An interesting question:

Which is the leading cause of death worldwide among boys 5 to 14 years of age?

In the United States, this cause of death is the second leading cause of injury-related death among children 1 to 4 years of age, with a death rate of 3 per 100,000, and in some countries, such as Thailand, the death rate among 2-year-old children is 107 per 100,000. In many countries in Africa and in Central America, the incidence of this cause of death is 10 to 20 times as high as the incidence in the United States. Key risk factors for this cause of death are male sex, age of less than 14 years,alcohol use, low income, poor education,  rural residency, risky behavior and lack of supervision. For people with epilepsy, the risk of this cause of death is 15 to 19 times as high as the risk for those who do not have epilepsy. For every person who dies from this cause of death, another four persons receive care in the emergency department for nonfatal incidences of this cause of death.

Give us your answer or guess in the Comments!

Missing slide: Indirect i.v. effect of ACh

Somehow, a slide seems to have disappeared from one of my lectures, dealing with the i.v. effect of acetylcholine. I inserted it into the ANS2 lecture and it says this:

• Injecting ACh i.v., interaction with vascular smooth muscle should cause contraction and rise in BP.
• BUT: Muscarinic receptors on endothelial cells, when stimulated, will cause Ca-mediated activation of nitric oxide synthase and formation of nitric oxide: This will overcome the contractile s.m. effect and lead to vasodilation and fall in BP/shock.
• This is referred to as an "indirect" action of ACh.

HB

Read after the exam: A rare dysautonomia

Shely sent an interesting reference to me that you might enjoy reading after the exam: A very rare disease that may first present right after birth, namely, when the newborn does not open its eyes for several days and later will cause the affected to have frequent orthostatic hypotension-like events all the way to short term coma... Actually this deficiency disease caught my eye when I looked at the list of dysautonomias in my ANS3 lecture today, slide #57, where it is listed - and I thought to myself that I should look up sometime what it entails!

Thanks, Shely!
HB

Success in Life

Many people will give you advice on how to become successful in life - beginning with your parents and now maybe continuing with your professors....
The formula below, however, is all I can tell you and promise you it will be highly effective!

Agonists, inverse, partial and full

Let's see whether you understand inverse antagonists etc:

1. I you combine an agonist with a competitive antagonist you will
   A) never obtain a maximal response
   B) get a negative response like with an inverse agonist alone.
   C) eventually will obtain a maximal effect when increasing the agonist concentration.
   D) get no or only a very small effect.

2. If you combine an antagonist with an inverse agonist you will
   A) get a positive response instead of a negative one as you would in the absence of the inverse agonist.
   B) get no response when increasing the antagonist concentration.
   C) will get an increased negative effect.
   D) will form a black hole.

3. If you combine a partial agonist with an inverse agonist you will get
   A) a maximal effect.
   B) a negative effect if you keep increasing the inverse agonist concentration.
   C) a negative effect if you keep increasing the partial agonist concentration.
   D) will precipitate a Big Bang.

Goods luck: I want to see responses by each of you in the comment section!

Inverse agonist

I found a very nice and clear description of what an inverse agonist is - right in the Wikipedia (just one example of how things are described there sometimes clearer and better than anywhere else.... Go ahead and google "inverse agonist"! Here is a nice graphic and the descriptive text"

"....an inverse agonist is an agent that binds to the same receptor as anagonist but induces a pharmacological response opposite to that agonist.

A prerequisite for an inverse agonist response is that the receptor must have a constitutive (also known as intrinsic or basal) level activity in the absence of any ligand. An agonist increases the activity of a receptor above its basal level while an inverse agonist decreases the activity below the basal level. A neutral antagonist has no activity in the absence of an agonist or inverse agonist but can block the activity of either.

The efficacy of a full agonist is by definition 100%, a neutral antagonist has 0%, while an inverse agonist has < 0% (i.e., negative) efficacy...."

NB" I noted with some pleasure that the first author quoted in the references is a Terry Kenakin: he was student in my department at the U. of Alberta back in 1970/72 or so and has made a big name for himself when it comes to classical analysis of dose response curves (although coming up with hypothesis most have trouble following or seeing the relevance of with respect to medicine...).

A dosing question

You are giving some one a drug, say, penicillin G, and you inject i.v. and you inject a total of 1 g. What would you think the plasma concentration is going to (make it in terms of g/L). Give me your thoughts as a Comment below.

Whatever you guestimate, would it be the same answer if you gave the drug orally?

Don't be afraid to give a wrong answer - I won't remember within a day who said what!

Too much acid - acidosis

When someone takes an overdose of a drug that is a carboxylic acid, then its buildup in the plasma can contribute to a borderline acidotic metabolic problem (due to whatever derangement of metabolism) and contribute to the overall metabolic acid build up in plasma and precipitate an acute metabolic acidosis (characterized diagnostically by a large anion gap - in case you know what this is).

Can you think of a way to accelerate the excretion of the acid drug and save the patient from serious trouble?

A rectal question for you

A very young patient is treated with an antibiotic at 2 mg every 4 hours, but the kid does not like the taste and rejects taking his drug, causing a "compliance" problem and a flare-up of his infection. His doctor decides to make use on a rectal preparation of the same drug and thus prescribes the same dose for this formulation and frequency of administration.

Do you see a problem with this or would you have done the same or what information would you require before proceeding in any way? 

Please explain via a comment below!

Don't forget to recreate!

Here in this vacation paradise of St. Vincent and the Grenadines you are supposed to lay the foundations for becoming a great physician...but you are also supposed to be a bit of a tourist and enjoy some of the outdoors, the beaches, the jungle and whatever: Here are links to some videos you might enjoy and maybe they will animate you to go and do some of that live:

http://youtu.be/hUHlWQKtEUA

http://youtu.be/p-PzLpfcV_M

http://youtu.be/spSSlzdMe8A

Welcome to Spring 2012 Class

Hello eager students:

On the side bar of this blog you will find places to

• sign on to this blog
• register your email for notifications on new entries
• get some background information on your new lecturer

Once we are underway in this course, it will make sense for you to scan through the archive all the way - there will be lots of entries that will have relevance to what we are doing in this course and your education in general. There is a bit entertainment as well. I know you have lots of things to do - but I still expect that you will "participate" in this blog dialogue by entering comments (such as lousy entry, excellent information or whatever) and enter questions - that way we can share the answers and the issues that may arise! Also, it would be terrific if you could provide some material for this blog to share with the class! Just send me the info by email, I will enter it.
Below is a shot from just across the border - Mt. Shuksan in the Mt. Baker Park of just some 3 weeks ago - but now I am happy to join you for some sunny and warm days in the Caribbean....