Summary contains all lectures and important parts discussed in the interactive lectures and workgroups / case studies. NOT JUST THE POWERPOINT SLIDES! Made this summary and used it to study for the course and got an 8.5 on the exam.
Lecture personalized healthcare
Molecular biomarkers: Omics (biomarkers). → The omics sciences share the overarching aim of
identifying, describing, and quantifying the biomolecules and molecular processes that contribute to
the form and function of cells and tissues. Clinical omics are used to drive personalized healthcare.
Diagnosis:
1. Genetic screening
2. Metabolic screening (urine) : Genetic metabolic disorder: something with a genetic origin
that causes changes in metabolics.
Analysis of dynamic biomarkers is key in monitoring Minimal Residual Disease (MRD). Mass
spectrometry has good potential.
Digital biomarkers (smart watch etc.) is growing and enables personalized health monitoring.
Advantages:
- Continuous monitoring versus 1 snapshot observation
- Real world data versus data from clinically controlled circumstances
- More comprehensive and rich data sets
- Truely personalized
- Strong potential in molecular + clinical + digital + environmental biomarkers for optimal
insight in complex biological systems
- Better basis to drive Personalized health(care)
- Better support for phase 1, 2, 3, 4 clinical trials
Primary prevention: preventing illness
Secondary prevention: preventing illness when someone has an increased risk (diabetes etc.)
Tertiary prevention: after disease
,Speech hearth attack app
Sounds great however, research to research, research to clinic or society is a big different → there is a
big gap.
There are a lot of biomarkers being worked on (5 each day) but only some of them get approved and
actually are used in diagnostic tests.
Lecture pharmacology and drug disposition
Pharmacology is the science that is concerned with the uses, effects and modes of action of
chemicals on the function of living system.
What does the patient do with the drug? Pharmacokinetics (the pathway of the drug to the
bloodstream via intestines and with the use of enzymes)
What does the drug do to the patient? Pharmacodynamics (when drug binds to receptor/ target →
what does it change)
Rational pharmacotherapy: finding out the mechanism and the principles of the drug → use this in
the creation of new drugs etc. the drug might not be functional but is promising.
Evidence-based pharmacotherapy: it does not matter how it works, studies show that it works
(paracetamol).
3 different phases that can be investigated in pharmacotherapy:
There are different types of receptors, these determine the speed in which the reaction occurs.
Examples:
,The interaction between the drug and the receptor can differ. From strongest to weakest:
1. Covalent
2. Ionic
3. Hydrogen
4. Hydrophobic
5. Van der Waals
Covalent bonds cannot easily? be broken.
Intracellular: lot of K+ little of Na+
Extracellular: lot of Na+ and little of K+
K+ in and Na+ out.
Receptor occupation (how much it binds) can be showed in a graph having concentration (log scale)
on the x-axis and fractional occupancy on the y-axis.
The more the graph moves to the left, the stronger the binding (green line).
EC50: effective concentration at 50%
,Partial agonist = orange line: not everything is stimulated.
If you have an agonist (no antoganist) you have the blue line. If you add an agonist the graph moves
to the right. Because there is competition.
If there is non-competitive inhibition of the antagonist the graph will differ.
Allosteric antagonist (non-competitive): doesn’t bind to the binding pocket but somewhere else → no
competition.
ADME: absorption, distribution, biotransformation and excretion.
Nerve agents: Organophosphates are acetylcholinesterase inhibitors and disrupt the signal
transduction at the cholinergic synapse. In the body, this leads to loss of function of the respiratory,
cardiovascular and skeletal muscles. The standard antidote is an injection of the acetylcholine
antagonist atropine inhibitor.
First pass effect:
How much of a compound reaches the general circulation? And how much is broken down. Only
when drugs are taken orally there is a first pass effect.
Vd (volume of distribution) = if the drug is evenly distributed through the blood and tissues than the
vd will be 100 (if there is 100L blood for instance). Protein binding can influence this: if drug binds to
proteins in the blood it stays longer in the blood and is less in the tissues (lower Vd). Total amount of
drug in the body / drug concentration in the plasma.
(V) Vd= F (bio availability) x D (dose) / C0 (concentration at time 0 in the blood)
Elimination of the drug is dependent on the concentration of the drug and is exponential. The higher
the concentration the more rapidly the enzymes work → faster elimination.
,T1/2 time in which half of the drug is removed.
First order kinetics: the higher the concentration the more of the compound is removed.
Repeated administration of a drug:
These curves determine the dose interval that will be used during therapy.
Delta T= time interval
Css= concentration at steady state
, F= AUc PO (orally taken) / AUC iv (taken intravenously).
Therapeutic index: difference between effect and unwanted effect. The smaller this window is the
more dangerous the drug.
Zero order pharmacokinetics (alcohol): the same amount is removed over time but not the same
percentage. Red line: would be first order (what we like). At a very low concentration the line is also
first order kinetics. In the linear line, the enzymes can not work any harder (there are at their limit).
The reaction happens independent on the concentration of the drug (overtoxication alcohol)
Un charged (neutral): it can pass the membrane
Charged: it cannot pass the membrane
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