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Nursing Pharmacology
08/11/23- Dr. grageda
• Pharmacology
o Study of biological effects of chemicals
o Pharma known as “above drugs.”
o All drugs are chemicals, and they are introduced into the body.
o If drugs are introduced to the body, there are always change. Two types of change:
§ Desirable – these are the therapeuDc (also known as cure) effect of the
medicaDon.
§ Undesirable – side effects or adverse effects of drugs.
o Tips
§ Review the sympatheDc (fight or flight situaAon) and parasympatheDc
nervous system
o Basic concept of pharmacology
§ Pharmacodynamics:
• Drug à body cells à there will be receptors (to receive the drug.
à once received there will acDvaDon in the hormones à changes
occur in the body.
§ Pharmacokine;cs (it is known as the movement of the drug)
• Response of the body to the drugs.
• Process:
o LiberaDon à absorpDon à distribuDon à metabolism à
excreDon
§ Note: drug is considered as foreign in the body.
• Pharmacodynamics
o AcDon of the drug to the body. Such as the following:
§ Replace a missing substance that is absent in the body. Ex: insulin from DM
paAents; or levothyroxine.
§ Increase cellular acDviDes. Ex: digoxin for HF paAents.
§ Depress cellular acDviDes.
§ Interfere with the growth of a foreign cell.
o Drugs acDon maybe through:
§ Receptors
• Drug receptor interacDons:
1. Agonist
a. AcDvates a receptor; Ex: digoxin (for HF), epinephrine
(adrenergic agonist)
2. Antagonist – it is against the agonist.
a. Compe;;ve antagonist – bind to the same receptor
which there will be compeDDon. Potency of an
agonist is blocked.; Ex: overdosed to morphine and
naloxone.
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b. Non-compe;;ve antagonist – binds to different

receptor sites. Potency of agonist is reduced.; Ex:
cefuroxime and omeprazole.

3. Adrenergic – sympatheDc receptors

a. Alpha
i. Alpha 1
ii. Alpha 2
b. Beta
i. beta 1
ii. Beta 2
§ Enzymes
• Drug enzyme interacDon
o Ex: Cholinesterase inhibitor – when inhibiAng cholinesterase
à result to breakdown acetylcholine
o Process:
§ Electrical impulse à travel through the axon
terminal à acDvates the effector cells à movement
of muscle every effector cell has muscle) à acDvates
acetylcholine à muscle relaxaDon occurs à when
paDent takes cholinesterase à it will breakdown
acetylcholine à muscle contracDon happens.
§ Pumps
• InhibiDng pumps
o Ex: proton pumps inhibitors
o Process:
§ Electrical impulse à release of 5HT which is
serotonin à bind to the receptor à impulse
transmission occurs à serotonin will be reuptake
and go back to where it belongs.
§ If, SSR given to the paDent – it inhibit/blocks the
reuptake the serotonin which will make serotonin
available when the body needs it and serotonin level
will increase.
§ Chemical interac;on
o Ex: antacids
§ Altering metabolic process
o Ex: insulin and levothyroxine
o Addi$onal:
§ Biogenic amine theory – there is decrease level of NE, DOPA, and SHT
which causes depression; thus paDent takes anD-depressant which is to
increase.
• Pharmacokine;cs
o Response of the body to the drugs
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§ Drugs enters the body à swallowed à passes through the esophagus and
stomach à release of acDve ingredients (when the chemical drugs is
released) there will be (1) libera;on.
§ Then (2) absorp;on of the drug occurs aYer liberaDon à it should cross
along the blood stream.
§ From the blood stream à (3) Distribu;on of the drugs occurs to the target
cells (it is the purpose of the drugs.)
§ It should cross the liver à a protein will be released from the liver à (4)
(4) metabolism occurs à then new drugs are produced and makes it less
acDve à also it will detoxify the drugs to lessen the toxicity of the drug to
the body.
• Ex: from 500mg taken drugs, when metabolized in the liver, 400mg only will be
back to the blood, detoxified and it is less ac@ve.
§ AYer metabolism à (5) excre;on occurs through the sweats in the skin,
urine, and feces.
• Note: this is why liver is very important to be healthy as it helps in
metabolizing the drugs taken by paDents; and usually if liver
(metabolizing the drugs) problem, kidney (filtering of the drugs for excre;on)
problem occurs, or the paDent is too young à lowering of the dose
is IMPORTANT!
o Types of drug transportaDon:
§ Passive transport
• Diffusion – drug moves from higher to lower concentraDon; most
drugs use diffusion.
§ AcDve transport
• Require a carrier (enzyme protein)
• Lower to higher concentraAon
o Dose
§ number of drugs to be administered to the paDent
o Schedule
§ Time, frequency, how many dose per day.
o Recommended dose
§ The number of drugs administered to reach the criDcal, concentraDon.
§ Right dose = right Dme
o CriDcal concentraDon
§ Level of drugs in the blood which produces a therapeuDc effect.
o TherapeuDc effect
§ Favorable response aYer a treatment of any kind
§ CURE
o Loading dose
§ IniDal dose or known as the immediate response.
§ Given during emergencies.
§ Higher than recommended dose
o Half-life (Ame)
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§ Time it takes for a drug to become half of its previously peaked level.
§ Ex: amoxicillin 500mg, q 8H for 7 days, T ½

§ Giving the right dose and right Ame results to recommended dose is given
to the paAent.

• Nervous system
o Backbone of pharmacology is the nervous system.
o Process of communicaDon:
§ Neurons – funcDonal unit of the nervous system
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• Electrical impulse carries informaDon (message) à it should reach

the effector cells (it can be a muscle, gland or another nerve) à it results of
muscle to contracts, or producDon of hormones.
o Types of neurotransmiLers: body’s chemical “messenger”
1. Acetylcholine (Ach) – it is for muscle contracDon
and memory. à CHOLINERGIC NERVES
2. Norepinephrine and epinephrine (NE/E) –
produced in adrenal gland; they are known as the
adrenalines of the body; it affects the behavior. à
ADRENERGIC NERVES
3. Dopamine (Dopa) – known as the excitatory; motor
and it can be inhibitory; it also tackles cogniDon such
as thinking, learning, and reasoning. à
DOPAMINERGIC NERVES
a. Too much dopamine – schizophrenia
b. Low dopamine – depression
4. Serotonin (5HT) – it is for arousal and sleep; it is for
moDvaDon, and it prevents depression; it can be get
from chocolates. à SEROTONERGIC NERVES
5. Gamma Amino butyric Acid (GABA) – it is inhibitory
neurotransmiaer and used for seizures. à
GABAMINERGIC NERVES
a. anD-epilepDc drugs (anxiolyAc drugs) which
sDmulates GABA.
o Two branches
§ Sympathe;c nervous system (fight or flight)
• Adrenergic nervous system
• FuncDons:
o Dilate pupils
o Inhibit salivaDon
o Increase HR
o Relax airways
o Inhibit acDvity in stomach
o SDmulate release of glucose; inhibit gallbladder
o Inhibit acDvity of intesDne
o Secrete epinephrine and norepinephrine
o Relax bladder
o Promote ejaculaDon and vaginal contracDon
• Neurotransmiaer
1. Preganglionic nerve: acetylcholine
2. Postganglionic nerve: Norepinephrine
§ Parasympathe;c (rest and digest)
• Cholinergic nervous system
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• FuncDons:
o Constrict pupils
o SDmulate saliva
o Slow HR
o Constrict airway
o SDmulate acDvity of stomach
o Inhibit release of glucose/sDmulate gallbladder
o SDmulate acDvity of intesDne
o Contract bladder
o Promote erecDon
o Contract bladder
• Neurotransmiaer
1. Preganglionic: acetylcholine
2. Postganglionic: acetylcholine
Autonomic nervous system Sympathe;c Parasympathe;c
(Adrenergic) (Cholinergic)
Response to: Increased Heart rate Decreased heart rate
• Heart contracDlity contracDlity
Lungs Increased RR Decreased RR
• Bronchus BronchodilaDon bronchoconstricDon
Pupils Dilate mydriasis Constrict meiosis
GIT
(blood flow, moAlity, consDpaDon Diarrhea
secretory)
Kidney
• Blood flow Decrease à urine formed Increase à more urine
formed
Urinary bladder
• Sphincter Contracted (retenAon of Relaxed (emptying of
urine) bladder)

• Detrusor muscle Relaxed Contract

Blood vessels
• Smooth muscles VasoconstricDon VasodilaDon

Agonist – sDmulate. Antagonist – block

Mime;c – mimic; gaya-gaya Ly;c – block, destroy. Dissolve

Alpha Beta

o During surgery medicaDon such as the following:

§ AnxiolyDc
§ Anesthesia
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§ Atropine – it has anDcholinergic effect which has sympatheDc effects.

• 3 components to know
o Receptors
o Agonist or antagonist
o LocaDon of the expected response

• Summary:
o Alpha 1 – found in urinary bladder, blood vessels, and iris.
§ Alpha 1 adrenergic agonist – it is expected to have sympatheDc effect.
1. Phenylephrine: which is a nasal decongestant and vasopressor (it
increases TPR which is good for pa;ent with hypotension.) and used for the paDent
with eye procedures (for dila;on effect in the eyes); effect of this drug is
sympatheDc; it has no effect in the heart because its effect can only
be seen in the specific locaDon which is in urinary bladder, blood vessels, and
iris not in the heart.
a. Effect: vasoconstricDon à Decreased BF and O2 à cell
shrinks
b. Alterna;ve: sinupret especially for paDent with
hypertensive.
c. SE: reflex bradycardia (no effect of heart)
i. heart senses BP is higher, slows itself down thinking
there is too much adrenalin.
ii. HTN
§ Alpha 1 Adrenergic antagonist – it is expected to have parasympatheDc
effect.
1. Prazosin: it will bind on the blood vessels only à vasodilaDon à
decreases the TPR thus it is used for hypertensive paDent.
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2. Doxazosin: it will be used for hypertensive paDent, but it also has

effect on the urinary bladder which its emptying bladder effect
used for paDent with BPH.
3. Terazosin: it has direct effect on the urinary bladder which there is
also emptying of the bladder and used for BPH paDents.
4. Alfuzosin: the same effect with terazosin.
5. Tamsulosin
o Alpha 2 – sympatheDc adrenergic found in CNS nerve membrane, pancreas.
§ Alpha 2 adrenergic agonist
1. Clonidine: it crosses the BBB (blood brain barrier) and use for
paDent with hypertension because it decreases BP (though it is
sympathe;c by effect, but this medica;on it decreases the s;mula;on of epinephrine in
the body in which when epinephrine is decreased through this medica;on, it decreases
the TPR, so, it decreases the blood pressure.)
a. Decreased SNS and BP
b. SE: orthostaDc hypotension
c. Note: remember that in alpha 2 the sympatheDc effect is
decreased unlike alpha 1.
2. Methyldopa: this is taken oral and It can be given to pregnant
paDent and has same effect with the clonidine.
§ Alpha adrenergic Agonist – it has effect in both alpha 1 and alpha 2
1. Midodrine (alpha 1): this is used for chronic orthostaDc
hypotension
o Beta 1 – it can be seen in the heart.
§ Beta 1 adrenergic agonists
1. Dobutamine: it is a syntheDc dopamine, and it is used for chronic
heart failure and shock paDents; also paDent in cardiogenic shock.
a. SE: hypertension because of its sympatheAc effect which
is to increase the HR.
b. Low dose: vasoconstricDon of splanchnic bed, increase
blood pressure, and used in ICU for renal perfusion.
c. Medium dose: B receptors – CO increases
d. High dose: alpha receptors and it increases TPR thus
increases the BP.
e. Renin release: with the involvement of angiotensin it
affects the increase of HR and BP.
o Beta 2 – it can be seen in the lungs.
§ Beta 2 adrenergic agonist
1. Albuterol/salbutamol: it causes bronchoconstricDon à for
asthmaDc and COPD pt. arteriolar vasodilaDon in skeletal
muscles; SABA
a. Onset: 5 mins,
b. Dura;on: 6 h
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c. SE: palpitaDon and tremors (because of its beta 1 effects

aside from beta 2)
2. Terbutaline: this is for asthma and COPD pt. because it causes
bronchodilaDon; SABA
a. Onset: 5 mins, duraDon 6 h
b. Tocoly;c (tone of the muscle): this is to relax the uterine
contracDon.
3. Isoxsuprine: tocolyDc, for preterm labor, and dysmenorrhea
4. Formeterol: LABA and this is prevenDon for asthma and use for
emergencies.
a. Onset: <3 mins
b. Dura;on: 12 h
5. Salmeterol: LABA
§ Beta 1 selec;ve adrenergic
1. Bisoprolol
2. Esmolol
3. Acebutolol
4. Atenolol
5. Metoprolol
o Alpha adrenergic antagonist
§ Phentolamine: used for hypertensive crises due to
o Beta adrenergic blockers
§ Propranolol: it is used for paDent with hyperthyroidism because with this
disease everything is increased especially the tachycardia, it is used for
stage fright; also used for prophylaxis for migraine.
§ Nadolol: drug of choice in angina + HTN
§ Labetalol: mostly used in pregnant women for blood pressure; it has alpha
receptor effect which increases blood flow.
• SE: bradycardia, hypotension, bronchoconstricDon, hypoglycemia
• CI: pt. with bradycardia, asthma, hypotensive, diabeDc paDent and
COPD.
• Nursing management:
1. monitor vital signs especially the heart rate and blood
pressure.
2. hold if HR is < 60 bpm.
3. call if the BP is less than 90/60 mmHg.
4. CauDon with paDent who has diabetes mellitus (DM)
• MAOIs – monoamine oxidase and known to be anD-depressant.
o Its funcDon is to breakdown the amines which are the following (1)
norepinephrine, (2) dopamine, and (3) serotonin.
o If you give MAOs inhibitor it blocks the MAO, and no breakdown that will occur,
thus amine increases.
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-----diseases related topics-----

Myasthenia gravis

• Women who are in 20-40 years old

• Ascending paralysis is present.
• Descending muscle weakness
• Nursing management:
o Ensure that airway is patent.
o Nurses should also look always assess for sudden aspiraDon.
o With weaknesses, assist the paDent for Immobility.
§ Myasthenic crisis (improvement of paralysis)
1. Weakness/paralysis
2. Cause: Underdose of cholinergic drugs
3. Treatment: cholinergic such as PyridosDgmine and physosDgmine
4. Test: tensilon test
§ Cholinergic crisis (worsening of paralysis)
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1. Weakness paralysis
2. Cause: Overdose of cholinergic drugs
3. Treatment: anDcholinergic such as atropine
4. Test: tensilon test
o Slow IV administraDon to avoid sever cholinergic effects
• Goal: is to have temporary strengthening of the muscles.
• Drugs are given 30 minutes before meals to ensure the tone of muscles in swallowing is
good.
• Drug process for MG pa;ents:

o The cholinergic effect of the medicaDon protects the acetylcholine (Ach), through
blocking the anDcholinesterase.
• PharmacotherapeuDcs
o Cholinergic or an;cholinesterase agents
§ Pyridos;gmine (MesDnon): it is the first line drug for MS paDent, it is used
for atropine toxicity.
§ Neos;gmine (prosDgmin): it is used for long term and it increases
acetylcholine – receptor binding
• Side effects: peripheral nervous system effects
o Cor;costeroids – to suppress the immune response
§ Decadron (dexamethasone)

Alzheimer disease
• No producDon of acetylcholine (which controls the muscle and memory, with a cholinergic nerve but with this
disease there is no produc;on of cholinergic nerves thus affects the memory of the pa;ent.)
• Symptoms:
o Amnesia – loss of memory
o Apraxia – unable to determine funcDon and purpose of the object.
o Aphasia
§ Expressive aphasia – paDent is unable to speak.
1. Frontal lobe
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2. Broccas area
§ Recep;ve aphasia – unable to understand spoken words. COMMON
1. Temporal lobe
2. Wernicke’s area
o Agnosia – unable to recognize familiar objects.

• No cure for Alzheimer’s disease because it is degeneraDve disease; it is also important to

ensure the remaining acetylcholine is prolong its life through anDcholinesterase.
• Cholinergic agonists known as the parasympathomimeDc.
o Bethanechol
§ SelecDvely acDvates bladder muscarinic receptor.
§ Emptying of the bladder
§ Use
1. Relief of urinary retenDon
2. Post-partum
3. Neurogenic atony of bladder
§ SE: asthma à for constrict airways; cardiac problems à slow HR; PepDc
ulcer à increase GI acDvity; intesDnal obstrucDon
• Cholinergic antagonists known as the parasympatholyDc.
o Atropine
§ AnDdotes to cholinergic criss
§ Pre-op
§ SE: dryness of mouth, consDpaDon, retenDon of urine, and tachycardia
o Dicyclomine
§ AnDspasmodic, anDmuscarinic
§ For hyperacDve bowel in adults
o Scopolamine (hyoscine butylbromide)
§ MoDon sickness
§ Decrease secreDons.
§ Pupil dilaDon
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§ PONV
Parkinson disease
• Progressive disorder
• DegeneraDon of dopaminergic neurons – there is decrease level of dopamine in the body
so to manage, there should be addiDonal dopamine in the body through medicaDon.
• The acetylcholine will conDnue to contract, while the dopamine relaxes, also as
acetylcholine contracts there is no one who can inhibit it.
• Goal: is to balance both the dopamine and acetylcholine, and to increase the dopamine
level
• The drugs will block the acetylcholine to aaain balance.

• Two types of drugs for PD:

o Dopaminergic – increase the level of dopamine.
o An;cholinergic – this is to block the producDon of Ach.
• Classes of an;-Parkinson’s drug
o Goal:
1. Improve motor control.
2. Improve quality of life
3. Increase dopamine and decrease acetylcholine.

• Dopaminergic agents
o Dopamine precursors
§ L-dopa (levodopa) – main stay of treaDng Parkinson’s disease but it has
many side effects to the paDent; BUT IT IS NOT DOPAMINE.
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• When taking levodopa, it travels through the brain and there is

decarboxylase which help in produces dopamine.
• Note: dopamine cannot cross the BBB or blood brain barrier

• the funcAon of carbidopa when taken with levodopa it blocks the

decarboxylase which stops the producAon of dopamine in the
periphery.
• Carbidopa cannot travel the BBB so only the decarboxylase in the
periphery is blocked. Therefore, the conversion of levodopa to
dopamine conAnues in the brain.
o Dopamine receptor agonists
§ Bromocrip;ne, pergolide
o MAO-B inhibitors
§ Selegiline
• Classes of anD-Parkinson’s disease
o Dopaminergic agents
§ Catechol---methyl transferase (COMT) inhibitor
• Entacapone, Tolcapone
• Blocks COMT
• Prolongs “on Dme”
§ Others
• Amantadine
• AnDretroviral drugs
• Improves bradykinesias.
• SE: anorexia and postural hypotension
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• Respiratory drugs
upper respiratory tract
Medica;on to treat allergic rhini;s
1. AnDhistamines – oral and intranasal
2. GlucocorDcoids – intranasal
3. SympathomimeDcs – decongestants
a. Which of these categories contains an OTC medicaAon to
used make crystal meth?
o An6histamine
§ It blocks the histamine 1 (this is for the allergies and histamine 2 is in the
stomach which causes to produce hydrochloric acid.)
• 1st generaDon – usually has drowsiness side effects.
1. Diphenhydramine (usually given before bedAme
because of its drowsiness effects)
• 2 generaDon – it does not have drowsiness side effects.
nd

1. Ce;rizine
2. Loratadine
3. Desloratadine
• Intranasal anDhistamine
1. Azelas;ne
o Intranasal Glucocor6coids
§ It blocks the immune response and anD-inflammatory.
• 1st generaDon
1. Beclomethasone
2. Budesonide
3. Triamcinolone
• 2 generaDon
nd

1. Flu;casone propionate
2. Ciclesonide
§ Nursing consideraDons:
• Avoid crowded.
• Avoid raw foods.
• Do not stop abruptly à Addisonian crisis
o Sympathomime6cs
§ Pharmacodynamics
• VasoconstricDon à shrink membranes
§ Phenylephrine – nasal spray or oral
§ Pseudoephedrines
• Oral
• Use with cauDon in CV paDents.
• Shrinks swollen membranes à eases breathing.
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• Ingredients in crystal meth

Medica;on to treat cough.
o Cough suppressants
§ Pharmacodynamics:
• Suppress the cough reflex in the CNS
§ Dextromethorphan
• Opioid derivaDves without euphoria in normal dosage
• Found in combinaDon with other cold medicaDons.
§ Codeine
• Opioid derivaDves with euphoria
• Most effecDve for treaDng cough
• 1/10th the dose used for pain
o Mucoly6c
§ Reduce the adhesiveness of the mucus bonds.
§ Dissolve the phlegm.
§ Use for producDve cough.
§ Acetylcysteine (Fluimucil)
• AnDdote to acetaminophen toxicity (it increase glutathione)
§ Ambroxol
§ S-carboxymethyl carbocisteine
§ Dornase alfa
o Expectorants
§ More cough but easier to expectorate.
§ It causes producDve cough when taken.
§ Guaifenesin (Robitussin expectorant)
• Inflammatory response
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Lower respiratory tract

Medica;on to treat both asthma airway problems
o Problem:
§ BronchoconstricDon
§ InflammaDon
o Goal
§ BronchodilaDon
§ Blocks the inflammaDon.
o Note: we can give anDcholinergic drugs if it is “lyDc”.
o Bronchoconstrictors
§ SABA – emergency rescuer inhaler
1. Albuterol
2. Levalbuterol
3. Terbutaline
§ LABA – long-term inhaler
1. Formoterol
2. Salmeterol
§ Xanthine – directly relax the smooth muscle.
1. Caffeine
2. Aminophylline
3. Theophylline
§ AnDcholinergic – blocks the muscarinic receptors in lungs
1. Ipratropium
o Bronchodilators
§ AnDcholinergics – it blocks the muscarinic receptors in the lungs, reduces
vagal cholinergic tone, reduce mucous hypersecreDons, and off label use
for asthma à more use with COPD; AE: dry mouth and irritaDon of pharynx
• Ipratropium
• Tiotropium
§ Methylxanthines: directly relaxes the bronchial smooth muscles à
increases vital capacity; less effecDve than beta 2 agonist but longer
duraDon; narrow window target 5-15 mcg/ml
• Nursing consideraDon:
1. Administer oral drug with food or milk.
2. Monitor for side effects such as palpitaDon and tremors.
3. Dietary control of caffeine
a. Coffee, soda, and tea
4. Serious SE
a. Dysrhythmia, convulsion
5. AnDdote: NONE
6. Monitor serum theophylline levels
a. > 20 mcg/ml = Nausea (1st sign)
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b. > 30 mcg/ml = tremor (later sign

o Asthma and meds in a nutshell
§ A chronic disease process.
§ Smooth muscle causes bronchoconstricDon of already narrowed airway.
§ Inflammatory response causes excess mucus.
§ Medicines need to address both the following
• InflammaDon
• BronchoconstricDon
§ During acute aaacks – periodize SABA
§ For prevenDon of aaacks use – LABA, Glucocor;coids, leukotrienes
modifiers
Treatment of inflamma;on
o Leukotrienes modifiers
§ Leukotrienes – promotes smooth muscle constricDon and inflammatory
response. Added on when glucocorDcoids aren’t enough.
§ Adverse effects
1. Neuropsychiatric effects
2. Mild GI distress
3. Montelukast
4. Zafirlukast
5. Zileuton may impact liver.
o Cromolyn
§ Inhaled meds
§ Mast cells stabilize.
§ Suppress inflammaDon.
§ “preventer”
§ Also used for exercise induced asthma: SABA can also be used.
§ Adverse effects: NONE
o Omalizumab
§ IgE antagonist
§ Route: SQ
§ 2nd line drug for allergy – related asthma
§ High cost (Xolair)
§ Adverse effect
1. Anaphylaxis
2. Risk for cancer
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Nursing Pharmacology
08/12/23- Dr. grageda

• Cardiovascular drugs
o Basic concept:
§ Preload – all the blood that will be going back to the heart through superior
and inferior vena cava.
• If paAent is given vasodilator there will be venous pooling in which
its effect to the preload is decrease. The stroke volume will also
decrease thus the blood pressure will also decrease.
• If paAent is given alpha 1 agonist such as phenylephrine the effect
is vice versa to the vasodilator.
§ Aaerload – away from the heart.
• Is the pressure of the leY ventricle so it can push the blood away
from the heart. If the blood pressure is high, the heart will have
difficulty.
Angina
o It is known as “chest pain.”
§ because there is lacDc acid caused by cells that undergoes anaerobic
metabolism, there is ischemia due to obstrucDon because of atheroma or
faay tumors.
§ There is increase in oxygen demand, so the goal is to decrease the oxygen
demand.
o Nursing priority: Oxygen
o Vasodilators
§ Nitrates
• Acts directly on vascular smooth muscles (primarily in veins)
• Drug of choice for instable angina and unstable angina; this is to
decrease cardiac O2 demand.
o Nitroglycerine
o Isosorbide mononitrate
o Isosorbide dinitrate
• Pharmacodynamics
o VasodilaDon of blood vessels à venous pooling à
decreased preload à decreased workload à DECREASE
OXYGEN DEMAND
o Also, there will be… arteriolar vasodilaDon à decrease in
TPR à decrease in aYerload à decreased workload à
Decrease in oxygen demand à INCREASE OXYGEN SUPPLY
• Nursing considera;on
o Route: Sublingual (SB) – because it will be faster for the
medicaDon to travel to the blood, and it can bypass the liver
thus there will be no first pass effects.
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its effects in 1-3 minutes.

§
Every 5 minutes, another dose if given because of its
§
half-life.
o Give 1 tab q 5 minutes up to 3 doses. – aDer 3 doses the angina
should be relieved if there is no relief felt then it is possible for MI instead of
angina.
o PaDent should not sip water because of the possibility of it
becoming oral than SB, and there it will not bypass the liver
thus the effect of medicaDon will be affected.
o Storage: dry, amber-colored container
o Shelf life: 3 months
o SE:
1. Headache – it is caused by cerebral vasodila;on.
2. Hypotension
o Patches:
§ body heat slowly releases nitrate into skin and
absorbed through skin à blood.
§ its effects in 30-60 minutes.
§ applied in hairless skin.
§ rotate sites – to prevent skin irritaAon.
§ 24 h/7 days to avoid tolerance – nitrate free for 10-12
hours/day (evening) at least 8h, because it s;ll has a half-life that will
take care the angina in the evening.
§ Calcium channel blockers
• Calcium is for muscle contracDon.
• Known as VNAFD
o Very – Verapamil
o Nice – Nifedipine blood vessels
o And – Amlodipine blood vessels
o Friendly – Felodipine blood vessels
o Drugs – Dil;azem
• Pharmacodynamics
o No calcium influx à heart à decrease HR à it’ll relax
vasospasm of coronary artery (drug of choice is prinametal
A.) à increase blood flow to myocardium à INCREASE
OXYGEN SUPPLY
o No calcium influx à blood vessels à arteriolar vasodilaDon
à decrease aYerload à decrease workload of heart à
DECREASE OXYGEN DEMAND
o Cardiac depressants
§ Beta blockers
• Beta adrenergic blockers
• Drugs involved:
o Propranolol
Cute si dims J

o Nadolol
o Metoprolol
• SympatholyDc effect
o à decrease heart rate à decrease workload of hear à
decrease O2 demand à INCREASE OXYGEN SUPPLY
o à VasodilaDon à increase blood flow à INCREASE
OXYGEN SUPPLY
§ Ranolazine
• Treatment of chronic angina in adults
• A newer drug with limited indicaDon
• Can be combined with other drugs.
Myocardial infarc6on
o There is chest pain, it is irreversible and Dssue death is present.
o Nursing priority: pain
o Drugs used in MI:
§ Morphine
• Opioid agonist
• Pharmacodynamics
o SDmulates opioid receptors in central nervous system and
gastrointesDnal.
• Uses
o Moderate to severe pain
o Vasodilator
o It causes venous pooling à decrease preload à decrease
workload heart à DECREASE OXYGEN DEMAND
• Contraindica;ons
o HypersensiDvity
o ICP and suspected head injuries
• Side effects:
o Euphoria
o ConsDpaDon
o Bradycardia as compensatory mechanism
o Respiratory depression
o For morphine overdose check for pinpoint pupils
§ Nitrates (check above for nitrate)
§ Drug affec;ng coagula;ons.
Cute si dims J

o FibrinolyDc cascade – it is where the fibrin is blocked by

the plasmin to stop clovng,
1. An;platelets
a. Blocks the formaDon of platelet plugs.
b. Permanently inhibit platelets.
c. Replacement restores overall funcDon in 3-7 days
d. Interac;on
i. NSAIDs interfere with aspirins effects.
e. Drugs involved.
i. Aspirin
ii. clopidogrel
iii. Dipyridamole

f. SE:
i. Tinnitus
ii. Gastric irritaDon à PUD
iii. Bleeding
g. Nursing interven;on:
i. watch out for signs of bleeding.
ii. use soY bristled.
iii. avoid taking in viral infecDons.
Cute si dims J

2. An;coagulants
a. Warfarin
i. Pharmacodynamics
1. Blocks the vitamin K dependent clovng
factors.
ii. Route: oral
iii. Therapeu;c test: PT or prothrombin Dme (is the ;me it takes
for the liver to produce prothrombin aDer an injury because if there will be
presence of thrombin, and fibrin thus there is cloOng.)

iv. Therefore, if there is warfarin then prothrombin

producDon will be delayed but be cauDous the delayed
Dme should not be prolonged as there will be bleeding.
v. Therapeu;c margin: 1.5 to 2.0 X normal
vi. Side effects: bleeding
vii. An;dote: vitamin K – in order to bring back the fibrin à
clovng will occur.
b. Heparin
i. Pharmacodynamics
1. Blocks the formaDon of thrombin
ii. Route: IV/SQ
iii. Therapeu;c test: aPTT
iv. Therapeu;c margin: 1.5 to 2.5 X normal
v. Side effects: bleeding
vi. An;dote: protamine sulfate

3. Thromboly;cs
a. Pharmacodynamics
i. AcDvate the conversion of plasminogen to plasmin à no
fibrin à no Clot
Cute si dims J

b. Nursing priority: restore the blood flow there will be less chance
of damage.
c. Golden period: 3 hours
d. Side effects: bleeding
4. An;fibrinoly;cs
a. anDfibrinolyDcs such as aminocaproic acid and tranexamic acid
– to restore the clocng and stop bleeding
o Summary of an;coagula;on

• An;hypertensive drugs
o Basic concept
§ BP = HR X SV X TPR
• SV – stroke volume
• BP – blood pressure
• HR – heart rate
• TPR – total peripheral resistance systemic vascular resistance
• Note: HR X SV = CO (cardiac output)
§ Therefore, BP = CO x TPR if the TPR increase the blood pressure will also
increase.
o Mean arterial pressure (MAP)
§ Average pressure throughout each cycle of the heartbeat
§ Normal: 70 - 100 mmHg
§ Formula:
• MAP = SBP + 2(DBP)/3
§ Interpreta;on for BP/MAP: if the answer is within…
• Normal range – it means that the cells are gevng sufficient oxygen.
• Abnormal low range – it means that the cells are not gevng
enough sufficient oxygen which can cause hypoxia, increases the
risk for Dssue death à possible for death.
Cute si dims J

•Abnormal high range – it means the cells are gevng too much
oxygen because if there is hypertensive crisis then the aYerload is
affected which makes it high, and the heart is working much harder
than it should be. If it’s not controlled there can be damage to the
heart. It will also acDvate coagulaDon cascade which there is risk for
formaDon of blood clot there will dislodge then possible for CVA.
§ Clinical significance: Dssue perfusion
§ Addi;onal:
• Baroreceptors – it is found in the caroAd and aorta, so if the blood
pass through the caroAd and aorta the baroreceptors present on
that area will sense if the blood pressure is high or not, then it will
send signals to the brain to control the blood pressure.
• Fluid volume – during hypertension, the paAent is limited with salt
content because it afracts water which causes increase in blood
pressure.
o Renin Angiotensin Aldosterone System
§ It is regulator of blood pressure, and it starts in the kidneys
§ Process: (kidney à liver à lungs à adrenal cortex à hypothalamus)
• Whenever there is decrease in blood flow which decreases the
oxygen supply going to the kidney (known as hypoxia) then this will
be trigger for the kidney to produce renin; renin goes to the liver in
which there is the angiotensinogen, which is inacDve, but with the
presence of renin it will be converted to angiotensin I and goes to
the lungs in which the ACE (angiotensin converAng enzyme). It will
release angiotensin II (potent vasoconstrictors it binds to the blood
vessels where there is angiotensin II receptors; ager binding, it will
vasoconstrict thus the TPR will increase resulAng to increase of BP.)
it will signal the kidney to stop producing renin
• Adrenal cortex there is angiotensin II it will bind to the receptor
converDng the angiotensin II to angiotensin III which will sDmulate
the cortex to produce aldosterone as it will perform sodium
retenDon thus resulDng to water retenDon and eliminates
potassium, with this it will increase everything and eliminate
hypoxia. à kidney stops producing renin.
• osmolality will increase due to the salt retenDon as it is solute from
the adrenal cortex which will make the blood more viscous, and if
the blood is more viscous it will sDmulate the hypothalamus to
produce ADH (anAdiureAc hormone) and its funcDon is to retain
water to avoid sDckiness of the blood, it will increase TPR and it will
increase blood pressure à kidney tops producing renin.
Cute si dims J

o Drugs that will act on RAAS

§ ACE inhibitors – it blocks the ACE in the lungs thus it stops producDon of
angiotensin II and conversion of angiotensin I. so, if there is no angiotensin
II, then the blood volume will decrease thus resulDng for blood pressure to
decrease; it is risk for hyperkalemia because there is no retenDon of the
sodium.
• Drug involved:
o Captopril
o Enalapril
o Lisinopril
§ ARBs angiotensin 2 receptor blocker – it blocks the angiotensin II receptors
in the blood vessels. the angiotensin II it will not goes inside the receptor
thus vasodilaDon occurs and resulDng for the blood pressure to decrease
thus relieves the hypertension.
• Drug involved:
o Losartan
o Valsartan
o Telmisartan
• Advantage
o Reno-protecDve – DM
o HTN with cardiomegaly – it prevents stroke.
§ Direct renin inhibitors – it will block the renin in the kidneys therefore
there is no angiotensin I and II, thus the blood vessels will dilate, and it will
decrease the blood pressure and relieves the hypertension.
• Drug involved:
o Aliskeren
§ Selec;ve aldosterone antagonist – its targets is in the adrenal cortex thus
no aldosterone then it will stop the sodium retenDon and it will cause
vasodilaDon thus decrease blood pressure and relieves the hypertension.
• Drug involved:
o Eplerenone
o Drugs that will act on ANS receptors
§ Alpha 1 adrenergic antagonist (known as sympatholyAc) – it has the
vasodilaDon effect thus it will decrease the blood pressure.
• Drug involved:
o Prazosin
o Doxazosin
o Teraxosin
§ Alpha 2 adrenergic agonist (known as sympathomimeAc) – it is centrally
acDng on the hypertensive drugs.
• Drugs involved:
o Clonidine
o Methyldopa
Cute si dims J

§ Beta blockers (known as the sympatholyAc) – two ways for the beta
blockers to decrease the BP (1) heart, (2) blood, and (3) kidney. Secondary
only for blood pressure.
• Drug involved:
o Metoprolol
o Propranolol
o Nadolol
o Drugs that cause vasodila;on
§ Calcium channel blockers – it stops calcium which helps decrease the heart
rate and causes vasodilaDon in the blood.
§ Vasodilators
• Drug involved:
o Nitroglycerine
o Nitroprusside – drug of choice for hypertensive crisis; fast
onset: IV
o Hydralazine – PSH
o Diazoxide
o Minoxidil
§ Diure;cs
• Drug involved:
o Thiazides
o Loop diure;cs
o K sparring
o Osmo;c diure;cs
o CAH inhibitor
SUMMARY: “An#hypertensive drugs”
o Angiotensin conver;ng Enzyme (ACE) inhibitor – “pril”
§ Captopril
§ Enalapril
o Angiotensin’s 2 receptor blockers (ARB) – “sartan”
§ Losartan
§ Valsartan
o Alpha 1 adrenergic antagonist – “zosin”
§ Prazosin
§ Dozacosin
§ Terazosin
o Alpha 2 adrenergic agonist –
§ Clonidine
§ Methyldopa
o Vasodilators
§ Indirect:
• Calcium channel blockers
o Verapamil
Cute si dims J

o Nidedipine
o Nicardipine
o Amlodipine
o Felodipine
o DilDazem
§ Direct:
• Vasodilators
o Hydralazine (apresoline)
o Nitrates
§ Nitroglycerine
§ Isosorbide dinitrate or mononitrate
o Nitroprusside
o Minoxidil
o First line drugs
§ Ace inhibitors
§ ARB
§ Thiazide
o Second line drugs
§ Beta blockers (BB)
§ Calcium channel blockers (CCB)
o Third line drugs
§ Vasodilators
• Minoxidil
§ Alpha agonist
• Clonidine
§ Alpha blockers
• Prazosin
Cute si dims J

o Drug used for heart failure.

§ The heart is not pumping properly.
§ Goal: help the heart pump
Inotropes Vasodilators/preloading Cardiac remodeling/neuro-
reduces hormonal ac;vity
Pharmacodynamics:
Increases intracellular
Na+/Ca+ levels in the heart à
increase contracDlity and (+)
inotropy
Cardiac glycosides: Digoxin Loop diure;cs: furosemide

Purpose: Pharmacodynamics:
most commonly used for HF,
also used in A-fib paDent; Increase UO à decrease blood volume à decrease preload à
reduces symptoms of HF decrease workload

narrows therapeuDc index à

monitor serum level (N=0.5
2mg/ml)

Effects:
+ inotropic effects; -
chronotropic effect; increases
CO and renal perfusion.

SE:
Halo and visual disturbance
which is the hallmark of
digoxin toxicity, dysrhythmias
can be bradycardia or
irregular pulse.

An;dote:
Digoxin immune Fab
(DigiBIND)

Digoxin toxicity:
it can be serious, there is
increase in hypoK+, hypoMg2,
hyperCa2+

serum level > 10ng/mL with

K+ >5mEq/L
Cute si dims J

N/V, malaise, diarrhea,

depression

arrhythmia (Ca+ overload)

Beta-1 Agonist: Dobutamine Nitroprusside nitrates: Spironolactone
Hydralazine
It is IV drugs only. Nesiri;de
Used in ICU/CCU Pharmacodynamics:
No appropriate for chronic HF
Possible tolerance to the Dilates BV à decrease
medicaDon can occuer preload à decrease workload
à improved cardiac funcDon
à decrease aYerload à
decrease workload
Phosphodiesterase inhibitors: Milrinone Ace inhibitors

Pharmacodynamics: Pharmacodynamics:
Blocks the enzyme phosphodiesterase à increase cAMP à Blocks ACE à no A2 à
increase Ca+ levels à increase contracDlity à inotropy vasodilaDon

ARB

Beta blockers

Gastrointes6nal system
o Basic concepts:
§ Mucus – coats the lining.
§ Bicarbonate – neutralizes the gastric acid.
§ Adequate blood flow – nourishes the mucosa.
§ Prostaglandins – sDmulate mucus and bicarbonate secreDon.
§ Ulcer – an erosion in the mucosal lining
o Pep;c ulcer disease
§ Causes: Heliobacter pylori (H. pylori)
• Gran negaDve bacillus
• Hides in between mucus and epithelial cells
• Most common cause of PUD
§ NSAIDs – it blocks the prostaglandin in the stomach which decreases the
mucus and bicarbonate which are both the protector of the stomach it
gives chances for hydrochloric acid to increase.
• Inhibit prostaglandins:
o Mefenamic acid
o Ibuprofen
o Naproxen
Cute si dims J

§ Gastric acid (hydrochloric acid) – it injures the mucosa cells and acDvates
the pepsin when there is pepsin then there is H.acid.
§ Smoking and alcohol
• Increases gastric acid.
• Increases bicarbonate producDon.
• It delays healing.
o Drugs affec;ng gastric secre;ons.
§ Drugs for PUD, GERD, and GastriDs
• Antacid
• H2 receptor blockers
• Proton pump inhibitors
• GI protec;ves
o Sucralfate
• Prostaglandins
o Misoprostol
o Management for H. pylori
§ Use of minimum of 2 anDbioDcs
• Clarithromycin
• Amoxicillin
• Tetracycline
• Metronidazole
§ PUD drugs
• Bismuth subsalicylate
• PPI
• H2 blockers
o Management of PUD
§ Heliobacter pylori
• An;bio;c
§ NSAIDs
• Limit use
• Consider misoprostol
§ Gastric acid
• H2 receptor antagonist
• PPI
• Mucosal protectants
• Antacids
§ Smoking
• Encourage to stop
o Antacids
§ It neutralizes the producDon of hydrochloric acid.
§ InacDvate pepsin.
§ Enhance mucosal protecDon.
§ Dose: 1 tab PC and HS for 6 months
Cute si dims J

§ 1-2 hours pc (ager meals) and hs (hours of sleep) for 6 months

• 4 Dmes a day for 6 months to cure the PUD
§ Drug involved
• Aluminum hydroxide
o SE: consDpaDon
• Magnesium hydroxide
o SE: diarrhea
• Mafaldrate
§ Tabs: should be chewed thoroughly with glass of H2O
§ Susp: shake
§ Allow 1 h between antacid administraDon and other meds to prevent
interacDons.
§ Common SE: rebound acidity
o Histamine 2 antagonist
§ Blocks histamine 2 receptors in the stomach lining (parietal cells)
§ It suppresses the gastric acid secDons; therefore, it stops the producDon of
the hydrochloric acid.
§ Dose: 1 tab BID x 2 months
§ OTC medica;ons:
• Cime;dine – gynecomasDa
• Rani;dine
• Famo;dine
• Niza;dine
o Proton pump inhibitors
§ It blocks the proton pump and suppress the gastric acid secreDons.
§ MOST EFFECTIVE and COST EFFECTIVE
§ It uses:
• PUD
• Erosive esophagiDs
§ OTC medica;ons
• Omeprazole
• Lansoprazole
§ Dose: 1 tab OD x 14 days
o Sucralfate
§ SDcky gel coaDng the ulcer.
§ ProtecDve barrier against pepsin and gastric acid
§ Small risk for consDpaDon
§ It should take before meals (AC)
o Misoprostol (prostaglandins agonist or cycotec)
§ Acts as a replacement for endogenous PG.
• Increase mucus and bicarbonate.
§ Prophylaxis against PUD due to NSAIDs and ASA
§ Contraindicated in pregnancy.
Cute si dims J

• aborDfacient
• Cervical dilaDon

Endocrine system
• Drugs for endocrine
o Diabetes mellitus
§ A metabolic disorder where there is hyperglycemia due to either absence
or deficiency of insulin (facilitates transport of glucose, K+, Mg+ into cell)
§ Types of DM:
• DM I – no insulin
o Mgt: insulin
• DM II – insufficient insulin; insulin receptor resistance
o Mgt: OHA or oral hypoglycemic agent, paAent can shig to
insulin if OHA has insufficient effect.
• Gesta;onal DM – insulin receptor resistance it is because of the
HPL or human placental lactogen produced by the placenta which
makes it resistant to insulin.
o Mgt: insulin à then ager pregnancy go back to OHA
§ Oral Hypoglycemic agents (OHA)
• Goal: decrease the blood glucose level
• Pharmacodynamics:
o Liver – producing glucose.
o Pancreas – producing insulin.
o Muscles – uptake of glucose through using of muscles as it
uses glucose in order for it to funcAon.
o Stomach – absorpDon of glucose
• Drug involved:
o Sulfonylureas – more insulin producDon
o Megli;nides – more insulin secreDons
o Thiazolidinediones (glitazones) – decrease hepaDc glucose
producDon.
o Biguanides (METFORMIN) – suppress hepaDc producDon of
glucose and increases insulin sensiDvity.
§ Commonly the 1st type of drug prescribed for new
type 2 diabetes mellitus
§ Lifestyle medicaDon + mehormin now used.
§ Pre-diabeDcs
§ Monotherapy or in combinaDon with other
medicaDon if needed
§ SE: weight loss
§ Lac;c acid with mehormin
1. CimeDdine + mewormin
2. Alcohol + mewormin
Cute si dims J

3. Iodine based radiocontrast dye + mewormin.

§ Considera;ons
1. DisconDnue mewormin 1-2 days before the
test and for 48 hours aYerwards.
2. Do not restart unless kidney funcDon is at
paDent baseline
§ Early signs of lacDc acidosis
1. Unusual sleepiness or drowsiness
2. HypervenDlaDon
3. Myalgia
o Alpha-glucosidase inhibitors – delay absorpDon of ingested
CHO
Type Example Onset Peak of Dura;on
hypoglycemia
Rapid ac;ng Log rolls rapidly
1. Lispro
(Humalog) 15 mins 1 hour 3 hours
2. Aspart
(Novalog)
Short ac;ng Clear
1. Humulin R 30 mins 2 hours 8 hours
2. Novolin R
Intermediate Cloudy
1. NPH
(neutral
pH 2 hours 8 hours 16 hours
protamine
Hagedorn)
Long ac;ng 1. Glargine
(lantus) 2 hours No peak 24 hours
2. Detamir
(levamir)

o Key points of insulin

§ Rotate sites to prevent lipodystrophy (scar Dssue)
§ Adverse effect: hypoglycemia which includes tachycardia, diaphoresis, shakiness,
headache, and weakness.
§ May need extra doses of insulin during illness or stress.
§ Do not skip doses of insulin.
§ Hypoglycemia: 15g of FAC (4oz orange juice, 8 oz milk, regular soda)
§ Mixing: draw up from clear
• Inject into cloudy, remove needle, inject air into clear, draw up clear,
draw up cloudy.
• RN: regular first, then NPH
Cute si dims J

§ AdministraDon:
• suspension = gently rotate vial
• if short acDng looks cloudy/discolored à dispose
o hypoglycemia
§ glucagon
• sDmulates glycogenolysis in the liver.
• use: hypoglycemia in insulin induced semiconscious or
unconscious.
• Site: SQ, IM, or IV
• Onset: 5 to 20 minutes
• Thyroid hormones
o Func;ons:
§ Control metabolic rate of Dssues
§ Accelerate heat producDon.
§ Accelerate oxygen consumpDon.
§ Development of secondary sexual characterisDc
§ Brain development
§ Growth
o Pharmacodynamics:
§ Iodine (DIET) à trapped in thyroid gland à binds with protein
(thyroglobulin – tyrosine) à organificaAon/iodinizaAon à
monoiodotyrosine (MIT) à coupling à …
• MIT + MIT = DIT
• MIT + DIT = T3
• DIT + DIT = T4
o Drugs for hyperthyroidism
§ Thioamides – blocks producDon of thyroid hormone
• Drug involved
o Propylthiouracil (PTU)
- Blocks conversion of T4 to T3
- Oral administraDon peak in 1 h
- Biaer taste
- Euthyroid status may take up to 1 month.
- Given every 8-12 hours.
- Nursing intervenDon
1. Take on an empty stomach.
2. BedDme dosing as effecDve as AM dosing
3. Pregnancy
a. Increase dose
b. 9 doses/week
c. Recheck labs every 6 weeks
4. Breasweeding
a. Not secreted in breastmilk
Cute si dims J

b. No adverse events in children

5. Ischemic heart disease
a. Start at half dose
o Methimazole
- Blocks producDon of thyroid hormones
- Adverse Effect: agranulocytosis and
thrombocytopenia
- Nursing care:
1. avoid in pregnancy
a. choanal atresia
b. aplasia cuDs congenta
c. prenatal goiter
§ Iodide salts
• Lugol solu;on – inhibits iodinaDon of tyrosine also thyroid release;
decrease vascularity of thyroid rapid onset (2-7 days).
o SE: rash, drug fever, anaphylaxis, metallic taste, and
bleeding disorder
• 131 I – destroy thyroid gland permanently.
o Nursing consideraDon: need thyroid hormone replacement
to prevent hypothyroidism.
o DefiniDve treatment for hyperthyroidism
§ Graves disease
§ MulDnodular goiter
o Route: oral
o SE: inferDlity and thyroidiDs
• An;microbials
o An;microbials classifica;on according to site of ac;on
§ Block cell wall synthesis
1. Beta lactams
a. Penicillins
b. Cephalosporins
c. Carbapenems
d. Monobactam
2. Glycopep;des
a. Vancomycin
§ Block protein synthesis
1. Macrolides
2. Chloramphenicol
3. Lincosamines
4. Aminoglycosides
5. Tetracycline
§ Folic acid synthesis inhibitor
1. Sulfonamides
2. Trimethoprim
Cute si dims J

§ Nucleic acid synthesis inhibitor

1. Fluoroquinolones
o Basic concept:
§ Bacteria cell wall
• Overall strength of the cell
• Growth
• ReproducDon
• Obtaining nutriDon
• ProtecDon
o Bacterial cell wall synthesis inhibitor
§ Beta lactams
• Penicillin: “cillins”
- Known as miracle drug
- G (+) and G (-) bacteria
- Bactericidal
- Resistant develops due to indiscriminate use
- Drug involved:
1. Penicillin
a. Penicillin V
b. Penicillin G
2. Extended-spectrum penicillins
a. Carbenicillin
b. Piperacillin – tazobactam
3. Penicillinase resistant PCN
a. Nafcillin
b. Oxacillin
4. Beta-lactamase inhibitors
a. Amoxicillin – clavulanic acid
b. Ampicillin – sulbactam
• Penicillinase – enzyme produced by bacteria and destroy internal
structure of PCN; no effect.
• Beta-lactamase – enzyme produced by bacteria; breaks open the
beta-lactam ring; inacDvates beta lactams
o Side effects / adverse effects:
§ Most commonly cause of medicaDon allergy
§ HypersensiDvity such as
1. Hives
2. Rash
3. Itching
4. Angioedema
5. Anaphylaxis
o Nursing care:
§ ST
Cute si dims J

§ When the paDent shows sign of an allergic reacDon,

take immediate acDon is to STOP!
§ AlternaDves:
1. Erythromycin
2. Vancomycin
3. Clindamycin
§ Glycopep;de
• Vancomycin
- NO BL RING ANTIBIOTIC
- Bactericidal this directly kills the bacteria itself
- G (+)
- IndicaDon
1. MRSA
2. AlternaDve to PCN allergy
3. Pseudomembranous coliDs
- Route: slow IV
- Adverse effect: Red man syndrome caused by fast
administraAon and toxic effect.
o Protein synthesis inhibitor
§ Protein is vital for bacterial cell replicaDon à growth
§ If bacteria cant synthesize protein no growth will occur and it’ll cause cell
death.
§ Macrolides
• Erythromycin
- 1st macrolide from funguslike bacteria
- Drug of choice is mycoplasma pneumonia.
- AlternaDve PCN allergy
• Azithromycin
- Eliminated slowly
- Give 3 days but lasts for 10 days
- Taken before meals
• Clarithromycin
§ Lincosamines
• Bactericidal and bacteriostaDc
• Gram (+) and anaerobic
• Clindamycin
§ Chloramphenicol
• Broad spectrum
• Used to treat serious infecDons.
• Used in eye infecDons and typhoid fever
• Side effects:
1. Gray baby syndrome – in intravenous use of chloramphenicol
Cute si dims J

2. This causes several adverse effects including hypotension and

cyanosis.
§ Aminoglycosides – “mycin” / “cin”
• Streptomycin – anA tb drug and its side effect is ototoxicity
• Kanamycin
• Neomycin – used in cirrhosis to prevent hepaAc encephalopathy
• Gentamycin – its side effects is nephrotoxic
§ Tetracyclines
• Indicated:
1. H. pylori in PUD
2. Acne vulgaris, oral, and topical preparaDon
3. Chlamydial infecDons
• Adverse effects
1. Staining of teeth
2. GI symptoms
3. Fetal exposure: dental enamel dysplasia
4. Hepatotoxicity
5. Dizziness, verDgo à doxycycline and minocycline
• Tetracyclines
• Doxycycline’s – drug of choice for prevenAon and treatment of
leptospirosis
• Demeclocyclines – has a diureAc effect and used in SIADH
o Folic acid synthesis inhibitors
§ Sulfasalazine
§ Sulfamethoxazole
§ Trimethoprim
o Nucleic acid synthesis inhibitors
§ Fluoroquinolones – “oxacin”
- Broad spectrum
- Bactericidal against g (-) and some g (+)
- Respiratory and urinary infecDon
- Drug involved:
1. Ciprofloxacin
2. Ofloxacin
3. Rifampicin
Cute si dims J