April 14th, 2012
medicaljourney
From The Human Body and Health by Alvin Davison, published in 1908

From The Human Body and Health by Alvin Davison, published in 1908

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anatomy vintage medicine Neuroscience science Physiology
April 14th, 2012
medicaljourney
“Pre-med students become accustomed to waiting for an uncertain payoff, especially while painstakingly running experiments and analyzing results. They have all waited for something to grow in a beaker or for a centrifuge to slow down before removing the tubes; patiently titrated solutions in the chemistry lab; waited for bacteria to incubate, DNA strands to replicate, or proteins to migrate across a polarized gel. Clever management of time and a high threshold for frustration accompany such pursuits. In fact, the entire protracted course of medical training entails persistence, or what psychiatrists lightheartedly refer to as ‘stick-to-it-iveness’” -Dr. Jeremy Spiegel, The Mindful Medical Student *I highly recommend this book for anyone who is pursuing medicine. It’s a great read and provides many strategies for the challenges that pre-medical and medical students face.

“Pre-med students become accustomed to waiting for an uncertain payoff, especially while painstakingly running experiments and analyzing results. They have all waited for something to grow in a beaker or for a centrifuge to slow down before removing the tubes; patiently titrated solutions in the chemistry lab; waited for bacteria to incubate, DNA strands to replicate, or proteins to migrate across a polarized gel. Clever management of time and a high threshold for frustration accompany such pursuits. In fact, the entire protracted course of medical training entails persistence, or what psychiatrists lightheartedly refer to as ‘stick-to-it-iveness’”

-Dr. Jeremy Spiegel, The Mindful Medical Student

*I highly recommend this book for anyone who is pursuing medicine. It’s a great read and provides many strategies for the challenges that pre-medical and medical students face.

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April 14th, 2012
medicaljourney
Zoom All day, every day (Taken with instagram)

All day, every day

(Taken with instagram)

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pre-med premed science
April 14th, 2012
medicaljourney

Reflections from clinic

At my clinic session today, the clinic was extremely busy and I was able to see many patients by shadowing pre-clinical students in triage and then following clinical students through the physical exam. I learned many new things from this clinic session, particularly about tuberculosis and non-Hodgkin lymphomas. One of the first patients triaged came in with a positive PPD test, which is a diagnostic tool for tuberculosis. The patient recently had a chest X ray that showed nodules, called tuberculomas, which are abnormal findings and can suggest tuberculosis. This was not the patient’s first positive PPD, she had one a few years ago and was going to begin treatment when she became pregnant and had to postpone treatment due to her pregnancy. She came to the clinic for treatment and also to have her chest X ray analyzed and explained to her because that was not done at the hospital where the radiology was performed. The patient was also at high risk as many of her family members had tuberculosis and a few had passed away from the disease. I learned a lot about tuberculosis from the attending physician and the pre-clinical and clinical students I shadowed. Tuberculosis is caused by mycobacterium, which normally attacks the lungs, but can also spread to other organs; it is spread through the air when an infected individual sneezes or coughs and saliva is transmitted. The infection can stay dormant for many years, but occasionally reactivates. Symptoms include cough, particularly coughing up mucus or blood, night sweats, weight loss, fever, fatigue, difficulty breathing and chest pain. The patient we saw had a number of these symptoms, including a chronic cough, night sweats, fatigue and difficulty breathing. The general treatment for TB uses antibiotics, often a combination of four antibiotics. The patient seemed very comfortable and appreciative of the care she received at HOME as she stated she did not receive that level of care when she went to the hospital.     

Another patient who had non-Hodgkin lymphoma came in for a follow up and phlebotomy. I shadowed pre-clinical students in triaging this patient. After the patient was triaged, I had some questions about Non-Hodgkin lymphoma and was given a quick lecture that I gained a lot of knowledge from. I learned about the distinction between non-Hodgkin (NHLs) and Hodgkin’s lymphomas – while they are both lymphomas, which is cancer involving white blood cells called lymphocytes, they each involve different specific lymphocytes. When a biopsy is taken and examined by a pathologist, if an abnormal cell called a Reed-Sternberg cell is present then it is classified as Hodgkin’s lymphoma, but if Reed-Sternberg cells are absent then it is non-Hodgkin’s. I learned that this is very important because these lymphomas have different treatments and general outcomes.      

After spending some more time shadowing preclinical students, I shadowed a clinical student performing a physical exam. It was suspected that the patient had a thyroid condition. The patient had symptoms of hypothyroidism including weight gain, dry skin, fatigue and cold intolerance. The clinical student had to draw blood for the thyroid function test, which is called TSH. She went through the steps involved in drawing blood with the standard venepuncture procedure so I could learn how blood is drawn. When the attending physician came in to examine the patient, she spent a lot of time discussing lifestyle changes with him. This was important as he was at risk for a number of diseases in which preventative lifestyle changes are vital. Some recommendations she had included increasing physical activity, adopting a new eating plan and reducing sodium consumption. These recommendations were presented in a respectful and empathetic way that made the patient feel comfortable and motivated.

5 notes
premed personal
February 18th, 2012
medicaljourney
great blog! I'm considering applying to pre-med post bacc programs and was wondering how long on average do they take to complete? thanks
Anonymous

How long it will take you to complete a post-bacc program depends on a few different factors such as how many pre-reqs you need to take. For example, some post-bacc students did not take any science or math courses in college, while other post-bacc students may have already taken certain courses. Another factor is how many courses you plan to take each semester - some people take a full course load and others may have to work full time and go to school part time. It also depends on whether or not you plan to only take the minimum pre-req coursework or if you plan to take some upper level science courses as well. Most of the people I’ve met in my program at Stony Brook take between 1 1/2 years to 2 1/2 years - although I also know someone who took only 1 year and another person who is taking ~3 years.

Thanks and good luck!

questions ask
February 18th, 2012
medicaljourney
Dr. Leonard Laster, Life After Medical School: Thirty-Two Doctors Describe How They Shaped Their Medical Careers

Dr. Leonard Laster, Life After Medical School: Thirty-Two Doctors Describe How They Shaped Their Medical Careers

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February 18th, 2012
medicaljourney

As part of my clinical education program at Stony Brook Health Outreach and Medical Education (HOME), after every clinic session we write a reflection about our experience. This is what I wrote after my very first session at the clinic, around late November or early December of last year:

On the first day of clinic, I woke up feeling excited and energized in anticipation of what I would learn and do that day. Upon arriving at clinic and meeting the Stony Brook medical students and attending physicians working that day, I felt fortunate to be contributing to this remarkable team. There is a very genuine and powerful sense of camaraderie amongst these students and doctors who teach and support one another and spend perhaps the only day they have off helping those who are underserved and in need of medical care. Early that day, a patient stopped by with homemade sweets for the staff and showed such an appreciation for the health services she received from Stony Brook HOME – a telling gesture.

It was not long before the clinic became very busy as the waiting room filled with patients. I began by shadowing preclinical students in triaging patients. During triage I learned about the primary four vital signs – blood pressure, heart rate (pulse), respiratory rate, and body temperature. I learned how and why these measurements are taken and how to interpret the readings. For example, I learned when measuring blood pressure that a systolic pressure, which is the contraction of the heart, that is persistently over 140-160 mmHg indicates hypertension. I also learned the differences between hypertensive urgency, hypertensive emergency and hypertensive crisis. This information proved very valuable when I later went to the comprehensive lecture on hypertension. Triaging patients also involved determining the reason for the visit and if the patient was experiencing any pain. In addition to the primary four vital signs, height and weight were measured and used to calculate BMI.     

After the patients were triaged, I shadowed clinical students who performed physical exams. I learned how a thorough physical exam is performed. One aspect of this was the diabetic foot screen, which was vital as some patients had type 2 diabetes. Some patients also had hypertension, or were at high risk for developing hypertension, so checking for identifiable causes of hypertension and other cardiovascular risk factors was very important. Discussing therapeutic lifestyle changes with these patients was another aspect of the comprehensive physical exam. The physical exam also involved taking social and family history. I learned that most patients had not received any medical care in years.

The clinical students then gave case presentations to the attending physicians. Case presentations involved going over the reasons for the visit, the patients’ chief complaints, past medical and surgical history, current medications and allergies, family and social history, the results of the physical exam and any labs that were taken. In their case summaries, the clinical students gave their impressions and outlined plans for treatment, management and follow up. The attending physicians asked questions, provided their input and then performed their own exams on the patients and discussed medication and treatment options. From this experience I learned the principles of differential diagnosis. I also learned how certain diagnostic tests are interpreted, such as the fasting plasma glucose (FPG) test, which was used to diagnose a patient with diabetes.     

My first experience at Stony Brook HOME provided me with new insights into how medicine is practiced and it also further solidified my belief that medicine is the path for me. The work at Stony Brook HOME is fundamentally what practicing medicine is all about – committed individuals working together to provide compassionate and competent care to those in need.

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February 18th, 2012
medicaljourney
The fundamental tool of science is doubt
Professor Paul Bingham
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February 18th, 2012
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Zoom Most human tumors, about 90%, are of epithelial origin. Cancers that are derived from epithelial cells are carcinomas. Epithelial cells are found in many tissues and organs and they are a sheet-like lining that can serve a number of functions including secretion, protection, absorption and permeability.   Epithelial cells sit on top of a structure called the basement membrane or basal lamina. Under the basement membrane/basal lamina is the mass of tissue called the stroma. The basal lamina is part of the ECM. The stroma or mesenchyme (connective tissue) provides strength through fibrous proteins called collagens. The cells that produce collagen and are found in the stroma/connective tissue are fibroblasts.   Epithelial cells are in very close contact with each other. The space between them contains several junctions, including tight junctions that seal the space between the cells to prevent leakage. In addition, adherens junctions and desmosomes also bind epithelial cells to one another. Both adherens junctions and desmosomes require transmembrane proteins called cadherins. At adherens junctions the cadherins are attached to actin microfilaments of the cytoskeleton. While at the desmosomes, cadherins connect to intermediate filaments such as keratins.   Epithelial cells are also attached to the basal lamina (ECM layer) by transmembrane proteins that are attached to the cytoskeleton called integrins.   This is very important in understanding what makes cancer cells invasive and metastatic. Epithelial cells are normally locked into place, sitting on top of the basement membrane and attached to each other by tight junctions, adherens junctions and desmosomes. In order to line the cavity effectively and function they need to be locked into place. For cells to become invasive and metastatic, these anchors have to become dysfunctional.   There are four major types of new tissue growth – Hypertrophy, Hyperplasia, Dysplasia and Neoplasia.   Hypertrophy – An increase in cell size, normal organization Hyperplasia – An increase in cell number, normal organization. Epithelium invades lumen, but not basement membrane or stroma. Cells appear normal in terms of organization, but they are growing when they shouldn’t be growing. Thus they are deregulated in terms of proliferation. Dysplasia – Disorganized growth. Transition between benign and malignant. In addition to there being too many cells, they are disorganized and they don’t look like normal epithelial cells – they are piling up. Neoplasia – Disorganized growth, net increase in the number of dividing cells. The cells are incredibly disorganized and they have broken through the basal lamina and invaded the stroma. These cells are invasive/malignant.  A growth that has stayed within the epithelial compartment is not technically considered cancer, it’s considered to be a benign growth. It becomes cancer/malignant/invasive/neoplastic only when it has broken out of the epithelial zone and invaded the underlying stroma.

Most human tumors, about 90%, are of epithelial origin. Cancers that are derived from epithelial cells are carcinomas. Epithelial cells are found in many tissues and organs and they are a sheet-like lining that can serve a number of functions including secretion, protection, absorption and permeability.  

Epithelial cells sit on top of a structure called the basement membrane or basal lamina. Under the basement membrane/basal lamina is the mass of tissue called the stroma. The basal lamina is part of the ECM. The stroma or mesenchyme (connective tissue) provides strength through fibrous proteins called collagens. The cells that produce collagen and are found in the stroma/connective tissue are fibroblasts.  

Epithelial cells are in very close contact with each other. The space between them contains several junctions, including tight junctions that seal the space between the cells to prevent leakage. In addition, adherens junctions and desmosomes also bind epithelial cells to one another. Both adherens junctions and desmosomes require transmembrane proteins called cadherins. At adherens junctions the cadherins are attached to actin microfilaments of the cytoskeleton. While at the desmosomes, cadherins connect to intermediate filaments such as keratins.  

Epithelial cells are also attached to the basal lamina (ECM layer) by transmembrane proteins that are attached to the cytoskeleton called integrins.  

This is very important in understanding what makes cancer cells invasive and metastatic. Epithelial cells are normally locked into place, sitting on top of the basement membrane and attached to each other by tight junctions, adherens junctions and desmosomes. In order to line the cavity effectively and function they need to be locked into place. For cells to become invasive and metastatic, these anchors have to become dysfunctional.  

There are four major types of new tissue growth – Hypertrophy, Hyperplasia, Dysplasia and Neoplasia.  

Hypertrophy – An increase in cell size, normal organization

Hyperplasia – An increase in cell number, normal organization. Epithelium invades lumen, but not basement membrane or stroma. Cells appear normal in terms of organization, but they are growing when they shouldn’t be growing. Thus they are deregulated in terms of proliferation.

Dysplasia – Disorganized growth. Transition between benign and malignant. In addition to there being too many cells, they are disorganized and they don’t look like normal epithelial cells – they are piling up.

Neoplasia – Disorganized growth, net increase in the number of dividing cells. The cells are incredibly disorganized and they have broken through the basal lamina and invaded the stroma. These cells are invasive/malignant. 

A growth that has stayed within the epithelial compartment is not technically considered cancer, it’s considered to be a benign growth. It becomes cancer/malignant/invasive/neoplastic only when it has broken out of the epithelial zone and invaded the underlying stroma.

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February 2nd, 2012
medicaljourney
Medicine is only for those who cannot imagine doing anything else.
Dr. Luanda Grazette, Doctors’ Diaries
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medicine doctors' diaries Dr. Luanda Grazette quote
January 29th, 2012
medicaljourney
Zoom A few interesting things I’ve learned in my cancer bio course: Tumor Viruses and Cellular Oncogenes: -Tumor viruses have very little to do with human cancer -Human cancers result from non-viral activation of cellular proto-oncogenes -A proto-oncogene is a normal gene that can become an oncogene (a gene that has the potential to cause cancer) as a result of mutations or increased expression -Chemical carcinogenesis vs. tumor virology - 2 schools of thought – chemicals cause cancer vs viruses cause cancer; truth: viruses don’t “cause” human cancers other than a few certain viruses - Study of tumor viruses lead scientists to identify the first oncogenes. The animal tumor viruses that cause cancer don’t cause cancer because of one of the viruses own genes, the viruses don’t have their own oncogenes – what they do is they activate or capture one of the host’s genes (proto-oncogenes) and that’s what makes them cancer causing viruses. - About 100-200 genes in the human genome are proto-oncogenes: these are genes whose normal function is involved in normal regulation of cell growth, cell division, cell signaling, if they are left alone our cells grow normally. Because their normal job has to do with regulating growth, these are the genes that if they are changed in some way (for example, if the protein they encode is mutated or if the gene is over-expressed) that will change the growth properties of the cell. - If a retrovirus (an RNA virus that uses reverse transcriptase to turn their genome into DNA and integrate into the host cell genome) inserts and disrupts, sometimes the virus makes a mistake when it’s copying its own genome, it takes a little bit too much, it runs off and into the oncogene as well. In that way, a virus has “captured” or “kidnapped” a host oncogene and now it has become part of that virus. When that virus goes and infects another cell it has its own viral genes and a host gene, but because all of these genes are being expressed under the control of a strong viral promoter, these genes are being expressed at very high levels. The infected cell now has an oncogene because it was originally a proto-oncogene whose expression has been wildly de-regulated. Cell is not going to regulate its growth properly because an oncogene has been de-regulated. The viruses that cause cancer do so by de-regulating host cell genes (with the exception of cervical cancer/HPV; liver cancer/hepatitis virus). -Chemical carcinogens cause cancer also by damaging and de-regulating the same subset of genes (proto-oncogenes) that can be kidnapped by tumor viruses. Thus both approaches, Chemical carcinogenesis and tumor virology, look at the same small subset of genes that can be de-regulated if they are captured by a virus and wildly over-expressed, or they can be mutated by a chemical carcinogen.  -New working hypothesis: there’s some subset of cellular genes that are normal proto-oncogenes (normal genes involved in growth and regulation) these genes can contribute to cancer either if they are kidnapped by a virus and wildly over-expressed or damaged in some way by chemical mutagens (thus they become oncogenes).

A few interesting things I’ve learned in my cancer bio course:

Tumor Viruses and Cellular Oncogenes:

-Tumor viruses have very little to do with human cancer

-Human cancers result from non-viral activation of cellular proto-oncogenes

-A proto-oncogene is a normal gene that can become an oncogene (a gene that has the potential to cause cancer) as a result of mutations or increased expression

-Chemical carcinogenesis vs. tumor virology - 2 schools of thought – chemicals cause cancer vs viruses cause cancer; truth: viruses don’t “cause” human cancers other than a few certain viruses

- Study of tumor viruses lead scientists to identify the first oncogenes. The animal tumor viruses that cause cancer don’t cause cancer because of one of the viruses own genes, the viruses don’t have their own oncogenes – what they do is they activate or capture one of the host’s genes (proto-oncogenes) and that’s what makes them cancer causing viruses.

- About 100-200 genes in the human genome are proto-oncogenes: these are genes whose normal function is involved in normal regulation of cell growth, cell division, cell signaling, if they are left alone our cells grow normally. Because their normal job has to do with regulating growth, these are the genes that if they are changed in some way (for example, if the protein they encode is mutated or if the gene is over-expressed) that will change the growth properties of the cell.

- If a retrovirus (an RNA virus that uses reverse transcriptase to turn their genome into DNA and integrate into the host cell genome) inserts and disrupts, sometimes the virus makes a mistake when it’s copying its own genome, it takes a little bit too much, it runs off and into the oncogene as well. In that way, a virus has “captured” or “kidnapped” a host oncogene and now it has become part of that virus. When that virus goes and infects another cell it has its own viral genes and a host gene, but because all of these genes are being expressed under the control of a strong viral promoter, these genes are being expressed at very high levels. The infected cell now has an oncogene because it was originally a proto-oncogene whose expression has been wildly de-regulated. Cell is not going to regulate its growth properly because an oncogene has been de-regulated. The viruses that cause cancer do so by de-regulating host cell genes (with the exception of cervical cancer/HPV; liver cancer/hepatitis virus).

-Chemical carcinogens cause cancer also by damaging and de-regulating the same subset of genes (proto-oncogenes) that can be kidnapped by tumor viruses. Thus both approaches, Chemical carcinogenesis and tumor virology, look at the same small subset of genes that can be de-regulated if they are captured by a virus and wildly over-expressed, or they can be mutated by a chemical carcinogen. 

-New working hypothesis: there’s some subset of cellular genes that are normal proto-oncogenes (normal genes involved in growth and regulation) these genes can contribute to cancer either if they are kidnapped by a virus and wildly over-expressed or damaged in some way by chemical mutagens (thus they become oncogenes).

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science cancer biology bio 314 courses premed
January 21st, 2012
medicaljourney
Zoom I got this syringe pen from a med school fair and whenever I use it in class somebody always does a double-take. I also got an eraser in the shape of a doctor wearing a lab coat. If you’re interested in med school, you should definitely try to go to a med school fair. The med school reps are very helpful and you really get a feel for the school by talking to them.

I got this syringe pen from a med school fair and whenever I use it in class somebody always does a double-take. I also got an eraser in the shape of a doctor wearing a lab coat. If you’re interested in med school, you should definitely try to go to a med school fair. The med school reps are very helpful and you really get a feel for the school by talking to them.

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medical school syringe pen personal
January 21st, 2012
medicaljourney
Medicine is not only a science; it is also an art. It does not consist of compounding pills and plasters; it deals with the very processes of life, which must be understood before they may be guided.
Paracelsus
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quote medicine science Paracelsus
January 21st, 2012
medicaljourney

Notes from Bio 208

Headaches:

sinus (forehead, cheekbones), cluster (around eye), tension (squeezing forehead), migraine (one sided)

Migraine:

-common migraine without aura

-classic migraine with aura

-silent (ocular) migraine – aura without headache

often misclassified as sinus headache

trigger factors: stress, weather changes, estrogen withdrawal, fatigue, sleep disturbance, OTC pain meds

aura – sensation before a migraine (can be visual disturbances, nausea)

trigeminal and cervical nerves of the head/types of headaches:

trigeminal nerve – face – frontal headache, migraine headache

cervical nerves  (c2 and c3) – neck and back of head – occipital headache, meningitis headache with stiff neck

migraine involves the trigeminal vascular system of the face, scalp and brain surface

most headaches caused by muscle contraction, vascular problems or both

phases of migraine:

phase 1 – prodromal phase – food cravings, heightened or dull perceptions, irritability, can occur up to 24 hours before migraine

phase 2 – the aura (visual disturbances, nausea)

phase 3 – the headache (aching, intolerance of light and noise, vomiting, often between 4-72 hours)

ocular migraine – vascular effects in visual cortex

ocular migraine takes place in brain, not eye. Some individuals see a bright light due to projected sensation

ocular migraine caused by electrical activity due to ionic disturbances in brain

prodromal and aura phases

waves of depolarization followed by depression of nerve impulses moving through the visual cortex, resulting in visual dark patches; these waves move toward the frontal cortex, they produce ionic disturbances and vasodilatation

-caused by wave of excitation such as in a seizure

-electrical wave starts in occipital lobe

-as different part of brain is activated (and excitation moves) the visual effects move

early treatment of migraines was vasoconstriction to treat the vasodilation. However the vasodilation is an effect that triggers the neurons, but what causes the vasodilation?

Aura phase – progresses from occipital to frontal

Headache phase – pain progresses from frontal to occipital

-pain centers located in brainstem. Electrical impulses cause abnormally active brain cell and inflamed blood vessels

-vasodilation – this is what causes pain

-serotonin receptors on trigeminal nerve are the target of ergot drugs

headache phase: peptides cause vasodilation and allodynia

-release of neuroinflammatory peptides from the trigeminal vascular system in response to some environmental stimulus

-these peptides cause vasodilation and

-sensitize nerve fibers of the trigeminal that respond to innocuous stimuli like blood vessel pulsing (allodynia) that leads to pain

migraine drugs imitrex/sumatriptan bind to:

1D and 1B 5HT (serotonin) receptors; prevent release of CGRP peptide, therefore no vasodilation

imitrex mimics seratonin which is how it prevents CGRP peptide

CGRP – inflammatory peptide blocked by migraine drugs

During migraine, CGRP peptide is released and binds on blood vessels. This causes blood vessels to vasodilate. This leads to sensitization. Imitrex/sumatripton binds to serotonin receptors, mimic serotonin, prevents the release of peptide - no vasodilation, pain is controlled

Migraine treatment:

Ergot alkaloids vasoconstrict blood vessels

Ergots activate and or inhibit all dopamine, serotonin and norepinephrine receptors

-       serotonin (5HT) is released from blood platelets and is a powerful vasoconstrictor

-       migraine is related to 5hT 1b and 5HT 1d receptors that control capillary blood flow in the brain

-       sumatriptan (imitrex) specific agonist for these receptors, blocks the release of inflammatory CGRP peptides in trigeminal ganglion and prevents vasodilation

-       first designer drug for migraine – 1974

other ergot medical uses:

-Parkinson’s disease – action on dopamine receptors

drugs parolodel and permax can be more effective than L-Dopa

-controls vomiting at 5hT3 receptors in brain: zofran/Ondansetron, used to prevent nausea and vomiting resulting from chemotherapy

-control of postpartum hemorrhage by vasoconstriction

-future in tumor suppression – targeted anoxia by shutting down blood supply

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bio 208 biology headaches medicine migraine courses
January 21st, 2012
medicaljourney
The life of a pre-med student…

The life of a pre-med student…

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personal pre-med books science premed

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I am a student in the postbaccalaureate pre-medical program at Stony Brook University. This blog chronicles my journey through my pre-med program and beyond. I plan to continue this blog throughout med school.

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