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Pharmacology Flashcards

1
Q

Pharmacology

A

Uses and effects of drugs

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2
Q

Clinical Pharmacology

A

How this applies to a clinical context
E.G. effects of a drug across a population

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3
Q

Therapeutics

A

Treatment and care of a patient to prevent, suppress or cure disease / alleviate pain and injury

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4
Q

Drug

A

Chemical which produces a biological effect when introduced to the body
Can be natural or manufactured

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5
Q

Medicine

A

Chemical preparation containing one or more drugs plus other substances
Given to produce a therapeutic effect

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6
Q

Pharmacodynamics

A

Effect of a drug on the body

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7
Q

Pharmacokinetics

A

What the body does to a drug

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8
Q

What are the 4 phases of pharmacokinetics?

A

1) Absorption
- from site of administration into the blood
2) Distribution
- drug leaves the bloodstream and goes in
3) Metabolism
- body inactivates the drug through enzymatic modification
4) Excretion
- drug is eliminated from the body in urine, bile or faeces

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9
Q

What is the interaction of a drug with a target dependent on?

A

Shape - ‘lock and key’ mechanism
Charge distribution - the type of bonds that hold the drug to the target

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10
Q

What are the 4 main targets of drug action?

A

Receptors
- agonists activate the receptor
- antagonists block the action of agonists
Ion channels
- block or modulate the opening/closing
Enzymes
- inhibit or act as a false substrate
Carriers
- transported in the place of the endogenous substrate or inhibit transport

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11
Q

What are the 4 major receptor subtypes?

A

1) Ligand gated ion channel
2) G-protein
3) Enzyme linked receptor
4) Intracellular receptor

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12
Q

What is an agonist, describe how an agonist and receptor work together and describe the relationship between potency and affinity

A

A ligand that combines with the receptor to elicit a cellular response
Agonist + receptor <–> agonist-receptor complex –> action –> effect
High potency tends to mean high affinity

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13
Q

What is an antagonist and describe its efficacy and affinity

A

A drug which inhibits the action of an agonist but has no effect in the absence of an agonist
They have no efficacy
They do have affinity

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14
Q

What is a competitive antagonist and how do they affect an agonist curve?

A

Competes with the agonist for the binding site
Agonist curves have the same form, are displaced to the right and have the same maximal response

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15
Q

How do irreversible antagonists affect agonist curves?

A

Agonist curves don’t have the same form and have a reduced maximal response

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16
Q

Efficacy

A

Maximal drug effect a drug can elicit from that system

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17
Q

What is potency and what is it dependent on?

A

Concentration of drug needed to produce an effect
Dependent on affinity, efficacy, the number of receptors and the efficiency of stimulus-response mechanisms used

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18
Q

What is a dose-response curve / concentration-effect curve used to determine?

A

Used to determine efficacy and potency

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19
Q

Affinity

A

Strength with which a ligand binds to the receptor
Measured with Kd - the concentration of ligand at which 50% of the available receptors are occupied (measure from agonist-binding curve)
Inverse relationship between Kd and affinity

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20
Q

EC50

A

Concentration of ligand where 50% of its maximal effect is observed
A measure of potency
Inverse relationship between EC50 and potency

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21
Q

Full and Partial Agonist

A

AR* = activated receptor
AR = unactivated receptor
Full agonist means AR* is very likely
Partial agonist means AR* is less likely

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22
Q

Drug Selectivity and Specificity

A

Selectivity - many drugs act preferentially on receptors or subtypes
Specificity - no drug is specific to only one receptor subtype
Because no drug is specific, as the dose increases the desired response in a patient rises to a maximum which induces toxic effects

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23
Q

Therapeutic Window

A

Measure of drugs safety
Difference between effective and toxic dose

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24
Q

Therapeutic Index

A

Comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxicity
A measure of drug safety
TD50 - dose that causes a toxic response in 50% of the population
ED50 - dose that is therapeutically effective in 50% of the population
Therapeutic Index = TD50 / ED50
Larger value suggests a wide margin between effective and toxic doses

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25
Tolerance
Reduction in response to a drug after repeated administration
26
Routes of Administration
Oral Parenteral (injection) - Intravenous - Intramuscular - Subcutaneous Inhalation Topical - Creams - Ointments - Transdermal - Patches Sublingual Rectal
27
Advantages of Oral Administration
Easy and convenient Non-invasive Less risk of infection Painless Cheapest Self-administered
28
Disadvantages of Oral Administration
Slower absorption Some patients can't swallow Patient compliance is necessary Some drugs (e.g. proteins) destroyed by gut acid/flora Some drugs can be irritant if taken orally
29
Factors affecting gastrointestinal absorption
Gut motility - decreased motility can increase drug absorption Gut pH - poor absorption of strong acids and bases Physiochemical interactions - interactions with food and other drugs Competition for carriers/transporters
30
Absorption across physiological barriers
Main site of absorption of oral drugs is the small intestine Drugs must cross cell membranes: - Passive diffusion through lipid bilayer - Diffusion through aqueous channel - Carrier mediated transport
31
Passive Diffusion
Lipid solubility is an important determinant of rate of absorption Non-polar/unionised substances dissolve in lipid Ionised species have low lipid solubility Many drugs exist in ionised and unionised forms as many are weak acids and bases
32
pH and pKa
Ratio of ionised : unionised determined by pH Proportion of a drug that is ionised depends on the pH of the solution and the pKa of the drug When pH = pKa, 50% of the drug is ionised
33
Drug Distribution
Reversible transfer of a drug from one location to another within the body For most drugs this occurs through passive diffusion of the unionised form across the cell membrane until equilibrium is reached
34
Factors Affecting Rate of Distribution
Membrane permeability - Drugs perfuse faster through a more permeable membrane Blood perfusion - Drugs reach highly vascularised tissues more rapidly
35
Factors Affecting Extent of Distribution
Lipid Solubility - Ionised lipid is insoluble so drugs can't easily enter cells Plasma protein binding Tissue binding
36
Plasma Protein Binding
Drugs can bind reversibly to plasma proteins in the blood Some drugs are ~1% ppb, while some are ~99% Albumin is the most important plasma protein as it binds many acidic and some basic proteins Acid-glycoprotein and beta-globulin plasma proteins bind basic drugs PPB drugs are not pharmacologically active Extensive ppb slows drug action and elimination (slower acting but with prolonged therapeutic effects)
37
Tissue Binding
Drugs diffuse from the plasma into tissues Tissues can bind drugs: - their composition --> lipid soluble drugs will accumulate in fat - binding to cellular components --> proteins, pigments, minerals
38
Volume of Distribution
Distribution of a drug between plasma and the rest of the body If drugs are confined to the plasma, Vd is low If drugs accumulate outside the plasma, Vd is high
39
Bioavailability
Proportion of a drug that passes into the systemic circulation after administration Dependent on absorption and metabolism - metabolism in the gut/liver = first pass metabolism High first pass metabolism leads to low bioavailability
40
First Pass Metabolism
Liver and gut wall have drug metabolising enzymes For certain drugs extensive metabolism occurs before the drug reaches the systemic circulation Only a small proportion of the dose reaches the systemic circulation Can be countered with a larger oral dose or a different route of administration (IV, inhalation, sublingual)
41
Drug Metabolism: Reducing Lipid Solubility
Most drugs are lipophilic - allows absorption of drugs across membranes to reach site of action Lipophilic compounds not efficiently eliminated by kidney so they need to be made hydrophilic so they can be excreted via urine Metabolism introduced hydrophilic components onto drug to aid excretion Hydrophilic drugs tend to be excreted unchanged
42
Drug Metabolism: Altering Biological Activity
End result of metabolism is usually the abolition of biological activity Various steps in between may cause: - Conversion of a pharmacologically active to an inactive substance (most drugs) - Conversion of one pharmacologically active substance to another (prolongs drug action) - Conversion of a pharmacologically inactive substance to an active substance
43
Phase 1 Metabolism
Reactions involve oxidation, reduction and hydrolysis - form more chemically reactive products - involves cytochrome P450 enzymes in liver Reactions create functional groups that allow the drugs to be acted upon by phase 2 conjugative mechanisms Main function is to prepare chemicals for phase 2 metabolism and then excretion
44
Phase 2 Metabolism
Conjugation reaction (e.g. glucuronidation) Conjugations lead to inactive and polar products that are readily excreted First pass metabolism reduces bioavailability of many drugs when orally administered
45
How are drugs removed from the body?
By the processes of metabolism and excretion --> elimination Major systems concerned with excretion: - kidneys (urine) - hepato-biliary system (faeces) - lungs (for volatile compounds such as anaesthetics) - liver (bile)
46
Enterohepatic Circulation
Glucuronide conjugates (more water soluble) excreted in bile may undergo enterohepatic circulation 1) Drug is metabolised to conjugate in liver 2) Conjugate is excreted in the bile from gallbladder into the gut 3) Conjugate undergoes bacterial hydrolysis in gut back into drug and free glucuronide 4) Drug is reabsorbed into hepatic portal vein and transported to liver 5) Drug is reabsorbed into the blood causing a prolonged duration of action
47
What does EHC create?
A reservoir of recirculating drug and increases the half life
48
Renal Excretion
Drugs differ greatly in the rate at which they are excreted by the kidney Metabolites are nearly always cleared quicker than the parent drug 3 processes for renal drug excretion: 1) Glomerular filtration - not affected by lipid solubility and pH - pbp almost completely held back 2) Active tubular secretion 3) Passive diffusion across tubular epithelium
49
Prodrug
Biologically inactive compound which can be metabolised in the body to produce a drug
50
Internal Factors affecting Variability in Response to Drugs
Disease Age Genetics
51
External Factors affecting Variability in Response to Drugs
Drug formulation Drug interactions Smoking/alcohol Diet Environment
52
What can tablets be manufactured for so the rate of disintegration and dissolution varies?
Rapid effect Sustained release Controlled release Delayed release
53
Drugs can be manufactured so the drug disintegrates in?
Duodenum Jejunum Colon
54
CYP1A
Important for paracetamol metabolism
55
CYP2C
CYP2C9 = important isoform It metabolises ibuprofen and warfarin
56
CYP2D
Major isoform CYP2D6 metabolises codeine, propranolol, many SSRIs (antidepressants)
57
CYP2E
Metabolises alcohol and paracetamol
58
CYP3A
Main isoform in liver and intestine It metabolises ~ 50% of current drugs
59
Substrate
The drug being metabolised
60
Inhibitors
Drugs which inhibit the activity of the P450 enzyme
61
Inducers
Drugs which increase the activity of the P450 enzyme

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