PCAT Critical Reading Practice Test

The primary seat of tubercular infection is generally in the upper part of the lung. The invading organisms settle on the surface here and cause a multiplication of the cells and an inflammatory exudate in a small area. With the continuous growth of the bacilli in the localized region, adjoining areas of the lung become affected, and there is further extension into the immediate vicinity by means of the lymphatics. Small nodules form and then coalesce to create a larger area. The body primarily defends itself with the formation of dense masses of cicatricial tissue, which function to wall off the affected area. This results in unfavorable growth conditions for the bacilli. This mode of defense, combined with the production of substances antagonistic to the toxins produced by the bacilli, is so efficacious that in the great majority of cases no further extension of the process takes place. In certain cases, however, the growth of the bacilli in the focus area is unchecked, then the surrounding tissue is killed and converted into a soft semi-fluid material; further extension then takes place. All parts of the enormous surface of the lungs are connected by a system of air tubes or bronchi, and as a result, the bacilli have favorable opportunity for distribution. This opportunity is facilitated by sudden movements of the air currents in the lung produced by coughing. The body’s defense; however, can still keep pace with the attack, and even in an advanced stage, the infection can sometimes be permanently checked; in other cases the check is temporary, the process of softening continues, and large cavities are produced by the destruction of the tissue. On the inner surface of these cavities there may be a rapid growth of bacilli.

From the lungs, the bacilli are carried by the lymphatics to the lymph nodes at the root of the lungs, in which a similar process takes place; this, on the whole, is favorable, because further extension by this route is for a time blocked. The extension across surfaces continues and the abundant sputum, which is formed in the lungs and contains large numbers of bacilli, becomes the vehicle of transportation. The windpipe and larynx may become infected, as the back parts of each are more closely in contact with the sputum and are the parts most generally infected. A large part of the sputum is swallowed and infection of the intestine takes place with the lesions taking the form of large ulcers. From the intestinal ulcers there is further extension by means of the lymphatics to the large lymph nodes in the back of the abdominal cavity.

The primary seat of tubercular infection is generally in the upper part of the lung. The invading organisms settle on the surface here and cause a multiplication of the cells and an inflammatory exudate in a small area. With the continuous growth of the bacilli in the localized region, adjoining areas of the lung become affected, and there is further extension into the immediate vicinity by means of the lymphatics. Small nodules form and then coalesce to create a larger area. The body primarily defends itself with the formation of dense masses of cicatricial tissue, which function to wall off the affected area. This results in unfavorable growth conditions for the bacilli. This mode of defense, combined with the production of substances antagonistic to the toxins produced by the bacilli, is so efficacious that in the great majority of cases no further extension of the process takes place. In certain cases, however, the growth of the bacilli in the focus area is unchecked, then the surrounding tissue is killed and converted into a soft semi-fluid material; further extension then takes place. All parts of the enormous surface of the lungs are connected by a system of air tubes or bronchi, and as a result, the bacilli have favorable opportunity for distribution. This opportunity is facilitated by sudden movements of the air currents in the lung produced by coughing. The body’s defense; however, can still keep pace with the attack, and even in an advanced stage, the infection can sometimes be permanently checked; in other cases the check is temporary, the process of softening continues, and large cavities are produced by the destruction of the tissue. On the inner surface of these cavities there may be a rapid growth of bacilli.

From the lungs, the bacilli are carried by the lymphatics to the lymph nodes at the root of the lungs, in which a similar process takes place; this, on the whole, is favorable, because further extension by this route is for a time blocked. The extension across surfaces continues and the abundant sputum, which is formed in the lungs and contains large numbers of bacilli, becomes the vehicle of transportation. The windpipe and larynx may become infected, as the back parts of each are more closely in contact with the sputum and are the parts most generally infected. A large part of the sputum is swallowed and infection of the intestine takes place with the lesions taking the form of large ulcers. From the intestinal ulcers there is further extension by means of the lymphatics to the large lymph nodes in the back of the abdominal cavity.

The primary seat of tubercular infection is generally in the upper part of the lung. The invading organisms settle on the surface here and cause a multiplication of the cells and an inflammatory exudate in a small area. With the continuous growth of the bacilli in the localized region, adjoining areas of the lung become affected, and there is further extension into the immediate vicinity by means of the lymphatics. Small nodules form and then coalesce to create a larger area. The body primarily defends itself with the formation of dense masses of cicatricial tissue, which function to wall off the affected area. This results in unfavorable growth conditions for the bacilli. This mode of defense, combined with the production of substances antagonistic to the toxins produced by the bacilli, is so efficacious that in the great majority of cases no further extension of the process takes place. In certain cases, however, the growth of the bacilli in the focus area is unchecked, then the surrounding tissue is killed and converted into a soft semi-fluid material; further extension then takes place. All parts of the enormous surface of the lungs are connected by a system of air tubes or bronchi, and as a result, the bacilli have favorable opportunity for distribution. This opportunity is facilitated by sudden movements of the air currents in the lung produced by coughing. The body’s defense; however, can still keep pace with the attack, and even in an advanced stage, the infection can sometimes be permanently checked; in other cases the check is temporary, the process of softening continues, and large cavities are produced by the destruction of the tissue. On the inner surface of these cavities there may be a rapid growth of bacilli.

From the lungs, the bacilli are carried by the lymphatics to the lymph nodes at the root of the lungs, in which a similar process takes place; this, on the whole, is favorable, because further extension by this route is for a time blocked. The extension across surfaces continues and the abundant sputum, which is formed in the lungs and contains large numbers of bacilli, becomes the vehicle of transportation. The windpipe and larynx may become infected, as the back parts of each are more closely in contact with the sputum and are the parts most generally infected. A large part of the sputum is swallowed and infection of the intestine takes place with the lesions taking the form of large ulcers. From the intestinal ulcers there is further extension by means of the lymphatics to the large lymph nodes in the back of the abdominal cavity.

The primary seat of tubercular infection is generally in the upper part of the lung. The invading organisms settle on the surface here and cause a multiplication of the cells and an inflammatory exudate in a small area. With the continuous growth of the bacilli in the localized region, adjoining areas of the lung become affected, and there is further extension into the immediate vicinity by means of the lymphatics. Small nodules form and then coalesce to create a larger area. The body primarily defends itself with the formation of dense masses of cicatricial tissue, which function to wall off the affected area. This results in unfavorable growth conditions for the bacilli. This mode of defense, combined with the production of substances antagonistic to the toxins produced by the bacilli, is so efficacious that in the great majority of cases no further extension of the process takes place. In certain cases, however, the growth of the bacilli in the focus area is unchecked, then the surrounding tissue is killed and converted into a soft semi-fluid material; further extension then takes place. All parts of the enormous surface of the lungs are connected by a system of air tubes or bronchi, and as a result, the bacilli have favorable opportunity for distribution. This opportunity is facilitated by sudden movements of the air currents in the lung produced by coughing. The body’s defense; however, can still keep pace with the attack, and even in an advanced stage, the infection can sometimes be permanently checked; in other cases the check is temporary, the process of softening continues, and large cavities are produced by the destruction of the tissue. On the inner surface of these cavities there may be a rapid growth of bacilli.

From the lungs, the bacilli are carried by the lymphatics to the lymph nodes at the root of the lungs, in which a similar process takes place; this, on the whole, is favorable, because further extension by this route is for a time blocked. The extension across surfaces continues and the abundant sputum, which is formed in the lungs and contains large numbers of bacilli, becomes the vehicle of transportation. The windpipe and larynx may become infected, as the back parts of each are more closely in contact with the sputum and are the parts most generally infected. A large part of the sputum is swallowed and infection of the intestine takes place with the lesions taking the form of large ulcers. From the intestinal ulcers there is further extension by means of the lymphatics to the large lymph nodes in the back of the abdominal cavity.

The primary seat of tubercular infection is generally in the upper part of the lung. The invading organisms settle on the surface here and cause a multiplication of the cells and an inflammatory exudate in a small area. With the continuous growth of the bacilli in the localized region, adjoining areas of the lung become affected, and there is further extension into the immediate vicinity by means of the lymphatics. Small nodules form and then coalesce to create a larger area. The body primarily defends itself with the formation of dense masses of cicatricial tissue, which function to wall off the affected area. This results in unfavorable growth conditions for the bacilli. This mode of defense, combined with the production of substances antagonistic to the toxins produced by the bacilli, is so efficacious that in the great majority of cases no further extension of the process takes place. In certain cases, however, the growth of the bacilli in the focus area is unchecked, then the surrounding tissue is killed and converted into a soft semi-fluid material; further extension then takes place. All parts of the enormous surface of the lungs are connected by a system of air tubes or bronchi, and as a result, the bacilli have favorable opportunity for distribution. This opportunity is facilitated by sudden movements of the air currents in the lung produced by coughing. The body’s defense; however, can still keep pace with the attack, and even in an advanced stage, the infection can sometimes be permanently checked; in other cases the check is temporary, the process of softening continues, and large cavities are produced by the destruction of the tissue. On the inner surface of these cavities there may be a rapid growth of bacilli.

From the lungs, the bacilli are carried by the lymphatics to the lymph nodes at the root of the lungs, in which a similar process takes place; this, on the whole, is favorable, because further extension by this route is for a time blocked. The extension across surfaces continues and the abundant sputum, which is formed in the lungs and contains large numbers of bacilli, becomes the vehicle of transportation. The windpipe and larynx may become infected, as the back parts of each are more closely in contact with the sputum and are the parts most generally infected. A large part of the sputum is swallowed and infection of the intestine takes place with the lesions taking the form of large ulcers. From the intestinal ulcers there is further extension by means of the lymphatics to the large lymph nodes in the back of the abdominal cavity.

The primary seat of tubercular infection is generally in the upper part of the lung. The invading organisms settle on the surface here and cause a multiplication of the cells and an inflammatory exudate in a small area. With the continuous growth of the bacilli in the localized region, adjoining areas of the lung become affected, and there is further extension into the immediate vicinity by means of the lymphatics. Small nodules form and then coalesce to create a larger area. The body primarily defends itself with the formation of dense masses of cicatricial tissue, which function to wall off the affected area. This results in unfavorable growth conditions for the bacilli. This mode of defense, combined with the production of substances antagonistic to the toxins produced by the bacilli, is so efficacious that in the great majority of cases no further extension of the process takes place. In certain cases, however, the growth of the bacilli in the focus area is unchecked, then the surrounding tissue is killed and converted into a soft semi-fluid material; further extension then takes place. All parts of the enormous surface of the lungs are connected by a system of air tubes or bronchi, and as a result, the bacilli have favorable opportunity for distribution. This opportunity is facilitated by sudden movements of the air currents in the lung produced by coughing. The body’s defense; however, can still keep pace with the attack, and even in an advanced stage, the infection can sometimes be permanently checked; in other cases the check is temporary, the process of softening continues, and large cavities are produced by the destruction of the tissue. On the inner surface of these cavities there may be a rapid growth of bacilli.

From the lungs, the bacilli are carried by the lymphatics to the lymph nodes at the root of the lungs, in which a similar process takes place; this, on the whole, is favorable, because further extension by this route is for a time blocked. The extension across surfaces continues and the abundant sputum, which is formed in the lungs and contains large numbers of bacilli, becomes the vehicle of transportation. The windpipe and larynx may become infected, as the back parts of each are more closely in contact with the sputum and are the parts most generally infected. A large part of the sputum is swallowed and infection of the intestine takes place with the lesions taking the form of large ulcers. From the intestinal ulcers there is further extension by means of the lymphatics to the large lymph nodes in the back of the abdominal cavity.

The primary seat of tubercular infection is generally in the upper part of the lung. The invading organisms settle on the surface here and cause a multiplication of the cells and an inflammatory exudate in a small area. With the continuous growth of the bacilli in the localized region, adjoining areas of the lung become affected, and there is further extension into the immediate vicinity by means of the lymphatics. Small nodules form and then coalesce to create a larger area. The body primarily defends itself with the formation of dense masses of cicatricial tissue, which function to wall off the affected area. This results in unfavorable growth conditions for the bacilli. This mode of defense, combined with the production of substances antagonistic to the toxins produced by the bacilli, is so efficacious that in the great majority of cases no further extension of the process takes place. In certain cases, however, the growth of the bacilli in the focus area is unchecked, then the surrounding tissue is killed and converted into a soft semi-fluid material; further extension then takes place. All parts of the enormous surface of the lungs are connected by a system of air tubes or bronchi, and as a result, the bacilli have favorable opportunity for distribution. This opportunity is facilitated by sudden movements of the air currents in the lung produced by coughing. The body’s defense; however, can still keep pace with the attack, and even in an advanced stage, the infection can sometimes be permanently checked; in other cases the check is temporary, the process of softening continues, and large cavities are produced by the destruction of the tissue. On the inner surface of these cavities there may be a rapid growth of bacilli.

From the lungs, the bacilli are carried by the lymphatics to the lymph nodes at the root of the lungs, in which a similar process takes place; this, on the whole, is favorable, because further extension by this route is for a time blocked. The extension across surfaces continues and the abundant sputum, which is formed in the lungs and contains large numbers of bacilli, becomes the vehicle of transportation. The windpipe and larynx may become infected, as the back parts of each are more closely in contact with the sputum and are the parts most generally infected. A large part of the sputum is swallowed and infection of the intestine takes place with the lesions taking the form of large ulcers. From the intestinal ulcers there is further extension by means of the lymphatics to the large lymph nodes in the back of the abdominal cavity.

The primary seat of tubercular infection is generally in the upper part of the lung. The invading organisms settle on the surface here and cause a multiplication of the cells and an inflammatory exudate in a small area. With the continuous growth of the bacilli in the localized region, adjoining areas of the lung become affected, and there is further extension into the immediate vicinity by means of the lymphatics. Small nodules form and then coalesce to create a larger area. The body primarily defends itself with the formation of dense masses of cicatricial tissue, which function to wall off the affected area. This results in unfavorable growth conditions for the bacilli. This mode of defense, combined with the production of substances antagonistic to the toxins produced by the bacilli, is so efficacious that in the great majority of cases no further extension of the process takes place. In certain cases, however, the growth of the bacilli in the focus area is unchecked, then the surrounding tissue is killed and converted into a soft semi-fluid material; further extension then takes place. All parts of the enormous surface of the lungs are connected by a system of air tubes or bronchi, and as a result, the bacilli have favorable opportunity for distribution. This opportunity is facilitated by sudden movements of the air currents in the lung produced by coughing. The body’s defense; however, can still keep pace with the attack, and even in an advanced stage, the infection can sometimes be permanently checked; in other cases the check is temporary, the process of softening continues, and large cavities are produced by the destruction of the tissue. On the inner surface of these cavities there may be a rapid growth of bacilli.

From the lungs, the bacilli are carried by the lymphatics to the lymph nodes at the root of the lungs, in which a similar process takes place; this, on the whole, is favorable, because further extension by this route is for a time blocked. The extension across surfaces continues and the abundant sputum, which is formed in the lungs and contains large numbers of bacilli, becomes the vehicle of transportation. The windpipe and larynx may become infected, as the back parts of each are more closely in contact with the sputum and are the parts most generally infected. A large part of the sputum is swallowed and infection of the intestine takes place with the lesions taking the form of large ulcers. From the intestinal ulcers there is further extension by means of the lymphatics to the large lymph nodes in the back of the abdominal cavity.

Sickle cell disease (SCD) affects millions of individuals worldwide, and the Sickle Cell Disease Association of America estimates that 70,000 to 100,000 individuals have SCD and 3 million individuals have the sickle cell trait. While SCD is known to primarily affect individuals of African American descent, individuals from South America, the Caribbean, Central America, the Middle East, and the Mediterranean can also have SCD or the SCD trait. SCD is estimated to affect 1 in 500 African American infants, and 1 in 12 African Americans are estimated to have the sickle cell trait. SCD is characterized by episodes of acute and chronic pain. By increasing awareness about SCD and promoting patient education, health care professionals can help patients and their families cope with SCD and better manage the associated pain.

Recurring episodes of acute and/or severe pain are hallmarks of SCD. SCD pain can often be debilitating, and episodes of pain vary from patient to patient in both frequency and intensity. SCD pain can be classified as acute, chronic, or mixed. At some point, most SCD patients experience episodes of pain often referred to as vaso-occlusive crisis (sickle cell crisis), the duration of which may range from hours to days. Some patients seldom have a sickle cell crisis, while others may experience crises several times a year. Some episodes may be so severe that hospitalization is warranted to manage the pain.

An acute pain event is the most common type of pain, and the onset is typically abrupt. It is often the result of an ischemic tissue injury, which is due to the occlusion of microvascular beds by sickled erythrocytes during an acute crisis. Acute pain episodes can also be triggered by factors including extreme temperature changes, changes in altitude, physical and emotional stress, illnesses, infections, dehydration, cold climates, menstruation, and fatigue.

Chronic pain is pain that lasts for 3 to 6 months or longer. Chronic pain often results from the destruction of bones, joints, and visceral organs due to recurrent crises. Sources of chronic sickle cell pain include aseptic necrosis, leg ulcerations, and osteomyelitis. Unfortunately, acute and chronic pain associated with SCD are commonly undertreated or inappropriately managed due to patient fear of potential addiction and adverse effects. Many studies report that some health care professionals are also concerned about the potential for addiction. When appropriate, pharmacologic management of SCD pain may involve the use of 3 major pharmacologic classes: nonopioids, opioids, and adjuvants.

Sickle cell disease (SCD) affects millions of individuals worldwide, and the Sickle Cell Disease Association of America estimates that 70,000 to 100,000 individuals have SCD and 3 million individuals have the sickle cell trait. While SCD is known to primarily affect individuals of African American descent, individuals from South America, the Caribbean, Central America, the Middle East, and the Mediterranean can also have SCD or the SCD trait. SCD is estimated to affect 1 in 500 African American infants, and 1 in 12 African Americans are estimated to have the sickle cell trait. SCD is characterized by episodes of acute and chronic pain. By increasing awareness about SCD and promoting patient education, health care professionals can help patients and their families cope with SCD and better manage the associated pain.

Recurring episodes of acute and/or severe pain are hallmarks of SCD. SCD pain can often be debilitating, and episodes of pain vary from patient to patient in both frequency and intensity. SCD pain can be classified as acute, chronic, or mixed. At some point, most SCD patients experience episodes of pain often referred to as vaso-occlusive crisis (sickle cell crisis), the duration of which may range from hours to days. Some patients seldom have a sickle cell crisis, while others may experience crises several times a year. Some episodes may be so severe that hospitalization is warranted to manage the pain.

An acute pain event is the most common type of pain, and the onset is typically abrupt. It is often the result of an ischemic tissue injury, which is due to the occlusion of microvascular beds by sickled erythrocytes during an acute crisis. Acute pain episodes can also be triggered by factors including extreme temperature changes, changes in altitude, physical and emotional stress, illnesses, infections, dehydration, cold climates, menstruation, and fatigue.

Chronic pain is pain that lasts for 3 to 6 months or longer. Chronic pain often results from the destruction of bones, joints, and visceral organs due to recurrent crises. Sources of chronic sickle cell pain include aseptic necrosis, leg ulcerations, and osteomyelitis. Unfortunately, acute and chronic pain associated with SCD are commonly undertreated or inappropriately managed due to patient fear of potential addiction and adverse effects. Many studies report that some health care professionals are also concerned about the potential for addiction. When appropriate, pharmacologic management of SCD pain may involve the use of 3 major pharmacologic classes: nonopioids, opioids, and adjuvants.

Sickle cell disease (SCD) affects millions of individuals worldwide, and the Sickle Cell Disease Association of America estimates that 70,000 to 100,000 individuals have SCD and 3 million individuals have the sickle cell trait. While SCD is known to primarily affect individuals of African American descent, individuals from South America, the Caribbean, Central America, the Middle East, and the Mediterranean can also have SCD or the SCD trait. SCD is estimated to affect 1 in 500 African American infants, and 1 in 12 African Americans are estimated to have the sickle cell trait. SCD is characterized by episodes of acute and chronic pain. By increasing awareness about SCD and promoting patient education, health care professionals can help patients and their families cope with SCD and better manage the associated pain.

Recurring episodes of acute and/or severe pain are hallmarks of SCD. SCD pain can often be debilitating, and episodes of pain vary from patient to patient in both frequency and intensity. SCD pain can be classified as acute, chronic, or mixed. At some point, most SCD patients experience episodes of pain often referred to as vaso-occlusive crisis (sickle cell crisis), the duration of which may range from hours to days. Some patients seldom have a sickle cell crisis, while others may experience crises several times a year. Some episodes may be so severe that hospitalization is warranted to manage the pain.

An acute pain event is the most common type of pain, and the onset is typically abrupt. It is often the result of an ischemic tissue injury, which is due to the occlusion of microvascular beds by sickled erythrocytes during an acute crisis. Acute pain episodes can also be triggered by factors including extreme temperature changes, changes in altitude, physical and emotional stress, illnesses, infections, dehydration, cold climates, menstruation, and fatigue.

Chronic pain is pain that lasts for 3 to 6 months or longer. Chronic pain often results from the destruction of bones, joints, and visceral organs due to recurrent crises. Sources of chronic sickle cell pain include aseptic necrosis, leg ulcerations, and osteomyelitis. Unfortunately, acute and chronic pain associated with SCD are commonly undertreated or inappropriately managed due to patient fear of potential addiction and adverse effects. Many studies report that some health care professionals are also concerned about the potential for addiction. When appropriate, pharmacologic management of SCD pain may involve the use of 3 major pharmacologic classes: nonopioids, opioids, and adjuvants.

Sickle cell disease (SCD) affects millions of individuals worldwide, and the Sickle Cell Disease Association of America estimates that 70,000 to 100,000 individuals have SCD and 3 million individuals have the sickle cell trait. While SCD is known to primarily affect individuals of African American descent, individuals from South America, the Caribbean, Central America, the Middle East, and the Mediterranean can also have SCD or the SCD trait. SCD is estimated to affect 1 in 500 African American infants, and 1 in 12 African Americans are estimated to have the sickle cell trait. SCD is characterized by episodes of acute and chronic pain. By increasing awareness about SCD and promoting patient education, health care professionals can help patients and their families cope with SCD and better manage the associated pain.

Recurring episodes of acute and/or severe pain are hallmarks of SCD. SCD pain can often be debilitating, and episodes of pain vary from patient to patient in both frequency and intensity. SCD pain can be classified as acute, chronic, or mixed. At some point, most SCD patients experience episodes of pain often referred to as vaso-occlusive crisis (sickle cell crisis), the duration of which may range from hours to days. Some patients seldom have a sickle cell crisis, while others may experience crises several times a year. Some episodes may be so severe that hospitalization is warranted to manage the pain.

An acute pain event is the most common type of pain, and the onset is typically abrupt. It is often the result of an ischemic tissue injury, which is due to the occlusion of microvascular beds by sickled erythrocytes during an acute crisis. Acute pain episodes can also be triggered by factors including extreme temperature changes, changes in altitude, physical and emotional stress, illnesses, infections, dehydration, cold climates, menstruation, and fatigue.

Chronic pain is pain that lasts for 3 to 6 months or longer. Chronic pain often results from the destruction of bones, joints, and visceral organs due to recurrent crises. Sources of chronic sickle cell pain include aseptic necrosis, leg ulcerations, and osteomyelitis. Unfortunately, acute and chronic pain associated with SCD are commonly undertreated or inappropriately managed due to patient fear of potential addiction and adverse effects. Many studies report that some health care professionals are also concerned about the potential for addiction. When appropriate, pharmacologic management of SCD pain may involve the use of 3 major pharmacologic classes: nonopioids, opioids, and adjuvants.

Sickle cell disease (SCD) affects millions of individuals worldwide, and the Sickle Cell Disease Association of America estimates that 70,000 to 100,000 individuals have SCD and 3 million individuals have the sickle cell trait. While SCD is known to primarily affect individuals of African American descent, individuals from South America, the Caribbean, Central America, the Middle East, and the Mediterranean can also have SCD or the SCD trait. SCD is estimated to affect 1 in 500 African American infants, and 1 in 12 African Americans are estimated to have the sickle cell trait. SCD is characterized by episodes of acute and chronic pain. By increasing awareness about SCD and promoting patient education, health care professionals can help patients and their families cope with SCD and better manage the associated pain.

Recurring episodes of acute and/or severe pain are hallmarks of SCD. SCD pain can often be debilitating, and episodes of pain vary from patient to patient in both frequency and intensity. SCD pain can be classified as acute, chronic, or mixed. At some point, most SCD patients experience episodes of pain often referred to as vaso-occlusive crisis (sickle cell crisis), the duration of which may range from hours to days. Some patients seldom have a sickle cell crisis, while others may experience crises several times a year. Some episodes may be so severe that hospitalization is warranted to manage the pain.

An acute pain event is the most common type of pain, and the onset is typically abrupt. It is often the result of an ischemic tissue injury, which is due to the occlusion of microvascular beds by sickled erythrocytes during an acute crisis. Acute pain episodes can also be triggered by factors including extreme temperature changes, changes in altitude, physical and emotional stress, illnesses, infections, dehydration, cold climates, menstruation, and fatigue.

Chronic pain is pain that lasts for 3 to 6 months or longer. Chronic pain often results from the destruction of bones, joints, and visceral organs due to recurrent crises. Sources of chronic sickle cell pain include aseptic necrosis, leg ulcerations, and osteomyelitis. Unfortunately, acute and chronic pain associated with SCD are commonly undertreated or inappropriately managed due to patient fear of potential addiction and adverse effects. Many studies report that some health care professionals are also concerned about the potential for addiction. When appropriate, pharmacologic management of SCD pain may involve the use of 3 major pharmacologic classes: nonopioids, opioids, and adjuvants.

Sickle cell disease (SCD) affects millions of individuals worldwide, and the Sickle Cell Disease Association of America estimates that 70,000 to 100,000 individuals have SCD and 3 million individuals have the sickle cell trait. While SCD is known to primarily affect individuals of African American descent, individuals from South America, the Caribbean, Central America, the Middle East, and the Mediterranean can also have SCD or the SCD trait. SCD is estimated to affect 1 in 500 African American infants, and 1 in 12 African Americans are estimated to have the sickle cell trait. SCD is characterized by episodes of acute and chronic pain. By increasing awareness about SCD and promoting patient education, health care professionals can help patients and their families cope with SCD and better manage the associated pain.

Recurring episodes of acute and/or severe pain are hallmarks of SCD. SCD pain can often be debilitating, and episodes of pain vary from patient to patient in both frequency and intensity. SCD pain can be classified as acute, chronic, or mixed. At some point, most SCD patients experience episodes of pain often referred to as vaso-occlusive crisis (sickle cell crisis), the duration of which may range from hours to days. Some patients seldom have a sickle cell crisis, while others may experience crises several times a year. Some episodes may be so severe that hospitalization is warranted to manage the pain.

An acute pain event is the most common type of pain, and the onset is typically abrupt. It is often the result of an ischemic tissue injury, which is due to the occlusion of microvascular beds by sickled erythrocytes during an acute crisis. Acute pain episodes can also be triggered by factors including extreme temperature changes, changes in altitude, physical and emotional stress, illnesses, infections, dehydration, cold climates, menstruation, and fatigue.

Chronic pain is pain that lasts for 3 to 6 months or longer. Chronic pain often results from the destruction of bones, joints, and visceral organs due to recurrent crises. Sources of chronic sickle cell pain include aseptic necrosis, leg ulcerations, and osteomyelitis. Unfortunately, acute and chronic pain associated with SCD are commonly undertreated or inappropriately managed due to patient fear of potential addiction and adverse effects. Many studies report that some health care professionals are also concerned about the potential for addiction. When appropriate, pharmacologic management of SCD pain may involve the use of 3 major pharmacologic classes: nonopioids, opioids, and adjuvants.

Sickle cell disease (SCD) affects millions of individuals worldwide, and the Sickle Cell Disease Association of America estimates that 70,000 to 100,000 individuals have SCD and 3 million individuals have the sickle cell trait. While SCD is known to primarily affect individuals of African American descent, individuals from South America, the Caribbean, Central America, the Middle East, and the Mediterranean can also have SCD or the SCD trait. SCD is estimated to affect 1 in 500 African American infants, and 1 in 12 African Americans are estimated to have the sickle cell trait. SCD is characterized by episodes of acute and chronic pain. By increasing awareness about SCD and promoting patient education, health care professionals can help patients and their families cope with SCD and better manage the associated pain.

Recurring episodes of acute and/or severe pain are hallmarks of SCD. SCD pain can often be debilitating, and episodes of pain vary from patient to patient in both frequency and intensity. SCD pain can be classified as acute, chronic, or mixed. At some point, most SCD patients experience episodes of pain often referred to as vaso-occlusive crisis (sickle cell crisis), the duration of which may range from hours to days. Some patients seldom have a sickle cell crisis, while others may experience crises several times a year. Some episodes may be so severe that hospitalization is warranted to manage the pain.

An acute pain event is the most common type of pain, and the onset is typically abrupt. It is often the result of an ischemic tissue injury, which is due to the occlusion of microvascular beds by sickled erythrocytes during an acute crisis. Acute pain episodes can also be triggered by factors including extreme temperature changes, changes in altitude, physical and emotional stress, illnesses, infections, dehydration, cold climates, menstruation, and fatigue.

Chronic pain is pain that lasts for 3 to 6 months or longer. Chronic pain often results from the destruction of bones, joints, and visceral organs due to recurrent crises. Sources of chronic sickle cell pain include aseptic necrosis, leg ulcerations, and osteomyelitis. Unfortunately, acute and chronic pain associated with SCD are commonly undertreated or inappropriately managed due to patient fear of potential addiction and adverse effects. Many studies report that some health care professionals are also concerned about the potential for addiction. When appropriate, pharmacologic management of SCD pain may involve the use of 3 major pharmacologic classes: nonopioids, opioids, and adjuvants.

Sickle cell disease (SCD) affects millions of individuals worldwide, and the Sickle Cell Disease Association of America estimates that 70,000 to 100,000 individuals have SCD and 3 million individuals have the sickle cell trait. While SCD is known to primarily affect individuals of African American descent, individuals from South America, the Caribbean, Central America, the Middle East, and the Mediterranean can also have SCD or the SCD trait. SCD is estimated to affect 1 in 500 African American infants, and 1 in 12 African Americans are estimated to have the sickle cell trait. SCD is characterized by episodes of acute and chronic pain. By increasing awareness about SCD and promoting patient education, health care professionals can help patients and their families cope with SCD and better manage the associated pain.

Recurring episodes of acute and/or severe pain are hallmarks of SCD. SCD pain can often be debilitating, and episodes of pain vary from patient to patient in both frequency and intensity. SCD pain can be classified as acute, chronic, or mixed. At some point, most SCD patients experience episodes of pain often referred to as vaso-occlusive crisis (sickle cell crisis), the duration of which may range from hours to days. Some patients seldom have a sickle cell crisis, while others may experience crises several times a year. Some episodes may be so severe that hospitalization is warranted to manage the pain.

An acute pain event is the most common type of pain, and the onset is typically abrupt. It is often the result of an ischemic tissue injury, which is due to the occlusion of microvascular beds by sickled erythrocytes during an acute crisis. Acute pain episodes can also be triggered by factors including extreme temperature changes, changes in altitude, physical and emotional stress, illnesses, infections, dehydration, cold climates, menstruation, and fatigue.

Chronic pain is pain that lasts for 3 to 6 months or longer. Chronic pain often results from the destruction of bones, joints, and visceral organs due to recurrent crises. Sources of chronic sickle cell pain include aseptic necrosis, leg ulcerations, and osteomyelitis. Unfortunately, acute and chronic pain associated with SCD are commonly undertreated or inappropriately managed due to patient fear of potential addiction and adverse effects. Many studies report that some health care professionals are also concerned about the potential for addiction. When appropriate, pharmacologic management of SCD pain may involve the use of 3 major pharmacologic classes: nonopioids, opioids, and adjuvants.

For most Americans, the words “Alzheimer’s disease” (AD)—often mispronounced purposefully or accidentally as “old timers’ disease”—signify devastating memory loss and stigma. The information about AD—often learned solely through the media—may lead individuals to believe that AD is inevitable (it isn’t), and possibly think that all AD patients receive poor care (there are many remarkably good AD units). Many individuals may envision a future burdened with more dementia patients and fewer societal resources to help support them (a real possibility). In general, pharmacists are well aware of what AD is and isn’t. AD is complex and relentlessly progressive; it affects patients, loved ones, and caregivers adversely. Pharmacists can provide pertinent information about AD’s myths, realities, and available symptomatic treatments.

AD’s harbinger is language difficulties, which include aphasia (language disturbance), apraxia (inability to carry out motor functions), and agnosia (failure to recognize or identify objects). Consequently, those with AD will often create new words for items. They may call a pencil a “list writer,” or a key a “door turner.” Clinicians stage AD as mild, moderate, or severe depending on the patient’s cognitive and memory impairment, communication problems, personality changes, behavior, and loss of control of bodily functions. People often dismiss mild AD as normal cognitive decline or senility—in other words, “normal” aging. For this reason, most people don’t seek treatment and are diagnosed in the late-mild to early-moderate stage.

In the severe stage, difficulty swallowing elevates the risk of aspiration pneumonia, which often marks the beginning of the downward spiral that ultimately ends with death; AD has no cure. A handful of pharmacologic treatments—acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists—alter the decline trajectory. These treatments slow disease progression, enhance cognitive function, delay cognitive decline, and decrease disruptive behaviors. Not all patients respond to these medications, but experts generally believe that those who do will show mild to moderate improvements for 6 months to a year. Although the drugs’ effects are short-lived, they improve patients’ quality of life and briefly enable independence.

Determining when medications stop providing a therapeutic benefit and should be discontinued is challenging. Clinicians use various methods to monitor decline, including mental status tools, patient self-report, and loved ones’ observations. Most clinicians continue drug treatment if the patient seems to tolerate the medication well, can afford it, and if there seems to be a benefit. With disease progression, specific behavioral symptoms including depression, agitation, hallucinations, and sleep disturbances become concerns. Antianxiety drugs, antipsychotics, and antidepressants are sometimes used to alleviate symptoms, but effective behavioral strategies are much preferred.

For most Americans, the words “Alzheimer’s disease” (AD)—often mispronounced purposefully or accidentally as “old timers’ disease”—signify devastating memory loss and stigma. The information about AD—often learned solely through the media—may lead individuals to believe that AD is inevitable (it isn’t), and possibly think that all AD patients receive poor care (there are many remarkably good AD units). Many individuals may envision a future burdened with more dementia patients and fewer societal resources to help support them (a real possibility). In general, pharmacists are well aware of what AD is and isn’t. AD is complex and relentlessly progressive; it affects patients, loved ones, and caregivers adversely. Pharmacists can provide pertinent information about AD’s myths, realities, and available symptomatic treatments.

AD’s harbinger is language difficulties, which include aphasia (language disturbance), apraxia (inability to carry out motor functions), and agnosia (failure to recognize or identify objects). Consequently, those with AD will often create new words for items. They may call a pencil a “list writer,” or a key a “door turner.” Clinicians stage AD as mild, moderate, or severe depending on the patient’s cognitive and memory impairment, communication problems, personality changes, behavior, and loss of control of bodily functions. People often dismiss mild AD as normal cognitive decline or senility—in other words, “normal” aging. For this reason, most people don’t seek treatment and are diagnosed in the late-mild to early-moderate stage.

In the severe stage, difficulty swallowing elevates the risk of aspiration pneumonia, which often marks the beginning of the downward spiral that ultimately ends with death; AD has no cure. A handful of pharmacologic treatments—acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists—alter the decline trajectory. These treatments slow disease progression, enhance cognitive function, delay cognitive decline, and decrease disruptive behaviors. Not all patients respond to these medications, but experts generally believe that those who do will show mild to moderate improvements for 6 months to a year. Although the drugs’ effects are short-lived, they improve patients’ quality of life and briefly enable independence.

Determining when medications stop providing a therapeutic benefit and should be discontinued is challenging. Clinicians use various methods to monitor decline, including mental status tools, patient self-report, and loved ones’ observations. Most clinicians continue drug treatment if the patient seems to tolerate the medication well, can afford it, and if there seems to be a benefit. With disease progression, specific behavioral symptoms including depression, agitation, hallucinations, and sleep disturbances become concerns. Antianxiety drugs, antipsychotics, and antidepressants are sometimes used to alleviate symptoms, but effective behavioral strategies are much preferred.

For most Americans, the words “Alzheimer’s disease” (AD)—often mispronounced purposefully or accidentally as “old timers’ disease”—signify devastating memory loss and stigma. The information about AD—often learned solely through the media—may lead individuals to believe that AD is inevitable (it isn’t), and possibly think that all AD patients receive poor care (there are many remarkably good AD units). Many individuals may envision a future burdened with more dementia patients and fewer societal resources to help support them (a real possibility). In general, pharmacists are well aware of what AD is and isn’t. AD is complex and relentlessly progressive; it affects patients, loved ones, and caregivers adversely. Pharmacists can provide pertinent information about AD’s myths, realities, and available symptomatic treatments.

AD’s harbinger is language difficulties, which include aphasia (language disturbance), apraxia (inability to carry out motor functions), and agnosia (failure to recognize or identify objects). Consequently, those with AD will often create new words for items. They may call a pencil a “list writer,” or a key a “door turner.” Clinicians stage AD as mild, moderate, or severe depending on the patient’s cognitive and memory impairment, communication problems, personality changes, behavior, and loss of control of bodily functions. People often dismiss mild AD as normal cognitive decline or senility—in other words, “normal” aging. For this reason, most people don’t seek treatment and are diagnosed in the late-mild to early-moderate stage.

In the severe stage, difficulty swallowing elevates the risk of aspiration pneumonia, which often marks the beginning of the downward spiral that ultimately ends with death; AD has no cure. A handful of pharmacologic treatments—acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists—alter the decline trajectory. These treatments slow disease progression, enhance cognitive function, delay cognitive decline, and decrease disruptive behaviors. Not all patients respond to these medications, but experts generally believe that those who do will show mild to moderate improvements for 6 months to a year. Although the drugs’ effects are short-lived, they improve patients’ quality of life and briefly enable independence.

Determining when medications stop providing a therapeutic benefit and should be discontinued is challenging. Clinicians use various methods to monitor decline, including mental status tools, patient self-report, and loved ones’ observations. Most clinicians continue drug treatment if the patient seems to tolerate the medication well, can afford it, and if there seems to be a benefit. With disease progression, specific behavioral symptoms including depression, agitation, hallucinations, and sleep disturbances become concerns. Antianxiety drugs, antipsychotics, and antidepressants are sometimes used to alleviate symptoms, but effective behavioral strategies are much preferred.

For most Americans, the words “Alzheimer’s disease” (AD)—often mispronounced purposefully or accidentally as “old timers’ disease”—signify devastating memory loss and stigma. The information about AD—often learned solely through the media—may lead individuals to believe that AD is inevitable (it isn’t), and possibly think that all AD patients receive poor care (there are many remarkably good AD units). Many individuals may envision a future burdened with more dementia patients and fewer societal resources to help support them (a real possibility). In general, pharmacists are well aware of what AD is and isn’t. AD is complex and relentlessly progressive; it affects patients, loved ones, and caregivers adversely. Pharmacists can provide pertinent information about AD’s myths, realities, and available symptomatic treatments.

AD’s harbinger is language difficulties, which include aphasia (language disturbance), apraxia (inability to carry out motor functions), and agnosia (failure to recognize or identify objects). Consequently, those with AD will often create new words for items. They may call a pencil a “list writer,” or a key a “door turner.” Clinicians stage AD as mild, moderate, or severe depending on the patient’s cognitive and memory impairment, communication problems, personality changes, behavior, and loss of control of bodily functions. People often dismiss mild AD as normal cognitive decline or senility—in other words, “normal” aging. For this reason, most people don’t seek treatment and are diagnosed in the late-mild to early-moderate stage.

In the severe stage, difficulty swallowing elevates the risk of aspiration pneumonia, which often marks the beginning of the downward spiral that ultimately ends with death; AD has no cure. A handful of pharmacologic treatments—acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists—alter the decline trajectory. These treatments slow disease progression, enhance cognitive function, delay cognitive decline, and decrease disruptive behaviors. Not all patients respond to these medications, but experts generally believe that those who do will show mild to moderate improvements for 6 months to a year. Although the drugs’ effects are short-lived, they improve patients’ quality of life and briefly enable independence.

Determining when medications stop providing a therapeutic benefit and should be discontinued is challenging. Clinicians use various methods to monitor decline, including mental status tools, patient self-report, and loved ones’ observations. Most clinicians continue drug treatment if the patient seems to tolerate the medication well, can afford it, and if there seems to be a benefit. With disease progression, specific behavioral symptoms including depression, agitation, hallucinations, and sleep disturbances become concerns. Antianxiety drugs, antipsychotics, and antidepressants are sometimes used to alleviate symptoms, but effective behavioral strategies are much preferred.

For most Americans, the words “Alzheimer’s disease” (AD)—often mispronounced purposefully or accidentally as “old timers’ disease”—signify devastating memory loss and stigma. The information about AD—often learned solely through the media—may lead individuals to believe that AD is inevitable (it isn’t), and possibly think that all AD patients receive poor care (there are many remarkably good AD units). Many individuals may envision a future burdened with more dementia patients and fewer societal resources to help support them (a real possibility). In general, pharmacists are well aware of what AD is and isn’t. AD is complex and relentlessly progressive; it affects patients, loved ones, and caregivers adversely. Pharmacists can provide pertinent information about AD’s myths, realities, and available symptomatic treatments.

AD’s harbinger is language difficulties, which include aphasia (language disturbance), apraxia (inability to carry out motor functions), and agnosia (failure to recognize or identify objects). Consequently, those with AD will often create new words for items. They may call a pencil a “list writer,” or a key a “door turner.” Clinicians stage AD as mild, moderate, or severe depending on the patient’s cognitive and memory impairment, communication problems, personality changes, behavior, and loss of control of bodily functions. People often dismiss mild AD as normal cognitive decline or senility—in other words, “normal” aging. For this reason, most people don’t seek treatment and are diagnosed in the late-mild to early-moderate stage.

In the severe stage, difficulty swallowing elevates the risk of aspiration pneumonia, which often marks the beginning of the downward spiral that ultimately ends with death; AD has no cure. A handful of pharmacologic treatments—acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists—alter the decline trajectory. These treatments slow disease progression, enhance cognitive function, delay cognitive decline, and decrease disruptive behaviors. Not all patients respond to these medications, but experts generally believe that those who do will show mild to moderate improvements for 6 months to a year. Although the drugs’ effects are short-lived, they improve patients’ quality of life and briefly enable independence.

Determining when medications stop providing a therapeutic benefit and should be discontinued is challenging. Clinicians use various methods to monitor decline, including mental status tools, patient self-report, and loved ones’ observations. Most clinicians continue drug treatment if the patient seems to tolerate the medication well, can afford it, and if there seems to be a benefit. With disease progression, specific behavioral symptoms including depression, agitation, hallucinations, and sleep disturbances become concerns. Antianxiety drugs, antipsychotics, and antidepressants are sometimes used to alleviate symptoms, but effective behavioral strategies are much preferred.

For most Americans, the words “Alzheimer’s disease” (AD)—often mispronounced purposefully or accidentally as “old timers’ disease”—signify devastating memory loss and stigma. The information about AD—often learned solely through the media—may lead individuals to believe that AD is inevitable (it isn’t), and possibly think that all AD patients receive poor care (there are many remarkably good AD units). Many individuals may envision a future burdened with more dementia patients and fewer societal resources to help support them (a real possibility). In general, pharmacists are well aware of what AD is and isn’t. AD is complex and relentlessly progressive; it affects patients, loved ones, and caregivers adversely. Pharmacists can provide pertinent information about AD’s myths, realities, and available symptomatic treatments.

AD’s harbinger is language difficulties, which include aphasia (language disturbance), apraxia (inability to carry out motor functions), and agnosia (failure to recognize or identify objects). Consequently, those with AD will often create new words for items. They may call a pencil a “list writer,” or a key a “door turner.” Clinicians stage AD as mild, moderate, or severe depending on the patient’s cognitive and memory impairment, communication problems, personality changes, behavior, and loss of control of bodily functions. People often dismiss mild AD as normal cognitive decline or senility—in other words, “normal” aging. For this reason, most people don’t seek treatment and are diagnosed in the late-mild to early-moderate stage.

In the severe stage, difficulty swallowing elevates the risk of aspiration pneumonia, which often marks the beginning of the downward spiral that ultimately ends with death; AD has no cure. A handful of pharmacologic treatments—acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists—alter the decline trajectory. These treatments slow disease progression, enhance cognitive function, delay cognitive decline, and decrease disruptive behaviors. Not all patients respond to these medications, but experts generally believe that those who do will show mild to moderate improvements for 6 months to a year. Although the drugs’ effects are short-lived, they improve patients’ quality of life and briefly enable independence.

Determining when medications stop providing a therapeutic benefit and should be discontinued is challenging. Clinicians use various methods to monitor decline, including mental status tools, patient self-report, and loved ones’ observations. Most clinicians continue drug treatment if the patient seems to tolerate the medication well, can afford it, and if there seems to be a benefit. With disease progression, specific behavioral symptoms including depression, agitation, hallucinations, and sleep disturbances become concerns. Antianxiety drugs, antipsychotics, and antidepressants are sometimes used to alleviate symptoms, but effective behavioral strategies are much preferred.

For most Americans, the words “Alzheimer’s disease” (AD)—often mispronounced purposefully or accidentally as “old timers’ disease”—signify devastating memory loss and stigma. The information about AD—often learned solely through the media—may lead individuals to believe that AD is inevitable (it isn’t), and possibly think that all AD patients receive poor care (there are many remarkably good AD units). Many individuals may envision a future burdened with more dementia patients and fewer societal resources to help support them (a real possibility). In general, pharmacists are well aware of what AD is and isn’t. AD is complex and relentlessly progressive; it affects patients, loved ones, and caregivers adversely. Pharmacists can provide pertinent information about AD’s myths, realities, and available symptomatic treatments.

AD’s harbinger is language difficulties, which include aphasia (language disturbance), apraxia (inability to carry out motor functions), and agnosia (failure to recognize or identify objects). Consequently, those with AD will often create new words for items. They may call a pencil a “list writer,” or a key a “door turner.” Clinicians stage AD as mild, moderate, or severe depending on the patient’s cognitive and memory impairment, communication problems, personality changes, behavior, and loss of control of bodily functions. People often dismiss mild AD as normal cognitive decline or senility—in other words, “normal” aging. For this reason, most people don’t seek treatment and are diagnosed in the late-mild to early-moderate stage.

In the severe stage, difficulty swallowing elevates the risk of aspiration pneumonia, which often marks the beginning of the downward spiral that ultimately ends with death; AD has no cure. A handful of pharmacologic treatments—acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists—alter the decline trajectory. These treatments slow disease progression, enhance cognitive function, delay cognitive decline, and decrease disruptive behaviors. Not all patients respond to these medications, but experts generally believe that those who do will show mild to moderate improvements for 6 months to a year. Although the drugs’ effects are short-lived, they improve patients’ quality of life and briefly enable independence.

Determining when medications stop providing a therapeutic benefit and should be discontinued is challenging. Clinicians use various methods to monitor decline, including mental status tools, patient self-report, and loved ones’ observations. Most clinicians continue drug treatment if the patient seems to tolerate the medication well, can afford it, and if there seems to be a benefit. With disease progression, specific behavioral symptoms including depression, agitation, hallucinations, and sleep disturbances become concerns. Antianxiety drugs, antipsychotics, and antidepressants are sometimes used to alleviate symptoms, but effective behavioral strategies are much preferred.

For most Americans, the words “Alzheimer’s disease” (AD)—often mispronounced purposefully or accidentally as “old timers’ disease”—signify devastating memory loss and stigma. The information about AD—often learned solely through the media—may lead individuals to believe that AD is inevitable (it isn’t), and possibly think that all AD patients receive poor care (there are many remarkably good AD units). Many individuals may envision a future burdened with more dementia patients and fewer societal resources to help support them (a real possibility). In general, pharmacists are well aware of what AD is and isn’t. AD is complex and relentlessly progressive; it affects patients, loved ones, and caregivers adversely. Pharmacists can provide pertinent information about AD’s myths, realities, and available symptomatic treatments.

AD’s harbinger is language difficulties, which include aphasia (language disturbance), apraxia (inability to carry out motor functions), and agnosia (failure to recognize or identify objects). Consequently, those with AD will often create new words for items. They may call a pencil a “list writer,” or a key a “door turner.” Clinicians stage AD as mild, moderate, or severe depending on the patient’s cognitive and memory impairment, communication problems, personality changes, behavior, and loss of control of bodily functions. People often dismiss mild AD as normal cognitive decline or senility—in other words, “normal” aging. For this reason, most people don’t seek treatment and are diagnosed in the late-mild to early-moderate stage.

In the severe stage, difficulty swallowing elevates the risk of aspiration pneumonia, which often marks the beginning of the downward spiral that ultimately ends with death; AD has no cure. A handful of pharmacologic treatments—acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists—alter the decline trajectory. These treatments slow disease progression, enhance cognitive function, delay cognitive decline, and decrease disruptive behaviors. Not all patients respond to these medications, but experts generally believe that those who do will show mild to moderate improvements for 6 months to a year. Although the drugs’ effects are short-lived, they improve patients’ quality of life and briefly enable independence.

Determining when medications stop providing a therapeutic benefit and should be discontinued is challenging. Clinicians use various methods to monitor decline, including mental status tools, patient self-report, and loved ones’ observations. Most clinicians continue drug treatment if the patient seems to tolerate the medication well, can afford it, and if there seems to be a benefit. With disease progression, specific behavioral symptoms including depression, agitation, hallucinations, and sleep disturbances become concerns. Antianxiety drugs, antipsychotics, and antidepressants are sometimes used to alleviate symptoms, but effective behavioral strategies are much preferred.

Coughs that linger after a cold or sinus problem cause constant disruption in the home, school, and workplace. Often, these dry, nonproductive coughs become increasingly troublesome although other symptoms—fever, congestion, and fatigue—resolved days or weeks ago. This stubborn cough persists for weeks, and plagues its victim and the victim’s family night and day. The diagnosis might be a common, but overlooked cause of lingering cough: atypical pneumonia caused by mycoplasma.

Mycoplasma—pleomorphic bacteria that lack a cell wall—are the smallest and simplest self-replicating organisms known to humans. They probably evolved from gram-positive, walled eubacteria by degenerative evolution. Smaller than amoebas, these 0.1-micrometer organisms grow and reproduce slowly and require no oxygen or host cell. They also change shapes asymmetrically, appearing as long, thin filaments, tiny spheres, or branches. Scientists have identified more than 100 mycoplasma species. Fifteen species are known to live in humans, most as normal symbiotic flora. Mycoplasma pneumoniae, previously called “walking pneumonia,” is pathogenic in humans.

Mycoplasma pneumoniae glides freely and uses its specialized filamentous tips to burrow between cilia within the respiratory epithelium, causing the respiratory epithelial cells to slough. It also produces hydrogen peroxide, which causes initial cell disruption in the respiratory tract and damages erythrocyte membranes. Researchers have determined that more than 40% of infants younger than 1 year old have had a mycoplasma infection. By age 5, approximately 65% of children have been infected. Nearly all adults have been infected at least once, often repeatedly. Mycoplasma pneumonia usually affects people younger than 40 years of age. The highest incidence is found in the 5- to 9-year age group.

The risk of contracting mycoplasma pneumonia is greatest for people who live or work in crowded areas, such as daycare facilities, schools, homeless shelters, long-term care units, and military and prison environments. However, many people who develop mycoplasma infections have no identifiable risk factor. Most mycoplasma infections cause mild to moderate clinical symptoms, but the infection incubates over 3 weeks and can last weeks without treatment. This infection cannot be diagnosed based on symptoms alone; laboratory testing is essential. Infection can also cause ear infections, sinus infections, bronchitis, croup, severe sore throats, infectious asthma, and 1 type of the common cold. When mycoplasma infects children, about 25% of them develop nausea, vomiting, or diarrhea.

Coughs that linger after a cold or sinus problem cause constant disruption in the home, school, and workplace. Often, these dry, nonproductive coughs become increasingly troublesome although other symptoms—fever, congestion, and fatigue—resolved days or weeks ago. This stubborn cough persists for weeks, and plagues its victim and the victim’s family night and day. The diagnosis might be a common, but overlooked cause of lingering cough: atypical pneumonia caused by mycoplasma.

Mycoplasma—pleomorphic bacteria that lack a cell wall—are the smallest and simplest self-replicating organisms known to humans. They probably evolved from gram-positive, walled eubacteria by degenerative evolution. Smaller than amoebas, these 0.1-micrometer organisms grow and reproduce slowly and require no oxygen or host cell. They also change shapes asymmetrically, appearing as long, thin filaments, tiny spheres, or branches. Scientists have identified more than 100 mycoplasma species. Fifteen species are known to live in humans, most as normal symbiotic flora. Mycoplasma pneumoniae, previously called “walking pneumonia,” is pathogenic in humans.

Mycoplasma pneumoniae glides freely and uses its specialized filamentous tips to burrow between cilia within the respiratory epithelium, causing the respiratory epithelial cells to slough. It also produces hydrogen peroxide, which causes initial cell disruption in the respiratory tract and damages erythrocyte membranes. Researchers have determined that more than 40% of infants younger than 1 year old have had a mycoplasma infection. By age 5, approximately 65% of children have been infected. Nearly all adults have been infected at least once, often repeatedly. Mycoplasma pneumonia usually affects people younger than 40 years of age. The highest incidence is found in the 5- to 9-year age group.

The risk of contracting mycoplasma pneumonia is greatest for people who live or work in crowded areas, such as daycare facilities, schools, homeless shelters, long-term care units, and military and prison environments. However, many people who develop mycoplasma infections have no identifiable risk factor. Most mycoplasma infections cause mild to moderate clinical symptoms, but the infection incubates over 3 weeks and can last weeks without treatment. This infection cannot be diagnosed based on symptoms alone; laboratory testing is essential. Infection can also cause ear infections, sinus infections, bronchitis, croup, severe sore throats, infectious asthma, and 1 type of the common cold. When mycoplasma infects children, about 25% of them develop nausea, vomiting, or diarrhea.

Coughs that linger after a cold or sinus problem cause constant disruption in the home, school, and workplace. Often, these dry, nonproductive coughs become increasingly troublesome although other symptoms—fever, congestion, and fatigue—resolved days or weeks ago. This stubborn cough persists for weeks, and plagues its victim and the victim’s family night and day. The diagnosis might be a common, but overlooked cause of lingering cough: atypical pneumonia caused by mycoplasma.

Mycoplasma—pleomorphic bacteria that lack a cell wall—are the smallest and simplest self-replicating organisms known to humans. They probably evolved from gram-positive, walled eubacteria by degenerative evolution. Smaller than amoebas, these 0.1-micrometer organisms grow and reproduce slowly and require no oxygen or host cell. They also change shapes asymmetrically, appearing as long, thin filaments, tiny spheres, or branches. Scientists have identified more than 100 mycoplasma species. Fifteen species are known to live in humans, most as normal symbiotic flora. Mycoplasma pneumoniae, previously called “walking pneumonia,” is pathogenic in humans.

Mycoplasma pneumoniae glides freely and uses its specialized filamentous tips to burrow between cilia within the respiratory epithelium, causing the respiratory epithelial cells to slough. It also produces hydrogen peroxide, which causes initial cell disruption in the respiratory tract and damages erythrocyte membranes. Researchers have determined that more than 40% of infants younger than 1 year old have had a mycoplasma infection. By age 5, approximately 65% of children have been infected. Nearly all adults have been infected at least once, often repeatedly. Mycoplasma pneumonia usually affects people younger than 40 years of age. The highest incidence is found in the 5- to 9-year age group.

The risk of contracting mycoplasma pneumonia is greatest for people who live or work in crowded areas, such as daycare facilities, schools, homeless shelters, long-term care units, and military and prison environments. However, many people who develop mycoplasma infections have no identifiable risk factor. Most mycoplasma infections cause mild to moderate clinical symptoms, but the infection incubates over 3 weeks and can last weeks without treatment. This infection cannot be diagnosed based on symptoms alone; laboratory testing is essential. Infection can also cause ear infections, sinus infections, bronchitis, croup, severe sore throats, infectious asthma, and 1 type of the common cold. When mycoplasma infects children, about 25% of them develop nausea, vomiting, or diarrhea.

Coughs that linger after a cold or sinus problem cause constant disruption in the home, school, and workplace. Often, these dry, nonproductive coughs become increasingly troublesome although other symptoms—fever, congestion, and fatigue—resolved days or weeks ago. This stubborn cough persists for weeks, and plagues its victim and the victim’s family night and day. The diagnosis might be a common, but overlooked cause of lingering cough: atypical pneumonia caused by mycoplasma.

Mycoplasma—pleomorphic bacteria that lack a cell wall—are the smallest and simplest self-replicating organisms known to humans. They probably evolved from gram-positive, walled eubacteria by degenerative evolution. Smaller than amoebas, these 0.1-micrometer organisms grow and reproduce slowly and require no oxygen or host cell. They also change shapes asymmetrically, appearing as long, thin filaments, tiny spheres, or branches. Scientists have identified more than 100 mycoplasma species. Fifteen species are known to live in humans, most as normal symbiotic flora. Mycoplasma pneumoniae, previously called “walking pneumonia,” is pathogenic in humans.

Mycoplasma pneumoniae glides freely and uses its specialized filamentous tips to burrow between cilia within the respiratory epithelium, causing the respiratory epithelial cells to slough. It also produces hydrogen peroxide, which causes initial cell disruption in the respiratory tract and damages erythrocyte membranes. Researchers have determined that more than 40% of infants younger than 1 year old have had a mycoplasma infection. By age 5, approximately 65% of children have been infected. Nearly all adults have been infected at least once, often repeatedly. Mycoplasma pneumonia usually affects people younger than 40 years of age. The highest incidence is found in the 5- to 9-year age group.

The risk of contracting mycoplasma pneumonia is greatest for people who live or work in crowded areas, such as daycare facilities, schools, homeless shelters, long-term care units, and military and prison environments. However, many people who develop mycoplasma infections have no identifiable risk factor. Most mycoplasma infections cause mild to moderate clinical symptoms, but the infection incubates over 3 weeks and can last weeks without treatment. This infection cannot be diagnosed based on symptoms alone; laboratory testing is essential. Infection can also cause ear infections, sinus infections, bronchitis, croup, severe sore throats, infectious asthma, and 1 type of the common cold. When mycoplasma infects children, about 25% of them develop nausea, vomiting, or diarrhea.

Coughs that linger after a cold or sinus problem cause constant disruption in the home, school, and workplace. Often, these dry, nonproductive coughs become increasingly troublesome although other symptoms—fever, congestion, and fatigue—resolved days or weeks ago. This stubborn cough persists for weeks, and plagues its victim and the victim’s family night and day. The diagnosis might be a common, but overlooked cause of lingering cough: atypical pneumonia caused by mycoplasma.

Mycoplasma—pleomorphic bacteria that lack a cell wall—are the smallest and simplest self-replicating organisms known to humans. They probably evolved from gram-positive, walled eubacteria by degenerative evolution. Smaller than amoebas, these 0.1-micrometer organisms grow and reproduce slowly and require no oxygen or host cell. They also change shapes asymmetrically, appearing as long, thin filaments, tiny spheres, or branches. Scientists have identified more than 100 mycoplasma species. Fifteen species are known to live in humans, most as normal symbiotic flora. Mycoplasma pneumoniae, previously called “walking pneumonia,” is pathogenic in humans.

Mycoplasma pneumoniae glides freely and uses its specialized filamentous tips to burrow between cilia within the respiratory epithelium, causing the respiratory epithelial cells to slough. It also produces hydrogen peroxide, which causes initial cell disruption in the respiratory tract and damages erythrocyte membranes. Researchers have determined that more than 40% of infants younger than 1 year old have had a mycoplasma infection. By age 5, approximately 65% of children have been infected. Nearly all adults have been infected at least once, often repeatedly. Mycoplasma pneumonia usually affects people younger than 40 years of age. The highest incidence is found in the 5- to 9-year age group.

The risk of contracting mycoplasma pneumonia is greatest for people who live or work in crowded areas, such as daycare facilities, schools, homeless shelters, long-term care units, and military and prison environments. However, many people who develop mycoplasma infections have no identifiable risk factor. Most mycoplasma infections cause mild to moderate clinical symptoms, but the infection incubates over 3 weeks and can last weeks without treatment. This infection cannot be diagnosed based on symptoms alone; laboratory testing is essential. Infection can also cause ear infections, sinus infections, bronchitis, croup, severe sore throats, infectious asthma, and 1 type of the common cold. When mycoplasma infects children, about 25% of them develop nausea, vomiting, or diarrhea.

Coughs that linger after a cold or sinus problem cause constant disruption in the home, school, and workplace. Often, these dry, nonproductive coughs become increasingly troublesome although other symptoms—fever, congestion, and fatigue—resolved days or weeks ago. This stubborn cough persists for weeks, and plagues its victim and the victim’s family night and day. The diagnosis might be a common, but overlooked cause of lingering cough: atypical pneumonia caused by mycoplasma.

Mycoplasma—pleomorphic bacteria that lack a cell wall—are the smallest and simplest self-replicating organisms known to humans. They probably evolved from gram-positive, walled eubacteria by degenerative evolution. Smaller than amoebas, these 0.1-micrometer organisms grow and reproduce slowly and require no oxygen or host cell. They also change shapes asymmetrically, appearing as long, thin filaments, tiny spheres, or branches. Scientists have identified more than 100 mycoplasma species. Fifteen species are known to live in humans, most as normal symbiotic flora. Mycoplasma pneumoniae, previously called “walking pneumonia,” is pathogenic in humans.

Mycoplasma pneumoniae glides freely and uses its specialized filamentous tips to burrow between cilia within the respiratory epithelium, causing the respiratory epithelial cells to slough. It also produces hydrogen peroxide, which causes initial cell disruption in the respiratory tract and damages erythrocyte membranes. Researchers have determined that more than 40% of infants younger than 1 year old have had a mycoplasma infection. By age 5, approximately 65% of children have been infected. Nearly all adults have been infected at least once, often repeatedly. Mycoplasma pneumonia usually affects people younger than 40 years of age. The highest incidence is found in the 5- to 9-year age group.

The risk of contracting mycoplasma pneumonia is greatest for people who live or work in crowded areas, such as daycare facilities, schools, homeless shelters, long-term care units, and military and prison environments. However, many people who develop mycoplasma infections have no identifiable risk factor. Most mycoplasma infections cause mild to moderate clinical symptoms, but the infection incubates over 3 weeks and can last weeks without treatment. This infection cannot be diagnosed based on symptoms alone; laboratory testing is essential. Infection can also cause ear infections, sinus infections, bronchitis, croup, severe sore throats, infectious asthma, and 1 type of the common cold. When mycoplasma infects children, about 25% of them develop nausea, vomiting, or diarrhea.

Coughs that linger after a cold or sinus problem cause constant disruption in the home, school, and workplace. Often, these dry, nonproductive coughs become increasingly troublesome although other symptoms—fever, congestion, and fatigue—resolved days or weeks ago. This stubborn cough persists for weeks, and plagues its victim and the victim’s family night and day. The diagnosis might be a common, but overlooked cause of lingering cough: atypical pneumonia caused by mycoplasma.

Mycoplasma—pleomorphic bacteria that lack a cell wall—are the smallest and simplest self-replicating organisms known to humans. They probably evolved from gram-positive, walled eubacteria by degenerative evolution. Smaller than amoebas, these 0.1-micrometer organisms grow and reproduce slowly and require no oxygen or host cell. They also change shapes asymmetrically, appearing as long, thin filaments, tiny spheres, or branches. Scientists have identified more than 100 mycoplasma species. Fifteen species are known to live in humans, most as normal symbiotic flora. Mycoplasma pneumoniae, previously called “walking pneumonia,” is pathogenic in humans.

Mycoplasma pneumoniae glides freely and uses its specialized filamentous tips to burrow between cilia within the respiratory epithelium, causing the respiratory epithelial cells to slough. It also produces hydrogen peroxide, which causes initial cell disruption in the respiratory tract and damages erythrocyte membranes. Researchers have determined that more than 40% of infants younger than 1 year old have had a mycoplasma infection. By age 5, approximately 65% of children have been infected. Nearly all adults have been infected at least once, often repeatedly. Mycoplasma pneumonia usually affects people younger than 40 years of age. The highest incidence is found in the 5- to 9-year age group.

The risk of contracting mycoplasma pneumonia is greatest for people who live or work in crowded areas, such as daycare facilities, schools, homeless shelters, long-term care units, and military and prison environments. However, many people who develop mycoplasma infections have no identifiable risk factor. Most mycoplasma infections cause mild to moderate clinical symptoms, but the infection incubates over 3 weeks and can last weeks without treatment. This infection cannot be diagnosed based on symptoms alone; laboratory testing is essential. Infection can also cause ear infections, sinus infections, bronchitis, croup, severe sore throats, infectious asthma, and 1 type of the common cold. When mycoplasma infects children, about 25% of them develop nausea, vomiting, or diarrhea.

Coughs that linger after a cold or sinus problem cause constant disruption in the home, school, and workplace. Often, these dry, nonproductive coughs become increasingly troublesome although other symptoms—fever, congestion, and fatigue—resolved days or weeks ago. This stubborn cough persists for weeks, and plagues its victim and the victim’s family night and day. The diagnosis might be a common, but overlooked cause of lingering cough: atypical pneumonia caused by mycoplasma.

Mycoplasma—pleomorphic bacteria that lack a cell wall—are the smallest and simplest self-replicating organisms known to humans. They probably evolved from gram-positive, walled eubacteria by degenerative evolution. Smaller than amoebas, these 0.1-micrometer organisms grow and reproduce slowly and require no oxygen or host cell. They also change shapes asymmetrically, appearing as long, thin filaments, tiny spheres, or branches. Scientists have identified more than 100 mycoplasma species. Fifteen species are known to live in humans, most as normal symbiotic flora. Mycoplasma pneumoniae, previously called “walking pneumonia,” is pathogenic in humans.

Mycoplasma pneumoniae glides freely and uses its specialized filamentous tips to burrow between cilia within the respiratory epithelium, causing the respiratory epithelial cells to slough. It also produces hydrogen peroxide, which causes initial cell disruption in the respiratory tract and damages erythrocyte membranes. Researchers have determined that more than 40% of infants younger than 1 year old have had a mycoplasma infection. By age 5, approximately 65% of children have been infected. Nearly all adults have been infected at least once, often repeatedly. Mycoplasma pneumonia usually affects people younger than 40 years of age. The highest incidence is found in the 5- to 9-year age group.

The risk of contracting mycoplasma pneumonia is greatest for people who live or work in crowded areas, such as daycare facilities, schools, homeless shelters, long-term care units, and military and prison environments. However, many people who develop mycoplasma infections have no identifiable risk factor. Most mycoplasma infections cause mild to moderate clinical symptoms, but the infection incubates over 3 weeks and can last weeks without treatment. This infection cannot be diagnosed based on symptoms alone; laboratory testing is essential. Infection can also cause ear infections, sinus infections, bronchitis, croup, severe sore throats, infectious asthma, and 1 type of the common cold. When mycoplasma infects children, about 25% of them develop nausea, vomiting, or diarrhea.

Lead—non-biodegradable, soft, malleable, as well as heat and corrosion resistant—is environmentally omnipresent. Its known properties make it an ideal metal for automobiles, paint, smelting, ceramics, and plastics. Not many years ago, it was also utilized in the toy industry. Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004. In 2002, around 10 out of every 100,000 of adults had lead toxicity.

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL were considered toxic in children and adults, respectively. But, since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability. Approximately 450,000 American children have BLLs >5 mcg/dL. Consequently, lead poisoning is still a problem.

Lead exposure can start with prenatal maternal-fetal transmission. Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint. Lead-based paint was phased out in the 1970s, lowering, but not eliminating, risk of exposure. Old pipes sometimes leach lead into drinking water. Lead hazards are disproportionately found in low-income housing. Adults rarely develop lead poisoning, but risk is increased for industrial workers who use or manufacture lead-based products.

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters. Increased urinary aminolevulinic acid concentrations are also reliable indicators. Plain film radiographs can reveal visible lead lines in patients’ long bones. Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.

Lead affects every organ system and causes an unpredictable variety of symptoms. The nervous system is most sensitive (centrally in children, peripherally in adults), but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion). Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Lead—non-biodegradable, soft, malleable, as well as heat and corrosion resistant—is environmentally omnipresent. Its known properties make it an ideal metal for automobiles, paint, smelting, ceramics, and plastics. Not many years ago, it was also utilized in the toy industry. Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004. In 2002, around 10 out of every 100,000 of adults had lead toxicity.

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL were considered toxic in children and adults, respectively. But, since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability. Approximately 450,000 American children have BLLs >5 mcg/dL. Consequently, lead poisoning is still a problem.

Lead exposure can start with prenatal maternal-fetal transmission. Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint. Lead-based paint was phased out in the 1970s, lowering, but not eliminating, risk of exposure. Old pipes sometimes leach lead into drinking water. Lead hazards are disproportionately found in low-income housing. Adults rarely develop lead poisoning, but risk is increased for industrial workers who use or manufacture lead-based products.

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters. Increased urinary aminolevulinic acid concentrations are also reliable indicators. Plain film radiographs can reveal visible lead lines in patients’ long bones. Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.

Lead affects every organ system and causes an unpredictable variety of symptoms. The nervous system is most sensitive (centrally in children, peripherally in adults), but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion). Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Lead—non-biodegradable, soft, malleable, as well as heat and corrosion resistant—is environmentally omnipresent. Its known properties make it an ideal metal for automobiles, paint, smelting, ceramics, and plastics. Not many years ago, it was also utilized in the toy industry. Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004. In 2002, around 10 out of every 100,000 of adults had lead toxicity.

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL were considered toxic in children and adults, respectively. But, since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability. Approximately 450,000 American children have BLLs >5 mcg/dL. Consequently, lead poisoning is still a problem.

Lead exposure can start with prenatal maternal-fetal transmission. Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint. Lead-based paint was phased out in the 1970s, lowering, but not eliminating, risk of exposure. Old pipes sometimes leach lead into drinking water. Lead hazards are disproportionately found in low-income housing. Adults rarely develop lead poisoning, but risk is increased for industrial workers who use or manufacture lead-based products.

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters. Increased urinary aminolevulinic acid concentrations are also reliable indicators. Plain film radiographs can reveal visible lead lines in patients’ long bones. Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.

Lead affects every organ system and causes an unpredictable variety of symptoms. The nervous system is most sensitive (centrally in children, peripherally in adults), but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion). Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Lead—non-biodegradable, soft, malleable, as well as heat and corrosion resistant—is environmentally omnipresent. Its known properties make it an ideal metal for automobiles, paint, smelting, ceramics, and plastics. Not many years ago, it was also utilized in the toy industry. Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004. In 2002, around 10 out of every 100,000 of adults had lead toxicity.

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL were considered toxic in children and adults, respectively. But, since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability. Approximately 450,000 American children have BLLs >5 mcg/dL. Consequently, lead poisoning is still a problem.

Lead exposure can start with prenatal maternal-fetal transmission. Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint. Lead-based paint was phased out in the 1970s, lowering, but not eliminating, risk of exposure. Old pipes sometimes leach lead into drinking water. Lead hazards are disproportionately found in low-income housing. Adults rarely develop lead poisoning, but risk is increased for industrial workers who use or manufacture lead-based products.

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters. Increased urinary aminolevulinic acid concentrations are also reliable indicators. Plain film radiographs can reveal visible lead lines in patients’ long bones. Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.

Lead affects every organ system and causes an unpredictable variety of symptoms. The nervous system is most sensitive (centrally in children, peripherally in adults), but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion). Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Lead—non-biodegradable, soft, malleable, as well as heat and corrosion resistant—is environmentally omnipresent. Its known properties make it an ideal metal for automobiles, paint, smelting, ceramics, and plastics. Not many years ago, it was also utilized in the toy industry. Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004. In 2002, around 10 out of every 100,000 of adults had lead toxicity.

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL were considered toxic in children and adults, respectively. But, since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability. Approximately 450,000 American children have BLLs >5 mcg/dL. Consequently, lead poisoning is still a problem.

Lead exposure can start with prenatal maternal-fetal transmission. Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint. Lead-based paint was phased out in the 1970s, lowering, but not eliminating, risk of exposure. Old pipes sometimes leach lead into drinking water. Lead hazards are disproportionately found in low-income housing. Adults rarely develop lead poisoning, but risk is increased for industrial workers who use or manufacture lead-based products.

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters. Increased urinary aminolevulinic acid concentrations are also reliable indicators. Plain film radiographs can reveal visible lead lines in patients’ long bones. Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.

Lead affects every organ system and causes an unpredictable variety of symptoms. The nervous system is most sensitive (centrally in children, peripherally in adults), but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion). Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Lead—non-biodegradable, soft, malleable, as well as heat and corrosion resistant—is environmentally omnipresent. Its known properties make it an ideal metal for automobiles, paint, smelting, ceramics, and plastics. Not many years ago, it was also utilized in the toy industry. Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004. In 2002, around 10 out of every 100,000 of adults had lead toxicity.

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL were considered toxic in children and adults, respectively. But, since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability. Approximately 450,000 American children have BLLs >5 mcg/dL. Consequently, lead poisoning is still a problem.

Lead exposure can start with prenatal maternal-fetal transmission. Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint. Lead-based paint was phased out in the 1970s, lowering, but not eliminating, risk of exposure. Old pipes sometimes leach lead into drinking water. Lead hazards are disproportionately found in low-income housing. Adults rarely develop lead poisoning, but risk is increased for industrial workers who use or manufacture lead-based products.

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters. Increased urinary aminolevulinic acid concentrations are also reliable indicators. Plain film radiographs can reveal visible lead lines in patients’ long bones. Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.

Lead affects every organ system and causes an unpredictable variety of symptoms. The nervous system is most sensitive (centrally in children, peripherally in adults), but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion). Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Lead—non-biodegradable, soft, malleable, as well as heat and corrosion resistant—is environmentally omnipresent. Its known properties make it an ideal metal for automobiles, paint, smelting, ceramics, and plastics. Not many years ago, it was also utilized in the toy industry. Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004. In 2002, around 10 out of every 100,000 of adults had lead toxicity.

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL were considered toxic in children and adults, respectively. But, since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability. Approximately 450,000 American children have BLLs >5 mcg/dL. Consequently, lead poisoning is still a problem.

Lead exposure can start with prenatal maternal-fetal transmission. Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint. Lead-based paint was phased out in the 1970s, lowering, but not eliminating, risk of exposure. Old pipes sometimes leach lead into drinking water. Lead hazards are disproportionately found in low-income housing. Adults rarely develop lead poisoning, but risk is increased for industrial workers who use or manufacture lead-based products.

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters. Increased urinary aminolevulinic acid concentrations are also reliable indicators. Plain film radiographs can reveal visible lead lines in patients’ long bones. Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.

Lead affects every organ system and causes an unpredictable variety of symptoms. The nervous system is most sensitive (centrally in children, peripherally in adults), but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion). Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Lead—non-biodegradable, soft, malleable, as well as heat and corrosion resistant—is environmentally omnipresent. Its known properties make it an ideal metal for automobiles, paint, smelting, ceramics, and plastics. Not many years ago, it was also utilized in the toy industry. Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004. In 2002, around 10 out of every 100,000 of adults had lead toxicity.

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL were considered toxic in children and adults, respectively. But, since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability. Approximately 450,000 American children have BLLs >5 mcg/dL. Consequently, lead poisoning is still a problem.

Lead exposure can start with prenatal maternal-fetal transmission. Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint. Lead-based paint was phased out in the 1970s, lowering, but not eliminating, risk of exposure. Old pipes sometimes leach lead into drinking water. Lead hazards are disproportionately found in low-income housing. Adults rarely develop lead poisoning, but risk is increased for industrial workers who use or manufacture lead-based products.

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters. Increased urinary aminolevulinic acid concentrations are also reliable indicators. Plain film radiographs can reveal visible lead lines in patients’ long bones. Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.

Lead affects every organ system and causes an unpredictable variety of symptoms. The nervous system is most sensitive (centrally in children, peripherally in adults), but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion). Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Since 1997, the American Heart Association (AHA) has attempted to increase awareness about cardiovascular disease (CVD) among women. Fortunately, great progress has been made to educate individuals about CVD and its consequences. According to the AHA’s 2011 Guidelines for Prevention of Cardiovascular Disease in Women, the misconception that CVD is a “man’s disease” has been somewhat disproved, as awareness among the general public increased from 30% in 1997 to 54% in 2009.

Unfortunately, CVD continues to be the leading cause of death in the United States for both men and women. Since 1984, the number of deaths related to CVD in women exceeded those in men. In the United States, CVD death rates among women aged 35 to 54 years appear to be increasing by 1% annually, which is most likely attributable to the escalating obesity epidemic. According to the AHA, even though CVD is the number 1 cause of death among women, only 13% of women perceive CVD as a health threat. CVD is responsible for more deaths among women than the next 3 leading causes of death combined, including all forms of cancer.

Due to the ongoing prevalence of CVD, increasing awareness and understanding of CVD, especially among the female population, is still a top priority for many health care professionals. As one of the most accessible health care professionals, pharmacists are in a pivotal position to educate and inform their patients of the risks associated with CVD, possible drug therapies, and preventive measures. The AHA has set a goal for 2020 to improve cardiovascular health in all Americans by 20%, while reducing deaths from CVD and stroke by 20%.

According to the American Heart Association, in the United States a woman dies of some form of CVD every minute and more than 1 in 3 females have some form of CVD. Studies have demonstrated that gender differences may play an important role in the diagnosis, treatment, and prevention of CVD. Unfortunately, many women may not always recognize the warning signs and symptoms of a heart attack because they sometimes appear more subtle when compared with those typically experienced by men.

Results from a study of 515 women who had heart attacks report that 43% did not experience any type of chest pain or pressure during the heart attack. Although the classic symptoms include chest pain, tingling in the left arm, sweating, and shortness of breath, women may also experience some “atypical” symptoms, such as extreme fatigue, nausea, dizziness, indigestion, vomiting, and pain in the neck or back. By learning and recognizing the warning signs, women can take a proactive approach to their cardiovascular health and get treatment earlier to prevent further complications.

Since 1997, the American Heart Association (AHA) has attempted to increase awareness about cardiovascular disease (CVD) among women. Fortunately, great progress has been made to educate individuals about CVD and its consequences. According to the AHA’s 2011 Guidelines for Prevention of Cardiovascular Disease in Women, the misconception that CVD is a “man’s disease” has been somewhat disproved, as awareness among the general public increased from 30% in 1997 to 54% in 2009.

Unfortunately, CVD continues to be the leading cause of death in the United States for both men and women. Since 1984, the number of deaths related to CVD in women exceeded those in men. In the United States, CVD death rates among women aged 35 to 54 years appear to be increasing by 1% annually, which is most likely attributable to the escalating obesity epidemic. According to the AHA, even though CVD is the number 1 cause of death among women, only 13% of women perceive CVD as a health threat. CVD is responsible for more deaths among women than the next 3 leading causes of death combined, including all forms of cancer.

Due to the ongoing prevalence of CVD, increasing awareness and understanding of CVD, especially among the female population, is still a top priority for many health care professionals. As one of the most accessible health care professionals, pharmacists are in a pivotal position to educate and inform their patients of the risks associated with CVD, possible drug therapies, and preventive measures. The AHA has set a goal for 2020 to improve cardiovascular health in all Americans by 20%, while reducing deaths from CVD and stroke by 20%.

According to the American Heart Association, in the United States a woman dies of some form of CVD every minute and more than 1 in 3 females have some form of CVD. Studies have demonstrated that gender differences may play an important role in the diagnosis, treatment, and prevention of CVD. Unfortunately, many women may not always recognize the warning signs and symptoms of a heart attack because they sometimes appear more subtle when compared with those typically experienced by men.

Results from a study of 515 women who had heart attacks report that 43% did not experience any type of chest pain or pressure during the heart attack. Although the classic symptoms include chest pain, tingling in the left arm, sweating, and shortness of breath, women may also experience some “atypical” symptoms, such as extreme fatigue, nausea, dizziness, indigestion, vomiting, and pain in the neck or back. By learning and recognizing the warning signs, women can take a proactive approach to their cardiovascular health and get treatment earlier to prevent further complications.

Since 1997, the American Heart Association (AHA) has attempted to increase awareness about cardiovascular disease (CVD) among women. Fortunately, great progress has been made to educate individuals about CVD and its consequences. According to the AHA’s 2011 Guidelines for Prevention of Cardiovascular Disease in Women, the misconception that CVD is a “man’s disease” has been somewhat disproved, as awareness among the general public increased from 30% in 1997 to 54% in 2009.

Unfortunately, CVD continues to be the leading cause of death in the United States for both men and women. Since 1984, the number of deaths related to CVD in women exceeded those in men. In the United States, CVD death rates among women aged 35 to 54 years appear to be increasing by 1% annually, which is most likely attributable to the escalating obesity epidemic. According to the AHA, even though CVD is the number 1 cause of death among women, only 13% of women perceive CVD as a health threat. CVD is responsible for more deaths among women than the next 3 leading causes of death combined, including all forms of cancer.

Due to the ongoing prevalence of CVD, increasing awareness and understanding of CVD, especially among the female population, is still a top priority for many health care professionals. As one of the most accessible health care professionals, pharmacists are in a pivotal position to educate and inform their patients of the risks associated with CVD, possible drug therapies, and preventive measures. The AHA has set a goal for 2020 to improve cardiovascular health in all Americans by 20%, while reducing deaths from CVD and stroke by 20%.

According to the American Heart Association, in the United States a woman dies of some form of CVD every minute and more than 1 in 3 females have some form of CVD. Studies have demonstrated that gender differences may play an important role in the diagnosis, treatment, and prevention of CVD. Unfortunately, many women may not always recognize the warning signs and symptoms of a heart attack because they sometimes appear more subtle when compared with those typically experienced by men.

Results from a study of 515 women who had heart attacks report that 43% did not experience any type of chest pain or pressure during the heart attack. Although the classic symptoms include chest pain, tingling in the left arm, sweating, and shortness of breath, women may also experience some “atypical” symptoms, such as extreme fatigue, nausea, dizziness, indigestion, vomiting, and pain in the neck or back. By learning and recognizing the warning signs, women can take a proactive approach to their cardiovascular health and get treatment earlier to prevent further complications.

Since 1997, the American Heart Association (AHA) has attempted to increase awareness about cardiovascular disease (CVD) among women. Fortunately, great progress has been made to educate individuals about CVD and its consequences. According to the AHA’s 2011 Guidelines for Prevention of Cardiovascular Disease in Women, the misconception that CVD is a “man’s disease” has been somewhat disproved, as awareness among the general public increased from 30% in 1997 to 54% in 2009.

Unfortunately, CVD continues to be the leading cause of death in the United States for both men and women. Since 1984, the number of deaths related to CVD in women exceeded those in men. In the United States, CVD death rates among women aged 35 to 54 years appear to be increasing by 1% annually, which is most likely attributable to the escalating obesity epidemic. According to the AHA, even though CVD is the number 1 cause of death among women, only 13% of women perceive CVD as a health threat. CVD is responsible for more deaths among women than the next 3 leading causes of death combined, including all forms of cancer.

Due to the ongoing prevalence of CVD, increasing awareness and understanding of CVD, especially among the female population, is still a top priority for many health care professionals. As one of the most accessible health care professionals, pharmacists are in a pivotal position to educate and inform their patients of the risks associated with CVD, possible drug therapies, and preventive measures. The AHA has set a goal for 2020 to improve cardiovascular health in all Americans by 20%, while reducing deaths from CVD and stroke by 20%.

According to the American Heart Association, in the United States a woman dies of some form of CVD every minute and more than 1 in 3 females have some form of CVD. Studies have demonstrated that gender differences may play an important role in the diagnosis, treatment, and prevention of CVD. Unfortunately, many women may not always recognize the warning signs and symptoms of a heart attack because they sometimes appear more subtle when compared with those typically experienced by men.

Results from a study of 515 women who had heart attacks report that 43% did not experience any type of chest pain or pressure during the heart attack. Although the classic symptoms include chest pain, tingling in the left arm, sweating, and shortness of breath, women may also experience some “atypical” symptoms, such as extreme fatigue, nausea, dizziness, indigestion, vomiting, and pain in the neck or back. By learning and recognizing the warning signs, women can take a proactive approach to their cardiovascular health and get treatment earlier to prevent further complications.

Since 1997, the American Heart Association (AHA) has attempted to increase awareness about cardiovascular disease (CVD) among women. Fortunately, great progress has been made to educate individuals about CVD and its consequences. According to the AHA’s 2011 Guidelines for Prevention of Cardiovascular Disease in Women, the misconception that CVD is a “man’s disease” has been somewhat disproved, as awareness among the general public increased from 30% in 1997 to 54% in 2009.

Unfortunately, CVD continues to be the leading cause of death in the United States for both men and women. Since 1984, the number of deaths related to CVD in women exceeded those in men. In the United States, CVD death rates among women aged 35 to 54 years appear to be increasing by 1% annually, which is most likely attributable to the escalating obesity epidemic. According to the AHA, even though CVD is the number 1 cause of death among women, only 13% of women perceive CVD as a health threat. CVD is responsible for more deaths among women than the next 3 leading causes of death combined, including all forms of cancer.

Due to the ongoing prevalence of CVD, increasing awareness and understanding of CVD, especially among the female population, is still a top priority for many health care professionals. As one of the most accessible health care professionals, pharmacists are in a pivotal position to educate and inform their patients of the risks associated with CVD, possible drug therapies, and preventive measures. The AHA has set a goal for 2020 to improve cardiovascular health in all Americans by 20%, while reducing deaths from CVD and stroke by 20%.

According to the American Heart Association, in the United States a woman dies of some form of CVD every minute and more than 1 in 3 females have some form of CVD. Studies have demonstrated that gender differences may play an important role in the diagnosis, treatment, and prevention of CVD. Unfortunately, many women may not always recognize the warning signs and symptoms of a heart attack because they sometimes appear more subtle when compared with those typically experienced by men.

Results from a study of 515 women who had heart attacks report that 43% did not experience any type of chest pain or pressure during the heart attack. Although the classic symptoms include chest pain, tingling in the left arm, sweating, and shortness of breath, women may also experience some “atypical” symptoms, such as extreme fatigue, nausea, dizziness, indigestion, vomiting, and pain in the neck or back. By learning and recognizing the warning signs, women can take a proactive approach to their cardiovascular health and get treatment earlier to prevent further complications.

Since 1997, the American Heart Association (AHA) has attempted to increase awareness about cardiovascular disease (CVD) among women. Fortunately, great progress has been made to educate individuals about CVD and its consequences. According to the AHA’s 2011 Guidelines for Prevention of Cardiovascular Disease in Women, the misconception that CVD is a “man’s disease” has been somewhat disproved, as awareness among the general public increased from 30% in 1997 to 54% in 2009.

Unfortunately, CVD continues to be the leading cause of death in the United States for both men and women. Since 1984, the number of deaths related to CVD in women exceeded those in men. In the United States, CVD death rates among women aged 35 to 54 years appear to be increasing by 1% annually, which is most likely attributable to the escalating obesity epidemic. According to the AHA, even though CVD is the number 1 cause of death among women, only 13% of women perceive CVD as a health threat. CVD is responsible for more deaths among women than the next 3 leading causes of death combined, including all forms of cancer.

Due to the ongoing prevalence of CVD, increasing awareness and understanding of CVD, especially among the female population, is still a top priority for many health care professionals. As one of the most accessible health care professionals, pharmacists are in a pivotal position to educate and inform their patients of the risks associated with CVD, possible drug therapies, and preventive measures. The AHA has set a goal for 2020 to improve cardiovascular health in all Americans by 20%, while reducing deaths from CVD and stroke by 20%.

According to the American Heart Association, in the United States a woman dies of some form of CVD every minute and more than 1 in 3 females have some form of CVD. Studies have demonstrated that gender differences may play an important role in the diagnosis, treatment, and prevention of CVD. Unfortunately, many women may not always recognize the warning signs and symptoms of a heart attack because they sometimes appear more subtle when compared with those typically experienced by men.

Results from a study of 515 women who had heart attacks report that 43% did not experience any type of chest pain or pressure during the heart attack. Although the classic symptoms include chest pain, tingling in the left arm, sweating, and shortness of breath, women may also experience some “atypical” symptoms, such as extreme fatigue, nausea, dizziness, indigestion, vomiting, and pain in the neck or back. By learning and recognizing the warning signs, women can take a proactive approach to their cardiovascular health and get treatment earlier to prevent further complications.

Since 1997, the American Heart Association (AHA) has attempted to increase awareness about cardiovascular disease (CVD) among women. Fortunately, great progress has been made to educate individuals about CVD and its consequences. According to the AHA’s 2011 Guidelines for Prevention of Cardiovascular Disease in Women, the misconception that CVD is a “man’s disease” has been somewhat disproved, as awareness among the general public increased from 30% in 1997 to 54% in 2009.

Unfortunately, CVD continues to be the leading cause of death in the United States for both men and women. Since 1984, the number of deaths related to CVD in women exceeded those in men. In the United States, CVD death rates among women aged 35 to 54 years appear to be increasing by 1% annually, which is most likely attributable to the escalating obesity epidemic. According to the AHA, even though CVD is the number 1 cause of death among women, only 13% of women perceive CVD as a health threat. CVD is responsible for more deaths among women than the next 3 leading causes of death combined, including all forms of cancer.

Due to the ongoing prevalence of CVD, increasing awareness and understanding of CVD, especially among the female population, is still a top priority for many health care professionals. As one of the most accessible health care professionals, pharmacists are in a pivotal position to educate and inform their patients of the risks associated with CVD, possible drug therapies, and preventive measures. The AHA has set a goal for 2020 to improve cardiovascular health in all Americans by 20%, while reducing deaths from CVD and stroke by 20%.

According to the American Heart Association, in the United States a woman dies of some form of CVD every minute and more than 1 in 3 females have some form of CVD. Studies have demonstrated that gender differences may play an important role in the diagnosis, treatment, and prevention of CVD. Unfortunately, many women may not always recognize the warning signs and symptoms of a heart attack because they sometimes appear more subtle when compared with those typically experienced by men.

Results from a study of 515 women who had heart attacks report that 43% did not experience any type of chest pain or pressure during the heart attack. Although the classic symptoms include chest pain, tingling in the left arm, sweating, and shortness of breath, women may also experience some “atypical” symptoms, such as extreme fatigue, nausea, dizziness, indigestion, vomiting, and pain in the neck or back. By learning and recognizing the warning signs, women can take a proactive approach to their cardiovascular health and get treatment earlier to prevent further complications.

Since 1997, the American Heart Association (AHA) has attempted to increase awareness about cardiovascular disease (CVD) among women. Fortunately, great progress has been made to educate individuals about CVD and its consequences. According to the AHA’s 2011 Guidelines for Prevention of Cardiovascular Disease in Women, the misconception that CVD is a “man’s disease” has been somewhat disproved, as awareness among the general public increased from 30% in 1997 to 54% in 2009.

Unfortunately, CVD continues to be the leading cause of death in the United States for both men and women. Since 1984, the number of deaths related to CVD in women exceeded those in men. In the United States, CVD death rates among women aged 35 to 54 years appear to be increasing by 1% annually, which is most likely attributable to the escalating obesity epidemic. According to the AHA, even though CVD is the number 1 cause of death among women, only 13% of women perceive CVD as a health threat. CVD is responsible for more deaths among women than the next 3 leading causes of death combined, including all forms of cancer.

Due to the ongoing prevalence of CVD, increasing awareness and understanding of CVD, especially among the female population, is still a top priority for many health care professionals. As one of the most accessible health care professionals, pharmacists are in a pivotal position to educate and inform their patients of the risks associated with CVD, possible drug therapies, and preventive measures. The AHA has set a goal for 2020 to improve cardiovascular health in all Americans by 20%, while reducing deaths from CVD and stroke by 20%.

According to the American Heart Association, in the United States a woman dies of some form of CVD every minute and more than 1 in 3 females have some form of CVD. Studies have demonstrated that gender differences may play an important role in the diagnosis, treatment, and prevention of CVD. Unfortunately, many women may not always recognize the warning signs and symptoms of a heart attack because they sometimes appear more subtle when compared with those typically experienced by men.

Results from a study of 515 women who had heart attacks report that 43% did not experience any type of chest pain or pressure during the heart attack. Although the classic symptoms include chest pain, tingling in the left arm, sweating, and shortness of breath, women may also experience some “atypical” symptoms, such as extreme fatigue, nausea, dizziness, indigestion, vomiting, and pain in the neck or back. By learning and recognizing the warning signs, women can take a proactive approach to their cardiovascular health and get treatment earlier to prevent further complications.