INTRODUCTION Pneumonia is an inflammation of the lungs caused by an infection. It is also called Pneumonitis or Bronchopneumonia.

Pneumonia can be a serious threat to our health. Although pneumonia is a special concern for older adults and those with chronic illnesses, it can also strike young, healthy people as well. It is a common illness that affects thousands of people each year in the Philippines, thus, it remains an important cause of morbidity and mortality in the country. There are many kinds of pneumonia that range in seriousness from mild to life-threatening. In infectious pneumonia, bacteria, viruses, fungi or other organisms attack your lungs, leading to inflammation that makes it hard to breathe. Pneumonia can affect one or both lungs. In the young and healthy, early treatment with antibiotics can cure bacterial pneumonia. The drugs used to fight pneumonia are determined by the germ causing the pneumonia and the judgment of the doctor. Its best to do everything we can to prevent pneumonia, but if one do get sick, recognizing and treating the disease early offers the best chance for a full recovery. A case with a diagnosis of Pneumonia may catch ones attention, though the disease is just like an ordinary cough and fever, it can lead to death especially when no intervention or care is done. Since the case is a toddler, an appropriate care has to be done to make the patients recovery faster. Treating patients with pneumonia is necessary to prevent its spread to others and make them as another victim of this illness. ANATOMY AND PHYSIOLOGY The lungs constitute the largest organ in the respiratory system. They play an important role in respiration, or the process of providing the body with oxygen and releasing carbon dioxide. The lungs expand and contract up to 20 times per minute taking in and disposing of those gases. Air that is breathed in is filled with oxygen and goes to the trachea, which branches off into one of two bronchi. Each bronchus enters a lung. There are two lungs, one on each side of the breastbone and protected by the ribs. Each lung is made up of lobes, or sections. There are three lobes in the right lung and two lobes in the left one. The lungs are cone shaped and made of elastic, spongy tissue. Within the lungs, the bronchi branch out into minute pathways that go through the lung tissue. The pathways are called bronchioles, and they end at microscopic air sacs called alveoli. The alveoli are surrounded by capillaries and provide oxygen for the blood in these vessels. The oxygenated blood is then pumped by the heart throughout the body. The alveoli also take in carbon dioxide, which is then exhaled from the body. Inhaling is due to contractions of the diaphragm and of muscles between the ribs. Exhaling results from relaxation of those muscles. Each lung is surrounded by a two-layered membrane, or the pleura, that under normal circumstances has a very, very small amount of fluid between the layers. The fluid allows the membranes to easily slide over each other during breathing. PATHOPHYSIOLOGY

Pneumonia is a serious infection or inflammation of your lungs. The air sacs in the lungs fill with pus and other liquid. Oxygen has trouble reaching your blood. If there is too little oxygen in your blood, your body cells cant work properly. Because of this and spreading infection through the body pneumonia can cause death. Pneumonia affects your lungs in two ways. Lobar pneumonia affects a section (lobe) of a lung. Bronchial pneumonia (or bronchopneumonia) affects patches throughout both lungs. Bacteria are the most common cause of pneumonia. Of these, Streptococcus pneumoniae is the most common. Other pathogens include anaerobic bacteria, Staphylococcus aureus, Haemophilus influenzae, Chlamydia pneumoniae, C. psittaci, C. trachomatis, Moraxella (Branhamella) catarrhalis, Legionella pneumophila, Klebsiella pneumoniae, and other gram-negative bacilli. Major pulmonary pathogens in infants and children are viruses: respiratory syncytial virus, parainfluenza virus, and influenza A and B viruses. Among other agents are higher bacteria including Nocardia and Actinomyces sp; mycobacteria, including Mycobacterium tuberculosis and atypical strains; fungi, including Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis, Cryptococcus neoformans, Aspergillus fumigatus, and Pneumocystis carinii; and rickettsiae, primarily Coxiella burnetii (Q fever). The usual mechanisms of spread are inhaling droplets small enough to reach the alveoli and aspirating secretions from the upper airways. Other means include hematogenous or lymphatic dissemination and direct spread from contiguous infections. Predisposing factors include upper respiratory viral infections, alcoholism, institutionalization, cigarette smoking, heart failure, chronic obstructive airway disease, age extremes, debility, immunocompromise (as in diabetes mellitus and chronic renal failure), compromised consciousness, dysphagia, and exposure to transmissible agents. Typical symptoms include cough, fever, and sputum production, usually developing over days and sometimes accompanied by pleurisy. Physical examination may detect tachypnea and signs of consolidation, such as crackles with bronchial breath sounds. This syndrome is commonly caused by bacteria, such as S. pneumoniae and H. influenzae.

NURSING PROFILE a. Patients Profile Name: R.C.S.B. Age: 1 yr,1 mo.

Weight:10 kgs Religion: Roman Catholic Mother: C.B. Address: Valenzuela City b. Chief Complaint: Fever Date of Admission: 1st admission Hospital Number: 060000086199 c. History of Present Illness 2 days PTA (+) cough (+) nasal congestion, watery to greenish (+) nasal discharge Tx: Disudrin OD Loviscol OD Few hrs PTA - (+) fever, Tmax= 39.3 C (+) difficulty of breathing (+) vomiting, 1 episode Tx: Paracetamol Sought consultation at ER: Rx=BPN, Salbutamol neb. IE: T = 38.3C, CR= 122s, RR= 30s (+) TPC SCE, (-) retractions, clear BS, (-) cyanosis, (-) edema d. Past Illness (-) asthma (-) allergies e. Family History PMHx: (+) asthma (mother) f. Activities of Daily Living y Sleeping mostly at night and during afternoon y Usually wakes up early in the morning (5AM) to be milkfed. y Eats a lot (hotdogs, chicken, crackers, any food given to her) y Active, responsive y BM (1-2 times a day) y Urinates in her diaper (more than 4 times a day) y Likes to play with those around her g. Review of Systems Neuromuscular: weakness of muscles Integumentary: (-) cyanosis Respiratory: tavhypnea; (+) DOB; (+) coarse crackles, (+) wheezes, Digestive: food aversion, vomits ingested milk

DRUG STUDY View NCP NURSING ACTIONS

INDEPENDENT

   

positioning of the patient with head on mid line, with slight flexion rationale: to provide patent, unobstructed airway , maximum lung excursion auscultating patients chest rationale: to monitor for the presence of abnormal breath sounds provide chest and back clapping with vibration rationale: chest physiotheraphy facilitates the loosening of secretions considering that the patient is an infant, and has developed a strong stranger anxiety as manifested by white coat syndrome , it is a nursing action to play with the patient. rationale: to establish rapport, and gain the patients trust DEPENDENT administer due medications as ordered by the physician, bronchodilators, anti pyretics and anti biotics rationale: bronchodilators decrease airway resistance, secondary to bronchoconstriction, anti pyretics alleviate fever, antibiotics fight infection placing patient on TPN prn rationale: to compensate for fluid and nutritional losses during vomiting COLLABORATIVE assist respiratory therapist in performing nebulization of the patient rationale: nebulization is a favourable route of administering bronchodilators and aid in expectorating secretions, hence patients breathing

  

PHYSICIANS ORDER SHEET

11/19/06 Admit patient to ROC under the service of Dr. Vitan secure consent for admission and management, TPR every shift then record. May have diet for age with strict aspiration precaution, IVF D5 0.3NaCl 500cc to run at 62-63mgtts/min.May give paracetamol 125mg 1supp/rectum if oral paracetamol is not tolerated. 11/20/06 For urinalysis, IVF to follow D5 0.3 NaCl 500 at SR (62-63mgtt/m Use zinacef brand of cefuroxine 750mg- given vial 375mg every 8hours, nebulize nebule) every 6 hours, paracetamol drugs prn every 4hours (Temp 37.8). 11/21/06 Continue cefuroxine and nebulizer every 6 hours. May not reinsert IVF, revise Cefuroxine IV to Cefuroxine 500mg via deep Intramuscular BID,continue management. 11/22/06 Continue management and refer.

(Ventolin 1

DISCHARGE PLANNING
       
Take the entire course of any prescribed medications. After a patients temperature returns to normal, medication must be continued according to the doctors instructions, otherwise the pneumonia may recur. Relapses can be far more serious than the first attack. Get plenty of rest. Adequate rest is important to maintain progress toward full recovery and to avoid relapse. Drink lots of fluids, especially water. Liquids will keep patient from becoming dehydrated and help loosen mucus in the lungs. Keep all of follow-up appointments. Even though the patient feels better, his lungs may still be infected. Its important to have the doctor monitor his progress. Encourage the guardians to wash patients hands. The hands come in daily contact with germs that can cause pneumonia. These germs enter ones body when he touch his eyes or rub his nose. Washing hands thoroughly and often can help reduce the risk. Tell guardians to avoid exposing the patient to an environment with too much pollution (e.g. smoke). Smoking damages ones lungs natural defenses against respiratory infections. Give supportive treatment. Proper diet and oxygen to increase oxygen in the blood when needed. Protect others from infection. Try to stay away from anyone with a compromised immune system. When that isnt possible, a person can help protect others by wearing a face mask and always coughing into a tissue.


1.

Is an inflammation of the lower airways characterized by excessive secretion of mucus, hypertrophy of mucous glands, and recurring infection, progressing to narrowing and obstruction of airflow. Assessment: Signs and symptoms of chronic bronchitis(insidious onset): Productive cough lasting at least 3 months during a year for 2 successive years. Thick, gelatinous sputum (greater amounts produced during superimposed infections). Dyspnea and wheezing as disease progresses. Diagnostic Evaluation:

  
1.

Pulmonary function tests, to demonstrate airflow obstruction-reduced forced expiratory volume in 1 second (FEV1), FEV1 to forced vital capacity ratio; increased residual volume to total lung capacity (TLC) ration, possibly increased TLC. 2. Chest X-rays to detect hyperinflation, flattened diaphragm, increased retrosternal space, decreased vascular markings, possible bullae (all in late stages). 3. Arterial blood gases, to detect decreased arterial oxygen pressure (PaO2), pH, and increased arterial carbon dioxide pressure (Paco2). 4. Sputum smears and cultures to identify pathogens. Therapeutic and Surgical Interventions: 1. 2. 3. 4. 5. 6. 1. 2. 3. 4. 5. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Smoking cessation to stop the progression and preserve lung capacity. Low-flow oxygen to correct severe hypoxemia in a controlled manner and minimize carbon dioxide retention. Home oxygen therapy, especially at night to prevent turnal oxygen desaturation. Pulmonary rehabilitation to reduce symptoms that limit activity. Chest physical therapy, including postural drainage and breathing retraining. Lung transplant in severe cases of alpha1-antitrypsin deficiency. Pharmacologic Intervention: Bronchodilators to reduce dyspnea and control bronchospasm delivered by metered-dose inhaler, other handheld devices, or nebulization. Inhaled corticosteriods may be useful for some with severe airflow limitation and frequent exacerbations. Corticosteroids by mouth or I.V. in acute exacerbations. Antimicrobials to control secondary bacterial infections in the bronchial tree, thus clearing the airways. Alpha1-antitrypsin replacement delivered by I.V. infusion. Nursing Interventions: Monitor for adverse effects of bronchodilators-tremulousness, tachycardia, cardiac arrhythmias, central nervous system stimulation, hypertension. Monitor oxygen saturation at rest and with activity. Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation usually reduces pulmonary irritation, sputum production, and cough. Keep the patients room as dust-free as possible. Use postural drainage positions to help clear secretions responsible for airway obstruction. Teach controlled coughing. Encourage high level of fluid intake (8 to 10 glasses; 2 to 2.5 L daily) within level of cardiac reserve. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. Add moisture (humidifier, vaporizer) to indoor air. Avoid dairy products if these increase sputum production. Encourage the patient to assume comfortable position to decrease dyspnea. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and depth of respiration and improve respiratory muscle coordination.

11. 12. 13. 14. 15. 16.

Discuss and demonstrates relaxation exercises to reduce stress, tension, and anxiety. Encourage frequent small meals if the patient is dyspneic; en a small increase in abdominal contents may press on diaphragm and impede breathing. Offer liquid nutritional supplements to improve caloric intake and counteract weight loss. Avoid foods producing abdominal discomfort. Encourage use of portable oxygen system for ambulation for patients with hypoxemia and marked disability. Encourage the patient in energy conservation techniques.


1. 2. 3. 1. 1. 2. 1. 2. 3. 1. 2. 3. 4. 5. 6. 7.

Is an infection of the lower respiratory tract that generally follows an upper respiratory tract infection. As a result of this viral (most common) or bacterial infection, the airways become inflamed and irritated, and mucus production increases. Assessment: Fever, tachypnea, mild dyspnea, pleuritic chest pain (possible). Cough with clear to purulent sputum production. Diffuse rhonchi and crackles(contrast with localized crackles usually heard with pneumonia). Diagnostic Evaluation: Chest X-ray may rule out pneumonia. In bronchitis, films show no evidence of lung infiltrates or consolidation. Therapeutic Intervention: Chest physiotherapy to mobilize secretions, if indicated. Hydration to liquefy secretions. Pharmacologic Interventions: Inhaled bronchodilators to reduce bronchospasm and promote sputum expectoration. A course of oral antibiotics such as a macrolide may be instituted, but is controversial. Symptom management for fever and cough. Nursing Interventions: Encourage mobilization of secretion through ambulation, coughing, and deep breathing. Ensure adequate fluid intake to liquefy secretions and prevent dehydration caused by fever and tachypnea. Encourage rest, avoidance of bronchial irritant, and a good diet to facilitate recovery. Instruct the patient to complete the full course of prescribed antibiotics and explain the effect of meals on drug absorption. Caution the patient on using over-the-counter cough suppressants, antihistamines, and decongestants, which may cause drying and retention of secretions. However, cough preparations containing the mucolytic guaifenesin may be appropriate. Advise the patient that a dry cough may persist after bronchitis because of irritation of airways. Suggest avoiding dry environments and using a humidifier at bedside. Encourage smokingcessation. Teach the patient to recognize and immediately report early signs and symptoms of acutebronchitis.

Bronchitis is one of the top conditions for which patients seek medical care. It is characterized by inflammation of the bronchial tubes (or bronchi), the air passages that extend from the trachea into the small airways and alveoli. (See Clinical Presentation.) Chronic bronchitis is defined clinically as cough with sputum expectoration for at least 3 months a year during a period of 2 consecutive years. Chronic bronchitis is associated with hypertrophy of the mucus-producing glands found in the mucosa of large cartilaginous airways. As the disease advances, progressive airflow limitation occurs, usually in association with pathologic changes of emphysema. This condition is called chronic obstructive pulmonary disease. (See Clinical Presentation.) When a stable patient experiences sudden clinical deterioration with increased sputum volume, sputum purulence, and/or worsening of shortness of breath, this is referred to as an acute exacerbation of chronic bronchitis, as long as conditions other than acute tracheobronchitis are ruled out. (See Diagnosis.) Triggers of bronchitis may be infectious agents, such as viruses or bacteria, or noninfectious agents, such as smoking or inhalation of chemical pollutants or dust. Bronchitis typically occurs in the setting of an upper respiratory illness; thus, it is observed more frequently in the winter months. (See Etiology.) Allergens and irritants can produce a similar clinical picture. Asthma can be mistakenly diagnosed as acute bronchitis if the patient has no prior history of asthma. In one study, one third of patients who had been determined to have recurrent bouts of acute bronchitis were eventually identified as having asthma. Generally, bronchitis is a diagnosis made by exclusion of other conditions such as sinusitis, pharyngitis, tonsillitis, and pneumonia. (See Diagnosis.) Acute bronchitis is manifested by cough and, occasionally, sputum production that last for no more than 3 weeks. Although bronchitis should not be treated with antimicrobials, it is frequently difficult to refrain from prescribing them. Accurate testing and decision-making protocols regarding who might benefit from antimicrobial therapy would be useful but are not currently available. (See Treatment and Management, as well as Medication.) To see complete information on Pediatric Bronchitis, please go to the main

Pathophysiology
During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis.

In the case of mycoplasmal pneumonia, bronchial irritation results from the attachment of the organism (Mycoplasma pneumoniae) to the respiratory mucosa, with eventual sloughing of affected cells. Acute bronchitis usually lasts approximately 10 days. If the inflammation extends downward to the ends of the bronchial tree, into the small bronchi (bronchioles), and then into the air sacs, bronchopneumonia results. Chronic bronchitis is associated with excessive tracheobronchial mucus production sufficient to cause cough with expectoration for 3 or more months a year for at least 2 consecutive years. The alveolar epithelium is both the target and the initiator of inflammation in chronic bronchitis. A predominance of neutrophils and the peribronchial distribution of fibrotic changes result from the action of interleukin 8, colony-stimulating factors, and other chemotactic and proinflammatory cytokines. Airway epithelial cells release these inflammatory mediators in response to toxic, infectious, and inflammatory stimuli, in addition to decreased release of regulatory products such as angiotensin-converting enzyme or neutral endopeptidase. Chronic bronchitis can be categorized as simple chronic bronchitis, chronic mucopurulent bronchitis, or chronic bronchitis with obstruction. Mucoid sputum production characterizes simple chronic bronchitis. Persistent or recurrent purulent sputum production in the absence of localized suppurative disease, such as bronchiectasis, characterizes chronic mucopurulent bronchitis. Chronic bronchitis with obstruction must be distinguished from chronic infective asthma. The differentiation is based mainly on the history of the clinical illness: patients who have chronic bronchitis with obstruction present with a long history of productive cough and a late onset of wheezing, whereas patients who have asthma with chronic obstruction have a long history of wheezing with a late onset of productive cough. Chronic bronchitis may result from a series of attacks of acute bronchitis, or it may evolve gradually because of heavy smoking or inhalation of air contaminated with other pollutants in the environment. When so-called smoker's cough is continual rather than occasional, the mucus-producing layer of the bronchial lining has probably thickened, narrowing the airways to the point where breathing becomes increasingly difficult. With immobilization of the cilia that sweep the air clean of foreign irritants, the bronchial passages become more vulnerable to further infection and the spread of tissue damage

About these extrapolations of prevalence and incidence statistics for Chronic Bronchitis: These statistics are calculated extrapolations of various prevalence or incidence rates against the populations of a particular country or region. The statistics used for prevalence/incidence of Chronic Bronchitis are typically based on US, UK, Canadian or Australian statistics. This extrapolation calculation is automated and does not take into account any genetic, cultural, environmental, social, racial or other differences across the various countries and regions for which the extrapolated Chronic Bronchitis statistics below refer to. As such, these extrapolations may be highly inaccurate (especially for developing or third-world countries) and only give a general indication (or even a meaningless indication) as to the actual prevalence or incidence of Chronic Bronchitis in that region.
About prevalence and incidence statistics in general for Chronic Bronchitis: The word 'prevalence' of Chronic Bronchitis usually means the estimated population of people who are managing Chronic Bronchitis at any given time (i.e. people with Chronic Bronchitis). The term 'incidence' of Chronic Bronchitis means the annual diagnosis rate, or the number of new cases of Chronic Bronchitis diagnosed each year (i.e. getting Chronic Bronchitis). Hence, these two statistics types can differ: a short disease like flu can have high annual incidence but low prevalence, but a life-long disease like diabetes has a low annual incidence but high prevalence. For more information see about prevalence and incidence statistics.

Read more at http://www.cureresearch.com/c/chronic_bronchitis/stats-country.htm?ktrack=kcplink

Incidence (annual) of Acute Bronchitis: 4.6 per 100 (NHIS96: acute bronchitis); 14.2 million cases annually Incidence Rate for Acute Bronchitis: approx 1 in 21 or 4.60% or 12.5 million people in USA [about data] Extrapolation of Incidence Rate for Acute Bronchitis to Countries and Regions: WARNING! EXTRAPOLATION ONLY. NOT BASED ON COUNTRY-SPECIFIC DATA SOURCES. The following table attempts to extrapolate the above incidence rate for Acute Bronchitis to the populations of various countries and regions. As discussed above, these incidence extrapolations for Acute Bronchitis are only estimates and may have very limited relevance to the actual incidence of Acute Bronchitis in any region:

Country/Region Extrapolated Incidence Population Estimated Used Acute Bronchitis in North America (Extrapolated Statistics) USA 13,508,148 293,655,4051 Canada 1,495,362 WARNING! (Details) 32,507,8742 Mexico 4,828,141 WARNING! (Details) 104,959,5942 Acute Bronchitis in Central America (Extrapolated Statistics) Belize 12,555 WARNING! (Details) 272,9452 Guatemala 656,907 WARNING! (Details) 14,280,5962 Nicaragua 246,548 WARNING! (Details) 5,359,7592 Acute Bronchitis in Caribbean (Extrapolated Statistics) Puerto Rico 179,306 WARNING! (Details) 3,897,9602

Acute Bronchitis in South America (Extrapolated Statistics) Brazil 8,468,650 WARNING! (Details) 184,101,1092 Chile 727,902 WARNING! (Details) 15,823,9572 Colombia 1,946,295 WARNING! (Details) 42,310,7752 Paraguay 284,802 WARNING! (Details) 6,191,3682 Peru 1,267,038 WARNING! (Details) 27,544,3052 Venezuela 1,150,799 WARNING! (Details) 25,017,3872 Acute Bronchitis in Northern Europe (Extrapolated Statistics) Denmark 249,016 WARNING! (Details) 5,413,3922 Finland 239,867 WARNING! (Details) 5,214,5122 Iceland 13,522 WARNING! (Details) 293,9662 Sweden 413,374 WARNING! (Details) 8,986,4002 Acute Bronchitis in Western Europe (Extrapolated Statistics) Britain (United Kingdom) 2,772,452 WARNING! (Details) 60,270,708 for UK2 Belgium 476,020 WARNING! (Details) 10,348,2762 France 2,779,513 WARNING! (Details) 60,424,2132 Ireland 182,599 WARNING! (Details) 3,969,5582 Luxembourg 21,283 WARNING! (Details) 462,6902 Monaco 1,484 WARNING! (Details) 32,2702 Netherlands (Holland) 750,637 WARNING! (Details) 16,318,1992 United Kingdom 2,772,452 WARNING! (Details) 60,270,7082 Wales 134,227 WARNING! (Details) 2,918,0002 Acute Bronchitis in Central Europe (Extrapolated Statistics) Austria 376,039 WARNING! (Details) 8,174,7622 Czech Republic 57,324 WARNING! (Details) 1,0246,1782 Germany 3,791,531 WARNING! (Details) 82,424,6092 Hungary 461,489 WARNING! (Details) 10,032,3752 Liechtenstein 1,538 WARNING! (Details) 33,4362 Poland 1,776,812 WARNING! (Details) 38,626,3492 Slovakia 249,484 WARNING! (Details) 5,423,5672 Slovenia 92,527 WARNING! (Details) 2,011,473 2 Switzerland 342,739 WARNING! (Details) 7,450,8672 Acute Bronchitis in Eastern Europe (Extrapolated Statistics) Belarus 474,283 WARNING! (Details) 10,310,5202 Estonia 61,716 WARNING! (Details) 1,341,6642 Latvia 106,090 WARNING! (Details) 2,306,3062 Lithuania 165,963 WARNING! (Details) 3,607,8992 Russia 6,622,806 WARNING! (Details) 143,974,0592 Ukraine 2,195,675 WARNING! (Details) 47,732,0792

Acute Bronchitis in the Southwestern Europe (Extrapolated Statistics) Azerbaijan 361,945 WARNING! (Details) 7,868,3852 Portugal 484,110 WARNING! (Details) 10,524,1452 Spain 1,852,915 WARNING! (Details) 40,280,7802 Georgia 215,919 WARNING! (Details) 4,693,8922 Acute Bronchitis in the Southern Europe (Extrapolated Statistics) Italy 2,670,643 WARNING! (Details) 58,057,4772 Greece 489,786 WARNING! (Details) 10,647,5292 Acute Bronchitis in the Southeastern Europe (Extrapolated Statistics) Albania 163,061 WARNING! (Details) 3,544,8082 Bosnia and Herzegovina 18,749 WARNING! (Details) 407,6082 Bulgaria 345,826 WARNING! (Details) 7,517,9732 Croatia 206,855 WARNING! (Details) 4,496,8692 Macedonia 93,843 WARNING! (Details) 2,040,0852 Romania 1,028,355 WARNING! (Details) 22,355,5512 Serbia and Montenegro 497,991 WARNING! (Details) 10,825,9002 Acute Bronchitis in Northern Asia (Extrapolated Statistics) Mongolia 126,560 WARNING! (Details) 2,751,3142 Acute Bronchitis in Central Asia (Extrapolated Statistics) Kazakhstan 696,610 WARNING! (Details) 15,143,7042 Tajikistan 322,531 WARNING! (Details) 7,011,556 2 Uzbekistan 1,214,879 WARNING! (Details) 26,410,4162 Acute Bronchitis in Eastern Asia (Extrapolated Statistics) China 59,746,989 WARNING! (Details) 1,298,847,6242 Hong Kong s.a.r. 315,335 WARNING! (Details) 6,855,1252 Japan 5,857,317 WARNING! (Details) 127,333,0022 Macau s.a.r. 20,483 WARNING! (Details) 445,2862 North Korea 1,044,087 WARNING! (Details) 22,697,5532 South Korea 2,218,752 WARNING! (Details) 48,233,7602 Taiwan 1,046,492 WARNING! (Details) 22,749,8382 Acute Bronchitis in Southwestern Asia (Extrapolated Statistics) Turkey 3,169,120 WARNING! (Details) 68,893,9182 Acute Bronchitis in Southern Asia (Extrapolated Statistics) Afghanistan 1,311,629 WARNING! (Details) 28,513,6772 Bangladesh 6,501,661 WARNING! (Details) 141,340,4762 Bhutan 100,536 WARNING! (Details) 2,185,5692 India 48,993,246 WARNING! (Details) 1,065,070,6072 Pakistan 7,323,031 WARNING! (Details) 159,196,3362 Sri Lanka 915,637 WARNING! (Details) 19,905,1652

Acute Bronchitis in Southeastern Asia (Extrapolated Statistics) East Timor 46,885 WARNING! (Details) 1,019,2522 Indonesia 10,968,835 WARNING! (Details) 238,452,9522 Laos 279,133 WARNING! (Details) 6,068,1172 Malaysia 1,082,034 WARNING! (Details) 23,522,4822 Philippines 3,967,117 WARNING! (Details) 86,241,6972 Singapore 200,279 WARNING! (Details) 4,353,8932 Thailand 2,983,813 WARNING! (Details) 64,865,5232 Vietnam 3,802,488 WARNING! (Details) 82,662,8002 Acute Bronchitis in the Middle East (Extrapolated Statistics) Gaza strip 60,949 WARNING! (Details) 1,324,9912 Iran 3,105,147 WARNING! (Details) 67,503,2052 Iraq 1,167,235 WARNING! (Details) 25,374,6912 Israel 285,154 WARNING! (Details) 6,199,0082 Jordan 258,115 WARNING! (Details) 5,611,2022 Kuwait 103,847 WARNING! (Details) 2,257,5492 Lebanon 173,752 WARNING! (Details) 3,777,2182 Saudi Arabia 1,186,613 WARNING! (Details) 25,795,9382 Syria 828,776 WARNING! (Details) 18,016,8742 United Arab Emirates 116,100 WARNING! (Details) 2,523,9152 West Bank 106,315 WARNING! (Details) 2,311,2042 Yemen 921,143 WARNING! (Details) 20,024,8672 Acute Bronchitis in Northern Africa (Extrapolated Statistics) Egypt 3,501,401 WARNING! (Details) 76,117,4212 Libya 259,052 WARNING! (Details) 5,631,5852 Sudan 1,800,815 WARNING! (Details) 39,148,1622 Acute Bronchitis in Western Africa (Extrapolated Statistics) Congo Brazzaville 137,909 WARNING! (Details) 2,998,0402 Ghana 954,823 WARNING! (Details) 20,757,0322 Liberia 155,969 WARNING! (Details) 3,390,6352 Niger 522,584 WARNING! (Details) 11,360,5382 Nigeria 816,516 WARNING! (Details) 12,5750,3562 Senegal 499,198 WARNING! (Details) 10,852,1472 Sierra leone 270,658 WARNING! (Details) 5,883,8892 Acute Bronchitis in Central Africa (Extrapolated Statistics) Central African Republic 172,154 WARNING! (Details) 3,742,4822 Chad 438,773 WARNING! (Details) 9,538,5442 Congo kinshasa 2,682,583 WARNING! (Details) 58,317,0302 Rwanda 378,978 WARNING! (Details) 8,238,6732

Acute Bronchitis in Eastern Africa (Extrapolated Statistics) Ethiopia 3,281,482 WARNING! (Details) 71,336,5712 Kenya 1,517,176 WARNING! (Details) 32,982,1092 Somalia 382,011 WARNING! (Details) 8,304,6012 Tanzania 1,659,256 WARNING! (Details) 36,070,7992 Uganda 1,213,951 WARNING! (Details) 26,390,2582 Acute Bronchitis in Southern Africa (Extrapolated Statistics) Angola 505,013 WARNING! (Details) 10,978,5522 Botswana 75,404 WARNING! (Details) 1,639,2312 South Africa 2,044,629 WARNING! (Details) 44,448,4702 Swaziland 53,785 WARNING! (Details) 1,169,2412 Zambia 507,181 WARNING! (Details) 11,025,6902 Zimbabwe 168,905 WARNING! (Details) 1,2671,8602 Acute Bronchitis in Oceania (Extrapolated Statistics) Australia 916,004 WARNING! (Details) 19,913,1442 New Zealand 183,715 WARNING! (Details) 3,993,8172
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Acute Bronchitis This is one of the most common disorders seen in clinical practice. Bronchitis is generally caused by a virus, and does not respond to antibiotic therapy. Unfortunately, seventy percent of the time, the diagnosis usually leads to a prescription for antibiotics. This diagnosis is one of the leading causes of antibiotic abuse. Bronchitis often evolves from a severe cold. This disorder may also follow or accompany the flu, or it may begin without having had an infection. Bronchitis - an inflammation of the bronchial tubes; may be caused by smoking, air pollution and viral or bacterial infections. Complications of a cold or flu may lead to acute bronchitis, which can be treated with over the counter cold remedies and by drinking plenty of fluids. How can It be treated ? Suffering from a series of acute bronchitis attacks, smoking heavily or inhaling contaminated air for prolonged periods may result in chronic bronchitis. Since chronic bronchitis can be serious, it should receive professional medical attention, no matter what its underlying cause. There is no doubt that cigarette smoking is the chief cause of chronic bronchitis, and recent studies indicate that smoking marijuana causes similar damage. Unless some other factor can be isolated as the irritant that produces the symptoms, the first step in dealing with chronic bronchitis is to stop smoking. To alleviate any symptoms, your doctor may prescribe a combination of medications that will both open up obstructed bronchial airways and thin obstructive mucus so that it can be coughed up more easily. A steam vaporizer near the bed can also be helpful in easing chest congestion at night. Meanwhile, the primary cause of bronchitis is bacterial infections, but asthmatic bronchitis is thought to be activated by tiny specks that break through the safety walls made of cilia of the bronchial tubes. Asthmatic bronchitis also involves congestion of the respiratory tract. Bronchial tubes produce mucus under normal circumstances, this mucus covers the trachea, lungs and other organs in the respiratory system. Nonetheless, in the existence of irritants, an overproduction of mucus occurs, which consequently obstructs the airways. Continuous mucoid obstruction of the respiratory tract is fairly widespread among asthmatic bronchitis patients. General symptoms of asthmatic bronchitis includes dyspnoea or difficulty of breathing and shortness of breath, cough, chest discomforts, wheezing that lasts for several weeks, fatigue or general malaise, pain, weight loss, a general feeling of soreness, and high risk of susceptibility to infections. Although these are also observed among common asthmatic patients, individuals suffering from asthmatic bronchitis have symptoms that are more profound. Sufferers are advised to steer clear from irritants like dust, pollen, smoke, chemicals, and alcohol fumes. They are also advised to avoid bacterial infection, thus they should avoid crowds as much as possible. If it is unavoidable, patients are obliged to wear masks to cover their nose and mouth to prevent bacteria from entering the respiratory tract.

Of course, if an infection develops, it is important to seek medical attention and begin a course of treatment with antibiotics, if the infection is bacterial. If it is viral, there is not much that can be done except to make the patient comfortable and allow the infection to run its course. There are no antibiotics which can treat a virus. By following these techniques, it is possible to make the pain and respiratory difficulties of Asthmatic Bronchitis tolerable. Consulting your physician as soon as a problem develops is wise, and likewise, keeping him/her informed of your progress is important too. Getting plenty of rest helps the body to expend its energy in fighting off the possible infection, rather than doing other work which might worsen the condition. Cough is the most common of all the bronchitis symptoms. It can be dry the first time, because it doesn' t produce any mucus. After a couple of days, it might bring some mucus from the lungs. The color of the mucus as a result of acute bronchitis can be green, clear or yellow. Fever is another symptom for bronchitis, but in the case of acute bronchitis, it is a mild fever. If the temperature is high, that might indicate pneumonia. When suffering from acute bronchitis you will also feel a general tiredness. You will also feel pain in your chest when suffering from bronchitis, which can agravate especially when you cough. Shortness of breath is also another symptom that you might have when you have acute bronchitis. To fully understand all the acute bronchitis symptoms, you must understand what causes the disease. When you develop acute bronchitis, the tubes that are used to carry air to your lungs get inflamated. Acute bronchitis is usually caused by a virus and also bronchitis is the result of a respiratory infection that you probably had. This infection has a very well determined path. It moves from your nose, mouth to the bronchial tubes, causing bronchitis. Your improvement in health from bronchitis depends on a few factors, like age, if you are a smoker or not of whether the acute bronchitis was caused by a virus or bacteria. If bronchitis has been caused by a virus, you will get better sooner than if the acute bronchitis had been caused by bacteria. As many of the lung related diseases, acute bronchitis can also have complications if not treated. For example, if a case of acute bronchitis indicates ingcreased fatigue, a very high temperature, serious chest pain, it usually indicates that acute bronchitis has developed into pneumonia. Another problem would be repeated episodes of acute bronchitis caused by bacteria.This condition may lead to permanent damage of the bronchial tubes. This case of acute bronchitis gone wrong usually happens to people that smoke of those who have a weak immune system. So be careful how you treat your bronchitis case!

Acute bronchitis
From Wikipedia, the free encyclopedia

Acute Bronchitis

Classification and external resources

This image shows the consequences of acute bronchitis.

ICD-10

J20.-J21.

ICD-9

466

MeSH

D001991

Acute bronchitis is an inflammation of the large bronchi (medium-size airways) in the lungs that is usually caused by viruses or bacteria and may last several days or weeks.[1] Characteristic symptoms include cough, sputum (phlegm) production, and shortness of breath and wheezing related to the obstruction of the inflamed airways. Diagnosis is by clinical examination and sometimes microbiological examination of the phlegm. Treatment for acute bronchitis is typically symptomatic. As viruses cause most cases of acute bronchitis, antibiotics should not be used unless microscopic examination ofgram-stained sputum reveals large numbers of bacteria.
Contents
[hide]

1 Cause/etiology 2 Signs and symptoms 3 Diagnosis 4 Treatment

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4.1 Antibiotics 4.2 Smoking cessation 4.3 Antihistamines

5 Prognosis 6 Prevention 7 See also 8 References 9 External links

[edit]Cause/etiology

Acute bronchitis can be caused by contagious pathogens. In about half of instances of acute bronchitis, a bacterial or viral pathogen is identified. Typical viruses include respiratory syncytial virus,rhinovirus, influenza, and others.

  

Damage caused by irritation of the airways leads to inflammation and leads to neutrophils infiltrating the lung tissue. Mucosal hypersecretion is promoted by a substance released by neutrophils. Further obstruction to the airways is caused by more goblet cells in the small airways. This is typical of chronic bronchitis.

Although infection is not the reason or cause of chronic bronchitis, it is seen to aid in sustaining the bronchitis.

[edit]Signs

and symptoms

Bronchitis may be indicated by an expectorating cough, shortness of breath (dyspnea), and wheezing. On occasion, chest pains, fever, and fatigue or malaise may also occur. In addition, bronchitis caused by Adenoviridae may cause systemic and gastrointestinal symptoms as well. However, the coughs due to bronchitis can continue for up to three weeks or more even after all other symptoms have subsided. [edit]Diagnosis

A physical examination will often reveal decreased intensity of breath sounds, wheezing, rhonchi, and prolonged expiration. Most doctors rely on the presence of a persistent dry or wet cough as evidence of bronchitis.

A variety of tests may be performed in patients presenting with cough and shortness of breath:

A chest X-ray that reveals hyperinflation; collapse and consolidation of lung areas would support a diagnosis of pneumonia. Some conditions that predispose to bronchitis may be indicated by chest radiography.

A sputum sample showing neutrophil granulocytes (inflammatory white blood cells) and culture showing that has pathogenic microorganisms such as Streptococcus species

A blood test would indicate inflammation (as indicated by a raised white blood cell count and elevated C-reactive protein).

[edit]Treatment

[edit]Antibiotics

Only about 5-10% of bronchitis cases are caused by a bacterial infection. Most cases of bronchitis are caused by a viral infection and are "self-limited" and resolve themselves in a few weeks. Acute bronchitis should not be treated with antibiotics unless microscopic examination of the sputum reveals large numbers of bacteria. Treating non-bacterial illnesses with antibiotics leads to the promotion of antibiotic-resistant bacteria, which increase morbidity and mortality.[2] [edit]Smoking

cessation

For more details on this topic, see Smoking cessation.

Many physicians recommend that, to help the bronchial tree heal faster and not make bronchitis worse, smokers should quit smoking completely in order to allow their lungs to recover from the layer of tar that builds up over time. [edit]Antihistamines Using over-the-counter antihistamines may be harmful in the self-treatment of bronchitis.[3]

An effect of antihistamines is to thicken mucus secretions. Expelling infected mucus via coughing can be beneficial in recovering from bronchitis. Expulsion of the mucus may be hindered if it is thickened. Antihistamines can help bacteria to persist[citation needed] and multiply in the lungs by increasing its residence time in a warm, moist environment of thickened mucus.

Using antihistamines along with an expectorant cough syrup may be doubly harmful, encouraging the production of mucus and then thickening that which is produced. Using an expectorant cough syrup alone might be useful in flushing bacteria from the lungs. Using an antihistamine along with it works against the intention of using the expectorant. [edit]Prognosis

Acute bronchitis usually lasts a few days or weeks.[4] It may accompany or closely follow a cold or the flu, or may occur on its own. Bronchitis usually begins with a dry cough, including waking the sufferer at night. After a few days, it progresses to a wetter or productive cough, which may be accompanied by fever, fatigue, and headache. The fever, fatigue, and malaise may last only a few days; but the wet cough may last up to several weeks.

Should the cough last longer than a month, some doctors may issue a referral to an otorhinolaryngologist (ear, nose and throat doctor) to see if a condition other than bronchitis is causing the irritation. It is possible that having irritated bronchial tubes for as long as a few months may inspire asthmatic conditions in some patients.

In addition, if one starts coughing mucus tinged with blood, one should see a doctor. In rare cases, doctors may conduct tests to see whether the cause is a serious condition such as tuberculosis orlung cancer. [edit]Prevention

In 1985, University of Newcastle, Australia Professor Robert Clancy developed an oral vaccine for influenza. This vaccine was commercialised four years later.[5] [edit]See

also

Chronic bronchitis

[edit]References

1.

30. doi:10.1056/NEJMcp061493. PMID 17108344. 2. 3. 4. ^ Hueston WJ (March 1997). "Antibiotics: neither cost effective nor 'cough' effective". The Journal of Family Practice 44 (3): 2615. PMID 9071245. ^ http://www.merck.com/mmhe/sec04/ch039/ch039b.html ^ Bronchitis. Mayo Foundation for Medical Education and Research. 2007-04-20. Retrieved 2008-05-30

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Freuds Stages of Psychosexual Development

Sigmund Freud (1856-1939) is probably the most well known theorist when it comes to the development of personality. Freuds Stages of Psychosexual Developmentare, like other stage theories, completed in a predetermined sequence and can result in either successful completion or a healthy personality or can result in failure, leading to an unhealthy personality. This theory is probably the most well known as well as the most controversial, as Freud believed that we develop through stages based upon a particular erogenous zone. During each stage, an unsuccessful completion means that a child becomes fixated on that particular erogenous zone and either over or under-indulges once he or she becomes an adult.

Wenzel RP, Fowler AA (2006). "Clinical practice. Acute bronchitis". N. Engl. J. Med. 355 (20): 2125

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Oral Stage (Birth to 18 months). During the oral stage, the child if focused on oral pleasures (sucking). Too much or too little gratification can result in an Oral Fixation or Oral Personality which is evidenced by a preoccupation with oral activities. This type of personality may have a stronger tendency to smoke, drink alcohol, over eat, or bite his or her nails. Personality wise, these individuals may become overly dependent upon others, gullible, and perpetual followers. On the other hand, they may also fight these urges and develop pessimism and aggression toward others. Anal Stage (18 months to three years). The childs focus of pleasure in this stage is on eliminating and retaining feces. Through societys pressure, mainly via parents, the child has to learn to control anal stimulation. In terms of personality, after effects of an anal fixation during this stage can result in an obsession with cleanliness, perfection, and control (anal retentive). On the opposite end of the spectrum, they may become messy and disorganized (anal expulsive). Phallic Stage (ages three to six). The pleasure zone switches to the genitals. Freud believed that during this stage boy develop unconscious sexual desires for their mother. Because of this, he becomes rivals with his father and sees him as competition for the mothers affection. During this time, boys also develop a fear that their father will punish them for these feelings, such as by castrating them. This group of feelings is known as Oedipus Complex ( after the Greek Mythology figure who accidentally killed his father and married his mother). Later it was added that girls go through a similar situation, developing unconscious sexual attraction to their father. Although Freud Strongly disagreed with this, it has been termed the Electra Complex by more recent psychoanalysts. According to Freud, out of fear of castration and due to the strong competition of his father, boys eventually decide to identify with him rather than fight him. By identifying with his father, the boy develops masculine characteristics and identifies himself as a male, and represses his sexual feelings toward his mother. A fixation at this stage could result in sexual deviancies (both overindulging and avoidance) and weak or confused sexual identity according to psychoanalysts. Latency Stage (age six to puberty). Its during this stage that sexual urges remain repressed and children interact and play mostly with same sex peers. Genital Stage (puberty on). The final stage of psychosexual development begins at the start of puberty when sexual urges are once again awakened. Through the lessons learned during the previous stages, adolescents direct their sexual urges onto opposite sex peers, with the primary focus of pleasure is the genitals.

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Structure of the Respiratory System

The respiratory system is represented by the following structures, shown in Figure1 :

Figure 1

A view of the entire respiratory system and the upper respiratory tract.
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The nose consists of the visible external nose and the internal nasal cavity. The nasal septum divides the nasal cavity into right and left sides. Air enters two openings, the external nares (nostrils; singular, naris), and passes into the vestibule and through passages called meatuses. The bony walls of the meatuses, called concha, are

formed by facial bones (the inferior nasal concha and the ethmoid bone). From the meatuses, air then funnels into two (left and right) internal nares. Hair, mucus, blood capillaries, and cilia that line the nasal cavity filter, moisten, warm, and eliminate debris from the passing air.

The pharynx (throat) consists of the following three regions, listed in order through which incoming air passes:

The nasopharynx receives the incoming air from the two internal nares. The two auditory (Eustachian) tubes that equalize air pressure in the middle ear also enter here. The pharyngeal tonsil (adenoid) lies at the back of the nasopharynx. The oropharyrnx receives air from the nasopharynx and food from the oral cavity. The palatine and lingual tonsils are located here. The laryngopharynx passes food to the esophagus and air to the larynx.

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The larynx receives air from the laryngopharynx. It consists of the following nine pieces of cartilage that are joined by membranes and ligaments, shown in Figure 2 .

Figure 2

Anterior and sagittal section of the larynx and the trachea.

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The epiglottis, the first piece of cartilage of the larynx, is a flexible flap that covers the glottis, the upper region of the larynx, during swallowing to prevent the entrance of food. The thyroid cartilage protects the front of the larynx. A forward projection of this cartilage appears as the Adam's apple. The paired arytenoids cartilages in the rear are horizontally attached to the thyroid cartilage in the front by folds of mucous membranes. The upper vestibular folds (false vocal cords) contain muscle fibers that bring the folds together and allow the breath to be held during periods of muscular pressure on the thoracic cavity (straining while defecating or lifting a heavy object, for example). The lower vocal folds (true vocal cords) contain elastic ligaments that vibrate when skeletal muscles move them into the path of outgoing air. Various sounds, including speech, are produced in this manner. The cricoid cartilage, the paired cuneiform cartilages, and the paired corniculate cartilages are the remaining cartilages supporting the larynx.

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The trachea (windpipe) is a flexible tube, 10 to 12 cm (4 inches) long and 2.5 cm (1 inch) in diameter, whose wall consists of four layers, as shown in Figure2 :

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The mucosa is the inner layer of the trachea. It contains mucusproducing goblet cells and pseudostratified ciliated epithelium. The movement of the cilia sweep debris away from the lungs toward the pharynx. The submucosa is a layer of areolar connective tissue that surrounds the mucosa. Hyaline cartilage forms 16 to 20 C-shaped rings that wrap around the submucosa. The rigid rings prevent the trachea from collapsing during inspiration. The adventitia is the outermost layer of the trachea. It consists of areolar connective tissue.

The primary bronchi are two tubes that branch from the trachea to the left and right lungs. Inside the lungs, each primary bronchus divides repeatedly into branches of smaller diameters, forming secondary (lobar) bronchi, tertiary (segmental) bronchi, and numerous orders of bronchioles (1 mm or less in diameter), including terminal bronchioles (0.5 mm in diameter) and microscopic respiratory bronchioles. The wall of the primary bronchi are constructed like the trachea, but as the branches of the tree get smaller, the cartilaginous rings and the mucosa are replaced by smooth muscle. Alveolar ducts are the final branches of the bronchial tree. Each alveolar duct has enlarged, bubblelike swellings along its length. Each swelling is called an alveolus, and a cluster of adjoining alveolar is called an alveolar sac. Some adjacent alveoli are connected by alveolar pores. The respiratory membrane consists of the alveolar and capillary walls. Gas exchange occurs across this membrane. Characteristics of this membrane follow:

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Type I cells are thin, squamous epithelial cells that constitute the primary cell type of the alveolar wall. Oxygen diffusion occurs across these cells. Type II cells are cuboidal epithelial cells that are interspersed among the type I cells. Type II cells secrete pulmonary surfactant (a phospholipid bound to a protein) that reduces the surface tension of the moisture that covers the alveolar walls. A reduction in surface tension permits oxygen to diffuse more easily into the moisture. A lower surface tension also prevents the moisture on opposite walls of an alveolus or alveolar duct from cohering and causing the minute airway to collapse. Alveolar macrophage (dust cells) wander among the other cells of the alveolar wall removing debris and microorganisms. A thin epithelial basement membrane forms the outer layer of the alveolar wall. A dense network of capillaries surrounds each alveolus. The capillary walls consist of endothelial cells surrounded by a thin basement membrane. The basement membranes of the alveolus and the capillary are often so close that they fuse.

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PNEUMONIA. You would think that in the light of modern medical treatment and wide availability of antibiotics, Pneumonia would no longer kill us, right? Wrong! For adults, this occurs mainly as a complication of other chronic diseases like lung cancer, COPD, tuberculosis, and other debilitating illnesses that leave them bedridden most of the time. For children, this remains to be a major killer, either as a sole disease beginning with a respiratory infection, or as a complication of measles. This recent study from Cebu City concludes that most physicians do not adhere to the local guidelines in treating community-acquired pneumonia. Also, there's the other form of more fatal pneumonia --- the hospital-acquired type. This is the pneumonia you get when your length of stay in the hospital is long, and the antibiotics used to treat are the higher generations.