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Principles of Disease > Drug Therapy > Flashcards

Drug Therapy Flashcards

1
Q

Glyceryl nitrate (GTN) is administered by the sublingual route to avoid?

A

First pass metabolism.

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2
Q

A drug trial in which neither patient nor doctor is aware what treatment the patient is taking is called a?

A

Double trial

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3
Q

A drug trial which data is collected from case records after treatment is given is called a?

A

Retrospective trial.

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4
Q

A drug trial in which patients take both treatments being tested one after the other is called a?

A

Cross-over trial.

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5
Q

a drug trial in which patients are allowed to treatment groups using random number generation is called a?

A

Randomised trial.

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6
Q

What are the physiological barriers that affect the transfer of drugs across the cell membrane.

A
  1. Passive diffusion
  2. Filtration
  3. Bulk flow
  4. Active transport
  5. Facilitated diffusion
  6. Ion pair transport
  7. Endocytosis
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7
Q

What factors affect bioavailability?

A

Particle size, lipid solubility, pH and ionisation

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8
Q

Discuss lipid solubility.

A

Drugs must be lipid soluble to cross the membrane.

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9
Q

Give an example of a non-lipid soluble drug.

A

Gentamicin

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10
Q

Discuss ionisation and drug absorption.

A

Most drugs don’t completely ionise in water as most drugs are weak acids or bases and therefore depends on pH.

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11
Q

Do ionised drugs cross the lipid membrane?

A

No

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12
Q

What equation represents pH and degree of ionisation relationship.

A

Henderson-Hasslebach equation.

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13
Q

Discuss the factors that affect absorption of a drug from the GI tract.

A
  1. Motility (speed of gastric absorption will affect speed at which drug reaches site of absorption, can be affected by other drugs)
  2. Food (can enhance or impair rate of absorption)
  3. Illness
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14
Q

Define bioavailability.

A

Amount of drug which reaches circulation and is available for action.

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15
Q

Give examples of illnesses which affect drug absorption.

A
  1. Malabsorption e.g coeliac disease can increase or decrease rate of absorption.
  2. Migraine reduces rate of stomach emptying and therefore absorption of analgesic drugs.
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16
Q

Why are paediatric patients a high risk group?

A

Absorption different due to different GI pH changes, gastric emptying and enzymes, bile acids and biliary function, GI flora, food /formula etc.

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17
Q

Define first pass metabolism.

A

Concentration of drug reduced before it reaches the circulation.

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18
Q

What are the causes of first pass metabolism?

A

Gut lumen (acid, enzymes) and gut wall (metabolic enzymes)

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19
Q

What is the clinical importance of first pass metabolism?

A

Can be a limit on oral route of some drugs.

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20
Q

What administration routes avoid first pass metabolism?

A

Subcutaneous/intra-muscular, sublingual/buccal, rectal and transdermal.

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21
Q

What two factors should be considered when deciding route of administration?

A
  1. Local absorption

2. First pass metabolism

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22
Q

What are the benefits of IV administration?

A

Rapid onset of action, careful control of plasma levels, short half-life, can be given rapidly or continuous infusion.

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23
Q

What are the benefits of topical administration?

A

Least invasive, decreased risk of side-effects, rapid, localised treatment.

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24
Q

What are the benefits of inhaled medications?

A

Better for volatile agents, can be metabolised in lungs, relatively rapid effect, small dose used, reduced adverse events

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25
Q

What factors determine bioavailability?

A

Formulation, ability to pass physiological barriers, GI effects, first pass metabolism, route of administration.

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26
Q

What route of administration has 100% availability?

A

Intravenous

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27
Q

What factors determine drug distribution?

A
  • Chemical properties (lipid solubility and ionisation) determine of drug reaches volume of distribution.
  • Protein binding (more than 90% bound) - only unbound drugs are biologically active.
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28
Q

Discuss protein binding and give an example of proteins.

A

E.g albumin or alpha1-glycoprotein e.g phenytoin

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29
Q

What is the result of increased volume of distribution?

A

Increases ability of drug to diffuse.

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30
Q

How is binding reversed?

A

Renal function, hypoalbuminaemia, pregnancy, other drugs, satiability of binding.

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31
Q

What is the result of increased half-life with regard to drug distribution?

A

Increased accumulation of drug with increased toxicity.

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32
Q

Define the half-life of a drug.

A

Time take for drug concentration in blood to decline to half of the current volume.

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33
Q

Discuss the relevance of three mechanism of renal disease states to drug excretion.

A
  1. Glomerular filtration
  2. Passive tubular reabsorption
  3. Active tubular secretion
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34
Q

Describe glomerular filtration.

A

Most important - as EGFR decreases, toxicity increases due to accumulation ad decreased excretion.

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35
Q

Where are all unbound drugs filtered?

A
  • At the glomerulus (as long as charge, molecular size and shape are not excessively large)
  • Factors affecting glomerular filtrate decrease drug clearance
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36
Q

Discuss passive tubular reabsorption.

A
  • As filtrate moves down renal tube, any drug present is concentrated.
  • Passive diffusion allows drug to move back through the tubule and into the circulation.
  • Occurs in distal tubule and collecting duct
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37
Q

What can passive tubular reabsorption be affected by?

A

Renal failure.

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38
Q

Define active tubular secretion.

A
  • Some drugs actively secreted into proximal tubule (acidic and basic compounds)
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39
Q

What is the most important system for eliminating protein bound cationic and anionic drugs?

A

Active tubular secretion.

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40
Q

Define metabolism.

A

An essential pharmacokinetic process which limits the life of a substance by rendering lipid-soluble and non-polar compounds to water soluble and polar compounds for excretion.

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41
Q

What are the important sites of metabolism?

A

Liver, gut lining, kidneys and lungs.

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42
Q

Define prodrugs and give an example.

A

Activated following metabolism e.g simvastatin.

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43
Q

What are the two phases of metabolism?

A
  1. Phase I metabolism - increase polarity, cytochrome P450 enzymes)
  2. Phase II metabolism - increase water solubility and enhances excretion, conjugation
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44
Q

Define pharmacogenetics.

A
  • Drug metabolising enzymes expressed in multiple forms.
  • gene mutations and genetic polymorphisms
  • Decreased enzyme activity increase drug toxicity.
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45
Q

What factors affect bioavailability?

A
  • Metabolism
  • Age
  • Gender
  • Ethnicity
  • Foods
  • Illness etc
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46
Q

How does age affect drug metabolising enzymes?

A
  • Enzymes deficient in fetes or premature infant.

- 2yo metabolises more rapidly than adults.

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47
Q

How does gender affect drug metabolism?

A
  • Difference in ADME

- Pregnancy induces certain enzymes in 2nd and 3rd trimesters

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48
Q

How does ethnicity differences affect drug metabolism?

A

Difference in genetic expression of cytochrome P450 isoforms.

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49
Q

Describe ADME.

A

Absorption
Distribution
Metabolism
Excretion

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50
Q

What is ADME important for?

A
  1. Determing how to get drug to site of action
  2. Determining dose and frequency
  3. Making sure drug is present in effective dose
  4. Predicting and avoiding toxicity
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51
Q

Describe the different types of oral medications.

A
  1. Solutions and suspensions
  2. Tablets and capsules
  3. Enteric coated tablets
  4. Prolonged and delayed release formulations
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52
Q

What are solutions and suspensions useful for?

A

Swallowing difficulties, may be given via NG or PEG tube, absorbed very rapidly.

53
Q

What is a disadvantage of tablets and capsules?

A

Dissolution of tablet breakdown = rate-limiting step in absorption.

54
Q

What are the advantages of enteric coated tablets?

A
  • delays disintegration until it reaches SI
  • protects drug from stomach acid
  • protects stomach from other drugs e.g aspirin
55
Q

What are the advantages of prolonged and delayed release formulations?

A
  • maintains drug levels in therapeutic range
  • decrease need for frequent dosing
  • improved compliance
56
Q

What is the rectal route useful for?

A

Young and old, achieve systemic absorption.

57
Q

Discuss the strengths of topical treatments.

A

Local effect, transdermal bypass first pass metabolism.

58
Q

What is a disadvantage of inhalation?

A

Patient education required.

59
Q

Define “object drug”.

A

Drug whose activity is effected.

60
Q

Define “precipitant”.

A

Agent causing interaction.

61
Q

What factors predispose a patient to drug interactions?

A
  • potent drugs with narrow therapeutic index (require therapeutic drug monitoring)
62
Q

Give examples of drugs that require therapeutic drug monitoring.

A

Lithium, digoxin, warfarin, cyclosporin, phenytoin, gentamicin, SSRI, erythromycin

63
Q

Give an example of food and drug interactions.

A

Warfarin interacts with certain types of veg e.g asparagus and broccoli.

64
Q

What patients are susceptible to drug interactions?

A

Polypharmacy, elderly, young, critically ill, undergoing complex surgical procedures.

65
Q

What are the causes of absorption interactions?

A

Altered pH
Altered bacterial flora
Altered GI motility (some drugs bind to each other in GI tract)

66
Q

What causes distribution interactions?

A

Protein-protein displacement, protein-binding displacement

67
Q

What causes metabolism interactions?

A

When one drug induces or inhibits the metabolism of another.

  • can inhibit cytochrome P450 (e.g Rifampicin and St John’s Wort)
  • older patients have diminished metabolism
68
Q

What causes elimination/excretion interactions?

A

Changes in GFR or tubular secretion.

69
Q

Name two toxic agents eliminated by the kidneys.

A

Digoxin and Lithium.

70
Q

Define drug-drug interactions.

A

Modification of drug effect by prior concomitant administration of another drug, herbal foodstuff or drink.

71
Q

Are drug-drug interactions always detrimental?

A

No.

72
Q

Describe the three different types of drug-drug interactions.

A
  1. Antagonistic
  2. Additive
  3. Synergistic
73
Q

What are the main causes of interactions?

A
  • Changes in drug transport
  • Fluid and electrolyte disturbances
  • indirect pharmacodynamic interactions
  • when pharmacodynamic action of drug changes because of another acting directly on same receptor or indirectly on different receptor.
74
Q

List the different types of pharmacodynamic interactions.

A

Direct, indirect, antagonistic, synergistic/agonist

75
Q

Give an example of indirect agonism.

A

Warfarin and NSAIDs

76
Q

Give an example of indirect antagonistic pharmacodynamic interactions.

A

NSAIDs and antihypertensives

77
Q

Why is therapeutic drug monitoring important?

A

Small change in blood level can induce profound toxicity.

78
Q

What is the purpose of therapeutic drug monitoring?

A

Monitors plasma drug levels which are toxic and have narrow therapeutic index.

79
Q

What is the frequency of hospital admissions that are the result of ADRs?

A

6.5%

80
Q

What percentage of inpatients suffer an ADR?

A

10-20%

81
Q

Approximately how many deaths a year are cause by ADRs?

A

5000-12000

82
Q

What groups are most likely to suffer an ADR?

A

Age, multiple co-morbidities, polypharmacy, prior history of ADR, genetic predisposition

83
Q

What are the most common drugs that cause ADRs?

A

Antibiotics, antineoplastics, CNS drugs, CV drugs

84
Q

What are the main types of ADRs?

A 
Type A (augmented)
Type B (bizzarre)
Type C (Chronic/long term effects)
Type D (delayed effects)
Type E (end of treatment effects)
Type F (failure of therapy)
85
Q

What type of ADR is predictable?

A

Type A

86
Q

What type of ADR is dose-related and reversible?

A

Type A

87
Q

What type of ADR is unpredictable?

A

Type B

88
Q

What type of ADR is most common?

A

Type A

89
Q

What type of ADR can be life threatening?

A

Type B

90
Q

What are the two main effects of type A reactions?

A
  1. Augmented primary effect (e.g bradycardia with beta-blockers)
  2. Secondary effect
91
Q

What type of reaction is unrelated to dose and not readily reversible?

A

Type B

92
Q

What type of reaction is rare and has idiosyncratic mechanisms?

A

Type B

93
Q

What type of reaction is a drug allergy or hypersensitivity reaction?

A

Type B

94
Q

In type B reactions, the differences in response are due to what?

A

Genetic or immunological variations

95
Q

What type of reaction is related to the duration of treatment and dose?

A

Type C

96
Q

What type of reaction is semi-predictable?

A

Type C

97
Q

Give an example of a type C reaction.

A

Iatrogenic Cushing’s disease with excess steroids.

98
Q

What type of reaction occurs a long time after treatment?

A

Type D

99
Q

Teratogenesis and carcinogenesis are examples of what type of reaction?

A

Type D

100
Q

What type of reaction occurs when a drug is suddenly stopped after use?

A

Type E

101
Q

Give an example of a type E reaction.

A

Unstable angina and MI when beta-blocker stopped

102
Q

What type of reaction is commonly seen in children?

A

Type F

103
Q

What type of reaction is dose related and frequently caused by drug interactions.

A

Type F

104
Q

What are the main reasons for type A ADRs?

A
  • too high a dose
  • pharmaceutical variation
  • pharmacokinetic variation (ADME) most common cause
  • pharmacodynamic variation
  • pharmacogenetic (number of drugs metabolised via acetylation which is under genetic control.
105
Q

What methods are available to detect and report ADRs?

A

Yellow card (online reports)

106
Q

What does the yellow card system collect info on?

A

Side effects. medical device adverse incidents, defective medicines, counterfeit or fake medicines or devices.

107
Q

What are the common mechanisms of drug-drug interactions?

A
  1. Pharmaceutical

2. Pharmacokinetic (ADME)

108
Q

What group of patient’s have a diminished metabolism?

A

Elderly

109
Q

Give an example of drugs that induce the cytochrome P450 system.

A

Barbiturates, rifampicin, tobacco smoke, St John’s Wort

110
Q

Define medication error.

A

Any preventable event that may cause or lead to inappropriate medication use or patient harm.

111
Q

Why do medication errors occur?

A
  • increase in number and variety of drugs
  • patients have co-morbidities
  • complexity of care
  • need for high risk medications
  • errors in prescription writing
112
Q

What are the consequences of prescription errors?

A

On patients, family, colleagues, professional, legal and media.

113
Q

“Think before you ink”. What are the associated 5 R’s?

A

Right patient, drug, rate, time, dose

114
Q

How can we enhance safe prescribing?

A

Patient passports, handovers, medicines reconciliation, technology, simulation, reporting system, comms techniques, safe delivery systems.

115
Q

What is the purpose of clinical trials?

A
  • Provide evidence when much practice is evidence based
  • protects the public and provide evidence to help rationalise prescribing
  • test efficacy and safety
116
Q

What are the basic considerations involved in trial design?

A 
hypothesis
end-ponts
number and choice of subjects
power calculations
choice of control drug
exclusion and selection criteria
ethics
117
Q

Discuss the importance of statistical tests and statistical power for analysis and interpretation of results?

A

p<0.05 = significant (? are differences due to chance?)

  • detect difference between groups
  • make sure findings are not missed
  • probability that it will reject a false null hypothesis
118
Q

What are two of the main challenges in clinical trials?

A

Impaired renal function and co-morbidities

119
Q

Define a parallel control trial.

A

Compare outcomes or end-points in 2 groups (e.g 100 patients - 50 get drug and 50 get placebo)

120
Q

Define cross-over trial.

A

A longitudinal study which investigates transient effects of an intermittent exposure on the onset of acute outcomes.

121
Q

Why do some studies have statistical significance but lack clinical significance?

A
  • Don’t explain existing info about patient or provide useful direction for intervention.
  • differences common in population unlikely to be clinically significant because they simply reflect a level of normal variation
122
Q

What is a Phase I clinical trial?

A

Drug development, pre-clinical, animal pharmacology and toxicology, tissue culture.
Clinical development with 100 volunteer subjects

123
Q

What drugs bypass Phase I clinical trials?

A

Cytotoxic drugs

124
Q

What is a Phase II clinical trial?

A

Clinical investigation to confirm kinetics and dynamics in patients (approx 500) to provide some evidence of efficacy and identify likely dosage range.

125
Q

What is a Phase III clinical trial?

A

Formal therapeutic trial where efficacy is established and evidence of safety is obtained based on approx 1000-3000 patients.

126
Q

What happens upon completion of a Phase III clinical trial?

A

All data must be submitted to regulatory authority for a drug license to sell.

127
Q

What is a phase IV clinical trial?

A

Post-marketing surveillance to produce evidence of long-term safety based on tens or hundred of thousands of patients worldwide.

128
Q

How is aspirin absorbed by the stomach?

A

Ionised at acidic pH.

Principles of Disease (9 decks)

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