Tuberculosis (TB)

TUBERCULOSIS (TB)

Tuberculosis or TB (short for Tubercle Bacillus) is a common and often deadly infectious disease caused by mycobacteria, usually Mycobacterium tuberculosis in humans.^[1] Tuberculosis usually attacks the lungs but can also affect other parts of the body. It is spread through the air, when people who have the disease cough, sneeze, or spit. Most infections in humans result in an asymptomatic, latent infection, and about one in ten latent infections eventually progresses to active disease, which, if left untreated, kills more than 50% of its victims.

Watch closely…

TB - Infected

The classic symptoms are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss. Infection of other organs causes a wide range of symptoms.Diagnosis relies on radiology (commonly chest X-rays), a tuberculin skin test, blood tests, as well as microscopic examination and microbiological culture of bodily fluids.Treatment is difficult and requires long courses of multiple antibiotics. Contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in (extensively) multi-drug-resistant tuberculosis. Prevention relies on screening programs and vaccination, usually with Bacillus Calmette-Guérin vaccine.

A third of the world’s population are thought to be infected with M. tuberculosis,^[2] and new infections occur at a rate of about one per second.^[3] The proportion of people who become sick with tuberculosis each year is stable or falling worldwide but, because of population growth, the absolute number of new cases is still increasing.^[3] In 2007 there were an estimated 13.7 million chronic active cases, 9.3 million new cases, and 1.8 million deaths, mostly in developing countries.^[4] In addition, more people in the developed world are contracting tuberculosis because their immune systems are compromised by immunosuppressive drugs, substance abuse, or AIDS. The distribution of tuberculosis is not uniform across the globe; about 80% of the population in many Asian and African countries test positive in tuberculin tests, while only 5-10% of the US population test positive.^[1]

Classification

The current clinical classification system for tuberculosis (TB) is based on the pathogenesis of the disease.^{[citation needed]}

Classification System for TB
Class	Type	Description
0	No TB exposure Not infected	No history of exposure Negative reaction to tuberculin skin test
1	TB exposure No evidence of infection	History of exposure Negative reaction to tuberculin skin test
2	TB infection No disease	Positive reaction to tuberculin skin test Negative bacteriologic studies (if done) No clinical, bacteriologic, or radiographic evidence of TB
3	TB, clinically active	M. tuberculosis cultured (if done) Clinical, bacteriologic, or radiographic evidence of current disease
4	TB Not clinically active	History of episode(s) of TB or Abnormal but stable radiographic findings Positive reaction to the tuberculin skin test Negative bacteriologic studies (if done) and No clinical or radiographic evidence of current disease
5	TB suspect	Diagnosis pending TB disease should be ruled in or out within 3 months

Signs and symptoms

TB-Signs & Symptoms

When the disease becomes active, 75% of the cases are pulmonary TB, that is, TB in the lungs. Symptoms include chest pain, coughing up blood, and a productive, prolonged cough for more than three weeks. Systemic symptoms include fever, chills, night sweats, appetite loss, weight loss, pallor, and often a tendency to fatigue very easily.^[3]

In the other 25% of active cases, the infection moves from the lungs, causing other kinds of TB, collectively denoted extrapulmonary tuberculosis.^[7] This occurs more commonly inimmunosuppressed persons and young children. Extrapulmonary infection sites include the pleura in tuberculosis pleurisy, the central nervous system in meningitis, the lymphatic system in scrofula of the neck, the genitourinary system in urogenital tuberculosis, and bones and joints in Pott’s disease of the spine. An especially serious form is disseminated TB, more commonly known as miliary tuberculosis. Extrapulmonary TB may co-exist with pulmonary TB as well.^[8]

Causes

The primary cause of TB, Mycobacterium tuberculosis, is a small aerobic non-motile bacillus. High lipid content of this pathogen accounts for many of its unique clinical characteristics.^[9] It divides every 16 to 20 hours, an extremely slow rate compared with other bacteria, which usually divide in less than an hour.^[10] (For example, one of the fastest-growing bacteria is a strain of E. coli that can divide roughly every 20 minutes.) Since MTB has a cell wall but lacks a phospholipid outer membrane, it is classified as aGram-positive bacterium. However, if a Gram stain is performed, MTB either stains very weakly Gram-positive or does not retain dye due to the high lipid & mycolic acid content of its cell wall.^[11] MTB can withstand weak disinfectants and survive in a dry state for weeks. In nature, the bacterium can grow only within the cells of a host organism, but M. tuberculosis can be cultured in vitro.^[12]

Using histological stains on expectorate samples from phlegm (also called sputum), scientists can identify MTB under a regular microscope. Since MTB retains certain stains after being treated with acidic solution, it is classified as an acid-fast bacillus (AFB).^[1]^[11] The most common acid-fast staining technique, the Ziehl-Neelsen stain, dyes AFBs a bright red that stands out clearly against a blue background. Other ways to visualize AFBs include an auramine-rhodamine stain and fluorescent microscopy.

The M. tuberculosis complex includes four other TB-causing mycobacteria: M. bovis, M. africanum, M. canetti and M. microti.^[13] M. africanum is not widespread, but in parts of Africa it is a significant cause of tuberculosis.^[14]^[15] M. bovis was once a common cause of tuberculosis, but the introduction of pasteurized milk has largely eliminated this as a public health problem in developed countries.^[1]^[16] M. canetti is rare and seems to be limited to Africa, although a few cases have been seen in African emigrants.^[17] M. microti is mostly seen in immunodeficient people, although it is possible that the prevalence of this pathogen has been underestimated.^[18]

Other known pathogenic mycobacteria include Mycobacterium leprae, Mycobacterium avium and M. kansasii. The last two are part of the nontuberculous mycobacteria (NTM) group. Nontuberculous mycobacteria cause neither TB nor leprosy, but they do cause pulmonary diseases resembling TB.^[19]

Treatment

Treatment for TB uses antibiotics to kill the bacteria. Effective TB treatment is difficult, due to the unusual structure and chemical composition of the mycobacterial cell wall, which makes many antibiotics ineffective and hinders the entry of drugs.^[71]^[72]^[73]^[74] The two antibiotics most commonly used are rifampicin and isoniazid. However, instead of the short course of antibiotics typically used to cure other bacterial infections, TB requires much longer periods of treatment (around 6 to 24 months) to entirely eliminate mycobacteria from the body.^[8] Latent TB treatment usually uses a single antibiotic, while active TB disease is best treated with combinations of several antibiotics, to reduce the risk of the bacteria developing antibiotic resistance.^[75] People with latent infections are treated to prevent them from progressing to active TB disease later in life.

Drug resistant tuberculosis is transmitted in the same way as regular TB. Primary resistance occurs in persons who are infected with a resistant strain of TB. A patient with fully susceptible TB develops secondary resistance (acquired resistance) during TB therapy because of inadequate treatment, not taking the prescribed regimen appropriately, or using low quality medication.^[75] Drug-resistant TB is a public health issue in many developing countries, as treatment is longer and requires more expensive drugs. Multi-drug-resistant tuberculosis (MDR-TB) is defined as resistance to the two most effective first-line TB drugs: rifampicin andisoniazid. Extensively drug-resistant TB (XDR-TB) is also resistant to three or more of the six classes of second-line drugs.^[76] The DOTS (Directly Observed Treatment Short-course) strategy of tuberculosis treatment recommended by WHO was based on clinical trials done in the 1970s by Tuberculosis Research Centre, Chennai, India. The country in which a person with TB lives can determine what treatment they receive. This is because multidrug-resistant tuberculosis is resistant to most first-line medications, the use of alternative treatments, often referred to as “second-line” antituberculosis medications, is necessary to cure the patient. However, the price of these medications is high; thus poor people in the developing world have no or limited access to these treatments.^[77]

Research

The Mycobacterium Tuberculosis Structural Genomics Consortium is a global consortium of scientists conducting research regarding the diagnosis and treatment of tuberculosis. They are attempting to determine the 3-dimensional structures of proteins from M. Tuberculosis.^{[citation needed]}

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Infection of other animals

Tuberculosis can be carried by mammals; domesticated species, such as cats and dogs, are generally free of tuberculosis, but wild animals may be carriers.

Mycobacterium bovis causes TB in cattle. An effort to eradicate bovine tuberculosis from the cattle and deer herds of New Zealand is underway. It has been found that herd infection is more likely in areas where infected natural reservoir such as Australian brush-tailed possums come into contact with domestic livestock at farm/bush borders.^[145] Controlling the vectors through possum eradication and monitoring the level of disease in livestock herds through regular surveillance are seen as a “two-pronged” approach to ridding New Zealand of the disease.

In the Republic of Ireland and the United Kingdom, badgers have been identified as one vector species for the transmission of bovine tuberculosis. As a result, governments have come under pressure from some quarters, primarily dairy farmers, to mount an active campaign of eradication of badgers in certain areas with the purpose of reducing the incidence of bovine TB. The effectiveness of culling on the incidence of TB in cattle is a contentious issue, with proponents and opponents citing their own studies to support their position.^[146]^[147]^[148] For instance, a study by an Independent Study Group on badger culling reported on 18 June 2007 that it was unlikely to be effective and would only make a “modest difference” to the spread of TB and that “badger culling cannot meaningfully contribute to the future control of cattle TB”; in contrast, another report concluded that this policy would have a significant impact.^[149] On 4 July 2008, the UK government decided against a proposed random culling policy.^[150]

References

^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 516–522. ISBN 978-1-4160-2973-1.
^ Jasmer RM, Nahid P, Hopewell PC (December 2002). “Clinical practice. Latent tuberculosis infection”. N. Engl. J. Med. 347 (23): 1860–6. doi:10.1056/NEJMcp021045. PMID 12466511.
^ ^a ^b ^c ^d ^e “Tuberculosis”. World Health Organization. 2007. Retrieved 12 November 2009. Fact sheet N^o 104.
^ ^a ^b ^c World Health Organization (2009). “Epidemiology”. Global tuberculosis control: epidemiology, strategy, financing. pp. 6–33. ISBN 978 92 4 156380 2. Retrieved 12 November 2009.
^ Tuberculosis Symptoms From eMedicineHealth. Author: George Schiffman, MD, FCCP. Last Editorial Review: 1/15/2009
^ Additional symptoms for primary/early pulmonary infection: wrongdiagnosis.com –> Diseases » Tuberculosis » Symptoms Retrieved on 1 June 2009
^ Extrapulmonary Tuberculosis: An Overview MARJORIE P. GOLDEN, M.D., Yale University School of Medicine and Hospital of Saint Raphael, New Haven, Connecticut. HOLENARASIPUR R. VIKRAM, M.D., Mayo Clinic, Scottsdale, Arizona.
^ ^a ^b ^c ^d ^e ^f Centers for Disease Control and Prevention (CDC), Division of Tuberculosis Elimination. Core Curriculum on Tuberculosis: What the Clinician Should Know. 4th edition (2000). Updated August 2003.
^ Southwick, Frederick (10 December 2007). “Chapter 4: Pulmonary Infections”. Infectious Diseases: A Clinical Short Course, 2nd ed.. McGraw-Hill Medical Publishing Division. p. 104. ISBN 0071477225.
^ Cox R (2004). “Quantitative relationships for specific growth rates and macromolecular compositions of Mycobacterium tuberculosis, Streptomyces coelicolor A3(2) and Escherichia coli B/r: an integrative theoretical approach”. Microbiology150 (Pt 5): 1413–26. doi:10.1099/mic.0.26560-0. PMID 15133103.

January 27, 2010 Posted by Engr. Ardy Motos | Blood | 2 Comments

What is Cancer?

Cancer /ˈkænsə(r)/ ( listen) (medical term: malignant neoplasm) is a class of diseases in which a group of cells display uncontrolled growth (division beyond the normal limits), invasion (intrusion on and destruction of adjacent tissues), and sometimes metastasis (spread to other locations in the body via lymph or blood). These three malignant properties of cancers differentiate them from benign tumors, which are self-limited, and do not invade or metastasize. Most cancers form a tumor but some, likeleukemia, do not. The branch of medicine concerned with the study, diagnosis, treatment, and prevention of cancer is oncology.

Cancer affects people at all ages with the risk for most types increasing with age.^[1] Cancer caused about 13% of all human deaths in 2007^[2] (7.6 million).^[3]

Brain Cancer Cell

Cancers are caused by abnormalities in the genetic material of the transformed cells.^[4] These abnormalities may be due to the effects of carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents. Other cancer-promoting genetic abnormalities may randomly occur through errors in DNA replication, or are inherited, and thus present in all cells from birth. The heritability of cancers is usually affected by complex interactions between carcinogens and the host’s genome.

Genetic abnormalities found in cancer typically affect two general classes of genes. Cancer-promoting oncogenes are typically activated in cancer cells, giving those cells new properties, such as hyperactive growth and division, protection against programmed cell death, loss of respect for normal tissue boundaries, and the ability to become established in diverse tissue environments. Tumor suppressor genes are then inactivated in cancer cells, resulting in the loss of normal functions in those cells, such as accurate DNA replication, control over the cell cycle, orientation and adhesion within tissues, and interaction with protective cells of the immune system.

Definitive diagnosis requires the histologic examination of a biopsy specimen, although the initial indication of malignancy can be symptomatic or radiographic imaging abnormalities. Most cancers can be treated and some cured, depending on the specific type, location, and stage. Once diagnosed, cancer is usually treated with a combination of surgery, chemotherapy and radiotherapy. As research develops, treatments are becoming more specific for different varieties of cancer. There has been significant progress in the development of targeted therapy drugs that act specifically on detectable molecular abnormalities in certain tumors, and which minimize damage to normal cells. The prognosis of cancer patients is most influenced by the type of cancer, as well as the stage, or extent of the disease. In addition, histologic grading and the presence of specific molecular markers can also be useful in establishing prognosis, as well as in determining individual treatments.

Classification

Cancers are classified by the type of cell that resembles the tumor and, therefore, the tissue presumed to be the origin of the tumor. These are the histology and the location, respectively. Examples of general categories include:

Carcinoma: Malignant tumors derived from epithelial cells. This group represents the most common cancers, including the common forms of breast, prostate, lung and colon cancer.
Sarcoma: Malignant tumors derived from connective tissue, or mesenchymal cells.
Lymphoma and leukemia: Malignancies derived from hematopoietic (blood-forming) cells
Germ cell tumor: Tumors derived from totipotent cells. In adults most often found in the testicle and ovary; in fetuses, babies, and young children most often found on the body midline, particularly at the tip of the tailbone; in horses most often found at the poll (base of the skull).
Blastic tumor or blastoma: A tumor (usually malignant) which resembles an immature or embryonic tissue. Many of these tumors are most common in children. Tumor – A tumor or tumour is the name for a swelling or lesion formed by an abnormal growth of cells (termed neoplastic).^[1] Tumor is not synonymous with cancer. A tumor can bebenign, pre-malignant or malignant, whereas cancer is by definition malignant. Neoplastic tumor of the cheek skin, here a benign neoplasm of the sweat glands called Hidradenoma. —>>>

How Cancer develop???

Malignant tumors (cancers) are usually named using -carcinoma, -sarcoma or -blastoma as a suffix, with the Latin or Greek word for the organ of origin as the root. For instance, a cancer of the liver is calledhepatocarcinoma; a cancer of the fat cells is called liposarcoma. For common cancers, the English organ name is used. For instance, the most common type of breast cancer is called ductal carcinoma of the breastor mammary ductal carcinoma. Here, the adjective ductal refers to the appearance of the cancer under the microscope, resembling normal breast ducts.

Benign tumors (which are not cancers) are named using -oma as a suffix with the organ name as the root. For instance, a benign tumor of the smooth muscle of the uterus is called leiomyoma (the common name of this frequent tumor is fibroid). Unfortunately, some cancers also use the -oma suffix, examples being melanoma and seminoma.

Signs and symptoms

Roughly, cancer symptoms can be divided into three groups:

Local symptoms: unusual lumps or swelling (tumor), hemorrhage (bleeding), pain and/or ulceration. Compression of surrounding tissues may cause symptoms such as jaundice(yellowing the eyes and skin).
Symptoms of metastasis (spreading): enlarged lymph nodes, cough and hemoptysis, hepatomegaly (enlarged liver), bone pain, fracture of affected bones and neurologicalsymptoms. Although advanced cancer may cause pain, it is often not the first symptom.
Systemic symptoms: weight loss, poor appetite, fatigue and cachexia (wasting), excessive sweating (night sweats), anemia and specific paraneoplastic phenomena, i.e. specific conditions that are due to an active cancer, such as thrombosis or hormonal changes.

Every symptom in the above list can be caused by a variety of conditions (a list of which is referred to as the differential diagnosis). Cancer may be a common or uncommon cause of each item.

Causes

Active Cancer Cell inside the body!

Cancer is a diverse class of diseases which differ widely in their causes and biology. Any organism, even plants, can acquire cancer. Nearly all known cancers arise gradually, as errors build up in the cancer cell and its progeny (see mechanisms section for common types of errors).

Anything which replicates (our cells) will probabilistically suffer from errors (mutations). Unless error correction and prevention is properly carried out, the errors will survive, and might be passed along to daughter cells. Normally, the body safeguards against cancer via numerous methods, such as: apoptosis, helper molecules (some DNA polymerases), possibly senescence, etc. However these error-correction methods often fail in small ways, especially in environments that make errors more likely to arise and propagate. For example, such environments can include the presence of disruptive substances called carcinogens, or periodic injury (physical, heat, etc.), or environments that cells did not evolve to withstand, such as hypoxia^[5] (see subsections). Cancer is thus aprogressive disease, and these progressive errors slowly accumulate until a cell begins to act contrary to its function in the animal.

The errors which cause cancer are often self-amplifying, eventually compounding at an exponential rate. For example:

A mutation in the error-correcting machinery of a cell might cause that cell and its children to accumulate errors more rapidly
A mutation in signaling (endocrine) machinery of the cell can send error-causing signals to nearby cells
A mutation might cause cells to become neoplastic, causing them to migrate and disrupt more healthy cells
A mutation may cause the cell to become immortal (see telomeres), causing them to disrupt healthy cells forever

Cancer Cell being attached by the immune system!

Thus cancer often explodes in something akin to a chain reaction caused by a few errors, which compound into more severe errors. Errors which produce more errors are effectively the root cause of cancer, and also the reason that cancer is so hard to treat: even if there were 10,000,000,000 cancerous cells and one killed all but 10 of those cells, those cells (and other error-prone precancerous cells) could still self-replicate or send error-causing signals to other cells, starting the process over again. This rebellion-like scenario is an undesirable survival of the fittest, where the driving forces of evolution itself work against the body’s design and enforcement of order. In fact, once cancer has begun to develop, this same force continues to drive the progression of cancer towards more invasive stages, and is called clonal evolution.^[6]

Research about cancer causes often falls into the following categories:

Agents (e.g. viruses) and events (e.g. mutations) which cause or facilitate genetic changes in cells destined to become cancer.
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The precise nature of the genetic damage, and the genes which are affected by it.
The consequences of those genetic changes on the biology of the cell, both in generating the defining properties of a cancer cell, and in facilitating additional genetic events which lead to further progression of the cancer.

Pathophysiology

Cancer is fundamentally a disease of regulation of tissue growth. In order for a normal cell to transform into a cancer cell, genes which regulate cell growth and differentiation must be altered.^[29] Genetic changes can occur at many levels, from gain or loss of entire chromosomes to a mutation affecting a single DNA nucleotide. There are two broad categories of genes which are affected by these changes. Oncogenes may be normal genes which are expressed at inappropriately high levels, or altered genes which have novel properties. In either case, expression of these genes promotes the malignant phenotype of cancer cells. Tumor suppressor genes are genes which inhibit cell division, survival, or other properties of cancer cells. Tumor suppressor genes are often disabled by cancer-promoting genetic changes. Typically, changes in many genes are required to transform a normal cell into a cancer cell.^[30]

There is a diverse classification scheme for the various genomic changes which may contribute to the generation of cancer cells. Most of these changes are mutations, or changes in the nucleotide sequence of genomic DNA. Aneuploidy, the presence of an abnormal number of chromosomes, is one genomic change which is not a mutation, and may involve either gain or loss of one or more chromosomes through errors in mitosis.

Large-scale mutations involve the deletion or gain of a portion of a chromosome. Genomic amplification occurs when a cell gains many copies (often 20 or more) of a small chromosomal locus, usually containing one or more oncogenes and adjacent genetic material. Translocation occurs when two separate chromosomal regions become abnormally fused, often at a characteristic location. A well-known example of this is the Philadelphia chromosome, or translocation of chromosomes 9 and 22, which occurs in chronic myelogenous leukemia, and results in production of the BCR-abl fusion protein, an oncogenic tyrosine kinase.

Small-scale mutations include point mutations, deletions, and insertions, which may occur in the promoter of a gene and affect its expression, or may occur in the gene’s coding sequence and alter the function or stability of its protein product. Disruption of a single gene may also result from integration of genomic material from a DNA virus or retrovirus, and such an event may also result in the expression of viral oncogenes in the affected cell and its descendants.

Glossary

The following closely related terms may be used to designate abnormal growths:

Tumor or tumour: originally, it meant any abnormal swelling, lump or mass. In current English, however, the word tumor has become synonymous with neoplasm, specifically solid neoplasm. Note that some neoplasms, such as leukemia, do not form tumors.
Neoplasm: the scientific term to describe an abnormal proliferation of genetically altered cells. Neoplasms can be benign or malignant:
- Malignant neoplasm or malignant tumor: synonymous with cancer.
- Benign neoplasm or benign tumor: a tumor (solid neoplasm) that stops growing by itself, does not invade other tissues and does not form metastases.
Invasive tumor is another synonym of cancer. The name refers to invasion of surrounding tissues.
Pre-malignancy, pre-cancer or non-invasive tumor: A neoplasm that is not invasive but has the potential to progress to cancer (become invasive) if left untreated. These lesions are, in order of increasing potential for cancer, atypia, dysplasia and carcinoma in situ.

The following terms can be used to describe a cancer:

Screening: a test done on healthy people to detect tumors before they become apparent. A mammogram is a screening test.
Diagnosis: the confirmation of the cancerous nature of a lump. This usually requires a biopsy or removal of the tumor by surgery, followed by examination by a pathologist.
Surgical excision: the removal of a tumor by a surgeon.
- Surgical margins: the evaluation by a pathologist of the edges of the tissue removed by the surgeon to determine if the tumor was removed completely (“negative margins”) or if tumor was left behind (“positive margins”).
Grade: a number (usually on a scale of 3) established by a pathologist to describe the degree of resemblance of the tumor to the surrounding benign tissue.
Stage: a number (usually on a scale of 4) established by the oncologist to describe the degree of invasion of the body by the tumor.
Recurrence: new tumors that appear at the site of the original tumor after surgery.
Metastasis: new tumors that appear far from the original tumor.
Median survival time: a period of time, often measured in months or years, over which 50% of the cancer patients are expected to be alive.^[93]
Transformation: the concept that a low-grade tumor transforms to a high-grade tumor over time. Example: Richter’s transformation.
Chemotherapy: treatment with drugs.
Radiation therapy: treatment with radiations.
Adjuvant therapy: treatment, either chemotherapy or radiation therapy, given after surgery to kill the remaining cancer cells.
Prognosis: the probability of cure after the therapy. It is usually expressed as a probability of survival five years after diagnosis. Alternatively, it can be expressed as the number of years when 50% of the patients are still alive. Both numbers are derived from statistics accumulated with hundreds of similar patients to give a Kaplan-Meier curve.
Cure: A cancer patient is “cured” if they live past the time by which 95% of treated patients live after the date of their diagnosis of cancer. This period varies among different types of cancer; for example, in the case of Hodgkin’s disease this period of time is 10 years, whereas for Burkitt’s lymphoma this period would be 1 year.^[94] The phrase “cure” used in oncology is based upon the statistical concept of a median survival time and disease-free median survival time.^[95]

Notes

^ Cancer Research UK (January 2007). “UK cancer incidence statistics by age”. Retrieved 2007-06-25.
^ WHO (February 2006). “Cancer”. World Health Organization. Retrieved 2007-06-25.
^ American Cancer Society (December 2007). “Report sees 7.6 million global 2007 cancer deaths”. Reuters. Retrieved 2008-08-07.
^ Kinzler, Kenneth W.; Vogelstein, Bert (2002). “Introduction”. The genetic basis of human cancer (2nd, illustrated, revised ed.). New York: McGraw-Hill, Medical Pub. Division. p. 5. ISBN 978-0-07-137050-9.
^ Nelson DA, Tan TT, Rabson AB, Anderson D, Degenhardt K, White E (September 2004). “Hypoxia and defective apoptosis drive genomic instability and tumorigenesis”. Genes & Development 18 (17): 2095–107. doi:10.1101/gad.1204904. PMID 15314031.
^ Merlo LM, Pepper JW, Reid BJ, Maley CC (December 2006). “Cancer as an evolutionary and ecological process”. Nat. Rev. Cancer 6 (12): 924–35. doi:10.1038/nrc2013. PMID 17109012.
^ ^a ^b Sasco AJ, Secretan MB, Straif K (August 2004). “Tobacco smoking and cancer: a brief review of recent epidemiological evidence”. Lung cancer (Amsterdam, Netherlands) 45 Suppl 2: S3–9. doi:10.1016/j.lungcan.2004.07.998. PMID 15552776.
^ Biesalski HK, Bueno de Mesquita B, Chesson A, et al. (1998). “European Consensus Statement on Lung Cancer: risk factors and prevention. Lung Cancer Panel”. CA: a cancer journal for clinicians 48 (3): 167–76; discussion 164–6.doi:10.3322/canjclin.48.3.167. PMID 9594919.
^ O’Reilly KM, Mclaughlin AM, Beckett WS, Sime PJ (March 2007). “Asbestos-related lung disease”. American family physician 75 (5): 683–8. PMID 17375514.
^ Seitz HK, Pöschl G, Simanowski UA (1998). “Alcohol and cancer”. Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism 14: 67–95. PMID 9751943.

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Cells, Liver, Lungs | Leave a Comment

Sleep Disorders

SLEEP DISORDERS:

A sleep disorder (somnipathy) is a medical disorder of the sleep patterns of a person or animal. Some sleep disorders are serious enough to interfere with normal physical, mental and emotional functioning. A test commonly ordered for some sleep disorders is the polysomnogram.

Common sleep disorders

The most common sleep disorders include:

Primary insomnia: Chronic difficulty in falling asleep and/or maintaining sleep when no other cause is found for these symptoms.
Bruxism: Involuntarily grinding or clenching of the teeth while sleeping
Delayed sleep phase syndrome (DSPS): inability to awaken and fall asleep at socially acceptable times but no problem with sleep maintenance, a disorder of circadian rhythms. Other such disorders are advanced sleep phase syndrome (ASPS) and Non-24-hour sleep-wake syndrome (Non-24), both much less common than DSPS.
Hypopnea syndrome: Abnormally shallow breathing or slow respiratory rate while sleeping
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Narcolepsy: Excessive daytime sleepiness (EDS) often culminating in falling asleep spontaneously but unwillingly at inappropriate times.
Cataplexy, a sudden weakness in the motor muscles that can result in collapse to the floor.
Night terror, Pavor nocturnus, sleep terror disorder: abrupt awakening from sleep with behavior consistent with terror
Parasomnias: Disruptive sleep-related events involving inappropriate actions during sleep stages – sleep walking and night-terrors are examples.
Periodic limb movement disorder (PLMD): Sudden involuntary movement of arms and/or legs during sleep, for example kicking the legs. Also known as nocturnal myoclonus. See also Hypnic jerk, which is not a disorder.
Rapid eye movement behavior disorder (RBD): Acting out violent or dramatic dreams while in REM sleep
Restless legs syndrome (RLS): An irresistible urge to move legs. RLS sufferers often also have PLMD.
Situational circadian rhythm sleep disorders: shift work sleep disorder (SWSD) and jet lag
Obstructive sleep apnea: Obstruction of the airway during sleep, causing lack of sufficient deep sleep; often accompanied by snoring. Other forms of sleep apnea are less common.
Sleep paralysis is characterized by temporary paralysis of the body shortly before or after sleep. Sleep paralysis may be accompanied byvisual, auditory or tactile hallucinations. Not a disorder unless severe. Often seen as part of Narcolepsy.
Sleepwalking or somnambulism: Engaging in activities that are normally associated with wakefulness (such as eating or dressing), which may include walking, without the conscious knowledge of the subject.
Nocturia: A frequent need to get up and go to the bathroom to urinate at night. It differs from Enuresis, or bed-wetting, in which the person does not arouse from sleep, but the bladder nevertheless empties.[1]
Somniphobia, a dread of sleep

General principles of treatment

Treatments for sleep disorders generally can be grouped into four categories:

behavioral/ psychotherapeutic treatments
rehabilitation/management
medications
other somatic treatments

None of these general approaches is sufficient for all patients with sleep disorders. Rather, the choice of a specific treatment depends on the patient’s diagnosis, medical and psychiatric history, and preferences, as well as the expertise of the treating clinician. Often, behavioral/psychotherapeutic and pharmacological approaches are not incompatible and can effectively be combined to maximize therapeutic benefits. Management of sleep disturbances that are secondary to mental, medical, or substance abuse disorders should focus on the underlying conditions.

Sleep medicine

Due to rapidly increasing knowledge about sleep in the 20th century, including the discovery of REM sleep and sleep apnea, the medical importance of sleep was recognized. The medical community began paying more attention than previously to primary sleep disorders, such as sleep apnea, as well as the role and quality of sleep in other conditions. By the 1970s in the USA, clinics and laboratories devoted to the study of sleep and sleep disorders had been founded, and a need for standards arose.

Sleep Medicine is now a recognized subspecialty within internal medicine, family medicine, pediatrics, otolaryngology, psychiatry and neurology in the United States. Certification in Sleep Medicine shows that the specialist:

“has demonstrated expertise in the diagnosis and management of clinical conditions that occur during sleep, that disturb sleep, or that are affected by disturbances in the wake-sleep cycle. This specialist is skilled in the analysis and interpretation of comprehensive polysomnography, and well-versed in emerging research and management of a sleep laboratory.”^[3]

Competence in sleep medicine requires an understanding of a myriad of very diverse disorders, many of which present with similar symptoms such as excessive daytime sleepiness, which, in the absence of volitional sleep deprivation, “is almost inevitably caused by an identifiable and treatable sleep disorder”, such as sleep apnea, narcolepsy, idiopathic central nervous system (CNS) hypersomnia, Kleine-Levin syndrome, menstrual-related hypersomnia, idiopathic recurrent stupor, or circadian rhythm disturbances.^[4]Another common complaint is insomnia, a set of symptoms which can have a great many different causes, physical and mental. Management in the varying situations differs greatly and cannot be undertaken without a correct diagnosis.

Sleep dentistry (bruxism, snoring and sleep apnea), while not recognized as one of the nine dental specialties, qualifies for board-certification by the American Board of Dental Sleep Medicine (ABDSM). The resulting Diplomate status is recognized by the American Academy of Sleep Medicine (AASM), and these dentists are organized in the Academy of Dental Sleep Medicine (USA).^[5] The qualified dentists collaborate with sleep physicians at accredited sleep centers and can provide oral appliance therapy and upper airway surgery to treat or manage sleep-related breathing disorders.^[6]

In the UK, knowledge of sleep medicine and possibilities for diagnosis and treatment seem to lag. Guardian.co.uk quotes the director of the Imperial College Healthcare Sleep Centre: “One problem is that there has been relatively little training in sleep medicine in this country – certainly there is no structured training for sleep physicians.”^[7] The Imperial College Healthcare site^[8] shows attention to obstructive sleep apnea syndrome (OSA) and very few other sleep disorders.

References

^ www.sleepfoundation.org
^ Ivanenko A and Massey C (October 1, 2006). “Assessment and Management of Sleep Disorders in Children”. Psychiatric Times 23 (11).
^ “American Board of Medical Specialties : Recognized Physician Specialty and Subspecialty Certificates”. Retrieved 2008-07-21.
^ Mahowald, M.W. (March 2000). “What is causing excessive daytime sleepiness?: evaluation to distinguish sleep deprivation from sleep disorders” (Online, full text). Postgraduate Medicine 107 (3): 108–23. doi:10.3810/pgm.2000.03.932. Retrieved 2008-07-27.
^ “About AADSM”. Academy of Dental Sleep Medicine. 2008. Retrieved 2008-07-22.
^ “About the ADBSM”. American Board of Dental Sleep Medicine. Retrieved 2008-07-22.
^ Wollenberg, Anne (July 28 2008). “Time to wake up to sleep disorders”. Guardian News and Media Limited. Retrieved 2008-08-03.
^ “Sleep services”. Imperial College Healthcare NHS Trust. 2008. Retrieved 2008-08-02.

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Brain, Cells, Eyes, Heart | 1 Comment

Breast Cancer

Breast Cancer:

Breast cancer is a cancer that starts in the breast, usually in the inner lining of the milk ducts or lobules. There are different types of breast cancer, with different stages (spread), aggressiveness, and genetic makeup. With best treatment, 10-year disease-free survival varies from 98% to 10%. Treatment includes surgery, drugs (hormone therapy and chemotherapy), and radiation.[1].

Worldwide, breast cancer is the second most common type of cancer after lung cancer (10.4% of all cancer incidence, both sexes counted)[2] and the fifth most common cause of cancer death.[3] In 2004, breast cancer caused 519,000 deaths worldwide (7% of cancer deaths; almost 1% of all deaths).[3] Breast cancer is about 100 times as frequent among women as among men, but survival rates are equal in both sexes.

Click Here to see the image of Chronic Breast Cancer

Signs and symptoms

The first symptom, or subjective sign, of breast cancer is typically a lump that feels different from the surrounding breast tissue. According to the The Merck Manual, more than 80% of breast cancer cases are discovered when the woman feels a lump.[11] According to the American Cancer Society, the first medical sign, or objective indication of breast cancer as detected by a physician, is discovered bymammogram.[12] Lumps found in lymph nodes located in the armpits[11] can also indicate breast cancer.

Mammograms showing a normal breast (left) and a breast cancer (right).

Indications of breast cancer other than a lump may include changes in breast size or shape, skin dimpling, nipple inversion, or spontaneous single-nipple discharge. Pain (“mastodynia“) is an unreliable tool in determining the presence or absence of breast cancer, but may be indicative of other breast health issues.[11][12][13]

When breast cancer cells invade the dermal lymphatics—small lymph vessels in the skin of the breast—its presentation can resemble skin inflammation and thus is known as inflammatory breast cancer (IBC). Symptoms of inflammatory breast cancer include pain, swelling, warmth and redness throughout the breast, as well as an orange-peel texture to the skin referred to as peau d’orange.[11]

Another reported symptom complex of breast cancer is Paget’s disease of the breast. This syndrome presents as eczematoid skin changes such as redness and mild flaking of the nipple skin. As Paget’s advances, symptoms may include tingling, itching, increased sensitivity, burning, and pain. There may also be discharge from the nipple. Approximately half of women diagnosed with Paget’s also have a lump in the breast.[14]

Occasionally, breast cancer presents as metastatic disease, that is, cancer that has spread beyond the original organ. Metastatic breast cancer will cause symptoms that depend on the location of metastasis. Common sites of metastasis include bone, liver, lung and brain.[15] Unexplained weight loss can occasionally herald an occult breast cancer, as can symptoms of fevers or chills. Bone or joint pains can sometimes be manifestations of metastatic breast cancer, as can jaundice or neurological symptoms. These symptoms are “non-specific”, meaning they can also be manifestations of many other illnesses.[16]

Most symptoms of breast disorder do not turn out to represent underlying breast cancer. Benign breast diseases such as mastitis andfibroadenoma of the breast are more common causes of breast disorder symptoms. The appearance of a new symptom should be taken seriously by both patients and their doctors, because of the possibility of an underlying breast cancer at almost any age.

Risk factors

The primary risk factors that have been identified are sex,^[21] age,^[22] lack of childbearing or breastfeeding,^[23]^[24] and higher hormone levels,^[25] ^[26].

In a study published in 1995, well-established risk factors accounted for 47% of cases while only 5% were attributable to hereditary syndromes.^[27] In particular, carriers of the breast cancer susceptibility genes,BRCA1 and BRCA2, are at a 30-40% increased risk for breast and ovarian cancer, depending on in which portion of the protein the mutation occurs.^[28].

In more recent years, research has indicated the impact of diet and other behaviors on breast cancer. These additional risk factors include a high-fat diet,^[29] alcohol intake,^[30]^[31] obesity,^[32] and environmental factors such as tobacco use, radiation^[33], endocrine disruptors and shiftwork.^[34] Although the radiation from mammography is a low dose, the cumulative effect can cause cancer.^[35] ^[36]

In addition to the risk factors specified above, demographic and medical risk factors include:

Personal history of breast cancer: A woman who had breast cancer in one breast has an increased risk of getting cancer in her other breast.
Family history: A woman’s risk of breast cancer is higher if her mother, sister, or daughter had breast cancer. The risk is higher if her family member got breast cancer before age 40. Having other relatives with breast cancer (in either her mother’s or father’s family) may also increase a woman’s risk.
Certain breast changes: Some women have cells in the breast that look abnormal under a microscope. Having certain types of abnormal cells (atypical hyperplasia and lobular carcinoma in situ [LCIS]) increases the risk of breast cancer.
Race: Breast cancer is diagnosed more often in Caucasian women than Latina, Asian, or African American women.

Abortion has not been found to be a risk factor for breast cancer. The breast cancer abortion hypothesis, however, continues to be promoted by some pro-life groups.^[37]^[38]^[39]

The United Kingdom is the member of International Cancer Genome Consortium that is leading efforts to map breast cancer’s complete genome.

.

Pathophysiology

Breast cancer, like other cancers, occurs because of an interaction between the environment and a defective gene. Normal cells divide as many times as needed and stop. They attach to other cells and stay in place in tissues. Cells become cancerous when mutations destroy their ability to stop dividing, to attach to other cells and to stay where they belong. When cells divide, their DNA is normally copied with many mistakes. Error-correcting proteins fix those mistakes. The mutations known to cause cancer, such as p53,BRCA1 and BRCA2, occur in the error-correcting mechanisms. These mutations are either inherited or acquired after birth. Presumably, they allow the other mutations, which allow uncontrolled division, lack of attachment, and metastasis to distant organs.^[33]^[40] Normal cells will commit cell suicide (apoptosis) when they are no longer needed. Until then, they are protected from cell suicide by several protein clusers and pathways. One of the protective pathways is the PI3K/AKT pathway; another is the RAS/MEK/ERK pathway. Sometimes the genes along these protective pathways are mutated in a way that turns them permanently “on”, rendering the cell incapable of committing suicide when it is no longer needed. This is one of the steps that causes cancer in combination with other mutations. Normally, the PTEN protein turns off the PI3K/AKT pathway when the cell is ready for cell suicide. In some breast cancers, the gene for the PTEN protein is mutated, so the PI3K/AKT pathway is stuck in the “on” position, and the cancer cell does not commit suicide.^[41]

Society and culture

The widespread acceptance of second opinions before surgery, less invasive surgical procedures, support groups, and other advances in patient care have stemmed, in part, from the breast cancer advocacy movement.^[87]

October is recognized as National Breast Cancer Awareness Month by the media as well as survivors, family and friends of survivors and/or victims of the disease.^[88] A pink ribbon is worn to recognize the struggle that sufferers face when battling with the cancer.^[89]

The patron saint of breast cancer is Agatha of Sicily.^[90]

In the fall of 1991, Susan G. Komen for the Cure handed out pink ribbons to participants in its New York City race for breast cancer survivors. ^[91]

The pink and blue ribbon was designed in 1996 by Nancy Nick, President and Founder of the John W. Nick Foundation to bring awareness that “Men Get Breast Cancer Too!”^[92]
In 2009 the male breast cancer advocacy groups Out of the Shadow of Pink, A Man’s Pink and the Brandon Greening Foundation for Breast Cancer in Men joined together to globally establish the third week of October as “Male Breast Cancer Awareness Week”^[93]

References

^ “Merck Manual Online, Breast Cancer”.
^ CancerMath.net Calculates survival with breast cancer based on prognostic factors and treatment. From the Laboratory for Quantitative Medicine, Massachusetts General Hospital.
^ ^a ^b “World Cancer Report”. International Agency for Research on Cancer. June 2003. Retrieved 2009-03-26.
^ ^a ^b “Fact sheet No. 297: Cancer”. World Health Organization. February 2006. Retrieved 2009-03-26.
^ “Male Breast Cancer Treatment”. National Cancer Institute. 2006. Retrieved 2006-10-16.
^ “Breast Cancer in Men”. Cancer Research UK. 2007. Retrieved 2007-11-06.
^ “What Are the Key Statistics About Breast Cancer in Men?”. American Cancer Society. September 27, 2007. Retrieved 2008-02-03.
^ Muss HB, Berry DA, Cirrincione CT, et al. Adjuvant chemotherapy in older women with early-stage breast cancer. N Engl J Med. 2009 May 14;360(20):2055-65.
^ Buchholz TA. N Engl J Med. 2009 Jan 1;360(1):63-70. Radiation therapy for early-stage breast cancer after breast-conserving surgery.
^ Merck Manual, Professional Edition, Ch. 253, Breast Cancer.

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Cancers, Cells, Muscles | Leave a Comment

Goiter

GOITER:

A goitre (BrE), or goiter (AmE) (Latin gutteria, struma), also called a bronchocele, is a swelling in the thyroid gland,[1] which can lead to a swelling of the neck or larynx (voice box). Goitre usually occurs when the thyroid gland is not functioning properly.

Classification

They are classified in different ways:

A “diffuse goiter” is a goiter that has spread through all of the thyroid (and can be a “simple goitre”, or a “multinodular goitre”).
“Toxic goiter” refers to goiter with hyperthyroidism. These most commonly due to Graves’ disease, but can be caused by inflammation or a multinodular goiter.
“Nontoxic goiter” (associated with normal or low thyroid levels) refers to all other types (such as that caused by lithium or certain otherautoimmune diseases).

Other type of classification:

I – palpation struma – in normal posture of head it cannot be seen. Only found when palpating.
II – struma is palpative and can be easily seen.
III – struma is very big and is retrosternal. Pressure and compression marks.

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Causes

Worldwide, the most common cause for goiter is iodine deficiency. In countries that use iodized salt, Hashimoto’s thyroiditis becomes the most common cause.

Other causes are:

Hypothyroid

Inborn errors of thyroid hormone synthesis, causing congenital hypothyroidism (E03.0)
Ingestion of goitrogens, such as cassava.
Side-effects of pharmacological therapy (E03.2)

Hyperthyroid

Graves’ disease (E05.0)
Thyroiditis (acute, chronic) (E06)
Thyroid cancer

Symptoms

In general, goiter unassociated with any hormonal abnormalities will not cause any symptoms aside from the presence of anterior neck mass. However, for particularly large masses, compression of the local structures may result in difficulty in breathing or swallowing. In those presenting with these symptoms, malignancy must be considered.

Meanwhile, toxic goiters will present with symptoms of thyrotoxicosis such as palpitations, hyperactivity, weight loss despite increased appetite, and heat intolerance.

Treatment

Treatment may not be necessary if the goiter is small. Goiter may be related to hyper- and hypothyroidism (especially Graves’ disease) and may be reversed by treatment. Graves’ disease can be corrected with antithyroid drugs (such as propylthiouracil and methimazole), thyroidectomy (surgical removal of the thyroid gland), and iodine-131 (¹³¹I – a radioactive isotope of iodine that is absorbed by the thyroid gland and destroys it). Hypothyroidism may raise the risk of goitre because it usually increases the production of TRH and TSH. Levothyroxine, used to treat hypothyroidism, can also be used in euthyroid patients for the treatment of goitre. Levothyroxine suppressive therapy decreases the production of TRH and TSH and may reduce goitre, thyroid nodules, and thyroid cancer. Blood tests are needed to ensure that TSH is still in range and the patient has not become subclinically hyperthyroid. If TSH levels are not carefully monitored, it is alleged that levothyroxine may increase the risk of osteoporosis but no peer reviewed studies on levothyroxine replacement of Hypothyroid patients causing this effect have actually been produced.

Thyroidectomy with ¹³¹I may be necessary in euthyroid goitrous patients who do not respond to levothyroxine treatment, especially if the patients have difficulty breathing or swallowing. ¹³¹I, with or without the pre-injection of synthetic TSH, can relieve obstruction and reduce the size of the goitre by thirty to sixty-five percent. Depending on how large the goiter is and how much of the thyroid gland must be removed or destroyed, thyroidectomy or ¹³¹ may produce hypothyroidism requiring life-long treatment and may eventually lead to death.

References

^ goiter at Dorland’s Medical Dictionary
^ “Mortality and Burden of Disease Estimates for WHO Member States in 2002″ (xls). World Health Organization. 2002.
^ Temple, Robert. (1986). The Genius of China: 3,000 Years of Science, Discovery, and Invention. With a forward by Joseph Needham. New York: Simon and Schuster, Inc. ISBN 0671620282. Pages 133–134.
^ Temple, Robert. (1986). The Genius of China: 3,000 Years of Science, Discovery, and Invention. With a forward by Joseph Needham. New York: Simon and Schuster, Inc. ISBN 0671620282. Page 134.
^ Temple, Robert. (1986). The Genius of China: 3,000 Years of Science, Discovery, and Invention. With a forward by Joseph Needham. New York: Simon and Schuster, Inc. ISBN 0671620282. Pages 134–135
^ Basedow’s syndrome or disease at Who Named It? – the history and naming of the disease
^ Ljunggren JG (August 1983). “[Who was the man behind the syndrome: Ismail al-Jurjani, Testa, Flagani, Parry, Graves or Basedow? Use the term hyperthyreosis instead]“. Lakartidningen 80 (32-33): 2902. PMID 6355710.
^ Nabipour, I. (2003), “Clinical Endocrinology in the Islamic Civilization in Iran”, International Journal of Endocrinology and Metabolism 1: 43–45 [45]
^ Robert James Graves at Who Named It?

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Cells, Thyroid | Leave a Comment

Rheumatoid Arthritis

RHEUMATOID ARTHRITIS:

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks the joints producing an inflammatory synovitis that often progresses to destruction of the articular cartilage and ankylosis of the joints. Rheumatoid arthritis can also produce diffuse inflammation in the lungs, pericardium, pleura, and sclera, and also nodular lesions, most common in subcutaneous tissue under the skin. Although the cause of rheumatoid arthritis is unknown, autoimmunity plays a pivotal role in its chronicity and progression.

About 1% of the world’s population is afflicted by rheumatoid arthritis, women three times more often than men. Onset is most frequent between the ages of 40 and 50, but people of any age can be affected. It can be a disabling and painful condition, which can lead to substantial loss of functioning and mobility. It is diagnosed chiefly on symptoms and signs, but also with blood tests (especially a test called rheumatoid factor) andX-rays. Diagnosis and long-term management are typically performed by a rheumatologist, an expert in the diseases of joints and connective tissues.[1]

Various treatments are available. Non-pharmacological treatment includes physical therapy,orthoses and occupational therapy. Analgesia(painkillers) and anti-inflammatory drugs, including steroids, are used to suppress the symptoms, while disease-modifying antirheumatic drugs(DMARDs) are often required to inhibit or halt the underlying immune process and prevent long-term damage. In recent times, the newer group of biologics has increased treatment options.[1]

Signs and symptoms

While rheumatoid arthritis primarily affects joints, problems involving other organs of the body are known to occur. Extra-articular (“outside the joints”) manifestations other than anemia (which is very common) are clinically evident in about 15-25% of individuals with rheumatoid arthritis.[3] It can be difficult to determine whether disease manifestations are directly caused by the rheumatoid process itself, or from side effects of the medications commonly used to treat it – for example, lung fibrosis from methotrexate or osteoporosis from corticosteroids.

.

Joints

The arthritis of joints known as synovitis is inflammation of the synovial membrane that lines joints and tendon sheaths. Joints become swollen, tender and warm, and stiffness limits their movement. With time RA nearly always affects multiple joints (it is a polyarthritis), most commonly small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved. Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss of function.[1]

Rheumatoid arthritis typically manifests with signs of inflammation, with the affected joints being swollen, warm, painful and stiff, particularly early in the morning on waking or following prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of the disease and may last for more than an hour. Gentle movements may relieve symptoms in early stages of the disease. These signs help distinguish rheumatoid from non-inflammatory problems of the joints, often referred to as osteoarthritis or “wear-and-tear” arthritis. In arthritis of non-inflammatory causes, signs of inflammation and early morning stiffness are absent, and movements induce pain due to the wear-and-tear.[4]

In RA, the joints are often affected in a fairly symmetrical fashion, although this is not specific, and the initial presentation may be asymmetrical.

Hands affected by RA

As the pathology progresses the inflammatory activity leads to tendon tethering and erosion and destruction of the joint surface, which impairs range of movement and leads to deformity. The fingers may suffer from almost any deformity depending on which joints are most involved. Medical students are taught to learn names for specific deformities, such as ulnar deviation, boutonniere deformity, swan neck deformity and “Z-thumb,” but these are of no more significance to diagnosis or disability than other variants.

Skin

The rheumatoid nodule, which is often subcutaneous, is the feature most characteristic of rheumatoid arthritis. The initial pathologic process in nodule formation is unknown but may be essentially the same as the synovitis, since similar structural features occur in both. The nodule has a central area of fibrinoid necrosis that may be fissured and which corresponds to the fibrin-rich necrotic material found in and around an affected synovial space. Surrounding the necrosis is a layer of palisading macrophages and fibroblasts, corresponding to the intimal layer in synovium and a cuff of connective tissue containing clusters of lymphocytes and plasma cells, corresponding to the subintimal zone in synovitis. The typical rheumatoid nodule may be a few millimetres to a few centimetres in diameter and is usually found over bony prominences, such as the olecranon, the calcaneal tuberosity, the metacarpophalangeal joint, or other areas that sustain repeated mechanical stress. Nodules are associated with a positive RF (rheumatoid factor) titer and severe erosive arthritis. Rarely, these can occur in internal organs or at diverse sites on the body.

Several forms of vasculitis occur in rheumatoid arthritis. A benign form occurs as microinfarcts around the nailfolds. More severe forms include livedo reticularis, which is a network (reticulum) of erythematous to purplish discoloration of the skin caused by the presence of an obliterative cutaneous capillaropathy.

Other, rather rare, skin associated symtoms include:

pyoderma gangrenosum, a necrotizing, ulcerative, noninfectious neutrophilic dermatosis.
Sweet’s syndrome, a neutrophilic dermatosis usually associated with myeloproliferative disorders
drug reactions
erythema nodosum
lobular panniculitis
atrophy of digital skin
palmar erythema
diffuse thinning (rice paper skin), and skin fragility (often worsened by corticosteroid use).

Pathophysiology

Rheumatoid arthritis is a form of autoimmunity, the causes of which are still incompletely known. It is a systemic (whole body) disorder principally affecting synovial tissues.

The key pieces of evidence relating to pathogenesis are:

1. A genetic link with HLA-DR4 and related allotypes of MHC Class II and the T cell-associated protein PTPN22.

2. A link with cigarette smoking that appears to be causal.

3. A dramatic response in many cases to blockade of the cytokine TNF (alpha).

4. A similar dramatic response in many cases to depletion of B lymphocytes, but no comparable response to depletion of T lymphocytes.

5. A more or less random pattern of whether and when predisposed individuals are affected.

6. The presence of autoantibodies to IgGFc, known as rheumatoid factors (RF), and antibodies to citrullinated peptides (ACPA).

These data suggest that the disease involves abnormal B cell – T cell interaction, with presentation of antigens by B cells to T cells via HLA-DR eliciting T cell help and consequent production of RF and ACPA. Inflammation is then driven either by B cell or T cell products stimulating release of TNF and other cytokines. The process may be facilitated by an effect of smoking on citrullination but the stochastic (random) epidemiology suggests that the rate limiting step in genesis of disease in predisposed individuals may be an inherent stochastic process within the immune response such as immunoglobulin or T cell receptor gene recombination and mutation. (See entry under autoimmunity for general mechanisms.)

If TNF release is stimulated by B cell products in the form of RF or ACPA – containing immune complexes, through activation of immunoglobulin Fc receptors, then RA can be seen as a form of Type III hypersensitivity.^[13] ^[14] If TNF release is stimulated by T cell products such as interleukin-17 it might be considered closer to type IV hypersensitivity although this terminology may be getting somewhat dated and unhelpful.^[15] The debate on the relative roles of immune complexes and T cell products in inflammation in RA has continued for 30 years. There is little doubt that both B and T cells are essential to the disease. However, there is good evidence for neither cell being necessary at the site of inflammation. This tends to favour immune complexes (based on antibody synthesised elsewhere) as the initiators, even if not the sole perpetuators of inflammation. Moreover, work by Thurlings and others in Paul-Peter Tak’s group and also by Arthur Kavanagh’s group suggest that if any immune cells are relevant locally they are the plasma cells, which derive from B cells and produce in bulk the antibodies selected at the B cell stage.^{[citation needed]}

Although TNF appears to be the dominant, other cytokines (chemical mediators) are likely to be involved in inflammation in RA. Blockade of TNF does not benefit all patients or all tissues (lung disease and nodules may get worse). Blockade of IL-1, IL-15 and IL-6 also have beneficial effects and IL-17 may be important. Constitutional symptoms such as fever, malaise, loss of appetite and weight loss are also caused by cytokines released in to the blood stream.

As with most autoimmune diseases, it is important to distinguish between the cause(s) that trigger the process, and those that may permit it to persist and progress.

References

^ ^a ^b ^c Majithia V, Geraci SA (2007). “Rheumatoid arthritis: diagnosis and management”. Am. J. Med. 120 (11): 936–9. doi:10.1016/j.amjmed.2007.04.005. PMID 17976416.
^ ^a ^b Landré-Beauvais AJ (1800). La goutte asthénique primitive (doctoral thesis). Paris. reproduced in Landré-Beauvais AJ (March 2001). “The first description of rheumatoid arthritis. Unabridged text of the doctoral dissertation presented in 1800″.Joint Bone Spine 68 (2): 130–43. doi:10.1016/S1297-319X(00)00247-5. PMID 11324929.
^ Turesson C, O’Fallon WM, Crowson CS, Gabriel SE, Matteson EL (2003). “Extra-articular disease manifestations in rheumatoid arthritis: incidence trends and risk factors over 46 years”. Ann. Rheum. Dis. 62 (8): 722–7. doi:10.1136/ard.62.8.722.PMID 12860726.
^ Jijith Krishnan,Document on Rhuematoid arthritis
^ de Groot K (August 2007). “[Renal manifestations in rheumatic diseases]“. Internist (Berl) 48 (8): 779–85. doi:10.1007/s00108-007-1887-9. PMID 17571244.
^ Wolfe F, Mitchell DM, Sibley JT, et al (April 1994). “The mortality of rheumatoid arthritis”. Arthritis Rheum. 37 (4): 481–94. doi:10.1002/art.1780370408. PMID 8147925.
^ Westwood OM, Nelson PN, Hay FC (April 2006). “Rheumatoid factors: what’s new?”. Rheumatology (Oxford) 45 (4): 379–85. doi:10.1093/rheumatology/kei228. PMID 16418203.
^ ^a ^b Nishimura K, Sugiyama D, Kogata Y, et al (June 2007). “Meta-analysis: diagnostic accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid factor for rheumatoid arthritis” (PDF). Ann. Intern. Med. 146 (11): 797–808. PMID 17548411.

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Cells, Muscles, Thyroid | Leave a Comment

Scoliosis

SCOLIOSIS:

Scoliosis (from Greek: skolíōsis meaning “crooked”)[1] is a medical condition in which a person’s spine is curved from side to side, shaped like an “s”, and may also be rotated. To adults it can be very painful. It is an abnormal lateral curvature of the spine. On an x-ray, viewed from the rear, the spine of an individual with a typical scoliosis may look more like an “S” or a “C” than a straight line. It is typically classified as congenital (caused by vertebral anomalies present at birth), idiopathic (sub-classified as infantile, juvenile, adolescent, or adult according to when onset occurred) or as neuromuscular, having developed as a secondary symptom of another condition, such as spina bifida, cerebral palsy, spinal muscular atrophy or due tophysical trauma.

Cause

In the case of the most common form of scoliosis, adolescent idiopathic scoliosis, there is no clear causal agent [6]. Various causes have been implicated, but none have consensus among scientists as the cause of scoliosis. The role of genetic factors in the development of this condition is widely accepted[7]. Scoliosis is more often diagnosed in females and is often seen in patients with cerebral palsy or spina bifida,which is a birth defect that involves the incomplete development of the spinal cord and its coverings[8][citation needed], although this form of scoliosis is different from that seen in children without these conditions.

Symptoms

Patients aged from 18 or older are less likely to worsen their case due to their mature spines and body system. Pain is often common in adulthood, especially if the scoliosis is left untreated.[citation needed] Though doctors do not always recommend surgery as the solution to scoliosis, it is still the most efficient way to completely strengthen the spine. Scoliosis surgery is often performed for cosmetic reasons rather than pain alone as the surgery cannot guarantee pain loss but it can stabilize a curvature and prevent worsening therefore improving one’s quality of life. Pain can occur because the muscles try to conform to the way the spine is curving often resulting in muscle spasms. Some of the severe cases of scoliosis can lead to diminishing lung capacity, putting pressure on the heart, and restricting physical activities.

Patients who have reached skeletal maturity are less likely to have a worsening case. Some severe cases of scoliosis can lead to diminishing lung capacity, putting pressure on the heart, and restricting physical activities.

The symptoms of scoliosis can include:

Uneven musculature on one side of the spine
A rib prominence and/or a prominent shoulder blade, caused by rotation of the ribcage in thoracic scoliosis
Uneven hips / leg lengths
Asymmetric size or location of breast in females
Slow nerve action (in some cases)

Surgery

Surgery is usually indicated for curves that have a high likelihood of progression (i.e., greater than 45 to 50 degrees magnitude), curves that would be cosmetically unacceptable as an adult, curves in patients withspina bifida and cerebral palsy that interfere with sitting and care, and curves that affect physiological functions such as breathing.

Surgery for scoliosis is done by a surgeon who specializes in spine surgery. For various reasons it is usually impossible to completely straighten a scoliotic spine, but in most cases very good corrections are achieved.

Prognosis

The prognosis of scoliosis depends on the likelihood of progression. The general rules of progression are that larger curves carry a higher risk of progression than smaller curves, and that thoracic and double primary curves carry a higher risk of progression than single lumbar or thoracolumbar curves. In addition, patients who have not yet reached skeletal maturity have a higher likelihood of progression (i.e., if the patient has not yet completed the adolescent growth spurt).

Scoliosis Research Society

The Scoliosis Research Society is a professional organization of physicians and allied health personnel. Their primary focus is on providing continuing medical education for health care professionals and on funding/supporting research in spinal deformities. Founded in 1966, the SRS has gained recognition as one of the world’s premier spine societies. Strict membership criteria ensure that the individual Fellows support that commitment. Current membership includes over 1,000 of the world’s leading spine surgeons as well as some researchers, physician assistants, and orthotists who are involved in research and treatment of spinal deformities. The purpose of the Scoliosis Research Society is to foster the optimal care of all patients with spinal deformities.^[20]

References

^ Online Etymology Dictionary. Douglas Harper, Historian. Accessed 27 December 2008. Dictionary.com http://dictionary.reference.com/browse/scoliosis
^ Christopher Good, M.D “The Genetic Basis of Adolescent Idiopathic Scoliosis,” Journal of the Spinal Research Foundation, Spring 2009 Vol 4.1 http://www.spinemd.com/publications/articles/the-genetic-basis-of-adolescent-idiopathic-scoliosis
^ Kouwenhoven, J & Castelein, R, 2008, ‘The Pathogenesis of Adolescent Idiopathic Scoliosis’, Spine, vol. 33, no. 26, pp. 2898-2908. 10.1097/BRS.0b013e3181891751
^ Ogilvie JW, Braun J, Argyle V, Nelson L, Meade M, Ward K, 2006, ‘The Search for Idiopathic Genes’, Spine, vol. 31, no. 6, pp. 679-81. March 2006
^ [1]
^ Texas Scottish Rite Hospital for Children: [2]
^ Gao X, Gordon D, Zhang D, Browne R, Helms C, Gillum J, Weber S, Devroy S,Swaney S, Dobbs M, Morcuende J, Sheffield V, Lovett M, Bowcock A, Herring J, Wise C (2007). [http://www.ncbi.nlm.nih.gov/pubmed/17436250?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum "CHD7 gene polymorphisms are associated with susceptibility to idiopathic scoliosis."]. Am J Hum Genet 80 (5): 957-65.PMID 17436250.

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Bones, Cells, Muscles | 3 Comments

Urinary Tract Infection (U.T.I)

URINARY TRACT INFECTIONS:

A urinary tract infection (UTI) is a bacterial infection that affects any part of the urinary tract.The main causitive agent is:Escherichia coli. Although urine contains a variety of fluids, salts, and waste products, it usually does not have bacteria in it.[1] When bacteria get into the bladderor kidney and multiply in the urine, they cause a UTI. The most common type of UTI is a bladder infection which is also often called cystitis. Another kind of UTI is a kidney infection, known as pyelonephritis, and is much more serious. Although they cause discomfort, urinary tract infections can usually be quickly and easily treated with a short course of antibiotics.[2]

“Multiple white cells at urinary microscopy from a patient with urinary tract infection.”

Symptoms

For bladder infections

Frequent urination along with the feeling of having to urinate even though there may be very little urine to pass.
Nocturia: Need to urinate during the night.
Urethritis: Discomfort, irritation or pain at the urethral meatus or a burning sensation throughout the urethra with urination (dysuria).
Pain in the midline suprapubic region.
Pyuria: Pus in the urine or discharge from the urethra.
Hematuria: Blood in urine (not always seen to the naked eye, but often revealed during urine tests).
Pyrexia: Mild fever
Cloudy and foul-smelling urine
Increased confusion and associated falls are common presentations to Emergency Departments for elderly patients with UTI.
Some urinary tract infections are asymptomatic.

For kidney infection

All of the above symptoms.
Emesis: Vomiting is common.[3]
Back, side (flank) or groin pain.
Abdominal pain or pressure.
Shaking chills and high spiking fever.
Night sweats.
Extreme fatigue.
Excessive thirst.

Multiple bacilli (rod-shaped bacteria, here shown as black and bean-shaped) shown between white cells at urinary microscopy. This is called bacteriuria and pyuria, respectively. These changes are indicative of a urinary tract infection.

Diagnosis

A patient with dysuria (painful voiding) and urinary frequency generally has a spot mid-stream urine sample sent for urinalysis, specifically the presence ofnitrites, leukocytes or leukocyte esterase. If there is a high bacterial load without the presence of leukocytes, it is most likely due to contamination. The diagnosis of UTI is confirmed by a urine culture.

If the urine culture is negative:

symptoms of urethritis may point at Chlamydia trachomatis or Neisseria gonorrheae infection.
symptoms of cystitis may point at interstitial cystitis.
in men, prostatitis may present with dysuria.

A negative urine test can also suggest the presence of unusual bacteria or viruses causing symptoms of UTI.

In severe infection, characterized by fever, rigors or flank pain, urea and creatinine measurements may be performed to assess whether renal function has been affected.

Most cases of lower urinary tract infections in females are benign and do not need exhaustive laboratory work-ups. However, UTI in young infants must receive some imaging study, typically a retrograde urethrogram, to ascertain the presence/absence of congenital urinary tract anomalies. Males too must be investigated further. Specific methods of investigation include x-ray, Nuclear Medicine, MRI and CAT scan technology.

References

^ “Adult Health Advisor 2005.4: Bacteria in Urine, No Symptoms (Asymptomatic Bacteriuria)”. Retrieved 2007-08-25.
^ “Urinary Tract Infections”. Retrieved 2007-08-25.
^ askdrsears.com
^ Urethra length is approximately 25–50 mm / 1-2 inches long in females, versus about 20 cm / 8 inches in males.
^ “Fluroquinolone Drug Class Review”. Oregon State University College of Pharmacy. 2002. Retrieved 4 September 2009.
^ ^a ^b http://findarticles.com/p/articles/mi_m0689/is_2_52/ai_97724151/
^ “BestBets: Cranberry Juice for the treatment of UTIs”.
^ Urinary Tract Infection – Alternative medicine. Accessed October 4, 2008.
^ Urinary Tract Infection – eMedicine Health. Accessed December 26, 2008.
^ Toxic Shock Syndrome: Bacterial Infections by Matthew E. Levison, MD(September 2008)Merck Manual Home Edition

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Cells, Pancreas | Leave a Comment

Bronchitis

BRONCHITIS:

Bronchitis is inflammation of the mucous membranes of the bronchi, the airways that carry airflow from the trachea into the lungs. Bronchitis can be classified into two categories, acute and chronic, each of which has unique etiologies, pathologies, and therapies.

1Acute bronchitis is characterized by the development of a cough, with or without the production of sputum, mucus that is expectorated (coughed up) from the respiratory tract. Acute bronchitis often occurs during the course of an acute viral illness such as the common cold or influenza. Viruses cause about 90% of cases of acute bronchitis while bacteriaaccount for less than 10%.[1]

Chronic bronchitis, a type of chronic obstructive pulmonary disease, is characterized by the presence of a productive cough that lasts for 3 months or more per year for at least 2 years. Chronic bronchitis most often develops due to recurrent injury to the airways caused by inhaled irritants. Cigarette smoking is the most common cause, followed by air pollution and occupational exposure to irritants, and cold air.

.

Acute bronchitis

Main article: Acute bronchitis

Acute bronchitis is most often caused by viruses that infect the epithelium of the bronchi, resulting in inflammation and increased secretion of mucus. Cough, a common symptom of acute bronchitis, develops in an attempt to expel the excess mucus from the lungs. Other common symptoms include sore throat, runny nose, nasal congestion (coryza), low-grade fever, malaise, and the production of sputum.[1]

Acute bronchitis often develops during the course of an upper respiratory infection (URI) such as the common cold or influenza.[1] About 90% of cases of acute bronchitis are caused by viruses, including rhinoviruses,adenoviruses, and influenza. Bacteria, including Mycoplasma pneumoniae, Chlamydia pneumoniae, and Bordetella pertussis, account for about 10% of cases.[1]

Treatment for acute bronchitis is primarily symptomatic. Non-steroidal anti-inflammatory drugs (NSAIDs) may be used to treat fever and sore throat. Decongestants can be useful in patients with nasal congestion, andexpectorants may be used to loosen mucus and increase expulsion of sputum. Cough suppressants may be used if the cough interferes with sleep or is bothersome, although coughing may be useful in expelling sputum from the airways. Even with no treatment, most cases of acute bronchitis resolve quickly.[1]

As most cases of acute bronchitis are caused by viruses, antibiotics should not be used since they are only effective against bacteria. Using antibiotics in patients who do not have bacterial infections promotes the development of antibiotic-resistant bacteria, which may lead to greater morbidity and mortality. Antibiotics should only be prescribed if microscopic examination of Gram stained sputum shows large numbers of bacteria present.[1]

Chronic Brochitis

Chronic bronchitis, a type of chronic obstructive pulmonary disease, is defined by a productive cough that lasts for 3 months or more per year for at least 2 years.^[3] Other symptoms may include wheezing andshortness of breath, especially upon exertion. The cough is often worse soon after awakening, and the sputum produced may have a yellow or green color and may be streaked with blood.^[1]

Chronic bronchitis is caused by recurring injury or irritation to the respiratory epithelium of the bronchi, resulting in chronic inflammation, edema (swelling), and increased production of mucus by goblet cells.^[1] Airflow into and out of the lungs is partly blocked because of the swelling and extra mucus in the bronchi or due to reversible bronchospasm.^[4]

Most cases of chronic bronchitis are caused by smoking cigarettes or other forms of tobacco. Chronic inhalation of irritating fumes or dust from occupational exposure or air pollution may also be causative. About 5% of the population has chronic bronchitis, and it is two times more common in males than females.^[1]

Chronic bronchitis is treated symptomatically. Inflammation and edema of the respiratory epithelium may be reduced with inhaled corticosteroids. Wheezing and shortness of breath can be treated by reducingbronchospasm (reversible narrowing of smaller bronchi due to constriction of the smooth muscle) with bronchodilators such as inhaled β-Adrenergic agonists (e.g., albuterol) and inhaled anticholinergics (e.g.,ipratropium bromide). Hypoxemia, too little oxygen in the blood, can be treated with supplemental oxygen.^[1] However, oxygen supplementation can result in decreased respiratory drive leading to increased blood levels of carbon dioxide and subsequent respiratory acidosis.

The most effective method of preventing chronic bronchitis and other forms of COPD is to avoid smoking cigarettes and other forms of tobacco.^[1]

On pulmonary tests, a bronchitic (bronchitis) may present a decreased FEV1 and FEV1/FVC. However, unlike the other common obstructive disorders, asthma and emphysema, bronchitis rarely causes a high residual volume. This is because the air flow obstruction found in bronchitis is due to increased resistance, which does not generally cause the airways to collapse prematurely and trap air in the lungs.^{[citation needed]}

References

^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k Cohen, Jonathan and William Powderly. Infectious Diseases. 2nd ed. Mosby (Elsevier), 2004. “Chapter 33: Bronchitis, Bronchiectasis, and Cystic Fibrosis”
^ Hueston WJ (March 1997). “Antibiotics: neither cost effective nor ‘cough’ effective”. The Journal of Family Practice 44 (3): 261–5. PMID 9071245.
^ “CDC Definition of Chronic Bronchitis from NIOSH HAZARD REVIEW, Health Effects of Occupational Exposure to Respirable Crystalline Silica”
^ “Ross and Wilson: Anatomy and Physiology (tenth edition)”

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Cells, Lungs, Muscles | Leave a Comment

Asthma

ASTHMA:

Asthma is a predisposition to chronic inflammation of the lungs in which the airways (bronchi) are reversibly narrowed. Asthma affects 7% of the population of the United States,[1][2] and 300 million worldwide.[3] During asthma attacks (exacerbations of asthma), the smooth muscle cells in the bronchi constrict, the airways become inflamed and swollen, and breathing becomes difficult.

Asthma causes 4,000 deaths a year in the United States. Medicines such as inhaled short-acting beta-2 agonists may be used to treat acute attacks. Attacks can also be prevented by avoiding triggering factors such as allergens or rapid temperature changes and through drug treatment such as inhaled corticosteroids and then long-acting β2-agonists if necessary.[4][5] Leukotriene antagonists are less effective than corticosteroids, but have no side effects. Monoclonal antibodies, such as mepolizumab andomalizumab, are sometimes effective. Prognosis is good with treatment.

In contrast to chronic obstructive pulmonary disease and chronic bronchitis, the inflammation of asthma is reversible. In contrast to emphysema, asthma affects the bronchi, not the alveoli.

The National Heart, Lung and Blood Institute defines asthma as a common chronic disorder of the airways characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness (bronchospasm), and an underlying inflammation.[6]

Signs and symptoms

Because of the spectrum of severity within the asthma, some people with asthma only rarely experience symptoms, usually in response to triggers, where as other more severe cases may have marked airflow obstruction at all times.

Asthma exists in two states: the steady-state of chronic asthma, and the acute state of an acute asthma exacerbation. The symptoms are different depending on what state the patient is in.

Common symptoms of asthma in a steady-state include: nighttime coughing, shortness of breath with exertion but no dyspnea at rest, a chronic ‘throat-clearing’ type cough, and complaints of a tight feeling in the chest. Severity often correlates to an increase in symptoms. Symptoms can worsen gradually and rather insidiously, up to the point of an acute exacerbation of asthma. It is a common misconception that all people with asthma wheeze—some never wheeze, and their disease may be confused with another Chronic obstructive pulmonary disease such as emphysema or chronic bronchitis.

An acute exacerbation of asthma is commonly referred to as an asthma attack. The cardinal symptoms of an attack are shortness of breath (dyspnea), wheezing and chest tightness.[9] Although the former is often regarded as the primary symptom of asthma,[10] some patients present primarily with coughing, and in the late stages of an attack, air motion may be so impaired that no wheezing may be heard.[11] When present the cough may sometimes produce clear sputum. The onset may be sudden, with a sense of constriction in the chest, breathing becomes difficult, and wheezing occurs (primarily upon expiration, but can be in bothrespiratory phases). It is important to note inspiratory stridor without expiratory wheeze however, as an upper airway obstruction may manifest with symptoms similar to an acute exacerbation of asthma, with stridor instead of wheezing, and will remain unresponsive to bronchodilators.

Bronchial inflammation

The mechanisms behind allergic asthma—i.e., asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both people with asthma and people who are free of the disease, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen-presenting cells, or APCs. APCs then “present” pieces of the allergen to other immune systemcells. In most people, these other immune cells (T_H0 cells) “check” and usually ignore the allergen molecules. In asthma patients, however, these cells transform into a different type of cell (T_H2), for reasons that are not well understood.

The resultant T_H2 cells activate an important arm of the immune system, known as the humoral immune system. The humoral immune system produces antibodies against the inhaled allergen. Later, when a patient inhales the same allergen, these antibodies “recognize” it and activate a humoral response. Inflammation results: chemicals are produced that cause the wall of the airway to thicken, cells which produce scarring to proliferate and contribute to further ‘airway remodeling’, causes mucus producing cells to grow larger and produce more and thicker mucus, and the cell-mediated arm of the immune system is activated. Inflamed airways are more hyper-reactive, and will be more prone to bronchospasm.

The “hygiene hypothesis” postulates that an imbalance in the regulation of these T_H cell types in early life leads to a long-term domination of the cells involved in allergic responses over those involved in fighting infection. The suggestion is that for a child being exposed to microbes early in life, taking fewer antibiotics, living in a large family, and growing up in the country stimulate the T_H1 response and reduce the odds of developing asthma.^[78]

Acute asthma exacerbation

When an asthma attack is unresponsive to a patient’s usual medication, other treatment options available for emergency management include:^[135]

Oxygen to alleviate the hypoxia that results from extreme asthma attacks (but not the asthma attack itself).
Nebulized salbutamol or terbutaline (short-acting beta-2-agonists), often combined with ipratropium (an anticholinergic).
Systemic steroids, oral or intravenous (prednisone, prednisolone, methylprednisolone, dexamethasone, or hydrocortisone). Some research has looked into an alternative inhaled route.^[136] A non tapered 5 – 10 day course seems to be sufficient.^[137]
Other bronchodilators that are occasionally effective when the usual drugs fail:
- Intravenous salbutamol
- Nonspecific beta-agonists, injected or inhaled (epinephrine, isoetharine, isoproterenol, metaproterenol)
- Anticholinergics, IV or nebulized, with systemic effects (glycopyrrolate, atropine, ipratropium)
- Methylxanthines (theophylline, aminophylline)
- Inhalation anesthetics that have a bronchodilatory effect (isoflurane, halothane, enflurane)
- The dissociative anaesthetic ketamine, often used in endotracheal tube induction
- Magnesium sulfate, intravenous
Intubation and mechanical ventilation, for patients in or approaching respiratory arrest.
Heliox, a mixture of helium and oxygen, may be used in a hospital setting. It has a more laminar flow than ambient air and moves more easily through constricted airways.

References

^ Merck Manual Home Edition
^ Merck Manual Professional Edition
^ http://content.nejm.org/cgi/content/full/360/10/1002 Asthma, Christopher H. Fanta, N Engl J Med, 360:1002-1014, March 5, 2009
^ AAAAI article on avoiding asthma symptoms
^ Section in “The Asthma Sourcebook” discussing air temperature and asthma symptoms
^ http://www.nhlbi.nih.gov/guidelines/asthma/03_sec2_def.pdf Retrieved March 11, 2009
^ Lilly CM (2005). “Diversity of asthma: evolving concepts of pathophysiology and lessons from genetics”. J. Allergy Clin. Immunol. 115 (4 Suppl): S526–31. doi:10.1016/j.jaci.2005.01.028. PMID 15806035.
^ ^a ^b Yawn, BP (September 2008). “Factors accounting for asthma variability: achieving optimal symptom control for individual patients”. Primary Care Respiratory Journal 17 (3): 138–147. doi:10.3132/pcrj.2008.00004. PMID 18264646.
^ Kumar, Vinay; A. N. J., Abbas, Fausto, Aster (2010). Robbins and Cotran Pathologic Basis of Disease (8th ed.). Saunders. p. 688. ISBN 9781416031215.
^ ^a ^b ^c ^d ^e Saunders (2005). “Asthma”. Mason: Murray & Nadel’s Textbook of Respiratory Medicine (Homer A. Boushey Jr. M.D. David B. Corry M.D. John V. Fahy M.D. Esteban G. Burchard M.D. Prescott G. Woodruff M.D. et al. (eds)) (4th ed.). Elsevier.
^ ^a ^b ^c McFadden ER, Jr (2004). “Asthma”. Harrison’s Principles of Internal Medicine (Kasper DL, Fauci AS, Longo DL, et al. (eds)) (16th ed.). New York: McGraw-Hill. pp. 1508–16.
^ ^a ^b Document on severe acute asthma and emergency management.. Guide for assessment of severity of exacerbation.
^ Longmore, Murray et al. (2007). Oxford Handbook of Clinical Medicine (7^th ed.). Oxford University Press. ISBN 978-0198568377.

January 27, 2010 Posted by Engr. Ardy Motos | Blood, Cells, Heart, Lungs | 2 Comments

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TUBERCULOSIS (TB)

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URINARY TRACT INFECTIONS:

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For bladder infections

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