wiseflow exam 1 Flashcards
Explain the following terms (in a pharmacology context).
Pharmacokinetic interactions (1.5p)
What the body does to the drug
Bioavailability
The ability of a drug or other substance to be absorbed and used by the body. If it has low bioavailability lots of it will be metabolized in the gut, by the liver etc and little will reach the target.
First passage metabolism
The degree of metabolic breakdown of an orally administered drug that occurs in the intestine or liver before it reaches the systemic circulation.
Affinity
Affinity can be defined as the extent or fraction to which a drug binds to receptors at any given drug concentration or the firmness with which the drug binds to the receptor.
a. Which drug or drugs is/are most potent?
The drug with the lowest e50. a highly potent drug will induce a strong effect even at low concentrations.
Which drug(s) has highest efficacy?
Efficacy is the maximum effect of the drug at the same amount of receptors. So the drug that has te highest Emax
partial agonists
when comparing multiple drugs in a effect concentraiton graph all drugs that can’t reach the Emax (the highest effect at least one drug can reach) is a partial agonist
Is any of the drugs an inverse agonist?
An inverse agonist in a concentration effect graph will give a decrease in response so the curve will go below 0
Looking at a concentration response curve how can we characterize the antagonist if we have a reduce in Emax with increasing concentrations
a competetive antagonist has a decreased e50 but not Emax since it decreaases the potency but not the efficacy. Competitive receptor antagonist compete with the agonist of the endogenous ligand. They bind to the same site and bind reversibly. So looking at a graph the the curve moves to the right, but the emax doesn’t decrease with an increasing concentraiton.
If it’s a on competitive antagonist the emax decreases. They bind either irreversibly or o an allosteric site.
Looking at a plasma concentration curve how can we identify zero and first order kinetics
First order kinetics is a type of reaction rate that is dependent on the concentration of one reactant. This means that the rate of the reaction is proportional to the concentration of one reactant. For example, if the concentration of a reactant doubles, then the rate of the reaction will double as well. First order kinetics gives curved line sines the system never becomes saturated.
Zero order kinetics is a type of reaction rate that is independent of the concentration of any reactants. This means that the rate of the reaction does not change with changes in concentration. The rate remains constant regardless of how much reactant is present. For example, if you double the amount of reactant, the rate will remain unchanged. Zero-order kinetics undergo constant elimination regardless of the plasma concentration, following a linear elimination phase as the system becomes saturated. Zero order kinetics gives straight line. Zero order is usually due to excess medication causing the reaction to become saturated.
A kinetic reaction can start as a zero order and become a first order but not the other way around.
Patients having increased risk of thrombosis can be treated with anticoagulants
and/or anti-platelet drugs.
a. Vitamin K is important for normal blood coagulation. Give an example of a drug that
interferes with the normal function of vitamin K and explain how this results in
inhibition of blood coagulation.
Warfarin blocks the availability of vitamin K and thus limits the amount of clotting factors produced in the liver.
Warfarin (brand name Coumadin) is an example of a drug that interferes with normal function of vitamin K. Warfarin is an anticoagulant, or blood thinner, that works by blocking the action of vitamin K in the body.
Vitamin K is required for the production of several proteins involved in clotting, including prothrombin, which is necessary for the conversion of fibrinogen to fibrin, the main component of a clot. Vitamin K also helps activate other clotting factors such as factor VII, IX and X.
b. Propose that you have investigated the effect of acetylsalicylic acid on platelet
function in a laboratory experiment. The results of the experiment showed that
acetylsalicylic acid partially inhibits collagen induced platelet activation. Explain,
based on the mechanism of action of acetylsalicylic acid, why the platelet activation
induced by collagen was partially inhibited.
acetylsalicylic acid is a common pain killer and partially inhibit platelet activation by irreversibly inhibiting COX 1/2 as a non competetive antagonist.
Acetylsalicylic acid (ASA) partially inhibits collagen-induced platelet activation by blocking the activity of cyclooxygenase-1 (COX-1). COX-1 is an enzyme that catalyzes the conversion of arachidonic acid to prostaglandin H2, which is a precursor for thromboxane A2. Thromboxane A2 is a potent vasoconstrictor and prothrombotic agent that stimulates platelet aggregation. By blocking the activity of COX-1, ASA prevents the formation of thromboxane A2, thus inhibiting platelet aggregation. Additionally, ASA has been shown to inhibit other pathways involved in platelet activation, such as the glycoprotein IIb/IIIa receptor pathway and the phospholipase C pathway.
Which receptors does “betablockers” act on in the heart (for full point the correct
receptor nomenclature needs to be used)? Which effects does “betablockers” have
on the function of the heart (for full point the cell types and related function must
be given)?
The effects via the sympathetic branch of the autonomic nervous system on the heart is mediated via beta 1 adrenoceptors and it will increase the frequency of the heart by effects on autorhythmic cells, its gonna increase the force by effects on cardiomyocytes
Betablockers act on beta-adrenergic receptors in the heart. These receptors are located on the surface of cardiac muscle cells and are responsible for mediating the effects of the hormones epinephrine and norepinephrine. When these hormones bind to the beta-adrenergic receptors, they cause an increase in heart rate, contractility, and conduction velocity. Betablockers work by blocking these receptors, thus preventing the hormones from binding and reducing their effects on the heart. This can help to reduce blood pressure, slow down a rapid heart rate, and reduce the risk of arrhythmias.
The beta-adrenergic receptors in the heart are divided into two subtypes: β1 and β2.
The β1 receptors are located mainly in the sinoatrial node, atrioventricular node, and ventricular myocardium. They are responsible for increasing heart rate, contractility, and conduction velocity.
The β2 receptors are located mainly in the atria and coronary arteries. They are responsible for vasodilation of the coronary arteries, which increases blood flow to the heart muscle.
In the heart, beta-adrenergic receptors are primarily located on the sinoatrial node (SA node), atrioventricular node (AV node), and ventricular myocytes. Beta-adrenergic receptors are also found in the coronary arteries, where they regulate blood flow to the heart muscle.
a. Describe the pharmacological treatment principles at allergic asthma.
The main treatmeant options for asthma is aimed to reduce inflammation using glucocorticoids and broncho dilators that target adrenergic B2 receptors in the lungs to increase blood flow and sometimes anti allergic drugs for allergic astham that targets IgE.
The anit inflammatory asthma medications are: Loratadine, budesonide. Budesonide works by binding to glucocorticoid receptors in the body. This binding causes a decrease in the production of inflammatory mediators such as cytokines and leukotrienes. This reduces inflammation and swelling in the affected area.
The broncho dialotrs astham emdications are: Salbutamol the mechanism of action of salbutamol involves binding to beta2-adrenergic receptors on airway smooth muscle cells, leading to activation of the cAMP-PKA pathway and inhibition of smooth muscle contraction. These effects contribute to the bronchodilatory and anti-inflammatory effects of salbutamol.
The medication targeting IgE is: Omalizumab
Budesonide is one drug used in the treatment of asthma.
b. Describe the mechanism of action and pharmacological effect of Budesonide.
Budesonide works by binding to glucocorticoid receptors in the body. This binding causes a decrease in the production of inflammatory mediators such as cytokines and leukotrienes. This reduces inflammation and swelling in the affected area.
Budesonide also has an anti-proliferative effect, which means it can help prevent the growth of certain cells that can cause inflammation. It also has an immunosuppressive effect, which means it can reduce the activity of the immune system and reduce inflammation.
The pharmacological effects of Budesonide include reduced inflammation, decreased airway hyperresponsiveness, improved lung function.
