Pharmacology and fluid therapy PART 1 Flashcards

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1
Q

The word pharmacology comes from the Greek words

A

Pharmakon meaning drug or poisonlogos meaning word or discourse

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2
Q

The goal of emergency pharmacology in the prehospital setting is

A

to use medication’s to reverse, prevent or control various diseases and illnesses, chronic and acute

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3
Q

Ancient Health Care

A

Ancient Egyptian healthcare was heavily influenced by spiritual beliefs however it incorporated Basic first aid and chemical compounds to treat certain ailments

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4
Q

The Pre-Renaissance and Post- Renaissance Periods

A

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

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5
Q

Modern Health Care

A

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

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6
Q

Pharmacology is defined as

A

the study of drugs and their effects on the body

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7
Q

Common Pharmacology Abbreviations -IV-IM-SQ-ET

A

IV (intravenous) IM (intramuscular) SQ or SC (subcutaneously) ET (endotracheal)

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8
Q

Common Pharmacology Abbreviations -IO-PO-PRN-NEB

A

IO (intraosseous) PO (per os or by mouth) PRN (pro re nata or as needed) NEB (nebulized)

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9
Q

Common Pharmacology Abbreviations -o.d -b.i.d-t.i.d-q.i.d 

A

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)

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10
Q

Common Pharmacology Abbreviations -q-IN-p.r.

A

q (every) IN (Intra Nasal) p.r. (Per Rectum)

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11
Q

Pharmaceutical preparations

A

are preparations that make a drug suited to certain method(s) of administration.

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12
Q

characteristics or properties that dictate in what form drugs will be manufactured

A

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.

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13
Q

Today, drug companies try to prepare drugs in forms that:

A

Can be easily administered. Contain the exact dose that a physician prescribes.

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14
Q

Extract

A

Concentrated preparation of a drug made by putting the drug into a solution and evaporating the excess solvent

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15
Q

Powder

A

A drug that has been ground into a pulverized form

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16
Q

Capsule

A

 A gelatin container that encloses a dose of medication

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17
Q

Pulvule

A

 Similar to a capsule except that it is not made of gelatin

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18
Q

Tablet

A

 A powdered drug that has been pressed into a small disk

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19
Q

Suppository

A

A drug in a firm base that is designed to melt at body temperature

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20
Q

Ointment

A

 A semisolid preparation that is designed for external application

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21
Q

Patch

A

Contains medication on the surface of an adhesive patch

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22
Q

Solution

A

 A liquid containing one or more chemicals dissolved in water

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23
Q

Suspension

A

Supplied as a powder and requiring the addition of water

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24
Q

Fluid extract

A

Concentrated form of the drug prepared by dissolving the drug in the fluid

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25
Q

Tincture

A

Dilute alcoholic extract of a drug

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26
Q

Spirits

A

Preparation of a volatile substance dissolved in alcohol

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27
Q

Elixir

A

Solution with alcohol and flavoring added

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28
Q

Milk

A

Aqueous suspension of an insoluble drug

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29
Q

Emulsion

A

One liquid (usually oil) distributed in small globules in another liquid (usually water)

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30
Q

Liniments

A

A lotion that is designed for external use

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31
Q

Vapour

A

Liquid form that when placed in a device that allows vaporization, allows the patient to inhale the medication

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32
Q

drug use: -define-examples Prevention

A

A drug used to prevent the occurrence of a disease. Heptavax B® Tetanus toxoid

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33
Q

drug use: -define-examplesDiagnosis

A

A drug used to determine the nature of an illness or disease. Radiopaque dyes  

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34
Q

drug use: -define-examplesTreatment

A

A drug used in the management of a disease or disorder. Lidocaine Atropine

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35
Q

drug use: -define-examplesCure

A

A drug used to eliminate the disease process. Ampicillin Cloxacillin

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36
Q

drug use: -define-examplesContraception

A

A drug used to prevent pregnancy. Ortho® 7/7/7 28 days Norinyl® 1/50

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37
Q

drug use: -define-examplesHealth Maintenance

A

A drug taken to maintain homeostasis and supplement deficient body chemistry. Vitamins B12 Vitamin C Humulin N Novolin® ge Toronto

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38
Q

Sources of Medications

A

plantanimalmineralsynthetic

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39
Q

plant meds

A

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)

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40
Q

animal meds

A

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.

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41
Q

mineral meds

A

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

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42
Q

synthetic meds

A

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

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43
Q

Health Canada’s Therapeutic Products Directorate (TPD)

A

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

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44
Q

Compendium of Pharmaceuticals and Specialties (CPS)

A

complies data on most medication’s available in Canada uses; includes info on indications, dosages, contraindications and adverse reactions

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45
Q

Hospital formulary

A

a list of medication’s, dosage forms, package sizes and medication strength stocked by particular hospitals and it’s pharmacies

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46
Q

Drug inserts

A

printed document included in the packaging provided by medication to manufacture often referred to as product monograph

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47
Q

American Hospital Formulary Service Drug Info

A

provides another source of useful in miscellaneous drug info for pharmacist and medical practitioners includes generic and trade names

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48
Q

Epocrates, Lexi-Comp, Micromedex

A

reliable and popular resources online easy to use great source of drug info

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49
Q

Every medication is assigned 4 names

A

Chemical name Trade name Generic name Official Name

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50
Q

define medication

A

is a drug that has been approved by the government agency that regulates pharmaceuticals

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51
Q

Health Products and Food Branch (HPFB)

A

is the Canadian agency that regulate pharmaceuticals The Food and Drugs Act is the applicable legislation that ensures public safety with regard to medication

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52
Q

A drug as defined by health Canada

A

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

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53
Q

Pharmaceutical companies protect their investments by obtaining patents on their new drugs

A

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

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54
Q

The chemical name

A

describes the drugs chemical makeup, it’s composition and molecular structure

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55
Q

The generic name

A

is a general name for a drug and is usually created by the company that first manufactures the chemical

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56
Q

International Nonproprietary Name Program

A

1950s the world health organization initiated to standardize generic names

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57
Q

The trade name or brand name

A

is the unique name under which the original manufacture registers the new drug with the HPFB

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58
Q

Drug legislation

A

responsible for ensuring that standards are maintained

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59
Q

Every health worker must have a working knowledge of the legal implications associated with giving drugs so that he/she will be able to

A

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

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60
Q

Canadian Regulation of Pharmaceuticals

A

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

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61
Q

Manufacturing Related Regulations

A

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

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62
Q

AssayBioassay

A

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

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63
Q

The HPFB

A

is Canada’s federal authority responsible for regulation of health products and food through enforcement of the food and drug act

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64
Q

Within HPFP there are three directorates:

A

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

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65
Q

The Office of Controlled Substances

A

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

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66
Q

The Pharmaceutical Advertising Advisory Board and Advertising Standards Canada

A

independently review pharmaceutical advertisements to determine compliance with the Food and Drug Act

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67
Q

The Marketed Health Products Directorate is responsible for post marketing surveillance of adverse events secondary to market and drugs

A

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

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68
Q

The Drug Approval Process

A

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

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69
Q

Clinical trials proceed in four phases

A

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

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70
Q

The Canadian Health Protection Branch of the Department of National Health and Welfare

A

is responsible for administration and enforcement of federal legislation for the Food and Drugs Act and the Controlled Drugs and Substances Act

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71
Q

Canadian Drug Legislation

A

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

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72
Q

The Canadian Food and Drugs Act

A

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.

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73
Q

There are three major classifications of drugs under the Food and Drugs Act:

A

Non-prescription drugs Prescription drugs, and Restricted drugs.

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74
Q

The Canadian Controlled Drugs and Substances Act 

A

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

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75
Q

The  Controlled Drugs and Substances Act  organizes drugs into eight schedules, depending on

A

their dependence and abuse potential and their usefulness in medical therapy:

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76
Q

The  Controlled Drugs and Substances Act: Schedule i

A

Includes narcotics such as opium, heroin, morphine, and cocaine

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77
Q

The  Controlled Drugs and Substances Act: Schedule ii

A

Includes cannabis and cannabis resin

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78
Q

The  Controlled Drugs and Substances Act: Schedule iii

A

Includes stimulants and hallucinogens

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79
Q

The  Controlled Drugs and Substances Act: Schedule iv

A

Includes anabolic steroids, barbiturates, and benzodiazepines

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80
Q

The  Controlled Drugs and Substances Act: Schedule v

A

Includes phenylpropanolamine

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81
Q

The  Controlled Drugs and Substances Act: Schedule vi

A

Includes precursors that can be converted or used to produce “designer drugs” or other controlled substances

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82
Q

The  Controlled Drugs and Substances Act: Schedule vii

A

Defines limits associated with application of cannabis — related penalties, cannabis (3 kg), and cannabis resin (3 kg)

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83
Q

The  Controlled Drugs and Substances Act: Schedule viii

A

Defines limits associated with application of cannabis — related penalties, cannabis (30 kg), and cannabis resin (1 g)

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84
Q

MedSask

A

provides health care professionals and consumers with objective, concise and unbiased information on drug therapy

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85
Q

Canada Vigilance Regional Office (Saskatchewan)

A

Report adverse drug reactions to the Canadian Vigilance Program

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86
Q

RxFiles Academic Detailing Program

A

The RxFiles provides objective comparative drug information to promote optimal drug therapy

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87
Q

The Saskatchewan Formulary

A

is a list of the drugs of proven high quality that have been approved for coverage under the Drug Plan

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88
Q

Pharmacokinetics

A

what the body does to the drug

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89
Q

ADME

A

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

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90
Q

Absorption

A

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

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91
Q

factors affecting the absorption of a medication including

A

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)

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92
Q

Distribution

A

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

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93
Q

bound drugfree drug

A

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

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94
Q

metabolism (biotransformation)

A

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

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95
Q

Excretion

A

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.

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96
Q

Drug Half-Life

A

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

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97
Q

The  minimum effective concentration (MEC) or therapeutic index

A

is a term indicating the lowest concentration of drug in the blood able to produce a therapeutic effect useful in determining adequate dosages

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98
Q

The therapeutic range describes

A

the range between MEC and the toxic concentration where the drug can seriously harm the client

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99
Q

Onset of Action

A

is the time after administration when the drug reaches the MEC and begins to produce its effects

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100
Q

Principles Related to Onset of Action

A

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

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101
Q

The duration of actionThe termination of action

A

–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

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102
Q

Duration of action of : -fentanyl (Sublimaze®),-meperidine (Demerol®), -morphine, -acetaminophen (Tylenol®),

A

fentanyl (Sublimaze®), 1–2 hours meperidine (Demerol®), 2–4 hours morphine, 3-7 hours acetaminophen (Tylenol®), 4–6 hours

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103
Q

Principles Related to Duration of Action

A

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.

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104
Q

Sites of Elimination

A

Kidneys (main site of elimination) GI tract Perspiration Respiration

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105
Q

Pharmacodynamics

A

what the drug does to the body

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106
Q

Drugs either alter the ——- —- or change the —— — — — —-

A

Drugs either alter the cell environment or change the rate of cell functions

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107
Q

the receptor theory of drug action

A

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.

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108
Q

the cell is said to be receptive to the drug if…

A

If at least three sites on the surfaces of both drug and cell match

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109
Q

what are receptors usually made of

A

cellular proteins or nucleic acids but can be enzymes, carbohydrate residues, and lipids

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110
Q

Agonist

A

a drug that directly alters the rate of a cellular process

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111
Q

Affinity for the target tissue

A

An agonist has a natural tendency to bind with the receptor

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112
Q

Efficacy

A

ability to initiate drug action

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113
Q

Partial agonists 

A

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.

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114
Q

Antagonists

A

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

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115
Q

Numerous factors affect an individual’s response to drugs, including:

A

Age Weight Gender Environment Time of administration Condition of the patient Genetic factors Psychologic factors

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116
Q

Types of Responses

A

predictableunpredictableiatrogenic

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117
Q

Predictable response

A

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

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118
Q

Unpredictable response

A

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

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119
Q

 idiosyncrasy

A

an abnormal or unusual response to a drug

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120
Q

Tolerance

A

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

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121
Q

Cross-tolerance

A

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

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122
Q

Tachyphlaxis

A

condition where patient rapidly becomes tolerant to a medication

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123
Q

Drug dependence

A

a physical or emotional need for drug

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124
Q

Cumulative effect

A

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

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125
Q

Summative effect

A

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

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126
Q

Synergism

A

combined action of two drugs that is greater than the sum of their individual responses

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127
Q

Potentiation

A

enhanced action of the drug by another administered concurrently

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128
Q

Iatrogenic response

A

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.

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129
Q

in the metabolic phase The liver can act on a drug in 2 phases

A

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)

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130
Q

excretion occurs primarily through the kidneys 3 mechanisms

A

Glomelur filtration Tubular secretion Partial reabsorption

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131
Q

Glomelur filtration

A

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

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132
Q

Tubular secretion

A

an active transport process in which medications are bound to specific transporters aiding in their elimination

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133
Q

Partial reabsorption

A

this occurs when some amount of the drug is reabsorbed after being filtered

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134
Q

Medications cause their action on the body by four mechanisms:

A

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

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135
Q

A medication molecule witll have 1 of 2 effects when it binds to a receptor site

A

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)

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136
Q

The autonomic nervous system

A

is composed of nerve fibers that send impulses from the CNS to smooth muscles, cardiac muscles, and glands

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137
Q

The autonomic nervous system (ANS) consists of two further subdivisions:

A

Parasympathetic  nervous system Sympathetic  nervous system

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138
Q

Nerve fibers associated with the parasympathetic system originate

A

from the spinal cord at the level of the cervical and sacral regions

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139
Q

Parasympathetic nervous system is responsible for actions such as:

A

Decreased heart rate Decreased cardiac contractile force Decreased blood pressure Increased circulation to digestive organs Increased peristalsis Constriction of the pupils Bronchoconstriction

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140
Q

The principle neurotransmitter of the parasympathetic nervous system is

A

acetylcholineuh·seh·tuhl·kow·leen

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141
Q

acetylcholine

A

Acetylcholine is very short lived. within seconds of release it is deactivated by another chemical called acetylcholinesterase

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142
Q

Within the parasympathetic nervous system there are two main types of acetylcholine receptors

A

nicotinic and muscarinic

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143
Q

Muscarinic receptors

A

are primarily responsible for parasympathetic overactivity responses

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144
Q

Muscarinic responses and what reverses them

A

including bradycardia, miosis (pinpoint pupils), sweating, blurred vision, tearing, wheezing, SOB, coughing, vomiting, abdominal cramps, diarrhea atropine reverses them

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145
Q

nicotinic receptors

A

are primarily responsible for sympathetic overactivity response and neuromuscular disfunction causes muscular contractionsopened by nicotine

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146
Q

nicotinic responses

A

responses include tachycardia, hypertension, dilated pupils, muscle fasciculation (involuntary twitching etc) and muscle weakness

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147
Q

cholinergic receptors

A

these receptors respond to acetylcholinenicotinic and muscarinic

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148
Q

parasympathomimetic  or cholinergic agonists

A

producing effects that resemble (mimic) the stimulation of the parasympathetic nervous system If a medication binds to and stimulates those receptors

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149
Q

parasympatholytic  or anticholinergic

A

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

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150
Q

Nerve fibers associated with the sympathetic system originate

A

from the spinal cord at the level of the thoracic and lumbar regions

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151
Q

Sympathetic nervous system is responsible for actions such as:

A

Increase heart rate Increase blood pressure Peripheral vasoconstriction Increase circulation to vital organs Sweat gland stimulation

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152
Q

The principle neurotransmitters of the sympathetic nervous system are

A

catecholamines norepinephrine epinephrine

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153
Q

Within the sympathetic nervous system there are two main types of receptors

A

adrenergic  and  dopaminergic.

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154
Q

Dopaminergic receptors

A

are believed to cause renal, coronary, and cerebral artery dilation

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155
Q

Adrenergic receptors

A

are the receptors that are most common within the sympathetic nervous systemthe receptors stimulated by prehospital medications

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156
Q

Adrenergic receptors 4 classes

A

Alpha1 Alpha2 Beta1 Beta2

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157
Q

where are the following receptors primarily locatedAlpha 1Alpha 2Beta 1Beta 2

A

Alpha 1: on peripheral blood vesselsAlpha 2: on nerve endingsBeta 1: within the cardiovascular systemBeta 2: on bronchial smooth muscle

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158
Q

Alpha 1 stimulation results in:

A

Peripheral vasoconstriction Mild bronchoconstriction Increased metabolism Stimulation of sweat glands

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159
Q

Alpha 2 stimulation results in:

A

Control release of neurotransmitters

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160
Q

Beta 1 stimulation results in:

A

Increased heart rate (positive chronotropic) Increased strength of cardiac contraction (positive inotropic) Increased cardiac conduction (positive dromotropic)

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161
Q

Beta 2 stimulation results in:

A

Bronchodilation Peripheral vasodilation

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162
Q

sympathomimetic  or adrenergic agonists

A

If a medication binds to and stimulates any of the adrenergic receptors

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163
Q

what do sympathomimetic or adrenergic agonists do

A

producing effects that resemble the stimulation of the sympathetic nervous system

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164
Q

sympatholytic or adrenergic antagonist

A

blocking effects or producing effects that resemble interruption of the sympathetic nervous system

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165
Q

Selective beta blockers

A

bind and block only beta 1 or beta 2 receptors

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166
Q

non-selective beta blockers

A

would block both beta 1 and beta 2 receptors

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167
Q

Drugs are organized into classifications according to

A

the body system they affect, their therapeutic use or clinical indication, and/or their physiologic or chemical action

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168
Q

13 classifications of drugs

A

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

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169
Q

Opioid

A

binds to opioid receptors to provide analgesic effects

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170
Q

Analgesic

A

medication that relieves pain

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171
Q

Anesthetics

A

medication that makes the body less sensitive to the perception of pain

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172
Q

Bronchodilators

A

medication which increases airflow to lungs by dilating the bronchi and bronchioles

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173
Q

Antiangina

A

medication to manage or reduce the heart condition angina

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174
Q

Anticoagulants

A

medication to prevent blood clots

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175
Q

Platelet inhibitors

A

medications which reduce blood clotting by preventing platelet cohesion

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176
Q

Uterotonics

A

medication to induce contraction of uterus

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177
Q

Antihypoglycemic

A

counteracting low blood glucose  

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178
Q

Antimicrobials

A

medication to destroy or slow growth of microorganisms

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179
Q

Antidotes

A

medication to counteract poison

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180
Q

The CNS

A

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

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181
Q

The classifications that you are going to study that affect the central nervous system are:

A

Opioid antagonists Non-narcotic analgesics Inhalation anesthetics

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182
Q

Opioid Antagonist

A

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

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183
Q

Mechanism of Action of Opioid Antagonist

A

Opioid antagonists attach to opioid receptors and displace the narcotic, thereby rapidly reversing the effects of the narcotic

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184
Q

Types of Opioid Antagonists

A

Pure antagonists Partial antagonists

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185
Q

Pure antagonists

A

Competitive blocking drugs Occupy a receptor site so that narcotic cannot, but do not have any effect themselves

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186
Q

Partial antagonists

A

Bind with receptor sites Produce weak narcotic-like effects in the absence of other narcotics

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187
Q

common uses of Opioid Antagonists

A

Narcotic induced respiratory depression Narcotic addictions

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188
Q

common examples of Opioid Antagonists

A

*Naloxone Nalmefene Butorphanol Nalbuphine Pentazocine

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189
Q

cautions of Opioid Antagonists

A

Partial antagonists may cause worsening of respiratory depression Use caution when administering to individuals that are addicted to narcotics due to resulting withdrawal symptoms

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190
Q

Non-Narcotic Analgesics

A

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

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191
Q

Mechanism of Action of Non-Narcotic Analgesics

A

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

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192
Q

Common Uses of Non-Narcotic Analgesics

A

Mild pain management Reduce fever Pain from inflammation

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193
Q

Common Examples of Non-Narcotic Analgesics

A

Nonsteroidal anti-inflammatory drugs (NSAID) *Ibuprofen *Ketorolac Naproxen Salicylates *Aspirin® Analgesic/Antipyretic *Acetaminophen (Tylenol®)

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194
Q

Cautions of Non-Narcotic Analgesics

A

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

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195
Q

Anesthetics

A

An anesthetic is any drug that has the capability of causing loss of all sensations, not only the sensation of pain

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196
Q

two types of general anesthetics:

A

Inhalation  anesthetic Injection  anesthetic

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197
Q

Mechanism of Action of general anesthetics

A

There are 4 stages to anesthesia, and mechanism of action depends on the stage that is achieved by the drug.

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198
Q

4 stages of Anesthetics

A

Stage 1: AnalgesiaStage 2: Involuntary movementStage 3: Surgical anesthesiaStage 4: Medullary paralysis

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199
Q

Stage 1 of anesthetics

A

Stage 1: Analgesia. Cerebral cortex is inhibited causing a decreased response to pain, a feeling of euphoria, and possible unconsciousness.

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200
Q

stage 2 of anesthetics

A

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.

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201
Q

stage 3 of anaesthetics

A

Stage 3: Surgical anesthesia. The hypothalamus is depressed, and cardiac and respiratory function returns to normal. Spinal reflexes are blocked and skeletal muscles relax.

202
Q

stage 4 of anesthetics

A

Stage 4: Medullary paralysis. The medulla is paralyzed, thus cardiac and respiratory centres are affected, and death may occur.

203
Q

common uses of anesthetics

A

Surgeries Dental procedures Pain control (nitrous oxide’s main use)

204
Q

Common Types of Inhalation Anesthetics

A

Volatile liquids –Ether –Enflurane –Halothane

205
Q

Gases

A
  • Nitrous oxide -Penthrox 
206
Q

cautions of anesthetics

A

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

207
Q

non-opiod analgesics

A

have antipyretic properties

208
Q

3 main types of non-opiod analgesics

A

Salicylates (asprin) Non steroidal anti-inflammatory medications (NSAIDs) (ibuprofen) Para-aminophenol derivatives (tylenol)

209
Q

Sedation

A

used to couteract anxiety before procedure

210
Q

Hypnosis

A

medications that ensure they sleep through event

211
Q

Benzodiazepines and MOA

A

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

212
Q

Midazolam (Versed)

A

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

213
Q

Diazepam (Vilum)

A

moderatley longer acting benzodiazepine 30-90 min duration of action Onset of action 5mins

214
Q

Barbiturates and MOA

A

believed to work similarto benzo’s; MOA: increase affinity between receptor sites and the inhibitory neurotransmitter GABA

215
Q

Thiopental (pentothal)

A

short acting barbiturate Onset action of 10-20secs Duration of action 5-10mins

216
Q

Nonbarbiturate hypnotics

A

almost identical properties to benzo’s and barbiturates

217
Q

Etomidate(Amidate/Lipuro)

A

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

218
Q

Propofol (diprivan)

A

Onset of 10-20 secs Duration lasts 10 to 15mins

219
Q

Anticonvulsants and MOA

A

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

220
Q

Classes of anticonvulstants include

A

hydantoins (phenytoin [Dilantin]),iminostilbenes (carbamazepine) valproic acid

221
Q

Stimulation of CNS can be acomplished in 2 ways

A

increasing excitatory neurotransmitters by decreasing inhibatory neurotransmitters

222
Q

Amphetamines

A

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

223
Q

Methylphenidate (Ritalin)

A

intended to allow pts to better focus and avoid distraction

224
Q

Psychotherapeutic Medications and MOA

A

MOA: work by blocking dopamine receptors

225
Q

Depression often treated with

A

seretonin reuptake inhibitors

226
Q

Monoamine oxidase inhibitors

A

block the metabolism of monoamines in the brain

227
Q

Tricyclic antidepressants (TCAs)

A

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

228
Q

CNS Agents

A

a class of drugs that produce physiological and psychological effects through a variety of mechanisms

229
Q

specific agents

A

which bring about an identifiable mechanism with unique receptors for the agent

230
Q

Nonspecific agents

A

which produce effects on different cells through a variety of mechanisms and are generally classified by the focus of action or specific therapeutic use

231
Q

Stimulants

A

exert their action by excitation of the CNS some of the specific drugs included in this group are caffeine, cocaine and various amphetamines

232
Q

Patient may be prescribed CNS depressants which

A

slow brain activity to treat anxiety, muscle tension, pain, insomnia, stress, panic attacks and sometimes seizures

233
Q

CNS depressant examples

A

lorazepam (Atrivan) triazolam (Halcion), chlordiazepoxide (Librium). Diazepam (Valium), alprazolam (xanax) opiclone (Imovane)

234
Q

the sympathetic branch of the ANS is based on… the parasympathetic branch function is to…

A

The sympathetic branch of the ANS is based on the parasympathetic branch function is to return the body to balance (homeostasis)

235
Q

neurotransmitters for the adrenergic (sympathetic) response

A

epinephrine and norepinephrine

236
Q

Medications that affect the ANS will…

A

either trigger or block an autonomic response

237
Q

Adrenergic Agonists

A

often referred to as sympathomimetic drugs because they “mimic” the actions of the sympathetic nervous system.

238
Q

Mechanism of Action of Adrenergic Agonists

A

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.

239
Q

Non-selective α and β Agonists uses and action

A

*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

240
Q

α1 agonist uses and action

A

Decongestants -Stimulate α1 receptors causing vasoconstriction and thereby decreasing congestion in the area

241
Q

α2 Agonists uses and action

A

Treatment of glaucoma -Stimulates α2 receptors causing a decrease in intraocular pressure

242
Q

β1 Agonists: uses and action

A

Treatment of cardiac arrest and hypotension -Stimulates β1 receptors causing an increase in heart rate, force of cardiac contraction, and cardiac conduction

243
Q

β2 Agonists: uses and actions

A

Bronchodilators -Stimulate β2 receptors, decreasing bronchoconstriction and causing bronchodilation

244
Q

adrenergic drug cautions and side effects

A

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)

245
Q

Beta-receptor - general(non-specific)ex: eye-effect-beta agonist-beta antagonist

A

-effectrelaxes ciliary muscle-beta agonistnon specific agonists: isoproterenol epinephrine-beta antagonistpropranololtimololnadolol

246
Q

b1 selective drugsex: myocardium-effect-beta agonist-beta antagonist

A

-effectincreases contractility increases heart rate-beta agonistnorepinephrine-beta antagonistmetoprololatenolol

247
Q

b2 selective adrenergic drugsex: lungs -effect-beta agonist

A

-effectbronchodilation-beta agonistbronchodilators:fenoterolalbuterolterbutaline

248
Q

Alpha-receptor - generalex: vascular smooth muscle-effect-beta agonist-beta antagonist

A

-effectskin and skeletal muscle vessel constriction-beta agonistepinephrinenorepinephrine-beta antagonistphentolamine

249
Q

a1 drugsex: vascular smooth muscle-effect-beta agonist-beta antagonist

A

-effectvasoconstriction-beta agonistphenylephrine-beta antagonistprazosin

250
Q

a2 drugsex: vascular smooth muscle-effect-beta agonist-beta antagonist

A

-effectOpposes α1 vasoconstriction Inhibits NE release Decreases adrenergic activity-beta agonistclonidine-beta antagonistyohimbine

251
Q

Neuromuscular blocking agents

A

affect the somatic nervouse system by inducing paralysis

252
Q

Depolarizing neuromuscular blocking agents

A

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

253
Q

Nondepolarizing neuromuscular blocking agents

A

find in a competitive but non-stimulatory manner to part of the ACH receptor as a result these drugs do not cause muscle twitches

254
Q

Succinycholine

A

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

255
Q

Vecuronium

A

a non-depolarizing neuromuscular blocker that produces paralysis Onset action of 30 seconds Duration of action of 30 minutes

256
Q

Pancuronium

A

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

257
Q

Adrenergic Agonists (sympathomimetics)

A

stimulates the adrenal medulla to release norepinephrine and epinephrin which stimulate one of two types of sympathetic receptors dopaminergic receptors and adrenergic receptors

258
Q

Dopiminergic receptors

A

produce dilation of renal, coronary and cerebral arteries there are no medication’s that specifically target these receptors

259
Q

3 categories of bronchodilators

A

β2 agonists  Anticholinergics Xanthines

260
Q

β2 Agonists

A

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

261
Q

short acting β2 Agonists

A

can be used about 15 minutes prior to exercise or exposure to a known trigger as a preventative measure common examples: *salbutamol,terbutaline,salmeterol

262
Q

long acting β2 Agonists

A

onset is slower but effects last 12 hours common example: formoterol

263
Q

Anticholinergics

A

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

264
Q

common anticholinergics

A

ipratropium bromide  combined  ipratropium bromide salbutamol

265
Q

Xanthines

A

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

266
Q

common Xanthines

A

theophylline, aminophylline

267
Q

common uses of all bronchodilators

A

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

268
Q

bronchodilator cautions

A

Short acting β2 agonists should only be used as required; not as a regular or daily drug

269
Q

bronchodilator Side Effects

A

CNS stimulation — anxiety, insomnia, restlessness, tremors Cardiac stimulation — tachycardia, palpitations, hypertension May precipitate angina, myocardial infarction, and dysrhythmias Nausea and vomiting Abdominal cramps

270
Q

bronchodilator drug interactions

A

Beta blockers may block the effect Monoamine oxidase inhibitors and tricyclic antidepressants may potentiate effects

271
Q

what is the preferred receptor to treat respiratory emergencies

A

beta 2 because they produce smaller increases in heart rate and force of contraction which decreases the body’s rate of oxygen consumption

272
Q

what is a well known CNS Stimulant which is also a Xanthine

A

caffeine

273
Q

common decongestants and cold products

A

pseudoephedrinedextromethorphandiphenhydramine

274
Q

Antianginal agents

A

are used to treat a cardiac condition called angina

275
Q

Angina

A

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

276
Q

Three main classes of antianginal agents are:

A

*Nitrates (currently only class that can be administered by PCP) Beta-blockers Calcium channel blockers

277
Q

Nitrates

A

can relieve symptoms of ischemic heart disease, but are not a cure for it.

278
Q

nitrates MOA

A

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

279
Q

Vasodilation results in:

A

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

280
Q

common uses of nitrates

A

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

281
Q

common examples of nitrates

A

*Nitroglycerin 

282
Q

cautions of nitrates

A

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

283
Q

drug interactions with nitrate

A

Viagra® Cialis® Levitra®

284
Q

Beta Blockers

A

another treatment and management used for angina.They are effective with angina pectoris, but are not effective when used for vasospastic angina.

285
Q

Beta Blockers MOA

A

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.

286
Q

common uses of beta blockers

A

Reducing the severity and frequency of exertional angina attacks Post myocardial infarction

287
Q

common examples of beta blockers

A

Metoprolol Atenolol Timolol

288
Q

cautions of beta blockers

A

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

289
Q

Calcium Channel Blockers

A

Calcium channel blockers are another treatment used to help treat and manage angina.

290
Q

Calcium Channel Blockers MOA

A

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

291
Q

Calcium Channel Blockers common uses

A

Angina Variant angina (Prinzmetal’s angina and vasospastic angina)

292
Q

Common Examples of Calcium Channel Blockers

A

Verapamil Diltiazem Nifedipine 

293
Q

cautions of Calcium Channel Blockers

A

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.

294
Q

Chronotropic effectInotropic effectsDromotropic effects

A

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

295
Q

Cardiac glycosides

A

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

296
Q

Antidysrhythmic medications

A

used to treat and prevent cardiac rhythm disorders further classified into four groups according to the fundamental mode of action on the heart

297
Q

four groups of antidysrhythmic medications

A

Sodium channel blockersBeta blockersPotassium chanel blockersCalcium channel blocker’s

298
Q

Sodium channel blockers effect on heart

A

slow the conduction through the heart (negative dromotropic effect)

299
Q

Beta blockers effect on heart

A

reduce the adrenergic stimulation of the beta receptors

300
Q

Potassium channel blockers effect on heart

A

increase the heart contractility (positive inotrophy) and work against the reentry of blocked impulses

301
Q

Calcium channel blockers effect on heart

A

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)

302
Q

thrombolytics

A

designed to break down (lyse) the clot and improve client outcomes if given shortly after the development of the clot

303
Q

Anticoagulants

A

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

304
Q

MOA of anticoagulants

A

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

305
Q

Common Examples of anticoagulants

A

*Heparin (monitor only) Low molecular weight heparins Warfarin

306
Q

common uses of coagulants

A

During or after surgeries A combination of anticoagulants may be used when a patient is first beginning oral anticoagulant therapy

307
Q

anticoagulants cautions

A

When doses are too high the following bleeding may result: Bleeding gums Nosebleeds Easy bruising

308
Q

Platelet inhibitors

A

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.

309
Q

MOA of platelet inhibitors

A

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

310
Q

TXA2

A

thromboxane A2 a type of thromboxane with prothrombotic properties

311
Q

Common Examples platelet inhibitors

A

*ASA Dipyridamole Ticlopidine Clopidogrel

312
Q

Common Uses platelet inhibitors

A

Primary prevention of a myocardial infarction Prevention of a reinfarction in patients with previous myocardial infarction history Prevention of thrombotic stroke

313
Q

Cautions platelet inhibitors

A

Increased risk of gastrointestinal bleeding and hemorrhagic stroke Increased risk of bleeding

314
Q

fibrolytic agent

A

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

315
Q

two different classifications of medications used to stop preterm labour, induce labour, or control postpartum hemorrhage

A

uterine stimulants and uterine relaxants.

316
Q

Uterotonics

A

given to facilitate uterine contraction

317
Q

MOA of uterotonics

A

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.

318
Q

Common Uses of uterotonics

A

Induce or speed up labour Facilitate contractions following a spontaneous abortion Treat postpartum hemorrhage

319
Q

Common Examples of uterotonics

A

*Oxytocin® (monitor only) Misoprostol Syntometrine Ergometrine

320
Q

Cautions of uterotonics

A

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.

321
Q

oxytocin

A

Naturally occurring hormone that has multiple reproductive functions it increases the force and frequency of contractions used to reduce postpartum haemorrhage

322
Q

tocolytic medication

A

Suppress the force and frequency metre and contractionsex: magnesium sulfateex: terbutaline

323
Q

magnesium sulfate

A

Relaxes the smooth muscles including those in the uterus

324
Q

terbutaline

A

Beta agonist that has been used as a tocolytic agent

325
Q

Vitamin and Electrolyte Supplements

A

The body is unable to synthesize vitamins and electrolytes and must, therefore, rely on an adequate and constant supply through diet

326
Q

MOA of Vitamin and Electrolyte Supplements

A

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

327
Q

Vitamin A

A

Required for production of rhodopsin which enables specialized retinal cells (rods) to adapt to dim light

328
Q

Vitamin D

A

Regulates serum calcium levels in conjunction with parathormone and calcitonin

329
Q

Vitamin E

A

Prevents formation and accumulation of toxic metabolites; maintenance of red blood cell membranes

330
Q

Vitamin K

A

Synthesis of blood clotting factors II, VII, IX, X

331
Q

Vitamin B

A

Necessary for cell reproduction and maturation

332
Q

Vitamin C

A

Involved in formation of catecholamines, steroids, and conversion reactions

333
Q

Sodium

A

Helps to maintain normal fluid balance

334
Q

*Potassium

A

Maintains cell structure and function; regulates muscle function (monitor only)

335
Q

Calcium

A

Plays role in muscle contraction, blood coagulation and bone formation

336
Q

Hydrogen

A

Regulates acidity and alkalinity of body fluids

337
Q

Cautions of Vitamin and Electrolyte Supplements

A

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.

338
Q

Antihypoglycemic Agents

A

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.

339
Q

MOA of Antihypoglycemic Agents

A

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

340
Q

common uses of Antihypoglycemic Agents

A

Hypoglycemia

341
Q

Common Examples of Antihypoglycemic Agents

A

*Glucagon *D5/D10 *D50W *Oral glucose

342
Q

Cautions of Antihypoglycemic Agents

A

Ensure that glucose levels are monitored before and after administration

343
Q

Antimicrobials

A

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

344
Q

General Guidelines for Use of Antimicrobials

A

Take as directed for the full course of treatment  Space doses evenly apart Be aware of compliance issues, reinfection, and superinfection

345
Q

Antibiotics

A

Antibiotics or antibacterial drug classes are used to treat bacterial infections Each antibiotic drug is generally effective for only certain pathogenic bacteria

346
Q

Types of Antibiotics

A

Beta-lactam Sulfonamide Tetracycline Macrolide Aminoglycoside Fluoroquinolone Miscellaneous

347
Q

type of Beta-lactam antibiotics

A

Penicillins Cephalosporin antibiotics Carbapenem antibiotics

348
Q

MOA of antibiotics

A

Preventing cell wall synthesis (penicillins) Blocking the synthesis of folic acid (sulfonamides) Interfering with protein synthesis (tetracyclines, macrolides, aminoglycosides) Interfering with DNA synthesis (quinolones)

349
Q

common uses of antibiotics

A

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

350
Q

cautions of antibiotics

A

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.

351
Q

Antivirals

A

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

352
Q

Types of Antivirals

A

Viral DNA Polymerase Inhibitors Antiretrovirals –RNA Reverse Transcriptase Inhibitors –Protease Inhibitors Viral Uncoating Blockers

353
Q

MOA of antivirals

A

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).

354
Q

Common Uses of antivirals

A

Treatment of herpes Decrease HIV virus production (antiretrovirals) Influenza A prophylaxis

355
Q

Cautions of antivirals

A

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.

356
Q

Antifungals

A

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.

357
Q

Types of Antifungals

A

Azole Nystatin Amphotericin B Terbinafine

358
Q

MOA of antifungals

A

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.

359
Q

Common Uses of antifungals

A

Skin and mucus membrane infections Systemic fungal infections Nail fungal infections

360
Q

Cautions

A

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

361
Q

Medications used to treat HIV

A

Classified as antiretrovirals -Nucleoside reverse transcriptase inhibitors: -Non nucleoside reverse transcriptase inhibitors: -Protease inhibitors

362
Q

Antidotes and Neutralizing Agents

A

Antidotes and neutralizing agents are administered in poisoning and overdose situations in an attempt to antagonize or inactivate the substance

363
Q

MOA of Antidotes and Neutralizing Agents

A

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

364
Q

Common Uses of Antidotes and Neutralizing Agents

A

Intentional and accidental overdose and poisonings

365
Q

Common Examples of Antidotes and Neutralizing Agents

A

-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

366
Q

cautions of Antidotes and Neutralizing Agents

A

Most poisons have no specific antidote, so care must be supportive in nature, focus on prevention of further absorption, and promote poison elimination

367
Q

common medication classifications that affect the gastrointestinal system

A

Antacids, Antiflatulents, Digestants, Antiemetics, LaxativesAntidiarrheals

368
Q

Antiemetics

A

Antiemetic is a classification of medication used to control nausea and vomiting in patients

369
Q

N/V is typically triggered by four main mechanisms:

A

Stimulation of the cerebral cortex and limbic system.  Stimulation of the chemoreceptor trigger zone (CTZ). Stimulation of the vestibular system.  Stimulation of peripheral pathways. 

370
Q

how Stimulation of the cerebral cortex and limbic system. cause n/v

A

The common causes of this type of N/V are increasing intracranial pressure, irritation of the meninges and emotional stress

371
Q

how Stimulation of the chemoreceptor trigger zone (CTZ). cause N/V

A

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.

372
Q

primary neurotransmitters within the chemoreceptor trigger zone (CTZ)

A

Dopamine (D2), Serotonin (5HT3) and Neurokinin (NK1) are the primary neurotransmitters within this area of the brain.

373
Q

How Stimulation of the vestibular system.  cause n/v

A

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.

374
Q

how Stimulation of peripheral pathways.  causes N/V

A

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.

375
Q

5-HT3 receptor antagonist

A

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.

376
Q

H1 Histamine antagonist

A

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.    

377
Q

Some common examples of antiemetics are:

A

*Gravol (H1 Histamine antagonist) *Ondansetron (5-HT3 receptor antagonist)

378
Q

Acetaminophen-Generic name-Trade name-Classification

A

Generic name:-AcetaminophenTrade name: -Tylenol®Classification-Analgesic, antipyretic

379
Q

Acetaminophen-Mechanism of action

A

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

380
Q

Acetaminophen-Indications-Contraindications

A

Indications-Pyrexic child-Severe sepsis-septic shockContraindications-hypersensitivity-Acetaminophen-induced liver disease

381
Q

Acetaminophen-precautions- side effects

A

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

382
Q

Acetaminophen-route-dose-pharmacokinetics

A

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

383
Q

SKIP FOR NOWAcetaminophen-how supplied

A

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)

384
Q

Activated Charcoal-Generic name-Trade name-Classification

A

Generic:-Activated charcoalTrade names:- Liqui-Char®, Actidose®, Charcodote®Classification-Antidote

385
Q

Activated Charcoal-Mechanism of action

A

Mechanism of Action-Binds and adsorbs ingested toxins from the gastrointestinal tract

386
Q

Activated Charcoal-Indications-Contraindications

A

Indications-Oral poisoning or overdoseContraindications-Caustic or corrosive substances-petroleum distillates

387
Q

Activated Charcoal-precautions- side effects

A

Precautions-decreased LOC.-If ipecac has been administered, wait 10 minutes.Side Effects-Nausea, vomiting-Constipation, cramping, bloating

388
Q

Activated Charcoal-route-dose-pharmacokinetics

A

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

389
Q

SKIP FOR NOWActivated Charcoal-how supplied

A

-Premixed with water or sorbitol-25 g / 125 mL bottle (200 mg/mL)-50 g / 250 mL bottle (200 mg/mL)

390
Q

Amyl Nitrate-trade name-classification

A

Trade name: -Amyl Nitrate®Classification-Vasodilator-Antidote

391
Q

Amyl Nitrate-Mechanism of Action

A

-Binds with hemoglobin to help biodegrade cyanide

392
Q

Amyl Nitrate-indications-contraindications

A

Indications-Acute cyanide poisoning with impaired LOCContraindications-no concrete proof of cyanide poisoning

393
Q

Amyl Nitrate-precautions-side effects

A

Precautions-FlammableSide Effects-Drowsiness

394
Q

Amyl Nitrate-route-dose-pharmacokinetics

A

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

395
Q

SKIP FOR NOWAmyl Nitrate-how supplied

A

0.2 mL or 0.3 mL glass ampoule

396
Q

Amyl Nitrate-Special Considerations

A

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.

397
Q

Acetylsalicylic Acid (ASA)-generic names-trade name-classification

A

Generic name:-Acetylsalicylic Acid (ASA)Trade name:-Aspirin®Classification-Platelet inhibitor-anti-inflammatory

398
Q

Acetylsalicylic Acid (ASA)- mechanism of action

A

Reduces production of thromboxane which mediates platelet aggregation.

399
Q

Acetylsalicylic Acid (ASA)- indications-contraindications

A

Indications-Chest pain, cardiac in originContraindications-Hypersensitivity to ASA or other NSAIDs-active peptic ulcers

400
Q

Acetylsalicylic Acid (ASA)-precautions-side effects

A

Precautions-Asthma patientSide Effects-Heartburn,-nausea/vomiting, -wheezing, -prolonged bleeding

401
Q

Acetylsalicylic Acid (ASA)-route-dose-pharmacokinetics

A

Route-PO, chewedDose-160–325 mgPharmacokinetics-Onset: Within 20 min-Peak effects: Varies-Duration: 2–3 hours

402
Q

SKIP FOR NOWAcetylsalicylic Acid (ASA)-how supplied

A

81 mg and 325 mg tablets

403
Q

Acetylsalicylic Acid (ASA)-special considerations

A

Administer regardless whether patient has taken their daily ASA dose

404
Q

Glucose-trade name-classification

A

Trade name: -Dextrose 50% (D50W), -Dextrose 25% (D25W),-Dextrose 10% (D10W),- Dextrose 5% (D5W)Classification-Carbohydrate, -Antihypoglycemic agent

405
Q

Glucose- mechanism of action

A

Increases blood sugar levels rapidly

406
Q

glucose-indications-contraindications

A

IndicationsHypoglycemiaContraindicationsHyperglycemia

407
Q

glucose-precautions-side effects

A

Precautions-Intracranial pressure – may worsen cerebral edemaSide Effects-Tissue necrosis-local venous irritation

408
Q

glucose-route-dose-pharmacokinetics

A

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

409
Q

SKIP FOR NOWglucose-how supplied

A

-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)

410
Q

glucose-special considerations

A

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.

411
Q

Dimenhydrinate-generic name-trade name-classification

A

Generic name:-DimenhydrinateTrade name: -Gravol®, Dramamine®Classification-Antiemetic (med for N/V)

412
Q

Dimenhydrinate-mechanism of action

A

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.

413
Q

Dimenhydrinate-indications-contraindications

A

Indications-Relief of nausea and vomitingContraindications-Hypersensitivity to dimenhydrinate or tartrazine.

414
Q

Dimenhydrinate-interactions

A

-Narcotics, sedatives or hypnotics, and alcohol – potentiates CNS depression

415
Q

Dimenhydrinate-side effects

A

Drowsiness, dizziness, blurred visionDry mouth, dry nose and bronchiTinnitus

416
Q

Dimenhydrinate-route-dose

A

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.

417
Q

Dimenhydrinate-pharmacokinetics

A

Excreted in urine, crosses placentaOnset: Immediate (IV), 20–30 minutes (IM)Peak effects: VariesDuration: 3–6 hours

418
Q

SKIP FOR NOWDimenhydrinate- how supplied

A

50 mg/mL

419
Q

Dimenhydrinate-special considerations

A

-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.

420
Q

Epinephrine 1 mg/mL-generic name-trade name-classification

A

Generic Name: -EpinephrineTrade name:-AdrenalineClassification-Sympathomimetic

421
Q

Epinephrine 1 mg/mL-mechanism of action

A

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

422
Q

Epinephrine 1 mg/mL-indications-contraindications

A

Indications-Anaphylaxis, status asthmaticus, and croupContraindications-Hypersensitivity

423
Q

Epinephrine 1 mg/mL-precautions-side effects

A

Precautions-Patients with cardiac history, pregnancySide Effects-Tachycardia, palpitations, arrhythmiasHeadache, anxiety, nausea/ vomiting

424
Q

Epinephrine 1 mg/mL-route -

A

IM, SQ, Nebulized

425
Q

Epinephrine 1 mg/mL-dose adult anaphylaxis

A

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

426
Q

Epinephrine 1 mg/mL-dose adult status asthmaticus

A

0.3 – 0.5 mg SC/IM (of 1 mg/mL concentration) q 5 – 10 minutes prn to a total of 1 mg

427
Q

Epinephrine 1 mg/mL- dose Peds anaphylaxis

A

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

428
Q

Epinephrine 1 mg/mL- dose Peds status asthmaticus

A

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

429
Q

Epinephrine 1 mg/mL- dose Peds croup

A

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)

430
Q

Epinephrine 1 mg/mL-pharmacokinetics

A

Onset: ImmediatePeak effects: VariesDuration: 5–10 min

431
Q

Epinephrine 1 mg/mL-how supplied-special considerations

A

1 mg/mLCan be deactivated by alkaline solutions

432
Q

Glucagon-trade name-classification

A

Trade name:-GlucagonClassification-Hormone-anti-hypoglycemic agent

433
Q

Glucagon-mechanism of action

A

Increases blood glucose levels by causing breakdown of glycogen to glucose, increases heart rate and cardiac contractility

434
Q

glucagon-indications-contraindications

A

Indications-LOC due to hypoglycemia where an IV cannot be establishedContraindications-Hypersensitivity,-hyperglycemia

435
Q

glucagon -precautions-side effects

A

Precautions-Hepatic or renal insufficiencySide Effects-Tachycardia,-nausea/vomiting,-hypertension

436
Q

glucagon-route-dose-pharmokinetics

A

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

437
Q

glucagon-how supplied SKIP FOR NOW-special considerations

A

How Supplied-1 mg/mL (requires reconstitution)Special Considerations-Ineffective if glycogen stores are depleted

438
Q

Ibuprofen -generic name-trade name-class

A

Generic name: -Ibuprofen Trade name: -Motrin®, Advil®Classification -NSAID, Analgesic, Antipyretic

439
Q

Ibuprofen -MOA

A

-Anti-Inflammatory, analgesic, and antipyretic activities by inhibiting prostaglandin synthesis in the central nervous system.  -Inhibits both COX-1 and COX-2

440
Q

Ibuprofen -Indications -Contraindications

A

Indications -Mild to moderate pain, fever reduction Contraindications -Hypersensitivity

441
Q

Ibuprofen -precautions-side effects

A

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

442
Q

Ibuprofen -side effects

A

GI upset, epigastric pain, heartburn, and abdominal pain

443
Q

Ibuprofen -route-dose-pharmacokinetics

A

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

444
Q

SKIP FOR NOWIbuprofen - how supplied

A

-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)

445
Q

Ipratropium Bromide -generic name-trade name-class

A

Generic name:-Ipratropium Bromide Trade name:-Atrovent® Classification -Anticholinergic

446
Q

Ipratropium Bromide -MOA

A

-Bronchodilation, smooth muscle relaxation

447
Q

Ipratropium Bromide -indications -contraindications

A

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

448
Q

Ipratropium Bromide -precautions-side effects

A

Precautions -Monitor vitals -Caution in elderly Side Effects -Dry mouth, metallic taste -Headache, dizziness -Anxiety, palpitations

449
Q

Ipratropium Bromide - route-dose-pharmockinetics

A

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

450
Q

Ipratropium Bromide-how supplied SKIP FOR NOW-Special Considerations

A

How Supplied -250 mcg in 2 mL Special Considerations -Patients with glaucoma should wear goggles while administered

451
Q

Ketorolac -generic name-trade name-class

A

Generic name: -Ketorolac Trade name:-Toradol® Classification -Nonsteroidal Anti-Inflammatory Drug (NSAID)

452
Q

Ketorolac -MOA

A

-Exhibits peripherally acting non-narcotic analgesia activity by inhibiting prostaglandin synthesis

453
Q

Ketorolac -indications-contraindications

A

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

454
Q

Ketorolac -precautions-side effects

A

Precautions -Can cause peptic ulcers, should not use for abdominal or chest pain Side Effects -Headache, heartburn, nausea, vomiting, diarrhea, stomach pain, bloating

455
Q

Ketorolac -route-dose-pharmacokinetics

A

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

456
Q

Ketorolac -How Supplied SKIP FOR NOW-special considerations

A

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.

457
Q

Naloxone -generic name-trade name-class

A

Generic name:-Naloxone Trade name: -Narcan® Classification Opioid Antagonist

458
Q

Naloxone -MOA

A

Reverses effects of narcotics by competing and displacing narcotic from opiate receptors in the brain

459
Q

Naloxone -indications-contraindications

A

Indications  -Suspected narcotic overdose with respiratory depression Contraindications -Hypersensitivity

460
Q

Naloxone -precautions-side effects

A

Precautions -Use with caution with narcotic-dependent patients and neonates of narcotic-addicted mothers Side Effects -Acute withdrawal symptoms

461
Q

Naloxone -route-dose-pharmocokinetics

A

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

462
Q

Naloxone - how supplied SKIP FOR NOW-Special Considerations

A

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

463
Q

Nitroglycerin -generic name-trade name-class

A

Generic name: -nitroglycerin Trade name: -Nitrostat®, Nitrolingual® Classification -Vasodilator, antianginal

464
Q

Nitroglycerin -MOA

A

Relaxes vascular smooth muscle causing vasodilation (increases blood flow and decreases preload)

465
Q

Nitroglycerin -indications-contraindications

A

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

466
Q

nitroglycerin-Precautions -side effects

A

Precautions -Continuously monitor vitals Side Effects -Syncope, dizziness, hypotension, headache,

467
Q

nitroglycerin-route-dose-pharmocokinetics

A

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

468
Q

nitroglycerin-How Supplied SKIP FOR NOW-Special Considerations

A

How Supplied -Spray: 0.4 mg -Tablet: 0.3 mg, 0.6 mg Special Considerations -Keep out of heat and light 

469
Q

Nitrous Oxide (N20) -generic name-trade name-class

A

Generic name: -Nitrous Oxide (N20) Trade name: -Nitronox®, Entonox® Classification -Analgesic gas

470
Q

Nitrous Oxide (N20) -MOA

A

Depresses the central nervous system and relieves pain

471
Q

Nitrous Oxide (N20) -indications-contraindications

A

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)

472
Q

Nitrous Oxide (N20) -precautions-side effects

A

Precautions -Use in well-ventilated area Side Effects -Headache, nausea, vomiting

473
Q

Nitrous Oxide (N20) -route-dose-pharmacokinetics

A

Route -Inhalation Dose -Self-administered via demand valve Pharmacokinetics -Onset: 2–5 min -Peak effects: Varies -Duration: 2–5 min

474
Q

Nitrous Oxide (N20) -How Supplied SKIP FOR NOW-Special Considerations

A

How Supplied -Cylinder containing 50% nitrous oxide and 50% oxygen Special Considerations -May not work in low temperatures -Monitor SpO2

475
Q

Ondansetron -generic name-trade name-class

A

Generic name: -Ondansetron Trade name:- Zofran®, Zofran ODT®, Zuplenz® Classification -Antiemetic, selective 5-HT3 antagonist

476
Q

Ondansetron -MOA

A

-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.

477
Q

Ondansetron -indications-contraindications

A

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

478
Q

Ondansetron -cautions-side effects

A

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

479
Q

Ondansetron -route-pharmacokinetics

A

Route -IM, IV, Orally Pharmacokinetics -Onset: 30 mins -Peak effects:  1–2 hours (IV) -Duration: 3–6 hours (IV)

480
Q

Ondansetron -dose

A

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.

481
Q

Ondansetron -how supplied SKIP FOR NOW-special considerations

A

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.

482
Q

Oral Glucose -generic name-trade name-class

A

Generic name:- Oral glucose Trade name: -Glutose®, Insta-Glucose® Classification -Carbohydrate, monosaccharide

483
Q

Oral Glucose -MOA

A

Provides prompt increase in circulating blood sugar

484
Q

Oral Glucose -indications-contraindications

A

Indications -Hypoglycemia Contraindications -Hyperglycemia

485
Q

Oral Glucose -precautions-side effects

A

Precautions -If patient has decreased level of consciousness, patient must be placed on side and glucose applied buccally Side Effects -Nausea and vomiting

486
Q

Oral Glucose -route-dose-pharmacokinetics

A

Route -PO Dose -15–45 g Pharmacokinetics -Onset: Immediate -Peak effects: Varies -Duration: Varies

487
Q

Oral Glucose -how supplied-special considerations

A

How Supplied -In tubes and tablets of varying concentrations Special Considerations -Always ensure that a blood glucose reading is obtained before administration

488
Q

oxygen-trade name-class

A

Trade name: -Oxygen Classification -Gas

489
Q

oxygen-MOA

A

Reverses hypoxemia, necessary for cellular metabolism

490
Q

oxygen-indications-contraindications

A

Indications -Hypoxia, signs of inadequate tissue perfusion Contraindications -None

491
Q

oxygen-precautions-side effects

A

Precautions -Chronic obstructive pulmonary disease (COPD) Side Effects -Drying of mucus membranes

492
Q

oxygen-route-dose-pharmacokinetics

A

Route -Inhalation Dose -2–15 lpm (titrate to effect) Pharmacokinetics -Onset: Immediate -Duration: Less than 2 min

493
Q

oxygen-how supplied-special considerations

A

How Supplied -Oxygen cylinders containing 100% compressed gas Special Considerations -Humidify if using for long periods of time

494
Q

Methoxyflurane (Penthrox®) -generic name-trade name-class

A

Generic name:-Methoxyflurane Trade name: -Penthrox® Classification Analgesic gas -

495
Q

Methoxyflurane (Penthrox®) -MOA

A

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.

496
Q

Methoxyflurane (Penthrox®) -indications-contraindications

A

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

497
Q

Methoxyflurane (Penthrox®) -precautions-side effects

A

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

498
Q

Methoxyflurane (Penthrox®) -route-dose-pharmacokinetics

A

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

499
Q

Methoxyflurane (Penthrox®) -how supplied SKIP FOR NOW-special notes

A

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

500
Q

Salbutamol -generic name-trade name-class

A

Generic name: -Salbutamol Trade name: -Ventolin® Classification -Bronchodilator