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OPTOM > OPTOM 345 > Flashcards

OPTOM 345 Flashcards

1
Q

What is a drug

A

Chemical substance that produces a biological effect and interacts with Receptors, Ion channels, Carriers and Enzymes

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2
Q

What is Pharmacokinetics

A

How drug moves in body and how well it reaches parts of the body

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3
Q

What is pharmacodynamics

A

The effect the drug has on the body

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4
Q

Name the axis on a Dose Response Curve

A

X axis = Drug Concentration
Y axis = Drug Response

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5
Q

What does a dose response curve tell us

A

Measures how well a drug binds to a receptor, and the point where it reaches maximum effect

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6
Q

What is maximum effect

A

The point where increasing drug concentration does not increase drug response

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7
Q

What is affinity

A

Drug interaction strength at the target site

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8
Q

What is Potency

A

Drug concentration needed for 50% maximal effect

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9
Q

Efficacy

A

The ability of the drug to produce a response once bound to a target site

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10
Q

When to use Bioequivalence

A

Used to determine which drug is better to use when compared to each other

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11
Q

How do we compare drugs

A

Risk v Benefit ratio

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12
Q

How does the risk v benefit ratio work

A

Uses the Toxic dose and Effective dose to calculate a therapeutic index

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13
Q

How to calculate the therapeutic index

A

TI = TD50 / ED50

The higher TI the safer the drug

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14
Q

What is the toxic dose

A

The toxic dose in 50% of the population

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15
Q

What is the effective dose

A

The effective dose in 50% of the population

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16
Q

What is the Therapeutic window

A

The dose range where the drug effect has minimal adverse effect

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17
Q

Different between specificity and selectivity

A

Specificity is where the drug targets in the body

Selectivity is how exclusive the drug is to certain receptors

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18
Q

Important of binding specificity

A

A drug must be specific for certain cells and tissues but in reality, no drug is completely specific.

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19
Q

Importance of binding selectivity

A

important for drugs to bind exclusively to certain receptors to reduce unwanted effects

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20
Q

What happens if we increase drug dose

A

It decreases drug specificity resulting in adverse effects

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21
Q

How do we make a drug more selective

A

By changing its size or having stereoisomerism where a drug has a different geometric structure so it will be selective to certain receptors increasing the potency for that receptor

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22
Q

What do Bioassays do

A

compare new drugs to existing drugs

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23
Q

What are the requirements for an assay

A

Should be reproducible, reliable indicator of its response and able to effectively comapre two or more drugs/formulations

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24
Q

Describe In-Vitro, Ex-Vivo and In-Vivo

A

In-vitro = Outside of body in Petri dish

Ex-vivo = Extract tissue from living organism

In-vivo = Perform study inside living organism

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25
Q

Explain the Transgenic animal models

A

They are use genetic manioulation to inactivate individual genes, mutate genes to pathological genotypes, introduce new genes and to over express genes such as parkinsons with increased synuclein expression

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26
Q

What is a requirement for animal models

A

Should be similar to human disease model where the pathophysiological phenotypes, causation and response to the treatment are similar

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27
Q

Why do many drugs fail clinical trials

A

Due to lack of clinical efficacy unmanageable toxicity, poor drug like properties, lack of commercial interest and poor strategic planning

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28
Q

What are clinical trials

A

Research studies that see if a medical strategy, treatment or device is safe and effective for humans

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29
Q

Briefly explain the procedures in clinical testing

A

Preclinical testing, 4 phases of clinical research and final data analysis with followups

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30
Q

What occurs in Phase 1 trial

A

Determine drug safety in healthy volunteers

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31
Q

What occurs in phase 2 trials

A

Pharmaco-kinetic/dynamic studies in healthy volunteers. There is also intital assessment of efficacy and continued assessment of safety in volunteers

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32
Q

What occurs in phase 3 trials

A

Assess longer-yerm efficacy and safety of the drug in the patient

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33
Q

What occurs in phase 4 trials

A

Post-marketing surveillance, ongoing assessment of safety and the likelihood of approval

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34
Q

What is a biomarker

A

Something that is objectively measured and evaluated as an indicator of normal biological process, pathogenic process or pharcologic response to a therapeuti intervention

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35
Q

What do biomarkers do

A

Indicate the prognosis of disease and monitor clinical response to an intervention

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36
Q

What do we measure in Bioassays when comparing drugs

A

The drugs efficacy, not potency

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37
Q

Strategies to avoid bias in drug testing

A

Controlled, Randomised and Double-blind testing

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38
Q

What is controlled testing

A

Compare A with B ( B is a control or placebo )

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39
Q

What is randomised testing

A

Patients assigned to group A or B randomly

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40
Q

What is double blind testing

A

Common in Phase 1-3 and sometimes 4, here neither participants or researchers know which participants belong to the control or test group. This minimises subjective bias

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41
Q

What is simple randomisation

A

When patients are assigned randomly to each group

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42
Q

What is stratified randomisation

A

When you divide participants into smaller group, then randomise each group with both the treatments and allocated similar overall demographics

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43
Q

What is Pharmacogenomics

A

Study the role of genes in drug response

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44
Q

Why do we do Pharmacogenomics

A

People of different ethnics have different genetic backgrounds that changes how the drug is metabolised and varies its efficacy

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45
Q

How to calculate Risk and Odds in a test

A

Risk for patients = Number of affected divided by the total number of paticipants

Odds for patients = Number of affected divided by the difference between the total number of participants and the affected

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46
Q

How to calculate relative risk ( RR )

A

Ratio of risk in treatment group and the risk in the control

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47
Q

How to calculate relative risk reduction ( RRR )

A

1 - RR

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48
Q

How to calculate Absolute Risk Reduction ( ARR )

A

Control risk - Treatment risk

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49
Q

How to calculate the number needed to treat ( NNT )

A

1/ARR

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50
Q

What is the number needed to treat ( NNT )

A

Number of people needed to treat to show the given effect of the drug

Lower NNT is more valuable

A drug that halves a mortality from 50% to 25% is more valuable than a drug that halves a mortality from 5% to 2.5%

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51
Q

What is the null hypothesis

A

States that there is no effect between comparisons

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52
Q

What is the P-Value

A

The probability that the null hypothesis is true. A statistically signficant P value is a value less that 0.05. When significant, we can reject the null hypothesis ( Ho )

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53
Q

What is the confidence interval

A

Range of values where the true parameter falls in, usually at 95%

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54
Q

What is Type 1 error

A

Rejection of a null hypothesis when it is true in the population

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55
Q

What is Type 2 error

A

Accepting null hypothesis when it is false in the population

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56
Q

What is power in statistics

A

The probability of detecting a difference when present where a larger sample size gives more power

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57
Q

What is the goal in a statistical tests regarding the number of participants

A

Recruit the minimum number of subjects to reject the null hypothesis ( usually 80% power )

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58
Q

How to calculate the power of a study

A

1 - Beta

Beta is the probability of a type 2 error

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59
Q

What does sample size of a study depend on

A

Power, magnitude of the difference you want to see and the statistical tests you plan to run

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60
Q

What are the 4 main targets for drugs

A

Receptors, Ion Channels, Carriers and Enzymes

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61
Q

Function of a receptor

A

Recognise and respond to endogenous chemical signals known as ligands and are found on cell surfaces

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62
Q

What happens when a receptor is bound

A

It activates and causes downstream effects

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63
Q

How do GPCRs work

A

Ligand binds giving conformational change in the GPCR causing the Alpha subunit to exchange GDP for GTP resulting in the alpha subunit and the beta-gamma dimer to dissociate and regulates the target proteins. Then the GTP hydrolyses to GDP and the cycle continues

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64
Q

How do Receptor Tyrosine Kinases work ( RTKs )

A

These have two receptors, when both are bound they come together forming one receptor causing the tyrosine residue to phosphorylate causing downstream effects

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65
Q

Name the 4 receptor types

A

Ligand gates ion channels, GPCRs, Kinase linked receptor and Nuclear receptors

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66
Q

How quickly do Ligand gated ion channels act

A

Milliseconds

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67
Q

How quickly do GPCRs act

A

Seconds

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68
Q

How quickly do Kinase linked receptors act

A

Hours

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69
Q

How quickly do nuclear receptors act

A

Hours

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70
Q

Why do nuclear receptors take so long to act

A

They are intracellular receptors so the ligand has to diffuse into the cell membrane to bind to the receptor

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71
Q

Function of ligand gated ion channels

A

When bound, the gate open or closes which either increases or decreases permeability to select ions. When membrane potential is changed by depolarisation or hyperpolarisation

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72
Q

Function of GPCRs

A

In eurkaryotes with 7 transmembrane domains coupled with G proteins which bind to GDP or GTP. These are also Muscarinic ACH receptors. It is for therapeutic drugs and causes downstream activation of other membrane targets

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73
Q

Structure of GPCRs

A

These are heterotrimeric so it has 3 subunits known as alpha, beta and gamma subunits which interact with GDP and GTP

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74
Q

Function of Kinase Linked Receptors

A

Includes RTKs, and Cytokine receptors. When bound is cuases phosphorylation of the intracellular domain and signals downstream processes

Also mediates growth factors, cytokines and hormones. The effects are exerted at the gene transcirption level and controls cell division, growth, differentiation, inflammation, immune responses, tissue repair and apoptosis

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75
Q

Function of Nuclear receptors

A

Found in cytoplasm ( Class 1 ), Nucleus ( Class 2 ) and Endocrine system ( Hybrid class ) known as steroid receptors

Activated by cell-permeating or lipophilic molecules and leads to the signalling cascades affecting gene expression

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76
Q

What is affinity and what does it depend on

A

The tendency of the drug to bind to a receptor, it depends on the Van der waals forces, hydrophobic, ionic, hydrogen and covalents

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77
Q

What is an agonist

A

acts as ligand and can activate or deactivate receptors

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78
Q

What is an antagonist

A

Acts as ligand and binds to receptor and causes no change in activity as it stops other molecules binding to the receptor but does not interact with active site

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79
Q

What is a partial agonist

A

Has an intermediate efficacy when bound even when all receptors are occupied

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80
Q

What are full agonists

A

Has full efficacy

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81
Q

What are inverse agonists

A

Drug that shows selectivity for resting states instead of activation of a receptor

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82
Q

What are antagonists

A

Have affinity but zero efficacy

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83
Q

Classes of Antagonists

A

Competitive reversible, Competitive irreversible and Non-competitive

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84
Q

What are competitive reversible antagonists and its effect on the dose respone curve

A

Competes with agonist, whichever concentration is higher will be favoured

Curve shifts to the right as more agonists needed to displace antagonist

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85
Q

What are competitive irreversible antagonists and its effect on the dose response curve

A

Competes with agnostic but has higher affinity for receptor so it requires new receptors to reverse its effects. Increasing concentration of agonist does not reverse its effect

Shifts curve to the right and reduces efficacy on the curve

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86
Q

What is a non-competitive antagonistm and its effect on the dose response curve

A

Does not bind to active site, binds to allosteric site

Shifts curve to the right and decreases efficacy

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87
Q

What are secondary messengers

A

Have receptors for ligand gated ion channels. When bound it causes a conformational change in the channel and ions move down their concentration gradients causing hyper or a depolarised state giving a cellular effect

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88
Q

Name the two ligand gated ion channels

A

Nicotinic acetylcholine receptor and the GABA receptor

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89
Q

What is the Nicotinic Acetylcholine receptor

A

ACH or Nicotine bnids giving influx of sodium which depolarises the cells increasing the chance of an action potential

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90
Q

What are GABA receptors

A

GABA binds causing influx of chloride ions into the cell and hyperpolarises the membrane reducing chance of an action potential

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91
Q

Name the types of GPCRs

A

Adenylyl Cyclase, Phospholipase C, Ion Channels, Rho A / Pho Kinase and Mitogen-Activated Protein Kinase

92
Q

What is Adenylyl cyclase

A

Enzyme for cAMP formation

93
Q

What is Phospholipase C

A

Enzyme for Inositol Phosphate and DAG formation

94
Q

Ion channels

A

Calcium and Potassium channels

95
Q

What are Rho A and Pho Kinase

A

System regulating activity of signal pathways for cell growth, proliferation, motility and smooth muscle contraction

96
Q

What are Mitogen activated Protein Kinases

A

System controlling cell functions like cell division, and also a target of several kinase linked receptors

97
Q

Name the subunits in G Proteins

A

Gas, Gai, Gao, Gaq and Ga12/13

98
Q

What does Gas do

A

Stimulate Adenylyl cyclase increasing cAMP formation

99
Q

What does Gai do

A

Inhibit Adenylyl cyclase decreasing cAMP formation

100
Q

What does Gaq do

A

activate phospholipase C increasing production of secondary messengers and releases Ca2+ form its stores

101
Q

What goes Ga12/13 do

A

Activate Rho and thus Rho kinase

102
Q

What does adenylyl cyclase do and its downstream effects

A

Produce cAMP which activate protein kinase inreasing lipolysis, reduced glycogen synthesis and increased glycogen breakdown. It also phosphorylates other enzymes for sugnalling cascades

103
Q

What does Phospholipase C do

A

Cause IP3 to be released resulting in IP3 gated calcium channels in the smooth endoplasmic reticulum to open which activates protein kinase C and binds to DAG

104
Q

What does DAG do

A

Remains in cell membrane and activates membrane bound protein kinase C that catalyses the phosphorylation of intracellular proteins

105
Q

How does GPCR control channel function

A

With G-protein via activation of effector proteins like adenyly cylclase or phospholipase C

106
Q

What do enzyme linked receptors do

A

Govern action of protein mediators like GF, cytokines and hormones

Receptors like RTKs and cytokine receptors

107
Q

What do nuclear receptors do

A

regulate gene transcription where ligands are lipophilic like hormones and fatty acid class 2

108
Q

Characteristics of Ion Channels

A

Polar molecules cannot penetrate the lipid bilayer unless there is an ion channel or transporter

Ion channels are water filled pores across the lipid membrane where the rate and direction of ion omvement is dependent on the electrochemical gradient for the ion

109
Q

What are ion channels selective for

A

Cations or Anions

110
Q

What does Phenytoin do

A

Blocks sodium channels to prevent excessive firing of neutrons during seizures

111
Q

What does phenobarbital do

A

Activates GABA receptors which opens chloride channels and reduces chances of action potentials

112
Q

What do blockers do

A

Block permeation of ions

113
Q

What do Modulators do

A

Increase or decrease the opening probability of a channel

114
Q

Ways enzymes can be inhibited

A

Competitive or non-competitive drugs

115
Q

What is a false substrate

A

A substrate that produces an abnornal response

116
Q

What is a competitive inhibitor for acetylcholinesterase and what is its acting duration

A

Neostigmate and is a medium duraton inhibitor

117
Q

What does Neostigmate do

A

Improves muscle tone in people with MG and reverses effects of non-depolaring muscle relaxants after surgery

118
Q

Which drug needs to be metabolised to be converted to an active state

A

Codeine

119
Q

What effect does Neostigmate have on muscles

A

It prolongs the effects of muscarinic and nicotinic receptors as it stops ACH from binding and also prevents the degradation of ACH

120
Q

How is codeine metabolised and to what

A

Metabolised to morphine by CYP2D6 when codeine reaches the liver

121
Q

Why is drug activation like codeine good

A

It reduces the interaction with opioid receptors in the GI tract and used for mild moderate pain with minimal side effects

122
Q

Methods of transporting molecules across membranes

A

Facilitated diffusion, Active transport, Na/K/Cl co transporters and Na/K ATPase

123
Q

How does Na/K ATPase work

A

Pumps Na to extracellular side and K to the intracellular side

124
Q

What is co-transport

A

Transports two things together in the same direction

125
Q

What are anti-porters

A

Transports two things in opposite directions

126
Q

How is pharmacokinetics measured

A

With ADME

127
Q

What is ADME

A

Absorption, Distribution, Metabolism and Elimination

128
Q

Why do we study pharmacokinetics

A

To see how much and how often we should supply a drug to maintain drug efficacy

129
Q

Why should we keep a drug in the therapeutic range

A

Otherwise it could get too toxic or the drug may not work well

130
Q

Methods of absorption

A

Oral, Parenteral ( IV ), Inhaled and topical

131
Q

What does absorption depend on

A

Membrane properties, drug characteristics and dosage form

132
Q

Characteristics of the Cornea regarding drug penetration

A

A mechanical barrier where drugs smaller than molecular weight of 5kDa can pass.

The corneas epithelium and endothelium is lipophilic and the stroma is hydrophilic

133
Q

What does Drug distribution depend on

A

The drugs characteristics, plasma protein binding and the patients weight. Other factors include permeability of barriers and the binding capacity of the drug.

134
Q

At what conditions do most drugs penetrate the lipophilic epithelium

A

pH 7 with drug in unionised form

When more than pH7 the ionised drug can easilt diffuse through the hydrophilic stroma

135
Q

What does drug metabolism depend on

A

The first pass, the enzyme inhibition and inducton, and drug activation.

136
Q

What drugs are more lipophilic and what does it mean for it

A

Ester prodrugs are more lipophilic so they are better at being absorbed and penetrates the cornea from the activation of esterases

137
Q

Where does metabolism mainly occur

A

In the liver and either activates or inactivates the drug

138
Q

Where does Elimination of drugs occur

A

In the kidneys in the GFR

139
Q

Describe the kinetics in elimination of a drug

A

Starts with first order or zero order where drugs decrease in concentration by half in the same time peroid, or has decreased reduction in concentration in the same time period

140
Q

What does washout mean

A

Tear fluid turnover after eyedrop application

141
Q

What is reflex tearing

A

From irritation from pH or foreign body sensation

142
Q

Where do most eyedrops drugs leave

A

In the nasolacrimal duct

143
Q

Where do most absorption of eyedrop drugs occur

A

In the nose where there is a high surface area and blood supply, this gives side effects which is a type of elimination we want to reduce

144
Q

Name the main routes of drug administration

A

Oral, sublingual, transdermal, rectal, inhalation, intranasal and parenteral

145
Q

What is bioavailability

A

The fraction of the administered dose that reaches the systemic circulation

146
Q

Oral administration characteristics

A

At least 80% drugs use this as its convenient and economical. Drug absorbed in stomach or intestines and enters the hepatic portal circulation into the liver for first pass. Then enters to general circulation giving longer onset of action and lower bioavailability

147
Q

Sublingual Administration characteristics

A

Drug dissolves under toungue and absorbs through mucous membranes into
blood stream, here there is no first pass. This makes it convenient and
economical and this method isnt suitable for all drugs

148
Q

Transdermal administration characteristics

A

Drug absorbed through skin, no first pass. Drug dosage here is continuous
and long acting. This is expensive and causes local irritation sometimes.

149
Q

Rectal administration characteristics

A

Drug absorbed through the mucous membranes. Suitable for children,
unconscious or vomiting patients. BUT there can be incomplete or irregular
absorption. This method has some First Pass

150
Q

Inhalation administration characteristics

A

Drug inhaled as gas to act in lung, so no first pass. This has a rapid onset of
action but can irritate lung tissue

151
Q

Intranasal administration characteristics

A

Drug absorbed through nasal mucous so no first pass, rapid onset of action
and this isnt suitable for all drugs. Drugs like Tyrvaya which increases tear
production

152
Q

Parenteral administration characteristics

( IV, IM and SC )
( Intravenous/muscular and
subcutaneous )

A

Bioavailability ( IV > IM > SC ). This gives more rapid response and avoids
unpredictable absorption processes in the GIT and is useful in unconcious or
uncooperative px. BUT must be sterile to prevent infection, drug cannot be
retrieved once injected, more expensive vs other routes and pain at the
injection site so px compliance goes down

153
Q

Types of ocular routes for drug administration

A

Intravitreal, intraocular, topical, periocular and systemic

154
Q

How do tonical eye drops work

A

Direct application to target site, a smaller dose is required and has rapid onset of
action. This method can have contamination and has limited corneal absorption
and fast nasolacrimal elimination giving systemic absorption giving side effects

155
Q

How do intravitreal injections work

A

Injection close to target site, a smaller drug doe required and has rapid onset of
action. This is an invasive procedure giving complications, also limited volume of
injection and has a short half life

156
Q

Compare solid and liquid dose drugs

A

Either way the drug needs to be in a solution for it to be absorbed. Solid excipents determine the tablet disintegration

157
Q

What do smaller particles mean for drugs

A

Higher surface area giving faster dissolution

158
Q

How do drugs get extended release formulations

A

Enteric coating

159
Q

Describe dosage forms as a solution

A

It is a homogenous mixture composed of only one phase where the solute is dissolved in the solvent

160
Q

Name examples of solution doses for ophthalmic formulations

A

Beta blockers and alpha agonists

161
Q

Pros and Cons of drugs as a solution

A

Pros –> Good stability, easy to prepare and low cost

Cons –> Fast drainage, low drug permeability through cornea and low drug bioavailability

162
Q

Describe dosage forms as a suspension

A

It is a heterogenous mixture composed of two phases where it has an internal solid phase which is dispersed throughout the external liquid phase such as steroids

163
Q

Pros and Cons of drugs as a suspension

A

Pros –> Reduced drainage as particles remain in lower lid, prolonged residence time giving higher drug availability

Cons –> Higher cost, larger particle size giving foreign body sensation and that suspensions need to be shaken before use

164
Q

Name the types of drug properties

A

Molecular weight, Partition coefficient and the acid dissociation constant

165
Q

Name the characteristics of class 1, 2, 3 and 4 drugs

A

Class 1 –> High solubility and permeability

Class 2 –> Low solubility and high permeability

Class 3 –> High solubility and low permeability

Class 4 –> Low solubility and low permeability

166
Q

Where does a drug need to be in order to be absorbed in regards to solubility

A

In a solution

167
Q

What dictates solubility

A

The solid state properties and the affinity for the solvent where like dissolves like

168
Q

What is the Henderson-Hasselbalch equation

A

pH = pKa - Log (Unionised)/(Ionised)

169
Q

Regarding permeability, explain the path for a drug to get to its site

A

Drug must penetrate the enterocytes lining the GIT

170
Q

What dictates permeability in passive diffusion

A

The drugs molecular weight, lipophilicity and the ionisation

171
Q

Which transport mechanism is more important for drug

A

Passive diffusion where it is driven by the concentration gradient

172
Q

What does active transport require

A

Energy as it transports things against its concentration gradient

173
Q

What does the rate of passive diffusion depend on

A

Concentration gradient between the GIT and the plasma, Surface area, thickness of the membrane and the diffusion coefficient of the molecule

174
Q

Rate of diffusion equation

A

((Cg - Cp) x A x D ) / d

175
Q

What is first pass metabolism

A

Occurs before the drug reaches the systemic circulation, mainly in the liver

176
Q

How to calculate oral dose

A

(Drug mass administered ) / (Bioavailability of that drug)

177
Q

How to ocular bioavailability increased in suspensions

A

Shaking the bottle before use and applying one drop into the lower lid pocket and close eyes, obstruct duct so the cornea can absorb it

178
Q

How long should we wait before applying another drop

A

5 minutes

179
Q

Why do we wait 5 mins before applying a second drop

A

Washout effect takes 5 mins for the drug to clear

180
Q

What does less washout mean

A

Higher absorption of drug

181
Q

How to increase compliance of px when multiple eye drops needed

A

Use a product that has a combination of both drugs in the same eye drop

182
Q

How is corneal permeability increased

A

By using penetration enhancers, prodrugs, colloidal delivery systems and increasing the contact time with the ocular surface by using viscosity enhancing

183
Q

Requirement for two pharmaceutical drugs to be bioequivalent

A

Both drugs need to be pharmaceutically equivalent and have the same bioavailability

184
Q

What is pharmaceutical equivalence

A

Same amount of same active form in same dosage for the same route of administration

185
Q

Are two different drops of the same drug bioequivalent

A

no

186
Q

Why arent the two drops bioequivalent

A

May have different pH giving different solubility and permeation, the particle size of the drug in the suspension can change its drainage and solubility. The addition of preservatives can vary the corneal penetration and absorption

187
Q

Where do drugs go

A

Places like blood, fat, intracellular and extracellular fluids

188
Q

What does drug absorption depend on

A

Drug properties, plasma protein binding and the disease state / age

189
Q

What is volume distribution ( Vd ) and how its calculated

A

Its a constant value for a drug in the average person. Here the total amount of drug absorbed is divided by the plasma concentration

It depends on Drug properties, plasma protein binding and the disease state / age

190
Q

What does a low plasma concentration mean for Volume distribution

A

A higher volume distribution, and vice versa.

191
Q

What decreases volume distribution

A

Increased molecular weight and plasma protein binding

192
Q

What increases volume distribution

A

Increased LogP and lipophilic drugs

193
Q

How is LogP and lipophilic drugs related

A

Higher LogP the more Lipophilic the drug is

194
Q

Compare Chloroquine and Warfarin

A

Chloroquine has longer half life as Warfarin binds to proteins like albumin

They have similar LogP and Molecular Weight

195
Q

What is the loading dose ( LD )

A

The amount of drug needed to achieve target concentration

196
Q

How to calculate loading dose ( LD )

A

LD = (Desired steady state concentration) x (Volume Distribution)

197
Q

How does increased age affect the drug in the body

A

Less plasma proteins in older people so more free drugs and possible increase in volume distribution. Diseases also increases permeability of capillary walls increasing volume distribution

198
Q

What does volume distribution affect

A

The time for a drug to reach a steady state and the time for the drug to be completely eliminated

199
Q

What is steady state ( Css )

A

The rate where drug administration equals drug elimination

200
Q

How to calculate steady state of a drug

A

Css = ( Maintanence dose rate ) / CL

CL = Clearance of drug

Can use to calculate Maintanence dose rate ( MDR ) where MDR = Css x CL

201
Q

What does does a higher volume distribution mean for Steady state

A

Longer time to reach steady state concentration ( Css )

202
Q

What does increasing the loading dose mean for Steady state

A

Decreases the time to the steady state concentration ( Css )

203
Q

What is Clearance ( CL )

A

The volume of plasma irreversibly cleared of drug per unit time.

Can be excretion of unchanged drug and metabolic conversion

204
Q

How are most drugs removed

A

Urinated out

205
Q

How does Renal clearance of a drug occur and how to calculate excretion

A

Drugs filtered into the bowmans capsule and then some components are reabsorbed and secreted

Excretion = Filtration - Reabsorption + Secretion

206
Q

What is the glomerular filtration rate ( GFR )

A

Total volume of filtrate produced per unit time by all functioning nephrons

207
Q

Explain the two phases in Hepatic clearance

A

Phase 1 –> Modification by oxidation, reduction, hydrolysis

Phase 2 –> Conjugation by sulphates, amino acids and Gluathione Acetylation

208
Q

What can occur in hepatic clearance

A

Can be eliminated by renal elimination of if drug goes through the hepatic circulation then that is not good for the liver

209
Q

How to calculate CLtotal

A

CLrenal + CLhepatic + CLother

210
Q

What affects GFR ( Glomerular filtration rate )

A

Renal diseases and failure reduces clearance

211
Q

How is GFR measured

A

By the creatinine clearance ( Multiply 0.85 for females )

212
Q

How to calculate creatinine clearance

A

[(140 - age in years) x Body mass in kg] / 814 x serum creatinine

213
Q

Which order kinetics do most drugs get eliminated

A

First order, where decline is constant over time

214
Q

What drugs are zero order kinetics regards to rate of elimination

A

Aspirin, Phenytoin and Ethanol

215
Q

What is a first order elimination

A

Exponential, where it is the amount of drug eliminated per unit time is proportional to a constant % of drug is eliminated per unit time

In other words, it is the constant fraction of drug eliminated per unit time

216
Q

What is a zero order elimination

A

A constant amount of drug is eliminated per unit time and is seen as a straight and declining line

217
Q

Characteristics of Zero order elimination

A

Metabolism dependent on enzyme saturation, more easily overdoes and the half life is not constant

218
Q

What is t 1/2

A

The time taken to eliminate 50% of the drug

219
Q

How to calculate the half life of a drug

A

t1/2 = (0.693 x Vd) / CL

or 0.693 / Ke

220
Q

How long does it take to eliminate a given drug dose

A

4-5x the half life of that drug , this is where 95% of the drug is out

221
Q

How long does it take to reach a drugs Css ( Steady state concentration )

A

Also 4-5x the half life of that drug

222
Q

Which equation is more relevant for drugs with higher half lifes

A

LD = Desired Css x Vd

223
Q

Which equation is more relevant for drugs with lower half lifes

A

MDR = Desired Css x CL

224
Q

What is the half life of most drugs

A

8-24 hours, hence dose is 1-3x per day

225
Q

Why do we do all these pharmaceutical calculations for drugs

A

To prevent no response and unwanted response and aim for desired response

We want the drug effect to be therapeutic, not toxic or sub-therapeutic

226
Q
A

OPTOM (6 decks)

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