Showing posts with label Clinical Manifestation. Show all posts
Showing posts with label Clinical Manifestation. Show all posts

COPD - Definition, Causes, Clinical Manifestation, Classification and Pathophysiology


Chronic Obstructive Pulmonary Disease

DEFINITIONS

Chronic Obstructive Pulmonary Disease (COPD) is a chronic lung disease characterized by the air flow resistance in the airway that is progressive nonreversibel or partially reversible. COPD consists of chronic bronchitis and emphysema or both. Chronic bronchitis is a respiratory disorder characterized by chronic cough with phlegm at least 3 months of the year, at least two consecutive years, is not caused by other diseases. while emphysema is an anatomical abnormality characterized by a widening lung airspaces distal to the terminal bronchioles, accompanied by destruction of the alveoli walls.


CAUSES

There are three factors that affect the incidence of COPD is cigarette, infection and pollution, but it is also associated with heredity, allergies, age and genetic predisposition, but it is not yet clear whether these factors play a role or not.

  • Smoking: According to the report of the WHO expert committee on smoking control, smoking is the main cause of COPD. Physiologically cigarettes directly related to hiperflasia bronchial mucous glands and squamous metaplasia of the respiratory tract. Can also cause acute bronchoconstriction. According Crofton and Doouglas smoke cause too inhibition activity vibrating hair cells, alveolar macrophages and surfactants.
  • Infections: upper respiratory tract infection in a patient with chronic bronchitis is almost always causes lower respiratory tract infection, and cause lung damage increases. Estimated exacerbation of chronic bronchitis is most often preceded by a viral infection, which then lead to secondary infection by bacteria.
  • Pollution: pollution chemical substances that can also cause bronchitis is a reducing agent such as CO2, oxidising agents such as N2O, hydrocarbons, aldehydes and ozone.


CLINICAL MANIFESTATION

Common signs and symptoms appear in patients with COPD are as follows:
  • Productive cough, initially intermittent and occurs almost every day over time.
  • White or mucoid sputum, if there is an infection becomes purulent or mukopurulent, shortness of breath to use additional respiratory muscles to breathe, cough and expectoration, which tends to increase and the maximum in the morning.
  • Shortness of breath after strenuous activity occurred along with the development of disease in the case of weight, shortness of breath occurs even with minimal exertion and even at rest due to the deterioration of gas exchange abnormalities.
  • In the moderate-to-severe disease, physical examination may show a decrease in breath sounds, expiratory elongated, Ronchi, and hyperresonance on percussion.
  • Anorexia.
  • Weight loss and weakness.
  • Tachycardia, sweating.
  • Hypoxia.
All respiratory disease characterized by chronic obstruction of the airflow. The main cause of the obstruction assortment, for example:

  • Airway inflammation.
  • Mucosal adhesions.
  • Narrowing of the airway lumen.
  • Damage to the airway.
  • Tachypnea.
  • Orthopnea. (Doenges, 1999: 152)


CLASSIFICATION

Classification of COPD can be divided into three, namely:

  • Bronchial asthma: a disease characterized by increased reaction response of the trachea and bronchi to various kinds of stimulation with manifestations such as difficulty in breathing caused by narrowing of the airways thorough.
  • Chronic bronchitis: a clinical disorder characterized by the formation of excessive mucus in the bronchi and manifested in the form of chronic cough and sputum formed during 3 months of the year, a minimum of 2 years continuously.
  • Emphysema: changes in the anatomy of the lung parenchyma characterized by widening the walls of the alveoli, alveolar ducts and alveolar wall destruction (Muttaqin, 2008).


PATHOPHYSIOLOGY

Inhalation of cigarette smoke or other harmful gases activates macrophages and epithelial cells to release chemotactic factors that recruit more macrophages and neutrophils. Then, macrophages and neutrophils release proteases that destroy these structural elements in the lungs. Proteases can actually be overcome by endogenous antiproteases, but the imbalance antiproteases against the dominance of protease activity that will eventually become a predisposition to the development of COPD. The formation of highly reactive oxygen species such as superoxide, hydrogen peroxide hydroxyl free radicals have been identified as factors that contribute to the pathogenesis because these substances can increase the destruction antiproteases.

Chronic inflammation result metaplasia on the walls of the bronchial epithelium, mucous hypersecretion, increased smooth muscle mass and fibrosis. There is also the epithelial ciliary dysfunction, causing disruption clearance excessive mucus production. Clinically, this process manifests as chronic bronchitis, characterized by a chronic productive cough. In the lung parenchyma, destruction of structural elements
mediated protease causes emphysema. Alveolar septum damage leads to reduced elasticity of the recoil of the lungs and airways dynamics failure due to damage to the small airways support non-cartilage. This whole process results in a patent airway obstruction and other symptoms characteristic pathophysiological for COPD.

Obstruction of the airways produce alveoli are not ventilated or less ventilated; Continuous perfusion of the alveoli will cause hypoksemia (low PaO 2) by a mismatch between ventilation and blood flow (V / Q is not appropriate). Ventilation of the alveoli are not perfused or less pefusi increase the space of the appendix (Vd), causing inefficient disposal of CO2. Hyperventilation would normally occur to compensate for this situation, which in turn will increase the work required to overcome airway resistance has increased, in the end this process fails, and there was retention of CO2 (hypercapnia) in some patients with severe COPD.

Clinical Manifestation of Systemic Lupus Erythematosus (SLE)

Course of the disease Systemic Lupus Erythematosus (SLE) is highly variable. The disease can arise suddenly accompanied by signs exposed to various systems in the body. Can also be chronic with symptoms in a system that gradually followed by symptoms that affected the immune system. In the chronic type there are remissions and exacerbations. Remission may last for years.

Onset of the disease can be spontaneous or preceded by precipitation factors such as sun exposure, viral infections / bacterial remedy. Each attack is usually accompanied by a clear common symptoms such as fever, poor appetite, weakness, weight loss, and irritability. The most prominent is fever, sometimes with chills.



Musculoskeletal symptoms

The most common symptom of SLE is; musculoskeletal symptoms, such as arthritis (93%). The most commonly affected are the proximal interphalangeal joints followed by knee, wrist, metacarpophalangeal, elbow and ankle. Besides swelling and pain may also include joint effusion. Arthritis is usually symmetrical, without causing deformity, contractures or ankylosis. Sometimes there are rheumatoid nodules. Vascular necrosis can occur in various places, and was found in patients receiving treatment with high-dose streroid. The most commonly affected is the femoral head.


Mucocutaneous symptoms

Abnormalities of the skin, hair or mucous membrane was found in 85% of cases of SLE. Skin lesions are most commonly found in SLE is ; skin lesions of acute, subacute, discoid, and reticular livido .
Skin rash butterfly-shaped form rather edamatus erythema on the nose and cheeks. With proper treatment, this disorder can be healed without scarring. On the part of the body exposed to the sun can skin rash that occurs due to hypersensitivity. These lesions include acute skin lesions. Skin lesions typical subacute annular shaped.

Discoid lesions progressed through three stages: erythema, hyperkeratosis and atrophy . Usually presents as erythematous patches of elevated, covered by keratin scales with the blockage of the follicle. If it lasts longer be shaped silikatriks.
Vasculitis can cause ulceration of the skin in the form of small to large. Often also seemed bleeding and periungual erythema. Reticular Livido a mild form of vasculitis, it is often found in SLE.


Kidney

Renal insufficiency was found in 68% of cases of SLE. The most frequent manifestation is proteinuria or hematuria. Hypertension, renal failure nephrotic syndrome is rare, only found in 25% of cases of SLE urine showed abnormalities.
There are 2 kinds of pathological abnormalities in the kidneys, which diffuse lupus nephritis, and membranous lupus nephritis. Lupus nephritis is the most severe disorder. Usually appear clinically as nephrotic syndrome, hypertension and impaired renal function with moderate to severe. Membranous lupus nephritis are less common. Marked with nephrotic syndrome, impaired renal function and mild course of the disease may be rapid or slow but progressive.
Other renal abnormalities that may be found in SLE is chronic pyelonephritis, renal tuberculosis. Kidney failure is one cause of death chronic SLE.


Central Nervous

Disorders of central nervous system consists of two main abnormalities organic psychosis and convulsions.
Organic brain disease is usually found in conjunction with active SLE symptoms in others systems. Patients showing symptoms of hallucinations in addition to the typical symptoms of organic brain as difficult to calculate and could not recall the pictures ever seen.
Steroid psychosis also include organic brain syndrome which is clinically indistinguishable from lupus psychosis. The difference between the two can only be known by lowering or raising the dose of steroids used. Lupus psychosis improved if the steroid dose is increased and vice versa.
Seizures arising grandmal type normally included. Other abnormalities that may be found is aphasia, hemiplegia.


Eye

Eye disorders may include conjunctivitis, sub - conjunctival hemorrhage and the body sitoid in the retina.


Heart

Inflammation of various parts of the heart can occur, such as pericarditis, endocarditis and myocarditis. Chest pain and arrhythmia may occur as a result of these circumstances.


Lungs

Can occur in lupus pleurisy (inflammation of the lining of the lungs) and pleural effusion (accumulation of fluid between the lung and the wrapper). As a result of these events often arise chest pain and shortness of breath.

Gastrointestinal tract

Abdominal pain present in 25 % of cases of SLE , may be accompanied by nausea and diarrhea. Symptoms disappear quickly if systemic disorders receive adequate treatment. Pain that may arise due to the sterile peritonitis or arteritis of small blood vessels that lead to bowel mesentery and intestinal ulceration. Arteritis can also cause pancreatitis.


Hemic - Lymphatic

Lymph nodes are commonly affected are the axillary and cervical, with the characteristics of non-tender and soft. Splenomegaly other lymphoid organs is usually accompanied by an enlarged heart. Lien in the form of myocardial damage or thrombosis associated with lupus anticoagulant. Anemia can be found in the period of disease progression LES, which is mediated by the immune and non-immune.

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