|Define the term pharmacology
|the study of substances that interact with living systems through chemical processes
|How do substances interact with living things?
|by binding to regulatory molecules and activating or inhibiting normal body processes
|Define the term drug
|any substance that interacts with a molecule or protein that plays a regulatory role in living organisms
|Define the term poison
|drugs that have almost exclusively harmful effects
|Define the term toxins
|poisons of biological origin, usually synthesised by plants or animals
|Define the term receptor
|a specific molecule, usually a protein that interacts with a specific chemical causing a change in the receptor that produces a regulated function
|Define the term agonist
|any drug that binds to a receptor and activates the receptor mimics the natural ligand of the receptor
|What is the difference between agonists and antagonists?
|agonists initiate changes in cell function, producing effects of various types whereas the latter bind to the receptor without initiating such changes
|What happens when the ligand leaves the receptor?
|this usually deactivates the receptor and stops effect although some receptors are permanently activated even after ligand has gone (covalent change in receptor)
|Define the term partial agonist
|binds to receptor at active site but produces only a partial response, even when all receptors are occupied have intermediate efficacy so produce only submaximal effects
|Define the term efficacy
|the ability once bound to initiate changes that lead to effects the >effect the more efficacious the drug a.k.a intrinsic activity
|Define the term affinity
|tendency to bind to receptors
|What sort of affinity do partial agonists have for the receptor? Explain the effects of this
|lower affinity for receptor so don't bind as strongly as full agonist have reduced intrinsic activity occupies receptor so can prevent other agonists from binding
|Describe how a partial agonist binds to and activates the receptor
|binds to the receptor and activates it with a smaller shape change in the receptor that induces a partial receptor response
|Define the term pharmacologic antagonist
|any drug that binds to a receptor and prevents activation of the receptor
|State the names of the four different types of pharmacologic antagonist
|competitive non-competitive chemical physiologic
|How does a competitive antagonist work?
|fits into lock but does not activate receptor and competes for binding site reduce agonist potency
|How does a non-competitive antagonist work?
|binds to a site that is not the agonist binding site modulates function of receptor reduce agonist efficacy
|How does a chemical antagonist work?
|binds directly to an agonist and prevents it binding to receptor
|What is a physiologic antagonist?
|when two substances have exactly opposite actions via different pathways
|What are the two ways drugs can be administered?
|oral or intravenous oral - absorption then distribution (enteric transport, enteric metabolism) intravenous - distribution (intravascular space, extravascular space, protein binding)
|What two processes follow the distribution of drugs in the body?
|metabolism and elimination metabolism - hepatic influx transport, phase I metabolism, phase II metabolism elimination - biliary excretion, intestinal excretion or renal excretion
|Define the terms enteric and efflux
|enteric - relating to or occurring in the intestines efflux - the flowing out of a substance or particle
|Define the terms intravascular and extravascular
|intravascular - situated or occurring within a blood vessel or blood vascular system extravascular - situated or occurring outside the vascular system
|What do drugs tend to be?
|weak acids or weak bases
|What is the difference between the dissociated and un-dissociated form of a drug?
|former is water soluble, later is lipid soluble
|What is meant by the term 'weak' acid? Use aspirin as an example
|incomplete dissociation in water R-COOH --> R-COO- H+ acidic solution: >[H+], shifts p.o.e. to left, more R-COOH forms alkali solution: >[OH-], shifts p.o.e to right, more ionic aspirin
|What is meant by the term pKa?
|pH at which the drug is completely balanced between the uncharged (lipid soluble) and charged (water soluble) form
|What are other terms for fat-soluble and water-soluble?
|What is TCA? What sort of acid is it? What are two damaging effects of TCA overdose?
|tricylic antidepressant weak acid causes cardiovascular and neurological toxicity
|What should be done in the event of TCA overdose?
|give person activated charcoal to absorb TCA in GI tract alkalinize the blood with sodium bicarbonate to change the drugs effect on the body dissociates to charged form in alkaline solutions so doesn't diffuse back into blood from renal tubules
|What is activated charcoal?
|normal charcoal heated in the presence of a gas, causing it to develop lots of internal spaces which can trap chemicals
|How can amphetamine excretion be speeded up?
|acidifying the urine by administration of ammonium chloride
|Explain what is meant by drug specificity
|drug-receptor structure drug solubility in water and the plasma membrane receptor function
|Explain what is meant by drug selectivity
|drug's ability to preferentially produce a particular effect is related to the structural specificity of the drug binding to receptors
|What are receptors responsible for - specificity or selectivity of drug action?
|Drugs interact with receptors by means of chemical forces or bonds. What are the four different types? Comment on their relative strength also
|covalent - very strong and usually irreversible electrostatic - fairly strong ionic groups and hydrogen bonds lipophilic - weak Van der waals -very weak
|What is pharmacodynamics?
|actions of a drug on the body e.g. propranolol lowers blood pressure and heart rate
|What is pharmacokinetics?
|actions of the body on the drug (ADME) e.g. propranolol is metabolised and eliminated by the liver and kidneys
|Explain the shape of a standard dose response curve
|as dose increases response increases as dose increases further response increment diminishes dose reached in which no further increase in response; maximal response reached
|What is half of a maximum response?
|EC50 half maximal effective concentration (ED50 - dose) the concentration of a drug which induces a response halfway between the baseline and maximum after a specified exposure time
|What's the difference between the shape of a dose response curve with a competitive and non-competitive antagonist?
|competitive - need to add more drug to get to EC50 non-competitive - maximal effect reduced, EC50 same dose as for agonist alone
|What is meant by the term potency?
|refers to concentration of a drug needed for that effect have same efficacy
|Explain what is meant by 'spare receptors'
|relationship between receptor occupancy and response is not linear not all receptors need to be occupied to produce full response so some receptors are 'spare'
|What are two functional benefits of spare receptors?
|increase sensitivity and speed of a tissue's responsiveness to a ligand
|How are spare receptors useful with competitive antagonists?
|competitive antagonists shift the 'curve' to the right but the maximal effect can still be achieved by the agonist interacting with spare receptors