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Introduction to Pharmacodynamics | Pharmacology — Transcript

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0:00foreign
0:07introduction to pharmacology and
0:10introduce you to one of the fundamental
0:12concepts which is pharmacodynamics we're
0:14going to break down what a drug is how
0:17drugs produce their effects on the body
0:18and introduce you to the different types
0:21of drug targets and then in later
0:23pharmacodynamics lectures we're going to
0:25expand on these topics all right so
0:28first of all
0:29what is a drug in Pharmacology a drug is
0:32a chemical substance that when
0:34administered to a living organism
0:36produces a biological effect
0:38drugs can be used for therapeutic
0:41purposes to treat diseases or they can
0:43be used for non-therapeutic purposes
0:45such as recreational or experimental use
0:49this also includes the caffeine in your
0:51coffee on an ice latte now and it also
0:55includes experimental tools that are
0:57used in researching diseases or finding
1:00new therapeutic treatments
1:02now medicine is what we usually refer to
1:05as a drug that is used to treat cure or
1:08alleviate a diseases symptoms these are
1:12what we refer to as therapeutic drugs or
1:14therapeutic agents and a lot of
1:16medicines actually contain more than one
1:19active ingredient so there will be a lot
1:21of other things in a therapeutic
1:23formulation so it may contain other
1:25substances such as stabilizers or
1:28solvents for example a brand of
1:32medication used to treat high blood
1:33pressure might contain two different
1:35types of blood pressure lowering drugs
1:37in a single pill okay
1:40another example that we might consider a
1:43drug might be something like a Venom or
1:45a toxin because these substances produce
1:48a biological effect on a living organism
1:51so a poison is a substance that causes a
1:53harmful effect on the body but the thing
1:55is the difference between a drug or
1:57medicine and a poison might be in the
2:00dose if a substance is taken at
2:02therapeutic levels it's very safe and
2:05effective but if taken in overdose it
2:08can lead to dangerous outcomes such as
2:10liver damage and failure and we're going
2:13to break this down in later lectures
2:15where we cover concentration response
2:17relationships and the relationship
2:19between the dose of a drug that's given
2:21and the effect it has so that's the
2:23definition of a drug the question now is
2:25how are drugs classified
2:28drugs can be classified in different
2:30ways based on their chemical structure
2:32mechanism of action which is how the
2:34drug achieves its biological effects
2:36okay so how the drug does what it does
2:39for example going back to lowering blood
2:42pressure how does it lower blood
2:44pressure
2:45another way is based on therapeutic use
2:49so what is the drug designed to do for
2:51example drugs can be classified as
2:53depressants analgesics or antibiotics
2:56based on their effects on the body
2:59okay so then how do you name drugs
3:02because many drugs have multiple
3:04different names there are three main
3:06systems for naming drugs we have
3:08chemical generic and proprietary
3:11chemical names are based on the Drug's
3:14chemical structure and are often complex
3:16and difficult to remember they are
3:18primarily used by chemists and
3:21researchers so it's not really used when
3:23talking about the medications that are
3:25given to patients next are generic names
3:27which are simpler names given to drugs
3:30by Regulatory Agencies ones that have
3:33been approved for use
3:35these names are not owned by any
3:37particular company and are used by
3:39multiple manufacturers
3:41now it's really important for these
3:43approved names to be different from each
3:45other this is to avoid confusion with
3:47other drugs that are already approved
3:50and on the market because we don't want
3:52to prescribe One Drug to a patient who
3:54ends up being given another drug that
3:56has similar sound or spelling to it that
3:59is a completely different effect
4:01and then we have proprietary names also
4:04known as brand names okay so these are
4:07created by drug companies and are used
4:09to Market their products these names are
4:11protected by trademarks and are unique
4:13to a particular product essentially the
4:15naming systems have different
4:16characteristics and uses chemical names
4:20are important for research and
4:21development while generic names are
4:24important for prescribing and dispensing
4:26drugs and proprietary names are
4:28important for marketing and brand
4:30recognition
4:32let's go through an example
4:33so here we have an example for a very
4:36commonly used drug if you're a medicinal
4:38chemist then you will tell you a lot
4:40about the drug but if you aren't then
4:42not really
4:43now if we were to use a generic name or
4:46a trade name most people would be
4:48familiar with the drug the generic name
4:50for this compound is ibuprofen ibuprofen
4:53is the approved name suggested by the
4:55manufacturer and approved by the
4:58regulatory authority to use and describe
5:00the chemical entity if you aren't
5:02familiar with ibuprofen then you are
5:04likely to be familiar with at least one
5:06of the trade or brand names for this
5:08drug
5:09one of the trade names is nurofen
5:11another is Advil it's the same chemical
5:14entity but it is manufactured and
5:16marketed by two different pharmaceutical
5:19companies you can see the differences
5:21between chemical name generic name and
5:24trade name all right so if coveted water
5:26drug is and the different systems that
5:28are used to classify drugs let's now
5:30subtract complexity and start to look at
5:32how drugs produce their effects within
5:34the body we're going to introduce
5:36pharmacodynamics which is the study of
5:38how drugs produce their biological
5:40effects and how drugs will affect the
5:42different systems of the body
5:45it involves understanding the
5:47interactions between drugs and their
5:49target receptors enzymes and other
5:51molecules in the body and how these
5:54interactions lead to changes in cellular
5:56function organ function and ultimately
5:58the overall response of the organism
6:02but before we start breaking this down
6:04why is this important because there's no
6:06point in going through this without
6:08actually asking what our purpose is here
6:10so why is pharmacodynamics important
6:13well because understanding
6:16pharmacodynamics is important for the
6:18development of safe and effective drugs
6:20by studying how drugs interact with the
6:23body we can predict their effects
6:25optimize their thirsting regimenes and
6:28minimize their potential for adverse
6:30reactions okay so then how does a drug
6:33exert its effects on the body
6:36it does this by modifying existing
6:39processes including physiological or
6:42biochemical processes a lot of drugs
6:44exert their effects via specific
6:46chemical interactions or covalent bonds
6:48hydrophobic interactions or
6:50electrostatic okay with particular
6:53molecular targets drug targets can be
6:56proteins enzymes receptors or other
6:59cellular components which will break
7:00down later in this lecture
7:03so the drug is going to bind to the
7:05Target molecule which then modifies the
7:08function of its molecular Target to
7:10produce a biological effect so either
7:12activate or inhibit its function leading
7:15to a physiological response the ability
7:17of a particular drug to bind to its
7:19molecular Target is determined by both
7:21the structure of the drug and the
7:23structure of the molecular Target okay
7:25and the type of interactions formed
7:28between the drug and its Target is
7:30important as well one thing I want to
7:32point out is that there are drugs that
7:33produce their effects on the body by
7:35acting on simple physical or chemical
7:37processes these are called non-selective
7:40interactions or effects what this means
7:43is that these drugs aren't interacting
7:45with a specific molecular Target but
7:47instead are modifying a more General
7:49physical or chemical process let's go
7:52through some examples
7:54a great example are antacids like
7:57calcium carbonate or magnesium hydroxide
7:59which are commonly used for indigestion
8:02these don't have a particular molecular
8:04Target but rather they modify a chemical
8:07process within the body they work by
8:10neutralizing stomach acid through a
8:12simple chemical reaction
8:14so they don't Target any specific
8:16molecule or pathway there are weak base
8:19that acts on the acidic environment of
8:21the stomach because your stomach
8:22produces large amounts of hydrochloric
8:25acid which AIDS in the digestion of food
8:28so the hydrochloric acid in the stomach
8:30will react directly with the antacid and
8:33therefore the acid will become
8:35neutralized so you will end up with a
8:36reduction in the acidity of the stomach
8:39that's pretty cool okay so there's our
8:41antacids another example of a type of
8:44drug that exerts is effect by modifying
8:47a non-selective process
8:49are asthmatic agents an example is
8:52osmotic laxatives which you may know are
8:55useful the treatment of constipation
8:57okay but they're also used for the
8:59preparation of particular GI procedures
9:02such as a colonoscopy so what these
9:04osmotic laxatives do is they're going to
9:06draw water into the colon which
9:08increases the bulk and softness of stool
9:11promoting bowel movements this effect is
9:14not due to any specific interaction with
9:17a drug Target but rather to the physical
9:19process of water movement okay so these
9:23laxatives contain molecules that are
9:25difficult for the GI tract to absorb so
9:28there's going to be a higher
9:29concentration of these molecules that
9:31stay within the GI tract so there's
9:33going to be an increase in soil
9:35concentration inside the GI tract which
9:38then stimulates osmotic activity because
9:40water follows solute so what happens is
9:43it's going to cause water to move from
9:45the gut capillaries into the inside of
9:48the GI tract okay so that's how
9:50laxatives work
9:52both antacids and osmotic agents in this
9:55case osmotic laxatives are examples of
9:57drugs that have non-selective effects on
10:00the body so in summary some drugs can
10:02exert their effects through
10:03non-selective interactions with simple
10:06chemical and or physical processes
10:08without targeting any specific molecule
10:10or pathway all right so it's good to be
10:13aware of these types of drugs
10:16let's now move on and break down the
10:19different types of drug targets and how
10:20different drugs affect these targets
10:25all right now
10:28the majority of drugs produce their
10:30effects via selective interactions with
10:32proteins so they will bind to a protein
10:35and alter the function of that protein
10:39we refer to the site where a drug binds
10:42to exert its action as a molecular
10:44Target although protein molecules aren't
10:47always the molecular targets of drugs
10:49they just make up the majority of them
10:51and we can divide these protein targets
10:54for drug action into four main groups we
10:57have iron channels carrier proteins
11:00enzymes and receptors each of these
11:03targets play plays an important role in
11:05cellular function and can be targeted by
11:08drugs to achieve therapeutic effects
11:10so again drugs can enhance the activity
11:14of a protein inhibited or modify its
11:17normal function so let's go through each
11:20of these four different types of
11:21proteins and use examples of how drugs
11:24can act on that type of Target starting
11:26with iron channels ion channels are
11:29membrane proteins that allow the passage
11:31of ions such as sodium potassium and
11:34calcium across cell membranes so they
11:37are formed by a single protein or a
11:39group of proteins that are embedded
11:41within the plasma membrane these
11:44channels are really important in
11:46cellular cell communication between
11:47excitable cells so neurons muscles even
11:51cells that are involved in secretion
11:54so when iron channels are open they're
11:57going to create an open pore or passage
11:59between the extracellular fluid and the
12:02inside of the cell or intracellular
12:04fluid and they are characterized by
12:06having specificity or selectivity for
12:09different types of ions so for example
12:11there are channels that are selective
12:14for sodium ions potassium ions or
12:16calcium ions and the channel name will
12:19depend on the selection the different
12:21types of ions so a channel that is
12:23selective or only allows sodium to pass
12:26will be referred to as the sodium
12:28Channel and what determines whether an
12:31ion can move through the open pore is
12:33influenced by the charge of the iron as
12:35well as the size of the molecule okay
12:38now
12:40ion channels can exist in different
12:42types of States so they can either be in
12:45an open or closed State and these
12:47channels are regulated to make sure that
12:50they are open or closed in response to
12:53different types of physiological signals
12:55because cells such as neurons and muscle
12:57cells rely on ION channels to create the
13:00appropriate signals that allow those
13:02cell types to do their job effectively
13:05okay so we want to open or close these
13:08channels appropriately
13:10so this is known as gating of channels
13:13or Channel gating so the opening or
13:16closing of ion channels is determined by
13:19Channel gaming okay iron Channel gating
13:22can be regulated by various types of
13:24stimuli but we're going to go through
13:26two examples voltage-gated channels and
13:29ligand-gated channels starting with
13:31voltage-k channels these are regulated
13:34by changes in the cell's membrane
13:36potential so think your neurons and your
13:38muscle cells
13:40remember that membrane potential refers
13:43to the difference in electrical charge
13:45between the inside and the outside of
13:48the cell resting membrane potential is
13:50the voltage difference across the cell
13:52membrane when cells are at rest
13:56so with voltage-geated channels in this
13:59case we have sodium channels these have
14:02two gates there's an activation gate and
14:04an inactivation gate so the inactivation
14:07gate here can be described as a ball and
14:10chain-like structure okay so these
14:12channels have three states or
14:14conformations
14:16first it can be closed but capable of
14:19opening okay so the inactivation gate
14:21here is open because the ball is just
14:23hanging free it can be completely open
14:25and activated so both gates are open or
14:28it can be closed and not capable of
14:31opening it's inactivated this is the
14:33inactivation state
14:35so voltage-gated ion channels will be
14:38influenced by whether they're in an open
14:40state or a closed State okay so some of
14:43these channels will be stimulated to
14:45open will be stimulated to open by
14:48depolarization or hyperpolarization any
14:51changes in the membrane potential
14:53determine whether the channel is open or
14:55closed alright that's voltage-gated ion
14:58channels
15:00the other type are ligand gated channels
15:03these are also called ionotropic
15:06receptors so these are large protein
15:09complexes these are iron channels that
15:12open directly in response to ligand
15:14binding so they are regulated by The
15:16Binding of chemical ligands a great
15:19example are neurotransmitters that are
15:21involved in synaptic transmission once a
15:23neurotransmitter binds this will cause
15:26the child to change shape and it's going
15:28to open up allowing ions from the
15:30extracellular fluid to enter
15:32so here we have the nicotinic
15:35acetylcholine receptor and right now
15:37this channel is in its close state so
15:39it's not allowing any ions to pass
15:41through the channel now when the ligand
15:44acetylcholine binds to the channel it
15:46will change the confirmation of the
15:48channel and earthena and it's going to
15:51allow ions in this case sodium ions to
15:53flow into the cell and down its
15:55concentration gradient okay so these are
15:57the two main types of gating channels
15:59voltage gain and ligand gating there are
16:02also some other types of buying channels
16:05that are regulated by other types of
16:07physical changes such as stretch
16:09sensitive channels and temperature
16:11sensitive channels okay so these are
16:13just the two main types
16:15okay
16:16now
16:18there are multiple different ways in
16:20which drugs can affect the activity of
16:23iron channels so
16:25drugs that Target iron channels can
16:28either block or enhance their activity
16:30altering the flow of ions and impacting
16:33cellular signaling and communication
16:36so some drugs will directly alter ion
16:39channels by binding to different sites
16:41on the Ion channel modifying the state
16:44of the channel okay so a drug can bind
16:46to the channel in such a way that it
16:49prevents the ions from moving through
16:51the channel examples of drugs that
16:53Target ion channels include local
16:55anesthetics which block sodium channels
16:57and reduce pain sensation but let's look
17:00at a more specific example by looking at
17:03drugs that affect voltage-gated sodium
17:05channels
17:07if you've seen the action potentials
17:09lecture who talked about how important
17:11these channels are in generating Action
17:13potentials in cells like neurons and
17:15muscle cells these sodium channels are
17:18usually closed in the resting state and
17:20with the neuron depolarizes that
17:23triggers the opening of these channels
17:25What happens when the Childs are open
17:27it's going to allow sodium ions to flow
17:30into the cell which allows for the
17:32continuation of action potential of the
17:34action potential
17:36so one example of a drug that directly
17:39affects voltage-gated sodium channels is
17:41tetradotoxin
17:43it's drug directly blocks the channel
17:45here so this is a neurotoxin that's
17:47found in a range of different Marine
17:49creatures and causes inhibition of
17:51neurotransmission which leads to a loss
17:54of sensation and in higher
17:55concentrations paralysis so tetradotoxin
17:59blocks these channels which then inhibit
18:01Island movement through the channel
18:03directly sorry can't pass through ions
18:06can't pass through the channel the thing
18:07is it doesn't matter whether the channel
18:09is in the urban State the inactivated
18:11State or the closed State the actions of
18:14tetradotoxin are the same so its action
18:16is independent of the state of the
18:18channel
18:19now there are also drugs that affect
18:22voltage-gated sodium channels and are
18:24dependent on the channel state for their
18:27action an example is lignocaine which is
18:31a type of anesthesia that works by
18:33binding to open or recently open
18:35channels in the nerves so when neurons
18:38are firing frequently there are more
18:41open or inactivated channels or in
18:43active channels for lignicane to bind to
18:46in those areas this is important because
18:48it allows for more targeted anesthesia
18:51in these areas with more nerve activity
18:54which is especially useful since Sensory
18:57neurons increase their firing rate with
18:59the intensity of the stimuli causing
19:01them to fire so lignocaine's
19:04interactions with these channels is used
19:06dependent meaning it is more effective
19:09in areas with higher nerve activity okay
19:12so essentially there are different ways
19:15drugs can interact with ion channels
19:18either directly such as with
19:19tetrodotoxin or dependent on their
19:21Channel State like lignitine all right
19:24that's ion channels
19:27let's now move on to the second type of
19:29protein Target for drug action which is
19:32another type of transport protein
19:33carrier proteins carrier proteins are
19:36membrane proteins that transport
19:38molecules across cell membranes
19:41here's the thing
19:42they don't form an open Channel or pore
19:45between the inside and outside of the
19:47cell what carrier proteins do is they
19:51take different conformation shape okay
19:53and shuttle the molecule from one side
19:56to the other this process involves a
19:59series of changes in the structure of
20:01the carrier protein that influence its
20:03orientation towards the inside or
20:05outside of the cell as well as the
20:07ability of different molecules to bind
20:09to it
20:10so specifically when a soil molecule
20:13needs to be transported across the
20:15membrane it binds to the carrier protein
20:18causing a conformational change so here
20:21we have the molecule it's cured as
20:24molecule that needs to be transported
20:26and the gate to the inside of the cell
20:28is closed but open to the outside of the
20:31cell and so this is going to flip okay
20:33this flips the carrier protein so that
20:36it is no longer open to the outside of
20:38the cell but now open to the inside of
20:40the cell so the gate is close to the
20:43outside so there's a conformational
20:44change here okay the shape is changing
20:48so this change in conformation allows
20:51the solid molecule to move across the
20:53membrane and then eventually
20:54dissociating from the carrier protein
20:57inside the cell it's pretty cool right
20:59now one key feature of carrier proteins
21:02is that they're never open to both sides
21:05of the membrane at the same time
21:07this is because the solid molecule must
21:10bind to a specific site on the protein
21:12channel to be transported and this also
21:15means that the carrier proteins can be
21:17subject to competition and potential
21:19saturation of the transport mechanism
21:22okay so the binding Affinity of the
21:25solute to the carrier protein is also
21:27affected by conformational changes in
21:30that protein structure this means that
21:33the ability of different molecules to
21:35bind to a specific carrier protein can
21:38vary all right
21:39now
21:41carrier proteins can be classified in
21:43different ways one method involves
21:46characterizing them by the type of
21:48molecule they transport such as sodium
21:50glucose or potassium
21:53and there are also several types of
21:55carrier proteins including uniport
21:57Transporters that can only transport a
22:00single molecule and co-transporters that
22:03can carry multiple types of molecules
22:06simultaneously or at the same time such
22:08as sodium glucose protransporters or
22:11sodium potassium co-transporters okay if
22:14they're co-transporters move the
22:16molecules in the same direction across
22:18the membrane they are referred to as
22:19simple carriers however if the transport
22:23protein moves molecules in different
22:25directions they are known as antipod
22:28carriers
22:29so that's one method another method of
22:32characterizing carrier proteins is based
22:35on the energy source that powers the
22:37transport passive transport or
22:40facilitated diffusion occurs when
22:42molecules move down their concentration
22:44gradient without the need for external
22:46energy it doesn't require any energy
22:48whereas active transport involves the
22:50movement of molecules against their
22:52concentration gradient which requires
22:54external energy such as ATP okay
22:58so now that we've established what
23:00carrier proteins are let's look at some
23:02examples let's look at how drugs can
23:04influence this process can influence
23:07carrier proteins
23:09so drugs that Target carrier proteins
23:11can interfere with their ability to
23:13transport molecules altering cellular
23:16metabolism and function
23:18we're still looking at neurotransmission
23:19here
23:21so we have the presynaptic terminal and
23:23the person optic cell and we have a per
23:26synaptic receptor right here and what a
23:29substance binds you will produce a
23:31response in the per synaptic cell okay
23:34so remember what happens when an action
23:36potential reaches the axon terminal
23:39it's going to stimulate the
23:40voltage-gated calcium channels to open
23:42and calcium ions are going to flow into
23:45the synaptic knob where calcium triggers
23:47the release of neurotransmitters from
23:50the synaptic vesicles here which contain
23:52dopamine serotonin and noradrenaline
23:55so here we have neurotransmitters being
23:58released at the synapse where they can
24:00interact with a receptors to produce a
24:03response
24:04but what we're truly focused on here is
24:07the reuptake process
24:09these neurotransmitters are terminated
24:11their actions are terminated when they
24:13are removed from the synapse okay so
24:16generally the removal of the
24:18neurotransmitter occurs via reuptake
24:20into the presynaptic neuron via a
24:23carrier protein through the process of
24:25facilitated diffusion okay so reuptake
24:29is when the neurotransmitters are taken
24:31back up into the presynaptic neuron
24:34after they have been released into the
24:36synapse now why is this process
24:38important why are we talking about this
24:40because reuptake helps helps the
24:43regulation it helps to regulate the
24:46duration and strength of neuronal
24:48signaling it's important to the overall
24:51functioning of the nervous system
24:53and there are several different drugs
24:55that can interfere with this process and
24:58they do Serve by blocking the carrier
25:00proteins okay because if you block the
25:02carrier proteins what's going to happen
25:04you will get less of the
25:06neurotransmitter that gets taken back up
25:08into the presynaptic neuron and what
25:10happens okay so when this happens what
25:13do we do it means you've got more
25:15neurotransmitter present in the synapse
25:17and therefore you're going to enhance
25:19the actions of that neurotransmitter
25:21because remember the actions of the
25:24neurotransmitter are early terminated
25:25when they are removed from the synapse
25:28so if we're blocking the re-uptake
25:29protein okay this carrier protein here
25:32we're going to be leaving
25:33neurotransmitters in the synapse that
25:36therefore enhancing their activity so
25:38let's go through two examples including
25:40cocaine and Fluoxetine
25:42so first up cocaine so what cocaine does
25:46is it blocks the carrier proteins that
25:48are responsible for neurotransmitters
25:50such as dopamine and norepinephrine so
25:53then it has a stimulatory effect on
25:56those neurotransmitters because these
25:58transmitters are going to stay in the
26:00synapse for longer causing Euphoria and
26:03all the other effects that cocaine has
26:05so there's going to be a buildup of
26:06these neurotransmitters in the synapse
26:09okay so that's cocaine on the other hand
26:11fluoxetine is an example of a drug that
26:13is more selective for individual carrier
26:15protein mechanisms what fluoxetine does
26:18is blocks the carrier protein that is
26:21responsible for the reuptake of
26:22Serotonin into the nervous system this
26:25is an example of a selective serotonin
26:28react take with okay which blocks the
26:31reuptake of Serotonin and increases its
26:34availability these drugs are one of the
26:36most commonly used in the treatment of
26:38depression okay so these are the
26:41different ways in which drugs can
26:42interfere with carrier proteins to
26:44influence the actions of
26:46neurotransmitters
26:48let's now move on to the next type of
26:50drug targets enzymes
26:52so recall that enzymes are biological
26:55catalysts they speed up a reaction
26:57without being consumed other reaction
26:59and most enzymes are proteins enzymes
27:02are important for a whole range of
27:04biological processes their activity
27:07depends on their protein conformation
27:09including primary secondary tertiary and
27:12quaternary protein structures if an
27:15enzyme is denatured it's catalytic
27:17activity is gone okay so drugs that
27:19Target enzymes can either enhance or
27:21inhibit their activity
27:23altering cellular metabolism
27:25neurotransmission and function let's go
27:27through an example of a drug called near
27:29stigma that inhibits an enzyme involved
27:32in neurotransmission
27:34so you may have heard of acetylcholine
27:36okay so acetylcholine is a
27:38neurotransmitter that's important in the
27:40peripheral and central nervous system
27:42and synthesize from acetyl-coa and
27:45choline catalyzed by choline acetyl
27:48transferase now the actions of
27:50acetylcholine are terminated when
27:53acetylcholine is broken down similar to
27:55what we've just spoken about
27:57and it's broken down by an enzyme called
28:00acetylcholinesterase that is found in
28:02nerve terminals where acetylcholine is
28:05released okay so when acetylcholine is
28:07released it can then diffuse across the
28:08synapse and bind to per synaptic
28:11receptor proteins so then this
28:13acetylcholine receptor opens up allowing
28:16ions to flow inside so going back to
28:19acetylcholinesterase it breaks down the
28:21acetylcholine into choline and acetate
28:24in activating that neurotransmitter
28:26because the actions of a
28:27neurotransmitter is terminated when it's
28:29removed from the synapse so what we're
28:32doing here is we're going to break it
28:33down to choline and acetate there are
28:37several different drugs that can Target
28:38inhibit this acetylcholinesterase okay
28:41so different drugs can inhibit
28:43acetylcholinesterase and one example of
28:46a drug that inhibits
28:47acetylcholinesterase in a competitive or
28:50reversible manner is near stigma okay so
28:53neostigmine binds to and inhibits
28:56acetylcholinesterase so then what
28:58happens when we inhibit the activity of
29:00this enzyme well now we can't break down
29:02acetylcholine and so we're going to end
29:05up with increased levels of
29:07acetylcholine at the synapse so
29:09neostigmine is a drug that is involved
29:11in the treatment of myasthenia gravis
29:13which is our neuromuscular disease
29:15that's characterized by a failure of
29:17transmission at the neuromuscular
29:19Junction okay and the main
29:21neurotransmitter at the junction is
29:23acetylcholine so if we step back and
29:25think about that for a second
29:27by preventing the breakdown of
29:29acetylcholine we're going to increase
29:31the levels of acetylcholine at the
29:33neuromuscular Junction and what's this
29:35going to do it's going to enhance
29:37neuromuscular transmission okay so
29:40that's near stigma and we mentioned that
29:42this drug can bind to and inhibit this
29:44enzyme reversibly but there are also
29:47drugs that do this irreversibly which
29:49means we can't take it back okay and
29:51there's a name for this family of
29:53molecules that irreversibly inhibits
29:55this enzyme here they are known as
29:58organophosphates all right so this is an
30:01example of how enzymes can be the cause
30:03of drug action
30:05for either enhancing or inhibiting the
30:07activity altering its function okay
30:11the last type we're going to look at are
30:15receptors so these bad boys recognize
30:18and respond to the different types of
30:20chemical messages that our body uses to
30:22communicate they bind to specific
30:24signaling molecules such as hormones
30:26neurotransmitters and cytokines and
30:29transmit signals into cells
30:31so the effect of neurotransmitters
30:35hormones and other chemical mediators
30:37are controlled by receptors so drugs
30:40that Target receptors again can either
30:42enhance or block their activity altering
30:45cellular signaling and function
30:48and one common mechanism for influencing
30:51a recipe is through an activating drug
30:53which is known as an Agonist an Agonist
30:56is a drug that binds to and activates a
30:59receptor we're going to talk about this
31:00in more detail in further
31:02pharmacodynamic structure okay but just
31:04know an Agonist is a drug that binds to
31:07and activates a receptor whereas an
31:09antagonist is a drug that binds to the
31:11receptor but does not cause activation
31:14it combines to it but it doesn't
31:15activate it so when an Agonist binds to
31:17a receptor it's going to activate a
31:19signaling mechanism within the cell and
31:21which have a signaling mechanism is
31:23activated will determine the cellulite
31:25effects examples of drugs that Target
31:27receptors include beta Agonist which
31:30activate beta adrenergic receptors and
31:32increase heart rate and Airway dilation
31:35and we also have antihistamines which
31:37block histamine receptors and reduce
31:39allergic symptoms we'll break down the
31:41four main types of receptors in another
31:43lecture but for now understand that
31:45receptors are a very diverse group of
31:47proteins and can mediate a whole range
31:50of different types of effects in the
31:52body from quick responses like
31:54neurotransmission to much slower
31:56processes that are related to growth and
31:58development okay
32:00all right so we've covered a lot in this
32:03lecture so to summarize it okay drugs
32:06can affect the four main types of
32:07molecular targets for drug action we
32:10have iron channels carrier proteins
32:12enzymes and receptors by either
32:14enhancing or inhibiting their activity
32:17or altering cellular signaling and
32:19function to achieve therapeutic effects
32:21thank you for watching this video make
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32:26don't miss a single lecture and remember
32:28subtract complexity and slow down to
32:31study the next lecture simply click the
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