Wednesday, February 9, 2011

Obesity and Cardiovascular disease and Its management

Obesity and Heart disease
Introduction:
Obesity is major public health problem in the united states. In the National Health and Nutritional Examination Survey(NHANES III) form 1988 to !991 it was 36% of the total population which was 25% in NHANES II from 1976 to 1980. The prevalence of obesity has continued to rise. Compared to NHANES data from 1988 to 1994, data from NHANES 1999 to 2000 demonstrates an increase in the prevalence of overweight and obese adults from 55.9 to 64.5 percent for overweight and from 22.9 to 30.5 percent for obese adults .
Similar results have been noted in the United Kingdom. The percentage of the population with a body mass index (BMI) above 30 kg/m2 increased between 1986 and 1993 from 6 to 13 percent in men and from 8 to 16 percent in women . These data and those from other countries are indicative of a major international epidemic .
There is a relationship between obesity and age. Approximately 20 percent of Americans between the age of 25 and 34 are obese; another 10 percent of the population becomes obese with each succeeding decade up to the age of 55
Obesity has long been associated with an increased risk for coronary heart disease (CHD). A recent meta-analysis observed a 29 percent increase in CHD for each five-unit increase in BMI . This association was slightly attenuated after adjustment for blood pressure and cholesterol level. The risk is compounded by the common coexistence of other risk factors associated with obesity such as hypertension, dyslipidemia, and abnormal glucose metabolism. How much of the risk is due to obesity alone has been uncertain. Furthermore, the mechanisms by which obesity, particularly abdominal obesity, cause or accelerate coronary atherogenesis are also uncertain.
Evidence does exist to suggest that obesity, particularly visceral adipose, among adolescents is associated with acceleration of atherosclerosis . More recently, long-term follow-up from Denmark demonstrated BMI during childhood was positively associated with increased risk of CHD during adulthood

DEFINITION OF OBESITY


The body mass index (BMI) is the most practical way to evaluate the degree of obesity. It is calculated from the height and weight as follows:
BMI = body weight (in kg) ÷ square of stature (height, in meters)
The BMI can be obtained from a nomogram or a table. BMI is correlated with body fat and is relatively unaffected by height.
Overweight is defined as a BMI between 25 and 30 kg/m2 and obesity as a BMI greater than 30 kg/m2. However, when estimating cardiovascular and other risks associated with obesity, both regional fat distribution and comorbid conditions must also be taken into account.
A BMI of 20 to 25 kg/m2 is associated with little or no increased risk unless visceral fat is high, or the subject has gained more than 10 kg since age 18.
• Subjects with a BMI of 25 to 30 kg/m2 may be described as having low risk, while those with a BMI of 30 to 35 kg/m2 are at moderate risk.
• Subjects with a BMI of 35 to 40 kg/m2 are at high risk, and those with a BMI above 40 kg/m2 are at very high risk from their obesity.



OBESITY AND CARDIOVASCULAR DISEASE
Despite uncertainties about the relationship between obesity and CHD, the American Heart Association has identified obesity as an independent risk factor. This action should heighten physician awareness about the importance of obesity and stimulate a more vigorous approach to prevention and treatment.

Coronary disease — The 27th Bethesda Conference classified obesity as a category II risk factor, that is, a risk factor for which intervention was likely to lower the incidence of CHD events, based upon the current pathophysiologic understanding and epidemiologic and clinical trial evidence . There is strong, consistent epidemiologic evidence for an association between obesity and CHD, but supporting data from clinical trials are lacking.

Many studies have demonstrated a linear, longitudinal relationship between obesity and CHD incidence in univariate analyses, but the relationship has been less certain in multivariate analyses that included serum lipids, diabetes, and hypertension. As an example, the Munster Heart Study (PROCAM) followed 16,288 men and 7325 women for up to seven years [17]. There was a graded positive relationship between BMI and other CHD risk factors including age, total serum cholesterol, low density lipoprotein (LDL) cholesterol, and systolic and diastolic blood pressure in addition to markers of inflammation and thrombosis. The increase of CHD death associated with BMI was completely accounted for and mediated by these risk factors.

In contrast, other studies have found that obesity is an independent cardiovascular risk factor .
• The Nurses' Health Study evaluated the relationship between BMI and total and cause specific mortality in 115,195 United States women [18]. In multivariate analyses of women who had never smoked, there was a significant trend for increasing risk of death with increasing BMI; compared to women with a BMI <19 kg/m2, the relative risk of death was: 1.2 for a BMI 19 to 24.9 kg/m2; 1.3 for a BMI 25 to 26.9 kg/m2; 1.6 for a BMI 27 to 28.9 kg/m2; 2.1 to 2.2 for a BMI >29 kg/m2. The risk of death was increased at BMI levels well below those considered to indicate obesity, with a striking increase in risk for truly obese women. Weight gain of 10 kg or more after the age of 18 was associated with increased mortality in middle adulthood.
There was also an association between BMI and cardiovascular mortality. Among women with a BMI of 32 or higher who had never smoked, the relative risk of death from cardiovascular disease was 4.1 compared with women who had a BMI below 19.0.
• Obesity was also found to be an independent risk factor for all-cause mortality in the Framingham Heart Study, which analyzed 30 year follow-up data on male participants . Using Metropolitan Relative Weight criteria, the minimum mortality was seen in the group of men with desirable weight (100 to 109 percent "normal"). Multivariate analyses showed a strong positive relationship between baseline weight and death occurring at any interval; the 30 year mortality rate for nonsmoking men who were overweight (weight more than 110 percent desirable weight) was up to 3.9 times higher than men of desirable weight.
• Another prospective study of over one million adults followed for 14 years found that obesity was strongly associated with an increased risk of all-cause mortality and cardiovascular death among nonsmokers and those without a history of CHD . All-cause mortality was lowest in adults with a BMI between 23.5 and 24.9 kg/m2 in men and 22 and 23.4 kg/m2 in women; mortality rates progressively increased at higher indices and were highest in the heaviest men and women who had a BMI ≥40 kg/m2 (relative risk 2.7 and 1.9, respectively). A high BMI was most predictive of death from cardiovascular disease, especially in men (relative risk 2.9); significantly increased risks of death from cardiovascular disease were found at all indices greater than 26.5 kg/m2 in men and 25 kg/m2 in women. The risk associated with BMI was greater for whites than blacks.
Thus, in several large, prospective, long-term studies using multivariate analyses, obesity was an independent risk factor for all-cause mortality and death from CHD in both women and men. However, other studies have observed reduced mortality risk with increasing BMI among patients with a prior history of heart disease . Data from over 9000 patients undergoing cardiac catheterization suggest obese patients tend to be younger, and more likely to have single-vessel disease. At one year, patients with normal BMI had higher rates of mortality compared to overweight and obese patients

Obesity and Other Complications:
There are a number of physiological and metabolic changes associated with obesity that may contribute to an increased risk of cardiovascular disease .
• Insulin resistance and hyperinsulinemia .
• Type 2 diabetes mellitus .
• Lipid abnormalities, including low HDL level, high triglyceride level, increased apolipoprotein B level .
• Systolic and diastolic hypertension .
• Left ventricular hypertrophy .
• Sympathetic nervous system dysfunction
• Endothelial dysfunction .
• Obstructive sleep apnea .

Metabolic syndrome — Visceral or abdominal obesity is associated with insulin resistance and an array of metabolic and hemodynamic disorders, including hyperinsulinemia, atherogenic blood lipid changes, hypertension, and type 2 diabetes. This constellation of findings has been called the metabolic syndrome (or insulin resistance syndrome or syndrome X). The prevalence of the metabolic syndrome is significantly higher in patients with than without a history of cardiovascular disease. In addition, the metabolic syndrome is associated with a significant increase in the subsequent risk of cardiovascular events.
Type 2 diabetes mellitus — Type 2 diabetes mellitus is strongly associated with obesity in all ethnic groups. More than 80 percent of cases of type 2 diabetes can be attributed to obesity, which may also account for many diabetes-related deaths. CHD is more common in diabetics than in the general population, affecting as many as 55 percent of patients.

Hyperlipidemia — Obesity is associated with several deleterious changes in lipid metabolism, including high serum concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL)-cholesterol, and triglycerides, and a reduction in serum HDL cholesterol of about 5 percent . The last effect may be most important since a low serum HDL cholesterol concentration carries a greater relative risk of CHD than hypertriglyceridemia.
Central fat distribution also plays an important role in the serum lipid abnormalities. Waist circumference alone accounts for as much or more of the variance in serum triglyceride and HDL cholesterol concentrations as either the WHR .

Hypertension — Blood pressure is often increased in obese subjects . In the Swedish Obesity Study, for example, hypertension was present at baseline in approximately one-half of subjects. In a report from the Nurses' Health Study, the BMI at age 18 years and at midlife was positively associated with the occurrence of hypertension . Weight gain was also associated with an increased risk; the relative risk of hypertension in those women who gained 5.0 to 9.9 kg and ≥25.0 kg was 1.7 and 5.2, respectively .

Left ventricular hypertrophy — Obesity is associated with volume overload resulting in a high end-diastolic volume and increased filling pressure. This, coupled with hypertension, can lead to left ventricular hypertrophy (LVH) . LVH is important clinically because it is associated with an enhanced incidence of heart failure, ventricular arrhythmias, death following MI, and sudden cardiac death .

Sympathetic nervous system — Obesity may be associated with abnormalities in sympathetic nervous system control. This can predispose obese individuals to prolonged QT intervals and arrhythmia .

Sleep apnea — Sleep apnea is associated with obesity.The syndrome is related to excess mortality, hypertension, left and right ventricular dysfunction, and arrhythmias.

Heart failure — There is an important association between obesity and heart failure. In an analysis from the Framingham Heart Study in which almost 6000 individuals without a history of heart failure (mean age 55 years) were followed for a mean of 14 years . heart failure developed in 496 (8.4 percent). The risk of heart failure was increased approximately two-fold in obese (body mass index [BMI] ≥30 kg/m2) compared with nonobese subjects. After adjusting for established risk factors (eg, hypertension, coronary disease, diabetes, left ventricular hypertrophy), the risk of heart failure increased 5 percent in men and 7 percent in women for each increment of 1 kg/m2 in BMI. Approximately 11 percent of cases of heart failure in men and 14 percent in women could be attributed to obesity alone. The risk was also increased in overweight (BMI 25 to 29.9 kg/m2) women but not men. However, among patients with a history of heart failure, increasing BMI appears protective. Several studies have observed lower rates of rehospitalization and death among heart failure overweight and obese heart failure patients .

ECG in morbid obesity — Morbid obesity can produce changes in cardiac morphology that can alter the surface ECG. This was revealed in a study that compared the ECG of 100 obese subjects and 100 controls; none of the subjects had clinical, ECG, radiographic, or echocardiographic evidence of coronary heart disease, systemic hypertension, valvular heart disease, heart failure, cardiomyopathy, or pericardial disease .Compared to controls, obese patients had the following alterations on the ECG:
• P, QRS, and T wave axes were more leftward
• Low QRS voltage, multiple ECG criteria for left ventricular hypertrophy and left atrial abnormality, and T wave flattening in the inferior and lateral leads were more common

Abdominal obesity — At any given level of BMI, the risk of the development of cardiovascular disease in both men and women is increased by more abdominal fat (increased waist to hip ratio, WHR) .
The relationship between abdominal obesity and cardiovascular mortality was evaluated in a cohort of 44,636 women in the Nurses' Health Study . The relative risk increased significantly from the lowest to the highest waist circumference quintiles (1.00, 1.04, 1.04, 1.28 and 1.99 respectively) after adjustment for body mass index and other confounders during 16 years of follow-up. This relationship persisted even among normal weight women (body mass index 18.5 to <25kg/m2).

BENEFITS OF WEIGHT LOSS — Weight loss can improve or prevent many of the obesity-related risk factors for cardiovascular disease . Benefits include:
• Decreased blood pressure in hypertensive patients .
• Decreased incidence of diabetes mellitus .
• Improved lipid profile
• Decreased insulin resistance.
• Reduced C-reactive protein concentration .
• Improved endothelial function .
Management of obesity:
Obesity can be managed by medical and surgical treatment. Medical treatment have some limitations and not applicable for those BMI is more than 40 and also those have visceral deposition of fat. At that case surgical procedure give good and excellent result
No randomized controlled clinical trial has demonstrated that voluntary weight loss alone has any effect upon long-term outcomes such as total mortality or cardiovascular disease . However, one prospective study of 28,388 overweight women ages 40 to 64 who had no preexisting illness found that intentional weight loss of more than 20 lb (9.1 kg) was associated with a 25 percent decrease in all-cause, cardiovascular, and cancer mortality . Among 15,069 women with comorbid conditions such as heart disease or diabetes mellitus, any amount of intentional weight loss was associated with a 10 percent reduction in cardiovascular disease and a 20 percent reduction in all-cause mortality, primarily due to a reduction in mortality from obesity-related malignancy.
Achieving and maintaining weight loss is made difficult by the reduction in energy expenditure that is induced by weight loss. In addition, recidivism (regaining of lost weight) is a common problem; of those subjects who lose weight during any treatment program, most do not maintain the weight loss.
Despite the limited data regarding the long-term benefits of weight loss and the difficulties with achieving and maintaining weight loss, physicians should urge patients with known cardiovascular disease or cardiovascular risk factors (eg, hypertension, dyslipidemia, type 2 diabetes mellitus) to lose weight. For persons free of disease, prevention of obesity beginning in early life is a sound recommendation. For individuals older than 75, excess body weight does not appear to be an important risk factor.
Drug therapy may be a helpful component of treatment for overweight subjects. However, among patients with CVD, certain drugs (such as sibutramine) may be contraindicated. Anti-obesity drugs have been used as an adjunct to diet and exercise for obese subjects with a BMI greater than 30 kg/m2. The role of drug therapy has been questioned, however, because of concerns about efficacy, the potential for abuse, and side effects. .
Surgery (gastric bypass or banding) is another option for patients at high risk of complications from obesity.
Like dietary weight loss, gastrointestinal obesity surgery can reduce cardiovascular risk factors, including blood pressure, diabetes incidence, and lipid profile . However, this does not appear to occur with liposuction suggesting that the negative energy balance associated with decreased nutritional intake may be necessary for achieving the metabolic benefits of weight loss.
PREOPERATIVE CONSIDERATIONS — As discussed above, the prevalence of coronary heart disease (CHD) or its risk factors is increased in obese patients.
Patients with established CHD are at increased risk for cardiovascular events at the time of non-cardiac surgery. The preoperative approach to obese patients scheduled to undergo non-cardiac surgery is discussed elsewhere.

RECOMMENDATIONS — The 2007 ACC/AHA focused update of the 2002 guidelines for the management of patients with chronic stable angina made the following recommendations for weight management :
• Regular assessment of BMI and waist circumference.
• Counseling on weight management at each patient visit, with a goal of a BMI between 18.5 and 24.9 kg/m2.
• The initial goal of weight loss should be approximately 10 percent from baseline.
• Recommend lifestyle changes and consider treatment strategies for metabolic syndrome in women if the waist circumference is ≥35 inches (89 cm) or ≥40 inches (102 cm) in men.

Thursday, December 30, 2010

amazan

Wednesday, November 10, 2010

Urinary Bladder

large muscular bag, reservior of urine lies ant part of pelvic cavity.

Size shape and position:
varies in size , shape and position according to amount of urine contains
when empty lies in pelvis, reaches abdomen when filled with urine.

External features:
when empty:
tetra hedral. has apex, base, three surface, four boarder and one neck.

Ligaments of the bladder:

a. true ligaments:
lateral true ligaments of bladder.
lateral puboprostatic ligament
Medial puboprostatic ligament
median umblical ligaments

b.false ligaments
The median umblical fold
medial umblical fold
lateral false ligaments
Posteriaor false ligaments

Arterial supply:
Superior and inferior vesicular artery
additional supply from obturator and inferior gluteal artery.
acne treatments
Nerve supply:
parasympathetic s234
sympathetic T11-L2
Pudendal nerve s234

Thursday, November 4, 2010

The urinary bladder

Urinary Bladder:

Muscular reservior of urine which lies ant to

Ureters

Thick wall muscular tube which convey urine to Urinary bladder from Kidneys.

Lies in posterior abdominal wall.
Measures about 25 cm, 12.5 cm lies in Abdomen and 12.5 cm lies in pelvis.

It has three constrictions.

Course:
Starts from renal pelvis , gradually narrows and lower end of kidneys it become
ureter proper. It runs downwards and slightly medially over psoas major muscle
enters pelvis infront of termination of common internal iliac artery.

In lesser pelvis it runs bownwards and slightly backwards and laterally following
ant margin of greater sciatic notch. Opposite the ischial spine it runs forward
meidally towards urinary bladder.

Normal constriction:
1. At pelvic ureteric junction
2.at the brim of lesser pelvis
3.At its passage through its bladder wall.

Relations:


Blood supply:
It is supplied by three set of arteries:
1.Upper part receives branches from renal artery
2.Middle part receives branchs from the abdominal aorta
3.The pelvic part receives branches from vesical, middle rectal or uterine arteries.

Nerve supply:
Sympathetic N T10-L1
ParaSYMPATHETIC S2-4