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NCLEX Nephrotic Syndrome Review

NCLEX Nephrotic Syndrome Review

Nephrotic Syndrome

Nephrotic syndrome is a syndrome comprising signs of nephrosis, chiefly proteinuria, hypoalbuminemia, and edema.  It is a component of glomerulonephrosis, in which different degrees of proteinuria occur.  Essentially, loss of protein through the kidneys (proteinuria) leads to low protein levels in the blood (hypoproteinemia including hypoalbuminemia), which causes water to be drawn into soft tissues (edema). Very low hypoalbuminemia can also cause a variety of secondary problems, such as water in the abdominal cavity (ascites), around the heart or lung (pericardial effusion, pleural effusion), high cholesterol (hence hyperlipidemia), loss of molecules regulating coagulation (hence increased risk of thrombosis).

Large proteinuria is due to an increase in permeability of the filtering membrane of the kidney which normally separates the blood from the urinary space in Bowman’s capsule. This is composed of the capillary walls of the glomerulus which are wrapped by highly specialized cells called podocytes. Alterations in their capacity to filter the substances transported in the blood mean that proteins but not cells pass into the urine (hence no hematuria). By contrast, in nephritic syndrome red blood cells pass through the pores, causing hematuria.

Nephrotic Syndrome Signs and Symptoms

Nephrotic syndrome is characterized by large proteinuria, hypoalbuminemia, hyperlipidemia, and edema (which is generalized and also known as anasarca or dropsy) that begins in the face. Lipiduria (lipids in urine) can also occur, but is not essential for the diagnosis of nephrotic syndrome. Hyponatremia also occurs with a low fractional sodium excretion.

Hyperlipidemia is caused by two factors:

  • Hypoproteinemia stimulates protein synthesis in the liver, resulting in the overproduction of lipoproteins.
  • Lipid catabolism is decreased due to lower levels of lipoprotein lipase, the main enzyme involved in lipoprotein breakdown.  Cofactors, such as apolipoprotein C2 may also be lost by increased filtration of proteins.

A few other characteristics seen in nephrotic syndrome are:

  • The most common sign is excess fluid in the body due to the serum hypoalbuminemia. Lower serum oncotic pressure causes fluid to accumulate in the interstitial tissues. Sodium and water retention aggravates the edema. This may take several forms:
    • Puffiness around the eyes, characteristically in the morning.
    • Pitting edema over the legs.
    • Fluid in the pleural cavity causing pleural effusion. More commonly associated with excess fluid is pulmonary edema.
    • Fluid in the peritoneal cavity causing ascites.
    • Generalized edema throughout the body known as anasarca.
  • Most of the patients are normotensive but hypertension (rarely) may also occur.
  • Anemia (iron resistant microcytic hypochromic type) maybe present due to transferrin loss.
  • Dyspnea may be present due to pleural effusion or due to diaphragmatic compression with ascites.
  • Erythrocyte sedimentation rate is increased due to increased fibrinogen & other plasma contents.
  • Some patients may notice foamy or frothy urine, due to a lowering of the surface tension by the severe proteinuria. Actual urinary complaints such as hematuria or oliguria are uncommon, though these are seen commonly in nephritic syndrome.
  • May have features of the underlying cause, such as the rash associated with systemic lupus erythematosus, or the neuropathy associated with diabetes.

Nephrotic Syndrome Causes

Nephrotic syndrome is usually caused by damage to the clusters of tiny blood vessels (glomeruli) of your kidneys.

The glomeruli filter your blood as it passes through your kidneys, separating things your body needs from those it doesn’t. Healthy glomeruli keep blood protein (mainly albumin) — which is needed to maintain the right amount of fluid in your body — from seeping into your urine. When damaged, glomeruli allow too much blood protein to leave your body, leading to nephrotic syndrome.

Many diseases and conditions can cause glomerular damage and lead to nephrotic syndrome, including:

  • Minimal change disease. The most common cause of nephrotic syndrome in children, this disorder results in abnormal kidney function, but when the kidney tissue is examined under a microscope, it appears normal or nearly normal. The cause of the abnormal function typically can’t be determined.
  • Focal segmental glomerulosclerosis. Characterized by scattered scarring of some of the glomeruli, this condition may result from another disease or a genetic defect or occur for no known reason.
  • Membranous nephropathy. This kidney disorder is the result of thickening membranes within the glomeruli. The exact cause of the thickening isn’t known, but it’s sometimes associated with other medical conditions, such as hepatitis B, malaria, lupus and cancer.
  • Diabetic kidney disease. Diabetes can lead to kidney damage (diabetic nephropathy) that affects the glomeruli.
  • Systemic lupus erythematosus. This chronic inflammatory disease can lead to serious kidney damage.
  • Amyloidosis. This disorder occurs when substances called amyloid proteins accumulate in your organs. Amyloid buildup often affects the kidneys, damaging their filtering system.
  • Blood clot in a kidney vein. Renal vein thrombosis, which occurs when a blood clot blocks a vein connected to the kidney, can cause nephrotic syndrome.
  • Heart failure. Some forms of heart failure, such as constrictive pericarditis and severe right heart failure, can cause nephrotic syndrome.

Risk Factors

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, minimal change disease and other kidney diseases.
  • Certain medications. Examples of medications that can cause nephrotic syndrome include nonsteroidal anti-inflammatory drugs and drugs used to fight infections.
  • Certain infections. Examples of infections that increase the risk of nephrotic syndrome include HIV, hepatitis B, hepatitis C and malaria.

Complications

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 (thrombus) 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, but it may be masked by swelling. You may also have too few red blood cells (anemia) and low levels of vitamin D and calcium.
  • High blood pressure. Damage to your glomeruli and the resulting buildup of wastes in your bloodstream (uremia) can raise your blood pressure.
  • Acute kidney failure. If your kidneys lose their ability to filter blood due to damage to the glomeruli, waste products may build up quickly in your blood. If this happens, you may 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 may cause your kidneys to gradually lose their function over time. If kidney function falls low enough, you may require dialysis or a kidney transplant.
  • Infections. People with nephrotic syndrome have an increased risk of infections.

Treatments

Treatment for nephrotic syndrome involves treating any underlying medical condition that may be causing your nephrotic syndrome. Your doctor may also recommend medications that may help control your signs and symptoms or treat complications of nephrotic syndrome. Medications may include:

  • Blood pressure medications
  • Diuretics help control swelling by increasing your kidneys’ fluid output. Diuretic medications include furosemide (Lasix) and spironolactone (Aldactone).
  • Cholesterol-reducing medications. Medications called statins can help lower cholesterol levels. However, it’s currently unclear whether or not cholesterol-lowering medications can specifically improve the outcomes of people with nephrotic syndrome, such as avoiding heart attacks or decreasing the risk of early death. Statins include atorvastatin (Lipitor), fluvastatin (Lescol), lovastatin (Altoprev, Mevacor), pravastatin (Pravachol), rosuvastatin (Crestor) and simvastatin (Zocor).
  • Blood thinners. Medications called anticoagulants help decrease your blood’s ability to clot and reduce your risk of developing blood clots. Anticoagulants include heparin or warfarin (Coumadin).
  • Immune system-suppressing medications. Medications to control the immune system, such as corticosteroids, may decrease the inflammation that accompanies certain kidney disorders, such as minimal change disease.

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NCLEX Glomerulonephritis Review

NCLEX Glomerulonephritis Review

Glomerulonephritis Overview

Glomerulonephritis is inflammation of the tiny filters in your kidneys (glomeruli). Glomeruli remove excess fluid, electrolytes and waste from your bloodstream and pass them into your urine. Also called glomerular disease, glomerulonephritis can be acute — a sudden attack of inflammation — or chronic — coming on gradually.

Glomerulonephritis (GN), also known as glomerular nephritis, is a term used to refer to several kidney diseases (usually affecting both kidneys). Many of the diseases are characterized by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory component.

As it is not strictly a single disease, its presentation depends on the specific disease entity: it may present with isolated hematuria and/or proteinuria (blood or protein in the urine); or as a nephrotic syndrome, a nephritic syndrome, acute kidney injury, or chronic kidney disease.

They are categorized into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differs in different types. Primary causes are intrinsic to the kidney. Secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic disorders (SLE, vasculitis), or diabetes.

Signs and Symptoms

Signs and symptoms of glomerulonephritis depend on whether you have the acute or chronic form, and the cause. Your first indication that something is wrong may come from symptoms or from the results of a routine urinalysis.

Glomerulonephritis signs and symptoms may include:

  • Pink or cola-colored urine from red blood cells in your urine (hematuria)
  • Foamy urine due to excess protein (proteinuria)
  • High blood pressure (hypertension)
  • Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen
  • Fatigue from anemia or kidney failure

Causes

Infections

  • Post-streptococcal glomerulonephritis. Glomerulonephritis may develop a week or two after recovery from a strep throat infection or, rarely, a skin infection (impetigo). To fight the infection, your body produces extra antibodies that may eventually settle in the glomeruli, causing inflammation. Children are more likely to develop post-streptococcal glomerulonephritis than are adults, and they’re also more likely to recover quickly.
  • Bacterial endocarditis. Bacteria occasionally can spread through your bloodstream and lodge in your heart, causing an infection of one or more of your heart valves. You’re at greater risk of this condition if you have a heart defect, such as a damaged or artificial heart valve. Bacterial endocarditis is associated with glomerular disease, but the exact connection between the two is unclear.
  • Viral infections. Viral infections, such as the human immunodeficiency virus (HIV), hepatitis B and hepatitis C, may trigger glomerulonephritis.

 Immune diseases

  • Lupus. A chronic inflammatory disease, lupus can affect many parts of your body, including your skin, joints, kidneys, blood cells, heart and lungs.
  • Goodpasture’s syndrome. A rare immunological lung disorder that may mimic pneumonia, Goodpasture’s syndrome causes bleeding in your lungs as well as glomerulonephritis.
  • IgA nephropathy. Characterized by recurrent episodes of blood in the urine, this primary glomerular disease results from deposits of immunoglobulin A (IgA) in the glomeruli. IgA nephropathy can progress for years with no noticeable symptoms.

Vasculitis

  • Polyarteritis. This form of vasculitis affects small and medium blood vessels in many parts of your body, such as your heart, kidneys and intestines.
  • Wegener’s granulomatosis. This form of vasculitis affects small and medium blood vessels in your lungs, upper airways and kidneys.

Conditions likely to cause scarring of the glomeruli

  • High blood pressure. High blood pressure can damage your kidneys and impair their ability to function normally. Glomerulonephritis can also lead to high blood pressure because it reduces kidney function and may influence how your kidneys handle sodium.
  • Diabetic kidney disease. Diabetic kidney disease (diabetic nephropathy) can affect anyone with diabetes. Diabetic nephropathy usually takes years to develop. Good control of blood sugar levels and blood pressure may prevent or slow kidney damage.
  • Focal segmental glomerulosclerosis. Characterized by scattered scarring of some of the glomeruli, this condition may result from another disease or occur for no known reason.

Chronic glomerulonephritis sometimes develops after a bout of acute glomerulonephritis. In some people there’s no history of kidney disease, so the first indication of chronic glomerulonephritis is kidney failure. Infrequently, chronic glomerulonephritis runs in families. One inherited form, Alport syndrome, also may involve hearing or vision impairment.

Complications

  • Acute kidney failure. Loss of function in the filtering part of the nephron may cause waste products to accumulate rapidly. You may need emergency dialysis — an artificial means of removing extra fluids and waste from your blood — typically by an artificial kidney machine.
  • Chronic kidney disease. With chronic kidney disease, your kidneys gradually lose their filtering ability. If your kidney function deteriorates to less than 10 percent of normal capacity, you have end-stage kidney disease, which requires dialysis or a kidney transplant to sustain life.
  • High blood pressure. Damage to your kidneys and the resulting buildup of wastes in the bloodstream can raise your blood pressure.
  • Nephrotic syndrome. With nephrotic syndrome, you have too much protein in your urine, which results in too little protein in your blood. Nephrotic syndrome may also be associated with high blood cholesterol and swelling (edema) of the eyelids, feet and abdomen.

Treatments

Treatment of glomerulonephritis and your outcome depend on:

  • Whether you have an acute or chronic form of the disease
  • The underlying cause
  • The type and severity of your signs and symptoms

Treat high blood pressure and underlying cause

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NCLEX Coarctation of the Aorta

NCLEX Coarctation of the Aorta

Coarctation Of The Aorta

Coarctation of the aorta is a birth defect in which a part of the aorta is narrower than usual.If the narrowing is severe enough and if it is not diagnosed, the baby may have serious problems and may need surgery or other procedures soon after birth. For this reason, coarctation of the aorta is often considered a critical congenital heart defect. The defect occurs when a baby’s aorta does not form correctly as the baby grows and develops during pregnancy. The narrowing of the aorta usually happens in the part of the blood vessel just after the arteries branch off to take blood to the head and arms, near the patent ductus arteriosus, although sometimes the narrowing occurs before or after the ductus arteriosus. In some babies with coarctation, it is thought that some tissue from the wall of ductus arteriosus blends into the tissue of the aorta. When the tissue tightens and allows the ductus arteriosus to close normally after birth, this extra tissue may also tighten and narrow the aorta.

The narrowing, or coarctation, blocks normal blood flow to the body. This can back up flow into the left ventricle of the heart, making the muscles in this ventricle work harder to get blood out of the heart. Since the narrowing of the aorta is usually located after arteries branch to the upper body, coarctation in this region can lead to normal or high blood pressure and pulsing of blood in the head and arms and low blood pressure and weak pulses in the legs and lower body.

If the condition is very severe, enough blood may not be able to get through to the lower body. The extra work on the heart can cause the walls of the heart to become thicker in order to pump harder. This eventually weakens the heart muscle. If the aorta is not widened, the heart may weaken enough that it leads to heart failure. Coarctation of the aorta often occurs with other congenital heart defects.

Signs and Symptoms

Coarctation of the aorta symptoms depend on the severity of the condition. Most people don’t have symptoms. Children with serious aortic narrowing may show signs and symptoms earlier in life, but mild cases with no symptoms might not be diagnosed until adulthood. People may also have signs or symptoms of other heart defects that they have along with coarctation of the aorta.

Babies with severe coarctation of the aorta may begin having signs and symptoms shortly after birth. These include:
  • Pale skin
  • Irritability
  • Heavy sweating
  • Difficulty breathing
  • Difficulty feeding

Causes

The causes of heart defects, including coarctation of the aorta, among most babies are unknown. Some babies have heart defects because of changes in their genes or chromosomes. Heart defects, like coarctation of the aorta, are also thought to be caused by a combination of genes and other risk factors, such as things the mother comes in contact with in the environment, what the mother eats or drinks, or medicines the mother uses.

Complications

Untreated coarctation of the aorta frequently leads to complications. Several of the complications may be a result of long-standing high blood pressure caused by the aortic coarctation. Complications are also possible after treatment for coarctation of the aorta.

Complications of coarctation of the aorta may include:

  • High blood pressure
  • Stroke
  • Enlargement in a section of the wall of the aorta (aneurysm)
  • Aortic rupture or tear (dissection)
  • Premature coronary artery disease — narrowing of the blood vessels that supply the heart
  • Heart failure
  • A weakened or bulging artery in the brain (brain aneurysm) or bleeding in the brain (hemorrhage)

Treatments

Treatment options for coarctation of the aorta depend on your age at the time of diagnosis and the severity of your condition. Other heart defects might be repaired at the same time as aortic coarctation.

Treatment approaches usually consist of surgery or a procedure called balloon angioplasty.

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NCLEX Mitral Valve Prolapse Review

NCLEX Mitral Valve Prolapse Review

Mitral Valve Prolapse

Mitral valve prolapse (MVP) (a.k.a. floppy mitral valve syndrome, systolic click murmur syndrome or billowing mitral leaflet) is a valvular heart disease characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. It is the primary form of myxomatous degeneration of the valve. There are various types of MVP, broadly classified as classic and nonclassic. In its nonclassic form, MVP carries a low risk of complications and often can be kept minimal by dietary attention. In severe cases of classic MVP, complications include mitral regurgitation, infective endocarditis, congestive heart failure, and, in rare circumstances, cardiac arrest.

The mitral valve, so named because of its resemblance to a bishop’s mitre, is the heart valve that prevents the backflow of blood from the left ventricle into the left atrium of the heart. It is composed of two leaflets, one anterior and one posterior, that close when the left ventricle contracts.

Each leaflet is composed of three layers of tissue: the atrialis, fibrosa, and spongiosa. Patients with classic mitral valve prolapse have excess connective tissue that thickens the spongiosa and separates collagen bundles in the fibrosa. This is due to an excess of dermatan sulfate, a glycosaminoglycan. This weakens the leaflets and adjacent tissue, resulting in increased leaflet area and elongation of the chordae tendineae. Elongation of the chordae tendineae often causes rupture, commonly to the chordae attached to the posterior leaflet. Advanced lesions—also commonly involving the posterior leaflet—lead to leaflet folding, inversion, and displacement toward the left atrium.

Signs and Symptoms

  • A racing or irregular heartbeat (arrhythmia)
  • Dizziness or lightheadedness
  • Difficulty breathing or shortness of breath, often when lying flat or during physical activity
  • Fatigue
  • Chest pain that’s not caused by a heart attack or coronary artery disease

Causes

When your heart is working properly, the mitral valve closes completely during contraction of the left ventricle and prevents blood from flowing back into your heart’s upper left chamber (left atrium).

But in some people with mitral valve prolapse, one or both of the mitral valve’s flaps (leaflets) have extra tissue bulging (prolapsing) like a parachute into the left atrium each time the heart contracts.

The bulging may keep the valve from closing tightly. When blood leaks backward through the valve, it’s called mitral valve regurgitation.

This may not cause problems if only a small amount of blood leaks back into the atrium. More severe mitral valve regurgitation can cause symptoms such as shortness of breath, fatigue or lightheadedness.

Another name for mitral valve prolapse is click-murmur syndrome. When a doctor listens to your heart using a stethoscope, he or she may hear a clicking sound as the valve’s leaflets billow out, followed by a murmur resulting from blood flowing back into the atrium. Other names to describe mitral valve prolapse include:

  • Barlow’s syndrome
  • Floppy valve syndrome
  • Balloon mitral valve
  • Billowing mitral valve
  • Myxomatous mitral valve
  • Prolapsing mitral valve syndrome

Risk Factors

Mitral valve prolapse can develop in any person at any age.  Serious symptoms of mitral valve prolapse tend to occur most often in men older than 50.

Mitral valve prolapse can run in families and may be linked to several other conditions, such as:

  • Marfan syndrome
  • Ehlers-Danlos syndrome
  • Ebstein’s anomaly
  • Muscular dystrophy
  • Graves’ disease
  • Scoliosis

Complications 

Although most people with mitral valve prolapse never have problems, complications can occur. They may include:

  • Mitral valve regurgitation.The most common complication is a condition in which the valve leaks blood back into the left atrium (mitral valve regurgitation).
    Being male or having high blood pressure increases your risk of mitral valve regurgitation. If the regurgitation is severe, you may need surgery to repair or replace the valve in order to prevent the development of complications, such as stroke.
  • Heart rhythm problems (arrhythmias). Irregular heart rhythms can occur in people with mitral valve prolapse. These most commonly occur in the upper chambers of the heart, and while they may be bothersome, they aren’t usually life-threatening.People with severe mitral valve regurgitation or severe deformity of their mitral valve are most at risk of having serious rhythm problems, which affect blood flow through the heart.
  • Heart valve infection (endocarditis). The inside of your heart contains four chambers and four valves lined by a thin membrane called the endocardium. Endocarditis is an infection of this inner lining.An abnormal mitral valve increases your chance of getting endocarditis from bacteria, which can further damage the mitral valve. The risk is higher in older men.Doctors used to recommend that some people with mitral valve prolapse take antibiotics before certain dental or medical procedures to prevent endocarditis but not anymore.The American Heart Association advises that antibiotics aren’t necessary in most cases for someone with mitral valve regurgitation or mitral valve prolapse.

Treatments

Most people with mitral valve prolapse, particularly people without symptoms, don’t require treatment.

If you have mitral valve regurgitation but don’t have symptoms, your doctor may suggest you return regularly for follow-up examinations to monitor your condition, depending on the severity of your condition.

If you develop symptoms, your doctor might prescribe certain medications to treat mitral valve prolapse-related chest pain, heart rhythm abnormalities or other complications. Some medications you might be prescribed include:

  • Beta blockers
  • Diuretics
  • Heart rhythm medications
  • Aspirin

Surgery

  • Valve Replacement or Repair

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NCLEX Aortic Stenosis Review

 NCLEX Aortic Stenosis Review

Aortic Stenosis Overview

Aortic stenosis (AS or AOS) is the narrowing of the exit of the left ventricle of the heart, such that problems result. It may occur at the aortic valve as well as above and below this level. It typically gets worse over time. Symptoms often come on gradually with a decreased ability to exercise often occurring first. If heart failure, loss of consciousness, or heart related chest pain occurs due to AS the outcomes are worse. Loss of consciousness typically occurs with standing or exercise. Signs of heart failure include shortness of breath especially when lying down, at night, or with exercise, and swelling of the legs. Thickening of the valve without narrowing is known as aortic sclerosis.

Signs and Symptoms

Aortic valve stenosis ranges from mild to severe. Aortic valve stenosis signs and symptoms generally develop when narrowing of the valve is severe and can include:

  • Chest pain (angina) or tightness
  • Feeling faint or fainting with exertion
  • Shortness of breath, especially with exertion
  • Fatigue, especially during times of increased activity
  • Heart palpitations — sensations of a rapid, fluttering heartbeat
  • Heart murmur

Causes

  • As the aortic valve narrows, the left ventricle has to work harder to pump blood out through the valve. To do this extra work, the muscles in the ventricle walls become thicker. This can lead to chest pain.
  • As the pressure continues to rise, blood may back up into the lungs. Severe aortic stenosis can limit the amount of blood that reaches the brain and the rest of the body.
  • Aortic stenosis may be present from birth (congenital), but most often it develops later in life. Children with aortic stenosis may have other conditions present from birth.
  • Aortic stenosis mainly occurs due to the buildup of calcium deposits that narrow the valve. This is called calcific aortic stenosis. The problem mostly affects older people.
  • Calcification of the valve happens sooner in people who are born with abnormal aortic or bicuspid valves. In rare cases, calcification can develop more quickly when a person has received chest radiation (such as for cancer treatment).
  • Another cause is rheumatic fever. This condition can develop after strep throat or scarlet fever. Valve problems do not develop for 5 – 10 years or longer after rheumatic fever occurs. Rheumatic fever is becoming rarer in the United States.
  • Aortic stenosis occurs in about 2% of people over 65 years of age. It occurs more often in men than in women.

Risk Factors

Aortic valve stenosis isn’t considered preventable, and presently it’s not known why some people develop this condition. Some risk factors include:

  • A deformed aortic valve Some people are born with an already narrowed aortic valve or develop aortic valve stenosis later in life because they were born with a bicuspid aortic valve — one with two flaps (leaflets) instead of three. People may also develop aortic valve stenosis if they were born with one leaflet (unicuspid aortic valve) or four leaflets (quadricuspid aortic valve), but these are much more rare conditions.
    A bicuspid aortic valve is a major risk factor for aortic valve stenosis. A bicuspid aortic valve can run in families, so knowing your family history is important. If you have a first-degree relative — a parent, sibling or child — with a bicuspid aortic valve, it is reasonable to check to see if you have this abnormality.
  • Age Aortic valve stenosis may be related to increasing age and the buildup of calcium deposits on heart valves.
  • Previous rheumatic fever  Rheumatic fever can cause the flaps (leaflets) of your aortic valve to stiffen and fuse, eventually resulting in aortic valve stenosis.
  • Chronic kidney disease  Aortic valve stenosis is associated with chronic kidney disease.

Risk factors for aortic valve stenosis and atherosclerotic heart disease are similar — such as high blood pressure, high cholesterol, type 2 diabetes and smoking — which may indicate a link between the two.

Complications

Aortic valve stenosis — of any cause — can be a serious condition. If the aortic valve is narrowed, the left ventricle has to work harder to pump a sufficient amount of blood into the aorta and onward to the rest of your body.

In response, the left ventricle may thicken and enlarge. At first, these adaptations help the left ventricle pump blood with more force. But eventually it’s harder for the heart to maintain the blood flow to the body through the narrowed valve. Then you will start to experience symptoms. Eventually, the extra work of the heart can weaken the left ventricle — and your heart overall.

Left unchecked, aortic valve stenosis can lead to life-threatening heart problems, including:
  • Chest pain (angina)
  • Fainting (syncope)
  • Heart failure
  • Irregular heart rhythms (arrhythmias)
  • Cardiac arrest

Diagnosis

A heart murmur, click, or other abnormal sound is almost always heard through a stethoscope. The health care provider may be able to feel a vibration or movement when placing a hand over the heart. There may be a faint pulse or changes in the quality of the pulse in the neck.

Blood pressure may be low.

The following tests may also be performed:

  • ECG
  • ECHO
  • Chest X-Ray
  • CT Chest
  • Exercise stress testing
  • Left cardiac catheterization
  • MRI of the heart
  • Transesophageal echocardiogram (TEE)

Treatments

Treatment is generally not necessary in people without symptoms.  In moderate cases, echocardiography is performed every 1–2 years to monitor the progression, possibly complemented with a cardiac stress test.  In severe cases, echocardiography is performed every 3–6 months.  In both moderate and mild cases, the person should immediately make a revisit or be admitted for inpatient care if any new related symptoms appear.  There are no therapeutic options currently available to treat people with aortic valve stenosis; however, studies have indicated that the disease occurs as a result of active cellular processes, suggesting that targeting these processes may lead to viable therapeutic approaches.

Surgical Repair

  • Aortic Valve Repair and/or Replacement
  • Balloon valvuloplasty

 

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NCLEX Atrial Septal Defect

 NCLEX Atrial Septal Defect

Atrial Septal Defect

Atrial septal defect (ASD) is a congenital heart defect in which blood flows between the atria (upper chambers) of the heart. Normally, the atria are separated by a dividing wall, the interatrial septum. If this septum is defective or absent, then oxygen-rich blood can flow directly from the left side of the heart to mix with the oxygen-poor blood in the right side of the heart, or vice versa.  This can lead to lower-than-normal oxygen levels in the arterial blood that supplies the brain, organs, and tissues. However, an ASD may not produce noticeable signs or symptoms, especially if the defect is small.

A “shunt” is the presence of a net flow of blood through the defect, either from left to right or right to left. The amount of shunting present, if any, determines the hemodynamic significance of the ASD. A “right-to-left-shunt” typically poses the more dangerous scenario.

Signs and Symptoms

Atrial septal defect signs and symptoms may include:

  • Shortness of breath, especially when exercising
  • Fatigue
  • Swelling of legs, feet or abdomen
  • Heart palpitations or skipped beats
  • Frequent lung infections
  • Stroke
  • Heart murmur, a whooshing sound that can be heard through a stethoscope

Causes

An atrial septal defect (ASD) allows freshly oxygenated blood to flow from the left upper chamber of the heart (left atrium) into the right upper chamber of the heart (right atrium). There, it mixes with deoxygenated blood and is pumped to the lungs, even though it’s already refreshed with oxygen.

If the atrial septal defect is large, this extra blood volume can overfill the lungs and overwork the heart. If not treated, the right side of the heart eventually enlarges and weakens. If this process continues, the blood pressure in your lungs increases as well, leading to pulmonary hypertension.

Atrial septal defects can be several types, including:

  • Secundum. This is the most common type of ASD, and occurs in the middle of the wall between the atria (atrial septum).
  • Primum. This defect occurs in the lower part of the atrial septum, and may occur with other congenital heart problems.
  • Sinus venosus. This rare defect occurs in the upper part of the atrial septum.
  • Coronary sinus. In this rare defect, part of the wall between the coronary sinus — which is part of the vein system of the heart — and the left atrium is missing.

Risk Factors

It’s not known why atrial septal defects occur, but congenital heart defects appear to run in families and sometimes occur with other genetic problems, such as Down syndrome. If you have a heart defect, or you have a child with a heart defect, a genetic counselor can estimate the odds that any future children will have one.

Some conditions that you have or that occur during pregnancy may increase your risk of having a baby with a heart defect, including:
  • Rubella infection. Becoming infected with rubella (German measles) during the first few months of your pregnancy can increase the risk of fetal heart defects.
  • Drug, tobacco or alcohol use, or exposure to certain substances. Use of certain medications, tobacco, alcohol or drugs, such as cocaine, during pregnancy can harm the developing fetus.
  • Diabetes or lupus. If you have diabetes or lupus, you may be more likely to have a baby with a heart defect.
  • Obesity. Being extremely overweight (obese) may play a role in increasing the risk of having a baby with a birth defect.
  • Phenylketonuria (PKU). If you have PKU and aren’t following your PKU meal plan, you may be more likely to have a baby with a heart defect.

Complications

A small atrial septal defect may never cause any problems. Small atrial septal defects often close during infancy.

Larger defects can cause mild to life-threatening problems, including:

  • Right-sided heart failure
  • Heart rhythm abnormalities (arrhythmias)
  • Increased risk of a stroke
 Less common serious complications may include:
  • Pulmonary hypertension. If a large atrial septal defect goes untreated, increased blood flow to your lungs increases the blood pressure in the lung arteries (pulmonary hypertension).
  • Eisenmenger syndrome. In rare cases, pulmonary hypertension can cause permanent lung damage. This complication, called Eisenmenger syndrome, usually develops over many years and occurs only in a small percentage of people with large atrial septal defects.

Treatments

Many atrial septal defects close on their own during childhood. For those that don’t close, some small atrial septal defects don’t cause any problems and may not require any treatment. But many persistent atrial septal defects eventually require surgery to be corrected.  Once someone is found to have an atrial septal defect, a determination of whether it should be corrected has to be made.  Methods of closure of an ASD include surgical closure and percutaneous closure.

Surgical mortality due to closure of an ASD is lowest when the procedure is performed prior to the development of significant pulmonary hypertension. The lowest mortality rates are achieved in individuals with a pulmonary artery systolic pressure of less than 40 mm Hg.

 

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NCLEX Muscular Dystrophy Review

 NCLEX Muscular Dystrophy Review

Muscular Dystrophy Overview

Muscular dystrophy (MD) is a group of muscle diseases that weaken the musculoskeletal system and hamper locomotion (walking or moving ).  Muscular dystrophies are characterized by progressive skeletal muscle weakness, defects in muscle proteins, and the death of muscle cells and tissue.

Signs and Symptoms

The main sign of muscular dystrophy is progressive muscle weakness. Specific signs and symptoms begin at different ages and in different muscle groups, depending on the type of muscular dystrophy.

Duchenne muscular dystrophy

About half of people with muscular dystrophy have this variety. Although girls can be carriers and mildly affected, the disease typically affects boys.

About one-third of boys with Duchenne muscular dystrophy don’t have a family history of the disease, possibly because the gene involved may be subject to sudden abnormal change (spontaneous mutation).

Signs and symptoms typically appear between the ages of 2 and 3, and may include:

  • Frequent falls
  • Difficulty getting up from a lying or sitting position
  • Trouble running and jumping
  • Waddling gait
  • Walking on the toes
  • Large calf muscles
  • Muscle pain and stiffness
  • Learning disabilities

Causes

These conditions are generally inherited, and the different muscular dystrophies follow various inheritance patterns. Muscular dystrophy can be inherited by individuals as an X-linked disorder, a recessive or dominant disorder. Furthermore, it can be a spontaneous mutationwhich means errors in the replication of DNA and spontaneous lesions. Spontaneous lesions are due to natural damage to DNA, where the most common are depurination and deamination

Risk Factors

Muscular dystrophy occurs in both sexes and in all ages and races. However, the most common variety, Duchenne, usually occurs in young boys. People with a family history of muscular dystrophy are at higher risk of developing the disease or passing it on to their children.

Complications

The complications of progressive muscle weakness include:

  • Inability to walk. Some people with muscular dystrophy eventually need to use a wheelchair.
  • Shortening of muscles or tendons around joints (contractures). Contractures can further limit mobility.
  • Breathing problems. Progressive weakness can affect the muscles associated with breathing. People with muscular dystrophy may eventually need to use a breathing assistance device (ventilator), initially at night but possibly also in the day.
  • Curved spine (scoliosis). Weakened muscles may be unable to hold the spine straight.
  • Heart problems. Muscular dystrophy can reduce the efficiency of the heart muscle.
  • Swallowing problems. If the muscles involved with swallowing are affected, nutritional problems and aspiration pneumonia may develop. Feeding tubes may be an option.

Treatments

Currently, there is no cure for muscular dystrophy. Medications and various therapies help slow the progression of the disease and keep the patient mobile for the longest possible time.

Drugs

The two most commonly prescribed drugs for muscular dystrophy are:

  • Corticosteroids: although this type of medication can help increase muscle strength and slow progression, their long-term use can weaken bone and increase weight gain
  • Heart medications: if the muscular dystrophy impacts the heart, beta blockers and angiotensin-converting enzyme (ACE) inhibitors may be useful.

Physical therapy

  • General exercises: a range of motion and stretching exercises can help combat the inevitable inward movement of the limbs as muscles and tendons shorten. Limbs tend to become fixed in position and these types of activities can help keep them mobile for longer. Standard low-impact aerobic exercises such as walking and swimming can also help slow the disease’s progression
  • Breathing assistance: as the muscles charged with breathing become weaker, it may be necessary to use devices to help improve oxygen delivery through the night. In the most severe cases, a patient may need to use a ventilator to breathe on their behalf
  • Mobility aids: canes, wheelchairs and walkers
  • Braces: these keep muscles and tendons stretched and help slow their shortening. They also give added support to the user when moving.

 

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NCLEX Myasthenia Gravis Review

 NCLEX Myasthenia Gravis Review

Myasthenia Gravis Overview

Myasthenia gravis (MG) is a neuromuscular disease that leads to fluctuating muscle weakness and fatigue. In the most common cases, muscle weakness is caused by circulating antibodies that block nicotinic acetylcholine receptors at the post-synaptic neuromuscular junction. By blocking the ability of the neurotransmitter acetylcholine to bind to these receptors in the muscle, these antibodies keep motor neurons from signaling the muscle to contract. Alternatively, in a much rarer form, muscle weakness is caused by a genetic defect in some portion of the neuromuscular junction that is inherited at birth as opposed to developing through passive transmission from the mother’s immune system at birth or through autoimmunity later in life.

Myasthenia gravis is believed to be caused by variations in certain genes. The disorder occurs when the immune system malfunctions and attacks the body’s tissues. The antibody in myasthenia gravis attacks normal human protein, targeting a protein called an acetylcholine receptor, or a related protein called a muscle-specific kinase.

Human leukocyte antigens have been associated with MG susceptibility.  Many of these genes are present among other autoimmune diseases. Relatives of MG patients have a higher percentage of other immune disorders.

The thymus gland cells form part of the body’s immune system. In those with myasthenia gravis, the thymus gland is large and abnormal. It sometimes contains clusters of immune cells which indicate lymphoid hyperplasia, and it is believed the thymus gland may give wrong instructions to immune cells

Signs and Symptoms

Muscle weakness caused by myasthenia gravis worsens as the affected muscle is used repeatedly. Because symptoms usually improve with rest, your muscle weakness may come and go. However, myasthenia gravis 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 the 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 percent of people with myasthenia gravis, the first symptoms involve face and throat muscles, which can cause:

  • Altered speaking. Your speech may sound very soft or nasal, depending upon which muscles have been affected.
  • Difficulty swallowing. You may choke very easily, which makes it difficult to eat, drink or take pills. In some cases, liquids you’re trying to swallow may come out your nose.
  • Problems chewing. The muscles used for chewing may wear out halfway through a meal, particularly if you’ve been eating something hard to chew, such as steak.
  • Limited facial expressions. Your family members may comment that you’ve “lost your smile” if the muscles that control your facial expressions have been affected.

Neck and limb muscles

Myasthenia gravis can cause weakness in your neck, arms and legs, but this usually happens along with muscle weakness in other parts of your body, such as your eyes, face or throat.

The disorder usually affects arms more often than legs. However, if it affects your legs, you may waddle when you walk. If your neck is weak, it may be hard to hold up your head.

Causes

This neuromuscular disease is caused by transmission defects in nerve impulses to muscles. The neuromuscular junction is apparently affected: acetylcholine, which produces muscle contraction under normal conditions no longer produces the contractions necessary to muscle movement.[

Treatments

Treatment is by medication and/or surgery. Medication consists mainly of acetylcholinesterase inhibitors to directly improve muscle function and immunosuppressant drugs to reduce the autoimmune process. Thymectomy is a surgical method to treat MG.

Medications

  • Cholinesterase inhibitors
  • Corticosteroids
  • Immunosuppressants

Intravenous therapy

  • Plasmapheresis
  • Intravenous immunoglobulin (IVIG).
  • Monoclonal antibody

 

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NCLEX Tetralogy Of Fallot Review

tetralogy of fallot

Tetralogy Of Fallot Review For NCLEX

Tetralogy of Fallot (TOF) is a congenital heart defect which is classically understood to involve four anatomical abnormalities of the heart (although only three of them are always present). It is the most common cyanotic heart defect and the most common cause of blue baby syndrome.  TOF is usually a right-to-left shunt, in which higher resistance to right ventricular outflow results in more severe cyanosis symptoms.

These defects, which affect the structure of the heart, cause oxygen-poor blood to flow out of the heart and to the rest of the body. Infants and children with tetralogy of Fallot usually have blue-tinged skin because their blood doesn’t carry enough oxygen.

Tetralogy of Fallot is often diagnosed during infancy or soon after. However, tetralogy of Fallot might not be detected until later in life, depending on the severity of the defects and symptoms.

With early diagnosis followed by appropriate surgical treatment, most children who have tetralogy of Fallot live relatively normal lives, though they’ll need regular medical care and might have restrictions on exercise.

Signs and Symptoms

Tetralogy of Fallot symptoms vary, depending on the extent of obstruction of blood flow out of the right ventricle and into the lungs. Signs and symptoms may include:

  • A bluish coloration of the skin caused by blood low in oxygen (cyanosis)
  • Shortness of breath and rapid breathing, especially during feeding or exercise
  • Loss of consciousness (fainting)
  • Clubbing of fingers and toes — an abnormal, rounded shape of the nail bed
  • Poor weight gain
  • Tiring easily during play or exercise
  • Irritability
  • Prolonged crying
  • A heart murmur

Tet spells

Sometimes, babies who have tetralogy of Fallot will suddenly develop deep blue skin, nails and lips after crying or feeding, or when agitated.  These episodes are called tet spells and are caused by a rapid drop in the amount of oxygen in the blood. Tet spells are most common in young infants, around 2 to 4 months old. Toddlers or older children might instinctively squat when they’re short of breath. Squatting increases blood flow to the lungs.

Causes

Tetralogy of Fallot occurs during fetal growth, when the baby’s heart is developing. While factors such as poor maternal nutrition, viral illness or genetic disorders might increase the risk of this condition, in most cases the cause of tetralogy of Fallot is unknown.

The four abnormalities that make up the tetralogy of Fallot include:

  • Pulmonary valve stenosis. Pulmonary valve stenosis is a narrowing of the pulmonary valve — the valve that separates the lower right chamber of the heart (right ventricle) from the main blood vessel leading to the lungs (pulmonary artery).Narrowing (constriction) of the pulmonary valve reduces blood flow to the lungs. The narrowing might also affect the muscle beneath the pulmonary valve.
  • Ventricular septal defect. A ventricular septal defect is a hole in the wall that separates the two lower chambers of the heart — the left and right ventricle. The hole allows deoxygenated blood in the right ventricle — blood that has circulated through the body and is returning to the lungs to replenish its oxygen supply — to flow into the left ventricle and mix with oxygenated blood fresh from the lungs.Blood from the left ventricle also flows back to the right ventricle in an inefficient manner. This ability for blood to flow through the ventricular septal defect reduces the supply of oxygenated blood to the body and eventually can weaken the heart.
  • Overriding aorta. Normally the aorta — the main artery leading out to the body — branches off the left ventricle. In tetralogy of Fallot, the aorta is shifted slightly to the right and lies directly above the ventricular septal defect.In this position the aorta receives blood from both the right and left ventricles, mixing the oxygen-poor blood from the right ventricle with the oxygen-rich blood from the left ventricle.
  • Right ventricular hypertrophy. When the heart’s pumping action is overworked, it causes the muscular wall of the right ventricle to thicken. Over time this might cause the heart to stiffen, become weak and eventually fail.

Some babies who have tetralogy of Fallot may have other heart defects, such as a hole between their heart’s upper chambers (atrial septal defect).

Risk Factors

While the exact cause of tetralogy of Fallot is unknown, various factors might increase the risk of a baby being born with this condition. These risk factors include:

  • A viral illness during pregnancy, such as rubella (German measles)
  • Alcoholism during pregnancy
  • Poor nutrition during pregnancy
  • A mother older than age 40
  • A parent who has tetralogy of Fallot
  • The presence of Down syndrome or DiGeorge syndrome

Diagnosis

Tests may include:

  • Echocardiography – Echocardiograms use high-pitched sound waves to produce an image of the heart. Sound waves bounce off your baby’s heart and produce moving images that can be viewed on a video screen.This test is generally used to diagnose tetralogy of Fallot. It allows your baby’s doctor to determine if there is a ventricular septal defect and where it’s located, if the structure of the pulmonary valve and pulmonary artery is normal, if the right ventricle is functioning properly, and if the aorta is positioned properly. This test can also help your baby’s doctors to plan treatment for your baby’s condition.
  • Electrocardiogram – An electrocardiogram records the electrical activity in the heart each time it contracts. During this procedure, patches with wires (electrodes) are placed on your baby’s chest, wrists and ankles. The electrodes measure electrical activity, which is recorded on paper.This test helps determine if your baby’s right ventricle is enlarged (right ventricular hypertrophy), if your baby’s right atrium is enlarged and if the heart rhythm is regular.
  • Chest X-ray – A chest X-ray can show the structure of your baby’s heart and lungs. A common sign of tetralogy of Fallot on an X-ray is a “boot-shaped” heart, because the right ventricle is enlarged.
  • Oxygen level measurement (pulse oximetry) – This test uses a small sensor that can be placed on a finger or toe to measure the amount of oxygen in your baby’s blood.
  • Cardiac catheterization – Doctors may use this test to evaluate the structure of the heart and plan surgical treatment. During this procedure, your baby’s doctor inserts a thin, flexible tube (catheter) into an artery or vein in your baby’s arm, groin or neck and threads it up to his or her heart.Your baby’s doctor injects a dye through the catheter to make your baby’s heart structures visible on X-ray pictures. Cardiac catheterization also measures pressure and oxygen levels in the chambers of the heart and in the blood vessels.

Treatments

Surgery is the only effective treatment for tetralogy of Fallot. Surgical options include intracardiac repair or a temporary procedure that uses a shunt. However, most babies and older children have intracardiac repair.

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NCLEX Cirrhosis Online Review

 NCLEX Cirrhosis Online Review

NCLEX Cirrhosis Online Review

Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism. The liver carries out several necessary functions, including detoxifying harmful substances in your body, cleaning your blood and making vital nutrients.

Cirrhosis occurs in response to damage to your liver. Each time your liver is injured, it tries to repair itself. In the process, scar tissue forms. As cirrhosis progresses, more and more scar tissue forms, making it difficult for the liver to function.

Decompensated cirrhosis is the term used to describe the development of specific complications resulting from the changes brought on by cirrhosis. Decompensated cirrhosis is life-threatening.

The liver damage done by cirrhosis generally can’t be undone. But if liver cirrhosis is diagnosed early and the cause is treated, further damage can be limited and, rarely, reversed.

Signs and Symptoms

Cirrhosis often has no signs or symptoms until liver damage is extensive. When signs and symptoms do occur, they may include:

  • Fatigue
  • Bleeding easily
  • Bruising easily
  • Itchy skin
  • Yellow discoloration in the skin and eyes (jaundice)
  • Fluid accumulation in your abdomen (ascites)
  • Loss of appetite
  • Nausea
  • Swelling in your legs
  • Weight loss
  • Confusion, drowsiness and slurred speech (hepatic encephalopathy)
  • Spiderlike blood vessels on your skin
  • Redness in the palms of the hands
  • Testicular atrophy in men
  • Breast enlargement in men

Causes

A wide range of diseases and conditions can damage the liver and lead to cirrhosis. The most common causes are:

  • Chronic alcohol abuse
  • Chronic viral hepatitis (hepatitis B and C)
  • Fat accumulating in the liver (nonalcoholic fatty liver disease)

Other possible causes include:

  • Iron buildup in the body (hemochromatosis)
  • Cystic fibrosis
  • Copper accumulated in the liver (Wilson’s disease)
  • Poorly formed bile ducts (biliary atresia)
  • Inherited disorders of sugar metabolism (galactosemia or glycogen storage disease)
  • Genetic digestive disorder (Alagille syndrome)
  • Liver disease caused by your body’s immune system (autoimmune hepatitis)
  • Destruction of the bile ducts (primary biliary cirrhosis)
  • Hardening and scarring of the bile ducts (primary sclerosing cholangitis)
  • Infection such schistosomiasis
  • Medications such as methotrexate

Complications

  • High blood pressure in the veins that supply the liver (portal hypertension).Cirrhosis slows the normal flow of blood through the liver, thus increasing pressure in the vein that brings blood from the intestines and spleen to the liver.
  • Swelling in the legs and abdomen. Portal hypertension can cause fluid to accumulate in the legs (edema) and in the abdomen (ascites). Edema and ascites also may result from the inability of the liver to make enough of certain blood proteins, such as albumin.
  • Enlargement of the spleen (splenomegaly). Portal hypertension can also cause changes to the spleen. Decreased white blood cells and platelets in your blood can be a sign of cirrhosis with portal hypertension.
  • Bleeding. Portal hypertension can cause blood to be redirected to smaller veins, causing them to increase in size and become varices. Strained by the extra load, these smaller veins can burst, causing serious bleeding. Life-threatening bleeding most commonly occurs when veins in the lower esophagus (esophageal varices) or stomach (gastric varices) rupture. If the liver can’t make enough clotting factors, this also can contribute to continued bleeding. Bacterial infections are a frequent trigger for bleeding.
  • Infections. If you have cirrhosis, your body may have difficulty fighting infections. Ascites can lead to spontaneous bacterial peritonitis, a serious infection.
  • Malnutrition. Cirrhosis may make it more difficult for your body to process nutrients, leading to weakness and weight loss.
  • Buildup of toxins in the brain (hepatic encephalopathy). A liver damaged by cirrhosis isn’t able to clear toxins from the blood as well as a healthy liver can. These toxins can then build up in the brain and cause mental confusion and difficulty concentrating. Hepatic encephalopathy symptoms may range from fatigue and mild impairment in cognition to unresponsiveness or coma.
  • Jaundice. Jaundice occurs when the diseased liver doesn’t remove enough bilirubin, a blood waste product, from your blood. Jaundice causes yellowing of the skin and whites of the eyes and darkening of urine.
  • Bone disease. Some people with cirrhosis lose bone strength and are at greater risk of fractures.
  • Increased risk of liver cancer. A large proportion of people who develop liver cancer that forms within the liver itself have cirrhosis.
  • Acute-on-chronic liver failure. Some people end up experiencing multiorgan failure. Researchers now believe this is a distinct complication in some people who have cirrhosis, but they don’t fully understand its causes.

Treatments

Treatment for cirrhosis depends on the cause and extent of your liver damage. The goals of treatment are to slow the progression of scar tissue in the liver and to prevent or treat symptoms and complications of cirrhosis.

 

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If you are taking the NCLEX National Exam for the first time and need information about how to register in your state, go to NCBSN.org for more information.

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