AtoZ Diseases

What do Doctors call this Condition - Thromboangiitis obliterans

What is this Condition?

Buerger’s disease - an inflammatory, occlusive condition - causes segmental lesions and subsequent blood clot (thrombus) formation in the small and medium arteries (and sometimes the veins), thereby reducing blood flow to the feet and legs. This disorder may produce ulceration and, eventually, gangrene.

What Causes it?

Although the cause of Buerger’s disease is unknown, it has been linked to smoking, suggesting a hypersensitivity reaction to nicotine. Incidence is highest among men of Jewish ancestry between the ages of 20 and 40 who smoke heavily.

What are its Symptoms?

Buerger’s disease typically causes intermittent claudication (cramplike pains) of the instep, which is aggravated by exercise and relieved by rest. During exposure to low temperature, the feet initially become cold, pale, and numb; later, they redden, become hot, and tingle.

Occasionally, Buerger’s disease also affects the hands, possibly resulting in painful fingertip ulcers.

How is it Diagnosed?

The person’s history and physical exam strongly suggest Buerger’s disease. Supportive diagnostic tests include arteriography (X-ray of the artery) and an ultrasound scan.

How is it Treated?

The primary goals of treatment are to relieve symptoms and prevent complications. Such therapy may include an exercise program that uses gravity to fill and drain the blood vessels or, in severe disease, a surgical procedure called a lumbar sympathectomy (interruption of the sympathetic nervous system pathway) to increase blood supply to the skin. Amputation may be necessary for nonhealing ulcers, intractable pain, or gangrene.

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What do Doctors call this Condition - Myocardial infarction

What is this Condition?

In a heart attack, one of the heart’s arteries fails to deliver enough blood to the part of the heart muscle it serves. The reduced blood flow causes destruction of localized areas of heart tissue.

If treatment is delayed, the person may die; almost half of sudden deaths from heart attack occur before the victims reach the hospital, within 1 hour after symptoms arise. (Typically, death stems from severe tissue damage or from complications.) The prognosis is better if vigorous treatment begins immediately.

What Causes it?

Arteriosclerosis (hardening of the heart’s arteries), which reduces the artery’s blood flow, is usually the underlying cause of a heart attack. Risk factors include:

• a family history of heart disease

• high blood pressure

• smoking

• high cholesterol and triglyceride levels

• diabetes

• obesity or a diet high in saturated fats, carbohydrates, or salt

• a sedentary lifestyle

• aging

• drug use, especially cocaine

• stress or Type A personality.

Men are more susceptible to heart attacks than women, although the heart attack rate is rising in women - especially those who smoke or take oral contraceptives.

What are its Symptoms?

The chief symptom of a heart attack is persistent, crushing chest pain that may spread to the left arm, jaw, neck, or shoulder blades and may last 12 hours or longer. Typically, heart attack victims describe the pain as heavy, squeezing, or crushing. Bur some - particularly elderly people and those with diabetes - don’t experience pain. Others have mild pain that they, or their doctor, may mistake for indigestion. In people with hardening of the arteries, chest pain that grows more and more frequent, severe, or longer-lasting may signal an impending heart attack - especially if the pain isn’t triggered by exertion, a heavy meal, or cold and wind.

Some heart attack victims also have a feeling of impending doom, fatigue, nausea, vomiting, shortness of breath, coolness in the arms and legs, perspiration, anxiety, and restlessness. And some people have a “silent” heart attack, which causes no symptoms at all.

Complications

The most common complications of a heart attack are recurrent or persistent chest pain; irregular heart rhythms; failure of the heart’s main chamber (left ventricle), causing heart failure or massive fluid buildup in the lungs; and failure of the heart to pump enough blood, causing shock.

Soon after a heart attack, a few people have potentially fatal complications - a blood clot in a vein, heart valve malfunction, rupture of the partition between the heart’s chambers, and rupture of the heart muscle.

Up to several months after a heart attack, some people experience Dressler’s syndrome - inflammation of the sac around the heart, accompanied by chest pain, fever, and possibly lung inflammation.

How is it Diagnosed?

To confirm a heart attack, the doctor checks for persistent chest pain, characteristic electrocardiogram findings, and blood tests showing elevated levels of cardiac enzymes over a 72-hour period. A physical exam may reveal abnormal heart sounds.

When symptoms and physical exam results aren’t clear-cut, the doctor assumes that the person has had a heart attack - to be on the safe side - until tests rule it out. To investigate further, these tests may be ordered:

• 12-lead electrocardiogram - may reveal characteristic abnormalities during the first few hours after a heart attack

• echocardiography- (a study of the heart’s structure and motion) ­may show abnormal motion of the ventricular wall in a heart attack that involves the entire wall of the heart.

• technetium scans - can identify badly damaged heart muscle by detecting emissions from the radioactive marker, an isotope of technetium, which looks like a “hot spot” on film. These scans help to pinpoint a recent heart attack.

How is it Treated?

The goals of treatment are to relieve chest pain, stabilize the heart rhythm, ease the heart’s workload, restore blood to the heart’s arteries, and preserve heart muscle tissue. Irregular heart rhythms - the main problem during the first 48 hours after a heart attack - may require drugs and possibly a pacemaker. Rarely, a person requires car- dioversion, in which an electrical current is delivered to the heart in an attempt to restore a normal rhythm.

To preserve heart muscle tissue, the doctor may administer thrombolytics (drugs that break up clots in the arteries) within 6 hours after heart attack symptoms arise. These drugs include streptokinase, alteplase, and urokinase.

Percutaneous transluminal coronary angioplasty may be another option. In this procedure, the doctor threads a thin, balloon-tipped catheter into the narrowed heart artery (if narrowing has caused the heart attack). After injecting contrast dye through the catheter to pinpoint the narrowed site, the doctor inflates the balloon catheter to expand and reopen the artery. If this procedure is done soon after symptoms begin, a thrombolytic drug may be injected directly into the artery.

Other Treatments

After a heart attack, some people also receive:

• lidocaine, a drug used to control certain irregular heart rhythms

• other drugs, such as Pronestyl, Cardioquin, Bretylol, or Norpace

• the drug atropine or a temporary pacemaker if the heart rate is abnormally slow

• nitroglycerin, calcium channel blockers, or other drugs that relieve pain, redistribute blood to blood-starved areas of the heart, help the heart to pump more blood, and reduce the heart’s workload

• heparin to prevent clotting

• morphine for pain relief and sedation

• drugs that improve heart contractions or raise blood pressure

• beta blockers, such as Inderal or Blocadren, after an acute heart attack to help prevent another heart attack

• aspirin to prevent clot formation (should be started within 24 hours after symptoms arise)

• bed rest with a bedside commode to rest the heart

• oxygen administration for 24 to 48 hours

• pulmonary artery catheterization to detect failure of the heart’s left or right ventricle and to monitor the person’s response to treatment. In this procedure, the doctor threads a thin, hollow tube through the heart and into the pulmonary artery to measure various pressures.

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What do Doctors call this Condition - Erythroblastosis fetalis

What is this Condition?

When the fetus’s blood is incompatible with the mother’s, the mother produces antibodies against the fetus’s red blood cells. Intrauterine transfusions with human Rh(D) immune human globulin can save 40% of fetuses with this disorder. However, in severe, untreated blood incompatibility, the prognosis is poor, especially if kernicterus (infiltration of parts of the brain and spinal cord with bilirubin) develops. About 70% of these infants die, usually within the first week of life; survivors inevitably develop severe nervous system damage.

What Causes it?

Blood incompatibility between mother and fetus usually results from Rh isoimmunization - a condition that develops in approximately 7% of all pregnancies in the United States. Until treatment with human Rh(D) immune human globulin became available, this condition was an important cause of kernicterus and neonatal death.

During her first pregnancy, a woman with Rh-negative blood factors becomes sensitized (during delivery or abortion) by exposure to Rh-positive fetal blood factors inherited from the father. In the next pregnancy that produces an Rh-positive fetus, increasing amounts of maternal anti-Rh-positive antibodies cross the placental barrier, attach to Rh-positive cells in the fetal blood, and destroy them.

To compensate for this, the fetus steps up the production of new red blood cells, which are attacked in their turn. Escalating red cell destruction releases large amounts of unconjugated bilirubin (a red cell component), which the fetal liver cannot properly process and excrete.

ABO incompatibility, another form of blood incompatibility between mother and fetus, is less severe.

What are its Symptoms?

An infant with this incompatibility disorder has liver problems. Jaundice (resulting from the fetal liver’s failure to process bilirubin from the destroyed red cells) doesn’t usually appear at birth but may occur 30 minutes to 24 hours later. A mildly affected infant is pale and has a mildly to moderately enlarged liver and spleen. Severely affected infants who survive birth usually have pallor, swelling, small reddish skin spots, an enlarged liver and spleen, grunting respirations, abnormal breath sounds, poor muscle tone, nervous system unresponsiveness, possible heart murmurs, a bile-stained umbilical cord, and yellow or meconium-stained amniotic fluid.

How is it Diagnosed?

Diagnostic evaluation considers both prenatal and neonatal findings.

Important factors to consider are:

• maternal history (for blood incompatibility-related stillbirths, abortions, previously affected children, or previous anti-Rh blood levels)

• blood typing and screening

• father’s blood test results

• history of blood transfusion.

Other diagnostic tests that provide important information include amniotic fluid analysis and X-ray studies.

How is it Treated?

Treatment depends on the degree of maternal sensitization and the effects of hemolytic disease on the fetus or newborn .

• Intrauterine-intraperitoneal blood transfusion is performed when amniotic fluid analysis suggests that the fetus is severely affected and that delivery is inappropriate because the fetus will be premature. A transabdominal puncture under fluoroscopy into the fetal peritoneal cavity allows infusion of group 0, Rh-negative blood. This may be repeated every 2 weeks until the fetus is mature enough for delivery.

• Planned delivery is usually done 2 to 4 weeks before term date, depending on maternal history, serologic tests, and amniocentesis results; labor may be induced from the 34th to 38th week of gestation. During labor, the fetus should be monitored electronically; capillary blood scalp sampling determines acid-base balance. Any indication of fetal distress calls for an immediate cesarean delivery .

• The newborn’s serum bilirubin levels are brought down by phenobarbital administered during the last 5 to 6 weeks of pregnancy; or by an albumin infusion, which helps bind bilirubin; or by phototherapy with ultraviolet light .

• Administration of human Rh(D) immune globulin can provide passive immunization, which prevents maternal Rh isoimmunization in Rh-negative women. However, it’s ineffective if sensitization has already resulted from a previous pregnancy, abortion, or transfusion.

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What do Doctors call this Condition - Congenital hypothyroidism, infantile cretinism

What is this Condition?

Hypothyroidism in children is a deficiency of thyroid hormone secretion during fetal development or early infancy. Untreated hypothyroidism is characterized in infants by respiratory difficulties, persistent jaundice, and hoarse crying; in older children, by stunted growth (dwarfism), bone and muscle dystrophy, and mental deficiency.

Early diagnosis and treatment offer the best prognosis; infants treated before age 3 months usually grow and develop normally. However, hypothyroid children who remain untreated beyond age 3 months and children with acquired hypothyroidism who remain un­treated beyond age 2 years suffer irreversible mental retardation; their skeletal abnormalities are reversible with treatment. Hypothyroidism occurs three times more often in girls than in boys.

What Causes it?

In infants, hypothyroidism usually results from defective embryonic development that causes congenital absence or underdevelopment of the thyroid gland. The next most common cause can be traced to an inherited enzymatic defect in the synthesis of the thyroid hormone thyroxine. Less frequently, antithyroid drugs taken during pregnancy produce hypothyroidism in infants. In children older than age 2, hypothyroidism usually results from chronic autoimmune thyroiditis.

What are its Symptoms?

At birth, the weight and length of an infant with hypothyroidism appear normal, but characteristic signs of hypothyroidism develop by age 3 to 6 months. Breast-fed infants don’t show most symptoms until they’re weaned because breast milk contains small amounts of thyroid hormone.

Symptoms in Infants

Typically, an infant with hypothyroidism sleeps excessively, cries rarely (except for occasional hoarse crying), and is generally inactive.

Because of this, the parents may describe the child as a “good baby-no trouble at all.” However, such behavior actually results from a decreased metabolism and progressive mental impairment.

The infant with hypothyroidism also has abnormal deep-tendon reflexes; hypotonic abdominal muscles; a protruding abdomen; slow, awkward movements; feeding difficulties; constipation; and jaundice.

A large, protruding tongue obstructs respiration, making breathing loud and noisy and forcing the child to breathe through an open mouth. The child may have shortness of breath on exertion, anemia, abnormal facial features, and a dull expression, resulting from mental retardation. The skin is cold and mottled because of poor circulation, and the hair is dry, brittle, and dull. Teeth erupt late and tend to decay early; body temperature is below normal; and pulse rate is slow.

Symptoms in Children

In the child who gets hypothyroidism after age 2 years, appropriate treatment will likely prevent mental retardation. However, growth retardation becomes apparent in short stature, obesity, and a head that appears abnormally large because the arms and legs are stunted. An older child may show delayed or accelerated sexual development.

How is it Diagnosed?

Lab tests help determine levels of thyroid hormones. A high serum level of thyroid-stimulating hormone, associated with low levels of thyroxine and triiodothyronine, points to hypothyroidism. Since early diagnosis and treatment can minimize the effects of hypothyroidism, many states require measurement of thyroid hormone levels at birth.

Electrocardiography shows slow heart rate and electrocardiographic changes in untreated infants. Thyroid scan and radioactive iodine uptake tests show decreased uptake levels and confirm the absence of thyroid tissue in hypothyroid children. Hip, knee, and thigh X-rays reveal delayed skeletal development that is markedly inappropriate for the child’s age.

How is it Treated?

Early detection is mandatory to prevent irreversible mental retardation and permit normal physical development.

Treatment in infants under age 1 year consists of replacement therapy with oral Levoxine, starting with moderate doses. Dosage gradually increases to levels sufficient for lifelong maintenance. (However, a rapid increase in dosage may precipitate thyrotoxicity.)

Doses are proportionately higher in children than in adults because children metabolize thyroid hormone more quickly. Older children also receive Levoxine.

What can the Parents of a Child with Hypothyroidism do?

• Be aware that your child will require lifelong treatment with thyroid supplements. Stay alert for signs of overdose: rapid pulse, irritability, insomnia, fever, sweating, and weight loss. To prevent further mental impairment, be sure to comply with your child’s treatment program .

• Focus on your child’s strengths, not weaknesses. Provide stimulating activities to help the child reach maximum potential.

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