HypertensionSymptoms/ScreeningScreening of hypertension is done through routine measurement of blood pressure in order to increase the probability of early disease detection. A person with a systolic blood pressure of 140 mm Hg and/or a diastolic blood pressure of 90 mm Hg is qualified as hypertensive. Other symptoms include frequent headaches, visual impairment and indications of target organ damage. (Gonzales and Kutner, 2008).

Pathophysiology and Epidemiology Among the causes of cardiovascular diseases, hypertension is considered as the foremost contributor worldwide.The prevalence of hypertension is increasing among adolescents and adults, concomitant with obesity. The National Health and Nutrition Examination Survey (NHANES) reported an overall hypertension prevalence of 28. 7% in 2000 (Wang and Vasan, 2000).

The same increasing trend can be seen in other countries. Approximately 972 million people are suffering from hypertension. Depending on age, gender, body size, and ethnicity, the incidence of hypertension ranges between 3-18% around the world (Hajjar, Kotchen and Kotchen, 2006).Hypertension is usually higher in people with obesity, particularly android obesity and in people who are aged >40 years. Hypertension may also be found in people who are overweight, diabetic, and those who habitually smoke cigarettes (Ghannem and Fredj, 1997) Although about 2-5% of patients diagnosed with hypertension has an underlying disease that cause rises in blood pressure, its pathophysiology remains unclear and there is still no clear identifiable cause of hypertension.Physiological mechanisms that are related to the maintenance of normal blood pressure however, have already been identified (Beevers, Lip and O’Brien, 2001).

Among those that have already been intensively studied in connection with hypertension are: salt intake, insulin resistance and obesity, sympathetic nervous system and the renin-angiotensin system. Genetics, endothelial dysfunction, low birth weight and neurovascular anomalies are also said to be connected to the development of hypertension (Beevers, Lip and O’Brien, 2001).Increased peripheral resistance. Even while most patients with hypertension have normal cardiac output, their raised peripheral resistance that is the constriction of the arterioles usually caused by the rise in intracellular calcium concentration increases the blood pressure. If the smooth muscles of the arterioles are constricted at a long period of time, structural changes involving the thickening of the arteriolar vessels may cause an irreversible rise in peripheral resistance (Beevers, Lip and O’Brien, 2001).

During early hypertension, it is the rise of cardiac output, which is related to sympathetic overactivity, and not the rise in peripheral resistance that causes the elevation of blood pressure. Peripheral resistance develops only later to prevent the raised pressure transmitted to the capillary bed, thereby affecting cell homeostasis (Beevers, Lip and O’Brien, 2001). Renin-Angiotensin System.Although this factor (circulating) is not usually thought of as being directly responsible for high blood pressure, there is evidence that the non-circulating local renin-angiotensin system in the kidney, heart and the arterial tree may have significant roles in blood flow regulation (Beevers, Lip and O’Brien, 2001). Autonomic Nervous System. The stimulation of the sympathetic nervous system may cause either constriction or dilation of the arteries.

It is also important in causing the necessary changes in blood pressure during stress or physical activity. The theory is that hypertension is related to the interaction between the renin-angiotensin system the autonomic nervous system as well as other hormones (Beevers, Lip and O’Brien, 2001). Endothelial Dysfunction. Vascular endothelial cells produce local vasoactive agents such as nitric oxide (dilator) and endothelin (constrictor). In this way, the endothelium regulates the cardiovascular flow and therefore the blood pressure.Dysfunction of the endothelium may cause the impairment of the endothelium-dependent vascular relaxation or vascular response to endothelial agonists, resulting to irreversible hypertension (Beevers, Lip and O’Brien, 2001).

Hypercoagulability. People with hypertension are in a prothrombotic or hypercoagulable state. Such is demonstrated by the abnormalities in the walls of the vessels due to endothelial damage; abnormalities in the levels of hemostatic factors, increased platelet formation and fibrinolysis (Beevers, Lip and O’Brien, 2001).Insulin Sensitivity. The hazards of cardiovascular risk are synergistic rather than additive. The clustering of risk factors including hypertension, glucose intolerance, obesity, diabetes and hyperlipidemia leads to a common pathway that raises blood pressure and causes vascular damage (Beevers, Lip and O’Brien, 2001).

Treatment/Management Treatment of hypertension depends on a person’s individual health status. As a general rule, healthier persons do not require lower blood pressure goals compared to people with kidney or heart diseases.The usual treatment for people with hypertension includes diet modification as well as exercise in conjunction with prescription medications. Such medications may include: thiazide diuretics; beta blockers; angiotensin-converting enzyme inhibitors; calcium channel blockers; renin inhibitors, among others. (MayoClinic, 2009).

Obesity Symptoms/Screening Obesity is usually determined by calculating the ratio of weight to height or by using the Body Mass Index (BMI). The BMI is calculated by dividing the weight in kilograms by the square of the height in meters.As a rule, persons with BMIs of 25 and above are considered overweight according to the WHO classification (Gonzales and Kutner, 2009). Pathophysiology and Epidemiology A person is considered obese if he/she reaches a body mass index (BMI) of 30 kg/m2. Based on this standard, no less than 20% of adults in the United States may qualify as obese.

This percentage is continuously rising with the technological, social and economic advances that countries have been experiencing over the years.The Behavioral Risk Factor Surveillance System conducted by the Centers for Disease Control and Prevention (CDC) showed that there had been an increase in the prevalence of obesity between years 1991-1998 in 50 states. In 1991, only 4 states in the US reached 15% obesity rates. Six years after, in 1998, more than 30 states have reached such level. Meanwhile, the National Health and Nutrition Examination Surveys (NHANES) reported a gradual to a marked increase in the prevalence of obesity from 1960-1980 and from 1976-1994 wherein prevalence started from 14. 5% to a 22.

5%.Such increases in obesity rates apply regardless of gender, age and race-ethnic groups. Among all race-ethnic groups, women among minority groups, Black women, and Mexican-American men and women have the highest rates of overweight and obesity. Among many factors, environmental, behavioral and genetic factors are the most examined causes of obesity. This disease is known to be associated with metabolic abnormalities including insulin resistance, diabetes, hypertension, dyslipidemia, heart disease, hyperinsulinemia and gallbladder disease.

Genetics and Environment. Approximately 30-40% of the BMI can be attributed to genetics and to the environment, approximately 60-70%. In a certain population, there are people who are genetically predisposed to become obese but expression of genotype may only happen under certain environmental conditions including high-calorie diets and sedentary lifestyles. This is how genetics and environment interact. An increasing number of people may express the obesity genotype after being exposed to adverse environmental conditions.While environment may determine whether a person will develop obesity, a person’s genes will determine both the development of obesity and how much a person will gain given a set of adverse environmental factors.

(Pi-Sunyer, 2002) Metabolic Predictors. Obesity may develop when a person’s caloric intake is higher than his/her energy expenditure. Low adjusted sedentary energy expenditure, high respiratory quotient, and low level of physical activity are factors that induce weight gain. (Pi-Sunyer, 2002) Low resting metabolic rate (RMR) is related to higher rate of weight gain.

Predictors of RMR include total daily energy expenditure (thermic effect of food and physical activity) as well as the fat-free mass (FFM). (Pi-Sunyer, 2002) Lower respiratory quotients (RQ) (with values 0. 7 and below) mean that a person oxidizes more fat than carbohydrate. Meanwhile, a ratio of 1. 0 suggests the opposite, that is more carbohydrates are oxidized compared to fat.

Higher RQ’s therefore results to higher probability of gaining more weight than their counterparts (Pi-Sunyer, 2002). People with sedentary lifestyle are more likely to gain weight since they are more likely to take more calories than the amount that they expend.Naturally, expenditure of energy is limited by the amount or level of a person’s daily activity (Pi-Sunyer, 2002). Stress. Stress forces the production of the hormone cortisol. This hormone increases the rate of fat deposition.

Treatment/Management The goal of obesity treatment is the reduction of weight in order to reduce the risks of associated diseases. Treatment may vary from simple behavioral changes, calorie intake reduction, increased physical activity to medications and surgery. Sibutramine and Orlistat are the most common medications prescribed to treat obesity.These medications work either by changing a person’s brain chemistry, making his/her feel fuller or by blocking the absorption of fat.

Meanwhile, surgical methods such as gastric bypass, gastric banding and biliopancreatic diversion may be the fastest ways to lose weight but not without the risk of complications. Threats include pneumonia, infections, vomiting and gallstones among others. (MayoClinic, 2009). Depression Symptoms/Screening People who are suspected of being depressed are evaluated physically and psychologically usually through questionnaires, interview, physical examination and laboratory tests.Interviews and questionnaires are usually set to determine the presence of features such as feeling of hopelessness, suicidal thoughts, and absence of positive thoughts. Since other factors such as medications may artificially create symptoms of depression, questionnaires are tailored to rule out such factors.

(Gonzales and Kutner, 2009) Pathophysiology and Epidemiology Depression has the highest prevalence among any other disorder worldwide. From 1991-2002 alone, there has been a marked increase in the rates of depression from 3. 33% to 7. 06% in the United States.The importance of treatment of depression lies on the fact that it is considered as the most significant risk factor for suicide among adolescents, adults and the elderly. It is also considered as a risk factor for the development of CVD as well as for poor treatment response among patients.

Approximately 33% of the risk variance for the development of depression may be attributed to genetics, while the remaining 66% may be attributed to the environment. (Nemeroff, 2008). Depression is usually characterized by the interaction of complex diseases including hypertension, diabetes, cancer, etc. and three major monoamine systems including serotonin, norepinephrine and dopamine.Current evidence solidifies the role of the central nervous system DA circuits in the development of depression. DA neurons are known for its role in mediating the symptoms of depression.

Imaging studies have proven that depressed people have reduced DA transporter binding sites as well as reduced synaptic availability of DA. (Nemeroff, 2008). The role of serotonin (similar to norepinephrine) is evidenced by studies that show the reduced activity of serotonergic neurons among people diagnosed with depression, examined postmortem.Imaging studies also show a reduced number of serotonin transporter binding sites in both the amygdala and midbrain of depressed patients who have not taken drugs. There is also evidence of reduced presynaptic and postsynaptic serotonin receptor density among patients suffering from depression (Nemeroff, 2008).

A study that caused the reduction of serotonin availability through tryptophan depletion among patients who have just recovered from depression shows signs of reemergence of symptoms of depression within just a few hours (Charney, 1998; Nemeroff, 2008).The effect of genes in the risk of developing depression is shown by the results of some studies that demonstrate how individuals with the s allele of the promoter region of the SERT gene are more vulnerable to developing depression compared to those with the l allele. PET imaging studies in fact showed that those with s alleles have reduced SERT binding sites, causing less immunity to depression. (Nemeroff, 2008). Treatment/Management Standard options for the treatment of depression may include medications (antidepressants) , psychotherapy (counseling) and electroconvulsive therapy (ECT).Among these standard methods, ECT is the most controversial as it involves the deliberate introduction of currents through the brain in order to trigger a seizure.

Its side effects include confusion and even temporary memory loss. Despite these, it offers the fastest and most effective relief to depression. (MayoClinic, 2009) Other treatment methods, although less studied include brain stimulation and complementary and alternative treatments. (MayoClinic, 2009).