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pink puffer n blue bloater

If you are a smoker, past smoker, someone who worked around certain chemicals while breathing in the fumes for many years, worked in a dusty area over a period of time or worked where there is heavy exposure to air pollution, then you may illustrate the signs and symptoms of Chronic Obstructive Pulmonary Disease. COPD is a lung disease in which the lungs are damaged making it hard to breathe. Chronic Obstructive Pulmonary Disease patients have both chronic bronchitis and emphysema, but are classified as "blue bloaters" or "pink puffers." A "blue bloater" will suffer from chronic bronchitis and a "pink puffer" will suffer primarily from emphysema.

Patients suffering from chronic bronchitis are termed "blue bloaters". The term is traced from the bluish color of the lips and skin commonly seen in patients who have Type B Chronic Obstructive Pulmonary Disease (COPD). If a person has the chronic bronchitis COPD, the damaged airways will have become inflamed and thickened and there will also be an increase in the number and size of mucus producing cells. When the walls of the airways become thick or swollen, many of the air sacs are destroyed. The cells accumulate more mucus which tends to clog the airways and the person will develop a cough and difficulty inhaling and exhaling air through the lungs. A "blue bloater" will demonstrate the following signs and symptoms.

HISTORY OF COUGH WITH SPUTUM FOR 3 MONTHS TO A YEAR OR MORE
Coughing is one of the most common lung disease symptoms. When trying to clear the airways of toxins, mucus, or a foreign body, coughing is used as a defense mechanism. Coughing can be productive or unproductive depending on how its did and the result. Along with other mechanisms, coughing helps to protect the lungs from particles that have been inhaled and sometimes brings up sputum. Sputum is also known as phlegm which is a mixture of mucus, debris, and cells expelled by the lungs. Airway could easily be irritated by bacterial or viral respiratory infections, allergies, and smoke. Smoke damages the cells that line the airways, including the hairlike projections that normally cleanse the airways of debris. Coughing may result from gastroesophageal reflux, postnasal drip or drugs. When airways are narrowed below the windpipe, foreign bodies or tumors, it can cause coughing, wheezing or, both.

CYANOSIS DUE TO A DECREASE IN SUFFICIENT AMOUNTS OF OXYGEN IN THE BLOOD
Cyanosis is a condition in which the skin, lips and nails become bluish or purplish in color. When there is an insufficient amount of oxygen in the blood, Cyanosis occurs. It could result from blood vessel and heart malformations that allow blood to flow directly to the heart without ever flowing past air sacs of the lung where oxygen is taken from the air. Blood form oxygen-depleted veins may flow directly into the vessels returning blood form the lungs to the left side of the heart or directly into the left side which is called a shunt. As in acute lung disease, Cyanosis may appear suddenly or gradually over time as a lung disease progresses.

SWOLLEN ANKLES OR LEGS AND DISTENTION IN THE NECK VEINS
Pay attention to swelling of the face, legs, arms and ankles which may show lung disease. The swelling occurs because of an increase in pressure in the lungs blood vessels. Then, blood backs up in the body's vein which causes excess fluid to leak into surrounding tissues allowing gravity to take over. Normally accompanied by shortness of breath, swelling is associated with heart disease.

DEVELOP SIGNS OF RIGHT-SIDED HEART FAILURE
Right-sided heart failure is a condition in which the right side of the heart loses its ability to pump blood efficiently. The right ventricle loses it's pumping function and blood may back up into areas of the body, producing congestion. Congestion affects the liver, the gastrointestinal tract, and the limbs.

When "blue bloaters" are analyzed and tested, the Arterial Blood Gas results will show evidence of hypoxemia, carbon dioxide retention and compensated respiratory acidosis. The prognosis for blue bloaters is poor and most die within 2 to 4 years. Long-term oxygen therapy at home using concentrators is the only treatment shown to improve the prognosis of a "blue bloater."

Patients suffering from emphysema are called "pink puffer". The term is traced from the reddish complexion and the "puffing" or hyperventilation seen in patients who have Type A Chronic Obstructive Pulmonary Disease. Type A In a case of emphysema type COPD, the walls between most of the air sacs are destroyed which leads to a few number of large air sacs instead of the normal number of many tiny ones. These larger air sacs have less surface area for the exchange of oxygen and carbon dioxide and the lungs looks like a sponge with many large bubbles in it. The poor exchange of oxygen and carbon dioxide, result in shortness of breath. A "pink puffer" will demonstrate the following signs and symptoms.

TYPICALLY THIN
Weight loss is normally difficult to maintain on a healthy level. It is usually easier for a "pink puffer" to lose weigh and much harder for them to gain. Therefore, they remain typically thin in body size.

BREATHES WITH PURSED LIPS
Breathing for a "pink puffer" takes an extreme amount of effort. He or she will have rapid and very shallow breathing. Due to the high residual lung volume a "pink puffer" may have a barrel chest.

INCREASING RESPIRATORY RATE AND EXPERIENCES DIFFICULTY BREATHING
During exercise and high altitudes, an increase in the rate and depth of breathing occurs, but the increase should not cause discomfort. Dyspnea is a term used to describe difficulty in breathing and is a common symptom of many lung diseases. It is termed shortness of breath, or difficulty breathing. With Dyspnea the person feels a sensation of not being able to breathe fast or deep enough and the faster breathing is accompanied by the feeling of running out of air. Another sensation of Dyspnea is the increased muscle effort to expand the chest while breathing, which is described as tightness in the chest.

When "pink puffers" are analyzed and tested, the Arterial Blood Gas results show evidence of less hypoxemia than "blue bloaters" and no carbon dioxide retention. The prognosis for "pink puffers" is a lot better than for "blue bloaters."

http://www.helium.com/items/700295-copd-screening-quiz-are-you-a-pink-puffer-or-a-blue-bloater?page=3

From Williams haematology 7th Edition

I. Primary lymphocytosis A. Lymphocytic malignancies 1. Acute lymphocytic leukemia (Chap. 91) 2. Chronic lymphocytic leukemia and related disorders (Chap. 92) 3. Prolymphocytic leukemia (Chap. 92) 4. Hairy cell leukemia133 (Chap. 93) 5. Adult T cell leukemia (Chaps. 92 and 96) 6. Lymphoma cell leukemia134 (Chap. 96) 7. Large granular lymphocytic leukemia135 (Chap. 94) a. NK cell leukemia136 (Chap. 94) b. CD8+ T cell large granular lymphocytic leukemia137,138,139 c. CD4+ T cell large granular lymphocytic leukemia53,140 d. / T cell large granular lymphocytic leukemia141 B. Essential monoclonal B cell lymphocytosis6 (Chap. 92) C. Persistent polyclonal B cell lymphocytosis9,10

II. Reactive lymphocytosis A. Mononucleosis syndromes (Chap. 84) 1. Epstein-Barr virus38,142,143,144,145,146 2. Cytomegalovirus41,42,147,148,149,150,151,152 3. Human immunodeficiency virus153,154,155,156,157,158 4. Herpes simplex virus type II 5. Rubella virus 6. Toxoplasma gondii159 7. Adenovirus 8. Infectious hepatitis virus 9. Dengue fever virus160,161,162 10. Human herpes virus type 6 (HHV-6)77,163 11. Human herpes virus type 8 (HHV-8)164 12. Varicella zoster virus165 B. Bordetella pertussis45 C. NK cell lymphocytosis54,55,56,73,75,166,167,168,169 D. Stress lymphocytosis (acute)69 1. Cardiovascular collapse66 a. Acute cardiac failure b. Myocardial infarction 2. Staphylococcal toxic shock syndrome170 3. Drug-induced68,77,171 4. Major surgery 5. Sickle cell crisis172 6. Status epilepticus 7. Trauma65,66 E. Hypersensitivity reactions 1. Insect bites73,74,75 2. Drugs76,78,80,81,173 F. Persistent lymphocytosis (subacute or chronic) 1. Cancer84 2. Cigarette smoking15,174 3. Hyposplenism86 4. Chronic infection a. Leishmaniasis175 b. Leprosy176 c. Strongyloidiasis58,59,60 5. Thymoma83

Leucocytosis: Interpretation

http://drchasrani.typepad.com/family_medicine_updates/2005/07/leucocytosis_in.html

Leucocytosis: Interpretation

Leucocytosis - an elevation of the total number of white cells in blood, can be caused by a rise in the amount of one or more leucocyte types:
Ø Neutrophilia
Ø Lymphocytosis
Ø Monocytosis
Ø Eosinophilia
Ø Basophilia.

The division of leucocytoses (especially neutrophilias) according to their aetiology is directly useful in clinical diagnostics.

• Infections and inflammations
• Medication-related (corticosteroids, granulocyte growth factors, others)
• Stress-related (physical, emotional)
• Leukaemias (rare in comparison to the previous-mentioned)

Approach
If the clinical picture explains the occurrence and extent of leucocytosis, no specific investigations are required. If the underlying disease is unknown, the leucocyte differential count helps in orientation.

Neutrophilia (> 75% of total WBC count) is the most common form of leucocytosis. Neutrophilia occurs most frequently with infections; the neutrophil count is related to the severity of infection as well as to the microbiological aetiology. Pyogenic cocci (staphylococcus, streptococcus, pneumococcus, gonococcus and meningococcus) and bacilli (E. coli, Proteus and Pseudomonas) are common causes of neutrophilia. The leucocyte count is usually 15 – 30,000/dl, but sometimes even 50 – 80,000/dl. Immature neutrophils (bands, metamyelocytes) and "toxic" granulation are characteristic in the acute phase.

Neutrophilia is also relatively common in non-pyogenic infections. These include rheumatic fever, diphtheria, polio, typhoid fever, cholera, and shingles. The leucocyte count is usually 12 – 18,000/dl.

Sometimes neutrophil leucocytosis with immature granulocytes is so marked that it is called a leukaemoid reaction.

Other causes of neutrophil leucocytosis include:
- Bleeding
- Trauma
- Cardiac diseases (infarction, atrial fibrillation)
- Drugs (e.g. corticosteroids), poisonings
- Metabolic diseases (renal insufficiency, diabetic coma, gout attack, eclampsia)
- Blood diseases: myeloid leukaemias and polycythaemia vera
- Rheumatoid arthritis, vasculitis
- Blood transfusion

Eosinophilia is relatively common (> 6% of total WBC count). It is a manifestation of nasal/ respiratory allergy. The absolute count is more significant that % alone (Total WBC X eosinophil % = absolute count). A count above 700 is considered pathological and warrants treatment

Lymphocytosis (> 40% of total WBC count) is also relatively common. Infants and younger children have a high lymphocyte count with normal WBC count and may be as high as 50-60%

Marked lymphocytosis is seen in acute/ chronic lymphocytic leukaemia, infectious mononucleosis and in pertussis.

Milder lymphocytosis is common in various infections.

Monocytosis (> 0.8% of total WBC count) is uncommon. It can be associated with various infections (typhoid fever, brucellosis, tuberculosis, subacute endocarditis, malaria), rheumatoid arthritis and other connective tissue diseases, Hodgkin's disease and monocytic leukaemias.

Basophilia is rare. It is sometimes seen in the accelerated phase of chronic myeloid leukaemia (CML)

Further Investigations

Bone marrow examination is necessary if the aetiology of leucocytosis remains unknown, especially if the white cell differential count or the clinical picture indicates the possibility of a haematological malignancy.

If the symptoms and findings are unremarkable, follow-up of 1 - 2 weeks and a new leucocyte count may be the method of choice. A significant proportion of underlying conditions (infections) are harmless and temporary. Treatment is directed against the cause of leucocytosis.

Tips

• A severe infection as a cause of leucocytosis should be urgently recognized and therapy initiated.
• Leucopenia or a normal leucocyte count, on the other hand, does not necessarily exclude a severe infection.
• Leucocytosis of unknown origin may be associated with rheumatic diseases, other chronic inflammations or haematological malignancies. The cause of leucocytosis can usually be revealed with a small number of investigations.

Rapid tests for drug-resistant TB

• 30 June 2008
• 
  Rapid tests for drug-resistant TB
  to be available in developing countries
• 
  Geneva -- People in low-resource countries who are ill with multidrug-resistant TB (MDR-TB) will get a faster diagnosis -- in two days, not the standard two to three months -- and appropriate treatment thanks to two new initiatives unveiled today by the World Health Organization (WHO), the Stop TB Partnership, UNITAID and the Foundation for Innovative New Diagnostics (FIND).
  MDR-TB is a form of TB that responds poorly to standard treatment because of resistance to the first-line drugs isoniazid and rifampicin. At present it is estimated that only 2% of MDR-TB cases worldwide are being diagnosed and treated appropriately, mainly because of inadequate laboratory services. The initiatives announced today should increase that proportion at least seven-fold over the next four years, to 15% or more.
  
  "I am delighted that this initiative will improve both the technology needed to diagnose TB quickly, and increase the availability of drugs to treat highly resistant TB," said British Prime Minister Gordon Brown, who helped launch the Stop TB Partnership's Global Plan to Stop TB in 2006 and whose government is a founding member of UNITAID. "The UK is committed to stopping TB around the world, from our funding of TB prevention programmes in poor countries, to our support of cutting edge research to develop new drugs."
  
  In developing countries most TB patients are tested for MDR-TB only after they fail to respond to a standard treatments. Even then, it takes two months or more to confirm the diagnosis. Patients have to wait for the test results before they can receive life-saving second-line drugs. During this period, they can spread the multidrug-resistant disease to others. Often the patients die before results are known, especially if they are HIV-infected in addition to having MDR-TB.
  The initiative comes just one week after WHO recommended "line probe assays" for rapid MDR-TB diagnosis worldwide. This policy change was driven by data from recent studies, including a large field trial--conducted by FIND together with South Africa's Medical Research Council and National Health Laboratory Services--which produced evidence for the reliability and feasibility of using line probe assays under routine conditions.
  "Five months ago, WHO renewed its call to make MDR-TB an urgent public health priority," said WHO Director-General Dr Margaret Chan, "and today we have evidence to guide our response. Based on that evidence, we are launching these promising initiatives."
  The new initiative consists of two projects. The first, made possible through $26.1 million in funding from UNITAID*, will introduce a molecular method to diagnose MDR-TB that until now was used exclusively in research settings. These rapid, new molecular tests, known as line probe assays, produce an answer in less than two days.
  Over the next four years -- as lab staff are trained, lab facilities enhanced and new equipment delivered -- 16 countries** will begin using rapid methods to diagnose MDR-TB, including the molecular tests. The countries will receive the tests through the Stop TB Partnership's Global Drug Facility, which provides countries with both drugs and diagnostic supplies.
  As part of the project, WHO's Global Laboratory Initiative and FIND will help countries prepare for installation and use of the new rapid diagnostic tests, ensuring necessary technical standards for biosafety and the capacity to accurately perform DNA-based tests. One country, Lesotho, is already equipped to start using these tests; Ethiopia is expected to be ready by the end of 2008. The tests will be phased in from 2009-2011 in the remaining 14 countries.
  Under a second, complementary agreement with UNITAID for US$ 33.7
  million, the Global Drug Facility will boost the supply of drugs needed to treat MDR-TB in 54 countries, including those receiving the new diagnostic tests. This project is also expected to achieve price reductions of up to 20% for second-line anti-TB drugs by 2010. All the countries receiving this assistance have met WHO's technical standards for managing MDR-TB and already have treatment programmes in place. Some will use grants from the Global Fund against AIDS, Tuberculosis and Malaria to purchase the drugs.
  "Through the US$ 60 million support provided by UNITAID, these projects are expected to produce significant results in diagnosing and treating patients as well as reducing drug prices and the costs of diagnosis. These efforts illustrate the way in which innovative financing can be deployed for health and development," said Philippe Douste-Blazy, Chairman of UNITAID's Executive Board.-- Tam Wing Sun, EricLiaison Officer to WHOInternational Federation of Medical Students' Associations (IFMSA)

Treatment of MDR-TB

The treatment and prognosis of MDR-TB are much more akin to that for cancer than to that for infection. It has a mortality rate of up to 80%, which depends on a number of factors, including

1. How many drugs the organism is resistant to (the fewer the better),
2. How many drugs the patient is given (Patients treated with five or more drugs do better),
3. Whether an injectable drug is given or not (it should be given for the first three months at least),
4. The expertise and experience of the physician responsible,
5. How co-operative the patient is with treatment (treatment is arduous and long, and requires persistence and determination on the part of the patient),
6. Whether the patient is HIV positive or not (HIV co-infection is associated with an increased mortality).

Treatment courses are generally measured in months to years; it may require surgery, though death rates remain high despite optimal treatment. That said, good outcomes are still possible.

The treatment of MDR-TB must be undertaken by a physician experienced in the treatment of MDR-TB. Mortality and morbidity in patients treated in non-specialist centres is significantly inferior to those patients treated in specialist centres.

In addition to the obvious risks (i.e., known exposure to a patient with MDR-TB), risk factors for MDR-TB include male sex, HIV infection, previous incarceration, failed TB treatment, failure to respond to standard TB treatment, and relapse following standard TB treatment.

Treatment of MDR-TB must be done on the basis of sensitivity testing: it is impossible to treat such patients without this information. If treating a patient with suspected MDR-TB, the patient should be started on SHREZ+MXF+cycloserine pending the result of laboratory sensitivity testing.

A gene probe for rpoB is available in some countries and this serves as a useful marker for MDR-TB, because isolated RMP resistance is rare (except when patients have a history of being treated with rifampicin alone). If the results of a gene probe (rpoB) are known to be positive, then it is reasonable to omit RMP and to use SHEZ+MXF+cycloserine. The reason for maintaining the patient on INH is that INH is so potent in treating TB that it is foolish to omit it until there is microbiological proof that it is ineffective (even though isoniazid resistance so commonly occurs with rifampicin resistance).

When sensitivities are known and the isolate is confirmed as resistant to both INH and RMP, five drugs should be chosen in the following order (based on known sensitivities):

• An aminoglycoside (e.g., amikacin, kanamicin) or polypeptide antibiotic (e.g., capreomycin)
• PZA
• EMB
• a fluoroquinolones: moxifloxacin is preferred to ciprofloxacin or ofloxacin;
• rifabutin
• cycloserine
• a thioamide: prothionamide or ethionamide
• PAS
• a macrolide: e.g., clarithromycin
• linezolid
• high-dose INH (if low-level resistance)
• interferon-γ
• thioridazine

Drugs are placed nearer the top of the list because they are more effective and less toxic; drugs are placed nearer the bottom of the list because they are less effective or more toxic, or more difficult to obtain.

Resistance to one drug within a class generally means resistance to all drugs within that class, but a notable exception is rifabutin: rifampicin-resistance does not always mean rifabutin-resistance and the laboratory should be asked to test for it. It is only possible to use one drug within each drug class. If it is difficult finding five drugs to treat then the clinician can request that high level INH-resistance be looked for. If the strain has only low level INH-resistance (resistance at 1.0mg/l INH, but sensitive at 0.2mg/l INH), then high dose INH can be used as part of the regimen. When counting drugs, PZA and interferon count as zero; that is to say, when adding PZA to a four drug regimen, you must still choose another drug to make five. It is not possible to use more than one injectable (STM, capreomycin or amikacin), because the toxic effect of these drugs is additive: if possible, the aminoglycoside should be given daily for a minimum of three months (and perhaps thrice weekly thereafter). Ciprofloxacin should not be used in the treatment of tuberculosis if other fluoroquinolones are available.

There is no intermittent regimen validated for use in MDR-TB, but clinical experience is that giving injectable drugs for five days a week (because there is no-one available to give the drug at weekends) does not seem to result in inferior results. Directly observed therapy certainly helps to improve outcomes in MDR-TB and should be considered an integral part of the treatment of MDR-TB.

Response to treatment must be obtained by repeated sputum cultures (monthly if possible). Treatment for MDR-TB must be given for a minimum of 18 months and cannot be stopped until the patient has been culture-negative for a minimum of nine months. It is not unusual for patients with MDR-TB to be on treatment for two years or more.

Patients with MDR-TB should be isolated in negative-pressure rooms, if possible. Patients with MDR-TB should not be accommodated on the same ward as immunosuppressed patients (HIV infected patients, or patients on immunosuppressive drugs). Careful monitoring of compliance with treatment is crucial to the management of MDR-TB (and some physicians insist on hospitalisation if only for this reason). Some physicians will insist that these patients are isolated until their sputum is smear negative, or even culture negative (which may take many months, or even years). Keeping these patients in hospital for weeks (or months) on end may be a practical or physical impossibility and the final decision depends on the clinical judgement of the physician treating that patient. The attending physician should make full use of therapeutic drug monitoring (particularly of the aminoglycosides) both to monitor compliance and to avoid toxic effects.

XDR-TB

Extensively drug-resistant tuberculosis

Extensively drug-resistant tuberculosis (XDR-TB) is defined as tuberculosis that has evolved resistance to rifampicin and isoniazid (resistance to these first line anti-TB drugs defines Multi-drug-resistant tuberculosis, or MDR-TB), as well as to any member of the quinolone family and at least one of the following second-line TB treatments: kanamycin, capreomycin, or amikacin. The old case definition of XDR-TB is MDR-TB that is also resistant to three or more of the six classes of second-line drugs. This definition should no longer be used, but is included here because many older publications refer to it.

The principles of treatment for MDR-TB and for XDR-TB are the same. The main difference is that XDR-TB is associated with a much higher mortality rate than MDR-TB, because of a reduced number of effective treatment options. The epidemiology of XDR-TB is currently not well studied, but it is believed that XDR-TB does not transmit easily in healthy populations, yet is capable of causing epidemics in populations which are already stricken by HIV and therefore more susceptible to TB infection.

Epidemiology of drug-resistant TB

A 1997 survey of 35 countries found mortality rate above 2% in about a third of the countries surveyed. The highest rates were in the former USSR, Argentina, India and China, and was associated with poor or failing national tuberculosis control programs. Likewise, the appearance of high rates of MDR-TB in New York city in the early 1990s was associated with the dismantling of public health programmes.

MDR-TB strains appear to be less fit and less transmissible. It has been known for many years that INH-resistant TB is less virulent in guinea pigs, and the epidemiological evidence is that MDR strains of TB do not dominate naturally. A study in Los Angeles found that only 6% of cases of MDR-TB were clustered. MDR-TB has a mortality rate comparable to lung cancer. People who have weakened immune systems (because of diseases such as HIV or because of drugs) are more susceptible to catching TB.

South African epidemic

Since late 2006, there has been an epidemic of XDR-TB in South Africa. The outbreak was first reported as a cluster of 53 patients in a rural hospital in Kwa Zulu-Natal of whom 52 died. What was particularly worrisome was that the median survival from sputum specimen collection to death was only 16 days and that the majority of patients had never previously received treatment for tuberculosis. This is the epidemic for which the acronym XDR-TB was first used, and although TB strains that fulfill the current definition have been identified retrospectively, this was the largest group of linked cases ever found. Since the initial report in September 2006, cases have now been reported in most provinces in South Africa. As of 16 March 2007, there were 314 cases reported, with 215 deaths. It is clear that the spread of this strain of TB is closely associated with a high prevalence of Aids and poor infection control; in other countries where XDR-TB strains have arisen, drug resistance has arisen from mismanagement of cases or poor patient compliance with drug treatment instead of being transmitted from person to person. This strain of TB does not respond to any of the drugs currently available in South Africa for first- or second-line treatment. It is now clear that the problem has been around for much longer than health department officials have suggested, and is far more extensive. By 23 November 2006, 303 cases of XDR-TB had been reported, of which 263 were in KwaZulu-Natal. Serious thought has been put to isolation procedures that may deny some patients their mobility. This has been seen as unconstitutional by the government and patients come and go as they see fit. The few that do get quarantined start riots and stone security guards. Quarantining patients is necessary to prevent further spread of this strain of TB.