Professional Documents
Culture Documents
drugs
Week 2
DRUGS - a synthetic chemicals obtained from
Cornerstone – drug discovery process plants, animals, or product of genetic engineering
3. clinicians - doctors/physicians , experts Otzi – (copper age) carried fungus for medical purposes
Pharmacology – science of drugs HIPPOCRATES – Father of medicine
Greek word: pharmakon /pharmacos - drug/spell/poison was the first to attempt to separate the
logia - study/knowledge practice of medicine from religion and
superstition
-experimental science which has for its purpose the study Babylonia – prescription was written in clay tablets
of changes brought about in living organisms by chemically
acting substance (w/ the exception of food) whether used EGYPTIAN – Erb’s papyrus written document for herbal
for therapeutic purpose or not meds 1500 bc
Chinese - Pen Psao – Great herbal
effect exert Materia medica - 40 vol of plant remedies
MAIN FXN OF PHARMA: 17th century – Nicholas Culpeper translated and use
1. Screening for desired activity pharmacological texts
2. Determining the modes of action plants and disease they could treat
th
18 century – clinical pharmacology
3. Quantifying drug activity when clinical methods
are not available
drugs in humans and their optimal use in
patient
Ex : Amoxicillin – MATERIA MEDICA – first recorded reference to the world
of pharmacology
1. cure for strep throat
book containing information about pharmacy,
2. inhibits the synthesis of cell wall mucopeptide by the
pharmacognosy (concerned w/medical drugs
bacteria that cause infection
obtained from plants), posology and used of
3. measures the desirability drugs
Fredrich Serturner – first isolated morphine from opium
Pharmacy – is the study of drugs, its origin, chemical and injected himself and 3 other friends
structure, preparation, administration, action, metabolism
and excretion 18TH – 19TH CENTURY
THERAPEUTIC WINDOW
• Range based on the minimum effective
therapeutic concentration and the minimum toxic
concentration for a specific toxic effect
EX : Theophylline
Minimum therapeutic concentration is 8mg/L
therapeutic window is at 8-18mg/L
Toxic effect observed at 18mg/L LIBERATION
EX: Lithium is the first step in the process by which medication
enters the body and liberates the active ingredient
Minimum therapeutic concentration is 0.8 mmol/L
that has been administered
therapeutic window is at 0.8-1.2 mmol/L
The release of the drug from its dosage form
Toxic effect observed 1.2 mmol/L
2 phases:
TOLERANCE – decrease responsiveness to a drug over the
course of therapy Disintegration – breakdown into smaller parts
PLACEBO EFFECT – drug response not attributed to Pharmaceutic / Dissolution – amount of drug substance
chemical properties of drugs that goes into solution/ further breakdown into smaller
part in the GI
can be +/- and may be influence by
beliefs, attitudes and expectations Immediate – the medicine is formulated to release
the medicinal drug w/o delay
• ONSET – time it takes to reach the minimum
Delayed – the medicine is formulated to release
effective concentration (MEC) after the
sometime after it is taken
administration of drugs
Extended – the drug is formulated to make the
• PEAK – when the drug reaches the plasma drug available over an extended period allowing a
concentration / highest blood concentration reduction in dosing frequency compared to
immediate or delay.
Absorption Therefore higher drug dosage must be
administered to achieved the desired effect.
the process by which the drug is transferred
3. More blood, more absorption – increase blood
flow improves drug absorption. Reduced blood
flow decrease drug absorption. EX: gluteal
muscle can accommodate a larger volume of drug
than deltoid muscle but blood flows faster
through deltoid muscle that’s why the muscle
area selected for IM administration is the deltoid
1. PASSIVE TRANSPORT – process in which drugs Is the process by which the drug leaves the bloodstream
cross cell membranes. Exception are drugs and enters the instertitium or the cell of the tissue
administered IV or inhaler (asthma drugs) requires
Distribution is affected by following factors
no energy
1. Blood flow
2. ACTIVE TRANSPORT – when drugs move against a
concentration slope. It requires energy in the form 2. Capillary permeability
of ATP .
3. Binding of drugs to the protein
ex: ions, vitamins , sugars and amino acids that need to
be absorb in the small intestine 4. Lipid fat solubility
1. Facilitated Diffusion - it helps larger , water • After a drug has reached the bloodstream, its
soluble and polar medications moves across the distribution in the body depends on the blood
membrane through transport protein like carriers flow. The drug is distributed quickly to those
organs with a large supply of blood, including
2. Passive Diffusion – which helps small lipid soluble heart, liver and kidneys. Distribution to other
and non-polar medication moves across the internal organs, skin, fat and muscle is slower.
membrane from higher to lower concentration
Absorption occurs at slower rates when drug is BREACHING THE BARRIER
administered by the oral, IM, or subcutaneous • The ability of the drug to cross the cell membrane
routes because the complex membrane systems depends on whether the drug is water or lipid
of GI mucosal layers, muscle and skin delay drug soluble. Lipid soluble drugs easily cross cell
passage membranes, it can also cross the blood-brain
Sublingual, IV or inhaled drugs are usually barrier and enter the brain. Water soluble can’t.
absorbed much faster
Example of FACTORS THAT AFFECT ABSORPTION: IN A BIND
1. Intestinal interference – most absorption of • As a drug travels through the body, it comes in
oral drugs occurs in small Intestine. If a patient contact with proteins, such as plasma protein
has had large sections of small intestine surgically albumin. The portion of drug that’s bound to
removed, drug absorption decrease because of protein is inactive and can’t exert therapeutic
the reduced surface area effect. Only those that are free or unbound
portion remain active.
2. Liver lowered levels- drugs absorbed by the
small intestine are transported to the liver before
being circulated to the body (FIRST- PAST
EFFECT). Liver metabolism may inactivate the
drug; if so, the first pass effect lowers the amount
of active drug released into systemic circulation.
I. MODIFICATION - drugs are modified by means of
oxidation, reduction to be more excretable
II. CONJUGATION- those insufficiently polar
molecules may then pass to phase II in which it
will be conjugated by glutathione, sulfates and
glycerin groups
III. EXCRETION – metabolized further to aid their
transport
IV. Drug half-life is the time it takes for the amount of
drug in the body to be reduced by half.
Example:
4 major compartments: BLOOD PLASMA/
FAT/EXTRACELLULARFLUID/INTRACELLULAR Ibuprofen has a half life of about 2 hours.
if the patient takes 200 mg, in 2 hours, 50% of the drug will
be gone, leaving 100 mg.
after 2 hours - 50 mg.
after 2 hours – 25 mg
after 2 hours – 12.5 mg
after 2 hours – 6.25 mg
ex: Ethanol – that’s why it is used to measure Eg: Nursing admission assessment
concentration in breath of vehicle drivers 2. Problem-focused assessment : To
Application of nursing process determine the status of a specific problem identified in an
Nursing process is a critical thinking process that earlier assessment.
professional nurses use to apply the best available Eg: hourly checking of vital signs of fever patient
evidence to caregiving and promoting human functions
and responses to health and illness (American Nurses 3. Emergency assessment: During emergency
Association, 2010). situation to identify any life threatening situation.
Eg: Rapid assessment of an individual's airway, breathing
Purposes of nursing process status, and circulation during a cardiac arrest.
• To identify a client's health status and actual or potential 4. Time-lapsed reassessment: Several months after
health care problems or needs. initial assessment. To compare the client's current
To establish plans to meet the identified needs. health status with the data previously obtained.
Types of Data
• To deliver specific nursing interventions to meet those
needs. Two types: subjective data and objective data.
1. Subjective data, also referred to as symptoms or covert
data, are clear only to the person affected and can be
described only by that person.
Itching, pain, and feelings of worry are examples of
subjective data.
2. Objective data, also referred to as signs or overt data,
are detectable by an observer or can be measured or
tested against an accepted standard. They can be seen,
heard, felt, or smelled, and they are obtained by
observation or physical examination.
For example, a discoloration of the skin or a blood
Assessment pressure reading is objective data.
collecting data Sources of Data
organize data Sources of data are primary or secondary.
validate data 1. Primary : It is the direct source of information. The
client is the primary source of data.
document data
2. Secondary: It is the indirect source of information. All
sources other than the client are considered secondary
sources. Family members, health professionals, records
and reports, laboratory and diagnostic results are
secondary sources.
Example:
Nurse Kim is knowledgeable about volume excess
or fluid overload. She knows that findings
associated with this include cough, dyspnea,
crackles, tachypnea, tachycardia and elevated BP. Potential Errors in Choosing a Nursing Diagnosis
The nurse knows that which of the following Formulation of nursing diagnosis
clients has the lowest risk of obesity and Diabetes
A client reports discomfort at the insertion site of
Mellitus
an IV catheter, area is slightly reddened
Diagnosis The nurse formulates a nursing diagnosis ie
Discomfort.
Analyzing data But fail to consider the Risk for infection.
Identifying health problems, risk and strengths Don't use medical terms in nursing diagnosis
This is the nurse’s clinical •Self care deficit,Hygiene related to weakness secondary
to Stroke
Judgement about client’s experience
Errors in Choosing a Nursing Diagnosis
To health problem
Don't combine two problems at the same time
At low doses - B2 effects (vasodilation) on the vascular Also called sympathomimetic, are drugs that mimic the
system predominate, At high doses - al effects effects of the SNS and are used to stimulate the adrenergic
(vasoconstriction) are strongest. receptors within the SNS. The adverse effects associated
with these drugs are usually also a result of sympathetic
Actions stimulation.
1. Cardiovascular – Adrenergic agonists include;
Strengthens the contractility of the myocardium (positive 1. alpha- and beta-adrenergic agonists - which
inotropic: B1 action) and increases its rate of contraction stimulate both types of adrenergic receptors in
(positive chronotropic: ẞ 1 action). the SNS
Activates ẞ 1receptors on the kidney to cause renin 2. alpha-specific adrenergic agonists - stimulate
release. only alpha receptors
Constricts arterioles in the skin, mucous membranes, and 3. beta-specific adrenergic agonists - stimulate only
viscera (al effects), and it dilates vessels going to the liver beta-receptors
and skeletal muscle (B 2 effects).
CENTRAL ACTING ALPHA AGONIST (alpha 2 adrenergic)
Cumulative effect is an increase in systolic blood pressure
& slight decrease in diastolic pressure. Central-acting agents lower your heart rate and reduce
your blood pressure.
Therapeutic uses
Anaphylactic shock :
Blocks the signals from the brain to the nervous system
Intramuscular - 1: 1000 that speed up your heart and narrow your veins and
Subcutaneous - 1: 1000 arteries
Intravenous - 1:10000
As a result, heart doesn't pump as hard and your blood Dopamine
flows more easily through your blood vessels.
Immediate precursor of norepinephrine &
epinephrine
Endogenous dopamine may have more
important effects in regulating sodium
excretion and renal function.
Features distinguishing from norepinehrine &
epinephrine
- 8 2-5 µg/kg/min - D1 receptors - renal
vasodilation
- 3 5-10 µg/kg /min - ẞ1 receptors - ↑
cardiac output
- >10 µg/kg/min -a 1 receptors –
vasoconstriction
• Drug that blocks the effects of adrenergic Dopamine contd..
neurotransmitter Its deficiency in the basal ganglia leads to
• Mostly block the Alpha and Beta receptors Parkinson's disease, which is treated with its
precursor levodopa.
They block in 2 ways: Dopamine antagonists are antipsychotic drugs.
Therapeutic uses - used in conditions with low
1. By occupying the receptor
cardiac output with compromised renal function
2. By inhibiting the release of neurotransmitter Iv infusion regulated by monitoring of BP & rate of
norepinephrine and epinephrine urine formation.
Mixed-Acting Sympathomimetics
Why do we need to block adrenergic neurotransmitter?
Ephedrine
plays a major role in the regulation of arterial pressure.
Activation of these nerves to the heart The plant Ephedra vulgaris, has been used in
traditional Chinese medicine for 2,000 years for
1. increases the heart rate (positive chronotropy) the treatment of asthma and hay fever, as well as
2.contractility (positive inotropy) for the common cold
Ephedrine is a noncatechol,it has high
3. velocity of electrical impulse conduction (positive bioavailability and a relatively long duration.
dromotropy). It releases NE and activates ẞ2 receptors directly.
Crossess BBB, it is a powerful stimulant.
2 classification of adrenergic antagonist
Nowadays only used to treat hypotension with
spinal anaesthesia
Repeated dosing – tachyphylaxis
Norepinephrine
A hormone secreted by certain nerve endings of the
Sympathetic nervous system.
Released in response to stress, classified as a neuro
transmitter that is released from neurons
Side effects
Difficulty in breathing
Swelling of face (lips, tongue, or throat)
ALPHA-and-BETA ADRENERGIC AGONISTS • ALPHA-SPECIFIC ADRENERGIC AGONISTS
Epinephrine Alpha-1 specific Adrenergic Agonists:
Dopamine
Ephedrine Phenylephrine
Norepinephrine Midodrine
• Alpha-2 specific Adrenergic Agonists:
Clonidine
Methyldopa
• BETA-SPECIFIC ADRENERGIC AGONISTS : ( Beta1
and Beta2 )
ü Isoproterenol ü Albuterolü Arformoterolü Indacaterolü
Levalbuterolü Metaproterenolü Olodaterolü Salmeterol
• Beta-1 specific adrenergic agonists
ü Dobutamine INTRODUCTION TO DEPRESSION
• Beta-2 specific adrenergic agonists 1. Anxiety is an emotional state commonly caused by the
perception of real or danger that threatens the security of
ü Terbutaline
an individual.
ü Isoxsuprine
2.It allows a person to prepare for or react to
Alpha 1 specific adrenergic environmental changes.
3. Anxiety can produce uncomfortable nature.
The Symptoms of Anxiety
1. Sweating 5. GI Discomfort
2. Shaking 6. Lack Of Sleep
3. Palpitation 7. Lack Of Concentration
4. Blushing 8. Irritation
TYPES OF ANXIETY
• Panic Disorder-unreasonable fear spreading for
ALBUTEROL SULFATE
10-20min
• Beta, adrenergic agonist, is selective for beta2- • Generalized Anxiety Disorder-experienced when
adrenergic receptors , its response is relaxation of person thinking about no. of events
bronchial smooth muscle and bronchodilation • Social Anxiety Disorder-means fear about
interaction with social programs.
• Activates only the B2 receptor of smooth muscle • Obsessive Compulsive Disorder-repeated
in the lungs experience of specific image or thoughts.
• High dose : increase heart rate
• Half life : via oral inhalations 2.7 to 6 hours
DRUG INTERACTION:
1. Albuterol + MAOI = hypertensive crisis
2. Beta agonist (beta blockers) + albuterol = hinders/inhibit
the action of albuterol
SE: Tremors, restlessness, nervousness
• In 1977 benzodiazepines were globally the most
prescribed medications.
• They are in the family of drugs commonly known
as minor tranquilizers.
• resulting in sedative, hypnotic (sleep-inducing),
anxiolytic (anti-anxiety), anticonvulsant, and
muscle relaxant properties. High doses of many
shorter-acting benzodiazepines may also cause
anterograde amnesia and dissociation.
SEDATIVE/HYPNOTICS ANXIOLYTICS Non – Benzodiazepines
• Major therapeutic use is to relief anxiety EX: Paraldehyde, Meprobamate, Chloral hydrate,
(anxiolytics) or induce sleep (hypnotics). Zolpidem, Diphenhydramine
• Hypnotic effects can be achieved with most
anxiolytic drugs just by increasing the dose. • The first three nonbenzodiazepine drugs to enter
• The distinction between a "pathological" and the market were the "Z-drugs", zopiclone,
"normal" state of anxiety is hard to draw, but in zolpidem and zaleplon. These three drugs are all
spite of, or despite of, this diagnostic vagueness, sedatives used exclusively for the treatment of
anxiolytics are among the most prescribed mild insomnia. They are safer than the older
substances worldwide. barbiturates especially in overdosage and they
BARBITURATES may, when compared to the benzodiazepines,
have less of a tendency to induce physical
• Barbiturates is a sedative-hypnotics, a type of dependence and addiction, although these issues
central nervous system (CNS) depressant used to can still become a problem. This has led to the Z-
treat insomnia, seizures, and headaches. drugs becoming widely prescribed for the
• Available under the following different brand treatment of insomnia particularly in elderly
names: amobarbital (Amytal), secobarbital patients Non-benzodiazepines generally cause less
(Seconal), butabarbital (Butisol), pentobarbital disruption of normal sleep architecture than
(Nembutal), belladonna and phenobarbital benzodiazepines. Psychomotor and memory
(Donnatal), butalbital/acetaminophen/caffeine. impairment may be less problematic with non-
benzodiazepines, especially when compared to
• Barbiturates are classified as Schedule II longer-acting benzodiazepines..
substances, meaning they have definite potential
for physical and psychological dependence and NURSING CONSIDERATIONS
abuse. Barbiturates may be habit-forming. Avoid abrupt discontinuation after prolonged use
Tolerance, psychological dependence, and
physical dependence may occur especially Not given if BP is elevated, with renal and hepatic
following prolonged use of high doses of condition, with history of drug abuse
barbiturates.
Xanax(Alprazolam),Ativan(Lorazepam), Serax (Oxazepam)-
BENZODIAZEPINES brand names
• enhance GABA effect to cause inhibition of Increase in 3D’s – Drowsiness, dizziness, decrease in BP
impulse transmission.
Enhance action of GABA
Examples: Diazepam, Lorazepam, Clonazepam
Teach to rise slowly from supine
• are a class of psychoactive drugs whose core
Yes , Alcohol and caffeine should be avoided
chemical structure is the fusion of a benzene ring
and a diazepine ring. The first such drug, Antipsychotic drugs
chlordiazepoxide (Librium), was discovered
accidentally by Leo Sternbach in 1955, and made Antipsychotic drugs (also called neuroleptics or
available in 1960 by Hoffmann–La Roche, which, major tranquilizers) are used primarily to treat
since 1963, has also marketed the benzodiazepine schizophrenia (a biologic illness), but they are also
diazepam (Valium). effective in other psychotic states, including manic
states with psychotic symptoms such as
grandiosity, paranoia, and hallucinations, and Phenothiazines
delusions. • Aliphatic side chain: Chlorpromazine,
Antipsychotic drugs are not curative and do not triflupromazine
eliminate the chronic thought disorder, but they • Piperidine side chain: Thioridazine
often decrease the intensity of hallucinations and • Piperazine side chain: Trifluoperazine,
delusions and permit the person with fluphenazine
schizophrenia to function in a supportive Butyrophenones: Haloperidol, Trifluperidol,
environment. Penfluridol
History of antipsychotic drugs Thioxanthenes: Flupenthixol
Other heterocyclics: Pimozide, Loxapine
Antipsychotic drugs have been used in Western
Atypical antipsychotics: Clozapine, risperidone,
medicine for more than 50 years.
olanzapine, quetiapine, aripiprazole, ziprasidone
Chlorpromazine (1952) and Reserpine were the
PHARMACOTHERAPY FOR MENTAL ILLNESS
first drugs found to be useful in schizophrenia.
Tricyclic and MOA inhibitor antidepressant in First-generation antipsychotics
1957-58.
Major novel antipsychotics are selective serotonin • The first-generation antipsychotic drugs (also
reuptake inhibitor and it has been introduced in called conventional, typical, traditional
1980s. antipsychotics) are or competitive inhibitors at a
Little attention was paid to Cade's report in 1949 variety of receptors, but their antipsychotic effects
that Lithium could be used for excitement and reflect competitive blocking of D2 dopamine
mania: its effective use started in the 1960s and receptors.
now it has a unique place in psychiatry. • First-generation antipsychotics are more likely to
Classification of antipsychotic drugs be associated with movement disorders,
particularly for drugs that bind tightly to
PHARMACOLOGICAL CLASSIFICATION dopaminergic neuroreceptors, such as
haloperidol.
FIRST-GENERATION ANTIPSYCHOTIC (low potency) Pharmacotherapy of metal illness
• Chlorpromazine, Prochlorperazine, Thioridazine Second-generation antipsychotic drugs
FIRST-GENERATION ANTIPSYCHOTIC (high potency) • The second generation antipsychotic drugs (also
Fluphenazine, Haloperidol, Pimozide, Thiothixene referred to as "atypical" antipsychotics) have
fewer extrapyramidal symptoms (EPS) than the
SECOND GENERATION ANTIPSYCHOTIC first-generation agents, but are associated with a
higher risk of metabolic side effects, such as
Aripiprazole, Asenapin, Clozapine, Iloperidone
diabetes, hypercholesterolemia, and weight gain.
• Lurasidone, Olanzapine, Quetiapine, Paliperidone, • The second-generation drugs appear to owe their
Risperidone, Ziprasidone unique activity to blockade of both serotonin and
dopamine receptors.
CLASSIFICATION OF ANTIPSYCHOTIC DRUGS
Typical antipsychotics
Phenothiazines
• e.g. chlorpromazine, fluphenazine,
thioridazine
Butyrophenones
• e.g. haloperidol, droperidol
Thioxanthines
• e.g. chlorprotixen, thiothixene
atypical Antipsychotics
• Chozapine, Risperidone, sulpiride,
sertindole, Seroquel, olanzapine,
quetiapine
Classification of antipsychotic drugs
CHEMICAL CLASSIFICATION
b. cholinergic drugs should be administered to
prevent further complications associated with the
crisis
c. the clinical condition of the client usually improves
after several days of treatment
d. loss of body function creates high levels of
anxiety and fear
3. A client with myasthenia gravis reports the occurrence
of difficulty chewing. The physician prescribes
pyridostigmine bromide (Mestinon) to increase muscle
strength for this activity. The nurse instructs the client to
take the medication at what time, in relation to meals?
a. after dinner daily when most fatigued
b. before breakfast daily
c. as soon as arising in the morning
d. thirty minutes before each meal
2. Akinesia – loss of voluntary muscle movement a. It increases the discharge of noradrenergic neurons
1. Anticholinergic agents achieve their effect in c. Expected because therapeutic effectiveness takes
treating Parkinson’s disease by antagonizing which 2-4 weeks
nervous system? a. Autonomic b. Peripheral c.
d. Ineffective result because perhaps the drug's
Parasympathetic d. Sympathetic
dosage is inadequate
2. Myasthenia crisis and cholinergic crisis are the
6. A client who has been receiving amitriptyline (Elavil) for
major complications of myasthenia gravis. Which
1 week reports not having a bowel movement for 5 days.
of the following is essential nursing knowledge
The nurse would interpret this in which of the following
when caring for a client in crisis?
ways?
a. weakness and paralysis of the muscles for
a. The client is demonstrating somatic
swallowing and breathing occur in either crisis
preoccupations associated with depression
b. The client is experiencing memory loss associated The impulse is spread to A.V at this time we get
with TCA therapy “PR” interval on ECG paper.
c. The client may be constipated due to the Then impulse spread to Bundle of His, Bundle
anticholinergic effects of TCAs Branches & Purkinji fibers through AV node & both
ventricles start to depolarize & we can get a waves
d. The client would be more likely to be complex on ECG paper which is known as “QRS” complex.
experiencing diarrhea as a side effect
Then the both ventricles start to repolarize & in
7. The client is started on chlorpromazine (Thorazine) 200 early stage we can get “ST” segment & later “T” wave on
mg PO q.i.d. The client should be assessed for which of the graphic paper.
following high-incidence side effects?
Anti-hypertensive drugs
a. dry mouth, constipation and blurred vision c.
cogwheel rigidity and drooling IDIOPATHIC /ESSENTIAL/PRIMARY HYPERTENSION
b. severe agranulocytosis > 90 % , 15 – 40 YRS
c. increased anxiety Genetic inheritance
d. c. cogwheel rigidity and drooling SECONDARY HYPERTENSION
CARDIOVASCULAR Renal artery disease
Pheochromocytoma
Renal parenchymal disease
Toxemia of pregnancy
OTHER BETA BLOCKERS
1. NADOLOL non selective beta receptor /
blocks B1& B2 receptor site
2. CARTEOLOL
3. BISOPROLOL - B1 selective blocker
4. PINDOLOL , ACEBUTOLOL – a partial agonist beta
blocker w/ some intrinsic sympathomimetic
Inherent rate activity. This drugs a particularly beneficial for
patients w/ bradyarrythmias or peripheral
SA NODE 60-100 BPM vascular disease
AV NODE 40-60 BPM
BUNDLE OF HIS 40-60 BPM PRECAUTIONS: not given to patients w/ Heart block, Brady
LEFT AND RIGHT BUNDLE cardia, CHF, COPD
BRANCHES 20-40 BPM SE: Bradycardia, Hypotension, Rebound hypertension ( be
PURKINJE FIBERS 20-40 BPM cautious when abruptly stopped)
ELECTRICAL CONDUCTION OF THE HEART
Impotent when use w/ Inderal
The normal site of impulse formation in the heart
is S.A node & then it spread to A.V node, Bundle of His, OTHER BETA BLOCKER
Bundle Branches & Purkinji network. This is the complete
electrical activity of heart. 1. LABETELOL have both Beta blocking and
vasodilating effects
During all this procedure the heart is depolarizes
& repolarizes under the effect of the electrical impulse & 2. CARVEDILOL
we can get same waves on the graphic paper. 3. NEBIVOLOL
Initially when impulse is generating through the 4. ESMOLOL – B1 selective blocker that is rapidly
S.A node, both atria start to depolarize which result as a metabolized via hydrolysis by RBC.
deflection on ECG paper which is known as “P” wave.
used for management of intra and post 3. Long term has potential to reduce incidence of Type 2
operative hypertension and sometimes for DM
hypertensive emergencies, particularly when 4. No rebound hypertension on withdrawal
HTN is associated w/ Tachycardia.
Angiotensin antagonist/
If the problem is altered raas angiotensin receptor blockers (“sartan”)
RENIN-ANGIOTENSIN-ALDOSTERONE-SYSTEM
1. LOSARTAN 4. TELMISARTAN
2. CANDESARTAN 5. TELMISARTAN
3. VALSARTAN 6. IRBESARTAN
ARBS produce arteriolar and venous dilatation and block
aldosterone secretion, thus lowering BP and decreasing
salt and water retention
AE: HYPERKALEMIA
WOF: HYPOTENSION
CI: 1.( teratogenicity) Pregnant women
Role of raas in control of bp
2. Bilateral renal artery stenosis
Kidney Protection
Cardio Protection Interacts: K sparing diuretics
Vascular protection
Anti hypertensive drugs
Ace inhibitors (“ pril”)
nursing responsibilities
Recommended as first line treatment of
most common SE: orthostatic hypotension
hypertension in patients w/ a variety of
compelling indications including high coronary take meds on regular basis
disease risk or history of DM , stroke, heart
failure , MI assume sitting or lying position for a few minutes
nitrates cause the smooth muscle of the veins, and to 3. Absorption of sublingual nitrates may be delayed
lesser extent the arteries to relax and dilate. when taken with anticholinergic drugs (atropine,
scopolamine)
• When the veins dilate – less blood return to the
heart 4. CCB + nitrates may caused light headedness,
orthostatic hypotension, fainting or blurred vision
reduce the amount of blood in ventricles at the end
of diastole, when the ventricles are full Most common Adverse Reaction: HEADACHE
by reducing the preload, nitrates reduce the BETA –ADRENERGIC ANTAGONIST/BETA BLOCKERS
ventricular size and ventricular wall tension (the left ATENOLOL
ventricle doesn’t have to stretch as much to pump CARVEDILOL
blood) which reduce the oxygen requirement of the heart
METOPROLOL TARTRATE
FORMS OF NITRATES:
NADOLOL
1. Sublingual – Isosorbide Dinitrate (SL,Chewable)
PROPRANOLOL HYDROCHLORIDE
Pharmacokinetics: taken SL, absorbed rapidly
and directly into JV and Rt. Atrium
- can repeat dose if pain is not relieved w/in 5 minutes
but do not give more than 3 tabs
2. Topical – ointment and ( transdermal patch – longer
acting nitrates )
• should not removed w/ bare hands
• Do not defib when there is Nitroglycerin patch
3. Heart will respond to other impulses generated by
the cardiac cell (other than SA node)
4. Heart will respond to impulses travelling the extra
pathways
MOA:
1. Blocks the adrenergic stimulation of the heart
2. Depress the myocardial excitability and
contractility
3. Decrease conduction velocity in cardiac tissue
CLASSIFICATION OF CCB 4. Increase recovery time (repolarization/ resting)
INDIRECT ACTING VASODILATORS/ CALCIUM CHANNEL
BLOCKERS (“DIPINE”)
1. Relax the coronary artery spasm in variant angina
Relax peripheral arterioles in stable angina which
decrease O2 demand
2. Decrease the cardiac contractility , afterload and
peripheral resistance thus decreasing the workload of the
heart
3. Reduce the force contraction of the heart
RATE : RR interval
RHYTHM: R to R interval
P WAVE : Atrial Depolarization/Atrial activity / Atrial
contraction
QRS COMPLEX: Ventricular depolarization/Ventricular
activity/Ventricular contraction
------Atrial repolarization/resting
T WAVE: Ventricular repolarization/resting
ST SEGMENT : should be flat
-------- Indicative of ischemia, infarction, strain
Types
Antidysrhythmic drugs
Cardiac Dysrhythmias / Arrhythmia – abnormal beats
4 things happens:
1. Heart beats faster
2. Heart beats slow
HEART FAILURE
condition in which the heart can't pump enough blood to
meet the body's needs. Heart failure does not mean that
your heart has stopped or is about to stop working. It
means that your heart is not able to pump blood the way it
should. It can affect one or both sides of the heart.
Steroids
• When use for motion sickness – should be taken
30mins before travel
I: SELECTIVE ANTIHISTAMINE ANTI-EMETICS/H1
RECEPTOR ANTAGONIST
DRUGS: Cyclizine Hcl Meclizine Hcl
Promethazine
Diphenhydramine Hcl
Dimenhydrinate
Nursing considerations Use: it inhibits vestibular stimulation in the middle ear
Breathing and coughing techniques SE: similar to those of anti-cholinergics (drowsiness,
Relaxation techniques Dryness of the mouth , constipation)
Evaluate heart rate and BP Nsg Responsibilities: 1. Not to use with Alcohol
Adsorbents anti-diarrhea
Decrease absorption of many agents including
Digoxin, clindamycin, Quinidine and OHA
Acts by coating the wall of GI tract and adsorbing
bacteria or toxins that causes diarrhea
Take blood pressure, contraindicated to
patient with hypotension
Hematuria
Acute Urinary Retention Side effects: impotence, abnormal ejaculation, dizziness,
swelling in hands or feet, weakness, headache, skin rash.
Bladder Decompensation: normal mucosa→ trabeculation
→ cellules & sacules→ diverticulae→ detrusor muscle Anti muscarinic drugs
failure.
1.Trospium chloride - treat an overactive bladder.
Urinary Incontinence: overflow incontinence or urge
By relaxing the muscles in the bladder, Trospium improves
incontinence
your ability to control your urination. It helps to reduce
Upper Urinary Tract Deterioration and Azotemia leaking of urine, feelings of needing to urinate right away,
and frequent trips to the bathroom.
Drug for prostate
Administration: 1. Take tablet 1 hour before meals or on
• Tamsulosin Hcl (Tamsolin) – SUB TYPE SELECTIVE an empty stomach at least 1 hour before
Indication: Treatment of benign prostatic hyperplasia to meal
relieve symptoms of urinary obstruction
2.Alcohol should not be consumed within 2
Action: relaxes the bladder muscles, These medications hours of administration.
relax the muscle of the prostate and bladder neck, which
allows urine to flow more easily. Diuretics
Take 30 minutes following meals, do not diuretics, such hydrochlorothiazide and chlorthalidone,
open, chew, or crush lower blood as pressure initially by increasing sodium and
Contraindication to patient with history of water excretion. Thiazide diuretics can induce
orthostatic hypotension
hypokalemia, hyperuricemia and, to a lesser extent, Actions
hyperglycemia in some patients.
• Inhibits sodium and chloride reabsorption in the
Thiazide diuretics: Hydrochlorothiazide (HydroDIURIL, ascending loop of Henle, thus
Microzide)
increasing renal excretion of sodium, chloride, and water
Actions
• Increases excretion of potassium (like thiazide diuretics)
• Interferes with sodium transport across tubules of the
cortical diluting segment of the • Produces greater maximum diuresis and electrolyte loss
than a thiazide diuretic
nephron
Indications
• Increases renal excretion of sodium, chloride, water,
potassium, and calcium • Acute pulmonary edema
5. Keep in mind that it may take 1 to 2 weeks to • acute gouty arthritis (urate deposits in the joints)
achieve full anti-inflammatory effects • dysmenorrhea (painful menstruation)
Nonselective NSAIDs warning • migraines
Before administering an NSAID to a patient, be aware of its • tendinitis
risks to special populations:
• mild to moderate pain.
• Children: Some NSAIDs aren’t recommended for use in
children.
• Elderly people: The risk of ulcers increases with age.
• Pregnant women: Ketoprofen, naproxen, flurbiprofen,
and diclofenac are category B drugs. Etodolac, ketorolac,
meloxicam, nabumetone, and oxaprozin are category C
drugs.
• Nursing mothers: Most NSAIDs are excreted in breast
milk. In general, nonselective
• NSAIDs shouldn’t be administered to nursing
mothers
All in favor?
The following conditions respond favorably to treatment
with NSAIDs:
• Ankylosing spondylitis (an inflammatory joint disease
that first affects the spine)
• Moderate to severe rheumatoid arthritis (an
inflammatory disease of peripheral joints)
• Osteoarthritis (a degenerative joint disease) in the hip,
shoulder, or other large joints
• osteoarthritis accompanied by inflammation
• acute gouty arthritis (urate deposits in the joints)
Selective nsaid
CELECOXIB/CELEBREX – are highly protein bound, primarily
to albumin and is extensively distributed in the tissue
- Prostaglandin produce by COX 2 are associated
with pain and inflammation. The selective NSAIDs
also called COX 2 inhibitors, this are NSAIDs that
selectively blocks COX2, relieving pain and
inflammation.
- They produce fewer side effect such as stomach
damage
Morphine sulfate
- Used to treat osteoarthritis, rheumatoid arthritis,
acute pain, primary dysmenorrhea • Is the standard against which the effectiveness
and the adverse reaction of other pain medication
Drug Interactions: metabolized by the liver is measured.
1. Celecoxib decreases the clearance of lithium, ACTION: acts on opiate receptors in the CNS
which can result in lithium toxicity
INDICATION: for pain
2. Reduces the effect of ACE inhibitors and diuretics
NSG CONSIDERATIONS: 1. monitor the patient for adverse
3. Celecoxib + Warfarin = increase PT levels (so effects such as sedation, euphoria, seizures, dizziness,
bleeding may occur) nightmares, bradycardia, shock, nausea, constipation,
vomiting, cardiac arrest
4. Celecoxib interacts with herbal preparations,
garlic, ginger. Gingko, horse chestnut (bleeding ANTIDOTE: NALOXONE
will occur)
PHARMACODYNAMICS: reduce pain by binding to opiate
Opioid agonists & antagonist receptor site in the PNS & CNS.
Also called narcotic agonists include opium derivatives and They mimic the effect of endorphins
synthetic drugs with similar properties
- Used to relieve and decrease pain without causing
the person to lose consciousness
- Some opioid agonists also have antitussive and
anti diarrheal effects
OPIOID OPPONENT
Opioid antagonists aren’t pain medications. They block the
effects of opioid agonist and used to reverse adverse drug
reaction such as respiratory and CNS depression, produced
by those drugs.
• Besides reducing pain, opioid agonists, especially
OPIOID AGONIST
morphine, affect the smooth muscle of the GIand
1. Codeine genitourinary tracts (the organs of the
reproductive and urinary systems).
2. Fentanyl citrate
• These drugs also cause blood vessels to dilate,
3. Hydrocodone especially in the face, head, and neck. In addition,
they suppress the cough center in the brain,
4. Meperidine hydrochloride
producing antitussive effects and causing
5. Methadone hydrochloride constriction of the bronchial muscles.