Aortic stenosis (AS) is the obstruction of blood flow across the aortic valve. AS has several etiologies: congenital unicuspid or bicuspid valve, rheumatic fever, and degenerative calcific changes of the valve.
Pathophysiology
When the aortic valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta. Stenotic aortic valves have a decreased aperture that leads to a progressive increase in left ventricular systolic pressure. This leads to pressure overload in the left ventricle, which, over time, causes an increase in ventricular wall thickness (ie, concentric hypertrophy). At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic compliance may be affected.
Eventually, however, the left ventricle dilates. This, coupled with a decrease in compliance, is associated with an increase in left ventricular end-diastolic pressure, which is increased further by a rise in atrial systolic pressure. A sustained pressure overload eventually leads to myocardial decompensation. The contractility of the myocardium diminishes, which leads to a decrease in cardiac output. The elevated left ventricular end-diastolic pressure causes a corresponding increase in pulmonary capillary arterial pressures and a decrease in ejection fraction and cardiac output. Ultimately, congestive heart failure (CHF) develops.
Frequency
United States
Aortic stenosis is a relatively common congenital cardiac defect. Incidence is 4 in 1000 live births.
Mortality/Morbidity
Sudden cardiac death occurs in 3-5% of patients with AS. Adults with AS have a 9% mortality rate per year. Once symptoms develop, the incidence of sudden death increases to 15-20%, with average survival duration of less than 5 years. Patients with exertional angina or syncope survive an average of 3 years. After the development of left ventricular failure, life expectancy is slightly greater than 1 year.
Sex
Among children, 75% of cases of AS are in males.
Age
AS usually is not detected until individuals are school aged. AS exists in up to 2% of those who are younger than 70 years. The etiology of AS in those aged 30-70 years can be rheumatic disease or calcification of a congenital bicuspid valve. In those older than 70 years, degenerative calcification is the primary cause of AS. Among people older than 75 years, 3% have critical AS.
Read more HERE
Wednesday, 30 July 2008
Angina Pectoris
Angina pectoris (AP) represents the clinical syndrome occurring when myocardial oxygen demand exceeds supply. The term is derived from Latin; the literal meaning is "the choking of the chest;" angere, meaning "to choke" and pectus, meaning "chest." The first English-written account of recurrent angina pectoris was by English nobleman Edward Hyde, Earl of Clarendon. He described his father as having, with exertion, "a pain in the left arm…so much that the torment made him pale".1 The first description of angina as a medical disorder came from William Heberden. Heberden, a prodigious physician, made many noteworthy contributions to medicine during his career. He presented his observations on "dolor pectoris" to the Royal College of Physicians in 1768. Much of his classic description retains its validity today.2
Angina pectoris has a wide range of clinical expressions. The symptoms most often associated to angina pectoris are substernal chest pressure or tightening, frequently with radiating pain to the arms, shoulders, or jaw. The symptoms may also be associated with shortness of breath, nausea, or diaphoresis. Symptoms stem from inadequate oxygen delivery to myocardial tissue. No definitive diagnostic tools that capture all patients with angina pectoris exist. This, combined with its varied clinical expression, makes angina pectoris a distinct clinical challenge to the emergency physician. The disease state can manifest itself in a variety of forms:
Stable angina pectoris is classified as a reproducible pattern of anginal symptoms that occur during states of increased exertion.
Unstable angina pectoris (UA) manifests either as an increasing frequency of symptoms or as symptoms occurring at rest.
Prinzmetal angina or variant angina occurs as a result of transient coronary artery spasms. These spasms can occur either at rest or with exertion. Unlike stable or unstable angina, no pathological plaque or deposition is present within the coronary arteries that elicits the presentation. On angiography, the coronary arteries are normal in appearance.
Cardiac syndrome X occurs when a patient has all of the symptoms of angina pectoris without coronary artery disease or spasm.
Pathophysiology
The past 2 decades has greatly expanded our overall understanding of the pathophysiology of myocardial ischemic syndromes. The primary dysfunction in angina pectoris is decreased oxygen delivery to myocardial muscle cells. The 2 predominant mechanisms by which delivery is impaired appear to be coronary artery narrowing and endothelial dysfunction. Any other mechanism that affects oxygen delivery can also precipitate symptoms.
Extracardiac causes of angina include, but are by no means limited to, anemia, hypoxia, hypotension, bradycardia, carbon monoxide exposure, and inflammatory disorders.3 The end result is a shift to anaerobic metabolism in the myocardial cells. This is followed by a stimulation of pain receptors that innervate the heart. These pain receptors ultimately are referred to afferent pathways, which are carried in multiple nerve roots from C7 through T4. The referred/radiating pain of angina pectoris is believed to occur because these afferent pathways also carry pain fibers from other regions (eg, the arm, neck, and shoulders).
Coronary artery narrowing
Coronary artery narrowing appears to be the etiology of cardiac ischemia in the preponderance of cases. This has clinical significance when atherosclerotic disease diminishes or halts blood flow through the coronary arterial circulation, interfering with normal laminar blood flow. The significance of even a small change in the diameter of a blood vessel can be profound. The Poiseuille law predicts this outcome—the rate of flow is decreased exponentially by any change in the radius of the lumen. As with a smaller pediatric airway, even relatively minute changes in diameter have dramatic consequences in flow rates. Thus, when a lumen is narrowed by one fifth, the flow rate is decreased by about one half. This predicts that even a small change in a coronary artery plaque size can affect the oxygenation through that vessel's territory.
The epicardial vessel, where atherosclerosis often takes place, has the capacity to dilate via autoregulatory mechanisms to respond to increased demand. Angina occurs as this compensatory mechanism is overwhelmed either by large plaques (typically considered 70% or greater obstruction) or by significantly increased myocardial demand.4
Endothelial factors
Endothelial factors also play an important role in angina pectoris. During sympathetic stimulation, the endothelium is subjected to mediators of both vasoconstriction and vasodilatation. Alpha-agonists (catecholamines) directly cause vasoconstriction, while endothelial nitrous oxide synthase creates nitrous oxide (NO), which counteracts this constricting force via vasodilatation.
In the diseased coronary artery, NO production is reduced or absent. In this setting, the catecholamine drive can overwhelm the autoregulatory mechanisms. In addition, the endothelium of the plaque-laden artery may, in itself, be dysfunctional. This limits the ability of the intra-arterial endothelium to produce mediators, which, in a healthy artery, would protect against further vasoconstriction, assist dilatation, and provide protection from platelet aggregation. Small lesions in these vessels may produce incompletely obstructing aggregates of platelets. This would further impede flow through the affected vessel.4
In the diseased heart, these 2 factors, coronary artery narrowing and endothelial dysfunction, synergistically result in reduced oxygen delivery to the myocardium. The net result is angina pectoris.
Extrinsic factors
Extrinsic factors can also play a role in specific circumstances. The oxygen-carrying capacity of blood is based on a number of factors. The most important of which is the amount of hemoglobin. Any alteration in the ability of blood to carry oxygen can precipitate angina. Anemia of any degree can result in anginal symptoms. Given a scenario where demand is increased, such as climbing a flight of stairs, increased stress, or even sexual intercourse, the anginal symptoms may appear.5 Abnormal hemoglobin, such as methemoglobin, carboxyhemoglobin, or any of a number of hemoglobinopathies, creates an environment at greater risk for precipitating angina.
Other extrinsic factors that affect hemoglobin formation, such as lead poisoning or iron-deficiency states, also lead to a similar decrease in oxygen-carrying capacity. Any mechanism that impedes oxygen delivery to the red blood cells has a similar effect. Therefore, any number of pulmonary causes, such as pulmonary embolism, pulmonary fibrosis or scarring, pneumonia, or congestive heart failure, can exacerbate angina. A decreased oxygen environment, such as travel to a higher elevation, has similar consequences due to the decrease in concentration of atmospheric oxygen.
Variant angina
The etiology of variant angina is currently not well understood. Research suggests that inflammatory mediators may result in focal coronary artery vasospasm. Another possibility is that perfusion is decreased through microvascular circulation. Spasm or intermittent narrowing of this microscopic lumen may result in transient areas of hypoperfusion and oxygen deprivation.6
Syndrome X
Syndrome X is the triad of angina pectoris, a positive ECG stress test result, and a normal coronary angiogram. The pathophysiology of this disease is not well understood. Many theories exist as to the underlying pathology. Decreased oxygenation of the underlying myocardium may be the result of impaired vasodilatation, dysfunctional smooth muscle cells, poor or deficient microvascular circulation, or even structural problems on a cellular level (eg, an inappropriately functioning sodium ion channel).6
Frequency
United States
An estimated 6,500,000 people in the United States experience angina pectoris.
Each year 400,000 new cases of angina pectoris develop.
Mortality/Morbidity
More than 479,000 people died from coronary heart disease (both angina and myocardial infarction) in 2003.
The estimated direct and indirect cost for Americans with coronary heart disease in 2006 was $142.5 billion.
Race
The Centers for Disease Control and Prevention (CDC) note that the prevalence of angina and/or coronary heart disease is highest in Hispanics followed by whites and black non-Hispanics (5%, 4.2%, 3.7%, respectively). This information includes the 50 US states, the District of Columbia, Puerto Rico, and the US Virgin Islands.7
Sex
According to National Health and Nutrition Examination Survey (NHANES) data, the age-adjusted prevalence of self-reported angina appears to be higher in woman than in men. Although 2005 CDC data suggest that men (5.5%) have a higher prevalence of angina and/or coronary heart disease than women (3.4%).7
Age
The incidence of new and recurrent angina increases with age but then declines at around 85 years.
Statistics from American Heart Association and Centers for Disease Control and Prevention.
Read more HERE
Angina pectoris has a wide range of clinical expressions. The symptoms most often associated to angina pectoris are substernal chest pressure or tightening, frequently with radiating pain to the arms, shoulders, or jaw. The symptoms may also be associated with shortness of breath, nausea, or diaphoresis. Symptoms stem from inadequate oxygen delivery to myocardial tissue. No definitive diagnostic tools that capture all patients with angina pectoris exist. This, combined with its varied clinical expression, makes angina pectoris a distinct clinical challenge to the emergency physician. The disease state can manifest itself in a variety of forms:
Stable angina pectoris is classified as a reproducible pattern of anginal symptoms that occur during states of increased exertion.
Unstable angina pectoris (UA) manifests either as an increasing frequency of symptoms or as symptoms occurring at rest.
Prinzmetal angina or variant angina occurs as a result of transient coronary artery spasms. These spasms can occur either at rest or with exertion. Unlike stable or unstable angina, no pathological plaque or deposition is present within the coronary arteries that elicits the presentation. On angiography, the coronary arteries are normal in appearance.
Cardiac syndrome X occurs when a patient has all of the symptoms of angina pectoris without coronary artery disease or spasm.
Pathophysiology
The past 2 decades has greatly expanded our overall understanding of the pathophysiology of myocardial ischemic syndromes. The primary dysfunction in angina pectoris is decreased oxygen delivery to myocardial muscle cells. The 2 predominant mechanisms by which delivery is impaired appear to be coronary artery narrowing and endothelial dysfunction. Any other mechanism that affects oxygen delivery can also precipitate symptoms.
Extracardiac causes of angina include, but are by no means limited to, anemia, hypoxia, hypotension, bradycardia, carbon monoxide exposure, and inflammatory disorders.3 The end result is a shift to anaerobic metabolism in the myocardial cells. This is followed by a stimulation of pain receptors that innervate the heart. These pain receptors ultimately are referred to afferent pathways, which are carried in multiple nerve roots from C7 through T4. The referred/radiating pain of angina pectoris is believed to occur because these afferent pathways also carry pain fibers from other regions (eg, the arm, neck, and shoulders).
Coronary artery narrowing
Coronary artery narrowing appears to be the etiology of cardiac ischemia in the preponderance of cases. This has clinical significance when atherosclerotic disease diminishes or halts blood flow through the coronary arterial circulation, interfering with normal laminar blood flow. The significance of even a small change in the diameter of a blood vessel can be profound. The Poiseuille law predicts this outcome—the rate of flow is decreased exponentially by any change in the radius of the lumen. As with a smaller pediatric airway, even relatively minute changes in diameter have dramatic consequences in flow rates. Thus, when a lumen is narrowed by one fifth, the flow rate is decreased by about one half. This predicts that even a small change in a coronary artery plaque size can affect the oxygenation through that vessel's territory.
The epicardial vessel, where atherosclerosis often takes place, has the capacity to dilate via autoregulatory mechanisms to respond to increased demand. Angina occurs as this compensatory mechanism is overwhelmed either by large plaques (typically considered 70% or greater obstruction) or by significantly increased myocardial demand.4
Endothelial factors
Endothelial factors also play an important role in angina pectoris. During sympathetic stimulation, the endothelium is subjected to mediators of both vasoconstriction and vasodilatation. Alpha-agonists (catecholamines) directly cause vasoconstriction, while endothelial nitrous oxide synthase creates nitrous oxide (NO), which counteracts this constricting force via vasodilatation.
In the diseased coronary artery, NO production is reduced or absent. In this setting, the catecholamine drive can overwhelm the autoregulatory mechanisms. In addition, the endothelium of the plaque-laden artery may, in itself, be dysfunctional. This limits the ability of the intra-arterial endothelium to produce mediators, which, in a healthy artery, would protect against further vasoconstriction, assist dilatation, and provide protection from platelet aggregation. Small lesions in these vessels may produce incompletely obstructing aggregates of platelets. This would further impede flow through the affected vessel.4
In the diseased heart, these 2 factors, coronary artery narrowing and endothelial dysfunction, synergistically result in reduced oxygen delivery to the myocardium. The net result is angina pectoris.
Extrinsic factors
Extrinsic factors can also play a role in specific circumstances. The oxygen-carrying capacity of blood is based on a number of factors. The most important of which is the amount of hemoglobin. Any alteration in the ability of blood to carry oxygen can precipitate angina. Anemia of any degree can result in anginal symptoms. Given a scenario where demand is increased, such as climbing a flight of stairs, increased stress, or even sexual intercourse, the anginal symptoms may appear.5 Abnormal hemoglobin, such as methemoglobin, carboxyhemoglobin, or any of a number of hemoglobinopathies, creates an environment at greater risk for precipitating angina.
Other extrinsic factors that affect hemoglobin formation, such as lead poisoning or iron-deficiency states, also lead to a similar decrease in oxygen-carrying capacity. Any mechanism that impedes oxygen delivery to the red blood cells has a similar effect. Therefore, any number of pulmonary causes, such as pulmonary embolism, pulmonary fibrosis or scarring, pneumonia, or congestive heart failure, can exacerbate angina. A decreased oxygen environment, such as travel to a higher elevation, has similar consequences due to the decrease in concentration of atmospheric oxygen.
Variant angina
The etiology of variant angina is currently not well understood. Research suggests that inflammatory mediators may result in focal coronary artery vasospasm. Another possibility is that perfusion is decreased through microvascular circulation. Spasm or intermittent narrowing of this microscopic lumen may result in transient areas of hypoperfusion and oxygen deprivation.6
Syndrome X
Syndrome X is the triad of angina pectoris, a positive ECG stress test result, and a normal coronary angiogram. The pathophysiology of this disease is not well understood. Many theories exist as to the underlying pathology. Decreased oxygenation of the underlying myocardium may be the result of impaired vasodilatation, dysfunctional smooth muscle cells, poor or deficient microvascular circulation, or even structural problems on a cellular level (eg, an inappropriately functioning sodium ion channel).6
Frequency
United States
An estimated 6,500,000 people in the United States experience angina pectoris.
Each year 400,000 new cases of angina pectoris develop.
Mortality/Morbidity
More than 479,000 people died from coronary heart disease (both angina and myocardial infarction) in 2003.
The estimated direct and indirect cost for Americans with coronary heart disease in 2006 was $142.5 billion.
Race
The Centers for Disease Control and Prevention (CDC) note that the prevalence of angina and/or coronary heart disease is highest in Hispanics followed by whites and black non-Hispanics (5%, 4.2%, 3.7%, respectively). This information includes the 50 US states, the District of Columbia, Puerto Rico, and the US Virgin Islands.7
Sex
According to National Health and Nutrition Examination Survey (NHANES) data, the age-adjusted prevalence of self-reported angina appears to be higher in woman than in men. Although 2005 CDC data suggest that men (5.5%) have a higher prevalence of angina and/or coronary heart disease than women (3.4%).7
Age
The incidence of new and recurrent angina increases with age but then declines at around 85 years.
Statistics from American Heart Association and Centers for Disease Control and Prevention.
Read more HERE
Tuesday, 29 July 2008
Allergic Rhinitis
Rhinitis is defined as inflammation of the nasal membranes1 and is characterized by a symptom complex that consists of any combination of the following: sneezing, nasal congestion, nasal itching, and rhinorrhea. The eyes, ears, sinuses, and throat can also be involved. Allergic rhinitis is the most common cause of rhinitis. It is an extremely common condition, affecting approximately 20% of the population. While allergic rhinitis is not a life-threatening condition, complications can occur and the condition can significantly impair quality of life, which leads to a number of indirect costs. The total direct and indirect cost of allergic rhinitis was recently estimated to be $5.3 billion per year.
Pathophysiology
Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian tubes, middle ear, sinuses, and pharynx. The nose invariably is involved, and the other organs are affected in certain individuals. Inflammation of the mucous membranes is characterized by a complex interaction of inflammatory mediators but ultimately is triggered by an immunoglobulin E (IgE)–mediated response to an extrinsic protein.
The tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens (proteins capable of causing an allergic reaction) has a genetic component. In susceptible individuals, exposure to certain foreign proteins leads to allergic sensitization, which is characterized by the production of specific IgE directed against these proteins. This specific IgE coats the surface of mast cells, which are present in the nasal mucosa. When the specific protein (eg, a specific pollen grain) is inhaled into the nose, it can bind to the IgE on the mast cells, leading to immediate and delayed release of a number of mediators.
The mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin. The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. These mediators, via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction.
Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages. This results in continued inflammation, termed the late-phase response. The symptoms of the late-phase response are similar to those of the early phase, but less sneezing and itching and more congestion and mucus production tend to occur. The late phase may persist for hours or days.
Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory response. These symptoms often contribute to impaired quality of life.
Frequency
United States
Allergic rhinitis affects approximately 40 million people in the United States. Recent US figures suggest a 20% cumulative prevalence rate.
International
Scandinavian studies have demonstrated a cumulative prevalence rate of 15% in men and 14% in women. The prevalence of allergic rhinitis may vary within and among countries. This may be due to geographic differences in the types and potency of different allergens and the overall aeroallergen burden.
Mortality/Morbidity
While allergic rhinitis itself is not life-threatening (unless accompanied by severe asthma or anaphylaxis), morbidity from the condition can be significant. Allergic rhinitis often coexists with other disorders, such as asthma, and may be associated with asthma exacerbations. It is also associated with otitis media, eustachian tube dysfunction, sinusitis, nasal polyps, allergic conjunctivitis, and atopic dermatitis. Allergic rhinitis may also contribute to learning difficulties, sleep disorders, and fatigue.
A number of complications that can lead to increased morbidity or even mortality can occur secondary to allergic rhinitis. Possible complications include otitis media, eustachian tube dysfunction, acute sinusitis, and chronic sinusitis.
Allergic rhinitis can be associated with a number of comorbid conditions, including asthma, atopic dermatitis, and nasal polyps. Evidence now suggests that uncontrolled allergic rhinitis can actually worsen the inflammation associated with asthma or atopic dermatitis. This could lead to further morbidity and even mortality.
Allergic rhinitis can frequently lead to significant impairment of quality of life. Symptoms such as fatigue, drowsiness (due to the disease or to medications), and malaise can lead to impaired work and school performance, missed school or work days, and traffic accidents. The overall cost (direct and indirect) of allergic rhinitis was recently estimated to be $5.3 billion per year.
Race
Allergic rhinitis occurs in persons of all races. Prevalence of allergic rhinitis seems to vary among different populations and cultures, which may be due to genetic differences, geographic factors or environmental differences, or other population-based factors.
Sex
In childhood, allergic rhinitis is more common in boys than in girls, but in adulthood, the prevalence is approximately equal between men and women.
Age
Onset of allergic rhinitis is common in childhood, adolescence, and early adult years, with a mean age of onset 8-11 years, but allergic rhinitis may occur in persons of any age. In 80% of cases, allergic rhinitis develops by age 20 years. The prevalence of allergic rhinitis has been reported to be as high as 40% in children, subsequently decreasing with age. In the geriatric population, rhinitis is less commonly allergic in nature.
Read further HERE
Pathophysiology
Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian tubes, middle ear, sinuses, and pharynx. The nose invariably is involved, and the other organs are affected in certain individuals. Inflammation of the mucous membranes is characterized by a complex interaction of inflammatory mediators but ultimately is triggered by an immunoglobulin E (IgE)–mediated response to an extrinsic protein.
The tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens (proteins capable of causing an allergic reaction) has a genetic component. In susceptible individuals, exposure to certain foreign proteins leads to allergic sensitization, which is characterized by the production of specific IgE directed against these proteins. This specific IgE coats the surface of mast cells, which are present in the nasal mucosa. When the specific protein (eg, a specific pollen grain) is inhaled into the nose, it can bind to the IgE on the mast cells, leading to immediate and delayed release of a number of mediators.
The mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin. The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. These mediators, via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction.
Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages. This results in continued inflammation, termed the late-phase response. The symptoms of the late-phase response are similar to those of the early phase, but less sneezing and itching and more congestion and mucus production tend to occur. The late phase may persist for hours or days.
Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory response. These symptoms often contribute to impaired quality of life.
Frequency
United States
Allergic rhinitis affects approximately 40 million people in the United States. Recent US figures suggest a 20% cumulative prevalence rate.
International
Scandinavian studies have demonstrated a cumulative prevalence rate of 15% in men and 14% in women. The prevalence of allergic rhinitis may vary within and among countries. This may be due to geographic differences in the types and potency of different allergens and the overall aeroallergen burden.
Mortality/Morbidity
While allergic rhinitis itself is not life-threatening (unless accompanied by severe asthma or anaphylaxis), morbidity from the condition can be significant. Allergic rhinitis often coexists with other disorders, such as asthma, and may be associated with asthma exacerbations. It is also associated with otitis media, eustachian tube dysfunction, sinusitis, nasal polyps, allergic conjunctivitis, and atopic dermatitis. Allergic rhinitis may also contribute to learning difficulties, sleep disorders, and fatigue.
A number of complications that can lead to increased morbidity or even mortality can occur secondary to allergic rhinitis. Possible complications include otitis media, eustachian tube dysfunction, acute sinusitis, and chronic sinusitis.
Allergic rhinitis can be associated with a number of comorbid conditions, including asthma, atopic dermatitis, and nasal polyps. Evidence now suggests that uncontrolled allergic rhinitis can actually worsen the inflammation associated with asthma or atopic dermatitis. This could lead to further morbidity and even mortality.
Allergic rhinitis can frequently lead to significant impairment of quality of life. Symptoms such as fatigue, drowsiness (due to the disease or to medications), and malaise can lead to impaired work and school performance, missed school or work days, and traffic accidents. The overall cost (direct and indirect) of allergic rhinitis was recently estimated to be $5.3 billion per year.
Race
Allergic rhinitis occurs in persons of all races. Prevalence of allergic rhinitis seems to vary among different populations and cultures, which may be due to genetic differences, geographic factors or environmental differences, or other population-based factors.
Sex
In childhood, allergic rhinitis is more common in boys than in girls, but in adulthood, the prevalence is approximately equal between men and women.
Age
Onset of allergic rhinitis is common in childhood, adolescence, and early adult years, with a mean age of onset 8-11 years, but allergic rhinitis may occur in persons of any age. In 80% of cases, allergic rhinitis develops by age 20 years. The prevalence of allergic rhinitis has been reported to be as high as 40% in children, subsequently decreasing with age. In the geriatric population, rhinitis is less commonly allergic in nature.
Read further HERE
Cholera
The word cholera is derived from a Greek term that means "flow of bile." Cholera is caused by Vibrio cholerae, the most feared epidemic diarrheal disease because of its severity. Dehydration and death can occur within hours of infection.
Robert Koch discovered V cholerae in 1883 during an outbreak in Egypt. The organism is a comma-shaped, gram-negative aerobic bacillus whose size varies from 1-3 µm in length by 0.5-0.8 µm in diameter. Its antigenic structure consists of a flagellar H antigen and a somatic O antigen. The differentiation of the latter allows for separation into pathogenic and nonpathogenic strains. V cholerae O1 and V cholerae O139 are associated with epidemic cholera. V cholerae O1 is classified into 2 major biotypes: classic and El Tor. Currently, El Tor is the predominant cholera pathogen. Organisms in both biotypes are subdivided into serotypes according to the structure of the O antigen, as follows:
Serotype Inaba - O antigens A and C
Serotype Ogawa - O antigens A and B
Serotype Hikojima - O antigens A, B, and C
Pathophysiology
The infectious dose of bacteria required to cause clinical disease varies by the mode of administration. If ingested with water, the infectious dose is 103-106 organisms. When ingested with food, fewer organisms (102-104 organisms) are required to produce disease.
The use of antacids, histamine receptor blockers, and proton pump inhibitors increases the risk of cholera infection and predisposes patients to more severe disease as a result of reduced gastric acidity. The same applies to patients with chronic gastritis secondary to Helicobacter pylori infection or those who have undergone a gastrectomy.
V cholerae O1 and V cholerae O139 cause clinical disease by producing an enterotoxin that promotes the secretion of fluid and electrolytes into the lumen of the small intestine. The enterotoxin is a protein molecule composed of 5 B subunits and 2 A subunits. The B subunits are responsible for binding to a ganglioside (monosialosyl ganglioside, GM1) receptor located on the surface of the cells that line the intestinal mucosa.
The activation of the A1 subunit by adenylate cyclase is responsible for the net increase in cyclic adenosine monophosphate (cAMP). cAMP blocks the absorption of sodium and chloride by the microvilli and promotes the secretion of chloride and water by the crypt cells. The result is watery diarrhea with electrolyte concentrations isotonic to those of plasma.
Fluid loss originates in the duodenum and upper jejunum; the ileum is less affected. The colon is usually in a state of absorption because it is relatively insensitive to the toxin. However, the large volume of fluid produced in the upper intestine overwhelms the absorptive capacity of the lower bowel, resulting in severe diarrhea.
The enterotoxin acts locally and does not invade the intestinal wall. As a result, few neutrophils are found in the stool.
Frequency
United States
Among the millions of Americans who travel to endemic areas in foreign countries, only 42 imported cases of cholera were reported from 1965-1991. However, in August 1986, 4 cases of cholera were acquired in Louisiana and 1 case was acquired in Florida. These patients were hospitalized with severe diarrhea and had stool cultures that yielded toxigenic V cholerae O1 Inaba. Although the vehicle of transmission was not specifically identified, the patients had consumed seafood within 5 days prior to symptom onset. Toxigenic V cholerae O1 El Tor Inaba appears to have an environmental reservoir on the US Gulf Coast.
Sixty-one cases of cholera were reported from January 1, 1995, through December 31, 2000, in 18 states and 2 US territories. Thirty-seven were travel-associated cases; the other 24 cases were acquired in the United States.1 Individuals living in the United States most often acquire cholera through travel to cholera-endemic areas or through consumption of undercooked seafood from the Gulf Coast or foreign waters.
In 2005, 12 cases were reported to the World Health Organization (WHO) and, of these, 8 were imported.
International
Since 1817, 7 cholera pandemics have occurred. The first 6 occurred from 1817-1923 and were probably the result of V cholerae O1 of the classic biotype. The pandemics originated in Asia, with subsequent spread to Europe and the Americas.
The seventh pandemic was caused by V cholerae O1 El Tor, which was first isolated in Egypt in 1905. The pandemic originated from the Celebes Islands, Indonesia, in 1961; this pandemic affected more countries and continents than the previous 6 pandemics. The last extension of this pandemic was into Latin America. The total number of cases officially reported from 1997 through March 26, 1998, was 120,867; 89% of these cases were reported in Africa.
In 2002, all regions of the world continued to report cholera caused by V cholerae O1 El Tor; that year, 142,311 cases and 4564 deaths were reported to the WHO by 52 countries. Compared with 2001, the number of reported cases almost doubled.
Between 2002 and 2004, the number of cases reported to the WHO decreased worldwide. In 2005, however, the number reported increased 30% to a total of 131,943 cases in 52 countries.
In October 1992, an epidemic of cholera emerged from Madras, India, as a result of a new serogroup, O139 (also known as Bengal). This Bengal strain has now spread throughout Bangladesh and India and into neighboring countries in Asia. Some experts regard this as an eighth pandemic. Thus far, 11 countries in Southeast Asia have reported isolation of this Vibrio serogroup.
Mortality/Morbidity
If untreated, the disease rapidly results in dehydration and can result in death in more than 50% of infected individuals. The mortality rate is increased in pregnant women and children.
Age
People of all ages are susceptible, although infants are protected through maternally transmitted antibodies during breastfeeding. An attack of the classic biotype of V cholerae usually protects against recurrent infection by either biotype, but El Tor cholera does not protect against further attacks.
Read further HERE
Robert Koch discovered V cholerae in 1883 during an outbreak in Egypt. The organism is a comma-shaped, gram-negative aerobic bacillus whose size varies from 1-3 µm in length by 0.5-0.8 µm in diameter. Its antigenic structure consists of a flagellar H antigen and a somatic O antigen. The differentiation of the latter allows for separation into pathogenic and nonpathogenic strains. V cholerae O1 and V cholerae O139 are associated with epidemic cholera. V cholerae O1 is classified into 2 major biotypes: classic and El Tor. Currently, El Tor is the predominant cholera pathogen. Organisms in both biotypes are subdivided into serotypes according to the structure of the O antigen, as follows:
Serotype Inaba - O antigens A and C
Serotype Ogawa - O antigens A and B
Serotype Hikojima - O antigens A, B, and C
Pathophysiology
The infectious dose of bacteria required to cause clinical disease varies by the mode of administration. If ingested with water, the infectious dose is 103-106 organisms. When ingested with food, fewer organisms (102-104 organisms) are required to produce disease.
The use of antacids, histamine receptor blockers, and proton pump inhibitors increases the risk of cholera infection and predisposes patients to more severe disease as a result of reduced gastric acidity. The same applies to patients with chronic gastritis secondary to Helicobacter pylori infection or those who have undergone a gastrectomy.
V cholerae O1 and V cholerae O139 cause clinical disease by producing an enterotoxin that promotes the secretion of fluid and electrolytes into the lumen of the small intestine. The enterotoxin is a protein molecule composed of 5 B subunits and 2 A subunits. The B subunits are responsible for binding to a ganglioside (monosialosyl ganglioside, GM1) receptor located on the surface of the cells that line the intestinal mucosa.
The activation of the A1 subunit by adenylate cyclase is responsible for the net increase in cyclic adenosine monophosphate (cAMP). cAMP blocks the absorption of sodium and chloride by the microvilli and promotes the secretion of chloride and water by the crypt cells. The result is watery diarrhea with electrolyte concentrations isotonic to those of plasma.
Fluid loss originates in the duodenum and upper jejunum; the ileum is less affected. The colon is usually in a state of absorption because it is relatively insensitive to the toxin. However, the large volume of fluid produced in the upper intestine overwhelms the absorptive capacity of the lower bowel, resulting in severe diarrhea.
The enterotoxin acts locally and does not invade the intestinal wall. As a result, few neutrophils are found in the stool.
Frequency
United States
Among the millions of Americans who travel to endemic areas in foreign countries, only 42 imported cases of cholera were reported from 1965-1991. However, in August 1986, 4 cases of cholera were acquired in Louisiana and 1 case was acquired in Florida. These patients were hospitalized with severe diarrhea and had stool cultures that yielded toxigenic V cholerae O1 Inaba. Although the vehicle of transmission was not specifically identified, the patients had consumed seafood within 5 days prior to symptom onset. Toxigenic V cholerae O1 El Tor Inaba appears to have an environmental reservoir on the US Gulf Coast.
Sixty-one cases of cholera were reported from January 1, 1995, through December 31, 2000, in 18 states and 2 US territories. Thirty-seven were travel-associated cases; the other 24 cases were acquired in the United States.1 Individuals living in the United States most often acquire cholera through travel to cholera-endemic areas or through consumption of undercooked seafood from the Gulf Coast or foreign waters.
In 2005, 12 cases were reported to the World Health Organization (WHO) and, of these, 8 were imported.
International
Since 1817, 7 cholera pandemics have occurred. The first 6 occurred from 1817-1923 and were probably the result of V cholerae O1 of the classic biotype. The pandemics originated in Asia, with subsequent spread to Europe and the Americas.
The seventh pandemic was caused by V cholerae O1 El Tor, which was first isolated in Egypt in 1905. The pandemic originated from the Celebes Islands, Indonesia, in 1961; this pandemic affected more countries and continents than the previous 6 pandemics. The last extension of this pandemic was into Latin America. The total number of cases officially reported from 1997 through March 26, 1998, was 120,867; 89% of these cases were reported in Africa.
In 2002, all regions of the world continued to report cholera caused by V cholerae O1 El Tor; that year, 142,311 cases and 4564 deaths were reported to the WHO by 52 countries. Compared with 2001, the number of reported cases almost doubled.
Between 2002 and 2004, the number of cases reported to the WHO decreased worldwide. In 2005, however, the number reported increased 30% to a total of 131,943 cases in 52 countries.
In October 1992, an epidemic of cholera emerged from Madras, India, as a result of a new serogroup, O139 (also known as Bengal). This Bengal strain has now spread throughout Bangladesh and India and into neighboring countries in Asia. Some experts regard this as an eighth pandemic. Thus far, 11 countries in Southeast Asia have reported isolation of this Vibrio serogroup.
Mortality/Morbidity
If untreated, the disease rapidly results in dehydration and can result in death in more than 50% of infected individuals. The mortality rate is increased in pregnant women and children.
Age
People of all ages are susceptible, although infants are protected through maternally transmitted antibodies during breastfeeding. An attack of the classic biotype of V cholerae usually protects against recurrent infection by either biotype, but El Tor cholera does not protect against further attacks.
Read further HERE
Wednesday, 16 July 2008
Cardiac Cirrhosis
Background
Cardiac cirrhosis (congestive hepatopathy) includes a spectrum of hepatic derangements that occur in the setting of right-sided heart failure. Clinically, the signs and symptoms of congestive heart failure (CHF) dominate the disorder. Unlike cirrhosis caused by chronic alcohol use or viral hepatitis, the effect of cardiac cirrhosis on overall prognosis is unknown. Because of this, treatment is aimed at managing the patient's underlying heart failure.
Distinguish cardiac cirrhosis from ischemic hepatitis. The latter condition may involve massive hepatocellular necrosis caused by sudden cardiogenic shock or other hemodynamic collapse. Typically, sudden and dramatic serum hepatic transaminase elevations lead to its discovery. Although cardiac cirrhosis and ischemic hepatitis arise from distinct underlying cardiac lesions (right-sided heart failure in the former and left-sided failure in the latter), in clinical practice they may present together.
Despite its name, cardiac cirrhosis rarely satisfies strict pathologic criteria for cirrhosis. The terms congestive hepatopathy and chronic passive liver congestion are more accurate, but the name cardiac cirrhosis has become convention.
Pathophysiology
Decompensated right ventricular or biventricular heart failure causes transmission of elevated central venous pressures directly to the liver via the inferior vena cava and hepatic veins. At a cellular level, venous congestion impedes efficient drainage of sinusoidal blood flow into terminal hepatic venules. Sinusoidal stasis results in accumulation of deoxygenated blood, parenchymal atrophy, necrosis, collagen deposition, and, ultimately, fibrosis.
A separate theory proposes that cardiac cirrhosis is not simply a response to chronically increased pressure and sinusoidal stasis. That intrahepatic vascular lesions are confined to areas of the liver with higher fibrotic burden suggests that cardiac cirrhosis requires a higher grade of vascular obstruction, such as intrahepatic thrombosis, for its development. The theory proposes that thrombosis of sinusoids and terminal hepatic venules propagates to medium-sized hepatic veins and to portal vein branches, resulting in parenchymal extinction and fibrosis.
Frequency
United States
Cardiac cirrhosis rarely occurs in the United States. Its true prevalence is difficult to estimate, since the disease typically remains subclinical and undiagnosed. The incidence of cardiac cirrhosis at autopsy has decreased significantly over the past several decades. This may be due to lower rates of uncorrected rheumatic heart disease and constrictive pericardial disease.
Mortality/Morbidity
The effect of cardiac cirrhosis on mortality and morbidity rates is unknown. The severity of the patient's underlying cardiac disease, which is typically advanced and chronic, is the major determinant of overall outcome.
Sex
Comparative sex data for cardiac cirrhosis do not exist. However, because CHF is more common in men than women in the United States, the same is likely for cardiac cirrhosis.
Age
No published data exist. However, the prevalence of cardiac cirrhosis in the United States, like that of CHF, almost certainly increases with age.
Read more HERE
Cardiac cirrhosis (congestive hepatopathy) includes a spectrum of hepatic derangements that occur in the setting of right-sided heart failure. Clinically, the signs and symptoms of congestive heart failure (CHF) dominate the disorder. Unlike cirrhosis caused by chronic alcohol use or viral hepatitis, the effect of cardiac cirrhosis on overall prognosis is unknown. Because of this, treatment is aimed at managing the patient's underlying heart failure.
Distinguish cardiac cirrhosis from ischemic hepatitis. The latter condition may involve massive hepatocellular necrosis caused by sudden cardiogenic shock or other hemodynamic collapse. Typically, sudden and dramatic serum hepatic transaminase elevations lead to its discovery. Although cardiac cirrhosis and ischemic hepatitis arise from distinct underlying cardiac lesions (right-sided heart failure in the former and left-sided failure in the latter), in clinical practice they may present together.
Despite its name, cardiac cirrhosis rarely satisfies strict pathologic criteria for cirrhosis. The terms congestive hepatopathy and chronic passive liver congestion are more accurate, but the name cardiac cirrhosis has become convention.
Pathophysiology
Decompensated right ventricular or biventricular heart failure causes transmission of elevated central venous pressures directly to the liver via the inferior vena cava and hepatic veins. At a cellular level, venous congestion impedes efficient drainage of sinusoidal blood flow into terminal hepatic venules. Sinusoidal stasis results in accumulation of deoxygenated blood, parenchymal atrophy, necrosis, collagen deposition, and, ultimately, fibrosis.
A separate theory proposes that cardiac cirrhosis is not simply a response to chronically increased pressure and sinusoidal stasis. That intrahepatic vascular lesions are confined to areas of the liver with higher fibrotic burden suggests that cardiac cirrhosis requires a higher grade of vascular obstruction, such as intrahepatic thrombosis, for its development. The theory proposes that thrombosis of sinusoids and terminal hepatic venules propagates to medium-sized hepatic veins and to portal vein branches, resulting in parenchymal extinction and fibrosis.
Frequency
United States
Cardiac cirrhosis rarely occurs in the United States. Its true prevalence is difficult to estimate, since the disease typically remains subclinical and undiagnosed. The incidence of cardiac cirrhosis at autopsy has decreased significantly over the past several decades. This may be due to lower rates of uncorrected rheumatic heart disease and constrictive pericardial disease.
Mortality/Morbidity
The effect of cardiac cirrhosis on mortality and morbidity rates is unknown. The severity of the patient's underlying cardiac disease, which is typically advanced and chronic, is the major determinant of overall outcome.
Sex
Comparative sex data for cardiac cirrhosis do not exist. However, because CHF is more common in men than women in the United States, the same is likely for cardiac cirrhosis.
Age
No published data exist. However, the prevalence of cardiac cirrhosis in the United States, like that of CHF, almost certainly increases with age.
Read more HERE
Tuesday, 1 July 2008
Adrenal Carcinoma
Adrenocortical cancers (ACs) are uncommon malignancies that can have protean clinical manifestations. Adrenocortical masses are common; autopsy studies show that approximately 5-15% of the general adult population may have adrenal incidentalomas. Adrenal incidentalomas are biochemically and clinically asymptomatic adrenal masses found incidentally as a result of unrelated imaging investigations such as abdominal CT or MRI scans. Findings from abdominal CT scans suggest that the prevalence rate is 1-5%. Only a small number of adrenal tumors are functional and an even smaller number (approximately 1%) are malignant.
Regardless of size, approximately 1 per 1500 adrenal tumors is malignant. The evaluation of these incidentalomas, therefore, focuses on (1) identifying functional masses and treating them appropriately (including surgical removal); (2) identifying adrenal carcinomas early, with the intent of attempting complete surgical extirpation; and (3) reassuring the patients who do not fit either of these classes and arranging for their subsequent follow-up.
Although the means of identifying ACs from this subpopulation still are controversial, virtually all authorities agree about removing all nonfunctional adrenal tumors larger than or equal to 6 cm because of the significant potential cancer risk. Authorities also generally agree that nonfunctional adrenal tumors (£3 cm) have a very low probability of being adrenal cancer; therefore, they can be removed safely.
The management strategy for adrenal masses larger than 3 cm and less than 6 cm is disputed. Some authorities suggest lowering the threshold for surgical removal of nonfunctional masses from 6 cm to 4-5 cm. Others individualize the follow-up of these patients depending on their clinical status, CT scan characteristics, and age. Particularly important is the fact that these criteria do not apply to children, who generally have smaller ACs. A review of the available data suggests that the incidence rate of malignancy is small Frequency
International
AC tumors are uncommon. The incidence is approximately 0.6-1.67 cases per million persons per year. Some reports suggest an inordinately high frequency (up to 10-fold higher) of cases among children in southern Brazil, for unknown reasons. Overall, AC accounts for 0.02-0.2% of all cancer-related deaths; therefore, it is relatively rare.
Race
AC has no specific racial predilection.
Sex
The female-to-male ratio is approximately 2.5-3:1. Male patients tend to be older and have a worse overall prognosis than female patients. Female patients are more likely than male patients to have an associated endocrine syndrome. Nonfunctional ACs are distributed equally between the sexes.
Age
AC occurs in 2 major peaks: in the first decade of life and again in the fourth to fifth decades. Approximately 75% of the children with AC are younger than 5 years. Functional tumors also are more common in children, while nonfunctional tumors are more common in adults.
Read more HERE
Regardless of size, approximately 1 per 1500 adrenal tumors is malignant. The evaluation of these incidentalomas, therefore, focuses on (1) identifying functional masses and treating them appropriately (including surgical removal); (2) identifying adrenal carcinomas early, with the intent of attempting complete surgical extirpation; and (3) reassuring the patients who do not fit either of these classes and arranging for their subsequent follow-up.
Although the means of identifying ACs from this subpopulation still are controversial, virtually all authorities agree about removing all nonfunctional adrenal tumors larger than or equal to 6 cm because of the significant potential cancer risk. Authorities also generally agree that nonfunctional adrenal tumors (£3 cm) have a very low probability of being adrenal cancer; therefore, they can be removed safely.
The management strategy for adrenal masses larger than 3 cm and less than 6 cm is disputed. Some authorities suggest lowering the threshold for surgical removal of nonfunctional masses from 6 cm to 4-5 cm. Others individualize the follow-up of these patients depending on their clinical status, CT scan characteristics, and age. Particularly important is the fact that these criteria do not apply to children, who generally have smaller ACs. A review of the available data suggests that the incidence rate of malignancy is small Frequency
International
AC tumors are uncommon. The incidence is approximately 0.6-1.67 cases per million persons per year. Some reports suggest an inordinately high frequency (up to 10-fold higher) of cases among children in southern Brazil, for unknown reasons. Overall, AC accounts for 0.02-0.2% of all cancer-related deaths; therefore, it is relatively rare.
Race
AC has no specific racial predilection.
Sex
The female-to-male ratio is approximately 2.5-3:1. Male patients tend to be older and have a worse overall prognosis than female patients. Female patients are more likely than male patients to have an associated endocrine syndrome. Nonfunctional ACs are distributed equally between the sexes.
Age
AC occurs in 2 major peaks: in the first decade of life and again in the fourth to fifth decades. Approximately 75% of the children with AC are younger than 5 years. Functional tumors also are more common in children, while nonfunctional tumors are more common in adults.
Read more HERE
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