West Nile encephalitis

West Nile encephalitis, part of a family of vectorborne diseases that also includes malaria, yellow fever, and Lyme disease, is an infectious disease that primarily causes encephalitis (inflammation) of the brain. It’s caused by the West Nile virus (WNV), a flavivirus commonly found in humans, birds, and other vertebrates in Africa, West Asia, and the Middle East. The first documented cases of WNV in the Western Hemisphere didn’t occur until late in August 1999, when numerous dead birds in the New York, New Jersey, and Connecticut region tested positive for WNV after genetic sequencing. Scientists traced the Western Hemisphere origin of the disease to the vicinity of New York’s Bronx Zoo and believe that mosquitoes feeding on diseased birds helped to spread the disease.
In temperate areas, West Nile encephalitis occurs mainly in the late summer or early fall. In southern climates with milder temperatures, West Nile encephalitis can occur year round.
All persons living in endemic areas carry a risk of contracting West Nile encephalitis, but persons older than age 50 or those with compromised immune systems have the greatest risk.
The mortality rate of West Nile encephalitis is measured by case-fatality rates, which range from 3% to 15% (higher in the elderly population).
WNV is transmitted to humans by the bite of an infected mosquito (primarily the Culex species). Mosquitoes become infected by feeding on infected birds.
Ticks infected with WNV have been found in Africa and Asia, but their role in transmission and maintenance of the virus is uncertain; they aren’t considered vectors for WNV in the United States.
The Centers for Disease Control and Prevention has reported that there’s no evidence that a person can contract the virus from handling live or dead infected birds. However, barehanded contact when Continue reading “West Nile encephalitis”

Introduction to Allergic rhinitis

Allergic rhinitis
 An immune disorder, allergic rhinitis is a reaction to airborne (inhaled) allergens. Depending on the allergen, the resulting rhinitis and conjunctivitis may be seasonal (hay fever) or year-round (perennial allergic rhinitis). Allergic rhinitis is the most common atopic allergic reaction, affecting over 20 million Americans.
Hay fever reflects an immunoglobulin (Ig) E–mediated, type I hypersensitivity response to an environmental antigen (allergen) in a genetically susceptible individual. In most cases, it’s induced by wind-borne pollens: in spring, by tree pollens (oak, elm, maple, alder, birch, cottonwood); in summer, by grass pollens (crabgrass, bluegrass, fescue, and ryegrass); and in fall, by weed pollens (ragweed). Occasionally, hay fever is induced by allergy to fungal spores.
With perennial allergic rhinitis, inhaled allergens provoke antigen responses that produce recurring symptoms year-round.
The major perennial allergens and irritants include dust mites, feather pillows, mold, cigarette smoke, upholstery, and animal dander. Seasonal pollen allergy may exacerbate symptoms of perennial rhinitis.
Signs and symptoms
With seasonal allergic rhinitis, the key signs and symptoms are paroxysmal sneezing, profuse watery rhinorrhea, nasal obstruction or congestion, and pruritus of the nose and eyes, usually accompanied by pale, cyanotic, edematous nasal mucosa; red and edematous eyelids and conjunctivae; excessive lacrimation; and headache or sinus pain. Some patients also complain of itching in the throat and malaise.
With perennial allergic rhinitis, conjunctivitis and other extranasal effects are rare, but chronic nasal obstruction is common and often extends to eustachian tube obstruction, particularly in children.
With both types of allergic rhinitis, dark circles may appear under the patient’s eyes because of venous congestion in the maxillary sinuses. The severity of signs and symptoms may vary from season to season and from year to year.
Some patients may develop chronic complications, including sinusitis and nasal polyps.
Microscopic examination of sputum and nasal secretions reveals large numbers of eosinophils. Blood chemistry studies show normal or elevated IgE levels, possibly linked to seasonal overproduction of interleukin-4 and -5 (involved in the allergic inflammatory process). A firm diagnosis rests on the patient’s personal and family history of allergies and on physical findings during a symptomatic phase. Skin testing, paired with tested responses to environmental stimuli, Continue reading “Introduction to Allergic rhinitis”

Adrenal hypofunction

Primary adrenal hypofunction or insufficiency (Addison’s disease) originates within the adrenal gland itself and is characterized by decreased mineralocorticoid, glucocorticoid, and androgen secretion. Secondary adrenal hypofunction is due to impaired pituitary secretion of corticotropin and is characterized by decreased glucocorticoid secretion. Secretion of aldosterone, the major mineralocorticoid, is often unaffected.
Addison’s disease is relatively uncommon, though it can occur at any age, in either sex. Secondary adrenal hypofunction occurs when a patient abruptly stops taking an exogenous steroid after long-term therapy or when the pituitary is injured by a tumor or by infiltrative or autoimmune processes. With an early diagnosis and adequate replacement therapy, the prognosis for the person with adrenal hypofunction is good.
Adrenal crisis (addisonian crisis), a critical deficiency of mineralocorticoids and glucocorticoids, generally follows acute stress, sepsis, trauma, surgery, or omission of steroid therapy in patients who have chronic adrenal insufficiency. A medical emergency, adrenal crisis necessitates immediate, vigorous treatment.
The following are causes of primary and secondary adrenal hypofunction and adrenal crisis.
Primary hypofunction
Addison’s disease occurs when more than 90% of both adrenal glands are destroyed. Such destruction usually results from an autoimmune process (autoimmune adrenalitis) in which circulating antibodies react specifically against the adrenal tissue.
Other causes include tuberculosis (once the chief cause; now responsible for less than 10% of adult cases), bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, and infections (histoplasmosis, cytomegalovirus). Rarely, a family history of autoimmune disease predisposes the patient to Addison’s disease and other endocrinopathies.
Secondary hypofunction
Secondary hypofunction, which results in glucocorticoid deficiency, can stem from hypopituitarism (causing decreased corticotropin secretion), abrupt withdrawal of long-term corticosteroid therapy (long-term exogenous corticosteroid stimulation suppresses pituitary corticotropin secretion and results in adrenal gland atrophy), or the removal of a corticotropin-secreting tumor. Continue reading “Adrenal hypofunction”

Brief Summary of Acute tubular necrosis

Also known as acute tubulointerstitial nephritis, acute tubular necrosis (ATN) is the most common cause of acute renal failure in critically ill patients, and it accounts for about 75% of all cases of acute renal failure. ATN injures the tubular segment of the nephron, causing renal failure and uremic syndrome. Mortality ranges from 40% to 70%, depending on complications from underlying diseases. Patients with non-oliguric forms of ATN have a better prognosis.
ATN results from ischemic or nephrotoxic injury, most commonly in debilitated patients, such as the critically ill and those who have undergone extensive surgery.
With ischemic injury, disruption of blood flow to the kidneys may result from circulatory collapse, severe hypotension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, or reactions to transfusions. Ischemic ATN can damage the epithelial and basement membranes and can cause lesions in the renal interstitium.
With nephrotoxic injury, damage may follow ingestion of certain chemical agents or result from a hypersensitive reaction of the kidneys. Because nephrotoxic ATN doesn’t damage the basement membrane of the nephron, it’s potentially reversible.
ATN may result from:
  • diseased tubular epithelium that allows leakage of glomerular filtrate across the membranes and reabsorption of filtrate into the blood
  • obstruction of urine flow by the collection of damaged cells, casts, red blood cells (RBCs), and other cellular debris within the tubular walls
  • ischemic injury to glomerular epithelial cells, resulting in cellular collapse and decreased glomerular capillary permeability Continue reading “Brief Summary of Acute tubular necrosis”

Acute Respiratory Distress Syndrome

A form of pulmonary edema that causes acute respiratory failure, acute respiratory distress syndrome (ARDS, shock lung, stiff lung) results from increased permeability of the alveolocapillary membrane. Fluid accumulates in the lung interstitium, alveolar spaces, and small airways, causing the lung to stiffen. Effective ventilation is thus impaired, prohibiting adequate oxygenation of pulmonary capillary blood. Severe ARDS can cause intractable and fatal hypoxemia; however, patients who recover may have little or no permanent lung damage.
ARDS can result from any one of several respiratory and nonrespiratory causes:
  • aspiration of gastric contents
  • sepsis (primarily gram-negative), trauma (lung contusion, head injury, long bone fracture with fat emboli), or oxygen toxicity
  • viral, bacterial, or fungal pneumonia or microemboli (fat or air emboli or disseminated intravascular coagulation)
  • drug overdose (barbiturates, glutethimide, narcotics) or blood transfusion
  • smoke or chemical inhalation (nitrous oxide, chlorine, ammonia)
  • pancreatitis, hypertransfusion, cardiopulmonary bypass
  • near drowning.
Altered permeability of the alveolocapillary membranes causes fluid to accumulate in the interstitial space. If the pulmonary lymphatics can’t remove this fluid, interstitial edema develops. The fluid collects in the peribronchial and peribronchiolar spaces, producing bronchiolar narrowing.
Hypoxemia occurs as a result of fluid accumulation in alveoli and subsequent alveolar collapse, causing the shunting of blood through nonventilated lung regions. In addition, regional differences in compliance and airway narrowing cause regions of low ventilation and inadequate perfusion, which also contribute to hypoxemia.
Signs and symptoms
ARDS initially produces rapid, shallow breathing and dyspnea within hours to days of the initial injury (sometimes after the patient’s condition appears stable). Hypoxemia develops, causing an Continue reading “Acute Respiratory Distress Syndrome”