By: BigFudge
Breast cancer organizations in the United States receive more funding than any other disease,
despite the fact that Heart Disease is the number one killer in the United States. Heart Disease
kills more than ten times as many people as breast cancer, while breast cancer organizations
receive about 5 times the amount of funding compared to heart disease (6). One fatal result of
heart disease is a heart attack, which the medical community calls a myocardial infarction (MI).
Many have heard of a heart attack, but a large proportion of them do not know exactly what they
are.
To understand what is going on in a heart attack, we need to understand the basics of the heart in normal situation. The heart pumps the blood around the body, bringing nutrients and oxygen to
all the cells in your body. Because the cells can’t use any nutrients from the blood on the inside
being pumped, the heart has very specific blood vessels that receive the freshest blood. These
blood vessels go around the heart, making sure it is always supplied with oxygen.
The way the heart pumps blood is very similar to the way one pushes toothpaste out of the tube:
from the bottom of the tube. The only difference is the mechanical action pushes the blood in
the heart from the top to bottom, and then out. As for the actual contraction, the cells use tiny
electrical currents to contract. As the electricity travels top to bottom, the heart contracts, forcing
blood to get pushed out. It is important to know that this electrical current is very organized and
travels and a very specific pattern in healthy individuals. Thus, the blood circulates and the body
and heart is happy.
Understanding a myocardial infarction goes back to the blood vessels surrounding the heart,
because the heart cells cannot receive oxygen from the blood inside being pumped. Before a
heart attack even happens, the blood throughout the body has plaque and fat naturally circulating. If there is too much plaque and fat in the blood, it will deposit on the walls of the vessels, limiting the blood flow through it. Fat and plaque can also stick together and form little balls which can become lodged and cut off blood flow as vessels become narrow, which is called ischemia. An MI is where these fat and plaque deposits cut off blood flow to the blood vessels surrounding the heart, preventing blood from oxygenating the heart tissue. Without the oxygen from the blood, the heart tissue begins to die in the area affected. In severe heart attacks, damage to the heart from ischemia progresses and the electrical conduction, which is normally extremely organized, becomes extremely chaotic. This causes the heart to quiver, rather than rhythmically pumping. Blood stops moving, and the body runs out of oxygen, including more heart tissue. Net result: death.
Signs and symptoms are provided in textbooks, but in reality, they are very diverse and vary
person to person. Most commonly, patients express the following complaints: chest pain which
radiates to other parts of the body, profuse sweating, nausea, vomiting, shortness of breath or
difficulty breathing, and/or abdominal pain. Some show none of these signs, and an MI is
diagnosed by an electrocardiogram or levels of troponin in the blood.
As for treatments, there are anticoagulants like heparin and coumadin, and platelet aggregation
inhibitors like aspirin. Nitroglycerin is commonly prescribed to patients who have a history of
heart problems, and makes the blood vessels bigger which can alleviate the chest pain associated. Antihypertensives like Lisinopril and Amlodipine are showing limited long term benefits (5). Improvements to diet and activity level are important, both to prevent initial and future MI’s. Once an MI is discovered within the hospital, it is critical to get the patient to a catheterization lab, where there are a few options. One option is using blood vessels from elsewhere in the body to replace or redirect the blood flow around the blockage. Another way is to put a stent in, a metal object which forces the vessel wide enough for blood flow. Lastly, they can pass a wire through the blood vessels and destroy the clot mechanically or with chemicals.
According to the American Heart Association, Mayo Clinic, and the National Heart, Lung, and
Blood Association, the best way to prevent an MI is through diet and exercise (1) (3) (4). A
healthy lifestyle may not completely prevent it, especially with a family history of heart disease,
but use of blood thinners is more common to prevent it. Avoiding other risk factors is important
as well, including but not limited to smoking, drinking, stress, and lack of sleep,
Here are some numbers to scare you into making healthier choices. According to the CDC, heart
disease claims over 610,000 victims every year in the United States alone, attributing to over a
quarter of all the deaths in the country. Furthermore, “Every year about 735,000 Americans have
a heart attack. Of these, 525,000 are a first heart attack and 210,000 happen in people who have
already had a heart attack” (2). They go on to note that almost half of the country has at least
one high risk factor for heart disease, such as high blood pressure, high cholesterol, or smoking.
Hopefully by now you get a sense of what a myocardial infarction is, some common signs, and
some treatments. If the numbers of how prevalent didn’t scare you, millions of americans share
the same disposition. Now I recognize that not all have access to the information or the financial
means to necessarily act on this, but that doesn’t mean you can’t use this information to help
your loved ones. I should also note that I am not saying breast cancer shouldn’t receive less, but
merely pointing out the discrepancy in how common the diseases are.
Bibliography
1) American Heart Association. (2014, April). How to Help Prevent Heart Disease At
Any Age. Retrieved February 01, 2016, from http://www.heart.org/HEARTORG/HealthyLiving/HowtoHelpPreventHeartDiseaseAtAnyAge_
UCM_442925_Article.jsp#.VqoFLIrLIU
2) Center for Disease Control. (2015, August 10). Heart Disease Facts. Retrieved February
01, 2016, from http://www.cdc.gov/heartdisease/facts.htm
3) Mayo Clinic. (2014, November 15). Heart attack. Retrieved February 01, 2016, from
http://www.mayoclinic.org/diseasesconditions/heartattack/basics/prevention/con20019520
4) National Heart, Lung, and Blood Institute. (2015, November 6). How Can a Heart Attack
Be Prevented? Retrieved February 01, 2016, from http://www.nhlbi.nih.gov/health/healthtopics/topics/heartattack/prevention
5) Psaty, B. M. (2003). Major outcomes in high-risk hypertensive patients randomized to
angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial
(ALLHAT). American College of Physicians Journal Club, 139 , 7. Retrieved February
11, 2016, from acpjc.acponline.org/Content/139/1/issue/ACPJC20031391007.htm
6) Vox. (2014, August 20). The truth about the Ice Bucket Challenge: Viral memes
shouldn't dictate our charitable giving. Retrieved February 01, 2016, from
http://www.vox.com/2014/8/20/6040435/alsicebucketchallengeandwhywegivetocharitydonate
Wednesday, February 24, 2016
Long QT Syndrome: Scared to Death
By: Pretty Momma
Imagine yourself as the parent of a child. Your hopes and dreams take shape as you see them grow and conquer their fears. You feel success from their successes and when they fall your heart aches to console them. Imagine yourself the parent of a young teenager. You see the frustration in them on a daily basis, trying desperately to cope with expectations, stress, and pressure in a rapidly changing environment, while they themselves are racing to grow into their own shoes. Imagine yourself as a proud, attentive mother of an athletic teenage son nearing the prime of his life. One morning you find that your son has slept in. You call and knock at his door to no response. You open the door, and panic, finding the son you have raised and nurtured, cared for, and disciplined lying lifeless and cold; a result of Sudden Arrhythmia Death Syndrome. Heart conditions such as Long QT Syndrome need to be advocated more for patient education to raise awareness in preventing such sudden deaths.
Long QT syndrome is a condition that affects the heart's rhythm that can cause fast and chaotic heartbeats. The heart can only beat erratically for so long before it causes sudden death. Prolonged QT, “LQTS” can be an inherited dormant error in a person’s genetic code or can be acquired due to certain medications and medical conditions. Inherited LQTS has been associated with 17 genes so far, with hundreds of mutations. Although genetic test can identify those with this disease, it does not pick up 20% of people who do have the disease. A known parent with LQTS has a 50% chance of passing the gene down to their child. LQTS may also be acquired. Acquired LQTS can be caused by certain medications of medical conditions. There are more than 75 medications that are known to lengthen the QT interval causing drug induced Long QT Syndrome (Mayo).
Often LQTS is discovered by accident by being picked up on an ECG. An ECG measures the electrical impulse as they travel through the heart. Long QT syndrome results from abnormalities in the heart’s electrical charging system (Mayo). Imagine each heart muscle has tiny holes called ion
channels. These holes open and close to allow important substances (sodium, calcium and potassium) to flow in and out of the heart muscle cells. In LQTS the holes in the cells that allow these important substances either do not properly open and close, or there is not enough holes to allow for the proper amount of substances or more through the cell to create the heart’s electrical activity (NHLBI).
A person with LQTS may not experience any symptoms and may be diagnosed posthumously. When diagnosis does occur it is usually after a person has some type of event such as: unexplained fainting, drowning or near-drowning (due to fainting while swimming) or unexplained cardiac arrest (NHLBI). This could cause a patient to seek diagnosis; however the first symptom could be the only symptom as LQTS can cause sudden death.
Treatments include education for awareness, lifestyle changes and medications. Lifestyle changes include avoiding medications that could cause prolonged QT intervals, staying well hydrated during illness, reducing loud or startling noises (including alarm clocks), staying away from situations that make you angry or excited, and avoiding prolonged strenuous activity (especially swimming). The most common medication class used for treatment is beta blockers. These drugs slow the heart rate and work by blunting the way the heart reacts to adrenaline, which can cause the heart to beat faster in times of fear, stress and/or exertion (Mayo). LQTS cannot be cured but these treatments can help to prevent these dangerous arrhythmias.
Long QT syndrome is an under-diagnosed disorder. The prevalence of LQTS is difficult to estimate. It may be expected to occur in 1 in 10,000 individuals. LQTS is more prevalent in female patients and usually presents in childhood, adolescence and early adulthood. Sudden death occurs more in boys than girls. LQTS is thought to cause about 4,000 deaths in the United States each year (Sovari).
To reduce the cases of sudden death by LQTS, first degree family members should be offered genetic testing, clinical evaluation, and treatment with the ultimate goal to prevent sudden death (Statton); this will identify those who have the genetic code for LQTS so they may take preventative measures to reduce their chance of this deadly arrhythmia. Raising awareness of this disease is paramount for individuals to gain the knowledge they need in order to watch for the tell-tale signs and symptoms in themselves and their family members. Once this disease is well known we can start to identify those who carry the gene, and we can create personalized medicine for each individual. This would help reduce the number of children suddenly dying at the hands of this disease.
References
Mayo Clinic Staff. (2015, October 27). Long QT syndrome. Retrieved February 10, 2016, from <http://www.mayoclinic.org/diseases-conditions/long-qt-syndrome/basics/definition/con-20025388>
NHLBI. (2011, September 21). Long QT Syndrome. Retrieved February 10, 2016, from
<https://www.nhlbi.nih.gov/health/health-topics/topics/qt>
Sovari, A. A., MD. (2015, December 31). Long QT Syndrome. Retrieved February 10, 2016, from <http://emedicine.medscape.com/article/157826-overview>
Statton, EL, IM Weston, K. Cederquist, J. Jonasson, BA Jonasson, S. Mörner, A. Norberg, P. Krantz, and A. Wisten. "Genetic Screening in Sudden Cardiac Death in the Young Can save Future Lives." Int J Legal Med (2015): 59-66. Jan. 2016. Web. 10 Feb. 2016. <http://www.ncbi.nlm.nih.gov/pubmed/26228265>
Imagine yourself as the parent of a child. Your hopes and dreams take shape as you see them grow and conquer their fears. You feel success from their successes and when they fall your heart aches to console them. Imagine yourself the parent of a young teenager. You see the frustration in them on a daily basis, trying desperately to cope with expectations, stress, and pressure in a rapidly changing environment, while they themselves are racing to grow into their own shoes. Imagine yourself as a proud, attentive mother of an athletic teenage son nearing the prime of his life. One morning you find that your son has slept in. You call and knock at his door to no response. You open the door, and panic, finding the son you have raised and nurtured, cared for, and disciplined lying lifeless and cold; a result of Sudden Arrhythmia Death Syndrome. Heart conditions such as Long QT Syndrome need to be advocated more for patient education to raise awareness in preventing such sudden deaths.
Long QT syndrome is a condition that affects the heart's rhythm that can cause fast and chaotic heartbeats. The heart can only beat erratically for so long before it causes sudden death. Prolonged QT, “LQTS” can be an inherited dormant error in a person’s genetic code or can be acquired due to certain medications and medical conditions. Inherited LQTS has been associated with 17 genes so far, with hundreds of mutations. Although genetic test can identify those with this disease, it does not pick up 20% of people who do have the disease. A known parent with LQTS has a 50% chance of passing the gene down to their child. LQTS may also be acquired. Acquired LQTS can be caused by certain medications of medical conditions. There are more than 75 medications that are known to lengthen the QT interval causing drug induced Long QT Syndrome (Mayo).
Often LQTS is discovered by accident by being picked up on an ECG. An ECG measures the electrical impulse as they travel through the heart. Long QT syndrome results from abnormalities in the heart’s electrical charging system (Mayo). Imagine each heart muscle has tiny holes called ion
channels. These holes open and close to allow important substances (sodium, calcium and potassium) to flow in and out of the heart muscle cells. In LQTS the holes in the cells that allow these important substances either do not properly open and close, or there is not enough holes to allow for the proper amount of substances or more through the cell to create the heart’s electrical activity (NHLBI).
A person with LQTS may not experience any symptoms and may be diagnosed posthumously. When diagnosis does occur it is usually after a person has some type of event such as: unexplained fainting, drowning or near-drowning (due to fainting while swimming) or unexplained cardiac arrest (NHLBI). This could cause a patient to seek diagnosis; however the first symptom could be the only symptom as LQTS can cause sudden death.
Treatments include education for awareness, lifestyle changes and medications. Lifestyle changes include avoiding medications that could cause prolonged QT intervals, staying well hydrated during illness, reducing loud or startling noises (including alarm clocks), staying away from situations that make you angry or excited, and avoiding prolonged strenuous activity (especially swimming). The most common medication class used for treatment is beta blockers. These drugs slow the heart rate and work by blunting the way the heart reacts to adrenaline, which can cause the heart to beat faster in times of fear, stress and/or exertion (Mayo). LQTS cannot be cured but these treatments can help to prevent these dangerous arrhythmias.
Long QT syndrome is an under-diagnosed disorder. The prevalence of LQTS is difficult to estimate. It may be expected to occur in 1 in 10,000 individuals. LQTS is more prevalent in female patients and usually presents in childhood, adolescence and early adulthood. Sudden death occurs more in boys than girls. LQTS is thought to cause about 4,000 deaths in the United States each year (Sovari).
To reduce the cases of sudden death by LQTS, first degree family members should be offered genetic testing, clinical evaluation, and treatment with the ultimate goal to prevent sudden death (Statton); this will identify those who have the genetic code for LQTS so they may take preventative measures to reduce their chance of this deadly arrhythmia. Raising awareness of this disease is paramount for individuals to gain the knowledge they need in order to watch for the tell-tale signs and symptoms in themselves and their family members. Once this disease is well known we can start to identify those who carry the gene, and we can create personalized medicine for each individual. This would help reduce the number of children suddenly dying at the hands of this disease.
References
Mayo Clinic Staff. (2015, October 27). Long QT syndrome. Retrieved February 10, 2016, from <http://www.mayoclinic.org/diseases-conditions/long-qt-syndrome/basics/definition/con-20025388>
NHLBI. (2011, September 21). Long QT Syndrome. Retrieved February 10, 2016, from
<https://www.nhlbi.nih.gov/health/health-topics/topics/qt>
Sovari, A. A., MD. (2015, December 31). Long QT Syndrome. Retrieved February 10, 2016, from <http://emedicine.medscape.com/article/157826-overview>
Statton, EL, IM Weston, K. Cederquist, J. Jonasson, BA Jonasson, S. Mörner, A. Norberg, P. Krantz, and A. Wisten. "Genetic Screening in Sudden Cardiac Death in the Young Can save Future Lives." Int J Legal Med (2015): 59-66. Jan. 2016. Web. 10 Feb. 2016. <http://www.ncbi.nlm.nih.gov/pubmed/26228265>
Shingles (Herpes zoster)
By: The Patient
Shingles is reactivation of the chickenpox virus. When you have chickenpox as a young child the virus stays inactive, it becomes a dormant in certain nerves in the body. Shingles occur after the virus becomes active again years later. The virus is activated when stress, aging, certain diseases and medicine weakens the immune system. Shingles can develop in any age group but usually develops in people who are 60 years and older and had chickenpox before they were one year old. Statistic has shown that one in three people will have shingles. Symptoms can happen in stages before any rash appear, usually it starts with one-sided pain, tingling or burning sensation, itching, flu like symptoms and headache. When rash appears it looks like red patches on the skin or small blisters that can stay on the skin for 2 to 3 weeks. The rash is usually around the spine, belly area and chest area but it can also be around face, eyes, mouth, ears and neck. Sometimes the blisters can leave permanent scars and nerve pain can be long-term. Shingles is treated with antiviral and pain medications. If detected in early stage shingles can be treated with antiviral medication to help with rash and pain relief. Shingles cannot be passed on unless a person is in direct contact with liquid from the blisters and didn’t have chickenpox as young child or chickenpox vaccine.
Shingle vaccine is recommended for people 60 and older, younger than that will need a prescription from the doctor.
Work Cited:
PubMedHealth. (2015, November 19). Shingles. Retrieved February 09, 2016, from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001861/
WebMD. (2014, September 11). Shingles. Retrieved February 10, 2016, from http://www.webmd.com/skin-problems-and-treatments/shingles/shingles-topic-overview
Cdc. (2015, August 05). Prevent Shingles. Retrieved February 10, 2016, from http://www.cdc.gov/features/shingles/
Dental Caries
By: Seahawks Gal
Dental caries is a clinical term for tooth decay. Dental caries starts as buildup of plaque that is formed by tiny bacteria and food particles built up on the tooth surface. Bacteria adhere to the tooth surface in a biofilm called dental plaque. The two main types of bacteria responsible for most tooth decay is Streptococcus Mutans and Lactobacillus. A professor at a University says "Teeth become susceptible to decay when the enamel is softened.”(Academic Onefile) Although there are different types of bacteria that cause tooth decay there are several ways to both treat it and prevent it.
I didn’t realize how serious of a problem tooth decay was in this country until I went to school for dental assisting ten years ago. After working in both pediatric dentistry as well as oral surgery I have seen some of the worst cases both in children as well as adults. I have also seen firsthand how quickly tooth decay can develop and how bad it can get in a short amount of time. Dental caries is a topic that more people need to be aware of and more education needs to be provided about it.
Statistics show that only 56.8% of women and 49% of men actually follow the ADA recommended guidelines and brush their teeth twice a day, along with flossing once a day and using fluoridated mouth wash. I have seen severe dental decay in children as young as 10 months and if not taken care of and prevented this can lead to a life time of dental problems. “Among 4-year-olds in 2005, approximately 37 percent of children had at least one decayed baby tooth. On average, there were 1.84 decayed, missing or filled baby teeth, of which 84 percent comprised of untreated dental decay.”
Tooth Decay-Treatment Overview
Starting at the age of about one when a child gets their first teeth it is vital to start good oral hygiene. Children should be seen by a Pedodontist as soon as they get their first tooth and continue to see a dentist every six months for regular checkups, cleaning and x rays. At the child’s first dental appointment their dentist will cover proper nutrition, proper brushing technique, oral habits as well as any concerns the parent may have. (Your Child's First Visit to the Dentist) Children should also have help with brushing until about the age of eight or when they can write cursive because before that they lack the ability to reach all areas that need to be brushed properly. (“What Is Good Oral Hygiene?") It is essential that parents make it a priority to teach their children good dental habits when they are young, so they are able to continue with good oral hygiene throughout their adult lives.
Untreated tooth decay can lead to a lot of more serious problems. A simple cavity that may just need a filling, if left un treated can lead to needing a root canal which involves removing the nerves from the tooth just like you would in trying to kill a tree. This process is one option to try and save the tooth. Another option is a crown placed over the tooth, or even extraction of the tooth. Also if dental caries is left untreated it can lead to the tooth becoming infected which can spread to other parts of the body through the blood stream. As we can see dental decay is nothing to mess around with as it can be very serious.
As we can see tooth decay also known as dental Caries is a very serious problem. This is a problem that affects people all over the world on a day to day basis. Dental decay can be easily prevented with the use of good oral hygiene. If a person does develop dental decay they need to make sure it is properly taken care of as soon as possible to avoid further problems. Simple steps can be taken to keep your teeth looking and feeling their best. With the proper knowledge and resources there should be no excuse for so many people to be living with dental decay which is both unattractive as well a painful and dangerous.
Work Cited
Aarow Peter, Raheb Joseph, Miller Margret. “Brief oral health promotion intervention among parents of young children to reduce early childhood dental decay.” BMC Public Health. 20 March. 2014. Academic Onefile . Web. 08 Feb. 2016
Edelstein Burton. “New approach needed to reduce caries in children” Public Health Reports. July-August 1997.Web. Academic Onefile. 08. Feb 2016
"Foods and Drinks Best for Your Teeth." WebMD. WebMD, n.d. Web. 09 Feb. 2016.
Journal of family health care. “Early Nutrition and Dental Health” June. 2009. Pavilion Publishing and Media Ltd. Web. Acedemic Onefile. 09. Feb. 2016.
"Tooth Decay-Treatment Overview." WebMD. WebMD, 10 Dec. 2014. Web. 10 Feb. 2016.
"Your Child's First Visit to the Dentist." WebMD. WebMD, 04 Jan. 2014. Web. 09 Feb. 2016.
"What Is Good Oral Hygiene?" Oral Hygiene Basics. N.p., n.d. Feb. 10 Feb. 2016.
Most people do not know what the word caries means. Dental Caries is another word for tooth decay or cavities. In the United States children between the ages of 6-19, with untreated dental caries was 16.2% during the years 2005-2008, and for adults over the age of 19 with untreated dental caries that were untreated were 23.7%. Dental Caries is a currently huge problem in the United States. Many people have a lack of knowledge, along with not caring or taking proper care of their teeth. Dental caries is one of the most common diseases seen in the human body second to the common cold. There must be more education taught to try and prevent this problem.
Dental caries is a clinical term for tooth decay. Dental caries starts as buildup of plaque that is formed by tiny bacteria and food particles built up on the tooth surface. Bacteria adhere to the tooth surface in a biofilm called dental plaque. The two main types of bacteria responsible for most tooth decay is Streptococcus Mutans and Lactobacillus. A professor at a University says "Teeth become susceptible to decay when the enamel is softened.”(Academic Onefile) Although there are different types of bacteria that cause tooth decay there are several ways to both treat it and prevent it.
I didn’t realize how serious of a problem tooth decay was in this country until I went to school for dental assisting ten years ago. After working in both pediatric dentistry as well as oral surgery I have seen some of the worst cases both in children as well as adults. I have also seen firsthand how quickly tooth decay can develop and how bad it can get in a short amount of time. Dental caries is a topic that more people need to be aware of and more education needs to be provided about it.
Statistics show that only 56.8% of women and 49% of men actually follow the ADA recommended guidelines and brush their teeth twice a day, along with flossing once a day and using fluoridated mouth wash. I have seen severe dental decay in children as young as 10 months and if not taken care of and prevented this can lead to a life time of dental problems. “Among 4-year-olds in 2005, approximately 37 percent of children had at least one decayed baby tooth. On average, there were 1.84 decayed, missing or filled baby teeth, of which 84 percent comprised of untreated dental decay.”
Tooth Decay-Treatment Overview
Starting at the age of about one when a child gets their first teeth it is vital to start good oral hygiene. Children should be seen by a Pedodontist as soon as they get their first tooth and continue to see a dentist every six months for regular checkups, cleaning and x rays. At the child’s first dental appointment their dentist will cover proper nutrition, proper brushing technique, oral habits as well as any concerns the parent may have. (Your Child's First Visit to the Dentist) Children should also have help with brushing until about the age of eight or when they can write cursive because before that they lack the ability to reach all areas that need to be brushed properly. (“What Is Good Oral Hygiene?") It is essential that parents make it a priority to teach their children good dental habits when they are young, so they are able to continue with good oral hygiene throughout their adult lives.
Untreated tooth decay can lead to a lot of more serious problems. A simple cavity that may just need a filling, if left un treated can lead to needing a root canal which involves removing the nerves from the tooth just like you would in trying to kill a tree. This process is one option to try and save the tooth. Another option is a crown placed over the tooth, or even extraction of the tooth. Also if dental caries is left untreated it can lead to the tooth becoming infected which can spread to other parts of the body through the blood stream. As we can see dental decay is nothing to mess around with as it can be very serious.
As we can see tooth decay also known as dental Caries is a very serious problem. This is a problem that affects people all over the world on a day to day basis. Dental decay can be easily prevented with the use of good oral hygiene. If a person does develop dental decay they need to make sure it is properly taken care of as soon as possible to avoid further problems. Simple steps can be taken to keep your teeth looking and feeling their best. With the proper knowledge and resources there should be no excuse for so many people to be living with dental decay which is both unattractive as well a painful and dangerous.
Aarow Peter, Raheb Joseph, Miller Margret. “Brief oral health promotion intervention among parents of young children to reduce early childhood dental decay.” BMC Public Health. 20 March. 2014. Academic Onefile . Web. 08 Feb. 2016
Edelstein Burton. “New approach needed to reduce caries in children” Public Health Reports. July-August 1997.Web. Academic Onefile. 08. Feb 2016
"Foods and Drinks Best for Your Teeth." WebMD. WebMD, n.d. Web. 09 Feb. 2016.
Journal of family health care. “Early Nutrition and Dental Health” June. 2009. Pavilion Publishing and Media Ltd. Web. Acedemic Onefile. 09. Feb. 2016.
"Tooth Decay-Treatment Overview." WebMD. WebMD, 10 Dec. 2014. Web. 10 Feb. 2016.
"Your Child's First Visit to the Dentist." WebMD. WebMD, 04 Jan. 2014. Web. 09 Feb. 2016.
"What Is Good Oral Hygiene?" Oral Hygiene Basics. N.p., n.d. Feb. 10 Feb. 2016.
Sickle-Cell Disease
By: OMGmbz
Affecting approximately 90,000 to 100,000 Americans, Sickle Cell Disease (SCD) is a genetic disorder that affects hemoglobin in red blood cells. Though commonly found in people of African, Hispanic, Mediterranean and Middle Eastern ancestry, SCD is relatively rare. Because of its rareness, doctors may not know how to properly treat this disease or how to generate a cure. Nevertheless, more information about the disease is surfacing. Information such as the cause, treatment, and how common it is will help those affected better understand their disease and potentially improve their quality of life.
In order for your red blood cells (RBC) to carry oxygen to the rest of your body, the hemoglobin protein found in RBC must be soluble. Hemoglobin transports oxygen from the lungs to the rest of the body. Normal hemoglobin (hemoglobin-A) is smooth and round, allowing easily movement through the blood vessels. In people with sickle cell disease, there is a mutation in the hemoglobin-beta gene found on chromosome 11, which results in the production of abnormal hemoglobin molecules (hemoglobin-S). When hemoglobin-S is deoxygenated, interaction with other hemoglobin cells become hydrophobic, which trigger polymerization of deoxygenated hemoglobin-S allowing them to stick together. This creates their long, rod-like shape. These hemoglobin structures cause RBC to become stiff, maintaining their sickle shape. These irregular shaped cells can stick to the walls of the blood vessels, which can slow or block blood flow and oxygen to the rest of the body. It is like trying to spray water and sand through a hose. Some will get through, but eventually the sand will stop the water from escaping.
Some clinical manifestations of sickle cell disease include anemia, periodic pain, frequent infections, delayed growth, and vision problems. Anemia is a lack of healthy RBC in the blood. Sickle cells are fragile due to its shape. They break apart easily and die, leaving your blood with inadequate RBC supply. Because sickle cells die at a faster rate than normal RBC, a person with SCD is left with lasting anemia. This decreases the amount of oxygen in your body, which in turn can cause fatigue and potentially organ failure.
Episodes of pain can occur because sickle cells can block blood flow in tiny vessels in your chest, bones, muscles, and joints. Some people experience this pain for up to a few hours, while others experience it up to weeks. Depending on the severity, some people may need to be hospitalized.
Due to lack of oxygenated blood to the organs, the immune system may also be compromised. Organs such the spleen plays a vital part in your immune system. It helps fight infection. People with SCD are more prone to infections. In addition, vision problems can occur because tiny blood vessels to your eye can be clogged by sickle cells. This blockage can damage the retina, which is the part of your eye that processes images.
Because this is a genetic mutation of the hemoglobin- beta gene, it can be passed on to offspring. It is an autosomal recessive inheritance, which means that both parents must pass on the mutated gene in order for the child to be affected. If only one parent passes on the mutation, then the child will produce both normal and sickle cells. Though they have sickle cells in their blood, they usually do not show any symptoms.
As previously stated, approximately 100,000 Americans have SCD. The number of cases in the world is unknown. However, according to the CDC, SCD occurs in 1 out of every 500 African-American births, 1 out of every 36,000 Hispanic-American births, and 1 in every 12 African-American.
Unfortunately, there is no cure for SCD and because it is a genetic disease, there is no way of preventing it if you have the mutated gene. However, there are some treatments that could subdue the symptoms of SCD. Bone marrow transplant, though very difficult process and procedure, could help for the body to produce healthy RBCs, which can reduce some of the symptoms of SCD. Antibiotics and vaccines are used to help fight infections due to the compromised immune cells. Doctors may begin to administer antibiotics as early as 2 months and continue administering it until they are 5 years old. Pain relieving medications are used when patients are experiencing episodes of pain from the disease.
A new drug being studied is Hydroxyurea. Studies suggest that it could help reduce the frequency of pain and the need for blood transfusions. It seems to work by stimulation the production of fetal hemoglobin, which is found in newborns. It helps prevent the formation of sickle cells. However, this is still being tested.
Interventions can also be taken to help reduce the symptoms and prevent other conditions. Maintaining a healthy diet may reduce the risk of a stroke due to blockage. Exercise could increase circulation, and help reduce pain. Avoiding infectious areas and maintaining cleanliness could help prevent infections among other things.
It is important to understand as much as possible about the disease. Though there is no cure and it cannot be prevented, education can help those with SCD live a sustainable lifestyle. There are many sources that could help those with the disease deal with its ramifications. Studies today are focused on finding a way to alter this mutation, and hopefully prevent this disease.
References
Brousseau, D. C., Scott, J. P., Badaki-Makun, O., Darbari, D. S., Chumpitazi, C. E., Airewele, G. E., Panepinto, J. A. (2015). A multicenter randomized controlled trial of intravenous magnesium for sickle cell pain crisis in children. Blood, 126(14), 1651-1657. doi:10.1182/blood-2015-05-647107
Data & Statistics. (2015, July 08). Retrieved from http://www.cdc.gov/ncbddd/sicklecell/data.html
Epstein, F. H., & Bunn, H. F. (1997). Pathogenesis and Treatment of Sickle Cell Disease. New England Journal of Medicine N Engl J Med, 337(11), 762-769. doi:10.1056/nejm199709113371107
Rees, D. C., FRCP, Williams, T. N., PhD, & Gladwin, M. T., MD. (2010). Sickle-cell Disease. The Lancet, 376(9757), 2018-2031. doi:10.1016/S0140-6736(10)61029-X
Schultz, C. L., Tchume-Johnson, T., Schapira, M. M., Bellamy, S., Smith-Whitley, K., & Ellison, A. (2015). Adherence to prompt fever evaluation in children with sickle cell disease and the health belief model. Pediatric Blood & Cancer Pediatr Blood Cancer, 62(11), 1968-1973. doi:10.1002/pbc.25634
Sickle cell anemia. (2014, June 11). Retrieved from http://www.mayoclinic.org/diseases-conditions/sickle-cell-anemia/basics/prevention/con-20019348
In order for your red blood cells (RBC) to carry oxygen to the rest of your body, the hemoglobin protein found in RBC must be soluble. Hemoglobin transports oxygen from the lungs to the rest of the body. Normal hemoglobin (hemoglobin-A) is smooth and round, allowing easily movement through the blood vessels. In people with sickle cell disease, there is a mutation in the hemoglobin-beta gene found on chromosome 11, which results in the production of abnormal hemoglobin molecules (hemoglobin-S). When hemoglobin-S is deoxygenated, interaction with other hemoglobin cells become hydrophobic, which trigger polymerization of deoxygenated hemoglobin-S allowing them to stick together. This creates their long, rod-like shape. These hemoglobin structures cause RBC to become stiff, maintaining their sickle shape. These irregular shaped cells can stick to the walls of the blood vessels, which can slow or block blood flow and oxygen to the rest of the body. It is like trying to spray water and sand through a hose. Some will get through, but eventually the sand will stop the water from escaping.
Some clinical manifestations of sickle cell disease include anemia, periodic pain, frequent infections, delayed growth, and vision problems. Anemia is a lack of healthy RBC in the blood. Sickle cells are fragile due to its shape. They break apart easily and die, leaving your blood with inadequate RBC supply. Because sickle cells die at a faster rate than normal RBC, a person with SCD is left with lasting anemia. This decreases the amount of oxygen in your body, which in turn can cause fatigue and potentially organ failure.
Episodes of pain can occur because sickle cells can block blood flow in tiny vessels in your chest, bones, muscles, and joints. Some people experience this pain for up to a few hours, while others experience it up to weeks. Depending on the severity, some people may need to be hospitalized.
Due to lack of oxygenated blood to the organs, the immune system may also be compromised. Organs such the spleen plays a vital part in your immune system. It helps fight infection. People with SCD are more prone to infections. In addition, vision problems can occur because tiny blood vessels to your eye can be clogged by sickle cells. This blockage can damage the retina, which is the part of your eye that processes images.
Because this is a genetic mutation of the hemoglobin- beta gene, it can be passed on to offspring. It is an autosomal recessive inheritance, which means that both parents must pass on the mutated gene in order for the child to be affected. If only one parent passes on the mutation, then the child will produce both normal and sickle cells. Though they have sickle cells in their blood, they usually do not show any symptoms.
As previously stated, approximately 100,000 Americans have SCD. The number of cases in the world is unknown. However, according to the CDC, SCD occurs in 1 out of every 500 African-American births, 1 out of every 36,000 Hispanic-American births, and 1 in every 12 African-American.
Unfortunately, there is no cure for SCD and because it is a genetic disease, there is no way of preventing it if you have the mutated gene. However, there are some treatments that could subdue the symptoms of SCD. Bone marrow transplant, though very difficult process and procedure, could help for the body to produce healthy RBCs, which can reduce some of the symptoms of SCD. Antibiotics and vaccines are used to help fight infections due to the compromised immune cells. Doctors may begin to administer antibiotics as early as 2 months and continue administering it until they are 5 years old. Pain relieving medications are used when patients are experiencing episodes of pain from the disease.
A new drug being studied is Hydroxyurea. Studies suggest that it could help reduce the frequency of pain and the need for blood transfusions. It seems to work by stimulation the production of fetal hemoglobin, which is found in newborns. It helps prevent the formation of sickle cells. However, this is still being tested.
Interventions can also be taken to help reduce the symptoms and prevent other conditions. Maintaining a healthy diet may reduce the risk of a stroke due to blockage. Exercise could increase circulation, and help reduce pain. Avoiding infectious areas and maintaining cleanliness could help prevent infections among other things.
It is important to understand as much as possible about the disease. Though there is no cure and it cannot be prevented, education can help those with SCD live a sustainable lifestyle. There are many sources that could help those with the disease deal with its ramifications. Studies today are focused on finding a way to alter this mutation, and hopefully prevent this disease.
References
Brousseau, D. C., Scott, J. P., Badaki-Makun, O., Darbari, D. S., Chumpitazi, C. E., Airewele, G. E., Panepinto, J. A. (2015). A multicenter randomized controlled trial of intravenous magnesium for sickle cell pain crisis in children. Blood, 126(14), 1651-1657. doi:10.1182/blood-2015-05-647107
Data & Statistics. (2015, July 08). Retrieved from http://www.cdc.gov/ncbddd/sicklecell/data.html
Epstein, F. H., & Bunn, H. F. (1997). Pathogenesis and Treatment of Sickle Cell Disease. New England Journal of Medicine N Engl J Med, 337(11), 762-769. doi:10.1056/nejm199709113371107
Rees, D. C., FRCP, Williams, T. N., PhD, & Gladwin, M. T., MD. (2010). Sickle-cell Disease. The Lancet, 376(9757), 2018-2031. doi:10.1016/S0140-6736(10)61029-X
Schultz, C. L., Tchume-Johnson, T., Schapira, M. M., Bellamy, S., Smith-Whitley, K., & Ellison, A. (2015). Adherence to prompt fever evaluation in children with sickle cell disease and the health belief model. Pediatric Blood & Cancer Pediatr Blood Cancer, 62(11), 1968-1973. doi:10.1002/pbc.25634
Sickle cell anemia. (2014, June 11). Retrieved from http://www.mayoclinic.org/diseases-conditions/sickle-cell-anemia/basics/prevention/con-20019348
Monday, February 15, 2016
Dupuytren’s Disease
By: Zombieland
Although many factors may contribute to the predisposition of Dupuytren’s Disease, there has been conflicting evidence of correlation and causation found in relation to alcoholism or hard-labor work. Many studies over history have failed to establish a definitive link between alcoholism, hard-labor work and Dupuytren’s Disease, but rather the only proven correlating link is solely heredity.
Dupuytren’s Disease, also known as “Viking’s Disease”, is a condition causing debilitating contractures (flexing, rigidity, or clawing) of the fingers and can progress to limited or full loss of hand function. The disease occurs most often in men of Northern European decent that are over the age of 60 (women can also develop the disease, but are less likely than men). Dupuytren’s is estimated to affect about 10% of the population of men aged over 65 currently living in Northern Europe 4. Dupuytren’s Disease has a well-established history, whose transmission is believed to stem from the 10th century invasions by Scandinavian Vikings. Once colonization of Scotland, Ireland, England, France, Holland and Belgium was established by the Vikings, the disease began to be passed on through intercultural relationships1.
Dupuytren’s Disease was first described by Swiss physician Felix Plater in 1614 2, but its namesake is derived from Baron Guillaume Dupuytren who, later in 1831, recorded multiple lectures regarding the disease and its origin and also performed the first surgery on a hand contracture of this type. Dupuytren, known as the greatest French surgeon of the 19th century, described seeing an increase of male patients of Irish descent presenting with permanent flexed fingers. Through research of his own, he concluded that the disorder was caused by an increase or thickening in the palmar fascia (a tough, fibrous layer of tissue in the palm of the hand5). Dupuytren also concluded that there were strong indicating factors such as Irish descent, alcoholism, and manual labor contributing to the cause of the disease, as most of his presenting patients were immigrant Irish manual laborers who drank excessively. This foundation of knowledge also brought to light “The Curse of the Mac Crimmons”, which was a belief that the Mac Crimmon family, who ran The College of Bagpiping in Scotland from the 15th century to the 18th century, had a curse laid upon the men in the family that inflicted bent fingers in the adult male bagpipers and prevented them from playing later in life1.
These bent fingers were described by Dupuytren in his lectures as a bend of the finger (contracture). Contractures can develop in a variety of number of digits, but most occur in the ring and small fingers. The degree of contracture can vary greatly depending on each individual’s disease process. Along with these contractures, nodules (small lumps) were described to be present on the palms of the hands. These nodules are usually firm and round and may cause the skin of the palm to pucker or pit. Although these hallmark characteristics observed in someone with Dupuytren’s Disease is often debilitating, it is usually not painful. The rate of development of contractures and nodules is different with each individual. Some patients may have nodules but never develop contractures and some patients may have both that progressively and rapidly worsen. Variabilities exist between the least severe case and the worst severe case. Patients often seek medical advice when the bent finger(s) impedes normal, everyday functions. Patients often describe that the contracted finger will snag on the pocket of their pants or that the finger will poke them in the face as they are attempting to wash. Many seek what treatments are available from an Orthopedic Hand Surgeon, who has specialized training in the diagnosis and treatment of Dupuytren’s Disease. Treatments include injections to dissolve collagen and multiple degrees of surgery, but there is no cure. Dupuytren’s Disease does recur and the rate of recurrence is dependent upon the individuals’ disease process 3.
Guillaume Dupuytren may have monumentally described the basic origin and characteristics of the disease, but many discoveries have been made regarding the actual process of development. It is widely agreed upon that the formation of contractures results from a tight cord that forms from an increase in collagen growth, promoted by cells called myofibroblasts (a cell that shares characteristics of both smooth muscle cells and fibroblast cells). This tight cord can be likened to a rope and is comprised mostly of collagen type III; normal palmar fascia is predominantly made up of collagen type II. The nodules that form, likened to a knot, are dense, highly cellular (many cells) masses of tissue. Cords and nodules can be exclusive from each other but nodules may also present on or within the cord, like knots in a rope 3.
The evolution of the discovery of Dupuytren’s Disease and its cause has been controversial for hundreds of years. Many researchers believe that the previously stated predicting factor of alcohol use was simply an oversight on behalf of Guillaume Dupuytren, who assumed that alcohol was a causative agent in the development of the disease, and failed to recognize a factor of culture in Irish and Scottish descent where heavy alcohol use was widely accepted and practiced. Other researchers, more recently in the last century, believe they have found a link that does relate to alcohol use being a contributing factor, by means of exciting myofibroblast cells and in turn increasing collagen growth in the hand 3. Controversy also surrounds the original idea that manual labor contributes to Dupuytren’s contractures. Some researchers have documented that the correlation that Guillaume Dupuytren made based on his Irish immigrant patients was, again, an oversight of coincidence; most Irish immigrants in France during the 19th century were manual laborers. On the other hand, some recent research indicates that trauma to the hand may trigger a repair process to begin where cytokines (small proteins that aid in cell signaling) are released and tell the myofibroblast cells to increase their number to repair the injury. This subject is loosely discussed in relationship with the original idea that manual labor contributes to the disease process, but more-over believed to be a possibility that repetitive, hard labor of the hand causes small injuries to occur, which in-turn trigger this process of repair 3.
There may be controversy and argument surrounding the causation of Dupuytren’s Disease but three things are widely agreed upon: (1) the cause of the disease is multifactorial in nature 4, (2) onset and prevention of progression has yet to be discovered 4 and (3) congenital predisposition is the only confirmed correlation of transmission, causation and recurrence although no specific gene has yet to be isolated 3.
Citations:
1 Flatt, A. E., MD. (2001). The Vikings and Baron Dupuytren’s disease. Baylor University Medical Center Proceedings, 14(4), 378-384. Retrieved February 10, 2016, from www.ncbi.nlm.nih.gov/pmc/articles/PMC1305903
2 Desai, S. S., MD. (2011). The Treatment of Dupuytren Disease. Journal of Hand Surgery, 36(A), 936-942. Retrieved February 10, 2016 from www.jhandsurg.org
3 Black, E. M., MD, & Blazar, P. E., MD. (2011). Dupuytren Disease: An Evolving Understanding of an Age-old Disease. Journal of the American Academy of Orthopaedic Surgeons, 19,746-757. Retrieved February 10, 2016 from www.aaos.org/jaaos
4 Frey, M., MD. (1997). Risks and prevention of Dupuytren’s Contracture. The Lancet, 350, 1568. Retrieved February 10, 2016
5 Krames. (2014). Dupuytren’s Contracture- Restoring Movement in Your Hand. www.kramesstaywell.com
Although many factors may contribute to the predisposition of Dupuytren’s Disease, there has been conflicting evidence of correlation and causation found in relation to alcoholism or hard-labor work. Many studies over history have failed to establish a definitive link between alcoholism, hard-labor work and Dupuytren’s Disease, but rather the only proven correlating link is solely heredity.
Dupuytren’s Disease, also known as “Viking’s Disease”, is a condition causing debilitating contractures (flexing, rigidity, or clawing) of the fingers and can progress to limited or full loss of hand function. The disease occurs most often in men of Northern European decent that are over the age of 60 (women can also develop the disease, but are less likely than men). Dupuytren’s is estimated to affect about 10% of the population of men aged over 65 currently living in Northern Europe 4. Dupuytren’s Disease has a well-established history, whose transmission is believed to stem from the 10th century invasions by Scandinavian Vikings. Once colonization of Scotland, Ireland, England, France, Holland and Belgium was established by the Vikings, the disease began to be passed on through intercultural relationships1.
Dupuytren’s Disease was first described by Swiss physician Felix Plater in 1614 2, but its namesake is derived from Baron Guillaume Dupuytren who, later in 1831, recorded multiple lectures regarding the disease and its origin and also performed the first surgery on a hand contracture of this type. Dupuytren, known as the greatest French surgeon of the 19th century, described seeing an increase of male patients of Irish descent presenting with permanent flexed fingers. Through research of his own, he concluded that the disorder was caused by an increase or thickening in the palmar fascia (a tough, fibrous layer of tissue in the palm of the hand5). Dupuytren also concluded that there were strong indicating factors such as Irish descent, alcoholism, and manual labor contributing to the cause of the disease, as most of his presenting patients were immigrant Irish manual laborers who drank excessively. This foundation of knowledge also brought to light “The Curse of the Mac Crimmons”, which was a belief that the Mac Crimmon family, who ran The College of Bagpiping in Scotland from the 15th century to the 18th century, had a curse laid upon the men in the family that inflicted bent fingers in the adult male bagpipers and prevented them from playing later in life1.
These bent fingers were described by Dupuytren in his lectures as a bend of the finger (contracture). Contractures can develop in a variety of number of digits, but most occur in the ring and small fingers. The degree of contracture can vary greatly depending on each individual’s disease process. Along with these contractures, nodules (small lumps) were described to be present on the palms of the hands. These nodules are usually firm and round and may cause the skin of the palm to pucker or pit. Although these hallmark characteristics observed in someone with Dupuytren’s Disease is often debilitating, it is usually not painful. The rate of development of contractures and nodules is different with each individual. Some patients may have nodules but never develop contractures and some patients may have both that progressively and rapidly worsen. Variabilities exist between the least severe case and the worst severe case. Patients often seek medical advice when the bent finger(s) impedes normal, everyday functions. Patients often describe that the contracted finger will snag on the pocket of their pants or that the finger will poke them in the face as they are attempting to wash. Many seek what treatments are available from an Orthopedic Hand Surgeon, who has specialized training in the diagnosis and treatment of Dupuytren’s Disease. Treatments include injections to dissolve collagen and multiple degrees of surgery, but there is no cure. Dupuytren’s Disease does recur and the rate of recurrence is dependent upon the individuals’ disease process 3.
Guillaume Dupuytren may have monumentally described the basic origin and characteristics of the disease, but many discoveries have been made regarding the actual process of development. It is widely agreed upon that the formation of contractures results from a tight cord that forms from an increase in collagen growth, promoted by cells called myofibroblasts (a cell that shares characteristics of both smooth muscle cells and fibroblast cells). This tight cord can be likened to a rope and is comprised mostly of collagen type III; normal palmar fascia is predominantly made up of collagen type II. The nodules that form, likened to a knot, are dense, highly cellular (many cells) masses of tissue. Cords and nodules can be exclusive from each other but nodules may also present on or within the cord, like knots in a rope 3.
The evolution of the discovery of Dupuytren’s Disease and its cause has been controversial for hundreds of years. Many researchers believe that the previously stated predicting factor of alcohol use was simply an oversight on behalf of Guillaume Dupuytren, who assumed that alcohol was a causative agent in the development of the disease, and failed to recognize a factor of culture in Irish and Scottish descent where heavy alcohol use was widely accepted and practiced. Other researchers, more recently in the last century, believe they have found a link that does relate to alcohol use being a contributing factor, by means of exciting myofibroblast cells and in turn increasing collagen growth in the hand 3. Controversy also surrounds the original idea that manual labor contributes to Dupuytren’s contractures. Some researchers have documented that the correlation that Guillaume Dupuytren made based on his Irish immigrant patients was, again, an oversight of coincidence; most Irish immigrants in France during the 19th century were manual laborers. On the other hand, some recent research indicates that trauma to the hand may trigger a repair process to begin where cytokines (small proteins that aid in cell signaling) are released and tell the myofibroblast cells to increase their number to repair the injury. This subject is loosely discussed in relationship with the original idea that manual labor contributes to the disease process, but more-over believed to be a possibility that repetitive, hard labor of the hand causes small injuries to occur, which in-turn trigger this process of repair 3.
There may be controversy and argument surrounding the causation of Dupuytren’s Disease but three things are widely agreed upon: (1) the cause of the disease is multifactorial in nature 4, (2) onset and prevention of progression has yet to be discovered 4 and (3) congenital predisposition is the only confirmed correlation of transmission, causation and recurrence although no specific gene has yet to be isolated 3.
Citations:
1 Flatt, A. E., MD. (2001). The Vikings and Baron Dupuytren’s disease. Baylor University Medical Center Proceedings, 14(4), 378-384. Retrieved February 10, 2016, from www.ncbi.nlm.nih.gov/pmc/articles/PMC1305903
2 Desai, S. S., MD. (2011). The Treatment of Dupuytren Disease. Journal of Hand Surgery, 36(A), 936-942. Retrieved February 10, 2016 from www.jhandsurg.org
3 Black, E. M., MD, & Blazar, P. E., MD. (2011). Dupuytren Disease: An Evolving Understanding of an Age-old Disease. Journal of the American Academy of Orthopaedic Surgeons, 19,746-757. Retrieved February 10, 2016 from www.aaos.org/jaaos
4 Frey, M., MD. (1997). Risks and prevention of Dupuytren’s Contracture. The Lancet, 350, 1568. Retrieved February 10, 2016
5 Krames. (2014). Dupuytren’s Contracture- Restoring Movement in Your Hand. www.kramesstaywell.com
ZIKA: Balancing Fear with Facts
By: OCR-Mama
You have heard about Zika virus. You have seen the heart-wrenching images of babies born with microcephaly or an abnormally small head. The World Health Organization is talking about it. The Centers for Disease Control and Prevention is talking about it. Your grandma is calling you to talk about it. Zika is spreading rapidly and can have dire health effects. Even as I write this new stories are popping up by the minute, but what are the facts about Zika? What is the real risk for you as a pregnant mom in the US? Before you finish your gestation in a DEET-filled cave, let’s look at what is known and unknown about Zika.
What is Zika virus and how do you get it?
Zika virus disease or ZIKV or Zika fever is caused by a mosquito-borne virus that was first identified in 1947 in a caged rhesus monkey in Africa. In humans the first cases were identified in 1952. In 2013 and 2014 French Polynesia had a ZIKV outbreak with an uptick in central nervous system malformations including microcephaly.
In 2015 a Zika virus outbreak swept through Brazil. 2016 has seen no end to the outbreak and Zika continues to spread through the Americas. So although this disease is not new, the areas of the world that have been impacted by the Zika virus are expanding and the effects on these naive populations are getting attention.
Mosquitos carry the virus and infect the human by acting as a vector for transmission. Mosquitos are excellent vectors because they break through the top layer of skin or epidermis and get into the dermis below. They do this because blood is their meal, but this also allows the virus to make it’s way into the host’s blood. The skin, like a suit of armor, protects against most dangers but a poisonous needle piercing through a chink can cause grave harm.
The cells of the dermis called dendritic cells and fibroblasts have receptors that allow Zika to enter the cell and replicate. The virus has other factors contributing to the rapid spread in areas with many mosquitos. A mosquito can pick up Zika from an infected person and then pass it along to another person. Meaning, a mosquito can become a carrier by biting someone who is sick.
Transmission is no longer thought to be limited to the work of mosquitos either. There is growing evidence that Zika virus disease can be transmitted sexually and remains in semen longer than it has cleared from the blood in an infected person. So if your partner has travelled to a region with Zika it is wise to use condoms or abstain until he has been cleared from the disease whether or not symptoms occur. This route of transmission, however, is much less likely than from a mosquito. So while unlikely to be an issue, better safe than sorry.
Not all mosquitoes carry the Zika virus. In fact, transmission is mainly by Aedes mosquitoes which are most commonly found in tropical environments. For US women concerns about contracting Zika are mainly around travel to area that have cases of Zika and sexual contact with partners that have experienced Zika virus disease. The CDC and WHO are actively tracking the disease and issuing travel guidelines for pregnant women or women who may become pregnant. Currently no locally-acquired cases of this disease have presented in the US, but travel-related cases have. Tracking of the disease and its spread are ongoing and if you have travel plans check with these sources for the latest recommendations.
What are the symptoms of Zika virus disease?
If Zika virus disease occurs symptoms are likely to begin around a couple days after exposure and symptoms are generally mild, lasting 2-7 days. These symptoms include fever, skin rash, discomfort, headache, joint and muscle pain, and eye redness. Most people infected with Zika virus will have no lasting harm from the disease. If a woman is pregnant when the Zika virus is contracted, however, the virus may cause severe brain damage to the unborn and is linked to a condition called microcephaly. The relationship between Zika virus and microcephaly is not fully understood by scientists.
How is Zika virus disease treated?
Symptoms of Zika virus can be eased with rest, drinking plenty of water, and taking pain relievers like ibuprofen. No antiviral medications are recommended at this time for Zika and no vaccination is available. If you are pregnant and suspect you have Zika virus talk to your doctor about what tests are available. Blood, urine, and saliva tests may be used to find viral RNA and the CDC has released an algorithm for testing. Ultrasound may be used to look for calcifications in the fetal skull and microcephaly. Recommended testing is still controversial and not widely available. The reality is that if you haven’t travelled to a region currently affected by Zika or live in that region then you aren’t considered to be at risk for Zika.
What is microcephaly and does Zika cause it?
Microcephaly is a condition that literally means small head. The head grows in a developing fetus because the brain is growing. In microcephaly the brain is not growing normally and this can be linked to a range of serious difficulties. Many causes of microcephaly are known such as infections like rubella, toxoplasmosis, and cytomegalovirus. Malnutrition or toxic exposures in development like alcohol can also cause microcephaly. ZIKV genetic material has been found in the brain tissue samples of a fetus with microcephaly whose mother was exposed to ZIKV during her pregnancy and experienced symptoms of ZIKA fever in her 13th week of pregnancy. ZIKV genetic material has also been found through amniocentesis. It is not proven that Zika causes microcephaly, but researchers think that the virus may target and replicate in the developing brain of a fetus. Zika doesn’t seem to cause lasting harm in other organs or tissues but stays and replicates in the brain stem.
The best prevention for ZIKV is to not get bit by a mosquito. Consider guidelines and consult with your doctor about travel plans. Look at the EPA’s recommendation for mosquito repellants and follow the directions carefully if you are expecting exposure. If you do they are safe to use during pregnancy. Wearing long pants and shirts can help as well. Standing water is prime breeding ground for mosquitos and can become a safety risk so care should be taken to prevent this. So the ZIKV media frenzy may be inducing worries in your pregnant mind, but fear is a beast that thrives on attention. Arm yourself with facts and be well.
What is Zika virus and how do you get it?
Zika virus disease or ZIKV or Zika fever is caused by a mosquito-borne virus that was first identified in 1947 in a caged rhesus monkey in Africa. In humans the first cases were identified in 1952. In 2013 and 2014 French Polynesia had a ZIKV outbreak with an uptick in central nervous system malformations including microcephaly.
In 2015 a Zika virus outbreak swept through Brazil. 2016 has seen no end to the outbreak and Zika continues to spread through the Americas. So although this disease is not new, the areas of the world that have been impacted by the Zika virus are expanding and the effects on these naive populations are getting attention.
Mosquitos carry the virus and infect the human by acting as a vector for transmission. Mosquitos are excellent vectors because they break through the top layer of skin or epidermis and get into the dermis below. They do this because blood is their meal, but this also allows the virus to make it’s way into the host’s blood. The skin, like a suit of armor, protects against most dangers but a poisonous needle piercing through a chink can cause grave harm.
The cells of the dermis called dendritic cells and fibroblasts have receptors that allow Zika to enter the cell and replicate. The virus has other factors contributing to the rapid spread in areas with many mosquitos. A mosquito can pick up Zika from an infected person and then pass it along to another person. Meaning, a mosquito can become a carrier by biting someone who is sick.
Transmission is no longer thought to be limited to the work of mosquitos either. There is growing evidence that Zika virus disease can be transmitted sexually and remains in semen longer than it has cleared from the blood in an infected person. So if your partner has travelled to a region with Zika it is wise to use condoms or abstain until he has been cleared from the disease whether or not symptoms occur. This route of transmission, however, is much less likely than from a mosquito. So while unlikely to be an issue, better safe than sorry.
Not all mosquitoes carry the Zika virus. In fact, transmission is mainly by Aedes mosquitoes which are most commonly found in tropical environments. For US women concerns about contracting Zika are mainly around travel to area that have cases of Zika and sexual contact with partners that have experienced Zika virus disease. The CDC and WHO are actively tracking the disease and issuing travel guidelines for pregnant women or women who may become pregnant. Currently no locally-acquired cases of this disease have presented in the US, but travel-related cases have. Tracking of the disease and its spread are ongoing and if you have travel plans check with these sources for the latest recommendations.
What are the symptoms of Zika virus disease?
If Zika virus disease occurs symptoms are likely to begin around a couple days after exposure and symptoms are generally mild, lasting 2-7 days. These symptoms include fever, skin rash, discomfort, headache, joint and muscle pain, and eye redness. Most people infected with Zika virus will have no lasting harm from the disease. If a woman is pregnant when the Zika virus is contracted, however, the virus may cause severe brain damage to the unborn and is linked to a condition called microcephaly. The relationship between Zika virus and microcephaly is not fully understood by scientists.
How is Zika virus disease treated?
Symptoms of Zika virus can be eased with rest, drinking plenty of water, and taking pain relievers like ibuprofen. No antiviral medications are recommended at this time for Zika and no vaccination is available. If you are pregnant and suspect you have Zika virus talk to your doctor about what tests are available. Blood, urine, and saliva tests may be used to find viral RNA and the CDC has released an algorithm for testing. Ultrasound may be used to look for calcifications in the fetal skull and microcephaly. Recommended testing is still controversial and not widely available. The reality is that if you haven’t travelled to a region currently affected by Zika or live in that region then you aren’t considered to be at risk for Zika.
What is microcephaly and does Zika cause it?
Microcephaly is a condition that literally means small head. The head grows in a developing fetus because the brain is growing. In microcephaly the brain is not growing normally and this can be linked to a range of serious difficulties. Many causes of microcephaly are known such as infections like rubella, toxoplasmosis, and cytomegalovirus. Malnutrition or toxic exposures in development like alcohol can also cause microcephaly. ZIKV genetic material has been found in the brain tissue samples of a fetus with microcephaly whose mother was exposed to ZIKV during her pregnancy and experienced symptoms of ZIKA fever in her 13th week of pregnancy. ZIKV genetic material has also been found through amniocentesis. It is not proven that Zika causes microcephaly, but researchers think that the virus may target and replicate in the developing brain of a fetus. Zika doesn’t seem to cause lasting harm in other organs or tissues but stays and replicates in the brain stem.
The best prevention for ZIKV is to not get bit by a mosquito. Consider guidelines and consult with your doctor about travel plans. Look at the EPA’s recommendation for mosquito repellants and follow the directions carefully if you are expecting exposure. If you do they are safe to use during pregnancy. Wearing long pants and shirts can help as well. Standing water is prime breeding ground for mosquitos and can become a safety risk so care should be taken to prevent this. So the ZIKV media frenzy may be inducing worries in your pregnant mind, but fear is a beast that thrives on attention. Arm yourself with facts and be well.
References:
Akpan, Nsikan (January 29, 2016 updated February 1, 2016) How does Zika virus
shrink a baby’s brain and other FAQs. PBS NewsHour. Retreived from: http://www.pbs.org/newshour/updates/zika-virus-faqs-ultrasound-detection/
Centers for Disease Control and Prevention. (February 12,
2016).
Facts about Microcephaly (article). Retreived from: http://www.cdc.gov/ncbddd/birthdefects/microcephaly.html
Centers for Disease Control and Prevention. (January 29,
2016).
Possible Association Between Zika Virus Infection and
Microcephaly — Brazil, 2015
(Morbidity and Mortality Weekly Report). Retreived from: http://www.cdc.gov/mmwr/volumes/65/wr/mm6503e2.htm
Mlakar, J M.D., Korva, M Ph.D., Tul, N M.D., Ph.D., Popović,
M M.D., Ph.D., Poljšak-Prijatelj, M
Ph.D., Mraz, J M.Sc.,... Avšič Županc, T
Ph.D. (February 10, 2016) Zika Virus Associated with Microcephaly. The New
England Journal of Medicine. DOI:
10.1056/NEJMoa1600651
McNeiL, D.G.
Jr., Saint Louis,
C. & St. Fleur, N. ( February 16,
2016). Short Answers to Hard Questions
about Zika Virus. The New York Times. Retreived
at: http://www.nytimes.com/interactive/2016/health/what-is-zika-virus.html?_r=0
World Health Organization.
(February 2016). Zika Virus (fact
sheet). Retreived from: http://www.who.int/mediacentre/factsheets/zika/en/
USE THIS CC VIDEO: https://commons.wikimedia.org/wiki/File:Zika_virus_video_osmosis.webm
And this image: http://d3hjf51r9j54j7.cloudfront.net/wp-content/uploads/sites/5/2013/01/pregnant-worried.jpg
Aplastic Anemia
By: Ragujo
Under normal
circumstances, our bone marrow pumps out up to one trillion (Gordon Lewis &
Marley, 2002) new blood cells each day! It functions like a very efficient
factory, housing tens of thousands (Gordon,Lewis & Marley, 2002) of amazing
machines (pluripotent hematopoetic stem cells) that can churn out three of the
most highly demanded consumer goods (red blood cells, white blood cells, and
platelets). Different chemicals in the
body function as foremen, telling the machines what type of cell to produce. Occasionally a person’s bone marrow will fail
and the factory slows production dramatically.
The products are still made well, but the factory just can’t keep up
with demand. This type of marrow failure
is called aplastic anemia and is a very rare and serious condition.
Reducing numbers of all three blood cell types can have a
profoundly negative impact on one’s quality of life. Our red blood is responsible for carrying
oxygen throughout the body, and when those counts are low (anemia) people
commonly experience dizziness, fatigue, shortness of breath, irregular
heartbeats and pallor. Our white blood
cells are strong players in our immune system, keeping us safe from viral and
bacterial infections. When we lack white
blood cells (neutropenia) then our risk of infection increases immensely, and
any infection requires medical intervention.
Platelets are part of the clotting process and when they are reduced (thrombocytopenia)
an individual is at risk for heavy bleeding and may bruise easily. Nosebleeds, bleeding gums and petichiae
(pinpoint red spots on the skin) are common signs of low platelet counts
(Aplastic Anemia, 2014b). If untreated, these conditions will lead to
death.
In most cases of aplastic anemia the first course of
treatment is to alleviate symptoms of anemia and thrombocytopenia by
transfusing platelets and red blood.
Hand washing, antibiotics and avoiding densely populated areas can help
keep a neutropenic individual avoid infection. These will help meliorate an
immediate situation but long-term recovery is often achieved through a
combination of immunosupressive therapies and/or bone marrow transplant. Because aplastic anemia is thought to be
caused by abnormal expression of T cells that attack the hematopeitic stem
cells, the immunotherapies used interfere with the activity of T cells
(Bacigulpo, 2007). T cells are a type of
white blood cell that are trained to
attack foreign cells in order to keep us healthy, and should know to
leave our cells alone. Stopping the activity of
abnormal T cells allows bone marrow to rebuild its supply of stem cells
and then blood cells. Antithymocyte globulin is the most successful immune
therapy and when used with cyclosporine will improve blood counts in 7 out of
10 cases (Aplastic Anemia, 2015). Bone marrow transplantation will often be
performed before immunosuppressive therapy if a matched sibling donor is
available. If immunotherapy does not
improve counts, and no sibling match is available, then an unrelated donor will
be sought. Survival rates after bone marrow transplants are much higher when
the donor is a relative, but success rates for unrelated donor transplants are
improving. Both treatments show higher
success rates in younger patients and when started soon after diagnosis
(Bacigulpo, 2007).
Aplastic anemia is very rare, affecting roughly 2.0
individuals/million population in Europe and around 4.0 individuals/million
population in Asian countries (Young & Kaufman, 2008). Because the incidence rate for people of
Asian descent living in the U.S. or Europe is comparable to the European
incidence rate, the increased number of cases in Asia suggests that
environmental factors could be more influential than genetic factors in disease
development (Young & Kaufman, 2008).
Toxins, such as solvents and pesticides, as well as medical drugs have
been linked to several cases of aplastic anemia. In other cases, bone marrow failure is
thought to have been caused by infection – infectious mononucleosis, hepatitis,
HIV and leukemia are conditions that can sometimes lead to aplastic
anemia. Overall, however, 75% of
aplastic anemia cases are idiopathic, which means the cause is unknown
(Aplastic Anemia, 2014a; Young & Kaufman, 2008). Because the underlying
cause of marrow failure is typically unknown, there is no sure way to prevent
it. Minimizing exposure to harsh
chemicals and infectious diseases can minimize risk of developing aplastic
anemia.
References
Aplastic Anemia & MDS International Foundation. (2014a).
Aplasatic anemia:
causes. Retrieved from:
http://www.aamds.org/about/aplastic-anemia/causes
Aplastic Anemia & MDS International Foundation. (2014b).
Aplasatic anemia:
symptoms.
Retrieved from:
http://www.aamds.org/about/aplastic-anemia/symptoms
Aplastic Anemia & MDS International Foundation. (2015).
Immunosuppressive drug
therapy. Retrieved from:
http://www.aamds.org/about/aplastic- anemia/treatment/immunosuppressives
Bacigulpo, A. (2007) . Aplastic anemia: pathogenesis and treatment.
ASH Education Book, 1, 23-28.
DOI: 10.1182/asheducation-2007.1.23
Gordon, M.,Lewis, J. & Marley, S. (2002). Of mice and
men and elephants. Blood: 100
(13), 4679. DOI: http://dx.doi.org/10.1182/blood-2002-08-2517
Johns Hopkins Sydney Kimmel Comprehensive Cancer
Center. (n.d). Aplastic anemia.
Retrieved from:
http://www.hopkinsmedicine.org/kimmel_cancer_center/types_cancer/aplastic_anemia.html
Young, N. & Kaufman, D. (2008).
The epidemiology of acquired aplastic anemia.
Hematologica,
93, 489-492. DOI: 10.3324/haematol.12855
Raynaud's Disease
By: TheGreenLabCoat
Working in Family Medicine, you see several chronic diseases
on a daily basis: diabetes mellitus 2, hypertension, and osteoporosis - Or as
one of our elderly patients jokingly refers to them, “all these old people
diseases.” Recently during a new patient visit, I noticed that this patient’s
fingers were a different color from the rest of her hand; fleshy, pink hands
but with almost paper white fingers. At first I thought it might have been a
skin discoloration that naturally occurs in some people, but through the course
of the visit her hand gradually turned blue, and then a bright shade of red. I
couldn’t help but to ask the patient, “Are you aware that your fingers have
been changing colors since you sat down in here?” The patient waved her
unusually colorful hand in the air, stating “Oh honey, I have Raynaud’s, it's
fine. I was just holding my soda.” Not knowing exactly what she meant at the
time, I decided to educate myself on the subject: What is Raynaud’s?
Raynaud’s Disease, named after Maurice Raynaud in 1862, is a
disorder of the blood vessels that causes them to overreact, predominantly in
the hands and feet. Our body has an internal thermostat with many locations of
thermometers. When we are cold, the sensors in our body tell us “Hey, we need
to keep the heat up so that all of our organs continue to function.” It sends
out a signal that binds to receptors on our blood vessels, instructing them to
secrete vasoconstriction hormones. When this happens, our blood vessels
constrict, kind of like shutting all the windows around the house to keep the
heat in. In this situation there is less blood going to our extremities,
keeping the core of our bodies warmer. People who have Raynaud’s disease are
unable to regulate the appropriate blood flow when exposed to cold
temperatures. Their blood vessels spasm, which can cause pain, numbness, and
tingling. Color changes in fingers are the most observable symptoms when an
attack is happening. Emotional distress may also be a trigger of this
phenomenon.
Though the exact cause of Raynaud’s is still unknown,
scientists have been able to separate this disease into two major
classifications: Primary Raynaud’s Phenomenon (PRP) and Secondary Raynaud’s
(SR). PRP is the most common type in most people. Development can occur at any
age but happens most frequently between the ages of 15 - 30, and it typically
affects women more often than men. If a family member has PRP, there is a 33%
chance that their offspring will develop the disease as well.
Secondary Raynaud’s (SR) has been associated with rheumatic
disorders such as Lupus and scleroderma. Depending
on severity of SR, it could be life threatening due to the hardening of blood
vessels which down the road could be a contributing factor of heart issues such
as ischemia or plaque buildup in the arteries.
Neural abnormalities, hormonal
and genetic factors, and smoking all have been noted as potential causes of
this disease. A few blood tests and observing capillaries of the
fingernails under a microscope are the common methods of diagnosing Raynaud’s
Disease. There currently are no medications to cure
Raynaud’s. Outcomes for patients with PRP are usually very good. No reported
mortality and little morbidity. In very rare cases, ischemia of the affected
body part can result in necrosis.
Following the guidelines below
can help prevent an attack:
●
Keep warm - Manually
regulating body temperature can help to prevent an attack. For instance, avoid
moving from a hot summer day to a cold air conditioned room. Wearing mittens
and socks to bed during winter, or changing out of wet clothing items a rainy
day are both good preventative measures.
●
Do not smoke -
Nicotine in cigarettes causes the body temperature to lower, which may trigger
an attack.
●
Control stress -
Emotional well being can prevent an attack. Relaxation methods such as
meditation has been reported useful.
●
Avoid stimulating
medications, foods - Vasoconstrictor medications such as narcotics, beta
blockers (blood pressure medication) OTC cold medication, and caffeine.
As for SR, there is no FDA-approved medication
specifically, but this type of Raynaud’s is usually treated with calcium
channel blockers such as amlodipine (norvasc) and felodipine which work by relaxing the
smooth muscle and dilating the small blood vessels.
When my patient returns to the clinic, hopefully just for a routine
check up, I will be able to have a conversation with her about this disease and
not look like a deer caught in headlights. I might be able to learn a few
pointers from her to potentially offer future patients with this disease some
information.
References
Peer-Reviewed
Herrick, A. L. (2005, May 01). Pathogenesis of Raynaud’s phenomenon.
Retrieved February 12, 2016, from
http://rheumatology.oxfordjournals.org/content/44/5/587.full.pdf html
Wigley, F. M., MD. (2002, September 26). Raynaud's Phenomenon. Retrieved
February 12, 2016, from http://www.nejm.org/doi/full/10.1056/nejmcp013013
Non-Peer-Reviewed
Hansen-Dispenza, H., MD, & Lisse, J. R., MD,FACP. (2015, November
17). Raynaud Phenomenon. Retrieved February 12, 2016, from
http://emedicine.medscape.com/article/331197-overview
Mayo Clinic Staff. (2015, March 04). Diseases and Conditions Raynaud's
disease. Retrieved February 12, 2016, from http://www.mayoclinic.org/diseases-conditions/raynauds-disease/basics/definition/con-20022916
Friday, February 12, 2016
Blog-o-genesis perfecta
By: The Doctor
As an instructor, I'm beyond ecstatic to roll out the fruits of my students' labor - their blog posts! Biology 241 - i.e., pathophysiology - is new curriculum for me this term and because I'm creating a lot as I go, I viewed this class as a "golden opportunity" to try an idea I've wanted to try for some time - an instructional blog.
As an instructor, I'm beyond ecstatic to roll out the fruits of my students' labor - their blog posts! Biology 241 - i.e., pathophysiology - is new curriculum for me this term and because I'm creating a lot as I go, I viewed this class as a "golden opportunity" to try an idea I've wanted to try for some time - an instructional blog.
What is an instructional blog?
While blogs serve many purposes (entertainment, information, product reviews, recipes, etc), the instructional blog serves as a tool of the learning process that can be shared with the world! It is intended to complement and extend classroom lectures and discussions beyond the canned powerpoint-based lecture/textbook format, which is widely used yet isn't necessarily the most effective teaching method for helping students retain information long-term.
The impetus for this is simple. Drawing on my own experiences as an undergraduate student (over 15 years ago now - eek!), the things I remember most were never the lectures, but rather assignments where I was "forced" to explore ideas and create something with those ideas. I have "learned" and forgotten the details of the Kreb's cycle numerous times throughout my career as both student and teacher, yet I have never forgotten how muscles fatigue with continued stimulation. I mean, I still have visions of stringing up a frog gastrocnemius muscle and then zapping it into action (or diminishing action?)! I was "forced" to experiment and then write the details of this experiment and here I am 15 years later recalling this experience in a blog post. In a sense, I'm trying to permanently root some detail of health and disease into my own student's long-term memory stores. More importantly, however, I'm trying to "teach" how to research, understand, and communicate biomedical information (and by "teach" I really mean "learn by doing"). We can only scratch the surface on all there is to learn about human disease in one term. Heck - there's still so much I don't know! What I hope to provide are the skills necessary to discern all the material I can't possibly cover.
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| Image source: Pixabay (CC0 license - public domain) |
The first of two blog posts
Teaching others is an incredibly effective method for learning, and my hope is that the first student blog post essentially allows them to teach their peers (and the world) about a disease process. The target audience is informed, but not a health care professional or individual with a background in biology/biomedical science. To communicate well, the student needs to understand the disease at a deep level in order to clearly and concisely pull out the important details. Creative explanations and metaphors are highly encouraged (not your typical science class for sure!). I can't wait to see their creations!
Assessment of the assignment
At the end of this, I sincerely hope my students share whether this assignment actually achieves what I hope it does and if they have suggestions for how it could be improved.
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