How I aced a college physics course while learning almost no physics

The basic game plan for the pre-med students was to get good grades and get into medical school.In some ways, many ways, getting a education was secondary, perhaps a side effects of getting the grades.

My college physics  course was in some ways rather idiosyncrasy- there were  weekly tests that consisted of several problems which were graded on a no partial credit basis. It the correct answer was 17.5 seconds 17.3 got no credits. There was instance feedback on the results. You took the paper to the Prof who quickly graded it and you knew the results.

The prof had taught for over twenty years and his pattern was to repeat questions .So that if you had access to an "Old test file" to  which all fraternity members had access and somehow the non-frat folks also had access You could review the type of problems that were in the files that related to the lecture material for that week and focus on those.

It was matter of learning how to solve each type problem,recognizing the patterns,and practicing the steps so you could set the problem up quickly,go through the steps and have amble time to recheck the math ( remember it was no partial credit).

An example problem was someone drops a rock in a well and hears the splash n seconds later, how deep is the well. (It is amazing how often that and other " well posed " problems come up in the daily practice of medicine)

This trip down memory lane was stimulated by a blog entry  by the ever interesting and insightful Dr. Scott Aberegg on his blog ,Status Iatrogenicus.

He discussed the difference between intelligence and common sense and how often the two are not well correlated. The physics course "success" was due to the application of the basic mechanisms that underlie the "intelligence" tested on such things as the SAT and ACT. Pattern recognition, learning the rules or technique of solving the particular problem and practice practice practice.The latter of which is the well recognized way to Carnegie Hall , It was clearly the way to ace the course and finish with a grade significantly higher that the rest of the class (  number 2 was not even close) all of whom were hand picked by the prof who seemed to enjoy giving pre med students a hard time.

This story can also be thought about in terms of Goodhart's Law.When a measure become a target it looses its value as a measure. I remember that the most common question asked by the medical school classmate who was first in the class was "Will that be on the test?"


h/t to and a firm recommendation to read and think about Dr. Aberegg's essay entitled "Book Smarts and Common Sense  in Medicine " . It is more than well worth the time spent. See here.




    
                         
 

Does the two-phase concept for treatment of Thromboembolic disease make sense?

Dr. Clive Kearon,from McMaster University, has suggested the concept of a two-phase anticoagulant treatment of  of vein thrombosis and pulmonary embolism.See here. A full text  version can be accessed from J Thromb Haemostis  2012;19: 507-511 entitled A conceptual Framework for two phases of anticoagulant treatment of venous thromboembolism.

Kearon , and his coworkers at McMaster University in Canada are accomplished researchers  in the field of thromboembolism and his thoughts deserve serious attention.

Kearon proposes that  four observations provide strong support for this  two-phase concept:

1.Treatment for less than 3 months is associated with a higher recurrence rate
2.Treatment for 6 months has the same recurrence risk as treatment for 3 months.
3.The recurrence after too short a treatment predominately occurs at the site of the original thrombus.
4.The recurrence after too short a treatments typically occurs immediately after stopping treatment.

These observations suggest to the author that at first the anticoagulant therapy treats or somehow"turns off" the acute thrombotic process and prevents extension of the clot and reduces the risk of a pulmonary embolus. This theory is consistent with his observations listed above as 3 and 4.

Kearon's two phases are :

1. active treatment phase during which there is a rapid decrease in the risk of recurrence
2.secondary prevention phase, which is as long as the anticoagulation is continued.

 Obviously the two phases overlap.

 In some patients there are recurrence DVTs when anticoagulant therapy is stopped, whether it be at 3 months or 6 months or several years.So now the way of thinking is changing from should we treat for 3 months or 6 months to three months or extended anticoagulation  with periodic reassessment of risks versus benefits, a process that is at best often a semi-educated guess with with broad error terms and is euphemistically described as "determining". Maybe followup D-dimer testing has some role here.

Pulmonary emboli after pacemaker implantation -symptomatically rare maybe more commonly silent

 Case reports of pulmonary embolism following pacemaker implantation are rare.

One 1986 paper  reported  a "15% incidence of asymptomatic perfusion defects on V/Q lung scans". Forty patients were studied after PM implants. 20  were given low dose heparin and twenty were not. In the non-heparin treatment arm there were 3  asymptomatic  cases of high probability positive studies, normal ventilation,normal xray and decreased perfusion. In other words, the typical pattern of a pulmonary embolus on lung scan. So the number of 15% of silent PE post PM implantation is typically quoted in the literature on the basis of this single, small study .

 A prospective study of 150 consecutive was published ,apparently a thesis at the University of Turku in Finland. There were five cases of PE. The abstract doesn't indicate if these were symptomatic or not.

My understanding is that routine post procedure anticoagulation is not widely done because of concern of pocket hematomas which is turn increases the risk of an infection.

Full disclosure-my interests in this stems from having pulmonary emboli, clincally manifest six days after the implantation of a bi-ventricular pacemaker and after being treated for a pulmonary embolus with apixaban I developed a pacemaker pocket hematoma.

A physician can learn a great deal about a condition when he develops that condition.Talk about generating limbic valence.

One take home message I discovered was how variable radiologists' reading of CTPA
can be.  A recent American Journal of Radiology article claimed that as many as 26% of CTPA are "false positive". In my case, the "official" reading indicated segmental emboli in the lingula and in the medial basal and anterior basal segments of the left lung.A second "unofficial" reading came from a friend, who is  recently retired radiologist -no clots seen. Another unofficial reading  done by a radiologist from the same institution as the EP cardiologist who was treating me  was read as showing some artifacts and "one or two emboli". Three radiologists produced three significantly  different readings and a 4th radiologist ( from another institution reading a 3 months follow up CTPA said of the earlier film there were some equivocal findings of possible subsegmental emboli.


addendum : 7/30/19 some comments and reference to new data  added.

Mayo Clinic did a retrospective review of 5646 pacemaker implantation done between 2000 and 2010.There were 88 cases of diagnosis of clinical PE which is 1.6% most of whom had a predisposing factor such as post of surgery status,DVT,immobility etc.

Ref: Nolteria, Amit, Pulmonary emboli in patients with transvenous cardiac implantable  electronic device leads. Europace 2016, Feb 18 (2), 246-252

So clinical PE seems rare and one small study suggested a 15% incidence of asymptomatic PE.

New ACCP guidelines on VTE-stockings out, NOACs solidly in -outpatient treatment of pulmonary emboli for some patients

The American College of Chest Physicians (ACCP) has issued its tenth set of recommendations regarding venous thrombo embolic disease (VTE) .See full  free text.

Noteworthy is the solid recommendation for the New (or novel) oral anticoagulants (NOACs) over the old favorite Warfarin which was the oral anticoagulant of choice (the only one in the U.S.)) for over fifty years.NOACs were first approved by the FDA for treatment of non-valvular atrial fibrillation and more recently for DVTs and PEs.

Recommendation wise the four NOACs currently approved are not created equal. Rivaroxaban and Apixaban can be used without pre treatment with a parenteral anticoagulant,typically low molecular weight heparin,  while dabigaran and endoxaban cannot.

The ACCP panel lead by Clive Kearon of McMaster University rescinded their earlier recommendation for the use of compression stocking to prevent the post thrombotic syndrome.

The outpatient treatment of some patients with PE is a game changer or sea change  or whatever the current cliche of choice is  for major changes in medical practice.Prior to the NOACs the standard of care was several days in the hospital overlapping  with heparin until the patient was safely anticoagulated with a reasonably stable INR . Now  patients who are hemodynamically stable with a suitable home environment can be either discharged after a brief time in the hospital or sent home from  the ER on either rivaroxaban or apicaban with a double dose for the first week.

The distinction between provoked and  unproved continues to be emphasized. With provoked DVT or PE three months seems to be the standard of care , while for unprovoked- reassessment at the end of three months is recommended at which time  the nebulous balancing of bleeding and clots risk is somehow determined.

The problem of  pulmonary emboli in the subsegmental pulmonary arteries is addressed without a clear cut definite recommendation being made .Watch and wait with follow up testing or treat-for patients with a subsegmental embolus and a negative leg vein study.

Subsegmental emboli are often asymptomatic and also are CT angiogram are more likely to be false positive and subject to varying readings when the study is interpreted by more than one radiologist


The argument of 3 months versus six months of anticoagulation has morphed into three months versus extended anticoagulation.