Investigation for Pneumonia

Imaging Test
1. X-ray
-A chest X-ray should be obtained to confirm the diagnosis of pneumonia, help guide initial treatment, and exclude other etiologies.

Chest X-ray showing right inferior lobar pneaumonia

For more info, go to this link http://www.accessmedicine.com.ezproxy.lib.monash.edu.au/content.aspx?aID=3111487&searchStr=pneumonia#3111487




2. CT Scan
-may be helpful in differentiating between lung abscess and empyema* when the chest X-ray is equivocal
*Empyema is a collection of pus in the space between the lung and the inside of the chest wall (pleural space).


Laboratory Test
1. Blood test- access white blood cell count
-An individual's white blood cell count can often give a hint as to the severity of the pneumonia and whether it is caused by bacteria or a virus. An increased number of neutrophils is seen in bacterial infections, whereas an increase in lymphocytes, is seen in viral infections, fungal infections, and some bacterial infections (like tuberculosis).

2. Culture of sputum/Gram’s staining-Sputum samples can be collected and examined under the microscope. If the pneumonia is caused by bacteria or fungi, the organisms can often be detected by this examination

3. Arterial blood gases-access for oxygen saturation to determine severity of respiratory illness.

Prognosis & Complications

• Prognosis depends on:
o Severity of lung disease
o Smoking status of patient
• FEV1 > 50% predicted: survival only slightly less than patients without COPD
• FEV1 < 0.75 L (very severe obstruction, < 30% predicted): 1-year mortality rate of 30% and a 10-year mortality rate of 95%
• At any level of lung impairment, prognosis improves when the patient quits smoking.

Cor Pulmonale
- an increase in bulk of the right ventricle of the heart, generally caused by chronic diseases or malfunction of the lungs (e.g. COPD). This condition can lead to heart failure.

Acute Exacerbations
Acute exacerbations of COPD are characterized by an abrupt increase of symptoms:
• Cough and sputum production increases
• Wheezing is often increased or noted for the first time
• Dyspnea is increased or apparent for the first time.

During an acute exacerbation, there is increased airway narrowing due to:
• Bronchospasm
• Edema
• Excessive mucus production.

If narrowed airways cause an extreme increase in the work of breathing that cannot be maintained, the patient will die, unless there is intervention (e.g. mechanical ventilation).

End-stage lung disease
- The final stages of lung disease, when the lung can no longer keep the blood supplied with oxygen.

When respiratory failure occurs in a patient who has end-stage lung disease, there is a slow decline in lung function and rising levels of carbon dioxide in the blood. The increasing carbon dioxide creates a narcotic effect in the patient, who slowly loses consciousness and stops breathing.

Pneumonia
Streptococcus pneumoniae is the most common cause of bacterial pneumonia in patients with COPD. This can lead to respiratory failure.

Pneumothorax
Patients with COPD are at increased risk for spontaneous penumothorax because of weakened lung structure. This can lead to severe respiratory distress and is treated by inserting a tube into the pleural cavity to allow the air to escape out and re-expanding the lung.

Polycythemia
The body attempts to adjust to decreased amounts of blood oxygen by increasing the production of erythrocytes. While this may be helpful in the short term, overproduction eventually clogs small blood vessels.

http://www.pulmonologychannel.com/copd/complications.shtml

definition incidence and pravelence

Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible. The more familiar terms 'chronic bronchitis' and 'emphysema' are no longer used, but are now included within the COPD diagnosis. COPD is not simply a "smoker's cough" but an under-diagnosed, life-threatening lung disease.

A COPD diagnosis is confirmed by a simple test called spirometry, which measures how deeply a person can breathe and how fast air can move into and out of the lungs. Such a diagnosis should be considered in any patient who has symptoms of cough, sputum production, or dyspnea (difficult or labored breathing), and/or a history of exposure to risk factors for the disease. Where spirometry is unavailable, the diagnosis of COPD should be made using all available tools. Clinical symptoms and signs, such as abnormal shortness of breath and increased forced expiratory time, can be used to help with the diagnosis. A low peak flow is consistent with COPD, but may not be specific to COPD because it can be caused by other lung diseases and by poor performance during testing. Chronic cough and sputum production often precede the development of airflow limitation by many years, although not all individuals with cough and sputum production go on to develop COPD.

prevalence of COPD of men in malaysia is 4.72 by ministry of health malaysia

COPD is estimated to be 6.2 percent in 11 Asian countries surveyed by the Asian Pacific Society of Respiratory Diseases

The WHO estimates that in 2000, 2.74 million people died of COPD worldwide

The prevalence of stage II or higher COPD was 10·1% (SE 4·8) overall, 11·8% (7·9) for men, and 8·5% (5·8) for women

The WHO estimates that passive smoking is associated with a 10 to 43 percent increase in risk of COPD in adults.

Pathophysiology of COPD

Role of Inflammation :
• The cellular composition of the airway inflammation in COPD is predominantly mediated by the neutrophils.
• Cigarette smoking induces macrophages to release neutrophil chemotactic factors and elastases, thus unleashing tissue destruction.
• Severity of airflow obstruction has correlated with greater induced sputum neutrophilia
• Macrophages also play an important role through macrophage-derived matrix metalloproteinases (MMPs).
• Pathological changes in chronic obstructive pulmonary disease (COPD) occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma.
• The increased number of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction.
• The primary offender has been human leukocyte elastase, with a possible synergistic role suggested for proteinase 3 and macrophage-derived matrix proteinases, cysteine proteinases, and a plasminogen activator.
• Additionally, increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells.
• Remodeling.
The Lungs :
• The walls of the bronchioles are weak and have a tendency to collapse, especially while exhaling.
• Normally, the bronchioles are kept open by the elasticity of the lung.
• Elasticity of the lung is supplied by elastic fibers which surround the airways and line the walls of the alveoli.
• When lung tissue is destroyed, as it is in patients with COPD who have emphysema, there is loss of elasticity and the bronchioles can collapse and obstruct the flow of air.
Emphysema
• There is permanent enlargement of the alveoli due to the destruction of the walls between alveoli in emphysema.
• The destruction of the alveolar walls reduces the elasticity of the lung overall.
• the collapse of the bronchioles obstructing airflow out of the alveoli. Air becomes "trapped" in the alveoli and reduces the ability of the lung to shrink during exhalation.
• This trapped air takes up space and results in a reduced amount of air that can be taken in during the next breath.
• As a result, less air gets to the alveoli for the exchange of gasses.
• The exchange of carbon dioxide and oxygen between air and the blood in the capillaries takes place across the thin walls of the alveoli.
• Destruction of the alveolar walls decreases the number of capillaries available for gas exchange.
Chronic Bronchitis:
• involves inflammation and swelling of the lining of the airways that leads to narrowing and obstruction of the airways.
• The inflammation also stimulates production of mucous (sputum), which can cause further obstruction of the airways.
• Obstruction of the airways, especially with mucus, increases the likelihood of bacterial lung infections.

Etiology of COPD

Cigarette smoking and second-hand smoke

Smoking is responsible for 90% of COPD in the United States. Although not all cigarette smokers will develop COPD, it is estimated that 15% will. Smokers with COPD have higher death rates than nonsmokers with COPD. They also have more frequent respiratory symptoms (coughing, shortness of breath, etc.) and a more rapid deterioration in lung function than non-smokers. It is important to note that when a COPD patient stops smoking, their decline in lung function slows to the same rate as a nonsmoker. Therefore, it is never "too late" to quit.

Effects of passive smoking or "second-hand smoke" on the lungs are not well-known; however, evidence suggests that respiratory infections, asthma, and symptoms are more common in children who live in households where adults smoke.

Cigarette smoking damages the lungs in many ways. For example, the irritating effect of cigarette smoke attracts cells to the lungs that promote inflammation. Cigarette smoke also stimulates these inflammatory cells to release elastase, an enzyme that breaks down the elastic fibers in lung tissue.

Air pollution

Air pollution can cause problems for persons with lung disease, but it is unclear whether outdoor air pollution contributes to the development of COPD. However, in the non-industrialized world, the most common cause of COPD is indoor air pollution. This is usually due to indoor stoves used for cooking.

Occupational pollutants

Some occupational pollutants such as cadmium and silica do increase the risk of COPD. Persons at risk for this type of occupational pollution include coal miners, construction workers, metal workers, cotton workers, etc. (Most of this risk is associated with cigarette smoking and these occupations, an issue not well controlled for. These occupations are more often associated with interstitial lung diseases, especially the pneumoconioses) Nevertheless, the adverse effects of smoking cigarettes on lung function are far greater than occupational exposure.

Alpha-1 antitrypsin deficiency

Another well-established cause of COPD is a deficiency of alpha-1 antitrypsin (AAT). AAT deficiency is a rare genetic (inherited) disorder that accounts for less than 1% of the COPD in the United States.

As discussed previously, normal function of the lung is dependent on elastic fibers surrounding the airways and in the alveolar walls. Elastic fibers are composed of a protein called elastin. An enzyme called elastase that is found even in normal lungs (and is increased in cigarette smokers) can break down the elastin and damage the airways and alveoli. Another protein called alpha-1 antitrypsin (AAT) (produced by the liver and released into the blood) is present in normal lungs and can block the damaging effects of elastase on elastin.

The manufacture of AAT by the liver is controlled by genes which are contained in DNA-containing chromosomes that are inherited. Each person has two AAT genes, one inherited from each parent. Individuals who inherit two defective AAT genes (one from each parent) have either low amounts of AAT in the blood or AAT that does not function properly. The reduced action of AAT in these individuals allows the destruction of tissue in the lungs by elastase to continue unopposed. This causes emphysema by age 30 or 40. Cigarette smoking accelerates the destruction and results in an even earlier onset of COPD.

Individuals with one normal and one defective AAT gene have AAT levels that are lower than normal but higher than individuals with two defective genes. These individuals MAY have an increased risk of developing COPD if they do not smoke cigarettes; however, their risk of COPD probably is higher than normal if they smoke. Though their Alpha-1 antitrypsin blood levels may be in the normal range, the function of this enzyme is impaired relative to normal patient. Some may even develop bronchiectasis instead of emphysema.

Investigation for COPD

Investigation for COPD (similar to asthma)

Pulmonary function test or Lung function test
-Measure the size of your lungs
-how much air you can breathe in and out
-how fast you can breathe air out
-how well your lungs deliver oxygen to your blood.

Type of Pulmonary function test

1) Spirometry (main)
-how much air you breathe in and out and how fast you blow it out.
-peak expiratory flow rate (PEFR): amount of air you can blow air out as quickly as possible
-forced expiratory volume in 1 second (FEV1): amount of air you can blow out in 1 second.
- FVC: forced vital capacity
- A diagnosis of airflow obstruction can be made if the FEV1/FVC less than 0.7 (i.e. 70%) and FEV1 less than 80% predicted

2) Peak flow meter
- How well air moves out of your lungs.

3) Lung Volume Measurement
- Size of your lungs and how much air you can breathe in and out
- During the test, you sit inside a glass booth and breathe into a tube that's hooked to a computer.Sometimes you breathe in nitrogen or helium gas and then blow it out. The gas you breathe out is then measured to test how much air your lungs can hold.
- Help diagnose lung tissue scarring or a stiff and/or weak chest wall.

4) Lung Diffusion Capacity
- How well oxygen passes from your lungs to your bloodstream.
- You breathe in a gas through a tube. You hold your breath for a brief moment and then blow the gas out.
- Abnormal test results: loss of lung tissue, emphysema (a type of COPD), very bad scarring, or problems with blood flow through the body's arteries.

Chest X Ray / Computerized tomography (CT) scan
- Can show emphysema (one of the causes of COPD)
- Show sign of COPD
- To rule out other causes

Blood test

1) Arterial Blood Gas Analysis
- How well your lungs are bringing oxygen into your blood and removing carbon dioxide.
-find out whether you may need supplemental oxygen therapy.

2) Full blood count
- To identify anaemia or polycythaemia

Sputum Examination
-Analysis of the cells in your sputum can help identify the cause of your lung problems and help rule out some lung cancers.


Additional investigations (tbc):
-Alpha-1 antitrypsin: if early onset, minimal smoking history or family history
-Transfer factor for carbon monoxide (TLCO): to investigate symptoms that seems disproportionate to the spirometric impairment
-ECG and echocardiogram: to assess cardiac status if features of cor pulmonale


References:
http://www.nhlbi.nih.gov/health/dci/Diseases/Copd/Copd_Diagnosis.html
http://www.nhlbi.nih.gov/health/dci/Diseases/lft/lft_whatare.html
http://www.nhlbi.nih.gov/health/dci/Diseases/lft/lft_types.html
http://www.mayoclinic.com/print/copd/DS00916/DSECTION=all&METHOD=print
http://www.patient.co.uk/doctor/Diagnosing-COPD.htm

Anatomy Practical - Orbit and Ear

Task 1 - Timothy and Wen Jye
Task 2 - Yi Zhen and Rebekah
Task 3 - Xin Yi and Nabilah
Task 4 - Nicholas and Pey Chien
Task 5 - Da Wei
Task 6 - Chesvin/ Fahad/ Nabeela