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Lungs

Structure and Function

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Structure

Respiratory Tract

The bronchi pass into the lungs at the hilum (the point at which all the main vessels, nerves, etc enter the lung) and begin to divide, first into the lobar bronchi (one for each lobe), then the segmental bronchus. These all contain cartilage, to keep them open when pressure in the lungs falls.

Eventually after 19 divisions, it reaches the terminal brionchioles, which do not contain cartilage or submucosal glands. The final bronchioles are called the respiratory bronchioles, which lead into the alveolar ducts, which have thin walled outpouchings called alveolar sacs. These sacs consist of several alveoli opening into a single chamber.

Lungs

The lungs are very elastic and spongy. They should be pink, but they go black in places in smokers, city dwellers, coal miners and fire breathing dragons.

They are placed either side of the mediastinum (the area containing the heart and the great vessels). The right lung has three lobes and is larger than the left lung which has only two - this is because the heart takes up more space on the left side of the thoracic cavity. The right lung is split up by the horizontal fissure and the oblique fissure, the left lung by just the oblique fissure.

Each lung has a blunt apex, a concave base on the diaphragm, a convex costal surface which corresponds to the convex chest wall, and a concave mediastinal surface, moulded to the pericardium. In the middle is the hilum, where all the bronchi, vessels and nerves go in.

Functions

Gas exchange occurs in the alveoli, and the reoxygenated blood runs into the venules, then the veins and eventually to the pulmonary vein which takes the blood to the left atrium.

The ventilation/perfusion ratio: Vasocontriction occurs with hypoxia to divert blood from underventilated to well ventilated regions.

Arterial and Venous supply

There are two blood circulations in the body; pulmonary and systemic. The lungs have two blood supplies – the pulmonary vascular system and the bronchial system (which is part of systemic). The pulmonary one is the important one, as it has the capillary network and gaseous exchange. The bronchial system merely supplies the larger components (first few bronchi).

The pulmonary arteries enter at the hilum with the bronchi, and follow the same course as the airways, dividing pretty much at the same times. It ends in the massive capillary network surrounding the alveoli.

Pulmonary artery systolic pressure is low (22mmHg), whereas systemic is high (110-135mmHg). Because of this the structure of the vessels is significantly different. The proximal arteries (up until the bronchi become bronchioles) are elastic. The distal arteries (up until the respiratory bronchioles) are muscular. After this they have neither and are arterioles.

Nervous Supply

At the root (part of the lung by the hilum) of each lung is a pulmonary plexus composed of efferent (going in) and afferent (coming out) autonomic nerve fibres. The plexus is made from branches of the sympathetic trunk of the vagus nerve and it receives parasympathetic fibres from the same nerve. The nerve supply to the lungs is down the bronchial tree, and the majority of the supply is to bronchi and bronchioles, since little signal is given to or from alveoli.

Sympathetic efferent fibres control:

  • Bronchodilation

Parasympathetic efferent fibres control:

  • Bronchoconstriction
  • Increased glandular secretion

Afferent impulses in both come from:

  • Bronchial mucous membrane
  • Stretch receptors in alveolar walls

Lymph

The fluid that is in the air spaces in the alveoli is absorbed into the walls, and diffuses into the interstitium (a small space in tissue or between parts of body), until it reaches the lymph vessels of the respiratory bronchioles. These vessels merge forming larger ones, that follow the bronchiole tree back up to the hilum.

The other lymphatic system lies in the visceral pleura and in the fibrocollagenous septae (network that divides lobules in the lung), and they both drain into the pleural space.

Histology

There are two types of alveoli: Type 1 pneumocytes (pavement cells) and Type II pneumocytes (surfactant producers).

Clinical Conditions

Asthma

About: Increased irritability of the bronchial tree with paroxysmal narrowing of the airways. It may reverse spontaneously or after treatment. Rarely causes death. Split into atopic (allergic) and non-atopic. Look for an allergen causing the problem. Aspirin is a commonly missed one – NEVER give someone aspirin if they have asthma, around 10-20% of people with asthma may be allergic to aspirin. Symptoms: Breathlessness/cough/wheeze, variable from day to day. Most commonly between attacks it will be symptom free. Investigations: Respiratory function test:what result? Treatment:

  • Preventors (anti-inflammatories are common, corticosteroids)
  • Relievers (bronchodilators such as salbutamol)
  • Allergen avoidance

COPD

Chronic obstructive airways disease is pretty common. Find out more on the COPD page:

About: It is actually two conditions: chronic bronchitis and chronic emphysema. Bronchitis is "chronic cough and sputum for at least 3 months each year for 2 consecutive years". Emphysema is "permanent enlargement of airspaces distal to the terminal bronchioles together with destruction of their walls".

Symptoms: Basically, look for breathlessness, cough and wheeze, with no return to normal between attacks. It will be getting progressively worse too.

With severe bronchitis it is accompanied with hypercapnia, hypoxaemia and cyanosis. This leads to them being called blue bloaters. With severe emphysema there is just overventilation in order to produce normal levels of pO2 and pCO2 – hence the term pink puffers. The amount of cough and sputum is always related to the degree of bronchitis.

Investigations: Pulmonary function tests:

  • Reduced vital capacity
  • Reduced FEV1:FVC ratio
  • Reduced Peak Expiratory Flow Rate

Treatment: Not much, just go on oxygen as it gets worse. For acute exacerbations of COPD, you can use similar treatment to asthma. See the page for more details.

Lung Cancer

Over 90% of lung cancers are carcinomas (it's a cancer that's in the epithelium). Around 5% 5 year survival, and the most common primary malignant tumour in the world. The only hope of survival comes from complete surgical resection, which can only happen if the tumour is operable at presentation.

The main causes are:

  • Smoking
  • Occupation hazards (asbestos, other dusts)
  • Radioactive gases
  • Pulmonary fibrosis

There are four main types of carcinoma:

  • Squamous Cell Carcinoma (20-30%) Most strongly associated with cigarette smoking. Tumours are almost always hilar (at the hilum). They are thought to originate in the squamous metaplasia after grades of dysplasia (abnormal development of tissues, bone or skin). It tends to metastatise (spread) locally to hilar lymph nodes. There is often haemorrhage and/or necrosis (non programmed cell death).
  • Small Cell Lung Carcinoma (15-20%) Also known as oat cell, because the small nuclei are thought to resemble oat grain. SSLC usually arise in a hilar bronchus. Unlike squamous, they metastatise very early, producing widespread bulky deposits – in fact the primary tumour is often pretty hard to find. It is aggressive and highly malignant. Almost always inoperable on presentation. Very, very bad news. Anyone reading this who smokes, STOP NOW!!
  • Adenocarcimona (30-40%) Usually peripheral. Linked to pulmonary fibrosis and asbestosis (which is a pneumoconiosis, a disease caused from inhaling dust – in this case, cancer). It's a malignant epithelial tumour arising from the glandular structures. This is the most common lung cancer in non smokers.
  • Large Cell Undifferentiated Carcinoma (10-15%) LCUC are usually central, highly destructive lesions with necrosis and haemorrhage.

Pneumonia

Inflammation of the lung caused by bacteria in which the alveoli become filled with inflammatory cells. Two types, bronchial and lobar:

Bronchial

About: It is a patchy distribution of infection centred on small bronchi and bronchioles with a random spread to alveoli. Seen in the elderly, in infants and in those with debilitating diseases. May also occur in patients with acute bronchitis, COPD or cystic fibrosis. Caused by low virulence pathogens, where it would not cause disease in a young healthy individual.

Symptoms: Patients often become septicaemic and toxis, with fever and reduced consciousness.

Investigations: The area of lung can be identified by hearing crepitations on auscultation (crackles through a stephoscope)

Treatment: Antibiotics and physiotherapy. It may heal cleanly, or leaving some scarring.

Lobar

About: Only affects a lobe. Typically affects healthy adults between 20 and 50 years of age. 90% of cases caused by streptococcus pneumonieae (which is why it's also known as pneumococcal pneumonia).

Symptoms: Cough, fever and production of sputum (often containing specks of blood, so called "rusty sputum"). Fever can be very high (upto 40°C). Acute pain on respiration reflects that the pleura have been affected too.

Investigations: As the lung becomes consolidated (alveoli are filled with fluid from inflamed tissue) the chest signs are dullness to percussion with increased whispering pectoriloquy (abnormal transmission of patients voice sounds through chest wall so they can be clearly heard through a stethoscope. this is a symptom specific to pneumonia!) and bronchial breathing.

Pulmonary Embolism

Thromboembolism is the most common pulmonary vascular problem. This is where a blood clot forms on a vessel wall at one point in the circulation and becomes detached and lodges at another point and obstructs blood flow. They usually originate from the deep pelvic veins or the deep veins of the calf (Hence DVT).

Sizes of Emboli:

  • Main pulmonary artery occlusion: a clot of one main pulmonary artery, or at the bifurcation of the left and right pulmonary arteries usually causes sudden death, or severe chest pain, dyspnoea (breathlessness/difficulty breathing) and shock. Most patients die within a few hours.
  • Lobar or segmental artery occlusion: Causes chest pain, and may lead to distal lung infarction (tissue death due to inadequate blood and therefore oxygen supply) – especially if there is already mitral stenosis (narrowing) or left ventricular failure, since this causes raised pulmonary venous pressure, which makes it worse.
  • Arteriole occlusion: results in gradual occlusion of the pulmonary arterial bed. This leads to pulmonary arterial hypertension.

Types of Emboli:

  • Fat emboli: comes from fractures of bones containing fatty marrow, or from massive injury of fatty marrow. Globules of lipid enter the torn veins and thereby lead to embolism.
  • Air emboli: Occurs occasionally in childbirth or with abortion, or from when dissolved nitrogen coming out of solution after rapid decompression (the bends).
  • Amniotic fluid emboli: Amniotic fluid emboli can occur during abortion or delivery. Flakes of keratin and vernix from foetal skin.
  • Tumour emboli: Very common, this is an important mechanism in the development of metastases.

Pulmonary Fibrosis

Fibrosis is the thickening and scarring of connective tissue,. In lungs it refers to the alveolar sacs, so oxygen transfer is harder, and compression, expansion also. It's not really a condition in itself, just remember it happens. There are theories that cancer is more common in heavily fibrosized areas (fibrosized is not a real word, but you get the picture)

ARDS(Acute Respiratory Distress Syndrome)

Happens after a trauma or injury. Leads to a massive diffuse inflammation of lung parenchyma, which leads to loads of pulmonary oedema

Pulmonary Oedema

Excessive fluid accumulation in the lungs resulting in swelling. Its generally caused by:

  • increased venous hydrostatic pressure (usually from left ventricular failure, mitral stenosis, etc)
  • blockage of lymphatic drainage (usually due to cancer)
  • lowered plasma oncotic pressure (rare)
  • injury to the alveolar-capillary wall (no idea, smoking? Usually a good guess)

Fluid gets forced out of the venous circulation into the alveoli to form pulmonary oedema. This happens only after the lymph system is overloaded – it can take 10x the normal amount before there is a problem, so the oedema is a sign of a problem with the lymph, or of fluid production. Clinically, there is dyspnoea with a cough, producing bubbly fluid. Auscultation (listening to sounds produced by movement of gas or liquid in the body) reveals fine crackles in the chest due to air bubbling through fluid soaked airways. There can be hypoxaemia (pO2 in arterial blood < 60mmHg = respiratory failure). The lungs are prone to secondary infection.

Tuberculosis

About: An infectious disease characterised by the formation of nodular lesions in the tissues. In pulmonary TB, the infectious bacteria is inhaled into the lungs. Here, it sets up a primary tubercle which spreads to lymph nodes. Can be passed from person to person by coughing and sneezing. Leading cause of death from a single infectious agent worldwide. A third of the world's population has been infected with TB. Disease occurs in only 10% of infections.

Symptoms: May vary from insidious weight loss, night sweating, mild chronic cough all the way up to rampant bronchopneumonia, fever, dyspnoea and respiratory distress. In most early cases, it does not present.

Investigations: Detected on x-ray. Vulnerable patients ought to be innoculated with BCG vaccine (a strain of TB bacteria that is unable to cause TB)