MEDICAL ALMIGHTY

Study Shows Poor Hearing May Cause False-Positive Results on Cognitive Tests

noreply@blogger.com (DevilX) — Sat, 06 Aug 2011 13:04:00 +0000

July 21, 2011 (Paris) -- If you're going to take your elderly parents in for a memory checkup, you may want to have their hearing tested first.

So suggest researchers who found that a substantial number of people may have false-positive results on cognitive tests designed to detect dementia due to undiagnosed hearing problems.

"A hearing test should be imperative prior to cognitive testing," says study researcher Michael Lerch, MD, of Diakonia Mark-Ruhr Hospital in Hagen, Germany.

Hearing problems can be overlooked, especially if they are mild, says William Thies, PhD, chief medical and scientific officer at the Alzheimer's Association.

"Just missing one word can distinctly affect performance on a cognitive test, particularly if it's done in a hurried fashion," he tells WebMD.

Thies' advice: If dementia is suspected, make sure cognitive testing is performed by a doctor with experience treating Alzheimer's disease patients.

Hearing Loss and Dementia

It's not uncommon for hearing loss and dementia to coexist, Lerch says. One in eight people over age 65 have dementia. And more than half of people over age 70 have hearing loss, he says.

The new study involved 1,600 patients in a geriatric practice. About 900 had scores suggestive of dementia on the Mini-Mental State Exam, a brief test of cognitive skills, including attention span and memory. Then, patients underwent hearing testing, with treatment if needed.

One-third of those with possible dementia were found to have a relevant hearing impairment and showed an improvement in cognitive testing results after treatment, Lerner reports.

The findings were presented here at the Alzheimer's Association International Conference 2011.

About 5.4 million Americans and 35 million people worldwide have Alzheimer's disease, the most common form of dementia.

What Is Astigmatism?

noreply@blogger.com (DevilX) — Fri, 05 Aug 2011 04:45:00 +0000

Astigmatism is a common eye condition that's easily corrected by eyeglasses, contact lenses or surgery.

Astigmatism is characterized by an irregular curvature of the cornea. This is one type of refractive error. Astigmatism occurs in nearly everybody to some degree. For significant curvature, treatment is required.

A person's eye is naturally spherical in shape. Under normal circumstances, when light enters the eye, it refracts evenly, creating a clear view of the object. However, the eye of a person with astigmatism is shaped more like a football or the back of a spoon. For this person, when light enters the eye it is refracted more in one direction than the other, allowing only part of the object to be in focus at one time. Objects at any distance can appear blurry and wavy.

What Causes Astigmatism?

Astigmatism can be hereditary and is often present at birth. It can also result from pressure from the eyelids on the cornea, incorrect posture or an increased use of the eyes for close work.

What Are the Symptoms of Astigmatism?

People with undetected astigmatism often experience headaches, fatigue, eyestrain andblurred vision at all distances. While these symptoms may not necessarily be the result of astigmatism, you should schedule an eye exam if you are experiencing one or more symptoms.

Allergy facts

noreply@blogger.com (DevilX) — Mon, 01 Aug 2011 05:47:00 +0000

Allergy facts

Allergy involves an exaggerated response of the immune system.
The immune system is the body's organized defense mechanism against foreign invaders, particularly infections.
Allergens are substances that are foreign to the body and can cause an allergic reaction.
IgE is the allergy antibody.
Allergies can develop at any age.
Your risk of developing allergies is related to your parents' allergy history.

Introduction

In this review you will learn how allergy relates to the immune system. You will begin understanding how and why certain people become allergic. The most common allergic diseases are discussed briefly in this article.

What does an allergy mean?

An allergy refers to an exaggerated reaction by our immune system in response to bodily contact with certain foreign substances. It is exaggerated because these foreign substances are usually seen by the body as harmless and no response occurs in non- allergic people. Allergic people's bodies recognize the foreign substance and one part of the immune system is turned on. Allergy-producing substances are called "allergens." Examples of allergens include pollens, dust mite, molds, danders, and foods. To understand the language of allergy it is important to remember that allergens are substances that are foreign to the body and can cause an allergic reaction in certain people.

When an allergen comes in contact with the body, it causes the immune system to develop an allergic reaction in persons who are allergic to it. When you inappropriately react to allergens that are normally harmless to other people, you are having an allergic reaction and can be referred to as allergic or atopic. Therefore, people who are prone to allergies are said to be allergic or "atopic."

Austrian pediatrician Clemens Pirquet (1874-1929) first used the term allergy. He referred to both immunity that was beneficial and to the harmful hypersensitivity as "allergy." The word allergy is derived from the Greek words "allos," meaning different or changed and "ergos," meaning work or action. Allergy roughly refers to an "altered reaction." The word allergy was first used in 1905 to describe the adverse reactions of children who were given repeated shots of horse serum to fight infection. The following year, the term allergy was proposed to explain this unexpected "changed reactivity."

Allergy Fact

It is estimated that 50 million North Americans are affected by allergic conditions.

The cost of allergies in the United States is more than $10 billion dollars yearly.

Allergic rhinitis (nasal allergies) affects about 35 million Americans, 6 million of whom are children.

Asthma affects 15 million Americans, 5 million of whom are children.

The number of cases of asthma has doubled over the last 20 years.

What causes allergies?

To help answer this question, let's look at a common household example. A few months after the new cat arrives in the house, dad begins to have itchy eyes and episodes of sneezing. One of the three children develops coughing and wheezing, especially when the cat comes into her bedroom. The mom and the other two children experience no reaction whatsoever to the presence of the cat. How can we explain this?

The immune system is the body's organized defense mechanism against foreign invaders, particularly infections. Its job is to recognize and react to these foreign substances, which are called antigens. Antigens are substances that are capable of causing the production of antibodies. Antigens may or may not lead to an allergic reaction. Allergens are certain antigens that cause an allergic reaction and the production of IgE.

The aim of the immune system is to mobilize its forces at the site of invasion and destroy the enemy. One of the ways it does this is to create protective proteins called antibodies that are specifically targeted against particular foreign substances. These antibodies, or immunoglobulins(IgG, IgM, IgA, IgD), are protective and help destroy a foreign particle by attaching to its surface, thereby making it easier for other immune cells to destroy it. The allergic person however, develops a specific type of antibody called immunoglobulin E, or IgE, in response to certain normally harmless foreign substances, such as cat dander. To summarize, immunoglobulins are a group of protein molecules that act as antibodies. There are five different types; IgA, IgM, IgG, IgD, and IgE. IgE is the allergy antibody.

(In 1967, the husband and wife team of Kimishige and Teriko Ishizaka detected a previously unrecognized type of immunoglobulin in allergic people. They called it gamma E globulin or IgE.)

In the pet cat example, the dad and the youngest daughter developed IgE antibodies in large amounts that were targeted against the cat allergen, the cat dander. The dad and daughter are now sensitized or prone to develop allergic reactions on subsequent and repeated exposures to cat allergen. Typically, there is a period of "sensitization" ranging from months to years prior to an allergic reaction. Although it might occasionally appear that an allergic reaction has occurred on the first exposure to the allergen, there must have been a prior contact in order for the immune system to be poised to react in this way.

IgE is an antibody that all of us have in small amounts. Allergic persons, however, produce IgE in large quantities. Normally, this antibody is important in protecting us from parasites, but not from cat dander or other allergens. During the sensitization period, cat dander IgE is being overproduced and coats certain potentially explosive cells that contain chemicals. These cells are capable of causing an allergic reaction on subsequent exposures to the dander. This is because the reaction of the cat dander with the dander IgE irritates the cells and leads to the release of various chemicals, including histamine. These chemicals, in turn, cause inflammation and the typical allergic symptoms. This is how the immune system becomes exaggerated and primed to cause an allergic reaction when stimulated by an allergen.

On exposure to cat dander, the mom and the other two children produce other classes of antibodies, none of which cause allergic reactions. In these non-allergic members of the family, the dander particles are eliminated uneventfully by the immune system and the cat has no effect on them.

Figure 1

The Immune System Foreign Substance alt="-" (cat dander, pollen, virus, bacteria)

Normal Immune Response IgM, IgG, IgA, IgD and various immune cells respond to attack.		Exaggerated Immune Response IgE is overproduced in response to cat dander, pollens, and other harmless allergens.

Foreign substance is eliminated.		Subsequent exposure results in an allergic reaction.

Non-Allergic Individual		Allergic Individual

Who is at risk and why?

Allergies can develop at any age, possibly even in the womb. They commonly occur in children but may give rise to symptoms for the first time in adulthood. Asthma may persist in adults while nasal allergies tend to decline in old age.

Why, you may ask, are some people "sensitive" to certain allergens while most are not? Why do allergic persons produce more IgE than those who are non-allergic? The major distinguishing factor appears to be heredity. For some time, it has been known that allergic conditions tend to cluster in families. Your own risk of developing allergies is related to your parents' allergy history. If neither parent is allergic, the chance that you will have allergies is about 15%. If one parent is allergic, your risk increases to 30% and if both are allergic, your risk is greater than 60%.

Although you may inherit the tendency to develop allergies, you may never actually have symptoms. You also do not necessarily inherit the same allergies or the same diseases as your parents. It is unclear what determines which substances will trigger a reaction in an allergic person. Additionally, which diseases might develop or how severe the symptoms might be is unknown.

Another major piece of the allergy puzzle is the environment. It is clear that you must have a genetic tendency and be exposed to an allergen in order to develop an allergy. Additionally, the more intense and repetitive the exposure to an allergen and the earlier in life it occurs, the more likely it is that an allergy will develop.

There are other important influences that may conspire to cause allergic conditions. Some of these include smoking, pollution, infection, and hormones.

What are common allergic conditions, and what are allergy symptoms and signs?

The parts of the body that are prone to react to allergies include the eyes, nose, lungs, skin, and stomach. Although the various allergic diseases may appear different, they all result from an exaggerated immune response to foreign substances in sensitive people. The following brief descriptions will serve as an overview of common allergic disorders.

Claudication

noreply@blogger.com (DevilX) — Sun, 31 Jul 2011 14:03:00 +0000

Claudication is pain and/or cramping in the lower leg due to inadequate blood flow to the muscles. The pain usually causes the person to limp. The word "claudication" comes from the Latin "claudicare" meaning to limp. Claudication typically is felt while walking, and subsides with rest. It is commonly referred to as "intermittent" claudication because it comes and goes with exertion and rest. (In severe claudication, the pain is also felt at rest.)

What causes claudication?

Several medical problems can cause claudication, but the most common is peripheral artery disease. Peripheral artery disease (PAD) is caused by atherosclerosis, which is a hardening of the arteries from accumulation of cholesterol plaques form on the inner lining of the arteries. This is especially common at branching points of the arteries in the legs. Blockage of the arteries from these plaques cause low blood flow to the muscles in the legs. When walking or exercising the muscles in the legs require more blood flow to increase oxygen to the cells. Atherosclerotic plaques cause decreased blood flow and decreased oxygen. The muscles of the legs can ache and burn as a result of inadequate oxygen. This is felt as cramping in the legs.

What are the symptoms of claudication?

Pain and cramping in the legs is the main symptom of claudication. Pain can be sharp or dull, aching or throbbing, or burning. The severity of the peripheral artery disease, the location of the plaque, and the activity of the muscles determine the severity of symptoms and location of pain. Calf pain is the most common location for leg cramps. This is because the atherosclerotic plaques often begin in the arteries farthest from the heart. If the blockage or plaque formation is farther up the leg, the pain from claudication may be in the thigh. If the blockage is in the aorta (the main artery from the heart to the legs) then symptoms may include pain in the buttocks, groin, or erectile dysfunction.

Why does claudication come and go?

The usually intermittent nature of the pain of claudication is due to a temporary inadequate supply of oxygen to the muscles of the leg. The poor oxygen supply is a result of narrowing of the arteries that supply the leg with blood. This limits the supply of oxygen to the leg muscles and is especially noticeable when the oxygen requirement of these muscles rises with exercise or walking. Claudication that comes and goes is often referred to as intermittent claudication.

What can cause the artery narrowing that leads to claudication?

Intermittent claudication can be due to temporary artery narrowing due to spasm of the artery (vasospasm), permanent artery narrowing due to atherosclerosis, or from the complete blockage of an artery of the leg.

Who typically is affected by claudication?

Intermittent claudication is more common in men than in women. The condition affects 1%-2% of the population under 60 years of age, increasing in incidence with age, to affect over 18% of persons over 70 years of age, according to the American Academy of Family Physicians.

What are the risk factors for claudication and peripheral vascular disease?

Risk factors for peripheral artery disease and claudication include:

Smoking
Diabetes
High blood pressure
High cholesterol
African American descent
Heart disease

How is claudication diagnosed?

A physician will take a history and the diagnosis will be based on the patient's symptoms.

Testing for claudication may include:

Ultrasound is most commonly used to determine location and severity of the narrowing in the blood vessels.
Ankle-arm index measures the blood pressure at the ankle compared with the blood pressure in the arm. An abnormal result is an indication of peripheral artery disease.
Segmental blood pressure measures blood pressure in different parts of the leg (calf, low thigh, high thigh) to detect a blockage that is causing decreased blood flow.
Computed tomography (CT) and magnetic resonance angiography(MRA) are other noninvasive tests that can help a doctor map the blood flow in the affected areas. These tests may be considered if the patient's doctor thinks that a procedure (revascularization) to treat peripheral artery disease may be helpful.

What is the treatment for claudication?

There are two main ways to treat claudication: medication and a surgical treatment, called revascularization.

Medication therapies are often used initially as they are non-invasive. The two most commonly used medications include:

Cilostazol (Pletal) reduces the pain of intermittent claudication by widening (dilating) the arteries, thereby improving the flow of blood and oxygen to the legs.
Pentoxifylline (Trental) decreases the "stickiness" (viscosity) of blood and thereby improves its flow through arteries. This increases the flow of blood and oxygen to muscles.

A surgical procedure called a revascularization is used in patients who do not respond to medications. There are two types of revascularization procedures: endovascular (inside the blood vessel) and surgically grafting or bypassing the artery.

Endovascular procedures include
- Angioplasty: A balloon is placed in the blocked area and inflated to widen the diameter of the artery and increase blood flow
- Stenting: Wire mesh used to hold a blood vessel open after angioplasty and prevents scar tissue from narrowing the blood vessel
Surgical grafting or bypassing an artery involves an open surgery with an incision and sewing in a graft using either the patient's vein or a synthetic tube to increase blood flow around the blocked area.
Can claudication be prevented?
Some of the risk factors for claudication are behaviors that can be modified such as:
- quit smoking,
- managing diabetes and high blood pressure, and
- maintaining a healthy diet to keep cholesterol levels normal.
Medications that help thin the blood can be used to help prevent symptoms of claudication, but they do not treat the underlying cause. Medications include:
- aspirin,
- clopidogrel (Plavix),
- ticlopidine (Ticlid), and
- dipyridamole (Permole, Persantine, Aggrenox).
Exercise is recommend for patients with claudication symptoms. Frequent exercise, especially walking, greatly reduces symptoms and increases symptom-free walking distance and is one of the most effective preventive measures.
What is the prognosis and treatment for patients with intermittent claudication?
The prognosis of claudication is generally favorable with treatment. Without treatment, 26% of patients worsen over time. Over 5 years, 4% to 8% will progress to require a revascularization procedure.
The underlying cause of claudication, peripheral vascular disease, does put patients at risk for other atherosclerotic diseases. A finding of claudication or peripheral artery disease should be considered a warning sign of other potential atherosclerotic blockages in the body.

Predicting Who Will -- and Won't -- Survive a Heart Attack

noreply@blogger.com (DevilX) — Sun, 31 Jul 2011 13:41:00 +0000

-- It may be possible to predict who will survive or die as the result of a first heart attack, researchers have found.

They analyzed data from more than 18,000 people in two of the largest U.S. cardiovascular studies and pinpointed certain traits that could predict the risk that a heart attack would be fatal. Those traits included having high blood pressure, being black and having a very high body mass index (BMI) -- a measurement based on height and weight.

"For some people, the first heart attack is more likely to be their last," lead author Dr. Elsayed Z. Soliman, director of the Epidemiological Cardiology Research Center (EPICARE) at Wake Forest Baptist Medical Center, said in a center news release. "For these people especially, it is important that we find ways to prevent that first heart attack from ever happening because their chances of living through it are not as good."

Among the researchers' findings:

Blacks are at higher risk than non-blacks of sudden cardiac death, in which the heart suddenly stops beating, but are at less risk of coronaryheart disease.
High blood pressure and increased heart rate were stronger predictors of sudden cardiac death than coronary heart disease.
Extreme high or low BMI was predictive of increased risk of sudden cardiac death, but not of coronary heart disease.
Certain markers that can be identified by doctors evaluating patients' electrocardiograms (ECGs) are associated with increased risk of sudden cardiac death.

The study was released online July 20 in advance of publication in an upcoming print issue of the journal Heart.

If the findings are validated and confirmed in future research, doctors will be able to identify patients who are at greater risk of dying if they suffer a heart attack and prescribe ways to reduce their risk, Soliman said.

What is insomnia and what causes it?

noreply@blogger.com (DevilX) — Sun, 31 Jul 2011 13:37:00 +0000

Insomnia is difficulty in falling or staying asleep, the absence ofrestful sleep, or poor quality of sleep. Insomnia is a symptom and not a disease. The most common causes of insomnia are:
- medications,
- psychological conditions (for example, depression,anxiety),
- environmental changes (travel, jet lag, or altitude changes), and
- stressful events or a stressful lifestyle.
Insomnia can also be caused by poor sleeping habits such as excessive daytime naps orcaffeine consumption and poor sleep hygiene.
The National Center for Sleep Disorders Research at the National Institutes of Health estimates 30%-40% of adults report some symptoms of insomnia each year, and about 10%-15% report they have chronic insomnia.
Insomnia may be classified by how long the symptoms are present.
- Transient insomnia usually is due to situational changes such as travel, extreme climate changes, and stressful events. It lasts for less than a week or until the stressful event is resolved.
- Short-term insomnia usually is due to ongoing stressful lifestyle or events, medication side effects or medical conditions and lasts for one to three weeks.
- Chronic insomnia (long-term insomnia) often results from depression, digestive problems, sleep disorders, or substance abuse and continues for more than three weeks.
Transient insomnia may progress to short-term insomnia and without adequate treatment, and short-term insomnia may become chronic insomnia.
Among the medications and substances that can contribute to insomnia are:
caffine and coffee,
tobacco,
alcohol,
decongestants (for example, pseudoephedrine),
diuretics (for example, furosemide [Lasix], hydrochlorothiazide[Dyazide]) especially if taken in the evening or at bedtime,
antidepressants (for example, bupropion [Wellbutrin, Wellbutrin SR, Wellbutrin XL, Zyban], fluoxetine [Prozac]),
appetite suppressants (for example, sibutramine [Meridia], phentermine[Fastin]), and
amphetamines.

Insomnia also may be the result of withdrawal from:

benzodiazepines (for example, diazepam [Valium], chlordiazepoxide[Librium], lorazepam [Ativan]),
alcohol,
antihistamines,
amphetamines,
cocaine,
marijuana, and
other addicting drugs.

Insomnia can also result from poor sleep-related habits (poor sleep hygiene).

Fracture facts

noreply@blogger.com (DevilX) — Sun, 31 Jul 2011 13:33:00 +0000

Bone fracture, broken bone, bone crack all mean he same thing. The bone has been damaged such that. None of these terms indicate the severity of the bone damage.
Bones are the body's storage place for calcium. Under hormone control, calcium content of bone is constantly increasing or decreasing.
Bones break when they cannot withstand a force or trauma applied to them. Sometimes the bones are so weak that force may be just gravity, like compression fractures of the back in the elderly.
Fracture descriptions help explain how the breakage appears. For examples, whether or not the fragments are aligned (displaced fracture) and whether or not there is skin overlying the injury is damaged (compound fracture).
Fractures may be complicated by damage to nearby blood vessels, nerves and muscles and joints.
Children's fractures may be more difficult to diagnose because their bones lack enough calcium to be seen on X-ray and because growth plates in the bones may disguise or hide the fracture.
Diagnosis of a fracture includes a history and physical examination. X-rays are often taken. Occasionally, CT or MRI is used to find an occult or hidden fracture or provide more information regarding the damage to the bone and adjacent tissues.
Fractures of the skull, spine and ribs have their own unique diagnosis and treatment issues.

Introduction to fracture

Bones form the skeleton of the body and allow the body to be supported against gravity and to move and function in the world. Bones also protect some body parts, and bone marrow is the production center for blood products.

Bone is not a stagnant organ. It is the body's reservoir of calcium and is always undergoing change under the influence of hormones. Parathyroid hormone increases blood calcium levels by leeching calcium from bone, while calcitonin has the opposite effect, allowing bone to accept calcium from the blood.

What causes a fracture?

When outside forces are applied to bone it has the potential to fail. Fractures occur when bone cannot withstand those outside forces. Fracture, break, or crack all mean the same thing. One term is not better or worse than another. The integrity of the bone has been damaged and the bone structure fails and a fracture occurs.

Broken bones hurt for a variety of reasons including:

The nerve endings that surround bones contain pain fiber. These fibers may become irritated when the bone is broken or bruised.
Broken bones bleed, and the blood and associated swelling (edema) causes pain.
Muscles that surround the injured area may go into spasm when they try to hold the broken bone fragments in place, and these spasms may cause further pain.

Often a fracture is easy to detect because there is obvious deformity. However, at times it is not easily diagnosed. It is important for the physician to take a history of the injury to decide what potential problems might exist. Moreover, fractures don't always occur in isolation, and there may be associated injuries that need to be addressed.

Fractures can occur because of direct blows, twisting injuries, or falls. The type of forces or trauma applied to the bone may determine what type of injury that occurs. Some fractures occur without any obvious trauma due toosteoporosis, the loss of calcium in bone (for example a compression fracture of the vertebrae of the back).

Descriptions of fractures can be confusing. They are based on:

Where in the bone the break has occurred
How the bone fragments are aligned
Whether any complications exist
Whether the skin is intact

The first step in describing a fracture is to decide if it is open or closed. If the skin over the break is disrupted, then an open fracture exists. The skin can be cut, torn, or abraded (scraped), but if the skin's integrity is damaged, the potential for an infection to get into the bone exists. Since the fracture site in the bone communicates with the outside world, these injuries often need to be cleaned out aggressively and many times require anesthesia in the operating room to do the job effectively. Compound fracture was the previous term used to describe an open fracture.

Next, there needs to be a description of the fracture line. Does the fracture line go across the bone (transverse), at an angle (oblique) or does itspiral? Is the fracture in two pieces or is it comminuted, in multiple pieces?

A greenstick fracture describes the situation when the bone partially breaks. This often occurs in infants and children where the bone hasn't completely calcified and has the potential to bend instead of breaking completely through. It is similar to trying to break off a young branch or shoot from a tree (a green stick). Other fracture terms include torus or buckle fracture, again when only part of a bone breaks, but this may occur in adults as well.

Finally, the fracture's alignment is described as to whether the fracture fragments are displaced or in their normal anatomic position. If the bones fragments aren't in the right place, they need to be reduced or placed back into their normal alignment.

ALL INDIA MEDICAL PG QUESTIONS 2008

noreply@blogger.com (DevilX) — Sun, 31 Jul 2011 13:25:00 +0000

1. Paclitaxel-- increase microtubule polymerisation
2. amyloidosis in dialysis---Beta 2 microglobin
3. Vibrio cholera 0139--- does not have 01 antigen
4. SYPHILITIC Aortitis-- calcification of ascending aorta
5. m.c. seizure in neonate---Subtle seizure
6. Crypt abscess-ulcerative colitis
7. MOA Clomiphene---INHIBIT NEGATIVE FEEDBACK OF estrogen
8. -BEST VIEW FOR c1 c2 fracture- Odontoid veiw
9. Cervix cancer- hpv
10. MC CAUSE OF Maternal mortality- haemorrhage

11. DOC FOR Cml-imitanib
12. MC PANCREATIC TUMOR IN Men-1 -- gastrinoma
13. FUNCTION OF Apolipoprotein c --- lipoprotein lipase activator
14. INV OF CHOICE FOR Interstitial lung ds- hrct
15. Ab IN Cold autoimmune hemolytic anemia-donath landsteiner
16. Torsion testis A/E—GIVE ANTIBIOTIC & CONSERVATIVE T/T
##17. Probiotics- used in necrotising enterocolitis (WHAT WERE THE OTHR OPTIONS?)
18. Spermatogenesis ---require low temp
19. Erythropoetin--- does not cause reticulocytopenia
20.m.c. cause Puberty delay - constitutional

21. Ear ossicle joint- synovial
22. Basement membrane degeneration- metalloproteinase
23. Synovial sarcoma translocation- t(x-18)
24. Hodgkin ds - cd15,30
25. Hmp shunt- no atp
26. Psychrometer- humidity
27. Pancytopenia with cellular bone marrow-cong dyserythropoetic anaemia
28. Penicillin in pseudomonas- piperacillin
29. Bacterial index/dharmendhra--- leprosy/dharmendra
30. Thyroid cancer m.c. - papillary

31. Hmb 45 - melanoma
32. Lepra-2 REACTION treatment OF CHOICE - steroids
33. Okazaki fragment-- ds dna replicatiom
34. Diffuse axonal injury- white matter lesions AT GREY WHITE INTERFACE
35. Vitamin b12 and folic acid given together because-- folic alone unmask neurotoxicity
36. Yaws- not sexually transmitted
37. P53a/e- wild type causes cancer
38. Phase 2 clinical trial IS FOR - efficacy
39. Flumazenil- benzodiazepine antagonist
40. EARLIEST SIGN OF Puberty IN girl - thelarche braest bud

41. NOT A Zoonosis - hiv
42. Rib notching- coarctation of aorta
43. NEONATAL Alveolar proteinosis (REPEAT q FROM NOV AIIMS )
44. diaghragmatic hernia –INSERTION OF NASOGATRIC TUBE(SPEED IS WRONG IN THIS q)
45. Volvulus A/E- sigmoidoscopy is C/I
46. Biliary obstruction-not by ancyclostoma duodenale
47. Henoch schonlein purpura-girl with purpura and abdominal symptoms
48. Genetic imprinting
49. Drug contraindicated in renal failure-streptomycin
50. female with acantholysis--Pemphigus vulgaris

51. aml Worse prognosis- monosomy 7
52. Prion -infectious
53. Prion- most resistant to sterilisation
54. Vaccine c/I in pregnancy-mmr
55. low vision who--6/18 to 3/60
56. Soil borne a/e - brucella
57. Sarcoidosis- band keratopathy
58. Ferruginous body- asbestosis
59. Pick disease- tau
60. LEAST RECUURENCE RATE IN Enuresis-alarm THERAPY

61. Golgi body--- cell compartment decider
62. Ipratropium bromide c/i- urinary retention
63. Vein in paraduodenal fossa- inferior mesentric
64. 55 yr with uterine atypia- hysterectomy
65. Saturated fatty acids- palm oil
##66. Bilateral torticollis, heterotopic calcification A/E-prognosis IS GOOD
67. NOT A SIDE EFFECT OF Tacrolimus- hirsutism
##68. Hirscprung, no meconium for 48 hrs- MANOMETRY
69. bp measured by spyghmomanometer—DIRECTL Y PROPERTIONAL TO VELOCIT OF BLOOD
70. T/T OF Bartholin abscess- EXCISON(REPEAT FROM PRETEST)
71. Fatty yellow liver- arsenic
72. MC ASSOSIATED ANOMALY WITH Coarctation of aorta- bicuspid valve
73. Resistant malaria-drug used doxycycline (REF-HARRISON)
74. Torsades de pointes- quinine
75. Alkalisation of urine -BARBITURATE
76. epispadias ASSOSIATED WITH-SEPRATION OF Symphysis pubis-
77. Nigro protocol- ONLY anal chemoradiation IN PLACE OF SURGERY
##78. PRETERM Induction of labour- a/e heart ds
79. SyntoMETRIN- not given in heart ds
80. Isotretinoin used in acute promyelocytic leukemia
81. Sensory supply from masseter goes to - mesencephalic nucleus
82. Lachman test- BEST FOR acute knee injury
83. Crohn disease- mycobacterium PARA TB
84. Pollicisation- thumb reconstruction FROM FINGER
85. Leukovorin-methotrexate
86. Mullerian dysgenesis a/e- absent ovary
87. Antiphospholipid syndrome a/e-PANCYTOPENIA
88. Glucose 6 phosphate breaking enzyme absent in- muscle
89. Von-gierke disease
90. Biologically active calcium is- ionised

91. Isolation use in- pneumonic plague
92. HYPERLUCENCY ON X-RAY & OBSTRUTIVE PATTERN-Bronchiolitis obliterans
93. Stabilises new clot- factor 13
##94. Placenta accreta m.c predisposing factor--- previous c.s. scar /CURRETAGE/PLACENTA PREVIA

95. post partum haemorrhage--not used mifepristone
##96. ABOUT Rubella A/E-pda IS THE MOST COMMON CONGENITAL ANOMALY(DEAFNESS IS MC,BUT CONTROVERSY ABOUT SEX RATIO ALSO PERSISTS)
97. Protein synthesis inhibitor- tetracycline
[snip]. Thymoma - myasthenia gravis
99. Most common site for bone graft- iliac crest
#100. Allergic fungal sinusitis—ORBITAL PENETRATION

##101. Rh factor is- MUCOPOLYSACCHRIDE
102. Water soluble vitamin- folic acid
103. Streptococcos antigen shared with synovium - hyaluronic acid
104. Photoelectric effect--outermost electron
105. Live vaccines-2 cannot be given together
106. Normal heart-denervation leads to tachycardia
107. Neck penetrating trauma--platysma breach
108. Nasal septum- no lacrimal bone
109. Growth factor like protooncogene- sis
110. Posterior mediastinal tumour- neuroenteric cyst
111. Therapeutic index-safety
112. Persistent hyperplastic primary vitreous--patau
113. Enterococci a/e- sensitive to penicillin
114. Death due to suffocation in a/e - throttling
115. Drug of choice for supraventricular tachycardiaVERAPRAMIL
##116. Retinoblastoma with second primary osteosarecoma D/T A/E- P53 MUTATION>CHEMOTHERAPY
117. Triple response-Axon reflex
118. Congenital nephrotic syndrome mutation- nephrin
119. Pneumocystis jevorici-- affects only immunocompromised >CULTURED FROM SPUTUM
120. MC CAUSE OF Ocular morbidity in india – REFRACTIVE ERROR
##121. Alcoholic with acute pancreatitis with stone IN DISTAL PANCREATIC DUCT- DISTAL PANCREATECTOMY/LONGITUDNAL P.J./ENDOSCOP????????????????

##122. Fat lady asymptomatic cholecystitis with stone with dyspepsia- LAP CHOLEY AFTER2 MONTH /T/T WITH IV ANALGESIC WHEN PAIN OCCURS/LAP.CHOLEY IMMEDIATE/
123 BEST TEST FOR Diffuse oesophageal spasm -- manometry
124 DUCT PAPPILOMA BRESTT/T-MICRODOCETOMY
125. Isoflurane vs desflurane A/E- ISOFLURANE IS MORE CARDIODEPRRESENT THEN DES
126 Tubectomy with highest recanalisation rate- isthmo-isthmic
127. Posterior column TRANSMITS A/E- temparature
128. TRIAL OF LABOUR c/I - previous classical cs
129. Vocal nodule- voice therapy & PPI
130. Locking of knee- tibia fixed.femur medial rotation
131 Community health centre chc- 1 st referral
132 Tuberculosis of ileocecal region a/e- applecore
##133 Nutritional surveillance a/e ---it is diagnostic
134. Liver lobes resected LEFT TO FALCIFORM LIGAMENT- 2 and 3
135. Diptheria prophylaxis- erythromycin

136. Man with headache and son with leukemia-adjustment
137. Panic attack- 25 yr man ,NO ECG CHANGES
##138. 1ST TEST FOR Erectile dysfunction in opd- sildenafil >CAVERNOSOMETRY
139. Horizontal gaze controlled by- abducents
140.. Special efferent A/E- facial nerve
141. Type b impedance, CONDUCTIVE DEAFNESS,lymph node IN POST.GROUP- nasopharyngeal cancer
142. Transverse lines nails, skin pigment- arsenic poison
143. Right sided aortic arch-TRUNCUS ARTERIOSUS>tof
144. Route of sperms-- straight-rete-epidydimis
145. CRESENTIC glomerulopathy A/E- ALPORT
146. Ring sideroblast- myelodysplastic syndrome
147. Sarcolemmal protein a/e --perlocan
148. Diploic veins A/E—APPEAR BY 8 WKS
149. Cavernous sinus tributary A/E-- deep MIDDLE CVEREBELLAR VEIN
150. Intractable glaucoma- melanoma of ant iris
151. Sibling with cah, present preagnancy management- steroid WHEN DIAGNOSIS OF PREGNANCY then cvs
152. Health is only central government responsibility- false
153. Alcoholic smoker –ATROPHIC GLLOSITIS-ANS IS CHECK B12 LEVELS
154 PATCHES OF GREY HAIR………………..-----alopecia areata
155. Heparin in pregnancy- calcium prophylaxis

156. Mitral stenosis ist sign- ELEVATION OF LEFT BRONCHUS>double ATRIAL shadow

157. Umbilical artery DOPPLER- S/D RATIO INCRESED IN NICOTINE & TOBBACO SMOKING
158. Premenstrual symptoms d.o.c.- ssri
159. Phosphorylase b inactivated state by- atp
160. Pulmonary hypertension first sign- upper lobe vein dilatation
161. Migratory thrombophlebitis in a/e- /prostate ca
162. Mip-2 in lens--- water out
163 Concurrent list a/e-- resposinble for mangement of medical education and profession
164. Digastric muscle A/E-STERNOCLEIDOMASTOID

165. Not a COMPOSITE muscle- RECTUS FEMORIS

166. Abdomen trauma hemodynamically stable rib fracture NEXT STEP- imaging
167 Ureteric stone pain is due to- RENAL CAPSULE DISTENTION>EXCEESIVE PERISTALSIS
168. Lateral corticospinal tract –PAIN,TEMP.
169 Extramedullary spinal tumour A/E-EARLY UPPER MOTOR N. LESION
170 Uro surgery bladder spasm given a/e- ipratropium
171. Conus medullarisA/E- absent knee jerk
172. Hiv patient on anti retroviral plus hip pain 6 months- AVASCULAR NECROSIS(OSTEONECROSIS)

173. ENDOSalpingitis investigation- hysterosALPINGOGRAPHY
174. Gfr measurement- dtpa
175. Peptide chemotherapeutic- bleomycin
##176 Bilateral gas in infant under diaphragm- PERFORATION OF STOMACH
177 LOOSE BODIESIN SYNOVIAL FLUID,charcots JOINT IN DIABETIS T/T a/e- ARTHROCENTESIS

178. CARPOBasal index- sex
179. Equal duration of interview eliminate which bias-RECALL BIAS
180. 6 yr old with 2 yr hematuria,no other abnormality-iga
181. child with anal atresia and passage of meconuria –SIGMOID COLOSTOMY
182. effect of exercise on cerebral blood flow-- no change
183. Hepatitis carrier- follow up
184. what helps in lymph drainage from foot –LEG MASSAGE
##185. upto what level does bronchial artery supplies blood- respiratory bronchiole/TERMINAL
186. Tb osteomyelitis A/E- ABUNDANT PERIOSTEAL REACTION
187. Most common teratogenic CNS infections-- CMV and toxoplasmosis
188. Meningitis in elderly a/e- GRAM NEGATIVE BACILLI
##189. Delphis method –FOR REACHING TO CONCLUSION/QUALITATIVE
190. Enteric fever a/e- amikacin
191 ac pancreatitis preferred route of nutrition -post jejunostomy feeding tube
192. FEMALE,25R,SpherocytoES,INV.- coombs test
193. Graft vs host ds A/E- gvhd moRE common With plasma components then whole blood
194. NOT A Facial nv pointer EXCEPT – TRAGAL(CARTILAGENOUS POINTER)
{{{{{{{SHOCKED,NO ITS NOT A TYPING MISTAKE ,PLZ READ THE q VERY CAREFULLY,IT ULTIMATLY MEANT WHICH ONE IS A FACIAL N.POINTER,& IAM QUIET SURE ABOUT IT}}}}}}}
195.LEAST IMP IN Non communicable ds- SPECIFICITY OF ASSO.

196. T/T OF PERFORATED Necrotising enterocolitis-PUT PERITONEAL DRAIN
(IF IT WAS AMONGST THE OPTIONS THEN SURELY IT IS THE ANS NEXT BEST WUD BE STABLISATION THEN DEF.SURGEY LATTER)
197. Acute cholecystitis- bladder invisible on hida (CAN NYBODY TELL ALLTHE OPTIONS)

198. trauma in region of pancreas,DISTAL STMACH,DUODENUM --Whipple procedure
199. Whipple disease seen are- histiocytosis IN LAMINA PROPRIA
200. Recurrent abortions a/e --torch
201. Iceberg-- apparent and non apparent disease
202. what is the correct age of surgical treatment in a child with microtia- 5 YR
203. Low radial nerve palsy- no weakness of brachioradialis
204 not included in IMNCI- neonatal tetanus
205 -No langerhans cells in lungs

206 G6pd hemolysis a/e- pyrimethamine >CHLOROQUINE
207 . Floatation test can be negative- atelectasis
208 Kap system WAS STARTED AFTER- FAMIL PLANNING PROGRAM
##209 TRUE Morula –TRANSPORTED ACTIVELY IN TUBE
210. Tetracycline A/E- not teratogenic
211 Splenectomy on child on ventilator itp, when to give platelets-withLIGATION of splenic pedicle
212 Ocular neurofibromatosis causes--glaucoma
#213 Cerebellar astrocytoma a/e-poor prognosis
214-INCRESED CHLOMICRION & VLDL RENANT Familial hypercholesterolemia--type 3
215. Action of Bradykinin –MEDIATES Pain

216. Chaperones- protein folding
##217 Superantigen A/E- ACTIVATION RTEQUIRES BINDING TO BOTH TCR & MHC
218. Cvs sampling a/e --neural tube defect
219. Flared ribs-- rickets
220. Pyelonephritis & uti CAN BE DIFFRETIATED B A/E-- >(10)8 BACTERIA
221. Testicular feminisation syndrome A/E- ABUNDANT pubic hair
##222. Cushing- high adh
*223. C3 normal glomerulonephritis
*224 Staph saprophyticus
*225. Methicillin resistance a/e

226. Recommended dietary allowance rda a/e- take care of needs of ALL PEPOLE
227. Carboxylation- vit k
228. Penicillin g A/E- EFFECTIVE AGAINST BOTH G+ & G-
229. DOC 4 NEURO(CNS) syphilis- procaine penicillin >BENZATHINE
230- Std, 5 day sloughing ulcer- chancroid
231 Not a Complication of hemithyroidectomy-- Low Ca
232 Pralidoxime MOA? Reactivation OF ACHESTERASE
233. Cervix cancer staging- no ct scan
234. ACHLASIA CARDIA on xray
235 propofol--c/i in porphyria

236 MALIGNANT hypertension histology A/E-- hyaline arteriosclerosis
237.contrast allergy-- anaphylACTOID
238. train of 4- nmdr
239 All are tocolytics except.. KETAMINE(OTHR OPTIONS WERE SALBUTAMOL,RITODRINE,ISOFLURANE)
##240. ALL ARE DISADVANTAGES OF calender method EXCEPT- ???
241 true about lactation mastitis.—ABSCESS CAN FORM & MAY REQUIRE DRAINAGE
242 LEAST CONTAMINATION for urine collection IN-- suprapubic aspiration
243 trus in prostate--- biopsy >VOLUME
244 MC posterior mediastinal tumour.. neurofibroma
245 best guide to operate in blunt thorax trauma—CHEST TUBE OUTPUT

246 anal fissure IS diagnosed by--- HISTORY & SUP.INSPECTION>anoscopy
247 not true about congenital adrenal hyperplasia –BOYS DEVELOP SYMPTOM AT PUBERTY
248 male with sudden death at basketball found hypertrophied septum.. repeat Q - HOCM
249 hitselberger sign loss of sensation in external auditary canal- acoustic neuroma
250 standard deviation is for.-DISPERSION AROUND MEAN
251 complete family size..tfr
252 abortion sticks - mechanism - repeat Q - stimulation of uterine contraction
253 polychlorinated hydrocarbon is..—eneldrin
254. Severe hypertension preeclampsia -NIFEDEPINE>labetelol >METHYLDOPA
255 Reactive oxygen intermediates- nadph OXIDASE
256. Soft tick TRANSMITS-RELAPSING FEVER>KFD
257 - CYCLOSPORINE ??
##258. Tubectomy with least failure- hulka clip /UNIPOLAR CAUTERY
259. TERM Dementia precox WAS GIVEN BY- kraeplin
260 Secretin a/e -increases acidity of bile
261. Most radiosensitive phase- g2m
262. Vas deferens blood supply- superior vesical
263. Facial colliculus at which level- pons
264. AntifungalA/E--CLOFASAMINE
265. Genital wart immunomodulator used- imiquimod
266. Urine discoloration IN A/E quinine
267 m.c. occupational cancer- skin
268. Rape, vaginal epithelial cells- lugols iodine
269. Not an Antidepressant- Resperidone
270. Ebbe estlander flap- lip
271 Kawasaki disease- 25% coronary artery aneurysm
272. Not a cancer- FIBROMATOSIS
273. SKIN NEAR large Saphenous vein IS SUPPLIED BY- FEMORAL NERVE(SAPHENOUS N. WAS NOT AMONGST THE OPTIONS
274. Hereditary haemochromatosis A/E-DESFERRIOXAMINE IS THE T/T OF CHOICE
275. Post traumatic stress disorder A/E-NUMBNESS OF EMOTIONS
276. MC CAUSE OF Conn syndrome- adrenal adenoma
277. Meniscal tear location repair preffered- OUTER1/3
278. Coronary ligament in knee joint –B/N MENISCUS & TIBIA
279. Diptheritic colitis like poison- mercury
280. H5n1- bird flu
281. Dying back neuropathy IN A/E-GBS
282. Blood supply cruciate ligament- MIDDLE GENICULAR
283. Compound not seen in photoreceptor complex matrix- MIMECAN
284. Gomez criteria A/E-BASED ON HEIGHT
285. ELECTRODES IN Cochlear implant PLACED ON-ROUND WINDOW
286. boyndi ring-- choroid plexus

Questions of All India PG Entrance Exam 2006

noreply@blogger.com (DevilX) — Sat, 30 Jul 2011 18:59:00 +0000

1.    All of the following are features of prematurity in a neonate, except:



    1.    No creases on sole.

    2.    Abundant lanugo.

    3.    Thick ear cartilage.

    4.    Empty scrotum.

2.    A normally developing 10 month old child should be able to do all of the following except :



    1.    Stand alone.

    2.    Play peek a boo.

    3.    Pick up a pellet with thumb and index finger.

    4.    Build a tower of 3-4 cubes.

3.    The following are characteristic of autism except :



    1.    Onset after 6 years of age.

    2.    Repetitive behaviour.

    3.    Delayed language development.

    4.    Severe deficit in social interaction.

4.    The earliest indicator of response after starting iron in a 6- year-old girl with iron deficiency is:



    1.    Increased reticulocyte count.

    2.    Increased hemoglobin.

    3.    Increased ferritin.

    4.    Increased serum iron.

5.    A 1 month old boy is referred for failure to thrive. On examination, he shows features of congestive failure. The femoral pulses are feeble as compared to branchial pulses. The most likely clinical diagnosis is :



    1.    Congenital aortic stenosis.

    2.    Coarctation of aorta.

    3.    Patent ductus arteriosus.

    4.    Congenital aortoiliac disease.

6.    All of the following statements regarding subendocardinal infarction are true, except :



    1.    These are multifocal in nature.

    2.    These often result from hypotension or shock.

    3.    Epicarditis is not seen.

    4.    These may result in aneurysm.

7.    All of the following are true for mitral valve prolapse, except :



    1.    Transmission may be as an Autosomal dominant trait.

    2.    Majority of the case present with features of mitral regurgitation.

    3.    The value leaflets characteristically show myxomatous degeneration.

    4.    The disease is one of the common cardiovascular manifestations of Marfan Syndrome.

8.    The following diseases are associated with Epstein â€“ Barr virus infection, except :



    1.    Infectious mononucleosis.

    2.    Epidermodysplasia verruciformis.

    3.    Nasopharyngeal carcinoma.

    4.    Oral Hairy leukoplakia

9.    Megaloblastic anaemia due to folic acid deficiency is commonly due to :



    1.    Inadequate dietary intake.

    2.    Defective intestinal absorption.

    3.    Absence of folic acid binding protein in serum.

    4.    Absence of glutamic acid in the intestine.

10.    The most important prognostic factor in breast carcinoma is :



    1.    Histological grade of the tumour.

    2.    Stage of the tumour at the time of diagnosis.

    3.    Status of estrogen and progesterone receptors.

    4.    Over expression of p-53 tumour suppressor gene.

11.    Smoking is generally not associated as a risk factor with :



    1.    Small cell carcinoma.

    2.    Respiratory bronchiolitis.

    3.    Emphysema.

    4.    Bronchiolitis obliterans organizing pneumonia.

12.    The tumour, which may occur in the residual breast or overlying skin following wide local excision and radiotherapy for mammary carcinoma, is :



    1.    Leiomyosarcoma.

    2.    Squamous cell carcinoma.

    3.    Basal cell carcinoma.

    4.    Angiosarcoma.

13.    The type of mammary ductal carcinoma in situ (DCIS) most likely to result in a palpable abnormality in the breast is :



    1.    Apocrine DCIS.

    2.    Neuroendocrine DCIS.

    3.    Well differentiated DCIS.

    4.    Comedo DCIS.

14.    Acinic cell carcinomas of the salivary gland arise most often in the :



    1.    Parotid salivary gland.

    2.    Minor salivary glands.

    3.    Submandibular salivary gland.

    4.    Sublingual salivary gland.

15.    All of the following statements regarding primary effusion lymphoma are true except :



    1.    It generally presents in elderly patients.

    2.    There is often an association with HHV-8.

    3.    The proliferating cells are NK cells.

    4.    Patients are commonly HIV positive.

16.    Mantle cell lymphomas are positive for all of the following, except :



    1.    CD 23.

    2.    CD 20.

    3.    CD 5.

    4.    CD 43.

17.    Fine needle aspiration cytology is not suitable for diagnosing :



    1.    Tubercular lymphadenitis.

    2.    Papillary carcinoma thyroid.

    3.    Plasmacytoma.

    4.    Aneurymal bone cyst.

18.    All of the following immunohistochemical markers are positive in the neoplastic cells of granulocytic sarcoma, except :



    1.    CD 45 RO.

    2.    CD 43.

    3.    Myeloperoxidase.

    4.    Lysozyme.

19.    B cell prolymphocytic leukemia patients differ from those with B cell chronic lymphocytic leukemia in :



    1.    Presenting at a younger age.

    2.    Having a lower total leucocyte count.

    3.    Having prominent lymphadenopathy.

    4.    Having a shorter survival.

20.    Which of the following statements is incorrect about pthisis bulbi?



    1.    The intraocular pressure is increased.

    2.    Calcification of the lens is common.

    3.    Sclera is thickened.

    4.    Size of the globe is reduced.

21.    Which one of the following statements is incorrect about Optic glioma?



    1.    Has a peak incidence in first decade.

    2.    Arises from oligodendrocytes.

    3.    Causes meningeal hyperplasia.

    4.    Is associated with type I neurofirbromatosis.

22.    Which one of the following stromal dystrophy is a recessive condition ?



    1.    Lattice dystrophy.

    2.    Granular dystrophy.

    3.    Macular dystrophy.

    4.    Fleck dystrophy.

23.    In which of the following conditions Parakeratosis most frequently occurs?



    1.    Actinic Keratoses.

    2.    Seborrheic keratoses.

    3.    Molluscum contagiosum.

    4.    Basal cell carcinoma.

24.    Which one of the following is the most significant risk factor for development of gastric carcinoma?



    1.    Paneth cell metaplasia.

    2.    Pyloric metaplasia.

    3.    Intestinal metaplasia.

    4.    Ciliated metaplasia.

25.    Which of the following is the most common presenting symptom of non-cirrhotic portal hypertension?



    1.    Chronic liver failure.

    2.    Ascites.

    3.    Upper gastrointestinal bleeding.

    4.    Encephalopathy.

26.    Ethosuximide is used in the treatment of :



    1.    Tonic-clonic seizure.

    2.    Absence seizure.

    3.    Myoclonic seizure.

    4.    Simple partial seizure.

27.    Which of the following statements is not true about etomidate?



    1.    It is an intravenous anesthetic.

    2.    It precipitates coronary insufficiency.

    3.    It inhibits cortisol synthesis.

    4.    It causes pain at site of injection.

28.    Which one of the following antibacterials should not be used with d-tubocurarine?



    1.    Norfloxacin.

    2.    Streptomycin.

    3.    Doxycycline.

    4.    Cefotaxime.

29.    Which one of the following drugs is an antipseudomonal penicillin?



    1.    Cephalexin.

    2.    Cloxacillin.

    3.    Piperacillin.

    4.    Dicloxacillin.

30.    The following statements regarding benzodiazephines are true except:



    1.    Binds to both GABAA and GABAB receptors.

    2.    They have active metabolites.

    3.    Decreases nocturnal gastric secretion in human being.

    4.    Extensively metabolized by CYP enzymes.

31.    One of the following statements regarding mycophenolate mofetil is incorrect:



    1.    It is a prodrug.

    2.    It is a selective uncompetitive and reversible inhibitor of inosine monophosphate dehydrogenase.

    3.    It also inhibits calcineurin.

    4.    Selectivity inhibits lymphocyte proliferation.

32.    All of the following mechanisms of action of oral contraceptive pill are true, except :



    1.    Inhibition of ovulation.

    2.    Prevention of fertilization.

    3.    Interference with implantation of fertilized ovum.

    4.    Interference with placental functioning.

33.    Which one of the following drugs does not interfere with folic acid metabolism?



    1.    Phenytoin.

    2.    Gabapentin.

    3.    Phenobarbitone.

    4.    Primidone.

34.    Which one of the following drugs causes constipation?



    1.    Propranolol.

    2.    Verapamil.

    3.    Nitroglycerin.

    4.    Captopril.

35.    Which of the following drugs is not used topically for treatment of open angle glaucoma:



    1.    Latanoprost.

    2.    Brimonidine.

    3.    Acetazolamide.

    4.    Dorzolamide.

36.    Concomitant administration of clonazepam with which of the following antiepileptic drug can precipitate absence status?



    1.    Sodium valproate.

    2.    Phenobarbitone.

    3.    Carbamazepine.

    4.    Phenytoin.

37.    Which one of the following agents has been associated with hemorrhagic stroke?



    1.    Phenylpropanolamine.

    2.    Terfenadine.

    3.    Quinidine.

    4.    Fenfluramine.

38.    All of the following are therapeutic uses of Penicillin G, except :



    1.    Bacterial meningitis.

    2.    Rickettsial Infection.

    3.    Syphilis.

    4.    Anthrax.

39.    All of the following are major complications of massive transfusion, except:



    1.    Hypokalemia.

    2.    Hypothermia.

    3.    Hypomagnesemia.

    4.    Hypocalcemia.

40.    Which one of the following muscle relaxant has the maximum duration of action ?



    1.    Atracurium.

    2.    Vecuronium.

    3.    Rocuronium.

    4.    Doxacurium.

41.    Which enzyme is inhibited by Aminophylline?



    1.    Monoamine Oxidase.

    2.    Alcohol dehydrogenase.

    3.    Phjosphodiesterase.

    4.    Cytochrome P-450.

42.    Which one of the following local anaesthetics belongs to the ester group?



    1.    Procaine.

    2.    Bupivacaine.

    3.    Lignocaine.

    4.    Mepivacaine.

43.    The following are the benozodiazepines of choice in elderly and those with liver disease, except:



    1.    Lorazepam.

    2.    Oxazepam,

    3.    Temazepam.

    4.    Diazepam.

44.    Which one of the following agents sensitises the myocardium to catecholamines?



    1.    Isoflurane

    2.    Ether.

    3.    Halothane.

    4.    Propofol.

45.    Which of the following is the muscle relaxant of choice in renal failure?



    1.    Rapacurium

    2.    Pancuronium

    3.    Atracurium

    4.    Rocuronium

46.    Ovulation is primarily caused by preovulatory surge of :



    1.    Estradiol.

    2.    Luteinizing hormone.

    3.    Progesterone.

    4.    Follicle stimulating hormone.

47.    Most afferent fibers from the lateral geniculate nucleus terminate in the primary visual cortex in :



    1.    Layer 1.

    2.    Layer 2 & 3.

    3.    Layer 4.

    4.    Layer 5 & 6.

48.    The blobs of the visual cortex are associated with :



    1.    Ocular dominance.

    2.    Orientation.

    3.    Color processing.

    4.    Saccadic eye movements.

49.    The parvocellular pathway, from the lateral geniculate nucleus to the visual cortex, carries signals for the detection of :



    1.    Movement, depth and flicker.

    2.    Color vision, shape and fine details.

    3.    Temporal frequency.

    4.    Luminance contrast.

50.    A pilot in Sukhoi aircraft is experiencing negative G. Which of the following physiological events will manifest in such situation?



    1.    The hydrostatic pressure in veins of lower limb increases.

    2.    The cardiac output decreases.

    3.    Black out occurs.

    4.    The cerebral arterial pressure rises.

BRAIN TUMORS

noreply@blogger.com (DevilX) — Sat, 30 Jul 2011 18:40:00 +0000

What are primary brain tumors?

Tumors that begin in brain tissue are known as primary tumors of the brain. (Information about secondary brain tumors appears in the following section.) Primary brain tumors are named according to the type of cells or the part of the brain in which they begin.

The most common primary brain tumors aregliomas. They begin in glial cells. There are many types of gliomas:

Astrocytoma - The tumor arises from star-shaped glial cells called astrocytes. In adults, astrocytomas most often arise in the cerebrum. In children, they occur in the brain stem, the cerebrum, and the cerebellum. A grade III astrocytoma is sometimes called an anaplasticastrocytoma. A grade IV astrocytoma is usually called a glioblastoma multiforme.
Brain stem glioma - The tumor occurs in the lowest part of the brain. Brain stem gliomas most often are diagnosed in young children and middle-aged adults.
Ependymoma - The tumor arises from cells that line the ventricles or the central canal of the spinal cord. They are most commonly found in children and young adults.
Oligodendroglioma - This rare tumor arises from cells that make the fatty substance that covers and protects nerves. These tumors usually occur in the cerebrum. They grow slowly and usually do not spread into surrounding brain tissue. They are most common in middle-aged adults.

Some types of brain tumors do not begin in glial cells. The most common of these are:

Medulloblastoma - This tumor usually arises in the cerebellum. It is the most common brain tumor in children. It is sometimes called aprimitive neuroectodermal tumor.
Meningioma - This tumor arises in the meninges. It usually grows slowly.
Schwannoma - A tumor that arises from a Schwann cell. These cells line the nerve that controls balance and hearing. This nerve is in the inner ear. The tumor is also called an acoustic neuroma. It occurs most often in adults.
Craniopharyngioma - The tumor grows at the base of the brain, near the pituitary gland. This type of tumor most often occurs in children.
Germ cell tumor of the brain - The tumor arises from a germ cell. Most germ cell tumors that arise in the brain occur in people younger than 30. The most common type of germ cell tumor of the brain is agerminoma.
Pineal region tumor - This rare brain tumor arises in or near thepineal gland. The pineal gland is located between the cerebrum and the cerebellum.
What are secondary brain tumors?
When cancer spreads from its original place to another part of the body, the new tumor has the same kind of abnormal cells and the same name as the primary tumor. Cancer that spreads to the brain from another part of the body is different from a primary brain tumor. When cancer cells spread to the brain from another organ (such as the lung or breast), doctors may call the tumor in the brain a secondary tumor or metastatic tumor. Secondary tumors in the brain are far more common than primary brain tumors.
What causes and who is at risk for brain tumors?
No one knows the exact causes of brain tumors. Doctors can seldom explain why one person develops a brain tumor and another does not. However, it is clear that brain tumors are not contagious. No one can "catch" the disease from another person.
Research has shown that people with certainrisk factors are more likely than others to develop a brain tumor. A risk factor is anything that increases a person's chance of developing a disease.
The following risk factors are associated with an increased chance of developing a primary brain tumor:
- Being male - In general, brain tumors are more common in males than females. However, meningiomas are more common in females.
- Race - Brain tumors occur more often among white people than among people of other races.
- Age - Most brain tumors are detected in people who are 70 years old or older. However, brain tumors are the second most common cancer in children. (Leukemia is the most common childhood cancer.) Brain tumors are more common in children younger than 8 years old than in older children.
- Family history - People with family members who have gliomas may be more likely to develop this disease.
- Being exposed to radiation or certain chemicals at work:
  - Radiation - Workers in the nuclear industry have an increased risk of developing a brain tumor.
  - Formaldehyde - Pathologists and embalmers who work withformaldehyde have an increased risk of developing brain cancer. Scientists have not found an increased risk of brain cancer among other types of workers exposed to formaldehyde.
  - Vinyl chloride - Workers who make plastics may be exposed to vinyl chloride. This chemical may increase the risk of brain tumors.
  - Acrylonitrile - People who make textiles and plastics may be exposed to acrylonitrile. This exposure may increase the risk of brain cancer.
Scientists are investigating whether cell phones may cause brain tumors. Studies thus far have not found an increased risk of brain tumors among people who use cell phones.
Scientists also continue to study whether head injuries are a risk factor for brain tumors. So far, these studies have not found an increased risk among people who have had head injuries.
Most people who have known risk factors do not get brain cancer. On the other hand, many who do get the disease have none of these risk factors. People who think they may be at risk should discuss this concern with their doctor. The doctor may be able to suggest ways to reduce the risk and can plan an appropriate schedule for checkups.

Traumatic Brain Injury Could Raise Stroke Risk Tenfold, Study Says

noreply@blogger.com (DevilX) — Sat, 30 Jul 2011 18:32:00 +0000

People who have had a traumatic brain injury face a tenfold increase in the risk of having a stroke within three months, according to a new study.

Traumatic brain injury occurs when a blow or jolt to the head causes changes in a person's normal brain function. It can result from injuries such as falls, vehicle accidents, and violence.

Although previous research has shown that traumatic brain injury can be associated with the future development of epilepsy, Alzheimer's disease, and psychiatric conditions, this the first study to link it to the future risk of stroke. The study appears in the July 28 online issue of Stroke: Journal of the American Heart Association.

Traumatic Brain Injury and Stroke

To conduct the study, researchers used records from a nationwide Taiwanese database. They examined the records of 23,199 patients who received a diagnosis of traumatic brain injury between 2001 and 2003 and compared them to 69,597 people who did not have a traumatic brain injury. Each person was then followed for five years to identify whether they had a stroke.

In the three-month follow-up period, researchers found that 2.91% of patients with traumatic brain injury had a stroke compared with 0.30% of those who didn't have a traumatic brain injury, a tenfold difference. After one year, the risk of stroke went down, but those who had a traumatic brain injury were still at significantly higher risk for stroke than those in the comparison group; they had about a 4.6 times higher risk. After five years, traumatic brain injury sufferers were 2.3 times more likely than those without such an injury to have a stroke.

Results further showed that a person who had a traumatic brain injury in which the skull bone was fractured was more at risk for a stroke than a person who had the injury but the skull bone remained intact.

In the article, the authors state that it is not known how traumatic brain injury may influence the incidence of strokes. However, they noted several possibilities, including the idea that a traumatic brain injury may damage the blood vessels in the brain, disturbing the blood supply to the brain and leading to a stroke.

In a news release, Herng-Ching Lin, PhD, senior study author and professor at the School of Health Care Administration in the College of Medicine at Taipei Medical University in Taiwan, calls for the use of imaging examinations, like MRI, and intensive medical monitoring support and intervention following a traumatic brain injury, especially in the first few months and years. He also says there is a need for initiatives to increase public awareness about the risk factors that cause stroke and the signs and symptoms of stroke in patients with traumatic brain injuries.

In the U.S., an estimated 1.7 million traumatic brain injuries occur each year, according to the CDC.

"Stroke is the most serious and disabling neurological disorder worldwide," Lin notes in the news release. "Our study leads the way in identifying stroke as an additional neurological problem that may arise following traumatic brain injury."

What is a kidney stone?

noreply@blogger.com (DevilX) — Sat, 30 Jul 2011 18:24:00 +0000

A kidney stone is a hard, crystalline mineral material formed within the kidney or urinary tract. Kidney stones are a common cause of blood in the urine (hematuria) and often severe pain in the abdomen, flank, or groin. Kidney stones are sometimes called renal calculi.

The condition of having kidney stones is termed nephrolithiasis. Having stones at any location in the urinary tract is referred to asurolithiasis, and the termureterolithiasis is used to refer to stones located in the ureters.

Who is at risk for kidney stones?

Anyone may develop a kidney stone, but people with certain diseases and conditions (see below) or those who are taking certain medications are more susceptible to their development. It is estimated that one out of every 10 people in the U.S. will develop stones in the urinary tract at some point in their lives. Most urinary stones develop in people 20-49 years of age, and those who are prone to multiple attacks of kidney stones usually develop their first stones during the second or third decade of life.

In residents of industrialized countries, kidney stones are more common than stones in the bladder. The opposite is true for residents of developing areas of the world, where bladder stones are the most common. This difference is believed to be related to dietary factors. Urinary tract stones are about three times more common in males than in females. The prevalence of kidney stones begins to rise when men reach their 40s, and it continues to climb into their 70s. A Caucasian male has a one in eight chance of developing a kidney stone by age 70. People who have already had more than one kidney stone are prone to developing further stones.

A family history of kidney stones is also a risk factor for developing kidney stones. Kidney stones are more common in Asians and Caucasians than in Native Americans, Africans, or African Americans.

Uric acid kidney stones are more common in people with chronically elevated uric acid levels in their blood.

A small number of pregnant women (about one out of every 1,500-3,000 pregnancies) develop kidney stones, and there is some evidence that pregnancy-related changes may increase the risk of stone formation. Factors that may contribute to stone formation during pregnancy include a slowing of the passage of urine due to increased progesterone levels and diminished fluid intake due to a decreasing bladder capacity from the enlarging uterus. Healthy pregnant women also have a mild increase in their urinary calcium excretion. However, it remains unclear whether the changes of pregnancy are directly responsible for kidney stone formation or if these women have another underlying factor that predisposes them to kidney stone formation.

What causes kidney stones?

Kidney stones form when there is a decrease in urine volume and/or an excess of stone-forming substances in the urine. The most common type of kidney stone contains calcium in combination with either oxalate or phosphate. Other chemical compounds that can form stones in the urinary tract include uric acid and the amino acid cystine.

Dehydration from reduced fluid intake or strenuous exercise without adequate fluid replacement increases the risk of kidney stones. Obstruction to the flow of urine can also lead to stone formation. In this regard, climate may be a risk factor for kidney stone development, since residents of hot and dry areas are more likely to become dehydrated and susceptible to stone formation.

Kidney stones can also result from infection in the urinary tract; these are known as struvite or infection stones.

A number of different medical conditions can lead to an increased risk for developing kidney stones:

Gout results in chronically increased amount of uric acid in the blood and urine and can lead to the formation of uric acid stones.
Hypercalciuria (high calcium in the urine), another inherited condition, causes stones in more than half of cases. In this condition, too much calcium is absorbed from food and excreted into the urine, where it may form calcium phosphate or calcium oxalate stones.
Other conditions associated with an increased risk of kidney stones include hyperparathyroidism, kidney diseases such as renal tubular acidosis, and some inherited metabolic conditions, including cystinuriaand hyperoxaluria. Chronic diseases such as diabetes and high blood pressure (hypertension) are also associated with an increased risk of developing kidney stones.
People with inflammatory bowel disease or who have had an intestinal bypass or ostomy surgery are also more likely to develop kidney stones.
Some medications also raise the risk of kidney stones. These medications include some diuretics, calcium-containing antacids, and the protease inhibitor indinavir (Crixivan), a drug used to treat HIVinfection.
Dietary factors and practices may increase the risk of stone formation in susceptible individuals. In particular, inadequate fluid intake predisposes to dehydration, which is a major risk factor for stone formation. Other dietary practices that may increase an individual's risk of forming kidney stones include a high intake of animal protein, a high-salt diet, excessive sugar consumption, excessive vitamin D supplementation, and possible excessive intake of oxalate-containing foods such as spinach. Interestingly, low levels of dietary calcium intake may alter the calcium-oxalate balance and result in the increased excretion of oxalate and a propensity to form oxalate stones.

What is high blood pressure?

noreply@blogger.com (DevilX) — Sat, 30 Jul 2011 18:12:00 +0000

High blood pressure (HBP) or hypertension means high pressure (tension) in the arteries. Arteries are vessels that carry blood from the pumping heart to all the tissues and organs of the body. High blood

pressure does not mean excessive emotional tension, although emotional tension and stress can temporarily increase blood pressure. Normal blood pressure is below 120/80; blood pressure between 120/80 and 139/89 is called "pre-hypertension", and a blood pressure of 140/90 or above is considered high.

The top number, the systolic blood pressure, corresponds to the pressure in the arteries as the heart contracts and pumps blood forward into the arteries. The bottom number, the diastolic pressure, represents the pressure in the arteries as the heart relaxes after the contraction. The diastolic pressure reflects the lowest pressure to which the arteries are exposed.

An elevation of the systolic and/or diastolic blood pressure increases the risk of developing heart (cardiac) disease, kidney (renal) disease, hardening of the arteries (atherosclerosis or arteriosclerosis), eye damage, and stroke(brain damage). These complications of hypertension are often referred to as end-organ damage because damage to these organs is the end result of chronic (long duration) high blood pressure. For that reason, the diagnosis of high blood pressure is important so efforts can be made to normalize blood pressure and prevent complications.

It was previously thought that rises in diastolic blood pressure were a more important risk factor than systolic elevations, but it is now known that in people 50 years or older systolic hypertension represents a greater risk.

The American Heart Association estimates high blood pressure affects approximately one in three adults in the United States - 73 million people. High blood pressure is also estimated to affect about two million Americanteens and children, and the Journal of the American Medical Association reports that many are under-diagnosed. Hypertension is clearly a major public health problem.

What are vitamins, and why are they important?

noreply@blogger.com (DevilX) — Sat, 30 Jul 2011 18:01:00 +0000

There are six nutrients that are considered essential to life: proteins, carbohydrates, fats, vitamins, minerals, and water. These nutrients are needed for your body to function properly, and your diet is the source of them. Vitamins and minerals are considered micronutrients because they are needed in smaller quantities than the macronutrients (protein, carbohydrates, and fat). Micronutrients do not provide calories. When your body does not absorb an adequate amount of any of the micronutrients, diseases can occur. It's important to understand what your nutritional needs are and how to reach them.

Vitamins are broken down into two categories: water-soluble and fat-soluble. Water-soluble vitamins dissolve in water. Leftover amounts are not stored and will leave your body through your urine. For this reason, you must consume them on a continuous basis. The water-soluble vitamins are the B vitamins and vitamin C. Fat-soluble vitamins dissolve in fat, not water. These vitamins need dietary fat in order to be absorbed in the small intestines. They are then stored in the liver and fatty tissues (adipose tissues) and can accumulate to toxic levels when consumed in excess quantities. The fat-soluble vitamins are vitamins A, D, E, and K.

Recommendations for essential nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Institute of Medicine of the National Academies. Dietary Reference Intakes is the general term for a set of reference values used for planning and assessing nutrient intake for healthy people. There are three important types of DRI reference values; Recommended Dietary Allowances (RDA), Adequate Intakes (AI), and Tolerable Upper Intake Levels (UL). The RDA is set to meet the nutrient requirements for the average daily intake of nearly all (97%-98%) healthy individuals in each age and gender group. When there is insufficient data to set an RDA for a nutrient, an AI is set. AIs meet or exceed the amount needed to maintain an adequate nutritional state in nearly everyone of a specific age and gender group. Some nutrients can cause health problems when consumed in excessive quantities. The UL was set to provide the maximum daily intake that is unlikely to result in adverse health effects. Numerous health conditions, however, can impact your nutritional needs. A registered dietitian or physician can help you determine your specific needs based upon your overall health and condition.

What is rickets?

noreply@blogger.com (DevilX) — Sat, 30 Jul 2011 17:36:00 +0000

What is rickets?

Rickets is a disorder caused by a deficiency of vitamin D, calcium, or phosphate. Rickets leads to softening and weakening of the bones and is seen most commonly in children 6-24 months of age. There are several subtypes of rickets, includinghypophosphatemic rickets(vitamin-D-resistant rickets),kidney rickets (renal osteodystrophy), and, most commonly, nutritional rickets (caused by dietary deficiency of vitamin D, calcium, or phosphate). Classic nutritional rickets is also medically termedosteomalacia.

What is the history of rickets?

Roman descriptions of individuals with rickets can be found as early as the second century, and in the 1640s, the condition was well documented as a common bone ailment across England. Unfortunately, the scientifically proven cause of rickets was not identified until the 1920s, and by the 1930s, public-health initiatives recommend fortifying milk with vitamin D and cod-liver oil as a nutritional supplement for young infants and children. This led to a near eradication of rickets in the United States and other industrialized nations. Unfortunately, rickets has made a comeback and is still common in less-developed nations. Moreover, for a variety of reasons, rickets is seen more frequently amongst infants and children living in industrialized nations, often among more affluent populations.

What causes rickets?

Regardless of the type of rickets, the cause is always either due to a deficiency of vitamin D, calcium, or phosphate. Three common causes of rickets include nutritional rickets, hypophosphatemic rickets, and renal rickets.

Nutritional rickets

Nutritional rickets, also called osteomalacia, is a condition caused by vitamin D deficiency. Vitamin D is a fat-soluble vitamin that is essential for the normal formation of bones and teeth and necessary for the appropriate absorption of calcium and phosphorus from the bowels. It occurs naturally in very small quantities in some foods such as saltwater fish (salmon, sardines, herring, and fish-liver oils). Vitamin D is also naturally synthesized by skin cells in response to sunlight exposure. It is necessary for the appropriate absorption of calcium from the gut.

Infants and children most at risk for developing nutritional rickets include dark-skinned infants, exclusively breastfed infants, and infants who are born to mothers who are vitamin D deficient. In addition, older children who are kept out of direct sunlight or who have vegan diets may also be at risk.

Hypophosphatemic rickets

Hypophosphatemic rickets is caused by low levels of phosphate. The bones become painfully soft and pliable. This is caused by a genetic dominant X-linked defect in the ability for the kidneys to control the amount of phosphate excreted in the urine. The individual affected is able to absorb phosphate and calcium, but the phosphate is lost in the urine. This is not caused by a vitamin D deficiency. Patients with hypophosphatemic rickets typically have obvious symptoms by 1 year of age. Treatment is generally through nutritional supplements of phosphate and calcitriol (the activated form of vitamin D).

Renal (kidney) rickets

Similar to hypophosphatemic rickets, renal rickets is caused by a number of kidney disorders. Individuals suffering from kidney disease often have decreased ability to regulate the amounts of electrolytes lost in the urine. This includes calcium and phosphate, and therefore the affected individuals develop symptoms almost identical to severe nutritional rickets. Treatment of the underlying kidney problem and nutritional supplementation are recommended for these patients.

Effect of Aspirin on Mortality in the Primary Prevention of Cardiovascular Disease

noreply@blogger.com (DevilX) — Thu, 21 Jul 2011 15:10:00 +0000

In patients without a history of cardiovascular disease, aspirin prevents deaths as well as myocardial infarction and ischemic stroke but increases hemorrhagic stroke and major bleeding when used in primary prevention of cardiovascular disease.

Abstract

Objective
The lack of a mortality benefit of aspirin in prior meta-analyses of primary prevention trials of cardiovascular disease has contributed to uncertainty about the balance of benefits and risks of aspirin in primary prevention. We performed an updated meta-analysis of randomized controlled trials of aspirin to obtain best estimates of the effect of aspirin on mortality in primary prevention.

Methods
Eligible articles were identified by searches of electronic databases and reference lists. Outcomes of interest were all-cause mortality, cardiovascular mortality, myocardial infarction, stroke, and bleeding. Data were pooled from individual trials using the DerSimonian-Laird random-effects model, and results are presented as relative risk (RR) and 95% confidence intervals (CIs).

Results
Nine randomized controlled trials enrolling 100,076 participants were included. Aspirin reduced all-cause mortality (RR 0.94; 95% CI, 0.88-1.00), myocardial infarction (RR 0.83; 95% CI, 0.69-1.00), ischemic stroke (RR 0.86; 95% CI, 0.75-0.98), and the composite of myocardial infarction, stroke, or cardiovascular death (RR 0.88; 95% CI, 0.83-0.94), but did not reduce cardiovascular mortality (RR 0.96; 95% CI, 0.84-1.09). Aspirin increased the risk of hemorrhagic stroke (RR 1.36; 95% CI, 1.01-1.82), major bleeding (RR 1.66; 95% CI, 1.41-1.95), and gastrointestinal bleeding (RR 1.37; 95% CI, 1.15-1.62). A lack of availability of patient-level data precluded exploration of benefits and risks of aspirin in key subgroups.

Conclusion

Aspirin prevents deaths, myocardial infarction, and ischemic stroke, and increases hemorrhagic stroke and major bleeding when used in the primary prevention of cardiovascular disease.

Should the Affordable Care Act of 2010 Be Repealed? Another viewpoint from an AJM reader

noreply@blogger.com (DevilX) — Thu, 21 Jul 2011 15:08:00 +0000

In the July 2011 issue, The American Journal of Medicine publishedShould the Affordable Care Act of 2010 Be Repealed? by James E. Dalen, MD, MPH, AJM associate editor and Dean Emeritus of the University of Arizona College of Medicine, in the Journal . AJM has received several e-mails and a few phone calls (pro and con) related to this article. Here is one commentary that takes issue with Dalen's commentary supporting the Affordable Care Act.

Should the Affordable Care Act of 2010 Be Repealed? A Fuller Picture

Dr. Dalen’s commentary in the July 2011(1) issue simply repeats the longstanding arguments supporting the Patient Protection and Affordable Care Act (PPACA), without shedding any new light on it since its passage in March of 2010. I take issue with his one-sided view of the law and its subsequent impact, and supply responses to contentions while describing some underpinnings of the opposition.

The Politics of Passage
Table 1 (below) delineates the votes of the health care bill, beginning with the initial version crafted from three House committees and passed on November 7, 2009.(2) Then, on December 24, 2009, the Senate passed its version on a party-line vote.(3) Because the Senate bill differed from that of the House, it needed to return there for ultimate approval. After much politicking, and the inability to alter anything, it was ultimately brought to the floor late Sunday evening on March 21, 2010, and narrowly saved the President from scathing defeat.(4) Table 1 also shows Medicare’s passage for comparison.(5)

After claiming that Americans would watch the health care debate occur on C-SPAN, in the most transparent government, President Obama failed to deliver on either. Most Americans did not envision back-room deals tantamount to bribery to secure votes, or accounting gimmicks to seemingly keep the price tag below the $1 trillion ceiling. They did not expect to hear Nancy Pelosi (D-CA) tell them that they needed to pass it to find out what was in it 6 or have no time to actually digest the monstrosity before rendering a well-read opinion. And they certainly did not expect a vote on an issue that consumes nearly 20% of our GDP to occur in such a clearly partisan fashion on Christmas Eve or late one Sunday night. The ends do not justify the means.

The World’s Best Health Care System
The commentary resurrects the issue of health outcomes by solely touting those statistics that satisfy the author’s premise. Some noteworthy others – according to the WHO’s 2010 World Health Statistics, the USA ranks as the 3rd lowest (best) country in those under age 5 who are underweight. To immunization rates, the Americas have the lowest incidence of measles and mumps in the world, a significantly higher percentage of neonates protected at birth against neonatal tetanus compared to our European colleagues, and the highest rates of hepatitis B vaccination among 1-year olds in the world. Further, according to the Organization for Economic Co-operation and Development (OECD) Health Care Quality Indicators Project, the US has the highest five-year relative survival rates in the world for breast cancer, and the third highest rate for colorectal cancer.(7)

The Americas have 23 physicians and 55 nursing and midwifery personnel per 10,000 population compared to 33 and 68, respectively, for the European region. Perhaps some statistics touted by others as better are simply a result of a larger healthcare workforce, thereby increasing access to care.(8)

The Uninsured
Dr. Dalen writes “22% of our citizens were uninsured or had inadequate health insurance in 2007,” and then lists “50+ million uninsured Americans” intable 3. Not all uninsured people in this country are in-fact American, or even legal residents. According to 2005 census data, 45.8 million people were uninsured. While non-citizens represented 7% of the population, they accounted for 21% of this group, or more than 9.5M individuals. Further, 20% (9.16M) were uninsured for less than 3 months. And, 28% (12.8M) were above 300% of the federal poverty line (FPL). [Federal Poverty Level chart] At that level, single coverage premiums would account for 2% of annual income and premiums for a family of four would amount to 4.7%. This leaves a legitimate number of 14.2M US citizens making less than 300% of the FPL who were uninsured for more than 3 months – 5% of all US inhabitants.(9)

In the description of table 3, it states that “all uninsured Americans will certainly benefit by receiving coverage.” Yet under the section on ACA and the uninsured, the figure is “95% of legal US residents…” Based on a population of 300 million, this 5% disparity accounts for some 15 million people and does not satisfy the claim of insuring everyone, as originally billed in the run-up to the bill’s final passage.

Does Coverage Equal Access?
Dr. Dalen claims that by expanding coverage to the uninsured, “the US would finally…[ensure] that nearly all of its citizens have access to health care.” He makes the colossal mistake of equating coverage to access. The nation’s current physician shortage already results in delays to access. Add to this some 30 million newly-insured patients, and the delay simply becomes longer. Coverage does not equal access. Just look at Massachusetts.(10, 11)

The Devil is in the Details
The paper purports that nearly everyone stands to benefit from the government’s attempt at healthcare overhaul. It conveniently neglects to highlight what needs to be replaced, or simply repealed. (1) The 1099 tax reporting requirement under PPACA for all vendors receiving more the $600 was repealed earlier this year. (2) CMS recently disseminated its proposed rule regarding accountable care organizations (ACOs). When most of the institutions it touted as successful examples publicly stated their resistance, CMS promulgated new rules to entice participation. Still far from making any significant impact on the nation’s healthcare expenditures, ACOs will not likely meet their January 1, 2012 implementation target date because of inherent design flaws. (3) The independent payment advisory board (IPAB) is being attacked at present with bills in both houses of Congress calling for repeal. In bipartisan fashion, it appears likely that this will be eliminated. (4) Above all else is the individual mandate, currently under legal attack. The Supreme Court will rule on its constitutionality.

There appear to be aspects of the law that may benefit patients, namely insurance industry reforms. But these come at a cost, one that will certainly be borne by those insured in the nature of higher premiums.

While obvious is the massive expansion of entitlement programs (read government takeover), glaringly missing from PPACA is meaningful tort reform and a fix to the sustainable growth rate (SGR). Physicians who care for Medicare beneficiaries continue to be shackled to this failed reimbursement calculation. Faced with a nearly 30% cut in reimbursement rates on January 1, 2012, some physicians have stopped accepting Medicare patients, while others have opted to retire early or leave medicine altogether because they cannot run their business under the constant threat of disastrous cuts. Combine the increased number of newly-insured patients clamoring for access, the growth of the baby boomer population, and a decreasing supply of physicians, and a perfect storm is brewing leading to an incredible gap between supply and demand.

The PPACA should be repealed and replaced with a real attempt at addressing our nation’s issues, without exceptions for unions, bribes for lawmakers, or back-room deals in the middle of the night in a strictly partisan fashion. The Democrats had a golden opportunity to put everything on the table, but squandered it to save face for the President. This came at a price, one that was only partially paid in November of 2010, but whose debt will be fulfilled next November.

-- Joshua D. Lenchus, DO, RPh
University of Miami Miller School of Medicine

References
1. Dalen JE. Should the affordable care act of 2010 be repealed? Am J Med. 2011;124(7):575-577.

2. H.R.3962 – Affordable Health Care for America Act. Available at: http://www.opencongress.org/bill/111-h3962/show. Accessed June 21, 2011.

3. H.R.3590 – Patient Protection and Affordable Care Act. Available at: http://www.senate.gov/legislative/LIS/roll_call_lists/roll_call_vote_cfm.cfm?congress=111&session=1&vote=00396#position. Accessed June 21, 2011.

4. H.R.3590 – Patient Protection and Affordable Care Act. Available at: http://clerk.house.gov/evs/2010/roll165.xml. Accessed June 21, 2011.

5. H.R.6675 – The Social Security Amendments of 1965. Available at: http://www.ssa.gov/history/tally65.html. Accessed June 21, 2011.

6. Roff P. Pelosi: Pass Health Reform So You Can Find Out What’s In It. US News and World Report, March 9, 2010. Available at: http://www.usnews.com/opinion/blogs/peter-roff/2010/03/09/pelosi-pass-health-reform-so-you-can-find-out-whats-in-it. Accessed June 23, 2011.

7. Organisation for Economic Co-operation and Development (OECD). Health care quality indicators. Available at: http://www.oecd.org/document/34/0,3746,en_2649_37407_37088930_1_1_1_37407,00.html. Accessed June 22, 2011.

8. World Health Organization (WHO). World health statistics 2010. Available at: http://www.who.int/whosis/whostat/EN_WHS10_Full.pdf. Accessed June 21, 2011.

9. U.S. Department of Health and Human Services. Overview of the uninsured in the United States: An analysis of the 2007 current population survey. Available at: http://aspe.hhs.gov/health/reports/07/uninsured/report.pdf. Accessed June 22, 2011.

10. Access to Massachusetts health care still tight. GazetteNet.com, Daily Hampshire Gazette. 2010 Nov 16. Available at: http://www.gazettenet.com/2010/11/16/report-health-access-still-tight. Accessed June 22, 2011.

11. Massachusetts Medical Society. 2011 Patient access to health care study: A survey of Massachusetts physicians’ offices. Available at: http://www.massmed.org/AM/Template.cfm?Section=Research_Reports_and_Studies2&CONTENTID=54336&TEMPLATE=/CM/ContentDisplay.cfm. Accessed June 22, 2011.

The DRESS Syndrome: A Literature Review

noreply@blogger.com (DevilX) — Thu, 21 Jul 2011 15:05:00 +0000

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) is a potential life-threatening syndrome including severe eruption, fever, hypereosinophilia and internal organ involvement. Although 50 drugs can induce DRESS, the main culprit drugs are carbamazepine and allopurinol.

Abstract
The Drug Reaction with Eosinophilia and Systemic Symptom (DRESS) is a severe adverse drug-induced reaction. Diagnosing DRESS is challenging due to the diversity of cutaneous eruption and organs involved. We used the RegiSCAR scoring system that grades DRESS cases as “no,” “possible,” “probable,” or “definite” to classify cases reported in the literature. We also analyzed the clinical course and treatments of the cases. A total of 44 drugs were associated with the 172 cases reported between January 1997 and May 2009 in PubMed and MEDLINE. The most frequently reported drug was carbamazepine, and the vast majority of cases were classified as “probable/definite” DRESS cases. Hypereosinophilia, liver involvement, fever, and lymphadenopathy were significantly associated with “probable/definite” DRESS cases, whereas skin rash was described in almost all of the cases, including “possible cases.” Culprit drug withdrawal and corticosteroids constituted the mainstay of DRESS treatment. The outcome was death in 9 cases. However, no predictive factors for serious cases were found. This better knowledge of DRESS may contribute to improve the diagnosis and management of this syndrome in clinical practice.

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Should the Affordable Care Act of 2010 Be Repealed? Another viewpoint from an AJM reader

The DRESS Syndrome: A Literature Review