Pharmacology Flashcards
What is pharmacology?
Explains what drugs are, what effect they have on the body and the effect the body has on the drug.
Explains why side effects may occur and why different people may react differently to drugs.
The science of the interaction of chemical agents with living systems. It encompasses the study of biochemical and physiological aspects of drug effects, including absorption, distribution, metabolism, elimination, toxicity and specific mechanisms of drug actions
What is a drug?
A substance that affects a biological system. Used in prevention, diagnosis, treatment of a disease.
Once the chemicals are absorbed into systemic circulation they bind with a target to change the function of the cell.
What is an active ingredient?
The chemical in the drug that affects physiological functioning
What is an inactive ingredient?
They have no effect on the cells. Act as a filler to bind the drug together, make it taste or smell pleasant, to lubricate the drug.
Where do drugs come from?
Plants- aspirin, opiates Microbes- penicillin, chloramphenicol Animals- heparin, insulin (usually now made synthetically or by genetic engineering) Minerals- calcium, magnesium Can be synthesised by chemists
Advantages of synthetic drugs?
Easier quality control Process easier and cheaper Safer Large scale production Drugs can be modified to improve properties
How are biological drugs made?
A product that is formed from living organisms or contain components of living organisms
These drugs are often large and difficult to generate synthetically
Types of drug names:
1) chemical: includes information on molecular structure
2) trivial: a common name, sometimes arising from historical uses
3) generic: non-proprietary drug name adopted by an officially recognised organisation in a country. E.g. BAN (British approved name) from the British Pharmacopeia or USP (United states pharmacopeia)
4) trade names: owned by a company
Reasons why adverse affects may occur?
Drug has additional effects on the body due to lack of specificity
Patient is sensitive to the drug given
Patient is not taking the prescribed dose
Dose incorrectly proscribed
Drug-drug interactions
Why so drugs effect people differently?
Age Genes Disease state Tolerance Dependence
What is a poison?
Any chemical agent that produces harmful effects
What is a toxin?
A poison of biological origin
What did Paul Ehrlich say?
A drug will not work unless bound
Types of drug targets?
Proteins- most common
Nucleic acids- some drugs bind to DNA, such as cancer therapies that interfere with DNA replication, e.g. doxorubicin
Others- such as protons, e.g. antacids
Types of drug target proteins?
Receptors, e.g. GPCRs
Enzymes
Ion channels
Transporters
Receptor definition?
A protein that, when bound to an agonist, transmits a signal which turns on or off a specific biological/physiological response
What is the name of the endogenous molecule that binds to a receptor?
Ligand
Examples of endogenous ligands?
Hormones Neurotransmitters Growth factors Cytokines Metabolites
Different classes of receptors?
Cell surface receptors Intracellular receptors (nuclear receptors)
Cell surface receptors?
G protein-coupled receptors (GPCR) (metabotropic): ligand binding to receptor activates a G-protein which then activates or inhibits an enzyme or ion channel
Ligand gated ion channels (ionotropic): ligand binding to the ion channel causes opening or closing of the channel and modulates passage of ions
Enzyme-coupled receptors: ligand binding activates the enzyme activity
Intracellular receptors?
Either cytoplasmic or nucleolus.
Binding of ligand activates receptor and alters gene expression
How does an agonist work?
Bind to and activates the receptor to produce biological response
They have affinity and efficacy
They often mimic or are the endogenous ligand
Examples of agonists
Salbutamol: beta 2 adrenergic receptor agonists (GPCR). Very similar chemical structure to adrenaline
Insulin: insulin receptor agonist (enzyme-linked receptor)
How does an antagonist work?
Binds to the receptor and prevents the agonist from producing a biological response
They have affinity but not efficacy
Types of antagonist?
Competitive: bind with the same site as the agonist
Non-competitive: binds to allosteric site on receptor to stop agonist from being able to bind
Can be reversible or irreversible
Example of antagonists?
Propranolol: antagonist of beta adrenergic receptors (GPCR)
Tamoxifen: antagonist of the oestrogen receptor (intracellular receptor)
How do ion channels blockers work?
The blocker sits in the channel to affect permeation (passage of ions)
Example of ion channel blocker?
Tetrodoxin: blocks voltage gated sodium channel. A poison isolated from Japanese puffer fish but in trials for analgesia purposes
How do ion channel modulators work?
Bind to the channel proteins to affect gating
Example of ion channel modulator?
Sulfonylureas: target ATP-sensitive potassium channel and promote insulin release
How do enzyme inhibitors work?
Bind to substrate binding site to inhibit normal reactions
Can be competitive or non-competitive
Can be reversible or irreversible
Examples of enzyme inhibitors?
Aspirin: a non-competitive inhibitor of cyclooxyrgenase
Sildenafil: a competitive inhibitor of cGMP phosphodiesterase type 5
How do pro-drugs work?
Drugs that first require modification by an enzyme before being active
Example of a pro-drug?
Enalapril: ACE inhibitor that needs to first be activated by an enzyme to enalaprilat
How do false substrates work?
Drugs that bind to the substrate binding site and are converted to an abnormal product by the enzyme. The product then subverts the normal metabolic pathway
False substrate example?
Methyldopa: catalysed by DOPA decarboxylase to methylnorepinephrine
How do transporter inhibitors work?
Block the channel or inhibit the activity
Example of transporter inhibitors?
SSRIs: they block the transporters responsible for the reuptake of serotonin meaning more is available to pass further messages to nerve cells
Amphetamines: compete with noradrenaline for NA-uptake 1 transporter. Meaning more noradrenaline is available to bind to receptors
Drug binding to a receptor is determined by what forces?
Hydrogen bonds
Van der Waals forces
Ionic bonds
Covalent bonds
Affinity meaning in pharmacology?
The strength of attraction between the drug and its receptor
It’s the ability to associate and dissociate from the receptor
What type of bond causes irreversible competition?
Covalent
Two most common types of forces between receptors and ligands?
Hydrogen bonds
Van der Waals forces
In terms of affinity, at equilibrium, the rate of associate is equal to?
Rate of dissociation
Drug binding to receptor formula?
[drug/receptor complex]
Which is equal to
K dissociation
———————-
K association
Which is equal to Kd
What is Kd?
The dissociation constant.
This is when 50% of the receptors are occupied
What does Kd measure?
Affinity
50% occupancy of receptors
What does a low Kd mean?
High affinity, so smaller concentrations of the drug are needed
Implying a strong binding of the receptors
What does a high Kd mean?
Low affinity, so higher drug concentrations are needed
Implying a weak binding of the receptors
What is a radioligand assay used for?
To measure affinity
How does a radioligand assay work?
1) conducted in vitro
2) cells in the dish have the receptors you are interested in
3) radiolabelled ligand is added to the dish
4) watch binding over time and record the steady-state at different concentrations
5) plot this against time
6) add excess non-radioactive ligands to complete and remove labelled ligands from the receptors; this measures the nonspecific binding
7) minus the nonspecific binding from the total binding to work out the specific binding of that drug
What does occupancy mean?
The proportion of receptors bound or occupied by the drug
What is Bmax?
The maximum number of receptors bound
When plotted on a linear scale a concentration-occupancy relationship is?
Hyperbolic
When plotted on a log scale a concentration-occupancy relationship is?
Sigmoidal (S-shaped)
What is Ka?
The reciprocal of Kd; 1/Kd
Measure of the affinity of the drug for the receptor
Low Kd would mean high Ka
How can efficacy be determined?
Plotting the concentration of a drug against its response
Usually in vitro as in humans the concentration at the site of action would not be the same as the concentration administered
When plotted on a linear scale a concentration-response relationship is?
Hyperbolic
When plotted on a log scale a concentration-response relationship is?
Sigmoidal (S-shaped)
Why do drug responses saturate?
Amplification of signals
What is Emax?
The maximum effect which can be expected from the drug
What is EC50?
The effective concentration that produces 50% of the maximal effect/response
It is a measure of potency
What is ED50?
The effective dose of a drug producing 50% of a maximal effort OR the dose required to produce a therapeutic response in 50% of the population
What is the difference between EC50 and ED50?
EC is measured in vitro as we can measure specific concentrations
ED is measured in vivo as we cannot measure the concentration of the drug at the site of action, but we can give a dose
What is TD50?
The dose required to produce a toxic effect in 50% of the population
What is therapeutic index?
Measurement of drug safety
The relationship between the therapeutic and the toxic dose of a drug
How to calculate the therapeutic index?
TD50/ED50
A drug with a high therapeutic index is?
Usually safer- maximal benefit with minimal risk
A drug with a low therapeutic index is?
More dangerous. May require regular monitoring of drug levels
What is the therapeutic window?
The range of doses between efficacy and toxicity. Achieving the greatest benefit without resulting in toxicity
What do full agonists do?
Produce a 100% response
Have high efficacy
What do partial agonists do?
Produces less than a full response when fully occupying their receptors
Have a lower efficacy
What values can efficacy take?
Between 0 and 1
1 being a maximum response
0 being no response
Potency meaning?
The amount of drug required to produce an effect of given intensity
The product of both affinity and efficacy
How to compare drug potency?
Using the EC/ED50 values
What does a low ED/EC 50 mean?
High potency
What does a high ED/EC50 show?
Low potency
Why is EC50 usually much lower than Kd?
Signal amplification
Drugs can produce a full response without full occupancy; some receptors are spare
Where do competitive antagonists bind?
Reversibly or irreversibly to the orthosteric site
Where do non-competitive antagonists bind?
Irreversible to the orthosteric site or to an allosteric site
The majority of clinically used drugs are what type?
Reversible competitive antagonists
What happens if you add more agonist to a reversible competitive antagonist?
No change in efficacy
A rightward shift of the concentration-response for the agonists (increased EC50)
The higher the affinity of the antagonist, the greater the shift
Can be inhibitory effects of an antagonist be surmounted by the addition of the agonist?
Yes
What happens if you add more agonist to an irreversible competitive antagonist?
The action of an irreversible antagonist cannot be surmounted
A reduction in efficacy- Emax
It may or may not affect EC50
What are the barriers to oral/dermal/pulmonary absorption?
Mainly the epithelium as cells are tightly packed; plasma membranes are lipid based
Effux proteins
Mucosal enzymes that may degrade the drug
Highly viscous layers that cover the epithelium
How can drugs cross the epithelium?
Passive diffusion
Active transport
How are most oral drugs absorbed?
Passive diffusion
Which kind of drugs can absorb by passive diffusion?
Small
lipophilic
What kind of drugs can enter cells by carrier proteins?
Small and hydrophilic molecules or ions
It may be passive or active
What is intracellular diffusion?
The movement of small (<600 Da) hydrophilic molecules through the right junction of cells
What is transcytosis?
How larger hydrophilic molecules may penetrate the epithelium
What is the pKa of a substance?
The pH at which ionised and unionised forms are equal
Why is pKa important in drug absorption?
So you can predict ionisation behaviour in different parts of the body that have different pHs
What happens if the pH is lower than the pKa?
In acids: the unionised form will dominate
In bases: the ionised form will dominate
What happens if the pH is higher than the pKa?
In acids: the ionised form will dominate
In bases: the unionised form will dominate
What happens if the pH is the same as the pKa?
50% will be ionised, and 50% will be unionised irrespective if acid or base
What does the partition coefficient measure?
Tests the hydrophilic/phobic properties
To what degree the molecule prefers to be in octanol or water
How is the partition coefficient measured?
Drug placed in a flask of octanol and water
Shaken
Analyse the amount of substance in each layer
What is log-P?
The partition coefficient is when none of the substance is ionised. The ratio of the concentrations of unionised compounds in octanol and water at equilibrium
Log-P equation?
P= [drug] octanol
——————–
[drug] water
What does log-P of 0 show?
50/50 in octanol and water
What does log-P of 1 show?
10x more in octanol
What does log-P of 2 show?
100x more in octanol
What does log-P of 3 show?
1000x more in octanol
What does log-P of -1 show?
10x more in water
What does log-P of -2 show?
100x more in water
What does log-P of -3 show?
1000x more in water
What is log-D?
Distribution coefficient
Includes the amount of ionised compound in the aqueous stage
The partition changes with pH
Weak bases are mainly absorbed at…… pH’s?
Higher
Weak acids are mainly absorbed at…… pH’s?
Lower
What is the pH of the stomach?
1-2
around 4 in neonates
What is the pH of the duodenum?
5-6
What is the pH of the jejunum/ileum?
6.5-7.6
What is the pH of the colon?
8
If the pKa of aspirin is 3.5 where will it be absorbed?
Stomach
If the pKa of morphine is 8 where will it be absorbed?
Duodenum
Why are ionised drugs not absorbed?
There are surrounded with a water sphere and therefore no lipophilic
What is faster passive diffusion or facilitated diffusion?
Facilitated diffusion
What is transported by facilitated diffusion?
Charged molecules
Polar substances
What are the two types of membrane transporters?
ATP-binding cassette (ABC)
Solute carrier transporters (SLC)
Which type of membrane transporters use energy from ATP?
ABCs
SLCs do not but after often couples to other energy-dependent mechanisms
What does the Biopharmaceutical Classification System do?
Categorises drug molecules based on intestinal permeability and aqueous solubility
Four possible categories
Barriers for oral absorption?
Rate of gastric emptying
The acidic environment of the stomach
Presence of enzymes
Advantages of the pulmonary administration route?
Non-invasive Delivers to a large surface area Thin alveolar epithelial cells Avoidance of first-pass metabolism Minimal enzymatic activity in the lungs
Factors that may limit the use of pulmonary administration?
Lung disease
Smoking
Necessity to control the breathing rate
How are drugs transported through the skin?
Passive diffusion
1) via hair follicles with their associated sebaceous glands
2) through sweat ducts
3) across the continuous stratum corneum between these appendages
What kinds of molecules are absorbed well by the dermal route?
High log-P, so lipophilic
Low molecular weight
Types of plasma proteins?
Albumin
Immunoglobulin
Fibrinogen
Why are plasma proteins important in drug distribution?
All drugs bind to plasma proteins to some degree, meaning only a certain amount can enter cells
Warfarin 99% bound
Digoxin less than 10% bound
What is extracellular fluid?
Blood plasma
Interstitial fluid
Lymph
22% total body weight
What is intracellular fluid?
Total fluid contents of all cells
30-40% of total body weight
What is transcellular fluid?
Cerebrospinal Intraocular Peritoneal Pleural Synovial Digestive secretions Around 2.5% of total body weight
What factors can affect distribution?
LogP Blood flow to organ/tissue Binding to blood and plasma proteins Size of molecules Membrane transporters
Volume of distribution definition?
The volume of fluid required to contain the total amount of drug throughout the body, at the same concentration as that present in the plasma
It provides a measure of the extent of distribution
What does a low volume of distribution indicate?
Distribution is restricted to a particular compartment such as the plasma
What could cause a low volume of distribution?
Large molecular weight drugs
High levels of protein binding 
What kind of drugs can have a high volume of distribution?
Lipid soluble or bind extensively to tissues
What is the blood brain barrier?
It functions as a physical, metabolic and immunological barrier maintaining the homoeostasis of the brain
What is the main type of cell in the blood brain barrier?
Brain capillary endothelial cells, these limit the movement of material from the blood to the brain
What kind of drugs can cross the blood brain barrier?
Highly lipid soluble
Molecules less than 400 Da and that form less than eight hydrogen bonds can pass via passive diffusion
Formula for protein binding?
Fu=Cu/C
Fu fraction unbound
Cu concentration unbound in plasma
C total plasma drug concentration
How can plasma proteins cause drug interactions?
Some drugs can push other drugs off the proteins.
What is metabolism?
Biotransformation of xenobiotics to more water-soluble compounds to facilitate excretion
What happens in phase 1 metabolism?
Low molecular weight functional groups are added
What happens in phase 2 metabolism?
Xenobiotic is conjugated with higher molecular weight adducts
What happens in phase 3 metabolism?
Further processing of phase 2 products
What part of the bloodstream does a drug enter?
The hepatic portal vein
What are the there most important conjugates? 
Glucuronides, glutathione and sulfate
What type of reactions are involved in phase 1 metabolism?
Oxidation, reduction, hydration, hydrolysis and other reactions
What enzymes are involved in oxidation reactions?
Cytochrome p450 enzymes (CYPs) Flavin monooxygenases Monoamine oxidases Alcohol dehydrogenase Xanthine oxidase
What enzymes are involved in reduction reactions?
DT-diaphorase
Cytochrome p450 (CYPs)
What kind of enzymes are involved in hydrolysis reactions?
Peptidases, carboxylesterases
What type of enzymes are involved in hydration reactions?
Epoxide hydrolase
What is the most common type of phase 1 metabolism reaction?
Oxidation
How do flavin monooxygenases work?
Tertiary amines to N-oxides
Secondary amines to hydroxylamines or N–oxides
Primary amines to hydroxylamine or oximes
sulfur atoms oxidised to disulfides or S-oxides
How do monoamine oxidase work?
They catalyse the oxidative deamination is monoamines
What is the most common CYP enzyme?
CYP3A4
What is the naming system for CYP enzymes?
The first number is the family.
The letter is the subfamily.
The second number is the isoform
How do CYP enzymes work?
A substrate binds to the active site.
This reduces redox potential.
this leads to a flow of electrons from NADPH to FAD to FMN and then into cytochrome
 oxygen binds to heme, which reacts with solvent hydrogen forming water and a Fe03 complex
Followed by the transfer of the oxygen to the substrate
Where are CYPs found?
All over the body but concentrated in SER of hepatocytes
How many CYPs are there?
57 in humans, 15 implicated in xenobiotic transformation
Are CYPs always expressed?
No, some are but not all
Some are induced/inhibited by food or drugs
How can CYPs be involved in drug interactions?
For example hyperforin in St johns wort can induce CYP3A4 leading to an increase in metabolism wheres ketoconazole can inhibit CYP3A4 leading to a decrease in metabolism
What are CYP polymorphisms?
Genetics from person to person
Some people have higher activity CYPs than others
What type of function group does histamine have?
Amine
Where is histamine most concentrated?
In the lungs, skin, and gastrointestinal tract
How is calcium involved with made cells?
When the antibodies of the mast cell bind to an antigen this caused an influx of calcium causing release of the histamine
What is the triple response?
Red
Flare
Wheal
What happens at a histamine plasma concentration of 0-1ng/ml?
Nothing
What happens at a histamine plasma concentration of 1-2ng/ml?
Enhanced gastric acid secretion
What happens at a histamine plasma concentration of 3-5ng/ml?
Tachycardia
Skin reactions
What happens at a histamine plasma concentration of 6-8ng/ml?
Decreased arterial pressure
What happens at a histamine plasma concentration of 7-12ng/ml?
Bronchospasm
What happens at a histamine plasma concentration of ~100ng/ml?
Cardiac arrest
Death
Examples of localised histamine release?
Urticaria/ angioedema
Allergic rhinitis
Allergic conjunctivitis
What to use in an anaphylactic emergency?
Adrenaline as it is a physiological reversal of histamine
What does of adrenaline to use for anaphylaxis?
0.5ml of 1:1000 (0.5mg)
Or 0.3ml if selfadminstered
How many types of histamine receptor?
4
But only 1 and 2 are therapeutically important
What type of receptors are histamine receptors?
G-protein couples receptors
Transduction mechanism of H1 receptors?
Two second messengers, IP3 and diacyglycerol (DAG)
Transduction mechanism of H2 receptors?
Stimulates production of cAMP from ATP by stimulating adenylate cyclase. cAMP activates protein kinase A
Transduction mechanism of H3 receptors?
Inhibits the productions of cAMP from ATP
First H2 receptor antagonist and who discovered it?
Cimetidine and James Black
Antihistamine drug therapy problems?
Hepatic disease Sometimes renal impairment Some can have CNS effects Anticholinergic burden- especially in elderly Urinary retention Long QT syndrome Interactions with CNS medications
Where are the adrenal glands?
Top of the kidneys
What are the parts of the adrenal gland?
Adrenal medulla and adrenal cortex
What does the adrenal medulla secrets?
Noradrenaline and adrenaline
What does the adrenal cortex release?
Corticosteroids
What are the three main corticosteroids secreted by the adrenal cortex?
Cortisol (hydrocortisone) a glucocorticoid for carbohydrate and protein metabolism
Aldosterone a mineralocorticoid for water and electrolyte balance
Dihydroepiandrostone (DHEA) for sexual development
Therapeutic uses of corticosteroids?
Replacement (in Addison’s disease) Asthma IBD Rheumatoid arthritis Eczema Post transplant
What controls secretion from the adrenal cortex?
Hypothalamic-pituitary axis which secretes adrenocoricotropin (ACTH)
What factors can influence the level of circulating cortisol?
Time of day (circadian rhythm) levels drop when you go to bed and is highest when you wake up in the morning
Stress such as hypoglycaemia, trauma, infection, extensive exercise, anxiety and fear
Cortisol secretion pathway?
Stress/circadian rhythm -> hypothalamus -> corticosteroid releasing hormone (CRH) -> anterior pituitary-> andrenocorticotrophic hormone (ACTH) -> adrenal cortex-> cortisol
Molecular action of glucocorticoids?
Easily crossed cell membrane
Attaches to cytoplasmic receptor which induces conformation change
Steroid/receptor complex enters nucleus
Binds to DNA and affects transcription and therefore translation
Pharmacological affects of mineralocorticoids?
Increase Na reabsorption in kidney
Increase K and H excretion
Increase water retention
Increase blood volume
Physiological affects of glucocorticoids?
Decrease the uptake and utilisation of glucose
Increase gluconeogenesis
Increase glycogen synthesis and storage
Decrease protein synthesis
Increase protein breakdown
Increase lipolysis and redistribution of fat
Pharmacological affects of therapeutic concentrations of corticosteroids?
Anti-inflammatory
Immunosuppressive
Mineralocorticoid activity and K loss
Effect on a a balance and bone metabolism
Atrophy of adrenal cortex (so treatment must not be stopped suddenly)
What causes cushing’s disease?
Excessive production of glucocorticoids usually due to a pituitary tumour which increases production of ACTH
What causes Addison’s disease?
Deficiency of glucocorticoids and mineralocorticoids due to atrophy of the adrenal cortex
Symptoms of Addison’s disease?
Hypoglycaemia
Hypotension
Weight loss
Muscular weakness
What causes Conn’s disease?
Excess of mineralocorticoids usually due to a tumour
Symptoms of Conn’s disease?
Oedema
Hypokalaemia
Alkalosis
Hypertension
Symptoms of cushings disease?
Same as corticosteroid side effects Hyperglycaemia Diabetes Muscle weakness Thin skin Fat redistribution to face and torso Poor wound healing Infection Infection of growth in children Hypertension
What is a polymorphism?
A gene mutation that occurs in more than 1% of the population
Benefits of pharmacogenomics?
maximise drug effectiveness
Minimise drug toxicity
Minimise PD and PK variability
Avoid unnecessary treatment
what is an SNP?
single nucleotide polymorphism
What does *1 in genetics mean?
wild-type (normal)
Types of polymorphism?
SNP
Variable number tandem repeat
Gene deletion
Copy number variant
What drug, according to the BNF, requires a patient’s DPD gene to be tested?
Fluorouracil
What drugs, according to the BNF, requires a patient’s TPMT gene to be tested?
Azathioprine
Mercaptopurine
Thioguanine
What is the HLA complex?
Human Leukocyte Antigen system. Can cause idiosyncratic drug reactions if gene mutations.
What drugs require HLA-B*1502 allele tests and why?
Carbamazepine and phenytoin in patients of Han Chinese or Thai origin due to the risk of Stevens-johnson syndrome
What drug requires HLA-B*5701 allele tests?
Abacavir
What are barriers to implementing pharmacogenomics?
Test issues IT Educational Ethical Legal Social Cost-effectiveness Clinical utility
What is zero order elimination?
A constant amount of drug is eliminated per unit time independent of drug concentration
What is first order elimination?
A constant fraction of the drug is eliminated per unit time which is dependent upon the drug concentration
What shape is a first order drug elimination on a graph?
Curved
What shape is a first order drug elimination on a semi-log graph?
Straight line
Examples of drugs cleared via zero order?
Ethanol
Phenytoin
What is Cmax?
The maximum concentration after a single oral dose
What is Tmax?
The time Cmax occurs
What does Kel stand for?
Elimination rage constant
What is Kel?
The fraction of drug eliminated per hour, with first order elimination
How to calculate Kel?
use the terminal data from a concentration-time plot
What is half-life?
The time it takes for drug concentration to half
What does t1/2 stand for?
half-life
Equation to work out half-life?
t1/2 = 0.693
———
Kel
What does area under the curve show?
The exposure to the drug
How to calculate AUC?
Use the trapezoid rules
What does F stand for?
Absolute oral bioavailability
What is absolute oral bioavailability?
The fraction of the drug that reaches the system circulation
What to calculate absolute oral bioavailability?
Compare AUCs from an oral dose and an IV dose
AUC oral
————-
AUC IV
What does V stand for?
Volume of distribution
How to calculate volume of distribution?
the total amount of drug in body/ plasma concentration
Volume of distribution definition?
the volume of distribution is the volume of plasma that would be necessary to account for the total amount of drug in the patient’s body, if that drug were present throughout the body at the same concentration as found in the plasma.
What PK parameters can only be determined by an IV dose?
Volume of distribution
Clearance
What does CL stand for?
Clearance
Clearance definition?
The efficiency that a drug is eliminated from the circulation. The volume of blood cleared of drug per unit time.
How to calculate clearance?
Does/ AUC
