To put the current disintegration of Medical education and practice into context, we need to first understand individual patient requirements and societal requirements to gain further insights into medical practice and how it can be integrated with medical education.
We share below an illustrative example from one of our online expert patients that we have published before here: https://pubmed.ncbi.nlm.nih.
The layer of Individual patient experience
(Medical practice) :
Patient’s voice – (in italics)
It all started in the summer of... when I
returned from a long weekend . . . it was
cool and rainy there.
I ate too many gravy coated potato fries,
drove home in damp clothes, and caught
what I thought was the flu.
It didn’t respond to my usual cure of lying on
the sofa and watching four rented videos.
In a few weeks I noticed some black and
blue marks on my arm and panicked when
I didn’t stop bleeding from a small cut.
My days became a struggle to continue life,
as I once knew it and understand why
my body was betraying me.
(Medical Education) A medical students related lecture notes although apparently distant from the above patient context:
Physiology of Haemostasis
The cessation of bleeding from damaged
blood vessel. After vessel injury, process of
haemostasis takes place in two phases:
Primary:
1. Vessel wall contraction
2. Platelet aggregation & plugging of injured
area
Secondary:
3. Formation of an insoluble fibrin clot
because of activation of clotting system
What are the abnormalities of haemostasis
that may have caused abnormal bleeding
in this patient?
Haemorrhagic diseases can result from
abnormalities of:
Blood vessels
Platelets
Clotting systems
Diseases affecting the smaller blood vessels
& platelets produce the clinical picture of
purpura.
Integrating medical education and practice:
The practice passage above begins an individual
clinical encounter with an audience (us) and we
notice that the initial queries generated
even by a patient are always something
like:
Where is the problem? (a physician’s
morphologic diagnosis)
Why is the problem (a physician’s etiologic
diagnosis)
and this is mostly answered by
pathophysiologic rationale that patients are
not expected to know (and may not
understand even through Internet
searches).
However, this is what physician’s are
expected to know as a result of their
training (and improve on with experience).
The most basic of these is the knowledge
of anatomy that takes time to change
unlike empirical evidence in medicine that
has proven to have a very short shelf life.
A physician by virtue of this basic knowledge
of macro- and microanatomy is able to
quickly grasp other information that keeps
adding to his lifelong day-to-day learning in
medicine.
It can often happen that what the physician had held as rote memorized facts (education) to apply to the current patient at hand (practice) may often fall short when it actually comes to deal with diagnostic and therapeutic uncertainty.
Let's return to the same patient centered example to check the challenges around integrating therapeutic uncertainty
Patient voice 2:
"The haematologist suggested prednisone,
the drug of choice. I was wary of the
side effects, but this seemed to be the
best option.
For three weeks I endured the brain fog,
sleepless nights, and anxiety, hoping the
drug would be a quick fix. It wasn’t.
There was only a slight rise in my platelet
count, then a fall. He then suggested IVIg."
Most physicians elect to not treat patients
unless their platelet count is below
50 000 L-1 or bleeding manifestations are
present.
Only 15%-25% of patients on steroids are
expected to have lasting remission;
The remainders have disease characterized by
frequent relapses and remissions.
Thiagarajan, P. (2006) Platelet disorders, E-medicine from web MD,
Web document last downloaded on August 16, 2007.
We enter the zone of empirical evidence that
tells us what intervention to choose for our
patient at hand utilizing population-based
data from collective experimentation.
The layer of Individual experience
Surviving and healing phase
Patient voice :
"The next round of IVIg was less successful in
raising my counts. The round after that had
almost no effect. I agreed to have my
spleen removed, hoping again for a quick
fix and to put an end to the endless round
of doctor appointments, hospitalizations
and the constant fear of bumping my head
and dying. Before I left for the hospital I
placed my will on my dresser."
Collective experience and its
conceptual layers
IV (Intravenous) IgG (Immunoglobulin G)
(0.8–1 g kg-1 for 2 d) can cause adverse
effects of IgG include fever, nausea,
vomiting, and, occasionally, renal failure.
Chronic ITP patients who fail to maintain
normal platelet count are eligible for Elective
Splenectomy. Splenectomy is effective
because it removes the major
site of destruction and the major source
of antiplatelet antibody synthesis.
Approximately 10%-20% of patients
who undergo splenectomy remain
thrombocytopenic and continue to have a
bleeding risk.
Patient voice :
My surgery was successful in that I survived,
my spleen was removed and the wound
eventually healed. However, it was not
successful in raising my platelet count.
Three weeks after the surgery I had as few
platelets as before the operation. Now I
was without a spleen bruised, and still on
the seizure meds.
Collective experience and its
conceptual layers:
A number of treatments have been
proposed for splenectomy and steroid
failures. Most of them are not based on placebo-
controlled studies, and evaluating the
efficacy of these treatments in a disease
associated with spontaneous remissions
and relapse is difficult.
Other treatment regimes:
High dose corticosteroids (iv)
High dose iv Ig
Rituximab
iv Anti-RhD
Danazol, colchicine
Vinca alkaloids
Immunosuppresive drugs: Azathioprine,
Cyclosporine, Dapsone
Patient Voice
My hematologist recommended Danazol...
No luck . . . Colchicine failed too. We even
tried another course of IVIg hoping that my
body would respond to it differently now
that I didn’t have a spleen. It responded
differently all right. I was hospitalized
following one of the treatments for a
nosebleed that didn’t stop. I went to an ITP
specialist in . . . and he berated my local
hematologist for not putting me in the
hospital.
I reluctantly agreed to a course of vincristine
(chemotherapy) followed by a series of Prosorba.
A blood cleansing treatments. They sneaked
in more of the dreaded prednisone.
At the same time I also took up alternative wellness techniques that gradually began to enrich my life. I returned to work at the end of March, part time wearing a wig, on the day that my short-term disability insurance ended. My counts were still low, but I was thrilled to have parts of my life back. In a few weeks, I began full time work again.
The above expert patient has subsequently published another paper with our team members where she elaborated on her cure and the integration of multidisciplinary interventions that was brought about to effect it. She subsequently utilized the power of online integration to provide a voice to similar stories from many patients around the world.
Reference link:
https://www.irma-
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