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Chapter 15 Respiratory disease
Structure of the respiratory system
Physiology of the respiratory system
Defence mechanisms of the respiratory tract
Examination of the respiratory system
Investigation of respiratory disease
Smoking and air pollution
Air pollution and epidemiology
Diseases of the upper respiratory tract
Diseases of the lower respiratory tract
Types of pneumonia
Complications of pneumonia
Pneumonia in other settings
Rare causes of pneumonia
Diffuse diseases of the lung parenchyma
Granulomatous lung disease
Granulomatous lung disease with vasculitis
Pulmonary autoimmune rheumatic disease
Idiopathic interstitial pneumonia (IIP)
Other types of diffuse lung disease
Pulmonary infiltration with eosinophilia
Hypersensitivity pneumonitis
Occupational lung disease
Lung cysts
Tumours of the respiratory tract
Malignant tumours
Benign tumours
Disorders of the chest wall and pleura
Disorders of the diaphragm
Mediastinal lesions
The main role of the respiratory system is to extract oxygen from the external environment and dispose of waste gases, principally carbon dioxide. This requires the lungs to function as efficient bellows, bringing in fresh air and delivering it to the alveoli, and expelling used air at an appropriate rate. Gas exchange is achieved by exposing thin-walled capillaries to the alveolar gas and matching ventilation to blood flow through the pulmonary capillary bed. In doing this, the lungs expose a large area of tissue, which can be damaged by dusts, gases and infective agents. Host defence is therefore a key priority for the lung and is achieved by a combination of structural and immunological defences.
The nose, pharynx and larynx
See Chapter 21 (p. 1052).
The trachea, bronchi and bronchioles
The trachea is 10–12 cm in length. It lies slightly to the right of the midline and divides at the carina into right and left main bronchi. The carina lies under the junction of the manubrium sterni and the second right costal cartilage. The right main bronchus is more vertical than the left and, hence, inhaled material is more likely to end up in the right lung.
The right main bronchus divides into the upper lobe bronchus and the intermediate bronchus, which further subdivides into the middle and lower lobe bronchi. On the left the main bronchus divides into upper and lower lobe bronchi only. Each lobar bronchus further divides into segmental and subsegmental bronchi. There are about 25 divisions in all between the trachea and the alveoli.
The first seven divisions are bronchi that have:
walls consisting of cartilage and smooth muscle
epithelial lining with cilia and goblet cells
submucosal mucus-secreting glands
endocrine cells – Kulchitsky or APUD (amine precursor and uptake decarboxylation) containing 5-hydroxytryptamine.
The next 16–18 divisions are bronchioles that have:
no cartilage and a muscular layer that progressively becomes thinner
a single layer of ciliated cells but very few goblet cells
granulated Clara cells that produce a surfactant-like substance.
The ciliated epithelium is a key defence mechanism. Each cell bears approximately 200 cilia beating at 1000 beats per minute in organized waves of contraction. Each cilium consists of nine peripheral parts and two inner longitudinal fibrils in a cytoplasmic matrix (Fig. 15.1). Nexin links join the peripheral pairs. Dynein arms consisting of ATPase protein project towards the adjacent pairs. Bending of the cilia results from a sliding movement between adjacent fibrils powered by an ATP-dependent shearing force developed by the dynein arms (see also p. 22). Absence of dynein arms leads to immotile cilia. Mucus, which contains macrophages, cell debris, inhaled particles and bacteria, is moved by the cilia towards the larynx at about 1.5 cm/min (the 'mucociliary escalator', see below).
Figure 15.1 Cross-section of a cilium. Nine outer microtubular doublets and two central single microtubules are linked by spokes, nexin links and dynein arms.
The bronchioles finally divide within the acinus into smaller respiratory bronchioles that have alveoli arising from the surface (Fig. 15.2). Each respiratory bronchiole supplies approximately 200 alveoli via alveolar ducts. The term 'small airways' refers to bronchioles of <2 mm; the average lung contains about 30 000 of these.
Figure 15.2 Branches of a terminal bronchiole ending in the alveolar sacs.
The alveoli
There are approximately 300 million alveoli in each lung. Their total surface area is 40–80 m2. The epithelial lining consists mainly of type I pneumocytes (Fig. 15.3). These cells have an extremely thin layer of cytoplasm, which only offers a thin barrier to gas exchange. Type I cells are connected to each other by tight junctions that limit the movements of fluid in and out of the alveoli. Alveoli are not completely airtight – many have holes in the alveolar wall allowing communication between alveoli of adjoining lobules (pores of Kohn).
Figure 15.3 The structure of alveoli, showing the pneumocytes and capillaries.
Type II pneumocytes are slightly more numerous than type I cells but cover less of the epithelial lining. They are found generally in the borders of the alveolus and contain distinctive lamellar vacuoles, which are the source of surfactant. Type I pneumocytes are derived from type II cells. Large alveolar macrophages are present within the alveoli and assist in defending the lung.
The lungs
The lungs are separated into lobes by invaginations of the pleura, which are often incomplete. The right lung has three lobes, whereas the left lung has two. The positions of the oblique fissures and the right horizontal fissure are shown in Figure 15.4. The upper lobe lies mainly in front of the lower lobe and therefore physical signs on the right side in the front of the chest are due to lesions of the upper lobe or the middle lobe.
Figure 15.4 Surface anatomy of the chest.
Each lobe is further subdivided into bronchopulmonary segments by fibrous septa that extend inwards from the pleural surface. Each segment receives its own segmental bronchus.
The bronchopulmonary segment is further divided into individual lobules approximately 1 cm in diameter and generally pyramidal in shape, the apex lying towards the bronchiole that supplies it. Within each lobule a terminal bronchus supplies an acinus, and within this structure further divisions of the bronchioles eventually give rise to the alveoli.
The pleura
The pleura is a layer of connective tissue covered by a simple squamous epithelium. The visceral pleura covers the surface of the lung, lines the interlobar fissures, and is continuous at the hilum with the parietal pleura, which lines the inside of the hemithorax. At the hilum the visceral pleura continues alongside the branching bronchial tree for some distance before reflecting back to join the parietal pleura. In health, the pleurae are in apposition apart from a small quantity of lubricating fluid.
The diaphragm
The diaphragm is covered by parietal pleura above and peritoneum below. Its muscle fibres arise from the lower ribs and insert into the central tendon. Motor and sensory nerve fibres go separately to each half of the diaphragm via the phrenic nerves. Fifty per cent of the muscle fibres are of the slow-twitch type with a low glycolytic capacity; they are relatively resistant to fatigue.
Pulmonary vasculature and lymphatics
The lung has a dual blood supply, receiving deoxygenated blood from the right ventricle via the pulmonary artery and oxygenated blood via the bronchial circulation.
The pulmonary artery divides to accompany the bronchi. The arterioles accompanying the respiratory bronchioles are thin-walled and contain little smooth muscle. The pulmonary venules drain laterally to the periphery of the lobules, pass centrally in the interlobular and intersegmental septa, and eventually join to form the four main pulmonary veins.
The bronchial circulation arises from the descending aorta. These bronchial arteries supply tissues down to the level of the respiratory bronchiole. The bronchial veins drain into the pulmonary vein, forming part of the normal physiological shunt.
Lymphatic channels lie in the interstitial space between the alveolar cells and the capillary endothelium of the pulmonary arterioles.
The tracheobronchial lymph nodes are arranged in five main groups: pulmonary, bronchopulmonary, subcarinal, superior tracheobronchial and paratracheal. For all practical purposes these form a continuous network of nodes from the lung substance up to the trachea.
Nerve supply to the lung
The innervation of the lung remains incompletely understood. Parasympathetic and sympathetic fibres (from the vagus and sympathetic chain respectively) accompany the pulmonary arteries and the airways. Airway smooth muscle is innervated by vagal afferents, postganglionic muscarinic vagal efferents and vagally derived non-adrenergic non-cholinergic (NANC) fibres which use a range of neurotransmitters including substance P, neurokinins A and B, calcitonin gene-related peptide, vasoactive intestinal polypeptide and various adenine and guanine phosphates. Three muscarinic receptor subtypes have been identified: M1 receptors on parasympathetic ganglia, a smaller number of M2 receptors on muscarinic nerve terminals, and M3 receptors on airway smooth muscle. The parietal pleura is innervated from intercostal and phrenic nerves but the visceral pleura has no innervation.
Albert RK, Spiro SG, Jett JR. Clinical Respiratory Medicine, 3rd edn. Chicago: Mosby; 2008.
The major functions of nasal breathing are:
To heat and moisten the air
To remove particulate matter.
About 10 000 L of air are inhaled daily. The relatively low flow rates and turbulence of inspired air in the nose mean that few particles greater than 10 microns (µm) diameter pass through the nose. Particles deposited on the nasal mucosa are removed within 15 minutes, compared with 60–120 days for particles that reach the alveoli. Nasal secretion contains IgA antibodies, lysozyme and interferons. In addition, the cilia of the nasal epithelium move the mucous gel layer rapidly back to the oropharynx where it is swallowed. Bacteria have little chance of settling in the nose. Mucociliary protection is less effective against viral infections because viruses bind to receptors on epithelial cells. The majority of rhinoviruses bind to an adhesion molecule, intercellular adhesion molecule 1 (ICAM-1), which is shared by neutrophils and eosinophils. Many noxious gases, such as SO2, are almost completely removed by nasal breathing.
Lung ventilation can be considered in two parts:
The mechanical process of inspiration and expiration
The control of respiration to a level appropriate for metabolic needs.
Mechanical process
The lungs have an inherent elastic property that causes them to tend to collapse away from the thoracic wall, generating a negative pressure within the pleural space. The strength of this retractive force relates to the volume of the lung: at higher lung volumes the lung is stretched more, and a greater negative intrapleural pressure is generated. Lung compliance is a measure of the relationship between this retractive force and lung volume. At the end of a quiet expiration, the retractive force exerted by the lungs is balanced by the tendency of the thoracic wall to spring outwards. At this point, respiratory muscles are resting. The volume of air remaining in the lung after a quiet expiration is called the functional residual capacity (FRC).
Inspiration from FRC is an active process: a negative intrapleural pressure is created by descent of the diaphragm and movement of the ribs upwards and outwards through contraction of the intercostal muscles. During tidal breathing in healthy individuals, inspiration is almost entirely due to contraction of the diaphragm. More vigorous inspiration requires the use of accessory muscles of ventilation (sternomastoid and scalene muscles). Respiratory muscles are similar to other skeletal muscles but are less prone to fatigue. However, inspiratory muscle fatigue contributes to respiratory failure in patients with severe chronic airflow limitation and in those with primary neurological and muscle disorders.
At rest or during low-level exercise, expiration is passive and results from the natural tendency of the lung to collapse.
Forced expiration involves activation of accessory muscles, chiefly those of the abdominal wall, which help to push up the diaphragm.
The control of respiration
Coordinated respiratory movements result from rhythmical discharges arising in an anatomically ill-defined group of interconnected neurones in the reticular substance of the brainstem, known as the respiratory centre. Motor discharges from the respiratory centre travel via the phrenic and intercostal nerves to the respiratory musculature.
In healthy individuals, the main driver for respiration is the arterial pH, which is closely related to the partial pressure of carbon dioxide in arterial blood. Oxygen levels in arterial blood are usually above the level which triggers respiratory drive. In a typical normal adult at rest:
The pulmonary blood flow of 5 L/min carries 11 mmol/min (250 mL/min) of oxygen from the lungs to the tissues.
Ventilation at about 6 L/min carries 9 mmol/min (200 mL/min) of carbon dioxide out of the body.
The normal pressure of oxygen in arterial blood (PaO2) is between 11 and 13 kPa.
The normal pressure of carbon dioxide in arterial blood (PaCO2) is 4.8–6.0 kPa.
Ventilation is controlled by a combination of neurogenic and chemical factors (Fig. 15.5).
Figure 15.5 Chemical and neurogenic factors in the control of ventilation. The strongest stimulant to ventilation is a rise in PaCO2 which increases [H+] in CSF. Sensitivity to this may be lost in COPD. In these patients hypoxaemia is the chief stimulus to respiratory drive; oxygen treatment may therefore reduce respiratory drive and lead to a further rise in PaCO2. An increase in [H+] due to metabolic acidosis as in diabetic ketoacidosis will increase ventilation with a fall in PaCO2 causing deep sighing (Kussmaul) respiration. The respiratory centre is depressed by severe hypoxaemia and sedatives (e.g. opiates) and stimulated by doxapram, large doses of aspirin and pyrexia. COPD, chronic obstructive pulmonary disease.
Breathlessness on physical exertion is normal and not considered a symptom unless the level of exertion is very light, such as when walking slowly. Surveys of healthy western populations reveal that over 20% of the general population report themselves as breathless on relatively minor exertion. Although breathlessness is a very common symptom, the sensory and neural mechanisms underlying it remain obscure. The sensation of breathlessness is derived from at least three sources:
Changes in lung volume. These are sensed by receptors in thoracic wall muscles signalling changes in their length.
Tension developed by contracting muscles. This is sensed by Golgi tendon organs.
Central perception of the sense of effort.
The airways of the lungs
From the trachea to the periphery, the airways decrease in size but increase in number. Overall, the cross-sectional area available for airflow increases as the total number of airways increases. The airflow rate is greatest in the trachea and slows progressively towards the periphery (since the velocity of airflow depends on the cross-sectional area). In the terminal airways, gas flow occurs solely by diffusion. The resistance to airflow is very low (0.1–0.2 kPa/L in a normal tracheobronchial tree), steadily increasing from the small to the large airways.
Airways expand as the lung volume increases. At full inspiration (total lung capacity, TLC) they are 30–40% larger in calibre than at full expiration (residual volume, RV). In chronic obstructive pulmonary disease (COPD), the small airways are narrowed but this can be partially compensated by breathing closer to TLC.
Control of airway tone
Bronchomotor tone is maintained by vagal efferent nerves and can be reduced by atropine or β-adrenoceptor agonists. Adrenoceptors on the surface of bronchial muscles respond to circulating catecholamines – there is no direct sympathetic innervation. Airway tone shows a circadian rhythm, which is greatest at 04.00 and lowest in the mid-afternoon. Tone can be increased transiently by inhaled stimuli acting on epithelial nerve endings, which trigger reflex bronchoconstriction via the vagus. These stimuli include cigarette smoke, solvents, inert dust and cold air. Airway responsiveness to these stimuli increases following respiratory tract infections even in healthy subjects. In asthma, the airways are very irritable and as the circadian rhythm remains the same, asthmatic symptoms are usually worse in the early morning.
Movement of air through the airways results from a difference between atmospheric pressure and the pressure in the alveoli; alveolar pressure is negative in inspiration and positive in expiration. During quiet breathing, the pleural pressure is negative throughout the breathing cycle. With vigorous expiratory efforts (e.g. cough), the pleural pressure becomes positive (up to 10 kPa). This compresses the central airways, but the smaller airways do not close off because the driving pressure for expiratory flow (alveolar pressure) is also increased.
Alveolar pressure (PALV) is equal to the pleural pressure (PPL) plus the elastic recoil pressure (Pel) of the lung.
When there is no airflow (i.e. during a pause in breathing), the tendency of the lungs to collapse (the positive recoil pressure) is exactly balanced by an equivalent negative pleural pressure.
As air flows from the alveoli towards the mouth there is a gradual drop of pressure owing to flow resistance (Fig. 15.6a).
Figure 15.6 Diagrams showing ventilatory forces. (a) During resting at functional residual capacity. (b) During forced expiration in normal subjects. (c) During forced expiration in a patient with COPD. The respiratory system is represented as a piston with a single alveolus and the collapsible part of the airways within the piston (see text). C, collapse point; PALV, alveolar pressure; PEL, elastic recoil pressure; PPL, pleural pressure.
In forced expiration, as mentioned above, the driving pressure raises both the alveolar pressure and the intrapleural pressure. Between the alveolus and the mouth, there is a point (C in Fig. 15.6b) where the airway pressure equals the intrapleural pressure, and the airway collapses. However, this collapse is temporary, as the transient occlusion of the airway results in an increase in pressure behind it (i.e. upstream) and this raises the intra-airway pressure so that the airways open and flow is restored. The airways thus tend to vibrate at this point of 'dynamic collapse'.
As lung volume decreases during expiration, the elastic recoil pressure of the lungs decreases and the 'collapse point' moves upstream (i.e. towards the smaller airways – see Fig. 15.6c). Where there is pathological loss of recoil pressure (as in chronic obstructive pulmonary disease, COPD), the 'collapse point' is located even further upstream and causes expiratory flow limitation. The measurement of the forced expiratory volume in 1 second (FEV1) is a useful clinical index of this phenomenon. To compensate, patients with COPD often 'purse their lips' in order to increase airway pressure so that their peripheral airways do not collapse. During inspiration, the intrapleural pressure is always less than the intraluminal pressure within the intrathoracic airways, so increasing effort does not limit airflow. Inspiratory flow is limited only by the power of the inspiratory muscles.
Flow-volume loops
The relationship between maximal flow rates and lung volume is demonstrated by the maximal flow-volume (MFV) loop (Fig. 15.7a).
Figure 15.7 (a, b) Maximal flow-volume loops, showing the relationship between maximal flow rates on expiration and inspiration. (a) In a normal subject. (b) In a patient with severe airflow limitation. Flow-volume loops during tidal breathing at rest (starting from the functional residual capacity (FRC)) and during exercise are also shown. The highest flow rates are achieved when forced expiration begins at total lung capacity (TLC) and represent the peak expiratory flow rate (PEFR). As air is blown out of the lung, so the flow rate decreases until no more air can be forced out, a point known as the residual volume (RV). Because inspiratory airflow is only dependent on effort, the shape of the maximal inspiratory flow-volume loop is quite different, and inspiratory flow remains at a high rate throughout the manoeuvre. (c, d) Flow-volume loops of patients with large airway (tracheal) obstruction, showing plateauing of maximal expiratory flow. (c) Extrathoracic tracheal obstruction with a proportionally greater reduction of maximal inspiratory (as opposed to expiratory) flow rate. (d) Intrathoracic large airway obstruction; the expiratory plateau is more pronounced and inspiratory flow rate is less reduced than in (c). In severe airflow limitation the ventilatory demands of exercise cannot be met (cf. a, b), greatly reducing effort tolerance.
In subjects with healthy lungs, maximal flow rates are rarely achieved even during vigorous exercise. However, in patients with severe COPD, limitation of expiratory flow occurs even during tidal breathing at rest (Fig. 15.7b). To increase ventilation these patients have to breathe at higher lung volumes and allow more time for expiration, both of which reduce the tendency for airway collapse. To compensate they increase flow rates during inspiration, where there is relatively less flow limitation.
The volume that can be forced in from the residual volume in 1 second (FIV1) will always be greater than that which can be forced out from TLC in 1 second (FEV1). Thus, the ratio of FEV1 to FIV1 is below 1. The only exception to this occurs when there is significant obstruction to the airways outside the thorax, such as tracheal tumour or retrosternal goitre. Expiratory airway narrowing is prevented by tracheal resistance and expiratory airflow becomes more effort-dependent. During forced inspiration this same resistance causes such negative intraluminal pressure that the trachea is compressed by the surrounding atmospheric pressure. Inspiratory flow thus becomes less effort-dependent, and the ratio of FEV1 to FIV1 exceeds 1. This phenomenon, and the characteristic flow-volume loop, is diagnostic of extrathoracic airways obstruction (Fig. 15.7c).
Ventilation and perfusion relationships
For optimum gas exchange there must be a match between ventilation of the alveoli ( ) and their perfusion ( ). However, in reality there is variation in the ( ) ratio in both normal and diseased lungs (Fig. 15.8). In the normal lung both ventilation and perfusion are greater at the bases than at the apices, but the gradient for perfusion is steeper, so the net effect is that ventilation exceeds perfusion towards the apices, while perfusion exceeds ventilation at the bases. Other causes of ( ) mismatch include direct shunting of deoxygenated blood through the lung without passing through alveoli (e.g. the bronchial circulation) and areas of lung that receive no blood (e.g. anatomical deadspace, bullae and areas of underperfusion during acceleration and deceleration, e.g. in aircraft and high performance cars).
Figure 15.8 Relationships between ventilation and perfusion: a schematic diagram showing the alveolar–capillary interface. The centre (b) shows normal ventilation and perfusion. On the left (a) there is a block in perfusion (physiological deadspace), while on the right (c) there is reduced ventilation (physiological shunting).
An increased physiological shunt results in arterial hypoxaemia since it is not possible to compensate for some of the blood being underoxygenated by increasing ventilation of the well-perfused areas. An increased physiological deadspace just increases the work of breathing and has less impact on blood gases since the normally perfused alveoli are well ventilated. In more advanced disease this compensation cannot occur, leading to increased alveolar and arterial PCO2 (PaCO2), together with hypoxaemia which cannot be compensated by increasing ventilation.
Hypoxaemia occurs more readily than hypercapnia because of the different ways in which oxygen and carbon dioxide are carried in the blood. Carbon dioxide can be considered to be in simple solution in the plasma, the volume carried being proportional to the partial pressure. Oxygen is carried in chemical combination with haemoglobin in the red blood cells, with a non-linear relationship between the volume carried and the partial pressure (Fig. 15.5, p. 341). Alveolar hyperventilation reduces the alveolar PCO2 (PACO2) and diffusion leads to a proportional fall in the carbon dioxide content of the blood (PaCO2). However, as the haemoglobin is already saturated with oxygen, there is no significant increase in the blood oxygen content as a result of increasing the alveolar PO2 through hyperventilation. The hypoxaemia of even a small amount of physiological shunting cannot therefore be compensated for by hyperventilation.
In individuals who have mild degrees of mismatch, the PaO2 and PaCO2 will still be normal at rest. Increasing the requirements for gas exchange by exercise will widen the mismatch and the PaO2 will fall. mismatch is by far the most common cause of arterial hypoxaemia.
Alveolar stability
Pulmonary alveoli are essentially hollow spheres. Surface tension acting at the curved internal surface tends to cause the sphere to decrease in size. The surface tension within the alveoli would make the lungs extremely difficult to distend were it not for the presence of surfactant, an insoluble lipoprotein largely consisting of dipalmitoyl lecithin, which forms a thin monomolecular layer at the air-fluid interface. Surfactant is secreted by type II pneumocytes within the alveolus and reduces surface tension so that alveoli remain stable.
Fluid surfaces covered with surfactant exhibit a phenomenon known as hysteresis; that is, the surface-tension-lowering effect of the surfactant can be improved by a transient increase in the size of the surface area of the alveoli. During quiet breathing, small areas of the lung undergo collapse, but it is possible to re-expand these rapidly by a deep breath; hence the importance of sighs or deep breaths as a feature of normal breathing. Failure of this mechanism, e.g. in patients with fractured ribs – gives rise to patchy basal lung collapse. Surfactant levels may be reduced in a number of diseases that cause damage to the lung (e.g. pneumonia). Lack of surfactant plays a central role in the respiratory distress syndrome of the newborn. Severe reduction in perfusion of the lung impairs surfactant activity and this may explain the characteristic areas of collapse associated with pulmonary embolism.
Fahy JV, Dickey BF. Airway mucus function and dysfunction. N Engl J Med 2010; 363:2233–2247.
Pulmonary disease often results from a failure of the normal host defence mechanisms of the healthy lung (Fig. 15.9). These can be divided into physical, physiological, humoral and cellular mechanisms.
Figure 15.9 Defence mechanisms present at the epithelial surface.
Physical and physiological mechanisms
This prevents dehydration of the epithelium.
Over 90% of particles greater than 10 µm diameter are removed in the nostril or nasopharynx. This includes most pollen grains, which are typically >20 µm in diameter. Particles between 5 and 10 µm become impacted at the carina. Particles smaller than 1 µm tend to remain airborne, thus the particles capable of reaching the deep lung are those in the 1–5 µm range.
Particle expulsion
This is effected by coughing, sneezing or gagging.
Respiratory tract secretions (Fig. 15.9)
The mucus of the respiratory tract is a gelatinous substance consisting of water and highly glycosylated proteins (mucins). The mucus forms a thick gel that is relatively impermeable to water and floats on a liquid or sol layer found around the cilia of the epithelial cells. The gel layer is secreted from goblet cells and mucous glands as distinct globules that coalesce increasingly in the central airways to form a more or less continuous mucus blanket. In addition to the mucins, the gel contains various antimicrobial molecules (lysozyme, defensins), specific antibodies (IgA) and cytokines, which are secreted by cells in airways and get incorporated into the mucus gel. Bacteria, viruses and other particles get trapped in the mucus and are either inactivated or simply expelled before they can do any damage. Under normal conditions the tips of the cilia engage with the undersurface of the gel phase and by coordinated movement they push the mucus blanket upwards and outwards to the pharynx where it is either swallowed or coughed up. While it only takes 30–60 minutes for mucus to be cleared from the large bronchi, it can be several days before mucus is cleared from respiratory bronchioles. One of the major long-term effects of cigarette smoking is a reduction in mucociliary transport. This contributes to recurrent infection and prolongs contact with carcinogenic material. Air pollutants, local and general anaesthetics and products of bacterial and viral infection also reduce mucociliary clearance.
Congenital defects in mucociliary transport lead to recurrent infections and eventually to bronchiectasis. For example, in the 'immotile cilia' syndrome there is an absence of the dynein arms in the cilia themselves, while in cystic fibrosis there is ciliary dyskinesia and abnormally thick mucus.
Humoral and cellular mechanisms
Nonspecific soluble factors
α-Antitrypsin (α1-antiprotease, see p. 341) in lung secretions is derived from plasma. It inhibits chymotrypsin and trypsin and neutralizes proteases including neutrophil elastase.
Antioxidant defences include enzymes such as superoxide dismutase and low-molecular-weight antioxidant molecules (ascorbate, urate) in the epithelial lining fluid. In addition, lung cells are protected by an extensive range of intracellular defences, especially members of the glutathione S-transferase (GST) superfamily.
Lysozyme is an enzyme found in granulocytes that has bactericidal properties.
Lactoferrin is synthesized from epithelial cells and neutrophil granulocytes and has bactericidal properties.
Interferons are produced by most cells in response to viral infection and are potent modulators of lymphocyte function.
Complement in secretions is also derived from plasma. In association with antibodies, it plays a major role in cytotoxicity.
Surfactant protein A (SPA) is one of four species of surfactant proteins which opsonizes bacteria/particles, enhancing phagocytosis by macrophages.
Defensins are bactericidal peptides present in the azurophil granules of neutrophils.
Dimeric secretory IgA targets specific antigens (p. 262).
Innate and adaptive immunity
These mechanisms act as a defence against microbes, inorganic substances, e.g. asbestos, particulate matter, such as dust, and other antigens. They act by aiding opsonization so that macrophages can better ingest foreign material.
With infection, neutrophils migrate out of pulmonary capillaries into the air spaces and phagocytose and kill microbes with, for example, antimicrobial proteins (lactoferrin), degradative enzymes (elastase) and oxidant radicals. In addition, neutrophil extracellular traps (NET) ensnare and kill extracellular bacteria. Neutrophils also generate a variety of mediators, e.g. TNF-α, IL-1 and chemokines which activate dendritic cells and B cells and produce the T-cell-activating cytokine IL-12. The latter enhances neutrophil-mediated defence during pneumonia. Dendritic cells are antigen presenting cells and are key to the adaptive immune response (p. 58).
Microbes are detected by host cells by pattern recognition receptors, e.g. toll-like receptors. These act via NF-κB transcription factors in the epithelial cells to produce adhesion molecules, chemokines and colony stimulating factors to initiate inflammation. Inflammation is necessary for innate immunity and host defence but can lead to lung damage: there is a fine line between defence and injury.
Runny, blocked nose and sneezing
Nasal symptoms (see also p. 691) are extremely common and both common colds and allergic rhinitis cause 'runny nose' (rhinorrhoea), nasal blockage and attacks of sneezing. In allergic rhinitis, symptoms may be intermittent, following contact with pollens or animal danders, or persistent, especially when house-dust mite is the allergen. Colds are frequent during the winter but if the symptoms persist for weeks the patient probably has perennial rhinitis rather than persistent viral infection.
Nasal secretions are usually thin and runny in allergic rhinitis but thicker and discoloured with viral infections. Nose bleeds and blood-stained nasal discharge are common and rarely indicate serious pathology. However, a blood-stained nasal discharge associated with nasal obstruction and pain may be the presenting feature of a nasal tumour (p. 1051). Nasal polyps typically present with nasal blockage and loss of smell.
Cough (see also p. 822) is the commonest symptom of lower respiratory tract disease. It is caused by mechanical or chemical stimulation of cough receptors in the epithelium of the pharynx, larynx, trachea, bronchi and diaphragm. Afferent receptors go to the cough centre in the medulla where efferent signals are generated to the expiratory musculature. Smokers often have a morning cough with a little sputum. A productive cough is the cardinal feature of chronic bronchitis, while dry coughing, particularly at night, can be a symptom of asthma. Cough also occurs in asthmatics after mild exertion or following forced expiration. Cough can also occur for psychological reasons without any definable pathology.
A worsening cough is the most common presenting symptom of lung cancer. The normal explosive character of the cough is lost when a vocal cord is paralysed, usually as a result of lung cancer infiltrating the left recurrent laryngeal nerve – sometimes termed a bovine cough. Cough can be accompanied by stridor in whooping cough or if there is laryngeal or tracheal obstruction.
Tarlo SM. Cough: occupational and environmental considerations: ACCP evidence-based clinical practice guidelines. Chest 2006; 129(Suppl 1):186S–196S.
Sputum
Approximately 100 mL of mucus is produced daily in a healthy, non-smoking individual. This flows gradually up the airways, through the larynx, and is then swallowed. Excess mucus is expectorated as sputum. Cigarette smoking is the commonest cause of excess mucus production.
Mucoid sputum is clear and white but can contain black specks resulting from the inhalation of carbon. Yellow or green sputum is due to the presence of cellular material, including bronchial epithelial cells, or neutrophil or eosinophil granulocytes. Yellow sputum is not necessarily due to infection, as eosinophils in the sputum, as seen in asthma, can give the same appearance. The production of large quantities of yellow or green sputum is characteristic of bronchiectasis.
Haemoptysis (blood-stained sputum) varies from small streaks of blood to massive bleeding.
The commonest cause of mild haemoptysis is acute infection, particularly in exacerbations of chronic obstructive pulmonary disease (COPD) but it should not be attributed to this without investigation.
Other common causes are pulmonary infarction, bronchial carcinoma and tuberculosis.
In lobar pneumonia, the sputum is usually rusty in appearance rather than frankly blood-stained.
Pink, frothy sputum is seen in pulmonary oedema.
In bronchiectasis, the blood is often mixed with purulent sputum.
Massive haemoptyses (>200 mL of blood in 24 hours) are usually due to bronchiectasis or tuberculosis.
Uncommon causes of haemoptyses are idiopathic pulmonary haemosiderosis, Goodpasture's syndrome, microscopic polyangiitis, trauma, blood disorders and benign tumours.
Haemoptysis should always be investigated. Although a diagnosis can often be made from a chest X-ray, a normal chest X-ray does not exclude disease. However, if the chest X-ray is normal, CT scanning and bronchoscopy are only diagnostic in about 5% of patients with haemoptysis.
Firm plugs of sputum may be coughed up by patients suffering from an exacerbation of allergic bronchopulmonary aspergillosis. Sometimes such sputum looks like casts of inflamed bronchi.
Dyspnoea is a sense of awareness of increased respiratory effort that is unpleasant and that is recognized by the patient as being inappropriate. Patients often complain of tightness in the chest; this must be differentiated from angina.
Breathlessness should be assessed in relation to the patient's lifestyle. For example, a moderate degree of breathlessness will be totally disabling if the patient has to climb many flights of stairs to reach home.
Orthopnoea (see p. 675) is breathlessness on lying down. While it is classically linked to heart failure, it is partly due to the weight of the abdominal contents pushing the diaphragm up into the thorax. Such patients may also become breathless on bending over.
Tachypnoea and hyperpnoea are, respectively, an increased rate of breathing and an increased level of ventilation. These may be appropriate responses (e.g. during exercise).
Hyperventilation is inappropriate overbreathing. This may occur at rest or on exertion and results in a lowering of the alveolar and arterial PCO2 (see p. 1178).
Paroxysmal nocturnal dyspnoea (see p. 798) is acute episodes of breathlessness at night, typically due to heart failure.
Wheezing is a common complaint and results from airflow limitation due to any cause. The symptom of wheezing is not diagnostic of asthma; other causes include vocal chord dysfunction, bronchiolitis and chronic obstructive pulmonary disease (COPD). Conversely, wheeze may be absent in the early stages of asthma.
The most common type of chest pain reported in respiratory disease is a localized sharp pain, often termed pleuritic. It is made worse by deep breathing or coughing and the patient can usually localize it. Localized anterior chest pain with tenderness of a costochondral junction is caused by costochondritis. Shoulder tip pain suggests irritation of the diaphragmatic pleura, while central chest pain radiating to the neck and arms is likely to be cardiac. Retrosternal soreness is associated with tracheitis, while malignant invasion of the chest wall causes a constant, severe, dull pain.
(see p. 1051)
The chest
Examination of the chest
Assess mental alertness, cyanosis, breathlessness at rest, use of accessory muscles, any deformity or scars on the chest and movement on both sides. CO2 intoxication causes coarse tremor or flap of the outstretched hands. Prominent veins on the chest may imply obstruction of the superior vena cava.
Cyanosis (see p. 676) is a dusky colour of the skin and mucous membranes, due to the presence of more than 50 g/L of desaturated haemoglobin. When due to central causes, cyanosis is visible on the tongue (especially the underside) and lips. Patients with central cyanosis will also be cyanosed peripherally. Peripheral cyanosis without central cyanosis is caused by a reduced peripheral circulation and is noted on the fingernails and skin of the extremities with associated coolness of the skin.
Finger clubbing is present when the normal angle between the base of the nail and the nail fold is lost. The base of the nail is fluctuant owing to increased vascularity, and there is an increased curvature of the nail in all directions, with expansion of the end of the digit. Some causes of clubbing are given in Table 15.1. Clubbing is not a feature of uncomplicated COPD.
Table 15.1 Some causes of finger clubbing
Bronchial carcinoma, especially epidermoid (squamous cell) type (major cause)
Chronic suppurative lung disease:
Lung abscess
Empyema
Pulmonary fibrosis (e.g. idiopathic lung fibrosis)
Pleural and mediastinal tumours (e.g. mesothelioma)
Cryptogenic organizing pneumonia
Cyanotic heart disease
Subacute infective endocarditis
Congenital – no disease
Palpation and percussion
Check the position of the trachea and apex beat. Examine the supraclavicular fossa for enlarged lymph nodes. The distance between the sternal notch and the cricoid cartilage (three to four finger breadths in full expiration) is reduced in patients with severe airflow limitation. Check chest expansion. A tape measure is used if precise or serial measurements are needed, e.g. in ankylosing spondylitis. Local discomfort over the sternochondral joints suggests costochondritis. In rib fractures, compression of the chest laterally and anteroposteriorly produces localized pain. On percussion, liver dullness is usually detected anteriorly at the level of the sixth rib. Liver and cardiac dullness disappear when lungs are over-inflated (Table 15.2).
Table 15.2 Physical signs of respiratory disease
Ask the patient to take deep breaths through the mouth. Inspiration should be more prolonged than expiration. Normal breath sounds are caused by turbulent flow in the larynx and sound harsher anteriorly over the upper lobes (particularly on the right). Healthy lungs filter out most of the high-frequency component, and the resulting sounds are called vesicular.
If the lung is consolidated or collapsed, the high-frequency hissing components of breath are not attenuated, and can be heard as 'bronchial breathing'. Similar sounds may be heard over areas of localized fibrosis or bronchiectasis. Bronchial breathing is accompanied by whispering pectoriloquy (whispered, high-pitched sounds can be heard distinctly through a stethoscope).
Added sounds
Wheeze. Wheeze results from vibrations in the collapsible part of the airways when apposition occurs as a result of the flow-limiting mechanisms. Wheeze is usually heard during expiration and is commonly but not invariably present in asthma and in chronic obstructive pulmonary disease. In acute severe asthma wheeze may not be heard, as airflow may be insufficient to generate the sound. Wheezes may be monophonic (single large airway obstruction) or polyphonic (narrowing of many small airways). An end-inspiratory wheeze or 'squeak' may be heard in obliterative bronchiolitis.
Crackles. These brief crackling sounds are probably produced by opening of previously closed bronchioles – early inspiratory crackles are associated with diffuse airflow limitation, while late inspiratory crackles are characteristically heard in pulmonary oedema, lung fibrosis and bronchiectasis.
Pleural rub. A creaking or groaning sound that is usually well localized. It indicates inflammation and roughening of the pleural surfaces, which normally glide silently over one another.
Vocal resonance. Healthy lung attenuates high-frequency notes, as compared to the lower-pitched components of speech. Consolidated lung has the reverse effect, transmitting high frequencies well; the spoken word then takes on a bleating quality. Whispered (and therefore high-pitched) speech can be clearly heard over consolidated areas, as compared to healthy lung. Low-frequency sounds such as 'ninety-nine' are well transmitted across healthy lung to produce vibration that can be felt over the chest wall. Consolidated lung transmits these low-frequency noises less well, and pleural fluid severely dampens or obliterates the vibrations altogether. Tactile vocal fremitus is the palpation of this vibration, usually by placing the edge of the hand on the chest wall. For all practical purposes this duplicates the assessment of vocal resonance and is not routinely performed as part of the chest examination.
Cardiovascular system examination (p. 676) gives additional information about the lungs.
Additional bedside tests
Since so many patients with respiratory disease have airflow limitation, airflow should be routinely measured using a peak flow meter or spirometer. This is a much more useful assessment of airflow limitation than any physical sign.
Radiology is essential in investigating most chest symptoms. Some diseases such as tuberculosis or lung cancer may be undetectable on clinical examination but are obvious on the chest X-ray. Conversely, asthma or chronic bronchitis may be associated with a normal chest X-ray. Always try to get previous films for comparison.
When viewing films consider:
Centring of the film. The distance between each clavicular head and the spinal processes should be equal
Penetration (check film is not too dark)
View. Routine films are taken postero-anterior (PA), i.e. the film is placed in front of the patient with the X-ray source behind. Anteroposterior (AP) films are taken only in very ill patients who are unable to stand up or be taken to the radiology department; the cardiac outline appears bigger and the scapulae cannot be moved out of the way. Lateral chest X-rays were often performed in the past to localize pathology, but CT scans have replaced these.
Look at:
The shape and bony structure of the chest wall
Whether the trachea is central
Whether the diaphragm is elevated or flat
The shape, size and position of the heart
The shape and size of the hilar shadows
The size and shape of any lung abnormalities and vascular shadowing.
X-ray abnormalities
Collapse and consolidation
Simple pneumonia is easy to recognize (see Fig. 15.33) but look carefully for any evidence of collapse (Fig. 15.10, Table 15.3). Loss of volume or crowding of the ribs are the best indicators of lobar collapse. The lung lobes collapse in characteristic directions. The lower lobes collapse downwards and towards the mediastinum, the left upper lobe collapses forwards against the anterior chest wall, while the right upper lobe collapses upwards and inwards, forming the appearance of an arch over the remaining lung. The right middle lobe collapses anteriorly and inward, obscuring the right heart border. If a whole lung collapses, the mediastinum will shift towards the side of the collapse. Uncomplicated consolidation does not cause mediastinal shift or loss of lung volume, so any of these features should raise the suspicion of an endobronchial obstruction.
Figure 15.10 Collapse of the left upper lobe. Chest X-ray showing triangular shadow in the left upper zone, next to the mediastinum.
Table 15.3 Causes of collapse of the lung
Enlarged tracheobronchial lymph nodes due to malignant disease, tuberculosis
Inhaled foreign bodies (e.g. peanuts) in children, usually in the right main bronchus
Bronchial casts or plugs (e.g. allergic bronchopulmonary aspergillosis)
Retained secretions – postoperatively and in debilitated patients
Pleural effusions (see Fig. 15.45) need to be larger than 500 mL to cause much more than blunting of the costophrenic angle. On an erect film they produce a characteristic shadow with a curved upper edge rising into the axilla. If very large, the whole of one hemithorax may be opaque, with mediastinal shift away from the effusion.
Localized fibrosis causes streaky shadowing, and the accompanying loss of lung volume causes mediastinal structures to move to the same side. More generalized fibrosis can lead to a honeycomb appearance (see p. 849), seen as diffuse shadows containing multiple circular translucencies a few millimetres in diameter.
Round shadows
Lung cancer is the commonest cause of large round shadows but many other causes are recognized (Table 15.4).
Table 15.4 Causes of round shadows (>3 cm) in the lung
Miliary mottling
This term, derived from the Latin for millet, describes numerous minute opacities, 1–3 mm in size. The commonest causes are tuberculosis, pneumoconiosis, sarcoidosis, idiopathic pulmonary fibrosis and pulmonary oedema (see Fig. 14.15), although pulmonary oedema is usually perihilar and accompanied by larger, fluffy shadows. Pulmonary microlithiasis is a rare but striking cause of miliary mottling.
CT provides excellent images of the lungs and mediastinal structures (Fig. 15.11). Narrow slice, high-resolution CT scans show the lung parenchyma well, while thicker slice staging CT scans are used for diagnosis of malignant disease. Mediastinal structures are shown more clearly after injecting intravenous contrast medium.
Figure 15.11 CT scans of the lung. (a) Lung setting – showing normal lung markings. 1, right hilum; 2, mediastinum; 3, left hilum; 4, lung vessels; 5, left main bronchus; 6, right main bronchus; 7, peripheral lung vessels. (b) Mediastinal (soft tissue) setting – showing normal mediastinal structures following intravenous contrast enhancement. 1, rib; 2, descending left pulmonary artery; 3, scapula; 4, subcutaneous fat; 5, left main bronchus; 6, descending aorta; 7, spinal canal; 8, vertebral body; 9, oesophagus; 10, right main bronchus; 11, right pulmonary artery; 12, muscle; 13, right superior pulmonary vein; 14, superior vena cava; 15, costal cartilage; 16, ascending aorta; 17, sternum; 18, thymic remnant; 19, pulmonary trunk; 20, left superior pulmonary vein. (c) Post-contrast scan showing large right upper zone carcinoma with enlarged lymph nodes in the mediastinum surrounding the trachea.
CT is essential in staging bronchial carcinoma by demonstrating tumour size, nodal involvement, metastases and invasion of mediastinum, pleura or chest wall. CT-guided needle biopsy allows samples to be obtained from peripheral masses. Staging scans should assess liver and adrenals, which are common sites for metastatic disease.
High-resolution CT (HRCT) scanning samples lung parenchyma with 1–2 mm thickness scans at 10–20 mm intervals and are used to assess diffuse inflammatory and infective parenchymal processes. It is valuable in:
Evaluating diffuse disease of the lung parenchyma, including sarcoidosis, hypersensitivity pneumonitis, occupational lung disease, and any other form of interstitial pulmonary fibrosis.
Diagnosis of bronchiectasis. HRCT has a sensitivity and specificity >90%.
Distinguishing emphysema from diffuse parenchymal lung disease or pulmonary vascular disease as a cause of a low gas transfer factor with otherwise normal lung function.
Suspected opportunistic lung infection in immunocompromised patients
Diagnosis of lymphangitis carcinomatosa.
Multi-slice CT scanners can produce detailed images in two or three dimensions in any plane. This detail is particularly useful for the detection of pulmonary emboli. Pulmonary nodules and airway disease are more easily defined and the technique makes HRCT less necessary.
MRI is less valuable than CT in assessing the lung parenchyma. In the mediastinum, MRI with ECG-gating allows accurate imaging of the heart and aortic aneurysms, and MRI has been used in staging lung cancer, for assessing tumour invasion in the mediastinum, chest wall and at the lung apex, because it produces good images in the sagittal and coronal planes. Vascular structures can be clearly differentiated as flowing blood produces a signal void on MRI.
Positron emission tomography (PET)
Tumours take up labelled fluorodeoxyglucose (FDG), which emits positrons that can be imaged and helps to differentiate benign from malignant tumours. In bronchial carcinoma, PET scanning combined with CT is now the investigation of choice for assessing lymph nodes and metastatic disease.
Hansell DM, Lynch DA, Page McAdams H et al. Imaging of Diseases of the Chest, 5th edn. Chicago: Elsevier Mosby; 2010.
Endocrine disease
Rheumatology and bone disease
Haematological disease
Tags: Kumar and Clarks Clinical Medicine
Mar 31, 2017 | Posted by admin in GENERAL & FAMILY MEDICINE | Comments Off on Respiratory disease


text:
Oklahoma State Sen. Nathan Dahm thinks all gun violence is caused by "sin nature"
9:15 AM EST on January 31, 2014
Sometimes I think this site should have one of those little counters like you see in the workplace, only instead of listing the number of days since a workplace injury it should be "number of days since an Oklahoma politician made national headlines for saying something dumb." Enter Broken Arrow Republican Nathan Dahm.
Last week Dahm went on Piers Morgan's popular CNN show British Guy Interrupts People to argue with Morgan about gun control. Dahm has introduced a bill that would get rid of all basically all licensing requirements including background checks for mental illness and criminal records. His reasoning is that all gun violence is caused by sin, and not by guns.
From Tulsa World:
"Sin nature in mankind" causes gun violence, not the guns themselves or mental illness, state Sen. Nathan Dahm, R-Broken Arrow, told combative CNN commentator Piers Morgan on Monday night.
Dahm appeared on Morgan's program in connection with a bill Dahm introduced for the upcoming legislative session.
The legislation is called the "Piers Morgan Act," a dig at Morgan's outspoken criticism of the United States' relatively lax gun laws.
Dahm's bill essentially would eliminate all handgun licensing requirements in Oklahoma. Dahm said he opposes all background checks, including those for mental illness and criminal records, as unconstitutional....
"If the key issue in gun deaths is not the guns and it's not mental health, what is it?" Morgan asked.
"It is the sin nature of mankind," replied Dahm. "It's that somebody is willing to take someone else's life."
I don't know what to say other than that is just objectively not true. Some gun violence is caused by sin, sure, but some gun violence is the result of other things, like mental illness. Or something else entirely.
Here are just a handful of the shootings that took place in Oklahoma in 2013. Read them carefully, because contrary to what Senator Dahm claims, it doesn't appear that anyone was willing to take someone else's life.
Rocky Point -- According to authorities, a woman was wounded when a gun accidentally discharged inside the residence.
Tulsa -- Cheyenne Monique Cunningham, 22, told police that her boyfriend, DeAndre Wilson, 22, had recently purchased a gun and wanted to show her how to use it, Solomon said. The small semi-automatic weapon accidentally fired, striking Wilson once in the stomach, police said.
Chickasha -- "Bingaman began to spin the gun on his finger, playing around when the gun fired," said Hendrix. "The bullet entered the top right of his head bouncing off the skull and exiting from the top of his head."
Tulsa -- The victim's friend, a 16-year-old who thought the weapon was not functional, tossed the gun to the victim, and the gun fired when it struck the floor, they told Tulsa police.
A Bartlesville gun shop -- "The victim had taken a pre-1950 .22 revolver in to have it looked at, and it accidentally went off and shot the customer in the groin."
Milton -- "At this point, I don't believe there was any foul play in her death," Seale said. "It looks like maybe the gun hit the floor and just went off or that sort of thing."
Jay -- Gardner and James were playing with a small handgun, passing it back and forth and twirling it "cowboy style" as they cruised down New Life Ranch Road between Colcord and West Siloam Springs, Wells said. Gardner was playing with the gun when it discharged, and the bullet passed through the front seat into the back of James, he said.
Edmond -- Today at the Edmond Police Department firing range there was an accidental discharge of a gun. The accident resulted in a minor injury to one of the officers. The officer was treated and released from Integris Hospital with a "burn" wound on the leg. At the time of the incident there were eight officers and two instructors conducting firearms training. There was another accidental shooting at this facility January of this year.
Midwest City -- ...she was getting ready for a birthday party around 5 p.m. Saturday inside the Chestnut Square Apartments when an old rifle fell, discharged and shot Destanie. Her family says she was painting her nails with a friend at their neighbor's apartment, who kept an old rifle from 1891 loaded on his dresser. Destanie's friend said the rifle fell and hit the wall and shot Destanie.
Tahlequah -- Chennault said it appears Lane was cleaning the handgun when it fired, and the bullet struck him in the chest.
Logan County -- A teenager remains in the hospital after investigators said he stuck a gun in his mouth and it accidentally went off.
Spiro -- LeFlore County Sheriff Rob Seale said Saylor Slone Martine and her 12-year-old sister were handling a .380-caliber semi-automatic handgun when one of the girls placed the gun on a counter. When the 15-year-old reached down to get her cell phone, Seale said the gun discharged.
Seale said the girl sustained life-threatening injuries and was immediately flown to a hospital in Tulsa where she later died.
Chickasha -- The minor then grabbed the barrel of the gun, identified as a 12 gauge Mossberg 500A shotgun, when it went off hitting the minor in the right hand. -
Braggs -- The Muskogee Phoenix reports that 54-year-old Steve Williams died at about 9 p.m. Thursday at his home in Greenleaf State Park. Muskogee County Sheriff Charles Pearson says Williams was cleaning his gun when it went off.
Spencer -- The sheriff's office was doing some routine training when two deputies went inside a classroom. At some point, sheriff's officials said, one of the deputies checked his weapon and it discharged.
Miami -- "After thorough review of the OSBI's reports, it would appear that the evidence is consistent with the fact that the gun accidentally discharged one time into the chest of Mr. Largent," Ottawa County District Attorney Eddie Wyant said. "Therefore, the State of Oklahoma will not pursue any charges surrounding Mr. Largent's death."
Tulsa -- At the scene, police discovered a 21-year-old male with a gunshot wound, the report said. Investigators said the men were playing with the .45-caliber assault rifle when it discharged.
You can find stories like these almost every day. These incidents are all always described in the passive voice, as if nothing caused them except for the gun just accidentally shooting out of nowhere. The weapon "accidentally fired." The gun "just went off." My personal "favorite" is the one talking about how there was no foul play, but "It looks like maybe the gun hit the floor and just went off or that sort of thing." Oopsie daisy, the gun just happened to hit the floor and go off! You know, like happens sometimes!
Guns don't kill people, people kill people, we're told time and time again. Until a person accidentally gets shot and then it's all the gun's fault.
I don't think you'll find sin as the cause for any of these. Basic human stupidity is a pretty common thing, but I don't remember my Sunday School teacher telling me Thou Shalt Not Be Dumb was one of the Ten Commandments.
Teaching personal responsibility is great and preaching responsible gun ownership is all well and good, but these are guns and when mistakes are made with them people often die. I'm not sure what the entire answer to gun violence is, but eliminating all restrictions and trusting anyone that wants to use one to do so responsibly doesn't seem like a great way to go. Neither does just shrugging your shoulders and saying, "Sin, man. What can you do about it?"
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Louis Fowler

redpajama_set_name: RedPajamaCommonCrawl


text:
Q: Mysqli query with zerofill Hello stackoverflow community, I need help with this mysqli query. My auto increase column in database is ZERO-FILL element for example 00001 so when I try to query like this:
$stmt = $mysqli->query("UPDATE ".$db_table_prefix."korteles
    SET
    vardas = '".$this->clean_k_name."',
    pavard = ".$this->clean_k_surname.",
    WHERE korteles_nr = '00001'");

And I get error:

You have an error in your SQL syntax; check the manual that
  corresponds to your MariaDB server version for the right syntax to use
  near 'WHERE korteles_nr = 00001' at line 18

I was searching Internet for solving this problem. But can't find so please help!

A: Query should be like this:-
$stmt = $mysqli->query("UPDATE ".$db_table_prefix."korteles
    SET
    vardas = '$this->clean_k_name',
    pavard = '$this->clean_k_surname'
    WHERE
      korteles_nr = '00001'");

You have to remove the comma after $this->clean_k_surname variable

redpajama_set_name: RedPajamaStackExchange


GIBRALTAR — Armenia beat Gibraltar 6-2 in UEFA Nations Cup D division game keeping a slim chance of promotion to Division C alive. Four-goal Yura Movsisyan quelled a Gibraltar side who initially led through Tjay De Barr. The Chicago Fire forward cancelled out that breakaway goal, then hit a seven-minute hat-trick soon after half-time. Artur Kartashyan and Aleksandre Karapetyan added further strikes to eliminate Gibraltar, avenging Armenia's shock home loss last month.
Armenia needs to beat Liechtenstein on Monday and hope that FYR Macedonia lose to Gibraltar to have a chance.
Despite the comfortable scoreline, Armenia were rattled early on, seeing two players booked inside the opening seven minutes and the locals were then sent potty on 10 minutes when Gibraltar took the lead.
A rapid breakaway saw Lee Casciaro pinch possession on the halfway line and he released 18-year-old Tjay De Barr, who sped beyond the Armenia defence, skipped past the goalkeeper and coolly slotted the ball into the empty goal.
Yet Armenians slowly asserted control and equalized when Yura Movsisyan scuffed the ball in from close range and Movsisyan scored again as he finished off a fine move early in the second half.
Movsisyan, who plays for Chicago Fire, scored a third and fourth before Artur Kartashyan added the fifth as Armenia scored four goals in 18 second-half minutes to take the game away from Gibraltar.
Gibraltar reduced the arrears to 5-2 on 77 minutes when Adam Priestley, who plays for Ossett United in the English Northern Premier League Division One East, stormed through and drove in a consolation goal to trigger more rapturous celebrations.
Armenia's Aleksandre Karapetyan ran through in injury time to restore the four goal advantage and seal the 6-2 win.


I think I have an obsession with grey. Just putting it out there. I don't know if it's the grey weather, me getting older or what, but lately I've found that I've been particularly drawn to grey. According to color psychology (if such a thing can be true), grey is the color of compromise, it's detached, neutral, impartial and indecisive – the fence-sitter. It's interesting to reflect on the meaning of this color. The one word that does stick out in this color analysis is "neutral", I often feel in life that I'm the "neutral" person, whether that directly reflects in what colors I wear, I doubt it but it's an interesting exercise to figure out why I've been drawn to this color lately.
I've noticed over the past couple of months, I've been shying away from bright colors and prints for my every day clothes but have opted for that color scheme when working out. Maybe it's a workout motivator to wear bright and fun colors and prints? Either way, I find it fascinating to see how my own personal style is evolving. Anything you've noticed in your way of dressing these past couple of months?


text:
Home Innovation Smartphones Mobility
Samsung unwraps skinny, octacore, full-metal 5.5-inch Galaxy A7
New eight-core smartphone fills out Samsung's A-series line-up.
Written by Liam Tung, Contributing Writer on Jan. 12, 2015
The Samsung Galaxy A7.
Samsung has followed up its full metal-bodied Galaxy A3 and A5 handsets with a slightly larger 5.5-inch sibling, the Galaxy A7.
The Galaxy A7 rounds out Samsung's line of Galaxy A-series smartphones, introduced last year, aimed at buyers who prefer metal over plastic, and "sophisticated design" over cutting-edge specs.
Looks-wise, the A7 is basically the same as the Galaxy A3 and A5, two nearly identical devices featuring full aluminum, unibody construction. The phones referenced design elements from the Galaxy Note 4 and Galaxy Alpha, but lacked their higher-end specs and fell well short of any comparison to the iPhone 6.
Samsung has, however, given the A7 more grunt than the A3 and A5, both of which had 1.2GHz quadcore processors. Instead, the Galaxy A7 has an octacore processor, consisting of 1.8GHz quadcore and 1.3GHz quadcore processors, while the dual SIM variant has 1.5GHz and 1GHz quadcore processors.
Samsung's Tizen smartphone OS: Dead or alive?
The A7's 5.5-inch HD super AMOLED display is on par with the A5's. Like its siblings, the A7 also comes with LTE Category 4, supporting download speeds of up to 150Mbps and uploads of 50Mbps to help consumers upload selfies tweaked with Samsung's 'wide selfie' or 'beauty face' features. Other key features include its 13-megapixel auto-focus front camera and five-megapixel rear camera.
The device also comes with 2GB RAM, 16GB of in-built storage, and a microSD slot on the side that supports up to 64GB additional memory. To support the larger screen and extra power, the phone comes with a 2600 mAh capacity battery. Notably, the A3 and A5 came with non-removable batteries.
The A7 is on the slim side: at 6.3mm deep, it's half a millimetre thinner than the iPhone 6 and slimmer than the A5 and A3. Still, it doesn't quite crack the Oppo R5's 4.85mm depth. Otherwise, the A7 weighs in at 141g with dimensions of 151mm long and 76.2 mm wide.
The Galaxy A7 is available in black, white, and gold and will ship with Android KitKat, though presumably it will get a Lollipop update at some point in the future.
The latest device from Samsung comes as the company attempts to deal with falling profits from its smartphone business and places greater emphasis on the Chinese and Indian markets. The A3 and A5 were both launched in China first, and got a second launch in India last week alongside the new mid-range Galaxy E5 and Galaxy E7.
Samsung hasn't said which markets Galaxy A7 will be available in, and hasn't given a release date yet.
Read more on this story
Samsung releases mid-range Galaxy E5 and E7 with Android onboard
Samsung expects to suffer annual profit drop
CES 2015: Samsung unveils tiny SSD that packs 1TB
Samsung unveils flagship Exynos 2100 smartphone chip
Samsung just showed off this 200-megapixel smartphone image sensor
Which Samsung phone is the best? The top Galaxy models compared


Now that you're opening up the possibility of bananas you should try my favourite smoothie. I cup chocolate almond milk, 1 frozen banana and a spoonful of PB2. I such a delicious treat, and pretty low cal if you use the unsweetened stuff!
Sounds delish! I should make that for Sawyer – I don't know if I'm ready for chocolate + banana yet, baby steps over here!
Oooh I have a packet of this protein at home. I can't wait to try out this recipe with it…been wondering what do make with it Thanks for posting!


Recently-released GDP data confirms that the battered Brazilian economy has entered a tentative recovery phase. GDP rose 0.3% annually in Q2, the first positive reading in over three years and a notable contrast to the 0.4% contraction recorded in Q1. The figure exceeded analysts' projections. Although the result is positive for the Brazilian economy, it remains to be seen whether a strong recovery will take hold as political uncertainty remains high.
The economy's upturn was driven by a rise in consumer spending. Private consumption grew 0.7% annually, the best result since Q4 2014. Falling inflation is helping underpin real disposable income, while the government's decision to allow workers to make early withdrawals from the employee severance fund, a scheme in place since 1994 that is known by its acronym "FGTS", also likely boosted the result. Outside of household consumption, the other components of domestic demand remained in freefall. Government spending dropped 2.4% in Q2, a multi-year low, and fixed investment plunged 6.5% (Q1: -3.7% year-on-year). The government continues to grapple with a large fiscal deficit and budget shortfalls, while the still-bleak economic panorama and large debt loads are likely behind the lack of investment.
On the external side, improving demand and stabilizing commodities prices boosted overseas sales. Exports grew at a robust pace of 2.5% annually in Q2 (Q1: +1.9% yoy). Meanwhile, imports dropped 3.3%, reflecting the weakness of the domestic economy and falling investment.
On a quarterly basis, GDP expanded a seasonally-adjusted 0.2%, the second consecutive quarter of growth, meaning the economy exited technical recession (Q1: +1.0% quarter-on-quarter).
Although the second-quarter GDP release points to improvements in the Brazilian economy, conditions remain discouraging. The unemployment rate continues to rest in double-digits, and falling investment shows no signs of bottoming out. Moreover, political noise worsened in Q3 as corruption allegations against President Michel Temer were in the spotlight. The turbulence is likely to continue holding back investment activity and prevent a stronger recovery from taking hold, as the trajectory for government reforms has become more uncertain in the wake of Temer's abysmal approval ratings.
LatinFocus Consensus Forecast panelists see GDP expanding a meagre 0.4% in 2017, which is unchanged from last month's estimate. For 2018, the panel sees the economy growing 2.0%.
Looking for forecasts related to GDP in Brazil? Download a sample report now.
Source: Brazilian Institute of Statistics and Geography (IBGE) and FocusEconomics Consensus Forecast.


text:
Hunting seasons heating up in Twin Tiers
Many hunting seasons are already under way in the Twin Tiers, and another popular season opens this weekend.
Saturday marks opening day of pheasant hunting season in both New York and Pennsylvania.
In both states, most of the hunting opportunities are provided by state-raised ring-necked pheasants that are released on land open to public hunting prior to and during the hunting season.
New York releases about 30,000 adult pheasants statewide for hunting, some on state-owned land and the rest on private property that owners agree to open to the public.
All of the birds released are raised at the Reynolds Game Farm near Ithaca.
Study: Outdoor recreation huge for New York's economy
Pennsylvania will release nearly 170,000 pheasants statewide, all raised at two rearing facilities. Most of the birds in the Northern Tier are released on state game lands.
For the first time, ringneck hunters in Pennsylvania have to buy an additional pheasant stamp for $25 in addition to a hunting license.
The state Game Commission approved creation of the new stamp this spring because revenues from hunting license sales weren't enough to sustain the pheasant propagation program.
In New York, a valid hunting license is all that is required to hunt pheasants.
Archery season for deer opened Sept. 30 in Pennsylvania and Oct. 1 in New York. Several small game seasons are also open in both states.
The regular, or gun season, for deer opens Nov. 18 in New York and Nov. 27 in Pennsylvania.
Follow @SGJeffMurray on Twitter.
For more information about hunting seasons and regulations in New York, go to www.dec.ny.gov/outdoor/hunting.html.
To learn more about hunting in Pennsylvania, go to www.pgc.pa.gov.


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Photoshop requires a lot of time and effort. What if there is a complex utility? Of course, use a simpler and more convenient program. This is the version that has been selected. The compositions of the compositions of the complex software.
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"Making the Word of God of none effect through your tradition, which ye have delivered: and many such like things do ye" (Mark 7:13).
In Israel, it was found that a great deal of emphasis was placed upon that which one generation passed on to the other; that is, what father passed on to son. It was found in Israel, at the time of Christ, that layer-upon-layer of tradition had been superimposed over the Word of God. These traditions were the opinions, the doctrines, the practices, the rites, and the customs that were handed down from one generation, in Israel, to the next. As a matter of fact, the word, tradition, means the handing-down, or transmitting of any opinions, or practices from forefathers to descendants without written memorials.
Thus, in the religious sense, or in the Biblical sense, "tradition" means that which is passed on to others as truth, but not based upon the Word of God, and that which has some sense of antiquity about it. That is, some opinion, practice, rite, or ceremony which dates back in time and, thus, carries with it some weight of authority because of its age.
Now, at the time the Lord Jesus Christ was being proclaimed as the long-awaited Anointed One (the Messiah) in Israel, He was confronted on every hand by the religious leaders in Israel because He failed to pay any attention, whatsoever, to their tradition.
"Then came together unto Him the Pharisees, and certain of the scribes, which came from Jerusalem. And when they saw some of His disciples eat bread with defiled, that is to say, with UNWASHEN, HANDS, they found fault" (Mk. 7:1-2).
One of the chief characteristics of tradition-worshipping Pharisees and scribes is that they find fault. They point out things that are contrary to their tradition. They are fault-finders. They tear down; they do not edify; they do not build up. "Why do thy disciples transgress the tradition of the elders?" The Lord answered, "Why do ye transgress the commandment of God by your tradition?"
"For the Pharisees and all the Jews, except they wash their hands oft, eat not, holding the TRADITIONS OF THE ELDERS. And when they come from the market, except they wash, they eat not. And many other things there be, which they have received to hold, as the washing of cups, and pots, and brasen vessels. and of tables. Then the Pharisees and scribes asked Him. Why walk not thy disciples according to the TRADITION OF THE ELDERS, but eat bread with UNWASHEN HANDS?"(Mk.7:3-5).
They are offended at the disciples because they are a little crude. They wash not their hands before they eat. But, they paid more attention to the Word of God than they did the tradition.
"He answered and said unto them, Well hath Esaias prophesied of you hypocrites, as it is written, This people honoreth me with their lips, but their heart is far from me. Howbeit in vain do they worship me (note that it is in VAIN, but they do worship), TEACHING FOR DOCTRINES THE COMMANDMENTS OF MEN. For laying aside the COMMANDMENT OF GOD, ye hold the TRADITION OF MEN, as the washing of pots and cups: and many other such like things ye do. And He said unto them. Full well ye reject the commandment of God, that ye may keep your own tradition" (Mk. 7.6-9).
". . . hold fast that which is good" (1 Thess. 5:21).
"Hold fast the form of sound words, which thou hast heard of me, in faith and love which is in Christ Jesus" (2 Tim. 1:23).
"Seeing then that we have a great high priest, that is passed into the heavens, Jesus the Son of God. let us hold fast our profession" (Heb. 4: 14).
"But I have a few things against thee, because thou (the church of Pergamos) hast there them that hold the doctrine of Balaam. . . " (Rev. 2:14).
"So hast thou also them that hold the doctrine of the Nicolaitans" (Rev. 2:15).
This is contrasted by the exhortation that the believer is to HOLD TO THE WORD OF GOD.
"Holding forth the word of life" (Phil. 2:16).
"Holding fast the faithful word" (Titus 1:9).
"Holding faith. and a good conscience: which some having put away concerning faith have made shipwreck" (1 Tim. 1:19).
"Holding the mystery of the faith in a pure conscience" (1 Tim. 3:9).
The believer is to hold to that which has been reported from the Word of God. He is not to reject the Word of God, nor is he to do as did the Pharisees and scribes: for the Lord Jesus Christ told them, in Mark 7:13, that they made the Word of God of none effect through their TRADITION.
"Making the word of God of none effect through your tradition, which ye have delivered:"
Here, we see the chief characteristic of tradition as something delivered by men and not by God. There is great danger in this. Remember what the Apostle Paul said in Galatians 1:13-14.
"For ye have heard of my conversation in time past in the Jews' religion, how that beyond measure I persecuted the church of God, and wasted it: And profited in the Jews' religion, how that above many my equals in mine own nation, being more exceedingly zealous of the TRADITIONS OF MY FATHERS. "
They were not zealous of the Word of God but of TRADITION. Watch out for religious tradition, for it is the seed bed for persecution. You ask why? When churches, Christians, or people hold to their tradition, and they are confronted with the fact that the Word of God is contrary to their tradition, it causes them to become angry with the one who calls attention to their error. Then, those who are exceedingly zealous about their tradition want to rise up and gnash on you with their teeth.
Being very zealous of the tradition of his fathers, Paul was able to place a great deal of confidence in the flesh when he had been a "blasphemer, and a persecutor, and injurious" (1 Tim. 1:13). The reason being; at that very time, he was as "touching the law blameless." He was a Hebrew of the Hebrews, a Pharisee who lived after the most straitest sect. If anyone had a standing in the flesh, in religion, or in the traditions of the elders, Paul could say, "I more." Those who are zealous toward their tradition are very sincere. But, sincerity with God does not count if your sincerity is not in harmony with God's Word.
In 1 Timothy, the Apostle Paul refers to himself when he had been a zealot of TRADITION. He states that "he did it ignorantly IN UNBELIEF." This; therefore, must be the Divine commentary on TRADITION. Folks do it, maintain it, observe it, or practice it, ignorantly, in unbelief.
The Lord Jesus Christ stated that individuals, full well, reject the commandment of God in order to keep "YOUR OWN TRADITION." It must be, then, considered a very important thing for Christians to examine the traditions to which they hold. It may very well be that they make "the word of God of none effect through (their) tradition."
Simon Peter makes mention of the fact that believing Israel, during the Book of Acts, was redeemed by the precious Blood of Christ from the vain traditions which Israel had passed on to them from their fathers.
"Forasmuch as ye know that ye were not redeemed with corruptible things. as silver and gold, from YOUR VAIN CONVERSATION (i.e. behavior) RECEIVED BY TRADITION FROM YOUR FATHERS: But with the precious Blood of Christ. as of a Lamb without blemish and without spot" (1 Peter 1:18-19).
Note what it took to redeem them from the TRADITION OF THE FATHERS - THE PRECIOUS BLOOD OF THE LORD JESUS CHRIST. That ought to speak to the heart of the Christian concerning tradition.
Lest it be ignored, it must be pointed out that during the Acts economy, the Apostle Paul delivered to the saints, certain traditions. This is tradition in the good sense of the word. That is, he delivered to them something that he had received from the Lord which he did not put in writing. There are two references to this. The first reference is found in 2 Thessalonians 2:15.
"Therefore, brethren, stand fast, and hold the traditions which ye have been taught, (notice, carefully) whether by word (what he told them, verbally), or by our epistle (i.e., what he wrote). "
"Now we command you, brethren, in the name of our Lord Jesus Christ, that ye withdraw yourselves from every brother that walketh disorderly, AND NOT AFTER THE TRADITION WHICH YE HAVE RECEIVED OF US."
"When ye received the Word of God which ye heard of us, ye received it not as the word of men, but as it is in truth, the Word of God, which effectually worketh also in you that believe"(1 Thess. 2:13).
Therefore, in the sense implied in the letter to the Thessalonians, "traditions" received from Paul were appropriate for that dispensation. Thus, traditions had the idea, only, of the "act of delivering over from one to another." There is no idea, here, of antiquity; only the transmitting of truth from Paul to others. At the time of the writing of the Thessalonian Epistle, the Bible was not, yet, complete; thus, much of the New Testament truth was, of necessity, passed by word of mouth (i.e. tradition) until such time as Pentecostal truth (i.e. N.T.) was committed to writing.
"Beware lest any man spoil you through philosophy and vain deceit. AFTER THE TRADITION OF MEN, after the rudiments of the world, and not after Christ" (Col. 2:8).
1. They find fault (Mk. 7:2).
2. They are offended if tradition is not kept (Mk. 7:5).
3. They honor God with their lips (Mk.7:6). They draw nigh to God with their mouth ( Matt. 15:8).
4. They have an affinity for ceremony (Mk.7:4).
5. They worship, but in vain (Mk.7:7; Matt. 15:9).
6. They keep their own tradition, and ignore the Word of God (Mk. 7:8).
Some of the writings of "our fathers," to wit, dispensational fathers, have become "tradition," and we must adhere to their traditional teaching, or we stand in jeopardy of being "ex-communicated" from the "Right Division Fellowship." This fate is equivalent to that of the Jews who were fearful that they should "be put out of the synagogue" (John 9:22).
There was a time when men embraced the Dispensational view that Acts 28:28 was the dividing line for Present Truth. Christian individualism, as Bible teachers, flourished from around 1830 to 1940. However, that time has past. Many Acts Twenty-eight believers now act as custodians, ever watchful for those who might "transgress the tradition" of the Dispensational Elders.


Published: Mar 18 at 10:45 a.m.
Updated: Mar 18 at 10:47 a.m.
Better late than never describes the Town of Kentville's Weekend of Winter's mini scavenger hunt held on Saturday, March 9, at Memorial Park. The event was originally scheduled for mid-February, but had to be postponed due to inclement weather.
"We try our best to think of events that don't rely on having snow so we can have them in case we don't get any," said organizer Ashley Alders, the communications and resource co-ordinator for the Town of Kentville. But what staff didn't count on was having too much ice, which created unsafe conditions in the park.
The concept for the event is based on the larger scavenger hunts created by co-organizer Chris Dorman last summer, in which he placed jars with $5 gift cards across the Valley and posted hints on yard sale sites. Within a few weeks, businesses across the region were contacting him to donate prizes and his Facebook page, Annapolis Valley Scavenger Hunt, attracted 2,000 followers.
About 14 teams consisting of approximately 45 people gathered at the town's Visitor Information Centre to register and get their first challenge: answering a list of questions based on information found around the park, such as when the park was established and how many swings are in the park's playground. Then off the teams went, trudging through the snow in various directions depending on what answers they sought first. Following that task, the participants had to solve a riddle in sequence in order to find a jar with another riddle to find the next jar and so on in the sequence until the third, final jar was found.
"It's pretty fun to watch. Once one person finds a jar, they all follow," said Dorman, who hid the jars and wrote the riddles. "I'm used to writing them, so that the rhyming and that comes easy. It's finding new ways to manipulate the game itself. This one is different because there is snow; I can use that in a different way to redirect people the wrong way," he laughs. In other words, sometimes tracks in the snow don't always lead participants where they think.
Alders said they kept three jars in total so it didn't take a whole afternoon, but just long enough to give participants some great fresh-air fun. Most teams were done in an hour, each expressing they were getting good exercise as they arrived back into the centre at each stage of the hunt.


Jessica Beardsley is passionate about nutrition and wellness. After earning a Bachelor's degree from NC State and a Master's from UC San Diego in biomedical engineering, she returned to graduate school to pursue a career in dietetics. With a Master's degree in nutrition from Georgia State University she enjoys helping her patients meet their health goals. Jessica works with patients in weight management, sports nutrition, prenatal health, diabetes and other chronic diseases. She is continuously reading up on the latest evidence-based medicine so she can best serve her patients. In her spare time you can find her developing new recipes, playing with her two young daughters, and training for her next race.


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Home Cargo Handling News Swissport to acquire Heathrow Cargo Handling
Swissport to acquire Heathrow Cargo Handling
Swissport will acquire Heathrow Cargo Handling from Air France, which it held in a joint venture, subject to regulatory approval.
The ground service provider will acquire the remaining 50% stake to fully own the handling company, which has provided cargo handling services at London's Heathrow Airport since 1995.
The completion of the sale is subject to Competition and Markets Authority approval and is expected in the first half of 2019.
The acquisition will enable Swissport to invest in its air cargo operations and services at Heathrow, where it operates two warehouses with a total surface of 15,300 square metres.
Last year, the joint venture had a workforce of 120 employees and handled over 150,000 tonnes of cargo, up 7% on 2017.
Luzius Wirth, executive vice president Europe, Middle East and Africa for Swissport says: "We are very satisfied that we can strategically round off our global cargo business with this selective acquisition. On the basis of over 20 years of successful business, jointly with Air France, Swissport now has the right setup to further develop and enhance its service offering at London's Heathrow airport."
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