Obesity

Obesity
Obesity is an excess of body fat frequently resulting in a significant impairment of health.
Adipose tissue is a normal constituent of the human body that serves the function of storing energy as fat. The fat may be used by the body in response to various metabolic demands. The excess fat accumulation is associated with increased fat cell size.A very important reason for obesity is the overconsumption of carbohydrates. When carbohydrates enter our body they are rapidly broken down into glucose (a sugar). Glucose raises blood sugar levels causing pancreas to make the hormone insulin. Insulin inhibits fat already stored in our body from being broken down and it also promotes the storage of new fat in the body; and increases cholesterol levels.In many forms of severe childhood-onset obesity, the total number of fat cells is increased.Formerly, obesity was explained by the single adverse behaviour of inappropriate eating in the setting of attractive foods. But now it has been established that obesity has multiple causes and is of different types. Both genetic and environmental factors are likely to be involved in the pathogenesis of obesity. These include excess caloric intake, decreased physical activity, and metabolic and endocrine abnormalities.Genetic determinants can either play a major role in the pathogenesis of obesity or enhance susceptibility to its development.The conditions in which genetics may play a role are Prader-Willi syndrome, Ahlstrom’s syndrome, the Laurence-Moon-Biedl syndrome, Cohen’s syndrome, and Carpenter’s syndrome.Over weight can be estimated by Body mass index (BMI), which is weight/height square, where weight is in kilograms and height is in meters.
Obesity is defined as a body mass index above 30 kg/square meter.
Weight gain may confer increased health risks even if the BMI does not exceed 25. In women a weight gain of more than 5 kg (11 lb) is associated with increased risks of diabetes and heart disease, and in men any weight gain after age 25 appears to carry increased health risks.
More than 30% of Americans are 20% or more overweight, and one third of women and more than one quarter of men are trying to lose weight at any given time.

Obesity related topics

Noonan Syndrome

Noonan Syndrome
Synonyms:

  • webbed neck syndrome
  • male Turner syndrome
  • female pseudo-Turner syndrome

Jacqueline Noonan, paediatrician and heart specialist in 1963, published a report on a small group of patients with typical facies, congenital heart defect, and some clinical features similar to Turner syndrome, but with normal chromosomes. Its after her that this syndrome has been named.

Noonan syndrome is inherited as an autosomal dominant condition. This means that the Noonan gene is on a non-sex (autosomal) chromosome and is transmitted from parent with a 50% probability to child. Although one dose of the Noonan gene is enough to cause the syndrome. A gene for Noonan syndrome (NS1) has been mapped to chromosome number 12. There are several different Noonan genes.

The frequency of the Noonan syndrome is estimated to be between 1:1,000 and 1:2,500 in the general population

 
Main features of this syndrome are:

  • Pulmonary Stenosis
  • Short stature after birth
  • Webbing of Neck
  • Caved in Chest Bones
  • In boys, Testes that do not descend into the scrotum.

Other possible heart defects are hypertrophic cardiomyopathy (thickened heart muscle), atrial septum defect (hole in the wall separating the anterior heart chambers), ventricular septum defect(hole in the wall separating the main heart chambers), septal hypertrophy or a combination of all these defects.

 
Other Facial features that may be present in this syndrome are:

  • Drooping of eyelids.
  • Downwards slanting eyes with arched eyebrows
  • Extra skin fold at the inner angle of the eyes.
  • Increased distance between the eyes.
  • Broad forehead
  • Very Blue or blue green eyes
  • Curly hair
  • Flat broad root of the nose.
  • Short broad neck with skin folds
  • Many pigmented birth marks

Variations occur in the facial features and they change with the age. As the child grows, the face gradually becomes more normal, often more triangular with a high forehead.

 
Other features of this syndrome

  • The birth length and weight of children with Noonan syndrome are often normal. The increase in height in both boys and girls is less than normal throughout the whole growing period.
  • On an average, puberty is delayed by about two years in both sexes.
  • During the first years of life the children may have great feeding and nutrition problems and frequent respiratory tract infections.
  • Only a few children with Noonan syndrome are seriously handicapped. Delayed motor development and speech may be seen in about 25% of the children.
  • Studies have shown that these children’s IQ was within normal limits, though in most cases in the lower range of normal. Mental retardation in approx. 35 %
  • Many of those with Noonan syndrome have a form of visual disturbance, squinting, near sight, or long sight, which may necessitate use of spectacles. The visual disturbance is usually mild.
  • A mild type of hearing impairment has been reported.
  • Children with Noonan syndrome often have dental problems. 1/3 of them have wrongly positioned teeth. The teeth often appear late and in an abnormal order.
  • Repeated attacks of epilepsy have been described in a few cases
  • Reduced fertility in men. Women’s fertility is normal.
 

Nitric Oxide

Nitric Oxide
  • Nitric oxide is a naturally occurring molecule found in a variety of cell types and organ systems. In the cardiovascular system, NO is an important determinant of basal vascular tone, prevents platelet activation, limits leukocyte adhesion to the endothelium, and regulates myocardial contractility. NO may also play a role in the pathogenesis of common cardiovascular disorders, including hypotension accompanying shock states, essential hypertension, and atherosclerosis.
  • It was first identified as endothelial-derived relaxing factor in blood vessels and as the mediator of the bactericidal actions of macrophages. NO’s role as a neural messenger may be even more prominent. NO is a likely transmitter of nonadrenergic, noncholinergic neurons.  Excess release of NO appears to account for a major portion of neural damage following vascular stroke.
  • Nitric oxide is a cytotoxic agent of macrophages, a messenger molecule of neurons, and a vasodilator produced by endothelial cells.
  • Nitric Oxide has been shown to be a mediator of Erectile function.
  • NO is a critical determinant of basal vascular tone, and a deficiency of NO is associated with hypertension.
  • Common disorders that promote atherosclerosis, such as hypertension, hyperlipidemia, smoking, and diabetes, are all associated with abnormal endothelial function. Deficiency of bioactive NO is associated with Abnormal Endothelial Function.
  • A deficiency of NO producing neurons in the gastrointestinal tract is believed to be responsible for certain abnormalities in gastrointestinal motility, such as Hirschsprung’s disease, achalasia, and chronic intestinal pseudo-obstruction.
  • Drugs like nitroglycerin, isosorbide mononitrate and dinitrate, and nitroprusside, promote vasodilation and platelet inhibition in dysfunctional coronary arteries by being metabolized to NO.
  • NO can be useful in the treatment of persistent pulmonary hypertension of the newborn, the pulmonary vasoconstriction that accompanies congenital diaphragmatic hernia, primary pulmonary hypertension, and adult respiratory distress syndrome.

Nausea & Vomiting

Nausea & Vomiting
NAUSEA is the sensation that precedes vomiting.VOMITING is the involuntary forced expulsion of stomach contents through the mouth. In most cases, the explanation is simple like irritation of the stomach by food or overindulgence in food and alcohol. Both are common complaints and are usually self-limiting. However, attention has to be paid to fluid balance and referral to hospital should be considered in case of dehydration and weight loss. If symptoms persist, a full examination of the patient is mandatory to look for serious underlying pathologies.Stimulation of the vomiting centre causes hypo-motility and reverse- motility of the digestive tract. The diaphragm presses down on the stomach and the abdominal walls move inwards, forcing the stomach contents out through the oesophagus. As this happens, the epiglottis clamps down upon the voice-box, thus preventing vomit from entering the wind-pipe. 

What causes Nausea and Vomiting?

Both nausea and vomiting result from stimulation of the vomiting centre located in the brain stem. This centre can be activated in two ways – chemically and neutrally. Chemical activation is mediated via the chemoreceptor trigger zone (CTZ) that is sensitive to the presence of toxins and poisons in the blood stream. Neural activation occurs as a result of information coming directly from the frontal lobes of the brain, the digestive tract and balancing mechanism of the inner ear.

Stimulation of the vomiting centre causes hypo-motility and reverse- motility of the digestive tract. The diaphragm presses down on the stomach and the abdominal walls move inwards, forcing the stomach contents out through the oesophagus. As this happens, the epiglottis clamps down upon the voice-box, thus preventing vomit from entering the wind-pipe.

Identification of Cause

The seriousness of vomiting depends upon its cause. It may be caused by overeating or drinking too much or by a viral infection. Alternatively, it may follow head injury or poisoning. Careful attention has to be paid in the following situations:

  • Head injury
  • Blood in the vomit
  • Temperature is more than 38degreeCelcius
  • Diarrhoea and continuous stomach pain
  • Stomach pain not relieved by vomiting
  • Chronic and unresponsive

Situation & Conditions to be suspected

  • Overindulgence in food, drinks or intake of drugs — Gastric Irritation
  • Consumption of bad food, similar symptoms seen in those who shared the food — Food Poisoning
  • Diarrhoea with or without rise in temperature – Gastoentiritis
  • Vomit contains blood or brown-black material resembling coffee grounds — Bleeding in the Gastroentestinal tract.
  • Abdominal pain not relieved by vomiting — Appendicitis, Perforation of duodenal ulcer, Pancreatitis.
  • Colicky pain — Gall Stones.
  • Jaundice – Hepatitis
  • Headache, drowsiness, difficulty in looking towards light; pain when bending the neck – Meningitis
  • Pain in and around one eye with blurred vision — Glaucoma.
  • Young woman who has missed her period – Pregnancy
  • While travelling — Motion Sickness
  • Accident, trauma — Head Injury, hematoma in the stomach
  • Vomiting during pregnancy: usually begins in the sixth week and peaks during the tenth week. Drug therapy should be avoided as far as possible. In severe cases  promethazine and doxylamine can be used as they are apparently free from teratogenic effects.

Drugs that commonly cause nausea and vomiting

  • Allopurinol
  • Antibiotics
  • Bromocriptine
  • Cytotoxics
  • Digoxin
  • Gold
  • Iron
  • Levopa
  • NSAIDS( Nonsteroid anti inflamatory drugs)
  • Oestrogens
  • Opiates
  • Penicillamine
  • Quinidine
  • Sulphasalazine
  • Theophyline
  • Thiazides

Management

The patient must be asked not to eat any solid food until nausea and vomiting subsides. He must be encouraged to take small sips of water to prevent dehydration. When the stomach settles, he should be advised to eat dry food like biscuits and toast before resuming normal diet. Attention has to be paid to fluid and electrolyte balance. Signs of dehydration include severe thirst, dry lips and tongue, sunken eyes, loss of skin elasticity, increased heart and respiratory rate, muscle cramps, lethargy, confusion and headache. If patient cannot take anything by mouth, intravenous fluids should be considered and the water salt balance should be carefully monitored by blood tests.

Medication

Drugs to manage nausea and vomiting are of two types: those that act directly on the digestive tract and those that act centrally. Drugs that act on the digestive tract increase intestinal contraction and accelerate transit. Centrally acting agents act at the vomiting centre or chemoreceptor trigger zone (CTZ) located in the brainstem and block impulses that induce nausea and Vomiting.

DOPAMINE ANTAGONISTS (prochlorperazinemetoclopramidedomperidone) act against D2 receptors in the brain stem (CTZ).

Prochlorperazine is a phenothazine possessing powerful antiernetic activity. In addition to CTZ, it also acts at the vomiting centre. It is used for nausea and vomiting due to various causes including migraine. Metoclopramide has a peripheral action on the gut and enhances gastric hurrying in addition to its effect on CTZ. Domperidone, unlike metoclopramide, does not cross the blood-brain barrier and may cause fewer extrapyramidal side-effects at high doses, eg. dystonia in children and parkinsonism in elderly.

ANTIHISTAMINES (promethazinediphenhydraminecyclizinecinnarizine) act on the vestibular apparatus of the inner ear and are useful in motion sickness and vomiting due to vestibular disease.

ANTISEROTONIN agents like ondansetron act on peripheral and central serotonin Acceptors and are valuable in the management of nausea and vomiting not relieved by conventional, less expensive agents.

ANTICHOLINERGICS act on the vomiting centre and digestive tract and reduce gastrointestinal hyperactivity. They help in the management of motion sickness but can cause dry mouth, drowsiness and blurred vision. All motion sickness drugs are effective if given before the journey. Once the sickness has started, the symptoms are more difficult to control.

 

 

Mustard agents

Mustard agents
Mustard agent was produced for the first time in 1822 but its harmful effects were not discovered until 1860.Mustard agents are usually classified as “blistering agents”. They also cause severe damage to the eyes, respiratory system and internal organs.

The effect of mustard agent is delayed and the first symptoms do not occur until 2-24 hours after exposure. A typical result of warfare with mustard agent is that the medical system is overloaded with numerous victims who require long and demanding care.

 

Mustard agent attacks the skin, eyes, lungs and gastro-intestinal tract. Internal organs may also be injured, mainly blood-generating organs, as a result of mustard agent being taken up through the skin or lungs and transported into the body. Mustard agent gives no immediate symptoms upon contact and consequently a delay of between two and twenty-four hours may occur before pain is felt and the victim becomes aware of what has happened. By then cell damage has already been caused.Mustard Agents as chemical weapons were first used towards the end of World War I. It was most commonly used chemical weapon, used to cause severe eye and lung damage.

 Mustard Agent-blistering of skin from exposure to mustard

 United States, Russia, Germany and Iraq are all said to have produced mustard agents during the 20th century. Iraq used it against Iran and the Kurdish civilians in the Iran-Iraq war. They are easy to make. They have rotten mustard or onion odour.
 Chemical Weapons