23

Short answer LSD appears to be enzymatically broken down in the liver. Background First off, hormones do not break down anything; enzymes are the work horses that mediate metabolism. According to a review paper (Passie et al., 2008), humans metabolize LSD into structurally similar metabolites (Fig. 1) by NADH-dependent microsomal liver enzymes to the ...


9

This question asks about the urinary excretion of THC. Before answering the question I think you're getting at, I'll first note that cannabinoids (of which THC is one) are primarily metabolized by hepatic cytochromes rather than being excreted directly. This article is a classical pharmacokinetic paper on the topic if you’re able to access it; this one is a ...


8

LSD is metabolized in the liver in humans by enzymes of the Cytochrome P450 hemoprotein. The specific enzymes are CYP3A4 and CYP2D6. CYP2D6 is generally regarded as non-inducible (meaning there appears to be no way to boost its production in humans), and can only be inhibited by other drugs that would cost more than LSD and be dangerous to take anyway. ...


6

You have done the calculation correctly it is just the answer you have is in hours, try dividing by 24. A good method of checking answers is to use a trick which is horribly called "Dimensional Analysis". This basically means writing out your equations but use the units of each value rather than the value itself so in this case you have T1/2 = Vd/Cl ...


5

Short answer: Yes. Diazepine is a ring-structure that forms the basis for the class of drugs called benzodiazepines. This class includes long acting and short acting agents. If you're actually talking about diazepam, it's one of the long acting agents, which means the half-life of the metabolite in your body (and it's detection) is long. The National ...


5

Fluorine has a combination of unique chemical properties, which makes it very useful in drug design : It is small, such that replacing a C-H with a C-F is often possible, from a sterical point of view. Halogens, which share some of the other desirable properties of fluorine, are much larger. It is very electronegative: it will attract electrons strongly, ...


4

Short answer: different people have different amount of active receptors. In treatment, combination scores of Pharmacodynamics and Pharmacokinetics determine the final effect of the drug. Receptors determine many effects of the drug in many pathways. Different people also sense pains differently (Psychology). Review answer The purpose of treatment is ...


4

Short answer No, orally taken painkillers act systemically. Background Taking a painkiller orally results in the drug being taken up into the bloodstream by the digestive system. From there it can potentially reach all tissues. In other words, a pain response does not act as a chaperone. A hypothetical drug that would home in on tissues with a pain ...


4

Short answer Chemical reversible shielding of the aminogroup in GABA seems to be sufficient to get it into the brain as a Trojan horse. Background Given that you ask ...how to make GABA pass the blood brain barrier? I assume that You wish to elevate GABA by exogenously administering a compound; That compound has to cross the blood-brain barrier (...


4

Well, $Cl = R/Cp$ is correct, but $R$ is not $Cp \cdot k$. Given $X(t)$, the actual quantity (ie weight or moles) of drug in the system, $R$ should have the dimension of $\frac{dX(t)}{dt}$, that is $weight \cdot time^{-1}$ or $mole \cdot time^{-1}$ because the base definition of clearance is given by $$- \frac{dX(t)}{dt} = Cl \cdot C(t)$$. The volume of ...


3

I plotted your data using MATLAB and it looks like this:                    Most degradation or clearance processes happen via first order kinetics. However when the clearance/degradation machinery gets saturated then degradation proceeds via a zeroth order kinetics i....


3

Regarding the tissue partition coefficient, Li et al. said: "By using such a parameter, it is assumed that there is the same transfer kinetics of nanoparticles from blood into tissues as from tissues back into blood circulation, and an equilibrium of concentrations between blood and tissue exists. These assumptions may not be appropriate for nanoparticles." ...


3

As Christiaan already pointed out, this depends on the pharmacokinetic and pharmacodynamic parameters. The effective drug concentration depends on the drug-receptor association constant and the drug degradation constant (for a highly simplified model). The degradation/removal depends on the abundance of the enzyme catalyzing this reaction. Ethanol is ...


3

Short answer Hormones act in the order of minutes or hours. Neurotransmitters in the order of milliseconds. Moreover, hormones are blood-born, neurotransmitters are confined to the synaptic cleft or in the extracelular space directy surrounding the neuron. Hence, their mechanisms of inactivation are different. Background The distinguishing feature of ...


3

The following is one of the many elegant statements in General Anesthetic Actions on GABAA Receptors: It is the fervent view of the authors that general anesthesia is no different from any other pharmacological process: exogenously administered drugs interact with key sites on cellular proteins in the body which results directly in the alteration in the ...


3

Basically any compound in concentrations sufficient to saturate its metabolization machinery will show zero-order pharmacokinetics. This reflects the fact that metabolization is taking place at full speed while facing a comparatively enormous amount of substrate (just as @WYSIWYG pointed out). This effect can also be shown in vitro with pure substrate/enzyme ...


2

I don't know of any interesting mechanism that is specific to pain killers, so I will instead answer for drugs in general. Drug action is a complex process consisting of many steps. Let's take a simple example: A systemic direct inhibitor of a kinase. This drug would need to*: Be absorbed into your bloodstream Remain in your bloodstream for sufficient time ...


2

Most NSAIDs derive their analgesic effects from inhibit the cyclooxygenase (COX) enzymes that produce the prostaglandin-H2 precursor to the prostaglandins that sensitize neurons to pain. Edit: With respect to where this takes place, the COX enzymes are expressed in inflamed tissues as well as constitutively in the stomach and kidney. The prostaglandins ...


2

I think you are after the slope of the dose-response curve: Dose-response curve. Souce: Merck The slope indicates the change in response per unit dose, which translates to sensitivity.


2

That is lysergic acid piperidide, an analog of lysergic acid diethylamide (LSD). According to Wikipedia, it is an agonist of the 5-HT2A receptor, but is much less potent than LSD.


2

Irreversible antagonism is like removing receptors. If there are spare receptors, maximum effect, or any effect level, can be recovered with more ligand (because displacing the irreversible ligand is not necessary, when there are other sites to fill). $$K_D = \frac{R*L}{RL}$$ A given effect level corresponds to a given $RL$, but with less receptor $R$ ...


2

To go the PBPK route: I would recommend using the organism parameters and structure from the whole body platform model by Shah and Betts. Shah, D.K. & Betts, A.M. J Pharmacokinet Pharmacodyn (2012) 39: 67. doi:10.1007/s10928-011-9232-2 They have assigned a plasma space volume, plasma flow, blood cell space volume and blood cell flow for each organ and ...


2

As noted in a comment, a truly thorough answer to this question would require one or more books (1,2) or scientific journals (3), but a simpler, necessarily incomplete answer can be provided. The short answer is: transmembrane drug transporters of the ABC family (4) But what are those? Well, you should read the wikipedia article for a detailed description, ...


2

Does body fat percentage effect storage of fat soluble compounds? Generally, yes. Phenytoin, an anti-seizure drug, provides a good and well studied example. The key issue here is that, for phenytoin, plasma half-life is proportional to the apparent volume of distribution of the drug. (Apparent) volume of distribution is a pharmacokinetic property of a ...


2

There is a huge misconception here. Morphine overdose is treated with Narcan (naloxone). Phenobarbiton overdose is treated with artificial respiration (in extreme cases), blood pressure medication, and management of low heart rate. The concept of lowering the pH of the urine to increase a drug excretion is (to my knowledge) never used in emergency ...


2

Your source (DrugBank via PubChem) is describing the typical pharmacokinetic information (ADME, absorption, distribution, metabolism, excretion) on Providine-Iodine, under the assumption it is not absorbed. It's true, a thing that is not absorbed has no volume of distribution, is not metabolized, and is not eliminated. Though Providine-Iodine is not ...


1

Basic sigmoidal curve looks like that: zero at $-\inf$ and one at $+\inf$. All in between should look like an integral of gaussian distribution. Take a look on this wiki page for more information. Now, the question, why sigmoidal curve is integral of gaussian function, I will leave out for now. My understanding is that gaussian distribution tells you how ...


1

You can use this equation to very generally describe the one-compartment pharmacokinetics of a drug: Cplasma = (Dose*F/Vd)e^(-kt) Where F is the fraction that is bioavailable and Vd is the volume of distribution of the drug. These values can be obtained from the Lexi-comp monograph. If a drug is administered i.v., F = 1. k in this equation is your ...


1

Antibodies are a unique case. I recommend reading PubMedID: 26726925 regarding the pharmacokinetics of ranibizumab (Lucentis), a Fab fragment, after intravitreal administration. "We assume that the principal pathway for the ocular clearance of large molecules is by a first-order transfer process from the vitreous to the aqueous chambers, from which the ...


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