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Pharmacology Units 1-10 > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

Why do dental hygienists need a working knowledge of pharmacology

A
  • obtain a good health history with regards to drug history
  • know which drugs are used in dentistry
  • assist in emergencies
  • explain medications to patients including herbal supplements
  • recognize side effects of medication
  • planning appts - diabetes, premeds - hman needs
  • part of being a well rounded indibidual
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2
Q

Define chemical name

A

chemical structure code name given during initial production

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3
Q

Define trade or proprietary name

A

chosen by the registering company

name is protected for 20 years

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4
Q

Define generic name

A

the official name (nonproprietary, approved) which is capitalized - after 20 years companies may market generic name

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5
Q

Define chemical equivalent

A

meet the chemical standards of a drug

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6
Q

Define biological equivalent

A

create similar concentrations of the drug in the blood

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7
Q

Define therapeutic equivalent

A

create equal therapeutic levels in clinical trials

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8
Q

List reputable resources a DH could use to access current trug information

A

RxTx - not specific for dentistry
Health Canada
Lexicomp: Drug Information Handbook
Mosby: Dental Drug Reference

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9
Q

How are drugs regulated in Canada

A

scheduled drug regulations: The National Association of Pharmacy Regulatory Authroties (NAPRA) uses a drug scheduling model which reflects the risk to the public and establishes the level of professional control required

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10
Q

Who can prescribe in BC

A

Hygienists may write a prescription but a dentist/physician must sign

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11
Q

What information must be included in a prescription?

A
  • date
  • patients first and last name, birthdate and personal health number
  • drug name (generic)
  • drug strenth with unts
  • drug dosage form and specify if sustained release
  • quantity and/or duration of therapy
  • directions for the patient (can no longer write as needed)
  • refills if permitted
  • physicians/dentists printed name, registration number and signature
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12
Q

What is the purpose of the Canada Vigilance Program?

A
  • collects and assess reports of suspected adverse reactions to health products marketed in Canada
  • post market surveillance ensures Health Canada monitor the safety profile of health produce once they are marketed
  • information collected is on Health Canada and often RxTx
  • reporting can be online, by phone or by email and fax
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13
Q

Define pharmacodynamics

A 
actions of drugs on the body
what kinds of effects
mechanism of action
beneficial and adverse effects
drug application
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14
Q

Define pharmacokinetics

A

study of how the drug enters the body, circulates, is changed itn

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15
Q

Define pharmacokinetics

A

study of how the drug enters the body, circulates, is changed in the body, and leaves the body (absorption, distribution and metabolism then excretion)

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16
Q

Define pharmacogenomics

A

study of how genetics affects the pharmacodynmaics and pharmacokinetics of the drug and thus the selection for individual patients

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17
Q

What is the mechanism of action of drugs to exert an effect?

A
  • fundamental principle is that drugs must interact with a molecular target (receptor) to exert an effect
  • many receptors are proteins found on cell membranes or inside the cell
  • molecues are activate/inhibit receptors are called ligonds - hormones, neurotransmitters, cytokines or growth factors
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18
Q

How doe the ‘law of mass’ apply to drug therapy

A
  • combinations of the drug and receptor depends on the concentration of each
  • the amount of drug-receptor complex determines the magnitude of the response
  • a minimum (threshold) number of drug-receptor complexes must form to initiate response
  • as drug concentrations increase, # of drug-receptor complexes increase therefore increasing drug effector
  • a point occurs when receptors are bound (saturation) and response cannot increase further
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19
Q

What factors can impact drug-target interaction?

A
  • drug binding controls the strength, duration and type of drug-receptor interaction (also known as the affinity - size and shape, types, # and special relationship; bonds - Van der Waals, hydrogen & covalent bonds)
  • selection of drug response (greater affinity for once receptor, the more selective a drug action will be therefore decreasing side effects; increase affinity and efficacy = smaller amount of drug needed)
  • tissue distribution of receptors: only tissues with receptors will response therefore the more restrictive the distribution of receptors = the more selective a drug
  • activation of the molecular target (amplification can occur - when the D-R bond intitiates other reactions which can potentiate the drug effect)
  • once distributed to the site of action, drugs either mimic or block therefore either speeding up a reaction or retarding the action - does not come in and do anything different
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20
Q

Define an agonist

A
  • mimics

- binds to receptor, produces the maximum activation of the receptor and maximum effect

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21
Q

Define antagonist

A
  • blocks

- binds to receptor but does not produce activation

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22
Q

Define partial antagonist

A

-binds and produces weaker activation of the receptor and subsequent downstream effects

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23
Q

Define inverse antagonist

A
  • inhibits rather than activates the receptor
  • can function like an antagonist however some diseases cause changes to the receptors
  • with suppression rather than blocking being a more favorable response (chemotherapy)
  • competitive
  • change receptor
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24
Q

Define chemical antagonist

A
  • do not act on the receptor but rather there is a chemical reaction with a target endogenous substance
  • eg. antacids for heartburn - neutralize gastric acids
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25
Q

Define physiologic antagonist

A
  • substances that create opposite effects

- eg. histamine and epinephrine

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26
Q

Define competitive reversible

A

-binds to receptor but produces no effect

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27
Q

Define competitive irreversible

A

-strongly binds ‘permanently’ reducing the number of receptors available

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28
Q

What is a dose/effect curve

A

indicates the increasing effect of a drug over the dose

-when the line flattens, it is the maximum response

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29
Q

What is the log dose effect curve?

A

-as the dose increases, the effect is 0, then a small effect (variable), and finally the effect is quickly increases which is the therapeutic range. Again, when the curve flatlines, it is the maximum response

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30
Q

What is ED50?

A

effective does where 50% of the patients responded

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31
Q

What is EDmax

A

all patients response - efficacy

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32
Q

What is TD50

A

50% of patients show toxic effect

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33
Q

What is LD50

A

50% of people died

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34
Q

Define potency

A 
function of the amount of drug needed to produce an effect
(potency and efficacy are unrelated!)
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35
Q

Define efficacy

A

maximum intensity of effect or response that can be produced by a drug
-how effective is that drug’s ability to achieve desired effect
(potency and efficacy are unrelated!)

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36
Q

What are advantages of enteral (oral or via the GI tract) administration?

A
  • least expensive
  • safest
  • slowest onset
  • most convenient though requires greater patient cooperation
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37
Q

What are disadvantages of enteral (oral or via the GI tract) administration?

A
  • absorbed in GI therefore nausea and vomiting can occur
  • require greater patient cooperation
  • amount absorbed is less predictable
  • rectal = poorly and irregularly absorbed, creams, gels and enemas
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38
Q

what are parental ways of administering pharm?

A
  • injection
  • topical - usually for local effects
  • inhalation - metered doses, quick onset, no needles
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39
Q

What type of injections are available for pharm?

A
  • IV
  • IM
  • subcutaneous
  • intradermal
  • intrathecal
  • intraperitoneal
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40
Q

What are some disadvantages to using transdermal patches

A

skin acts as a barrier therefore require increased concentrations

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41
Q

What is the definition of absorption?

A

process by which drug molecules are transferred from the site of administration to the rest of the body
-drug must pass through the biologic membrane

42
Q

What factors affect enteral absorption?

A
  • ionization - ionized and non ionized will exist (non ionized readily crossed membranes; pH of tissue and pKa determine the amount of drug present in ionized form)
  • disruption -encasing needs disruption
  • disintegration - capsule needs to break apart
  • dispersion - must disperse
  • dissolution - must dissolve in gastrointestinal fluid
43
Q

What factors affect parental absorption?

A
  • dpeends on solubility of drug and blood flow to the site
  • affected by dose
  • in suspension slows dose - miss the first step and therefore absorbed more quickly
44
Q

Describe distribution of drugs

A

drugs occur as either bound to splasma proteins or as free drug (active), influence by oran size, solubility, plasma binding capability, presence of barriers (BBB, placenta)

45
Q

Define plasma protein binding. Why is binding strength relevant?

A

-drugs bound to albumin and globulin - reversible
-does not contribute to intensity of drug
-bound is considered stoage site
-highly bound drug can be replaced by another highly bound drug therefore increasing the effect of the first drug - one form of drug interaction
(drug B can knock drug A from bind therefore increasing the free amount of drug A in the system)

46
Q

Define half life. How does a half life contribute to possible toxicity concerns?

A

amount of time it takes for the concentration of a drug to fall to 1/2 of its blood level

  • short half life = quickly removed from body and short duration
  • long half life = slowly removed from body
  • talkes 4-5 half lives for drug to be considered eliminated from body
47
Q

What is an agonist?

A

binds to receptor, produces the maximum activation of the receptor and maximum effect
-mimics

48
Q

What is an antagonist?

A

binds to receptor and does not produce activation - essentially blocking

49
Q

Define competitive antagonist

A

affinity for receptor; combines with receptor; produces no effect

  • antagonist competes with agonist for receptor and the outcome depends on relative affinity and concentration of each agent
  • increased concentrations increase the chances of overcoming and winning the receptor site
50
Q

Define noncompetitive antagonist

A
  • binds to a different receptor site than agonist therefore reducing maximum response of agonist
  • alters the shape of the activation site
51
Q

What are enzymes (transferase)

A

causes drug to become more polar (ionized) therefor less lipid soluble than original parent compound

  • this causes a decreased renal tubular reabsorption because reabsorption favors lipid soluble compounds
  • the metabolites are less likely to bind to plasma or tissue proteins and less likely to be stored in fat tissue therefore causing it to be excreted more easily
52
Q

What is biotransformation?

A
  • how the body changes the drug so it can be excreted (liver most common site, enzyme dependent process)
  • conversion to more polar water soluble compounds
  • ionized forms (less lipid soluble) are more likely excreted
53
Q

Who do enzymes metabolize druges?

A

active to inactive
inactive to active
active to active
-metabolites less likely to be lipid soluble, or stored in fat tissue

54
Q

Where are most microsomal enzymes located?

A

liver

P450 enzyme

55
Q

What is a phase 1 reaction?

A
  • lipid reactions occur, by oxidation, reduction or hydrolysis
  • p-450 enzyems - 80% of oxidation (mised function oxidases in the liver)
56
Q

What is phase 2 reaction?

A
  • involve conjugation adding a functional group
  • most common is with glucuronic acid
  • allows the body to convert a lipid soluble drug to a more polar compound
  • enzymes are known as trnasferases
57
Q

What is enzyme induction?

A
  • enzymes can be induced by drugs and smoking tobacco which cause other drugs to be metabolized more quickly
  • the metabolized drugs will have a more therapeutic affect
  • eg. phenobarbital stimulates microsomal enzymes that normally metabolize anticoagulant warfarin therefore decreasing warfarin response because the phenobarbital stimulated the metabolism of warfarin
58
Q

What is enzyme inhibition?

A

-blood levels and actions of the drugs metabolized by these enzymes will be increased therefore inhibiting the microsomal enzymes which would result in an increased effect of the drugs metabolized by the liver function

59
Q

What are the pathways for excretion of drugs? Which is the most common?

A
  • can be excreted unchanged or as metabolites
  • mainly by kidneys (but alos lungs, bile, gi tract, sweat, saliva, gingival crevicular fluid and milk)
  • renal route: glumular filtration, active tubular secretion, passibe tubular diffusion
60
Q

How would disease of the kidneys impact excretion? What could this lead to?

A
  • disease state respond differently
  • increased reactions
  • hepatic/renal influences metabolism and excretion of drugs therefore would increase the duration of action
  • repeated doses would increase serum levels therefore becoming toxic
61
Q

List the factors that may alter a drug’s effect

A
  • patient adherence
  • psychological factors (placebo effect, attitude of patient or prescriber)
  • tolerance - end up with less receptors therefore requires increased dose for desired effect
  • pathologic state - liver or kidney function
  • time of administration
  • route of administration
  • sex - estrogen messes everything up
  • genetic variations
  • drug interactions
  • age and weight
  • environmental (smoking - decreases blood flow; releases enzymes)
62
Q

List the factors that may alter a drug’s effect

A
  • patient adherence
  • psychological factors (placebo effect, attitude of patient or prescriber)
  • tolerance - end up with less receptors therefore requires increased dose for desired effect
  • pathologic state - liver or kidney function
  • time of administration
  • route of administration
  • sex - estrogen messes everything up
  • genetic variations
  • drug interactions
  • age and weight
  • environmental (smoking - decreases blood flow; releases enzymes)
63
Q

List some adverse effects of drugs

A

-exaggerated effect on target tissues (oversensitivity or overreaction)
-effect on non-target tissue; GI
-teratogenetic effects
-local effects: irritation (contact dermatitis), necrosis
-drug interactions: effect of one drug impacts another
-idiosynaratic (its in me): genetically related abnormal reactions
-drug allergy
-interference with natural defense
NAUSEA - VOMITING - SEIZURE - COMA - DEATH

64
Q

List some adverse effects of drugs

A

-exaggerated effect on target tissues (oversensitivity or overreaction)
-effect on non-target tissue; GI
-teratogenetic effects
-local effects: irritation (contact dermatitis), necrosis
-drug interactions: effect of one drug impacts anothWreactions
-drug allergy
-interference with natural defense
NAUSEA - VOMITING - SEIZURE - COMA - DEATH

65
Q

What are the four categories of allergy? Which can be most life threatening?

A 
Type I
Type II
Type III
Type IV
Type I is most life threatening
66
Q

What is type I allergy?

A

immediate hypersensitivty reaction

  • releases histamine, leukotrienes, and prostogrlandins producing vasoldialtion, edema, and inflammation when drug antigen bind sot IgE antibody
  • anaphylaxis
67
Q

What is anaphylaxis

A

acute, life threatening allergic reaction characterized by hypotension, bronchospasm, laryngeal edema, cardiac arrhythmias

68
Q

What is type II allergy

A

antigen 0antibody complex is attached to a criculating red blood cell resulting in lysis

  • complement dependent reaction
  • cytotoxic/cytolytic
69
Q

What is type III allergy

A

drug antigen-antibody complex fixes complement and deposts in vascular endothelium

  • increase serum sickness: urticarial skin eruption,s arthralgia, arthritis, lymphadenopathy and fever
  • mediated by IgG antibodies
70
Q

What is type IV allergy

A

when cells contact eh antigen

  • produced by lymphokines, neutrophils, macrophages
  • eg. contact dermatitis caused by topical application of medications
71
Q

What is therapeutic index?

A
  • small (narrow) = increased risk of toxicity
  • large (wide) = safer drugs
  • T1 > than 10 is usually needed to produce a therapeutically useful drug
72
Q

What are three questions you can ask yourself when reviewing drugs on a client’s medical history?

A
  1. how might this drug affect treatment in a dental office?
  2. for what condition is the drug being prescribed? is the patient following the doctor’s orders?
  3. how might this condition affect treatment in a dental office?
73
Q

What is a requirement for a drug substitution?

A

generic drugs must enter the bloodstream at the same rate as the trade name

74
Q

How does the food and drug act define a drug?

A

any substance or mixture of substances manufactured or sold for:

  • diagnosis, treatment or modification, of a disease, disorder, abnormal physical state or its symptoms
  • restoring, correcting or modifying organic functions
  • disinfection in premises in which food is manufactured, prepared or kept
75
Q

What is the role of Health Canada’s Therapeutic Products Directorate

A

regulates, evaluates and monitors with safety, efficacy, and quality of therapeutic and diagnostic products in Canada

76
Q

What is contained on package inserts?

A

must contain information including the chemical makeup, contraindications, warnings, adverse reactions, drug interactions, dose and administration….now contain a ‘highlights’ section of critical information

77
Q

What are labeled and off label uses

A

information or use of a drug not listed or labeled on the package inserts

  • prescribers are allowed to use a drug for an off labeled use if good medical evidence based research is available
  • drug manufactureres are not allowed to market off lable uses
78
Q

What are orphan drugs?

A

used to treat rare diseases

-approval process different

79
Q

What is affinity?

A

drug binding controls the strength, duration, and type of drug-receptor interaction
-size and shape
-types, number and spatial relationship
-bonds - van der waals, hydrogen, covalent
(the binding of most drugs is weak….therefore not static…continuously associating/diassociating….in general a drug with a higher affinity/bond stength requires a lower concentration

80
Q

What are factors affecting drug-target interactions?

A
  • affinity
  • selectivity of drug response
  • tissue distribution of receptors
  • activation of the molecular target
81
Q

How does selectivity of drug response affect drug-target interaction?

A
  • the greater the affinity for one receptor, the more selective a drug’s action will be, with lower side effects
  • the higher the affinity and efficacy of a given drug, the smaller amount of the drug needed
82
Q

How does tissue distribution of receptors affect drug-target interaction?

A

only tissues with receptors will respond….therefore the more restrictive the distribution of receptors are…the more selective a drug

83
Q

How does activation of the molecular target affect drug-target interaction?

A
  • amplification can occur…when the drug-receptor bond initiates other reactions which can potentiate the drug effect
  • once distributed to the site of action, drugs either produce the same action as an endogenous agent or block the action of an endogenous agent…this can speed up a reaction or retard the reaction
84
Q

Describe the receptor mechanisms

A

-drug must bind (transduction) to receptor site on the cell membrane or intracellularily (lock and key) to generate biologic response. drugs with greater binding strength are more potent

85
Q

what is transmembrane transduction mechanisms

A

some drugs can amplify extracellurlar enzyme action (kinases), or alter ion channels. transporter substances can control movement between intracellular and extracellular spaces

86
Q

What is amplification of drug responses

A

only small amounts o f a drug are necessary to elicit responses (such as hormones, neurotransmitters depending on the sensitivity of tissues)

87
Q

what can alter drug reception number and function?

A
  • repeated drug administration
  • diseases
  • age
  • desensitization (rapid) and tolerance (longer time days/or longer) lead to a reduction in responsiveness (eg nitrates)
88
Q

What are the different types of antagonists?

A
  • chemical
  • physiologic
  • pharmacokinetic
  • competitive reversible
  • competitive irreversible
89
Q

What is our role in pharmacodynamics?

A
  • ultimately need to understand the relationship between the amount of drug given and expected effect
  • drug-response curves, potency and efficacy are terms used to measure the drug response
  • slope of curve provides information: steep narrow therapeutic dose, shallow…variable response
90
Q

How do you determine which drug is the least effective on a log drug dose curve

A

be able to look at a graph and determine this

  • closest to the Y axis is most potent
  • Y axis = efficacy
91
Q

Which drug is most potent on a log drug dose curve

A

be able to look at a graph and determine this

  • closest to the Y axis is most potent
  • Y axis = efficacy
92
Q

What is passive tubular diffusion

A

nonionized less lipid soluble metabolites less likely to be reabsorbed and therefore will be excreted
-alteration of urine pH can favour the formation of nonionized forms and therefor exchanges in pH can be used to help decrease the amount of drug in the system in cases of toxicity

93
Q

What are the different forms of drug metabolism

A
  • excretion
  • glomerular filtration
  • active tubular secretion
  • passive tubular diffusion
94
Q

What are extrarenal routes of excreting drugs?

A

-lungs
-bile
milk
sweat
saliva
gingival crevilar fluid

95
Q

What are the pros and cons of parenteral administration of drugs?

A
  • injection, inhalation, topical
  • fast, uncomfortable, self medication challenging
  • good in emergencies, unconscious, uncooperative, nauseated
  • caution due to risk of infection, intravascuarl risk
96
Q

What are the clinical aspects of pharmacokinetics

A
  • ultimate goal is produce drug concetnratsions at the site o faction the exert beneficial effects with minimal advers effects
  • absorption, distribution and elimination occur simultaneously (can be charted using plasma conc. curves)
  • goal is to exceed the minimal therapeutic concentration and not exceed the minimal toxic concentration
  • drugs are eliminated by either first or der of zero order kinetics
97
Q

What are the different orders of drug elimination?

A

first order - constant fraction (eg 25%) of the drug is eliminated/unit of time(concentration dependent)

98
Q

What is an adverse reaction?

A

an undesired effect

99
Q

What is toxicity

A

when the desired effect is excessive

100
Q

What is a side effect?

A

dose related reaction

  • some side effects can be seen orally
  • gingival enlargement (can be caused by calcium channel blockers), xerostomia
101
Q

What is idiosyncroatic

A

genetically related abnormal reactions (it is in me)

Pharmacology Units 1-10 (13 decks)

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