Skin Cancer — Recognizing Skin Cancer and Preventing it in the First Place!

Tis the season for excessive sun exposure and excessive sun exposure = risk for skin cancer. Yes, that’s right, that sun exposure that gives you your sexy tan is also the #1 preventable risk factor for all three of the main types of skin cancer. Dermatologists (doctors who specialize in the skin) uniformly recommend protecting your skin when you are outdoors with a sunblock of at least SPF 30 and hopefully that is old news to you, especially if you are a parent, because sunburns when you are young (i.e. in your kids) are an even greater risk factor for skin cancer than they are once you are a crusty old bastard like me. Another good tip is to wear dark clothing and a good broad-brimmed hat when you’re outside and to limit your sun exposure between the hours of 10:00am and 4:00pm, which is the time of day that the sun is most directly overhead in the temperate latitudes (like the U.S. and the U.K.), most intense, and most damaging. Remember that UV light doesn’t only damage your skin, it also damages your eyes and can cause cataracts (commonly) and potentially fatal intraocular melanoma (cancer inside the eye) — wear sunglasses! The CDC has an excellent, and short, webpage on sunprotection here: http://www.cdc.gov/cancer/skin/basic_info/prevention.htm

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Sunlight is composed of a broad spectrum of lightwaves (hang with me here) including the visible light that you can see and ultraviolet light (UV) that you can’t. UV light is further composed of UVA and UVB and both of these types of UV light are damaging to your skin, causing it to look old and wrinkled, and potentially can cause skin cancer in people with excessive sun exposure. The SPF of a sunscreen is a measure of how much UVB light the sunscreen blocks under laboratory conditions. Under laboratory conditions an SPF 30 sunblock blocks out approximately 97% of damaging UVB light — the take home message being that if you really want the level of protection that the sunscreen is supposed to provide you better follow the instructions on the bottle. If you think that you’re doing your skin any favors by applying a light coat of SPF 30 sunblock in the morning and then spending 10 hours in the sun without reapplying it every two hours (or whatever the bottle says) you should think again! Remember that SPF only is a rating of protection against UVB light, but UVA is damaging too! Look for a sunscreen that specificially says that it protects against UVA + UVB and don’t settle for anything less.

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This is good sunscreen because it has UVA and UVB coverage and it clearly states this on the label. Whether or not an SPF of greater than 30 actually provides greater protection is debatable, but use at least SPF 30 to be safe.

All of this talk about SPF (that’s Sun Protective Factor) immediately begs the question, at least in my mind, as to what the SPF of your skin naturally is and whether the SPF 30 sunscreen recommendation holds for dark skinned people as well as for those of us with lighter complexions. It surprised me to learn that a tanned persons skin only has an SPF of about 4 and an extremely dark skinned person (a black person with very dark skin) still only naturally carries an SPF of about 13 naturally! That’s right, even if you’re as dark as they come you still need to wear sunblock when your outside in the sun or you’re placing yourself at risk of getting skin cancer. While it is true that very light skinned people, especially redheads, are at higher risk for developing a skin cancer (approximately 7x higher risk) than the rest of us, everyone is at risk for this disease and dark skin people tend to be diagnosed later (and with more advanced cancers) because they don’t realize that they can get skin cancer too!

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How much protection does this guy’s nice dark tan provide against the sun? Only about SPF 4 — better than nothing, but still pretty darn mediocre.

The Major Types of Skin Cancer

1. Basal Cell Carcinoma: If you absolutely must have a cancer, this is the one to have because it virtually never metastasizes (spreads throughout the body) and it is the metastases that generally make cancers deadly. The downside is that basal cell carcinoma loves to grow in places that are highly visible, like your nose and cheek for instance (notice that these are also highly sun exposed areas!!!), and they can be extremely disfiguring. The only way to get rid of a basal cell carcinoma is to have it surgically cut of your body — and they only get bigger with time, not smaller!

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There probably won’t be much of a nose left after this is resected. Keep the plastic surgeon’s in business anyhow…

2. Squamous Cell Carcinoma: Unlike the classic raised and pearly appearing lesion of a basal cell carcinoma, squamous cell carcinoma of the skin likes to form ulcerations. This cancer does metastasize but it is generally slow growing and tends to be curable unless people choose to ignore the large ulceration on their face — which happens more often than you would think (??!!!??!!!??).

Squamous_Cell_Carcinoma[1]

Ditto.

3. Melanoma: The granddaddy of all skin cancers and one of the worst cancers that you can possibly get, period. Melanoma loves to spread through the body with a rapidity that is difficult to imagine, being especially fond of migrating to the bone (extremely painful) and the brain (causes delirium, seizures, etc.). This cancer is CURABLE if caught early and surgically resected. There has been some medical progress in the past few years for treating metastatic melanoma but once this cancer migrates out of the skin it remains a death sentence.

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Given the size of this unfortunate fellow’s melanoma it is unlikely that it hadn’t metastasized by the time the second photo was taken. Given that the second photo was taken in 2009, it is also unlikely that he is still alive. Melanoma is a devasting disease.

4. Actinic Keratosis and Xeroderma pigmentosa: The girl in the picture below has a genetic condition called xeroderma pigmentosa, or “XP” for short. Everytime you step outside into the sun the sun’s powerful UV rays damage your skin, causing genetic mutations (changes in your skin cells’ DNA). Most of the time your body is pretty good about repairing these mutations, the problem being that every once in a while one slips through the natural repair mechanisms and sticks around inside your skin cells, which then pass it on to new skin cells. Over a lifetime of sun exposure these mutations buildup, just like mutations slowly accumlate in the lungs of long time smokers, and skin cancer (or lung cancer in the case of the smoker) is often the result.

Child_suffering_from_Xeroderma_Pigmentosa_(_Rukum_Nepal)[1]

People with the genetic disease xeroderma pigmentosa are born with a defective DNA repair mechanism in their skin and all of that sun damage rapidly results in mutations that, unlike in a healthy person (most of the time, anyhow), don’t get fixed. The result in skin cancer in childhood. People with this disease also suffer from early cataracts, which is why the girl in the picture has cloudy appearing eyes. This unfortunate girl is a potent example of what sun damage does to your skin over time if you don’t take care of yourself — it just happened to her a lot sooner! By the way, the crusted appearing skin lesions on this girl’s face are actinic keratoses, precancerous lesions that each have a 10% chance (in a healthy person) of developing into a skin cancer.

An Important Note: All forms of skin cancer can present in atypical forms, some of which look nothing like the lesions demonstrated above (especially certain types of melanomas). If you have any skin mark/lesion/mole/etc. that is or might be changing, or that is or might be suspicious, get it checked out by your physician!!!

As an aside, the CDC has an excellent webpage detailing the risk factors for skin cancer here: http://www.cdc.gov/cancer/skin/basic_info/risk_factors.htm

Dr. Leonardo Noto

Physician and Author of Medical School 101, Intrusive Memory, The Life of a Colonial Fugitive, and The Cannabinoid Hypothesis. Amazon Link to Doc’s Writing:  http://www.amazon.com/Leonardo-Noto/e/B00ATVOMCW/ref=ntt_dp_epwbk_0

NOTE: The Life of a Colonial Fugitive — my dark historical thriller — is free for your ereader at http://www.smashwords.com/books/view/215272. Thanks for reading!

Author Bio: Dr. Leonardo Noto is the nom de plume of a former airborne battalion surgeon who is now in civilian practice. Dr. Noto is the author of four books and he also writes for a medical education corporation that assists medical students, interns, and residents as they prepare for the medical board examinations. Dr. Noto is the proud father of an extremely spoiled 16-month-old American Bulldog who enjoys slobbering everywhere and tearing up things that he is not supposed to! Dr. Noto is an amateur practitioner of muay Thai and Brazilian jiu jitsu and he recently began learning to play the guitar (but he is currently a quite terrible musician, as his neighbors will readily attest).

Remember to discuss all health concerns with your personal physician (I don’t count!) before making any medical decisions. www.leonardonoto.com is intended to present general medical information for entertainment purposes and not as specific guide to any medical treatment. The author has made every effort to present accurate information; however, due to the ever-changing nature of medicine and the intrinsic caveats that are inherent in any particular case, no medical decisions should ever be made based on information gleaned from the internet (duh!). The internet and self-education are great, but they don’t replace your Doc!

The opinions voiced on this medical blog are solely the author’s own and they do not reflect the opinions or values of Dr. Noto’s employers, past or present. Dr. Noto’s medical blogs should never be used as supporting evidence for legal testimony — this is of course obvious to anyone who isn’t a complete moron, but some people are rather stupid.

References:

1. Sunscreen SPF: http://www.skincancer.org/skin-cancer-information/ask-the-experts/does-a-higher-spf-sunscreen-always-protect-your-skin-better

2. SPF of Black Skin: http://news.bbc.co.uk/2/hi/health/5219752.stm

3. With Sunscreen, Without Sunscreen: http://commons.wikimedia.org/wiki/File:UV_and_Vis_Sunscreen.jpg

4. UVA/UVB Protection Sunblock: http://www.google.com/imgres?imgurl=&imgrefurl=http%3A%2F%2Fwww.walmart.com%2Fip%2FCoppertone-Sport-High-Performance-Ultra-Sweatproof-Sunscreen-SPF-100-4-oz%2F17619676&h=0&w=0&sz=1&tbnid=B65Fwr6SBHb5iM&tbnh=225&tbnw=225&zoom=1&docid=ul9nyaTgmWXhEM&hl=en&ei=yhEdUtzQMYa4qQG7q4DACQ&ved=0CAEQsCU

5. Darkly Tanned Skin: http://en.wikipedia.org/wiki/Human_skin_color

6. Basal Cell Carcinoma: http://en.m.wikipedia.org/wiki/File:BCC_Nodular_type.jpg

7. Squamous Cell Carcinoma: http://commons.wikimedia.org/wiki/File:Squamous_Cell_Carcinoma.jpg

8. Melanoma: http://commons.wikimedia.org/wiki/File:NodularMelanomaEvolution.jpg

9. Xeroderma Pigmentosa: http://commons.wikimedia.org/wiki/File:Child_suffering_from_Xeroderma_Pigmentosa_(_Rukum_Nepal).jpg

Are Genetic Diseases Evolutionarily Beneficial?

Are genetic diseases evolutionarily beneficial? It sounds like a crazy question, but the answer is “yes, some are.” In my blog post, “Why are Black People Black and White People White,” we discussed how sickle cell trait (primarily in people of African descent) and thalassemia (a group of diseases that is mostly found in Southern Europeans and in Asians) are both protective against malaria. Inherit one copy of the sickle cell gene and you gain substantial and lifelong protection against malaria, historically one of the most deadly diseases to afflict mankind, the downside being that the rare person who inherits two copies of the sickle cell gene ends up dying from a horrible genetic disease. The genetics of thalassemia follow this concept, although the actual inheritance patterns are more complicated and not something that I’m going to bore you with. The take home message is that on a population level, at least historically, having the sickle cell gene and the thalassemia genes floating around in the population did a lot more good than harm (on a net basis) and that this is the reason why these genes are still with us today!

The impetus for my writing “Why are Black People Black and White People White” was the excellent book The World Until Yesterday, by Jared Diamond (he’s also the author of Guns, Germs, and Steel — another exceptionally great read), which reminded me of some things that I’d learned years ago in medical school, found fascinating, and just never gotten around to blogging about. Following on this theme, I thought that it would be interesting to briefly explore some additional genetic diseases that are present today because they were evolutionarily beneficial, at least on the population level, to people in the past. Most of these diseases work in the same basic way — lots of people inherit one copy of the defective gene and gain protection against something in the environment with little downside. Unfortunately, a few people inherit two copies of the defective gene and end up suffering from a full blown genetic disease.

Cystic Fibrosis: The mutation that causes cystic fibrosis causes your body to retain salt from the gut. Inheriting one copy of the mutated gene provides protection against cholera, a bacteria that is contracted by drinking contaminated water and that causes your gastrointestinal system to waste salt which results in profuse diarrhea. Cholera killed millions upon millions of people in Europe during the 19th century and this terrible disease recently reared its ugly head in the Western Hemisphere when Nepalese U.N. Peacekeepers inadvertently carried cholera with them to Haiti during their earthquake relief mission, unfortunately causing a deadly epidemic in the worst possible place at the worst possible time. While having one copy of the cystic fibrosis gene protects against “King Cholera” at little cost to the carrier of the defective gene by making the carrier resistant to loss of salt through the gastrointestinal tract, inheriting two copies of this defective gene causes cystic fibrosis, a terrible disease. Patients with cystic fibrosis cannot excrete adequate amounts of salt into their bowels or their airways and, since water follows salt, this results in the accumulation of thick and dry mucus that clogs up the airways and the gut and that causes all sorts of really awful problems, eventually resulting in early death in most cases (although this outlook is slowly improving with advances in medical science).

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This is a cholera clinic in India with patients lined on “cholera cots (cots coated with easily cleanable plastic).” Notice the white buckets below each cot — those are for diarrhea. Cholera is caused by a bacterium that causes profuse diarrhea. Cholera kills its victims by dehydration. This deadly pathogen has been largely eradicated in the developed world due to effective water sanitation efforts.

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A diagram of the effects of cystic fibrosis. Mucus plugs in the lungs provide an excellent habitat for difficult to eradicate bacterial infections, especially by the pathogen Pseudomonas aeruginosa, a bacterium that is notoriously resistant to antibiotics. Patient’s with cystic fibrosis also suffer from mucus plugging in the gastrointestinal tract and this causes a range of complications including potentially fatal pancreatitis.

HIV Resistance: CCR5 is the name of a gene on a group of your white blood cells called CD4+ T cells, and these are the cells that the HIV virus loves to work its mischief inside. Approximately 10% of people of European descent have inherited one mutated copy of the CCR5 gene and these lucky people are resistant to the HIV virus, and thus resistant to getting AIDS even if they are exposed to HIV. People with two copies of the mutated CCR5 gene — about 1% of Europeans — are immune to HIV (as far as we know) and apparently can’t get AIDS even if they are exposed to HIV. The CCR5 mutation is not found in non-European peoples and it is thought that this mutation was selected for hundreds of years ago because it provided some protection against either bubonic plague (“The Black Death”) or smallpox, both of which were major killers in medieval Europe. Since people with the CCR5 mutation were less likely to die from the above said diseases, the gene eventually became widespread in Europe because people dying from smallpox or from bubonic plague (people without the mutation) are a heck of a lot less likely to have children than healthy people for obvious reasons! The downside of having the CCR5 mutation is that it probably weakens immunity to some other infectious diseases, including the West Nile Virus, which is an avian (bird) virus that causes meningoencephalitis (an infection of the brain and its supporting tissues, the meninges) in humans.

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A man dying from AIDS. In and of itself HIV does not typically directly kill its victims. Rather, the HIV virus destroys the immune system and leaves its victim vulnerable to environmental pathogens that people with intact immune systems are able to easily ward off.

So that’s a few more examples of predominantly genetic diseases/mutations that are, at least at times, beneficial on the population level, which is why they are still floating around in our gene pool. While a few select genetic diseases fit into this category, most are simply bad diseases and we’ll discuss the “hows and whys” of these afflictions next time (in English!) — hope that you join us!

Doc’s Fiction!

The Life of a Colonial FugitiveThe Cannabinoid Hypothesis

 

Dr. Leonardo Noto

Physician and Author of Medical School 101, Intrusive Memory, The Life of a Colonial Fugitive, and The Cannabinoid Hypothesis.

NOTE: The Life of a Colonial Fugitive — my dark historical thriller — is free for your ereader at http://www.smashwords.com/books/view/215272. Thanks for reading!

Author Bio: Dr. Leonardo Noto is the nom de plume of a former airborne battalion surgeon who is now in civilian practice. Dr. Noto is the author of four books and he also writes for a medical education corporation that assists medical students, interns, and residents as they prepare for the medical board examinations. Dr. Noto is the proud father of an extremely spoiled 16-month-old American Bulldog who enjoys slobbering everywhere and tearing up things that he is not supposed to! Dr. Noto is an amateur practitioner of muay Thai and Brazilian jiu jitsu and he recently began learning to play the guitar (but he is currently a quite terrible musician, as his neighbors will readily attest).

Remember to discuss all health concerns with your personal physician (I don’t count!) before making any medical decisions. www.leonardonoto.com is intended to present general medical information for entertainment purposes and not as specific guide to any medical treatment. The author has made every effort to present accurate information; however, due to the ever-changing nature of medicine and the intrinsic caveats that are inherent in any particular case, no medical decisions should ever be made based on information gleaned from the internet (duh!). The internet and self-education are great, but they don’t replace your Doc!

The opinions voiced on this medical blog are solely the author’s own and they do not reflect the opinions or values of Dr. Noto’s employers, past or present. Dr. Noto’s medical blogs should never be used as supporting evidence for legal testimony — this is of course obvious to anyone who isn’t a complete moron, but some people are rather stupid.

References:

1. HIV Resistance Via CCR5 Mutation. Stanford at the Tech: http://genetics.thetech.org/original_news/news13

2. Cholera Clinic. Flickr.com. https://www.google.com/search?as_st=y&tbm=isch&hl=en&as_q=cholera&as_epq=&as_oq=&as_eq=&cr=&as_sitesearch=&safe=images&tbs=sur:fc&biw=1366&bih=622&sei=JlUSUt2DKYro2QX-noHYCw#facrc=_&imgdii=_&imgrc=8PiUOA3RqTPBIM%3A%3BZvgjzhUR9-GmxM%3Bhttp%253A%252F%252Ffarm1.staticflickr.com%252F32%252F66832397_c3d1224de7_o.jpg%3Bhttp%253A%252F%252Fwww.flickr.com%252Fphotos%252Fknobil%252F66832397%252F%3B800%3B600

3. Cystic Fibrosis. Children’s Hospital.org. http://www.google.com/imgres?imgurl=&imgrefurl=http%3A%2F%2Fwww.childrenshospital.org%2Faz%2FSite2934%2FmainpageS2934P0.html&h=0&w=0&sz=1&tbnid=ijQWsIiGnCSJJM&tbnh=225&tbnw=225&zoom=1&docid=PRJDSxdx5tiO8M&hl=en&ei=l1USUsL_E-2yygHEyoFQ&ved=0CAEQsCU

4. AIDS Patient. www.gsdmc.com.

What is COPD? On Emphysema, Chronic Bronchitis, and Obstructive Airway Disease.

Chronic obstructive pulmonary disease (COPD) kills 120,000 Americans every year and approximately 25 million Americans have this disease. In comparison, 4,500 Americans died in the entire Iraq War, 30-40,000 die in automobile accidents annually, and 150,000 die from lung cancer every year — the take home message being that this disease is a big deal. In addition to the large numbers of people that COPD outright kills in any given year, the overwhelming majority  of persons living with this disease are at least minimally disabled and many of these unfortunate people are severely disabled. ever seen that guy tugging around an oxygen tank everywhere he goes? Chances are that he has COPD.

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Hopefully she doesn’t still smoke. Quitting smoking is the only intervention that actually slows the inevitable downward spiral of COPD.

COPD is a catchall term that covers two disease processes that were formerly known as emphysema and as chronic bronchitis. Since it turns out that just about everyone who has emphysema also has symptoms that are consistent with chronic bronchitis and vice versa, and since both are caused by the same inciting factor (smoking!), it just makes sense to bundle the disease into one name and to quit confusing everyone!

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Left — the blue bloater. The blue bloater of chronic bronchitis (Note: acute bronchitis is a completely different disease) is obese and constantly hacks up copious amounts of phlegm. He is blue because his body is starving for oxygen. Right — the pink puffer. The pink puffer of emphysema is wasting away because he burns all of his calories trying to breath through his diseased lungs. It is extremely rare to see a patient who actually fits either stereotype — most people with COPD have a combination of these traits.

Normal lungs work by sucking in air and then allowing this inhaled air to come into close contact with blood, which “grabs” ahold of the oxygen in the inhaled air and transports it to the rest of the body. The blood that flows through the blood vessel network in the lungs also dumps off waste gases, especially carbon dioxide, which is then exhaled by the lungs, getting rid of waste gases whilst simultaneously making room for a new breath of oxygen containing new air. The core problem in COPD is inflammation, usually caused by smoking or by chronic exposure to a smoky environment. This inflammation results in destruction of the lungs, causing the formation of large air pockets that trap air. To aid fuel to the fire, the lungs try to protect themselves from the damage caused by inhaling hot smoke by producing copious amounts of mucus. People with COPD end up with giant “holes” (air pockets) in their lungs that don’t properly allow for the proper exchange of oxygen and carbon dioxide between the inhaled air in the lungs and that don’t allow the lungs to efficiently exhale the old air to make room for a new breath — this dysfunction is known as “air trapping.” The mucus that the damaged lungs produce in a vain attempt to protect themselves makes the problem even worse by clogging up the small airways with thick mucus.

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Left — a normal/healthy lung. Right — a lung diseased with COPD.

COPD is a progressive disease and once you have COPD it will get worse over time. The only treatment known to slow the progression (worsening) of COPD is quitting smoking. There are several medications that are useful for treating COPD, but quitting smoking is the only treatment that actually changes the course of the disease.

Types of Medications used in the Treatment of COPD:

1. Oxygen: By increasing the amount of oxygen in the air that someone with COPD inhales, oxygen tanks can somewhat offset the lousy exchange of oxygen between the blood and the COPD-ravaged lungs. The downside is that the patient has to lug around an oxygen tank, which are heavy and also have the potential to explode (e.g. if exposed to a lit cigarette!).

2. Bronchodilators: A quick and very short-acting “fix” for COPD air trapping that have a rapid onset and also rapidly quit working if they are the only treatment being used. Bronchodilators like albuterol work by widening the airways and make it easier for the patient to exhale through their anatomically distorted and mucus plugged bronchioles (small airways).

3. Corticosteroids: These powerful drugs work by decreasing inflammation in the lungs. After quitting smoking, corticosteroids are the cornerstone of effective COPD treatment and can be either inhaled (preferably), taken orally (lots of nasty side-effects), or injected (ditto). The side-effects of corticosteroids include predisposing patient to gastrointestinal bleeds, to fluid retention (some people do a pretty good impression of the StayPuff Marshmellow man when on these drugs), and even to psychosis — most of these potential side-effects are very limited with inhaled corticosteroids and much more common when they are prescribed in the oral or injectable formulations.

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Advair is a combination of an inhaled bronchodilator and an inhaled corticosteroid.

4. Anticholinergics: Inhaled medications that work by both decreasing inflammation (but less than corticosteroids do) in the lungs and by causing bronchodilation (but less than bronchodilators do).

In a nutshell, please consider quitting smoking!

 #MedFacts: A predisposition to storing eaten food as fat probably was evolutionarily beneficial in pre-times — ironically, this body type is now dangerous to your health in a world of plenty!

Doc’s Novels! Just click on the book cover!

The Life of a Colonial FugitiveThe Cannabinoid Hypothesis

Dr. Leonardo Noto

Physician and Author of Medical School 101, Intrusive Memory, The Life of a Colonial Fugitive, and The Cannabinoid Hypothesis.

Author Bio: Dr. Leonardo Noto is the nom de plume of a former airborne battalion surgeon who is now in civilian practice. Dr. Noto is the author of four books and he also writes for a medical education corporation that assists medical students, interns, and residents as they prepare for the medical board examinations. Dr. Noto is the proud father of an extremely spoiled 16-month-old American Bulldog who enjoys slobbering everywhere and tearing up things that he is not supposed to! Dr. Noto is an amateur practitioner of muay Thai and Brazilian jiu jitsu and he recently began learning to play the guitar (but he is currently a quite terrible musician, as his neighbors will readily attest).

Remember to discuss all health concerns with your personal physician (I don’t count!) before making any medical decisions. www.leonardonoto.com is intended to present general medical information for entertainment purposes and not as specific guide to any medical treatment. The author has made every effort to present accurate information; however, due to the ever-changing nature of medicine and the intrinsic caveats that are inherent in any particular case, no medical decisions should ever be made based on information gleaned from the internet (duh!). The internet and self-education are great, but they don’t replace your Doc!

The opinions voiced on this medical blog are solely the author’s own and they do not reflect the opinions or values of Dr. Noto’s employers, past or present. Dr. Noto’s medical blogs should never be used as supporting evidence for legal testimony — this is of course obvious to anyone who isn’t a complete moron, but some people are rather stupid.

References:

1.The National Institutes of Health:  http://www.nhlbi.nih.gov/health/public/lung/copd/campaign-materials/html/copd-atrisk.htm

Lady with an Oxygen Tank — Courtesy of Flickr.com: https://www.google.com/search?as_st=y&tbm=isch&hl=en&as_q=COPD&as_epq=&as_oq=&as_eq=&cr=&as_sitesearch=&safe=images&tbs=sur:fc&biw=1109&bih=552&sei=8QsNUqK7KYfP2QWK4oHoBQ#as_st=y&bav=on.2,or.r_qf.&fp=ff81f272d7d29692&hl=en&q=oxygen+tank+smoking&sa=1&tbm=isch&tbs=sur:fc&facrc=_&imgdii=_&imgrc=2tpTUU9WpZliRM%3A%3B2t5tKnOAISbkUM%3Bhttp%253A%252F%252Ffarm4.staticflickr.com%252F3188%252F3067282492_72968a122a_o.jpg%3Bhttp%253A%252F%252Fwww.flickr.com%252Fphotos%252Fchrstphre%252F3067282492%252F%3B2448%3B3264

COPD Lung — Courtesy of Flickr.com: https://www.google.com/search?as_st=y&tbm=isch&hl=en&as_q=COPD&as_epq=&as_oq=&as_eq=&cr=&as_sitesearch=&safe=images&tbs=sur:fc&biw=1109&bih=552&sei=8QsNUqK7KYfP2QWK4oHoBQ#as_st=y&bav=on.2,or.r_qf.&fp=ff81f272d7d29692&hl=en&q=COPD&sa=1&tbm=isch&tbs=sur:fc&facrc=_&imgdii=_&imgrc=xULziWdbzXyd7M%3A%3BmhQbILXJvRyI4M%3Bhttp%253A%252F%252Ffarm4.staticflickr.com%252F3507%252F4563270966_37970c937f_o.jpg%3Bhttp%253A%252F%252Fwww.flickr.com%252Fphotos%252Fpulmonary_pathology%252F4563270966%252F%3B2069%3B1367

Pink Puffer/Blue Bloater: http://www.google.com/imgres?imgurl=&imgrefurl=http%3A%2F%2Fnakisarin.livejournal.com%2F&h=0&w=0&sz=1&tbnid=CKq57JzBHdsxXM&tbnh=194&tbnw=260&zoom=1&docid=2boT4gr1NTT0mM&hl=en&ei=Kw4NUoORIIisyAHP24HACw&ved=0CAMQsCU

Normal Lung: http://www.google.com/imgres?imgurl=&imgrefurl=http%3A%2F%2Fcal.vet.upenn.edu%2Fprojects%2Flgcardiac%2Fnormal_cases%2Fequine_normals%2Fpost_mortem%2Fpmortem_8.htm&h=0&w=0&sz=1&tbnid=NNzLncAT3J_izM&tbnh=184&tbnw=274&zoom=1&docid=bfYarPzifhn0oM&hl=en&ei=dw4NUpydGaXiyAGUloG4AQ&ved=0CAIQsCU

Advair Inhaler: http://www.google.com/imgres?imgurl=&imgrefurl=https%3A%2F%2Fhealthy.kaiserpermanente.org%2Fhealth%2Fcare%2F!ut%2Fp%2Fc4%2FHYvRCsIwDEW_qASnA9mb3zBE68sIaayBJinVCf79VrlP99xz4QF7DL-S8SNuWOAOUTkJiXEQe3rT_zKltubARj8qXncB4da_xQkLQ2QL67sDSRCHcTwNh95qw6wI0TwQ0othZluuM1TV81GXywbp7iCt%2F&h=0&w=0&sz=1&tbnid=AEH-kEAnKwuU_M&tbnh=172&tbnw=230&zoom=1&docid=ZxTd_wbreJjFmM&hl=en&ei=wQ4NUrTIHuPkyQHFuIDQDg&ved=0CAIQsCU

The World Until Yesterday — By Jared Diamond. This great book jogged my memory about the topic of my #MedFact above and it also served as a great reference for my last blog post. http://www.amazon.com/The-World-Until-Yesterday-Traditional/dp/0670024813

How do you Become a Doctor?

Don’t worry, I’m still in the world of the living — I’ve just been working really long hours as of late and it’s hard to find time to blog when you’re having trouble finding time for basic body functions like eating and sleeping! But enough of my griping, let’s get back into the swing of things by quickly going over a topic that I personally know very well — How the heck did my doctor become a doctor?

Medical training consists of three to four distinct phases: Undergraduate, Doctoral, and Postgraduate Training. Some docs also go through a fourth phase of training called a “Fellowship.” Let’s walk through the process by following the career of “Premed Priss,” our stereotypical doctor wannabe — and yes, since the majority of blooming doctors are now female our stereotype is both politically and factually correct.

Undergraduate Training:

This is just college with a premed twist. Premed Priss majors in whatever she wants to while simultaneously also taking the “premed core” classes — General Chemistry, Biology, Organic Chemistry, and Physics. These four classes provide a good background in the basic sciences that Premed Priss will need in order to understand her medical school classes and to score a high enough mark on the dreaded “MCAT” (Medical Colleges Admissions Test) to actually get her foot in the door. Unfortunately for Premed Priss, her chances of getting accepted into a medical school are not very high (on average). Most premeds bomb out of the core classes before they ever think about taking the MCAT and even folks who make it far enough to duke it out with the MCAT exam have a less than 50% chance of getting accepted into a school (Probably much less than 50%. It’s hard to come by accurate figures, but the overwhelming majority of freshman premed students don’t ever become a doctor.).

Doctoral Training:

Medical school takes four years to complete and it is divided equally into a two year “didactic” (classroom and laboratory learning) period that is followed by two years of rotations (essentially a clinical apprenticeship in the hospital). Most premeds who are lucky enough to become medical students end up graduating from medical school (>90%). That’s the good news. The bad news is that most of them can also plan on hating their life for at least the next seven years. The hours that the average medical student works would make most slavedrivers blush and it only gets worse during postgraduate training. Medical school is also unfortunately cutthroat and postgraduate training (“residency”) is the reason why. Some specialties and residencies are extremely competitive, like orthopedic surgery, and since just about all medical schools grade there students on a curve there is a huge incentive to screw your buddies.

Postgraduate Training:

The last year of medical school consists of “audition rotations” and of applying for a residency. Residency “matches” are announced at a big ceremony at most schools and even the students who don’t “match” have to show up for it — sort of like pouring salt into a wound while everyone is staring at you! Just about all medical students eventually land a residency one way or another and that’s a very good thing because the average medical student is several 100K in debt by the time they graduate and they aren’t employable despite the fact that they are officially doctors now! In order to get a medical license, that precious document that allows a doctor to actually ply their trade, they have to complete at least one year of residency — the intern year. The intern year was until recently the hardest year of postgraduate training, a year full of 80+ hour work weeks and 30hr calls with no sleep. Unfortunately these pesky little interns kept doing stupid things, like accidentally killing patients or slamming their cars into the walls of overpasses after falling asleep at the wheel. The good news is that The-Powers-That-Be developed a brillant solution to this dilemma — restricting intern work hours and passing on the workload to senior residents so that they’re now the who are having the accidents!

While a doctor is officially employable after completing their internship and getting their medical license, the reality is that unless you want to work in flyover country or as a physician for the military you have to finish residency training to land a job. Residency postgraduate training last 3-7 years depending on the medical specialty and many specialties require a 2-3 year fellowship after residency before you can actually practice.

So in grand total, here is how long it takes to become a physician (a few examples, listed by specialty):

1. Family Medicine/General Internal Medicine/General Pediatrics: 11 years — 4 yrs of college, 4 yrs of medical school, 1 yr of internship, 2 yrs of residency.

2. Cardiology (a subspecialty of Internal Medicine): 14 years — 4 yrs of college, 4 yrs of medical school, 1 yr of internship, 2 yrs of residency, 3 yrs of fellowship training.

3. Neurosurgery: 15 years — 4 yrs of college, 4 yrs of medical school, 1 yr of internship, 6 yrs of residency.

My guide to medical school (click on the book cover below) is on sale! $0.99 for Kindle and ~$5 in paperback!

Medical School 101

Dr. Leonardo Noto

Physician and Author of Medical School 101, Intrusive Memory, The Life of a Colonial Fugitive, and The Cannabinoid Hypothesis.

Author Bio: Dr. Leonardo Noto is the nom de plume of a former airborne battalion surgeon who is now in civilian practice. Dr. Noto is the author of four books and he also writes for a medical education corporation that assists medical students, interns, and residents as they prepare for the medical board examinations. Dr. Noto is the proud father of an extremely spoiled 16-month-old American Bulldog who enjoys slobbering everywhere and tearing up things that he is not supposed to! Dr. Noto is an amateur practitioner of muay Thai and Brazilian jiu jitsu and he recently began learning to play the guitar (but he is currently a quite terrible musician, as his neighbors will readily attest).

Remember to discuss all health concerns with your personal physician (I don’t count!) before making any medical decisions. www.leonardonoto.com is intended to present general medical information for entertainment purposes and not as specific guide to any medical treatment. The author has made every effort to present accurate information; however, due to the ever-changing nature of medicine and the intrinsic caveats that are inherent in any particular case, no medical decisions should ever be made based on information gleaned from the internet (duh!). The internet and self-education are great, but they don’t replace your Doc!

The opinions voiced on this medical blog are solely the author’s own and they do not reflect the opinions or values of Dr. Noto’s employers, past or present. Dr. Noto’s medical blogs should never be used as supporting evidence for legal testimony — this is of course obvious to anyone who isn’t a complete moron, but some people are rather stupid.