Human Anatomy at Colby

Calvin Robbins: My Celiac Disease Story

February 24th, 2015 · Comments Off on Calvin Robbins: My Celiac Disease Story

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Every year, the BI 265 Jan Plan class holds student run Grand Rounds presentations. A Grand Round presentation is usually done by a doctor and patient (or actor) in front of other doctors to educate them of a surprising finding or elusive diagnosis, thereby helping the doctors in attendance better diagnose the problem in the future. This year a group presented about a man who had Celiac disease but presented as a cardiac patient (check out Ari, Danielle, and Laurel’s Grand Rounds presentation on celiac disease). It inspired me to tell my own story of being diagnosed with Celiac disease.

When I was 10 years old, I started to notice that when I coughed, there were small specks of blood in the mucous. Originally this was dismissed as an issue with dry air, as it was winter at the time, but as time passed, it was recognized as a larger problem.

The obvious assumption was a respiratory issue, so I had X-rays done which showed a very mild case of pneumonia. Soon the Pneumonia was treated but the blood in the mucous remained. Next came a series of blood tests, consultations, more blood tests, MRIs, X-rays, and still more blood tests, of which the only result was slight anemia. Guesses ranged from Acute Interstitial Pneumonia to tuberculosis to cancer, to a stomach ulcer, but every test came back negative. Doctors wanted to do a lung biopsy to check for AIP but my parents elected to wait for the Celiac results as a lung biopsy is invasive, carries a high risk of infection and would have had a long recovery period for an active 10 year old.

Finally, after about 3 months into an attempted diagnosis, a blood test was performed to test for Celiac Disease. The test was positive. An endoscopy was performed to verify Celiac Disease, as blood tests are not 100% accurate. The doctors discovered an abnormality in the small intestine: the villi were heavily flattened. Given this new insight, and after about a month of a gluten free diet, the blood speckling disappeared.

Celiac Disease is a genetic disease in which the body has an immune reaction to the presence of gluten, a protein found in wheat, rye, and barley. After blood testing it was found that my father and sister, who was asymptomatic, both have Celiac Disease, while my mother does not. From my family you might guess that it is recessive, but the actual inheritance mechanism is still unknown. Worldwide, it is estimated that about 1% of people are diagnosed with Celiac disease while most people with Celiac Disease actually remained undiagnosed.

Sticking with the theme of Grand Rounds, my case was actually presented as a Grand Rounds discussion by Dr. Andrew Filderman once the diagnosis was reached. It is thought that these types of atypical situations go undiagnosed or are improperly diagnosed most of the time they are presented, so spreading information about Celiac Disease is an important step in providing better care to patients.

Tags: Human Health

Calvin Robbins: Lyme’s Disease

February 23rd, 2015 · Comments Off on Calvin Robbins: Lyme’s Disease

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In the last decade, occurrences of Lyme Disease in Maine have been increasing at shocking rates. Colby is a school with a very outdoor-oriented student body, so information regarding Lyme Disease and its effects on the human body is something that everybody should take the time to look at.

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Maine.gov reference

Lyme Disease is a bacteria based disease which affects several body systems. The bacteria is transferred via the bite from an infected tick, usually (although not always) resulting in a rash in the surrounding area. The classic sign of Lyme disease is this “bull’s eye” shaped rash, although recently many cases have gone undiagnosed as people with a solid rash do not suspect Lyme Disease.

The first stage of the disease is called the Early localize stage, which begins with the rash which can take up to 30 days to appear after being bitten. Early symptoms tend to present similarly to the flu, with fatigue and joint pain being key identifiers.

The next stage, Early Dissemination begins around a week to a few months after the bite. During this stage, the disease spreads from the muscles, joints and skin into the nervous and cardiac systems. Heart problems due to Lyme disease can include blockages and weak heart muscles, thus creating symptoms such as easily induced fatigue that you would expect from poor heart function. Nervous system effects, while relatively rare, are generally serious. Common issues include meningitis and numbness or pain in certain affected nerves. If treated in or before Early Dissemination, the disease generally has no lasting effects. If the disease progresses past Early Dissemination, the patient is likely to experience lasting effects.

The Late Disease is generally many months or years after the bite. The most common symptom at this stage is arthritis of the joints, usually one or both knees.

When Lyme disease is suspected, a simple blood test can confirm Lyme Disease, although they are rarely effective within the first six weeks of the disease, and even after that can often read as a false positive. If the patient is experiencing Late Disease symptoms, they are tested for septic arthritis which presents similarly, but generally with a higher fever. A final decision on this can be achieved with an analysis of the synovial fluid, which, as we learned in BI 265, is produced by the synovial membranes, which line joints. The synovial fluid is used as a lubricant for the joint.

Treatment is relatively simple and consists of a regiment of antibiotics, which are administered via IV in more severe cases. Most patients experience lasting symptoms even after antibiotics have killed the bacteria, these patients often experience joint pain and nervous system problems for months after treatment. For patients with severe joint swelling, a synovectomy (removal of a portion of the synovium from the damaged joint) is recommended to ease some of the pain.

Fortunately, this is a very easily preventable disease. When you go outside, make sure you cover your lower extremities by wearing pants. On top of this you can also use tick repellants to deter ticks from even getting on you to begin with. At the end of any outdoor activity, make sure to check all areas of the body (especially inside joints and other warm moist places). If you ever find a tick attached to you, carefully remove it with tweezers and continue to monitor the area of the bite over the course of the next few weeks. There is no vaccine for Lyme Disease so the best way to prevent it is to be aware of the signs and symptoms and to avoid tick exposure in the first place.

Tags: Human Health

Calvin Robbins: The Science Behind Run Til You Puke

February 23rd, 2015 · Comments Off on Calvin Robbins: The Science Behind Run Til You Puke

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Have you ever heard of somebody exercising to the point of vomiting? Or have you done it yourself? I never have, but during the digestive system lecture of the BI 265 Human Anatomy and Physiology class this Jan plan I had a sudden realization as to why this happens.

While nausea may be a common feeling when working out due to food or liquids in the stomach being bounced around, that is not usually why we actually end up vomiting during hard exercise. In fact, one of the biggest causes starts with the respiratory system. The job of the respiratory system is to remove CO2 from the blood and replace it with O2. During exercise, cells produce CO2 as sugars are broken apart to make ATP, which the cell uses for energy. Some of the CO2 byproduct goes into the blood and attaches to hemoglobin, but the vast majority of CO2 is actually transported as carbonic acid, which induces respiratory acidosis. When a person is doing anaerobic activity, such as running at full speed for a long enough time, their lungs are unable to get all of this accumulating CO2 and carbonic acid out of the bloodstream thus creating increasingly acidic blood. It is not due solely to lactic acid as many people believe, but the inability to exchange enough gas in the lungs.

As the blood gets increasingly acidic, the body has to find a way to get rid of all of this acid. One of the main ways the body has of releasing acid, as you may have already guessed, is through vomiting. As you vomit, the hydrochloric acid used for digestion is expelled from the stomach, which is lined with highly vascularized rugae. As the acid is forced out of the stomach, the acidic contents of the blood are pulled out to replace the Hydrochloric acid that was lost from vomit. Following the same thought process, this is why excessive puking will produce alkalosis (high pH) in the blood.

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If you vomit frequently after heavy exercise you should take a few steps to achieve a healthier and more beneficial workout:

  1. Base your workouts on a heart rate range.  This will force you to stay within a set range for aerobic exercise, which can be roughly calculated based on your age. Usually 85% of max heart rate is the highest you should be going for an aerobic workout to prevent acidosis.
  2. Drink plenty of water; if you are vomiting due to dehydration, it is a much more severe issue than acidosis. Steadily drinking water before, during, and after exercise will help, as well as a small amount of sports drink to replace some of the ions lost during the work out.

It takes a lot of anaerobic exercise for the body to get to the point of vomiting. This kind of activity, contrary to what some may think, is very bad for your body, and is not something to strive for in a hard workout. Remember to drink plenty of water and keep a reasonable heart rate target in mind for a healthy and effective workout.

Tags: Human Health · Lab · Special Activities

Grand Rounds: Postpartum Coronary Artery Dissection

January 28th, 2015 · Comments Off on Grand Rounds: Postpartum Coronary Artery Dissection

Lauren Shirley, Allison O’Connor, Cal Robbins

Grand Rounds Synopsis

Case 28-2010 A 32-Year-Old, 3 Weeks Postpartum with Substernal Chest Pain

Grand Rounds Case Presentation powerpoint pdf

Onset

A 32-year old woman had an uncomplicated, spontaneous vaginal delivery after 39 weeks of gestation. This was the patient’s second pregnancy. During her first pregnancy, she was diagnosed with preeclamptic toxemia which was treated with magnesium sulfate. Mild hypertension (systolic 120-140 mm Hg) was reported during the first and third trimesters of her second pregnancy followed by a return to normal blood pressure. Upon delivery, it was noted that her placenta weighed 340 g (below the fifth percentile for gestational age, mean 540 g) with increased amounts of perivillous fibrin (suggesting placental ischemia- lack of blood and thus oxygen and glucose to tissue).

The patient was admitted three weeks post partum when she developed pain in the left jaw and substernal area. The patient called EMS and was given oxygen which resolved her symptoms after 20 minutes and EMS personnel left. The pain returned shortly and EMS returned whereupon the pt scored her pain as a 7 out of 10. Blood pressure was noted as 148/74 and an electrocardiogram (ECG) revealed normal sinus rhythm of 90-100 bpm and ST-segment elevation of 4 mm in leads V2 and V3 (Abnormalities in ECG). Oxygen, acetyl-salicylic acid, nitroglycerin and morphine were administered. When examined at the hospital, the pt’s blood pressure was 143/92 mm Hg in her left arm and 137/81 mm Hg in her right arm with a pulse of 83-92 bpm.

Diagnosis

With a chief complaint of chest pain the patient could have been experiencing cardiovascular, pulmonary, gastrointestinal or musculoskeletal complications. Since the patient was 32 years old, cardiovascular complications would seem unlikely, however, since the patient was three weeks postpartum cardiovascular complications need to be considered more carefully since the risk of acute myocardial infarction is increased during pregnancy and the postpartum period and since pregnancy is a risk factor for aortic dissection. The risk of pulmonary embolism (a blockage of an artery in the lungs) is also increased during the postpartum period.

Since the patient’s ECG showed ST-segment elevation in conjunction with chest pain, an acute myocardial infarction would be suspected. Approximately 35% of postpartum women who present with myocardial infarction have a coronary artery dissection. There are two main types of coronary artery dissections, those that are caused by mechanical precipitation and those that are spontaneous. A spontaneous dissection is a tear in the artery where the tunica media and tunica externa separate, allowing blood to pool in between these layers. SCAD are rare, however 75% of patients who present with spontaneous aortic dissections are women and 30%  of those women are peripartum, suggesting that this patient’s coronary artery dissection was spontaneous. There are four subgroups of spontaneous coronary artery dissections, however peripartum status and idiopathic spontaneous coronary-artery dissections or those caused by coronary shear stress are the two subgroups relevant to this case. Since the chest pain began after the patient picked up her toddler, there is a high index of suspicion that this dissection may have been caused by the patient’s peripartum status and coronary shear stress caused by lifting her toddler. Angiographic projections showed 35mm long segment of narrowing in the left anterior descending coronary artery.  The lack of vascular disease in other coronary arteries along with the patient’s postpartum status as well as her test results are consistent with the diagnosis of a postpartum coronary-artery dissection.

Treatment Options

Unlike aortic dissections, the usual chest pain drugs (asprin, nitroglycerin, etc) which thin the blood can actually help, keeping the true lamen patent. Beta-blockers and nitrates are often used to prevent superimposed vapospasm.  In cases of myocardial ischemia or compromised coronary flow, reperfusion therapy is used.  In patients with severe ischemia, coronary-artery bypass  grafting is done. In this case, the patient was given an intra aortic balloon pump which helps to increase myocardial oxygen supply by being placed in the aorta where it inflates and decreases based on the heart beat.  Since the patient had no pain and the Percutaneous Coronary Intervention could have entered the false lumen, and since coronary dissections can heal by themselves, the balloon pump makes the most sense.  This increased blood flow to the coronary artery.  Aspirin as an antiplatelet, ß-blockers, and statins were used in case of intramural hematoma in the coronary vessel.  Because of the potential for emergency cardiac surgery, the patient was not given glycoprotein IIb/IIIa inhibitors.

 

After 2 days a significant improvement was noted, the pump was terminated, and since surgery was now unlikely, glycoprotein inhibitors were initiated  for a minor myocardial infarction discovered during treatment of the aortic dissection. This would be discontinued in a year, while aspirin was recommended indefinitely. The patient was able to return to her normal life with no further complications.

 

Little evidence exist in terms of the cause of spontaneous coronary artery dissections, but the current theory is that  inflammation is caused by hormones, which explains the prevalence in post partum women.  Several studies also included women taking oral contraceptives as being at risk for coronary artery dissections.  The eosinophils release the histolytic agents between the tunica media and the tunica adventitia, which cause dissections in coronary arteries.

 

References

  1. Sabatine, Marc S., Farouc A. Jaffer, Paul N. Statts, and James R. Stone. “Case 28-2010: A 32-Year-Old Woman, 3 Weeks Post Partum, with Substernal Chest Pain.”The New England Journal of Medicine (2010): n. pag. Web.
  2. James, A. H. “Acute Myocardial Infarction in Pregnancy: A United States Population-Based Study.” Circulation 113.12 (2006): 1564-571. Web.
  3. Koul, Ashok K., Gerald Hollander, Norbert Moskovits, Robert Frankel, Leo Herrera, and Jacob Shani. “Coronary Artery Dissection during Pregnancy and the Postpartum Period: Two Case Reports and Review of Literature.” Catheterization and Cardiovascular Interventions 52.1 (2001): 88-94. Web.
  4. Mcintyre-Spatar, Leslie, and Kevin H. Silver. “Spontaneous Coronary Artery Dissection in a Postpartum Woman: Literature Review.” The Journal for Nurse Practitioners 7.9 (2011): 770-73.
  5. Oliveira Marta Silvia, Goncalves Alexandra, Dias Paula, Maciel Júlia Maria. “Spontaneous Coronary Artery Dissection: a Diagnosis to consider in Acute Coronary Artery Syndromes” Artigos de Revisão. (2009): 28 (6): 707-713
  6. Heart Assist Devices. Texas Heart Institute, 2015. (Accessed January 20, 2015 at http://www.texasheart.org/Research/Devices/iabp.cfm)
  7. CBC. MedlinePlus, 2015. (Accessed Janury 25, 2015 at http://www.nlm.nih.gov/medlineplus/ency/article/003642.htm)
  8. Placental Pathology. University of Chicago. (Accessed January 20, 2015 at https://pathology.uchicago.edu/sites/pathology.uchicago.edu/files/uploads/PDFs/Placental%20Pathology%20Notes%20Aspen%202014%20-Fritsch%20final.pdf)
  9. Electrolytes. AACC, 2013. (Accessed January 25, 2015 at http://labtestsonline.org/understanding/analytes/electrolytes/tab/test/)
  10. CK-MB. AACC, 2013. (Accessed January 25, 2015 at http://labtestsonline.org/understanding/analytes/ckmb/tab/sample/)

 

Tags: Grand Rounds