Bonus Episode: Learn exactly what is in the Health Care bill. In this video, Dr. Dan explains exactly how he will unveil the full contents of the Health Care bill so that you don’t have to read it yourself.

Unbiased

Actually bipartisan (is that still possible?)

Register for the conference:

Page 183   Establishment of Community Health Insurance Option (CHIO)

Page 204  At least 85% of money must go toward actual health care costs

Page 132  Establishment of Small Business Health Options Program (SHOP)

Health Care Reform Bill

That’s right, I’m reading the entire 2,409 – page health care bill in preparation for this year’s conference.

Which new government program is poised to replace the Health Insurance industry?

Find out at May 29-30, 2010 in Dallas, Texas.

How will Health Care Reform affect medically underserved communities?

Dr. Robert Bowman, M.D., a foremost expert in Health Disparities, will present a thorough case for the medically underserved patients in the U.S. that led to such sweeping reform.

Register for the conference:

Episode 48: In this episode, you’ll learn about cell death, types of necrosis and lots of examples of pathophysiologic states that exemplify each condition.

Listen to the podcast here…

Apoptosis – Programmed cell death

Normal functions of apoptotic genes – “programmed to die” (theory).

(1) embryo – small bowel got lumens from apoptosis.

(2) King of the body – Y c’some (for men); MIF very imp b/c all mullarian structures (uterus, cervix, upper 1/3 of vagina) are gone, therefore, no mullarian structures. MIF is a signal working with apoptosis, via caspasases. They destroy everything, then wrap everything in apoptotic bodies to be destroyed, and lipofuscin is left over.

(3)For woman – X c’some; only have one functioning one b/c the other is a barr body. Absence of y c’some caused germinal ridge to go the ovarian route, therefore apoptosis knocked off the wolfian structures (epidydymis, seminal vesicles, and vas deferens).

(4) Thymus in anterior mediastinum – large in kids; if absent, it is DiGeorge syndrome (absent thymic shadow), and would also have tetany; cause of thymus to involute is apoptosis.

(5) Apoptosis is the major cancer killing mechanism.

(6) Process of atrophy and reduced cell or tissue mass is due to apoptosis. Ex. Hepatitis – councilman body (looks like eosinophilic cell without apoptosis) of apoptosis (individual cell death with inflammation around it). Just needs a signal (hormone or chemical) which activate the caspases, and no inflammation is around it. Apoptosis of neurons – loss brain mass and brain atrophy, and leads to ischemia. Red cytoplasm, and pycnotic nucleas.

Atherosclerotic plaque. Therefore, apoptosis is involved in embryo, pathology, and knocking off cancer cells.

IV. Types of necrosis – manifestations of tissue damage.

A. Coagulation Necrosis:

Results often from a sudden cutoff of blood supply to an organ i.e. Ischemia (definition of ischemia = decrease in arterial blood flow). In ischemia, there is no oxygen therefore lactic acid builds up, and leads to coagulation necrosis. Gross manifestation of coagulation necrosis is infarction. Under microscope, looks like cardiac muscle but there are no striations, no nuclei, bright red, no inflammatory infiltrate, all due to lactic acid that has denatured and destroyed all the enzymes (cannot be broken down – neutrophils need to come in from the outside to breakdown). Therefore, vague outlines = coagulation necrosis (see color change in heart).

Pale vs hemorrhagic infarctions: look at consistency of tissue. Good consistency = grossly look pale: infarct: heart, kidney, spleen, liver (rarest of the organ to infarct b/c dual blood supply); ie coagulation necrosis. Example of a pale infarction of the spleen, most likely due to emboli from left side of heart; causes of emboli: vegetations (rarely embolize in acute rheumatic endocarditis); infective endocarditis; mitral stenosis (heart is repeatedly attacked by group A beta hemolytic streptococcus); and clots/thrombi.

The worst arrhythmia associated with embolization in the systemic circulation is atrial fib b/c there is stasis in the atria, clot formation, then it vibrates (lil pieces of clot embolize).

B. Gangrenous Necrosis: dry and wet gangrene:

Picture of a dry gangrene – not wet/no pus. This commonly occurs in diabetic’s with atherosclerosis of popliteal artery and possible thrombosis; (dry gangrene related to coagulation necrosis related with ischemia (definition of ischemia = decrease in arterial blood flow), which is due to atherosclerosis of the popliteal artery. Pathogenesis of MI: coronary thrombosis overlying the atheromatous plaque, leading to ischemia, and lumen is blocked due to thrombosis. MCC nontraumatic amputation = diabetes b/c enhanced atherosclerosis (popliteal artery = dangerous artery).

Coronary is also dangerous b/c small lumen.

Episode 47:  This week I interviewed Carvell Nguyen, MD, PhD from Princeton Review. He is a Master Trainer for the USMLE.

Listen here for the full podcast…

For 15 years, Dr. Nguyen has been teaching for Princeton Review – ever since he took his MCAT!

Now, he travels the globe training Princeton Review’s trainers and teaching thousands of international medical students in Mexico, the Dominican Republic, Caribbean, and Puerto Rico.

There are several options that Princeton Review offers for the USMLE:

US Nationals:

* USMLE Step 1 Classroom Course: 7 hours of classroom instruction of Step 1 highlights to master, which includes their online review and Q-bank

* USMLE Online Review, which includes the Q-bank

* USMLE Q-bank

“The biggest difference is the intensity of the classroom instruction.”

International Medical Students:

* 150-hours of classroom instruction over 6-8 weeks!

* Same Online review and Q-bank options are available

Dr. Nguyen’s top 3 recommendations for the second year medical schools:

* Have a good study strategy, including using multiple senses to learn.

* Have a good study schedule.

* Emphasize quality of  conceptual understanding the material more than the average student, not only the quantity.

Episode 46: Learn all about bronchopulmonary dysplasia’s pathophysiology, tylenol overdoses and treatment, and hydroxyl free radicals.

Listen to the podcast here…

Free Radicals

The liver’s brownish pigment is lipofuscin (seen on gross pic; can also be hemosiderin, bilirubin, etc; therefore need to have a case with the gross pic); end products of free radical damage are lipofuscin b/c certain things are not digestible (include lipids).

A. Definition of free radical

A compound with unpaired electron that is out of orbit, therefore it’s very unstable and it will damage things.

B. Types of Free Radicals:

1. Oxygen:

We are breathing O2, and O2 can give free radicals. If give a person 50% O2 for a period of time, will get superoxide free radicals, which lead to reperfusion injury, esp after giving tPA when trying to rid a damaged thrombus. Oxygentated blood goes back into the damaged cardiac muscle=reperfusion injury. Kids with resp distress syndrome can get free radical injury and go blind b/c they destroy the retina – called retinopathy prematurity; also leads to bronchopulmonary dysplasia, which leads to damage in the lungs and a crippling lung disease.

2. Hydroxyl Free Radicals

Water in tissues converted to hydroxyl free radicals, leading to mutations in tissues.Complication of radiation therapy is CANCER (MC cancer from radiation is leukemia, due to hydroxyl free radicals). Fe2+ produces hydroxyl free radicals b/c of the Fenton rxn. This is what makes Fe overload diseases so dangerous, b/c wherever Fe is overloaded, leads to hydroxyl free radicals which will damage that tissue (therefore, in liver leads to cirrhosis, in heart leads to restrictive cardiomyopathy, in pancreas leads to failure, and malabsorption, along with diabetes).

3. Tylenol (aka acetaminophen):

MCC drug induced fulminant hepatitis b/c free radicals (esp targets the liver, but also targets the kidneys). Cytochrome P450 in liver metabolizes drugs, and can change drugs into free radicals. Drugs are often changed in the liver to the active metabolite – ie phenytoin. Where in the liver does acetaminophen toxicity manifest itself? – right around central vein.

Treatment: n-acetylcysteine; how? Well, the free radicals can be neutralized. Superoxide free radicals can be neutralized with supraoxide dismutase (SOD). Glutathione is the end product of the hexose/pentose phosphate shunt and this shunt also generates NADPH. Main function is to neutralize free radicals (esp drug free radicals, and free radicals derived from peroxide). Glutathione gets used up in neutralizing the acetaminophen free radicals.

Therefore, when give n-acetylcysteine (aka mucamist); you are replenishing glutathione, therefore giving substrate to make more glutathione, so you can keep up with neutralizing acetaminophen free radicals. (like methotrexate, and leukoverin rescue – using up too much folate, leukoverin supplies the substrate to make DNA, folate reductase).

4. Carbon tetrachloride:

CCl4 can be converted to a free radical in the liver (CCl3) in the liver, and a free radical can be formed out of that (seen in dry cleaning industry).

c. Effect of NSAIDS on the Kidney

Aspirin + Tylenol = very bad for kidney (takes a long time for damage to be seen). Free radicals from acetaminophen are destroying the renal medulla *only receives 10% of the blood supply-relatively hypoxic) and renal tubules. Aspirin is knocking off the vasodilator PGE2, which is made in the afferent arteriole. Therefore Angiotensin II (a vasoconstrictor) is left in charge of renal blood flow at the efferent arteriole. Either sloughing of medulla or destroyed ability to concentrate/dilute your urine, which is called analgesic nephropathy (due mainly to acetaminophen).

Episode 45: Sample this preventive medicine from the USMLE Audio Series at Medical-School-Podcast.com

Preventive Medicine

Preventive medicine, basically, has three tasks – screening, counseling, and immunization.  We are going to be focusing on screening and immunization.  About 15 minutes we’ll go over some screening principles, 15 minutes we’ll go over some principles regarding immunization.

Primary Prevention

So when you talk about preventive medicine and prevention, you can talk about it and think about it as primary prevention, secondary prevention, and tertiary prevention.  In primary prevention, you are actually working on reducing risk factors before a disease or a condition has occurred – so, immunizing somebody so they don’t get tetanus, you know, treating somebody who doesn’t have coronary artery disease with hyperlipidemia therapy to prevent them from getting heart disease.

Secondary Prevention

Secondary prevention talks about detecting a disease or a condition to improve prognosis – to do a mammogram to get an early stage breast cancer where that disease will be treatable and curable.

Tertiary Prevention

Tertiary prevention is another concept we don’t think about that much, but that would involve reducing risks of getting a second event.  So, if somebody has coronary artery disease, you put them on a high dose hyperlipidemic therapy to prevent their – or reduce their incidence of getting a follow-up disease.

There are a number of terms that you need to know in preventive medicine – that are listed up here.  These are covered very nicely in your book in chapter four.  And I believe Dr. (Stoller) will be reviewing some of these at the end of the day as well.  So, I’m not going to touch on these.

Screening Tests

So let’s talk about screening.  What are the general principles of screening?  Well, the disease that you’re screening for or condition should be important – meaning it should have a significant morbidity or mortality.  It should also be common.  It should have a high prevalence and a high incidence.  The disease that you screen for, you should be able to treat.  And the tests that you use to screen should be accurate, getting at the sensitivity, specificity, and predictive value.

Costs of Screening

And, finally, the screening tests should have a reasonable cost, not only financial in regards to quality of the life you’ll save, but also to the patient.  A screening test should be a low-risk test.

So when you look at the – number one – two causes of mortality in United States in 2002, you can see that the big players are heart disease and cancer.  So these are the ones who we would want to screen for the most.  And, obviously, the age where you screen somebody or practice preventive medicine varies.  So, obviously, in your older population, heart disease and cancer will be much higher on the list, whereas in your younger population, accidents, suicide, homicide, unfortunately, has a higher prevalence.

This very interesting slide shows the change in the United States death rates by cause between the years 1950 and 2002.  You can see that there has been a marked decrease in the rate per thousand deaths for heart disease, cerebral vascular disease, and also infection disease.  But the curve or the bar graph for cancer is relatively flat.

So let’s talk about, briefly, a couple of slides about cardiovascular screening.  We don’t have time today, but I think this will be covered at other sessions during the course about screening for blood pressure, lipid guidelines, diabetes guidelines.

EKG Screening?

I wanted to just make sure that you are aware.  According to the United States Preventive Services Task Force, if you have a 40-year-old patient who comes in without any risk factor who is healthy, there is no indication to do routine stress te...

Episode 44: Welcome to this bi-weekly series of Goljan-inspired USMLE review MP3’s. I’ll go through my personal notes that I used to prepare for Step 1 first, then Step 2 Clinical Knowledge. My style is more direct, no stories or shame on you if you’re not studying enough. Get access to all of the MP3’s and high yield notes by joining Medical-Mastermind-Community.com and study on-the-go!

Listen to the sample here…

I. Hypoxia = inadequate oxygenation of tissue (same definition of as shock). Need O2 for

oxidation phosphorylation pathway – where you get ATP from inner Mito membrane (electron transport system, called oxidative phosphorylation). The last rxn is O2 to receive the electrons. Protons are being kicked off, go back into the membrane, and form ATP, and ATP in formed in the mitochondria.

A. Terms:

1. Oxygen content = Hb x O2 satn + partial pressure of arterial oxygen (these are the 3 main things that carry O2 in our blood) In Hb, the O2 attaches to heme group (O2 sat’n)

Partial pressure of arterial O2 is O2 dissolved in plasma. In RBC, four heme groups (Fe must be +2; if Fe+ is +3, it cannot carry O2). Therefore, when all four heme groups have an O2 on it, the O2 sat’n is 100%.

2. O2 sat’n is the O2 IN the RBC is attached TO the heme group = (measured by a pulse oximeter)

3. Partial pressure of O2 is O2 dissolved in PLASMA  O2 flow: from alveoli through the interphase, then dissolves in plasma, and increases the partial pressure of O2, diffuses through the RBC membrane and attaches to the heme groups on the RBC on the Hb, which is the O2 sat’n. Therefore – if partial pressure of O2 is decreased, O2 sat’n HAS to be decreased (B/c O2 came from amount that was dissolved in plasma)

B. Causes of tissue hypoxia:

1. Ischemia (decrease in ARTERIAL blood flow ……NOT venous). MCC Ischemia is thrombus in muscular artery (b/c this is the mcc death in USA = MI, therefore MI is good example of ischemia b/c thrombus is blocking arterial blood flow, producing tissue hypoxia).

Other causes of tissue ischemia: decrease in Cardiac Output (leads to hypovolemia and cardiogenic shock) b/c there is a decrease in arterial blood flow.

2. 2nd MCC of tissue hypoxia = hypoxemia

Hypoxia = ‘big’ term

Hypoxemia = cause of hypoxia (they are not the same); deals with the partial pressure of O2 in the tissues.

3. Arterial O2 (O2 dissolved in arterial plasma, therefore, when the particle pressure of O2 is decreased, this is called hypoxemia).

C. Here are 4 causes of hypoxemia:

1. Resp acidosis (in terms of hypoxemia) – in terms of Dalton’s law, the sum of the partial pressure of gas must = 760 at atmospheric pressure (have O2, CO2, and nitrogen; nitrogen remains constant – therefore, when you retain CO2, this is resp acidosis; when CO2 goes up, pO2 HAS to go down b/c must have to equal 760. Therefore, every time you have resp acidosis, from ANY cause, you have hypoxemia b/c low arterial pO2; increase CO2= decrease pO2, and vice versa in resp alkalosis).

2. Ventilation defects – best example is resp distress syndrome (aka hyaline membrane dz in children). In adults, this is called Adult RDS, and has a ventilation defect. Lost ventilation to the alveoli, but still have perfusion; therefore have created an intrapulmonary shunt. Exam question: pt with hypoxemia, given 100% of O2 for 20 minutes, and pO2 did not increase, therefore indicates a SHUNT, massive ventilation defect.

3. Perfusion defects – knock off blood flow

MCC perfusion defect = pulmonary embolus, especially in prolonged flights, with sitting down and not getting up. Stasis in veins of the deep veins, leads to propagation of a clot and 3-5 days later an embolus develops and embolizes. In this case, you have ventilation, but no perfusion; therefore there is an increase in dead space.

Episode 43: Learn about the 5 residency options for osteopathic students, osteopathic board certification, malignant residency programs, and the full NRMP Match and Scramble Course.

Watch the full video podcast here…

There are two certifying agencies for Osteopathic and Allopathic residency programs:

•AOA: American Osteopathic Assn. (osteopathic D.O.)

•ACGME: Accreditation Council for GME (allopathic M.D.)

Here are the 5 different pathways Osteopathic medical students have to choose from:

1.AOA Residency (internship incl.)

2.AOA Prelim. (mostly at same institution)

3.AOA Traditional Internship (stand-alone)

4.ACGME (internship)

5.ACGME (residency)

AOA approval for an allopathic internship?

Yes, it is possible to get AOA approval for doing ACGME (allopathic) internship. This is useful for students who still want osteopathic board certification.

In 2006, there were only 90 dual ABMS-AOA programs out of over 8,000 allopathic residencies.

Download the full JOAO report and full AAMC report here.

From July 2007 to December 2007:

–1,603 D.O. petitions

–1,217 (76%) approved

–369 (23%) pending completion

____________

–99% total

–<1% denied or withdrew app.

In 2007, there were 3,103 D.O. graduates. This was the first time that number surpassed 3,000.

Add in about 70 previous grads and you have the full residency application pool. Therefore, 3,173 for 2007, the most recent full data set released by the AOA.

If you assume that all of them applied to either an AOA or ACGME program, then use ACGME data to complete the picture. AOA doesn’t release all the necessary data, so I’ve made some calculations of my own:

OVERALL D.O. MATCH RATE:

76% match rate of D.O. grads and previous grads match at either AOA or ACGME.

•3,173 applicants to AOA + ACGME

•1,136 matched allopathic with ACGME – 68.8% (69.9%, 2009)

•1,267* matched osteopathic with AOA – 62.2%

COMPARISON OF D.O.’s TO OTHER BACKGROUNDS MATCHING ALLOPATHIC:

•Overall allopathic applicants – 71.4%

•US Allopaths Grads/Students – 93.1%

•US Osteopaths Grads/Students – 69.9%

•US Nationals at International Medical Schools – 47.8%

•International Medical Graduates 41.6%

For further reading, click here.

Episode 42: Learn how to get insider access to the FULL version of this Match and Scramble Course. Doctor Dan unveils intimate parts of his medical education journey and gives Mastermind members exclusive access to behind-the-scenes video tutorials on the Scramble and Electronic Residency Application Service.

Watch the full video podcast here…

Every year there are over a hundred vacant residency positions after the match.

Watch the Anatomy of a Malignant Residency Program course to figure out why some of these programs don’t fill.

At exactly that time, the Scramble begins – the stressful cramming full of all these programs nationally, simultaneously.

Practically speaking, the programs themselves get flooded with inquiries:

•University email servers CRASH

•Fax machines are busy and run out of ink, with people faxing 15-20 pages each of required documents.

•The phone systems JAM.

•The unprepared applicant suffers!

Here’s a great solution to this problem that you can employ BEFORE the match. Medical Mastermind membership gives you a 20% discount to www.ElectronicResidency.com:

•Pre-Load all relevant documents into their software

•Send cover page with relevant facts, not 20 pages to jam the system

•Last year, submitted 500 applicant summaries by 12:05 PM with 97+% deliverability!

Episode 41: In this video podcast Doctor Dan unveils hidden residency program requirements that affect previous graduates and those that attended medical schools outside the United States. Also, there is a 4-step process for how to apply to U.S. Residencies if you don’t have U.S. citizenship or a green card.

Watch the full video podcast here…

We’re down to the 5th reason residency applicants don’t match every year:

* Not enough interviews

* Ranking unvetted programs

* Failure to certify the Rank Order List

* Competitiveness (USMLE scores, med school performance)

* Incomplete documentation

If you are a green card holder, then you have nothing to worry about.

If you require a visa, then you need to get either:

• a J1 sponsorship from ECFMG, or

•residency program to sponsor you with an H1 visa.

4 Step Process For IMG’s Entering U.S. Residencies:

1. Get Permission To Register for United States Medical Licensing Exam (USMLE)

–Have your credentials transmitted to ECFMG so that you can get the ok to take the USMLE exams.

–When the credentials are verified by ECFMG, you can register for the exams at ECFMG.org using the IWA link:

https://secure2.ecfmg.org/emain.asp?app=iwa

2. Register for the USMLE Exams:

http://www.nbme.org/

3. Prepare for the USMLE Exams:

• USMLE Step 1, Step 2 Question Banks

• Complete MCAT Video Lectures

• U.S. Medical School Exams

• U.S. Medical Student Class summaries

All are now available with Mastermind membership.

4. When done with the exams and now ECFMG certified, then you can apply for residency.

–Get the “token” from ECFMG.org

–Register through ERAS:

http://www.aamc.org/programs/eras/programs/registration/start.htm

–Register with the NRMP:

https://services.nrmp.org/r3/home/login/login.cfm

Episode 40: Every year there are empty residency positions left over after Match Day. In this video podcast, learn the average USMLE scores for matched and unmatched NRMP applicants, as well as how competitive different residencies are.

Watch the full video podcast here…

In the last 18 years, competition has been rising:

–1,100 new residency positions

–10,300 increase of applicants

Interestingly, 53% of applicant growth comes from non-US medical schools (Download the full NRMP report).

With rising competition, higher USMLE scores are expected over time. Here is a snapshot of current USMLE scored for matched and unmatched US and IMG residency applicants:

Another question I get a lot is about the relative competitiveness of different medical specialties.