100% tevredenheidsgarantie Direct beschikbaar na betaling Zowel online als in PDF Je zit nergens aan vast
logo-home
Medical pharmacology lecture 1-8 notes (2022) €13,39
In winkelwagen

College aantekeningen

Medical pharmacology lecture 1-8 notes (2022)

 84 keer bekeken  7 keer verkocht

The notes include elaborate explanations of all lectures except the last lecture (lecture 9) which is about chapter 12.

Voorbeeld 4 van de 46  pagina's

  • 26 mei 2022
  • 46
  • 2021/2022
  • College aantekeningen
  • Mmm wilhelmus
  • Lecture 1 - 8
Alle documenten voor dit vak (4)
avatar-seller
obblub
Lecture 1 – introduction to pharmacology
Pharmacology = explanation of action of pharmaca in the human (or animal) body (what drugs do
and how they do it)
- Pharmaca = biologically active substances
o It is a chemical that is usually used to treat disease. But it can also mean other stuff
such as toxic compounds.
o Toxicology = is a subdiscipline of pharmacology
- Medicine = pharmacon (‘drug’) specifically applied for therapy
o They intended to have a selective action but this ideal is seldom achieved.
▪ There is always a risk of adverse (side) effects as well as a benefit connected
with using any drug --> toxic effects. This is why selective action is usually not
always achieved.
▪ Therefore knowledge of pharmacology is needed for using drugs effectively
in therapy.
- Two main areas of investigation into the action of pharmaca
o Pharmacodynamics = “What does the drug do with the body”
o Pharmacokinetics = “What does the body do with the drug”

Pharmacotherapy = applied pharmacology Use of knowledge and insights gained from
pharmacology for the treatment of diseased humans in a responsible, effective and safe manner.
- Each pharmaca has:
o Minimum toxic concentration
o Therapeutic window
o Minimum effective concentration

- There is a direct relationship between
concentration of drug in blood plasm and
its therapeutic effects.
o The concentration in blood plasm
(Cp) has to be in between the
minimum toxic concentration and
Minimum effective concentration

- Primary effect = effect(s) for which the compound is administered
- Side effect = adverse/unwanted effect(s)
o The distinction between primary and side effect is determined by the aim for which
the medicine is administered
▪ I.e. acetylsalicylic acid (aspirin) can be used as a pain killer or against blood
clotting.

- Placebo = a preparation without any pharmacologically active substance
o It may have a therapeutic effect
o The expectation(s) of the patient determine the strength of the placebo effect
o Randomized, placebo-controlled clinical trials = The contribution of the placebo
effect to the overall effects of a drug are investigated in this
- Nocebo = a placebo with unwanted effects (side effects)

, o Nausea = the most common nocebo effect when taking in oral medication even
though the medication does not have this side effect

Phases of making drug:
1. Discovery: takes 2-5 years
2. Development: takes 5-9 years
▪ Phase 1: safety exposure
▪ Phase 2: Efficacy and dose selection
▪ Phase 3: Registration trials
▪ Phase 4: Post approval regulation = after the approval of use they still have
to check how it is going and what the side effects are

Lecture 2 – PD

Pharmacodynamics = what does the drug do to the body

The 4 levels of drug action
1. System level effects = an effect on system function (a system in a body: organs,
cardiovascular system)
o I.e. Blood pressure medication on the system
o But it does not say anything about how to make a better medication
2. Tissue level = effect on tissue function
o i.e. looking at the heart tissue or metabolic activity
3. Cellular level = looking at transduction metabolisms --> the biochemicals linked to drug
target
o I.e. looking at amount of cyclic AMP after giving the drug
4. Molecular level = establish interaction of drug with the molecular targets
o Molecular targets = proteins most of the times --> the drug target
o You can now see what the compound does and interferes with in the body and
develop a better drug --> pharmacodynamics

Molecular level = fourth level and consists of:
Drug targets can be (so drugs can interact with: ) =
- Receptors:
o 2 main groups of drug:
1. Agonist: drug binds to receptor and changes the conformation and
activates thereby the receptors --> has effect on the cell in which this
happens and activates or deactivates transduction mechanisms:
o Enzyme is being activated or inhibited
o Ion channels modulation --> open up or close
o DNA transcription changes
2. Antagonist: drug bind to receptor but conformation does not change of
the receptor
o Does not has effect
o Does have a biological effect
▪ It prevents the binding of endogenous mediators to
the receptor

, - Ion channels as drug targets
o Ion channel = a hole in the membrane through which ions can pass (pores). The hole
is formed by insertions of proteins
▪ They can be either opened or closed
1. Ion channel blockers = permeation is blocked of the ions from inside to
outside of other way around
2. Modulators = they modulate by binding to the protein --> change the
probability of the channel being open of closed
- Enzymes
o They catalyze reactions = turn a substrate into a product
1. Enzyme inhibitors = normal reaction is inhibited
2. Drug that act as false substrate = they look like the substrate and can
bind to the enzyme --> the enzyme thinks it is a normal substrate and
turns it into a product
o So the normal reaction is inhibited AND also a new product is
being formed --> this new product might have a biological
effect that the body did not want.
3. Pro-drug = are inactive by themselves --> recognized by enzyme -->
activates the drug
o They only activate in specific places (organs) that express the
specific enzyme
o i.e. treating Parkinson’s disease with levodopa = tyrosine
hydroxylase (enzyme) activates this drug --> dopamine
- Carrier molecules = transporters
o They transport a substrate form one side of the membrane to the other side of the
membrane




1. Inhibitor = bind to the binding site of the transporter --> the compound
cannot be transported anymore
2. False substrate = accumulation of an abnormal compound happens
because the substrate is carried by the transporter

Types of receptors on which and (ant)agonist can bind = all receptors have different time scales in
which the reaction happens
1. Type 1: Ligand-gated ion channels = ionotropic receptors
o These are present in cell membranes
o They are proteins, so a receptor, and have also ion channels inside the protein
structure
▪ So they are: receptors and ion channels
o When something binds on the binding domain --> the ion channels open up or close
o I.e. nicotinic Ach receptor
receptors
▪ Very fast = depolarization
or hyperpolarization (ms)

, 2. Type 2: G-protein-coupled receptors = metabotropic receptors
o Expressed inside membranes
o When drug binds to binding domain --> G-proteins are directed towards the
receptors --> activity is altered of second messenger proteins (cyclic AMP for
example)




o Takes a bit more time for the effect to be seen --> protein phosphorylation takes
time
▪ i.e. muscarinic ACH receptors
3. Type 3: Kinase-linked receptors
o Are proteins in membranes + have a catalytic domain
o When drug bind to binding domain --> kinase activity is altered (blocked or
stimulated)




o Receptors is also an enzyme --> leads immediately to alteration of protein
phosphorylation --> gene transcription which takes a lot of time
▪ i.e. cytokine receptors --> takes hours
▪ I.e. insulin
4. Type 4: nuclear receptors
o Located = in cell nucleus membrane
▪ Inactive = in cytosol
▪ Binding of ligand --> they move in cell nucleus --> bind to DNA parts -->
modify DNA transcription
o So they are: transcription factors
▪ All type 4 receptors are transcription factors but not all transcription factors
are type 4 receptors




o I.e. oestrogen receptors
▪ The activation takes time and gene transcription takes time --> takes hours

Voordelen van het kopen van samenvattingen bij Stuvia op een rij:

Verzekerd van kwaliteit door reviews

Verzekerd van kwaliteit door reviews

Stuvia-klanten hebben meer dan 700.000 samenvattingen beoordeeld. Zo weet je zeker dat je de beste documenten koopt!

Snel en makkelijk kopen

Snel en makkelijk kopen

Je betaalt supersnel en eenmalig met iDeal, creditcard of Stuvia-tegoed voor de samenvatting. Zonder lidmaatschap.

Focus op de essentie

Focus op de essentie

Samenvattingen worden geschreven voor en door anderen. Daarom zijn de samenvattingen altijd betrouwbaar en actueel. Zo kom je snel tot de kern!

Veelgestelde vragen

Wat krijg ik als ik dit document koop?

Je krijgt een PDF, die direct beschikbaar is na je aankoop. Het gekochte document is altijd, overal en oneindig toegankelijk via je profiel.

Tevredenheidsgarantie: hoe werkt dat?

Onze tevredenheidsgarantie zorgt ervoor dat je altijd een studiedocument vindt dat goed bij je past. Je vult een formulier in en onze klantenservice regelt de rest.

Van wie koop ik deze samenvatting?

Stuvia is een marktplaats, je koop dit document dus niet van ons, maar van verkoper obblub. Stuvia faciliteert de betaling aan de verkoper.

Zit ik meteen vast aan een abonnement?

Nee, je koopt alleen deze samenvatting voor €13,39. Je zit daarna nergens aan vast.

Is Stuvia te vertrouwen?

4,6 sterren op Google & Trustpilot (+1000 reviews)

Afgelopen 30 dagen zijn er 52510 samenvattingen verkocht

Opgericht in 2010, al 14 jaar dé plek om samenvattingen te kopen

Start met verkopen
€13,39  7x  verkocht
  • (0)
In winkelwagen
Toegevoegd