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INTRODUCTION-

Arteriosclerosis occurs when the blood vessels that carry oxygen and nutrients from your heart to the rest of your body (arteries) become thick and stiff — sometimes restricting blood flow to your organs and tissues. Healthy arteries are flexible and elastic, but over time, the walls in your arteries can harden, a condition commonly called hardening of the arteries.

Atherosclerosis is a specific type of arteriosclerosis, but the terms are sometimes used interchangeably. Atherosclerosis refers to the buildup of fats, cholesterol and other substances in and on your artery walls (plaque), which can restrict blood flow.

The plaque can burst, triggering a blood clot. Although atherosclerosis is often considered a heart problem, it can affect arteries anywhere in your body. Atherosclerosis may be preventable and is treatable.

Atherosclerosis is a narrowing of the arteries caused by a buildup of plaque. Arteries are the blood vessels that carry oxygen and nutrients from your heart to the rest of your body.

As you get older, fats, cholesterol, and calcium can collect in your arteries and form plaque. The buildup of plaque makes it difficult for blood to flow through your arteries. This buildup may occur in any artery in your body, including your heart, legs, and kidneys.

It can result in a shortage of blood and oxygen in various tissues of your body. Pieces of plaque can also break off, causing a blood clot. If left untreated, atherosclerosis can lead to heart attack, stroke, or heart failure.

Atherosclerosis is a fairly common problem associated with aging. This condition can be prevented and many successful treatment options exist.

CAUSES-

Plaque buildup and subsequent hardening of the arteries restricts blood flow in the arteries, preventing your organs and tissues from getting the oxygenated blood they need to function.

The following are common causes of hardening of the arteries:

High cholesterol

Cholesterol is a waxy, yellow substance that’s found naturally in the body as well as in certain foods you eat.

If the levels of cholesterol in your blood are too high, it can clog your arteries. It becomes a hard plaque that restricts or blocks blood circulation to your heart and other organs.

Diet

It’s important to eat a healthy diet. The American Heart Association (AHA) recommends that you follow an overall healthy dietary pattern that stresses:

• a wide range of fruits and vegetables
• whole grains
• low-fat dairy products
• poultry and fish, without skin
• nuts and legumes
• non-tropical vegetable oils, such as olive or sunflower oil

Some other diet tips:

• Avoid foods and drinks with added sugar, such as sugar-sweetened beverages, candy, and desserts. The AHA recommends no more than 6 teaspoons or 100 calories of sugar a day for most women, and no more than 9 teaspoons or 150 calories a day for most men.
• Avoid foods high in salt. Aim to have no more than 2,300 milligrams (mg) of sodium per day. Ideally, you’d consume no more than 1,500 mg a day.
• Avoid foods high in unhealthy fats, such as trans fats. Replace them with unsaturated fats, which are better for you. If you need to lower your blood cholesterol, reduce saturated fat to no more than 5 to 6 percent of total calories. For someone eating 2,000 calories a day, that’s about 13 grams of saturated fat.

Aging-

As you age, your heart and blood vessels work harder to pump and receive blood. Your arteries may weaken and become less elastic, making them more susceptible to plaque buildup.

SYMPTOM-

Atherosclerosis develops gradually. Mild atherosclerosis usually doesn’t have any symptoms.

You usually won’t have atherosclerosis symptoms until an artery is so narrowed or clogged that it can’t supply adequate blood to your organs and tissues. Sometimes a blood clot completely blocks blood flow, or even breaks apart and can trigger a heart attack or stroke.

Symptoms of moderate to severe atherosclerosis depend on which arteries are affected. For example:

• If you have atherosclerosis in your heart arteries, you may have symptoms, such as chest pain or pressure (angina).
• If you have atherosclerosis in the arteries leading to your brain, you may have signs and symptoms such as sudden numbness or weakness in your arms or legs, difficulty speaking or slurred speech, temporary loss of vision in one eye, or drooping muscles in your face. These signal a transient ischemic attack (TIA), which, if left untreated, may progress to a stroke.
• If you have atherosclerosis in the arteries in your arms and legs, you may have symptoms of peripheral artery disease, such as leg pain when walking (claudication).
• If you have atherosclerosis in the arteries leading to your kidneys, you develop high blood pressure or kidney failure.

When to see a doctor

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If you think you have atherosclerosis, talk to your doctor. Also pay attention to early symptoms of inadequate blood flow, such as chest pain (angina), leg pain or numbness.

Early diagnosis and treatment can stop atherosclerosis from worsening and prevent a heart attack, stroke or another medical emergency.

Risk factors

Hardening of the arteries occurs over time. Besides aging, factors that increase the risk of atherosclerosis include:

• High blood pressure
• High cholesterol
• Diabetes
• Obesity
• Smoking and other tobacco use
• A family history of early heart disease
• Lack of exercise
• An unhealthy diet

DIAGNOSIS-

Your doctor will perform a physical exam if you have symptoms of atherosclerosis. They’ll check for:

• a weakened pulse
• an aneurysm, an abnormal bulging or widening of an artery due to weakness of the arterial wall
• slow wound healing, which indicates a restricted blood flow

A cardiologist may listen to your heart to see if you have any abnormal sounds. They’ll be listening for a whooshing noise, which indicates that an artery is blocked. Your doctor will order more tests if they think you may have atherosclerosis.

Tests can include:

• a blood test to check your cholesterol levels
• a Doppler ultrasound, which uses sound waves to create a picture of the artery that shows if there’s a blockage
• an ankle-brachial index (ABI), which looks for a blockage in your arms or legs by comparing the blood pressure in each limb
• a magnetic resonance angiography (MRA) or a computed tomography angiography (CTA) to create pictures of the large arteries in your body
• a cardiac angiogram, which is a type of chest X-ray that’s taken after your heart arteries are injected with radioactive dye
• an electrocardiogram (ECG or EKG), which measures the electrical activity in your heart to look for any areas of decreased blood flow
• a stress test, or exercise tolerance test, which monitors your heart rate and blood pressure while you exercise on a treadmill or stationary bicycle

Complications

The complications of atherosclerosis depend on which arteries are blocked. For example:

• Coronary artery disease. When atherosclerosis narrows the arteries close to your heart, you may develop coronary artery disease, which can cause chest pain (angina), a heart attack or heart failure.
• Carotid artery disease. When atherosclerosis narrows the arteries close to your brain, you may develop carotid artery disease, which can cause a transient ischemic attack (TIA) or stroke.
• Peripheral artery disease. When atherosclerosis narrows the arteries in your arms or legs, you may develop circulation problems in your arms and legs called peripheral artery disease. This can make you less sensitive to heat and cold, increasing your risk of burns or frostbite. In rare cases, poor circulation in your arms or legs can cause tissue death (gangrene).
• Aneurysms. Atherosclerosis can also cause aneurysms, a serious complication that can occur anywhere in your body. An aneurysm is a bulge in the wall of your artery. Most people with aneurysms have no symptoms. Pain and throbbing in the area of an aneurysm may occur and is a medical emergency. If an aneurysm bursts, you may face life-threatening internal bleeding. Although this is usually a sudden, catastrophic event, a slow leak is possible. If a blood clot within an aneurysm dislodges, it may block an artery at some distant point.
• Chronic kidney disease. Atherosclerosis can cause the arteries leading to your kidneys to narrow, preventing oxygenated blood from reaching them. Over time, this can affect your kidney function, keeping waste from exiting your body.

Prevention

The same healthy lifestyle changes recommended to treat atherosclerosis also help prevent it. These include:

• Quitting smoking
• Eating healthy foods
• Exercising regularly
• Maintaining a healthy weight

Just remember to make changes one step at a time, and keep in mind what lifestyle changes are manageable for you in the long run.

TREATMENT-

Treatment involves changing your current lifestyle to decrease the amount of fat and cholesterol you consume. You may need to exercise more to improve the health of your heart and blood vessels.

Unless your atherosclerosis is severe, your doctor may recommend lifestyle changes as the first line of treatment. You may also need additional medical treatments, such as medications or surgery.

Medications

Medications can help prevent atherosclerosis from worsening.

Medications for treating atherosclerosis include:

• cholesterol-lowering medications, including statins and fibrates
• angiotensin-converting enzyme (ACE) inhibitors, which may help prevent narrowing of your arteries
• beta-blockers or calcium channel blockers to lower your blood pressure
• diuretics, or water pills, to help lower your blood pressure
• anticoagulants and antiplatelet drugs such as aspirin to prevent blood from clotting and clogging your arteries

Aspirin is particularly effective for people with a history of atherosclerotic cardiovascular disease (e.g., heart attack and stroke). An aspirin regimen can reduce your risk of having another health event.

If there’s no prior history of atherosclerotic cardiovascular disease, you should only use aspirin as a preventive medication if your risk of bleeding is low and your risk of atherosclerotic cardiovascular disease is high.

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Surgery

If symptoms are especially severe or if muscle or skin tissue are endangered, surgery may be necessary.

Possible surgeries for treating atherosclerosis include:

• bypass surgery, which involves using a vessel from somewhere else in your body or a synthetic tube to divert blood around your blocked or narrowed artery
• thrombolytic therapy, which involves dissolving a blood clot by injecting a drug into your affected artery
• angioplasty, which involves using a catheter and a balloon to expand your artery, sometimes inserting a stent to leave the artery open
• endarterectomy, which involves surgically removing fatty deposits from your artery
• atherectomy, which involves removing plaque from your arteries by using a catheter with a sharp blade at one end

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INTRODUCTION

Nephritic syndrome is characterized by glomerular damage leading to hematuria, pyuria, water retention, and subsequent hypertension and edema. It can be caused by a variety of conditions including autoimmune, hereditary, and infectious diseases. This article provides an overview of nephritic syndrome; Nephritic diseases can present in varying degrees of severity, ranging from asymptomatic hematuria to systemic involvement as in rapidly progressive glomerulonephritis. The urine sediment is typically characterized by red blood cell (RBC) casts, mild to moderate proteinuria (< 3.5 g/day), and sterile pyuria. Diagnosis of the underlying disease is often based on presentation and laboratory values, although renal biopsy may be indicated for confirmation.

Nephritic syndrome is not a disease but a syndrome. A syndrome is a group of symptoms that often and predictably occur together, and which develop as a result of another condition. Syndromes are not necessarily specific to any disease or disorder. Nephritic syndrome has many potential triggers, therefore, successfully treating it involves identifying the underlying causes.

Nephritic syndrome has both acute and chronic forms. Acute, or rapidly-progressing, nephritic syndrome usually comes on suddenly and, because of acute and painful symptoms, seldom goes undetected. Chronic nephritic syndrome typically progresses slowly and often goes undetected for some time.

Chronic inflammation of the kidneys can cause scarring, which may negatively impact kidney function and lead to high blood pressure and, eventually, if left undiagnosed and untreated, to a need for dialysis (renal replacement therapy, when a dialysis machine replaces the kidneys’ function and filters waste products from the blood), and possibly kidney transplantation.

CAUSES-

Nephritic syndrome is the result of inflammation affecting small groups of blood vessels, known as glomeruli, in the kidneys. As the glomeruli are the kidneys’ main filter units, this inflammation disrupts the kidneys’ ability to adequately filter blood. The inflammation can originate in the kidneys themselves or be the result of infection or injury elsewhere in the body.

It can occur in people of any age, including children.

Nephritic syndrome can develop as a result of any of the following:

Primary glomerular diseases: Such as IgA nephropathy (Berger’s disease) or membranoproliferative glomerulonephritis. IgA nephropathy is a very common cause of nephritic syndrome.

Bacterial infections: Such as methicillin-resistant staphylococcus aureus (MRSA), pneumococcal pneumonia, typhoid, infective endocarditis, or secondary syphilis. Nephritic syndrome following a streptococcal throat infection is fairly common, especially in children.

Viral infections: Such as hepatitis B, mumps, measles, chickenpox or glandular fever (mononucleosis).

Multisystem systemic/inflammatory diseases: Such as vasculitis, Goodpasture’s Syndrome, granulomatosis with polyangiitis, Henoch-Schönlein purpura, or lupus (systemic lupus erythematosus).

	Associations	Findings	Treatment
Poststreptococcal glomerulonephritis	Occurs weeks after group A β-hemolytic streptococci infections Pharyngitis/tonsillitis (most common): 1–2 weeks Skin infections: 3–4 weeks Usually affects children between the ages of 3–12 years Can lead to RPGN in some cases	Positive antistreptococcal antibodies (ASO, ADB) ↓ Serum C3 complement levels Tea- or cola-colored urine LM: glomeruli appear enlarged and hypercellular IM: granular subepithelial immune complex depositions (IgG, IgM, C3) → “lumpy-bumpy” appearance EM: dome-shaped, subepithelial deposits (“humps”)	Usually self-limiting Supportive therapy (see “Treatment” below)
IgA nephropathy (Berger’s disease)	Most common idiopathic glomerulonephritis worldwide Episodic gross hematuria during or directly after upper respiratory tract (URT), gastrointestinal (GI) infections, or strenuous exercise Occurrence: ♂ > ♀ Peak incidence: 2nd to 3rd decade of life ∼ 25-30% of the patients progress to end-stage renal disease (ESRD) within 20–25 years	Asymptomatic microhematuria with intermittent gross hematuria ↑ Serum IgA Normal C3 complement levels LM: mesangial proliferation IM: mesangial IgA deposits EM: mesangial immune complex deposits	Supportive therapy (see “Treatment” below) Glucocorticoids in severe cases
Small vessel vasculitis	Granulomatosis with polyangiitis (Wegener’s)	Pulmonary and nasopharyngeal involvement is common → hemoptysis, nasal ulcers	c-ANCA Renal biopsy: segmental necrotizing glomerulonephritis EM: immune complex depositions	Supportive therapy (see “Treatment” below) Immunosuppressive therapy
Microscopic polyangiitis	Usually only mild respiratory symptoms	p-ANCA
Churg-Strauss syndrome	Patients present with: Asthma Allergic rhinitis Purpura Peripheral neuropathy	p-ANCA (∼ 50% of cases) Peripheral eosinophilia Focal segmental necrotizing glomerulonephritis
Goodpasture syndrome (Anti–GBM antibody disease)	Two peaks of occurrence: 3rd decade of life (♂ > ♀) and ≥ 60 years of age (♀ > ♂) Caused by antibodies against type IV collagen Antibodies can cross-react with basement membrane of pulmonary capillaries and lead to pulmonary hemorrhage and hemoptysis Can lead to RPGN	Pulmonary infiltrates on chest x–ray IM: linear deposition of immunoglobulin (IgG) along the glomerular basement membrane	Immunosuppressive therapy Plasmapheresis
Thin basement membrane disease	Hereditary disorder Abnormalities of type IV collagen Good prognosis	Persistent microhematuria Possible episodic gross hematuria, typically occurring during or directly after an upper respiratory tract infection or exercise EM: diffuse thinning of glomerular basement membrane	Renal function monitoring Supportive therapy (see “Treatment” below)
Alport syndrome	X-linked (usually affects males) Mutation in gene for type IV collagen Often leads to ESRD	Persistent microhematuria with intermittent gross hematuria Associated with sensorineural hearing loss and abnormalities of the eye EM: splitting and alternating thickening and thinning of the glomerular basement membrane	Supportive therapy (see “Treatment” below) Renal transplant can lead to development of Goodpasture syndrome
Lupus nephritis	Complication of systemic lupus erythematosus Can be nephritic or nephrotic Can lead to RPGN in some cases	ANA, anti-dsDNA antibodies Histologic changes are very variable	Supportive therapy (see “Treatment” below) Immunosuppressive therapy
Rapidly progressive glomerulonephritis (RPGN)	Glomerular diseases that progress to ESRD within weeks to months	Can be caused by a variety of diseases: Goodpasture syndrome (anti-GBM disease) Poststreptococcal glomerulonephritis Systemic lupus erythematosus (SLE) Microscopic polyangiitis Granulomatosis with polyangiitis (Wegener’s) LM, IM, EM: crescent formation, monocytes, macrophages	Immunosuppressive therapy Plasmapheresis

PATHOPHYSIOLOGY-

• Inflammation → cytokine release → glomerular capillary damage
  • Porous glomerular basement membrane → leakage of proteins and RBCs → nephritic sediment (all blood components are detectable on urinalysis)
    • Proteinuria (< 3.5 g/24h): leakage of proteins
    • Hematuria: leakage of RBCs, which stick together and form red blood cell casts in the renal tubules
  • Oliguria: inflammatory infiltrates reduce fluid movement across the membrane (↓ GFR)
  • Azotemia: inflammation prevents sufficient filtering and excretion of urea
  • Salt retention → intravascular volume expansion → hypertension and edema

SYMPTOM-

Typical symptoms include passing less urine than normal, having blood in the urine and swelling of the feet or face (edema). Other possible symptoms are flank pain, back pain, headache, shortness of breath and symptoms related to the underlying cause, for example a skin rash and joint pain.

The symptoms of nephritic syndrome differ, depending on whether the acute or chronic form of the syndrome is present.

Symptoms of acute nephritic syndrome include:

• Edema in the face and legs: Edema is the accumulation of fluids in the body, usually under the skin, leading to a puffy appearance.
• Low urine volume: Known as oliguria, this is defined as less than 500ml of urine being produced in a 24-hour period.
• Hematuria: Blood in the urine which often, but not necessarily, leads to red discoloration. There are two types of hematuria: microhematuria, which indicates unseen blood, and macrohematuria, in which the blood is visible to the eye.
• High blood pressure: Hypertension, which results from the disruption of kidney function, may also occur. High blood pressure is generally defined as a resting blood pressure of 140/90 mmHg or higher in adults,

. In children, what constitutes hypertension depends on the age and size of the child. Fever, weakness and fatigue

• Appetite loss, vomiting and abdominal pain
• Malaise (a feeling of general unwellness) and nausea may also be present.

Chronic nephritic syndrome usually presents with fairly mild or even undetectable symptoms, which can include:

• Edema
• Hypertension/high blood pressure
• Kidney failure in later stages

Symptoms of kidney failure can include:

• Edema
• Hypertension/high blood pressure
• Kidney failure in later stages

Symptoms of kidney failure can include:

• Itchy skin and/or rash
• Decreased appetite
• Nausea
• Vomiting
• Fatigue
• Difficulty breathing

In both chronic and acute nephritic syndrome, the urine will usually contain high concentrations of red blood cells, as the blood cells leak out of the damaged glomeruli.

DIAGNOSIS-

The diagnosis of nephritic syndrome is typically based on a physical examination of the person and analysis of their urine (urinalysis). People with nephritic syndrome tend to have high blood pressure, so a doctor will check this. A doctor will also look for signs of:

• Abnormalities, such as dark color or cloudiness in the urine
• Protein in the urine (proteinuria), which may indicate nephrotic syndrome
• Uremia, an excess of urea or creatinine in the blood, or azotemia, an excess of nitrogen-rich waste compounds in the blood
• Increased fluid volume in the body, which may lead to edema
• Reduced filtration in the kidneys, specifically the glomeruli

A kidney biopsy (tissue sample from the kidney) may be performed to investigate the cause of the nephritic syndrome.

Urinalysis, blood tests and diagnostic procedures

Because nephritic syndrome is a cluster of symptoms rather than a disease in itself, much of the testing that makes up the diagnosis is aimed at determining what the underlying cause is. Another important element in diagnosis is differential diagnosis, as the illness may be nephrosis rather than nephritis.

In examining a person with potential nephritic syndrome, a doctor might carry out the following tests:

Take patient history: A doctor will ask the affected person about the time at which their symptoms began and attempt to determine the point at which the kidneys began to excrete protein into the urine.

Check appearance and colour of urine: Urine that is dark in colour may be very concentrated and contain blood.

Blood pressure: Hypertension can be a sign of disrupted kidney function.

Edema assessment: Edema, or fluid gathering in the tissues, can be a sign that there is not enough protein in the blood and may suggest proteinuria.

Urine dipstick test: A simple form of urinalysis that is used as a quick test for blood and protein in the urine. They will use a dipstick test, in which a test-strip of paper is immersed in a urine sample, to check for blood and protein in the urine

Urinalysis: A urine sample will be sent to a laboratory to do a precise check for protein levels and red blood cells.

Blood tests: To check levels of electrolytes, creatinine, blood urea nitrogen, immunoglobulins, antibodies, and other substances.

Kidney biopsy: This relatively straightforward procedure may be performed as an outpatient procedure or after hospital admission, depending on the patient’s particular circumstances. It uses only local anesthetic and is done using ultrasound and specialized biopsy needles to remove a small sample of tissue. Kidney biopsies are a very reliable way of distinguishing chronic glomerulonephritis from other, similar, disorders.

TREATMENT–

Treatment depends on the underlying causes. Medications (such as ramipril, benazepril, candesartan, or valsartan) are typically used to treat the high blood pressure. Medications will also be administered to reduce inflammation in the kidneys.

Generally, doctors will recommend:

• Bed rest
• A diet that is restricted in salt, potassium and fluid
• Medication to control blood pressure, if necessary
• Medication to reduce inflammation
• Medication to remove fluids from the body
• Dialysis to replace kidney function in severe cases

The time it takes to recover from nephritic syndrome varies according to its severity and the underlying cause. Most patients begin to feel better fairly soon, especially if treatment is prompt.

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INTRODUCTION-

Nephrotic syndrome is a kidney disorder that causes your body to pass too much protein in your urine.

Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in your kidneys that filter waste and excess water from your blood. The condition causes swelling, particularly in your feet and ankles, and increases the risk of other health problems.

Treatment for nephrotic syndrome includes treating the condition that’s causing it and taking medications. Nephrotic syndrome can increase your risk of infections and blood clots. Your doctor might recommend medications and dietary changes to prevent complications.

Nephrotic syndrome isn’t a disease. It’s a group of symptoms that can appear if your kidneys aren’t working right.

Small blood vessels in your kidneys function as a filter, clearing out waste and extra water from your blood. That waste and water ends up in your bladder and leaves your body as urine. These vessels are part of what’s called “glomeruli,” the filtering part of your kidney.

When they’re damaged, too much protein slips through the filters into your urine. The result is nephrotic syndrome.

Nephrotic syndrome can affect both adults and children. It is treatable.

Practice Essentials

Nephrotic syndrome is the combination of nephrotic-range proteinuria with a low serum albumin level and edema. Nephrotic-range proteinuria is the loss of 3 grams or more per day of protein into the urine or, on a single spot urine collection, the presence of 2 g of protein per gram of urine creatinine.

Nephrotic syndrome has many causes, including primary kidney diseases such as minimal-change disease, focal segmental glomerulosclerosis, and membranous glomerulonephritis. Nephrotic syndrome can also result from systemic diseases that affect other organs in addition to the kidneys, such as diabetes, amyloidosis, and lupus erythematosus.

CSUSES-

You might have a condition that affects only your kidneys. Doctors call that a “primary” cause of nephrotic syndrome.

Or you might have an issue with another part of your body that also affects your kidneys. That’s called a “secondary” cause of nephrotic syndrome.

Some of the conditions that can damage your glomeruli include:

Minimal change disease, which is the main cause of nephrotic syndrome in children. Kidney tissue from people with this disease looks relatively normal under a microscope. Doctors don’t know why this disease stops the kidneys from working properly. Some potential causes of the disease include infections from viruses, allergic reactions, taking certain medications, and using non-steroidal anti-inflammatory drugs (NSAIDs)

Focal segmental glomerulosclerosis, or FSGS, is a disease that scars the glomeruli. It’s the most common primary cause of nephrotic syndrome in adults. FSGS can be caused by a virus, such as HIV, or medications.

Membranous nephropathy, in which the membranes of the glomeruli thicken. Causes may include cancer, malaria, hepatitis B, and lupus.

Diabetes, which is the most common secondary cause of nephrotic syndrome in adults. It can cause kidney damage, known as diabetic nephropathy.

Lupus (systemic lupus erythematosus), a chronic disease of the immune system, can seriously damage the kidneys.

Amyloidosis, which happens when you have a buildup of substances called amyloid proteins in your blood. This can damage your kidney.

RISK FACTOR-

Factors that can increase your risk of nephrotic syndrome include:

• Medical conditions that can damage your kidneys. Certain diseases and conditions increase your risk of developing nephrotic syndrome, such as diabetes, lupus, amyloidosis, reflux nephropathy and other kidney diseases.
• Certain medications. Medications that might cause nephrotic syndrome include nonsteroidal anti-inflammatory drugs and drugs used to fight infections.
• Certain infections. Infections that increase the risk of nephrotic syndrome include HIV, hepatitis B, hepatitis C and malaria.

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SYMPTOM-

Signs and symptoms of nephrotic syndrome include:

• Severe swelling (edema), particularly around your eyes and in your ankles and feet
• Foamy urine, a result of excess protein in your urine
• Weight gain due to fluid retention
• Fatigue
• Loss of appetite

COMPLICATION-

possible complications of nephrotic syndrome include:

• Blood clots. The inability of the glomeruli to filter blood properly can lead to loss of blood proteins that help prevent clotting. This increases your risk of developing a blood clot in your veins.
• High blood cholesterol and elevated blood triglycerides. When the level of the protein albumin in your blood falls, your liver makes more albumin. At the same time, your liver releases more cholesterol and triglycerides.
• Poor nutrition. Loss of too much blood protein can result in malnutrition. This can lead to weight loss, which can be masked by edema. You may also have too few red blood cells (anemia), low blood protein levels and low levels of vitamin D.
• High blood pressure. Damage to your glomeruli and the resulting buildup of excess body fluid can raise your blood pressure.
• Acute kidney injury. If your kidneys lose their ability to filter blood due to damage to the glomeruli, waste products can build up quickly in your blood. If this happens, you might need emergency dialysis — an artificial means of removing extra fluids and waste from your blood — typically with an artificial kidney machine (dialyzer).
• Chronic kidney disease. Nephrotic syndrome can cause your kidneys to lose their function over time. If kidney function falls low enough, you might need dialysis or a kidney transplant.
• Infections. People with nephrotic syndrome have an increased risk of infections.

DIAGNOSIS-

Tests and procedures used to diagnose nephrotic syndrome include:

• Urine tests. A urinalysis can reveal abnormalities in your urine, such as large amounts of protein. You might be asked to collect urine samples over 24 hours.
• Blood tests. A blood test can show low levels of the protein albumin and often decreased levels of blood protein overall. Loss of albumin is often associated with an increase in blood cholesterol and blood triglycerides. The creatinine and urea nitrogen levels in your blood also might be measured to assess your overall kidney function.
• Kidney biopsy. Your doctor might recommend removing a small sample of kidney tissue for testing. During a kidney biopsy, a needle is inserted through your skin and into your kidney. Kidney tissue is collected and sent to a lab for testing.

TREATMENT-

Treatment for nephrotic syndrome involves treating any medical condition that might be causing your nephrotic syndrome. Your doctor might also recommend medications and changes in your diet to help control your signs and symptoms or treat complications of nephrotic syndrome.

Medications might include:

• Blood pressure medications. Drugs called angiotensin-converting enzyme (ACE) inhibitors reduce blood pressure and the amount of protein released in urine. Medications in this category include lisinopril (Prinvil, Qbrelis, Zestril), benazepril (Lotensin), captopril and enalapril (Vasotec). Another group of drugs that works similarly is called angiotensin II receptor blockers (ARBs) and includes losartan (Cozaar) and valsartan (Diovan). Other medications, such as renin inhibitors, also might be used, though ACE inhibitors and ARBs are generally used first.
• Water pills (diuretics). These help control swelling by increasing your kidneys’ fluid output. Diuretic medications typically include furosemide (Lasix). Others include spironolactone (Aldactone, Carospir) and thiazides, such as hydrochlorothiazide or metolazone (Zaroxolyn).
• Cholesterol-reducing medications. Statins can help lower cholesterol levels. However, it’s not clear whether cholesterol-lowering medications can improve the outcomes for people with nephrotic syndrome, such as avoiding heart attacks or decreasing the risk of early death. Statins include atorvastatin (Lipitor), fluvastatin (Lescol XL), lovastatin (Altoprev), pravastatin (Pravachol), rosuvastatin (Crestor, Ezallor) and simvastatin (Zocor).
• Blood thinners (anticoagulants). These might be prescribed to decrease your blood’s ability to clot, especially if you’ve had a blood clot. Anticoagulants include heparin, warfarin (Coumadin, Jantoven), dabigatran (Pradaxa), apixaban (Eliquis) and rivaroxaban (Xarelto).
• Immune system-suppressing medications. Medications to control the immune system, such as corticosteroids, can decrease the inflammation that accompanies some of the conditions that can cause nephrotic syndrome. Medications include rituximab (Rituxan), cyclosporine and cyclophosphamide.

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INTRODUCTION-

A urinary tract infection, or UTI, is an infection in any part of your urinary system, which includes your kidneys, bladder, ureters, and urethra.

If you’re a woman, your chance of getting a urinary tract infection is high. Some experts rank your lifetime risk of getting one as high as 1 in 2, with many women having repeat infections, sometimes for years. About 1 in 10 men will get a UTI in their lifetime.

Here’s how to handle UTIs and how to make it less likely you’ll get one in the first place.

Women are at greater risk of developing a UTI than are men. Infection limited to your bladder can be painful and annoying. However, serious consequences can occur if a UTI spreads to your kidneys.

Doctors typically treat urinary tract infections with antibiotics. But you can take steps to reduce your chances of getting a UTI in the first place.

A urinary tract infection (UTI) is an infection from microbes. These are organisms that are too small to be seen without a microscope. Most UTIs are caused by bacteria, but some are caused by fungi and in rare cases by viruses. UTIs are among the most common infections in humans.

A UTI can happen anywhere in your urinary tract. Your urinary tract is made up of your kidneys, ureters, bladder, and urethra. Most UTIs only involve the urethra and bladder, in the lower tract. However, UTIs can involve the ureters and kidneys, in the upper tract. Although upper tract UTIs are more rare than lower tract UTIs, they’re also usually more severe.

Types of UTIs

An infection can happen in different parts of your urinary tract. Each type has a different name, based on where it is.

• Cystitis (bladder): You might feel like you need to pee a lot, or it might hurt when you pee. You might also have lower belly pain and cloudy or bloody urine.
• Pyelonephritis (kidneys): This can cause fever, chills, nausea, vomiting, and pain in your upper back or side.
• Urethritis (urethra): This can cause a discharge and burning when you pee.

Part of urinary tract affected	Signs and symptoms
Kidneys (acute pyelonephritis)	Upper back and side (flank) pain High fever Shaking and chills Nausea Vomiting
Bladder (cystitis)	Pelvic pressure Lower abdomen discomfort Frequent, painful urination Blood in urine
Urethra (urethritis)	Burning with urination Discharge

CAUSES-

Urinary tract infections typically occur when bacteria enter the urinary tract through the urethra and begin to multiply in the bladder. Although the urinary system is designed to keep out such microscopic invaders, these defenses sometimes fail. When that happens, bacteria may take hold and grow into a full-blown infection in the urinary tract.

The most common UTIs occur mainly in women and affect the bladder and urethra.

• Infection of the bladder (cystitis). This type of UTI is usually caused by Escherichia coli (E. coli), a type of bacteria commonly found in the gastrointestinal (GI) tract. However, sometimes other bacteria are responsible. Sexual intercourse may lead to cystitis, but you don’t have to be sexually active to develop it. All women are at risk of cystitis because of their anatomy — specifically, the short distance from the urethra to the anus and the urethral opening to the bladder.
• Infection of the urethra (urethritis). This type of UTI can occur when GI bacteria spread from the anus to the urethra. Also, because the female urethra is close to the vagina, sexually transmitted infections, such as herpes, gonorrhea, chlamydia and mycoplasma, can cause urethritis.

SYMPTOM-

Symptoms of a UTI depend on what part of the urinary tract is infected.

Lower tract UTIs affect the urethra and bladder. Symptoms of a lower tract UTI include:

• burning with urination
• increased frequency of urination without passing much urine
• increased urgency of urination
• bloody urine
• cloudy urine
• urine that looks like cola or tea
• urine that has a strong odor
• pelvic pain in women
• rectal pain in men

Upper tract UTIs affect the kidneys. These can be potentially life threatening if bacteria move from the infected kidney into the blood. This condition, called urosepsis, can cause dangerously low blood pressure, shock, and death.

Symptoms of an upper tract UTI include:

• pain and tenderness in the upper back and sides
• chills
• fever
• nausea
• vomiting

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UTI symptoms in men

Symptoms of an upper tract urinary infection in men are similar to those in women. Symptoms of a lower tract urinary infection in men sometimes includes rectal pain in addition to the common symptoms shared by both men and women.

UTI symptoms in women

Women with a lower tract urinary infection may experience pelvic pain. This is in addition to the other common symptoms. Symptoms of upper tract infections among both men and women are similar.

Risk factors

Urinary tract infections are common in women, and many women experience more than one infection during their lifetimes. Risk factors specific to women for UTIs include:

• Female anatomy. A woman has a shorter urethra than a man does, which shortens the distance that bacteria must travel to reach the bladder.
• Sexual activity. Sexually active women tend to have more UTIs than do women who aren’t sexually active. Having a new sexual partner also increases your risk.
• Certain types of birth control. Women who use diaphragms for birth control may be at higher risk, as well as women who use spermicidal agents.
• Menopause. After menopause, a decline in circulating estrogen causes changes in the urinary tract that make you more vulnerable to infection.

Other risk factors for UTIs include:

• Urinary tract abnormalities. Babies born with urinary tract abnormalities that don’t allow urine to leave the body normally or cause urine to back up in the urethra have an increased risk of UTIs.
• Blockages in the urinary tract. Kidney stones or an enlarged prostate can trap urine in the bladder and increase the risk of UTIs.
• A suppressed immune system. Diabetes and other diseases that impair the immune system — the body’s defense against germs — can increase the risk of UTIs.
• Catheter use. People who can’t urinate on their own and use a tube (catheter) to urinate have an increased risk of UTIs. This may include people who are hospitalized, people with neurological problems that make it difficult to control their ability to urinate and people who are paralyzed.
• A recent urinary procedure. Urinary surgery or an exam of your urinary tract that involves medical instruments can both increase your risk of developing a urinary tract infection.

Complications

When treated promptly and properly, lower urinary tract infections rarely lead to complications. But left untreated, a urinary tract infection can have serious consequences.

Complications of a UTI may include:

• Recurrent infections, especially in women who experience two or more UTIs in a six-month period or four or more within a year.
• Permanent kidney damage from an acute or chronic kidney infection (pyelonephritis) due to an untreated UTI.
• Increased risk in pregnant women of delivering low birth weight or premature infants.
• Urethral narrowing (stricture) in men from recurrent urethritis, previously seen with gonococcal urethritis.
• Sepsis, a potentially life-threatening complication of an infection, especially if the infection works its way up your urinary tract to your kidneys.

PREVENTION

You can take these steps to reduce your risk of urinary tract infections:

• Drink plenty of liquids, especially water. Drinking water helps dilute your urine and ensures that you’ll urinate more frequently — allowing bacteria to be flushed from your urinary tract before an infection can begin.
• Drink cranberry juice. Although studies are not conclusive that cranberry juice prevents UTIs, it is likely not harmful.
• Wipe from front to back. Doing so after urinating and after a bowel movement helps prevent bacteria in the anal region from spreading to the vagina and urethra.
• Empty your bladder soon after intercourse. Also, drink a full glass of water to help flush bacteria.
• Avoid potentially irritating feminine products. Using deodorant sprays or other feminine products, such as douches and powders, in the genital area can irritate the urethra.
• Change your birth control method. Diaphragms, or unlubricated or spermicide-treated condoms, can all contribute to bacterial growth.

TREATMENT-

Antibiotics usually are the first line treatment for urinary tract infections. Which drugs are prescribed and for how long depend on your health condition and the type of bacteria found in your urine.

Simple infection

Drugs commonly recommended for simple UTIs include:

• Trimethoprim/sulfamethoxazole (Bactrim, Septra, others)
• Fosfomycin (Monurol)
• Nitrofurantoin (Macrodantin, Macrobid)
• Cephalexin (Keflex)
• Ceftriaxone

The group of antibiotic medicines known as fluoroquinolones — such as ciprofloxacin (Cipro), levofloxacin (Levaquin) and others — isn’t commonly recommended for simple UTIs, as the risks of these medicines generally outweigh the benefits for treating uncomplicated UTIs. In some cases, such as a complicated UTI or kidney infection, your doctor might prescribe a fluoroquinolone medicine if no other treatment options exist.

Often, symptoms clear up within a few days of treatment. But you may need to continue antibiotics for a week or more. Take the entire course of antibiotics as prescribed.

For an uncomplicated UTI that occurs when you’re otherwise healthy, your doctor may recommend a shorter course of treatment, such as taking an antibiotic for one to three days. But whether this short course of treatment is enough to treat your infection depends on your particular symptoms and medical history.

Your doctor may also prescribe a pain medication (analgesic) that numbs your bladder and urethra to relieve burning while urinating, but pain usually is relieved soon after starting an antibiotic.

Frequent infections

If you have frequent UTIs, your doctor may make certain treatment recommendations, such as:

• Low-dose antibiotics, initially for six months but sometimes longer
• Self-diagnosis and treatment, if you stay in touch with your doctor
• A single dose of antibiotic after sexual intercourse if your infections are related to sexual activity
• Vaginal estrogen therapy if you’re postmenopausal

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INTRODUCTION-

Encephalitis is an inflammation of the brain tissue. The most common cause is viral infections. In rare cases it can be caused by bacteria or even fungi.

There are two main types of encephalitis: primary and secondary. Primary encephalitis occurs when a virus directly infects the brain and spinal cord. Secondary encephalitis occurs when an infection starts elsewhere in the body and then travels to your brain.

Encephalitis is a rare yet serious disease that can be life-threatening. You should call your doctor immediately if you have symptoms of encephalitis.

Encephalitis often causes only mild flu-like signs and symptoms — such as a fever or headache — or no symptoms at all. Sometimes the flu-like symptoms are more severe. Encephalitis can also cause confused thinking, seizures, or problems with movement or with senses such as sight or hearing.

In some cases, encephalitis can be life-threatening. Timely diagnosis and treatment are important because it’s difficult to predict how encephalitis will affect each individual.

Types-

Different types of encephalitis have different causes.

• Japanese encephalitis is spread by mosquitoes
• Tick-borne encephalitis is spread by ticks
• Rabies can be spread through a bite from a mammal

There is also primary or secondary encephalitis.

Primary or infectious encephalitis can result if a fungus, virus, or bacterium directly infects the brain.

Secondary, or post-infectious, encephalitis is when the immune system responds to a previous infection and mistakenly attacks the brain.

SYMPTOM-

The patient typically has a fever, headache, and photophobia (excessive sensitivity to light). There may also be general weakness and seizures.

Less common symptoms

The individual may also experience nuchal rigidity (neck stiffness), which can lead to a misdiagnosis of meningitis. There may be stiffness of the limbs, slow movements, and clumsiness. The patient may also be drowsy and have a cough.

More serious cases

In more serious cases, the person may experience very severe headaches, nausea, vomiting, confusion, disorientation, memory loss, speech problems, hearing problems, hallucinations, as well as seizures and possibly coma. In some cases, the patient can become aggressive.

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Signs and symptoms in infants

Initially, encephalitis is harder to detect in young children and babies. Parents or guardians should look out for vomiting, a bulging fontanel (the soft area on the top center of the head), incessant crying that does not get better when the baby is picked up and comforted, and body stiffness.

The symptoms of encephalitis can range from mild to severe.

Mild symptoms include:

• fever
• headache
• vomiting
• stiff neck
• lethargy (exhaustion)

Severe symptoms include:

• fever of 103°F (39.4°C) or higher
• confusion
• drowsiness
• hallucinations
• slower movements
• coma
• seizures
• irritability
• sensitivity to light
• unconsciousness

Infants and young children show different symptoms. Call a doctor immediately if your child is experiencing any of the following:

• vomiting
• bulging fontanel (soft spot in the scalp)
• constant crying
• body stiffness
• poor appetite

CAUSES-

Encephalitis can develop as a result of a direct infection to the brain by a virus, bacterium, or fungus, or when the immune system responds to a previous infection; the immune system mistakenly attacks brain tissue.

Primary (infectious) encephalitis can be split into three main categories of viruses:

1. Common viruses, including HSV (herpes simplex virus) and EBV (Epstein-Barr virus)
2. Childhood viruses, including measles and mumps
3. Arboviruses (spread by mosquitoes, ticks, and other insects), including Japanese encephalitis, West Nile encephalitis, and tick-borne encephalitis

Secondary encephalitis: could be caused by a complication of a viral infection. Symptoms start to appear days or even weeks after the initial infection. The patient’s immune system treats healthy brain cells as foreign organisms and attacks them. We still do not know why the immune system malfunctions in this way.

In more than 50 percent of encephalitis cases, the exact cause of the illness is not tracked down.

Encephalitis is more likely to affect children, older adults, individuals with weakened immune systems, and people who live in areas where mosquitoes and ticks that spread specific viruses are common.

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Common viral causes

The viruses that can cause encephalitis include:

• Herpes simplex virus (HSV). Both HSV type 1 — associated with cold sores and fever blisters around your mouth — and HSV type 2 — associated with genital herpes — can cause encephalitis. Encephalitis caused by HSV type 1 is rare but can result in significant brain damage or death.
• Other herpes viruses. These include the Epstein-Barr virus, which commonly causes infectious mononucleosis, and the varicella-zoster virus, which commonly causes chickenpox and shingles.
• Enteroviruses. These viruses include the poliovirus and the coxsackievirus, which usually cause an illness with flu-like symptoms, eye inflammation and abdominal pain.
• Mosquito-borne viruses. These viruses can cause infections such as West Nile, La Crosse, St. Louis, western equine and eastern equine encephalitis. Symptoms of an infection might appear within a few days to a couple of weeks after exposure to a mosquito-borne virus.
• Tick-borne viruses. The Powassan virus is carried by ticks and causes encephalitis in the Midwestern United States. Symptoms usually appear about a week after a bite from an infected tick.
• Rabies virus. Infection with the rabies virus, which is usually transmitted by a bite from an infected animal, causes a rapid progression to encephalitis once symptoms begin. Rabies is a rare cause of encephalitis in the United States.
• Childhood infections. Common childhood infections — such as measles (rubeola), mumps and German measles (rubella) — used to be fairly common causes of secondary encephalitis. These causes are now rare in the United States due to the availability of vaccinations for these diseases.

Risk factors

Anyone can develop encephalitis. Factors that may increase the risk include:

• Age. Some types of encephalitis are more common or more severe in certain age groups. In general, young children and older adults are at greater risk of most types of viral encephalitis.
• Weakened immune system. People who have HIV/AIDS, take immune-suppressing drugs or have another condition causing a weakened immune system are at increased risk of encephalitis.
• Geographical regions. Mosquito- or tick-borne viruses are common in particular geographical regions.
• Season of the year. Mosquito- and tick-borne diseases tend to be more common in summer in many areas of the United States.

DIAGNOSIS

Your doctor will first ask you about your symptoms. They may perform the following tests if encephalitis is suspected.

Spinal tap or lumbar puncture

In this procedure, your doctor will insert a needle into your lower back to collect a sample of spinal fluid. They will test the sample for signs of infection.

Brain imaging with CT scan or MRI

CT scans and MRI detect changes in brain structure. They can rule out other possible explanations for symptoms, such as a tumor or stroke. Certain viruses have a tendency to affect certain areas of the brain. Seeing what parts of your brain are affected can help determine what type of virus you have.

Electroencephalograph (EEG)

An EEG uses electrodes (small metal discs with wires) attached to the scalp to record brain activity. An EEG does not detect the virus that causes encephalitis, but certain patterns on the EEG may alert your neurologist to an infectious source of your symptoms. Encephalitis can lead to seizures and coma in later stages. That’s why the EEG is important in determining the areas of the brain that are affected and the types of brain waves that occur in each area.

Blood tests

A blood test can reveal signs of a viral infection. Blood tests are rarely performed alone. They usually help diagnose encephalitis along with other tests.

Brain biopsy

In a brain biopsy, your doctor will remove small samples of brain tissue to test for infection. This procedure is rarely performed because there’s a high risk of complications. It’s usually only done if doctors can’t determine the cause the brain swelling or if treatment isn’t working.

When to see a doctor

Get immediate care if you are experiencing any of the more-severe symptoms associated with encephalitis. A severe headache, fever and altered consciousness require urgent care.

Infants and young children with any signs or symptoms of encephalitis should receive urgent care.

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Complications

The complications of encephalitis vary, depending on factors such as:

• Your age
• The cause of your infection
• The severity of your initial illness
• The time from disease onset to treatment

People with relatively mild illness usually recover within a few weeks with no long-term complications.

Complications of severe illness

Inflammation can injure the brain, possibly resulting in a coma or death.

Other complications — varying greatly in severity — may persist for months or be permanent. These complications can include:

• Persistent fatigue
• Weakness or lack of muscle coordination
• Personality changes
• Memory problems
• Paralysis
• hearing defect
• vision defect

TREATMENT-

Treatment for encephalitis focuses on alleviating symptoms. There are only a limited number of reliably tested specific antiviral agents that can help, one of which is acyclovir; success is limited for most infections except when the condition is due to herpes simplex.

Corticosteroids may be administered to reduce the brain’s inflammation, especially in cases of post-infectious (secondary) encephalitis. If the patient has severe symptoms, they may need mechanical ventilation to help them breathe and other supportive treatment.

Anticonvulsants are sometimes given to patients who have seizures. Sedatives can be effective for seizures, restlessness, and irritability. For patients with mild symptoms, the best treatment is rest, plenty of fluids, and Tylenol (paracetamol) for fever and headaches. Tylenol is available to purchase online.

Prevention

Keeping up-to-date with vaccines is the most effective way of reducing the risk of developing encephalitis. These include vaccines for measles, mumps, rubella, and if the virus exists in those areas, Japanese encephalitis and tick-borne encephalitis.

In areas known to have mosquitoes that carry encephalitis-causing viruses, individuals should take measures to reduce the risk of being bitten. This may include wearing appropriate clothing, avoiding mosquito-infested areas, avoiding going outside at specific times during the day when there are large numbers of mosquitoes about, keeping the home mosquito-free, using mosquito repellent, and making sure there is no stagnant water around the home.

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INTRODUCTION-

Meningitis is an inflammation of the membranes (meninges) surrounding your brain and spinal cord.

The swelling from meningitis typically triggers symptoms such as headache, fever and a stiff neck.

Most cases of meningitis in the United States are caused by a viral infection, but bacterial, parasitic and fungal infections are other causes. Some cases of meningitis improve without treatment in a few weeks. Others can be life-threatening and require emergency antibiotic treatment.

Seek immediate medical care if you suspect that someone has meningitis. Early treatment of bacterial meningitis can prevent serious complications.

CAUSES-

Meningitis is almost always caused by a bacterial or viral infection that begins somewhere else in your body, like your ears, sinuses, or throat.

Less common causes of meningitis include:

• Autoimmune disorders
• Cancer medications
• Syphilis
• Tuberculosis

Bacterial Meningitis

It’s an extremely serious illness. You or your child will need to get medical help right away. It can be life-threatening or lead to brain damage unless you get quick treatment.

Several kinds of bacteria can cause bacterial meningitis. The most common ones in the U.S. are:

• Streptococcus pneumoniae (pneumococcus)
• Neisseria meningitidis (meningococcus)

• Listeria monocytogenes (in older people, pregnant women, or those with immune system problems)

A bacteria called Haemophilus influenzae type b (Hib) was a common cause of meningitis in babies and young children until the Hib vaccine became available for infants. There are also vaccines for Neisseria meningitidis and Streptococcus pneumoniae. Experts recommend that all children get them, as well as all adults who are at a higher risk for the disease.

In many cases, bacterial meningitis starts when bacteria get into your bloodstream from your sinuses, ears, or throat. The bacteria travel through your bloodstream to your brain.

The bacteria that cause meningitis can spread when people who are infected cough or sneeze. If you or your child has been around someone who has bacterial meningitis, ask your doctor what steps you should take to avoid catching it.

Viral Meningitis

Viral meningitis is more common than the bacterial form and generally — but not always — less serious. A number of viruses can trigger the disease, including several that can cause diarrhea.

Fungal Meningitis

Fungal meningitis is much less common than the bacterial or viral forms. Healthy people rarely get it. Someone with a problem with their immune system — because they have AIDS, for example — is more likely to become infected with this form of meningitis.

Meningitis Diagnosis

Your doctor will ask about your medical history and do a physical exam, including checking your neck for stiffness and looking for a skin rash that might suggest a bacterial infection. They will also need to do tests that can include:

• Blood tests to find bacteria
• CT or MRI scans of your head to find swelling or inflammation
• Spinal tap, in which a health care worker uses a needle to take fluid from around your spinal cord. It can tell what’s causing your meningitis.

SYMPTOM-

The symptoms of viral and bacterial meningitis can be similar in the beginning. However, bacterial meningitis symptoms are usually more severe. The symptoms also vary depending on your age.

Viral meningitis symptoms

Viral meningitis in infants may cause:

• decreased appetite
• irritability
• sleepiness
• lethargy
• fever

In adults, viral meningitis may cause:

• headaches
• fever
• stiff neck
• seizures
• sensitivity to bright light
• sleepiness
• lethargy
• nausea and vomiting
• decreased appetite

Bacterial meningitis symptoms

Bacterial meningitis symptoms develop suddenly. They may include:

• altered mental status
• nausea
• vomiting
• sensitivity to light
• irritability
• headache
• fever
• chills
• stiff neck
• purple areas of skin that resemble bruises
• sleepiness
• lethargy

Seek immediate medical attention if you experience these symptoms. Bacterial and viral meningitis can be deadly. There’s no way to know if you have bacterial or viral meningitis just by judging how you feel. Your doctor will need to perform tests to determine which type you have.

Fungal meningitis symptoms

Symptoms of fungal meningitis resemble the other types of this infection. These may include:

• nausea
• vomiting
• sensitivity to light
• fever
• headache
• confusion or disorientation

Each type of meningitis has some distinguishing symptoms.

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Risk factors

Risk factors for meningitis include:

• Skipping vaccinations. Risk rises for anyone who hasn’t completed the recommended childhood or adult vaccination schedule.
• Age. Most cases of viral meningitis occur in children younger than age 5. Bacterial meningitis is common in those under age 20.
• Living in a community setting. College students living in dormitories, personnel on military bases, and children in boarding schools and child care facilities are at greater risk of meningococcal meningitis. This is probably because the bacterium is spread by the respiratory route, and spreads quickly through large groups.
• Pregnancy. Pregnancy increases the risk of listeriosis — an infection caused by listeria bacteria, which may also cause meningitis. Listeriosis increases the risk of miscarriage, stillbirth and premature delivery.
• Compromised immune system. AIDS, alcoholism, diabetes, use of immunosuppressant drugs and other factors that affect your immune system also make you more susceptible to meningitis. Having your spleen removed also increases your risk, and anyone without a spleen should get vaccinated to minimize that risk.

Complications

Meningitis complications can be severe. The longer you or your child has the disease without treatment, the greater the risk of seizures and permanent neurological damage, including:

• Hearing loss
• Memory difficulty
• Learning disabilities
• Brain damage
• Gait problems
• Seizures
• Kidney failure
• Shock
• Death

With prompt treatment, even patients with severe meningitis can have good recovery.

Prevention

Common bacteria or viruses that can cause meningitis can spread through coughing, sneezing, kissing, or sharing eating utensils, a toothbrush or a cigarette.

These steps can help prevent meningitis:

• Wash your hands. Careful hand-washing helps prevent the spread of germs. Teach children to wash their hands often, especially before eating and after using the toilet, spending time in a crowded public place or petting animals. Show them how to vigorously and thoroughly wash and rinse their hands.
• Practice good hygiene. Don’t share drinks, foods, straws, eating utensils, lip balms or toothbrushes with anyone else. Teach children and teens to avoid sharing these items too.
• Stay healthy. Maintain your immune system by getting enough rest, exercising regularly, and eating a healthy diet with plenty of fresh fruits, vegetables and whole grains.
• Cover your mouth. When you need to cough or sneeze, be sure to cover your mouth and nose.
• If you’re pregnant, take care with food. Reduce your risk of listeriosis by cooking meat, including hot dogs and deli meat, to 165 F (74 C). Avoid cheeses made from unpasteurized milk. Choose cheeses that are clearly labeled as being made with pasteurized milk.

Characteristics/Clinical Presentation

Headache, fever, vomiting, and rigidity of the neck are the most common symptoms that present with the onset of meningitis. Early symptoms include nausea, drowsiness and confusion. Pain in the posterior thigh or lumbar region may also be noted. Later symptoms can include seizures, photophobia and rapid breathing rate. In addition, a rash on the skin, scanty petechial (red or purple non-blanching macules smaller than 2mm in diameter) ,or a purpuric (larger than 2mm) appears on approximately 80-90% of individuals with bacterial meningitis.

Meningitis causes inflammation of the meningeal membranes; as a result nerve roots may endure tension as they pass through these inflamed membranes. Passive ROM of the neck into flexion will gradually become painful and limited. Also, neck extension and rotation may be painful as well, however not to the extent of flexion. In severe cases, Brudzinki’s sign, or Kernig’s may be presented.

Brudzinki’s sign is caused by passive neck flexion producing flexion of the hips or knees. Kernig’s sign presents, as restrictive passive extension of the knee while the hip is flexed. In cases when meningitis is not treated immediately (especially bacterial meningitis), the parenchyma within the brain may be involved. As a result i,ndividuals may present with lethargy, vomiting, seizures, papilledema, confusion, coma, focal deficits, and cranial nerve palsies.

Immunizations

Some forms of bacterial meningitis are preventable with the following vaccinations:

• Haemophilus influenzae type b (Hib) vaccine. Children in the United States routinely receive this vaccine as part of the recommended schedule of vaccines, starting at about 2 months of age. The vaccine is also recommended for some adults, including those who have sickle cell disease or AIDS and those who don’t have a spleen.
• Pneumococcal conjugate vaccine (PCV13). This vaccine also is part of the regular immunization schedule for children younger than 2 years in the United States. Additional doses are recommended for children between the ages of 2 and 5 who are at high risk of pneumococcal disease, including children who have chronic heart or lung disease or cancer.
• Pneumococcal polysaccharide vaccine (PPSV23). Older children and adults who need protection from pneumococcal bacteria may receive this vaccine. The Centers for Disease Control and Prevention recommends the PPSV23 vaccine for all adults older than 65; for younger adults and children age 2 and older who have weak immune systems or chronic illnesses such as heart disease, diabetes or sickle cell anemia; and for anyone who doesn’t have a spleen.
• Meningococcal conjugate vaccine. The Centers for Disease Control and Prevention recommends that a single dose be given to children ages 11 to 12, with a booster shot given at age 16. If the vaccine is first given between ages 13 and 15, the booster is recommended between ages 16 and 18. If the first shot is given at age 16 or older, no booster is necessary. This vaccine can also be given to children between the ages of 2 months and 10 years who are at high risk of bacterial meningitis or who have been exposed to someone with the disease. It’s also used to vaccinate healthy but previously unvaccinated people who have been exposed in outbreaks.

physical therapy management-

According to the American Physical Therapy Association’s Guide to Physical Therapist Practice infectious disorders of the central nervous system fall under the following preferred practice patterns; 5D: Impaired Motor Function and Sensory Integrity Associated with Nonprogressive Disorders of the Central Nervous System- Acquired in Adulthood or Adolescence and 5I: Impaired Arousal, Range of Motion, and Motor Control Associated with Coma, Near Coma, or Vegetative State.

Typically physical therapy treatment is initiated in the intensive care unit. While initiating a plan of care, it is crucial to keep in mind a patient’s chart information or contraindications to therapy such as intracranial pressure, cerebral perfusion pressure, and other lab values that determine rehabilitation guidelines. Meningitis may present with similar symptoms to brain injuries, neurological complications, immunological deficiency, vascular compromise, and additional secondary impairments.

Additionally understanding the various stages of consciousness or behavioural changes a patient with secondary complications may go through can guide the approach to treatment. The therapist should create an environment that would ease the patient’s hypersensitivity to sensory input such as light or sound thus creating a structured environment to eliminate behaviural outbursts. Close monitoring of the vital signs will allow the therapist to gauge the patient’s receptiveness to therapy. The therapist should be familiar with the Glasgow Coma Scale and monitor the patient’s progression through the levels of consciousness.

Proper positioning and range of motion exercise should be initiated as soon as safely possible in the acute phase. Proper positioning with pillows and towels will protect the skin integrity and prevention of contractures. Maintaining mobility of the trunk and neck are important to sustain functional mobility. The earlier therapy is initiated with a patient, the chances of secondary impairments are decreased allowing for a better prognosis.

A primary key component to treating a patient recovering from bacterial meningitis is proper education not only to the patient, but to the family and caregivers as well. Providing the patient and family with education on the disease, stages of the disease, secondary complications, warning sign,s and resources can encourage the patient and family to become more involved in the treatment. It is very important to educate on the effectsofm different systemic involvement and how the timeline of recovery may vary.

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INTODUCTION-

Osteomyelitis is an infection in a bone. Infections can reach a bone by traveling through the bloodstream or spreading from nearby tissue. Infections can also begin in the bone itself if an injury exposes the bone to germs.

Smokers and people with chronic health conditions, such as diabetes or kidney failure, are more at risk of developing osteomyelitis. People who have diabetes may develop osteomyelitis in their feet if they have foot ulcers.

Although once considered incurable, osteomyelitis can now be successfully treated. Most people need surgery to remove areas of the bone that have died. After surgery, strong intravenous antibiotics are typically needed.

Osteomyelitis can affect both adults and children. The bacteria or fungus that can cause osteomyelitis, however, differs among age groups. In adults, osteomyelitis often affects the vertebrae and the pelvis. In children, osteomyelitis usually affects the adjacent ends of long bones. Long bones (bones in the arms or legs) are large, dense bones that provide strength, structure and mobility. They include the femur and tibia in the legs and the humerus and radius in the arms.

Osteomyelitis is not more common in a particular race or gender. However, some people are more at risk for developing the disease, including:

• People with diabetes.
• Patients receiving hemodialysis.
• People with weakened immune systems.
• People with sickle cell disease.
• Intravenous drug abusers.
• The elderly.

CAUSES-

It can be caused by a variety of microbial agents (most common in staphylococcus aureus) and situations, including:

• An open injury to the bone, such as an open fracture with the bone ends coming out through the skin.
• A minor trauma, which can lead to a blood clot around the bone and then a secondary infection from seeding of bacteria.
• Bacteria in the bloodstream (bacteremia), which is deposited in a focal (localized) area of the bone. This bacterial site in the bone then grows, resulting in destruction of the bone. However, new bone often forms around the site.
• A chronic open wound or soft tissue infection can eventually extend down to the bone surface, leading to a direct bone infection.

Most cases of osteomyelitis are caused by staphylococcus bacteria, types of germs commonly found on the skin or in the nose of even healthy individuals.

Germs can enter a bone in a variety of ways, including:

• The bloodstream. Germs in other parts of your body — for example, in the lungs from pneumonia or in the bladder from a urinary tract infection — can travel through your bloodstream to a weakened spot in a bone.
• Injuries. Severe puncture wounds can carry germs deep inside your body. If such an injury becomes infected, the germs can spread into a nearby bone. Germs can also enter the body if you have broken a bone so severely that part of it is sticking out through your skin.
• Surgery. Direct contamination with germs can occur during surgeries to replace joints or repair fractures.

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Risk factors

Your bones are normally resistant to infection, but this protection lessens as you get older. Other factors that can make your bones more vulnerable to osteomyelitis may include:

Recent injury or orthopedic surgery

A severe bone fracture or a deep puncture wound gives bacteria a route to enter your bone or nearby tissue. A deep puncture wound, such as an animal bite or a nail piercing through a shoe, can also provide a pathway for infection.

Surgery to repair broken bones or replace worn joints also can accidentally open a path for germs to enter a bone. Implanted orthopedic hardware is a risk factor for infection.

Circulation disorders

When blood vessels are damaged or blocked, your body has trouble distributing the infection-fighting cells needed to keep a small infection from growing larger. What begins as a small cut can progress to a deep ulcer that may expose deep tissue and bone to infection.

Diseases that impair blood circulation include:

• Poorly controlled diabetes
• Peripheral artery disease, often related to smoking
• Sickle cell disease

Problems requiring intravenous lines or catheters

There are a number of conditions that require the use of medical tubing to connect the outside world with your internal organs. However, this tubing can also serve as a way for germs to get into your body, increasing your risk of an infection in general, which can lead to osteomyelitis.

Examples of when this type of tubing might be used include:

• Dialysis machine tubing
• Urinary catheters
• Long-term intravenous tubing, sometimes called central lines

Conditions that impair the immune system

If your immune system is affected by a medical condition or medication, you have a greater risk of osteomyelitis. Factors that may suppress your immune system include:

• Cancer treatment
• Poorly controlled diabetes
• Needing to take corticosteroids or drugs called tumor necrosis factor inhibitors

Illicit drugs

People who inject illegal drugs are more likely to develop osteomyelitis because they may use nonsterile needles and are less likely to sterilize their skin before injections.

Complications

Osteomyelitis complications may include:

• Bone death (osteonecrosis). An infection in your bone can impede blood circulation within the bone, leading to bone death. Areas where bone has died need to be surgically removed for antibiotics to be effective.
• Septic arthritis. Sometimes, infection within bones can spread into a nearby joint.
• Impaired growth. Normal growth in bones or joints in children may be affected if osteomyelitis occurs in the softer areas, called growth plates, at either end of the long bones of the arms and legs.
• Skin cancer. If your osteomyelitis has resulted in an open sore that is draining pus, the surrounding skin is at higher risk of developing squamous cell cancer.

SYMPTOM-

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The symptoms of osteomyelitis can include:

• Pain and/or tenderness in the infected area.
• Swelling, redness and warmth in the infected area.
• Fever.
• Nausea, secondarily from being ill with infection.
• General discomfort, uneasiness, or ill feeling.
• Drainage of pus (thick yellow fluid) through the skin.

Additional symptoms that may be associated with this disease include:

• Excessive sweating.
• Chills.
• Lower back pain (if the spine is involved).
• Swelling of the ankles, feet, and legs.
• Loss or decrease of motion of a joint.
• Changes in gait (walking pattern that is a painful, yielding a limp) or unwillingness to bear weight in children.

TREATMENT-

Treatment focuses on stopping infection in its tracks and preserving as much function as possible. Most people with osteomyelitis are treated with antibiotics, surgery, or both.

Antibiotics help bring the infection under control and often make it possible to avoid surgery. People with osteomyelitis usually get antibiotics for several weeks through an IV, and then switch to a pill.

More serious or chronic osteomyelitis requires surgery to remove the infected tissue and bone. Osteomyelitis surgery prevents the infection from spreading further or getting so bad that amputation is the only remaining option.

physical therapy approach-

Physical  therapists can play a vital role in the screening process for osteomyelitis.  Individuals who present with signs and symptoms of infection, possibly causing osteomyelitis, should be referred to a physician for further diagnostic testing.  These signs and symptoms are included in the above section. Prevention is another area in cases of osteomyelitis where physical therapists can play an important role.  Chronic osteomyelitis is often a result of complication of treatment with open fractures, therefore, prevention of infection is highly important^[3].  Since the role of nutrition is vital in cases of infection, patient need to be properly educated on proper nutrition in early post-surgical intervention due to the fact that most infections occur in the immediate post-operative period^[3].  Individuals who are at risk for developing osteomyelitis should also be taught proper preventative measures and be aware of early warning signs that infection may be present such as, excessive pus present coming from incision line, redness, extreme tenderness, increased skin temperature near area of injury or surgical procedure, and symptoms of nausea or vomiting. If treated surgically for osteomyelitis, physical therapy may be indicated post-operatively to address any impairments in strength, ROM, proprioception, etc. as well as treatment for any functional limitations or disability secondary to infection.

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The myopathies are neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber. Other symptoms of myopathy can include include muscle cramps, stiffness, and spasm. Myopathies can be inherited (such as the muscular dystrophies) or acquired (such as common muscle cramps). Myopathies are grouped as follows:
congenital myopathies: characterized by developmental delays in motor skills; skeletal and facial abnormalities are occasionally evident at birth
muscular dystrophies: characterized by progressive weakness in voluntary muscles; sometimes evident at birth
mitochondrial myopathies: caused by genetic abnormalities in mitochondria, cellular structures that control energy; include Kearns-Sayre syndrome, MELAS and MERRF
glycogen storage diseases of muscle: caused by mutations in genes controlling enzymes that metabolize glycogen and glucose (blood sugar); include Pompe’s, Andersen’s and Cori’s diseases
myoglobinurias: caused by disorders in the metabolism of a fuel (myoglobin) necessary for muscle work; include McArdle, Tarui, and DiMauro diseases
dermatomyositis: an inflammatory myopathy of skin and muscle
myositis ossificans: characterized by bone growing in muscle tissue
familial periodic paralysis: characterized by episodes of weakness in the arms and legs
polymyositis, inclusion body myositis, and related myopathies: inflammatory myopathies of skeletal muscle
neuromyotonia: characterized by alternating episodes of twitching and stiffness; and
stiff-man syndrome:  characterized by episodes of rigidity and reflex spasms
common muscle cramps and stiffness, and
tetany:  characterized by prolonged spasms of the arms and legs

Symptoms-

There are several different types of genetic myopathies, most of which have similar symptoms. These include:

• Muscle weakness
• Motor delay
• Respiratory impairment
• Bulbar muscle dysfunction (malfunction of the muscles responsible for swallowing and speech)

Bulbar muscle dysfunctions can be especially apparent in congenital myopathies (those present from birth), and can result in severe impairments to swallowing and speech abilities. Congenital myopathies also are characterized by developmental motor delays and, at times, facial or skeletal abnormalities.

Acquired myopathies may have symptoms similar to those of genetic myopathies and also may include:

• Muscle weakness
• Muscle soreness (myalgias)
• Cramps
• Stiffness
• Muscle wasting around the shoulders and hips

Causes and Risk Factors

Patients who have a blood relative with a genetic myopathy have an increased risk for developing the condition. Depending on how the myopathy is inherited, men can be at greater risk than women of developing the condition. Myopathies carried on the X chromosome affect more men than women, while those carried on chromosomes other than the sex chromosome affect both men and women equally.

Patients may be at increased risk of developing acquired myopathy if they have an autoimmune disorder, metabolic or endocrine disorder, are on certain drugs or are exposed to certain toxins.

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Classification

Myopathies may be divided into two main categories: inherited and acquired. The temporal course, the pattern of muscle weakness, and the absence or presence of a family history of myopathy help distinguish between the two types. An early age of onset with a relatively longer duration of disease suggests an inherited myopathy, and a sudden or subacute presentation at a later age is more consistent with an acquired myopathy. Inherited myopathies can be further subclassified as muscular dystrophies, congenital myopathies, mitochondrial myopathies, and metabolic myopathies. Acquired myopathies can be subclassified as inflammatory myopathies, toxic myopathies, and myopathies associated with systemic conditions. The more commonly seen inherited and acquired myopathies are listed in Box 1.

Box 1 Common Causes of Myopathy
Acquired Myopathies
Inflammatory Myopathy Polymyositis Dermatomyositis Inclusion body myositis
Infection Viral infections (HIV, influenza virus, Epstein-Barr virus) Bacterial pyomyositis (Staphylococcus aureus and streptococci are common organisms) Spirochete (Lyme disease) Parasitic infections such as trichinosis
Toxic Myopathy Medications Steroids Cholesterol-lowering medications: statins, fibrates, niacin, and ezetimibe Propofol Amiodarone Colchicine Chloroquine Antivirals and protease inhibitors Omeprazole Tryptophan Toxins Alcohol Toluene
Myopathy Associated with Systemic Diseases Endocrine disorders Thyroid Parathyroid Pituitary or adrenal dysfunction Systemic inflammatory diseases Systemic lupus erythematosus Rheumatoid arthritis Scleroderma Sjögren’s syndrome Mixed connective disease Sarcoidosis Electrolyte imbalance Potassium or magnesium abnormalities Hypophosphatemia Critical illness myopathy Nondepolarizing neuromuscular blocking agents Steroids Amyloid myopathy Primary amyloidosis Familial amyloidosis (TTR mutation)
Inherited Myopathies
Muscular Dystrophy Dystrophinopathy (Duchenne muscular dystrophy,Becker muscular dystrophy) Myotonic dystrophy 1 and 2 Facioscapulohumeral muscular dystrophy Oculopharyngeal muscular dystrophy Limb girdle muscular dystrophy
Congenital Myopathy Nemaline myopathy Central core myopathy
Metabolic Myopathy Acid maltase or acid alpha-1,4-glucosidase deficiency (Pompe’s disease) Glycogen storage disorders 3-11 Carnitine deficiency Fatty acid oxidation defects Carnitine palmitoyl transferase deficiency
Mitochondrial Myopathy Myoclonic epilepsy and ragged red fibers (MERRF) Mitochondrial myopathy, lactic acidosis, and strokes (MELAS) Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) Progressive external ophthalmoplegia (PEO)

DIAGNOSIS-

The clinical history is essential in identifying the presence of a myopathy and narrowing down the differential diagnosis. In particular, the patient should be questioned about medication and recreational drug history (especially alcohol), chemical exposures, exercise intolerance, childhood development, and family history of muscle disease or developmental motor delay.

Laboratory Testing

Serologic testing, which can indicate muscle damage, includes elevations in creatine phosphokinase (CPK), aldolase, lactate dehydrogenase (LDH), and liver function enzymes. A screening panel of laboratory tests may also be obtained to rule out more common causes of myopathy, which are listed in. In cases suspected to be a primary inflammatory myopathy, specific autoantibodies can be considered to determine the prognosis and rule out associated conditions. For example, the presence of anti-Jo antibody in dermatomyositis predicts a superimposed interstitial lung disease. In addition, these patients should also be evaluated for an underlying systemic autoimmune disease with an extensive autoimmune panel and angiotensin-converting enzyme (ACE) levels. In myopathies that are accompanied by polyneuropathy, renal involvement, and a restrictive cardiomyopathy, immunofixation electrophoresis studies in the serum and urine should be considered to rule out the possibility of amyloid disease. Genetic testing is available for some inherited myopathies. These are listed in

Box 2 Laboratory Evaluation for Suspected Myopathy
Confirm the Presence of Muscle Disease Creatine phosphokinase Aldolase Liver function tests Lactate dehydrogenase levels
Identify Etiology Complete blood count with differential Complete metabolic panel Thyroid function tests Parathyroid hormone level Sedimentation rate C-reactive protein and antinuclear antibody panel
Suspected Inflammatory Etiology Myositis-specific autoantibodies Anti–double stranded DNA antibody Anti-Scl 70 antibody Anti-SSA and SSB antibodies Anti-ribonucleoprotein antibody Rheumatoid factor Anti-PM1 antibody Angiotensin-converting enzyme levels
Suspected Mitochondrial or Metabolic Myopathy Serum lactate, pyruvate, ammonia, coenzyme Q10 levels Ischemic forearm lactate test Carnitine levels
Suspected Amyloid Myopathy Immunofixation electrophoresis of monoclonal proteins in serum and urine

Table 2 Commercially Available Genetic Tests in Diagnosis of a Myopathy

Myopathies with Known Genetic Defects	Gene Abnormalities	Pattern of Inheritance
Duchenne muscular dystrophy	Dystrophin gene	X-linked recessive
Becker muscular dystrophy	Dystrophin gene	X-linked recessive
Emery-Dreifuss muscular dystrophy	Emerin gene	X-linked recessive
Limb girdle muscular dystrophy	Lamin A/C Calpain Dysferlin Fukutin related protein	Some are autosomal dominant and others are recessive
Facioscapulohumeral muscular dystrophy	D4Z4 deletion	Autosomal dominant
Oculopharyngeal muscular dystrophy	GCG repeat expansion in poly A binding protein 2 gene	Autosomal dominant
Myotonic dystrophy 1 and 2	DMPK gene for type 1 CNBP (ZNF9) gene for type 2	Autosomal dominant
Mitochondrial myopathy	Specific point mutation analysis for diseases like MELAS POLG1 sequencing for MERRF available Southern blot analysis for mtDNA deletions and mtDNA sequencing	Maternally inherited. But other can be inherited as autosomal dominant or recessive disease
Amyloid myopathy from familial causes	Transthyretin mutation	Autosomal dominant
Statin myopathy (predictor of increased susceptibility)	SLCO1B1 gene	Unknown

MELAS, mitochondrial myopathy, lactic acidosis, and strokes; MERRF, myoclonic epilepsy and ragged red fibers; mtDNA, mitochondrial DNA.

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Ischemic Forearm Test

A traditional test used in the evaluation of a suspected metabolic myopathy is the ischemic forearm test. This is performed by obtaining baseline serum ammonia and lactate levels taken from the forearm. The patient then exercises that arm for 1 minute, after which repeat serum lactate and blood ammonia levels are measured. This is repeated at several intervals (1, 2, 5, and 10 minutes). In normal muscle, the resultant ischemia causes a 3- to 5-fold rise in lactate levels. In contrast, patients with glycogen storage disorders demonstrate no change in lactate levels after exercise.

Electrodiagnostic Studies

The electromyogram (EMG) is an electrical study of the nerves and muscles that plays an important role in confirming the presence, duration, and severity of a myopathy. The study can also disclose special findings such as myotonic potentials. This is the electrical equivalent of clinical myotonia, which is manifested as impaired relaxation of muscles after forceful contraction; for example, patients cannot release objects from their grip. Myotonic potentials have the characteristic sound of a dive bomb on EMG and can help point toward the diagnosis of myotonic dystrophy when found in the appropriate muscles.

Although integral in the evaluation of a myopathy, the EMG can be normal in mild myopathies, steroid myopathies, and a number of metabolic myopathies. Therefore, it is important to remember that a normal EMG does not exclude the presence of a myopathy.

Muscle Biopsy

Histopathologic examination of muscle may be helpful in determining the specific type of muscle disease, especially in patients with a suspected inflammatory or infectious myopathy. Selecting the optimal muscle to biopsy is very important because factors such as severe weakness and technical artifacts can hamper an accurate histologic diagnosis. The ideal muscle that should be sampled is one that is clinically involved but still antigravity in strength, because more-severe weakness can lead to unhelpful, nonspecific findings of fibrosis. Also avoid muscles that have been examined by an EMG because the needle portion of the electrical study might have caused local damage, which can result in spurious findings. Common biopsy sites include the biceps and deltoid muscles in the upper extremity and the quadriceps and gastrocnemius muscles in the lower extremity.

TREATMENT-

Treatments for the myopathies depend on the disease or condition and specific causes. Supportive and symptomatic treatment may be the only treatment available or necessary for some disorders. Treatment for other disorders may include drug therapy, such as immunosuppressives, physical therapy, bracing to support weakened muscles, and surgery.

The treatment of myopathies is multidisciplinary and depends on the type of myopathy. Certain types of myopathies can be treated with immune-suppressant agents and IVIG. Most myopathies require the use of supportive services, such as physical and occupational therapy, pulmonary medicine, cardiology, dietary management, and speech/swallowing therapists. Surgical treatment of spine and limb deformities is used in long-standing cases.

While there is no cure for genetic myopathy, many different treatment options are available to manage the symptoms. Treatments for both genetic and endocrine myopathy are most effective when the disease is diagnosed early and a comprehensive treatment plan is overseen by a knowledgeable medical team, such as those at Cedars-Sinai’s Neuromuscular Disorders Program.

For acquired myopathies due to the immune system, such as dermatomyositis and polymyositis, medications that work to reduce the body’s immune response and decrease inflammation, such as corticosteroids or other immunosuppressants, can help manage some symptoms. Physical therapy, supportive devices such as braces, and sometimes surgery may also be used as treatment tools.

Treatment of metabolic, toxic and endocrine-related myopathy generally focuses on the underlying cause of the condition. Medication or surgery may be used to address the symptoms.

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INTRODUCTION-

Myasthenia gravis (MG) is a relatively rare acquired, autoimmune disorder caused by an antibody-mediated blockade of neuromuscular transmission resulting in skeletal muscle weakness. The autoimmune attack occurs when autoantibodies form against the nicotinic acetylcholine postsynaptic receptors at the neuromuscular junction of skeletal muscles Although the chief target of the autoimmune attack in most cases is the skeletal muscle nicotinic acetylcholine receptor (nAChR), other antigenic targets that are components of the neuromuscular junction (NMJ) have also been implicated.

Myasthenia gravis (MG) is a neuromuscular disorder that causes weakness in the skeletal muscles, which are the muscles your body uses for movement. It occurs when communication between nerve cells and muscles becomes impaired. This impairment prevents crucial muscle contractions from occurring, resulting in muscle weakness.

According to the Myasthenia Gravis Foundation of America, MG is the most common primary disorder of neuromuscular transmission. It’s a relatively rare condition that affects between 14 and 20 out of every 100,000 people in the United States.

SYMPTOM-

Muscle weakness caused by myasthenia gravis worsens as the affected muscle is used. Because symptoms usually improve with rest, muscle weakness can come and go. However, the symptoms tend to progress over time, usually reaching their worst within a few years after the onset of the disease.

Although myasthenia gravis can affect any of the muscles that you control voluntarily, certain muscle groups are more commonly affected than others.

Eye muscles

In more than half of people who develop myasthenia gravis, their first signs and symptoms involve eye problems, such as:

• Drooping of one or both eyelids (ptosis)
• Double vision (diplopia), which may be horizontal or vertical, and improves or resolves when one eye is closed

Face and throat muscles

In about 15% of people with myasthenia gravis, the first symptoms involve face and throat muscles, which can:

• Impair speaking. Your speech might sound soft or nasal, depending on which muscles have been affected.
• Cause difficulty swallowing. You might choke easily, making it difficult to eat, drink or take pills. In some cases, liquids you’re trying to swallow come out your nose.
• Affect chewing. The muscles used for chewing might wear out halfway through a meal, particularly if you’ve been eating something hard to chew, such as steak.
• Change facial expressions. For example, your smile might look like a snarl.

Neck and limb muscles

Myasthenia gravis can also cause weakness in your neck, arms and legs. Weakness in your legs can affect how you walk. Weak neck muscles make it hard to hold up your head.

Weakness associated with MG typically gets worse with more activity and improves with rest. Symptoms of MG can include:

• trouble talking
• problems walking up stairs or lifting objects
• facial paralysis
• difficulty breathing due to muscle weakness
• difficulty swallowing or chewing
• fatigue
• hoarse voice
• drooping of eyelids
• double vision

Not everyone will have every symptom, and the degree of muscle weakness can change from day to day. The severity of the symptoms typically increases over time if left untreated.

When to see a doctor

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Talk to your doctor if you have difficulty:

• Breathing
• Seeing
• Swallowing
• Chewing
• Walking
• Using your arms or hands
• Holding up your head.

CAUSES-

Antibodies

Your nerves communicate with your muscles by releasing chemicals (neurotransmitters) that fit precisely into receptor sites on the muscle cells at the nerve-muscular junction.

In myasthenia gravis, your immune system produces antibodies that block or destroy many of your muscles’ receptor sites for a neurotransmitter called acetylcholine With fewer receptor sites available, your muscles receive fewer nerve signals, resulting in weakness.

Antibodies can also block the function of a protein called a muscle-specific receptor tyrosine kinase . This protein is involved in forming the nerve-muscular junction. Antibodies that block this protein can lead to myasthenia gravis.

Thymus gland

The thymus gland is a part of your immune system situated in the upper chest beneath your breastbone. Researchers believe the thymus gland triggers or maintains the production of the antibodies that block acetylcholine.

Large in infancy, the thymus gland is small in healthy adults. In some adults with myasthenia gravis, however, the thymus gland is abnormally large. Some people with myasthenia gravis also have tumors of the thymus gland (thymomas). Usually, thymomas aren’t cancerous (malignant), but they can become cancerous.

Other causes

Some people have myasthenia gravis that isn’t caused by antibodies blocking acetylcholine or the muscle-specific receptor tyrosine kinase. This type of myasthenia gravis is called antibody-negative myasthenia gravis. Antibodies against another protein, called lipoprotein-related protein 4, can play a part in the development of this condition.

Rarely, mothers with myasthenia gravis have children who are born with myasthenia gravis (neonatal myasthenia gravis). If treated promptly, children generally recover within two months after birth.

Some children are born with a rare, hereditary form of myasthenia, called congenital myasthenic syndrome.

Factors that can worsen myasthenia gravis

• Fatigue
• Illness
• Stress
• Some medications — such as beta blockers, quinidine gluconate, quinidine sulfate, quinine, phenytoin, certain anesthetics and some antibiotics
• Pregnancy
• Menstrual periods

DIAGNOSIS-

Your doctor will perform a complete physical exam, as well as take a detailed history of your symptoms. They’ll also do a neurological exam. This may consist of:

• checking your reflexes
• looking for muscle weakness
• checking for muscle tone
• making certain your eyes move properly
• testing sensation in different areas of your body
• testing motor functions, like touching your finger to your nose

Other tests that can help your doctor diagnose the condition include:

• repetitive nerve stimulation test
• blood testing for antibodies associated with MG
• edrophonium (Tensilon) test: a drug called Tensilon (or a placebo) is administered intravenously, and you’re asked to perform muscle movements under doctor observation
• imaging of the chest using CT scans or MRI to rule out a tumor

Treatment options for myasthenia gravis-

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There is no cure for MG. The goal of treatment is to manage symptoms and control the activity of your immune system.

Medication

Corticosteroids and immunosuppressants can be used to suppress the immune system. These medications help minimize the abnormal immune response that occurs in MG.

Additionally, cholinesterase inhibitors, such as pyridostigmine (Mestinon), can be used to increase communication between nerves and muscles.

Thymus gland removal

Removal of the thymus gland, which is part of the immune system, may be appropriate for many patients with MG. Once the thymus is removed, patients typically show less muscle weakness.

According to the Myasthenia Gravis Foundation of America, between 10 and 15 percent of people with MG will have a tumor in their thymus. Tumors, even those that are benign, are always removed because they may become cancerous.

Plasma exchange

Plasmapheresis is also known as a plasma exchange. This process removes harmful antibodies from the blood, which may result in an improvement in muscle strength.

Plasmapheresis is a short-term treatment. The body continues to produce the harmful antibodies and weakness may recur. Plasma exchange is helpful before surgery or during times of extreme MG weakness.

Intravenous immune globulin

Intravenous immune globulin (IVIG) is blood product that comes from donors. It’s used to treat autoimmune MG. Although it’s not entirely known how IVIG works, it affects the creation and function of antibodies.

Lifestyle changes

There are some things you can do at home to help alleviate symptoms of MG:

• Get plenty of rest to help minimize muscle weakness.
• If you’re bothered by double vision, talk to your doctor about whether you should wear an eye patch.
• Avoid stress and heat exposure, as both can worsen symptoms.

These treatments cannot cure MG. However, you’ll typically see improvements in your symptoms. Some individuals may go into remission, during which treatment is not necessary.

Tell your doctor about any medications or supplements you take. Some drugs can make MG symptoms worse. Before taking any new medication, check with your doctor to ensure it’s safe.

PHYSICAL THERAPY APPROACH-

Rehabilitation alone or in combination with other forms of treatment can relieve or reduce symptoms for some people with MG.

MG patients should find the optimal balance between physical activity and rest. It is not possible to cure the weakness by active physical training. However, most MG patients are more passive than they need to be. Physical activity and physical training of low to medium intensity is recommended.

One study showed a clear benefit from a strength training exercise program for a group of patients with mild to moderate MG, concluding “physical training can be carried out safely in mild MG and provides some improvement of muscle force”.

Physical exercise is well tolerated in patients with well regulated Myasthenia Gravis. Aerobic exercise and mild strength training can be advised and should be supervised.

Balance strategy training maybe effective in improving balance and more research into this domain has to be done

General advice for exercise programs for people with MG:

• Aim to strengthen large muscle groups, particularly proximal muscles of shoulders and hips
• Advise patient to do the exercises at their “best time of day” ie. when not feeling tired – for the majority of MG patients this will be morning
• If a patient is taking pyridostigmine, exercise at peak dose ie. 1.5 to 2 hours after taking a dose
• Moderate intensity of exercise only: the patient should not experience worsening of MG symptoms (eg. ptosis or diplopia) during exercise
• General aerobic exercise is also valuable, helping with respiratory function as well stamina

EXERCISE CONSIDERATIONS FOR INDIVIDUALS WITH MYASTHENIA GRAVIS–

When engaging in exercise, individuals with MG must be cautious. They must consider the time of day in which they exercise, type of exercise, duration of exercise, and the environment in which they exercise.

Because fatigue is a common symptom of MG, individuals with this condition should exercise in the morning when they have the most energy and are least fatigued, since muscular weakness is usually heightened in the evening. 4 Being conscious of timing to avoid fatigue not only applies to exercise, but also to the eating schedules of individuals with MG. Chewing is essentially an exercise which works the muscles of the jaw. If these muscles experience too much fatigue, individuals may be at greater risk of choking because their food is inadequately chewed. To combat this, meals should also be planned with the largest meals of the day coinciding with the time at which the individual is least fatigued.

Additionally, “Excessive heat can bring on muscle weakness as well as other MG symptoms.” 6 As a result, exercise sessions are best limited to the mornings when temperatures are lower, or performed in indoor facilities to avoid hot, humid outdoor environments.

To ensure safety while exercising, PACE is a suitable guideline to follow. 8

P- Planning daily activities
A- Adapting the home, adequate rest, assistive equipment, asking for help
C- Conserving energy, check-ups with doctor, cool temperature
E- Emotional stability, exercising in moderation, eliminating unnecessary daily tasks

EXERCISE PRESCRIPTION

Although there are no set guidelines for exercise intensity, duration and load for individuals with MG, regular to moderate exercise in the form of walking swimming, jogging or recreational sports can combat muscle weakness. 6 Exercise should be repeated, yet only performed at a level which falls short of muscular fatigue. 6

In a physiotherapy clinic, exercise progression should be based on the needs of each individual. Some cases of MG are less progressive, meaning individuals may be able to tolerate more exercise, while in other circumstances, less exercise may be advisable.

All strengthening exercises should progress first from range of motion exercises to emphasize flexibility to exercises using light resistance in the form of a thera-band and finally to full resistance exercises using machines and free weights. A general exercise prescription for an average individual is 3 sets of 10 repetitions, while no distinct guidelines exist for individuals with MG, starting with a lower prescription of 3 sets of 5 repetitions may be advisable.

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INTRODUCTION-

Bone fractures are a common injury and the healing process is complex. Bone is one of a few tissues that is able to heal without forming a fibrous scar. There are two types of fracture healing – indirect (secondary) and direct healing (primary)

Fracture of 4th Metacarpal Bone

Direct healing occurs when the bony fragments are fixed together with compression. There is no callus formation. The bony ends are joined and healed by osteoclast and osteoblast activity.

ndirect healing is more common than direct healing and involves both endochondral and intramembranous bone healing. Anatomical reduction and stable conditions are not required for indirect healing to occur. Rather, there is a small amount of motion and weight bearing at the fracture, which causes a soft callus to form, leading on to secondary bone formation. It should be noted though that too much load/movement can result in delayed healing or non-union, which occurs in 5-10% of all fractures.

Indirect healing usually occurs with:

• non operative fracture treatment
• operative treatments where some motion occurs at the fracture site, such as:
  • Intramedullary nailing
  • External fixation
  • Internal fixation of comminuted fractures.

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PHSESE OF FRACTURE HEALING-

Inflammatory phase (duration: hours–days): Broken bones result in torn blood vessels and the formation of a blood clot or haematoma. The inflammatory reaction results in the release of cytokines, growth factors and prostaglandins, all of which are important in healing. The fracture haematoma becomes organised and is then infiltrated by fibrovascular tissue, which forms a matrix for bone formation and primary callus.

Reparative phase (duration: days-weeks): A thick mass of callus forms around the bone ends, from the fracture haematoma. Bone-forming cells are recruited from several sources to form new bone, which can be seen on radiographs within 7-10 days after injury . Soft callus is organised and remodelled into hard callus over several weeks. Soft callus is plastic and can easily deform or bend if the fracture is not adequately supported. Hard callus is weaker than normal bone but is better able to withstand external forces and equates to the stage of “clinical union”, i.e. the fracture is not tender to palpation or with movement.

Remodelling phase (duration: months-years): This is the longest phase and may last for several years. During remodelling, the healed fracture and surrounding callus responds to activity, external forces, functional demands and growth. Bone (external callus) which is no longer needed is removed and the fracture site is smoothed and sculpted until it looks much more normal on an x-ray (Figure 9). The epiphyses gradually realign and residual angulation may be slowly corrected, in accordance with the rules of remodelling.

With the continued migration of osteoblasts and osteoclasts, the hard callus undergoes repeated remodeling – termed ‘coupled remodeling.’ This ‘coupled remodeling’ is a balance of resorption by osteoclasts and new bone formation by osteoblasts. The center of the callus is ultimately replaced by compact bone, while the callus edges become replaced by lamellar bone. Substantial remodeling of the vasculature occurs alongside these changes. The process of bone remodeling lasts for many months, ultimately resulting in regeneration of the normal bone structure.

An important point to expand on is endochondral ossification, which is the name given for the process of conversion of cartilage to bone. As described above, this occurs during the formation of bony callus, in which the newly formed collagen-rich cartilaginous callus gets replaced by immature bone. This process is also the key to the formation of long bones in the fetus, in which the bony skeleton replaces the hyaline cartilage model. The second type of ossification also occurs in the fetus; this is intramembranous ossification; this is the process by which mesenchymal tissue (primitive connective tissue) is converted directly to the bone, which no cartilage intermediate. This process takes place in the flat bones of the skull.

CLINICAL SIGNIFICANCE-

Primary bone healing is the reestablishment of the cortex without the formation of a callus. It occurs if a fracture is adequately “fixed” through reduction, immobilization, and rehabilitation. Secondary bone healing, as described above, occurs through the formation of a callus and subsequent remodeling.

By reducing and fixating, the clinician moves the two ends of the fracture into close apposition, which results in the minimal formation of granulation tissue and callus. ‘Cutting cones’ of osteoclasts cross the fracture site to the resorbed damaged bone, and ‘forming zones’ of osteoblasts lay down new bone.

Reduction and fixation of fractures can be either open or closed. If treated as closed, this happens without the need to make an incision into the skin. Open refers to the need/choice to open the skin with a surgical incision. If a fracture pattern appears stable, then the most appropriate method is closed. Options for this would be to use a cast (e.g., plaster of Paris), a brace or a splint. Open reduction tends to be the choice with unstable fractures and commonly occurs alongside internal fixation – hence the term ORIF. Internal fixation involves the use of surgical implants to hold the two ends of the fracture closely opposed. Commonly used methods of internal fixation include plating, screws, wires, and intramedullary nails. A final method of external fixation is also an option, and this involves the placing of pins through the skin, which are then held in place by an external ‘scaffold.’ This method tends to be used in complex fractures and can serve as a temporary option before internal fixation.

Multiple factors affect fracture healing, which can broadly categorize into local and systemic categories.

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Local factors:

• Fracture characteristics – excessive movement, misalignment, extensive damage and soft tissues caught within fracture ends can lead to delayed or non-union
• Infection – it can lead to poor healing and delayed or non-union.
• Blood supply – reduced blood supply to the fracture site can lead to delayed or non-union.

Systemic factors (the presence of any of these factors predisposes to poor healing)

• Advanced age
• Obesity
• Anemia
• Endocrine conditions – Diabetes mellitus, Parathyroid disease, and Menopause
• Steroid administration
• Malnutrition
• Smoking

Fractures have significant mortality and morbidity; therefore a multi-disciplinary approach is essential for good outcomes.

There are multiple methods that the interprofessional team can utilize to promote/stimulate fracture healing, including:

• Dietary supplements – calcium, protein, Vitamins C, and D
• Bone stimulators – which can be electrical, electromagnetic, and ultrasound. The current effectiveness of these methods is still equivocal, and this area requires further research.
• Bone graft – this involves the use of bone to help provide a scaffold to the newly forming bone. This graft can be from the patient’s body (autograft) or from a deceased donor (allograft).

What Can Hinder Bone Healing? 

A wide variety of factors can slow down the healing process. These include:

• Movement of the bone fragments; weightbearing too soon
• Smoking, which constricts the blood vessels and decreases circulation
• Medical conditions, such as diabetes, hormone-related problems or vascular disease
• Some medications, such as corticosteroids and other immunosuppressants
• Fractures that are severe, complicated or become infected
• Advanced age
• Poor nutrition or impaired metabolism
• Low levels of calcium and vitamin D
  

What Helps Promote Bone Healing?

If a bone will be cut during a planned surgical procedure, some steps can be taken pre- and postoperatively to help optimize healing. The surgeon may offer advice on diet and nutritional supplements that are essential to bone growth. Smoking cessation and adequate control of blood sugar levels in people living with diabetes are important. Smoking and high glucose levels interfere with bone healing. 

For all patients with fractured bones, immobilization is a critical part of treatment because any movement of bone fragments slows down the initial healing process. Depending on the type of fracture or surgical procedure, the surgeon may use some form of fixation (such as screws, plates or wires) on the fractured bone and/or a cast to keep the bone from moving. During the immobilization period, weightbearing is restricted as instructed by the surgeon. 

Once the bone is adequately healed, physical therapy often plays a key role in rehabilitation. An exercise program designed for the patient can help in regaining strength and balance and can assist in returning to normal activities.

PHYSICAL THERAPY FOR BONE HEALING-

Physiotherapy should start immediately after the fracture has been immobilised. Physiotherapy during fracture healing will concentrate on:

• Promoting healing
• Encouraging weight bearing
• Maintaining strength of weakened muscles
• Maintaining range of movement of the affected and surrounding joints
• Reducing pain
• Reducing swelling

After your fracture has healed and/or your cast has been removed physiotherapy is continued for 3-12 months or until you have regained your full level of function.The aims of physiotherapy are to:

• Progress weight bearing activities
• Return to full function
• Return strength and full range of movement to muscles / joints
• Focus on sport-specific rehabilitation
• Optimise the range of movement at the affected joint

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