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COPY BDS3 University of Adelaide Dentistry > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is Nexium commonly used to treat?

A

Acid Reflux or GORD

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2
Q

What is Cartia and what is it used for?

A

Low dosage Aspirin used to prevent blood clots for patients with high CVD risks

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3
Q

Usage of asthma inhalers without a spacer can result in what?

A

Oral Candidiasis from diffused corticosteroids

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4
Q

Isotretinoin (Accutane) is a commonly used drug to treat severe acne. What are the oral side effects?

A

Dryness of oral mucosa and xerostomia

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5
Q

What is the main dental issue that can occur from Bisphosphonate usage?

A

Bisphosphonate related osteonecrosis of the jaw (BRONJ)

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6
Q

What is Bisphosphonates commonly used for?

A

Treatment of Osteoporosis

Cancer treatment of multiple myeloma

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7
Q

A patient presents that is taking Oral Bisphosphonates. Is dental treatment contraindicated?

A

No

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8
Q

What preventions must be taken when treating a patient taking IV Bisphosphonates?

A

Pre/Post Operative AB Cover: Clindamycin

and Chlorhexadine mouthwash to reduce bacterial load

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9
Q

FOSAMAX (Alendronate sodium) what sort of drug?

A

Bisphosphonate

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10
Q

How does propanolol work to combat hypertension?

A

It is a non-selective beta-adrenergic blocker.

lt blocks beta-adrenergic receptor sites and therefore causes smooth and
skeletal muscle arteriole dilation (literally bIocks effect of adrenaline oh beta-adrenergic receptors which are part of the fight or flight response. lf these sites are blocked there is no contraction of smooth or skeletal muscle) It is a|so likely to have direct effects on the myocardium. For these reasons it is used to treat hypertension and abnormally fast heart rate.

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11
Q

Why is combining alcohol with sertraline (a SSRI antidepressant) a bad idea?

A 
Alcohol = decreased serotonin production
SSRI = decreased serotonin resorption

Overall effect, decreased neurotransmitter activity: slower reaction time, poorer motor skills, depressed heart rate/blood pressure

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12
Q

What is sertraline (a SSRI antidepressant) commonly known as?

A

Zoloft

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13
Q

What are 4 principles of rational drug prescribing?

A

Right drug
Right dose
Right frequency
Right duration: Acute vs Chronic

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14
Q

What informational sources should dentists use for pharmacological information?

A

Australian Medical Handbook (AMH) 2016 best practice
Therapeutic Guidelines 2012 (v2): Oral and Dental
MIMS is unreliable and not practical

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15
Q

What are the major classes of prescriptions that dentists can prescribe on PBS?

A 
Anti-infectives (Antibiotics)
Antispasmodics, propulsives: gastric issues
Antiemetics
Local anaesthetics 
Adrenergic/dopaminergics
Corticosteroids: soft tissue
Anti-inflammatory 
Opioids
Antiepileptics
Anticholinergics
Anxiolytics/sedatives
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16
Q

What does drug therapy hope to achieve?

A
  1. Prevent disease: influenza, measles/mumps
  2. Cure disease: pneumonia, some cancers
  3. Decrease mortality/prolong life: Heart attack / stroke
  4. Decrease sickness: Asthma, epilepsy
  5. Decrease symptoms of illness: Headache, cough/cold, pain
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17
Q

What are examples of non xenobiotic drugs that can be administered in the body?

A

Thyroxin, Insulin, Adrenaline

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18
Q

What is a xenobiotic?

A

Chemical substance not synthesised in the body and must be introduced into the body from outside

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19
Q

What is the smallest molecular weight drug?

A

Lithium - MW 7 (used for mania/bipolar)

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20
Q

What is Tissue plasminogen activator used for?

A

Emergency dissolving of blood clots for heart attacks

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21
Q

What is the lock and key concept?

A

A drug that has a good fit, high affinity, high specificity to a binding site

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22
Q

How does Allopurinol work?

A

Allopurinol has the same size and shape as Hypoxanthine (purine), binds to active site/receptor, blocking action of Xanthine Oxidase enzyme to produce urates which have inflammatory complications in joints (Gout)

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23
Q

When referring to medications to patients, which of the following nomenclature should be used?

A. Chemical Name
B. Non-proprietary/Generic Name
C. Official Name
D. Brand Name

A

Non-proprietary/Generic Name

Example: Paracetamol, rather than Panadol

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24
Q

What are the major ways that drugs can be named?

A

Plant name or Chemistry

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25
Q

What are the way drugs can be classified?

A

Chemical Group
Function
Target
International Nonproprietary Names

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26
Q

What is the International Nonproprietary Names given for anesthetics?

A

Drug name that ends in -caine

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27
Q

What is an example of a non-specific target for drugs?

A

Antacid preparations to neutralise H+ in stomach acid

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28
Q

What are 3 examples of specific drug targets?

A

Protein (very common)
RNA/DNA (less common)
Lipid cell membrane (uncommon)

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29
Q

What are 3 targets of drug action located on the cell surface?

A 
Membrane bound receptors (very common)
Ion channels 
Carrier proteins (pumps/transporters)
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30
Q

What are 3 intracellular targets of drug action?

A

Enzymes (very common)
RNA/DNA (cell nucleus)
Protein

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31
Q

A low Kd (dissociation constant) is indicative of what?

A

A low molar concentration needed for drug to work. Therefore the drug has a high affinity for the target receptor

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32
Q

A high Kd (dissociation constant) is indicative of what?

A

A high molar concentration needed for drug to work. Therefore the drug has a low affinity for the target receptor

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33
Q

What is the dissociation constant for a drug?

A

concentration at which 50% of binding sites (receptors) are occupied by drug

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34
Q

Would effects would there be if a drug had a similar high affinity for more than one target receptor?

A

Different action on a the different site

Outcome could be either helpful or an unintentional side effects

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35
Q

What is the preferred pharmacopoeia for dental prescribing?

A

Australian Medical Handbook (AMH) 2016
Therapeutic Guidelines 2012 (v2): Oral and Dental

MIMS is unreliable and not practical

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36
Q

What is Pharmacodynamics?

A

Effect of the Drug on the Body:

The pharmacological response or functional change in the body resulting from interaction of drug on the body

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37
Q

What is Pharmacokinetics?

A

Effect of the Body on the Drug:

Absorption
Distribution
Elimination: excretion/metabolism
Factors which alter the concentration of drug in body: disease, age, other drugs, genetics 
Used to design drug dosage
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38
Q

What is Toxicology?

A

The discipline dealing with undesirable effects of xenobiotics

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39
Q

What is an example of a non-specific drug target?

A

Antacid preparations to neutralise H+ in stomach acid

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40
Q

Which is more common: specific or non-specific drug tagets?

A

Specific Drug Targets

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41
Q

What are the 3 types of Specific Drug Targets?

A

Protein (very common)
RNA/DNA (less common)
Lipid cell membrane (uncommon)

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42
Q

What are the main classes of targets for drug action?

A
  1. Cell Surface Targets (Membrane Bound Receptors, Ion Channels, Carrier Proteins)
  2. Intracellular Targets (Enzymes, RNA/DNA, Proteins)
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43
Q

What are the sites of action for drugs targeting intracellularly?

A

Enzymes (very common)
RNA/DNA (cell nucleus)
Protein

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44
Q

What are the sites of action for drugs targeting the cell surface?

A 
Membrane bound receptors (very common)
Ion channels 
Carrier proteins (pumps/transporters)
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45
Q

What is a Ligand?

A

A substance (in this instance drug) that binds with a biomolecule for a functional purpose. Drugs are typically ligands that bind with receptors to induce a functional change (eg with Opioid or Adrenergic Receptors)

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46
Q

Would it be beneficial if a drug had a similar high affinity for more than one target receptor??

A

Probably not, it could have a helpful/unintentional side effects, or completely different action on a the different site

Example: Hay fever medication - additional high affinity to salivary glands induces dry mouth

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47
Q

What is drug affinity?

A

How tight the protein binds to the drug. Higher affinity requires lower molar concentration of the drug to work

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48
Q

What is the dissociation constant (Kd)?

A

The concentration at which 50% of binding sites (receptors) are occupied by drug

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49
Q

What is the clinical implication for drug prescribing for a drug with a low Kd?

A

A Low Kd drug is 50% dissociated at a lower molar concentration, making it a high affinity drug. Therefore a lower dosage is needed for the drug to work

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50
Q

What is the clinical implication for drug prescribing for a drug with a high Kd?

A

A Low Kd drug is 50% dissociated at a higher molar concentration, making it a lower affinity drug. Therefore a higher dosage is needed for the drug to work

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51
Q

Do small conformational changes in molecular shape/orientation affect the drug’s affinity?

A

Yes.

Codeine vs Morphine are almost chemically identical with the only difference a OH vs CH3O group, but yet have enormous difference in drug affinity.

Codeine Kd = 150nm (Weak Analgesic) vs Morphine ( Kd = 1000nm) (Strong Analgesic)

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52
Q

How do ligand-gated channels work?

A

Ligand binds to a binding domain on the channel, opening the channel for ion flow

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53
Q

How do voltage gated channels work?

A

Coordinated depolarisation (voltage change) triggers a ion channels to open

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54
Q

What types of ion efflux are common in drug action?

A

Cl-, Na+, K, H+, Ca2+

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55
Q

T/F: Local Anesthetics work as channel openers

A

False: they work as channel blockers

Local Anesthetics block sodium transduction and prevents membrane depolarisation and subsequent action potential

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56
Q

T/F: benzodiazepines, diazepam, oxazepam work as Channel Openers

A

True: they work as channel opener

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57
Q

What are the 2 mechanisms that a channel opener can have?

A
  1. Prolong duration of channel opening

2. Increase frequency of channel opening

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58
Q

What are the 3 types of carrier pumps

A
  1. Uniporters
  2. Antiporters
  3. Symporters
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59
Q

How does a Uniporter carrier pump work?

A

Facilitate transport of only one solute across the cell membrane

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60
Q

How does a Antiporters carrier pump work?

A

Facilitate transport of two dissimilar solutes in opposing direction across the membrane

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61
Q

How does a Symporters carrier pump work?

A

Facilitate transport of two dissimilar solutes in the same direction across the membrane

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62
Q

What type of carrier pump is involved with Diuretics, and how do they work on the kidney?

A

Symporter: diuretic drug blocks the Na/Cl symporter, increasing the sodium gradient into the distal tubule of the kidney. Water follows the sodium gradient to increase urine excretion

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63
Q

What is the role in diuretics in treating high blood pressure

A

Increasing excretion of urine decreases blood volume that decreases MAP.

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64
Q

What type of carrier pump is involved with anti stomach ulcer / reflux drugs?

A

Antiporter: Proton Pump Inhibitors (eg Omeprazole) inhibit H+/K+ exchange, so in turn decrease stomach lumen concentration of H+. This reduces the damaging effects of acid in stomach ulcers and acid reflux

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65
Q

What is the mechanism of action of SSRI-antidepressants?

A
  1. SSRIs antidepressants close membrane transports found on the end of the presynaptic neuron
  2. This limits re-absorption of serotonin into the presynaptic cell
  3. This increases the concentration of serotonin in synaptic cleft to bind to postsynaptic receptor
  4. People with depression typically have depressed levels of serotonin - this in effect allows for normal firing of neurons
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66
Q

What are 3 examples of drug classes that target enzymes?

A
  1. NSAIDS: anti-inflammatories
  2. ACE Inhibitors: address high blood pressure
  3. HMGCoA Reductase Inhibitors (Statins): address high LDL cholesterol
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67
Q

What is the difference in length of duration of competitive vs irreversible drugs

A

Irreversible: drug covalently binds to site, therefore inactivating enzyme. Therefore, the only way the body can recover is to create new enzymes.

This means the duration will be longer

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68
Q

What are the complications of aspirin being an irreversible inhibitor of cyclooxygenase (Cox) in platelets

A

Aspirin induces complete irreversible inhibition of cyclooxygenase (Cox) in platelets, therefore limiting platelet aggregation.

If this was an issue with treatment, the patient would have to wait 1 week after stopping aspirin in order for the body to synthesise new cyclooxygenase

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69
Q

What is the current clinical advise with regard to aspirin and post surgical bleeding complications

A

Risk of bleeding is less than the beneficial effect of preventing heart attack.

Warn patient of chance of bleeding for some time
Apply other hemostatic agents during surgery
Monitor patient for safety after treatment

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70
Q

A Ligand gated ion channel blocker for a nicotinic acetylcholine receptor would have what effect?

A
  1. Prevent Acetylcholine from binding to Ion Channel
  2. Prevents influx of sodium
  3. Depolarisation can’t occur
  4. No skeletal muscle Contraction
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71
Q

Would you expect drugs that work on 2nd Messengers to work immediately?

A

No, onset would occurs in minutes.

Ion Influx from 1st Messengers require action from intracellular enzymes

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72
Q

Would you expect drugs that work on Intracellular Nucleic receptors to work immediately

A

No, onset would be in hours as gene transcription/translation is involved

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73
Q

Would you expect drugs that work on Intracellular Nucleic receptors to keep working after the patient has ceased use of the drug?

A

Yes, RNA has already been altered, so RNA stimulation is still ongoing and Protein translation will still occur

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74
Q

Would you expect an Asthma preventer (Corticosteroid) to treat an acute asthma attack?

A

No, it’s action is slow as it alters transcription of inflammatory mediators. It would not provide immediate relief or target action on smooth muscle tissue on the lungs

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75
Q

What type of medication is an asthma reliever?

A

Salbutamol: bind to beta 2 receptor (G-protein coupled receptor)

Quick effect that is has affinity to beta 2 receptors: causes smooth muscle tissue in the lungs to dilate.

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76
Q

What are the 2 classes of asthma therapy drugs?

A
  1. Relievers (Selective Beta 2 agonists)

2. Preventers (Corticosteroids)

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77
Q

How can we quantify and classify the effect of a drug?

A
  1. Size of Response
  2. Reversibility of Action
  3. Graded-Dose Response Relationship
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78
Q

Dose Concentration/Effect work on a linear or log scale?

A

Typically a linear scale

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79
Q

What is ED50 and why is this significant

A

It is the dosage required to get 50% efficacy OR where 50% of people have 50% of max effect (Essentially the same thing)

A drug that reaches ED50 at a lower 5mg dosage is far more potent

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80
Q

What is the issue with a drug that has a very steep dose concentration/effect curve?

A

A small increase in concentration (where the curve is steepest) leads to a very large increase in response: making the risk of adverse effects/toxicity higher

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81
Q

T/F: 2 Drugs that work on the same target receptors will follow the same Dose-Response Curve Slope

A

True, as there are limited number of receptors of the same type to bind to

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82
Q

T/F: 2 Drugs that work on the different target receptors will follow the same Dose-Response Curve Slope

A

False, the drugs are independent of each other and will follow different slopes

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83
Q

Would you expect full agonist to reach 100% effect of a Dose-Response Curve Slope

A

Yes

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84
Q

Would you expect partial agonist to reach 100% effect of a Dose-Response Curve Slope

A

No, by definition a partial agonists are drugs that bind to and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist. It can not reach 100% effect

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85
Q

What is the Therapeutic Index?

A

The Toxic Dose / Effective Dose

High TI = toxic dose if substantially bigger than normal dose
Low TI = only a small increase in dose produces toxic effects

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86
Q

The interaction between St John’s wart and Cyclosporine is an example of what?

A

Altered Pharmacokinetics: St John’s Wart speeds up the metabolism of cyclosporine and other drugs, reducing it below a efficacious concentration = increasing risk of organ transplant failure.

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87
Q

What is the role of Cyclosporine?

A

It is an immunosuppressant drug that prevents organ transplant rejection

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88
Q

What are the dental side effects of Cyclosporine?

A

Gingival Hyperplasia

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89
Q

Dosage regimen is a vital part of pharmacokinetics. What are the 4 dosage regimen considerations when prescribing a drug?

A
  1. Route of administration (e.g. oral)
  2. Amount (dose)
  3. Frequency (how often)
  4. Duration (for how long)
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90
Q

What is the main measurement of an optimal drug concentration and why is this chosen?

A

Blood plasma concentration

  • Good correlation with target site concentration
  • Easy to access and test
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91
Q

What 4 factors influence the administered drug dose to the end blood concentration?

A

Absorption
Distribution
Metabolism
Excretion

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92
Q

Why might drug response differ between individuals?

A

Pharmacokinetic factors (Absorption, Distribution, Metabolism, Excretion) all affected by:

Age
Weight
Disease (type and severity)
Genetic
Environment 
Interaction with drugs
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93
Q

Why is there less difference in drug response in animals tests than human trials?

A
  • Less genetic variability in lab rat populations

- Very controlled environment: housing, food all same

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94
Q

What are different pharmacokinetic parameters that can chart drug plasma concentration over time?

A

Bioavailability (f)
Clearance (CL)
Volume of distribution (V)
Half-life (t ½)

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95
Q

What is the Therapeutic window?

A

The optimum drug concentration at the site of action to ellicit the desired effect

Too Low: No Effect
Too High: Toxicity

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96
Q

Which is more desirable: a wide or narrow therapeutic index window?

A

Wide Therapeutic Window: the jump in dosage between effective dose and toxicity / no effect is very large.

This means there is less risk in patients being able to suffer from dosage issues despite interpersonal variation in pharmakinetics

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97
Q

Why would the route of administration of a drug for acute and chronic disease be different?

A

Acute Disease: requires rapid response and quick bioavailability

Chronic Disease: may opts for a slow release administration route so there is less intervention needed by the patient for regular dosage

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98
Q

What are the 2 factors to consider when deciding on the route of drug administration?

A
  1. Properties of the Drug

2. Therapeutic Objective: Rapid response vs Chronic Dosage

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99
Q

What are 3 enteral drug administration sites?

A
  1. Oral (Tablets, Capsules, Mixtures)
  2. Sublingual
  3. Rectal (Suppositories)
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100
Q

What are the benefits of administering drugs sublingually as opposed to orally?

A

Drug avoids liver first pass

Some drugs they are completely metabolised by the liver so can’t enter the bloodstream (Glyceryl Trinitrate for Angina)

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101
Q

What are the benefits of administering drugs rectally as opposed to orally?

A
  1. If the illness is causing vomiting

2. Also partially avoids liver first pass

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102
Q

What is the most direct Parenteral drug administration route?

A

Intravenous Injection - results in very rapid onset at target tissue

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103
Q

What is the difference between aqueous solutions and oily suspensions used in intramuscular injections into skeletal muscle?

A

Aqueous solution → slow absorption

Oily suspension → very slow absorption

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104
Q

What are indications for a parenteral administration route?

A
  1. Poorly absorbed drugs
  2. Drug unstable in acid stomach
  3. Unconscious patient
  4. Can’t swallow orally
  5. Need very quick onset (IV only)
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105
Q

What are alternative non enteral or parenteral drug administration routes?

A 
Inhalers
Intranasal
Topical Creams/Oiltments
Transdermal Patches
Eye Drops
Ear Drops
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106
Q

T/F: Transdermal Patches are very slow acting drug delivery vehicles that are intended for systemic effects

A

True

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107
Q

What administration route does not involve Drug Absorption?

A

All types except for I/V injections:

Oral: Tablet, Capsule, Liquid
Sublingual
Transdermal
Rectal
Intramuscular / Subcutaneous Injection
Inhalers, Intranasal, Eye, Nose, Ear
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108
Q

What is Drug Absorption?

A

Process by which drug proceeds from site of administration to site of measurement (blood stream) within the body

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109
Q

What are the mechanisms of Drug Absorption in the GIT?

A
  1. Passive Diffusion

2. Carrier Mediated Update Transport

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110
Q

T/F: Lipophobic drugs are absorbed faster via passive diffusion

A

False, fat solubility is the key factor in rapid movement via the cell membrane.
Lipophobic (aka souble) drugs typically require Carrier Mediated Uptake Transport but are rate limited by the number of transporter located on the cell surface.

Therefore they are slower than lipophillic drugs that can freely move through the cell membrane

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111
Q

What are the properties of movement of drug molecules via passive diffusion?

A
  1. Movement from high to low concentration gradients
  2. No energy required for movement
  3. No saturation
  4. No competitive inhibition
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112
Q

What is Octanol/water partition ratio (O/W) used for?

A

It is a water solubility measure for estimation of drug distribution within the body

Lipophilic/Hydrophobic drugs
have O/W > 5 = high permeability / absorption
Example: codeine

Lipophobic/Hydrophillic drugs
O/W < 1 = low permeability/adsorption
Example: antibiotics

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113
Q

What is the clinical implication for dosage for Lipophobic drugs?

A

Typically require a far higher dosage as they have low cellular permeability/absorption

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114
Q

Why is taking large dosages of water soluble vitamins a waste of time?

A

Permeability of hydrophillic/lipophobic drugs on the cell membrane is rate limited by the number of efflux pump transporters (Carrier Mediated Uptake Transport) that can transport the drug at any time.

Any excess dosage not transported is simply excreted

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115
Q

What is the main purpose of Carrier Mediated Uptake Transports?

A

To support transport of very water soluble drugs

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116
Q

What are the properties of movement of drug molecules via carrier mediated uptake transports?

A
  1. Energy is Required
  2. Transports can be saturated
  3. Transports can be specific
  4. Competition for Transport can occur
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117
Q

What is P-glycoprotein (Pgp) an example of, and what is it’s function?

A

P-glycoprotein (Pgp) is a transmembrane glycoprotein that functions as efflux pump to push xenobiotics out of a cell.

In terms of drug absorption, it can pushes xenobiotics/toxins back into the intestinal lumen, thus acting as a protective mechanism against potentially toxic substances in our diet

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118
Q

What are the 3 physiological factors that impact on GIT absorption?

A
  1. Blood Flow
  2. Large Surface Area
  3. Gastric Emptying
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119
Q

Is blood flow typically a limiting factor in drug absorption?

A

Typically no: most drugs are not sufficiently fat soluble, therefore slow absorption via the GIT is what prevents it from taking effect

However, highly fat soluble drugs are rapidly absorbed (eg alcohol). In this instance, blood flow is the rate limiting factor in reaching the brain

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120
Q

How is surface area important in GIT absorption?

A

Microvilli in the small intestine provide 1000x more surface area than the stomach, meaning there are more surface cells to allow for absorption. This is why most drugs enter via the intestine and not the stomach.

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121
Q

Why is Gastric Emptying required for absorption?

A

Affects the speed/rate of absorption

If you’re backed up, the drug can’t be absorbed along GIT

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122
Q

How can a patient increase absorption via gastric emptying?

A
  1. Take a dump

2. Consume the drug with 250ml of water

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123
Q

What are different ingredients in oral medication designed to maximise absorption?

A
  1. Filler
  2. Lubricant
  3. Disintegration Agents: to correct disintegrate the tablet to maximise solution being absorbed, but not to be destroyed in the stomach
  4. Enteric Coating: to resist acid dissolution in the stomach
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124
Q

Why would a Sustained Release Tablets/Capsules be designed?

A

Reduce rate of dissolution
Reduce rate of absorption
Reduce frequency of dosing (helps in pt compliance)

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125
Q

What is the method of administration that would maximise drug bioavailability?

A

Intravenous Injection

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126
Q

What factors reduce bioavailability?

A
  1. Insufficient time for absorption (lipophobic/requires activity transport)
  2. Decomposition in gut lumen (Acid Hydrolysis, Complexation, Efflux Transport Out, Metabolism by Gut Wall)
  3. Hepatic first pass effect: liver metabolises/excretes much of the drug, reducing bioavailability
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127
Q

What are the 3 determinants for Drug Distribution?

A
  1. Rate of blood flow to tissue/organ
  2. Ability to cross the cell membrane wall
  3. Binding to plasma and tissue proteins
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128
Q

What are the 2 ways drugs can be transported in systemic circulation?

A
  1. Unbound/Free Drug

2. Protein Bound Drug

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129
Q

What determines the rate/speed of drug distribution in the blood stream?

A
  1. Blood flow to the organ - well perfused organs take up drugs more easily
  2. Protein Bounded Drugs: can’t cross small capillaries
  3. Blood Brain Barrier
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130
Q

What is volume of distribution a measure of?

A

The drugs ability to be distributed to target tissues

Volume of Distribution (V) = Amount in body (A) / Blood Concentration (C)

High V = High Tissue Binding (readily absorbed)
Low V = Low Tissue Binding (only low quantity is absorbed, most excreted)

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131
Q

What are the 2 routes of Drug Elimination?

A
  1. Metabolism: conversion to another chemical in the liver

2. Excretion: loss of a chemically unchanged drug via the kidney

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132
Q

What is the metabolism of alcohol in the liver?

A

Alcohol → Aldehyde via alcohol dehydrogenase) → CH3COOH (Acetic acid)

133
Q

What all the organs that are involved in drug metabolism?

A

Liver (primary), Lung, GIT

134
Q

What all the organs that are involved in drug excretion?

A

Kidney (primary), Glands: sweat, tears, bile

135
Q

T/F: Lipid soluble drugs are metabolised by liver

A

True

136
Q

T/F: Water soluble drugs are excreted by kidney

A

True

137
Q

How do you measure the Pharmacokinetic Measurement of Elimination?

A

Clearance = renal clearance (0-1200 mL/min) + Hepatic clearance (0-1500mL/min)

138
Q

What is the purpose of an acid resistant enteric coated tablet?

A

Avoid dissolution in pH 2 (acidic stomach)

139
Q

What is the purpose of an alkaline sensitive enteric coated tablet?

A

For dissolution in the upper intestine (pH > 6)

140
Q

T/F: Protein bound drugs are filtered in the glomerulus

A

False, only free unbounded drugs are filtered

141
Q

T/F: Only unbound fraction drugs exhibit pharmacological effects

A

True

142
Q

What is the main factors that inhibit clearance of unbounded fraction in the glomerulus

A
  • Older people have poorer kidney function

- Kidney Disease

143
Q

What is the maximum rate that a drug can be excreted?

A

The maximum rate of glomerular filtration (120mL/min in a healthy person)

144
Q

How much blood is filtered as plasma water in the glomerulus?

A

10% at 120mL/min

145
Q

How are drugs excreted in the proximal tubule?

A

They are secreted from blood capillaries into the tubule lumen via active transporters

146
Q

T/F: Is it possible for drugs to interact during drug secretion in the proximal tubule

A

True: high affinity to the same transporter can mean that one drug can prevent the secretion of another drug with slightly less affinity:

Example: probenecid can block the secretion of some acid based antibiotics such as penicillin, keeping the blood concentration of penicillin higher.

147
Q

What are examples of acidic transporters in the proximal tubule?

A

Organic Anion Transporter (OATs): secrete penicillin

148
Q

What are examples of basic transporters in the proximal tubule?

A

Organic Cation Transporter (OCTs), p-glycoprotein

149
Q

What affects the ability for drugs to be reabsorbed into the body at the distal tubule/collecting duct

A

If it is lipid soluble, if will follow the concentration gradient back into the body via passive diffusion until equilibrium is reached

150
Q

What determines whether a drug is reabsorbed or secreted

A

Secreted = If unbound fraction in plasma (fu) X GFR (120mL/min) is high

Reabsorbed = If unbound fraction in plasma (fu) X GFR (120mL/min) is low

151
Q

What is a metabolite?

A

Enzymatic converted chemical form of a drug

152
Q

What is the chemical strategy of drug metabolism?

A

Enzymes introduce or cleave a chemical group to increase polarity to make the molecule more water soluble, therefore able to be excreted by the kidney

153
Q

What chemical groups are typically exposed as part of drug metabolism?

A

Alcohol, Carboxylic Acid, Gluchoronic acid

Highly polar groups that increase the molecules water solubility

154
Q

What are the implications of active metabolites?

A
  1. Similar Functional Activity: Morphine → morphine-6-glucuronide → some analgesia
  2. Different Functional Activity (Side Effects):
    Pethidine → norpethidine → convulsions
155
Q

Who are at high risk for complications with active metabolites? Why is this important?

A
  1. The Elderly
  2. People with decreased kidney function:

Metabolites will remain in the body for longer increasing the chance of getting side effects

156
Q

What strategy is needed to minimise the effects of active metabolites?

A

Elderly/Kidney disease patients should be given lower dosages

157
Q

What are 2 Phase 1 (Functionalisation) drug metabolism systems?

A
  1. Oxidation

2. Microsomal Mixed Function Oxidase System

158
Q

Alcohol is metabolised by which Phase 1 metabolism reaction?

A

Oxidation via Alcohol Dehydrogenase to form acetic acid

159
Q

Briefly explain the Cytochrome P450 system

A

Cytochrome P450 (CYP450) system is a family of hemoprotein enzymes that bind to the drugs to insert an oxygen molecule and produce water.

As a result the xenobiotic becomes more hydrophillic.

160
Q

How can CYP450 be interrupted?

A
  1. Enzyme Induction: suppression of transcription factors so CYP450 enzymes aren’t produced (caused by St Johns Wort, Cigarette Smoke, Cabamazepine)
  2. Enzyme Inhibition: competition from higher affinity molecules to the same enzymes. Enzymes are depleted and xenobiotic concentration remains high (example: Grapefruit with Clarithromycin)
  3. Pharmacogenetic Factors: certain populations genes have missing/non-functional CYPs
161
Q

What sort of Therapeutic Index drugs are at the most risk of CYP450 interruption?

A

Low TI drugs: as a high concentration of the drug not being metabolised increases the risk of overdosing if the patient continues to take the drug at regular intervals.

162
Q

What are the 2 phases of Drug Metabolism?

A

Phase 1: Functionalisation

Phase 2: Conjugation

163
Q

What happens during Phase 2 Metabolism (Conjugation)?

A

Large polar chemical groups (donor compounds) are added on via enzymes called transferases

164
Q

What issues can occur during Phase 2 Metabolism (Conjugation) using Paracetamol as an example.

A

During toxic doses of Paracetamol, PAPS (the donor compound) is depleted, meaning that the body is unable to convert the phase 1 reactive electrophilic metabolite.

Since it can’t be conjugated, it attacks and destroys the liver cells resulting in death

165
Q

What are strategies to address paracetamol overdose?

A
  1. Increase Sulphate: not enough to overcome overdose. Also highly irritating to endothelium
  2. Giving CYP enzyme inhibitors: unlikely to work quickly
  3. Increasing Glutathione transferase: can work within 2 hours of overdose to convert Phase 1 Metabolites to Phase 2 Metabolites (Paracetamol Mercapturate)
166
Q

What kind of drugs that Phase 2 Conjugation Glucuronidation commonly work on?

A

Drugs with Carboxylic Acid or Alcohol end groups

167
Q

Why is Phase 2 Conjugation Glucuronidation very effective?

A

End product Glucoronide metabolites are very water soluble and are easily excreted

168
Q

What 4 factors does the Plasma Concentration-time Curve shape depend on?

A
  1. Dose (Double the dose should equal 2 x concentration)
  2. Route of administration (IV different to oral)
  3. Single dose versus chronic dose
  4. Patients elimination and distribution rates
169
Q

What curve shape should you expect to see on a Plasma Concentration-time Curve graph for a drug taken intravenously?

A

Maximum concentration at time 0 with a decrease concentration curve following a half life decay curve as the drug is distributed to tissues/organs and is eliminated

170
Q

What curve shape should you expect to see on a Plasma Concentration-time Curve graph for a drug taken intra-orally?

A

Increasing plasma concentration until the maximum rate of absorption occurs, then a decay rate over time as the drug is distributed to tissues/organs and is eliminated

171
Q

What is meant by steady state concentration?

A

Plasma concentrations increase between chronic dosages until there no difference between successive doses. This is where the rate of drug in (dosing rate) vs drug out (rate of elimination) is the same

172
Q

Why is determining the steady state concentration important for addressing chronic disease

A

Finding the optimum concentration that provides efficacy without risking toxicity

173
Q

How do you calculate drug clearance?

A

Clearance (CL) = rate of elimination (mg/min) /plasma concentration (mg/L)

Clearance (CL) = Dose (Single IV)/AUC

174
Q

How do you calculate total drug clearance?

A 
Total Clearance =
Renal Clearance (CLR) + Hepatic Clearance (CLNR)
175
Q

T/F: Drug clearance is dependent on dosage interval

A

False, is it dependent on individual factors (age, liver/kidney disease)

176
Q

What is maintenance dose rate and why is it helpful?

A

Maintenance dose achieves a desired/target plasma drug concentration and therapeutic effect on chronic dosing

177
Q

T/F: Steady State Concentration and Clearance are inversely proportional

A

True

If Clearance increases 2x (then Steady State Concentration is halved) => hyperthyroidism, other medications that ramp up enzymes involved with clearance

If Clearance is halved (then Steady State Concentration doubles) => due to hepatitis/kidney disease

178
Q

When does Clearance and Steady State Concentration calculations pose issues in the real world?

A

Where a patient’s clearance is compromised (age, liver disease), such that regular dosage is not adequately cleared, therefore becoming a toxic dosage

179
Q

How do you calculate Steady State Concentration (CSS)?

A

CSS (steady state concentration) = Dose Rate / Clearance

180
Q

What is drug half life? (t 1/2)

A

Time for blood concentration/amount of drug in the body to fall by 50% after a single dose

181
Q

What is an example of a drug with a long half life?

A

Bisphosphonates: 1-10 years

182
Q

What can drug half life help inform?

A

1) Time to reach steady state

2) Time taken to eliminate drug after dosing has stopped

183
Q

How many half lives are needed to completely eliminate a drug from the body

A

5 half lives

184
Q

How do you calculate half life (t 1/2)?

A

Half Life (t 1/2) = 0.69 x V / Clearance (CL)

185
Q

How would Steady State Concentration be different between the same drug being administered Intravenously or Orally?

A

IV: Clearance Rate Alone
Oral: Clearance Rate + Bioavailability

186
Q

What is Volume of Distribution (V)?

A

Proportionality factor that illustrates how much of a drug consumed is in the body vs how much of the drug is available in the blood

187
Q

Why is Volume of Distribution important?

A

Volume of Distribution indicates how much a loading dose should be.

A loading dose is an initial higher dosage that allows the drug to reach the optimum concentration in the blood faster to begin being effective.

188
Q

How do you determine oral bioavailability (F)?

A

Oral bioavailability (F) = [AUC (Oral) / AUC (IV)] x [Dose (IV) / Dose (Oral)]

189
Q

What does AUC represent?

A

AUC is the area under the Plasma Concentration-time Curve graph for IV Dose

AUC = Total amount of drug absorbed by body over time

190
Q

What is hepatic first pass?

A

The amount of drug that can become bioavailable after metabolism by the liver via oral administration

191
Q

What 2 factors can affect hepatic first pass?

A
  1. Blood Flow (Q)

2. Intrinsic Clearance (CLint)

192
Q

What is the significance of intrinsic clearance in hepatic first pass?

A

A measure of how efficient the enzymes in the liver are in metabolising the drug

193
Q

What are the characteristics of enzymes in low clearance drugs?

A

Enzymes are so sluggish that although the drug is metabolised it is so slow that most of it escapes the first pass

Examples: Caffeine, ibuprofen

194
Q

What are the characteristics of enzymes in high clearance drugs?

A

Enzymes are so efficient that nearly all drug is metabolised during first pass and little escapes

Examples: Morphine, Codeine

195
Q

T/F: A Low Clearance drug has high oral bioavailability

A

True. An example is caffeine

196
Q

What are issues with high clearance drugs and a patient with liver cirrhosis?

A

1) Cirrhosis = poor liver function
2) Decreased enzymes produced
3) Decreased hepatic first pass,
4) Increased the bioavailability of the drug
5) Higher chance of toxicity if dosage not changed

197
Q

How would a clinician overcome an issue with a drug that has high hepatic first pass clearance?

A

Choose a different administration method: Intravenous, Sublingual, Transdermal, Inhalation

198
Q

What factors can affect bioavailability?

A

1) Age
2) Liver Function
3) Drug Interactions: Induction/Inhibition effects

199
Q

What are 6 different ways that drugs can be discovered?

A
  1. Purification from natural sources
  2. Chemical Modification of active drug
  3. Rational Drug Design
  4. Serendipity: by chance (uncommon)
  5. New Indications from Clinical Observations
  6. Recombinant Proteins
200
Q

What are examples of drugs discovered from traditional natural sources?

A

Aspirin: willow bark (400 BC salicin) = > Analgesic
Morphine: opium poppy => Analgesic
Paclitaxel: bark of Yew tree (conifer) => Colon Cancer
Artemisinin: Artemesia annua (chinese wormwood) => Malaria

201
Q

What are examples of drugs discovered from chance observation?

A

Warfarin: spoiled cattle feed (toxic rotting clover contained dicumarol => reduces prothrombin)

202
Q

What are examples of drugs discovered from screening of biological sources?

A

Cyclosporin: immunosuppressant (from a moss in Southern Norway)

Rapamycin (Sirolimus): used in heart disease (stent), transplantation. Found in bacteria in Easter Island

Ziconotide: toxin found in marine snail -> pain control

203
Q

What are reasons for chemical modification of active drugs?

A

Synthesis of new analogues of active drugs, modification of existing molecules by addition/deletion & rearrangement of chemical groups in order to:

  1. Increase Specificity
  2. Decrease Toxicity
  3. Increase Spectrum of Activity
  4. Better Pharmacokinetics
  5. Exploitation of side effects
204
Q

What is an example of a drug that has new indications after long term clinical observations?

A

Aspirin

  1. Inflammation / pain / temperature (Original Indication)
  2. Stroke prophylaxis (Low Dose)
  3. Colon cancer prophylaxis (New Indication)
205
Q

What is meant by rational drug design?

A

Detailed knowledge of genomics/proteomics to design drugs around specific genetic factors that causes biochemistry deficiencies in proteins/enzymes in individuals

206
Q

What are used to make recombinant proteins are a source of drugs discovery

A

Bacteria to produce endogenous proteins

207
Q

What 2 methods are used for pre-clinical drug development?

A
  1. Laboratory (In Vitro)

2. Whole animal testing (In Vivo)

208
Q

What are limits to whole animal testing?

A
  1. Limits to measure CNS activity and disease
  2. Can’t extrapolate to human pharmacokinetics/dynamics
  3. Small test sample - unlikely to detect uncommon side effects
209
Q

What things can be tested in whole animal testing

A
  1. Pharmacokinetics to extrapolate human pharmacokinetics
  2. Carcinogenesis
  3. Acute / Chronic Toxicity
  4. Effects on Pregnancy + Lactation
210
Q

What are the 3 phases of Clinical Drug Development?

A

Phase I: Is it immediately safe? What doses are safe?
Phase II: Can it work? What dose does it work
Phase III: Is it Effective? What are side effects?

211
Q

What frequencies of side effects would be deemed common, infrequent or rare?

A

Common: >1%
Infrequent: 0.1-1%
Rare: < 0.1%

212
Q

What are the timeframes for drug development?

A

Preclinical: 3-4 years
Phase I-III: 8-10 years
Patent expires 20 years

213
Q

What are the aims of drug regulation?

A

Protect public from unsafe, ineffective & poor quality drugs

Serve the public interest in gaining timely access to new & possibly life-saving drugs

214
Q

Which body in Australia regulates drugs?

A

Therapeutic Goods Administration (TGA)

215
Q

What is a drug that isn’t on the

ARTG (Australian Register of Therapeutic Goods)?

A

It is illegal in Australia

216
Q

What 3 broad families of medicines are evaluated by the TGA?

A
  1. Prescription Medicines
  2. Non-prescription (Over the Counter)
  3. Complementary Medicines
217
Q

What are the two types of drugs on the ARTG (Australian Register of Therapeutic Goods)?

A
  1. AUST L (Listed): ~11,500 products in Australia

2. AUST R (Registered): ~13,500 products in Australia

218
Q

What are the 3 evaluation criteria when getting a drug approved by the TGA?

A
  1. Pharmaceutical/chemical data quality of product
  2. Preclinical pharmacology & toxicology
  3. Clinical pharmacology, Human efficacy, safety
219
Q

T/F: Scheduling of medicines is done at the federal level?

A

False: scheduling is done at the state level, recommending restrictions on sale, labelling and packaging and legislated accordingly.

Harmonization between states through ACMS (Advisory Committee on Medicines Scheduling)

220
Q

What are the 5 categories of scheduling?

A
  1. Unscheduled- General Sales
  2. Pharmacy Medicine (S2)
  3. Pharmacist Only Medicine (S3) [Also available at doctor/dentist] - requires professional advice given on dispensing
  4. Prescription Only Medicine (S4) - prescriptor can only give scripts within scope of practice
  5. Controlled Substances (S8)
221
Q

Can drugs exist on different scheduling categories?

A

Ibuprofen exists from S1-4 based on different dosages

222
Q

What are the annual financial limits for the PBS Safety Net Scheme?

A

$1421 general; $360- concessional]

223
Q

What are the end costs to general or concessional patients for prescription medications on PBS?

A
  1. General patients: $37.70 maximum/item
  2. Concessional patients: $6.10/item: Old age/disability pensions, entitled veterans, low income earners, healthcare assistance
224
Q

What information can be found on the TGA approved Product Information (API) sheets for prescription medications

A 
Pharmacology
Indications
Contraindications
Precautions
Interactions with Other Medicines
Adverse Effects
Dosage and Administration
Overdosage
Presentation and Storage Conditions
Poison Schedule of the Medicine
Name and Address of the Sponsor
Date of Approval
225
Q

What are S5, S6, S7, S9 drug schedules?

A

S5: Lower Harm Potential (household poisons)
S6: Poisons
S7: Dangerous Poisons (Commercial pesticides)
S9: Prohibited Substances (Heroin, MDMA, most recreational substances)

226
Q

How can you tell a dentist vs a GP prescription pad?

A

Blue edge on the form

227
Q

What prescription drugs can dentists prescribe?

A 
Antibiotics/antifungals
Local anaesthetics
Antiemetics
Cardiac stimulants
NSAIDs
Opioid Analgesics (some limits in some states)
Anti-inflammatories
Sedatives
228
Q

What indications can a dentist prescribe for?

A

Prescription must be for dental treatment only

229
Q

What information must be present when writing a script?

A 
Patient’s name (scripts not transferable)
Name &amp; address of practitioner (preprinted form)
Drug name (preferably generic name)
Drug form (tablets, capsules etc)
Drug strength (eg. 15 mg)
Drug Quantity (eg. 30)
Dose &amp; frequency of administration
Signature of Prescriber
Date of Prescription
230
Q

What are the qualities of a generic medicine

A
  1. Same quantitative composition of therapeutically active substances
  2. Same Pharmaceutical Form
  3. Bioequivalent
  4. Same safety and efficacy properties
231
Q

What is the minimum period of time before a drug can be rescheduled?

A

2 years

232
Q

Which drugs have been downwards rescheduled?

A 
H1 &amp; H2 antagonists
Nicotine replacements
Antifungals
Morning after pill
Statins
PPIs
Loperamide
Fexofenadine
Ibuprofen
233
Q

Which drugs have been upwards rescheduled?

A

Codeine: due to increased domestic abuse
Pseudoephedrine: use in manufacturing of meth

234
Q

What drug classification are blood thinning drugs?

A

Anticoagulation Drugs

235
Q

What drug classification are fluid tablets?

A

Diuretics

236
Q

What drug classification are reliever drugs?

A

Bronchodilators

237
Q

Are drugs that act on GABAA receptors responsive within seconds, minutes or hours?

A

Seconds - very rapid onset

Example: Ligand gated Cl Channel

238
Q

Are drugs that act on opioid receptors responsive within seconds, minutes or hours?

A

Minutes - rapid onset

Example: G-protein coupled receptor

239
Q

Are drugs that act on glucocorticoid receptors responsive within seconds, minutes or hours?

A

Hours - slow onset, as these receptors regulate gene transcription => proteins/enzyme creation

240
Q

T/F: Metabolic biotransformation lowers the plasma concentration of a drug

A

True

Increased elimination => decreased concentration

241
Q

Renal Tubular Resorption increases plasma concentration of a drug

A

True

Decreased elimination => increased concentration

242
Q

Renal Secretion lowers plasma concentration of a drug

A

True

Increased elimination => decreased concentration

243
Q

T/F: A drug has a 2% recovery from urine? Is the drug primarily cleared by the kidneys?

A

False

If it was cleaned by the renal system, we would expect a high recovery % in urine.

The drug is therefore metabolised in the liver

244
Q

What is a common way to bypass first pass effect?

A

Lingual administration tablets

245
Q

What are 4 mechanisms that reduce drug bioavailability?

A
  1. Poor Absorption: Fat Insoluble
  2. Active transport for absorption unavailable due to saturation
  3. Breakdown by stomach acid
  4. Liver First Pass Metabolism
246
Q

What is the implication of a narrow Therapeutic Index?

A

Increased likelihood of overdose in small changes in dosage

Example: Morphine

247
Q

What is the implication of a wide Therapeutic Index?

A

More likely to be easily available over-the-counter or legal drugs since toxicity dosage is relatively high

Example: Paracetamol, Ibuprofen, Caffeine

248
Q

What are 3 considerations for General Marketing of Medicines in Australia?

A

Drug Safety
Drug Efficacy
Quality of Tablet Formulation

249
Q

What are 2 predictable drug effects?

A

Bradycardia - slow heart action

Dry Mouth - due to effects on sympathetic nervous system

250
Q

What are complications with using Miconazole and Warfarin together?

A

Miconazole is a broad spectrum antifungal agent, absorbed through skin. When taken with warfarin inhibits P450 CYP2C9 pathway in the liver

  1. Warfarin metabolism reduced
  2. Increased Warfarin plasma concentration
  3. Increased anticoagulation effect (increased warfarin effectiveness)

Dangerous as warfarin has narrow TI
Big change in INR - measure for blood clotting

251
Q

How does Naloxone work as an antidote for morphine overdose

A

Works as an opioid receptor antagonist

252
Q

How does Neostigmine work as a treatment for Myasthenia Gravis?

A

Myasthenia Gravis is an autoimmune disease causing muscle weakness. It attacks Acetylcholine (ACh) receptors - hence poor muscle contraction

Neostigmine inhibits Acetylcholinesterase (enzyme that breaks down ACh) in Synaptic Cleft => hence more ACh to counteract effect of antibody

253
Q

What’s the difference between Sepsis and Septicaemia?

A

Septicaemia: systemic infection caused by microorganisms multiplying
in circulation

Sepsis: body’s inflammatory reaction to severe reaction

254
Q

What are origins of original antibiotics?

A

Natural Substances: Bacteria, Fungi/Moulds, Plants

255
Q

What are origins of modern antibiotics?

A

Synthetic / Semi-synthetic

256
Q

What are 2 actions that antibiotics can have on bacteria?

A

Bacteriostatic: Reduces multiplication rate allowing the body’s immune system to combat

Bacteriocidal: Direct kills and reduces population

257
Q

What groups are at risk of getting serious infections? How can antibiotics help?

A

People with reduced immune function:

  1. Age - Elderly
  2. Immunocompromised/suppressed: HIV, medication, organ transplant, malnutrition, stress

Antibiotics can reduce bacterial levels to a low enough level for the suppressed immune system to cope with clearing the infection

258
Q

What are the 4 mechanisms of action of Antibiotics and examples of each?

A
  1. Inhibit cell wall synthesis (bactericidal)
    Penicillins, cephalosporins
  2. Disrupt cell membrane (bactericidal)
    Anti-fungals
  3. Inhibit metabolism (folic acid) (bacteriostatic)
    Trimethoprim sulphamethoxazole
  4. Inhibit protein synthesis (bacteriostatic)
    Tetracyclines, macrolides (bacteriostatic), gentamicin (bacteriocidal)
259
Q

What are the 3 spectrums of action for antibiotics and which is preferred?

A
  1. Narrow spectrum: active against a few species
    Benzylpenicillin: mainly G +ve bacteria
  2. Moderate spectrum: active against several species
    Amoxicillin: G-ve cocci, some G+ve bacteria e.g. E. coli, salmonella, shigella
  3. Broad-spectrum: effective against many species
    Tetracyclines: G+ve and –ve bacteria, chlamydia

Clinical Application: narrow spectrum better: reduce harming native microflora + minimal side effects on body

260
Q

What is Minimum Inhibitory Concentration (MIC)?

A

The lowest concentration of an antimicrobial that will inhibit the visible growth of a microorganism in 24 hours, usually reported as mg/L

261
Q

What is the implication of an increase to MIC to pharmacokinetic efficacy?

A

Increased MIC indicates increased antibiotic resistance, reducing the efficacy of the antibiotic.

262
Q

What are the 2 methods used for antibiotic efficacy?

A
  1. Time Dependent Killing (dose/time above MIC)

2. Concentration-Dependent Killing (peak concentration level above MIC)

263
Q

What are the 3 unwanted side effects of antibiotics?

A
  1. Side Effects
  2. Hypersensitivity
  3. Resistance
264
Q

What are side effects that can occur from antibiotic use?

A 
Nausea (Most Common)
Vomiting
Diarrhea
Colitis (in chronic usage)
Opportunistic Infections (candida)
265
Q

What are Hypersensitivity reactions that can occur from antibiotic use?

A
  1. Type 1 Anaphylaxis (particularly in IV dose)

2. Delayed reaction (eg maculopapular or morbilliform rash)

266
Q

Why is antibiotic resistance a major health issue?

A
  1. Over usage / Incomplete usage
  2. Usage of potent AB in intensive agriculture spreading from animals => humans
  3. Globalisation: resistance travelling across countries due to human movement + air travel
267
Q

What are biochemical mechanisms that bacteria can use to create resistance against antibiotics?

A
  1. Enzymes that inactivate drug: beta-lactamase and penicillins
  2. Changes to drug binding site: penicillins, macrolides
  3. Drug pumped out of microbe: tetracyclines
  4. Microbe makes alternative enzyme bypass pathway: sulphonamides
268
Q

What is the antibiotic creed when determining antibiotic usage?

A

MIND ME

M: microbiology: knowledge of the infection/bacteria guides therapy wherever possible
I: Indications should be evidence based
N: Narrowest spectrum required
D: Dosage appropriate to the site and type of infection
M: Minimise duration of therapy
E: Ensure monotherapy in most situations

269
Q

What are the 3 types of antibiotic therapy?

A
  1. Prophylactic - prevent infection in clinical settings where there is a significant risk of infection
  2. Empirical [More important for dentists] - Causative bacteria not proven
  3. Directed - Culture susceptibility test results guide therapy
270
Q

When is Antibiotic Prophylaxis indicated?

A

In situations where an infection is likely and consequences would be disastrous:

1) Open Surgery
2) In dentistry: surgical operations to prevent endocarditis (risk groups -
Indigenous with Rheumatic Fever, prosthetic heart valve)

271
Q

What are the routes of administration for Antibiotics?

A

1) Oral: requires high bioavailability
2) IV (Parenteral): where oral route can’t be taken or urgent treatment needed
3) Topical
4) Intradental: Odontopaste and Ledermix in reducing bacteria in canal during RCT

272
Q

What antibiotics are used in Odontopaste?

A

Clindamycin

273
Q

What antibiotics are used in Ledermix?

A

Tetracycline

274
Q

What are the 7 major antibiotic families?

A
  1. β-lactams (Variable in Spectrum): Penicillins
  2. Cephalosporins (Moderate spectrum): cephalexin, cephazolin
  3. Glycopeptides:
    Parenteral Route : vancomycin and teicoplanin
  4. Macrolides: Roxithromycin
  5. Lincosamides: Clindamycin
    and lincomycin
  6. Tetracyclines: Doxycycline
  7. Nitroimidazole: Metronidazole. Tinidazole
275
Q

What are the 6 principles of antimicrobial selection?

A
  1. Use narrowest spectrum antibiotic to treat disease
  2. Safest
  3. Avoid topical administration of a drug used systemically
  4. Don’t use combinations unless proven usage
  5. Don’t give prophylactically unless benefit proven
  6. Lowest Cost
276
Q

Why should a narrow spectrum antibiotic be preferred?

A

Reduce impact on normal flora

Reduce selection pressure for resistance

277
Q

What groups require antibiotic prophylaxis if undergoing extractions, periodontal procedures, replanting avulsed teeth or any other surgical procedure?

A

1) Prosthetic heart valve
2) Previous Endocarditis
3) Congenital heart disease (if involves unrepaired cyanotic defects, unepitheliated prosthetics)
4) Cardiac Transplantation that develops cardiac valvulopathy
5) Rheumatic Heart Disease in Indigenous Australians only

278
Q

When might antibiotic prophylaxis be required in some circumstances?

A

If there is:

  1. Multiple procedures done at once
  2. Procedure is prolonged
  3. Periodontal disease present

Procedures include

  • Full Perio probing
  • Intraosseous/intraligamentary LA
  • Supragingival scaling
  • Rubber Dam placement
  • Restorative matrix band placement
  • Endodontics beyond apical foramen
  • Placement of orthodontic bands
  • Placement of intradental wedges
  • Retraction cord placement
279
Q

What 3 factors that alter pharmocokinetics?

A
  1. Clearance
  2. Bioavailability
  3. First Pass
280
Q

What other factors influence drug response over time?

A
  1. Disease - Liver + Kidney Disease
  2. Age
  3. Drug Interactions via medications, vitamins and supplements
  4. Diet/Food
  5. Environment
  6. Pregnancy
281
Q

T/F: Renal disease affects bioavailability

A

False - bioavailability has to do with GIT/liver function (first pass), not kidney (clearance)

282
Q

How is clearance affected in renal disease

A

Reduced filtration and secretion in parallel

283
Q

How is dosing regimen affected by renal disease?

A

Reduce maintenance dose - as major route of elimination is reduced by impaired renal excretion

284
Q

How does liver disease affect low clearance drugs?

A
  1. Bioavailability: No change
  2. Clearance: reduced due to reduced enzyme clearance
  3. Dosing regimen: reduce the maintenance dose
285
Q

How does liver disease affect high clearance drugs?

A
  1. Bioavailability: increased 2-5x
  2. Clearance: decreased due to decrease flow and enzyme activity
  3. Dosing regimen: reduce the maintenance dose
286
Q

What are principles for medication usage during pregnancy?

A

Avoid if possible. Potential damage includes:

  1. Foetal damage (1st trimester)
  2. Decreases growth and development in 2nd and 3rd trimester

Consult AMH and Product information leaflets for drug pregnancy category and any contraindications

287
Q

What is a Category A drug in the Australian Drug Pregnancy Categories?

A

No Risk

Drugs taken by large number of pregnant women with no increase in malformations or other direct harmful effects on foetus e.g. paracetamol

288
Q

What is a Category B1-B3 drug in the Australian Drug Pregnancy Categories?

A

Limited Risk

Drugs taken by limited number of pregnant women
B1: With no increase in malformations or other direct harmful effects on the foetus, animal studies no evidence of toxicity (ok) e.g. Amoxicillin
B2: With no increase in malformations or other direct harmful effects on foetus, animal studies inadequate but no toxicity (probably ok) e.g. Dicloxacillin (Another less common penicillin based AB)
B3: With no increase in malformations or other direct harmful effects on the foetus, animal studies show evidence of toxicity (avoid) e.g. Trimethoprim (AB for UTI, Middle Ear Infection)

289
Q

What is a Category C drug in the Australian Drug Pregnancy Categories?

A

Avoid

Drugs with pharmacological effects that cause/may be suspected of causing harmful effects on fetus without malformation - eg Ibuprofen

290
Q

What is a Category D drug in the Australian Drug Pregnancy Categories?

A

Avoid - increased chance of fetal damage

Drugs with pharmacological effects that cause/expected of causing increased incidence of human fetal malformation/irreversible damage - eg Fluconazole (anti-fungal)

291
Q

What is a Category X drug in the Australian Drug Pregnancy Categories?

A

Do not use - high risk of permanent fetal damage

Should not be used in pregnancy/possibility of pregnancy - eg Oral Isotretinoin for Acne

292
Q

What pharmacokinetic changes occur in pregnancy?

A
  1. Decreased GI motility:
    Slower absorption of drugs
  2. Kidney: GFR and secretion increased - eg higher dose needed for Amoxycillin due to 70% higher clearance rate
  3. Liver: Hepatic metabolism increased due to increased enzyme activity
  4. Maintenance dose of some drugs increased (Phenytoin or epilepsy)
293
Q

What pharmacokinetic changes occur in children?

A

Higher pharmacokinetics and pharmacodynamics - renal and hepatic clearance higher on kg basis compared in adults.

Therefore higher maintenance dose compared to adults

294
Q

Should teenagers be given children or adult doses for medication?

A

Pharmacokinetics and pharmacodynamics start to resemble adults so transition to adult versions of the medication

295
Q

What considerations should be given to the elderly in terms of medication usage?

A
  1. Likely to be using multiple medications
  2. Side effects from drug / drug interactions
  3. Altered pharmacokinetics
  4. Altered pharmacodynamics
296
Q

How are pharmacokinetics altered in the elderly?

A

Principle: start low and go slow

  1. Slower gut function: decreased absorption rate
  2. Decreased renal function → decreased renal clearance
  3. Decreased liver function and decreased enzyme activity (decreased clearance, increased bioavailability)
  4. Decreased normal maintenance dose
297
Q

How are pharmacodynamics altered in the elderly?

A

Principle: lower dosage

  1. Increased sensitivity to CNS acting drugs: Sedatives, antidepressants, opioids
  2. Decreased homeostasis: Postural hypotension from antihypertensives
298
Q

What are the clinical implications of codeine effectiveness in people with the CYP2D6 polymorphism?

A

Decreased drug effect as less codeine can be metabolised into the morphine active form.

However a smaller subset who are ultrarapid metabolisers could deliver toxic doses to their babies through breastfeeding, even though they themselves are safe

299
Q

What is the effect of Pharmacokinetics on those with a autosomal recessive version of CYP2D6 gene?

A

Autosomal Recessive are poor metabolisers - likely decreased clearance for some medications (Perphenazine for schizophrenia), toxic overdose for other medications (Dextromethorphan for dry-cough)

300
Q

What are the implications for a population where there higher epidemiological populations with poor metabolism as a result of the CYP2D6 gene?

A

Decreased dosage in medications to accommodate the poorer metabolism of that drug in the population

301
Q

Why can’t some Asians tolerate alcohol?

A

Alteration in ALDH2 gene - decreased activity of alcohol dehydrogenase => accumulation of alcohol => facial flushing, tachycardia, muscle weakness

302
Q

Why do some smokers drink more coffee?

A

Cigarette smoke => induces CYP1A2 enzyme in liver => increased caffeine clearance

303
Q

How does Grapefruit juice have drug/drug interactions?

A

Lower Metabolism = Inhibits CYP3A4 enzyme in gut wall

Therefore increases bioavailability of Cyclosporine (organ transplant immunosuppresant) + statins (cholesterol lowering drugs)

304
Q

T/F: The effect of drug/drug interactions on pharmacokinetics is primarily on bioavailability

A

False, drug drug interactions typically alter clearance. Bioavailability is rarely affected.

  • Hepatic clearance is increased or decreased
  • Renal clearance decreased
305
Q

T/F: The effect of drug/drug interactions on pharmacodynamics is the interacting drug altering the effect/response of the index drug without changing its concentrations

A

True - the interaction could result in an exaggerated or reduce response to the index drug

306
Q

What are the clinical implications of an enzyme induction drug/drug interaction?

A
  1. Inducer Drug A will induce the transcription of the enzyme that can metabolise Drug B
  2. Drug B plasma concentration decrease
  3. Disease returns as insufficient effect of Drug B
  4. If inducer drug ceased, Drug B dosage should be reduced as metabolism has slowed
307
Q

What are some examples of enzyme inducers?

A

Anticonvulsants

  • Carbamazepine
  • Phenytoin

Others

  • Rifampicin (tuberculosis)
  • Tobacco smoke
  • St John’s Wort (Depression)
  • Some Antivirals (AIDS)
308
Q

What are the clinical implications of an enzyme inhibition drug/drug interaction?

A
  1. Competition for same enzyme site
  2. Drug A blocks the metabolism of drug B in the liver
  3. Increased plasma concentration of Drug B - potentially toxic dose
309
Q

What are some examples of enzyme inhibitors?

A 
Anti-infectives/Antibiotics
- Metronidazole
- Erythromycin, clarithromycin
- Ketoconzaole/miconazole, -
 fluconazole (anti-fungals)
- Quinolones (ciprofloxacin, norfloxacin)
- Sulphonamides

Others

  • Grapefruit juice
  • Amiodarone
  • Omeprazole
  • Fluoxetine & other SSRIs antidepressants
  • Quinidine
310
Q

What are the characteristics of drugs that are susceptible to metabolic interactions?

A
  1. Cleared by metabolism

2. Narrow TI

311
Q

Why is the Interaction of ACEI + NSAID + Diuretics bad on Kidneys?

A
  1. Diuretics
    Reduced plasma volume => reduced renal blood flow
    Increased serum creatinine
  2. Kidney Compensation via RAAS
    Constriction of efferent renal arteriole => increased glomerular filtration pressure
    Favours water + sodium retention => increased plasma volume
  3. ACEI
    Inhibits constriction of efferent renal arteriole => lower glomerular filtration pressure
  4. NSAIDs
    Inhibits prostaglandins / bradykinin => vasoconstruction of afferent renal atteriole
    Reduce kid ability to increases glomerular blood flow

Result:
Combination of all 4 factors, RAAS can’t compensate for actions of 3x drugs
Acute reduction of glomerular filtration => rising serum creatinine levels
Constriction lowering blood pressure going into bowman’s capsule => kidney failure => death

312
Q

What would happen with the concurrent use of a:

  1. Beta blocker (for heart failure) e.g. propranolol
  2. Beta 2 agonist (for asthma) e.g. salbutamol
A

The antagonist and agonist counteract each other

313
Q

What is meant by a Potentiation Effect?

A

Also known as superadditive drug/drug interaction that can have two forms:

  1. Drug A + Drug B act on same target leading to increased mode of action or side effect: Amitriptyline + Ipratropium → very dry mouth
  2. Drug A + Drug B act on different target but same effect: Alcohol + Heyfever Medication (CNS Depressants)
314
Q

What is dangerous about St John’s Wart?

A

Powerful liver enzyme inducer => Lowers blood concentrations of other drugs.

Linked to inhibiting Cyclosporin (immunosuppressant) for heart/kidney transplant => kidney failure

315
Q

What sort of effects can grapefruit juice have on drugs?

A
  1. Inhibit CYP enzymes in the small intestine that create an active metabolite (lower bioavailability)
  2. Inhibit CYP enzymes in the small intestine that create an inactive metabolite (higher bioavailability) eg Statins
  3. Block protein transporters that carry the drug into the liver (lower bioavailability)
316
Q

What interactions can milk have on antibiotics?

A

Calcium binds to antibiotic molecule reducing the plasma concentration

317
Q

What interactions can antacids have on antibiotics?

A

Calcium binds to antibiotic molecule reducing the plasma concentration

318
Q

What interactions can iron tablets have on antibiotics?

A

Ferrous molecules binds to Ciprofloxacin (Fluoroquinolone Antibiotic) molecule reducing the plasma concentration

319
Q

How can we as clinicians avoid drug interactions?

A
  1. Look at patient’s drug list for any with narrow TI & prone to pharmacokinetic interactions
  2. Examine any drugs that have a superadditive (potentiating) or antagonistic effect
  3. Fully examine patient’s past medication usage
  4. Also examine herbal medicines, vitamins and supplements
320
Q

What is an Adverse Drug Reaction (ADR)?

A

Any response to a drug which is unintended, harmful and which occurs at a dose usually given to humans for management of disease

321
Q

What is an Adverse Drug Event (ADE)?

A

An injury resulting from medical intervention related to a drug

322
Q

What is an Type A ADE?

A

Augmented or increased effect

  • Effects are Predictable + Dose related
  • Manage by decreasing dosage
  • High risk of morbidity (disease)
  • Low risk of mortality

Examples

  • Caffeine → nervousness, palpitations
  • Benzodiazepines → excessive sedation
  • Codeine → constipation
323
Q

What is an Type B ADE?

A

Bizarre effect

  • Not predictable from known in pharmacology of drug
  • Not dose related
  • Low risk of morbidity (disease)
  • High risk of mortality
  • Example: Anaphylaxis / Allergies fpr Penicillin
324
Q

What is an Type C ADE?

A

Long Term Effects

1) Heroin: Dependence + Tolerance
2) Stilboestrol (to prevent miscarriage): caused vagina cancers, auto-immune disease (lupus) and infertility in daughters of the mothers taking the drug
3. Osteonecrosis in Jaw from long term bisphosphonate usage

325
Q

What is an Type D ADE?

A

Delayed Effect

Example: Thalidomide causing limb deformities in newborns

326
Q

What is an example of an unavoidable ADE?

A

Toxicity from Chemotherapy

327
Q

What is Pharmacovigilance?

A

The science of recording and studying adverse drug reactions

328
Q

Which groups are at risk of ADRs?

A
  1. Elderly: Altered pharmacokinetic & pharmacodynamics, multiple medications
  2. Infants: Immature organs for drug elimination
  3. Females > Males
  4. People on Multiple Medications
  5. Kidney / Liver Disease
  6. Ethnicity and Pharmacogenetics (CYP2D5 Poor Metabolisers)
329
Q

What are potential oral reactions to drugs?

A
  1. Local reactions: chemical burns (aspirin), opportunistic infections (asthma inhalers/topical antibiotics)
  2. Systemic reactions: immunesuppressions due to Systemic steroids → stomatitis (herpes simplex) or candida
  3. Stevens-Johnson Syndrome (Severe Erythema Multiforme): severe oral ulceration
  4. Drug induced Lichenoid Reaction: Allopurinol, Furosemide
  5. Gingival Hyperplasia: Calcium Channel Blockers, Cyclosporine, Phenytoin
  6. Xerostomia

COPY BDS3 University of Adelaide Dentistry (28 decks)

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