Pharmacology and fluid therapy PART 1 Flashcards
The word pharmacology comes from the Greek words
Pharmakon meaning drug or poisonlogos meaning word or discourse
The goal of emergency pharmacology in the prehospital setting is
to use medication’s to reverse, prevent or control various diseases and illnesses, chronic and acute
Ancient Health Care
Ancient Egyptian healthcare was heavily influenced by spiritual beliefs however it incorporated Basic first aid and chemical compounds to treat certain ailments
The Pre-Renaissance and Post- Renaissance Periods
Doctors had no concept of viruses or bacteria it was believed that sickness represents punishment for one sins Attempts to treat ailments centered on approaches intended to counteract the presenting symptoms Presenting symptoms were categorized based on their moisture and temperature blood was hot and wet, phlegm was cold and wet, black bile was cold and dry, and yellow bile was hot and dry
Modern Health Care
The modern pharmaceutical industry began in the 19 century with the discovery of highly active medicinal compounds that could be manufactured on a large scale Although not every condition has a cure virtually all diseases can be treated to some degree with medications
Pharmacology is defined as
the study of drugs and their effects on the body
Common Pharmacology Abbreviations -IV-IM-SQ-ET
IV (intravenous) IM (intramuscular) SQ or SC (subcutaneously) ET (endotracheal)
Common Pharmacology Abbreviations -IO-PO-PRN-NEB
IO (intraosseous) PO (per os or by mouth) PRN (pro re nata or as needed) NEB (nebulized)
Common Pharmacology Abbreviations -o.d -b.i.d-t.i.d-q.i.d
o.d (once a day) b.i.d (twice a day) t.i.d (three times a day) q.i.d (four times a day)
Common Pharmacology Abbreviations -q-IN-p.r.
q (every) IN (Intra Nasal) p.r. (Per Rectum)
Pharmaceutical preparations
are preparations that make a drug suited to certain method(s) of administration.
characteristics or properties that dictate in what form drugs will be manufactured
Some drugs deteriorate when dissolved in solution and are, therefore, manufactured in powder form and dissolved just prior to administration. —This is usually the case with injectable antibiotics. Some drugs are destroyed when taken by mouth. —For example, insulin can only be injected and is manufactured in a sterile liquid form that can be injected.
Today, drug companies try to prepare drugs in forms that:
Can be easily administered. Contain the exact dose that a physician prescribes.
Extract
Concentrated preparation of a drug made by putting the drug into a solution and evaporating the excess solvent
Powder
A drug that has been ground into a pulverized form
Capsule
A gelatin container that encloses a dose of medication
Pulvule
Similar to a capsule except that it is not made of gelatin
Tablet
A powdered drug that has been pressed into a small disk
Suppository
A drug in a firm base that is designed to melt at body temperature
Ointment
A semisolid preparation that is designed for external application
Patch
Contains medication on the surface of an adhesive patch
Solution
A liquid containing one or more chemicals dissolved in water
Suspension
Supplied as a powder and requiring the addition of water
Fluid extract
Concentrated form of the drug prepared by dissolving the drug in the fluid
Tincture
Dilute alcoholic extract of a drug
Spirits
Preparation of a volatile substance dissolved in alcohol
Elixir
Solution with alcohol and flavoring added
Milk
Aqueous suspension of an insoluble drug
Emulsion
One liquid (usually oil) distributed in small globules in another liquid (usually water)
Liniments
A lotion that is designed for external use
Vapour
Liquid form that when placed in a device that allows vaporization, allows the patient to inhale the medication
drug use: -define-examples Prevention
A drug used to prevent the occurrence of a disease. Heptavax B® Tetanus toxoid
drug use: -define-examplesDiagnosis
A drug used to determine the nature of an illness or disease. Radiopaque dyes
drug use: -define-examplesTreatment
A drug used in the management of a disease or disorder. Lidocaine Atropine
drug use: -define-examplesCure
A drug used to eliminate the disease process. Ampicillin Cloxacillin
drug use: -define-examplesContraception
A drug used to prevent pregnancy. Ortho® 7/7/7 28 days Norinyl® 1/50
drug use: -define-examplesHealth Maintenance
A drug taken to maintain homeostasis and supplement deficient body chemistry. Vitamins B12 Vitamin C Humulin N Novolin® ge Toronto
Sources of Medications
plantanimalmineralsynthetic
plant meds
can come from a root, leaf, flower or seed of a plant Morphine is generally accepted to be the first active ingredient isolated from a plant for pharmacological purposes; it was first isolated from the opium poppy in the early 1800s Digitalis for heart failure is prepared from the dried leaves of a flower called Purple Foxglove (Digitalis purpurea)
animal meds
Common medications that are derived from animal source are select types of insulin and a thyroid medication called Armour® Both of these medications are derived from pigs (porcine). —-Insulin is derived from the pig’s pancreas — Armour® from the pig’s thyroid.
mineral meds
Minerals can be used to treat many medical problems Common minerals that are used as part of a treatment for patients are calcium, potassium, iron, and magnesium
synthetic meds
derived from a synthetic source are created in a laboratory may provide an alternative source to those found in nature or be an entirely new medication A common medication that is derived from a synthetic source is Demerol
Health Canada’s Therapeutic Products Directorate (TPD)
ensures the safe and efficacious medication’s are available in Canada aims to balance potential health benefits with risk to patient safety post by drugs
Compendium of Pharmaceuticals and Specialties (CPS)
complies data on most medication’s available in Canada uses; includes info on indications, dosages, contraindications and adverse reactions
Hospital formulary
a list of medication’s, dosage forms, package sizes and medication strength stocked by particular hospitals and it’s pharmacies
Drug inserts
printed document included in the packaging provided by medication to manufacture often referred to as product monograph
American Hospital Formulary Service Drug Info
provides another source of useful in miscellaneous drug info for pharmacist and medical practitioners includes generic and trade names
Epocrates, Lexi-Comp, Micromedex
reliable and popular resources online easy to use great source of drug info
Every medication is assigned 4 names
Chemical name Trade name Generic name Official Name
define medication
is a drug that has been approved by the government agency that regulates pharmaceuticals
Health Products and Food Branch (HPFB)
is the Canadian agency that regulate pharmaceuticals The Food and Drugs Act is the applicable legislation that ensures public safety with regard to medication
A drug as defined by health Canada
is any substance or mixture of substances manufactured, sold or represented for use in: The diagnosis, treatment, mitigation, or prevention of a disease, disorder, or abnormal physical state or its symptoms in human beings are animals Restoring, corrected or modifying organic functions in human beings or animals Disinfection in premises in which food is manufactured, prepared or kept
Pharmaceutical companies protect their investments by obtaining patents on their new drugs
A patent gives its holder exclusive rights to produce and sell the drug until the patent expires After it loses its patent the medication may then be available as generic drug (nonpatented) from multiple sources
The chemical name
describes the drugs chemical makeup, it’s composition and molecular structure
The generic name
is a general name for a drug and is usually created by the company that first manufactures the chemical
International Nonproprietary Name Program
1950s the world health organization initiated to standardize generic names
The trade name or brand name
is the unique name under which the original manufacture registers the new drug with the HPFB
Drug legislation
responsible for ensuring that standards are maintained
Every health worker must have a working knowledge of the legal implications associated with giving drugs so that he/she will be able to
Interpret drug data Evaluate therapeutic (desired) response Recognize his/her responsibilities when administering narcotics and controlled drugs Remain within the necessary restrictions imposed by the laws Recognize their responsibilities when involved with clinical tests of experimental drugs
Canadian Regulation of Pharmaceuticals
They prohibit manufactures from making false claims about their medication benefits or advising patients to administer the medication’s incorrectly They seek to protect patients from medication’s that might cause harm and require drug manufacturers to publish information about side effects unknown potential harmful effects of their products Outline standards for drug manufacturers to ensure the medication is produced by different manufacturers are of uniform strength and purity
Manufacturing Related Regulations
Guarantee standardization of doses Standardization assures patients that when they take a medication with a stated amount of the active ingredient they will receive that amount of the medication The amount of active ingredient must be within 95% to 105% of that stated on the label AssayBioassay
AssayBioassay
Assay: an Analysis of the drug itself to evaluate its potency Bioassay: it’s a procedure for determining the concentration, purity and/or biological activity of a substance by measuring its effect on an organism, tissue, cell or enzyme
The HPFB
is Canada’s federal authority responsible for regulation of health products and food through enforcement of the food and drug act
Within HPFP there are three directorates:
The Therapeutic Products Directorate reviews the safety and efficacy of pharmaceuticals and medical devices and authorizes their use in Canada The National Health Products Directorate regulates natural health products such as vitamins or herbal supplements The Biologics and Genetic Therapies Directorate regulates biological and radiopharmaceutical drugs
The Office of Controlled Substances
ensures that controlled substances and drugs are not diverted for illegal use it developed legislation, regulations, policies and operations to support the control of illicit drug use
The Pharmaceutical Advertising Advisory Board and Advertising Standards Canada
independently review pharmaceutical advertisements to determine compliance with the Food and Drug Act
The Marketed Health Products Directorate is responsible for post marketing surveillance of adverse events secondary to market and drugs
In the event that a product quality or safety comes into question it can work with other health Canada directorates to remove the product from the market or provide safety information
The Drug Approval Process
the average time for a drug to be developed, tested and approved is approximately nine years All new drugs must go through animal studies and clinical trials in humans before they are approved for distribution
Clinical trials proceed in four phases
Phase 1: the new drug is tested in healthy volunteers to compare human data with those in animals to determine safe doses of drug and to assess its safety Phase 2: these trials are performed in homogeneous population of patients one group receives the drug in the other group receives the placebo Phase 3: in these clinical trials the drug is made available to a large group of patients Phase 4: after successful completion of phase 3 the drug company can submit a New Drug Submission to the HPFB for approval to market the drug
The Canadian Health Protection Branch of the Department of National Health and Welfare
is responsible for administration and enforcement of federal legislation for the Food and Drugs Act and the Controlled Drugs and Substances Act
Canadian Drug Legislation
the Food and Drugs Act and the Controlled Drugs and Substances Act together with provincial acts and regulations that govern the sale of poisons and drugs and those that govern the health professions, are designed to protect the Canadian consumer from health hazards, deceptive advertising of drugs, cosmetics, and devices, and adulteration of food and drugs
The Canadian Food and Drugs Act
First passed in 1920 and most recently revised in 1985 Aims to protect the public from mislabeled, poisonous or otherwise harmful foods and medications divide drugs into various categories.
There are three major classifications of drugs under the Food and Drugs Act:
Non-prescription drugs Prescription drugs, and Restricted drugs.
The Canadian Controlled Drugs and Substances Act
governs the possession, sale, manufacture, production, and distribution of narcotics in Canada Only authorized persons can be in possession of a narcotic and must keep a record of the name and quantity of all narcotics dispensed and they must ensure the safekeeping of narcotics
The Controlled Drugs and Substances Act organizes drugs into eight schedules, depending on
their dependence and abuse potential and their usefulness in medical therapy:
The Controlled Drugs and Substances Act: Schedule i
Includes narcotics such as opium, heroin, morphine, and cocaine
The Controlled Drugs and Substances Act: Schedule ii
Includes cannabis and cannabis resin
The Controlled Drugs and Substances Act: Schedule iii
Includes stimulants and hallucinogens
The Controlled Drugs and Substances Act: Schedule iv
Includes anabolic steroids, barbiturates, and benzodiazepines
The Controlled Drugs and Substances Act: Schedule v
Includes phenylpropanolamine
The Controlled Drugs and Substances Act: Schedule vi
Includes precursors that can be converted or used to produce “designer drugs” or other controlled substances
The Controlled Drugs and Substances Act: Schedule vii
Defines limits associated with application of cannabis — related penalties, cannabis (3 kg), and cannabis resin (3 kg)
The Controlled Drugs and Substances Act: Schedule viii
Defines limits associated with application of cannabis — related penalties, cannabis (30 kg), and cannabis resin (1 g)
MedSask
provides health care professionals and consumers with objective, concise and unbiased information on drug therapy
Canada Vigilance Regional Office (Saskatchewan)
Report adverse drug reactions to the Canadian Vigilance Program
RxFiles Academic Detailing Program
The RxFiles provides objective comparative drug information to promote optimal drug therapy
The Saskatchewan Formulary
is a list of the drugs of proven high quality that have been approved for coverage under the Drug Plan
Pharmacokinetics
what the body does to the drug
ADME
determine how and how much of a drug arrives at its target body tissues and how long it exerts its therapeutic effect(A) Absorption (D) Distribution (M) Metabolism (E) Excretion
Absorption
refers to the transfer of medication from its site of administration into the body to specific target organs and tissuesThe rate of absorption determines the onset of action The extent of absorption determines the intensity of action
factors affecting the absorption of a medication including
Solubility of the drug Concentration of the drug pH of the body Site of absorption Absorbing surface area Blood supply to absorption site Medication’s bioavailability (the amount of medication that is still active once it reaches it’s target tissue)
Distribution
As a drug passes through the body, its form and its concentration in the tissues influences the effect it will have Plasma protein binding is an important mechanism of distribution
bound drugfree drug
bound drug: Plasma protein binding is an important mechanism of distribution.Drugs are bound in variable degrees to proteins or become stored in fatty tissues free drug: Only those drug particles that are not bound can be active in the cells
metabolism (biotransformation)
changes a drug into forms that can be used by the body or which can be readily excreted (or both) Metabolism occurs immediately and most often in the liver. first pass effect: the liver inactivates some medications and some can only be given parenterally
Excretion
A drug and its metabolites must be excreted If a drug is excreted more slowly than it is administered, accumulation occurs causing adverse effects and toxicity.
Drug Half-Life
represents the time required for the amount of the drug in the blood serum to diminish by one-halfthe concentration (M) of a drug in the blood during a period of time after administration of a single dose
The minimum effective concentration (MEC) or therapeutic index
is a term indicating the lowest concentration of drug in the blood able to produce a therapeutic effect useful in determining adequate dosages
The therapeutic range describes
the range between MEC and the toxic concentration where the drug can seriously harm the client
Onset of Action
is the time after administration when the drug reaches the MEC and begins to produce its effects
Principles Related to Onset of Action
Route of administrationsometimes a loading or priming dose is given to achieve the MEC quicklySome drugs have a latency period peak effect occurs when blood level is highest
The duration of actionThe termination of action
–The duration of action–is usually defined as how long the medication can be expected to remain above the minimum level to provide the effectsit is the time the blood level is above the MEC -The termination of action-the amount of time after the concentration level falls below the minimum level to the time it is eliminated from the body
Duration of action of : -fentanyl (Sublimaze®),-meperidine (Demerol®), -morphine, -acetaminophen (Tylenol®),
fentanyl (Sublimaze®), 1–2 hours meperidine (Demerol®), 2–4 hours morphine, 3-7 hours acetaminophen (Tylenol®), 4–6 hours
Principles Related to Duration of Action
Short acting drugs must be given frequently. Duration of action can be maintained by giving drugs at regular intervals (maintaining the blood level). Duration can be used to help predict the time of next dose. Occasionally a drug’s effects may persist even after it has been excreted. Duration is influenced by pharmacokinetics and can vary with different routes of administration.
Sites of Elimination
Kidneys (main site of elimination) GI tract Perspiration Respiration
Pharmacodynamics
what the drug does to the body
Drugs either alter the ——- —- or change the —— — — — —-
Drugs either alter the cell environment or change the rate of cell functions
the receptor theory of drug action
Drugs “attach” to cells because their molecular structure matches All cell receptors will be exposed to the drug circulating in the blood stream but only those that fit (visualize a lock and key) will bind to each otherIf many receptors are available, we can increase the drug dosage and thus drug effect. If few receptors are available, increasing the drug dosage will have no effect.
the cell is said to be receptive to the drug if…
If at least three sites on the surfaces of both drug and cell match
what are receptors usually made of
cellular proteins or nucleic acids but can be enzymes, carbohydrate residues, and lipids
Agonist
a drug that directly alters the rate of a cellular process
Affinity for the target tissue
An agonist has a natural tendency to bind with the receptor
Efficacy
ability to initiate drug action
Partial agonists
are agonists that produce only moderate effect.They occupy a receptor site and produce moderate effect prevent any other drug from binding to those receptor sites.
Antagonists
do not alter cellular rates or environments. they compete with agonists to occupy the same receptor site If successful in binding more tightly, the antagonist will prevent the agonist from acting Antagonists are often given to act as antidotes excreted more rapidly than the agonist they oppose, therefore have short-lived actions and must be administered repeatedly to prevent toxicity from recurring
Numerous factors affect an individual’s response to drugs, including:
Age Weight Gender Environment Time of administration Condition of the patient Genetic factors Psychologic factors
Types of Responses
predictableunpredictableiatrogenic
Predictable response
extensive research to determine the therapeutic action (desired effect) of a drug in order for a response to be classed as predictable it must have occurred in 50% of the population going to be some potential negative results that may occur (side effects) Through research and testing, most side effects can be anticipated
Unpredictable response
If the response seen is unique to that patient and not seen in other patients in a similar setting, the response is classed as an idiosyncrasyWhen medications are given in successive doses or in conjunction with other medications, we can see unpredictable responses as well
idiosyncrasy
an abnormal or unusual response to a drug
Tolerance
decreased effects of a drug due to long term use These patients will build a tolerance to that medication resulting in the need for a higher than normal dose to achieve the same result
Cross-tolerance
drug tolerance in which patients who takes a medication for an extended period of time can build up a tolerance to other medications in the same class
Tachyphlaxis
condition where patient rapidly becomes tolerant to a medication
Drug dependence
a physical or emotional need for drug
Cumulative effect
occurs when several does of a medication are administered or when absorption occurs more quickly than elimination If repeat doses are given too quickly, a cumulative effect may result, causing possible nontherapeutic effects
Summative effect
the process where multiple medications can produce a response that the individual medications alone do not produce If two medications of similar effect are given to a patient
Synergism
combined action of two drugs that is greater than the sum of their individual responses
Potentiation
enhanced action of the drug by another administered concurrently
Iatrogenic response
is an adverse condition that is inadvertently induced in a patient by the treatment given An example of this would be a patient developing an urinary tract infection after the insertion of urinary catheter.
in the metabolic phase The liver can act on a drug in 2 phases
Phase1: the enzymes may oxidize the drug or bind it with oxygen molecules and can also hydrolyze the medication; both causes medication to be more soluble with water Phase 2: the medication molecules combine with a chemical found in the body (known as conjugation reaction)
excretion occurs primarily through the kidneys 3 mechanisms
Glomelur filtration Tubular secretion Partial reabsorption
Glomelur filtration
a passive process in which blood flows through the glomeruli of the kidneys a differential in pressure forces waste away from the blood into the capsule where it is transported for excretion
Tubular secretion
an active transport process in which medications are bound to specific transporters aiding in their elimination
Partial reabsorption
this occurs when some amount of the drug is reabsorbed after being filtered
Medications cause their action on the body by four mechanisms:
They may bind to a receptor site They may change physical properties of cells They may chemically combine with other chemicals They may alter a normal metabolic pathway
A medication molecule witll have 1 of 2 effects when it binds to a receptor site
It may stimulate the receptor site to cause the response it normally does (agonist) It may block the receptor site from being stimulated by other chemical mediators and inhibit the normal response (antagonist)
The autonomic nervous system
is composed of nerve fibers that send impulses from the CNS to smooth muscles, cardiac muscles, and glands
The autonomic nervous system (ANS) consists of two further subdivisions:
Parasympathetic nervous system Sympathetic nervous system
Nerve fibers associated with the parasympathetic system originate
from the spinal cord at the level of the cervical and sacral regions
Parasympathetic nervous system is responsible for actions such as:
Decreased heart rate Decreased cardiac contractile force Decreased blood pressure Increased circulation to digestive organs Increased peristalsis Constriction of the pupils Bronchoconstriction
The principle neurotransmitter of the parasympathetic nervous system is
acetylcholineuh·seh·tuhl·kow·leen
acetylcholine
Acetylcholine is very short lived. within seconds of release it is deactivated by another chemical called acetylcholinesterase
Within the parasympathetic nervous system there are two main types of acetylcholine receptors
nicotinic and muscarinic
Muscarinic receptors
are primarily responsible for parasympathetic overactivity responses
Muscarinic responses and what reverses them
including bradycardia, miosis (pinpoint pupils), sweating, blurred vision, tearing, wheezing, SOB, coughing, vomiting, abdominal cramps, diarrhea atropine reverses them
nicotinic receptors
are primarily responsible for sympathetic overactivity response and neuromuscular disfunction causes muscular contractionsopened by nicotine
nicotinic responses
responses include tachycardia, hypertension, dilated pupils, muscle fasciculation (involuntary twitching etc) and muscle weakness
cholinergic receptors
these receptors respond to acetylcholinenicotinic and muscarinic
parasympathomimetic or cholinergic agonists
producing effects that resemble (mimic) the stimulation of the parasympathetic nervous system If a medication binds to and stimulates those receptors
parasympatholytic or anticholinergic
blocking effects or producing effects that resemble interruption of the parasympathetic nervous system If a medication blocks the actions of the parasympathetic nervous system ex: atropine
Nerve fibers associated with the sympathetic system originate
from the spinal cord at the level of the thoracic and lumbar regions
Sympathetic nervous system is responsible for actions such as:
Increase heart rate Increase blood pressure Peripheral vasoconstriction Increase circulation to vital organs Sweat gland stimulation
The principle neurotransmitters of the sympathetic nervous system are
catecholamines norepinephrine epinephrine
Within the sympathetic nervous system there are two main types of receptors
adrenergic and dopaminergic.
Dopaminergic receptors
are believed to cause renal, coronary, and cerebral artery dilation
Adrenergic receptors
are the receptors that are most common within the sympathetic nervous systemthe receptors stimulated by prehospital medications
Adrenergic receptors 4 classes
Alpha1 Alpha2 Beta1 Beta2
where are the following receptors primarily locatedAlpha 1Alpha 2Beta 1Beta 2
Alpha 1: on peripheral blood vesselsAlpha 2: on nerve endingsBeta 1: within the cardiovascular systemBeta 2: on bronchial smooth muscle
Alpha 1 stimulation results in:
Peripheral vasoconstriction Mild bronchoconstriction Increased metabolism Stimulation of sweat glands
Alpha 2 stimulation results in:
Control release of neurotransmitters
Beta 1 stimulation results in:
Increased heart rate (positive chronotropic) Increased strength of cardiac contraction (positive inotropic) Increased cardiac conduction (positive dromotropic)
Beta 2 stimulation results in:
Bronchodilation Peripheral vasodilation
sympathomimetic or adrenergic agonists
If a medication binds to and stimulates any of the adrenergic receptors
what do sympathomimetic or adrenergic agonists do
producing effects that resemble the stimulation of the sympathetic nervous system
sympatholytic or adrenergic antagonist
blocking effects or producing effects that resemble interruption of the sympathetic nervous system
Selective beta blockers
bind and block only beta 1 or beta 2 receptors
non-selective beta blockers
would block both beta 1 and beta 2 receptors
Drugs are organized into classifications according to
the body system they affect, their therapeutic use or clinical indication, and/or their physiologic or chemical action
13 classifications of drugs
Opioid antagonists Non-narcotic analgesics Inhalation anesthetics Adrenergic agonists Bronchodilators Antianginal agents Anticoagulants Platelet inhibitors Uterotonics Vitamin and electrolyte supplementsAntihypoglycemic agents Antimicrobials Antidotes or neutralizing agents
Opioid
binds to opioid receptors to provide analgesic effects
Analgesic
medication that relieves pain
Anesthetics
medication that makes the body less sensitive to the perception of pain
Bronchodilators
medication which increases airflow to lungs by dilating the bronchi and bronchioles
Antiangina
medication to manage or reduce the heart condition angina
Anticoagulants
medication to prevent blood clots
Platelet inhibitors
medications which reduce blood clotting by preventing platelet cohesion
Uterotonics
medication to induce contraction of uterus
Antihypoglycemic
counteracting low blood glucose
Antimicrobials
medication to destroy or slow growth of microorganisms
Antidotes
medication to counteract poison
The CNS
which is comprised of the brain and spinal cord, receives signals from sensory receptors (e.g., pain, vision, cold, pressure, smell), processes these signals, and controls body responses to them
The classifications that you are going to study that affect the central nervous system are:
Opioid antagonists Non-narcotic analgesics Inhalation anesthetics
Opioid Antagonist
Narcotic medications elicit both analgesic and CNS effects Some patients experience a feeling of well-being with their use Opioid antagonists may be used to treat both narcotic abuse symptoms as well as therapeutic narcotic symptoms
Mechanism of Action of Opioid Antagonist
Opioid antagonists attach to opioid receptors and displace the narcotic, thereby rapidly reversing the effects of the narcotic
Types of Opioid Antagonists
Pure antagonists Partial antagonists
Pure antagonists
Competitive blocking drugs Occupy a receptor site so that narcotic cannot, but do not have any effect themselves
Partial antagonists
Bind with receptor sites Produce weak narcotic-like effects in the absence of other narcotics
common uses of Opioid Antagonists
Narcotic induced respiratory depression Narcotic addictions
common examples of Opioid Antagonists
*Naloxone Nalmefene Butorphanol Nalbuphine Pentazocine
cautions of Opioid Antagonists
Partial antagonists may cause worsening of respiratory depression Use caution when administering to individuals that are addicted to narcotics due to resulting withdrawal symptoms
Non-Narcotic Analgesics
Pain levels must be assessed before and after an analgesic is administered to determine its effectiveness Analgesics inhibit the body’s reaction to pain Non-narcotic analgesics differ from narcotic analgesics as they produce analgesia through both the CNS and peripheral mechanism of action at the site of injury
Mechanism of Action of Non-Narcotic Analgesics
provide analgesia by blocking prostaglandin stimulation in the CNS cause fever reduction by affecting the hypothalamic center to reduce temperature, and they increase sweating and peripheral blood flow in order to increase heat loss Select non-narcotic analgesics will also reduce inflammation by stabilizing cell membranes so that cells are less permeable, thus limiting edema formation
Common Uses of Non-Narcotic Analgesics
Mild pain management Reduce fever Pain from inflammation
Common Examples of Non-Narcotic Analgesics
Nonsteroidal anti-inflammatory drugs (NSAID) *Ibuprofen *Ketorolac Naproxen Salicylates *Aspirin® Analgesic/Antipyretic *Acetaminophen (Tylenol®)
Cautions of Non-Narcotic Analgesics
May cause gastric erosion and ulceration, increased risk of bleeding, and renal impairment Overdose of salicylates and acetaminophen may result in acidosis and respiratory complications
Anesthetics
An anesthetic is any drug that has the capability of causing loss of all sensations, not only the sensation of pain
two types of general anesthetics:
Inhalation anesthetic Injection anesthetic
Mechanism of Action of general anesthetics
There are 4 stages to anesthesia, and mechanism of action depends on the stage that is achieved by the drug.
4 stages of Anesthetics
Stage 1: AnalgesiaStage 2: Involuntary movementStage 3: Surgical anesthesiaStage 4: Medullary paralysis
Stage 1 of anesthetics
Stage 1: Analgesia. Cerebral cortex is inhibited causing a decreased response to pain, a feeling of euphoria, and possible unconsciousness.
stage 2 of anesthetics
Stage 2: Involuntary movement. Cerebral cortex is completely depressed and the hypothalamus takes over control of bodily functions. There is an increase in sympathetic tone which causes an increase in heart rate, blood pressure, respirations, and muscle tone.
stage 3 of anaesthetics
Stage 3: Surgical anesthesia. The hypothalamus is depressed, and cardiac and respiratory function returns to normal. Spinal reflexes are blocked and skeletal muscles relax.
stage 4 of anesthetics
Stage 4: Medullary paralysis. The medulla is paralyzed, thus cardiac and respiratory centres are affected, and death may occur.
common uses of anesthetics
Surgeries Dental procedures Pain control (nitrous oxide’s main use)
Common Types of Inhalation Anesthetics
Volatile liquids –Ether –Enflurane –Halothane
Gases
- Nitrous oxide -Penthrox
cautions of anesthetics
Oxygen must be included with all inhalation anesthetics or hypoxia will result They may cause nausea and vomiting in patients, so must monitor airway Potentially hepatotoxic May cause heart to be sensitive to catecholamines (naturally occurring hormones such as dopamine or epinephrine), thus resulting in possible dysrhythmias Potentially fatal malignant hyperthermia may result, characterized by temperatures as high as 43° C and muscle rigidity
non-opiod analgesics
have antipyretic properties
3 main types of non-opiod analgesics
Salicylates (asprin) Non steroidal anti-inflammatory medications (NSAIDs) (ibuprofen) Para-aminophenol derivatives (tylenol)
Sedation
used to couteract anxiety before procedure
Hypnosis
medications that ensure they sleep through event
Benzodiazepines and MOA
seditatives used to prepare pts for invasive procedures MOA: affect the inhibitory neurotransmitter gamma-aminobutyrate acid (GABA) in the brain causing brain activity to slow
Midazolam (Versed)
is a popular benzodiazepine has potent amnesic effect that inhibits patients ability to recall the procedure Onset of action is 1-3mins has a 30-60min duration of action
Diazepam (Vilum)
moderatley longer acting benzodiazepine 30-90 min duration of action Onset of action 5mins
Barbiturates and MOA
believed to work similarto benzo’s; MOA: increase affinity between receptor sites and the inhibitory neurotransmitter GABA
Thiopental (pentothal)
short acting barbiturate Onset action of 10-20secs Duration of action 5-10mins
Nonbarbiturate hypnotics
almost identical properties to benzo’s and barbiturates
Etomidate(Amidate/Lipuro)
ultra short common choice Onset action of 5-15 secs Duration of action of 3-5 mins Minimal effects on hemodynamic stability and decreases intracranial pressure and cerebral oxygen metabolism
Propofol (diprivan)
Onset of 10-20 secs Duration lasts 10 to 15mins
Anticonvulsants and MOA
anti seizure medsMOA: work by inhibiting the influx of sodium into cells enhancing the inhibitory GABA system reducing excitatory glutamingeric neurotransmission and reducing activity in calcium channels
Classes of anticonvulstants include
hydantoins (phenytoin [Dilantin]),iminostilbenes (carbamazepine) valproic acid
Stimulation of CNS can be acomplished in 2 ways
increasing excitatory neurotransmitters by decreasing inhibatory neurotransmitters
Amphetamines
are CNS stimulants They increase the release of dopamine and norepinephrine to increase wakefullness and awarness Increase tachycardia, hypertension and can cause seizures and psychosis
Methylphenidate (Ritalin)
intended to allow pts to better focus and avoid distraction
Psychotherapeutic Medications and MOA
MOA: work by blocking dopamine receptors
Depression often treated with
seretonin reuptake inhibitors
Monoamine oxidase inhibitors
block the metabolism of monoamines in the brain
Tricyclic antidepressants (TCAs)
have powerful inhibitory effects: They Block the neurotransmitters norepinephrine and serotonin from being reabsorbed in the brain They block ACH from reaching its receptors which may lead to tachycardia They block alpha 1 receptors which may produce orthostatic hypotension
CNS Agents
a class of drugs that produce physiological and psychological effects through a variety of mechanisms
specific agents
which bring about an identifiable mechanism with unique receptors for the agent
Nonspecific agents
which produce effects on different cells through a variety of mechanisms and are generally classified by the focus of action or specific therapeutic use
Stimulants
exert their action by excitation of the CNS some of the specific drugs included in this group are caffeine, cocaine and various amphetamines
Patient may be prescribed CNS depressants which
slow brain activity to treat anxiety, muscle tension, pain, insomnia, stress, panic attacks and sometimes seizures
CNS depressant examples
lorazepam (Atrivan) triazolam (Halcion), chlordiazepoxide (Librium). Diazepam (Valium), alprazolam (xanax) opiclone (Imovane)
the sympathetic branch of the ANS is based on… the parasympathetic branch function is to…
The sympathetic branch of the ANS is based on the parasympathetic branch function is to return the body to balance (homeostasis)
neurotransmitters for the adrenergic (sympathetic) response
epinephrine and norepinephrine
Medications that affect the ANS will…
either trigger or block an autonomic response
Adrenergic Agonists
often referred to as sympathomimetic drugs because they “mimic” the actions of the sympathetic nervous system.
Mechanism of Action of Adrenergic Agonists
are used to stimulate peripheral adrenergic receptors, alpha (α) and beta (β), and mimic the actions of the sympathetic nervous system Drugs that act directly on the receptor are direct-acting, and those that alter the release of norepinephrine are indirect-acting The drug can be either non-selective or selective to the receptor sites they stimulate.
Non-selective α and β Agonists uses and action
*Treatment of anaphylaxis/shock (currently only use for PCP) -Stimulates α1 receptors causing vasoconstriction, thus increasing blood pressure Treatment of cardiac arrest -Stimulates β1 receptors stimulate the heart, causing an increase in heart rate, force of contraction, and impulse contraction Treatment of glaucoma -Decreases intraocular pressure
α1 agonist uses and action
Decongestants -Stimulate α1 receptors causing vasoconstriction and thereby decreasing congestion in the area
α2 Agonists uses and action
Treatment of glaucoma -Stimulates α2 receptors causing a decrease in intraocular pressure
β1 Agonists: uses and action
Treatment of cardiac arrest and hypotension -Stimulates β1 receptors causing an increase in heart rate, force of cardiac contraction, and cardiac conduction
β2 Agonists: uses and actions
Bronchodilators -Stimulate β2 receptors, decreasing bronchoconstriction and causing bronchodilation
adrenergic drug cautions and side effects
CNS stimulation — anxiety, jitters, insomnia, tremors Cardiac stimulation (β1 effect) — increase heart rate, force of cardiac contraction, and cardiac impulse conduction; palpitations and arrhythmias can occur Increased blood pressure (α1 effect) Urinary retention (α1 effect)
Beta-receptor - general(non-specific)ex: eye-effect-beta agonist-beta antagonist
-effectrelaxes ciliary muscle-beta agonistnon specific agonists: isoproterenol epinephrine-beta antagonistpropranololtimololnadolol
b1 selective drugsex: myocardium-effect-beta agonist-beta antagonist
-effectincreases contractility increases heart rate-beta agonistnorepinephrine-beta antagonistmetoprololatenolol
b2 selective adrenergic drugsex: lungs -effect-beta agonist
-effectbronchodilation-beta agonistbronchodilators:fenoterolalbuterolterbutaline
Alpha-receptor - generalex: vascular smooth muscle-effect-beta agonist-beta antagonist
-effectskin and skeletal muscle vessel constriction-beta agonistepinephrinenorepinephrine-beta antagonistphentolamine
a1 drugsex: vascular smooth muscle-effect-beta agonist-beta antagonist
-effectvasoconstriction-beta agonistphenylephrine-beta antagonistprazosin
a2 drugsex: vascular smooth muscle-effect-beta agonist-beta antagonist
-effectOpposes α1 vasoconstriction Inhibits NE release Decreases adrenergic activity-beta agonistclonidine-beta antagonistyohimbine
Neuromuscular blocking agents
affect the somatic nervouse system by inducing paralysis
Depolarizing neuromuscular blocking agents
stimulate depolarization of muscle cells which manifests as muscle twitches the medication then produces continuous stimulation of muscle cell which does not allow it to return to its resting state
Nondepolarizing neuromuscular blocking agents
find in a competitive but non-stimulatory manner to part of the ACH receptor as a result these drugs do not cause muscle twitches
Succinycholine
a depolarizing neuromuscular blocking agents that is paralytic for prehospital airway management Rapid onset action less than 45 seconds Short duration of action 4 to 5 mins
Vecuronium
a non-depolarizing neuromuscular blocker that produces paralysis Onset action of 30 seconds Duration of action of 30 minutes
Pancuronium
neuromuscular blocking agents that may be used in prehospital setting Onset action of 90 to 120 seconds Duration of action of 45 minutes to 90 minutes
Adrenergic Agonists (sympathomimetics)
stimulates the adrenal medulla to release norepinephrine and epinephrin which stimulate one of two types of sympathetic receptors dopaminergic receptors and adrenergic receptors
Dopiminergic receptors
produce dilation of renal, coronary and cerebral arteries there are no medication’s that specifically target these receptors
3 categories of bronchodilators
β2 agonists Anticholinergics Xanthines
β2 Agonists
Act on the sympathetic nervous system “Fit and act” at β2 receptors in the lungs Stimulate bronchial smooth muscle causing bronchodilation and decreased respiratory secretions Stabilize inflammatory cells, but do not treat inflammation classified as short acting or long acting
short acting β2 Agonists
can be used about 15 minutes prior to exercise or exposure to a known trigger as a preventative measure common examples: *salbutamol,terbutaline,salmeterol
long acting β2 Agonists
onset is slower but effects last 12 hours common example: formoterol
Anticholinergics
Act on the parasympathetic nervous system Block action of acetacholine on bronchial smooth muscle resulting in bronchodilation and decreased respiratory secretions Stabilize inflammatory cells, but do not treat inflammation
common anticholinergics
ipratropium bromide combined ipratropium bromide salbutamol
Xanthines
Act directly on respiratory muscle to cause bronchodilation Most commonly used orally, but sometimes by injection Not very effective for acute management, used mainly as chronic or maintenance treatment to prevent asthma symptoms Have a narrow therapeutic range, which leads to a low safety margin
common Xanthines
theophylline, aminophylline
common uses of all bronchodilators
Treat acute asthmatic episodes –Short acting β2 agonists are used because they act quickly –Longer acting β2 agonists are of little value for acute episodes due to the length of onset Prevent acute asthmatic episodes Treat chronic obstructive pulmonary disease (COPD). –Best treatment involves anticholinergics, but other bronchodilators may be used
bronchodilator cautions
Short acting β2 agonists should only be used as required; not as a regular or daily drug
bronchodilator Side Effects
CNS stimulation — anxiety, insomnia, restlessness, tremors Cardiac stimulation — tachycardia, palpitations, hypertension May precipitate angina, myocardial infarction, and dysrhythmias Nausea and vomiting Abdominal cramps
bronchodilator drug interactions
Beta blockers may block the effect Monoamine oxidase inhibitors and tricyclic antidepressants may potentiate effects
what is the preferred receptor to treat respiratory emergencies
beta 2 because they produce smaller increases in heart rate and force of contraction which decreases the body’s rate of oxygen consumption
what is a well known CNS Stimulant which is also a Xanthine
caffeine
common decongestants and cold products
pseudoephedrinedextromethorphandiphenhydramine
Antianginal agents
are used to treat a cardiac condition called angina
Angina
is an ischemic heart disease that results in a decreased blood flow to the myocardium due to a buildup of atherosclerotic plaques, or coronary artery vasospasm
Three main classes of antianginal agents are:
*Nitrates (currently only class that can be administered by PCP) Beta-blockers Calcium channel blockers
Nitrates
can relieve symptoms of ischemic heart disease, but are not a cure for it.
nitrates MOA
is to relax vascular smooth muscles the vascular endothelium converts nitrates to nitric oxide (NO) which causes vasodilationDilation of veins is greater than arteriolar dilation at the lower dosage ranges of these drugs
Vasodilation results in:
Decreased amount of blood returning to the heart (preload); therefore, less blood for the heart to pump out Decreased pressure for the heart to pump against (afterload) Decreased afterload and preload decreases the hearts work; therefore, the heart requires less oxygen
common uses of nitrates
To prevent angina attacks –May be used as acute or long-term prophylaxis of angina To relieve acute angina attacks Treatment of myocardial infarctions To help decrease blood pressure –May be combined in hospital with other medications to control blood pressure
common examples of nitrates
*Nitroglycerin
cautions of nitrates
Vasodilatation may cause headaches or orthostatic hypotension (resulting in weakness, dizziness, or fainting) Alcohol potentiates the effects of nitrates Drug loses its effects when exposed to light or air Do not shake the spray as can affect dosage by displacing air in the bottle Tolerance can be developed if used 24 hours a day
drug interactions with nitrate
Viagra® Cialis® Levitra®
Beta Blockers
another treatment and management used for angina.They are effective with angina pectoris, but are not effective when used for vasospastic angina.
Beta Blockers MOA
in treatment of angina is to block beta 1 receptors in the heart, thus decreasing heart rate and contractility This in turn will help reduce oxygen demand by causing a decrease in afterload.
common uses of beta blockers
Reducing the severity and frequency of exertional angina attacks Post myocardial infarction
common examples of beta blockers
Metoprolol Atenolol Timolol
cautions of beta blockers
May produce bradycardia, decreased atrioventricular (AV) conduction, and reduced cardiac contractility Should not be administered to patients with sick sinus syndrome or an AV block. Use with caution in patients with heart failure Asthmatics should only receive beta blockers that are beta1 selective to reduce risk of bronchoconstriction May mask signs of hypoglycemia
Calcium Channel Blockers
Calcium channel blockers are another treatment used to help treat and manage angina.
Calcium Channel Blockers MOA
The mechanism of action of calcium channel blockers is to block calcium channels, primarily in arterioles, resulting in arteriolar dilation and reduction in peripheral resistance (afterload) They can also result in relaxation of coronary vasospasm, thus resulting in increased oxygen supply Select calcium channel blockers may also block calcium channels in the heart, causing a decrease in heart rate, AV conduction, and contractility
Calcium Channel Blockers common uses
Angina Variant angina (Prinzmetal’s angina and vasospastic angina)
Common Examples of Calcium Channel Blockers
Verapamil Diltiazem Nifedipine
cautions of Calcium Channel Blockers
Dilation of peripheral arterioles can cause hypotension and a resultant tachycardia. Use caution with administration of calcium channel blockers that cause depression of the heart to patients taking beta blockers or that have bradycardia, heart failure, or an AV block.
Chronotropic effectInotropic effectsDromotropic effects
Chronotropic effect: medications that affect the heart rate Inotropic effects: are changes in the force of contraction Dromotropic effects: when a drug alters the velocity of the conduction of electricity through the heart
Cardiac glycosides
our class of medications that are derived from plants These medication’s block certain ionic pumps in the heart cells membranes which increases calcium concentration
Antidysrhythmic medications
used to treat and prevent cardiac rhythm disorders further classified into four groups according to the fundamental mode of action on the heart
four groups of antidysrhythmic medications
Sodium channel blockersBeta blockersPotassium chanel blockersCalcium channel blocker’s
Sodium channel blockers effect on heart
slow the conduction through the heart (negative dromotropic effect)
Beta blockers effect on heart
reduce the adrenergic stimulation of the beta receptors
Potassium channel blockers effect on heart
increase the heart contractility (positive inotrophy) and work against the reentry of blocked impulses
Calcium channel blockers effect on heart
block the inflow of calcium into the cardiac cells decreasing the force of contraction in automaticity and may decrease the conduction velocity (negative dromotropic effect)
thrombolytics
designed to break down (lyse) the clot and improve client outcomes if given shortly after the development of the clot
Anticoagulants
may also be called antithrombotics most effective at preventing venous thrombosis, and are used to prevent formation of clots in veins and to stabilize an existing clot so it does not break off into circulation Anticoagulants do not dissolve existing clots
MOA of anticoagulants
anticoagulants disrupt the coagulation cascade and prevent the production of fibrin They block the action of certain clotting factors, which cause platelets to stick together and form blood clots, but the method of action differs for each anticoagulant as each one works at different points in the clotting cascade After addition of antiplatelet drugs, the formation of blood clots is reduced Anticoagulants may be given to patients undergoing surgery to prevent blood clots from forming and decrease the risk of embolism
Common Examples of anticoagulants
*Heparin (monitor only) Low molecular weight heparins Warfarin
common uses of coagulants
During or after surgeries A combination of anticoagulants may be used when a patient is first beginning oral anticoagulant therapy
anticoagulants cautions
When doses are too high the following bleeding may result: Bleeding gums Nosebleeds Easy bruising
Platelet inhibitors
also called antithrombotics inhibit the normal functioning of plateletsmost effective for preventing arterial thrombosis (blood clot in artery) taken by people with a tendency to form clots in the heart and arteries where blood flow is fastthey are used to prevent clot formation after certain types of surgery (clots can lead to myocardial infarctions, strokes, etc.). Platelet inhibitors do not dissolve existing clots.
MOA of platelet inhibitors
Platelet inhibitors act at the level of platelets to prevent clots in arteries They decrease the ability of platelets to stick together (therefore decreasing platelet aggregation) by inhibiting TXA2 or ADP. reduce the tendency of platelets to stick together when blood flow is disrupted and prevent clot formation
TXA2
thromboxane A2 a type of thromboxane with prothrombotic properties
Common Examples platelet inhibitors
*ASA Dipyridamole Ticlopidine Clopidogrel
Common Uses platelet inhibitors
Primary prevention of a myocardial infarction Prevention of a reinfarction in patients with previous myocardial infarction history Prevention of thrombotic stroke
Cautions platelet inhibitors
Increased risk of gastrointestinal bleeding and hemorrhagic stroke Increased risk of bleeding
fibrolytic agent
Once a blood clot has formed it may be administered to dissolve the thrombus and prevent it from breaking off and entering the bloodstreamPromote the digestion of fibrin
two different classifications of medications used to stop preterm labour, induce labour, or control postpartum hemorrhage
uterine stimulants and uterine relaxants.
Uterotonics
given to facilitate uterine contraction
MOA of uterotonics
is stimulation of uterine contractions and compression of maternal blood vessels at the placental site in an attempt to induce labour and control postpartum hemorrhage.
Common Uses of uterotonics
Induce or speed up labour Facilitate contractions following a spontaneous abortion Treat postpartum hemorrhage
Common Examples of uterotonics
*Oxytocin® (monitor only) Misoprostol Syntometrine Ergometrine
Cautions of uterotonics
Ergometrine is contraindicated in women with a history of hypertension, pre-eclampsia, eclampsia, or heart disease. Overstimulation of the uterus could result in uterine rupture, trauma to both mom and baby due to the fetus being forced through an incompletely dilated cervix, and decreased uterine perfusion.
oxytocin
Naturally occurring hormone that has multiple reproductive functions it increases the force and frequency of contractions used to reduce postpartum haemorrhage
tocolytic medication
Suppress the force and frequency metre and contractionsex: magnesium sulfateex: terbutaline
magnesium sulfate
Relaxes the smooth muscles including those in the uterus
terbutaline
Beta agonist that has been used as a tocolytic agent
Vitamin and Electrolyte Supplements
The body is unable to synthesize vitamins and electrolytes and must, therefore, rely on an adequate and constant supply through diet
MOA of Vitamin and Electrolyte Supplements
Vitamins and electrolytes are equally as important for the body to maintain normal function. If the demand is not met, body function will be compromised. Depending on what component is lacking will determine the body function that is affected
Vitamin A
Required for production of rhodopsin which enables specialized retinal cells (rods) to adapt to dim light
Vitamin D
Regulates serum calcium levels in conjunction with parathormone and calcitonin
Vitamin E
Prevents formation and accumulation of toxic metabolites; maintenance of red blood cell membranes
Vitamin K
Synthesis of blood clotting factors II, VII, IX, X
Vitamin B
Necessary for cell reproduction and maturation
Vitamin C
Involved in formation of catecholamines, steroids, and conversion reactions
Sodium
Helps to maintain normal fluid balance
*Potassium
Maintains cell structure and function; regulates muscle function (monitor only)
Calcium
Plays role in muscle contraction, blood coagulation and bone formation
Hydrogen
Regulates acidity and alkalinity of body fluids
Cautions of Vitamin and Electrolyte Supplements
There is specific balance that is required when administering certain electrolytes and vitamins, blood levels must be monitored as too much can be sometimes as detrimental as too little.
Antihypoglycemic Agents
The brain requires a certain level of glucose in order to sustain life; if the blood sugar drops below that level, coma, or death can result Antihypoglycemic agents are used when blood sugar levels drop and the patient’s needs are no longer met.
MOA of Antihypoglycemic Agents
Antihypoglycemic agents work in one of two ways to increase plasma glucose levels: Break down glycogen stores from the liver Supply usable glucose directly to the patient’s blood stream
common uses of Antihypoglycemic Agents
Hypoglycemia
Common Examples of Antihypoglycemic Agents
*Glucagon *D5/D10 *D50W *Oral glucose
Cautions of Antihypoglycemic Agents
Ensure that glucose levels are monitored before and after administration
Antimicrobials
Bacteria have only a few strategies to fight these drugs. However, bacteria often have the upper hand because of their high numbers and their ability to adapt and reproduce Antibiotics, antiviral, and anti-fungal agents are used to treat a variety of infections
General Guidelines for Use of Antimicrobials
Take as directed for the full course of treatment Space doses evenly apart Be aware of compliance issues, reinfection, and superinfection
Antibiotics
Antibiotics or antibacterial drug classes are used to treat bacterial infections Each antibiotic drug is generally effective for only certain pathogenic bacteria
Types of Antibiotics
Beta-lactam Sulfonamide Tetracycline Macrolide Aminoglycoside Fluoroquinolone Miscellaneous
type of Beta-lactam antibiotics
Penicillins Cephalosporin antibiotics Carbapenem antibiotics
MOA of antibiotics
Preventing cell wall synthesis (penicillins) Blocking the synthesis of folic acid (sulfonamides) Interfering with protein synthesis (tetracyclines, macrolides, aminoglycosides) Interfering with DNA synthesis (quinolones)
common uses of antibiotics
Skin and soft tissue infections Dental infections Respiratory tract infections Eye, ear, nose, and throat infections Urinary tract infections Gastrointestinal infections Some sexually transmitted diseases
cautions of antibiotics
Stopping too early can cause a relapse of symptoms, or it may cause the bacteria to become resistant to the medication, which could lead to ineffectiveness of the antibiotic at a later date. Dairy products, antacids, and iron preparations containing minerals such as calcium, iron, aluminum, and magnesium may interact with some antibiotics and prevent them from being properly absorbed into the body (tetracycline, ciprofloxacin, norflaxacin) May interfere with effectiveness of oral contraceptives Disruption of normal flora can be disrupted causing the bacteria Clostridium difficile to over grow. This results in pseudomembranous colitis that can cause bloody diarrhea, abdominal pain, fever, and cramps.
Antivirals
Antibiotics are not effective against viruses Antivirals are a type of antimicrobial drug used to treat viral infections. Their mechanism of action is to inhibit, not destroy, the growth of the virus. Since viruses insert themselves into a cell’s DNA, it is very difficult to make antiviral drugs that are effect against the virus, but do not harm the healthy cells
Types of Antivirals
Viral DNA Polymerase Inhibitors Antiretrovirals –RNA Reverse Transcriptase Inhibitors –Protease Inhibitors Viral Uncoating Blockers
MOA of antivirals
Antiviral drugs work by: Preventing virus from replicating, but do not destroy the virus. Inhibit reverse transcriptase, an enzyme used by RNA viruses to build their DNA (RNA Reverse Transcriptase Inhibitors). Inhibit protease, an enzyme used by RNA viruses in the final stages of creating new virus particles (Protease Inhibitors). Prevent the virus from incorporating into the host cells (Viral Uncoating Blockers).
Common Uses of antivirals
Treatment of herpes Decrease HIV virus production (antiretrovirals) Influenza A prophylaxis
Cautions of antivirals
Since viruses reproduce very quickly, treatment must be started immediately Possible adverse effects are nausea, headache, dizziness or drowsiness Antiretrovirals may have harmful side effects, so regular blood tests are required to monitor effects on the liver, pancreas, and bone marrow.
Antifungals
Fungi exist as yeasts or molds and can invade mucous membranes and the skin. Treatment of fungi is directed at destroying the fungal cell wall Antifungal medications are used to treat fungal infections such as athlete’s foot, diaper rash, and thrush. They can be administered either topically or systemically.
Types of Antifungals
Azole Nystatin Amphotericin B Terbinafine
MOA of antifungals
Inhibiting ergosterol synthesis in fungal cell membranes, thus inhibiting fungal cell membrane synthesis When fungal cell membrane synthesis does not occur, the membrane becomes permeable and cell contents leak out, causing the fungal cell to die.
Common Uses of antifungals
Skin and mucus membrane infections Systemic fungal infections Nail fungal infections
Cautions
Amphotericin B is very potent and has a narrow therapeutic range, so dose must be closely monitored and blood tests must be performed to monitor drug levels Some azole antifungals need an acidic environment in order to absorb, so no stomach acid neutralizing medications can be taken for two hours after taking it All systemic azoles are hepatotoxic, therefore patients must be monitored with blood tests
Medications used to treat HIV
Classified as antiretrovirals -Nucleoside reverse transcriptase inhibitors: -Non nucleoside reverse transcriptase inhibitors: -Protease inhibitors
Antidotes and Neutralizing Agents
Antidotes and neutralizing agents are administered in poisoning and overdose situations in an attempt to antagonize or inactivate the substance
MOA of Antidotes and Neutralizing Agents
Depending on the drug or poison they are working against, there are several ways that antidotes and neutralizing agents work. They may: -Compete and displace drug from receptor sites -Use a different cellular mechanism to overcome effects of poison -Prevent biotransformation -Bind and inactivate the poison
Common Uses of Antidotes and Neutralizing Agents
Intentional and accidental overdose and poisonings
Common Examples of Antidotes and Neutralizing Agents
-Antidotes *Narcan (Naloxone) for opioid overdose N-acetyl-L-cysteine for acetaminophen overdose Chelating agents for metal ion poisoning Glucagon for beta blocker overdose Flumazenil for benzodiazepine overdoses -Neutralizing agents *Activated charcoal
cautions of Antidotes and Neutralizing Agents
Most poisons have no specific antidote, so care must be supportive in nature, focus on prevention of further absorption, and promote poison elimination
common medication classifications that affect the gastrointestinal system
Antacids, Antiflatulents, Digestants, Antiemetics, LaxativesAntidiarrheals
Antiemetics
Antiemetic is a classification of medication used to control nausea and vomiting in patients
N/V is typically triggered by four main mechanisms:
Stimulation of the cerebral cortex and limbic system. Stimulation of the chemoreceptor trigger zone (CTZ). Stimulation of the vestibular system. Stimulation of peripheral pathways.
how Stimulation of the cerebral cortex and limbic system. cause n/v
The common causes of this type of N/V are increasing intracranial pressure, irritation of the meninges and emotional stress
how Stimulation of the chemoreceptor trigger zone (CTZ). cause N/V
The CTZ is an area within the ventricle of the brain that is outside of the blood brain barrier that is directly exposed to substances in the blood and Cerebral Spinal Fluid (CSF). Common causes of this type of N/V are metabolic abnormalities, toxins and medications.
primary neurotransmitters within the chemoreceptor trigger zone (CTZ)
Dopamine (D2), Serotonin (5HT3) and Neurokinin (NK1) are the primary neurotransmitters within this area of the brain.
How Stimulation of the vestibular system. cause n/v
This is part of the inner ear that controls balance. Stimulation of this system is mediated by Histamine. Common causes of this type of N/V are movement related, i.e. motion sickness, vertigo.
how Stimulation of peripheral pathways. causes N/V
This pathway is triggered by stimulation of receptors in the GI tract, heart and kidneys. Common causes of this type of N/V are toxins in the GI tract, blockage or decreased motility within the bowels.
5-HT3 receptor antagonist
This type of antiemetic drug blunts or blocks the effects of Serotonin. It is the most effective in controlling N/V associate with stimulation of the CTZ.
H1 Histamine antagonist
This type of antiemetic drug blunts or blocks the effects of H1 Histamine and blunts the vestibular inputs. this mechanism is effective in treating N/V associated with simulation of the vestibular system.
Some common examples of antiemetics are:
*Gravol (H1 Histamine antagonist) *Ondansetron (5-HT3 receptor antagonist)
Acetaminophen-Generic name-Trade name-Classification
Generic name:-AcetaminophenTrade name: -Tylenol®Classification-Analgesic, antipyretic
Acetaminophen-Mechanism of action
MOA-Antipyretic action by acting on heat regulating centers in the hypothalamus causing increased heat loss through vasodilation and sweating-Analgesic action by inhibiting prostaglandin synthesis in the central nervous system
Acetaminophen-Indications-Contraindications
Indications-Pyrexic child-Severe sepsis-septic shockContraindications-hypersensitivity-Acetaminophen-induced liver disease
Acetaminophen-precautions- side effects
Precautions- hepatotoxicity- medications that induce hepatic enzymes-All acetaminophen containing products taken by patient need to be accounted for during 24-hour period including cough and cold remedies, analgesic or arthritis formulations and antipyreticsSide Effects-Nausea / vomiting-Cramping: overdoses in children
Acetaminophen-route-dose-pharmacokinetics
Route-PO/PRDose-A: 325–650 mg p 4–6 hours, DNE 4000 mg/24 hrs-P: 10–15 mg/kg p 4–6 hours, DNE 5 doses in 24 hoursPharmacokinetics-Onset: 48 minutes-Peak effects: 48 minutes-Duration: 4–6 hours
SKIP FOR NOWAcetaminophen-how supplied
How Supplied-OralImmediate release tablet (325 mg, 500 mg), caplet (325 mg, 500 mg), extended release caplet (650 mg), gel cap (500 mg), chewable tablet (80 mg, 160 mg), rapidly-dissolving tablet (80 mg, 160 mg), suspension (80 mg/mL, 32 mg/mL)-Rectal – Suppository (120 mg, 160 mg, 325 mg, 650 mg)
Activated Charcoal-Generic name-Trade name-Classification
Generic:-Activated charcoalTrade names:- Liqui-Char®, Actidose®, Charcodote®Classification-Antidote
Activated Charcoal-Mechanism of action
Mechanism of Action-Binds and adsorbs ingested toxins from the gastrointestinal tract
Activated Charcoal-Indications-Contraindications
Indications-Oral poisoning or overdoseContraindications-Caustic or corrosive substances-petroleum distillates
Activated Charcoal-precautions- side effects
Precautions-decreased LOC.-If ipecac has been administered, wait 10 minutes.Side Effects-Nausea, vomiting-Constipation, cramping, bloating
Activated Charcoal-route-dose-pharmacokinetics
Route-PODose-1 g/kg-In massive overdoses, may consider 2 g/kg for adults**Requires Online Medical ControlPharmacokinetics-Onset: Immediate-Peak effects: Varies-Duration: Varies based on gastrointestinal function, will act until excreted
SKIP FOR NOWActivated Charcoal-how supplied
-Premixed with water or sorbitol-25 g / 125 mL bottle (200 mg/mL)-50 g / 250 mL bottle (200 mg/mL)
Amyl Nitrate-trade name-classification
Trade name: -Amyl Nitrate®Classification-Vasodilator-Antidote
Amyl Nitrate-Mechanism of Action
-Binds with hemoglobin to help biodegrade cyanide
Amyl Nitrate-indications-contraindications
Indications-Acute cyanide poisoning with impaired LOCContraindications-no concrete proof of cyanide poisoning
Amyl Nitrate-precautions-side effects
Precautions-FlammableSide Effects-Drowsiness
Amyl Nitrate-route-dose-pharmacokinetics
Route-InhalationDose-0.2–0.3 mL inhaled for 15–30 sec with breaks for 15–30 sec. -New ampoule every 3 min until arrival at emergency departmentPharmacokinetics-Onset: Immediate-Peak effects: 3-5 minutes-Duration: 20 minutes
SKIP FOR NOWAmyl Nitrate-how supplied
0.2 mL or 0.3 mL glass ampoule
Amyl Nitrate-Special Considerations
Only services that respond to industries where cyanide exposure can occur will stock drug.Retraining and certification is required by a physician every 2 years.
Acetylsalicylic Acid (ASA)-generic names-trade name-classification
Generic name:-Acetylsalicylic Acid (ASA)Trade name:-Aspirin®Classification-Platelet inhibitor-anti-inflammatory
Acetylsalicylic Acid (ASA)- mechanism of action
Reduces production of thromboxane which mediates platelet aggregation.
Acetylsalicylic Acid (ASA)- indications-contraindications
Indications-Chest pain, cardiac in originContraindications-Hypersensitivity to ASA or other NSAIDs-active peptic ulcers
Acetylsalicylic Acid (ASA)-precautions-side effects
Precautions-Asthma patientSide Effects-Heartburn,-nausea/vomiting, -wheezing, -prolonged bleeding
Acetylsalicylic Acid (ASA)-route-dose-pharmacokinetics
Route-PO, chewedDose-160–325 mgPharmacokinetics-Onset: Within 20 min-Peak effects: Varies-Duration: 2–3 hours
SKIP FOR NOWAcetylsalicylic Acid (ASA)-how supplied
81 mg and 325 mg tablets
Acetylsalicylic Acid (ASA)-special considerations
Administer regardless whether patient has taken their daily ASA dose
Glucose-trade name-classification
Trade name: -Dextrose 50% (D50W), -Dextrose 25% (D25W),-Dextrose 10% (D10W),- Dextrose 5% (D5W)Classification-Carbohydrate, -Antihypoglycemic agent
Glucose- mechanism of action
Increases blood sugar levels rapidly
glucose-indications-contraindications
IndicationsHypoglycemiaContraindicationsHyperglycemia
glucose-precautions-side effects
Precautions-Intracranial pressure – may worsen cerebral edemaSide Effects-Tissue necrosis-local venous irritation
glucose-route-dose-pharmacokinetics
Route-IVDose-Adult: 0.5 g/kg IV/IO max 10 g (if suspected head injury or stroke, give in 5-10g increments)-Pediatric: 2 mL/kg D10W IV/IOPharmacokinetics-Onset: Less than 1 min-Peak effects: Varies-Duration: Varies
SKIP FOR NOWglucose-how supplied
-How Supplied25 g in 50 mL prefilled syringe (D50W)12.5 g in 25 mL prefilled syringe (D25W)10 g/100 mL in 50 mL, 100 mL, 250 mL, 500 mL and 1000 mL IV bag (D10W)5 g/100 mL in 50 mL, 100 mL, 250 mL, 500 mL and 1000 mL IV bag (D5W)
glucose-special considerations
Always ensure that a blood glucose reading is obtained before administration.Since tissue necrosis can occur if IV is interstitial, you must aspirate blood to ensure IV is patent prior to medication administration.
Dimenhydrinate-generic name-trade name-classification
Generic name:-DimenhydrinateTrade name: -Gravol®, Dramamine®Classification-Antiemetic (med for N/V)
Dimenhydrinate-mechanism of action
Not precisely known, but evidence is that it acts to depress hyperstimulated labyrinthine functions or associated neural pathways. It is also thought to inhibit cholinergic stimulation in the vestibular and associated neural pathways.
Dimenhydrinate-indications-contraindications
Indications-Relief of nausea and vomitingContraindications-Hypersensitivity to dimenhydrinate or tartrazine.
Dimenhydrinate-interactions
-Narcotics, sedatives or hypnotics, and alcohol – potentiates CNS depression
Dimenhydrinate-side effects
Drowsiness, dizziness, blurred visionDry mouth, dry nose and bronchiTinnitus
Dimenhydrinate-route-dose
Route-IM, IVDoseIV-Adult: 50 mg over 2 minutes.-Peds: 1 mg/kg over 2 minutes, not to exceed 50 mg.-IM: Concentration 50 mg/1mL-Over 12 yrs: 50 mg q4 hrs.-8–12 yrs: 25–50 mg q8 hrs.-6–8 yrs: 12.5–25 mg q8 hrs.
Dimenhydrinate-pharmacokinetics
Excreted in urine, crosses placentaOnset: Immediate (IV), 20–30 minutes (IM)Peak effects: VariesDuration: 3–6 hours
SKIP FOR NOWDimenhydrinate- how supplied
50 mg/mL
Dimenhydrinate-special considerations
-Should be used cautiously ) in patients with: glaucoma, (COPD), asthma, prostatic hypertrophy, are intoxicated, decreased (LOC).patients with a head injury as it may result in a decreased level of consciousness. C-spine immobilized on a back board, emesis may result in aspiration and obstruction of the airway.
Epinephrine 1 mg/mL-generic name-trade name-classification
Generic Name: -EpinephrineTrade name:-AdrenalineClassification-Sympathomimetic
Epinephrine 1 mg/mL-mechanism of action
Mechanism of action: Alpha and beta agonist-Alpha-1: Systemic vasoconstriction-Beta-1: Positive inotropic, chronotropic, and dromotropic effects-Beta-2: Bronchial smooth muscle relaxation
Epinephrine 1 mg/mL-indications-contraindications
Indications-Anaphylaxis, status asthmaticus, and croupContraindications-Hypersensitivity
Epinephrine 1 mg/mL-precautions-side effects
Precautions-Patients with cardiac history, pregnancySide Effects-Tachycardia, palpitations, arrhythmiasHeadache, anxiety, nausea/ vomiting
Epinephrine 1 mg/mL-route -
IM, SQ, Nebulized
Epinephrine 1 mg/mL-dose adult anaphylaxis
Anaphylaxis:-Mild / Moderate: 0.3 mg IM (of a 1 mg/mL concentration) q 5 minutes prn to a total maximum of 0.9 mg-Severe: 0.5 mg IM (of a 1 mg/mL concentration) q 5 minutes prn to a total maximum of 1.5 mg
Epinephrine 1 mg/mL-dose adult status asthmaticus
0.3 – 0.5 mg SC/IM (of 1 mg/mL concentration) q 5 – 10 minutes prn to a total of 1 mg
Epinephrine 1 mg/mL- dose Peds anaphylaxis
Anaphylaxis-Mild / Moderate: 0.01 mg/kg (0.01 mL/kg of a 1 mg/mL concentration) IM to a single maximum dose of 0.3 mg q 5 minutes prn to a total maximum of 0.9 mg-Severe: 0.01 mg/kg (0.01 mL/kg of a 1 mg/mL concentration) IM to a single maximum dose of 0.5 mg q 5 minutes prn to a total maximum of 1.5 mg
Epinephrine 1 mg/mL- dose Peds status asthmaticus
0.01 mg/kg IM single minimum dose of 0.1 mg to a single maximum dose of 0.3 mg (of a 1 mg/mL concentration) q 5 minutes prn to a total maximum of 0.03 mg/kg
Epinephrine 1 mg/mL- dose Peds croup
0.5 mg/kg to a max of 5 mg diluted in 2-3 ml NaCl, repeat dose x 1 prior to Online Medical Control (OLMC)
Epinephrine 1 mg/mL-pharmacokinetics
Onset: ImmediatePeak effects: VariesDuration: 5–10 min
Epinephrine 1 mg/mL-how supplied-special considerations
1 mg/mLCan be deactivated by alkaline solutions
Glucagon-trade name-classification
Trade name:-GlucagonClassification-Hormone-anti-hypoglycemic agent
Glucagon-mechanism of action
Increases blood glucose levels by causing breakdown of glycogen to glucose, increases heart rate and cardiac contractility
glucagon-indications-contraindications
Indications-LOC due to hypoglycemia where an IV cannot be establishedContraindications-Hypersensitivity,-hyperglycemia
glucagon -precautions-side effects
Precautions-Hepatic or renal insufficiencySide Effects-Tachycardia,-nausea/vomiting,-hypertension
glucagon-route-dose-pharmokinetics
Route-SQ, IMDose-12 years and older: 1 mg with repeat in 15 min as needed-Under 12 years: 0.1 mg/kg to a max of 1 mg with repeat in 15 min as neededPharmacokinetics-Onset: 13-20 min-Peak effects: 30 min-Duration: 1–2 hours
glucagon-how supplied SKIP FOR NOW-special considerations
How Supplied-1 mg/mL (requires reconstitution)Special Considerations-Ineffective if glycogen stores are depleted
Ibuprofen -generic name-trade name-class
Generic name: -Ibuprofen Trade name: -Motrin®, Advil®Classification -NSAID, Analgesic, Antipyretic
Ibuprofen -MOA
-Anti-Inflammatory, analgesic, and antipyretic activities by inhibiting prostaglandin synthesis in the central nervous system. -Inhibits both COX-1 and COX-2
Ibuprofen -Indications -Contraindications
Indications -Mild to moderate pain, fever reduction Contraindications -Hypersensitivity
Ibuprofen -precautions-side effects
Precautions -Use caution with cardiovascular dysfunction, hypertension, peptic ulcers, GI bleeds, pregnancy, and impaired hepatic or renal function -When taken with lithium, may cause increase risk of lithium toxicity -If taken with a diuretic may cause diuretic to have a decreased effect -May cause a decreased antihypertensive effect of B-adrenergic blocking drugs
Ibuprofen -side effects
GI upset, epigastric pain, heartburn, and abdominal pain
Ibuprofen -route-dose-pharmacokinetics
Route-PODose-Adult: 200–400 mg every 4–6 hours, not to exceed 3200 mg/24 hours-Pediatric: 5–10 mg/kg every 6 hours, not to exceed 40 mg/kg in 24 hoursPharmacokinetics-Onset: 30 min-Peak effects: 1–2 hours-Duration: 4–6 hours
SKIP FOR NOWIbuprofen - how supplied
-Oral – tablet (100 mg, 200 mg, 400mg, 600mg, 800mg), chewable tablets (50 mg, 100 mg), capsules (200 mg), Suspension (100 mg/2.5mL, 100 mg/5mL), oral drops (40 mg/mL)
Ipratropium Bromide -generic name-trade name-class
Generic name:-Ipratropium Bromide Trade name:-Atrovent® Classification -Anticholinergic
Ipratropium Bromide -MOA
-Bronchodilation, smooth muscle relaxation
Ipratropium Bromide -indications -contraindications
Indications -Bronchial asthma that has not responded to salbutamol -Severe bronchospasm -Bronchospasm associated with Chronic Obstructive Pulmonary Disease (COPD) Contraindications -Hypersensitivity -Administered within last 4 hours
Ipratropium Bromide -precautions-side effects
Precautions -Monitor vitals -Caution in elderly Side Effects -Dry mouth, metallic taste -Headache, dizziness -Anxiety, palpitations
Ipratropium Bromide - route-dose-pharmockinetics
Route -Inhalation via nebulizer Dose -12 years and older: 250 mcg–500 mcg -5 to 12 years: 125 mcg - 250 mcg Pharmacokinetics -Onset: 5–15 min -Peak effects: Varies -Duration: 4–6 hours
Ipratropium Bromide-how supplied SKIP FOR NOW-Special Considerations
How Supplied -250 mcg in 2 mL Special Considerations -Patients with glaucoma should wear goggles while administered
Ketorolac -generic name-trade name-class
Generic name: -Ketorolac Trade name:-Toradol® Classification -Nonsteroidal Anti-Inflammatory Drug (NSAID)
Ketorolac -MOA
-Exhibits peripherally acting non-narcotic analgesia activity by inhibiting prostaglandin synthesis
Ketorolac -indications-contraindications
Indications -Pain refractory to opioids -Renal colic Contraindications -Hypersensitivity to ketorolac or other non-steroidal anti-inflammatory agents -Asthma -History of significant renal disease, except renal colic -Suspected intracranial bleed -History of GI bleeding -Subarachnoid hemorrhage (indicated by sudden onset/most severe ever headache/thunderclap) Pregnancy
Ketorolac -precautions-side effects
Precautions -Can cause peptic ulcers, should not use for abdominal or chest pain Side Effects -Headache, heartburn, nausea, vomiting, diarrhea, stomach pain, bloating
Ketorolac -route-dose-pharmacokinetics
Route -IV or IM Dose -30 mg IV/IM -15 mg IV/IM If the patient is over 65 years of age Pharmacokinetics -Onset: approx. 30 minutes -Peak effects: 45–60 minutes -Duration: 4–6 hours
Ketorolac -How Supplied SKIP FOR NOW-special considerations
How Supplied -Vials or Ampules doses per vial or ampule can vary from 10, 15, 30 or 60 mg/mL Special Considerations -Patient should be placed on the cardiac monitor after administration.
Naloxone -generic name-trade name-class
Generic name:-Naloxone Trade name: -Narcan® Classification Opioid Antagonist
Naloxone -MOA
Reverses effects of narcotics by competing and displacing narcotic from opiate receptors in the brain
Naloxone -indications-contraindications
Indications -Suspected narcotic overdose with respiratory depression Contraindications -Hypersensitivity
Naloxone -precautions-side effects
Precautions -Use with caution with narcotic-dependent patients and neonates of narcotic-addicted mothers Side Effects -Acute withdrawal symptoms
Naloxone -route-dose-pharmocokinetics
Route -IM, IV, IN Dose -Adult: 0.4–2 mg (titrate to effect) -Pediatric: 0.01 mg/kg–0.1 mg/kg to max of 2 mg (titrate to effect) Pharmacokinetics -Onset: Within 2 min -Peak effects: Varies -Duration: 45 min
Naloxone - how supplied SKIP FOR NOW-Special Considerations
How Supplied -0.02 mg/mL, 0.4 mg/mL, and 2 mg/2 mL Special Considerations -Short acting, may need a repeat dose in 5 min
Nitroglycerin -generic name-trade name-class
Generic name: -nitroglycerin Trade name: -Nitrostat®, Nitrolingual® Classification -Vasodilator, antianginal
Nitroglycerin -MOA
Relaxes vascular smooth muscle causing vasodilation (increases blood flow and decreases preload)
Nitroglycerin -indications-contraindications
Indications -Suspected cardiac chest pain, pulmonary edema Contraindications -Systolic blood pressure below 100 mmHg -Pulse less than 50/min -Viagra® (sildenafil), Levitra® (vardenafil), or Cialis® (tadalafil) within the last 24 hours
nitroglycerin-Precautions -side effects
Precautions -Continuously monitor vitals Side Effects -Syncope, dizziness, hypotension, headache,
nitroglycerin-route-dose-pharmocokinetics
Route -SL Dose -0.3–0.4 mg q 5 min to max of 3 Pharmacokinetics -Onset: 1–3 min -Peak effects: 5–10 min -Duration: 20–30 min
nitroglycerin-How Supplied SKIP FOR NOW-Special Considerations
How Supplied -Spray: 0.4 mg -Tablet: 0.3 mg, 0.6 mg Special Considerations -Keep out of heat and light
Nitrous Oxide (N20) -generic name-trade name-class
Generic name: -Nitrous Oxide (N20) Trade name: -Nitronox®, Entonox® Classification -Analgesic gas
Nitrous Oxide (N20) -MOA
Depresses the central nervous system and relieves pain
Nitrous Oxide (N20) -indications-contraindications
Indications -Musculoskeletal injuries, burns, active childbirth Contraindications -Abdominal pain indicative of a bowel obstruction -Pneumothorax -Head injury, impaired mental status, intoxication, decompression sickness, inability to follow commands -Severe Chronic Obstructive -Pulmonary Disease (COPD)
Nitrous Oxide (N20) -precautions-side effects
Precautions -Use in well-ventilated area Side Effects -Headache, nausea, vomiting
Nitrous Oxide (N20) -route-dose-pharmacokinetics
Route -Inhalation Dose -Self-administered via demand valve Pharmacokinetics -Onset: 2–5 min -Peak effects: Varies -Duration: 2–5 min
Nitrous Oxide (N20) -How Supplied SKIP FOR NOW-Special Considerations
How Supplied -Cylinder containing 50% nitrous oxide and 50% oxygen Special Considerations -May not work in low temperatures -Monitor SpO2
Ondansetron -generic name-trade name-class
Generic name: -Ondansetron Trade name:- Zofran®, Zofran ODT®, Zuplenz® Classification -Antiemetic, selective 5-HT3 antagonist
Ondansetron -MOA
-Not fully characterized; selective 5-HT3 receptor antagonist; binds to 5-HT3 receptors both in PNS and CNS with primary effect on GI tract. -It has no effect on dopamine receptors, therefore does not cause extrapyramidal symptoms.
Ondansetron -indications-contraindications
Indications -Nausea and vomiting (chemotherapy, postoperative, and radiation) -Nausea and vomiting NOT cause by vertigo, motion sickness or inner ear disturbances -Hyperemesis Contraindications -Hypersensitivity -Co-administration with apomorphine has been reported to cause profound hypotension and loss of consciousness
Ondansetron -cautions-side effects
Cautions -Reduce dose with severe hepatic impairment Side Effects -Gastrointestinal: nausea and vomiting -Anaphylaxis -General: flushing, rare cases of hypersensitivity reactions, sometimes severe (e.g., anaphylactic reactions, angioedema, bronchospasm, cardiopulmonary arrest, hypotension, laryngeal edema, laryngospasm, shock, shortness of breath or stridor) -Local reactions: pain, redness, burning feeling at site -Lower respiratory: hiccups -Neurological: oculogyric crisis -Integumentary: Urticaria, Stevens-Johnson syndrome and toxic epidermal necrosis -Ocular: transient blindness (mostly IV administration) reported to resolve within 48hrs -Musculoskeletal: arthralgia
Ondansetron -route-pharmacokinetics
Route -IM, IV, Orally Pharmacokinetics -Onset: 30 mins -Peak effects: 1–2 hours (IV) -Duration: 3–6 hours (IV)
Ondansetron -dose
Adult <65: 4–8 mg IV/IM-IV push over 2–5 min, repeat q 8 hours (can be diluted in 10 mLs of NS or undiluted) Adult >65:4–8 mg- IV/IM-IV is mixed in 50 mL bag and infused over 15–20 minutes, repeat q 8 hours Note: Can be given orally if necessary, when IV/IM not possible Pediatrics (8–15 kg): 2 mg IV/IM- IV push over 2–5 minutes (can be diluted in 10 mLs NS or undiluted) Pediatrics (over 15 kg): 4 mg IV/IM - IV push over 2–5 minutes (can be diluted in 10 mLs NS or undiluted), with one repeat.
Ondansetron -how supplied SKIP FOR NOW-special considerations
How Supplied -2 mg/mL (2 mL) OR 2 mg/mL (4 mL) Special Considerations -Ondansetron is generally given to patients undergoing Chemotherapy and/or radiation therapy to treat the nausea and vomiting. -Note: for children, it does not appear to be a drug of choice to treat nausea and vomiting. -Dose-dependent QT prolongation -Avoid in patient with congenital long QT syndrome -ECG monitoring recommended in patient who have electrolyte abnormalities, congestive heart failure (CHF) or bradycardia arrhythmias, or who are also receiving other medications that cause QT prolongation.
Oral Glucose -generic name-trade name-class
Generic name:- Oral glucose Trade name: -Glutose®, Insta-Glucose® Classification -Carbohydrate, monosaccharide
Oral Glucose -MOA
Provides prompt increase in circulating blood sugar
Oral Glucose -indications-contraindications
Indications -Hypoglycemia Contraindications -Hyperglycemia
Oral Glucose -precautions-side effects
Precautions -If patient has decreased level of consciousness, patient must be placed on side and glucose applied buccally Side Effects -Nausea and vomiting
Oral Glucose -route-dose-pharmacokinetics
Route -PO Dose -15–45 g Pharmacokinetics -Onset: Immediate -Peak effects: Varies -Duration: Varies
Oral Glucose -how supplied-special considerations
How Supplied -In tubes and tablets of varying concentrations Special Considerations -Always ensure that a blood glucose reading is obtained before administration
oxygen-trade name-class
Trade name: -Oxygen Classification -Gas
oxygen-MOA
Reverses hypoxemia, necessary for cellular metabolism
oxygen-indications-contraindications
Indications -Hypoxia, signs of inadequate tissue perfusion Contraindications -None
oxygen-precautions-side effects
Precautions -Chronic obstructive pulmonary disease (COPD) Side Effects -Drying of mucus membranes
oxygen-route-dose-pharmacokinetics
Route -Inhalation Dose -2–15 lpm (titrate to effect) Pharmacokinetics -Onset: Immediate -Duration: Less than 2 min
oxygen-how supplied-special considerations
How Supplied -Oxygen cylinders containing 100% compressed gas Special Considerations -Humidify if using for long periods of time
Methoxyflurane (Penthrox®) -generic name-trade name-class
Generic name:-Methoxyflurane Trade name: -Penthrox® Classification Analgesic gas -
Methoxyflurane (Penthrox®) -MOA
Active ingredient is methoxyflurane, works by decreasing the CNS and making patients less responsive to pain. Research is unsure how this drug effects the CNS.
Methoxyflurane (Penthrox®) -indications-contraindications
Indications -Moderate to severe pain related to trauma Contraindications -Inadequate understanding/patient cooperation -Decreased level of consciousness -Psychosis -Pre-eclampsia -Moderate to severe renal and/or liver impairment -Hypersensitivity/ family history of malignant hyperpyrexia without negative personal test -Significant cardiovascular compromise -Raised intracranial pressure
Methoxyflurane (Penthrox®) -precautions-side effects
Precautions -Used with care in patients with underlying hepatic conditions -Previous exposure to halogenated hydrocarbon anesthetic (methoxyflurane when used as an anesthetic agent) especially if the interval is less than 3 months. -May increase the potential for hepatic injury. Side Effects -Altered level of consciousness -Cough
Methoxyflurane (Penthrox®) -route-dose-pharmacokinetics
Route -Inhalation Dose -Self-administered -One bottle containing 3 mL of Penthrox® to be vaporized is a supplied inhaler -Maximum dose is 6 mL in a 48-hour period Pharmacokinetics -Onset 1 to 3 minutes -Duration 1 hour -Half-life unavailable
Methoxyflurane (Penthrox®) -how supplied SKIP FOR NOW-special notes
How Supplied -Bottle containing 3 mL Penthrox® Special Notes -When disposing Penthrox®, the inhaler and medication is to be placed in plastic bags provided, sealed and disposed
Salbutamol -generic name-trade name-class
Generic name: -Salbutamol Trade name: -Ventolin® Classification -Bronchodilator
