What are the differences and similarities between the Ewells and Cunninghams in Harper Lee's To Kill a Mockingbird?

One similarity shared between the Cunninghams and Ewells in Harper Lee's To Kill a Mockingbird is that they are both uneducated, low class families. They are also both presented as racist families. Other than that, they are mostly presented as character foils, meaning exact opposites.They are especially presented as character foils because the Cunninghams are very hardworking people, whereas the Ewells have never worked a day in their lives. We know...

One similarity shared between the Cunninghams and Ewells in Harper Lee's To Kill a Mockingbird is that they are both uneducated, low class families. They are also both presented as racist families. Other than that, they are mostly presented as character foils, meaning exact opposites.

They are especially presented as character foils because the Cunninghams are very hardworking people, whereas the Ewells have never worked a day in their lives. We know the Cunninghams are hardworking people because Walter Cunningham Sr. goes to Atticus for help about his entailed farmland and, as payment, brings Atticus whatever his poor farm is able to produce during the Great Depression. Scout describes the payments Atticus received from Mr. Cunningham in her following narration:

One morning Jem and I found a load of stovewood in the back yard. Later, a snack of hickory nuts appeared on the back steps. With Christmas came a crate of smilax and holly. That spring we found a crokersack full of turnip greens, Atticus said Mr. Cunningham had more than paid him. (Ch. 3)

Since the Cunninghams are such hardworking people, they are also prideful people, and their pride is demonstrated in their refusal to accept charity, despite being poor.

In contrast, not only have the Ewells never worked a day in their lives, Bob Ewell lives only off of charity in the form of government relief checks, which he mostly spends on alcohol. In addition, while the Cunninghams are respectful people who value loyalty, just as Mr. Cunningham showed loyalty to Atticus by breaking up the lynch mob, Bob Ewell is a generally evil person, so evil he is willing to try to kill innocent children for the sake of revenge.

What are anabolic steroids? |

History of Use

Although commonly called anabolic steroids, these drugs are more correctly identified as anabolic-androgenic steroids. They have both anabolic properties, which promote the growth of skeletal muscle, and androgenic properties, which promote the development of male sexual characteristics.

Synthetic testosterones were first developed in the 1930s in Europe. After World War II they were used by sports officials in the Soviet bloc, especially East Germany, to enhance athletic strength and performance in both males and females. In 1956, John Ziegler, a US Olympic Team physician, developed methandrostenolone, which in 1958 became the first anabolic steroid licensed in the United States for medical use. Eventually, the danger and long-term risk of the use of anabolic steroids as muscle enhancers became apparent. The steroids were banned from use in Olympic competitions in 1976.

The US Anabolic Steroids Control Act
was passed in 1990, making anabolic steroids a schedule III controlled substance in the United States. Anabolic steroids now are used in medicine primarily to treat men with hypogonadism (low production of testosterone by the testes) and to treat boys with delayed puberty. The steroids also are used to facilitate tissue regrowth in persons with severe burns and to treat severe weight loss in persons with acquired immune deficiency syndrome.

The illegal use of anabolic steroids, including among professional athletes, remains a major problem. Newer formulations based on molecules not screened by existing tests are always being developed. These newer steroids are popular among teenage boys, especially those participating in competitive sports, most notably wrestling, football, and weightlifting. Although anabolic steroids are banned by virtually all major amateur and professional sports organizations, there have been numerous cases of high-profile athletes revealed to have used the drugs to enhance their performance. Within Major League Baseball (MLB) especially, steroid use was rampant among players throughout the 1980s and 1990s, affecting the way baseball was played and leading to a public scandal. The US Drug Enforcement Administration has also noted a relatively high rate of steroid abuse among law enforcement officials, particularly police officers. Abusers take doses of anabolic steroids in quantities ten to one-hundred times greater than those doses used in medicine.

Anabolic steroids, including formulations of bolderone and nandrolone, are usually injected. Methandrostenolone, oxymetholone, and stanozole are taken as pills. Steroid gels, creams, and transdermal patches are less effective when used alone, but many abusers employ a “stacking” regimen, in which topical, oral, and injectable formulations are combined to increase the total effect and to avoid detection of high levels of any one steroid in testing. New formulations of anabolic steroids that are not specifically restricted or that are not detectable using current screening methods are being developed and distributed. Well over fifty anabolic steroids have been identified as controlled substances in the United States.

Effects and Potential Risks

Unlike most other abused drugs, anabolic steroids do not cause immediate euphoria or other pleasurable feelings. They are used to promote rapid muscle growth and weight gain (also called bulking up) and to increase strength and sports prowess over time. A common adverse effect of high, prolonged dosing is “roid rage,” in which one experiences mood swings, anxiety, irritability, and aggressiveness. Other psychological effects such as depression and psychosis may be observed, and some evidence suggests that the risk of suicide may be increased by prolonged steroid use.

Abusers do not become physically addicted to anabolic steroids, but they can develop a compulsive reliance on them. Depression, headache, fatigue, loss of appetite, and insomnia may result if the drugs are discontinued. Depression may be long-lasting and can lead to suicidal thoughts and actions. In males, long-term abuse suppresses the sex drive, lowers or halts sperm production, and causes shrinking of the testicles. Severe acne may develop. In general these adverse effects are reversible. Feminine characteristics, including breast development, may occur because some of the excess testosterone produced is converted into the female hormone estradiol. Such changes cannot be reversed.

In females, abuse leads to the emergence of masculine characteristics, including extra muscle deposits, deeper voice, thicker and coarser body hair, male-pattern baldness, disruption of the menstrual cycle, and enlargement of the clitoris. Some of these changes are irreversible. Among younger abusers, high testosterone levels in the body can prematurely signal bones to stop growing and, thus, can stunt growth. In both males and females, steroid abuse contributes to the risk of heart attack and stroke. High levels of testosterone negatively impact cholesterol levels. Levels of bad cholesterol (low-density lipoprotein, or LDL) are increased, while those of good cholesterol (high-density lipoprotein, or HDL) are decreased. This causes a buildup of plaque in the arteries (atherosclerosis), which decreases or eventually blocks blood flow to the heart, leading to a heart attack, or blood flow to the brain, leading to a stroke. Liver disease too is a rare but potential risk of steroid abuse. Blood-filled cysts that develop in the liver may rupture and cause life-threatening internal bleeding. Kidney failure also can occur. Abusers who share or use contaminated needles are at risk of infection with HIV (human immunodeficiency virus) or with the hepatitis B or C viruses. Anabolic steroids are also considered likely carcinogens by the International Agency for Research on Cancer (IARC), a branch of the World Health Organization (WHO).

Bibliography

"Anabolic Steroids." Center for Substance Abuse Research. U of Maryland, 29 Oct. 2013. Web. 28 Oct. 2015.

"Anabolic Steroids." MedlinePlus. US National Library of Medicine, 18 Sept. 2015. Web. 28 Oct. 2015.

Gold, Mark S., ed. Performance-Enhancing Medications and Drugs of Abuse. Binghamton, NY: Haworth, 2007. Print.

Kuhn, Cynthia, Scott Swartwelder, and Wilkie Wilson. Buzzed: The Straight Facts about the Most Used and Abused Drugs from Alcohol to Ecstasy. 3rd ed. New York: Norton, 2008. Print.

Minelli, Mark J. Drug Abuse in Sports: A Student Course Manual. 7th ed. Champaign, IL: Stipes, 2008. Print.

Rosen, Daniel M. Dope: A History of Performance Enhancement in Sports from the Nineteenth Century to Today. Westport, CT: Praeger, 2008. Print.

Yasalis, Charles E., ed. Anabolic Steroids in Sport and Exercise. Champaign, IL: Human Kinetics, 2000. Print.

If the lot size is 3000, the sample size is 140, and the probability of accepting each lot is 0.798, what is the ATI for this quality level of...

The ATI, or average total inspection, is the average number of items we end up inspecting per lot in the long run, assuming that we inspect a given sample from each lot every time, and then if one of those is bad we infer that the lot is bad and go on to inspect all of them.Thus the ATI is an expectation value, summing two possible events:(1) The sample goes well, in which...

The ATI, or average total inspection, is the average number of items we end up inspecting per lot in the long run, assuming that we inspect a given sample from each lot every time, and then if one of those is bad we infer that the lot is bad and go on to inspect all of them.

Thus the ATI is an expectation value, summing two possible events:

(1) The sample goes well, in which case we inspect 140 items.
(2) One or more items in the sample is defective, in which case we inspect the whole lot, 3000 items.

We are given that the probability of accepting a lot is 0.798, so the probability of rejecting a lot and inspecting all items must be one minus that, or 0.202. From there we can calculate our expectation value, which is the ATI:
`ATI = (0.798)(140) + (0.202)(3000) = 111.72 + 606 = 717.72`

We will, on average, expect to inspect about 717.72 items per lot, so for example if there were 100 lots we'd inspect somewhere around 71,772 items. (The actual figure could be more or less than this, but that is the long-run average we expect to converge toward by the Law of Large Numbers.)

Was Ancient Rome or Athens a better form of government?

The Roman system of government was a republic, which meant that citizens could vote for who would represent them in government. The Athenian system of government was a direct democracy, which meant that the entire body of citizens voted for virtually everything that was decided by the government. Both systems limited citizenship, but it was easier to acquire citizenship in Rome than in Athens.

The Roman system of government was more complex, but offered a...

The Roman system of government was a republic, which meant that citizens could vote for who would represent them in government. The Athenian system of government was a direct democracy, which meant that the entire body of citizens voted for virtually everything that was decided by the government. Both systems limited citizenship, but it was easier to acquire citizenship in Rome than in Athens.

The Roman system of government was more complex, but offered a more flexible and efficient form of government than in Athens. Since it was more efficient and allowed for greater flexibility, I believe it was the better form of political organization. Athens was often criticized by other city-states as being dictated by "mob" rule. In other words, the political climate changed often at the mood of the people. In Rome, greater stability existed and military and political officers were granted more power and influence as a result. The consequence of having powerful and influential leaders is that more can be achieved because political leaders can make decisions for the good of the state without fear of being replaced at the whims of the populace. For this reason, the Roman system of government can be considered superior to Athens.

What is hypertension? |

Causes and Symptoms

Hypertension is a higher-than-normal blood pressure (either systolic or diastolic). Blood pressure is usually measured using a sphygmomanometer and a stethoscope. The stethoscope is used to hear when the air pressure within the cuff of the sphygmomanometer is equal to that in the artery. When taking a blood pressure, the cuff is pumped to inflate an air bladder secured around the arm; the pressure produced will collapse the blood vessels within. As cuff pressure decreases, a slight thump is heard as the artery snaps open to allow blood to flow. At this point, the cuff pressure equals the systolic blood pressure. As the cuff pressure continues to fall, the sound of blood being pumped will continue but become progressively softer. At the point where the last sound is heard, the cuff pressure equals the diastolic blood pressure.

In hypertension, both
systolic and diastolic blood pressures are usually elevated. Blood pressures are reported as the systolic pressure over the diastolic pressure, such as 130/80 millimeters of mercury. It is important to recognize there are degrees of seriousness for hypertension. The higher the blood pressure, the more rigorous the treatment may be. When systolic pressures are in the high normal range, the individual should be closely monitored with annual blood pressure checks. Persistently high blood pressures (greater than 140–159/90–99 millimeters of mercury) require closer monitoring and may result in a decision to treat the condition with medication or other types of intervention.

The blood pressure in an artery is determined by the relationship among three important controlling factors: the blood volume, the amount of blood pumped by the heart (cardiac output), and the contraction of smooth muscle within blood vessels (arterial tone). To illustrate the first point, if blood volume decreases, the result will be a fall in blood pressure. Conversely, the body cannot itself increase blood pressure by rapidly adding blood volume; fluid must be injected into the circulation to do so.

A second controlling factor of blood pressure is cardiac output (the volume of blood pumped by the heart in a given unit of time, usually reported as liters per minute). This output is determined by two factors: stroke volume (the volume of blood pumped with each heartbeat) and the heart rate (beats per minute). As heart rate increases, output generally increases, and blood pressure may rise as well. If blood volume is low, such as with excessive bleeding, the blood returning to the heart per beat is lower and could lead to decreased output. To compensate, the heart rate increases to prevent a drop in blood pressure. Therefore, as cardiac output changes, blood pressure does not necessarily change.

Last, a major controlling factor of blood pressure is arterial tone. Arteries are largely tubular, smooth muscles that can change their diameter based on the extent of contraction (tone). This contraction is largely under the control of a specialized branch of the nervous system called the sympathetic nervous system. An artery with high arterial tone (contracted) will squeeze the blood within and increase the pressure inside. There is also a relaxation phase that will allow expansion and a decrease in blood pressure. Along with relaxation, arteries are elastic to allow some stretching, which may further help reduce pressure or, more important, help prevent blood pressure from rising.

There are two general types of hypertension: essential and secondary. Secondary hypertension is attributable to some underlying identifiable cause, such as a tumor or kidney disease, while essential hypertension has no identifiable cause. Therefore, essential hypertension is a defect that results in excessive arterial pressure secondary to poor regulation by any one of the three controlling factors discussed above. Each factor can serve as a focal point for treatment with medications.

The negative consequences of hypertension are mainly manifested in the deteriorating effect that this condition has on coronary heart disease (CHD). Cardiovascular risk factors for CHD are described as two types, unmodifiable and modifiable. Unmodifiable risk factors cannot be changed. This group includes gender, race, advanced age, and a family history of heart disease (hypertensive traits can be inherited). The modifiable risk factors are cigarette smoking (or other forms of tobacco abuse), high blood cholesterol levels, control over diabetes, and perhaps other factors not yet discovered. For example, additional factors are now recognized for their adverse effects on hypertension, including obesity, a lack of physical activity, and psychological factors.

There is no definitive blood pressure level at which a person is no longer at risk for CHD. While any elevation above the normal range places the person at increased risk for CHD, what are considered high normal blood pressures were previously defined as normal. (Looking back at older data, researchers noted that persons able to maintain pressures at or below 139/89 millimeters of mercury had less severe CHD.) The definition of normal blood pressure may change again in the future as new information is discovered. There is a practical limit as to how low pressure can be while maintaining day-to-day function.

In coronary heart disease, the blood supply to the heart is reduced, and the heart cannot function well. The common term for arteriosclerosis, “hardening of the arteries,” indicates the symptom of reduced blood flow, which is a major component of CHD. When the heart cannot supply itself with the necessary amount of blood (a condition known as ischemia), a characteristic chest pain called angina may be produced. The hardening aspect of this disease is the result of cholesterol deposits in the vessel, which decrease elasticity and make the vessel wall stiff. This stiffness will force pressures in the vessel to increase if cardiac output rises. As pressures advance, the vessel may develop weak spots. These areas may rupture or lead to the development of small blood clots that may clog the vessel; either problem will disrupt blood flow, making the underlying CHD worse. Eventually, if the blood supply is significantly reduced, a myocardial infarction(heart attack) may occur. Where the blood supply to the heart muscle itself is functionally blocked, that part of the heart will die.

Besides contributing to an increased risk of heart attack and coronary heart disease, hypertension is a major risk for other vascular problems, such as stroke, kidney failure, heart failure, and visual disturbances secondary to the effects on the blood vessels within the eye. Hypertension is a major source of premature death in the United States. According to the Centers for Disease Control and Prevention in 2014, over 67 million Americans, or 1 in 3 adults, have hypertension. Over forty percent of all African Americans and over 60 percent of those over the age of sixty-five are affected. Public awareness of hypertension is increasing, yet less than half of all patients diagnosed are treated or report having their condition under control. This lack of control is of particular concern when one considers the organs influenced by hypertension, most notably the brain, eyes, kidneys, and heart.

Although causative factors of hypertension cannot be identified, many physiological factors contribute to hypertension. They include increased sympathetic nervous activity (part of the autonomic nervous system), which promotes arterial contraction; overproduction of an unidentified sodium-retaining hormone or chronic high sodium intake; inadequate dietary intake of potassium or calcium; an increased or inappropriate secretion of renin, a chemical made by the kidney; deficiencies of arterial dilators, such as prostaglandins; congenital abnormalities (birth defects) of resistance vessels; diabetes mellitus or resistance to the effects of insulin; obesity; increased activity of vascular growth factors; and altered cellular ion transport of electrolytes, such as potassium, sodium, chloride, and bicarbonate.

The kidneys are greatly responsible for blood pressure control. They have a key role in maintaining both blood volume and blood pressure. When kidney function declines, secondary to problems such as a decrease in renal blood flow, the kidney will release renin. High renin levels result in activation of the renin-angiotensin-aldosterone system. The resulting chemical cascade produces angiotensin II, a potent arterial constrictor. Another chemical released is aldosterone, an adrenal hormone which causes the kidney to retain water and sodium. These two actions add to blood volume and increase arterial tone, resulting in higher blood pressure. Normally, the renin-angiotensin-aldosterone system protects kidney function by raising blood pressure when it is low. In hypertensives, the controlling forces seem to be out of balance, so that the system does not respond appropriately. The renin-angiotensin-aldosterone system has a negative effect on bradykinin, a chemical that protects renal function by producing vasodilating prostaglandins that help maintain adequate renal blood flow. This protection is especially important in elderly individuals, who may depend on this system to maintain renal function. The system can be inhibited by medications such as aspirin or ibuprofen, resulting in a recurrence of hypertension or less control over the existing disease.

Arteries are largely smooth muscles under the control of the autonomic nervous system, which is responsible for organ function. Yet there is often no conscious control of organs; for example, one can tell the lungs to take a breath, but one cannot tell the heart to beat. The autonomic nervous system has two branches, sympathetic and parasympathetic, that essentially work against each other. The sympathetic system exerts much control over blood pressure. Many chemicals and medicines, such as caffeine, decongestants, and amphetamines, affect blood pressure by mimicking the effects of increased sympathetic stimulation of arteries.

Numerous factors associated with blood pressure elevations will affect one or more of the key determinants of blood pressure; they affect one another as well. An example will show the extent of their relationship. Sodium and water retention will increase blood volume returning to the heart. As this return increases, the heart will increase output (to a point) to prevent heart failure. This higher cardiac output may also raise blood pressure. If arterial vessels are constricted, pressures may be even higher. This elevated pressure (resistance) will force the heart to try to increase output to maintain blood flow to vital organs. Thus, a vicious cycle is started; hypertension can be perceived as a merry-go-round ride with no exit.

Treatment and Therapy

Blood pressure reduction has a protective effect against cardiovascular disease. Generally, as blood pressure decreases, arteries are less contracted and are able to deliver more blood to the tissues, maintaining their function. Furthermore, this decreased blood pressure will help reduce the risk of heart attack in the patient with heart disease. With lower pressures, the heart does not need to work as hard supplying blood to itself or the rest of the body. Therefore, the demand for cardiac output to supply blood flow is less. This reduced workload lowers the incidence of angina.

Treatment of hypertensive patients may involve using one to four different medications to achieve the goal of blood pressure reduction. There are many types of medications from which to choose: diuretics, sympatholytic agents (also known as antiadrenergic drugs), beta-blockers (along with one combined-action alpha-beta blocker), calcium-channel blockers, peripheral vasodilators, angiotensin-converting enzyme inhibitors, and the newest class, angiotension receptor inhibitors. The list of available drugs is extensive; for example, there are fourteen different thiazide-type diuretics and another six diuretics with different mechanisms of action.

Patients prone to sodium and water retention are treated with diuretics, agents that prevent the kidney from reabsorbing sodium and water from the urine. Diuretics are usually added to other medications to enhance those medications’ activity. Research into thiazide-type diuretics has shown that these agents possess mild calcium-channel blocking activity, aiding their ability to reduce hypertension.

Beta-blocking agents are used less often than when they were first developed. They work by decreasing cardiac output through reducing the heart rate. Although they are highly effective, the heart rate reduction tends to produce side effects. Most commonly, patients complain of fatigue, sleepiness, and reduced exercise tolerance (the heart rate cannot increase to adapt to the increasing demand for blood in tissues and the heart itself). These agents are still a good choice for hypertensive patients who have suffered a heart attack. Their benefit is that they reduce the risk of a second heart attack by preventing the heart from overworking.

Calcium-channel blockers were originally intended to treat angina. These agents act primarily by decreasing arterial smooth muscle contraction. Relaxed coronary blood vessels can carry more blood, helping prevent the pain of angina. When calcium ions enter the smooth muscle, a more sustained contraction is produced; therefore, blocking this effect will produce relaxation. Physicians noted that this relaxation also produced lower blood pressures. The distinct advantage to these agents is that they are well tolerated; however, some patients may require increasing their fiber intake to prevent some constipating effects.

Peripheral vasodilators have been a disappointment. Theoretically, they should be ideal since they work directly to cause arterial dilation. Unfortunately, blood pressure has many determinants, and patients seem to become immune to direct vasodilator effects. Peripheral vasodilators are useful, however, when added to other treatments such as beta-blockers or sympatholytic medications.

The sympatholytic agents are divided into two broad categories. The first group works within the brain to decrease the effects of nerves that would send signals to blood vessels to constrict (so-called constrict messages). They do this by increasing the relax signals coming out of the brain to offset the constrict messages. The net effect is that blood vessels dilate, reducing blood pressure. Many of these agents have fallen into disfavor because of adverse effects similar to those of beta-blockers. The second group of sympatholytics works directly at the nerve-muscle connection. These agents block the constrict messages of the nerve that would increase arterial smooth muscle tone. Overall, these agents are well tolerated. Some patients, especially the elderly, may be very susceptible to their effect and have problems with low blood pressure; this issue usually resolves itself shortly after the first dose.

The renin-angiotensin-aldosterone system is a key determinant of blood pressure. Angiotensin-converting enzyme inhibitors (ACE inhibitors) work by blocking angiotensin II and aldosterone and by preserving bradykinin. They have been found quite effective for reducing blood pressure and are usually well tolerated. Some patients will experience a first-dose effect, while others may develop a dry cough that can be corrected by dose reductions or discontinuation of the medication. The angiotension receptor inhibitors work, instead, by blocking the effects of this substance on the target cells of the arteries themselves. They are proving to be excellent substitutes for people who cannot tolerate the related class of ACE inhibitors.

Unfortunately, and contrary to popular belief, no one can reliably tell when his or her own blood pressure is elevated. Consequently, hypertension is called a “silent killer.” It is extremely important to have regular blood pressure evaluations and, if diagnosed with hypertension, to receive treatment.

From 1950 through 1987, as advances in understanding and treating hypertension were made, the United States population enjoyed a 40 percent reduction in coronary heart disease and a more than 65 percent reduction in stroke deaths. (By comparison, noncardiovascular deaths during the same period were reduced little more than 20 percent.)

It is evident that blood pressure can be reduced without medications. Research in the 1980s led to a nonpharmacologic approach in the initial management of hypertension. This strategy includes weight reduction, alcohol restriction, regular exercise, dietary sodium restriction, dietary potassium and calcium supplementation, stopping of tobacco use (in any form), and caffeine restriction. Often, these methods can produce benefits without medication being prescribed. Stress is another common contributor to hypertension; therefore, stress reduction and management is another strategy to reduce blood pressure. This may be achieved through lifestyle changes, meditation, relaxation techniques, and exercise. Using this approach, medication is added to the therapy if blood pressure remains elevated despite good efforts at nonpharmacologic control.

Other aspects of hypertension and hypertensive patients have been identified to help guide the clinician to the proper choice of medication. With this approach, the clinician can focus therapy at the most likely cause of the hypertension: sodium and water retention, high cardiac output, or high vascular resistance. This pathophysiological approach led to the abandonment of the rigid step-care approach described in many texts covering hypertension. The pathophysiological approach to hypertension management is based on a series of steps that are taken if inadequate responses are seen.

The best strategy for controlling hypertension is to be informed. Each person needs to be aware of his or her personal risk for developing hypertension. One should have regular blood pressure evaluations, avoid eating excessive salt and sodium, increase exercise, and reduce fats in the diet. Maintaining ideal body weight may be a key control factor. Studies have shown that patients who have been successful at losing weight will require less stringent treatment. The benefits could be a need for fewer medications, reduced doses of medications, or both.

Bibliography

Cruickshank, J. M. Essential (Primary) Hypertension. New York: McGraw-Hill Medical, 2013. Print.

Elliott, William J., and Henry R. Black. Hypertension: A Companion to Braunwald's Heart Disease. Philadelphia: Elsevier Saunders, 2013. Print.

"High Blood Pressure Facts." Centers for Disease Control and Prevention. CDC, 7 July 2014. Web. 21 Aug. 2014.

McGowan, Mary P., and Jo McGowan-Chopra. The Hypertension Sourcebook. Chicago: Contemporary, 2001. Print.

Messerli, Franz H., ed. Cardiovascular Disease in the Elderly. 3d ed. Boston: Kluwer, 1993. Print.

Mancia, Giuseppe, and Adel E. Berbari. Special Issues in Hypertension. Milano: Springer-Verlag, 2012. Print.

Matthes, Jan, and Christian Albus. "Improving Adherence with Medication: A Selective Literature Review Based on the Example of Hypertension Treatment." Dtsch. Arztebl Int 111.4 (2014): 41–47. Print.

Messerli, Franz H. The Heart and Hypertension. New York: Yorke Medical, 1987. Print.

Piscatella, Joseph, and Barry Franklin. Take a Load Off Your Heart: 109 Things You Can Do to Prevent or Reverse Heart Disease. New York: Workman, 2003. Print.

Portman, Ronald J., Julie R. Ingelfinger, Joseph T. Flynn. "Pediatric Hypertension." Clinical Hypertension and Vascular Disease. 3d ed. New York: Humana, 2013. Print.

Rowan, Robert L. Control High Blood Pressure Without Drugs: A Complete Hypertension Handbook. Rev. ed. New York: Fireside, 2001. Print.

Seeley, Rod R., Trent D. Stephens, and Philip Tate. Anatomy and Physiology. 7th ed. New York: McGraw-Hill, 2006. Print.

Tierney, Lawrence M., Stephen J. McPhee, and Maxine A. Papadakis, eds. Current Medical Diagnosis and Treatment 2007. New York: McGraw-Hill, 2006. Print.

Zanchetti, Alberto. "Challenges of Hypertension and Hypertension Treatment." Journal of Hypertension. Lippincott Williams & Wilkins, 20 Aug. 2014. Web. 24 Aug. 2014.

What is Lynch syndrome? |

Risk Factors

Lynch syndrome poses an increased risk of colorectal, stomach, small bowel, gallbladder duct, upper urinary tract, brain, and skin cancers. Women with LS have additional risk of endometrial and ovarian cancer. A diagnosis can be made by family history and is typically confirmed with the finding of a genetic alteration (mutation) in a mismatch repair (MMR) gene.

Etiology and Genetics

Lynch syndrome is inherited in an autosomal dominant fashion, with most individuals inheriting this altered gene from their parent.

Lynch syndrome is most commonly associated with gene changes (mutations) found in mismatch repair genes. When functioning properly, MMR genes routinely repair damaged or erroneous sections of DNA (deoxyribonucleic acid). However, with only one functioning copy of the MMR gene, the cell is less able to repair the mistakes in DNA that accumulate. As abnormal cells continue to grow and divide, the mistakes are perpetuated, and can result in uncontrolled cell growth and possibly cancer.

Researchers best understand the significance of four MMR genes. Genetic variations in MMR genes named MLH1 (on chromosome 3), MSH2 and MSH6 (both on chromosome 2), and PMS2 (on chromosome 7) increase the risk of developing colorectal and LS-related cancers. Inactivation may result from deletions, mutations, or splicing errors occurring anywhere throughout the gene. The genes responsible for 20 to 25 percent of colorectal cancer cases are currently unknown and have not yet been discovered.

Having LS confers an increased risk of cancers. The lifetime risk of colorectal cancer for men with LS is currently estimated at 66 percent; the figure is 42 percent for women. Women also have an increased risk of 39 percent for endometrial cancer throughout the lifetime.

Symptoms

Despite the term “nonpolyposis,” patients with hereditary nonpolyposis colorectal cancer (HNPCC), another name for LS, do have polyps. Individuals with HNPCC tend to develop less than one hundred polyps, which is much fewer than other forms of inherited colorectal cancers. Polyp formation generally begins with patients between twenty and thirty years of age. The polyps are typically right-sided adenomas that can be more aggressive than nonhereditary colorectal cancers.

Screening and Diagnosis

Individuals with a strong family history of cancer are encouraged to seek genetic counseling to determine their personal risk status. Carrier testing via DNA analysis (called microsatellite instability testing) may be useful to confirm or rule out personal risks. DNA testing is not usually recommended for individuals under the age of eighteen; however, screening for colorectal cancer may be initiated.

Individuals with colorectal cancer or other LS-associated cancers often confirm the diagnosis of LS by testing the tumor directly. Current practices include DNA testing MMR genes for instability (microsatellite instability, or MSI testing). The tumor can also be tested by chemically staining thin sections (immunohistochemistry), which are later evaluated by a pathologist.

Full colonoscopy screenings should be performed every one to two years because of the aggressive nature of LS-associated colorectal cancers. Colonoscopy screening should be initiated between the ages of twenty and twenty-five, or ten years before the earliest age of diagnosis in the family (whichever comes first).

Endometrial and ovarian cancer surveillance is less established than screening for colorectal cancer. In addition to annual examinations, annual transvaginal ultrasounds and the CA-125 blood test are also available.

Other screening practices are also available for stomach and urinary tract cancers including gastroscopy and ultrasonography respectively. No specific screening recommendations are currently available for gallbladder and brain cancers.

Treatment and Therapy

Treatment of colorectal cancers and other LS-associated cancers is dependent upon the nature of the cancer. Typically chemotherapy, radiation therapy, and surgery are available as effective treatments.

Prevention and Outcomes

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin has been shown to be effective in preventing some colorectal cancers in patients with other types of hereditary colorectal cancer conditions. The efficacy in individuals with LS, however, is currently unknown.

Oral contraceptives have been shown to reduce the risk of ovarian and endometrial cancers in the general public; however it is not known whether they are as effective in risk reduction for individuals with LS.

Because routine colonoscopy is effective in detecting colon cancer, prophylactic surgery (removal of the colon) is generally not recommended for individuals with LS. Upon the finding of initial colorectal cancer, however, colectomies are recommended given the accelerated rate of carcinogenesis of LS-related colorectal cancers.

Prophylactic removal of the uterus and ovaries after childbearing years is optional for females with concerns with gynecologic cancers associated with LS.

In general, LS-associated cancers have the most positive outcome when detected early; thus adhering to recommended screening practices is essential to optimal care. Patients with Lynch syndrome have better rates of survival after colorectal cancer in comparison to patients with sporadic (nonhereditary) colorectal cancers.

Bibliography

Bonis, P. A., et al. “Hereditary Nonpolyposis Colorectal Cancer: Diagnostic Strategies and Their Implications.” Evidence Report/Technology Assessment 150 (2007): 1–180.

Jankowski, Janusz A. Z. Inflammation and Gastrointestinal Cancers. Heidelberg: Springer, 2011. Print.

Lindor, N. M., et al. “Recommendations for the Care of Individuals with an Inherited Predisposition to Lynch Syndrome: A Systematic Review.” JAMA 296.12 (2006): 1507–517.

Lynch, H. T., and J. F. Lynch. “What the Physician Needs to Know About Lynch Syndrome: An Update.” Oncology 19.4 (2005): 455–63.

McKusick, Victor A. “Lynch Syndrome I.” Online Mendelian Inheritance in Man. Johns Hopkins U, 12 Feb. 2014. Web. 1 Aug. 2014.

Munoz, Juan Carlos. “Hereditary Colorectal Cancer.” Medscape. WebMD, 18 Apr. 2013. Web. 1 Aug. 2014.

I don't understand the term standard atmospheric pressure. At sea level, is the pressure on mercury 760 mmHg? Why is a mercury column used as the...

The air in our atmosphere is made of molecules of gases such as oxygen and nitrogen gas. These molecules have a mass and are made of matter, thus gravity pulls them downward towards the earth's surface. We have the weight of the entire atmosphere (from space down to us) sitting on top of us our entire lives, and the exact weight of the atmosphere at any given time is referred to as atmospheric pressure. 

Normally...

The air in our atmosphere is made of molecules of gases such as oxygen and nitrogen gas. These molecules have a mass and are made of matter, thus gravity pulls them downward towards the earth's surface. We have the weight of the entire atmosphere (from space down to us) sitting on top of us our entire lives, and the exact weight of the atmosphere at any given time is referred to as atmospheric pressure. 

Normally we have around 1 atmosphere of pressure on us, or 1 atm. This number can go up or down based on a number of conditions including humidity, temperature, and altitude. The higher in the atmosphere you go the less air is above you, thus the lower the pressure. Sea level is used as the standard, as all other heights are also based off of this value. 

The current tool used to measure air pressure is the barometer, a large compass-like tool that can finely weigh the air and show the results as atmospheres, torr, or millimeters of mercury (mmHg for short). The first barometer, built in 1644 by Evangelista Torricelli, used a large glass tube and liquid mercury over a plate. Based on the air pressure each day the mercury would move up or down in the tube and it was measured in millimeters, thus millimeters of mercury (mmHg). The accepted "normal" air pressure at sea level is indeed about 760 mmHg or 1 atm of pressure. We may have created better technology than the large open tubes of mercury but the old standard unit still remains, even if no modern barometer uses mercury any more. 

What is Huntington's disease? |

Causes and Symptoms

The mutated gene responsible for Huntington’s disease is located on one arm of chromosome 4 and produces the protein huntingtin. The gene contains repeats of the triplet nucleotide sequence CAG. Normal individuals have between nine and thirty-five (on average eighteen or nineteen) CAG repeats in their genes; affected individuals have forty or more repeats, with an average of forty-six repeats. Individuals with between thirty-six and thirty-nine repeats may or may not develop Huntington’s disease. The disease always occurs if the expansion is forty or more repeats. The larger the number of repeats above forty, the earlier the onset of the disease. The disease-causing gene is dominant, so those who inherit the mutated gene develop the disease and have a 50 percent chance of passing the defective gene on to their children.

The triplet CAG codes for the amino acid glutamine. Mutant forms of the huntingtin proteins have forty or more glutamines in the protein. Huntington’s disease appears to be caused by a mutation involving a gain of function, in which the expanded polyglutamine region makes the mutant huntingtin protein toxic. Aggregates of mutant huntingtin are observed in the neurons of those who died from Huntington’s disease. Normal huntingtin appears to keep neurons alive by stopping programmed cell death.

The neuropathology of Huntington’s disease is primarily the degeneration of neurons of the striatum (part of the basal ganglia) and the motor cortex. Clinical manifestations of Huntington’s disease typically begin in midlife (thirties and forties), with characteristic motor abnormalities such as uncoordinated movements (chorea) and loss of muscle control (dystonias), personality changes, a gradual loss of cognition, and eventually, death. Huntington’s disease primarily affects the central nervous system, but most patients actually die of heart or respiratory complications from long confinement to bed or from head injuries caused by frequent falls.

Treatment and Therapy

The present treatment for Huntington’s disease is the use of drugs such as tricyclic antidepressants to control psychological problems and neuroleptics to treat the associated chorea. In 2003, clinical trials were examining the effects of implanting fetal neurons into the brains of Huntington’s disease patients.

Perspective and Prospects

In 1872, George Huntington first reported this hereditary disease that he observed in a Long Island, New York, family. Because of the uncoordinated movements of patients, he termed the condition “chorea,” from the Greek word for “dance.” In 1981, Nancy Wexler began to study a large extended family with Huntington’s disease in an isolated village on Lake Maracaibo, Venezuela. Studies of this family aided the work of localizing the gene responsible for this disease. In 1993, that gene was identified by the collaborative work of fifty-eight scientists, led by James R. Gusella and Francis S. Collins.

Bibliography

Alan, Rick. "Huntington's Disease." Health Library, September 10 , 2012.

Baréma, Jean. The Test: Living in the Shadow of Huntington’s Disease. New York: Franklin Square Press, 2005.

Bates, Gillian, Peter S. Harper, and Lesley Jones, eds. Huntington’s Disease. 3d ed. New York: Oxford University Press, 2007.

Cattaneo, Elena, Dorotea Rigamonti, and Chaiara Zuccato. “The Enigma of Huntington’s Disease.” Scientific American 287 (December, 2002): 92–97.

"Huntington's Disease." Mayo Clinic, May 5, 2011.

"Huntington's Disease: Hope Through Research." National Institute of Neurological Disorders and Stroke, April 24, 2013.

Lewis, Ricki. Human Genetics: Concepts and Applications. 9th ed. Dubuque, Iowa: McGraw-Hill, 2009.

Nussbaum, Robert L., Roderick R. McInnes, and Willard F. Huntington. Thompson and Thompson Genetics in Medicine. 7th ed. Philadelphia: Saunders/Elsevier, 2006.

Rubinsztein, David C. “Lessons from Animal Models of Huntington’s Disease.” Trends in Genetics 18 (April 4, 2002): 202–209.

What is rotator cuff surgery?

Indications and Procedures

The shoulder is considered to be the most flexible joint in the human body. It has a ball-and-socket structure that permits a wide range of motion, but this same structure also predisposes the shoulder to a very high risk of injury. To counter this risk, the shoulder is stabilized by a group of four muscles, collectively known as the rotator cuff: the subscapularis, the supraspinatus, the infraspinatus, and the teres minor. The signs and symptoms of rotator cuff injuries include point tenderness around the region of the humeral head deep within the deltoid muscle, pain and stiffness within the shoulder region within a day of participating in activities that involve shoulder movements, and difficulty in producing overhead motions involving the upper arm. Pain often occurs at night as a result of sleeping positions that put excess pressure on the joint. Occasionally, a clicking noise can be heard emanating from the joint upon movement or the patient may experience a “sticking point” when shoulder movements are attempted.

Injuries to the rotator cuff can mimic other common shoulder region problems, including bursitis
(inflammation of a bursa, a soft, fluid-filled sac that helps cushion surfaces that glide over one another) and tendinitis
(inflammation of a tendon). Injuries to the rotator cuff include impingement and tears. Impingement occurs when the rotator cuff tendons are pinched because of a narrowing of the space between the acromion (shoulder blade) process and the rotator cuff. This narrowing commonly occurs with aging, but it can also be traumatically induced. Sports that commonly put excess stress on the rotator cuff include baseball, swimming, and tennis. Besides a traumatic injury, chronic impingement of the rotator cuff tendons can cause partial or complete tears.

To evaluate the extent of shoulder dysfunction, the physician will conduct a physical examination to determine range of motion and use diagnostic procedures such as x-rays, an arthrogram (an x-ray after a tracer dye has been injected into the shoulder), magnetic resonance imaging (MRI), and ultrasound. Nonsurgical interventions include rest, ice immediately following an injury or heat twenty-four hours afterward, painkillers, anti-inflammatory medications, and physical therapy.

Rotator cuff surgery is usually recommended when there is little improvement in shoulder function or pain reduction after a course of noninvasive therapies. Surgery to correct rotator cuff tears is more successful if the procedure is performed within three months of the date of injury. Surgery can be a classic open procedure, requiring a 2- to 3-inch incision in the shoulder, or less traumatic arthroscopy, which requires only a small incision, half an inch or less, just large enough to accommodate the instruments and a video camera apparatus. Occasionally, the surgeon will use a combination of the open procedure and arthroscopy. Either general anesthesia, in which the patient is asleep, or local anesthesia, in which the region is “frozen” but the patient is awake, can be used for the procedure. With local anesthesia, a light sedative may also be used to put the patient at ease, but not asleep.

Acromioplasty reduces the impingement of the rotator cuff tendons. In this procedure, a portion of the bone underneath the acromion is shaved in order to give the tendons more room to move and prevent them from becoming pinched. This process is often included in rotator cuff surgical repairs. In rotator cuff repairs, the torn tendons are reattached to the humerus (upper arm bone). The open surgical procedure requires a relatively large incision through the shoulder as well as cutting through the deltoid muscle. Any scar tissue that has formed is removed, and a small ridge is cut into the top of the humerus. Small holes are drilled into the bone, and the tendons are sutured to the bone using these holes as anchors. The surgeon will also correct any other problems encountered, such as removing bone spurs, shaving down the acromion, or freeing up ligaments that may be pressing against the tendons.

During arthroscopic surgery, these extra procedures are not done. After the small incision is made into the shoulder, a thin tube is inserted. This tube contains the surgical instruments as well as a video camera that is used to guide the repair procedure. Arthroscopic surgery is becoming more common and is preferred for small tears, as it limits the amount of surgical intervention, reduces surgical risks, and quickens recovery time. If more extensive damage is discovered, then the surgeon may elect to combine the arthroscopic procedure with open surgery. However, arthroscopic tear repair has advanced tremendously, to the point that tears previously thought to be irreparable or too extensive are now being completed with arthroscopy.

Uses and Complications

The varying outcomes from rotator cuff surgery range from almost full recovery to no improvement at all. The degree of recovery is dependent upon the extent of damage to the rotator cuff as well as patient compliance with physical therapy after surgery. If the tendon has been torn for a long time, then it may not be reparable.

As with all surgical procedures, the patient may have an adverse reaction to the anesthesia. This risk is greater if the person is obese or has a cardiovascular, pulmonary, or metabolic condition. Surgical incisions always have the risk of infection, but this risk is minimized with the arthroscopic procedure because of the small incision size and the relatively short operative time (one to two hours). In rare instances, there is also the risk of nerve damage resulting in partial paralysis or temporary numbness at the incision area.

After surgery, the recovering arm will be put in a sling with a small shock-absorbing pillow placed behind the elbow. Extreme care should be taken with shoulder movements for the first three months following surgery. Reaching and lifting objects above the head should be avoided during this period. Passive range of motion exercises, in which the arm is moved by the physical therapist, should be started as soon as possible to prevent scar tissue formation and resultant stiffness. Exercises should be done several times a day so that within two to three weeks, the range of motion (flexibility) of the repaired shoulder should be equivalent to that of the uninjured shoulder. After six weeks, more advanced exercises are recommended in order to strengthen the rotator cuff as well as the surrounding shoulder muscles. Full recovery and rehabilitation from rotator cuff surgery can take up to a year.

Bibliography

Fongemie, A. E., D. D. Buss, and S. J. Rolnick. “Management of Shoulder Impingement Syndrome and Rotator Cuff Tears.” American Family Physician 57, no. 4 (1998): 667–674.

Lo, I. K., and S. S. Burkhart. “Current Concepts in Arthroscopic Rotator Cuff Repair.” American Journal of Sports Medicine 1, no. 2 (2003): 308–324.

Matsen, Frederick A., and Steven B. Lippitt. Shoulder Surgery: Principles and Procedures. Philadelphia: W. B. Saunders, 2003.

Pfeiffer, Ronald P., and Brent C. Mangus. Concepts of Athletic Training. 6th ed. Sudbury, Mass.: Jones and Bartlett, 2012.

Rockwood, Charles A., Frederick A. Matsen, and Michael Wirth. The Shoulder. 4th ed. 2 vols. St. Louis, Mo.: Saunders/Elsevier, 2009.

"Rotator Cuff Repair." Health Library, March 18, 2013.

"Rotator Cuff Repair." MedlinePlus, June 30, 2011.

Williams, G. R., and M. Kelley. “Management of Rotator Cuff and Impingement Injuries in the Athlete.” Journal of Athletic Training 35, no. 3 (2000): 300–315.

Yamaguchi, K., et al. “Transitioning to Arthroscopic Rotator Cuff Repair: The Pros and Cons.” Journal of Bone & Joint Surgery, American Volume 85, no. 1 (2003): 144–156.

What is teenage suicide? |

Introduction

The statistics on teenage suicide are shocking. Suicide is the fifth leading cause of death for those under age fifteen, and it is the second leading cause of death for those ages fifteen to twenty-four.

In 1960, the suicide rate among fifteen- to nineteen-year-olds was 3.6 per 100,000. By 1990, 11.1 out of every 100,000 teenagers fifteen and older committed suicide, according to the US Centers for Disease Control and Prevention (CDC). In 1997, about 9 percent of suicides in the United States were committed by people aged nineteen or younger. Suicide rates declined between 1990 and 2000, but rose back to their previous levels between 2000 and 2010. Perhaps even more disturbing are the statistics regarding the classification of attempted suicides. Although it is difficult to determine accurately, it is estimated that for every teenager who commits suicide there are approximately fifty teenagers who attempt to take their own lives. A nationwide survey by the CDC found that 16 percent of high school students had seriously considered suicide.

Females attempt suicide at higher rates than males but are less likely to succeed. Males are much more likely to use violent and lethal methods for trying to kill themselves, such as shooting or hanging. Females are more likely to use passive means to commit suicide; the use of drugs and poisons, for example, is more prevalent among females than males. Culture can also affect suicide rates, with the CDC's study finding that Native American, Alaskan Native, and Hispanic youth were more likely to report attempting suicide than their African American and white peers.

As alarming as these facts may be, it should be noted that suicide is still rare among the young. Nevertheless, preventing suicide would save thousands of adolescent lives each year. The problem of suicide is complex, and studying it has been especially difficult because suicidal death is often denied by both the medical professional and the victim’s family. The whole subject of suicide is carefully avoided by many people. As a result, the actual suicide rate among adolescents may be significantly higher than the official statistics indicate.

Contributing Factors

There are no simple answers to explain why adolescents attempt suicide, just as there are no simple solutions that will prevent its occurrence; however, researchers have discovered several factors that are clearly related to this drastic measure. These include family relations, depression, social interaction, and the adolescent’s concept of death.

Family factors have been found to be highly correlated with adolescent suicide. A majority of adolescent suicide attempters come from families in which home harmony is lacking. Often there is a significant amount of conflict between the adolescent and his or her parents and a complete breakdown in communications. Many suicidal youths feel unloved, unwanted, and alienated from the family. Almost every study of suicidal adolescents has found a lack of family cohesion.

Most adolescents who attempt suicide have experienced serious emotional difficulty prior to their attempt. For the majority, this history involves a significant problem with depression. The type of chronic depression that leads some adolescents to commit suicide is vastly different from the occasional “blues” most people experience from time to time. When depression is life-threatening, adolescents typically feel extremely hopeless and helpless and believe there is no way to improve their situation. These feelings of deep despair frequently lead to a negative self-appraisal in which the young person questions his or her ability to cope with life.

Further complicating the picture is the fact that clinically depressed adolescents have severe problems with relating to other people. As a result, they often feel isolated, which is a significant factor in the decision to end one’s life. They may become withdrawn from their peer group and develop the idea that there is something wrong with society. At the same time, they lack the ability to recognize how their inappropriate behavior adversely affects other people.

Another factor that may contribute to suicidal thoughts is the adolescent’s conception of death. Because of developmental factors, a young person’s cognitive limitations may lead to a distorted, incomplete, or unrealistic understanding of death. Death may not be seen as a permanent end to life and to all contact with the living; suicide may be viewed as a way to punish one’s enemies while maintaining the ability to observe their anguish from a different dimension of life. The harsh and unpleasant reality of death may not be realized. Fantasy, drama, and “magical thinking” may give a picture of death that is appealing and positive. Adolescents’ limited ability to comprehend death in a realistic manner may be further affected by the depiction of death in the songs they hear, the literature they read, and the films they watch. Frequently death is romanticized. Often it is presented in euphemistic terms, such as “gone to sleep” or “passed away.” At other times it is trivialized to such an extent that it is the stimulus for laughter and fun. Death and violence are treated in a remarkably antiseptic fashion.

Prevention Attempts

Suicide is a tragic event for both the victim and the victim’s family. It is also one of the most difficult problems confronting persons in the helping professions. In response, experts have focused their attention on trying to understand better how to prevent suicide and how to treat those who have made unsuccessful attempts to take their own lives.

It is believed that many suicides can be prevented if significant adults in the life of the adolescent are aware of various warning signals that often precede a suicide attempt. Most adolescents contemplating suicide will emit some clues or hints about their serious troubles or will call for help in some way. Some of the clues are easy to recognize, but some are very difficult to identify.

The adolescent may display a radical shift in characteristic behaviors related to academics, social habits, and relationships. There may be a change in sleeping habits; adolescents who kill themselves often exhibit difficulty in falling asleep or maintaining sleep. They are likely to be exhausted, irritable, and anxious. Others may sleep excessively. Any deviation from a usual sleep pattern should be noted. The individual may experience a loss of appetite with accompanying weight loss. A change in eating habits is often very obvious.

A pervasive feeling of hopelessness or helplessness may be observed. These feelings are strong indicators of suicide potential. Hopelessness is demonstrated by the adolescent’s belief that his or her situation will never get better. It is believed that current feelings will never change. Helplessness is the belief that one is powerless to change anything. The more intense these feelings are, the more likely it is that suicide will be attempted. The adolescent may express suicidal thoughts and impulses. The suicidal adolescent may joke about suicide and even outline plans for death. He or she may talk about another person’s suicidal thoughts or inquire about death and the hereafter. Frequently, prized possessions will be given away. Numerous studies have demonstrated that drug abuse
is often associated with suicide attempts. A history of drug or alcohol abuse should be considered in the overall assessment of suicide potential for adolescents.

A variable that is often mentioned in suicide assessment is that of recent loss. If the adolescent has experienced the loss of a parent through death, divorce, or separation, he or she may be at higher risk. This is especially true if the family is significantly destabilized or the loss was particularly traumatic. A radical change in emotions is another warning sign. The suicidal adolescent will often exhibit emotions that are uncharacteristic for the individual. These may include anger, aggression, loneliness, guilt, grief, and disappointment. Typically, the emotion will be evident to an excessive degree.

Any one of these factors may be present in the adolescent’s life and not indicate any serious suicidal tendency; however, the combination of several of these signs should serve as a critical warning and result in some preventive action.

Treatment

The treatment of suicidal behavior in young people demands that attention be given to both the immediate crisis situation and the underlying problems. Psychologists have sought to discover how this can best be done. Any effort to understand the dynamics of the suicidal person must begin with the assumption that most adolescents who are suicidal do not actually want to die. They want to improve their lives in some manner, they want to overcome the perceived meaninglessness of their existence, and they want to remove the psychological pain they are experiencing.

The first step in direct intervention is to encourage talking. Open and honest communication is essential. Direct questions regarding suicidal thoughts or plans should be asked. It simply is not true that talking about suicide will encourage a young person to attempt it. It is extremely important that the talking process include effective listening. Although it is difficult to listen to an individual who is suicidal, it is very important to do so in a manner that is accepting and calm. Listening is a powerful demonstration of caring and concern.

As the adolescent perceives that someone is trying to understand, it becomes easier to move from a state of hopelessness to hope and from isolation to involvement. Those in deep despair must come to believe that they can expect to improve. They must acknowledge that they are not helpless. Reassurance from another person is very important in this process. The young person considering suicide is so overwhelmed by his or her situation that there may seem to be no other way of escape. Confronting this attitude and pointing out how irrational it is does not help. A better response is to show empathy for the person’s pain, then take a positive position that will encourage discussion about hopes and plans for the future.

Adolescents need the assurance that something is being done. They need to feel that things will improve. They must also be advised, however, that the suicidal urges they are experiencing may not disappear immediately and that movement toward a better future is a step-by-step process. The suicidal young person must feel confident that help is available and can be called on as needed. The adolescent contemplating suicide should never be left alone.

If the risk of suicide appears immediate, professional help is indicated. Most desirable would be a mental health expert with a special interest in adolescent problems or in suicide. Phone-in suicide prevention centers are located in virtually every large city and many smaller towns, and they are excellent resources for a suicidal person or for someone who is concerned about that person. To address long-term problems, therapy for the adolescent who attempts suicide should ideally include the parents. Family relationships must be changed to assist the young person in feeling less alienated and worthless.

Suicidal Personalities

Suicide has apparently been practiced to some degree since the beginning of recorded history; however, it was not until the nineteenth century that suicide came to be considered a psychological problem. Since that time, several theories that examine the suicidal personality have been developed.

Émile Durkheim
was one of the first to offer a theoretical explanation for suicidal behavior. In the late nineteenth century, he conducted a now-classic study of suicide and published a book, Le Suicide: Étude de sociologie (1897; Suicide: A Study in Sociology, 1951). He concluded that suicide is often a severe consequence of the lack of group involvement. He divided suicide into three groupings: egoistic, altruistic, and anomic suicides.

The egoistic suicide is representative of those who are poorly integrated into society. These individuals feel set apart from their social unit and experience a severe sense of isolation. He theorized that people with strong links to their communities are less likely to take their lives. Altruistic suicide occurs when individuals become so immersed in their identity group that group goals and ideals become more important than their own lives. A good example of this type of suicide would be the Japanese kamikaze pilots in World War II: They were willing to give up their lives to help their country. The third type, anomic suicide, occurs when an individual’s sense of integration in the group has dissolved. When caught in sudden societal or personal change that creates significant alienation or confusion, some may view suicide as the only option available.

Psychologists with a psychodynamic orientation explain suicide in terms of intrapsychic conflict. Emphasis is placed on understanding the individual’s internal emotional makeup. Suicide is viewed as a result of turning anger and hostility inward. Sigmund Freud discussed the life instinct versus the drive toward death or destruction. Alfred Adler believed that feelings of inferiority and aggression can interact in such a way as to bring a wish for death to punish loved ones. Harry Stack Sullivan viewed suicide as the struggle between the “good me,” “bad me,” and “not-me.”

Other areas of psychology offer different explanations for suicidal behavior. Cognitive psychologists believe that suicide results from the individual’s failure to use appropriate problem-solving skills. Faulty assessment of the present or future is also critical and may result in a perspective marked by hopelessness. Behavioral psychologists propose that past experiences with suicide make the behavior an option that may be considered; other people who have taken their lives may serve as models. Biological psychologists are interested in discovering any physiological factors that are related to suicide. It is suggested that chemicals in the brain may be linked to disorders that predispose an individual to commit suicide.

Research in the area of suicide is very difficult to conduct. Identification of those individuals who are of high or low suicidal risk is complex, and ethical considerations deem many research possibilities questionable or unacceptable. Theory construction and testing will continue, however, and the crisis of adolescent suicide demands that research address the causes of suicide, its prevention, and treatment for those who have been unsuccessful in suicide attempts.

Bibliography

Boesky, Lisa. When to Worry: How to Tell If Your Teen Needs Help and What to Do About It. New York: AMACOM, 2007. Print.

Friedman, Myra. Buried Alive: The Biography of Janis Joplin. Updated ed. New York: Harmony, 1992. Print.

Huddle, Lorena, and Jay Schleifer. Teen Suicide. New York: Rosen, 2012. Print.

Hyde, Margaret O., and Elizabeth Held Forsyth. Suicide: The Hidden Epidemic. Rev. ed. New York: Watts, 1991. Print.

Kaplan, Cynthia S., and Blaise Aguirre. Helping Your Troubled Teen: Learn to Recognize, Understand, and Address the Destructive Behavior of Today’s Teens and Preteens. Beverly: Fair Winds, 2007. Print.

Miller, David Neil. Child and Adolescent Suicidal Behavior: School-Based Prevention, Assessment, and Intervention. New York: Guilford, 2011. Print.

Peck, Michael L., Norman L. Farberow, and Robert E. Litman, eds. Youth Suicide. New York: Springer, 1989. Print.

Petti, T. A., and C. N. Larson. “Depression and Suicide.” Handbook of Adolescent Psychology. Ed. Vincent B. Van Hassett and Michel Herson. New York: Free, 1995. Print.

Robbins, Paul R. Adolescent Suicide. Jefferson: McFarland, 1998. Print.

Wirchel, Dana, and Robin E. Gearing. “Child and Adolescent Suicide.” Suicide Assessment and Treatment: Empirical and Evidence-Based Practices. New York: Springer, 2010. 171–98. Print.

What is metabolic syndrome? |

Causes and Symptoms

Metabolic syndrome is a complex medical disorder. According to guidelines issued by the National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATP III), diagnosis of metabolic syndrome is made when an individual displays at least three of the following risk factors: abdominal obesity, elevated triglycerides, low levels of the high-density lipoprotein (HDL) type of cholesterol, high blood pressure, and the presence of more than 100 milligrams per deciliter (mg/dL) of glucose in the blood after fasting.

The National Heart, Lung, and Blood Institute (NHLBI) estimates that as many as forty-seven million adults in the United States suffer from metabolic syndrome, which is around 25 percent of the total adult population. A study published in National Health Statistics Reports in May 2009 reported that 34 percent of the study's 3,423 adults aged twenty and older met the criteria for metabolic syndrome. Age plays a large role in metabolic syndrome, with the likelihood of being diagnosed increasing as an individual gets older. Total body weight is also an indicator of the likelihood of the metabolic syndrome criteria being met. Males who are overweight are six times as likely as normal-weight males to be diagnosed with metabolic syndrome, and those who are obese are thirty-two times as likely.

In females, being overweight leads to a fivefold increase in the chances of being diagnosed with metabolic syndrome and obesity a seventeen-fold increase, compared to women of normal weight. Disturbingly, metabolic syndrome is now being recognized in children and adolescents; this is probably related to the increase in obesity and type 2 diabetes mellitus
seen in this age group over recent years. There is also evidence to demonstrate a genetic component to metabolic syndrome; further research will clarify this.

Key aspects of the metabolic syndrome are an energy imbalance and resultant altered metabolic pathways. The abnormal metabolic reactions seen in metabolic syndrome confer an increased risk for type 2 diabetes mellitus and cardiovascular
disease (CVD). Several other diseases—colon
cancer, Nonalcoholic steatohepatitis (NASH), polycystic ovary disease, and chronic renal failure—can also be a consequence of this syndrome.

The National Health and Nutrition Examination Survey determined that the most prevalent risk factor displayed by individuals with metabolic syndrome is abdominal obesity.
This is when fat is stored in the abdominal region of the body as opposed to in the buttocks and thighs. People with abdominally stored fat are often said to have “apple” type bodies; those with fat stored lower, in the buttocks and thighs, are said to be “pear” shaped. Men are typically apples and women are pears. Cortisol is a stress response hormone that promotes fat deposition in the abdominal area in individuals with chronic stress. Nearly all cases of overweight and obesity, including abdominal obesity, are due to excess calorific intake (overeating) combined with a sedentary lifestyle. In the United States, around one-third of the adult population is obese. Obesity greatly increases the risk for type 2 diabetes and cardiovascular disease.

Abnormal levels of fats in the blood is called dyslipidemia. In people who are overweight or obese, the levels of lipids in the body are so high that the pathways involved in fat synthesis and breakdown cannot keep up, and chronically high blood lipids are seen.

In addition, due to impaired insulin action and incorrect handling of glucose by their cells, individuals with type 2 diabetes tend to have high levels of blood triglyceride and low HDL cholesterol levels. This puts type 2 diabetics and obese individuals at high risk for CVD.

The second most prevalent factor seen in patients diagnosed with metabolic syndrome is hypertension, or high blood pressure. One in four Americans suffers from hypertension. If untreated, it can lead to CVD and kidney failure. The atherosclerotic process is accelerated in the metabolic syndrome and in type 2 diabetes because of the presence of multiple metabolic abnormalities. In insulin resistance, plaque formation may be enhanced because of the increased expression of adhesion molecules on endothelial cells and an increased rate of monocyte adhesion to endothelial cells. Circulating plasminogen is also more likely activated, which typically leads to increased clotting. In addition, hypertension may contribute to an increased risk of stroke in those with the metabolic syndrome.

The third most prevalent factor is hyperglycemia, or impaired fasting glucose. To satisfy the criterion for metabolic syndrome the glucose level in the blood after fasting must be over 100 mg/dl. A person with 100 to 125 mg/dl would be considered prediabetic, and diabetes is diagnosed when the fasting level of glucose is 126 mg/dl or above. Increases in blood glucose are indicative of a phenomenon called insulin resistance. Here, the cells of the body do not respond properly to insulin, and as a result glucose cannot enter the cells for use or storage so it remains in the circulating blood. Chronically elevated blood glucose concentration permits glucose molecules to combine with diverse proteins in the body, including hemoglobin within red blood cells, by a process known as glycation or glycosylation. Glycation also leads to blood vessels becoming rigid, a factor that contributes to CVD.

Any one of the risk factors listed on the NCEP/ATP III guidelines can cause chronic health problems, specifically type 2 diabetes mellitus and CVD. Diagnosis of metabolic syndrome requires that at least three out of the five criteria are met. This translates into a vastly increased risk for these chronic health problems; the reason why the life span of individuals diagnosed with metabolic syndrome is an average of fourteen years shorter than those without the disease.

Treatment and Therapy

Treatment strategies for the metabolic syndrome focus on weight loss through a comprehensive program utilizing behavioral changes, including improved nutrition and an increase in physical activities. The long-term goal of therapy is a better balance between the intake of food energy sources and energy expenditure, so that a healthier body weight can be achieved. Dietary treatment typically requires the involvement of nutritionists and registered dieticians to provide educational information and institute changes in food selection.

Physicians provide overall care, and concomitant with lifestyle changes use the prescription of medications for one or more of the components of metabolic syndrome. Metformin is a drug used to treat type 2 diabetes mellitus; it works by improving insulin action, and has also been shown to stop the development of impaired fasting glucose to type 2 diabetes in patients with metabolic syndrome. Angiotensin-converting enzyme (ACE) inhibitors are used in the treatment of hypertension. They are successful in treating hypertension and, in addition, have a beneficial effect on insulin resistance in metabolic syndrome. Another class of drugs is the statins, which are used to improve cholesterol levels in people with metabolic syndrome. Statins also appear to cause a reduction in inflammation seen in metabolic syndrome, leading to a reduction in CVD.

Since the emerging epidemic of the metabolic syndrome is expected to continue, both preventive and treatment strategies are needed. Prevention aimed toward reducing the development of this syndrome in children and adolescents should involve schools and community agencies.

Perspective and Prospects

Recognition of the metabolic syndrome essentially paralleled the increases in overweight and obesity in the United States in the early 1990’s. Physicians were diagnosing many overweight and obese patients with the major components of the metabolic syndrome without linking them to a major health trend. Other countries of affluence were also reporting cases.

The metabolic syndrome was first defined in 1998 by the World Health Organization (WHO). The WHO criteria included a BMI of more than thirty; a blood triglyceride level greater than or equal to 150 mg/dl; HDL cholesterol level under 35 mg/dl in men and 39 mg/dl in women; blood pressure over 140/90 mm Hg; impaired glucose tolerance, insulin tolerance or type 2 diabetes; insulin resistance; and microalbuminuria (protein in the urine). In 2001 the NCEP/ATP III released their guidelines for the diagnosis of metabolic syndrome, which quickly became the most widely accepted. These differed from the WHO guidelines in several ways. Firstly, BMI measurement was replaced with waist circumference measurement when it became clear that it was not necessarily the total body fat content, but the way in which it is deposited in the body that is important to pathogenesis. A waist circumference of over forty inches for men and over thirty-five inches for women is considered a risk factor for metabolic syndrome. Secondly, the HDL values were changed to less than 40 mg/dl for men and 50 mg/dl for women, and blood pressure limit was lowered to 130/85 mm Hg. A fasting glucose level of
over 110 mg/dl was defined as a risk for metabolic syndrome. Finally, insulin resistance and microalbumiuria were removed from the criteria. In 2005 the guidelines were updated by American Heart Association (AHA) and NHLBI; the fasting blood glucose level was lowered to 100 mg/dl. These are the currently used criteria for the diagnosis of metabolic syndrome.

The metabolic syndrome has deadly consequences because of the nature of the chronic diseases that it spawns. This problem will worsen in the future in the United States because excessive calorific intake, eating the wrong kinds of food (for example highly processed food containing high fructose corn syrup, trans fats, or too much salt), and too little physical activity continue to dominate society. The epidemic nature of this syndrome requires that new public health measures be initiated and implemented as soon as possible. Preventive strategies need to be instituted to reduce the enormous impact of this syndrome anticipated in the United States in the coming decades. The overall cost of treatment will be enormous.

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