4.05.2012

reflection upon exiting medical school


As I graduate medical school and begin my training I would like to reflect on some observations about the economics and practice of medicine I made while a student.
Physicians’ sensitivity to financial incentive is greater than I thought-
When I first came to medical school, I was more idealistic about the role of physicians in society. I had chosen this profession because I believed it was a path to living a just life. I had very little understanding regarding the economics of medicine. As I listened to conversations between my superiors on the wards, both residents and attending physicians, I was surprised by the preoccupation with money. This critique is more directed at the procedural specialties but can apply to us all. American physician reimbursement is the highest in the world, and it is creating a serious financial incentive to enter medicine, even in today’s more highly regulated healthcare setting. It is also creating an even more powerful incentive to specialize. This drive to use medicine for personal enrichment is supported by the preferences of competitive medical student applicants to enter highly reimbursed specialties. This financial incentive attracts those who prioritize financial reward; this adversely impacts the humanity and compassion of the profession as a whole. Those who choose lucrative specialties with minimal patient interaction offer much rationalization. Still, in doing so they stray from the classical definition of physician as a healer. Under the guise of a physician concerned with the sick and unhealthy, these specialists operate as highly skilled technical specialists. It is masquerade. The rational conclusion is that far too many doctors, and those entering the field are motivated by money.
The advent of hospitalists and salaried shift physicians will herald the loss of physician autonomy unless physicians become more organized politically.
As physicians continue to specialize, their interests have diverged greatly and solidarity has suffered both philosophically and politically. Desires for reductions in workload and relinquishing responsibilities of practice management have resulted in the creation of shift working physicians. Autonomy and controlling interest has been traded for better work hours and less administrative work, such that physicians are now managers without ownership. This phenomenon is compounded by narrowly focused specialist physicians, now more closely resembling technicians, blinded to both larger economic trends in healthcare delivery and the interests of their colleagues. Whereas allied health providers are strongly organized and unionized; organizing physicians has been likened to “herding cats”. Role confusion of specialist and shift physicians will adversely impact us all. Physician autonomy will now compete with newly established firmly adhered practice guidelines (to which practicing physicians may not have created). Finally, the much sought after salaried shift work no-call hospital physician position will face increased price pressure as the owners attempt to constrain costs of these generous salaries. Physicians now neither owners nor effectively organized will face these pressures divided and unleveraged.
The entitlement of subspecialty physicians in a fee for service model of inappropriately priced healthcare procedures-
Fee for service medicine creates financial incentive to increase procedural volume. Those sensitive to this incentive are subject to a conflict of interest in the administration of their service. They naturally pursue their rational interest to maximize profit. In the setting of increasing medical specialization, new medical technology (imaging, procedures, pharmaceuticals) is increasingly expensive and offers ostensibly better medical care yet possesses marginal utility in health outcomes. Though these procedures, improperly vetted by an underpowered governmental reimbursement body are still provided by third party payers. These payers in turn ultimately disperse the cost of these procedures onto that population whom comprise their risk pool. In combination with this, subspecialty physicians now with ever-narrowing scopes of practice proliferate and still require same broad physician privileges (in terms of patient contact, leadership, and management) afforded generalists in previous eras. Thus several “teams of doctors” may be involved in any single case many times voicing conflicting medical opinions. This is both confusing and exhausting as the parade of consulting physicians each have their 5 minutes with the patient, seldom altogether.
An ounce of prevention is worth a pound of cure, which is why if you want to make money it makes sense to sell cures by the pound.
Preventive medicine is inappropriately valued because prevention is too often not profitable for physicians and unpopular for patients. As well, these solutions many times reduce economic consumption and thus do not propagate a deficit-sustained society. They are of no interest to policy makers because their economic impact has not been believably quantified. Until real cost savings can be demonstrated, preventive medicine (especially where prevention means “doing nothing”) will not have a role in modern western medicine.
How healthcare expenditure is required for increased GDP and the necessity of increasing healthcare spending in maintaining American sovereignty.
Calls to reduce medical expenditure must account for the fact that healthcare spending is greater than 17% of GDP and increases every year. Therefore, significant reductions in spending would adversely affect GDP and increase federal budget deficits. Every dollar of health care spending eventually goes to someone, in some form. Reduction in federal health expenditure thus reduces "federally subsidized" economic output. Increased budget deficits (already scheduled for $1.2 trillion in 2012) decrease US borrowing capacity, which undermines US economic stability and sovereignty. Thus, much talked about reductions in healthcare spending and subsequent GDP reductions must be accounted for either by increased economic activity or further reductions in non-GDP contributing government spending.
The individual mandate is constitutional only in the setting of health insurance being purchased from a governmental body unconcerned with profit.
If healthcare is a public trust, then an individual mandate is a civil duty. However, the purchase of health insurance from private for profit corporations without allegiance to the citizenry violates the definition of a public trust. Thus, the only tenable means by which the individual mandate can be upheld is through compulsory purchase of government insurance or tax because it is the government who must by law serve its citizens and it will be the government who ultimately bears the cost burden of the uninsured.

3.27.2012

prohibition and cirrhosis

a comment was made in today's pharmacology lecture-


"US alcohol prohibition reduced rates of liver cirrhosis, and therefore was good for public health in this particular instance."


i think because none of use had ever looked into this question combined with the fact that it seemed so intuitive, we all took it as fact. however i was interested in seeing whether any data exist to support this claim.


national board of economic research published a paper, Alcohol Prohibition and Cirrhosis, by Dills and Miron, in 2003. The paper examined death rates in the context of state and federal prohibitions. All the cirrhosis death rates declined during the prohibition period by 10-20%, they caution concluding this solely to prohibition for the following reasons:

-there have been substantial fluctuations in cirrhosis death rates comparable to the ones seen during prohibition, outside of periods of prohibition

-cirrhosis did not increase to pre-prohibition levels upon repeal

-cirrhosis levels had declined by the time prohibition began, allow little time for this effect


you decide!


3.05.2012

random pharmacology notes

clinical pharmacology notes


takes 3 half lives of elimination to achieve steady state, so drugs w/long half lives o elimination (amiodarone - 40 days) can fool one into changing them before they've reached steady state. don't make any changes to meds unless they have been in patient for greater than 3 half lives.


aminoglycosides and fluoroquinolones are concentration dependent for bacterial infections


penicillins are time dependent


thus don't underdose fluoroquinolones, don't short course penicillins


quinidine is the most potent inhibitor of CYP2D6 in man


clinical clue: nail through the tennis shoe- think s. aureus or p. aeruginosa because these bacteria grow great in sneakers.


fluoroquinolone with Ca2+ (as in milk or iron fortified OJ) going to form Ca fluoroquinolone precipitates in the gut and less antibiotic will be available. this is bad because fluoroquinolones are concentration dependent anti-bacterial agents


interesting findings surrounding acetaminophen and EtOH. Chronic EtOH induces CYP2E1 for which acetaminophen is a substrate. the acetaminophen is metabolized to a hepatotoxic byproduct associated w/liver failure, thus the total recommended daily dosage for acetaminophen for someone who has at least 2 drinks a day is 2gms! interestingly, in binge drinking college kids - EtOH acutely inhibits CYP2E1, thus they are not bound by the same restriction of 2gm/day of acetaminophen-

2.20.2012

clinical pain management notes/ renal notes

random clinical notes from pain management and renal service






Epidural steroid injection

methylprednisolone or triamcinolone - less post injection flare


dilute w/local anesthetic for less atrohpy/rupture


3 causes of lumbar stenosis

1. ligamentum flavum hypertrophy

2. disc bulge

3. facet hypertrohpy/osteophyte



chief complaint: i have back pain.

clinical question: should you image?

in light of data indicating false positive findings on normals, one should image only in cases of:

history of trauma

unexplained weight loss

fever

immunosuppression

h/o neoplasm

steroid use

age >70

intravenous drug use

definite change in neurological status



chronic pain -76.2 million people in US

20% of outpatient office visits

12% of prescriptions


untreated pain estimated economic impact ~$100 billion/year


pain categories by etiology

nociceptive (somatic, visceral) - this pain is adaptive (keep you out of trouble)

musculoskeletal/inflammatory/mechanical


neuropathic - (this pain no longer helpful, lingers, remains past point of being informative)

sympathetically mediated

peripheral (post herpetic neuralgia, neuromas)

central (post stroke, phantom limb)


nociceptive afferents come in two categories

peptidergic - calcitonin gene related peptide (CGRP), somatostatin, trkA, trpV1

non-petidergic -purinergic ligand gated ion (Ca++) channels, scn9A (sodium channel)


ascending signals are subject to descending modulation from the following neuroanatomical structures

somatosensory cortex, hypothalamus, peri-aqueductal grey, pons, prefrontal, anterior cingulate, - these descend by DLF (dorsal longitudinal fasciculus)


COMPLEX REGIONAL PAIN SYNDROME

type 1 - RSD - reflex sympathetic dystrophy, no evidence of actual tissue damage

type 2 -causalgia - has an identifiable etiology

treatment - sympathetic block and PT/OT.

a sympathetic block is determined to be successful in the the ipsilateral the skin temperature increases >1 degree C in the distrubution of the nerve. the temperature increases presumably because sympathetics are responsible for sweat, which cool the body by transfer of heat to H2O. side effect - horners syndrome


cervical blocks be aware - 0.5cc of of local into the vertebral artery is all that it takes to cause a seizure


don't do b/l cervical blocks because you can knock out the phrenic nerve


3 things to do to decrease ICP

1. hyperventilate

2. mannitol

3. steroids


acute increased in ICP only 1/3-1/2 will get papilledema


old tenet in medicine, "the real problem is greater than the potential problem"

i don't know if i agree with this all the time!


RENAL STUFF


PTH - catabolic for cortical bone, anabolic for trabecular

osteocalcin - blast marker

c-telopeptide - breakdown product of collagen, an osteoclast marker

alk phos - blast product (marker of mineralization) not metabolized by kidney


SIADH

A - erratic, greatly increased levels of ADH

B- constant ADH leak

C - osmostat reset

D -genetic increase in V2 aquaporin


etiologies of SIADH

cns - stroke, hemorrhage, infection, trauma, psychosis

malignancy - ectopic ADH secretion (usually in small cell lung ca) - a neuroendocrine tumor

drugs - carbamazepine, cyclyophosphamide, SSRI, valproate, ecstasy, interferons

surgery - 2/2 pain, can see triphasic presentation 1. polyuria, 2. siadh, 3. diabetes insipidus

pulmonary - pneumonia (viral bacteria tb)

hormone def - adrenal insufficiency and hypothyroid!!

hiv


treatment

free water restrict

salt tabs and furosemide (to wash out intramedullary gradient and prevent the ability to concentrate urine)

hypertonic saline (only in emergency hyponatremia)

classic blunder: giving IVF to siadh patient, anything fluid given is hypotonic to the patient's urine will only exacerbate free water retention

tolvaptan - V2 receptor antagonist


potent pimpable!

what is the differential diagnosis for increased BUN in the setting of normal GFR?

prerenal

catabolic process

high protein diet

GI bleed or other hemorrhage - (tissue destruction)

glucocorticoids (increases tissue destruction)

tetracycline therapy (decreasing tissue anabolism)


cystatin - a ubiquitous cysteine protease inhibitor looking to challenge creatinine as clinical measure of GFR



patient all of the sudden gone into A-FIB? don't forget about PE on your differential.


40 & 5, 40% O2 and 5cm PEEP - lowest vent settings (either coming off or going on)


1.23.2012

drug discovery review

preclinical drug discovery methods

screening by target

phenotype screening

natural substance modification

biologics


259 agents approved by FDA between '99-08

75 w/new molecular mechanisms of action

50 small molecules

25 biologics

28 were developed using phenotype screening

17 were developed using target based


drug discovery main focus since 1990's has been on targets - clone the receptor or protein and modify it, the rational basis

tools that aid the discovery of compounds - high throughput, x-ray crystallography, computational modelling/screening


prior to molecular era of the 90's was phenotypic screening - less emphasis on mechanism of action


pros/cons of target vs phenotypic screening


target based discovery

pro

hypothesis driven based on molecular/chemical knowledge, all biologics are discovered this way

con

the hypothesis is not useful because it is not involved in pathophysiology


phenotype screening

pro

do not need to know mechanism of action

cons

without mechanism, designing is difficult because don't know which properties to modify, also - screening can be less efficient (low throughput)


the following is a list of CNS drugs approved for these years (taken from their table), most do not have an identifiable target, and 3/7 do not have a known MMOA



Target MMOA


Levetiracetam unknown unknown

Memantine receptor receptor kinetics

rufinamide unknown unknown

varenicline ion channel partial agonist

zonisamide unknown unknown

ramelteon receptor equilibrium binding


discoveries by modification of natural substance

acamprosate ion channel modulator


term

biochemical efficiency - binding affinity/functional response (Ki/EC50)


28 of the first in class small molecules were identified with phenotypic screening -

25 were intentionally targeted, 3 incidentally discovered

MOA were reversed engineered after observing physiological phenomena

18/50 first in class molecules came from natural substances


ramelteon - a melatonin receptor agonist approved for insomnia was discovered with a target specific strategy.


biologics - large peptide molecules - all created using target based approach

enzyme replacement

novel functioning

inhibition of normal function

augmentation of normal function


phenotypic approach worked best for CNS and ID, target based approach worked well for cancer, ID, and metabolic disease