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.

A 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

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.

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.

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.

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.