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Wednesday, December 7, 2011

Frequent adverse drug reactions

Which drugs do you think cause the most adverse drug reactions?

A recent study by the CDC it says that
  • warfarin, 
  • oral antiplatelet medications, 
  • insulins, 
  • and oral hypoglycemic agents 

account for 67% of emergency hospitalizations of adults 65 years and older, with warfarin being implicated in 33% of cases.

There you go - keep your ears open when these drugs will be discussed in future classes!

Thursday, November 17, 2011

Let's play doctor

I know: the course is over, the exam has been taken (and the results are not bad at all!) - but the following story is of some interest in your class, and i would expect at least one idea of what could have caused the symptoms in the lady...:
Yesterday I got an email from a lady from Brooklyn. She is about 30-35 years old, has an 11 yo son, works, seems to lead a healthy lifestyle...had no significant illnesses.
Here is what she wrote:
" ...I had some twitching on my tongue and neck accompanied with shortness of breath.  They did an EKG and my primary care physcian has referred me to see a cardiologist because "there is an abnormality in my EKG..."
She is very worried and scared.
So, what do you think? What would you do with this patient? What would you ask her, what are these symptoms about, what could her condition be...?
Send me your comment....
Meanwhile I will ask around, and I suppose I will also hear from her and see what came out of her referrals and maybe get a meaningful answer. I don't have her EKG and do not know what the "abnormality" was. What abnormality would you expect, in line with the above symptoms??

Wednesday, November 2, 2011

Propranolol and surgery performance

James Parker did some research and found us a neat reference for a study where they tested the hypothesis that use of propranolol (40 mg) would improve the performance of a resident surgeon. You may recall that this question was brougth up in class. Indeed, there was less nervous tremor and anxiety (note that this is the probably the cardiac rate consequence of anxiety, not the anxiety sense itself) after taking propranolol. Also note that the summary conclusions  carefully state that the ultimate outcome, namely improved surgery, was not tested in this study! I would add also that these were residents that were tested - seasoned surgeons probably would not show any more tremor or anxiety - I hope!


Thanks James, great job!

Monday, October 31, 2011

QT Lengthening or Long QT Syndrome

Please take a look at an earlier blog on QT lengthening. I think it is important you know about this unique adverse effects that is based, apparently, on a number of possible "Channelopathies", i.e. mutations in ion channel proteins!

Alpha-2 Receptors etc.

In the lecture I was a bit short on explaining issues regarding these receptors: The classification of such receptors of course is based on struture-activity studies, eventually confirmed by molecular biology/cloning. Initially these were seen to function as pre-synaptic receptors whose stimulation by norepinephrine (NE)  reduced NE discharge and thus represented a self-regulatory process. Later it was found that agonists of alpha-2 receptors were present in many tissues and functioned sometimes independent of innervation/neurotransmission pathways, both in the periphery and centrally. You just should be aware of this in principle, and you don't have to memorize the long list of individual functions I copied from theWikipedia:
  • decrease release of acetylcholine
  • decrease release of norepinephrine
  • Inhibit norepinephrine system in brain
  • inhibition of lipolsis in adipose tissue
  • inhibition of insulin release in pancreas
  • induction of glucagon release from pancreas
  • platelet aggregation
  • contraction of sphincters of the gastrointestinal tract
  • ↓ Secretion from salivary gland
  • relax gastrointestinal tract (presynaptic effect)
  • decreased aqueous humor fluid production from the ciliary body 
I am sure you are glad we are not telling you to remember this at this time!                                    

Friday, October 21, 2011

What is the TI re. alcohol lethality?

You may recall that in today's lecture I was asked what the TI for alcohol is and that I recommended to the student (James) to go and look it up. He did and sent me this (you will see that my general idea that a TI of 4 is not good enough for comfort is shared by the author of the site):


Dr. Baer, here is a link to some forums with information regarding thetherapeutic index of alcohol:
http://www.drugs-forum.com/forum/showthread.php?t=34430

Below is the direct quote from the website:

"From Pharmako/Poeia, a book I find myself often quoting these days:

Quote:
Ethanol, drinking alcohol, is far from harmless. Alcohol is a
protoplasmic poison. It kills bacteria, animals, and plants, even the
plant that produces it to begin with. The most effective concentration
for germicides is 140 proof, or 70 percent alcohol. This is the
concentration used in doctors offices as a disinfectant. Pure alcohol
is less effective, evidently because it gelatinizes the cellular walls
of the targeted microbes.

The toxicity of medicines and poisons is commonly expressed as the
LD50, the "lethal dose for 50 percent." Usually measured in grams per
kilogram of body weight, it signifies the amount of the substance
necessary to result in death for one-half of the unfortunate test
subjects. The relative safety or danger of a drug is denoted by its
therapeutic index, its margin of safety. The therapeutic index is the
ratio of the drug's LD50 to its effective dose, the dose necessary to
produce the desired effects. Since both the effective dose and the
LD50 are in grams per kilogram, the therapeutic index is a pure
number. The larger the therapeutic index, the safer the drug.

The therapeutic index of alcohol is only about five. That is, five
times the amount needed to get high can kill you. This puts alcohol,
as recreational drugs go, into the "highly dangerous" category. To
illustrate: if your child were going to overdose on a drug as part of
some rite of passage, say, turning twenty-one, would you rather he or
she overdose on alcohol or on marijuana? Either/or is not the point of
course. The point is that merely by drinking too much alcohol too
quickly, even once, you can die. Even cigarettes are safer than that."

Special Kinetics 2: Zoledronic acid

Zoledronic acid is a biphosphonate (related to phosphates - carrying negative charge(s) as an anion), and among the many derivatives of bipohosphonates used for treatment of bone diseases incl. osteoporosis, it has a long half-life of about 1 year. I want to point out that I think that the basic concepts we discussed in the course do not apply to this type of drug: As an anionic substance it should not distribute well (but it does act on bone - ho does it get there??), and its action starts of course long before 1 year, and there are questions about its reversibility (in case adverse effects appear). I am going to look into this and will see whether I can get some information on this interesting case and drug! If you run across something, let me know!

Wednesday, October 19, 2011

A dosing problem

This dosing problem we will come back to after having discussed dosing issues in general - it follows from the previous blog on appropriate pain management in a pain crisis.

Say that the time to maximum effect for morphine is 8 min (I hope I remember correctly...) and that you needed to double the dose (as per the recommendations in the reference in the preceding blog) successively, thus giving 2+4+8+16 mg to have the patient pain free. Now, what would be the maintenance dose for this patient? How often would you have to repeat your administration, and how much would you give each time? For that you need some parameters. Which one or which ones?
Lets assume the following, and you then pick:


Volume of distribution: 82 L
Half-life: 4 hours (if you needed to (do you) you can calculate from this the clearance or the rate constant of elimination, of course).


1,2,3 go!

Special kinetics: Pain Control

In our discussions on drug kinetics we could not cover all therapeutic situations. For example, I will not say anything or much on the parameter "time to maximal effect". But this seems to be a major concern when dealing with a pain crisis - as you can see by listening to the following recording. Make a note of it  - this is of importance to any of you and something you can throw into discussions on the subject anywhere. here is the link:
http://www.medscape.com/viewarticle/747777?src=mp&spon=17


Now, you may need a user account and password to view Medscape files (I will alert you often to new and interesting ones). Registration is free - so go and get it in any case!

Monday, October 17, 2011

How about rowing instead!

Who knows, one or the other of you may need a break from studying. And since you are down here in the Caribbean, how about an interlude described in this link: http://theadventureblog.blogspot.com/2011/10/want-to-row-across-caribbean-in-2012.html.


But watch it: yesterday we came back from Bequia in a speed boat - and a lunar tide threw up waves that even surprised me! 


Good luck

Welcome to Fall 2011 Class

OK: here we go! You might enjoy looking at some of the previous term's blogs, and from here on we will deal with your class - "Fall 2011".

Remember, if you sign up you would get email notifications of new entries, and you can make this blog lively by asking both stupid and intelligent or challenging questions (actually, both types could be challenging, right?) - just don't be afraid to ask and comment!

As I said already in one or the other of the preceding blogs, I will sometimes insert some stupid exam questions - knowing that this always attracts students magically...and then we can argue about things!

Welcome again!

Thursday, June 9, 2011

Friday, June 3, 2011

Oxygen or not?

Well, I had hardly finished my lunch and there was an answer already from Dr. Katz:


"There is no concern for oxygen toxicity since patients essentially can drown in their own secretions. So, therefore adequate oxygentation/ventilation is absolutely critical for treatment along with reversal of the toxicity with atropine/2-pam. Obviously it should be titrated to clinical effect especially if administered over days, but no different than any other patient in a critical illness situation."


(He is talking about oxygen toxicity - and the question really was concerned with whether or not there is an effect of oxygen on the distribution of drug (translocation to CNS)? I would love to see the original text the lady in class commented about.....)

Oxygen during treatment of organophosphate poisoning

I am still searching - and I also wrote an email to someone who published a rather detailed paper on the topic (http://emedicine.medscape.com/article/167726-overview) hoping for an authoritative answer to the question of whether oxygen should or should not be given. In his article the author has these statements:
  • Mortality rates depend on the type of compound used, amount ingested, general health of the patient, delay in discovery and transport, insufficient respiratory management, delay in intubation, and failure in weaning off ventilatory support.
  • Complications include severe bronchorrhea, seizures, weakness, and neuropathy. Respiratory failure is the most common cause of death.
  •  Airway control and adequate oxygenation are paramount in organophosphate (OP) poisonings. Intubation may be necessary in cases of respiratory distress due to laryngospasm, bronchospasm, bronchorrhea, or seizures.
  • Optimizing oxygenation prior to the use of atropine is recommended to minimize the potential for dysrhythmias.
Will let you know what else I can find.....thanks for raising questions like this!

Thursday, June 2, 2011

Special drug adverse effect: QT Lengthening

I won't have time to cover in any detail the topic of "adverse effects of drugs". I had suggested that you should read through the ppt file to get some ideas...
There is one type of adverse effects that has been observed with drugs with a great variety of functionally and chemically diverse features - and this made it difficult in the early days of its discovery to understand what is going on. But now we seem to know: I can only recommend that you do some self-studying, trying to comprehend this adverse effect that has been responsible for several drug withdrawals because of reports of death as the ultimate outcome (viz terfenadine, cisapride...others).
This adverse effect is referred to as QT-Lengthening or Long QT Syndrome. The initial phase is a lengthening of the QT interval on the EKG, and thus a bradycardia. This in itself may not be a serious problem but this condition may precipitate a tachycardia in form of ventricular arrhythmia referred to as Torsades de Pointes, and this indeed can be fatal.
Here are some points you should remember in connection with this topic:

  • Many drugs can cause the phenomenon.
  • It is now recognized that it is due to an effect (usually not predictable unless the drugs are known to affect excitable cells), involving mutated or genetically defective ion channels (one of the K-channels in particular). These ion channel defects - about 12 possibilities usually are listed (Na and K channels) although most cases involve only three of these - are referred to as "channelopathies".
  • Repolarization of the cardiac action potential is thus delayed by the drug that interacts somehow with these channels, causing a bradycardia.
  • During this extended, lengthened QT period, the likelihood of a spontaneous pacemaker cells kicking in is increased now leading to triggered tachyarrhythmia: the Torsades des Pointes.
  • Without coordinated and productiue ventricular contractions a perfusion deficit develops leading to weakness, temporary awareness or performance problems, and if this persists for more than a certain time (1 min or so?) it can be fatal.
  • Drugs can cause this effect on their own, but sometimes the problem is due to metabolism and drug interaction issues whereby a prodrug is not quickly metabolized to its active form, so that the prodrug plasma concentration remains too high and then can cause QT lengthening (case in point: terfenadine,  an old and now withdrawn H1-antihistamine). Such delays in metabolism can be due to co-administered drugs like erythromycin or ketoconazole which inhibit CYP enzymes.
  • Some individuals have a genetic condition (Long QT Syndrome) predisposing them to this adverse drug effect.
  • Nowadays, new drug applications require EKG data showing that they do not cause QT Lengthening.
Nice story? Now you know, in a nutshell, how it works!

Sunday, May 29, 2011

Information from the FDA - subscription services

The FDA of course has to be accessible and transparent, and they have several services a physician should subscribe to in order to remain up to date. I am using a service (https://mail.google.com/mail/?shva=1#inbox/1303ba92ab78b523) where I get information on new releases and approvals - but most of these turn out issues pertaining to foods. But today I received info on a newly approved antibiotic, and this information goes straight into one of my lectures..
This reference: http://www.fda.gov/Drugs/ResourcesForYou/Consumers/ucm054420.htm informs about drug approval procedural topics which also contains a link to information on currently approved drugs. Sometimes we hear about a "new drug" which often is just an extended use of a drug approved for other indications - and so I can check whether in fact the new indication is already official (viz. sildenafil and altitude sickness!). RSS services also are available - you may wish to make use of this for a while or may find it interesting for times to come.

Saturday, May 28, 2011

Sildenafil metabolism and clearance

Here is a follow-up on sildenafil – after a question in class. Some of this will make perfect sense to you after the coming drug metabolism lecture.

Firstly, I just discovered that the drug now has a third medical indication. I will have to check whether this indication is officially sanctioned by the FDA, but the drug apparently is useful for the prevention and treatment of high-altitude pulmonary edema associated with altitude sickness such as that suffered by mountain climbers. While this effect has only recently been discovered, sildenafil is already becoming an accepted treatment for this condition, in particular in situations where the standard treatment of rapid descent has been delayed for some reason. I recently read some blogs about climbing Everest (an 80-year old died when trying to set an age record!), but in none of the altitude sickness cases the drug was mentioned.
Metabolism:
Sildenafil is rapidly absorbed and distributed throughout tissues following oral ingestion. Maximum plasma concentration occurs between 30 minutes to 2 hours following oral administration. Absorption and plasma concentration can be reduced if taken with food.
Following absorption in the gut, sildenafil enters the hepatic vein in high concentration. As sildenafil makes its first pass through the liver, much of it is metabolized by the cytochrome P450 enzyme system. The P450 enzyme system breaks sildenafil into a number of metabolites. One of these metabolites is UK-103,320 which retains some PDE-5 inhibiting capacity. The sildenafil which is not metabolized and the UK-103,320 are then distributed throughout the body having the primary effect of blocking PDE-5 activity in the corpus cavernosum. Sildenafil and metabolites are cleared primarily through the biliary system with about 80% excreted in feces. The half-life of sildenafil is about 4 hours.
The P450 enzyme responsible for most sildenafil metabolism is CYP3A4. This enzyme is known to be inhibited by a number of substances. Some of the substances which have been demonstrated to interfere with the CYP3A4 metabolism of sildenafil include: ketoconazole, erythromycin, cimetidine and ritonavir. Inhibiting the action of CYP3A4 results in increased plasma sildenafil concentration and an extended half-life.
Grapefruit is a known intestinal CYP3A4 inhibitor. Research indicates that grapefruit can increase the bioavailability of sildenafil. While the effects are modest it may be wise to avoid concomitant use.
Protease inhibitors used in treatment of AIDS also are metabolized by the above CYP enzyme(s) and thus also give rise to higher plasma levels of sildenafil based on competition. I am sure that there may be issues sometimes also regarding drugs like warfarin used for blood coagulation control.
(NB: Some of the above was copied straight from the source such as Wikipedia.)

Wednesday, May 25, 2011

Want to know how we measured adenyly cyclase activity?

There were 2 problems to be overcome: Tinyest amounts of cyclic AMP had to be detected and quantitated, and ATPases had to be "neutralized" because they would eat up ATP so fast, there was nothing left for the adenylyl cyclase.
Enzyme preparation: We worked with fat cells. Homogenizing cells often destroyed the enzyme activity - so we treated fat pads with collagenase to obtain free cells that could then be lysed in hypotonic buffer, yielding membrane "ghosts" that proved to retain activity of membrane-associated enzymes like the cyclase.
Radioactive substrate - p32-labeled  ATP: This was obtained from a manufacturer that was able to custom produce ATP that had radioactive P32 only in the alpha postition, the one that of course was retained in the cAMP product. It had to have highest specific radioactivity to produce the sensitivity we needed. This was a new market for the manufacturer, and we managed to make them improve their product in terms of purity - initial 2-dimensional chromatography studies we did showed them and us that the preps contained radioactive impurities exceeding what we expected our enzyme product, P32 labeled cyclic AMP, to be.
New enzyme technology: To date (1967) enzyme studies always involved incubates of 1-10 ml - but that would waste radioactive substrates immensely - so we developed microassays in volumes of 50 uL. Fortuitously, the Eppendorf company was in the process of pioneering pushbutton pipetting devices with disposable tips for pipetting and transferring amounts down to 5 microliter to special propylene incubation vessels (before that we had to use tiny test tubes that needed siliconizing the glass surface so that the tiny volumes would mix and form one volume rather than scattering inside the tube). These pipettes were intended for hospital labs - and we may have been the first to use them for enzyme assays in research.
The assay: Now we combined, in 5-10 uL increments to a total of 50 uL, a Mg ion containing buffer solution, ATP-alpha-P32, various other components to be tested (hormone solutions), high concentrations of creatinine kinase and creatinine phosphate (supposed to regenerate any ATP hydrolyzed by ATPases)  and enzyme preparations (fat cell ghosts) - the latter added last to start the reaction. To stop the reaction we initially used immersion in boiling water - but then we just added  10 uL of a mix of high concentrations of Assays and evaluate ATP/ADP/AMP and unlabeled cyclic AMP plus EDTA (a Mg complexing agent). In  the next step we used a chromatographic separation method on thin-layer cellulose plates with poly-imine that served as an ion exchange system. After chromatographic separation we identified the location of cyclic AMP and of the other nucleotides uinder UV light, marked them with pencil and then cut out the areas containing these. The cut out strips were immersed in scintillation vials and counted in a common scintillation medium to count the radioactivity levels. This way we could determine how much of the radioactive ATP had been transformed into cyclic AMP and calculate the enzyme rates in proper units - pmol/min/mg protein.
The exciting thing was then that indeed the enzyme rates proved to be affected by various hormones such as epinephrine, glucagon, TSH, ACTH, FSH and others produced dose-dependent activation of the enzyme.
I cannot believe today that we went through all this trouble to study this enzyme, needing such an elaborate setup. Once you are able to develop a technology to measure something new and reproducibly so, you can crank out data and generate publications because every enzyme assay produces new findings and results!

And here is a little question for you: How come fat cells seem to respond to so many different hormones with lipolysis (mediated always by cyclic AMP? This is not seen in any other tissue or cell.

How to determine AUC (and then bioavailability)

We used to discuss in a small group some of the ways in which pharmacokinetic parameters were determined for a given drug. In the absence of such a time slot, let me explain here the issue of determining the AUC from experimental data (plasma concentration versus time, after giving a certain single dose of drug to a patient) – this being necessary of course for determining the bioavailability of a drug.
How can we determine the AUC for a curve obtained by experimental data points, not being linear but rather representing a Bateman function (first order exponential drug absorption plus first order exponential elimination...)?
Usually you would plot the data to see whether they look reasonable and represent a curve that you expect. Then there are several options.
  1. Draw the curve by hand or computer, using a grid as a background and count (estimate) the grid squares “under the curve”. The number of grids is all you need usually, but knowing the area for each grid, the grid count gives you the total area in the exact dimensions (say, [mg/mL times time]).
  2. After drawing a curve as above, cut out the area to be measured and weigh the paper (so-called “integration paper used to be available with a rather constant weight/area. The nice thing is that this method can take care of any shape of a cirver for which you otherwise may not have a descriptive formula. Of course, the weight is just something that is proportional to the AUC, but weiging a cutout of a rectangle or square for which you can calculate the exact are in [mg/L x time] can give you an absolute value.
  3. I have seen engineers using some x/y tracing gadgets that run up a counter number for you as you trace around an area.
  4. Mathematically, use the Batement equation to fit the data points to and calculate the parameters by iterative procedures (rate constants in and out): And, after inserting the parameter estimates into the formula, integrate it between the limits of time zero to somewhere when the curve almost touches the x-axis or maybe to infinity. This would be an enormous task without computers!The plotting program called “Sigmaplot” is tremendous for such a task. The obtained integral of course is the AUC.
  5. Fit the data point sto a polynomial (y = a + bx + cx 2 + dx3 .......) and after insertion of the parameter estimates integrate the function between the same limits as above.
  6. Use the experimental data and generate rectangles of time intervals times PC values that approximate the AUC, and this can be easily done by using a spreadsheet calculator. That is what I would be using nowadays where I do no longer have available Sigmaplot! You can try it out, it is fun: The spreadsheet is included in your ancillary files and available on the Student Drive under my name following the Basics lectures
  7. After drawing a curve as above, cut out the area to be measured and weigh the paper (so-called “integration paper used to be available with a rather constant weight/area). The nice thing is that this method can take care of any shape of a curve for which you otherwise may not have a descriptive formula.
  8. Mathematically, use the Batement equation to fit the data points to and calculate the parameters (rate constants in and out): And, after inserting the parameter estimates into the formula, integrate it between the limits of time zero to somewhere when the curve almost touches the x-axis or maybe to infinity. This would be an enormous task without computers!The plotting program called “Sigmaplot” is tremendous for such a task. The obtained integral of course is the AUC.
  9. Fit the data point to a polynomial (y = a + bx + cx 2 + dx3 .......) and after insertion of the parameter estimates integrate the function between the same limits.
  10. Use the experimental data and generate rectangles of time intervals times PC values that approximate the AUC, and this can be easily done by using a spreadsheet calculator. That is what I would be using nowadays where i do no longer have available Sigmaplot! You can try it out, it is fun: The spreadsheet is included in your ancillary files and available on the Student Drive under my name following the basics lectures. File name: “CP and AUC Calculations Spreadsheet”.
One you have values for AUC, exact or proportionally, you then of course take the AUC for the i.v. administration as 100% and calculate the bioavailability for your drug in relation to that. How many times in one patient, and how many patients total? I have no idea - ask the clinical pharmacologist of a company! I know one and will let you know what he says...

Monday, May 23, 2011

Treatment switch

A patient has been on the antibiotic ampicillin for some time (E. coli upper urinary tract infection; this would not be the correct therapy - i.e. one would not use ampicillin alone, and pl. ignore this point here). He now is stable enough to be switched to a drug that has the same mechanism of action and antibacterial spectrum, but it is commonly used orally. 
The infusion rate of ampicillin was 500 mg/kg/day.
You make the switch on day zero at 8 am, stopping ampicillin infusion and starting with amoxicillin oral 4 times a day.
How much amoxicillin should you give orally every 4 hours, and how long would it take for the switch to be complete, i.e. the patient being on full therapy with amoxicillin? The half life of ampicillin is about 1 hour.

Saturday, May 21, 2011

How much needed to get a desired plasma concentration?

Suppose you want to achieve a plasma concentration for a drug, say penicillin, of 1 mg/L. How much of the drug would you have to administer, say i.v., in a 70 kg person?


(Ignore the fact that as soon as you give something elimination kicks in right away so that you would be chasing an elusive point in time...).


If you feel that you cannot calculate or estimate this and need some more information to do so, what information do you need - or what assumptions are you making to make your estimate?

Determining the bioavailability of a drug

Below I am inserting a hand-drawn graph.  It represents two plasma concentration (PC) versus time curves, using in one case an oral dose of a drug X and in the other an i.v. dose of the drug (same amount in each case).

1) Which curve (A or B) represents the intravenous administration?

2) What is the oral bioavailability of drug X - estimated?
Or, if you like MCQ's better - the oral bioavailability is about
A.  120%
B.   50%
C.   80%
D.   10%

Protein phosphorylation - why?

Here is a small challenge question that will come up in class soon enough, pertaining to the observation that essentially all major intracellular regulation pathways (signaling pathways) for metabolism, cellular functions such as growth and cell cycling as well as typical activities of cells seem to involve the action of protein kinases. Just about any hormonal control mechanism involves either activation or inhibition of protein kinases (as well as phophoprotein phosphatases, the reverse event). So, do you have any idea why nature chose protein phosphorylation as a central and common controlling function?
Additionally, you will see that calcium ion (Ca2+) also is involved in just about any signaling pathway - why did nature choose to muse this ion?

Friday, May 20, 2011

More on cultural sensitivity

I mentioned to you that my daughter found some serious problem with my little "Sugar" video: She said nit was insensitive of me to have the "fat" one portrayed as an Indian (I know, I know:  Ishould not call the First Nations people Indians...more on that later). You did not seem to mind - but here is what happened:
Firstly, the online video program offered that option of characters, and I gave it no thought, just went ahead, no offenses intended. Secondly, I told her, it so happens that indeed our Indians in Canada are the worst affected when it comes to diet, obesity, and other metabolically promoted diseases such as Type 2 diabetes, hypertension and cardiovascular issues. Not to speak of additional factors such as alcohol, water quality etc. So, she says, now I am making the situation even worse.
Oh, my sweet daughter meant well, and I, stupid, old and culturally insensitive father, meant no evil. We left it at that! I am refraining, however, from publishing the clip on YouTube or sending copies to the Indian reserves!

Careful with humor in the office!

Humor is something culture specific: remember this when you deal with your patient, because what entertains one may annoy the other!
You found my little sugar video funny or hilarious. Well, I had sent it to a Vincentian friend as well, and the person asked me what is was about - saw no humor in it. That person would never be entertained by Seinfeld, my favored.
A friend once wanted to contribute to a round of jokes while in the company of a few Saudis in Riyadh. He told the one about the guy who, wanting to join a group of Canadian loggers, proved his ability by chopping down a tree or two in next to no time. "Man, where did you develop this skill?" "In Saudi Arabia". "But there are no tress". "Of course not, I was there long enough!"
The Saudis got up and left, obviously embarrassed or annoyed.
For you: careful with your jokes when dealing with patients! I, for one, would make a bad doctor.

Answer to question:

The answer to the question on the previous blog, briefly is that rectal drug absorption takes place via both the portal and the systemic circulation (50/50 about). Only the portion that goes into the portal one will be subject a first pass loss (via liver metabolism, not of course acid destruction in stomach). So rectal absorption indeed produces a higher plasma concentration. Nice to have had so many good answers, in principle! 
Oh, and to the person who asked whether there was a burp at the end of the preceding Xtra video: yes, indeed there was! Inserted via one of the sound options of the program - Do try the program and send your creations!
HB

Tuesday, May 17, 2011

A question for you...

Here is a question that maybe goes beyond what I covered in class so far, but how about doing some thinking and reasoning: 
What do you think will be the consequence of switching from oral administration of a drug to rectal administration, i.e. via a suppository?
And by "consequence" I mean whether you think it would make a difference to the eventual plasma concentration?
(This cannot easily be formulated in form of a multiple choice question. So your reply in the Comment section needs to be in form of a short statement.)


I like to see an answer from everyone - and you won't be punished if you say "I have no idea"..

Sunday, May 15, 2011

An artificial nose?

After watching this video I gained some new respect for the "complication" of other sciences. Doesn't this sound like having constructed a nose? How would you like it if yours beeped everytime it smells your favored parfume?
Incidentally, olfaction involves some interesting processes, right down the line we will be discussing in the lecture on Signaling.

Saturday, April 30, 2011

Sugar: a new teaching tool?

Recently I stumbled across a nice way to make funny videos. I immediately "created" one such video and wonder whether I could not use this regularly to provide some teaching content. LET ME KNOW, and maybe you could create some of your own
Here is my first (not quite polished) creation - and I would like you to tell me whether there is anything offensive in this video (as my daughter claimed there is): click on this link!

Friday, April 29, 2011

Welcome!

I started this course blog idea in the last term: Students used it and seemed to like it - but they did not really participate (via comments or blog suggestions or provision of images or other media files, or by asking questions). Hopefully this class will be more active and dynamic! I added a gadget feature that sends you emails about new entries (I believe). To attract you to the blog, I will use a dirty tool: I will insert some exam type questions from time to time! If that does not work, then  I don't know!
If you have some special ideas on how to enhance our communication and provide interesting, educational and entertaining content, talk to me and write comments - the more the better. I know of course that you are all busy with other lectures...but maybe this blog will provide for some relieve and un-stress you a bit. Welcome again, Handsbare (submitted from Burnaby/Vancouver BC).