Apr 29 2008

HOMOEOPATHY -THE FUTURE OF MEDICINE !

HOMOEOPATHY -THE FUTURE OF MEDICINE !

image001 HOMOEOPATHY THE FUTURE OF MEDICINE !

clip image001 HOMOEOPATHY THE FUTURE OF MEDICINE !

Dr Sreevals G. Menon

Medical treatment with Homoeopathic therapeutics, at its very outset aims at management of disease beyond the actual expectation of the sick humanity! The complete nature of this therapeutic science gets important around the globe year by year for reasons more that one. Gifted by clairvoyance, extreme linguistic skills and extraordinary intelligence, Dr Samuel Hahnemann, a leading Surgeon and Physician of Germany suffered from contempt towards his own allopathic school of medical studies and sets out into hunting literatures for the right alternatives. While exercising his linguistic abilities during a translation of medical literature he finds clues about a virgin concept in medicine which had not seen light until then. His desire to develop on those despite immense opposition was the reason for the birth of ‘Homoeopathy’ 200 years back. Post modern by its concept and inception 400 years after the so-called modern medicine took shape, Homoeopathy continues it triumph into time setting free the bindings of side-effects of drugs and delivering cure of a complete nature, avoiding many a surgical intervention and with a softer impact on ones medical expenses !

Discussing about the major domains of Homoeopathic efficiency I would first talk about ALLERGY. A difficult situation resulting from hyper-responsiveness to external and internal causes and at times from unfavorable descend through genetic inheritance, this multi-headed monster often has its impact on upper, lower respiratory tracts and skin, and nomenclatures by various disease names !. Be it Atopic Dermatitis, Bronchial Asthma, Allergic Bronchitis, Allergic Rhinitis, Contact Dermatitis, Allergic Nasal polyp, Allergic pharyngitis and laryngitis…., all find their roots at allergy. Homoeopathy by its novel idea of introspection of the case by the individualization mandate in case-taking diagnoses the person beyond the disease per se. The application of this holistic science in the form of therapeutics often compromises hyper-responsiveness setting him free from the clutches of allergic disorders and facilitating normal life.
The other major sectors of Homoeopathic excellence are Obstetrics & Gynecology, Trichology [hairfall and other related diseases], Dermatologic ailments, Gastro-intestinal disorders, Cancer, Neurological disorders, Psychiatry, Renal diseases, Male & Female Infertility, Diabetes, Rheumatology, Hypertension and Cholesterol related ailments. Homoeopathy also does immensely well in diseases related to the heart.

Among the Gastrointestinal disorders the best treated illnesses are those related to the stress factors, and other psycho-somatic disorders. The major conditions are Irritable Bowel Syndrome, Acid Peptic Disease, Flatulent Dyspepsia, Peptic Ulcer & Chronic gastritis. Disorders of Liver, Pancreas and Intestines often turn a major reason for suffering in many patients which are often corrected with ease using Homoeopathic Therapeutics. Here again the diagnosis is very vital in prescribing under various heads and approaches which entirely depends on the seat of the disease. Very often all major investigations are often sought for interpreting the disease in detail and also as prognostic criterions to assess development towards cure.

The approach in female disorders is very holistic where the individual is deeply assessed in terms of thermal reactions, reactive patterns of the mind, basic attitudes, meteorological reactions, factors modifying the illness, temperament etc. The stress factors are deeply assessed. Every disease related to the female genital organs, diseases related to the menstrual cycles and other organs can be treated well by the Homoeopathic system leaving absolutely negligible possibilities of recurrence.

Prophylaxis, or in other words the preventive aspects of diseases, mostly endemic and epidemic diseases has been proved off late as a major advancement in Homoeopathy. In the past decade Homoeopathy was solely responsible for limiting many outbreaks by the appropriate intervention of the Government sectors and the Homoeopathic Medical Colleges with support from the urban and rural private practitioners who shouldered the mission. The preventive medicines revealed by the ‘Genus Epidemicus’ study was widely used for Cholera, Japanese Encephalitis, Chikun Guniya, Dengue Hemorrhagic Fevers, Leptospirosis [Weil's Disease] etc. Preventive medicines were widely distributed by these bodies at the disease stricken areas and surrounding promptly reducing new outbreaks, incidences of cases and thus setting new standards in community health care.

The recent advancement in Science and Materials Labs, Arizona has helped interpret the extreme scientificity of Homoeopathic medicines through the explanations favoring the formation of nano-molecular bubbles in the vehicle [water, alcohol] as a part of the act of homoeopathic potentisation where the OH radicals present in these inherits the properties of the mother drug substance at its sp hybridization levels which remains in the vehicle much after the non- existence of the mother drug quantitatively, thus explaining the action of Homoeopathic medicines of higher dynamization status !

The recent development as a part of a conference in favor of NASA, at the Rutger’s University says that Homeopathy could be the next choice in their Lunar Settlement projects for future!! The conventional medicines of allopathy are found to fail for space conditions. This is because of problems related to absorption and solubility of such medicines in extreme environments, where there is no gravity. This is where our ultra-diluted medicines could come up as a possible substitute as they are easily absorbed by the body. The only system of medicine which uses ultra-diluted medicines is Homoeopathy which gives it a huge momentum into a futuristic medicine!!

The similarities in the Mitochondrial DNA concepts and the fundamentals of Homoeopathic philosophy about concepts of miasms, the formation of Psora in particular!, gives hope in a new direction, where the genetically inherited diseases could be added to Homoeopathic scope and domain with possibilities of efficient intervention. The observation also adds credibility to the Homoeopathic philosophy. The miasmatic assessment of individuals could be done and diseases could be anticipated, envisioned, treated and controlled efficiently abiding the concepts in the Homoeopathic Philosophy!

I therefore leave the readers to ponder on these and to assess if Homoeopathy is just a complementary & alternative system of medicine, or a post modern system of medicine which could also be addressed as the future of Medicine!

Dr Sreevals G Menon [PH-00919349117833, [email protected]]

Special Consultant, Allergy-Asthma & Respiratory Clinic

Director, AIHMS HOMOEOPATHY

[KANNUR-KOZHIKODE-COCHIN-TRIVANDRUM]

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Apr 28 2008

THE DELIBERATIONS AGAIST HOMOEOPATHIC MEDICINES – BASELESS AND ABSURD

THE DELIBERATIONS AGAIST HOMOEOPATHIC MEDICINES – BASELESS AND ABSURD

Dr.S.G.Biju

[email protected]

The report published by the Medical Journal LANCET that Homoeopathic medicines does not have any action and it has only placebo effect is baseless and absurd. We do not know what principle they have used in testing the efficacy of Homoeopathic medicine. The drug trials they are mentioning are not of the homoeopathic way. Homoeopathic treatment is based on individualization. Homoeopathy is not treating the disease or parts of the body. We treat the person as a whole and follow the cardinal principle law of similars. Any other tests targeting the diseased parts of the person using homoeopathic medicines will go wrong because they are not individualizing the person and not following the principle of Law of similars. So the claim of 110 drug trial is baseless. This is only to defame Homoeopathy , the noble system.

If you look into the reports we can find that they are trying to defame homoeopathy with some vested interests: last year the sale of homoeopathic medicines in Britain was 3,60,000 pound sterling causing fear to the multinational drug companies. According to the National daily ‘The Hindu’ dated August 27,the

same journal Lancet published another report from a draft prepared by Prof.Ernst,WHO comes to the conclusion that studies over the last 40 years have shown that homoeopathic medicines are found to be as effective as conventional medicine in the treatment of illness both in humans and animals. This report of WHO the world’s most leading health monitoring body is contradictory to the Swiss teams report about the efficacy of homoeopathic medicine.

Homoeopathic medical system is widely accepted as the first alternative medical system because it is the most effective medicine without any side effects. Homoeopathy is accepted as the first alternative system of medicine in 140 countries in the world. It is getting wide acceptance in Gulf countries too.

Homoeopathic medical system is gaining acceptance even among allopathic doctors so says “Good House keeping” a magazine published by India Today group dated January 25 and also its wide acceptance in England, France, Germany, Greece and USA. In USA the number of patients opting homoeopathy is growing at an annual rate of 20% per year claims this magazine.

In Kerala alone we have five homoeopathic medical colleges, 550 government dispensaries, 55 hospitals and 14 district hospitals. More than 3 lakh patients attend the hospitals daily for homoeopathic treatment.

During the out breaks of epidemics like cholera, viral encephalitis, dengue fever, hepatitis leptospirosis in the yester years it was homoeopathy which prevented the disease in Kerala. As an acceptance to the efficacy of homoeopathic medical system in the field of epidemic control, the state government has started an epidemic control cell for homoeopathy namely RAECH(Rapid Action Epidemic Control Cell in Homoeopathy), Govt.of Kerala.

During the Tsunami disaster the state government has directed us to take up the challenge of controlling the outbreak of epidemics in the region. Homoeopathic medical system has taken up the challenge and we have done a creditable job in the prophylactic treatment. No epidemic occurred in the area. Here I want to quote the Father of our nation Mahatma Gandhi” Homoeopathy Never fails”. I want to emphasize that the method adapted by the Swiss team to do the drug trial was not correct. The yard stick they used to do the drug trails for other system of medicines is not effective in homoeopathic medical science.

We the members of “The Institution of Homoeopaths Kerala” the one and only organization which represents all categories of institutionally qualified homoeopaths of Kerala comprising of more than 4000 members and having 51 units all over Kerala condemns this baseless statement against the homoeopathic medical system in the journal Lancet. The statement is baseless and absurd. It is only to defame the homoeopathic medical system for the sale of multinational drug companies.

Apr 27 2008

APPENDICITIS

APPENDICITIS

The appendix is a closed-ended, narrow tube up to several inches in length that attaches to the cecum (the first part of the colon) like a worm. (The anatomical name for the appendix, vermiform appendix, means worm-like appendage.) The inner lining of the appendix produces a small amount of mucus that flows through the open center of the appendix and into the cecum. The wall of the appendix contains lymphatic tissue that is part of the immune system for making antibodies. Like the rest of the colon, the wall of the appendix also contains a layer of muscle, but the muscle is poorly developed.

Appendicitis (or epityphlitis) is a condition characterized by inflammation of the appendix. While mild cases may resolve without treatment, most require removal of the inflamed appendix, either by laparotomy or laparoscopy. Untreated, mortality is high, mainly due to peritonitis and shock. Reginald Fitz first described acute appendicitis in 1886, and it has been recognized as one of the most common causes of acute abdomen pain worldwide.

It is thought that appendicitis begins when the opening from the appendix into the cecum becomes blocked. The blockage may be due to a build-up of thick mucus within the appendix or to stool that enters the appendix from the cecum. The mucus or stool hardens, becomes rock-like, and blocks the opening. This rock is called a fecalith (literally, a rock of stool). At other times, the lymphatic tissue in the appendix may swell and block the appendix. After the blockage occurs, bacteria which normally are found within the appendix begin to invade (infect) the wall of the appendix. The body responds to the invasion by mounting an attack on the bacteria, an attack called inflammation. An alternative theory for the cause of appendicitis is an initial rupture of the appendix followed by spread of bacteria outside the appendix.. The cause of such a rupture is unclear, but it may relate to changes that occur in the lymphatic tissue, for example, inflammation, that line the wall of the appendix.)

If the inflammation and infection spread through the wall of the appendix, the appendix can rupture. After rupture, infection can spread throughout the abdomen; however, it usually is confined to a small area surrounding the appendix (forming a peri-appendiceal abscess).

Sometimes, the body is successful in containing (”healing”) the appendicitis without surgical treatment if the infection and accompanying inflammation do not spread throughout the abdomen. The inflammation, pain and symptoms may disappear. This is particularly true in elderly patients and when antibiotics are used. The patients then may come to the doctor long after the episode of appendicitis with a lump or a mass in the right lower abdomen that is due to the scarring that occurs during healing. This lump might raise the suspicion of cancer.

Causes

Obstruction of the appendiceal lumen has been attributed to a number of common sources including from fecaliths (a hard mass of fecal matter), normal stool, viral induced ulcers, or lymphoid hyperplasia. Once this obstruction occurs the appendix subsequently becomes filled with mucus and distends, increasing intraluminal and intramural pressures, resulting in thrombosis and occlusion of the small vessels, and stasis of lymphatic flow. As these progress, the appendix becomes ischemic and then necrotic. Rarely, spontaneous recovery can occur at this point. As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). The end result of this cascade is appendiceal rupture causing peritonitis, which may lead to septicemia and eventually death.

A number of environmental factors involving diet and hygiene have been proposed to be alternate causes of appendicitis, none of which has been studied in detail. According to the Medical Journal of Australia, “Dietary theories, notably an inadequate fibre intake, have been advanced to account for the geography of the disease, but it is clear that diet can not fully explain the epidemiology.

Complications of Appendicitis

The most frequent complication of appendicitis is perforation. Perforation of the appendix can lead to a periappendiceal abscess (a collection of infected pus) or diffuse peritonitis (infection of the entire lining of the abdomen and the pelvis). The major reason for appendiceal perforation is delay in diagnosis and treatment. In general, the longer the delay between diagnosis and surgery, the more likely is perforation. The risk of perforation 36 hours after the onset of symptoms is at least 15%. Therefore, once appendicitis is diagnosed, surgery should be done without unnecessary delay.

A less common complication of appendicitis is blockage of the intestine. Blockage occurs when the inflammation surrounding the appendix causes the intestinal muscle to stop working, and this prevents the intestinal contents from passing. If the intestine above the blockage begins to fill with liquid and gas, the abdomen distends and nausea and vomiting may occur. It then may be necessary to drain the contents of the intestine through a tube passed through the nose and esophagus and into the stomach and intestine.

A feared complication of appendicitis is sepsis, a condition in which infecting bacteria enter the blood and travel to other parts of the body. This is a very serious, even life-threatening complication. Fortunately, it occurs infrequently.

Symptoms

Symptoms of acute appendicitis can be classified into two types, typical and atypical (Hobler, K., 1998). The typical history includes pain starting centrally (periumbilical) before localising to the right iliac fossa (the lower right side of the abdomen); this is due to the poor localizing (spatial) property of visceral nerves from the mid-gut, followed by the involvement of somatic nerves (parietal peritoneum) as the inflammation progresses. The pain is usually associated with loss of appetite and fever. Nausea or vomiting may or may not occur. With the typical type, diagnosis is easier to make, surgery occurs earlier and findings are often less severe (Hobler, K., 1998).

Atypical symptoms may include pain beginning in the right lower quadrant, diarrhea and a more prolonged, smoldering course. Being more difficult to diagnose, CT scans and ultrasound tests are more useful. Surgical findings are more apt to be severe (suppuration, abscess, perforation, etc.(Hobler,K., 1998).

In either type of history, physical findings of appendicitis usually include localized findings in the right lower quadrant suggesting peritonitis. The abdominal wall becomes very sensitive to gentle pressure (palpation)and tapping (percussion). Coughing causes point tenderness in this area (McBurney’s Point) and this is the least painful way to localize the inflamed appendix. If the abdomen on palpation is also involuntarily guarded (rigid), there should be a strong suspicion of peritonitis requiring urgent surgical intervention.

The main symptom of appendicitis is abdominal pain. The pain is at first diffuse and poorly localized, that is, not confined to one spot. (Poorly localized pain is typical whenever a problem is confined to the small intestine or colon, including the appendix.) The pain is so difficult to pinpoint that when asked to point to the area of the pain, most people indicate the location of the pain with a circular motion of their hand around the central part of their abdomen. A second, common, early symptom of appendicitis is loss of appetite which may progress to nausea and even vomiting. Nausea and vomiting also may occur later due to intestinal obstruction.

As appendiceal inflammation increases, it extends through the appendix to its outer covering and then to the lining of the abdomen, a thin membrane called the peritoneum. Once the peritoneum becomes inflamed, the pain changes and then can be localized clearly to one small area. Generally, this area is between the front of the right hip bone and the belly button. The exact point is named after Dr. Charles McBurney–McBurney’s point. If the appendix ruptures and infection spreads throughout the abdomen, the pain becomes diffuse again as the entire lining of the abdomen becomes inflamed.

Diagnosis

Diagnosis is based on history and physical examination backed by an elevation of neutrophilic white cells. Atypical histories often requires ultrasound and/or CT scanning (Hobler, K., 1998).

The classical history in appendicitis is diffuse pain in the periumbilical region which then localizes as pain and tenderness at McBurney’s point (associated with an inflamed appendix coming in contact with the surrounding parietal peritoneum). This point is located on the right-hand side of the abdomen one-third of the distance between the anterior superior iliac spine and the navel. Here, on gentle palpation, the abdominal muscles often feel firm to rigid because of involuntary spasm, and a cough also produces a localized soreness.

Other physical findings include right-side tenderness on a digital rectal exam. Since the appendix normally lies on the right, if a finger is inserted into the rectum and there may be tenderness when pressure is applied toward the right indicating an increased likelihood that the patient has a pelvic appendix.

Other signs used in the diagnosis of appendicitis are the psoas sign (useful in retrocecal appendicitis), the obturator sign (specifically the obturator internus muscle), Blumberg’s sign, and Rovsing’s sign.

Ultrasonography and Doppler sonography also provide useful means to detect appendicitis, especially in children. In some cases (15% approximately), however, ultrasonography of the iliac fossa does not reveal any abnormalities despite the presence of appendicitis. This is especially true of early appendicitis before the appendix has become significantly distended and in adults where larger amounts of fat and bowel gas make actually seeing the appendix technically difficult. Despite these limitations, in experienced hands sonographic imaging can often distinguish between appendicitis and other diseases with very similar symptoms such as inflammation of lymph nodes near the appendix or pain originating from other pelvic organs such as the ovaries or fallopian tubes.

In places where it is readily available, CT scan has become the diagnostic test of choice, especially in adults whose diagnosis is not obvious on history and physical. (The use of CT in pregnant women and children is significantly limited, however, by concerns regarding radiation exposure.) A properly performed CT scan with modern equipment has a detection rate (sensitivity) of over 95% and a similar specificity. Signs of appendicitis on CT scan include lack of contrast (oral dye) in the appendix and direct visualization of appendiceal enlargement (greater than 6 mm in diameter on cross section). The inflammation caused by appendicitis in the surrounding peritoneal fat (so called “fat stranding”) can also be observed on CT, providing a mechanism to detect early appendicitis and a clue that appendicitis may be present even when the appendix is not well seen. Thus, diagnosis of appendicitis by CT is made more difficult in very thin patients and in children, both of whom tend to lack significant fat within the abdomen. The utility of CT scanning is made clear, however, by the impact it has had on negative appendectomy rates. For example, use of CT for diagnosis of appendicitis in Boston, MA has decreased the chance of finding a normal appendix at surgery from 20% in the pre-CT era to only 3% according to data from the Massachusetts General Hospital.

The white blood cell count in the blood usually becomes elevated with infection. In early appendicitis, before infection sets in, it can be normal, but most often there is at least a mild elevation even early. Unfortunately, appendicitis is not the only condition that causes elevated white blood cell counts. Almost any infection or inflammation can cause this count to be abnormally high. Therefore, an elevated white blood cell count alone cannot be used as a sign of appendicitis.

Urinalysis is a microscopic examination of the urine that detects red blood cells, white blood cells and bacteria in the urine. Urinalysis usually is abnormal when there is inflammation or stones in the kidneys or bladder. The urinalysis also may be abnormal with appendicitis because the appendix lies near the ureter and bladder. If the inflammation of appendicitis is great enough, it can spread to the ureter and bladder leading to an abnormal urinalysis. Most patients with appendicitis, however, have a normal urinalysis. Therefore, a normal urinalysis suggests appendicitis more than a urinary tract problem.

The surgeon faced with a patient suspected of having appendicitis always must consider and look for other conditions that can mimic appendicitis. Among the conditions that mimic appendicitis are:

  • Meckel’s diverticulitis. A Meckel’s diverticulum is a small outpouching of the small intestine which usually is located in the right lower abdomen near the appendix. The diverticulum may become inflamed or even perforate (break open or rupture). If inflamed and/or perforated, it usually is removed surgically.
  • Pelvic inflammatory disease. The right fallopian tube and ovary lie near the appendix. Sexually active women may contract infectious diseases that involve the tube and ovary. Usually, antibiotic therapy is sufficient treatment, and surgical removal of the tube and ovary are not necessary.
  • Inflammatory diseases of the right upper abdomen. Fluids from the right upper abdomen may drain into the lower abdomen where they stimulate inflammation and mimic appendicitis. Such fluids may come from a perforated duodenal ulcer, gallbladder disease, or inflammatory diseases of the liver, e.g., a liver abscess.
  • Right-sided diverticulitis. Although most diverticuli are located on the left side of the colon, they occasionally occur on the right side. When a right-sided diverticulum ruptures it can provoke inflammation they mimics appendicitis.
  • Kidney diseases. The right kidney is close enough to the appendix that inflammatory problems in the kidney-for example, an abscess-can mimic appendicitis.

Treatment

Once a diagnosis of appendicitis is made, an appendectomy usually is performed. Antibiotics almost always are begun prior to surgery and as soon as appendicitis is suspected.

There is a small group of patients in whom the inflammation and infection of appendicitis remain mild and localized to a small area. The body is able not only to contain the inflammation and infection but to resolve it as well. These patients usually are not very ill and improve during several days of observation. This type of appendicitis is referred to as “confined appendicitis” and may be treated with antibiotics alone. The appendix may or may not be removed at a later time.

On occasion, a person may not see their doctor until appendicitis with rupture has been present for many days or even weeks. In this situation, an abscess usually has formed, and the appendiceal perforation may have closed over. If the abscess is small, it initially can be treated with antibiotics; however, the abscess usually requires drainage. A drain (a small plastic or rubber tube) usually is inserted through the skin and into the abscess with the aid of an ultrasound or CT scan that can determine the exact location of the abscess. The drain allows pus to flow from the abscess out of the body. The appendix may be removed several weeks or months after the abscess has resolved. This is called an interval appendectomy and is done to prevent a second attack of appendicitis.

The treatment begins by keeping the patient from eating or drinking anything, even water, in preparation for surgery. An intravenous drip is used to hydrate the patient. Antibiotics given intravenously such as cefuroxime and metronidazole may be administered early to help kill bacteria and thus reduce the spread of infection in the abdomen and postoperative complications in the abdomen or wound. Equivocal cases may become more difficult to assess with antibiotic treatment and benefit from serieal examinations. If the stomach is empty (no food in the past six hours) general anaesthesia is usually used. Otherwise, spinal anaesthesia may be used.

The surgical procedure for the removal of the appendix is called an appendicectomy (also known as an appendectomy). Often now the operation can be performed via a laparoscopic approach, or via three small incisions with a camera to visualize the area of interest in the abdomen. If the findings reveal suppurative appendicitis with complications such as rupture, abscess, adhesions, etc., conversion to open laparotomy may be necessary. An open laparotomy incision if required most often centers on the area of maximum tenderess, McBurney’s Point, in the right lower quadrant. A transverse or a gridiron diagonal incision is used most commonly.

According to a meta-analysis from the Cochrane Collaboration comparing laparoscopic and open procedures, laparoscopic procedures seem to have various advantages over the open procedure. Wound infections were less likely after laparoscopic appendicectomy than after open appendicectomy (odds ratio 0.45; CI 0.35 to 0.58), but the incidence of intraabdominal abscesses was increased (odds ratio 2.48; CI 1.45 to 4.21). The duration of surgery was 12 minutes (CI 7 to 16) longer for laparoscopic procedures. Pain on day 1 after surgery was reduced after laparoscopic procedures by 9 mm (CI 5 to 13 mm) on a 100 mm visual analogue scale. Hospital stay was shortened by 1.1 day (CI 0.6 to 1.5). Return to normal activity, work, and sport occurred earlier after laparoscopic procedures than after open procedures. While the operation costs of laparoscopic procedures were significantly higher, the costs outside hospital were reduced. Young female, obese, and employed patients seem to benefit from the laparoscopic procedure more than other groups.

Surgery may last from 15 minutes in typical appendicitis in thin patients to several hours in complicated cases. Hospital lengths of stay usually range from overnight to a matter of days (rarely weeks in complicated cases.) The pain is not always constant, in some cases it can stop for a day and then come back.

Prognosis

Most appendicitis patients recover easily with treatment, but complications can occur if treatment is delayed or if peritonitis occurs.

Recovery time depends on age, condition, complications, and other circumstances, including the amount of alcohol consumption, but usually is between 10 and 28 days. For young children (around 10 years old) the recovery takes three weeks.

The real possibility of life-threatening peritonitis is the reason why acute appendicitis warrants speedy evaluation and treatment. The patient may have to undergo a medical evacuation. Appendectomies have occasionally been performed in emergency conditions (i.e. outside of a proper hospital), when a timely medical evaluation was impossible.

Typical acute appendicitis responds quickly to appendectomy and occasionally will resolve spontaneously. If appendicitis resolves spontaneously, it remains controversial whether an elective interval appendectomy should be performed to prevent a recurrent episode of appendicitis. Atypical appendicitis (associated with suppurative appendicitis) is more difficult to diagnose and is more apt to be complicated even when operated early. In either condition prompt diagnosis and appendectomy yield the best results with full recovery in two to four weeks usually. Mortality and severe complications are unusual but do occur, especially if peritonitis persists and is untreated.

An unusual complication of an appendectomy is “stump appendicitis”: inflammation occurs in the remnant appendiceal stump left after a prior, incomplete appendectomy.

What is new about appendicitis?

Recently it has been hypothesized that some episodes of appendicitis-like symptoms, especially recurrent symptoms, may be due to an increased sensitivity of the intestine and appendix from a prior episode of inflammation. That is, the recurrent symptoms are not due to recurrent episodes of inflammation. Rather, prior inflammation has made the nerves of the intestines and appendix or the central nervous system that innervate them more sensitive to normal stimuli, that is, with stimuli other than inflammation. This will be a difficult, if not impossible, hypothesis to confirm.

[email protected]

Apr 27 2008

HEART ATTACK (MYOCARDIAL INFARCTION)

HEART ATTACK (MYOCARDIAL INFARCTION)

A heart attack (also known as a myocardial infarction) is the death of heart muscle from the sudden blockage of a coronary artery by a blood clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the heart muscle. Injury to the heart muscle causes chest pain and pressure. If blood flow is not restored within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for six to eight hours at which time the heart attack usually is “complete.” The dead heart muscle is replaced by scar tissue.

CAUSES OF HEART ATTACK

ha1 HEART ATTACK (MYOCARDIAL INFARCTION)

With advancing age, cholesterol and calcium are deposited gradually in the walls of the coronary arteries. These deposits are called plaques. The process is known as atherosclerosis, or “hardening of the arteries.”

  • A diet high in cholesterol combined with smoking and lack of exercise can accelerate this process.
  • As these plaques grow, they begin to impede the flow of blood.
  • The growing plaque is like a firm shell with a soft inner core containing cholesterol.
  • As blood hits a plaque during each heartbeat, the plaque may crack open and expose the inner cholesterol.
  • The cholesterol may cause a blood clot to begin to form.
  • The plaque and the blood clot block the artery partially or completely. The more the artery is blocked, the greater the resulting damage to the heart.

Atherosclerotic coronary artery disease

This most common type of heart disease is associated with several risk factors. The greater the number of risk factors you have, the more likely you are to have atherosclerosis. The most common risk factors are as follows:

  • Hereditary (runs in the family)
  • High cholesterol in blood, especially high levels of “bad cholesterol” (LDL, low-density lipoprotein) and low levels of “good cholesterol” (HDL, high-density lipoprotein)
  • Cigarette smoking or other tobacco use, including cigars and chewing tobacco
  • Obesity or excess weight
  • High blood pressure (hypertension)
  • Diabetes
  • Physical inactivity, lack of regular exercise (sedentary lifestyle)
  • High-fat diet
  • Emotional stress
  • Type-A personality (hard-driving, perfectionist)

Nonatherosclerotic coronary artery disease

Coronary arteries can be blocked by conditions other than atherosclerosis. These include inflammatory diseases of the arteries, trauma such as a cut or stab wound to the heart, and diseases that cause thickening of the coronary arteries.

Coronary embolization may cause a heart attack. Coronary embolization refers to a clot from elsewhere in the body breaking off and traveling to the heart.

Other causes of heart attack are blood or oxygen supply problems or outside influences such as cocaine abuse and complications from bypass or catheterization.

Certain heart problems leading to heart attack may be present from birth.

SYMPTOMS

Although chest pain or pressure is the most common symptom of a heart attack, heart attack victims may experience a diversity of symptoms that include:

  • Pain, fullness, and/or squeezing sensation of the chest
  • Jaw pain, toothache, headache
  • Shortness of breath
  • Nausea, vomiting, and/or general epigastric (upper middle abdomen) discomfort
  • Sweating
  • Heartburn and/or indigestion
  • Arm pain (more commonly the left arm, but may be either arm)
  • Upper back pain
  • General malaise (vague feeling of illness)
  • No symptoms (Approximately one quarter of all heart attacks are silent, without chest pain or new symptoms. Silent heart attacks are especially common among patients with diabetes mellitus.)

Even though the symptoms of a heart attack at times can be vague and mild, it is important to remember that heart attacks producing no symptoms or only mild symptoms can be just as serious and life–threatening as heart attacks that cause severe chest pain. Too often patients attribute heart attack symptoms to “indigestion,” “fatigue,” or “stress,” and consequently delay seeking prompt medical attention. One cannot overemphasize the importance of seeking prompt medical attention in the presence of symptoms that suggest a heart attack. Early diagnosis and treatment saves lives, and delays in reaching medical assistance can be fatal. A delay in treatment can lead to permanently reduced function of the heart due to more extensive damage to the heart muscle. Death also may occur as a result of the sudden onset of arrhythmias such as ventricular fibrillation.

Chest pressure, discomfort, or a bandlike sensation around the chest with squeezing or heaviness is a common symptom of heart attack.

  • About one fourth of people having a heart attack have no pain (”silent” heart attack).
  • Silent heart attacks are more frequent in people with diabetes.

The following symptoms suggest a heart attack:

  • Chest pain or pressure (heaviness)
  • Jaw pain, or extension of pain into the arms or shoulder, especially the left arm
  • Unexplained shortness of breath
  • Unexplained sweating
  • Heartburn or feeling of indigestion
  • Nausea or vomiting
  • Back pain or upper abdominal pain
  • General lethargy or listlessness (malaise)

COMPLICATIONS

Heart failure

If a large amount of heart muscle dies, the ability of the heart to pump blood to the rest of the body is diminished, and this can result in heart failure. The body retains fluid, and organs, for example, the kidneys, begin to fail

Ventricular fibrillation

Injury to heart muscle also can lead to ventricular fibrillation. Ventricular fibrillation occurs when the normal, regular, electrical activation of heart muscle contraction is replaced by chaotic electrical activity that causes the heart to stop beating and pumping blood to the brain and other parts of the body. Permanent brain damage and death can occur unless the flow of blood to the brain is restored within five minutes.

Most of the deaths from heart attacks are caused by ventricular fibrillation of the heart that occurs before the victim of the heart attack can reach an emergency room. Those who reach the emergency room have an excellent prognosis; survival from a heart attack with modern treatment should exceed 90%. The 1% to 10% of heart attack victims who die later include those victims who suffer major damage to the heart muscle initially or who suffer additional damage at a later time.

Deaths from ventricular fibrillation can be avoided by cardiopulmonary resuscitation (CPR) started within five minutes of the onset of ventricular fibrillation. CPR requires breathing for the victim and applying external compression to the chest to squeeze the heart and force it to pump blood. When paramedics arrive, medications and/or an electrical shock (cardioversion) can be administered to convert ventricular fibrillation back to a normal heart rhythm and allow the heart to pump blood normally. Therefore, prompt CPR and a rapid response by paramedics can improve the chances of survival from a heart attack. In addition, many public venues now have defibrillators that provide the electrical shock needed to restore a normal heart rhythm even before the paramedics arrive. This greatly improves the chances of survival.

DIAGNOSIS

A heart attack is not a quick event that lasts a few minutes and is over.

  • A heart attack is a process that continues over several hours.
  • Every minute that passes before treatment is begun, your heart sustains more damage.
  • You must seek medical attention as soon as you suspect you are having a heart attack.

If you arrive at the hospital in an ambulance, the staff will be ready for you.

  • They will evaluate your condition rapidly by examining you and, if you can answer, asking you questions about your symptoms.
  • They will obtain an electrocardiogram (ECG) right away to look for signs of heart attack.
  • A quick diagnosis is essential for starting treatment as soon as possible.

If you are thought to be having a heart attack, you may undergo the following tests upon arrival and/or during the next few days of your hospital stay.

Blood tests: Routine blood tests include blood cell counts, chemistry and electrolytes, and coagulation (clotting) function.

  • Cardiac enzymes: When heart muscle is damaged, certain muscle proteins are released into the bloodstream and can be measured. Elevations of the levels of certain of these proteins, known as cardiac enzymes, strongly suggest that a heart attack is in progress or has occurred recently. Repeated testing of blood samples for cardiac enzymes is helpful in making the diagnosis of a heart attack, especially when the ECG is not diagnostic.
  • Other enzymes: Some other enzymes tested include AST (SGOT, aspartate transferase) and LDH (lactate dehydrogenase).
  • The 2 most measured enzymes are creatine kinase (CK) and troponin.
    • Creatine kinase is released from the cardiac muscle cells as they die and as their membranes dissolve. The level of this enzyme takes a number of hours after the beginning of the heart attack to peak. It returns to normal by 24 hours after the beginning of the heart attack. A form of this enzyme called MB subform is quite specific in showing cardiac damage.
    • Troponin-I and troponin-T are very useful enzyme tests. The levels of these enzymes rise by 6-8 hours after the heart attack begins and remain elevated above normal for as long as a week. To some extent, the level of troponin can predict the likelihood of complications for a person with a heart attack. The levels may also helpful in deciding what treatments should be used.

Electrocardiogram: This test detects the electrical activity of the heart and records graphlike tracings of each heartbeat (waves).

  • It is safe and painless, and it takes only a few minutes.
  • An ECG is performed by taping electrodes on your arms, legs, and chest. The electrodes pick up the electrical impulses of your heart from different points of view in your chest.
  • ECG abnormalities diagnostic of heart attack are sometimes seen early in a heart attack, but the ECG may be normal at first and need to be repeated.
  • Sometimes existing ECG abnormalities may make the diagnosis difficult.

Chest x-ray: This is not always done, but it can show abnormalities in the size or shape of the heart and indicate if fluid is collecting in the lungs, a sign or poor circulation.

Echocardiogram (echo): This is an ultrasound examination of the heart. The ultrasound device uses sound waves to create a detailed “picture” of the heart, which are then transmitted to a video monitor.

  • This is a safe, noninvasive, and very helpful test.
  • Echo may show problems in the heart structure, such as abnormalities in the movements of the heart wall. A heart attack is a damaged heart wall.
  • It can show abnormal enlargement or pouching of the heart wall (aneurysm).
  • Echo may also visualize complications of heart attack including valve problems, rupture of the heart muscle, or accumulation of fluid in the cardiac sac (pericardial effusion).
  • The most important information obtained from the echo is the ejection fraction. This is a measurement of the strength of heart muscle. This information may be used to help predict outcome and to decide on treatment.

Coronary angiography: This is the best test for identifying blockages in the coronary arteries.

  • It often is performed for people with persistent pain and those who have not received “clot-busting” drugs to re-open their blocked artery.
  • At some hospitals, people are taken directly into the catheterization, or cath, lab from the emergency department after initial evaluation.
  • In the cath lab, a long, thin plastic tube (catheter) is put into the femoral artery (in the groin) or the brachial or radial artery (in the arm) and guided into the openings of the coronary arteries. Dye is injected into the arteries to make them stand out on x-ray. Pictures are recorded for later review.
  • Coronary angiography is an invasive test with potentially serious complications, but when performed by an experienced doctor, the risk of complications is relatively small.
  • An angiogram is the best test to determine which treatment is most appropriate: medication, angioplasty, stent placement, or bypass surgery.

A stress test may be performed before a person leaves the hospital, after the patient is stable and recovering from the heart attack and/or procedure.

  • Exercise stress testing involves recording an ECG while the heart is stressed and again at rest.
    • The “stress” is usually exercise, namely, walking on a treadmill.
    • Speed and elevation are gradually increased while recording the ECG.
    • Certain changes in the ECG indicate possible coronary artery blockage.
    • The exercise stress test is about 60-70% accurate in predicting increased risk of future heart attacks.
    • If the stress test indicates fairly severe blockage, coronary angiography may be needed to confirm the diagnosis and determine the need for further treatment.
  • Radionuclide stress testing is another type of stress testing.
    • It uses a special camera that sees blood flow after a tiny dose of a radioactive “dye” (isotope) is injected into the blood.
    • It measures the quantities of blood flow that reach the different parts of the heart muscle through the coronary arteries.
    • Like the exercise stress test, pictures are obtained with exercise on the treadmill and then with rest.
    • People who are unable to walk on the treadmill may be given medication to “stress” the heart muscle.
    • If a particular coronary artery is blocked partially or completely, the part of the heart supplied with blood by that artery would appear as a “cold spot” on the pictures because no radioactive isotope reaches that area.
    • This test is quite accurate in diagnosing coronary artery blockage. The small amount of radioactivity is not considered to be harmful.

TREATMENT

Medical treatment may be started immediately, before a definite diagnosis of a heart problem is made.

General treatment measures include the following:

  • Oxygen through a tube in the nose or face mask
  • Nitroglycerin under the tongue
  • Pain medicines (morphine or meperidine)
  • Aspirin: Those with allergy to aspirin may be given clopidogrel (Plavix).

Clot-dissolving medicines: The tissue plasminogen activators (tPAs) can actually dissolve clots.

  • The earlier these drugs are given, the better the chance of dissolving the clot and opening the blocked artery, protecting the heart muscle from further injury.
  • If more than 12 hours has passed since the onset of chest pain, these drugs are less helpful.
  • Potential risks of this therapy include bleeding.
  • The most serious risk is a stroke (bleeding into the brain).

Angioplasty: Emergency coronary angiography and coronary balloon angioplasty (percutaneous transluminal coronary angioplasty, or PTCA) are available in hospitals equipped with a full-service cardiac catheterization laboratory. This is the most direct method of removing blockage in a coronary artery.

  • Coronary balloon angioplasty is an extension of coronary angiography.
  • A long, thin tube (catheter) is inserted in an artery in the groin or arm.
  • At the tip of the catheter is a tiny, elongated balloon, which is threaded over a hair-thin guidewire into the narrowed coronary artery.
  • Once the balloon is positioned at the blockage in the coronary artery, it is inflated.
  • The balloon pushes aside the plaque and clot that are blocking the artery, allowing blood to flow more freely.
  • The balloon is then deflated and removed with the catheter.

Stenting: A stent is a small, metal springlike device that may be inserted into a coronary artery after balloon angioplasty. After the catheter and balloon are removed, the stent stays in place, holding the artery open. A stent is better than angioplasty alone at keeping the artery from narrowing again.

Atherectomy: Sometimes the plaques are too rigid, bulky, or calcified to be treated by balloon angioplasty. In these cases, the plaque often can be removed by cutting it out with a drill-like rotary blade or a laser or other tool.

Medications

If you are having a heart attack, you will almost certainly be given some or all of these medications while you are in the hospital. Some you will continue taking at home.

  • Intravenous (IV) nitroglycerin has been shown to improve blood flow to the heart muscle by relaxing (dilating) the coronary arteries and increasing blood flow. It is usually given for 24-48 hours continuously.
  • Heparin is a “blood thinner,” or anticoagulant, which may be given after a heart attack. Heparin does not remove an existing clot, but it reduces the tendency of blood to clot in the coronary arteries. Some newer forms of heparin have recently been introduced that can be given as a shot instead of through an IV line.
  • Beta-blockers are medications that decrease the heart rate and blood pressure. This reduces the heart’s workload and thus the amount of oxygen it needs. Beta-blockers may help prevent heart irregularities/life threatening rhythm disorders and future heart attacks.
  • Angiotensin-converting enzyme (ACE) inhibitors may prevent repeat heart attacks and other problems when started early during a heart attack. They are especially useful in people with diabetes and those with a weakened heart muscle congestive heart failure).

Surgery

  • Sometimes cardiac catheterization reveals extensive coronary artery disease. In such cases, you will need to undergo coronary bypass surgery.
  • Standard coronary artery bypass grafting (CABG) is performed if many coronary arteries are narrowed or blocked. This is especially recommended when the left main coronary artery shows significant blockage. This is “open heart surgery,” meaning that the chest wall is opened. When performing a bypass, heart surgeons use sections of the mammary artery from the chest, radial arteries from the arms, or veins from the legs to create detours around the blocked arteries. For this surgery, you will be connected to a bypass pump, which does the work of the heart during the operation. Although this sounds dangerous, this surgery is considered very safe and has a very low rate of complications.
  • Off-pump bypass surgery: Sometimes the surgeon can perform open heart surgery without using a bypass pump. The heart continues to beat during surgery. This type of surgery has even fewer complications than the standard procedure but is not always feasible.
  • Minimally invasive coronary bypass: If just the front or the right coronary artery needs bypass, the bypass may be performed via a small keyhole-type incision without a large incision in the chest. The internal mammary artery is used for the bypass.

Follow-up

If you have a heart attack, you will receive detailed instructions for your care after leaving the hospital. You should follow these instructions carefully. The following general guidelines apply to recovery from an uncomplicated heart attack.

You may return to work or prior activity levels after about 2 weeks, resume sexual activity in 7-10 days, drive a week after leaving the hospital, and continue commercial air travel after 2 weeks, if you are feeling fine and totally asymptomatic. Those with complicated heart attacks or who still have symptoms should wait at least 2-3 weeks after symptoms go away before driving.

After a heart attack, you will need close follow-up with your health care provider.

  • Coronary heart disease is a chronic (ongoing, long-term), progressive condition.
  • Changing your risk factors only slows its pace.
  • Angioplasty or bypass surgery only alleviates the symptoms and is not a cure. The disease may recur and progress.

Your health care provider will watch you carefully for the following developments:

  • Any new symptoms or signs of disease progression through clinical evaluation, physical examination, and periodic ECGs or stress tests
  • Silent ischemia by periodic treadmill or radionuclide stress tests or stress echocardiography

He or she will also manage the following aspects of your treatment and recovery:

  • Risk factor management by checking blood pressure and cholesterol levels periodically
  • Adjustment of medicines and management of their side effects
  • Prescription for an exercise program (cardiac rehabilitation)

What is new in heart attack?

Greater public awareness about heart attacks and changes in lifestyle have contributed to a dramatic reduction in the incidence of heart attacks during the last four decades. Improved anticoagulant drugs such as hirudin and hirulog, are being tested and may complement current therapies. The role of the “super aspirins” (Reopro and Integrilin) is currently being investigated as well. More effective versions of TPA are being developed. Increasingly, paramedics can do ECGs in the field, diagnose a heart attack, and take patients directly to hospitals that have the ability to do PTCA and stenting. This can save time and reduce damage to the heart. Recent data has shown that lowering blood LDL levels even further than previously suggested may further decrease the risk of heart attacks. Research also has shown that inflammation may play a role in the development of atherosclerosis, and this is an active area of current investigation. There also is early evidence that with genetic engineering it may be possible to develop a drug that can be administered to clear plaques from arteries (a “scavenger molecule”).

Apr 27 2008

CHIKUNGUNYA FEVER

CHIKUNGUNYA FEVER

aedes aegypti biting human CHIKUNGUNYA FEVER

Chikungunya fever is a viral disease acquired by humans through the bite of infected mosquitoes. Chikungunya virus (CHIKV) was first identified in Tanzania in 1953, and has since been found in west, central and southern Africa and many areas of Asia. Chikungunya virus has caused many human epidemics in those areas since that time. CHIKV infection can cause a severe illness, that most often includes symptoms such as fever, headache, fatigue, nausea, vomiting, muscle pain, rash, and joint pain. There is no vaccine or specific antiviral treatment for chikungunya fever available. The best way to avoid CHIKV infection is to prevent mosquito bites.

Chikungunya is a relatively rare form of viral fever caused by an alphavirus that is spread by mosquito bites from Aedes aegypti mosquitoes, though recent research by the Pasteur Institute in Paris claims the virus has suffered a mutation that enables it to be transmitted by Aedes albopictus (Tiger mosquito). This was the cause of the plague in the Indian Ocean and a threat to the Mediterranean coast at present, requiring urgent meetings of health officials in the region.

The name is derived from the Makonde word meaning “that which bends up” in reference to the stooped posture developed as a result of the arthritic symptoms of the disease.

Chikungunya is generally not fatal. However, in 2005-2006, 200 deaths were associated with chikungunya on Réunion island and a widespread outbreak in India, primarily in Tamil Nadu, Karnataka, Kerala, and Andhra Pradesh. After flood and heavy rains in Rajasthan, India in August 2006, thousands of cases were detected in Rajsamand, Bhilwara, Udaipur, and Chittorgarh districts and also in adjoining regions of Gujarat and Madhya Pradesh, and in the neighbouring country of Sri Lanka. In the southern Indian state of Kerala, 125 deaths were attributed to Chikungunya with the majority of the casualties reported in the district of Alapuzha, primarily in Cherthala. In December 2006, an outbreak of 3,500 confirmed cases occurred in Maldives, and over 60,000 cases in Sri Lanka, with over 80 deaths. [1]. In October 2006 more than a dozen cases of Chikungunya were reported in Pakistan. A recent outbreak of the disease during June 2007 in Pathanamthitta, Kottayam and Alappuzha districts of South Kerala, India claimed more than 50 lives. It is confirmed officially that there are 7000 confirmed Chikungunya patients in these areas. Unofficial reports suggest that more than one hundred thousand are suffering from symptoms of chikungunya. Rumors float around of radio active waste from Tamil Nadu being dumped at the outskirts of this region, which mutated the mosquitos and spread the disease. The European Network for Diagnostics of “Imported” Viral Diseases claims new phylogenetic variants of virus which are fatal have been identified on Réunion. In August/September 2007 some 160 people were infected in Italies northern Ravenna region, resulting in one fatality.

Acute chikungunya fever typically lasts a few days to a couple of weeks, but as with dengue, West Nile fever, o’nyong-nyong fever and other arboviral fevers, some patients have prolonged fatigue lasting several weeks. Additionally, some patients have reported
incapacitating joint pain, or arthritis which may last for weeks or months. The prolonged joint pain associated with CHIKV is not typical of dengue. Co-circulation of dengue fever in many areas may mean that chikungunya fever cases are sometimes clinically misdiagnosed as dengue infections, therefore the incidence of chikungunya fever could be much higher than what has been previously reported.

No deaths, neuroinvasive cases, or hemorrhagic cases related to CHIKV infection have been conclusively documented in the scientific literature.

CHIKV infection (whether clinical or silent) is thought to confer life-long immunity.

chiqun map map CHIKUNGUNYA FEVER

Cases of chikungunya fever (between 1952-2006) have been reported in the countries depicted in red on this map.
In Africa, these include Burundi; Central African Republic; Comoros; Democratic Republic of Congo; Guinea; Kenya; Nigeria; Madagascar; Malawi; Mauritius; Mayotte; Reunion; Senegal; Seychelles, South Africa; Tanzania; Uganda; Zimbabwe.In Asia, these include Australia; Burma; Cambodia; India; Indonesia; Malaysia; Pakistan; Philippines; Taiwan; Thailand; Timor; Vietnam.

Symptoms

The symptoms of Chikungunya include fever which can reach 39°C, (102.2°F) a petechial or maculopapular rash usually involving the limbs and trunk, and arthralgia or arthritis affecting multiple joints which can be debilitating. The symptoms could also include headache, conjunctival injection, and slight photophobia. In the present epidemic in the states of Andhra Pradesh and Tamil Nadu, India, high fever and crippling joint pain are the prevalent complaint. The fever typically lasts for two days and abruptly comes down. However, other symptoms, namely joint pain, intense headache, insomnia and an extreme degree of prostration last for a variable period, usually for about 5 to 7 days. But, patients have complained joint pains for much longer time periods depending on age of the patient. With younger patients recovering within 5 to 15 days and middle aged recovering in 1 to 2.5 months and more for old people. It has been observed that the severity of the disease as well as its duration is less in younger patients and pregnant women. No untoward effects of pregnancy is noticed following the infection.

Dermatological manifestations observed in a recent outbreak of Chikungunya fever in Southern India and Eastern Indiaincludes the following:

  • Maculopapular rash
  • Nasal blotchy erythema
  • Freckle-like pigmentation over centro-facial area
  • Flagellate pigmentation on face and extremities
  • Lichenoid eruption and hyperpigmentation in photodistributed areas
  • Multiple aphthous-like ulcers over scrotum, crural areas and axilla.
  • Lympoedema in acral distribution (bilateral/unilateral)
  • Multiple ecchymotic spots (Children)
  • Vesiculobullous lesions (infants)
  • Subungual hemorrhage
  • Photo Urticaria
  • Acral Urticaria
  • Cephalgia
  • Lumbago
  • Vomiting
  • Epistaxis and haemetemesis

Histopathologically, pigmentary changes, maculopapular rash, lichenoid rash, aphthous-like ulcers show lymphocytic infiltration around dermal blood vessels (Inamadar et al). Pedal oedema (swelling of legs) is observed in many patients, the cause of which remains obscure as it is not related to any cardiovascular, renal or hepatic abnormalities.

Prevention of CHIKV Infection

The best way to avoid CHIKV infection is to prevent mosquito bites. There is no vaccine or preventive drug. Prevention tips are similar to those for dengue or West Nile virus:

  • Use insect repellent containing an DEET or another EPA-registered active ingredient on exposed skin. Always follow the directions on the package.
  • Wear long sleeves and pants (ideally treat clothes with permethrin or another repellent).
  • Have secure screens on windows and doors to keep mosquitoes out.
  • Get rid of mosquito breeding sites by emptying standing water from flower pots, buckets and barrels. Change the water in pet dishes and replace the water in bird baths weekly. Drill holes in tire swings so water drains out. Keep children’s wading pools empty and on their sides when they aren’t being used.
  • Additionally, a person with chikungunya fever or dengue should limit their exposure to mosquito bites in order to avoid further spreading the infection. The person should stay indoors or under a mosquito net.
  • Homoeopathic medicines are found to be very effective in preventing the disease.

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Apr 27 2008

CHICKENPOX

CKICKENPOX (VARICELLA)

Chickenpox, also spelled chicken pox, is the common name for Varicella zoster, classically one of the childhood infectious diseases caught by and survived by almost every child.

Chickenpox is caused by the varicella-zoster virus (VZV), also known as human herpes virus 3 (HHV-3), one of the eight herpes viruses known to affect humans. It starts with conjunctival and catarrhal symptoms and then characteristic spots appearing in two or three waves, mainly on the body and head rather than the hands and becoming itchy raw pox (pocks), small open sores which heal mostly without scarring.

Most people contract chickenpox by age 15, the majority between age 5 and 9, but all ages can contract it. Chickenpox is usually more severe in adults than children. Winter and spring are the most common times of the year for chickenpox to occur.

Chickenpox has a 10-14 day incubation period and is highly contagious through physical contact two days before symptoms appear. Following primary infection there is usually lifelong protective immunity from further episodes of chickenpox. Recurrent chickenpox, commonly known as shingles, is fairly rare but more likely in people with compromised immune systems.

Chickenpox is very highly contagious. It is easily passed between members of families and school classmates through airborne particles, droplets in exhaled air and fluid from the blisters or sores. It also can be transmitted indirectly by contact with articles of clothing and other items exposed to fresh drainage from open sores. Patients are contagious up to five days (more commonly, one to two days) before and five days after the date that their rash appears. When the sores have crusted over, the person is usually no longer contagious.

Chickenpox is rarely fatal (usually from varicella pneumonia), with pregnant women and those with a suppressed immune systems being more at risk. Pregnant women not known to be immune and who come into contact with chickenpox may need urgent treatment as the virus can cause serious problems for the baby. This is less of an issue after 20 weeks.

Later in life, viruses remaining dormant in the nerves can reactivate causing localised eruptions of shingles. This occurs particularly in people with compromised immune systems, such as the elderly, and perhaps even those suffering sunburn. Unlike chickenpox which normally fully settles, shingles may result in persisting post-herpetic neuralgia pain.

Signs and Symptoms

child with chickenpox CHICKENPOX

Chickenpox is a highly contagious disease that spreads from person to person by direct contact or through the air from an infected person’s coughing or sneezing. Touching the fluid from a chickenpox blister can also spread the disease. A person with chickenpox is contagious from 1-2 days before the rash appears until all blisters have formed scabs. This may take 5-10 days. It takes from 10-21 days after contact with an infected person for someone to develop chickenpox.

Symptoms tend to appear 14 to 16 days after initial exposure but can occur any time from 10 days up to 21 days after contact with the virus. Chickenpox is characterized by one to two days of mild fever up to 102 degrees F, general weakness, and a rash, often the first sign of the disease. Rarely, a person may have the disease without the rash. The rash of chickenpox develops in crops with raised red spots arriving first, progressing to blisters that burst, creating open sores, before crusting over. This process usually starts on the scalp, then the trunk (its area of greatest concentration), and finally the arms and legs. Any area of skin that is irritated (by diaper rash, poison ivy, eczema, sunburn, etc.) is likely to be hard hit by the rash. The rash is typically very itchy (pruritic).

The chickenpox lesions (blisters) start as a 2–4 mm red papule which develops an irregular outline (rose petal). A thin-walled, clear vesicle (dew drop) develops on top of the area of redness. This “dew drop on a rose petal” lesion is very characteristic for chickenpox. After about 8–12 hours the fluid in the vesicle gets cloudy and the vesicle breaks leaving a crust. The fluid is highly contagious, but once the lesion crusts over, it is not considered contagious. The crust usually falls off after 7 days sometimes leaving a crater-like scar. Although one lesion goes through this complete cycle in about 7 days, another hallmark of chickenpox is the fact that new lesions crop up every day for several days. Therefore, it may take about a week until new lesions stop appearing and existing lesions crust over. Children are not to be sent back to school until all lesions have crusted over.

Second infections with chickenpox occur in immunocompetent individuals, but are uncommon. Such second infections are rarely severe. A soundly-based conjecture being carefully assessed in countries with low prevalence of chickenpox due to immunisation, low birth rates, and increased separation is that immunity has been reinforced by subclinical challenges and this is now less common.(Meaning is unclear please FIXME) This is more dangerous with shingles. There have been reported cases of repeat infections. Chickenpox is highly contagious and is spread through the air when infected people cough or sneeze, or through physical contact with fluid from lesions on the skin. Zoster, also known as shingles, is a reactivation of chickenpox and may also be a source of the virus for susceptible children and adults. It is not necessary to have physical contact with the infected person for the disease to spread. Those infected can spread chickenpox before they know they have the disease – even before any rash develops. In fact, people with chickenpox can infect others from about 2 days before the rash develops until all the sores have crusted over, usually 4-5 days after the rash starts.

Complications

Complications can and do occur from chickenpox. Infection of the open pox sore by bacteria can injure the skin, sometimes causing scarring, especially if the patient scratches the inflamed area. Bacterial skin infection is, in fact, the most common complication of chickenpox in children. The next most common complications in children affect the central nervous system and include a disorder of the cerebellar portion of the brain (cerebellar ataxia with wobbliness, dizziness, tremor, and altered speech), encephalitis (inflammation of the brain with headaches, seizures, and decreased consciousness), damaged nerves (nerve palsies) and Reye’s syndrome (a potentially fatal combination of liver and brain disease that can be associated with aspirin. Children with fever should not take aspirin.). Especially serious complications can occur in patients with AIDS, lupus, leukemia, and cancer. Complications also occur in people taking immune-suppressing drugs, such as cortisone-related medications. Newborn infants whose mothers have chickenpox in the last trimester of pregnancy are at increased risk from the disease. If the mother develops the disease from five days before to two days after delivery, the fatality rate for the baby is up to 30%.

Congenital defects in Babies

These may occur if the child’s mother was exposed to VZV during pregnancy. Effects on the foetus may be minimal in nature but physical deformities range in severity from under developed toes and fingers, to severe anal and bladder malformation. Possible problems include:

  • Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain
  • Damage to the eye (optic stalk, optic cap, and lens vesicles), microphthalmia, cataracts, chorioretinitis, optic atrophy.
  • Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner’s syndrome
  • Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction
  • Skin disorders: (cicatricial) skin lesions, hypopigmentation

Most people develop lifetime immunity to chickenpox after the first occurrence and never experience it again. But the virus can sometimes resurface later in life as shingles (zoster). The current aim in the U.S. and many other countries is to achieve universal (or nearly universal) immunization of children with the chickenpox vaccine. The vaccination requires only one shot given at about one year of age. If an older person has not had chickenpox, the shot may be given at any time. There have been few significant adverse reactions to the chickenpox vaccine. All children, except those with a compromised immune system, should have the vaccination.

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Apr 27 2008

SINUSITIS

SINUSITIS

sinusitis meditalk4all.thumbnail SINUSITIS

Sinuses are hollow air spaces within the bones surrounding the nose. They produce mucus, which drains into the nose. If your nose is swollen, this can block the sinuses and cause pain and infection. Infection of sinuses is known as Sinusitis. Sinusitis is one of the more common conditions that can afflict people throughout their lives. Sinusitis commonly occurs when environmental pollens irritate the nasal passages, such as with hay fever. Sinusitis can also result from irritants, such as chemicals or the use and/or abuse of over-the-counter nasal sprays and illegal substances that may be snorted through the nose. Sinusitis can also be caused by infection (by viruses or bacteria).

Sinusitis can be acute, lasting for less than four weeks, or chronic, lasting much longer. Acute sinusitis often starts as a cold, which then turns into a bacterial infection. Allergies, pollutants, nasal problems and certain diseases can also cause sinusitis.

Symptoms of sinusitis can include fever, weakness, fatigue, cough and congestion. There may also be mucus drainage in the back of the throat, called postnasal drip. Treatments include antibiotics, decongestants and pain relievers. Using heat pads on the inflamed area, saline nasal sprays and vaporizers can also help.

CAUSES

Anything that causes swelling in your sinuses or keeps the cilia from moving mucus can cause sinusitis. This can occur because of changes in temperature or air pressure. Using decongestant nasal sprays too much, smoking, and swimming or diving can also increase your risk of getting sinusitis. Some people have growths called polyps (say: “pawl-ips”) that block their sinus passages.

When sinusitis is caused by a bacterial or viral infection, you get a sinus infection. Sinus infections sometimes occurs after you’ve had a cold. The cold virus attacks the lining of your sinuses, causing them to swell and become narrow. Your body responds to the virus by producing more mucus, but it gets blocked in your swollen sinuses. This built-up mucus makes a good place for bacteria to grow. The bacteria can cause a sinus infection.

Sinuses can also become obstructed by tumors or growths which are in the proximity of the sinus ostia. The drainage of mucous from the sinuses can be impaired by thickening of the mucous secretions, by decrease in hydration (water content) of the mucous brought on by disease (cystic fibrosis), drying medications (antihistamines), and lack of sufficient humidity in the air. The mucous producing cells have small hairlike fibers, called cilia, which move back and forth to help the mucous move out of the sinuses. These small cilia may be damaged by many irritants, especially smoke, which then prevents them from assisting the mucous from draining from the sinuses. Stagnated mucous then provides a perfect environment for bacteria and in some circumstances (i.e.: AIDS) fungus to grow in the sinus cavities.

CLASSIFICATION

Sinus infection may be classified in at least two ways, based on the time span of the problem (acute, subacute, or chronic ) and the type of inflammation (either infectious or noninfectious). Acute sinus infection is usually defined as being of less than 30 days duration; subacute sinus infection as being over 1 month but less than 3 months; and chronic sinus infection as being greater than 3 months duration. Infected sinusitis is usually caused by uncomplicated virus infection. Far less frequently bacterial growth causes sinus infection. Noninfectious sinusitis can be caused by irritants and allergic conditions. Subacute and chronic forms of sinus infection usually are the result of incomplete treatment of an acute sinus infection.

SIGNS AND SYMPTOMS

Commonly the symptoms of sinus infection are headache, facial tenderness or pain, and fever. However, as few as 25% of patients may have fever associated with acute sinus infection. Other common symptoms include cloudy, discolored nasal drainage, a feeling of nasal stuffiness, a sore throat, and a cough. Some people notice an increased sensitivity or headache when they lean forward. In allergic sinusitis other associated allergy symptoms of itching eyes and sneezing may be common.

Some of the signs that a person may have bacterial sinusitis are:

  • a stuffy or runny nose with a daytime cough that lasts for 10 to 14 days without improvement
  • mucus discharge from the nose (this can occur with both viral and bacterial sinusitis but continuous thick discharge is more likely to be from bacterial sinusitis)
  • persistent dull pain or swelling around the eyes
  • tenderness or pain in or around the cheekbones
  • a feeling of pressure in your head
  • a headache when you wake up in the morning or when bending over
  • bad breath, even after brushing your teeth
  • pain in the upper teeth
  • a fever greater than 102 degrees Fahrenheit (39 degrees Celsius)

Some people also have dry coughs and find it hard to sleep. Others have upset stomachs or feel nausea.

Although many of these symptoms are similar to those you can get from viral sinusitis or allergic rhinitis (inflammation of the nose and sinuses due to allergy), it’s a good idea to see your doctor just in case. Viral sinusitis and allergic rhinitis are more common, but bacterial sinusitis often needs to be treated with antibiotics, and you can only get these with a doctor’s prescription.

PREVENTION

You can lower your risk of getting sinusitis by making some simple changes in your home environment. Try using a humidifier during cold weather to stop dry, heated air from irritating your sinuses, which can make them more susceptible to infection. Clean the humidifier regularly because mold, which can trigger allergies in some people, forms easily in moist environments.

If you have allergies, make an extra effort to keep them under control because they can make a person more prone to developing a sinus infection.

Although sinusitis itself is not contagious, it is often preceded by a cold, which can be spread to family members and friends. The most effective way to prevent the spread of germs is to wash your hands frequently and thoroughly. Steer clear of used tissues, and try to stay out of the line of fire when someone sneezes.

TIPS ON TAKING CARE OF SINUSITIS

  • Get plenty of rest. Lying down can make your sinuses feel more stopped-up, so try lying on the side that lets you breathe the best.
  • Sip hot liquids and drink plenty of fluids.
  • Apply moist heat by holding a warm, wet towel against your face or breathing in steam through a cloth or towel.
  • Talk with your doctor before using an over-the-counter cold medicine. Some cold medicines can make your symptoms worse or cause other problems.
  • Don’t use a nose spray with a decongestant in it for more than 3 days. If you use it for more than 3 days, the swelling in your sinuses may get worse when you stop the medicine.
  • Use an over-the-counter medicine such as acetaminophen (one brand name: Tylenol) for pain.
  • Rinse your sinus passages with a saline solution. You can buy an over-the-counter saline solution or ask your doctor how to make one at home.

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Apr 27 2008

Ten diseases that cannot be cured with Modern Medicine

Ten diseases that cannot be cured with Modern Medicine

Modern medicine has done much to eradicate and cure disease, but it has failed in some areas. Of those areas, at least one disease that cannot be cured is suffered by many people in the world every year – the common cold.

The following is a list of the top ten incurable diseases.

10. Ebola

ebola virus Ten diseases that cannot be cured with Modern Medicine

Ebola is a virus of the family Filoviridae that is responsible for a severe and often fatal viral hemorrhagic fever; outbreaks in primates such as gorillas and chimpanzees as well as humans have been recorded. The disease is characterized by extreme fever, rash, and profuse hemorrhaging. In humans, fatality rates range from 50 to 90 percent.

The virus takes its name from the Ebola River in the northern Congo basin of central Africa, where it first emerged in 1976. Outbreaks that year in Zaire (now Congo [Kinshasa]) and The Sudan resulted in hundreds of deaths, as did another outbreak in Zaire in 1995. Ebola is closely related to the Marburg virus, which was discovered in 1967, and the two are the only members of the Filoviridae that cause epidemic human disease. A third related agent, called Ebola Reston, caused an epidemic in laboratory monkeys in Reston, Virginia, but apparently is not fatal to humans.

9. Polio

Polio is known in full as poliomyelitis – also called infantile paralysis. It is an acute viral infectious disease of the nervous system that usually begins with general symptoms such as fever, headache, nausea, fatigue, and muscle pains and spasms and is sometimes followed by a more serious and permanent paralysis of muscles in one or more limbs, the throat, or the chest. More than half of all cases of polio occur in children under the age of five. The paralysis so commonly associated with the disease actually affects fewer than 1 percent of persons infected by the poliovirus.

Between 5 and 10 percent of infected persons display only the general symptoms outlined above, and more than 90 percent show no signs of illness at all. For those infected by the poliovirus, there is no cure, and in the mid-20th century hundreds of thousands of children were struck by the disease every year. Since the 1960s, thanks to widespread use of polio vaccines, polio has been eliminated from most of the world, and it is now endemic only in several countries of Africa and South Asia. Approximately 1,000–2,000 children are still paralyzed by polio each year, most of them in India.

8. Lupus Erythematosus

Also often referred to simply as lupus, this is an autoimmune disorder that causes chronic inflammation in various parts of the body. Three main types of lupus are recognized—discoid, systemic, and drug-induced.

Discoid lupus affects only the skin and does not usually involve internal organs. The term discoid refers to a rash of distinct reddened patches covered with grayish brown scales that may appear on the face, neck, and scalp. In about 10 percent of people with discoid lupus, the disease will evolve into the more severe systemic form of the disorder.

Systemic lupus erythematosus is the most common form of the disease. It may affect virtually any organ or structure of the body, especially the skin, kidneys, joints, heart, gastrointestinal tract, brain, and serous membranes (membranous linings of organs, joints, and cavities of the body.) While systemic lupus can affect any area of the body, most people experience symptoms in only a few organs. The skin rash, if present, resembles that of discoid lupus. In general, no two people will have identical symptoms. The course of the disease is also variable and is marked by periods when the disease is active and by other periods when symptoms are not evident (remission).

7. Influenza

Influenza, also known as the flu, or grippe, is an acute viral infection of the upper or lower respiratory tract that is marked by fever, chills, and a generalized feeling of weakness and pain in the muscles, together with varying degrees of soreness in the head and abdomen.

Influenza is caused by any of several strains of orthomyxoviruses, categorized as types A, B, and C. The three major types generally produce similar symptoms but are completely unrelated antigenically, so that infection with one type confers no immunity against the others. The A viruses cause the great influenza epidemics, and the B viruses cause smaller localized outbreaks; the C viruses are not important causes of disease in humans. Between pandemics, the viruses undergo constant, rapid evolution (a process called antigenic drift) in response to the pressures of human population immunity. Periodically, they undergo major evolutionary change by acquiring a new genome segment from another influenza virus (antigenic shift), effectively becoming a new subtype to which none, or very few, of the population is immune.

6. Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob disease is a rare fatal degenerative disease of the central nervous system. Creutzfeldt-Jakob disease occurs throughout the world at an incidence of one person in a million; however, among certain populations, such as Libyan Jews, rates are somewhat higher. The disease commonly occurs in adults between the ages of 40 and 70, although some young adults have been stricken with the disease. Both men and women are affected equally. The onset of the disease is usually characterized by vague psychiatric or behavioral changes, which are followed within weeks or months by a progressive dementia that is often accompanied by abnormal vision and involuntary movements. There is no known cure for the disease, which is usually fatal within a year of the onset of symptoms.

The disease was first described in the 1920s by the German neurologists Hans Gerhard Creutzfeldt and Alfons Maria Jakob. Creutzfeldt-Jakob disease is similar to other neurodegenerative diseases such as kuru, a human disorder, and scrapie, which occurs in sheep and goats. All three diseases are types of transmissible spongiform encephalopathies, so called because of the characteristic spongelike pattern of neuronal destruction that leaves brain tissue filled with holes.

5. Diabetes

Diabetes is a disorder of carbohydrate metabolism characterized by impaired ability of the body to produce or respond to insulin and thereby maintain proper levels of sugar (glucose) in the blood.

There are two major forms of the disease. Type I diabetes, formerly referred to as insulin-dependent diabetes mellitus (IDDM) and juvenile-onset diabetes, usually arises in childhood. It is an autoimmune disorder in which the diabetic person’s immune system produces antibodies that destroy the insulin-producing beta cells. Because the body is no longer able to produce insulin, daily injections of the hormone are required.

Type II diabetes, formerly called non-insulin-dependent diabetes mellitus (NIDDM) and adult-onset diabetes, usually occurs after 40 years of age and becomes more common with increasing age. It arises from either sluggish pancreatic secretion of insulin or reduced responsiveness in target cells of the body to secreted insulin. It is linked to genetics and obesity, notably upper-body obesity. People with type II diabetes can control blood glucose levels through diet and exercise and, if necessary, by taking insulin injections or oral medications.

4. HIV/AIDS

AIDS is the byname of acquired immunodeficiency syndrome – a transmissible disease of the immune system caused by the human immunodeficiency virus (HIV). HIV slowly attacks and destroys the immune system, the body’s defense against infection, leaving an individual vulnerable to a variety of other infections and certain malignancies that eventually cause death. AIDS is the final stage of HIV infection, during which time fatal infections and cancers frequently arise.

HIV/AIDS spread to epidemic proportions in the 1980s, particularly in Africa, where the disease may have originated. Spread was likely facilitated by several factors, including increasing urbanization and long-distance travel in Africa, international travel, changing sexual mores, and intravenous drug use. According to the United Nations 2004 report on AIDS, some 38 million people are living with HIV, approximately 5 million people become infected annually, and about 3 million people die each year from AIDS. Some 20 million people have died of the disease since 1981.

3. Asthma

Asthma is a chronic disorder of the lungs in which inflamed airways are prone to constrict, causing episodes of breathlessness, wheezing, coughing, and chest tightness that range in severity from mild to life-threatening. Inflamed airways become hypersensitive to a variety of stimuli, including dust mites, animal dander, pollen, air pollution, cigarette smoke, medications, weather conditions, and exercise. Stress can exacerbate symptoms.

Asthmatic episodes may begin suddenly or may take days to develop. Although an initial episode can occur at any age, about half of all cases occur in persons younger than 10 years of age, with boys being affected more often than girls. Among adults, however, the incidence of asthma is approximately equal in men and women. When asthma develops in childhood, it is often associated with an inherited susceptibility to allergens, substances such as pollen, dust mites, or animal dander that may induce an allergic reaction. In adults, asthma also may develop in response to allergens, but viral infections, aspirin, and exercise may cause the disease as well. Adults who develop asthma may have nasal polyps or sinusitis.

2. Cancer

Cancer refers to a group of more than 100 distinct diseases characterized by the uncontrolled growth of abnormal cells in the body. Cancer affects one in every three persons born in developed countries and is a major cause of sickness and death throughout the world. Though it has been known since antiquity, significant improvements in cancer treatment have been made since the middle of the 20th century, mainly through a combination of timely and accurate diagnosis, selective surgery, radiation therapy, and chemotherapeutic drugs. Such advances actually have brought about a decrease in cancer deaths (at least in developed countries), and grounds for further optimism are seen in laboratory investigations into elucidating the causes and mechanisms of the disease.

Owing to continuing advances in cell biology, genetics, and biotechnology, researchers now have a fundamental understanding of what goes wrong in a cancer cell and in an individual who develops cancer—and these conceptual gains are steadily being converted into further progress in prevention, diagnosis, and treatment of this disease.

1. The Common Cold

The common cold is an acute viral infection that starts in the upper respiratory tract, sometimes spreads to the lower structures, and may cause secondary infections in the eyes or middle ears. More than 100 agents cause the common cold, including parainfluenza, influenza, respiratory syncytial viruses, and reoviruses. Rhinoviruses, however, are the most frequent cause.

The popular term common cold reflects the feeling of chilliness on exposure to a cold environment that is part of the onset of symptoms. The feeling was originally believed to have a cause-and-effect relationship with the disease, but this is now known to be incorrect. The cold is caught from exposure to infected people, not from a cold environment, chilled wet feet, or drafts. People can carry the virus and communicate it without experiencing any of the symptoms themselves. Incubation is short — usually one to four days. The viruses start spreading from an infected person before the symptoms appear, and the spread reaches its peak during the symptomatic phase.

Source: listverse.com

Apr 27 2008

ASTHMA

ASTHMA

lungs meditalk4all ASTHMA

Asthma is a chronic disorder characterized by shortness of breath, wheezing, coughing and tightness of the chest.  It is a disease of the lungs. The airways of people with asthma are extra sensitive to the things they’re allergic to (called allergens) and to other irritating things in the air (called irritants).

asthma 2 meditalk4all ASTHMA

Asthma symptoms start when allergens or other irritants cause the lining of the airways to swell (become inflamed) and narrow. The muscles around the airways can then spasm, (contract rapidly), causing the airways to narrow even more. When the lining of the airways is inflamed, it produces more mucus. The mucus clogs the airways and further blocks the flow of air. This is called an “asthma attack.”

Asthma affects people differently. Each individual is unique in their degree of reactivity to environmental triggers. This naturally influences the type and dose of medication prescribed, which may vary from one individual to another.

Asthma is now the most common chronic illness in children, affecting one in every 15. In North America, 5% of adults are also afflicted. In all, there are about 1 million Canadians and 15 million Americans who suffer from this disease.

The number of new cases and the yearly rate of hospitalization for asthma have increased about 30% over the past 20 years. Even with advances in treatment, asthma deaths among young people have more that doubled.

Asthma cannot be cured with allopathic treatment but it will cure successfully with proper homeopathic treatment.

CAUSES

It is not clear exactly what makes the airways of people with asthma inflamed in the first place. Your inflamed airways may be due to a combination of things. We know that if other people in your family have asthma, you are more likely to develop it. New research suggests that being exposed to things like tobacco smoke, infections, and some allergens early in your life may increase your chances of developing asthma.

There are things in the environment that bring on your asthma symptoms and lead to asthma attacks. Some of the more common things include exercise, allergens, irritants, and viral infections. Some people have asthma only when they exercise or have a viral infection.

The list below gives some examples of things that can bring on asthma symptoms.

Allergens

  • Animal dander (from the skin, hair, or feathers of animals)
  • Dust mites (contained in house dust)
  • Cockroaches
  • Mold (indoor and outdoor)
  • “Seasonal” pollens
  • Year-round dust mites, molds, pets, and insect parts
  • Foods, such as fish, egg, peanuts, nuts, cow’s milk, and soy
  • Additives, such as sulfites
  • Work-related agents, such as latex

About 80% of children and 50% of adults with asthma also have allergies.

Irritants

  • Respiratory infections, such as those caused by viral “colds,” bronchitis, and sinusitis
  • Drugs, such as aspirin, other NSAIDs (nonsteroidal antiinflammatory drugs), and beta blockers (used to treat blood pressure and other heart conditions)
  • Tobacco smoke
  • Outdoor factors, such as smog, weather changes, and diesel fumes
  • Indoor factors, such as paint, detergents, deodorants, chemicals, and perfumes
  • Nighttime
  • GERD (gastroesophageal reflux disorder)
  • Exercise, especially under cold dry conditions
  • Work-related factors, such as chemicals, dusts, gases, and metals
  • Emotional factors, such as laughing, crying, yelling, and distress
  • Hormonal factors, such as in premenstrual syndrome

SYMPTOMS

The symptoms of asthma vary from person to person and in any individual from time to time. It is important to remember that many of these symptoms can be subtle and similar to those seen in other conditions. All of the symptoms mentioned below can be present in other respiratory, and sometimes, in heart conditions. This potential confusion makes identifying the settings in which the symptoms occur and diagnostic testing very important in recognizing this disorder.

The Four Major Recognized Symptoms:

  • Shortness of breath – especially with exertion or at night
  • Wheezing – a whistling or hissing sound when breathing out
  • Coughing – may be chronic; usually worse at night and early morning; and may occur after exercise or when exposed to cold, dry air
  • Chest tightness – may occur with or without the above symptoms

Not all people have these symptoms, and symptoms may vary from one asthma attack to another. Symptoms can differ in how severe they are: Sometimes symptoms can be mildly annoying, other times they can be serious enough to make you stop what you are doing, and sometimes symptoms can be so serious that they are life threatening.Symptoms also differ in how often they occur. Some people with asthma have symptoms only once every few months, others have symptoms every week, and still other people have symptoms every day. With proper treatment, however, most people with asthma can expect to have few or no symptoms.

Who is at risk for Asthma?

In the United States, about 20 million people have been diagnosed with asthma; nearly 9 million of them are children.

Asthma is closely linked to allergies. Most, but not all, people with asthma have allergies. Children with a family history of allergy and asthma are more likely to have asthma.

Although asthma affects people of all ages, it most often starts in childhood. More boys have asthma than girls, but in adulthood, more women have asthma than men.

Although asthma affects people of all races, African Americans are more likely than Caucasians to be hospitalized for asthma attacks and to die from asthma.

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Apr 27 2008

CARCINOMA OF CERVIX

CARCINOMA OF CERVIX

Dr.Sreeja L

Carcinoma of the cervix was one of the most common causes of cancer death in women, but over the past 30 years, mortality rate has decreased by 50% due to the widespread screening with the PAP smear. It remains the major gynecologic cancer in undeveloped countries. It is more common in lower socioeconomic groups, in women with early initial sexual activity and/or multiple sexual partners, and in smokers. Venereal transmission of human papilloma viruses has an important etiologic role. Over 66 types of HPV have been isolated, and many are associated with cervical carcinoma are 16,18,31,45, and 51 to 53. These along with many other types are also associated with cervical intra epithelial Neoplasia (CIN). Vaccination against pathologic HPV appears quite promising as a cervix cancer prevention strategy.

Uncomplicated HPV lower genital tract infection and Condylomatous atypia of the cervix can progress to CIN. This lesion precedes invasive cervical carcinoma and is classified as low grade squamous intraepithelial lesion (SIL), high-grade SIL, and carcinoma in situ. Carcinoma in situ demonstrates cytologic evidence of Neoplasia without invasion through the basement membrane can persist unchanged for 10 to 20 years, but eventually progresses to invasive carcinoma.

The PAP smear is 90-95% accurate in detecting early lesions such as CIN but is less sensitive in detecting cancer when frankly invasive cancer or fangating masses are present. Inflammation, necrosis, and haemorrhage may produce false-positive smears, and colposcopic directed biopsy is required when any lesion is visible on the cervix, regardless of PAP smear findings. The PAP smear can be reported as normal, atypical squamous cells of undetermined significance (ASCUS) or cannot exclude high grade SIL (ASEH); low-or high grade CIN; or frankly malignant. Women with ASCUS, ASC-H, or low-grade CIN should have repeat smears in 3-6 months and be tested for HPV. Women with high grade CIN or frankly malignant PAP smears should have colposcopic directed cervical biopsy.

Approximately 80% of invasive cervix cancers are squamous cell tumour, 10-15% are adenocarcinomas, 2-5% are adenosquamous with epithelial and glandular structures, and 1-2% are clear cell mesonephric tumours.

Patients with cervix cancer generally present with abnormal bleeding or post coital spotting that may increase to inter-menstrual of prominent menstrual bleeding. Yellowish vaginal discharge, lumbo-sacral back pain, and urinary symptoms can also be seen.

The staging of cervical carcinoma is clinical and generally completed with a pelvic examination under anesthesia with Cystoscopy and proctoscopy. Chest x-rays, intravenous pyelograms, and computed tomography are generally required and magnetic resonance imaging (MRI) may be used to asses extra-cervical extension.

Stage 0 is carcinoma in situ

Ø Stage I is disease confined to the cervix

Ø Stage II is disease invades beyond the cervix but not to the pelvic wall or lower third of the vagina

Ø Stage III-disease extends to the pelvic wall or lower third of vagina or causes hydronephrosis

Ø Stage IV is present when the tumour invades the mucosa of bladder or rectum or extends beyond the true pelvis.

Five year survivals are follows

Stage I- 85%

Stage II- 60%

Stage III- 33%

Stage IV- 7%

Carcinoma in situ (Stage 0) can be arranged successfully by biopsy or by abdominal hysterectomy. For Stage I disease, results appear equivalent for either radical hysterectomy or radiation therapy. Patients with Stage II to IV diseases are primarily managed with radical radiation therapy or combined modality therapy

Dr.Sreeja.L

Apr 27 2008

UTERINE CANCER

UTERINE CANCER

Synonyms of Uterine Cancer are Endometrial/uterine adenocarcinoma, Uterine cancer, Adenocarcinoma of the endometrium/uterus, Cancer – uterine, Cancer – endometrial & Uterine corpus cancer.

Endometrial cancer is cancer that starts in the endometrium, the lining of the uterus (womb).Uterine cancer usually occurs after menopause. Being obese and taking estrogen-alone hormone replacement therapy also increase your risk. Treatment varies depending on your overall health, how advanced the cancer is and whether hormones affect its growth. Treatment is usually a hysterectomy, which is surgery to remove the uterus. Other options include hormone therapy and radiation.

No one knows the exact causes of uterine cancer. However, it is clear that this disease is not contagious. No one can “catch” cancer from another person.

Women who get this disease are more likely than other women to have certain risk factors. A risk factor is something that increases a person’s chance of developing the disease.

Most women who have known risk factors do not get uterine cancer. On the other hand, many who do get this disease have none of these factors. Doctors can seldom explain why one woman gets uterine cancer and another does not.

Studies have found the following risk factors:

  • Age. Cancer of the uterus occurs mostly in women over age 50.
  • Endometrial hyperplasia. The risk of uterine cancer is higher if a woman has endometrial hyperplasia. This condition and its treatment are described above.
  • Hormone replacement therapy (HRT). HRT is used to control the symptoms of menopause, to prevent osteoporosis (thinning of the bones), and to reduce the risk of heart disease or stroke.

    • Women who use estrogen without progesterone have an increased risk of uterine cancer. Long-term use and large doses of estrogen seem to increase this risk. Women who use a combination of estrogen and progesterone have a lower risk of uterine cancer than women who use estrogen alone. The progesterone protects the uterus.

    Women should discuss the benefits and risks of HRT with their doctor. Also, having regular checkups while taking HRT may improve the chance that the doctor will find uterine cancer at an early stage, if it does develop.

  • Obesity and related conditions. The body makes some of its estrogen in fatty tissue. That’s why obese women are more likely than thin women to have higher levels of estrogen in their bodies. High levels of estrogen may be the reason that obese women have an increased risk of developing uterine cancer. The risk of this disease is also higher in women with diabetes or high blood pressure (conditions that occur in many obese women).
  • Tamoxifen. Women taking the drug tamoxifen to prevent or treat breast cancer have an increased risk of uterine cancer. This risk appears to be related to the estrogen-like effect of this drug on the uterus. Doctors monitor women taking tamoxifen for possible signs or symptoms of uterine cancer.The benefits of tamoxifen to treat breast cancer outweigh the risk of developing other cancers. Still, each woman is different. Any woman considering taking tamoxifen should discuss with the doctor her personal and family medical history and her concerns.
  • Race. White women are more likely than African-American women to get uterine cancer.
  • Colorectal cancer. Women who have had an inherited form of colorectal cancer have a higher risk of developing uterine cancer than other women.

Other risk factors are related to how long a woman’s body is exposed to estrogen. Women who have no children, begin menstruation at a very young age, or enter menopause late in life are exposed to estrogen longer and have a higher risk.

Women with known risk factors and those who are concerned about uterine cancer should ask their doctor about the symptoms to watch for and how often to have checkups. The doctor’s advice will be based on the woman’s age, medical history, and other factors.

Associated conditions include the following:

  • Obesity
  • Hypertension
  • Polycystic ovarian disease

Symptoms

Uterine cancer usually occurs after menopause. But it may also occur around the time that menopause begins. Abnormal vaginal bleeding is the most common symptom of uterine cancer. Bleeding may start as a watery, blood-streaked flow that gradually contains more blood. Women should not assume that abnormal vaginal bleeding is part of menopause.

  • Abnormal uterine bleeding, abnormal menstrual periods
    • Bleeding between normal periods before menopause
    • Vaginal bleeding or spotting after menopause
  • Extremely long, heavy, or frequent episodes of vaginal bleeding after age 40
  • Lower abdominal pain or pelvic cramping
  • Thin white or clear vaginal discharge after menopause

A woman should see her doctor if she has any of the following symptoms:

  • Unusual vaginal bleeding or discharge
  • Difficult or painful urination
  • Pain during intercourse
  • Pain in the pelvic area

These symptoms can be caused by cancer or other less serious conditions. Most often they are not cancer, but only a doctor can tell for sure.

Diagnosis

If a woman has symptoms that suggest uterine cancer, her doctor may check general signs of health and may order blood and urine tests. The doctor also may perform one or more of the exams or tests described on the next pages.

  • Pelvic exam — A woman has a pelvic exam to check the vagina, uterus, bladder, and rectum. The doctor feels these organs for any lumps or changes in their shape or size. To see the upper part of the vagina and the cervix, the doctor inserts an instrument called a speculum into the vagina.
  • Pap test — The doctor collects cells from the cervix and upper vagina. A medical laboratory checks for abnormal cells. Although the Pap test can detect cancer of the cervix, cells from inside the uterus usually do not show up on a Pap test. This is why the doctor collects samples of cells from inside the uterus in a procedure called a biopsy.
  • Transvaginal ultrasound — The doctor inserts an instrument into the vagina. The instrument aims high-frequency sound waves at the uterus. The pattern of the echoes they produce creates a picture. If the endometrium looks too thick, the doctor can do a biopsy.
  • Biopsy — The doctor removes a sample of tissue from the uterine lining. This usually can be done in the doctor’s office. In some cases, however, a woman may need to have a dilation and curettage (D&C). A D&C is usually done as same-day surgery with anesthesia in a hospital. A pathologist examines the tissue to check for cancer cells, hyperplasia, and other conditions. For a short time after the biopsy, some women have cramps and vaginal bleeding.

If cancer is found, other tests may be done to determine how widespread the cancer is and whether it has spread to other parts of the body. This is called staging.Stages of endometrial cancer:

  1. The cancer is only in the uterus.
  2. The cancer is in the uterus and cervix.
  3. The cancer has spread outside of the uterus but not beyond the true pelvis area. Cancer may involve the lymph nodes in the pelvis or near the aorta (the major artery in the abdomen).
  4. The cancer has spread to the inner surface of the bowel, bladder, abdomen, or other organs.

Treatment

Treatment options involve surgery, radiation therapy, and chemotherapy.

A hysterectomy may be performed in women with the early stage 1 disease. Removal of the tubes and ovaries (bilateral salpingo-oophorectomy) is also usually recommended.

Abdominal hysterectomy is recommended over vaginal hysterectomy. This type of hysterectomy allows the surgeon to look inside the abdominal area and remove tissue for a biopsy.

Surgery combined with radiation therapy is often used to treat women with stage 1 disease that could return and stage 2 disease. Chemotherapy may be considered in some cases, especially for those with stage 3 and 4 disease.

Expectations (prognosis)

Endometrial cancer is usually diagnosed at an early stage. The 1-year survival rate is about 94%.

The 5-year survival rate for endometrial cancer that has not spread is 96%. If the cancer has spread to distant organs, the 5-year survival rate drops to 25%.

Complications

Complications may include anemia due to blood loss. A perforation (hole) of the uterus may occur during a D and C or endometrial biopsy.

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Apr 27 2008

LUNG CANCER

LUNG CANCER

Cancer of the lung, like all cancers, results from an abnormality in the body’s basic unit of life, the cell. Normally, the body maintains a system of checks and balances on cell growth so that cells divide to produce new cells only when needed. Disruption of this system of checks and balances on cell growth results in an uncontrolled division and proliferation of cells that eventually forms a mass known as a tumor.

Tumors can be benign or malignant; when we speak of “cancer,” we refer to those tumors that are considered malignant. Benign tumors can usually be removed and do not spread to other parts of the body. Malignant tumors, on the other hand, grow aggressively and invade other tissues of the body, allowing entry of tumor cells into the bloodstream or lymphatic system which spread the tumor to other sites in the body. This process of spread is termed metastasis; the areas of tumor growth at these distant sites are called metastases. Since lung cancer tends to spread, or metastasize, very early in its course, it is a very life-threatening cancer and one of the most difficult cancers to treat. While lung cancer can spread to any organ in the body, certain organs—particularly the adrenal glands, liver, brain, and bone—are the most common sites for lung cancer metastasis.

lungcancer 300x227 LUNG CANCER

Lung cancer, or carcinoma of the lung, is a disease where epithelial (internal lining) tissue in the lung grows out of control. This leads to invasion of adjacent tissue and infiltration beyond the lungs (metastasis). Lung cancer, the most common cause of cancer-related death in men and the second most common in women, is responsible for 1.3 million deaths worldwide annually. The most common symptoms are shortness of breath, cough (including coughing up blood), and weight loss.

The main types of lung cancer are small cell lung cancer and non-small cell lung cancer. This distinction is important because non-small cell lung cancer is sometimes treated with surgery, while small cell cancer is not. Also, small cell lung cancer usually responds better to chemotherapy.

The most important cause of lung cancer is exposure to tobacco smoke. The occurrence of lung cancer in non-smokers, who account for less than 10% of cases, appears to be due to a combination of genetic factors. Radon gas, asbestos, and air pollution may also contribute to the development of lung cancer.

Lung cancer may be seen on chest x-ray and CT scan. The diagnosis is confirmed with a biopsy. This is usually performed via bronchoscopy or CT-guided biopsy.

Treatment and prognosis depend upon the histological type of cancer, the stage (degree of spread), and the patient’s performance status. Possible treatments include surgery, chemotherapy, and radiotherapy. Even with treatment, the overall five-year survival rate is 14%.

The lung is also a very common site for metastasis from tumors in other parts of the body. Tumor metastases are made up of the same type of cells as the original, or primary, tumor. For example, if prostate cancer spreads via the bloodstream to the lungs, it is metastatic prostate cancer in the lung and is not lung cancer.

Lung cancers can arise in any part of the lung, and 90%-95% of cancers of the lung are thought to arise from the epithelial, or lining cells of the larger and smaller airways (bronchi and bronchioles); for this reason, lung cancers are sometimes called bronchogenic carcinomas or bronchogenic cancers. Cancers can also arise from the pleura (the thin layer of tissue that surrounds the lungs), called mesotheliomas, or rarely from supporting tissues within the lungs, for example, blood vessels.

Causes of Lung Cancer

Smoking

The incidence of lung cancer is strongly correlated with cigarette smoking, with about 90% of lung cancers arising as a result of tobacco use. The risk of lung cancer increases with the number of cigarettes smoked over time; doctors refer to this risk in terms of pack-years of smoking history (the number of packs of cigarettes smoked per day multiplied by the number of years smoked). For example, a person who has smoked two packs of cigarettes per day for 10 years has a 20 pack-year smoking history. While the risk of lung cancer is increased with even a 10 pack-year smoking history, those with 30 pack-year histories or more are considered to have the greatest risk for the development of lung cancer. Among those who smoke two or more packs of cigarettes per day, one in seven will die of lung cancer.

Pipe and cigar smoking can also cause lung cancer, although the risk is not as high as with cigarette smoking. While someone who smokes one pack of cigarettes per day has a risk for the development of lung cancer that is 25 times higher than a nonsmoker, pipe and cigar smokers have a risk of lung cancer that is about five times that of a nonsmoker.

Tobacco smoke contains over 4,000 chemical compounds, many of which have been shown to be cancer-causing, or carcinogenic. The two primary carcinogens in tobacco smoke are chemicals known as nitrosamines and polycyclic aromatic hydrocarbons. The risk of developing lung cancer decreases each year following smoking cessation as normal cells grow and replace damaged cells in the lung. In former smokers, the risk of developing lung cancer begins to approach that of a nonsmoker about 15 years after cessation of smoking. For more, please read the Smoking and Quitting Smoking article.

Passive smoking

Passive smoking, or the inhalation of tobacco smoke from other smokers sharing living or working quarters, is also an established risk factor for the development of lung cancer. Research has shown that nonsmokers who reside with a smoker have a 24% increase in risk for developing lung cancer when compared with other nonsmokers. An estimated 3,000 lung cancer deaths occur each year in the U.S. that are attributable to passive smoking.

Asbestos fibers

Asbestos fibers are silicate fibers that can persist for a lifetime in lung tissue following exposure to asbestos. The workplace is a common source of exposure to asbestos fibers, as asbestos was widely used in the past for both thermal and acoustic insulation materials. Today, asbestos use is limited or banned in many countries, including the Unites States. Both lung cancer and mesothelioma (a type of cancer of the pleura or of the lining of the abdominal cavity called the peritoneum) are associated with exposure to asbestos. Cigarette smoking drastically increases the chance of developing an asbestos-related lung cancer in exposed workers. Asbestos workers who do not smoke have a fivefold greater risk of developing lung cancer than nonsmokers, and those asbestos workers who smoke have a risk that is 50 to 90 times greater than nonsmokers.

Radon gas

Radon gas is a natural, chemically inert gas that is a natural decay product of uranium. It decays to form products that emit a type of ionizing radiation. Radon gas is a known cause of lung cancer, with an estimated 12% of lung cancer deaths attributable to radon gas, or 15,000 to 22,000 lung cancer-related deaths annually in the U.S., making radon the second leading cause of lung cancer in the U.S. As with asbestos exposure, concomitant smoking greatly increases the risk of lung cancer with radon exposure. Radon gas can travel up through soil and enter homes through gaps in the foundation, pipes, drains, or other openings. The U.S. Environmental Protection Agency estimates that one out of every 15 homes in the U.S. contains dangerous levels of radon gas. Radon gas is invisible and odorless, but it can be detected with simple test kits.

Familial predisposition

While the majority of lung cancers are associated with tobacco smoking, the fact that not all smokers eventually develop lung cancer suggests that other factors, such as individual genetic susceptibility, may play a role in the causation of lung cancer. Numerous studies have shown that lung cancer is more likely to occur in both smoking and nonsmoking relatives of those who have had lung cancer than in the general population. Recent research has localized a region on the long (q) arm of the human chromosome number 6 that is likely to contain a gene that confers an increased susceptibility to the development of lung cancer in smokers.

Lung diseases

The presence of certain diseases of the lung, notably chronic obstructive pulmonary disease (COPD), is associated with a slightly increased risk (four to six times the risk of a nonsmoker) for the development of lung cancer even after the effects of concomitant cigarette smoking are excluded.

Prior history of lung cancer

Survivors of lung cancer have a greater risk than the general population of developing a second lung cancer. Survivors of non-small cell lung cancers (NSCLCs, see below) have an additive risk of 1%-2% per year for developing a second lung cancer. In survivors of small cell lung cancers (SCLCs), the risk for development of second cancers approaches 6% per year.

Air pollution

Air pollution from vehicles, industry, and power plants can raise the likelihood of developing lung cancer in exposed individuals. Up to 1% of lung cancer deaths are attributable to breathing polluted air, and experts believe that prolonged exposure to highly polluted air can carry a risk similar to that of passive smoking for the development of lung cancer.

Viruses

Viruses are known to cause lung cancer in animals and recent evidence suggests similar potential in humans. Implicated viruses include human papillomavirus, JC virus, simian virus 40 (SV40), BK virus and cytomegalovirus. These viruses may affect the cell cycle and inhibit apoptosis, allowing uncontrolled cell division.

Signs and symptoms

Symptoms that suggest lung cancer include:

  • dyspnea (shortness of breath)
  • hemoptysis (coughing up blood)
  • chronic coughing or change in regular coughing pattern
  • wheezing
  • chest pain or pain in the abdomen
  • cachexia (weight loss), fatigue and loss of appetite
  • dysphonia (hoarse voice)
  • clubbing of the fingernails (uncommon)
  • difficulty swallowing

If the cancer grows in the airway, it may obstruct airflow, causing breathing difficulties. This can lead to accumulation of secretions behind the blockage, predisposing the patient to pneumonia.

Many lung cancers have a rich blood supply. The surface of the cancer may be fragile, leading to bleeding from the cancer into the airway. This blood may subsequently be coughed up.

Depending on the type of tumor, so-called paraneoplastic phenomena may initially attract attention to the disease. In lung cancer, these phenomena may include Lambert-Eaton myasthenic syndrome (muscle weakness due to auto-antibodies), hypercalcemia or SIADH. Tumors in the top (apex) of the lung, known as Pancoast tumors, may invade the local part of the sympathetic nervous system, leading to changed sweating patterns and eye muscle problems (a combination known as Horner’s syndrome), as well as muscle weakness in the hands due to invasion of the brachial plexus.

Many of the symptoms of lung cancer (bone pain, fever, weight loss) are nonspecific; in the elderly, these may be attributed to comorbid illness. In many patients, the cancer has already spread beyond the original site by the time they have symptoms and seek medical attention. Common sites of metastasis include the bone, such as the spine (causing back pain and occasionally spinal cord compression), the liver and the brain. About 10% of people with lung cancer do not have symptoms at diagnosis; these cancers are incidentally found on routine chest x-rays.

Other changes that can sometimes occur with lung cancer may include repeated bouts of pneumonia, changes in the shape of the fingertips, and swollen or enlarged lymph nodes (glands) in the upper chest and lower neck.

These symptoms can happen with other illnesses, too. People with symptoms should talk to their doctor, especially if they smoke, but even if they don’t. Doctors can help find the cause.

When should one consult a doctor?

One should consult a health care provider if they develop the symptoms associated with lung cancer, in particular, if they have

  • a new persistent cough or worsening of an existing chronic cough

    • ,

  • blood in the sputum,
  • persistent bronchitis or repeated respiratory infections

    • ,

  • chest pain

    • ,

  • unexplained weight loss and/or fatigue

    • , and/or

  • breathing difficulties such as shortness of breath or wheezing.

Diagnosis and Treatment

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Picture 1: CT scan showing lung cancer in the left lung

Picture 2: Chest x-ray showing lung cancer in the left lung

A person’s lung cancer diagnosis depends on the type of lung cancer present. The two main types of lung cancer are small cell lung cancer and non-small cell lung cancer. Non-small cell lung cancer is more common than small cell lung cancer. These categories refer to what the cancer cells look like under a microscope.

Performing a chest x-ray is the first step if a patient reports symptoms that may be suggestive of lung cancer. This may reveal an obvious mass, widening of the mediastinum (suggestive of spread to lymph nodes there), atelectasis (collapse), consolidation (infection) and pleural effusion. If there are no X-ray findings but the suspicion is high (such as a heavy smoker with blood-stained sputum), bronchoscopy and/or a CT scan may provide the necessary information. In any case, bronchoscopy or CT-guided biopsy is often necessary to identify the tumor type.

The extent of disease is referred to as the stage. Information about how big a cancer is or how far it has spread is often used to determine the stage. Doctors use information about stage to plan treatment and to monitor progress.

The differential diagnosis for patients who present with abnormalities on chest x-ray includes lung cancer, as well as nonmalignant diseases. These include infectious causes such as tuberculosis or pneumonia, or inflammatory conditions such as sarcoidosis. These diseases can result in mediastinal lymphadenopathy or lung nodules, and sometimes mimic lung cancers.

There are several ways to treat lung cancer. The treatment depends on the type of lung cancer and how far it has spread. Treatments include surgery, chemotherapy, and radiation. People with lung cancer often get more than one kind of treatment.

Surgery
Doctors cut out and remove cancer tissue in an operation.

If investigations confirm lung cancer, CT scan and often positron emission tomography (PET) are used to determine whether the disease is localised and amenable to surgery or whether it has spread to the point where it cannot be cured surgically.

Blood tests and spirometry (lung function testing) are also necessary to assess whether the patient is well enough to be operated on. If spirometry reveals a very poor respiratory reserve, as may occur in chronic smokers, surgery may be contraindicated.

Surgery itself has an overall operative death rate of about 4.4%, depending on the patient’s lung function and other risk factors. Surgery is usually only an option in non-small cell lung cancer limited to one lung, up to stage IIIA. This is assessed with medical imaging (computed tomography, positron emission tomography). A sufficient pre-operative respiratory reserve must be present to allow adequate lung function after the tissue is removed.

Procedures include wedge resection (removal of part of a lobe), lobectomy (one lobe), bilobectomy (two lobes) or pneumonectomy (whole lung). In patients with adequate respiratory reserve, lobectomy is the preferred option, as this minimizes the chance of local recurrence. If the patient does not have enough functional lung for this, wedge resection may be performed. Radioactive iodine brachytherapy at the margins of wedge excision may reduce recurrence to that of lobectomy. Chemotherapy
Chemotherapy involves the use of drugs to shrink or kill the cancer. The drugs could be pills or medicines given through an IV (intravenous) tube. Sometimes chemotherapy includes both IV drugs and pills.

Small cell lung cancer is treated primarily with chemotherapy, as surgery has no demonstrable influence on survival. Primary chemotherapy is also given in metastatic non-small cell lung cancer.

The combination regimen depends on the tumor type. Non-small cell lung cancer is often treated with cisplatin or carboplatin, in combination with gemcitabine, paclitaxel, docetaxel, etoposide or vinorelbine. Combinations with carboplatin, gemcitabine, paclitaxel, vinorelbine, In small cell lung cancer, cisplatin and etoposide are most commonly used.topotecan and irinotecan are also used.Radiation
Radiation uses high-energy rays (similar to x-rays) to try to kill the cancer cells. The rays are aimed at the part of the body where the cancer is.

Radiotherapy is often given together with chemotherapy, and may be used with curative intent in patients with non-small cell lung cancer who are not eligible for surgery. For small cell lung cancer cases that are potentially curable, in addition to chemotherapy, chest radiation is often recommended. The use of adjuvant thoracic radiotherapy following curative intent surgery for non-small cell lung cancer is not well established and controversial. Benefits, if any, may only be limited to those in whom the tumor has spread to the mediastinal lymph nodes.

For both non-small cell lung cancer and small cell lung cancer patients, smaller doses of radiation to the chest may be used for symptom control (palliative radiotherapy). Unlike other treatments, it is possible to deliver palliative radiotherapy without confirming the histological diagnosis of lung cancer.

Patients with limited stage small cell lung carcinoma are usually given prophylactic cranial irradiation (PCI). This is a type of radiotherapy to the brain, used to reduce the risk of metastasis. More recently, PCI has also been shown to be beneficial in those with extensive small cell lung cancer. In patients whose cancer has improved following a course of chemotherapy, PCI has been shown to reduce the cumulative risk of brain metastases within one year from 40.4% to 14.6%.These treatments may be provided by different doctors on your medical team. Pulmonologists are doctors that are experts in diseases of the lungs. Surgeons are doctors that perform operations. Medical oncologists are doctors that are experts in cancer and treat cancers with medicines. Radiation oncologists are doctors that treat cancers with radiation.

Prognosis

Prognosis depends on the cell type (histology), stage (degree of spread), and the patient’s performance status. Overall 5 year survival rates vary from 8.9% in developing countries to 15% in the United States.

For non-small cell lung cancer, prognosis is poor. Following complete surgical resection of stage IA disease, five-year survival is 67%. With stage IB disease, five-year survival is 57%. The 5-year survival rate of patients with stage IV NSCLC is about 1%.

Patients with extensive-stage SCLC have an average five-year survival rate of less than 1%. The For small cell lung carcinoma, prognosis is also poor. The overall five-year survival for patients with SCLC is about 5%.median survival time for limited-stage disease is 20 months, with a five-year survival rate of 20%.

Prevention

Prevention is the most cost-effective means of fighting lung cancer. While in most countries industrial and domestic carcinogens have been identified and banned, tobacco smoking is still widespread. Eliminating tobacco smoking is a primary goal in the prevention of lung cancer, and smoking cessation is an important preventative tool in this process.

Policy interventions to decrease passive smoking in public areas such as restaurants and workplaces have become more common in many Western countries, with California taking a lead in banning smoking in public establishments in 1998, Ireland playing a similar role in Europe in 2004, followed by Italy and Norway in 2005, Scotland as well as several others in 2006, and England in 2007. New Zealand has also recently banned smoking in public places.

The state of Bhutan has had a complete smoking ban since 2005. In many countries, pressure groups are campaigning for similar bans. Arguments cited against such bans are criminalisation of smoking, increased risk of smuggling and the risk that such a ban cannot be enforced.

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Apr 27 2008

CANCER OF OESOPHAGUS

CANCER OF OESOPHAGUS

The Gastrointestinal tract is the second most common noncutaneous site for cancer and the second major cause of the cancer related mortality in the United Stated.

Incidence

Cancer of the Oesophagus is a relatively un-common but extremely lethal malignancy. It occurs frequently within a geographic region extending from the southern shore of the Caspian Sea on the west to northern China on the east and encompassing parts of Iran, Central Asia, Afghanistan, Siberia, and

Mongolia. The disease is more common in Blacks than whites and in males than females; it appears most often after age 50 and seems to be associated with a lower socioeconomic status.

Aetiology (Cause of Disease)

A variety of Causative factors have been implicated in the development of the disease. In the

United States, esophageal cancer cases are either squamous cell carcinomas or adenocarcinomas. The aetiology of squamous cell esophageal cancer is related to excess alcohol consumption and/or cigarette smoking. The relative risk increases with the amount of tobacco smoked or alcohol consumed, with these factors acting synergistically. The consumption of whiskey is linked to a higher incidence than the consumption off wine or beer. Squamous cell esophageal carcinoma has also been associated with the ingestion of nitrites, smoked opiates, and fungal toxins in pickled vegetables, as well as mucosal damage caused by such physical insults as long term exposure to extremely hot tea, the ingestion of lye, radiation induced strictures, and chronic achalasia. The presence of an esophageal web in association with glossitis and iron deficiency and congenital hyperkeratosis and pitting of the palms and soles have rich been linked with squamous cell esophageal cancer, as have dietary deficiencies of molybdenum, zinc, and vitamin A.

The rate of adenocarcinoma has risen dramatically, particularly in white males. Adenocarcinoma arises in the distal esophagus in the presence of chronic gastric reflux and gastric maetaplasia of the epithelium, which is more common in obese persons. Adenocarcinomas arise within dysplastic columnar epithelium in the distal esophagus. These adenocarcinomas behave clinically gastric adenocarcinomas and now account for >50% of esophageal cancer.

Clinical Features

About 15% of esophageal cancers occur in the upper third of the esophagus, 35% in the middle third, and 50% in the lower third. Squamous cell carcinoma and adenocarcinomas of the esophagus cannot be distinguished radiographically or endoscopically.

Progressive dysphagia and weight loss of short duration are the initial symptoms in the vast majority of cases. Dysphagia initially occurs with solid foods and gradually progresses to include semisolids and liquids. By the time these symptoms develop, the disease is usually incurable, since difficulty in swallowing does not occur until >60% of the esophagus circumference is infiltrated with cancer. Dysphagia may associate with pain on swallowing, pain radiating to the chest and/or back, regurgitation or vomiting, aspiration pneumonia. The disease most commonly spread to adjacent and supra-clavicular lymph nodes, liver, lungs, pleura. Tracheo-esophageal fistula may develop when the disease advances, and may lead in to severe suffering. As with other squamous cell carcinomas, hypercalemia may occur in the absence of osseous metastasis, probably from parathormone related peptides secreted by tumour cells.

Diagnosis

Various modern techniques are used to find out the carcinomas, some important tests are:

  1. Endoscopic and cytologic screening.
  2. Routine contrast Radiographs.
  3. Computed Tomography Scans.
  4. Positron emission Tomography Scanning

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Apr 27 2008

MESOTHELIOMA

MESOTHELIOMA

Mesothelioma is a rare form of cancer. The cancer cells (Malignant cells) are found in the lining of chest (Pleura), the lining of the abdominal cavity (Peritoneum) or the lining around the Heart (Pericardium).

Peritoneal Mesothelioma is a cancer of the lining of the abdominal cavity. It occurs in one fifth to one third of total number of mesothelioma.

Most people affected had a History of breathing of Asbestos. The exposure may be from their working environment or from their house itself. An exposure of Asbestos for just one or two months can result in Mesothelioma in 30 or 40 years later. The present diseased individual has a History of Asbestos exposure in the 1940s, 50s, 60s and 70s age. That is showing that it has a long latency period.

Like all cancers the prognosis of Mesothelioma is depend on the early diagnosis of the disease and how aggressively it is treated.

MAIN CAUSE OF MESOTHELIOMA- ASBESTOS EXPOSURE

At some point in our lives, nearly all of us have been exposed to asbestos in the air we breathe and the water we drink; from natural deposits in the earth, and from the deterioration of asbestos products around us. Most of us, however, do not become ill as a result of our exposure. More commonly, those who at some point are diagnosed with asbestos disease have worked in jobs where more substantial exposure occurred over longer periods of time. Nevertheless, cases of mesothelioma have been documented as the result of lesser exposure, affecting family members of workers who came into contact with asbestos and brought it home on their clothing, skin or hair, or affecting those who lived in close proximity to asbestos manufacturing facilities. Symptoms of asbestos disease usually are not be apparent until decades after exposure.

Asbestos are commonly used in the North America during 1800s itself. The use of asbestos enormously increased during Second World War, when shipyards produced massive number of ships for War purpose. Since that time the asbestos was commonly used in building construction automotive industry, etc. During that time about 5,000 products containing asbestos are used.

Although it is suggested that the number of mesothelioma cases in the U.S. has reached its peak and has begun to drop, a forecast released by the National Cancer Institute’s Surveillance, Epidemiology, and End Results Program (SEER), in April, 2003, projected the total number of American male mesothelioma cases from 2003-2054 to be approximately 71,000. This number, however, does not take into consideration events such as the World Trade Center disaster on September 11, 2001, when millions of New Yorkers were potentially exposed to air filled with carcinogenic asbestos particles. When the latency period for asbestos disease is factored in, cases of mesothelioma will continue to be diagnosed for years to come.

RACE AND MESOTHELIOMA:

Mesothelioma has no racial predilection. Asbestos exposure is the most important factor. Race is not a factor.

SEX AND MESOTHELIOMA:

Malignant mesothelioma is more common in men, with a male-to-female ratio of 3:1. It can also occur in children; however, these cases are not thought to be associated with asbestos exposure.

With regard to women with mesothelioma, a 1996 case series by Ascoli et al showed 86% of tumors arising from the pleura, of which most were the epithelial type. Of the patients in this series, 75% had a history of exposure to asbestos and more than half developed the malignancy secondary to household contact with a worker exposed to asbestos.

With regard to men with mesothelioma, the same case series demonstrated 45.5% with a history of exposure to asbestos and 53% with occupational exposure to asbestos. Most who were involved were construction workers, railroad workers, naval mechanics, bakers, explosive workers, and automobile mechanics.

AGE AND MESOTHELIOMA:

Malignant mesothelioma has a peak incidence 35-45 years after asbestos exposure. It commonly develops in the fifth to seventh decade of life.

MORTALITY/MORBIDITY:

Median survival for patients with malignant mesothelioma is 11 months. It is almost always fatal. Median survival based on histologic type is 9.4 months for sarcomatous, 12.5 months for epithelial and 11 months for mixed. Approximately 15% of patients have an indolent course.

Asbestos exposure is linked to at least 50% of patients developing malignant mesothelioma. Approximately 8 million people in the United States have been exposed to asbestos in the workplace. Family members are also exposed to asbestos embedded in the worker’s clothing. The combination of tobacco and asbestos exposure greatly increases the risk of developing pleural mesothelioma.

SYMPTOMS OF MESOTHELIOMA

The early symptoms of mesothelioma are generally non-specific, and may lead to a delay in diagnosis. Sometimes resembling viral pneumonia, pleural mesothelioma patients may present with shortness of breath, chest pain and/or persistent cough; some patients show no symptoms at all. A chest x-ray may show a build-up of fluid or pleural effusion. The right lung is affected 60% of the time, with involvement of both lungs being seen in approximately 5% of patients at the time of diagnosis. Less common symptoms of pleural mesothelioma include fever, night sweats and weight loss. Symptoms of peritoneal mesothelioma may include pain or swelling in the abdomen due to a build-up of fluid, nausea, weight loss, bowel obstruction, anemia or swelling of the feet.

PLEASE KEEP IN MIND THAT THESE SYMPTOMS MAY BE CAUSED BY MESOTHELIOMA OR BY OTHER LESS SERIOUS CONDITIONS. ONLY A DOCTOR CAN MAKE A DEFINITIVE DIAGNOSIS.

Pleural Effusion:-

One of the most common symptoms of mesothelioma is a pleural effusion, or an accumulation of fluid between the parietal pleura (the pleura covering the chest wall and diaphragm) and the visceral pleura (the pleura covering the lungs). Both of these membranes are covered with mesothelial cells which, under normal conditions, produce a small amount of fluid that acts as a lubricant between the chest wall and the lung. Any excess fluid is absorbed by blood and lymph vessels maintaining a balance. When too much fluid forms, the result is an effusion.

Types of Pleural Effusion:-

Pleural effusion is broken down into two categories, transudates and exudates. A transudate is a clear fluid that forms not because the pleural surfaces are diseased, but because of an imbalance between the normal production and removal of the fluid. The most common cause of transudative fluid is congestive heart failure. An exudate, which is often cloudy and contains many cells and proteins, results from disease of the pleura itself, and is common to mesothelioma. To determine whether a fluid is a transudate or exudate, a diagnostic thoracentesis, in which a needle or catheter is used to obtain a fluid sample, may be conducted.

Symptoms of Pleural Effusion:-

As the volume of fluid increases, shortness of breath, known as “dyspnea”, and sometimes pain, ranging from mild to stabbing, may occur. Some patients may experience a dry cough. When the doctor listens to the patient’s chest with a stethoscope, normal breath sounds are muted, and tapping on the chest will reveal dull rather than hollow sounds.

TREATMENT

Pleural effusion caused by heart failure or infection can usually be resolved by directing treatment at the cause, however, when testing has realized no diagnosis, and fluid continues to build or recur, doctors may recommend chest tube drainage and chemical pleurodesis. Chemical pleurodesis is a technique in which a sclerosing agent is used to abrade the pleural surfaces producing an adhesion between the parietal and visceral pleurae. This will prevent further effusion by eliminating the pleural space. Talc appears to be the most effective agent for pleurodesis, with a success rate of nearly 95%. It is highly effective when administered by either poudrage or slurry. Poudrage is the most widely used method of instilling talc into the pleural space. Before spraying the talc, the medical team removes all pleural fluid to completely collapse the lung. After the talc is administered, they inspect the pleural cavity to be sure the talc has been evenly distributed over the pleural surface. Some doctors prefer to use talc mixed with saline solution which forms wet slurry that can roll around the pleural cavity.

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Apr 27 2008

QUESTION BANK OF ANATOMY

QUESTION BANK OF ANATOMY

  1. Name the dural folds & describe the tentorium cerebelli
  2. Enumerate the dural venous sinuses & describe cavernous sinus
  3. Describe the anatomy of scalp. Write about its applied anatomy.
  4. Describe the intrinsic muscles of larynx
  5. Describe the movements of vocal chords & enumerate muscles producing them
  6. Name muscles of pharynx & describe the constrictors of pharynx
  7. Describe the extra ocular muscles of eyeball
  8. Describe the middle ear cavity.
  9. Describe the movements of temporo-mandibular joint & muscles of mastication.
  10. Describe the temporo-mandibular joint
  11. Describe anatomy of tongue. Add a note on its development.
  12. Describe anatomy of thyroid gland. Add a note on its development.
  13. Give the relations, blood supply, & development of the thyroid gland.
  14. Describe the anatomy of parotid gland
  15. Describe relations, nerve supply, histology, & applied anatomy of parotid gland
  16. Describe the submandibular salivary gland
  17. Describe relations, blood supply, histology, & nerve supply of submandibular salivary gland. Add a note on its applied anatomy.
  18. Describe the hypophysis cereberi. Add a note on its development.
  19. Describe the nerve supply of face.
  20. Describe the external carotid artery.
  21. Describe anatomy of palatine tonsil.
  22. Describe in details muscles of mastication,

Short Notes

  1. Posterior triangle
  2. Carotid triangle
  3. Digastric triangle
  4. External muscles of eye
  5. External carotid artery
  6. Movements of larynx
  7. Lachrymal apparatus
  8. Waldeyers ring
  9. Cavernous sinus
  10. Pharyngotympanic tube
  11. Lateral wall of nose
  12. Chordae tympanii nerve
  13. Recurrent laryngeal nerve (both sides)
  14. Boundaries of middle ear
  15. Relations, blood supply, & clinical anatomy of palatine tonsil
  16. Mylohoid muscle & its relations
  17. Sternocleidomastoid & its relations
  18. Tympanic membrane
  19. Hyoglossus
  20. Oblique muscles of eye
  21. Common carotid artery
  22. Internal jugular vein
  23. Interior of larynx
  24. Tonsil
  25. Vocal chords
  26. Submandibular salivary gland
  27. Medial wall of middle ear
  28. Maxillary air sinus
  29. Soft palate

Neuroanatomy

Full Questions

  1. Describe the internal capsule & its blood supply.
  2. Describe the lateral ventricle
  3. Describe the third ventricle
  4. Describe anatomy of the cerebellum
  5. Describe the corpus callosum
  6. Describe the third cranial nerve
  7. Describe the seventh cranial nerve. Write effects of its lesion at various levels
  8. Describe the seventh cranial nerve with a note on its clinical anatomy
  9. Describe the extra cranial part of facial nerve & its applied anatomy
  10. Describe the ninth cranial nerve
  11. Describe the twelveth cranial nerve
  12. Describe course, connections, nuclei, branches, & clinical anatomy of XII nerve
  13. Describe the auditory pathway. Write effects of its lesion at various levels
  14. Describe the auditory pathway
  15. Describe the visual pathway.

Short Notes

  1. Spino-thalamic tract
  2. Cortical spinal tract
  3. Inferior cerebellar peduncle
  4. Visual pathway & applied anatomy.
  5. Third ventricle
  6. Lateral ventricle
  7. Basal nuclei
  8. Midbrain section at superior colliculus
  9. Parietal lobe
  10. Post central gyrus
  11. Internal capsule
  12. Cerebellar peduncles
  13. Auditory pathway
  14. Floor of fourth ventricle
  15. Circle of Willis
  16. Thalamus
  17. Pones
  18. Mid brain section at inferior colliculus
  19. Frontal lobe
  20. Spino cerebellar pathway

Draw & label

  1. Cross section of medulla at level of fourth ventricle
  2. Draw & label medial surface of cerebrum
  3. Describe blood supply of superolateral surface of cerebrum
  4. Blood supply of cerebral cortex with its clinical anatomy
  5. Transverse section of spinal cord at mid-thoracic level
  6. Connections of thalamus
  7. Corpus callosum

Chest

Full Questions

  1. Describe the left ventricle & add a note on its blood supply
  2. Describe the right atrium. Write about its development.
  3. Describe the right lung.
  4. Describe the mediastinal surface of right lung. Give its bronchopulmonary segments.
  5. Describe the superior mediastinum. Write in details about any one of its contents
  6. Enumerate all structures of superior mediastinum. Describe arch of aorta
  7. Describe the arch of aorta & give its development
  8. Describe the thoracic part of oesophagus. Add a note on its development
  9. Describe the thoraco-abdominal diaphragm & give its development
  10. Describe a typical intercostal space. Add a note on mechanism of respiration
  11. Describe movements of the thoracic cage during respiration

Abdomen-Pelvis

Full Questions

  1. Describe the inguinal canal
  2. Describe the right kidney
  3. Describe the left kidney
  4. Describe the kidney
  5. Describe the urinary bladder
  6. Describe the suprarenal glands. Give their development
  7. Describe the stomach
  8. Describe the anatomy of pancreas
  9. Describe the anatomy of spleen
  10. Describe the duodenum & give its histology & development
  11. Describe the caecum & appendix and give their applied anatomy
  12. Describe the extra hepatic biliary apparatus
  13. Describe the anatomy of prostate
  14. Describe the anatomy of rectum & anal canal
  15. Describe the anal canal
  16. Describe the anatomy of uterus. Add a note on its supports
  17. Describe the anatomy of uterus.
  18. Describe the supports of uterus.
  19. Describe the perineal pouches

Short Notes

  1. Rectus sheath
  2. Gall bladder
  3. Male urethra
  4. Prostrate
  5. Rectum
  6. Left ureter
  7. Head of pancreas
  8. Broad ligament
  9. Urinary bladder
  10. Right Suprarenal gland
  11. Posterior relations of both kidneys
  12. Internal iliac artery
  13. Inferior vena cava
  14. Porto-systemic anastomosis & its clinical importance
  15. Inguinal canal
  16. Ischio rectal fossa
  17. Vas deferens
  18. Fallopian tube
  19. Anal canal
  20. Psoas major muscle
  21. Ovary
  22. Supports of uterus
  23. Appendix
  24. Suprarenal gland
  25. Spleen
  26. Superior mesenteric artery
  27. Portal vein

Superior Extremity

Full Questions

  1. Describe axilla.
  2. Describe the axillary artery
  3. Describe the mammary gland
  4. Describe in detail anatomy of female mammary gland. Add note on its lymphatic drainage
  5. Describe the radial nerve
  6. Describe the ulnar nerve in hand
  7. Describe the ulnar nerve. What are the effects of its lesion at wrist joint.
  8. Describe the medium nerve
  9. Describe the wrist joint
  10. Describe the elbow joint
  11. Describe the movements of thumb
  12. Describe the shoulder joint
  13. Describe the movements of the shoulder joint
  14. Name muscles which move the shoulder joint & describe deltoid in detail
  15. Describe pronation & supination of forearm

Short Notes

  1. Radial nerve in arm
  2. Movements of shoulder joint
  3. Axillary artery
  4. Give attachments, nerve supply, & actions of- Trapezius, Latissimus dorsi, Brachialis, Supinator
  5. Ulnar nerve in hand
  6. Elbow joint
  7. Axillary lymph nodes

Genetics

Short Notes

  1. Kleinefelter’s syndrome
  2. Turner’s syndrome
  3. Chromosome
  4. Y-Chromosome
  5. Chromosomal anomalies
  6. Meiosis
  7. Barr body
  8. Non disjunction
  9. Transcription
  10. Autosomal recessive inheritance
  11. X-linked recessive inheritance
  12. Hemophilia
  13. Genetics of ABO blood groups system
  14. Rh. Inheritance
  15. Prenatal diagnosis
  16. Ultrasonography
  17. Dermatoglyphics
  18. Genotype
  19. Mosaicism
  20. Down’s syndrome
  21. Ribosome
  22. Trisomy
  23. X-Chromosome
  24. Structural chromosomal anomalies
  25. Gene
  26. R.N.A.
  27. Mitosis
  28. Sex chromatin
  29. Mutation
  30. Lyon’s hypothesis
  31. Inheritance of color blindness
  32. Autosomal dominant inheritance
  33. X-linked inheritance
  34. Genetics of Rh blood group system
  35. Inheritance of ABO blood groups
  36. Multifactorial inheritance
  37. ABO blood groups
  38. Amniocentesis
  39. Karyotyping
  40. Genetic counseling
  1. Codon

Short Notes on Microscopic Structure of

  1. Tonsil.
  2. Lymph node
  3. White fibro cartilage
  4. Costal cartilage
  5. Hyaline cartilage
  6. Skeletal muscle
  7. Tendon
  8. Large size artery
  9. Transverse section Aorta
  10. Pancreas
  11. Loose connective tissue
  12. Scalp
  13. Oesophagus
  14. Large intestine
  15. Duodenum
  16. Trachea
  17. Super renal gland
  18. Thyroid
  19. Testis
  20. Vas deferens
  21. Eyelid
  22. Cornea
  23. Lens
  24. Myelinated nerve fiber
  25. Cerebellum
  26. Autonomic & Spinal ganglion
  27. Spleen
  28. Thymus
  29. Elastic cartilage
  30. Articular cartilage
  31. Compact bone
  32. Cardiac muscle
  33. Tendon
  34. Medium size artery
  35. Mixed salivary gland
  36. Skin
  37. Thick skin
  38. Lip
  39. Stomach
  40. Stomach-fundus
  41. Ileum
  42. Lung
  43. Pituitary gland
  44. Urinary bladder
  45. Prostate
  46. Ovary
  47. Retina
  48. Neuron
  49. Organ of Corti
  50. Cerebrum
  51. Autonomic ganglion

Embryology

Short Notes

  1. Oogenesis
  2. Fertilization
  3. Zygote
  4. Primitive streak
  5. Neural tube
  6. Chorionic villi
  7. Amnion
  8. Placenta
  9. Derivatives of three germ layers
  10. Mesonephric duct
  11. Kidney
  12. First pharyngeal arch
  13. Second pharyngeal arch
  14. Tooth
  15. Diaphragm
  16. Ductus arteriosus
  17. Inter-atrial septum
  18. Subclavian artery
  19. Stomach
  20. Liver
  21. Midgut & its rotation
  22. Palate
  23. Thyroid
  24. Testis
  25. Superior vena cava
  26. Face
  27. Spermatogenesis
  28. Implantation
  29. Yolk sac
  30. Notochord
  31. Neural crest
  32. Chorion
  33. Amniotic sac
  34. Functions of placenta
  35. Allantois
  36. Para mesonephric duct
  37. Urinary bladder
  38. Fate of first pharyngeal arch
  39. Fate of second pharyngeal arch
  40. Tongue
  41. Sinous venosus
  42. Inter-ventricular septum
  43. Right atrium
  44. Arch of aorta
  45. Meckel’s diverticulum
  46. Duodenum
  47. Large Intestine
  48. Spleen
  49. Supra renal
  50. Pituitary gland
  51. Middle ear
  52. Spinal cord
  53. Retina

Inferior Extremity

Full Questions

  1. Describe the knee joint
  2. Describe the movements of knee joint
  3. Describe the anatomy of hip joint
  4. Describe the movements of the hip joint. Name the muscles producing the movements
  5. Describe in details inversion & eversion of foot
  6. Describe the sciatic nerve
  7. Describe the femoral triangle
  8. Describe the anatomy of femoral sheath. Add a note of femoral hernia
  9. Describe the femoral artery
  10. Describe the popliteal fossa
  11. Describe venous drainage of lower limb. Add a note on varicose veins.
  12. Describe the great saphenous vein. Give its applied anatomy
  13. Describe two abductors & two flexors of hip joint
  14. Describe the gluteus maximus muscle. Describe the arches of the foot

Short Notes

  1. Gluteus maximus with its relations
  2. Plantar flexors
  3. Inversion & eversion of foot
  4. Intra Articular structures of knee joint
  5. Femoral nerve
  6. Abductors of hip joint
  7. Gluteus medius
  8. Ligaments of the knee joint
  9. Arches of the foot
  10. Longitudinal arches of foot
  11. Femoral artery

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QUESTION BANK OF ANATOMY

  1. Name the dural folds & describe the tentorium cerebelli
  2. Enumerate the dural venous sinuses & describe cavernous sinus
  3. Describe the anatomy of scalp. Write about its applied anatomy.
  4. Describe the intrinsic muscles of larynx
  5. Describe the movements of vocal chords & enumerate muscles producing them
  6. Name muscles of pharynx & describe the constrictors of pharynx
  7. Describe the extra ocular muscles of eyeball
  8. Describe the middle ear cavity.
  9. Describe the movements of temporo-mandibular joint & muscles of mastication.
  10. Describe the temporo-mandibular joint
  11. Describe anatomy of tongue. Add a note on its development.
  12. Describe anatomy of thyroid gland. Add a note on its development.
  13. Give the relations, blood supply, & development of the thyroid gland.
  14. Describe the anatomy of parotid gland
  15. Describe relations, nerve supply, histology, & applied anatomy of parotid gland
  16. Describe the submandibular salivary gland
  17. Describe relations, blood supply, histology, & nerve supply of submandibular salivary gland. Add a note on its applied anatomy.
  18. Describe the hypophysis cereberi. Add a note on its development.
  19. Describe the nerve supply of face.
  20. Describe the external carotid artery.
  21. Describe anatomy of palatine tonsil.
  22. Describe in details muscles of mastication,

Short Notes

  1. Posterior triangle
  2. Carotid triangle
  3. Digastric triangle
  4. External muscles of eye
  5. External carotid artery
  6. Movements of larynx
  7. Lachrymal apparatus
  8. Waldeyers ring
  9. Cavernous sinus
  10. Pharyngotympanic tube
  11. Lateral wall of nose
  12. Chordae tympanii nerve
  13. Recurrent laryngeal nerve (both sides)
  14. Boundaries of middle ear
  15. Relations, blood supply, & clinical anatomy of palatine tonsil
  16. Mylohoid muscle & its relations
  17. Sternocleidomastoid & its relations
  18. Tympanic membrane
  19. Hyoglossus
  20. Oblique muscles of eye
  21. Common carotid artery
  22. Internal jugular vein
  23. Interior of larynx
  24. Tonsil
  25. Vocal chords
  26. Submandibular salivary gland
  27. Medial wall of middle ear
  28. Maxillary air sinus
  29. Soft palate

Neuroanatomy

Full Questions

  1. Describe the internal capsule & its blood supply.
  2. Describe the lateral ventricle
  3. Describe the third ventricle
  4. Describe anatomy of the cerebellum
  5. Describe the corpus callosum
  6. Describe the third cranial nerve
  7. Describe the seventh cranial nerve. Write effects of its lesion at various levels
  8. Describe the seventh cranial nerve with a note on its clinical anatomy
  9. Describe the extra cranial part of facial nerve & its applied anatomy
  10. Describe the ninth cranial nerve
  11. Describe the twelveth cranial nerve
  12. Describe course, connections, nuclei, branches, & clinical anatomy of XII nerve
  13. Describe the auditory pathway. Write effects of its lesion at various levels
  14. Describe the auditory pathway
  15. Describe the visual pathway.

Short Notes

  1. Spino-thalamic tract
  2. Cortical spinal tract
  3. Inferior cerebellar peduncle
  4. Visual pathway & applied anatomy.
  5. Third ventricle
  6. Lateral ventricle
  7. Basal nuclei
  8. Midbrain section at superior colliculus
  9. Parietal lobe
  10. Post central gyrus
  11. Internal capsule
  12. Cerebellar peduncles
  13. Auditory pathway
  14. Floor of fourth ventricle
  15. Circle of Willis
  16. Thalamus
  17. Pones
  18. Mid brain section at inferior colliculus
  19. Frontal lobe
  20. Spino cerebellar pathway

Draw & label

  1. Cross section of medulla at level of fourth ventricle
  2. Draw & label medial surface of cerebrum
  3. Describe blood supply of superolateral surface of cerebrum
  4. Blood supply of cerebral cortex with its clinical anatomy
  5. Transverse section of spinal cord at mid-thoracic level
  6. Connections of thalamus
  7. Corpus callosum

Chest

Full Questions

  1. Describe the left ventricle & add a note on its blood supply
  2. Describe the right atrium. Write about its development.
  3. Describe the right lung.
  4. Describe the mediastinal surface of right lung. Give its bronchopulmonary segments.
  5. Describe the superior mediastinum. Write in details about any one of its contents
  6. Enumerate all structures of superior mediastinum. Describe arch of aorta
  7. Describe the arch of aorta & give its development
  8. Describe the thoracic part of oesophagus. Add a note on its development
  9. Describe the thoraco-abdominal diaphragm & give its development
  10. Describe a typical intercostal space. Add a note on mechanism of respiration
  11. Describe movements of the thoracic cage during respiration

Abdomen-Pelvis

Full Questions

  1. Describe the inguinal canal
  2. Describe the right kidney
  3. Describe the left kidney
  4. Describe the kidney
  5. Describe the urinary bladder
  6. Describe the suprarenal glands. Give their development
  7. Describe the stomach
  8. Describe the anatomy of pancreas
  9. Describe the anatomy of spleen
  10. Describe the duodenum & give its histology & development
  11. Describe the caecum & appendix and give their applied anatomy
  12. Describe the extra hepatic biliary apparatus
  13. Describe the anatomy of prostate
  14. Describe the anatomy of rectum & anal canal
  15. Describe the anal canal
  16. Describe the anatomy of uterus. Add a note on its supports
  17. Describe the anatomy of uterus.
  18. Describe the supports of uterus.
  19. Describe the perineal pouches

Short Notes

  1. Rectus sheath
  2. Gall bladder
  3. Male urethra
  4. Prostrate
  5. Rectum
  6. Left ureter
  7. Head of pancreas
  8. Broad ligament
  9. Urinary bladder
  10. Right Suprarenal gland
  11. Posterior relations of both kidneys
  12. Internal iliac artery
  13. Inferior vena cava
  14. Porto-systemic anastomosis & its clinical importance
  15. Inguinal canal
  16. Ischio rectal fossa
  17. Vas deferens
  18. Fallopian tube
  19. Anal canal
  20. Psoas major muscle
  21. Ovary
  22. Supports of uterus
  23. Appendix
  24. Suprarenal gland
  25. Spleen
  26. Superior mesenteric artery
  27. Portal vein

Superior Extremity

Full Questions

  1. Describe axilla.
  2. Describe the axillary artery
  3. Describe the mammary gland
  4. Describe in detail anatomy of female mammary gland. Add note on its lymphatic drainage
  5. Describe the radial nerve
  6. Describe the ulnar nerve in hand
  7. Describe the ulnar nerve. What are the effects of its lesion at wrist joint.
  8. Describe the medium nerve
  9. Describe the wrist joint
  10. Describe the elbow joint
  11. Describe the movements of thumb
  12. Describe the shoulder joint
  13. Describe the movements of the shoulder joint
  14. Name muscles which move the shoulder joint & describe deltoid in detail
  15. Describe pronation & supination of forearm

Short Notes

  1. Radial nerve in arm
  2. Movements of shoulder joint
  3. Axillary artery
  4. Give attachments, nerve supply, & actions of- Trapezius, Latissimus dorsi, Brachialis, Supinator
  5. Ulnar nerve in hand
  6. Elbow joint
  7. Axillary lymph nodes

Genetics

Short Notes

  1. Kleinefelter’s syndrome
  2. Turner’s syndrome
  3. Chromosome
  4. Y-Chromosome
  5. Chromosomal anomalies
  6. Meiosis
  7. Barr body
  8. Non disjunction
  9. Transcription
  10. Autosomal recessive inheritance
  11. X-linked recessive inheritance
  12. Hemophilia
  13. Genetics of ABO blood groups system
  14. Rh. Inheritance
  15. Prenatal diagnosis
  16. Ultrasonography
  17. Dermatoglyphics
  18. Genotype
  19. Mosaicism
  20. Down’s syndrome
  21. Ribosome
  22. Trisomy
  23. X-Chromosome
  24. Structural chromosomal anomalies
  25. Gene
  26. R.N.A.
  27. Mitosis
  28. Sex chromatin
  29. Mutation
  30. Lyon’s hypothesis
  31. Inheritance of color blindness
  32. Autosomal dominant inheritance
  33. X-linked inheritance
  34. Genetics of Rh blood group system
  35. Inheritance of ABO blood groups
  36. Multifactorial inheritance
  37. ABO blood groups
  38. Amniocentesis
  39. Karyotyping
  40. Genetic counseling
  1. Codon

Short Notes on Microscopic Structure of

  1. Tonsil.
  2. Lymph node
  3. White fibro cartilage
  4. Costal cartilage
  5. Hyaline cartilage
  6. Skeletal muscle
  7. Tendon
  8. Large size artery
  9. Transverse section Aorta
  10. Pancreas
  11. Loose connective tissue
  12. Scalp
  13. Oesophagus
  14. Large intestine
  15. Duodenum
  16. Trachea
  17. Super renal gland
  18. Thyroid
  19. Testis
  20. Vas deferens
  21. Eyelid
  22. Cornea
  23. Lens
  24. Myelinated nerve fiber
  25. Cerebellum
  26. Autonomic & Spinal ganglion
  27. Spleen
  28. Thymus
  29. Elastic cartilage
  30. Articular cartilage
  31. Compact bone
  32. Cardiac muscle
  33. Tendon
  34. Medium size artery
  35. Mixed salivary gland
  36. Skin
  37. Thick skin
  38. Lip
  39. Stomach
  40. Stomach-fundus
  41. Ileum
  42. Lung
  43. Pituitary gland
  44. Urinary bladder
  45. Prostate
  46. Ovary
  47. Retina
  48. Neuron
  49. Organ of Corti
  50. Cerebrum
  51. Autonomic ganglion

Embryology

Short Notes

  1. Oogenesis
  2. Fertilization
  3. Zygote
  4. Primitive streak
  5. Neural tube
  6. Chorionic villi
  7. Amnion
  8. Placenta
  9. Derivatives of three germ layers
  10. Mesonephric duct
  11. Kidney
  12. First pharyngeal arch
  13. Second pharyngeal arch
  14. Tooth
  15. Diaphragm
  16. Ductus arteriosus
  17. Inter-atrial septum
  18. Subclavian artery
  19. Stomach
  20. Liver
  21. Midgut & its rotation
  22. Palate
  23. Thyroid
  24. Testis
  25. Superior vena cava
  26. Face
  27. Spermatogenesis
  28. Implantation
  29. Yolk sac
  30. Notochord
  31. Neural crest
  32. Chorion
  33. Amniotic sac
  34. Functions of placenta
  35. Allantois
  36. Para mesonephric duct
  37. Urinary bladder
  38. Fate of first pharyngeal arch
  39. Fate of second pharyngeal arch
  40. Tongue
  41. Sinous venosus
  42. Inter-ventricular septum
  43. Right atrium
  44. Arch of aorta
  45. Meckel’s diverticulum
  46. Duodenum
  47. Large Intestine
  48. Spleen
  49. Supra renal
  50. Pituitary gland
  51. Middle ear
  52. Spinal cord
  53. Retina

Inferior Extremity

Full Questions

  1. Describe the knee joint
  2. Describe the movements of knee joint
  3. Describe the anatomy of hip joint
  4. Describe the movements of the hip joint. Name the muscles producing the movements
  5. Describe in details inversion & eversion of foot
  6. Describe the sciatic nerve
  7. Describe the femoral triangle
  8. Describe the anatomy of femoral sheath. Add a note of femoral hernia
  9. Describe the femoral artery
  10. Describe the popliteal fossa
  11. Describe venous drainage of lower limb. Add a note on varicose veins.
  12. Describe the great saphenous vein. Give its applied anatomy
  13. Describe two abductors & two flexors of hip joint
  14. Describe the gluteus maximus muscle. Describe the arches of the foot

Short Notes

  1. Gluteus maximus with its relations
  2. Plantar flexors
  3. Inversion & eversion of foot
  4. Intra Articular structures of knee joint
  5. Femoral nerve
  6. Abductors of hip joint
  7. Gluteus medius
  8. Ligaments of the knee joint
  9. Arches of the foot
  10. Longitudinal arches of foot
  11. Femoral artery

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Apr 27 2008

Question Bank of Forensic Medicine

QUESTION BANK OF FORENSIC MEDICINE

Full Questions

  1. Define and explain the term `Death’. How will you assess the time since death.
  2. Define and explain the term `Infanticide’. How will you establish the proof of live-birth by examining the dead body of a new born?
  3. Define `drowning.’ Describe the positive findings in a case of death due to drowning in sea.
  4. Describe the contractual relationship between a medical practitioner and patient.
  5. Define `Abortion’. What is `criminal abortion’? Describe the provisions of the M.T.P. Act of 1971.
  6. Describe the procedure of Coroner’s inquest. How is evidence recorded in a court of law?
  7. Define the Infanticide. How will you distinguish between a live-born and a still-born.
  8. Define `Identity.’ How will you establish the identity of a mutilated, decomposed body?
  9. Define Identity’. How is it established?
  10. Describe the nature of the professional relation between a medical practitioner and his patient.
  11. What precautions should a medical practitioner take to avoid charges of negligence?
  12. Define and discuss `Medical Negligence’. What precautions should a medical practitioner take in order to avoid charges of negligence?
  13. What do you mean by `unnatural sexual offences’? Describe the positive findings in the victim of sodomy.
  14. Define drowning. What are the types of drowning? Describe the post-mortem findings in a case of drowning in sea water.
  15. What is infamous conduct in a professional respect? Mention the circumstances under which the name of a medical practitioner can be erased from the State Medical Register.
  16. What is medical negligence? When does it become criminal in nature? What are the legal remedies available to a patient?
  17. Enumerate the differences between Unnatural sexual offense and sexual perversion. Write the report of the examination of the accused in case of `Sodomy’.
  18. Describe the circumstances under which the acts of a practitioner are called negligent.
  19. The dead body of a young girl is found in a suspended position with a ligature around the neck. How will you establish the cause of death?
  20. What is M.T.P. Act? When, where, by whom and on what grounds can the pregnancy be terminated under this act?
  21. Enumerate Grievous hurt. Describe in detail how an injury certificate is written.
  22. What is infanticide? What are the various acts of omission and commission. How will you establish that the child was born alive?
  23. Define rape. How would you examine a victim of rape? What laboratory investigations will help in establishing identity of the assailant in case of sexual assault?
  24. The dead body of a young female is recovered from a well. It has multiple injuries. Describe the post-mortem examination in such a case.
  25. Mention the various types of `witness’. Describe the procedure for recording evidence in a court of law.
  26. How will you determine the nature of injuries in a case of multiple injuries?
  27. Explain the terms “suffocation”. What are different types of suffocation & postmortem findings?
  28. Enumerate Grievous hurt. How do you determine age of Bruise (contusion).
  29. Compare and contrast (any two pairs).

(a) Dry drowning and classical drowning.

(b) Dying declaration and dying deposition.

(c) Contusion and hypostasis.

  1. Define “Consent”. Name different types of consents. Write in detail about “Informed” consent.

Short Notes

  1. Dry drowning
  2. Imprint abrasion
  3. Contributory negligence
  4. Suicidal cut throat
  5. Locard Principal
  6. Railway Spine
  7. Partial Hanging
  8. Expert Witness
  9. Diatoms
  10. Mummification
  11. Imprint Abrasions
  12. Professional Secrecy
  13. Defloration
  14. Molecular death
  15. Post-mortem lividity
  16. Burking
  17. Incest
  18. Age of contusion
  19. Adipocere
  20. Bestiality
  21. Defense injuries
  22. Magistrate’s quest
  23. Smothering.
  24. Age of viability
  25. Poroscopy
  26. Professional secret
  27. Pugilistic attitude
  28. Dying deposition
  29. Subpoena
  30. Viable infant
  31. P M Caloricity
  32. Mummification
  33. Inquest
  34. Ligature mark on neck
  35. Abrasion collar
  36. Dactylography
  37. Bruise
  38. Hymen
  39. Bestiality
  40. Fabricated injuries
  41. Anthropometry
  42. Hydrostatic test
  43. Privileged communication.
  44. Sexual offences
  45. Professional misconduct
  46. Virgin
  47. Mechanical injuries and their medicolegal importance
  48. Antemortem and Post mortem Burns
  49. Hesitation marks
  50. Medicolegal aspects of identity
  51. Insanity
  52. Determination of time of death
  53. Ante mortem and post mortem incised wound
  54. Cross examination

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Apr 27 2008

Question Bank of Homoeopathic Pharmacy

QUESTION BANK OF HOMOEOPATHIC PHARMACY

Full Questions

  1. What is an ideal vehicle? Write uses, properties & methods of preparation of commonly used solid vehicle in homoeopathy
  2. Describe properties, preparation, & uses or alcohol used in homoeopathic pharmacy.
  3. What are vehicles? Name different vehicles used in Homoeopathic pharmacy
  4. Describe in detail preparation of alcohol.
  5. Name different types of vehicles & describe alcohol in details
  6. Describe different types of alcohol you know in relation to homoeopathic pharmacy
  7. What are the varieties of vehicles used for homoeopathic Medicines State how they are to be selected in preparing medicine?
  8. What are vehicles? Classify them & give advantages & disadvantages of any four commonly used vehicles in homoeopathy.
  9. Give properties & uses of 4 vehicles commonly used in homoeopathic pharmacy
  10. Give preparation, properties, advantages & possible impurities of alcohol / sac lac
  11. Describe the preparation of sac lac. How will you detect impurities in it?
  12. What are vehicles? Give preparation, properties, & uses of Sac lac
  13. What are vehicles? Describe preparation of sugar of milk in homoeopathic pharmacy.
  14. What are globules? How will you prepare globules in homoeopathic pharmacy?
  15. Describe in detail the manufacturing process of globules & their uses.
  16. What are the impurities found in Sugar of milk? Describe in detail process of Staph’s method
  17. How will do prepare distilled water in homoeopathic pharmacy? When is it used in laboratory?
  18. How will you prepare distilled water in homoeopathic pharmacy? What are the impurities found in it?
  19. Name different types of utensils. Describe any 3 in details
  20. Name the instruments & appliances used in pharmacy. How will you clean them ? Describe in detail-Bottles, Water bath, Percolator/
  21. What is Prescription? Describe different parts of prescription. Give examples of two prescriptions
  22. What is prescription writing? Explain validity & utility of prescription writing
  23. What is the scope of ext. application in homoeopathic prescribing? How will you select its ingredients?
  24. What is the scope of ext. Applications in homoeopathic prescribing? How will you prepare arnica ointment
  25. How will you identify, select, collect & preserve a sample of calendula and prepare calendula ointment from it.
  26. Differentiate in detail between trituration or succussion
  27. What are the different sources of homoeopathic drugs? Describe each with example
  28. Explain sources of homoeopathic, drugs with their preservation
  29. What are the different scales in preparing homoeopathic medicines? Describe in detail 50 milliscimal scale
  30. Describe in detail different scales of preparing homoeopathic medicines Describe in detail 50 milliscimal scale
  31. Describe in detail different scales of preparing homoeopathic medicines
  32. Write an essay on drug standarisation
  33. What is standarisation? Describe the various parameters used to standardise a mother tincture
  34. What is standardization? Describe various parameters prepare a standard homoeopathic medicine
  35. What is official sampling describe the process of percolation
  36. Write scope of homoeopathic pharmacy in relation to Materia Medica & Organon of medicine.
  37. Discuss the provisions related to sale & manufacture of homoeopathic medicines
  38. Discuss the professions related to sale & manufacture of homoeopathic medicines
  39. What are nosodes? How are they prepared & preserved in lab.
  40. Describe the preparation of NI & N2 nosodes
  41. How will you proceed to prove a drug which in its natural form produces changes in body? Name few such drugs.
  42. How will you proceed to prove a drug which in its natural form does not effect the vital force? Name few such drugs. ,
  43. What is mother tincture? What is meant by drug power of mother tincture?
  44. Describe preparation of mother tincture from more juice & less juicy plants.
  45. Describe in detail preparation of mother tincture from class II III, IV, V-A with 3 examples of each
  46. Differentiate in detail between mother tincture & mother substance
  47. What is moisture content of plant Describe in detail preparation of mother tincture from dry plant
  48. What are the different methods of knowing moisture content plants? Describe any one of them
  49. What are the different methods of knowing moisture content of plants? How does it help in preparing mother tincture
  50. Why do homoeopaths potentise their medicines? What are the different methods of potentisation
  51. What is jumping potency? How will you convert insoluble substance into liquid potency
  52. Write significance of conversion so solid potency of liquid potency. How will you convert solid potency into liquid potency?
  53. Explain conversion of Cal carb. 6 X to 8 X. Explanation why 7x of this medicine can not be available
  54. How will you prepare liquid potency of cal carb? From this natural sources.
  55. How will you prepare Cal Cab? 1X (first potency) from its natural source?
  56. What is Scilla IC? Describe its preparation & how will you further potentise it.
  57. Give preparation, purification, impurity detection & uses of any one vehicle used for trituration.
  58. Describe the process of trituration. Why do we triturate drugs in homeopathy

Write identifying features, constituents, & various actions or monographs of

  1. Aconite
  2. Cantharis/Spanish Fly
  3. Nux vom/poison nut.
  4. Anacardium orientalis.
  5. Jamal gota/Croton tig.
  6. Hyoscyamus Nig.
  7. Chelidonium
  8. Coffea crud
  9. Calendula
  10. Arsenic alb
  11. Pulsatilla
  12. Colchicum
  13. Abrotanum
  14. Aurum met
  15. Bryonia
  16. Chamomilla
  17. Opium
  18. Lachesis
  19. Drosera
  20. Apis mel
  21. Nux mosh
  22. Carbo veg
  23. Baptisia tinctora
  24. Stramonium
  25. Berberis v.
  26. Sulphur
  27. Arnica
  28. Aloe
  29. Digitalis
  30. Datura
  31. China off.
  32. Sepia
  33. Cina

Short Notes

  1. Maceration
  2. Decantation
  3. Moisture content
  4. Mother tincture
  5. Sources of drugs
  6. Placebo
  7. Nosode
  8. Succussion
  9. Trituration
  10. Fluxion potency
  11. Doctrine of potentisation
  12. Scales of homoeopathy,
  13. Centesimal scale
  14. Pharmacodynamics
  15. Pharmacology
  16. Alcohol
  17. Aqueous solution
  18. Sublimation
  19. Filtration
  20. Remedy
  21. Sublimation
  22. Filtration sources
  23. Vegetable sources
  24. Preservation of drugs
  25. Ideal vehicle
  26. Calendula ointment
  27. Ointment
  28. External applications
  29. Doctrine of signature (with examples)
  30. Active principle
  31. Prescription writing
  32. Jumping potency
  33. Collection of medicinal plants
  34. Official sampling
  35. 50 Milliscimal potency
  36. Sarcodes
  37. Nosodes
  38. Dynamisation
  39. Potentisation
  40. Potency
  41. Pharmacy
  42. Decimal scale
  43. Pharmacopoea
  44. Legislation in Homoeopathy
  45. Distilled water
  46. Distillation
  47. Medicine
  48. Drug
  49. Mortar & Pestle
  50. Chemical balance
  51. Specific gravity
  52. Standardisation
  53. Arnica liniment
  54. Liniment

Differentiate between the following.

  1. Inscription & subscription writing
  2. Cane sugar & Milk
  3. Nosodes & Sarcodes
  4. Centesimal & Decimal scale

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Apr 27 2008

Question Bank of Materia Medica Set-3

MATERIA MEDICA QUESTIONS SET-3

Full Questions

  1. Give the drug picture of : Med, Lyco, Carcinosin, Rhus T, Kali Bi, Bell, Thuja, Lach, Kali C, Bacillinum Sepia, Caust, Cal C, Alum, Phos
  2. Write the short the group symptoms of Magnesium. Describe the drug picture of Mag carb. Compare Mag-Carb, Sulph, Mur, Phos
  3. Describe DP. of Mag C. Detail the Antidotal & Complementary relationship
  4. Write the common group symptoms of Acids. Describe the drug picture of Fluoric acid
  5. Write the group symptoms of Antimony
  6. Write the group symptoms of Halogens. Describe antiscrofulous & antisyphilitic action of Iodium. Discuss its relation with Carbolic Ac
  7. Write the group symptoms of Kali & differentiate the constitution of Kali C & Kali Bi
  8. Write common group symptoms of Ophidia. Describe drug picture of Crotalus Hor.
  9. In  a  given case of common cold the nasal discharge is “thick yellow” discuss the application of Puls, Kali Bi, Kali P. Sil, Arum triph
  10. Outline a CHAM child giving its differentiating features with its counter-part Staph.
  11. What are Nosodes? Write indications & contra-indications of nosodes
  12. Write the leading indication of Sul, Cal, C in psoric miasm
  13. Write the leading indications of Thuja, Med in sycotic miasm
  14. Describe Carb Veg as corpse reviver
  15. Describe Kali Mur as Biochemic Sulphur
  16. Describe Nat Sulph as king of hydro-genoid constitution

Compare & Contrast

  1. MIND – AmbraG & NatM
  2. RESPIRATORY-Euph & AlliumC
  3. SKIN – Sul & Graph
  4. FEMALE – Sep & NuxV
  5. CONVULSIONS-CicV CupM
  6. ŠSUN STROKE-Glon & Natc
  7. TRAUMA-Arn & BellisP
  8. THROAT-MercS & HepS
  9. URINARY-Apis & Canth
  10. HEADACHE-Bell & Bry
  11. JOINTS-Bry & RhusT
  12. RECTAL – Aescul & Collin
  13. G.I.T. – MagM & NatM
  14. HEMORRHAGE-Phos & NitAc

Differentiate the following:

  1. ALLERGY-Ferrum & Bov
  2. ABD. COLIC-Colo & Plb
  3. LIVER-SecCor & ArsA
  4. MENTALS-Phos & Plat
  5. LEUCORRHOEA-Kali Bi & Kreos
  6. CONSTIPATION-Alum & Plat


Short Notes

  1. CONSTITUTION of: AurM, Caps, Cal-Carb, Phos, Sulph, Fl, NatM
  2. BIOPHYSIOLOGICAL ACTION: Kali-P,M,S, Nat-P,M,S
  3. CHANGING MOODS: Alum, Puls Plat
  4. MENTALS: AmbraG, Con, Coff, Caust, Hyosc, Iod, Lach, NatC,  Puls, Petr, Sep, Thuj, Verat alb, Opium
  5. GLANDS: CarduusM CarbAn, Iod
  6. REDLINE MODALITY: CrotT, CupM, Cycl, Glon
  7. SKIN : Anth, CrotT, CarbAn, Graph, Hydroc, Mez, Maland
  8. HOME SICKNESS : Bry, Caps, Ign
  9. MOTION : Asaf, AdonisV, ArgM, AvenaS, AcalI, Anthr, Bry,  Bacil, Bufo, CarbAn, Cina, Cycl, Cham, EupPerf, Kreos, Med, RhusT, Sab, Lyssin
  10. CANCER : AsterR, CarbAn, Carcin, Condur, Hydras
  11. CONVULSIONS: AsterR, Bufo, Cic, CupM
  12. LIVER: Chel, China, NatS, MerS
  13. FEMALE: AmbraG, CoccI, CrocS, Grap, NuxM
  14. CARDIAC: Ado, Cact, Crat, Kal, LithC, Digitalis, Gels
  15. HAEMORRHAGES: Acal, Coll, Caulo, CrocS, Mell
  16. C.N.S. : Agar, ArtV, CupM, Cic, Hell, Lyssin
  17. RESPIRATORY: Ars, AmmM, Bry, Brom, CorRub, Dros, Dig, Meph, Phos, Spong, Sep, Lyco, AntT
  18. ASTHMA: AntArs, Blatta, lobelia
  19. COUGH: AntArs, CorR,
  20. BACKACHE : AescH, KaliC, NatM
  21. RHEUMATISM:  Arn, Colch, Calp, LithC, Led, Puls, Phyt, LacC, RhusT, Sul, Rad.br.
  22. POLYURIA: AmmM, Apis, AcetAc, CalArs, NatS
  23. G.I.T.: Phos, VertA, Abies Can
  24. ABD. COLIC : Bism, Coloc, Lyco, MagP, Plump, Spig
  25. FATIGUE : AvenaS
  26. TRAUMA : BellisP
  27. RECTAL : MagM
  28. ULCER : MercS
  29. INSOMNIA : Coff
  30. FILARIASIS: Hydras
  31. CAR SICKNESS: CoccI
  32. SCROFULA : CarbAn
  33. SEX : Calad
  34. GENERALS : CrocS
  35. DIPHTHERIA: Dipt
  36. TYPHOID: Bapt
  37. HEADACHE : Glon
  38. DIABETES: AcetAc
  39. BREAST : LacC
  40. CHARACTERISTIC SYMPTOMS OF: Aeth,  Agnus,  AbiesC., AmbraG, AntArs, Apocy, Acal, BerbV, Bov, Caps, chinaArs, CarboA, Caust, Con, CrocS, Coca, Dulc, Dios, Fl.Ac, Helonias, KaliBr, LacD, Lyssin, Melli, MercS, NuxM, NatC, Spong,Thuja, VertA, ArumT, Borax, Cinchona, Can. Ind, Medor, Lith. Carb.
  41. PRESCRIPTIVE TOTALITY OF: ArsI, Cyclamen, HepS, NuxV, VertA, Maland.

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Apr 27 2008

Question Bank of Materia Medica Set-2

MATERIA MEDICA QUESTION SET-2

Compare & Contrast

  1. Merc Sol. & Hep. Sulph in Throat complaints
  2. China & Gels in Fever
  3. Digitals & Acetic Acid in Dropsy
  4. Cantharis & Apis Mel in Urinary  complaints
  5. Ammonium Mur & Bromium in Coryza
  6. Conium & Phytolacca in indurations of Glands
  7. Nux  Vomica & Merc Sol in Rectal symptoms
  8. Ammonium  Mur & Bovista in Menstrual disorders
  9. Acetic  Acid  & Apis in Urinary symptoms
  10. Nux. Vom & Pulsatilla in Gastric disorders.
  11. CactG & Digitals in Heart
  12. China and Gels in Fever
  13. Ammonium Mur & Arsenic Iod. in Coryza
  14. Alumina & Platina in GIT
  15. Lycopodium & Gelsemium in Mind
  16. Nux.Moschata & Ambra Gr. in Hysteria
  17. Nat. Mur & Nat Carb. in Headache
  18. Anacardium & Phosphorus in Mental.
  19. Mercuris & Apis Mel in Throat
  20. Apis Mel & Apocynum in Dropsy
  21. Conium & Phytolacca in Glands
  22. Aloes & Podophyllum in Diarrhoea
  23. Ignatia & Lachesis in Throat trouble
  24. Cantharis & Berb. Vul in Renal colic
  25. Ant. Tart & Ipecac in cough
  26. Bryonia & Nux vomica in Constipation
  27. Colocynth & Mag. Phos in Colic
  28. Bryonia & Conium  in Vertigo
  29. Cactus & Gelsemium in Cardiac Manifestation
  30. Ipecac &  Ant. Tart in Respiratory complaints
  31. Veratrum Album & Camphor in Cholera
  32. Puls & Sep in Female
  33. Alumina & Opium in Constipation
  34. Lycopodium & Phosphorus in Respiratory field
  35. Phytolacca and Bromium in Glandular pathology
  36. Acetic acid & Apis Urinary
  37. Ambra gr  & Nat m in mentals
  38. Amm C, Sec C, Bov, Plat Menses.


Differentiate

  1. Opium, Alumina, phos – GIT
  2. Cardiac symptoms of Aur met. Cactus, Dig, Gels
  3. Marasmus of Abrot, BC, NM
  4. Lycopodium & Sepia – Renal colic
  5. Bromium and Ars. Iod – Asthma
  6. Lycopodium & Conium – Urinary disorders
  7. Mercury & Lachesis – Throat complaint
  8. Sepia & Conium – Urinary symptoms
  9. Ammonium mur & Bovista – Mental disorders
  10. Bovista & Ferr Met – Allergies
  11. Gelsemium & Pulsatilla – Fever
  12. Nat  mur & Petroleum  – Skin eruption
  13. Cinchona officinalis & Nat.Carb – Fever

Short Notes

  1. Marasmus – Abrotanum, Bar. C.
  2. Oedema – Apis, Apo, Digit, Cinch
  3. Abdomen – Thuja
  4. Heart – Cactus, Dig
  5. Collapse- Veratrum Alb, Camphor, Carb V
  6. Headache – Nat Mur
  7. Physical generals – Petroleum,  Ferr met
  8. Geriatric Age – Con
  9. Cough – Con
  10. Cholera – Agar
  11. Sexual Disorders – Agnus
  12. Whooping  Cough – Drosera
  13. Rectum – Silicea
  14. Pneumonia – Phos
  15. Liver Symptoms – Chelidonium, Podo
  16. Psychosis – Lach
  17. Constipation – Alumina, Opium, Platina
  18. Asthma – Ars. Alb, Kali. C, CV, AntT., Ip
  19. Eczema – Graphites, Pet
  20. Causation – Conium, RT
  21. Destructive Dimensions – Kali Bich
  22. CNS – Gels, Agar
  23. Suppurations – Sil
  24. Bleeding – Lach
  25. Diarrhoea Podo, Nat S
  26. Eyes – Euph
  27. Typhoid condition – Hyos, Bapt
  28. Food Allergies – Ferr met.
  29. Breast disorders – Con, Phyt, Bor, Bry
  30. Urinary Symp – Apis, Canth, Con, Lyco.
  31. Gastric Symptoms – Nux, Vom, Chel, Bis, Sep, Lyco, Kali Bi, Nat C.
  32. Sciatica – Kali Bichromicum, Colocynth, Magnesium Phosphorus, Phytolacca, Amm mur.
  33. Rheumatism – Causticum, Kali-Carb., Rhus-tox, Pulsatilla, Cal. P., Cimic, Phyt
  34. Dysentry – Merc-Sol., Canth, Kali-Bich, Bryonia, Merc. Cor, Nux-Vomica, Ipecac
  35. Children – Calcium Phosphorus, Silicea, Borax, Chamomilla, Cina, Aeth, Calc, Bar. C.
  36. Fever – Belladonna, Aconite, Arnica, Baptisia, Aethusa, Cinch.
  37. Skin Symptoms – Graphites, Silicea, Bovista, Petroleum, Ars-Iod.
  38. Mentals – Anac, Anacardium, Nat-carb, Platina, Phosphorus, Hellebores, Cantharis, Nat-mur, Aur M, Verat alb
  39. Modalities – Nitric Acid, Dulcamara, Bapt-Tinct., Colchicum, Chel, Aco, Cal. P.
  40. Respiratory symptoms – Antim tart, Carbo veg, Ipecac, Hepar Sulph, Amm C, Dros, Ars I, Bromium, Lyc, Spong, Phos, Ars Alb
  41. Causation and modalities – Lycopodium, Colocynth, Spon, Phos, Nat M.
  42. Anacardium – Split Personality
  43. Platina – Lilliputian hallucination.
  44. Sulphur – Personality

Full Questions

  1. Describe drug picture under following heading: Constitution, Physical generals, Causation, Mentals, Modalities, and Characteristic Particulars.
  2. Calc-carb, Baryta-carb, Phosphorus, Ferrum-met, Aconitum Napellus, Opium, Platina, Sepia, Sul.
  3. Leading Indications:-
  4. Actea Racemosa
  5. Agnus Castus
  6. Chelidonium
  7. Ammonium Carb
  8. Nitric acid
  9. Causticum
  10. Calc. F.
  11. Pulsatilla
  12. Phosphorus
  13. Platina
  14. Merc. Sol
  15. Calc. Ars.
  16. Secale Cor
  17. Ignatia
  18. Opium
  19. Lyco
  20. Lachesis
  21. Arg nit
  22. Ars alb.
  23. Hyos
  24. NV
  25. Describe the drug picture of Lachesis or Lycopodium and give important differentiating features of them in a tabular form. Compare & contrast : mentals, Reproductive, throat
  26. Describe in detail the Drug picture of SEPIA and compare with PULSATILLA. Give the main generalities of each and their differentiating points in mentals.
  27. Describe the leading indications of Sepia an Platina and differentiate them in mentals and rectal symptoms
  28. Give briefly the general sphere of action of Pulsatilla and how will you differentiate it in general with Nux-vomica
  29. Give broad generalisation of: Natrum mur and Silicea and give their differentiation
  30. Give broad generalisation of Sepia and NatM and give their differentiation.
  31. Give broad generalisation of Lycopodium and Lachesis and give their differentiation
  32. Give broad generalisation of Sepia and Nux-Vomica and give their differentiation.

Compare:

  1. Nux-Vom and Sepia
  2. Canth and Apis M.
  3. Lycopodium and Lachesis
  4. Give the Pathophysiology of Opium
  5. Describe leading indication of Lyco & NV & Compare & Contrast them in mentals, renal, GIT.
  6. Give only five leading indications each of Apis, Belladonna. Compare and Contrast them with Mentals, Urine, Stool, Females.
  7. Give only five leading indication each of Gelsemium and Bryonia. Compare and Contrast them with three indication of Head, Throat, Female Extremities

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Apr 27 2008

MATERIA MEDICA QUESTION SET-1

MATERIA MEDICA QUESTION SET-1

Full Questions

Give the “Drug Picture” of the following drugs:

  1. Arsenic alb
  2. Aurum met
  3. Bryonia
  4. Baryta carb
  5. Calc.C.
  6. Carbo veg
  7. Causticum
  8. Graphites
  9. Gelsemium
  10. Kali carb
  11. Lachesis
  12. Lycopodium
  13. Merc sol
  14. Nux vom
  15. Natrum mur
  16. Nitric acid
  17. Pulsatilla
  18. Rhus tox
  19. Sulphur
  20. Silica
  21. Thuja

Short Notes

Give the Generalities of

  1. Bryonia
  2. Cina
  3. Lycopodium
  4. Nitric acid
  5. Sulphur

Give the Leading Indications of:

  1. Arsenic alb
  2. Ant. Crud
  3. Ant. Tart
  4. Argentum nit
  5. Abrotanum
  6. Aethusa
  7. Baryta carb
  8. Calc. Carb.
  9. Causticum
  10. Carbo veg
  11. Graphites
  12. Ipecac
  13. Kali carb
  14. Lycopodium
  15. Natrum mur
  16. Nitric acid
  17. Pulsatilla
  18. Rhus tox
  19. Sulphur
  20. Thuja
  21. Baptisia

Other Short Notes

  1. Give the leading indications of Kali bi & compare Merc c. Merc.s & Nux v in dysentry
  2. Give the guiding indications of Bell & compare delirium of Bell., Hyosc., & Verat alb
  3. Climacteric irritability of Lachesis & compare it with Puls
  4. Indicate finer composition of Graphites & Silicea & differentiate their skin symptoms
  5. Write the mental, physical generals & modalities of Kali carb, Lachesis, Ars alb.
  6. Explain Baryta carb is an idiotic child
  7. Thuja is king of sycotic
  8. Ant. Tart. is a death rattle
  9. Causticum is an important consideration in paralysis

Give Biochemic indications of these drugs

  1. Calc Flour
  2. Calc Phos
  3. Calc Sulph
  4. Ferr Phos
  5. Kali Mur
  6. Kali Phos
  7. Kali Sulph
  8. Mag Phos
  9. Nat Mur
  10. Nat Phos
  11. Nat Sulph
  12. Silicea
  13. Give Biochemic indications of Kali mur in upper respiratory tract infection, Nat phos in gastric complaints
  14. Nat phos in allergic disorders
  15. Mag phos in colic
  16. Ferr phos in fever

Compare & contrast:

  1. Puls & Nat mur in mentals
  2. Arnica & Ledum in trauma
  3. Baryta C & Cal C in children disorders
  4. Ipecac Ant tart in respiratory disorders
  5. Ant C & Puls in gastric complains
  6. Nitric acid & Aesc in rectal complaints
  7. Colo & Mag phos in colic
  8. Carbo veg & Sec cor in collapse
  9. Borax & Nitric acid in mouth complaints.
  10. Biochemic & homoeopathic system of medicine
  11. Aconite & Ars alb in mentals
  12. Arnica & Rhus tox in injuries
  13. Spongia & Drosera in cough
  14. Hepar S & Merc s. in throat complaints
  15. ArsA & Apis in skin-mucus membrane.
  16. Bryonia & Rhus tox in joint pains
  17. Graph & Sulphur in skin disorder
  18. Aconite & Bell in fevers

Give indications of:

  1. Urinary symptoms: Apis, Berb V, Lyco
  2. Fever: Aconite, Bell, Bapt, Gels, Hell, Hyos, Puls, Nux V
  3. Injuries: Arn, Calendula, Rhus T
  4. Female disorders :Kali C, puls, Sec C
  5. Diarrhoea: Aloe, Podo
  6. Gastric complaints: Arg N, Ant C, Aeth, China, Ipec, Sulp.
  7. Irritability: Cina Cham
  8. Tenesmus/Dysentry :Merc cor
  9. Colic :Colo
  10. Pain: Aco, Cham, Ledum
  11. Catarrhal symptoms :Allium c, Euph
  12. Respiratory symptoms: Amm c, Ant t, Allium c, Dulc, Drosera, Ipec, Kali bi
  13. Cough: Spongia, Drosera
  14. Coryza: Euphr
  15. Rheumatism: Colch, Ledum, Puls, Rhus t
  16. Joint involvement: Caust, Ledum, Puls, Rhus t
  17. Skin(Mucous membrane):Apis, Ars, Graph, Hepar s, Nit acid, Sil, Sec C, Thuj
  18. Rectal complaints: Aloe, Aesc, Graph, Nit acid
  19. Piles: Aesc, Ign
  20. Headache: Bry, Sil.
  21. Collapse: Verat alb
  22. Oral cavity: Merc sol
  23. Dentition: Podo
  24. Eye symptoms: Euphr
  25. Child: Ant c, Abrot, Cina, Calc c, Cham
  26. Child milestones: Baryta c
  27. Destructive dimensions: Kali bi, Merc s
  28. Causation(A/F):Caust, Calc c
  29. S.O.A: Calendula, Kali c
  30. Modalities: Bry, Borax, Caust, China, Calc C, Merc S, Thuja
  31. Antidote: Bell, Ipec
  32. Delirium: Nat mur, Thuja, Bell, Bry
  33. Sensation as if: Thuja, Verat alb, Ign
  34. Insanity: Arg nig, Aurum met, Hyosc, Kali phos, Lach, Lyco, Nit acid,
  35. Mentals: Puls, Sulph, Thuja

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