Saturday 15 August 2015

TONSILLITIS : REVIEW

Tonsillitis

Tonsillitis is inflammation (swelling) of the tonsils.

Causes

The tonsils are lymph nodes in the back of the mouth and top of the throat. They help to filter out bacteria and other germs to prevent infection in the body.

A bacterial or viral infection can cause tonsillitis. Strep throat is a common cause.

The infection may also be seen in other parts of the throat. One such infection is called pharyngitis.

Tonsillitis is very common in children.

Symptoms

Common symptoms may be:

Difficulty swallowingEar painFever and chillsHeadacheSore throat, which lasts longer than 48 hours and may be severeTenderness of the jaw and throat

Other problems or symptoms that may occur are:

Problems breathing, if the tonsils are very largeProblems eating or drinking

Exams and Tests

Your health care provider will look in the mouth and throat.

The tonsils may be red and may have white spots on them.The lymph nodes in the jaw and neck may be swollen and tender to the touch.

rapid strep test can be done in most doctors' offices. However, this test may be normal, and you can still have strep. Your provider may send the throat swab to a laboratory for a strep culture. Test results can take a few days.

Treatment

Swollen tonsils that are not painful or do not cause other problems do not need to be treated. Your provider may not give you antibiotics. You may be asked to come back for a checkup later.

If tests show you do have strep, your doctor will give you antibiotics. It is important to finish all of your antibiotics as directed, even if you feel better. If you do not take them all, the infection can return.

The following tips may help your throat feel better:

Drink cold liquids or suck on fruit-flavored frozen bars.Drink fluids, and mostly warm (not hot), bland fluids.Gargle with warm salt water.Suck on lozenges (containing benzocaine or similar ingredients) to reduce pain (these should not be used in young children because of the choking risk).Take over-the-counter (OTC) medicines, such as acetaminophen (Tylenol) or ibuprofen to reduce pain and fever. DO NOT give a child aspirin. Aspirin has been linked to Reye syndrome.

Some people who have repeated infections may need surgery to remove the tonsils (tonsillectomy).

Outlook (Prognosis)

Tonsillitis symptoms due to strep will often get better within 2 or 3 days after you start the antibiotics.

Children with strep throat should be kept home from school or day care until they have been on antibiotics for 24 hours. This helps reduce the spread of illness.

Possible Complications

Complications from strep throat may be severe. They may include:

Abscess in the area around the tonsilsKidney disease caused by strepRheumatic fever and other heart problems

Sunday 9 August 2015

ORAL HYPOGLYCEMIC AGENTS - CLASSIFICATION

Oral hypoglycemic drugs are used only in the treatment of type 2 diabetes which is a disorder involving resistance to secreted insulin. Type 1 diabetes involves a lack of insulin and requires insulin for treatment. There are now four classes of hypoglycemic drugs:

SulfonylureasMetforminThiazolidinedionesAlpha-glucosidase inhibitors.

These drugs are approved for use only in patients with type 2 diabetes and are used in patients who have not responded to diet, weight reduction, and exercise. They are not approved for the treatment of women who are pregnant with diabetes.

SULFONYLUREAS – Sulfonylureas are the most widely used drugs for the treatment of type 2 diabetes and appear to function by stimulating insulin secretion. The net effect is increased responsiveness of ß-cells (insulin secreting cells located in the pancreas) to both glucose and non-glucose secretagogues, resulting in more insulin being released at all blood glucose concentrations. Sulfonylureas may also have extra-pancreatic effects, one of which is to increase tissue sensitivity to insulin, but the clinical importance of these effects is minimal.

Pharmacokinetics – Sulfonylureas differ mainly in their potency & their duration of action. Glipizide, glyburide (glibenclamide), and glimepiride are so-called second-generation sulfonylureas. They have a potency that allows them to be given in much lower doses.

Those drugs with longer half-lives (particularly chlorpropamide, glyburide, and glimepiride) can be given once daily. This benefit may be counterbalanced by a substantially increased risk of hypoglycemia.

Side effects – Sulfonylureas are usually well tolerated. Hypoglycemia is the most common side effect and is more common with long-acting sulfonylureas. Patients recently discharged from hospital are at the highest risk for hypoglycemia.

Patients should be cautioned about those settings in which hypoglycemia is most likely to occur. They are:

After exercise or a missed meal.When the drug dose is too high.With the use of longer-acting drugs (glyburide, chlorpropamide).In patients who are undernourished or abuse alcohol.In patients with impaired renal or cardiac function or inter-current gastrointestinal disease.With concurrent therapy with salicylates, sulfonamides, fibric acid derivatives (such as gemfibrozil), and warfarin.After being in the hospital.

Other, infrequent side effects that can occur with all sulfonylureas include nausea, skin reactions, and abnormal liver function tests. Weight gain can also occur unless the diabetic diet and exercise program are followed. Chlorpropamide has two unique effects: it can cause an unpleasant flushing reaction after alcohol ingestion and it can cause hyponatremia (low blood sodium), primarily by increasing the action of antidiuretic hormone.

Clinical use – Sulfonylureas usually lower blood glucose concentrations by about 20 percent. They are most likely to be effective in patients whose weight is normal or slightly increased. In contrast, insulin should be used in patients who are underweight, are losing weight, or are ketotic despite adequate caloric intake.

The choice of sulfonylurea is primarily dependent upon cost and availability, because their efficacy is similar. However, given the relatively high incidence of hypoglycemia in patients taking glyburide or chlorpropamide, shorter acting drugs should probably be used in elderly patients

Repaglinide – Repaglinide is a short-acting glucose-lowering drug recently approved by the Food and Drug Administration for therapy of type 2 diabetes alone or in combination with metformin. It is structurally different than sulfonylureas, but acts similarly by increasing insulin secretion.

The clinical efficacy of repaglinide is similar to that of the sulfonylureas. The recommended starting dose is 0.5 mg before each meal for patients who have not previously taken oral hypoglycemic drugs. The maximum dose is 4 mg before each meal; the dose should be skipped if the meal is missed. Hypoglycemia is the most common adverse effect.

Natiglinide – Natiglinide (Starlix) is a very short-acting glucose lowering drug whose mode of action is similar to the sulfonylureas and is nearing approval by the FDA. A potential advantage of this drug is that it seems to have it’s effect on the first phase of insulin release rather than the late phase of insulin release. The first phase of insulin release is brisk, of short duration and occurs within minutes of ingesting food. It is this first phase of insulin release that is abnormal in early diabetes & can often be found in patients with impaired glucose tolerance prior to the onset of diabetes. The usual dose is 120 mg before meals.

METFORMIN – Metformin has been used in Europe for over thirty years, and has been available in the United States since March 1995. It is effective only in the presence of insulin but, in contrast to sulfonylureas, it does not directly stimulate insulin secretion. Its major effect is to increase insulin action.

How metformin increases insulin action is not known but it is known to affect many tissues. One important effect appears to be suppression of glucose output from the liver.

Clinical use – Metformin is most often used in patients with type 2 diabetes who are obese, because it promotes modest weight reduction or at least weight stabilization. This is in contrast to the increased appetite and weight gain often induced by insulin and sulfonylureas.

Metformin typically lowers fasting blood glucose concentrations by approximately 20 percent, a response similar to that achieved with a sulfonylurea.

Metformin given in combination with a sulfonylurea lowers blood glucose concentrations more than either drug alone.

In addition to causing modest weight loss, metformin has two other advantages as compared with sulfonylureas. They are:

It is less likely to cause hypoglycemia.It has prominent lipid-lowering activity, producing a significant reduction in serum triglyceride and free fatty acid concentrations, a small reduction in serum low-density lipoprotein (LDL) cholesterol concentration, and an elevation in serum high-density lipoprotein (HDL) cholesterol concentration.

There are, however, two disadvantages to metformin: the risk for lactic acidosis described below and its prominent gastrointestinal side effects.

Pharmacokinetics – Metformin should be taken with meals and should be started at a low dose to avoid intestinal side effects. The dose can be increased slowly as necessary to a maximum of 2550 mg/day (850 mg TID).

Side effects – The most common side effects of metformin are gastrointestinal, including a metallic taste in the mouth, mild anorexia, nausea, abdominal discomfort, and diarrhea. These symptoms are usually mild, transient, and reversible after dose reduction or discontinuation of the drug.

A rare problem is lactic acidosis, which may be fatal in as many as one-half of cases. The risk is much less than with another biguanide, phenformin, which was withdrawn from use in the United States in the 1970s because of this complication. Serious lactic acid accumulation usually occurs only in the presence of a predisposing conditions including:

Renal insufficiency.Current liver disease or alcohol abuse.Heart failure.Past history of lactic acidosis.Severe infection with decreased tissue perfusion.Hypoxic statesSerious acute illnessHemodynamic instabilityAge 80 years or more

Drug interactions – A potential drug interaction exists between metformin and cimetidine (Tagamet) resulting in an increase in metformin blood levels. This interaction could increase the risk of hypoglycemia in patients taking metformin plus a sulfonylurea or insulin, and could increase the risk of lactic acidosis in those with impaired renal function. These risks could increase now that cimetidine is available over-the-counter. Other H2-blockers are less likely to cause this problem.

The manufacturer also recommends discontinuing metformin for 48 hours after any radiologic procedure involving the administration of iodinated contrast material into the blood. The rationale for this recommendation is to avoid the potential for high plasma metformin concentrations if the patient develops contrast-induced acute renal failure

THIAZOLIDINEDIONES – The thiazolidinediones such as Avandia (Rosiglitazone) and Actos (Pioglitazone) reverse insulin resistance by acting on muscle, fat and to a lesser extent liver to increase glucose utilization and diminish glucose production.

The mechanism by which the thiazolidinediones increase insulin action is not well understood but they may be acting by redistributing fat from the visceral compartment to the subcutaneous compartment. We know that visceral fat is associated with insulin resistance.

Efficacy – In one large study of 284 patients with type 2 diabetes treated with Rezulin, the fall in mean fasting blood glucose concentration was significant but not dramatic over 12 weeks; patients treated with placebo had a fall in blood glucose concentration of only 4 mg/dL. The HbA1c value in the troglitazone group fell from 8.6 to 8.1 percent.

Thiazolidinediones are also effective when given in combination with metformin, although they are not currently approved for this purpose.

Safety – There have been reports of severe liver injury in small numbers of patients receiving Rezulin and this product has now been removed from the market. Most cases of liver damage occured early in treatment with the drug and were reversible when it was stopped but there have been some deaths. The newer agents such as Actos and Avandia have a much lower incidence of this side effect.

ALPHA-GLUCOSIDASE INHIBITORS – The alpha-glucosidase inhibitors include acarbose (Precose) & Miglitol (Glycet) and are available in the United States. They inhibit the upper gastrointestinal enzymes that converts dietary starch and other complex carbohydrates into simple sugars which can be absorbed. The result is to slow the absorption of glucose after meals.

As in patients with type 2 diabetes, patients with type 1 diabetes have a reduction in the amplitude of glucose excursion and HbA1c and a possible reduction in nocturnal hypoglycemia with alpha-glucosidase inhibitors.

The main side effects of alpha-glucosidase inhibitors are flatulence and diarrhea. These symptoms are usually mild and do not necessitate cessation of therapy.

Thursday 6 August 2015

BILIRUBIN & BILIRUBIN TEST :

What Is a Bilirubin Blood Test?

Bilirubin is a yellow pigment that is in everyone’s blood and stool. If you notice a yellowing of your skin or the whites of your eyes, this is called jaundice, and it may be caused by high levels of bilirubin.

Bilirubin is made in the body when old red blood cells are broken down. The breakdown of old cells is a normal, healthy process. After circulating in your blood, bilirubin then travels to your liver. In the liver, bilirubin is excreted into the bile duct and stored in your gall bladder. Eventually, the bilirubin is released the small intestine as bile to help digest fats and ultimately excreted with your stool.

Bilirubin attached to sugar is called “direct” or “conjugated” bilirubin, and bilirubin without sugar is called “indirect” or “unconjugated” bilirubin. All the bilirubin in your blood together is called “total” bilirubin.

A bilirubin blood test will get an accurate count of all three bilirubin levels in your blood: direct, indirect, and total.

Common Reasons to Test for Bilirubin

If bilirubin is not being attached to sugars (conjugated) in the liver and/or is not being adequately removed from the blood, it can mean that there is damage to your liver. Testing for bilirubin in the blood is therefore a good test of damage to your liver.

Newborn infants often have some jaundice, and bilirubin in the blood may be tested several times in the first few days of an infant’s life to check that the liver is starting to work properly. Jaundice in a newborn can be very serious if left untreated.

Other reasons for high bilirubin levels could be that more blood cells are being destroyed than normal. This is called hemolysis.

Sometimes bilirubin is measured as part of a “panel” of tests. Often, the liver is evaluated with a group of tests that include bilirubin, alanine transaminase (ALT), asparate transaminase (AST), alkaline phosphatase (ALP), albumin, total protein, and others.

How Is the Bilirubin Blood Test Performed?

A small amount of your blood is needed to perform this test. The blood sample is obtained through venipuncture, where a needle is inserted into a vein through the skin in your arm or hand, and a small amount of blood comes out through the needle into tubing and is stored in a test tube.

How Do I Prepare for the Bilirubin Blood Test?

For this test, you will need to fast (not eat or drink anything other than water) for four hours before you have the test performed. Drink a normal amount of water before going to the laboratory or collection site.

You may have to stop taking certain medications before the test is performed, but only if your doctor tells you to do this. Examples of drugs that can affect bilirubin levels include antibiotics like penicillin G, sedatives like phenobarbital, diuretics like furosemide, and asthma medications like theophylline. However, there are many drugs that can influence bilirubin levels. Talk to your doctor before your test to see if you should stop or continue taking medication.

What Are the Risks of the Bilirubin Blood Test?

When the blood is collected, you may feel some moderate pain or a mild pinching sensation, though this is usually very short in duration and very slight. After the needle is taken out, you may feel a throbbing sensation, and you will be instructed to apply pressure to the site where the needle entered your skin. A bandage will be applied that needs to remain in place typically for 10 to 20 minutes, and you should avoid using that arm for heavy lifting for the rest of the day.

There are some very rare risks to taking a blood sample:

lightheadedness or faintinghematoma—a bruise where blood accumulates under the skininfection—usually prevented by the skin being cleaned before the needle is insertedexcessive bleeding—Bleeding for a long period afterward may indicate a more serious bleeding condition and should be reported to your doctor.

What Is a Normal Result for the Bilirubin Blood Test?

In an older child or adult, normal values of direct (conjugated) bilirubin are from 0 to 0.3 milligrams per deciliter (mg/dL). Normal values of total bilirubin (direct and indirect) are from 0.3 to 1.9 mg/dL.

In a newborn, higher bilirubin is normal due to the stress of birth. Normal bilirubin in a newborn would be under 5 mg/dL, but up to 60 percent of newborns have some kind of jaundice and bilirubin levels above 5 mg/dL.

What Is an Abnormal Result for the Bilirubin Blood Test?

Your doctor may want to perform further blood tests or an ultrasound if high levels of bilirubin are detected in your blood. In an adult, high bilirubin may be due to problems with the liver, bile ducts, or gallbladder. Examples include:

drug toxicityliver diseases like hepatitisGilbert’s disease (a genetic disease affecting some families)cirrhosis (scarring of the liver)biliary stricture (part of the bile duct is too narrow to allow fluid to pass)cancer of the gallbladder or pancreasgallstones

Another cause of high bilirubin may be due to problems in the blood instead of problems in the liver. Blood cells breaking down too fast can be caused by: hemolytic anemia (too many blood cells being destroyed from an autoimmune disease, genetic defect, drug toxicity, or infection); or transfusion reaction (your immune system can attack some blood given during a transfusion).

In an infant, high bilirubin and jaundice can be very dangerous, and may be caused by several factors. There are three common types:

physiological jaundice (at 2-4 days after birth, caused by a brief delay in the functioning of the liver, usually not serious)breast feeding jaundice (during first week of life, caused by a baby not nursing well or low milk supply in the mother)breast milk jaundice (after 2-3 weeks of life, caused by the processing of some substances in breast milk)

All of these can be easily treated and are usually harmless if treated. Some more serious conditions that cause high bilirubin and jaundice in the infant:

abnormal blood cell shapes (like sickle cell anemia)blood type mismatch between infant and mother (called erythroblastosis fetalis)lack of certain important proteins due to genetic defectsbleeding in the scalp due to a difficult deliveryhigh levels of red blood cells due to small size, prematurityinfections

In both adults and children, symptoms related to high bilirubin involve jaundice, a yellowing of the skin or eyes, fatigue, itchy skin, dark urine, and low appetite.

Sunday 2 August 2015

DIABETES INSIPIDUS :

Diabetes Insipidus

Pathophysiology

                   Diabetes insipidus is caused by abnormality in the functioning or levels of antidiuretic hormone (ADH), also known of as vasopressin. Manufactured in the hypothalamus and stored in the pituitary gland, ADH helps to regulate the amount of fluid in the body.

In healthy individuals, when the bodily fluids are depleted, ADH is released from the pituitary gland which prevents the excretion of fluids from the body in the form of urine. ADH acts on the kidneys to increase water permeability in the collecting duct and distal convoluted tubule. Specifically, ADH acts on transmembrane protein channels called aquaporins that open up to allow water into the collecting duct. Once the permeability rises, the water is re-absorbed into the blood, reducing urine volume and increasing its concentration.

The two forms of diabetes insipidus

In central (cranial) diabetes insipidus, the production or release of ADH is too low to stop the kidneys from passing dilute urine, which results in an increased loss of water and therefore more thirst. People with nephrogenic diabetes insipidus, however, have adequate amounts of ADH in the body but the kidneys fail to respond it, and again the urine is still not concentrated.

Causes of diabetes insipidus

Some of the causes of cranial diabetes insipidus include:

Genetic inheritance of a mutation in the vasopressin gene, AVP-NPII. The pattern of inheritance is autosomal.Brain tumors such as pituitary adenoma and craniopharyngiomasHead injury causing damage to the pituitary gland or hypothalamus. Injury may also result after brain surgery.Meningitis and encephalitis or brain infections may also affect the pituitary gland and the hypothalamus.Sheehan's syndrome, deposition of iron (haemochromotosis) in pituitary/hypothalamic tissue, Langerhans' cell histiocytosis and Wolfram syndrome are other causes.Blood vessel complications such as those during pregnancy where the blood supply to the hypothalamus and pituitary gland may be compromised.Stroke or sudden loss of oxygen to the brain (e.g. during anesthesia or drowning) may also result in diabetes insipidus.

Causes of nephrogenic diabetes insipidus

Familial or genetic causes resulting from mutation in the AQP2gene that codes for the aquaporin-2 protein. This genetic mutation is has an autosomal recessive pattern of inheritance.Metabolic causes such as high blood sugar, high blood calcium and low potassium.The use of drugs such as lithium used to treat bipolar disorder can decrease the expression of aquaporin-2.Diseases such as amyloidosis, obstructive uropathy, chronic kidney disease and polycystic kidney disease.

Saturday 1 August 2015

HIRSCHSPRUNG'S DISEASE :


 Hirschsprung's Disease

What is Hirschsprung's disease?

Hirschsprung's disease occurs when some of the nerve cells that are normally present in the intestine do not form properly while a baby is developing during pregnancy.

As food is digested, muscles move food forward through the intestines in a movement called peristalsis. When we eat, nerve cells that are present in the wall of the intestines receive signals from the brain telling the intestinal muscles to move food forward.

In children with Hirschsprung's disease, a lack of nerve cells in part of the intestine interrupts the signal from the brain and prevents peristalsis in that segment of the intestine. Because stool cannot move forward normally, the intestine can become partially or completely obstructed (blocked), and begins to expand to a larger than normal size.

The problems a child will experience with Hirschsprung's disease depend on how much of the intestine has normal nerve cells present.

What causes Hirschsprung's disease?

Between the 4th and the 12th weeks of pregnancy, while the fetus is growing and developing, nerve cells form in the digestive tract, beginning in the mouth and finishing in the anus. For unknown reasons, the nerve cells do not grow past a certain point in the intestine in babies with Hirschsprung's disease.

How often does Hirschsprung's disease occur?

Hirschsprung's disease occurs in 1 out of every 5,000 live births.

Who is at risk for Hirschsprung's disease?

Hirschsprung's disease occurs five times more frequently in males than in females, and children with Down syndrome have a higher risk of having the disease.

There is possibly a genetic, or inherited, cause for Hirschsprung's disease.

Why is Hirschsprung's disease a concern?

Because a segment of the intestine lacks normal nerve cells, digested food and stool cannot move forward through that portion of the digestive tract. The intestine becomes blocked with stool, and the baby will be constipated, or unable to have normal bowel movements.

The obstruction (blockage) causes pressure on the inside of the intestine, causing part of the intestinal wall to wear thin. Eventually, a bacterial infection can develop in the digestive tract, causing serious problems.

What are the symptoms of Hirschsprung's disease?

Most children with Hirschsprung's disease show symptoms in the first few weeks of life. Children who only have a short segment of intestine that lacks normal nerve cells may not show symptoms for several months or years. The following are the most common symptoms of Hirschsprung's disease. However, each person may experience symptoms differently. Symptoms may include:

Not having a bowel movement in the first 48 hours of life

Gradual bloating of the abdomen

Vomiting green or brown fluid

Children who do not have early symptoms may also present the following:

Constipation that becomes worse with time

Loss of appetite

Delayed growth

Passing small, watery, bloody stools

Loss of energy

Symptoms of Hirschsprung's disease may resemble other conditions or medical problems.

How is Hirschsprung's disease diagnosed?

A doctor will examine your child and obtain a medical history. Other tests may be done to evaluate whether your child has Hirschsprung's disease. These tests may include:

Abdominal X-ray. A diagnostic test which may show a lack of stool in the large intestine or near the anus and dilated segments of the large and small intestine.

Barium enema. A procedure performed to examine the large intestine for abnormalities. A fluid called barium (a metallic, chemical, chalky, liquid used to coat the inside of organs so that they will show up on an X-ray) is given into the rectum as an enema. An X-ray of the abdomen shows strictures (narrowed areas), obstructions (blockages), and dilated intestine above the obstruction.

Anorectal manometry. A test that measures nerve reflexes which are missing in Hirschsprung's disease.

Biopsy of the rectum or large intestine. A test that takes a sample of the cells in the rectum or large intestine and then looks for nerve cells under a microscope.

What is the treatment for Hirschsprung's disease?

Specific treatment for Hirschsprung's disease will be determined by your child's doctor based on the following:

The extent of the problem

Your child's age, overall health, and medical history

Your child's tolerance for specific medications, procedures, or therapies

Expectations for the course of the disorder

The opinion of the health care providers involved in the child's care

Your opinion and preference

An operation is usually necessary to deal with intestinal obstruction caused by Hirschsprung's disease. The surgeon removes the portion of the rectum and intestine that lacks normal nerve cells. When possible, the remaining portion is then connected to the anal opening. This is known as a pull-through procedure. At times, a child may need to have a colostomy done so stool can leave the body. With a colostomy, the upper end of the intestine is brought through an opening in the abdomen known as a stoma. Stool will pass through the opening and then into a collection bag. The colostomy may be temporary or permanent, depending on the amount of intestine that needs to be removed. After a healing period, many children can have the intestine surgically reconnected above to the anal opening and have the colostomy closed.

Thursday 30 July 2015

GLASGOW COMA SCALE (GCS) :

Glasgow Coma Scale ( GCS)

There are a few different systems that medical practioners use to diagnose the symptoms of Traumatic Brain Injury. This section discusses the Glasgow Coma Scale.
The Glasgow Coma Scale is based on a 15 point scale for estimating and categorizing the outcomes of brain injury on the basis of overall social capability or dependence on others.

The test measures the motor response, verbal response and eye opening response with these values:

I. Motor Response(M)

6 - Obeys commands fully
5 - Localizes to noxious stimuli
4 - Withdraws from noxious stimuli
3 - Abnormal flexion, i.e. decorticate posturing
2 - Extensor response, i.e. decerebrate posturing
1 - No response

II. Verbal Response(V) 
5 - Alert and Oriented
4 - Confused, yet coherent, speech
3 - Inappropriate words and jumbled phrases consisting of words
2 - Incomprehensible sounds
1 - No sounds

III. Eye Opening(E)
4 - Spontaneous eye opening
3 - Eyes open to speech
2 - Eyes open to pain
1 - No eye opening

The final score is determined by adding the values of (E+V+M = ? score).

This number helps medical practioners categorize the four possible levels for survival, with a lower number indicating a more severe injury and a poorer prognosis:

Mild (13-15):
More in-depth discussion on the Mild TBI Symptoms page.

Moderate Disability (9-12):
Loss of consciousness greater than 30 minutes
Physical or cognitive impairments which may or may resolve
Benefit from Rehabilitation

Severe Disability (3-8):
Coma: unconscious state. No meaningful response, no voluntary activities
Vegetative State (Less Than 3):

Sleep wake cycles
Aruosal, but no interaction with environment
No localized response to pain

Persistent Vegetative State:
Vegetative state lasting longer than one month

Brain Death:
No brain function
Specific criteria needed for making this diagnosis

Wednesday 22 July 2015

CONGESTIVE HEART FAILURE (CHF) : A BRIEF REVIEW

Congestive Heart Failure - Diastolic

Introduction

Congestive heart failure (CHF) occurs when the cardiac output is not adequate enough to meet the demands of the body. This can occur for several reasons as congestive heart failure is the predominant clinical presentation in multiple disease states. Heart failure can be due to:

Systolic dysfunction (reduced ejection fraction)Diastolic dysfunction (relaxation or filling abnormality)Valvular heart diseaseRight heart failureArrhythmiaHigh output CHF (i.e. severe anemia, arteriovenous malformations)

Review of diastolic congestive heart failure will be presented here. Review of systolic congestive heart failure, valvular heart disease, right heart failure and high output heart failure are presented elsewhere.

Pathophysiology

Diastolic dysfunction occurs when the left ventricular myocardium is non-compliant and not able to accept blood return in a normal fashion from the left atrium. This can be a normal physiologic change with aging of the heart or result in elevated left atrial pressures leading to the clinical manifestations of diastolic congestive heart failure.

While there is some degree of activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) in states of diastolic heart failure, it is not as dramatic as seen with systolic heart failure. Also, these neurohormonal systems do not exert the negative remodeling effect on the heart during diastolic heart failure as much as occurs with systolic congestive heart failure. Below is a schematic of the neurohormal mechanisms present in congestive heart failure:

Etiology

There are a number of causes of diastolic congestive heart failure:

Hypertensive heart diseaseAging of the heartRestrictive cardiomyopathyValvular heart diseaseTachyarrhythmiasConstrictive pericarditis

Hypertension causes left ventricular hypertrophy and impaired relaxation. Over time, this progressing resulting in higher degrees of diastolic dysfunction, low cardiac output and symptoms of congestive heart failure.

The aging process of the heart is not well understood, however fibrotic changes are seen within the myocardium. This results in a relaxation abnormality that is almost universally present by the age of 60. In the elderly, this can progress causing significant diastolic impairment and congestive heart failure.

Restrictive cardiomyopathies frequently cause deposition of substances (i.e. amyloid protein) within the myocardium causing diastolic relaxation abnormalities and when severe, diastolic congestive heart failure.

Valvular heart disease such as mitral stenosis, technically causes heart failure due to diastolic dysfunction of the left ventricle. Severe aortic stenosis causes left ventricular hypertrophy and when left ventricular pressures increase a significant amount, diastolic heart failure can occur.

When a tachyarrhythmia occurs such as atrial fibrillation with an uncontrolled ventricular response, congestive heart failure can occur in the setting of normal systolic function from a shortened diastolic filling time. This is technically a form of diastolic heart failure, however once ventricular rates are controlled, the cardiac hemodynamics should dramatically improve.

Symptoms

The general symptoms of congestive heart failure are the same regardless of the etiology (systolic or diastolic) and are attributed to either fluid retention (related to the activated RAAS) or low cardiac output. They can also be categorized as from left heart failure versus right heart failure.

Left heart failure will result in low cardiac output symptoms and transmission of the increased left-sided cardiac pressures into the lungs causing pulmonary edema and a sense of dyspnea. With physical exertion the heart demands increased cardiac output which is not able to be satisfied in states of heart failure and thus left heart pressures increase significantly causing this transient pulmonary edema.

As those increased pressures from the left heart affect the right ventricle, right heart failure can ensue. The most common cause of right heart failure is left heart failure.
Right heart failure symptoms include lower extremity dependant edema. When the legs are elevated at night, the fluid redistributes centrally causing pulmonary edema resulting in orthopnea (dyspnea while laying flat) or paroxysmal nocturnal dyspnea (PND). Hepatic congestion can occur causing right upper quadrant abdominal pain.

Symptoms related to low cardiac output include fatigue, weakness and in extreme cases, cardiac cachexia can occur.

The New york Heart Association (NYHA) functional class helps to classify patients based on their symptoms of heart failure.

Class I: No symptoms of heart failure
Class II: Symptoms of heart failure with moderate exertion such as ambulating 2 blocks or 2 flights of stairs
Class III: Symptoms of heart failure with minimal exertion such as ambulating 1 block or 1 flight of stairs, but no symptoms at rest
Class IV:  Symptoms of heart failure at rest

Note that the NYHA functional class differs from the ACC/AHA heart failure classification system in that the former allows movement from one class to the other while the ACC/AHA classification does not (see below).

Diagnosis

Echocardiography is the gold standard to diagnose diastolic dysfunction. There are four grades of diastolic dysfunction as described below. Clinical manifestations of congestive heart failure may start to occur once grade II diastolic dysfunction is present, however not in the presence of grade I diastolic dysfunction (impaired relaxation).

Grade I (impaired relaxation): This is a normal finding and occurs in nearly 100% of individuals by the age of 60. The E wave velocity is reduced resulting in E/A reversal (ratio < 1.0). The left atrial pressures are normal. The deceleration time of the E wave is prolonged measuring > 200 ms. The e/e’ ratio measured by tissue Doppler is normal.

Grade II (pseudonormal): This is pathological and results in elevated left atrial pressures. The E/A ratio is normal (0.8 +- 1.5), the deceleration time is normal (160-200 ms), however the e/e’ ratio is elevated. The E/A ratio will be < 1 with Valsalva. A major clue to the presence of grade II diastolic dysfunction as compared to normal diastolic function is the presence of structural heart disease such as left atrial enlargement, left ventricular hypertrophy or systolic dysfunction. If significant structural heart disease is present and the E/A ratio as well as the deceleration time appear normal, suspect a pseudonormal pattern. Valsalva distinguishes pseudonormal from normal as well as the e/e’ ratio. Diuresis can frequently reduce the left atrial pressure relieving symptoms of heart failure and returning the hemodynamics to those of grade I diastolic dysfunction.

Grade III (reversible restrictive): This results in significantly elevated left atrial pressures. Also known as a “restrictive filling pattern”, the E/A ratio is > 2.0, the deceleration time is < 160 ms, and the e/e’ ratio is elevated. The E/A ratio changes to  < 1.0 with Valsalva. Diuresis can frequently reduce the left atrial pressure relieving symptoms of heart failure and returning the hemodynamics to those of grade I diastolic dysfunction.

Grade IV (fixed restrictive): This indicates a poor prognosis and very elevated left atrial pressures. The E/A ratio is > 2.0, the deceleration time is low and the e/e’ ratio is elevated. The major difference distinguishing grade III from grade IV diastolic dysfunction is the lack of E/A reversal with the Valsalva maneuver (no effect will be seen with Valsalva). Diuresis will not have a major effect on the left atrial pressures and clinic heart failure is likely permanent. Grade IV diastolic dysfunction is present only in very advanced heart failure and frequently seen in end-stage restrictive cardiomyopathies such as amyloid cardiomyopathy.

Treatment

There is a relative lack of data to guide medical therapy in patients with diastolic congestive heart failure, especially when compared to systolic congestive heart failure.

The ACC/AHA guidelines give three class I recommendations to medically treat chronic diastolic congestive heart failure.

The first is to control the heart rate in patients with atrial fibrillation in order to improve diastolic filling. Tachycardia shortens diastolic filling time and so keeping heart rates < 100 beats per minute and preferably between 60-80 beats per minute will improve cardiac output when significant diastolic heart failure is present. Rate control can be achieved using beta-blockers, non-dihydropyridine calcium channel blockers, or digoxin.

The second recommendation is to control systolic and diastolic blood pressure using the standard treatment for hypertension.

The third is to use diuretics to control pulmonary congestion and peripheral edema.

Tuesday 21 July 2015

BASIC ANATOMY OF EYEBALL :

Cornea

The cornea is the clear window to the eye.  It is at the front of the eye just in front of the coloured part of the eye, the iris.  It has no blood vessels in it, and normally is completely transparent.  When it is scarred or infected, it may appear white in some areas.  When a person gets a "scratch" to the eye or a corneal abrasion, the superficial layer of the cornea is torn off.  This can be very painful but heals quickly with the proper treatment.  People who have permanent corneal scarring may be candidates for a corneal transplant.  When people wear contact lenses, these lenses sit on top of the cornea.  The cornea is the structure that is lasered during procedures like LASIK or PRK, which help people see without glasses (Refractive Laser).

Anterior Chamber

The anterior chamber is the area just in front of the iris inside the eye.  It is filled with watery fluid calledaqueous.  Aqueous is produced in the cilary body muscle (in the posterior chamber) and flows through the pupil, into the anterior chamber angle or drainage canal, to exit the eye.  This is a very important pathway of study in glaucoma research.

Posterior Chamber

The posterior chamber is behind the iris and includes the ciliary body muscle and the lens complex.  The aqueous is produced in this chamber and flows to the front of the eye to be drained in the anterior chamber angle.

 

Iris

The iris is the part of the eye that gives us the colour of the eye, whether it be blue, brown, green or hazel.  It acts like the diaphragm of a camera and expands (dilates) and contracts to allow more or less light into the eye.

 

Sclera

This is the white hard shell around the eye which is connected to the cornea.

 

Conjunctiva

The conjunctiva is a thin membranous layer of tissue on top of the sclera.  It covers the eyeball up to the lids and then folds under the lids and covers the underside of the upper and lower lids.  You can never lose a contact lens behind the eye, since the conjunctiva creates a natural barrier.  The conjunctiva is what gets inflamed and red when we have any infection or allergic reaction of the eyes giving the appearance of "pink eyes". Sometimes, people get a red spot under the conjunctiva, which can be a bit of blood, that can arise spontaneously or with minor trauma, and usually clears up within a few days.

 

Pupil

The pupil is the hole in the iris.  The pupil gets larger when it is dark letting more light into the eye, and smaller when it is bright letting less light into the eye.  When you eye doctor dilates your eyes with eye drops, the pupil becomes large for a few hours and it becomes blurry up close.  This allows more visibility inside your eyes to do a more thorough examination of the inside of your eyes.

 

Lens

This is the natural lens of the eye.  Just as a camera has a lens, so does the eye.  This lens is clear for most of our lives, and changes shape as we try to focus on things up close and things in the distance.  With some medications or diseases, the ability of our lenses to change shape becomes temporarily (or permanently)impaired.  For example, pregnant women may notice that their glasses prescription changes during pregnancy, and then stabilizes after giving birth.  This is due to hormonal changes that affect the shape of the lens during pregnancy.  Overtime, and earlier with some medications (like steroids) and diseases (like diabetes), or lifestyle issues (such as smoking or excessive exposure to UV radiation), clouding of our lenses develops which we call "cataract".  Cataracts blur our vision and can be treated with cataract surgery.

 

Ciliary Body and Ciliary Muscle

This is the muscle that enables the iris to move back and forth to change the shape of the pupil.  It also produces the fluid of the eye called "aqueous".  Diode laser is a treatment for glaucoma that targets the ciliary body to decrease the production of aqueous thereby decreasing the build-up of fluid and pressure in the eye.

 

Vitreous

The vitreous is a clear gel that fills the bulk of the eyeball.  It is solid when we are born and is attached to the inside of the eye.  As we get older, the vitreous becomes loose, and "floaters" are created.  These are just pieces of more solid vitreous, floating in the more liquid vitreous, and creating shadows on the retina.  Sometimes the vitreous falls off the back of the eye abruptly (posterior vitreous detachment), and creates sudden floaters and flashing light sensation.  The flashing is from the vitreous pulling on the retina.  Sometimes, the retina is torn during this spontaneous event (happens with aging).  This is called a retinal tearand can be a risk factor for a retinal detachment.  This can be lasered close to avoid further problems.

 

Retina

The retina is the "film" of the eye, if you think if the eye as a camera.  It is a very thin layer of nerve tissue.  If a person has a retinal detachment, this means that this layer has come loose and is not attached to the circulation.  This is an eye emergency that needs to be surgically treated to prevent permanent vision loss.

 

Macula

The macula is the centre of the retina that is responsible for our central, reading vision. The retina outside the macula provides us with our peripheral or side vision.  Macular degeneration is degeneration of this central, very important part of the retina.  Although people with macular degeneration may lose their central, reading vision, they will still have their peripheral vision, if the rest of the retina is okay.

 

Retinal vessels

The retina is provided with oxygen and nutrients by vessels both within it and underneath it (in the choroid).  The retinal layers need both sets of circulation to function properly.  Sometimes, people may have a "stroke" in the eye.  This means that the circulation an artery of the eye has been blocked.  This is often due to "atherosclerosis".  Veins can also become blocked, especially from uncontrolled high blood pressure.

 

Choroid

This is the layer of mostly blood vessels between the retina and the sclera.

 

Optic Nerve

The optic nerve is like a large fibreoptic cable, bringing together all the nerve endings from the retina and connecting them to the brain for interpretation of the pictures that have been taken by the eye.  The brain is our "super computer " that translates these photo messages for us.  In glaucoma, the optic nerve degenerates over time, and we lose this vital connection to the brain.  The result is weakening and loss of vision, without proper treatment.  HRT and OCT imaging is used to track changes in the optic nerve over time that may be too subtle for the naked eye to detect.

Friday 17 July 2015

ANAPHYLAXIS / HYPERSENSITIVITY / ALLERGY - OVERVIEW

What are allergies? What is an allergy?

                         Allergies are hypersensitive immune responses to substances that either enter or come in contact with the body, such as pet dander, pollen or bee venom. A substance that causes an allergic reaction is called an "allergen". Allergens can be found in food, drinks or the environment.

Most allergens are harmless, i.e. the majority of people are not affected by them.

If you are allergic to a substance, such as pollen, your immune system reacts to it as if it were a pathogen (a foreign harmful substance), and tries to destroy it.

Allergies are very common. Public health authorities estimate that about 20% of people in North America and Western Europe suffer from some degree of hay fever (allergic rhinitis, allergy to pollen).

A study published in JAMA Pediatrics (September 2013 issue) reported that kids' food allergies cost both families and the US as a whole nearly $25 billion annually.

The number of people worldwide with allergies is increasing. According to Allergy UK, about 30% to 40% of people have an allergy at some stage in their lives. Some years ago, this increase was only apparent in industrialized nations. However, middle-income nations are now reporting higher rates of allergies across their populations.

The steepest increase in allergies has been observed in children, particularly food allergies.

A team of researchers from Northwestern University Feinberg School of Medicine reported in Pediatrics that about 8% of American children have some kind of food allergy. 38.7% of those with food allergies have a history of anaphylaxis (severe allergic reactions), and 30.4% are allergic to more than one food.

Researchers from St. Luke's Roosevelt Hospital Center, New York, found that foreign-born children who live in the USA have a lower risk of allergies. This risk grows the longer they remain in America.

What are the signs and symptoms of allergies?

A symptom is something the patient feels and describes, while a sign can be detected by others too. Pain is a symptom and a rash is a sign.

When a person with an allergy comes into contact with an allergen, the allergic reaction is not immediate. The immune system gradually builds up sensitivity to the substance before overreacting to it.

The immune system needs time to recognize and remember the allergen. As it becomes sensitive to it, it starts making antibodies to attack it - this process is called sensitization.

Sensitization can take from a few days to several years. In many cases the sensitization process is not completed and the patient experiences some symptoms but never a full allergy.

When the immune system reacts to an allergen, there is inflammation and irritation. Signs and symptoms depend on the type of allergen. Allergic reactions may occur in the gut (digestive system), skin, sinuses, airways, eyes, and nasal passages.

Allergies from dust and pollen may have the following symptoms:

Blocked noseItchy eyesItchy noseRunny noseSwollen eyesWatery eyesCough.

Skin reactions, as in eczema (atopic dermatitis) may include:

Flaking skinItchy skinPeeling skinRed skin, rashes.

Food allergies may include several types of reactions:

VomitingTongue swellingTingling in the mouthSwelling of the lipsSwelling of the faceSwelling in the throatStomach crampsShortness of breathRectal bleeding (in children, rare in adults)Itchiness in the mouthDiarrheaAnaphylaxis - a very severe, often life-threatening allergic reaction.

The following allergic reactions are possible after an insect sting:

WheezingSwelling where the sting occurredSudden drop in blood pressureSkin itchingShortness of breathRestlessnessHives - a red and very itchy rash that spreadsDizzinessCoughChest tightnessAnxietyAnaphylaxis.

The following may be signs of an allergic reaction to medication:

WheezingSwollen tongueSwollen lipsSwelling of the faceSkin rashItchinessAnaphylaxis.

Signs and symptoms of anaphylaxis

Anaphylaxis is a serious allergic reaction of rapid onset. Anaphylaxis can be life-threatening and must be treated as a medical emergency.

This type of allergic reaction presents several different symptoms which can appear minutes or hours after exposure to the allergen. If the exposure is intravenous, onset is usually between 5 to 30 minutes. A food allergen will take longer.Anaphylaxis is a medical emergency

Researchers from the University of Manitoba, Canada, reported in The Journal of Allergy & Clinical Immunology that the most commonly affected areas in anaphylaxis are the skin (80-90%), respiratory (70%), gastrointestinal (30-45%), cardiovascular 10-45%) and the central nervous system (10-15%). In most cases two areas are affected simultaneously.

Anaphylaxis - skin symptoms

Hives all over the body, flushing and itchiness. The affected tissues may also become swollen (angioedema). Some patients may experience a burning sensation on the skin.

In about 20% of cases, there is swelling of the tongue and throat.

If the skin has a strange bluish color, it could be a sign of hypoxia (lack of oxygen).

Some patients may experience a runny nose. The membrane that covers the front of the eye and the inside of the eyelid (conjunctiva) may become inflamed.

Anaphylaxis - respiratory symptoms:

Shortness of breathWheezing - caused by bronchial muscle spasmsStridor - a high-pitched vibrating wheezing sound when breathing. Caused by upper airway obstruction due to swellingHoarsenessOdynophagia - pain when swallowingCough.

Anaphylaxis - cardiovascular symptoms

Coronary artery spasm - sudden tightening of the muscle in the artery wall (temporary) due to cells in the heart that release histamine. This can lead to myocardial infarction (heart attack), dysrhythmia (abnormal heart rhythm), or cardiac arrest (heart stops).

Low blood pressure can cause the heart rate to accelerate. In some cases a slow heart rate can occur as a result of low blood pressure (Bezold-Jarisch reflex).

Patients whose blood pressure suddenly drops can feel lightheaded and dizzy. Some may lose consciousness. In some rare cases, the only sign of anaphylaxis might be low blood pressure.

Anaphylaxis - gastrointestinal symptoms

Abdominal crampsDiarrheaVomitingLoss of bladder controlPelvic pain (like uterine cramps).

Patients may also have a sense of impending doom.

What are the causes of allergies?

The immune system of a person with an allergy reacts to the allergen as though it were a harmful pathogen - such as an undesirable bacterium, virus, fungus or toxin. However, the allergen is not harmful. The immune system has simply become oversensitive to that substance.

When the immune system reacts to an allergen, it releases immunoglobulin E (IgE), a type of antibody. IgE is released to destroy the allergen. IgE causes chemicals in the body to be produced. These chemicals cause the allergic reaction.

One of these chemicals is called histamine. Histamine causes tightening of the muscles, including those in the airways and the walls of blood vessels. It also makes the lining of the nose produce more mucus.

People with allergies blame the allergen for their symptoms - a friend's pet, pollen or dust mites. However, the allergens are not harmful. The problem is not the allergen but the allergic person's immune system which mistakes harmless substances for harmful ones.

What are the risk factors for allergies?

In medicine, a risk factor is something that raises the risk of developing a disease or condition. This risk can come from something a person does. For example, smoking is a risk factor for lung disease. It can also be something you are born with. For example, if your mother had breast cancer, her daughter has a higher risk of developing breast cancer too. A family history of breast cancer is a risk factor.

Below are some risk factors associated with allergies:

A family history of asthma - if your parents, grandparents or siblings have/had asthma, your risk of having an allergy is higher.

A family history of allergies - if a close relative has/had an allergy, your risk of having an allergy yourself is greater.
Being a child - a child is much more likely to have an allergy than an adult. On a positive note, this means that many children outgrow their allergies.
Having asthma - people with asthma are significantly more likely to develop allergies.
Not enough sunlight exposure - scientists from the European Centre for Environment & Human Health, together with researchers from various Australian centers found that children living in areas with less sunlight had higher rates of allergies.
Having an allergy - if you already have an allergy, there is a greater risk that you will develop an allergy to something else.
C-section babies - a team from the Henry Ford Hospital reported that C-section babies have a considerably higher risk of developing allergies compared to those born naturally.
Chemicals used in water purification - Elina Jerschow, M.D., M.Sc., a fellow of the American College of Allergy, Asthma and Immunology, said that pesticides in tap water could be partly to blame for the increased food allergy rates in the USA.

What are the most common allergens?

An allergen is a substance which causes an allergic reaction in some susceptible people.

Below are the most common allergens, apart from foreign proteins found in blood transfusions and vaccines:

Allergens from animals

Dust mites - their excrementCockroaches calyxWoolFurDander - skin flakes (dandruff)Fel d 1 - a protein found in cat saliva and sebaceous glands. Proteins from the urine, saliva or hair of household pets can cause allergic reactions in some people.

Medications

PenicillinSalicylates - a salt of salicylic acid commonly found in many medications, including aspirinSulfonamides

Foods - theoretically, any food can cause an allergy. The eight foods most likely to cause allergies are eggs (especially egg-white, albumen), fish, milk, nuts from trees, peanuts (groundnuts), wheat, soy, and shellfish.

Scott H. Sicherer, MD, Professor of Pediatrics, Jaffe Food Allergy Institute at Mount Sinai School of Medicine, and colleagues reported in the Journal of Allergy and Clinical Immunology that the number of kids with peanut allergies more than tripled between 1997 and 2008.

The following foods can also cause allergies:

Corn (maize)CeleryPumpkinBeansSesame.

Insect stings

wasp sting venommosquito stingsbee sting venomfire ants.

Insect bites

kissing bugshorsefliesfleasblackflies.

Insects that cause respiratory allergies

cockroachescaddis flieslake fliesmidgesmoths.

Mold spores

AlternariaAspergillusAureobasidium (Pullularia)Cladosporium (Hormodendrum)EpicoccumFusariumHelmin thosporiumMucorPenicilliumRhizopus.

Plant pollens - cause hay fever.

grass - the most common cause of hay fevertrees - including oak, ash, cedar, willow, and hazelweeds - such as mugwort and ragweed.

Other allergens

household chemicalsmetal - nickel, cobalt, chromium, and zinclatex.

Diagnosing allergies

The doctor will ask the patient questions regarding the allergy symptoms, when they occur, how often and what seems to cause them.

The patient will also be asked whether there is a family history of allergies, and whether other household members (who might not be relatives) have allergies.

The doctor, probably a primary care physician initially, may either recommend some tests to find out which allergen is causing the symptoms, or refer the patient to a specialist.

In the American College of Allergy, Asthma and Immunology's website there is a page called "Find an Allergist", where you can find a specialist who has been certified by the College.

On The British Society for Allergy & Clinical Immunology: BSACI homepage you can find an allergy clinic near you (UK only).

Even if the patient knows what causes his/her allergy, the doctor will wish to carry out tests to determine whether a particular substance within the food, drink, or something else is the culprit.

Below are some examples of allergy tests

Blood test - to measures levels of IgE antibodies released by the immune system. This test is sometimes called the radioallergosorbent test (RAST).
Skin prick test - also known as puncture testing or prick testing. The skin is pricked with a small amount of a possible allergen. If there is a skin reaction - itchy, red and swollen skin - it may mean there is an allergy.
Patch test - for patients with contact dermatitis (eczema). Special metal discs with trace amounts of a suspect allergen are taped onto the back. The doctor checks for a skin reaction 48 hours later, and then again after a couple of days.

The National Health Service says that commercial allergy-testing kits are not recommended and that patients should have these tests done by specialized health care professionals.

The National Institute for Health and Clinical Excellence (NICE), in the UK, found that the IgE antibody test and the skin prick test were cost effective compared with no test.

What are the treatment options for allergies?

The most effective treatment and management of an allergy is to avoid exposure to the allergen.

However, sometimes it is not possible to completely avoid an allergy. A person with hay fever cannot avoid exposure to pollens, unless he/she closes all the windows in the house and never goes out. Even then, there is a risk of other people bringing pollen into the house.

It is also important to educate patients so that they know how to identify their allergenic foods properly. Many people with peanut or tree nut allergy could not correctly identify which items they were allergic to in a study carried out at Ohio State University.

Study leader, Professor Todd Hostetler, said "When we ask patients to avoid peanuts and tree nuts, we shouldn't assume patients know what they're looking for, because they may not. It's worthwhile to do some education about what a tree nut is, what a peanut is, and what they all look like."

Medications for allergies

Drugs can help treat the symptoms of allergy, but do not cure it. The majority of allergy medications are OTC (over-the-counter, no prescription required). Before considering a medication, speak to a pharmacist or your doctor.

Antihistamines (histamine antagonists) - they block the action of histamine, a chemical released in the body as part of an allergic reaction. Some antihistamines are not suitable for children.
Decongestants - some patients say they help with a blocked nose in cases of hay fever, pet allergy or dust allergy. Decongestants are short-term medications.
Leukotriene receptor antagonists (anti-leukotrienes) - for asthma when other treatments have not worked. Anti-leukotrienes block the effects of leukotrienes, chemicals that cause swelling. Leukotrienes are released in the body when there is an allergic reaction.
Steroid sprays - applied to the inside lining of the nose. Corticosteroid sprays help reduce nasal congestion.

Immunotherapy

Also known as hyponsesitization. This type of therapy rehabilitates the immune system. The doctor administers gradually increasing doses of allergens over a period of years. The aim is to induce long-term tolerance by reducing the allergen's tendency to trigger IgE production.

Immunotherapy is only used in cases of severe allergies.

Thursday 16 July 2015

ANATOMY OF THE LIVER

 

Anatomy

The liver is the largest organ in the abdominal cavity and the most complex. It consists of a myriad of individual microscopic functional units call lobules. The liver performs a variety of functions including the removal of endogenous and exogenous materials from the blood, complex metabolic processes including bile production, carbohydrate homeostasis , lipid metabolism, urea formation, and immune functions. 

The liver arises from the ventral mesogastrium and only the upper posterior surface is outside of that structure. The ligamentum teres and falciform ligament connect the liver to the anterior body wall. The lesser omentum connects it to the stomach and the coronary and triangular ligaments to the diaphragm. The liver is smooth and featureless on the diaphragmatic surface and presents with a series of indentations on the visceral surface where it meets the right kidney, adrenal gland, inferior vena cava, hepatoduodenal ligament and stomach (Figure 4).

Figure . A, Normal gross anatomy of a liver; B, histological slide; B’, histological view.

The liver can be considered in terms of blood supply hepatocytes, Kupffer cells and biliary passages. The liver receives its blood supply from the portal vein and hepatic artery, the former providing about 75% of the total 1500 ml/min flow. Small branches from each vessel—the terminal portal venule and the terminal hepatic arteriole—enter each acinus at the portal triad. Pooled blood then flows through sinusoids between plates and hepatocytes in order to exchange nutrients. The hepatic vein carries efferent blood into the inferior vena cava and a supply of lymphatic vessels drains the liver. 

Parenchymal cells or hepatocytes comprise the bulk of the organ and carry out complex metabolic processes. Hepatocytes are responsible for the liver’s central role in metabolism (Figure 4B'). These cells are responsible for the formation and excretion of bile ; regulation of carbohydrate homeostasis ; lipid synthesis and secretion of plasma lipoproteins; control of cholesterol metabolism; and formation of urea, serum albumin, clotting factors, enzymes, and numerous proteins. The liver also aids in the metabolism and detoxification of drugs and other foreign substances. 

Kupffer cells line the hepatic sinusoids and are part of the reticuloendothelial system, filtering out minute foreign particles, bacteria, and gut-derived toxins. They also play a role in immune processes that involve the liver. 

Biliary passages begin as tiny bile canaliculi formed by hepatocytes. These microvilli -lined structures progress into ductules, interlobular bile ducts, and larger hepatic ducts. Outside the porta hepatis, the main hepatic duct joins the cystic duct from the gallbladder to form the common bile duct, which drains into the duodenum. 

Monday 13 July 2015

RHEUMATIC HEART DISEASE :

Rheumatic heart disease

Introduction

Rheumatic heart disease is a chronic condition that results years after acute rheumatic fever which is caused by group A beta-hemolytic Streptococcus (Streptococcus pyogenes). This organism produces a pharyngitis that can be followed by rheumatic fever in about 0.3-3% of cases and occurs several weeks after the pharyngitis resolves.

Rheumatic heart disease chronically manifests as congestive heart failure form valvular involvement. Most commonly the mitral valve is affected resulting in mitral stenosis or mitral regurgitation. Less commonly the aortic valve can be involved and tricuspid valve involvement is rare, but reported. In approximately 50% of cases of rheumatic heart disease, the patient does not give a history of having rheumatic fever as a child.

Symptoms

Rheumatic fever acutely causes symptoms of pericarditis and congestive heart failure depending on the degree of valvulitis and myocarditis present. Migratory polyarthritis is the most common symptom in acute rheumatic fever. Subcutaneous nodules arise over the bones and tendons. A rash that starts on the trunk and extends to the limbs. The rash has a characteristic erythematous ring with a pale center and is referred to as erythema marginatum. Sydenham's chorea (St. Vitus’ dance) occurs and is described as uncontrollable rapid movements of the arms and facial muscles.

Rheumatic heart disease chronically manifests as congestive heart failure from valvular heart disease including mitral stenosis, mitral regurgitation and aortic stenosis.

Diagnosis

Rheumatic fever is diagnosed with the Jones criteria:
 

Rheumatic valvular disease is diagnosed predominantly via echocardiography. The mitral valve will give a classic “hockey stick” appearance.

Physical Examination

Physical examination findings include inflamed joints, subcutaneous nodules, a pericardial friction rub, findings of congestive heart failure (edema, pulmonary rales, elevated jugular venous pressure), and the rash of erythema marginatum

The Carey Coombs Murmur occurs during acute rheumatic fever. Mitral valvulitis can occur causing thickening of the leaflets. A murmur is created by increased blood flow across the thickened mitral valve. This can be distinguished from rheumatic mitral valve stenosis by the absence of an opening snap. The murmur is described as a mid diastolic murmur heard at the mitral listening post with the bell of the stethoscope with the patient in the left lateral decubitus position at end expiration. As the rheumatic valvulitis resolves, the murmur disappears.

Rheumatic heart disease chronically will most commonly reveal the murmur of mitral valve stenosis:

 

Treatment

Reducing the inflammatory response with corticosteroids is the mainstay of therapy during acute rheumatic fever when there is significant cardiac involvement. Aspirin historically had been used however the risk of Reye’s syndrome causing fulminant hepatic failure and death in children has decreased its use.

Long-term therapy with penicillin is recommended as re-infection with group A beta-hemolytic Streptococcus can cause a serious recurrence.

See the review on mitral valve stenosis for treatment strategies for rheumatic mitral stenosis, the most common manifestation of rheumatic valvular disease.

Sunday 12 July 2015

KETOGENIC DIET GUIDE :

What to Eat and What to Avoid

In short, you should eat REAL food (meat, eggs, nuts, yogurt, vegetables and occasionally some fruits). Apart from the obvious limitation of net carbs content in food, it is also recommended to avoid processed food and any food that may contain preservatives and colourings.

KetoDiet is not just about losing weight at any cost; it's about adopting a healthier lifestyle.


Below is a list of the most common low-carb foods recommended for the ketogenic diet.

EAT Freely

Grass-fed and wild animal sources

grass-fed meat (beef, lamb, goat, venison), wild-caught fish & seafood (avoid farmed fish), pastured pork and poultry, pastured eggs, gelatin, ghee, butter - these are high in healthy omega 3 fatty acids (avoid sausages and meat covered in breadcrumbs, hot dogs, meat that comes with sugary or starchy sauces)offal, grass-fed (liver, heart, kidneys and other organ meats)

Healthy fats

saturated (lard, tallow, chicken fat, duck fat, goose fat, clarified butter / ghee, butter, coconut oil)monounsaturated (avocado, macadamia and olive oil)polyunsaturated omega 3s, especially from animal sources (fatty fish and seafood)You can find a complete guide to fats & oils in my post here. (which to use for cold use, which for high-heat cooking and which to avoid)

Non-starchy vegetables

leafy greens (Swiss chard, bok choy, spinach, lettuce, chard, chives, endive, radicchio, etc.)some cruciferous vegetables like kale (dark leaf), kohlrabi, radishescelery stalk, asparagus, cucumber, summer squash (zucchini, spaghetti squash), bamboo shoots

Fruits, Nuts and Seeds

avocado, coconut, macadamia nuts

Beverages and Condiments

water (still), coffee (black or with cream or coconut milk), tea (black, herbal)pork rinds (cracklings) for "breading"mayonnaise, mustard, pesto, bone broth (make your own), pickles, fermented foods (kimchi, kombucha and sauerkraut (make your own) - best home-made with no additives (my recipes for home-made condiments are here)all spices and herbs, lemon or lime juice and zestwhey protein (beware of additives, artificial sweeteners, hormones and soy lecithin), egg white protein and gelatin (grass-fed, hormone free)

Eat Occasionally

Vegetables, Mushrooms and Fruits

some cruciferous vegetables (white and green cabbage, red cabbage, cauliflower, broccoli, Brussels sprouts, fennel, turnips, rutabaga / swede)nightshades (eggplant, tomatoes, peppers)some root vegetables (parsley root), spring onion, leek, onion, garlic, mushrooms, winter squash (pumpkin)sea vegetables (nori, kombu), okra, bean sprouts, sugar snap peas, wax beans, globe or French artichokes, water chestnutsberries (blackberries, blueberries, strawberries, raspberries, cranberries, mulberries, etc.), rhubarb, olives

Grain-fed animal sources and Dairy

beef, poultry, eggs and ghee (avoid farmed pork, it's too high in omega 6s!)dairy products (plain full-fat yogurt, cottage cheese, cream, sour cream, cheese) - avoid products labeled "low-fat", most of them are packed with sugar and starch and have little sating effectbacon - beware of preservatives and added starches (nitrates are acceptable if you eat enough antioxidants)

Nuts and seeds

pecans, almonds, walnuts, hazelnuts, pine nuts, flaxseed, pumpkin seeds, sesame seeds, sunflower seeds, hemp seedsbrazil nuts (beware of very high level of selenium - don't eat too many of them!)

Fermented soy products

if eaten, only non GMO and fermented soy products (Natto, Tempeh, soy sauce or paleo-friendly coconut aminos)Edamame (green soy beans), black soybeans - unprocessed

Condiments

healthy "zero-carb" sweeteners (Stevia, Swerve, Erythritol, etc.)thickeners: arrowroot powder, xanthan gum (keep in mind xanthan gum is not paleo-friendly - some people following the paleo diet use it, as you only need a very little amount)sugar-free tomato products (puree, passata, ketchup)cocoa and carob powder, extra dark chocolate (more than 70%, better 90% and beware of soy lecithin), cocoa powderbeware of sugar-free chewing gums and mints - some of them have carbs

Some Vegetables, Fruits, Nuts and Seeds with Average Carbohydrates

root vegetables (celery root, carrot, beetroot, parsnip and sweet potato)apricot, watermelon, Cantaloupe / Galia / Honeydew melons, dragon fruit (Pitaya), peach, nectarine, apple, grapefruit, kiwifruit, kiwi berries, orange, plums, cherries, ears, figs (fresh)dried fruit (dates, berries, raisins, figs, etc.) – only in very small quantities (if any)pistachio and cashew nuts, chestnuts

Alcohol

dry red wine, dry white wine, spirits (unsweetened) - avoid for weight loss, only for weight maintenance

AVOID Completely: Food rich in carbohydrates, factory-farmed meat and processed foods

1) All grains, even whole meal (wheat, rye, oats, corn, barley, millet, bulgur, sorghum, rice, amaranth, buckwheat, sprouted grains), quinoa and white potatoes. this includes all products made from grains (pasta, bread, pizza, cookies, crackers, etc.) sugar and sweets (table sugar, HFCS, agave syrup, ice creams, cakes, sweet puddings and sugary soft-drinks)

2) Factory-farmed pork and fish are high ininflammatory omega 6 fatty acids and farmed fish may contain PCBs, avoid fish high in mercury.

3) Processed foods containing carrageenan (e.g. almond milk products), MSG (e.g. in some whey protein products), sulphites (e.g. in dried fruits, gelatin), BPAs (they don't have to be labeled!), wheat gluten

4) Artificial sweeteners (Splenda, Equal, sweeteners containing Aspartame, Acesulfame, Sucralose, Saccharin, etc.)

5) Refined fats / oils (e.g. sunflower, safflower, cottonseed, canola, soybean, grapeseed, corn oil), trans fats such as margarine.

6) "Low-fat", "low-carb" and "zero-carb" products (Atkins products, diet soda and drinks, chewing gums and mints may be high in carbs or contain artificial additives, gluten, etc.)

7) Milk (only small amounts of raw, full-fat milk is allowed). Milk is not recommended for several reasons. Firstly, from all the diary products, milk is difficult to digest, as it lacks the "good" bacteria (eliminated through pasteurization) and may even contain hormones. Secondly, it is quite high in carbs (4-5 grams of carbs per 100 ml). For coffee and tea, replace milk with cream in reasonable amounts. You may have a small amount of raw milk but be aware of the extra carbs.

8) Alcoholic, sweet drinks (beer, sweet wine, cocktails, etc.) - you can try my healthier versions of popular cocktails and drinks.

9) Tropical fruit (pineapple, mango, banana, papaya, etc.) and some high-carb fruit(tangerine, grapes, etc.) Also avoid fruit juices (yes, even 100% fresh juices!) - better to drink smoothies if any, but either way very limited. Juices are just like sugary water, but smoothies have fiber, which is at least more sating. This also includes dried fruit (dates, raisins, etc.) if eaten in large quantities.

10) Mainly for health reasons, avoid soy products apart from a few non-GMO fermented products which are known for their health benefits. Also avoid wheat gluten which may be used in low-carb foods. When you give up bread, you shouldn't eat any part of it. Beware ofBPA-lined cans. If possible, use naturally BPA-free packaging like glass jars or make my own ingredients such as ghee, ketchup, coconut milk or mayonnaise. BPA has been linked to many negative health effects such as impaired thyroid function and cancer. Other additives to avoid:carrageenan (e.g. almond milk products), MSG (e.g. in some whey protein products) andsulfites (e.g. in dried fruits, gelatin)

And here is everything in a nutshell...