1
Q
What is a drug
A
Chemical substance that produces a biological effect and interacts with Receptors, Ion channels, Carriers and Enzymes
2
Q
What is Pharmacokinetics
A
How drug moves in body and how well it reaches parts of the body
3
Q
What is pharmacodynamics
A
The effect the drug has on the body
4
Q
Name the axis on a Dose Response Curve
A
X axis = Drug Concentration
Y axis = Drug Response
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
6
Q
What is maximum effect
A
The point where increasing drug concentration does not increase drug response
7
Q
What is affinity
A
Drug interaction strength at the target site
8
Q
What is Potency
A
Drug concentration needed for 50% maximal effect
9
Q
Efficacy
A
The ability of the drug to produce a response once bound to a target site
10
Q
When to use Bioequivalence
A
Used to determine which drug is better to use when compared to each other
11
Q
How do we compare drugs
A
Risk v Benefit ratio
12
Q
How does the risk v benefit ratio work
A
Uses the Toxic dose and Effective dose to calculate a therapeutic index
13
Q
How to calculate the therapeutic index
A
TI = TD50 / ED50
The higher TI the safer the drug
14
Q
What is the toxic dose
A
The toxic dose in 50% of the population
15
Q
What is the effective dose
A
The effective dose in 50% of the population
16
Q
What is the Therapeutic window
A
The dose range where the drug effect has minimal adverse effect
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
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.
19
Q
Importance of binding selectivity
A
important for drugs to bind exclusively to certain receptors to reduce unwanted effects
20
Q
What happens if we increase drug dose
A
It decreases drug specificity resulting in adverse effects
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
22
Q
What do Bioassays do
A
compare new drugs to existing drugs
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
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
25
Explain the Transgenic animal models
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
26
What is a requirement for animal models
Should be similar to human disease model where the pathophysiological phenotypes, causation and response to the treatment are similar
27
Why do many drugs fail clinical trials
Due to lack of clinical efficacy unmanageable toxicity, poor drug like properties, lack of commercial interest and poor strategic planning
28
What are clinical trials
Research studies that see if a medical strategy, treatment or device is safe and effective for humans
29
Briefly explain the procedures in clinical testing
Preclinical testing, 4 phases of clinical research and final data analysis with followups
30
What occurs in Phase 1 trial
Determine drug safety in healthy volunteers
31
What occurs in phase 2 trials
Pharmaco-kinetic/dynamic studies in healthy volunteers. There is also intital assessment of efficacy and continued assessment of safety in volunteers
32
What occurs in phase 3 trials
Assess longer-yerm efficacy and safety of the drug in the patient
33
What occurs in phase 4 trials
Post-marketing surveillance, ongoing assessment of safety and the likelihood of approval
34
What is a biomarker
Something that is objectively measured and evaluated as an indicator of normal biological process, pathogenic process or pharcologic response to a therapeuti intervention
35
What do biomarkers do
Indicate the prognosis of disease and monitor clinical response to an intervention
36
What do we measure in Bioassays when comparing drugs
The drugs efficacy, not potency
37
Strategies to avoid bias in drug testing
Controlled, Randomised and Double-blind testing
38
What is controlled testing
Compare A with B ( B is a control or placebo )
39
What is randomised testing
Patients assigned to group A or B randomly
40
What is double blind testing
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
41
What is simple randomisation
When patients are assigned randomly to each group
42
What is stratified randomisation
When you divide participants into smaller group, then randomise each group with both the treatments and allocated similar overall demographics
43
What is Pharmacogenomics
Study the role of genes in drug response
44
Why do we do Pharmacogenomics
People of different ethnics have different genetic backgrounds that changes how the drug is metabolised and varies its efficacy
45
How to calculate Risk and Odds in a test
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
46
How to calculate relative risk ( RR )
Ratio of risk in treatment group and the risk in the control
47
How to calculate relative risk reduction ( RRR )
1 - RR
48
How to calculate Absolute Risk Reduction ( ARR )
Control risk - Treatment risk
49
How to calculate the number needed to treat ( NNT )
1/ARR
50
What is the number needed to treat ( NNT )
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%
51
What is the null hypothesis
States that there is no effect between comparisons
52
What is the P-Value
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 )
53
What is the confidence interval
Range of values where the true parameter falls in, usually at 95%
54
What is Type 1 error
Rejection of a null hypothesis when it is true in the population
55
What is Type 2 error
Accepting null hypothesis when it is false in the population
56
What is power in statistics
The probability of detecting a difference when present where a larger sample size gives more power
57
What is the goal in a statistical tests regarding the number of participants
Recruit the minimum number of subjects to reject the null hypothesis ( usually 80% power )
58
How to calculate the power of a study
1 - Beta
Beta is the probability of a type 2 error
59
What does sample size of a study depend on
Power, magnitude of the difference you want to see and the statistical tests you plan to run
60
What are the 4 main targets for drugs
Receptors, Ion Channels, Carriers and Enzymes
61
Function of a receptor
Recognise and respond to endogenous chemical signals known as ligands and are found on cell surfaces
62
What happens when a receptor is bound
It activates and causes downstream effects
63
How do GPCRs work
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
64
How do Receptor Tyrosine Kinases work ( RTKs )
These have two receptors, when both are bound they come together forming one receptor causing the tyrosine residue to phosphorylate causing downstream effects
65
Name the 4 receptor types
Ligand gates ion channels, GPCRs, Kinase linked receptor and Nuclear receptors
66
How quickly do Ligand gated ion channels act
Milliseconds
67
How quickly do GPCRs act
Seconds
68
How quickly do Kinase linked receptors act
Hours
69
How quickly do nuclear receptors act
Hours
70
Why do nuclear receptors take so long to act
They are intracellular receptors so the ligand has to diffuse into the cell membrane to bind to the receptor
71
Function of ligand gated ion channels
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
72
Function of GPCRs
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
73
Structure of GPCRs
These are heterotrimeric so it has 3 subunits known as alpha, beta and gamma subunits which interact with GDP and GTP
74
Function of Kinase Linked Receptors
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
75
Function of Nuclear receptors
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
76
What is affinity and what does it depend on
The tendency of the drug to bind to a receptor, it depends on the Van der waals forces, hydrophobic, ionic, hydrogen and covalents
77
What is an agonist
acts as ligand and can activate or deactivate receptors
78
What is an antagonist
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
79
What is a partial agonist
Has an intermediate efficacy when bound even when all receptors are occupied
80
What are full agonists
Has full efficacy
81
What are inverse agonists
Drug that shows selectivity for resting states instead of activation of a receptor
82
What are antagonists
Have affinity but zero efficacy
83
Classes of Antagonists
Competitive reversible, Competitive irreversible and Non-competitive
84
What are competitive reversible antagonists and its effect on the dose respone curve
Competes with agonist, whichever concentration is higher will be favoured
Curve shifts to the right as more agonists needed to displace antagonist
85
What are competitive irreversible antagonists and its effect on the dose response curve
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
86
What is a non-competitive antagonistm and its effect on the dose response curve
Does not bind to active site, binds to allosteric site
Shifts curve to the right and decreases efficacy
87
What are secondary messengers
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
88
Name the two ligand gated ion channels
Nicotinic acetylcholine receptor and the GABA receptor
89
What is the Nicotinic Acetylcholine receptor
ACH or Nicotine bnids giving influx of sodium which depolarises the cells increasing the chance of an action potential
90
What are GABA receptors
GABA binds causing influx of chloride ions into the cell and hyperpolarises the membrane reducing chance of an action potential
91
Name the types of GPCRs
Adenylyl Cyclase, Phospholipase C, Ion Channels, Rho A / Pho Kinase and Mitogen-Activated Protein Kinase
92
What is Adenylyl cyclase
Enzyme for cAMP formation
93
What is Phospholipase C
Enzyme for Inositol Phosphate and DAG formation
94
Ion channels
Calcium and Potassium channels
95
What are Rho A and Pho Kinase
System regulating activity of signal pathways for cell growth, proliferation, motility and smooth muscle contraction
96
What are Mitogen activated Protein Kinases
System controlling cell functions like cell division, and also a target of several kinase linked receptors
97
Name the subunits in G Proteins
Gas, Gai, Gao, Gaq and Ga12/13
98
What does Gas do
Stimulate Adenylyl cyclase increasing cAMP formation
99
What does Gai do
Inhibit Adenylyl cyclase decreasing cAMP formation
100
What does Gaq do
activate phospholipase C increasing production of secondary messengers and releases Ca2+ form its stores
101
What goes Ga12/13 do
Activate Rho and thus Rho kinase
102
What does adenylyl cyclase do and its downstream effects
Produce cAMP which activate protein kinase inreasing lipolysis, reduced glycogen synthesis and increased glycogen breakdown. It also phosphorylates other enzymes for sugnalling cascades
103
What does Phospholipase C do
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
What does DAG do
Remains in cell membrane and activates membrane bound protein kinase C that catalyses the phosphorylation of intracellular proteins
105
How does GPCR control channel function
With G-protein via activation of effector proteins like adenyly cylclase or phospholipase C
106
What do enzyme linked receptors do
Govern action of protein mediators like GF, cytokines and hormones
Receptors like RTKs and cytokine receptors
107
What do nuclear receptors do
regulate gene transcription where ligands are lipophilic like hormones and fatty acid class 2
108
Characteristics of Ion Channels
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
What are ion channels selective for
Cations or Anions
110
What does Phenytoin do
Blocks sodium channels to prevent excessive firing of neutrons during seizures
111
What does phenobarbital do
Activates GABA receptors which opens chloride channels and reduces chances of action potentials
112
What do blockers do
Block permeation of ions
113
What do Modulators do
Increase or decrease the opening probability of a channel
114
Ways enzymes can be inhibited
Competitive or non-competitive drugs
115
What is a false substrate
A substrate that produces an abnornal response
116
What is a competitive inhibitor for acetylcholinesterase and what is its acting duration
Neostigmate and is a medium duraton inhibitor
117
What does Neostigmate do
Improves muscle tone in people with MG and reverses effects of non-depolaring muscle relaxants after surgery
118
Which drug needs to be metabolised to be converted to an active state
Codeine
119
What effect does Neostigmate have on muscles
It prolongs the effects of muscarinic and nicotinic receptors as it stops ACH from binding and also prevents the degradation of ACH
120
How is codeine metabolised and to what
Metabolised to morphine by CYP2D6 when codeine reaches the liver
121
Why is drug activation like codeine good
It reduces the interaction with opioid receptors in the GI tract and used for mild moderate pain with minimal side effects
122
Methods of transporting molecules across membranes
Facilitated diffusion, Active transport, Na/K/Cl co transporters and Na/K ATPase
123
How does Na/K ATPase work
Pumps Na to extracellular side and K to the intracellular side
124
What is co-transport
Transports two things together in the same direction
125
What are anti-porters
Transports two things in opposite directions
126
How is pharmacokinetics measured
With ADME
127
What is ADME
Absorption, Distribution, Metabolism and Elimination
128
Why do we study pharmacokinetics
To see how much and how often we should supply a drug to maintain drug efficacy
129
Why should we keep a drug in the therapeutic range
Otherwise it could get too toxic or the drug may not work well
130
Methods of absorption
Oral, Parenteral ( IV ), Inhaled and topical
131
What does absorption depend on
Membrane properties, drug characteristics and dosage form
132
Characteristics of the Cornea regarding drug penetration
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
What does Drug distribution depend on
The drugs characteristics, plasma protein binding and the patients weight. Other factors include permeability of barriers and the binding capacity of the drug.
134
At what conditions do most drugs penetrate the lipophilic epithelium
pH 7 with drug in unionised form
When more than pH7 the ionised drug can easilt diffuse through the hydrophilic stroma
135
What does drug metabolism depend on
The first pass, the enzyme inhibition and inducton, and drug activation.
136
What drugs are more lipophilic and what does it mean for it
Ester prodrugs are more lipophilic so they are better at being absorbed and penetrates the cornea from the activation of esterases
137
Where does metabolism mainly occur
In the liver and either activates or inactivates the drug
138
Where does Elimination of drugs occur
In the kidneys in the GFR
139
Describe the kinetics in elimination of a drug
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
What does washout mean
Tear fluid turnover after eyedrop application
141
What is reflex tearing
From irritation from pH or foreign body sensation
142
Where do most eyedrops drugs leave
In the nasolacrimal duct
143
Where do most absorption of eyedrop drugs occur
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
Name the main routes of drug administration
Oral, sublingual, transdermal, rectal, inhalation, intranasal and parenteral
145
What is bioavailability
The fraction of the administered dose that reaches the systemic circulation
146
Oral administration characteristics
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
Sublingual Administration characteristics
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
Transdermal administration characteristics
Drug absorbed through skin, no first pass. Drug dosage here is continuous
and long acting. This is expensive and causes local irritation sometimes.
149
Rectal administration characteristics
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
Inhalation administration characteristics
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
Intranasal administration characteristics
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
Parenteral administration characteristics
( IV, IM and SC )
( Intravenous/muscular and
subcutaneous )
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
Types of ocular routes for drug administration
Intravitreal, intraocular, topical, periocular and systemic
154
How do tonical eye drops work
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
How do intravitreal injections work
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
Compare solid and liquid dose drugs
Either way the drug needs to be in a solution for it to be absorbed. Solid excipents determine the tablet disintegration
157
What do smaller particles mean for drugs
Higher surface area giving faster dissolution
158
How do drugs get extended release formulations
Enteric coating
159
Describe dosage forms as a solution
It is a homogenous mixture composed of only one phase where the solute is dissolved in the solvent
160
Name examples of solution doses for ophthalmic formulations
Beta blockers and alpha agonists
161
Pros and Cons of drugs as a solution
Pros --> Good stability, easy to prepare and low cost
Cons --> Fast drainage, low drug permeability through cornea and low drug bioavailability
162
Describe dosage forms as a suspension
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
Pros and Cons of drugs as a suspension
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
Name the types of drug properties
Molecular weight, Partition coefficient and the acid dissociation constant
165
Name the characteristics of class 1, 2, 3 and 4 drugs
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
Where does a drug need to be in order to be absorbed in regards to solubility
In a solution
167
What dictates solubility
The solid state properties and the affinity for the solvent where like dissolves like
168
What is the Henderson-Hasselbalch equation
pH = pKa - Log (Unionised)/(Ionised)
169
Regarding permeability, explain the path for a drug to get to its site
Drug must penetrate the enterocytes lining the GIT
170
What dictates permeability in passive diffusion
The drugs molecular weight, lipophilicity and the ionisation
171
Which transport mechanism is more important for drug
Passive diffusion where it is driven by the concentration gradient
172
What does active transport require
Energy as it transports things against its concentration gradient
173
What does the rate of passive diffusion depend on
Concentration gradient between the GIT and the plasma, Surface area, thickness of the membrane and the diffusion coefficient of the molecule
174
Rate of diffusion equation
((Cg - Cp) x A x D ) / d
175
What is first pass metabolism
Occurs before the drug reaches the systemic circulation, mainly in the liver
176
How to calculate oral dose
(Drug mass administered ) / (Bioavailability of that drug)
177
How to ocular bioavailability increased in suspensions
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
How long should we wait before applying another drop
5 minutes
179
Why do we wait 5 mins before applying a second drop
Washout effect takes 5 mins for the drug to clear
180
What does less washout mean
Higher absorption of drug
181
How to increase compliance of px when multiple eye drops needed
Use a product that has a combination of both drugs in the same eye drop
182
How is corneal permeability increased
By using penetration enhancers, prodrugs, colloidal delivery systems and increasing the contact time with the ocular surface by using viscosity enhancing
183
Requirement for two pharmaceutical drugs to be bioequivalent
Both drugs need to be pharmaceutically equivalent and have the same bioavailability
184
What is pharmaceutical equivalence
Same amount of same active form in same dosage for the same route of administration
185
Are two different drops of the same drug bioequivalent
no
186
Why arent the two drops bioequivalent
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
Where do drugs go
Places like blood, fat, intracellular and extracellular fluids
188
What does drug absorption depend on
Drug properties, plasma protein binding and the disease state / age
189
What is volume distribution ( Vd ) and how its calculated
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
What does a low plasma concentration mean for Volume distribution
A higher volume distribution, and vice versa.
191
What decreases volume distribution
Increased molecular weight and plasma protein binding
192
What increases volume distribution
Increased LogP and lipophilic drugs
193
How is LogP and lipophilic drugs related
Higher LogP the more Lipophilic the drug is
194
Compare Chloroquine and Warfarin
Chloroquine has longer half life as Warfarin binds to proteins like albumin
They have similar LogP and Molecular Weight
195
What is the loading dose ( LD )
The amount of drug needed to achieve target concentration
196
How to calculate loading dose ( LD )
LD = (Desired steady state concentration) x (Volume Distribution)
197
How does increased age affect the drug in the body
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
What does volume distribution affect
The time for a drug to reach a steady state and the time for the drug to be completely eliminated
199
What is steady state ( Css )
The rate where drug administration equals drug elimination
200
How to calculate steady state of a drug
Css = ( Maintanence dose rate ) / CL
CL = Clearance of drug
Can use to calculate Maintanence dose rate ( MDR ) where MDR = Css x CL
201
What does does a higher volume distribution mean for Steady state
Longer time to reach steady state concentration ( Css )
202
What does increasing the loading dose mean for Steady state
Decreases the time to the steady state concentration ( Css )
203
What is Clearance ( CL )
The volume of plasma irreversibly cleared of drug per unit time.
Can be excretion of unchanged drug and metabolic conversion
204
How are most drugs removed
Urinated out
205
How does Renal clearance of a drug occur and how to calculate excretion
Drugs filtered into the bowmans capsule and then some components are reabsorbed and secreted
Excretion = Filtration - Reabsorption + Secretion
206
What is the glomerular filtration rate ( GFR )
Total volume of filtrate produced per unit time by all functioning nephrons
207
Explain the two phases in Hepatic clearance
Phase 1 --> Modification by oxidation, reduction, hydrolysis
Phase 2 --> Conjugation by sulphates, amino acids and Gluathione Acetylation
208
What can occur in hepatic clearance
Can be eliminated by renal elimination of if drug goes through the hepatic circulation then that is not good for the liver
209
How to calculate CLtotal
CLrenal + CLhepatic + CLother
210
What affects GFR ( Glomerular filtration rate )
Renal diseases and failure reduces clearance
211
How is GFR measured
By the creatinine clearance ( Multiply 0.85 for females )
212
How to calculate creatinine clearance
[(140 - age in years) x Body mass in kg] / 814 x serum creatinine
213
Which order kinetics do most drugs get eliminated
First order, where decline is constant over time
214
What drugs are zero order kinetics regards to rate of elimination
Aspirin, Phenytoin and Ethanol
215
What is a first order elimination
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
What is a zero order elimination
A constant amount of drug is eliminated per unit time and is seen as a straight and declining line
217
Characteristics of Zero order elimination
Metabolism dependent on enzyme saturation, more easily overdoes and the half life is not constant
218
What is t 1/2
The time taken to eliminate 50% of the drug
219
How to calculate the half life of a drug
t1/2 = (0.693 x Vd) / CL
or 0.693 / Ke
220
How long does it take to eliminate a given drug dose
4-5x the half life of that drug , this is where 95% of the drug is out
221
How long does it take to reach a drugs Css ( Steady state concentration )
Also 4-5x the half life of that drug
222
Which equation is more relevant for drugs with higher half lifes
LD = Desired Css x Vd
223
Which equation is more relevant for drugs with lower half lifes
MDR = Desired Css x CL
224
What is the half life of most drugs
8-24 hours, hence dose is 1-3x per day
225
Why do we do all these pharmaceutical calculations for drugs
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
OPTOM III
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