Circadian rhythm

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Some features of the human circadian biological clock A circadian rhythm ( /srkedin/) is any biological process that displays an endogenous, entrainable oscillation of about 24 hours. These rhythms are driven by a circadian clock, and rhythms have been widely observed in plants, animals, fungi and cyanobacteria. The term circadian comes from the Latin circa, meaning "around" (or "approximately"), and diem or dies, meaning "day". The formal study of biological temporal rhythms, such as daily, tidal, weekly, seasonal, and annual rhythms, is called chronobiology. Although circadian rhythms are endogenous ("built-in", self-sustained), they are adjusted (entrained) to the local environment by external cues called zeitgebers, commonly the most important of which is daylight.

History
The earliest known account of a circadian process dates from the 4th century BC, when Androsthenes, a ship captain serving under Alexander the Great, described diurnal leaf movements of the tamarind tree.[1] The observation of a circadian or diurnal process in humans is mentioned in Chinese medical texts dated to around the 13th century, including the Noon and Midnight Manual and the Mnemonic Rhyme to Aid in the Selection of Acu-points According to the Diurnal Cycle, the Day of the Month and the Season of the Year.[2] The first recorded observation of an endogenous circadian oscillation was by the French scientist JeanJacques d'Ortous de Mairan in 1729. He noted that 24-hour patterns in the movement of the leaves of the plant Mimosa pudica continued even when the plants were kept in constant darkness, in the first experiment to attempt to distinguish an endogenous clock from responses to daily stimuli. [3][4] In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours.[5] In 1918, J.S. Szymanski showed

that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature.[6] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic component of a circadian clock.[7] Joseph Takahashi discovered the first mammalian 'clock gene' (CLOCK) using mice in 1994.[8][9] The term "circadian" was coined by Franz Halberg in the late 1950s.[10]

Criteria
To be called circadian, a biological rhythm must meet these four general criteria: 1. 2. The rhythms repeat once a day (they have a 24-hour period). In order to keep track of the time of day, a clock must be at the same point at the same time each day, i.e. repeat every 24 hours. The rhythms persist in the absence of external cues (endogenous). The rhythm persists in constant conditions with a period of about 24 hours. The rationale for this criterion is to distinguish circadian rhythms from simple responses to daily external cues. A rhythm cannot be said to be endogenous unless it has been tested in conditions without external periodic input. The rhythms can be adjusted to match the local time (entrainable). The rhythm can be reset by exposure to external stimuli (such as light and heat), a process called entrainment. The rationale for this criterion is to distinguish circadian rhythms from other imaginable endogenous 24-hour rhythms that are immune to resetting by external cues, and hence do not serve the purpose of estimating the local time. Travel across time zones illustrates the ability of the human biological clock to adjust to the local time; a person will usually experience jet lag before entrainment of their circadian clock has brought it into sync with local time. The rhythms maintain circadian periodicity over a range of physiological temperatures; they exhibit temperature compensation. Some organisms live at a broad range of temperatures, and differences in thermal energy will affect the kinetics of all molecular processes in their cell(s). In order to keep track of time, the organism's circadian clock must maintain a roughly 24-hour periodicity despite the changing kinetics, a property known as temperature compensation.

3.

4.

In the healthy lung the airsacs look like a bunch of grapes. Ventilation is the movement of air in and out of these airsacs. Each airsac is surrounded by blood vessels. Perfusion is the movement of blood through these vessels. The area where the airsacs and blood vessels meet is where the exchange of oxygen and carbon dioxide occur. Air is inhaled. The oxygen moves from the airsacs of the lung to the blood. It then travels to the cells of the body. Carbon dioxide travels from the cells of the body to the airsacs of the lung through the blood. The term COPD is an abbreviation for Chronic Obstructive Pulmonary Disease. COPD is a general term used to describe the chronic lung disease linked with cigarette smoking. When the lungs are affected by COPD there is a relatively irreversible decrease in airflow and permanent destruction of the airsacs in the lung. Over time this creates some areas where there is a blood supply without any airsac. This is considered a ventilation-perfusion mismatch. When airsacs of the lung are destroyed, there is less surface area for oxygen to get from the lungs into the blood and for carbon dioxide to get from the blood into the lungs to be exhaled. This can reach a point where the amount of oxygen in the blood is low. This is called hypoxemia. This can also reach a point where

the amount of carbon dioxide in the blood is high. This is called hypercarbia or hypercapnia.

Bronchitis

This diagram shows acute 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 divided into two categories, acute and chronic, each of which has two distinct etiologies, pathologies, and therapies. Acute 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, whereas bacteria account for fewer than 10%.[1] Chronic bronchitis, a type of chronic obstructive pulmonary disease, is characterized by the presence of a productive cough that lasts for three months or more per year for at least two 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.[1]

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, pleurisy, malaise, and the production of sputum.[1] Acute bronchitis often develops during 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, Chlamydophila pneumoniae, Bordetella pertussis, streptococcus pneumoniae, and haemophilus influenzae, 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, and expectorants 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] Only about 510% of bronchitis cases are caused by a bacterial infection. Most cases of bronchitis are caused by a viral infection and are "self-limiting" and resolve themselves in a few weeks.[2] As most cases of acute bronchitis are caused by viruses, antibiotics should not generally be used, since they are effective only against bacteria. Using antibiotics in patients without bacterial infections promotes the development of antibiotic-resistant bacteria, which may lead to greater morbidity and mortality. However, even in cases of viral bronchitis, antibiotics may be indicated in certain patients in order to prevent the occurrence of secondary bacterial infections.

Chronic bronchitis
Main article: Chronic bronchitis
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 and shortness 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 females than in males.[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 reducing bronchospasm (reversible narrowing of smaller bronchi due to constriction of the smooth muscle) with bronchodilators such as inhaled -Adrenergic agonists (e.g., salbutamol) 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, in general, does not cause the airways to collapse prematurely and trap air in the lungs.[citation needed]

Protracted bacterial bronchitis

Protracted bacterial bronchitis is defined as a chronic wet cough, with a positive bronchoalveolar lavage (BAL), that resolves with antibiotics.[5] It is usually caused by Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis.[5]

Dengan bantuan spirometer, resistensi pernapasan akibat tahanan gesekan terhadap aliran udara (resitensi nonelastik) dapat diperkirakan dengan mengukur volume eksipirasi paksa dan kecepatan aliran udara:

Kapasitas vital paksa (FVC) adalah pengukuran kapasitas vital yang didapat pada ekspirasi yang dilakukan secepat dan sekuat mungkin. Volume udara ini sangat penting dan dalam keadaan normal nilainya kurang lebih sama dengan VC, tetapi mungkin sangat berkurang pada pasien obstruksi saluran napas.

Volume ekspirasi paksa (FEV) adalah volume udara yang dapat diekspirasi dalam waktu standar selama tindakan FVC. Biasanya FEV diukur selama detik pertama ekspirasi yang paksa (FEV1) dan detik ketiga (FEV3). Pada keadaan normal, besar FEV1 adalah 83% (70-80%) dari VC dan FEV3 = 97% (85-100%) dari VC. FEV merupakan petunjuk penting untuk mengetahui adanya gangguan kapasitas ventilasi. Kapasitas Pernapasan Maksimal (Maximal Breath Capacity) ditentukan dengan cara mengukur volume hiperventilasi maksimal dalam 1 menit
(amplitudo x frekuensi 12 x 5). Untuk menetapkan KPM normal seseorang dapat kita gunakan rumus: Sex Females Males Males Formulae [71.3 (0.474 x age)] m2s. area [86.5 (0.522 x age)] x m2s.area 228 (182 x age) Reference Baldwin Baldwin Wright, normal 17,6%

KPM, sama seperti KV dapat dinyatakan dalam liter secara mutlak, akan tetapi dapat juga dinyatakan secara relative dalam % dari predicted MBCnya KPM Relatif = KPM mutlak x 100% Predicted CV Cara menetapkan volume cadangan pernapasan: Volume Cad. Pernafasan = KPM Volume Pernapasan Semenit x 100% RPM

Spirometri adalah pemeriksaan yang dilakukan untuk mengukur secara obyektif kapasitas/fungsi paru (ventilasi) pada pasien dengan indikasi medis. Alat yang digunakan disebut spirometer.

Tujuan : mengukur volume paru secara statis dan dinamik menilai perubahan atau gangguan pada faal paru

Prinsip spirometri adalah mengukur kecepatan perubahan volume udara di paru-paru selama pernafasan yang dipaksakan atau disebut forced volume capacity (FVC). Prosedur yang paling umum digunakan adalah subyek menarik nafas secara maksimal dan menghembuskannya secepat dan selengkap mungkin Nilai FVC dibandingkan terhadap nilai normal dan nilai prediksi berdasarkan usia, tinggi badan dan jenis kelamin.

Sebelum dilakukan spirometri, terhadap pasien dilakukan anamnesa, pengukuran tinggi badan dan berat badan. Pada spirometer terdapat nilai prediksi untuk orang Asia berdasarkan umur dan tinggi badan. Bila nilai prediksi tidak sesuai dengan standar Indonesia, maka dilakukan penyesuaian nilai prediksi menggunakan standar Indonesia. Volume udara yang dihasilkan akan dibuat prosentase pencapaian terhadap angka prediksi.

Spirometri dapat dilakukan dalam bentuk social vital capacity (SVC) atau forced vital capacity (FVC). Pada SCV, pasien diminta bernafas secara normal 3 kali (mouthpiece sudah terpasang di mulut) sebelum menarik nafas dalam-dalam dan dihembuskan secara maksimal. Pada FVC, pasien diminta menarik nafas dalam-dalam sebelum mouth piece dimasukkan ke mulut dan dihembuskan secara maksimal.

Pengukuran fungsi paru yang dilaporkan : 1. 2. Forced vital capacity (FVC) adalah jumlah udara yang dapat dikeluarkan secara paksa setelah inspirasi secara maksimal, diukur dalam liter. Forced Expiratory volume in one second (FEV1) adalah jumlah udara yang dapat dikeluarkan dalam waktu 1 detik, diukur dalam liter. Bersama dengan FVC merupakan indikator utama fungsi paru-paru.

3. 4. 5. 6.

FEV1/FVC merupakan rasio FEV1/FVC. Pada orang dewasa sehat nilainya sekitar 75% 80% FEF 25-75% (forced expiratory flow), optional Peak Expiratory Flow (PEF), merupakan kecepatan pergerakan udara keluar dari paru-paru pada awal ekspirasi, diukur dalam liter/detik. FEF 50% dan FEF 75%, optional, merupakan rata-rata aliran (kecepatan) udara keluar dari paru-paru selama pertengahan pernafasan (sering disebut juga sebagai MMEF(maximal midexpiratory flow)

Klasifikasi gangguan ventilasi (% nilai prediksi) : Gangguan restriksi : Vital Capacity (VC) < 80% nilai prediksi; FVC < 80% nilai prediksi

Gangguan obstruksi : FEV1 < 80% nilai prediksi; FEV1/FVC < 75% nilai prediksi Gangguan restriksi dan obstruksi : FVC < 80% nilai prediksi; FEV1/FVC < 75% nilai prediksi.

Bentuk spirogram adalah hasil dari spirometri. Beberapa hal yang menyebabkan spirogram tidak memenuhi syarat : 1. 2. 3. 4. 5. 6. Terburu-buru atau penarikan nafas yang salah Batuk Terminasi lebih awal Tertutupnya glottis Ekspirasi yang bervariasi Kebocoran

Setiap pengukuran sebaiknya dilakukan minimal 3 kali. Kriteria hasil spirogram yang reprodusibel (setelah 3 kali ekspirasi) adalah dua nilai FVC dan FEV1 dari 3 ekspirasi yang dilakukan menunjukkan variasi/perbedaan yang minimal (perbedaan kurang dari 5% atau 100 mL)

Indications
Spirometry is indicated for the following reasons:

to diagnose or manage asthma[1][2][3] to detect respiratory disease in patients presenting with symptoms of breathlessness, and to distinguish respiratory from cardiac disease as the cause[4] to measure bronchial responsiveness in patients suspected of having asthma[4] to diagnose and differentiate between obstructive lung disease and restrictive lung disease[4] to follow the natural history of disease in respiratory conditions[4] to assess of impairment from occupational asthma[4] to identify those at risk from pulmonary barotrauma while scuba diving[4] to conduct pre-operative risk assessment before anaesthesia or cardiothoracic surgery[4] to measure response to treatment of conditions which spirometry detects[4]

Peak expiratory flow

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Peak expiratory flow Diagnostics

A peak flow meter issued in the UK. MeSH D010366

The peak expiratory flow (PEF), also called peak expiratory flow rate (PEFR) is a person's maximum speed of expiration, as measured with a peak flow meter, a small, hand-held device used to monitor a person's ability to breathe out air. It measures the airflow through the bronchi and thus the degree of obstruction in the airways.

Function

Peak flow readings are higher when patients are well, and lower when the airways are constricted. From changes in recorded values, patients and doctors may determine lung functionality, severity of asthma symptoms, and treatment options. First measure of precaution would be to check patient for signs and symptoms of asthmatic hypervolemia. This would indicate whether or not to even continue with the Peak Flow Meter procedure. Measurement of PEFR requires training to correctly use a meter and the normal expected value depends on a patient's sex, age and height. It is classically reduced in obstructive lung disorders such as asthma. Due to the wide range of normal' values and high degree of variability, peak flow is not the recommended test to identify asthma. However, it can be useful in some circumstances. A small proportion of people with asthma may benefit from regular peak flow monitoring. When monitoring is recommended, it is usually done in addition to reviewing asthma symptoms and frequency of reliever medication use.[1] When peak flow is being monitored regularly, the results may be recorded on a peak flow chart. It is important to use the same peak flow meter every time.

obatnya NaCl, Bisolvon pengecer daha & ventolin).

Hyperinflated lungs can be caused by obstructions in the passages that deliver air to your lung tissue. Air gets trapped within the lung and causes it to overinflate. Hyperinflation can also occur when the air sacs in your lungs become less elastic, which interferes with the expulsion of air from your lungs. One of the most common causes of hyperinflated lungs is chronic obstructive pulmonary disease (COPD) a disorder that includes emphysema. Lung problems such as asthma and cystic fibrosis can also cause hyperinflation. In some cases, lungs may appear hyperinflated on X-rays for reasons unrelated to lung function. If you aren't experiencing shortness of breath, there's probably nothing to worry about. But the only way to know whether you have something that causes truly hyperinflated lungs is to do a lung function test. If your lung function is abnormal, you should see a lung specialist to identify and treat the underlying problem.

Classification and Clinical Diagnosis of Bronchial Asthma :

Classification of Bronchial Asthma : Asthma can be classified in many ways:(A) Usual Classification : A. On the basis of allergya. Allergic of Extrinsic asthma, b. Non allergic or Intrinsic asthma. B. Combination of allergic and non-allergic asthma. C. Factors relatinga. Exercise induced, b. Seasonal, c. Aspirin sensitive etc. D. On the basis of periodicitya. Acute b. Chronic E. On the basis of age of onseta. Early onset (usually allergic of Extrinsic type) b. late onset (usually Intrinsic type). (B) Classification by Naepp, USA. Another classification used by Nation asthma Education and preventive program NAEPP, USA in the following ways-

1) Intermittent asthma: In this form of asthma patient remains symptom free in between attack and peak flow meter recording is normal.

2) Persistent asthma: In this form patient has frequent attack eg, patient has coughing, wheezing or shortness of breath at least > 2 times in a month. There are 3 persistent varietya) Mild persistent variety: Here patient have > 2 times of nocturnal attack, baseline PEFR (peak expiratory flow rate) or FEV1 is usually less than 80% to 65% and also PFT occasionally normal in between attack. b) Moderate persistent asthma: Almost daily complain with baseline PEFR < 65%. c) Severe persistent asthma : Patient having some degree of dyspnea > 6 months and baseline PEFR < 50%. iii) Acute exacerbation : A condition of life threatening attack.

Mild: Moderate: Severe:

Dysponeic but can talk. Cannot complete a sentence. Severely dyspoenic, restless may be unconscious.

iv) Special variants : a) Seasonal asthma: Patients experience asthma only in a particular period of a year. Pollens, moulds are the causative factors. Inhaled corticosteroids, cromlyn sodium are the choice of drugs. b) Exercise induced asthma: Patient experience broncho-spasm during the period of exercise. An exercise challenge test can be used to establish the diagnosis. c) Cough variant asthma: Esonophilic bronchitis is the other name. This variety present with chronic cough and sputum with eosonophilia. d) Drug induced asthma: When drugs like aspirin, b-blocker etc invites broncho-spasm. e) Pregnancy and asthma : During pregnancy asthma follows the rule of one third eg. one third become worse, one third improve and one third remain same. The exact mechanism is unknown. (C) Classification Usually Used By Russian Medical Expertise: Mirror way classification

Extrinsic-non extrinsic (intrinsic) Atopic-Nonatopic Allergic-nonallergic Immunologic-non immunologic Infection -allergic versus Non infection-allergic. etc.

(D) Classification By Grading of Bronchial Asthma (Usually Used In Uk and Australia): a) Mild Asthma

Mild episode, Not more than one attack in a week Response to broncho dilator within 48 hours. Working hour or school time usually not lost, No sleep disturbance,

b) Moderate Asthma

Moderate episode, More than one attack in a week, In between episode cough and wheeze is present frequently, Sleep disturbance present, Working hour often loss.

c) Severe Asthma

Severe episode, Daily wheezing Frequent hospitalization, Frequent loss of working hour, Sleep disturbance is very common, Continuation of broncho dilators + steroids to relief from symptoms.

Difference Points Between Extrinsic And Intrinsic Asthma Common Symptoms: In medicine there are three common symptoms-cough, wheeze and respiratory difficulties. However people tell their experiences during their attack commonly as

Shortness of breath- Here one person complains that he can not finish his each breath before need another. Wheezing- Some one can here whistling noise catching inside the lung. Tightness of chest- Some one feels that an elastic band is placed around his chest. Cough-A cough is often a sign of asthma. Nocturnal cough is a common symptom of asthma.

It is to be remembered that above common symptoms of asthma patient occurs repeatedly. Therefore history is an important factor. During acute phase following signs and symptoms are presentHyperinflation of chest, tachypnea, tachycardia, bronchi, chest recession, use of accessory muscle, agitation, inability to speak, pule us paradoxical, trepoid sitting position etc. Interpretations: 0-4 = No immediate danger, 5-6= Impending respiratory failure, notify ICU and anesthesia,>7= respiratory failure. (Modified from wood DW, Downes JJ). Feathers of severity:

Pulse rate>100, Pulse us paradox us, Unable to speak in one sentence, Peak flow less than 50% of predicted.

Life threatening features:

Can not speak, Central cyanosis, Exhaustion, Bradicardia, Silent chest, Unrecordable peak flow.

Different diagnosis of asthma patientIt is wise to exclude other disease likePTB (pulmonary tuberculosis), CCF, recurrent pneumonia, GE reflux disorder, post nasal drip symptom, Bromchiolities, aspergilosis, tropical eosonophilia, foreign body impaction etc.