prinzmetal angina
○ 24/7 patch → TOLERANCE (need a higher dose for 3. BB
same effect)
○ Prevent tolerance by having NITRATE-FREE Ranolazine
HOURS (8 hours) HS or @ bedtime - New drug for angina
- FIRST LINE DRUG approved by FDA
NITRATES DRUGS: - For acute cases we still give Nitrates
● Nitroglycerine
● Isosorbide MONONITRATE
DRUGS AFFECTING BLOOD COAGULATION
● Isosorbide DINITRATE ANTIPLATELETS - prevents clot
● Aspirin
II. Calcium Channel Blockers ● Clopidogrel
- Calcium: muscle contraction ANTICOAGULANTS - prevents clot
- PISOCO (Potassium In, Sodium Out, Calcium Out) ● Warfarin
- NO CALCIUM INFLUX in the muscles (myocardium ♥ & ● Heparin
smooth muscle of bv) THROMBOLYTICS - dissolve clot
- DOC: Prinzmetal/ Variant Angina ● Alteplase
● Streptokinase
● Reteplase
● Urokinase
ANTIFIBRINOLYTIC - form a clot
● Aminocaproic Acid
● Tranexamic Acid
LOW-MOLECULAR WEIGHT HEPARINS
● Deakteoarub
● Enoxaparin
ANTICOAGULANT ADJUNCTIVE THERAPY
● Vitamin K
● Lepirudin
CCB DRUGS: ● Protamine Sulfate
“Very Nice And Friendly Drugs”
MYOCARDIAL INFARCTION “tissue death”
○ Verapamil
Nursing priority: PAIN (M, O2, N,A)
○ Nifedipine/Nicardipine
○ Amlodipine - can cause peripheral edema DRUGS USED IN MYOCARDIAL INFARCTION
- Elevate legs ● Morphine
- 1 pillow under feet @ hs - Opioid agonist/narcotic
- Limit salt intake - Stimulate opioid receptors in the brain and GIT
○ Felodipine - Uses:
○ Diltiazem ● moderate to severe pain
➔ -dipine - works in blood vessels ● generally safer than NSAIDS in older adults
➔ Verapamil & Diltiazem - works in the ♥ ● Vasodilator → venous pooling → dec
workload of heart → dec O2 demand →
inc O2 supply
III. Beta Adrenergic Blockers
- Contraindications:
- Sympatholytic = parasympathetic effect
● Hypersensitivity
- Beta 1 - found in the heart
● Inc ICP and suspected head injury (may
mask the pathology in the brain
- Side Effects:
● Euphoria - sedation
● Constipation - this also used in Inflammatory
Bowel disease (IBD)
● Bradycardia
● Addiction - (this is an S2 prescription)
● RESPIRATORY DEPRESSION (brain)
➔ the Antidote is Naloxone (Narcan)
an opioid antagonist
 ● Pinpoint Pupils - indication of morphine
overdose

● Nitrate

Coagulation Cascade

Nursing Considerations: ASA

- If there’s clot it may lead to dislodgement that will
become an embolus, resulting in obstruction.
Fibrinolytic cascade
1. Give with glass of milk or water because it is irritating
to the stomach
2. Teach WOF (watch out for) Toxicity, s/s:
- Bleeding gums
- Tinnitus
- Black tarry stool
- SALICYLISM: a result of too much aspirin
3. Increase risk of toxicity to elderly and children
4. AVOID in children with fever viral illness like Varicella,
chicken pox, Flu A or B → it may lead to REYE’S
SYNDROME

➔ REYE’S SYNDROME - progressive encephalopathy

with hepatic dysfunction (Fulminant hepatitis)

- This is when the clot is dissolved

Drugs affecting coagulation

● Antiplatelets “blood thinners”
- Pharmacodynamics: Blocks the formation of platelet plug
- Examples are Aspirin, Clopidogrel, Ticlopidine,
Dipyridamol
- This blocks vasospasm from injury that may result in
formation of platelet plug thus stopping its progression.

○ Aspirin (ASA)
Salicylate poisoning (SALICYLISM)
- Acetyl Salicylic Acid
Fatal dose: 150 mg/kg BW
- given indefinitely
S/S
- Uses: 4A’s (Antiplatelet, Analgesic,
● Nausea & Vomiting
Antiinflammatory, Antipyretic)
● Tinnitus: the most important sign in acute poisoning
- Blocks the prostaglandin
● Fever
- Side effects: bleeding so don’t give to
● Lethargy/Excitability
dengue pxns
● Hyperventilation leading to Respiratory Alkalosis
● Respiratory Alkalosis
➔ REYE’S SYNDROME - progressive encephalopathy
● Severe toxicity
with hepatic dysfuntion
○ Metabolic acidosis
○ Seizures
Nursing care:
- Avoid in foods with Iodine (important in the formation
of T3 and T4
- Blocks the formation of T3 and T4
 2. Rx: Warfarin
PT: 24 sec (N:8-12 sec)
Nursing Intervention: GIVE
12 x 1.5 = 18 sec
12 x 2.0 = 24 sec
Therapeutic margin : 18-24 sec
➔ ALWAYS HAVE A BASELINE
➔ Therapeutic margin will be applied on the
next order

3. 53 y/o, male, chest pain

5. AVOID in pxn’s w/ dengue, Rx: Warfarin
6. ASA toxicity: PT = 13 secs (N= 10-13 secs)
- STOP 13 x 1.5 = 19.5
- Flush ASAP = sodium bicarbonate + 13 x 2.0 = 26 secs
dextrose fluid Therapeutic margin = 19.5 to 26 secs
Nursing intervention: GIVE WARFARIN
○ Clopidogrel (plavix) — 2 months
○ Ticlopidine Rs: Warfarin
○ Dipyridamole PT = 26 secs (N=10-13 secs)
Nursing intervention: GIVE WARFARIN
● Anticoagulants
○ Warfarin
Nursing Considerations: WARFARIN
- Pharmacodynamics: Blocks the vit k dependent
1. Monitor PT and INR (up to 2-3)
clotting factors
2. Monitor I/O (bleeding - dec UO)
- Route: Oral
3. Monitor bleeding tendencies
- Side effect: bleeding
= petechiae, purpura, bruises etc.
- Antidote: Vit K
4. Dec intake of green leafy veggies (rich in vit. k)
- Therapeutic margin: 1.5 x 2.0 x N
- Therapeutic test:
○ Heparin
● Prothrombin Time (time it takes for the liver
- Pharmacodynamics: Blocks formation of thrombin
to produce prothrombin) N: 10-13secs or
- Route: IV/SC
8-12secs — In the presence of warfarin,
- Therapeutic Test: aPTT or PTT ( N= 25-35 secs)
expect PT to be higher or prolonged (mas
- Therapeutic Margin: 1.5 x 2.5 x N
matagal magform ng clot = there will be
- Side Effect: bleeding
bleeding)
- Antidote: Protamine Sulfate
- Therapeutic margin: 1.5 x 2.0 x N
- If it’s too prolonged or longer PT, there
will be bleeding and hemorrhage.
● INR (International Normalized Ratio)
Normal value: 1; best/average
- Side effect: bleeding?
- Antidote: Vit. K

Situation:
1. Rx: Heparin, IV
PTT= 33 secs (25-35 secs)
33 x 1.5 = 49.5
33 x 2.5 = 82.5 sec
Therapeutic margin: 39.5 - 85.2
Nursing intervention:= GIVE
Situation:
1. Rx: Warfarin Another PTT requested= 98 secs
PT: 12 sec (N:8-12 sec) IF 8 ni = next dose HOLD Nursing intervention: HOLD
Nursing Intervention: GIVE
 2. Rx: Warfarin b. Purpura
aPTT: 35 sec (N:25-35 sec) c. Bruising
Nursing Intervention: GIVE d. Bleeding gums
e. Black tarry stool
3. Rx: Warfarin 3. Use soft bristled toothbrush
aPTT: 87 sec (N:25-35 sec) 4. Avoid green leafy vegetables especially if we are
Nursing Intervention: GIVE taking warfarin because these vegetables are rich in
35 x 1.5 = 52.5 vitamin K which will block the action of warfarin
35 x 2.5 = 87
TM: 52.5-87 sec ANTIHYPERTENSIVE DRUGS
● Thrombolytics
- Pharmacodynamics: Activate the conversion of
plasminogen (liver) to plasmin
- Plasminogen is from the liver
- If with plasmin then no fibrin resulting to no
clotting
- Fibrinolysis - process of dissolving the clot
- GOAL: restore blood flow by dissolving the clot (activates
plasmin)
- Golden period: 3 hours – but the sooner you give the
better the outcome
- If the situation is when to give thrombolytics
and has choices such as 1 hour, 2 hours, or ● BP = resistance exerted by blood against the smooth
3 hours, choose 1 hour or the earliest time. muscle wall
- Side effect: Bleeding Antidote: antifibrinolytics ○ BP = Heart rate x Stroke Volume x Total
○ Urokinase Peripheral Resistance/ Systemic Vascular
○ Streptokinase Resistance or BP = CO x TPR
○ Alteplase ○ bleeding → decreased blood volume →
○ Recombinant tissue plasminogen activator (rTPA) decreased preload → decreased Stroke
Volume → decreased BP
● SV = Amount of blood ejected per beat
● Cardiac Output (CO) = Amount of blood ejected per
minute (HR x SV)
● SVR = Pressure exerted by the wall of the blood vessel
against the blood
● TPR = Total Peripheral Resistance
● MAP = Mean Arterial Pressure; N: 70-100 mmHg
➔ Clinical Significance of MAP: Tissue Perfusion
SBP: systolic blood pressure
DBP: diastolic blood pressure
● Antifibrinolytic
- We need to form a fibrin to form a clot and stop bleeding
○ Aminocaproic Acid (Amicar)
○ Tranexamic Acid (Hemostan)
■ Decreases melanin → lighten skin
Nursing Considerations:
1. Monitor VS
a. BP - it is down if there is bleeding
i. If there is bleeding → decreased
blood volume → decreased preload
→ decreased Stroke Volume →
decreased BP → compensate →
baroreceptor will compensate →
brain → increased heart rate
ii. Decrease o2 supply to tissues →
ischemia → tissue death
b. HR
2. Monitor signs of bleeding
a. Petechiae
 ● afterload=workload of the heart
*if there’s prolonged hypertensive crisis → activate the local
coagulation cascade → blood clot → give aspirin because it
has antiplatelet effect which prevents the formation of clot
*don’t give thrombolytic sa hemorrhagic stroke ANTIHYPERTENSIVE DRUGS ACTING ON RAAS
➢ DRUG ACTING ON RENIN
REGULATORS OF BP: ➢ ON ACE RECEPTOR
1. Baroreceptors ➢ ON THE ANGIOTENSIN 2 RECEPTORS
- Found in the aorta and carotid arteries ➢ ON ALDOSTERONE
- Sends signal brain → then send back the ➢ ON ALPHA 1 ADRENERGIC RECEPTORS
signal to the heart to inc/dec hr ➢ ON THE CNS ( ALPHA 2 RECEPTORS )
2. Vascular autoregulation ➢ ON BETA ADRENERGIC RECEPTORS
- Vasoconstriction (↑TPR; ↑BP)
- Vasodilation (↓TPR; ↓ BP) ANTIHYPERTENSIVE DRUGS
3. Regulation of body fluid volume ● ANGIOTENSIN CONVERTING ENZYME (ACE)
- Inc body fluid volume → inc blood volume → INHIBITORS “pril”
inc BP (↑TPR; ↑BP) - Nothing will convert angiotensin I to angiotensin II
- Salt → attracts water causing dilation to the blood vessels → dec TPR, BP,
4. RAAS and blood volume
- It starts in the kidneys - Site of action: LUNGS
- Hypoxia → stimulate the kidneys → production of - Blocks ACE
erythropoietin → bone marrow → erythropoiesis - ↓TPR; ↓ BP (blood volume ↓ )
(formation of RBC) ○ Captopril
- Hypoxia → stimulate the kidney to produce renin in ○ Enalapril
the blood stream then renin goes to the liver → ○ Lisinopril
angiotensinogen → converted to become angiotensin
I and goes back to the bloodstream and the blood will Side Effect: ACE
bring that back to the lungs → ACE (angiotensin ■ A: Angioedema
converting enzyme) → converts angiotensin I to ■ C: Cough - #1 side effect
angiotensin II (it is a potent vasoconstrictor if it will - Nursing Consideration: Don’t give to pt with asthma
bind to the blood vessel) → blood vessels has and COPD
angiotensin II receptors causing the blood vessels to - There is cough because the site of action is in the
constrict → inc TPR and BP → increase blood flow lungs.
back to the kidney which will eliminate hypoxia ■ E: Elevated potassium/hyperkalemia due to lack
- Adrenal cortex also has angiotensin II which can also of potassium excretion
bind to the blood vessel producing angiotensin III →
production of aldosterone → retains sodium (solute: ● ANGIOTENSIN 2 RECEPTOR BLOCKER (ARB) “sartan”
ang tinutunaw) causing potassium excretion → - Site of action: BLOOD VESSELS (naa diha ang
retains h2o causing BP, TPR, and blood volume to angiotensin 2 receptor)
increase - Advantages:
- Osmolarity: solute load in solution making the blood ● Renoprotective (protects kidneys) = DM pxns
more viscous (malapot ang dugo; results to clot) ● HTN with cardiomegaly = prevents stroke
- Increased osmolarity will stimulate the
hypothalamus to secrete ADH which retains Side Effects:
h20 leading to increase blood volume, TPR, ● Angioedema
and BP ● Elevated potassium
○ Losartan: has renoprotective action
○ Valsartan
● DIRECT RENIN INHIBITOR
- Site of action: kidney → eliminates renin
○ Drug: Aliskerin

● SELECTIVE ALDOSTERONE ANTAGONIST

○ Epelrone - S/E: Hyperkalemia

ANTIHYPERTENSIVE DRUGS ACTING ON ANS

RECEPTORS

● ALPHA 1 ADRENERGIC ANTAGONISTS “zosin” Nitroprusside

- Site of action: blood vessel causing vasodilation - DOC for hypertensive crisis
- They have first dose effect (severe orthostatic - IV onset 2-3 mins
hypotension) - Duration: 48 hrs (d/t cyanide poisoning)
- To prevent the first dose effect: Split the 1st Hydralazine - PIH
dose @ hs Minoxidil- SE: Hair growth
○ Prazosin
○ Doxazosin DIURETICS
○ Terazosin - increase urine output → decrease BV, TPR, BP
INDICATIONS
● ALPHA 2 ADRENERGIC AGONISTS 1. HF
- Site of action = CNS (parasympathetic) → dec hr → 2. Pulmonary edema
dec bp → vasodilation 3. Liver Failure (ascies)
○ Clonidine: given sublingual 4. Cirrhosis
○ Methyldopa: also used in hypertension in 5. Renal disease
pregnancy
■ Thiazide - most commonly used diuretic for HPN
● BETA ADRENERGIC BLOCKERS “olol” ○ Hydrochlorothiazide
- Dec TPR and BP ○ It will only give you a mild diuresis
○ Propranolol (hxn and hyperthyroidism) ■ Loop Diuretic
○ Metoprolol ○ Furosemide (Lasix)
○ Nadolol (can be used to pxn with angina)
Thiazide and Loop Diuretic S/E:
● BETA I SPECIFIC ADRENERGIC BLOCKERS “olol” - Hyperglycemia
○ Betaxolol - Hyperuricemia
○ Esmolol - Hypokalemia
○ Acebutolol
○ Metoprolol ■ Potassium-Sparing
○ Bisoprolol ○ Spironolactone
○ Atenolol ○ Amiloride
○ Triamterene
SE: Hyperkalemia
VASODILATOR ANTIHYPERTENSIVE DRUGS
● Indirect Acting Vasodilators
■ Osmotic Diuretics
○ Calcium Channel Blockers “Very Nice And
○ Mannitol
Friendly Drugs”
- Given if Increase ICP → Inc UO
○ Used for angina
● Direct Acting Vasodilators
■ Carbonic Anhydrase Inhibitors (CAH
○ Vasodilators
INHIBITORS)
○ Used for hypertensive crisis
○ Acetazolamide (Diamox)
- For acute angle glaucoma and
lithium toxicity

Calcium Channel Blockers DRUGS USED FOR HEART FAILURE

 - Heart Failure - pump failure (dec CO = dec O2 ANTIARRHYTHMIC DRUGS
supply) Action Potential
- Increases intracellular calcium levels in the - Electrical current occurring in nerves and muscles
heart → inc contractility → (+) INOTROPY - If we stimulate the muscles, the sodium gets in the
(force of contraction) cell
- GOAL: Help the ♥ pump
● Depolarization = contraction of muscles
● Repolarization = relaxation of muscles
I. CARDIOTONIC DRUGS ● Resting membrane potential = cardiac muscles ay
● Cardiac Glycosides nagpapahinga
○ Digoxin (Lanoxin)
- Pharmacodynamics: Increase CA+ in myocardial cells
→ (+) INOTROPIC effect
- Most commonly used for HF
- Also used in atrial fibrillation
- N: 0.5-2 ng/ml
- Effects:
● (+) inotropy → inc CO → inc renal
perfusion
● (-) chronotropy - rate of contraction

Side Effects of Digoxin:

- Bradycardia
- Visual disturbance “halo” - HALLMARK OF TOXICITY
- Digitalis/Digoxin Toxicity: most serious side effect
● Hypokalemia will increase the risk of toxicity ARRHYTHMIA
➔ Serum level >10 ng/ml with K+ >5 meq/l - Change in the automaticity or conductivity of heart
● Anorexia, N/V, Malaise, Depression and cells
arrhythmia - SA node (pacemaker of the heart): 60-100 electrical
● Antidote: Digitalis Immune Fab (Digibind) impulses/minute
- Results from:
● Phosphodiesterase Inhibitors • electrolyte imbalances - K+, Na+, Ca+
- Blocks the enzyme Phosphodiesterase • decreased O2 delivery - pnx w/ MI, Angina
○ Milrinone • acidosis alters Action Potential - met. acidosis
- Inc cAMP → inc CA+ levels → (+) inotropy • structural damage - valvular diseases →
arrhythmia → clot → embolus
II. OTHER DRUG THERAPIES • drugs
● Vasodilators: blocks ACE → no angio1 →
vasodilation → dec preload → dec heart workload → DRUGS USED FOR ARRHYTHMIA
more time to inc inotropy effect
- Venous pooling → dec preload → (+) inotropy →
dec afterload
○ ACE Inhibitors
○ Nitrates

● Beta Adrenergic Agonists: sympathomimetic of

choice
- SNS → inc CA+ flow → (+) inotropy
○ Dobutamine - sympathomimetic choice for
HF

● Diuretics
- Inc UO → dec blood volume → dec preload → (+)
CLASS I: blocks sodium channel which blocks phase 0
inotropy
(depolarization)
○ Furosemide
➢ CLASS 1a
○ Procainamide - HIPP → drug inducing SLE
● Human B-type Natriuretic Peptide
○ Quinidine
- Compensatory response → produced by myocardial
➢ CLASS 1b
cells → dec workload → (+) inotropy
○ Lidocaine: local anesthesia
○ Nesiritide ( Natrecor )
➢ CLASS 1c
 ○ Propafenone - Tetracycline
- Metronidazole
CLASS II: block the beta receptor; blocks phase 4
○ Propranolol PUD Drugs:
○ Esmolol - Bismuth subsalicylate
○ Nadolol - PPI
- H2 Blockers
CLASS III: blocks potassium channel; blocks phase 3
○ Amiodarone - recommended use during life
support measures
○ Sotalol

CLASS IV: blocks the calcium channel; blocks phase 2

○ Diltiazem
○ Verapamil

FOR HEART BLOCKS

● Anticholinergic Drugs
○ Atropine
MANAGEMENTS:
GIT ● H.Pylori
○ Antibiotic
● MUCUS - coats the lining and protects it from HCL
● NSAIDs
● BICARBONATE - neutralizes the gastric acid
○ Limit use
● ADEQUATE BLOOD FLOW - nourishes the mucosa
○ Consider misoprostol
● PROSTAGLANDIN - stimulate mucus and
● Gastric acid
bicarbonate secretion
○ H2 receptor antagonist
○ PPI
➔ Ulcer = an erosion in the mucosal lining d/t H. pylori
○ Mucosal protectants
○ Antacids
PEPTIC ULCER DISEASE
● Smoking
CAUSES:
○ Encourage to stop
➔ Helicobacter Pylori (H. Pylori)
- Gram negative bacillus
- Hides in between mucus and epithelial cells DRUGS FOR PUD, GERD & GASTRITIS
- Most common cause of PUD I. ANTACIDS
- Neutralize acid
➔ NSAIDs - Inhibit prostaglandin (prostaglandin - Inactivate pepsin
increase the mucus and bicarbonate) - Enhance mucosal protection
● Mefenamic acid (ponstan) - DOSE: 1 tab 1-2 hrs after meals and hs for 6 months
● Ibuprofen (alaxan) - SE: Rebound Acidity
● Naproxen (skelan) ● Am Hydroxide - SE: Constipation
(Alangluminu Tae)
➔ Gastric Acid (Hydrochloric Acid) ● Magnesium Hydroxide - SE: Diarrhea
- Injures the mucosa cells and activates (Magtatae)
pepsin ● Magaldrate

➔ Smoking and Alcohol Nursing Considerations:

- ↑ gastric acid 1. Take with a glass of water
- ↓ bicarbonate production 2. Tabs should be chewed thoroughly with a glass of
- Delays healing water
3. Suspension = shake well
Testing Options for H. Pylori 4. Allow 1h between antacid administration and other
- Serum antibody test med to prevent interaction
- Urea breath test
- Stomach biopsy II. H2 RECEPTOR BLOCKERS “tidine”
- Blocks histamine 2 receptors in the stomach lining
USE A MINIMUM OF 2 ANTIBIOTICS (parietal cells)
- Clarithromycin - OTC meds
- Amoxicillin - Suppresses gastric acid secretion
 ● Cimetidine - can result to gynecomastia
(because it binds to androgen receptor)
● Ranitidine HEPATIC ENCEPHALOPATHY: LACTULOSE
● Famotidine
● Nizatidine

III. PROTON PUMP INHIBITORS (PPI) “prazole”

- Suppress gastric acid secretion
- Most effective and cost-effective
- Uses: PUD, erosive esophagitis
- SE: headache, diarrhea, abdominal pain
● Omeprazole
- low protein diet sila so that ammonia won't
● Lansoprazole
accumulate the blood
- BBB: blood brain barrier
IV. GI PROTECTIVES & PROSTAGLANDIN - Lactulose can bind with ammonia so when lactulose
SUCRALFATE MISOPROSTOL is excreted kay ma excrete sad si ammonia
(Prostaglandin Agonist) - Route: Oral
(Cytotec) - Promotes increased peristalsis and bowel evacuation
➔ Expels ammonia
- Sticky gel coating the - Acts as replacement for
ulcer endogenous - Uses:
- Protective barrier prostaglandin (PG)→ ● Prevention and tx of portal systemic
against pepsin and enhance the effect of PG encephalopathy
gastric acid - Inc mucus and ● Hepatic precoma and coma
- Small risk for bicarbonate ● Chronic constipation
constipation - Prophylaxis against PUD HEPATIC ENCEPHALOPATHY: NEOMYCIN
- Coats the ulcer due to NSAIDs and ASA
- Given ac (before meals) - Contraindicated in ● An aminoglycoside antibiotic
to coat the ulcer and pregnancy – this is an ● Destroy bacteria in colon (so that it will not convert
hindi sha masyado abortifacient (could protein wastes to ammonia)
nasasaktan ig kaon cause cervical dilation so
mahuhulog ang baby) ANTIDIARRHEAL DRUGS
- May cause diarrhea ● Loperamide ( Diatabs )Imodium )
- Anticholinergic = sympathetic
- Side effects: constipation, dryness of the
mouth, retention of urine, mydriasis
LAXATIVES ● Opiate Related Diphenoxylate with Atropine
- Narcotic
Types of Laxatives:
- Can cause constipation
1. Chemical Stimulants
- Irritate the colon muscles → induce bowel
DIABETES MELLITUS
movement
- Metabolic disorder where there is hyperglycemia due
● Senna - ex: biguerlai, kankunis, biofitea
to either absence or disorder of insulin
● Bisacodyl (Dulcolax)
- INSULIN brings sugar from the blood to the cells; K+
● Castor oil
and Mg+ to the cell
- Dextrose solution + insulin
2. Bulk forming/ osmotic laxatives
- Hyperkalemia mgt: dextrose fluid plus insulin (insulin
- Absorbs water → add volume to stool
will bring glucose to the cell along with potassium)
- SAFEST of all laxatives
● Psyllium - mix in a glass of water and drink
● DM TYPE 1 - no insulin
immediately
○ DOC: Insulin
● DM TYPE 2 - insufficient insulin; insulin receptor
3. Stool softener/ Emollient laxative
resistance; common in obese
- Helps to wet and soften the stool
○ DOC: Oral hypoglycemic agents (OHA)
- Used in Hepatic Encephalopathy
○ We also give insulin if di kaya ng OHA
● Lactulose
● GDM (Gestational DM)
○ DOC: Insulin
○ If diagnosed with DM before pregnancy and
was prescribed with OHA, shift to insulin
when become pregnant
● SECONDARY DM
 - inhibits glucagon release →
lowering of blood glucose
DRUGS TO CONTROL BLOOD GLUCOSE
Liver - produces glucose
Pancreas - producing insulin (transports glucose to the cells)
Muscles - uptake and use glucose
Intestine - absorbs

INSULIN
- Action: liver, muscle, and adipose tissue → facilitates
the passage of glucose, K+, and Mg into cell
- INDICATIONS:
● DOC for DM Type 1, DM Type 2 & GDM
➔ DM type 2 DOC: OHA
● If pregnant and taking OHA (shift OHA to
insulin)
- Syringe: Tuberculin syringe, Gauge 27-29, ½ to 1
inch long
- Storage: ref (chiller) but not in the freezer; avoid
extremes of temp.
- Before injection, need e room temp (from ref then
iinject lahus maka cause lipodystrophy or scar)
- Open insulin = if vial will be use in 1 month - room
temp.
- Route: SC (45-90 degrees for a normal SC mass and
45-60 degrees for thin pxn); and pwede IV
- Administration: mix ingredients well → swirl vial gently
or rotate between palms

I. ORAL HYPOGLYCEMIC AGENTS: ( OHA )

- GOAL: dec blood glucose level
● Actions of OHA:
○ Liver - decrease production of glucose
○ Pancreas - increase production of insulin
(transports glucose to the cells)
○ Muscles - increases uptake and use glucose
○ Intestine - decrease absorption of glucose *The peak effect is taas ang possibility na magka hypoglycemia kay
● Sulfonylureas - more insulin production mao mani na taas iya insulin level
● Meglitinides - more insulin production *Glargine (lantus) - only insulin that should not be mixed
● Thiazolidinediones “glitazones” - dec hepatic *Regular - only insulin that can be given IV in emergency cases; clear
insulin
glucose production
*NPH- cloudy insulin
● Biguanides (METFORMIN)
*We can mix insulin together
- suppress hepatic production of glucose and
inc insulin sensitivity
How to prepare/ mix insulin:
- Also used in PCOS
1. Inject air from cloudy, remove syringe
- S/E: dec appetite → weight loss
2. Inject air from clear, draw from clear
- Delikado for lactic acidosis (if taken with
3. Draw from clear first and then draw from cloudy
alcohol)
4. Don’t shake just swirl or rotate between palms gently
● Alpha-glucosidase Inhibitors - delay absorption of
ingested CHO
● GLPT-1 and DPT-4 inhibitors
○ Incretins
- stimulates insulin release →
lowering of blood glucose
 - MIT + DIT = T3
- DIT + DIT = T4

Thyroid Hormone FUNCTIONS:

- control metabolic rate of tissues
- accelerate heat production
- accelerate oxygen consumption
- development of secondary sexual characteristics
- brain development

HYPOTHYROIDISM - metabolism is decreased

- Bradycardia
- Constipation
Key Points for INSULIN: - Decreased appetite but there’s weight gain
● Rotate sites to prevent lipodystrophy (scar - Cold intolerance
tissue) - Easy fatigability
- Male: Impotence
● Adverse effect: hypoglycemia
- Female: Amenorrhea
○ Tachycardia, diaphoresis, shakiness,
- Mental retardation
headache, weakness - Stunted growth
● May need extra doses of insulin during illness or
stress because of the release of cortisol HYPERTHYROIDISM - bali
● Not skip doses of insulin
● Hypoglycemia: 15g of FAC (4 oz orange juice, 8 *Iodine from the diet is very important (trapped in thyroid gland)
oz of milk, regular soda) → iodine + tyrosine (protein) → MonoIODOTyrosine = MIT
● Mixing: draw up from clear ↓ coupling
○ Inject air into cloudy, remove needle, MIT + MIT = DIT
MIT + DIT = T3
inject air into clear, draw up clear, draw
DIT + DIT = T4
up cloudy
○ RN: regular first, then NPH
THYROID REPLACEMENTS - for hypothyroidism (give t3
● Administration and t4)
○ Suspensions - S/E: Hyperthyroidism
■ gently rotate vial ● Levothyroxine (Synthroid) = T4
■ If short acting looks ● Liothyronine (Triostat) = T3
cloudy/discolored → discard ● Liotrix = T3 plus T4
● Thyroid Hormone
HYPOGLYCEMIA
Nursing Interventions:
● GLUCAGON
1. Should be given at least 4 hours apart from
- Stimulates glycogenolysis in the liver
- MULTIVITAMIN
- USE: Hypoglycemia in insulin induced, - ALMG (OH)
semiconscious and unconscious - SIMETHICONE
- Site: SQ, IM, IV - CALCIUM CARBONATE
- Onset: 5-20 mins - IRON
- SUCRALFATE
15/15 rule: ➔ Decreases absorption of the thyroid
First 15 grams of FAC (fast acting carbs) hormones
After 15 minutes give FAC again if wala gihapon na recover;
repeat until the patient is no longer hypoglycemic 2. Instruct to avoid foods:
- STRAWBERRIES
- PEACHES
DRUGS AFFECTING THE THYROID GLAND - PEARS
Triiodothyronine = T3 - CABBAGE
Tetraiodotyroxine = T4 - TURNIPS
Iodine Diet - CAULIFLOWER
- Trapped in the thyroid gland and iodine will bind with - RADISHES
the protein tyrosine and will form Monoiodotyrosine - PEAS
(MIT) ➔ These are thyroid hormone blockers or
- There will be a coupling meaning MIT + MIT blocks the production of T3 and T4
= DIT (two molecules of Iodine)
ANTI THYROID DRUGS - used for hyperthyroidism
- S/E: Hypothyroidism CLASSIFICATION OF ANTIMICROBIALS BASED ON
● Methimazole (Tapazole) SITE OF ACTION
● Propylthiouracil (PTU) used in pregnancy
● Lugol’s Solution (strong iodine sol.); blocks I. BLOCKS CELL WALL SYNTHESIS
the synthesis of thyroid hormone ● Beta Lactams: they have beta lactam ring in their
● Iodide I 131 (radioactive iodine) chemical structure
○ Penicillins
Propranolol - palpitations in hyperthyroidism ○ Cephalosporins
○ Carbapenems
Nursing Interventions for Antithyroid Drugs: ○ Monobactam
1. Monitor VS (bradycardia, constipation, intolerance to ● Vancomycin: no beta lactam ring
heat, hypotension)
2. Monitor T3 (low), T4 (low), TSH (high) II. BLOCKS PROTEIN SYNTHESIS
3. Monitor weight (wt. gain) - Targets the protein of the bacteria
4. Take with meals to avoid GI irritation ● Macrolides
5. Instruct how to measure PR (instruct to take PR in 1 ● Chloramphenicol
whole minute) ● Lincosamides
6. Instruct importance of medication compliance ● Aminoglycosides
7. Don’t abruptly stopping meds (to avoid rebound and ● Tetracyclines
thyroid storm)
S/S of thyroid storm III. FOLIC ACID SYNTHESIS INHIBITORS
- Fever, flushed skin, confusion, tachycardia, ● Sulfonamides
dysrhythmia, behavioral changes, and signs ● Trimethoprim
of HF (right or left)
8. Monitor sign of IODISM (excess iodine) IV. NUCLEIC ACID SYNTHESIS INHIBITORS
- N&V ● Fluoroquinolones
- Metallic taste
- Skin rash
BACTERIAL CELL WALL
- Sore gums
- Needed for the overall strength of the cell
- Hypersalivation
- Growth
- Halitosis or bad breath
- Reproducion
9. Consult MD before eating iodized salt and iodine-rich
- Obtaining nutrition
foods
- Protection
10. Avoid aspirin & meds with iodine
**if an antibiotic targets the cell wall of the bacteria, then the
- Aspirin blocks production of thyroid
bacteria will die
hormones
11. PTU causes agranulocytosis
- Immunocompromised BACTERIAL CELL WALL SYNTHESIS INHIBITORS
- Advise to contact MD or nurse if ever nay I. BETA LACTAMS
sore throat a. Penicillins: “CILLINS”
12. If euthyroid na = stop meds but continue to monitor T3 ➢ PENICILLINS: good for Gram (+) bacteria
and T4 ● Penicillin V - oral
● Penicillin G Benzathine - IV
DRUGS TO CONTROL BLOOD GLUCOSE ● Penicillin G Potassium - IV
● Glucose-elevating agents ● Penicillin G Procaine - IV
○ Diazoxide ➢ EXTENDED-SPECTRUM PENICILLINS
○ Glucagon For Gram (+) , (-)
● Amoxicillin - oral
ANTIMICROBIALS ● Ampicillin - IV
● BACTERICIDAL - kill ➢ PENICILLINASE-RESISTANT PCN
● BACTERIOSTATIC - prevents growth Penicillinase = enzyme produced by bacteria to
● NARROW SPECTRUM - limited coverage of bacteria destroy internal structure of PCN → no effect
● BROAD SPECTRUM - cover wide range of bacteria ● Nafcillin
● Oxacillin
➢ BETA-LACTAMASE INHIBITORS
 Beta-Lactamase = enzyme produced by bacteria that ➔ Usually used for Hospital Acquired
break open the beta lactam ring → inactivates beta Pneumonia
lactams - CEFEPIME, CEFTAROLINE
● Clavulanic Acid
● Sulbactam ● 5TH GENERATION: Gram (-) and Gram (+)
➔ Only cephalosporins used to treat MRSA
*CoAMOXICLAV (clavulanic acid + amoxicillin) - CEFTOBIPROLE

c. Carbapenems: Gram (-) and Gram (+)

- Broad spectrum
- Bactericidal
- Limited use due to its potential fatal GI
toxicity
- MEROPENEM

d. Monobactam: Gram (-) enterobacteria

- Used in UTI, skin and gyne infections
- IV/IM
- AZTREONAM

II. GLYCOPEPTIDE
● Vancomycin
- DOC for pseudomembranous
colitis (antibiotic-induced colitis)
- Used for serious infections
- Alternative drug for Penicillin allergy

Adverse Effects: hypersensitivity reactions:

- Possible allergic reaction or anaphylaxis
- RED MAN SYNDROME : occurs if u have fast IV
infusion
➔ Manifestations: red face,neck and trunk,
Nursing Considerations: itchy
1. High risk of hypersensitivity ➔ Prevention: slow IV infusion (30 mins to 1hr)
2. If px allergic to PCN, avoid other PCN
3. If px allergic to PCN, avoid cephalosporins and vice PROTEIN SYNTHESIS INHIBITORS
versa
- Vital for bacterial cell replication → growth
4. Give 1-2h ac or 2-3h pc
- If bacteria can’t synthesize protein
5. Give PROBENECID(uricosuric drug) - inc blood level
of PCN by decreasing excretion; given with penicillin
- No growth → death
to increase blood level of PCN

b. Cephalosporins “CEPH” or “CEF”

● 1ST GENERATION: Gram (+) and weak Gram (-)
coverage
- CEPHALEXIN, CEFAZOLIN

● 2ND GENERATION: Gram (+) and some Gram (-)

coverage
- CEFUROXIME, CEFACLOR

● 3RD GENERATION: Gram (-) and some Gram (+)

➔ Effective concentration in the CSF; can cross I. MACROLIDES
the blood brain barrier - Usually for URTI
➔ DOC for meningitis cause by Gram (-) ● Azithromycin
bacilli - Concentrates into macrophages and tissues
- CEFTRIAXONE, CEFTAZIDIME - Eliminated slowly (OD for 3 days)
- Give 3 days but lasts for 10 days
● 4TH GENERATION: Gram (-) and Gram (+) - Effective in gonorrhea
➔ Effective concentration in the CSF ● Clarithromycin
 ● Erythromycin ● Sulfamethoxazole
- Alternative drug for PCN allergy ● Trimethoprim

II. CHLORAMPHENICOL FLUOROQUINOLONES “oxacin”

- Broad spectrum - Broad spectrum
- Used to treat serious infections like typhoid fever, eye - Bactericidal against G(-) and some G(+)
infections, or any salmonella infections - Used for urinary tract infection
- Not given in children < 2 y/o = Gray baby syndrome ● Ciprofloxacin
(there is cardiovascular collapse) ● Ofloxacin
● Rifampicin - anti TB; S/E: red orange
discoloration of body fluids
C/I in pregnancy:
1. QUINOLONES
2. TETRACYCLINES

ANALGESICS AND ANTI INFLAMMATORY DRUGS

Antiinflammatory drugs - block one or more signs of
inflammation dolor (pain), calor(heat), rubor (redness), tumor
(swelling), pallor)

Inflammatory response: a normal response of a vascularized

III. LINCOSAMINES tissue to injury
● Clindamycin
- Allows Clostridium difficile to infect the Colon
which can result to Colitis
(pseudomembranous) or an
antibiotic-induced colitis
➔ DOC: Vancomycin

IV. AMINOGLYCOSIDES “mycin” / “cin”

- Always in combination with penicillin = synergistic effect
(help each other)
● Streptomycin - anti TB; S/E: ototoxic
● Kanamycin
● Neomycin - used in HE
● Gentamicin - nephrotoxic
Non-Opioids/Non-Narcotics
V. TETRACYCLINES “cyclines” - Antiinflammatory drugs
● Tetracyclines - Corticosteroids
- Indicated for PUD caused by H. Pylori - Nsaids
- Also used in acne vulgaris and chlamydial - Salicylates
infections - para-aminophenols
Adverse Effect:
- Staining of the teeth (avoid in children <8 y/o) Opioids/Narcotics
- GI symptoms - Opioids agonist - strong opioids
- C/I in pregnant: fetal exposure can cause - Opioids agonist-antagonist- weak opioids
dental enamel dysplasia - Opioid antagonist - antidote

● Doxycycline Analgesics
- DOC in the treatment and prophylaxis of - A/AN = absence, Algia/algus = pain
leptospirosis - Pain relievers

● Demeclocycline Gold Compounds

- An antibiotic that has a diuretic effect - Auric chloride
- Used in SIADH (increase in ADH → - Chloroauric acid
retention of water)
Anti Migraine Drugs
SULFONAMIDES “sulfa” - Ergots
- A/E: Steven Johnson’s Disease: nalapnos ang skin - Triptans
● Sulfasalazine
 ➢ Antihistamines
➢ Corticosteroids “one” *Give NSAIDS, Corticosteroids and ASA after meals = to
- Blocks the immune response prevent gastric irritation
- Blocks the arachidonic acid and histamine
- Uses: asthma and copd, arthritis, allergy,
immunosuppressants (organ transplant)
- S/E: hyperglycemia, immunosuppression, gastric
irritation (because it will block the PGE1 of the
stomach), cushing syndrome
● Prednisone - oral
● Hydrocortisone - IV/Topical
● Fluticasone - Inhalation

- Nursing considerations:
- Take with meals
- Don't stop abruptly
WHO ANALGESIC LADDER
- Watch out for S/E
- Assessment used: PAIN SCALE
- Avoid crowded places
- Avoid raw foods

Non-Narcotic Analgesic
Non-Steroidal Inflammatory Drugs

➢ NSAIDs
- Blocks prostaglandin
● Fenmates
○ Mefenamic Acid
● Propionic Acid
○ Ibuprofen
■ Can be given for fever
(antipyretic)
○ Naproxen
● Indole Acetic Acid
○ Indomethacin (most potent
inhibitor of COX)
● COX-2 Inhibitors
○ CeleCOXib Opioid Agonist - Antagonist
➔ Should not be given to pxn with kidney - Pharmacodynamics: blocks some opioid receptors
problems (may lead to ischemia and may and stimulates some opioid receptors
worsen the problem) - Nubain

➢ Salicylates a. OPIOID/ NARCOTICS

● ASA - Blocks prostaglandin and ● Morphine
thromboxane A2 ● Fentanyl
○ Most commonly used ● Codeine
○ Aspirin ● Tramadol
○ Least potent analgesic effect drug
○ Used as blood thinner ● Mild pain: 1-3
● Moderate pain: 4-6
➢ PARACETAMOL - weak antiinflammatory drug ● Moderate to severe pain: 7-10
➢ Para-Aminophenols
● Acetaminophen
○ Week anti inflammatory drug
○ Binds to the receptor in the
hypothalamus
○ Effects: lowers body temperature
and analgesic
○ Adverse effects: hemolytic anemia
and hepatic necrosis
○ Antidote to hepatic necrosis: NAC=
N-Acetyl-Cystein
 FRIED’S RULE
- Used only until 2 y/o

DOSAGE CALCULATIONS
A = AMOUNT
D = DESIRED DOSE
S = STOCK
Q = QUANTITY

CLARK’S RULE:

= 10 ml

YOUNG’S RULE:

Order: PARACETAMOL 15mg/kgBW q4h for fever prn

Weight: 25 lbs
Supply: Paracetamol 100 mg/ml

Steps:
1. Covert

2. desired dose = (recommended dose) x (weight in kg)

15mg/kg x 11.36 kg = 170.4 mg
 3. 170.4 / 100 = 1.7
For how long should the nurse a 1L of D5 0.9% NaCl running
at a rate of 32 gtts/min. IV set is labeled at 10 gtts/ml
= 5.2 hrs

What is the hourly rate?

63 ml/hr

If walay drop factor then infant = micro ang iuse (60gtts)

If wala jud nakaindicate = 15 gtts/min

Infuse 1L of IVF to a patient for 8 hrs using macroset. Rate?

= 31-32 gtts/min

Infuse 200 ml of IVF to a patent for 45 minutes. IV set is

labeled at 10 gtts/ml. Rate?
= 44 gtts/min

For how long should the nurse infuse a 1000ml of D5 0.9%

NaCl running at a rate of 32 gtts/min IV set is labeled at 15
gtts/ml

= 8 hours
BP = HR x Stroke Volume x Total Peripheral Resistance

*Don’t give neozep to hypertensive clients.

- You can give Sinupret 3x a day for 5 days