Occupational Asthma: Causes and Symptoms

Occupational asthma is a type of asthma that is caused by exposure to certain chemicals in the workplace. Patients may experience worsening asthma symptoms while at work or notice an improvement in symptoms when away from work. The most common cause of occupational asthma is exposure to isocyanates, which are found in spray painting and foam moulding using adhesives. Other chemicals associated with occupational asthma include platinum salts, soldering flux resin, glutaraldehyde, flour, epoxy resins, and proteolytic enzymes.

To diagnose occupational asthma, it is recommended to measure peak expiratory flow at work and away from work. If there is a significant difference in peak expiratory flow, referral to a respiratory specialist is necessary. Treatment may include avoiding exposure to the triggering chemicals and using medications to manage asthma symptoms. It is important for employers to provide a safe working environment and for employees to report any concerns about potential exposure to harmful chemicals.

The area of the vocal cords lacks lymphatic drainage, making it a lymphatic boundary. The upper portion above the vocal cords drains to the deep cervical nodes through vessels that penetrate the thyrohyoid membrane. The lower portion below the vocal cords drains to the pre-laryngeal, pre-tracheal, and inferior deep cervical nodes. The aryepiglottic and vestibular folds have a significant lymphatic drainage and are prone to early metastasis.

Anatomy of the Larynx

The larynx is located in the front of the neck, between the third and sixth cervical vertebrae. It is made up of several cartilaginous segments, including the paired arytenoid, corniculate, and cuneiform cartilages, as well as the single thyroid, cricoid, and epiglottic cartilages. The cricoid cartilage forms a complete ring. The laryngeal cavity extends from the laryngeal inlet to the inferior border of the cricoid cartilage and is divided into three parts: the laryngeal vestibule, the laryngeal ventricle, and the infraglottic cavity.

The vocal folds, also known as the true vocal cords, control sound production. They consist of the vocal ligament and the vocalis muscle, which is the most medial part of the thyroarytenoid muscle. The glottis is composed of the vocal folds, processes, and rima glottidis, which is the narrowest potential site within the larynx.

The larynx is also home to several muscles, including the posterior cricoarytenoid, lateral cricoarytenoid, thyroarytenoid, transverse and oblique arytenoids, vocalis, and cricothyroid muscles. These muscles are responsible for various actions, such as abducting or adducting the vocal folds and relaxing or tensing the vocal ligament.

The larynx receives its arterial supply from the laryngeal arteries, which are branches of the superior and inferior thyroid arteries. Venous drainage is via the superior and inferior laryngeal veins. Lymphatic drainage varies depending on the location within the larynx, with the vocal cords having no lymphatic drainage and the supraglottic and subglottic parts draining into different lymph nodes.

Overall, understanding the anatomy of the larynx is important for proper diagnosis and treatment of various conditions affecting this structure.

The oxygen dissociation curve can be shifted to the left by low pCO2, which increases haemoglobin’s affinity for oxygen and makes it less likely to release oxygen to the tissues. In contrast, acidosis, hypercapnia, and hyperthermia cause a right shift of the curve, making it easier for oxygen to be released to the tissues. Raised levels of 2,3-diphosphoglycerate also shift the curve to the right by inhibiting oxygen binding to haemoglobin.

Understanding the Oxygen Dissociation Curve

The oxygen dissociation curve is a graphical representation of the relationship between the percentage of saturated haemoglobin and the partial pressure of oxygen in the blood. It is not influenced by the concentration of haemoglobin. The curve can shift to the left or right, indicating changes in oxygen delivery to tissues. When the curve shifts to the left, there is increased saturation of haemoglobin with oxygen, resulting in decreased oxygen delivery to tissues. Conversely, when the curve shifts to the right, there is reduced saturation of haemoglobin with oxygen, leading to enhanced oxygen delivery to tissues.

The L rule is a helpful mnemonic to remember the factors that cause a shift to the left, resulting in lower oxygen delivery. These factors include low levels of hydrogen ions (alkali), low partial pressure of carbon dioxide, low levels of 2,3-diphosphoglycerate, and low temperature. On the other hand, the mnemonic ‘CADET, face Right!’ can be used to remember the factors that cause a shift to the right, leading to raised oxygen delivery. These factors include carbon dioxide, acid, 2,3-diphosphoglycerate, exercise, and temperature.

Understanding the oxygen dissociation curve is crucial in assessing the oxygen-carrying capacity of the blood and the delivery of oxygen to tissues. By knowing the factors that can shift the curve to the left or right, healthcare professionals can make informed decisions in managing patients with respiratory and cardiovascular diseases.

The patient’s prolonged smoking history and current symptoms suggest a diagnosis of chronic bronchitis and possibly emphysema, both of which are obstructive lung diseases. These conditions cause air to become trapped in the lungs, making it difficult to breathe out. Pulmonary function tests typically show a greater decrease in FEV1 than FVC in obstructive lung diseases, resulting in a lower FEV1/FVC ratio (also known as the Tiffeneau-Pinelli index). This is different from restrictive lung diseases, which may sometimes show an increase in the FEV1/FVC ratio due to a larger decrease in FVC than FEV1. Chest X-rays may reveal hyperinflated lungs in patients with obstructive lung diseases. An increase in FEV1 may occur in healthy individuals after exercise training or in patients with conditions like asthma after taking medication. Restrictive lung diseases, such as pneumoconioses, hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis, are typically associated with a decrease in the FEV1/FVC ratio.

Understanding Pulmonary Function Tests

Pulmonary function tests are a useful tool in determining whether a respiratory disease is obstructive or restrictive. These tests measure various aspects of lung function, such as forced expiratory volume in one second (FEV1) and forced vital capacity (FVC). By analyzing the results of these tests, doctors can diagnose and monitor conditions such as asthma, COPD, pulmonary fibrosis, and neuromuscular disorders.

In obstructive lung diseases, such as asthma and COPD, the FEV1 is significantly reduced, while the FVC may be reduced or normal. The FEV1% (FEV1/FVC) is also reduced. On the other hand, in restrictive lung diseases, such as pulmonary fibrosis and asbestosis, the FEV1 is reduced, but the FVC is significantly reduced. The FEV1% (FEV1/FVC) may be normal or increased.

It is important to note that there are many conditions that can affect lung function, and pulmonary function tests are just one tool in diagnosing and managing respiratory diseases. However, understanding the results of these tests can provide valuable information for both patients and healthcare providers.

Sarcoidosis is likely in this patient based on their symptoms and examination findings, including a neck lump, tender nodules on the shin, and a history of red-eye. Bilateral lymphadenopathy on chest X-ray further supports the diagnosis, as does the presence of elevated angiotensin-converting enzyme levels, which are commonly seen in sarcoidosis. Hypercalcemia, fatigue, and uveitis are also associated with sarcoidosis, while exposure to silica is not supported by this patient’s presentation.

Investigating Sarcoidosis

Sarcoidosis is a disease that does not have a single diagnostic test, and therefore, diagnosis is mainly based on clinical observations. Although ACE levels may be used to monitor disease activity, they are not reliable in diagnosing sarcoidosis due to their low sensitivity and specificity. Routine blood tests may show hypercalcemia and a raised ESR.

A chest x-ray is a common investigation for sarcoidosis and may reveal different stages of the disease. Stage 0 is normal, stage 1 shows bilateral hilar lymphadenopathy (BHL), stage 2 shows BHL and interstitial infiltrates, stage 3 shows diffuse interstitial infiltrates only, and stage 4 shows diffuse fibrosis. Other investigations, such as spirometry, may show a restrictive defect, while a tissue biopsy may reveal non-caseating granulomas. However, the Kveim test, which involves injecting part of the spleen from a patient with known sarcoidosis under the skin, is no longer performed due to concerns about cross-infection.

In addition, a gallium-67 scan is not routinely used to investigate sarcoidosis. CT scans may also be used to investigate sarcoidosis, and they may show diffuse areas of nodularity predominantly in a peribronchial distribution with patchy areas of consolidation, particularly in the upper lobes. Ground glass opacities may also be present, but there are no gross reticular changes to suggest fibrosis.

Overall, investigating sarcoidosis involves a combination of clinical observations, blood tests, chest x-rays, and other investigations such as spirometry and tissue biopsy. CT scans may also be used to provide more detailed information about the disease.

The most effective intervention to slow the decrease in FEV1 experienced by patients with COPD is to stop smoking. If the patient has no asthmatic/steroid-responsive features, the next step in management would be to add a long-acting beta2-agonist (LABA) and a long-acting muscarinic antagonist. If the patient has asthmatic/steroid-responsive features, the next step would be to add a LABA and an inhaled corticosteroid. Oral theophylline is only considered if inhaled therapy is not possible, and oral prednisolone is only used during acute infective exacerbations of COPD to help with inflammation and is not a long-term solution to slow the reduction of FEV1.

The National Institute for Health and Care Excellence (NICE) updated its guidelines on the management of chronic obstructive pulmonary disease (COPD) in 2018. The guidelines recommend general management strategies such as smoking cessation advice, annual influenzae vaccination, and one-off pneumococcal vaccination. Pulmonary rehabilitation is also recommended for patients who view themselves as functionally disabled by COPD.

Bronchodilator therapy is the first-line treatment for patients who remain breathless or have exacerbations despite using short-acting bronchodilators. The next step is determined by whether the patient has asthmatic features or features suggesting steroid responsiveness. NICE suggests several criteria to determine this, including a previous diagnosis of asthma or atopy, a higher blood eosinophil count, substantial variation in FEV1 over time, and substantial diurnal variation in peak expiratory flow.

If the patient does not have asthmatic features or features suggesting steroid responsiveness, a long-acting beta2-agonist (LABA) and long-acting muscarinic antagonist (LAMA) should be added. If the patient is already taking a short-acting muscarinic antagonist (SAMA), it should be discontinued and switched to a short-acting beta2-agonist (SABA). If the patient has asthmatic features or features suggesting steroid responsiveness, a LABA and inhaled corticosteroid (ICS) should be added. If the patient remains breathless or has exacerbations, triple therapy (LAMA + LABA + ICS) should be offered.

NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot use inhaled therapy. Azithromycin prophylaxis is recommended in select patients who have optimised standard treatments and continue to have exacerbations. Mucolytics should be considered in patients with a chronic productive cough and continued if symptoms improve.

Cor pulmonale features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, and loud P2. Loop diuretics should be used for oedema, and long-term oxygen therapy should be considered. Smoking cessation, long-term oxygen therapy in eligible patients, and lung volume reduction surgery in selected patients may improve survival in patients with stable COPD. NICE does not recommend the use of ACE-inhibitors, calcium channel blockers, or alpha blockers

Lung cancer can cause the hemidiaphragm on the same side to rise due to pressure on the phrenic nerve. Haemoptysis is a common symptom of lung cancer, along with significant weight loss and a history of smoking. A chest x-ray can confirm the presence of a mediastinal mass, which is likely to be lung cancer.

A rapidly expanding lung mass can cause compression of surrounding structures, leading to complications. For example, an apical tumor can compress the brachial plexus, causing sensory symptoms in the arms or Erb’s or Klumpke’s palsies. Compression of the cervical sympathetic chain can cause Horner’s syndrome, which includes meiosis, anhidrosis, ptosis, and enophthalmos.

A mediastinal mass can also compress the recurrent laryngeal nerve as it winds around the aortic arch, resulting in hoarseness of voice or aphonia. Superior vena caval syndrome is a medical emergency that can cause swelling of the face, neck, upper chest, and arms, as well as the development of collaterals on the chest wall. Malignancy is the most common cause, but non-malignant causes can include an aortic aneurysm, fibrosing mediastinitis, or iatrogenic factors.

The Phrenic Nerve: Origin, Path, and Supplies

The phrenic nerve is a crucial nerve that originates from the cervical spinal nerves C3, C4, and C5. It supplies the diaphragm and provides sensation to the central diaphragm and pericardium. The nerve passes with the internal jugular vein across scalenus anterior and deep to the prevertebral fascia of the deep cervical fascia.

The right phrenic nerve runs anterior to the first part of the subclavian artery in the superior mediastinum and laterally to the superior vena cava. In the middle mediastinum, it is located to the right of the pericardium and passes over the right atrium to exit the diaphragm at T8. On the other hand, the left phrenic nerve passes lateral to the left subclavian artery, aortic arch, and left ventricle. It passes anterior to the root of the lung and pierces the diaphragm alone.

Understanding the origin, path, and supplies of the phrenic nerve is essential in diagnosing and treating conditions that affect the diaphragm and pericardium.

The trachea divides into two branches at the fifth thoracic vertebrae, or sometimes the sixth in individuals who are tall.

Anatomy of the Trachea

The trachea, also known as the windpipe, is a tube-like structure that extends from the C6 vertebrae to the upper border of the T5 vertebrae where it bifurcates into the left and right bronchi. It is supplied by the inferior thyroid arteries and the thyroid venous plexus, and innervated by branches of the vagus, sympathetic, and recurrent nerves.

In the neck, the trachea is anterior to the isthmus of the thyroid gland, inferior thyroid veins, and anastomosing branches between the anterior jugular veins. It is also surrounded by the sternothyroid, sternohyoid, and cervical fascia. Posteriorly, it is related to the esophagus, while laterally, it is in close proximity to the common carotid arteries, right and left lobes of the thyroid gland, inferior thyroid arteries, and recurrent laryngeal nerves.

In the thorax, the trachea is anterior to the manubrium, the remains of the thymus, the aortic arch, left common carotid arteries, and the deep cardiac plexus. Laterally, it is related to the pleura and right vagus on the right side, and the left recurrent nerve, aortic arch, and left common carotid and subclavian arteries on the left side.

Overall, understanding the anatomy of the trachea is important for various medical procedures and interventions, such as intubation and tracheostomy.

Surgical resection is the preferred treatment for pleomorphic adenoma, a benign tumor of the parotid gland that may undergo malignant transformation. Chemotherapy and radiotherapy are not effective in managing this condition. Additionally, salivary stone removal is not relevant to the treatment of pleomorphic adenoma.

Understanding Pleomorphic Adenoma

Pleomorphic adenoma, also known as a benign mixed tumour, is a non-cancerous growth that commonly affects the parotid gland. This type of tumour usually develops in individuals aged 40 to 60 years old. The condition is characterized by the proliferation of epithelial and myoepithelial cells of the ducts, as well as an increase in stromal components. The tumour is slow-growing, lobular, and not well encapsulated.

The clinical features of pleomorphic adenoma include a gradual onset of painless unilateral swelling of the parotid gland. The swelling is typically movable on examination rather than fixed. The management of pleomorphic adenoma involves surgical excision. The prognosis is generally good, with a recurrence rate of 1-5% with appropriate excision (parotidectomy). However, recurrence may occur due to capsular disruption during surgery. If left untreated, pleomorphic adenoma may undergo malignant transformation, occurring in 2-10% of adenomas observed for long periods. Carcinoma ex-pleomorphic adenoma is the most common type of malignant transformation, occurring most frequently as adenocarcinoma.

Aminophylline works by binding to adenosine receptors and preventing adenosine-induced bronchoconstriction. This mode of action is different from antihistamines like loratadine, which is an incorrect option. Theophylline, a shorter acting form of aminophylline, competitively inhibits type III and type IV phosphodiesterase enzymes responsible for breaking down cyclic AMP in smooth muscle cells, leading to possible bronchodilation. Additionally, theophylline binds to the adenosine A2B receptor and blocks adenosine-mediated bronchoconstriction. In inflammatory conditions, theophylline activates histone deacetylase, which prevents the transcription of inflammatory genes that require histone acetylation for transcription to begin. Therefore, the last three options are incorrect. (Source: Drugbank)

Aminophylline infusions are utilized to manage acute asthma and COPD. In patients who have not received xanthines (theophylline or aminophylline) before, a loading dose of 5 mg/kg is administered through a slow intravenous injection lasting at least 20 minutes. For the maintenance infusion, 1g of aminophylline is mixed with 1 litre of normal saline to create a solution of 1 mg/ml. The recommended dose is 500-700 mcg/kg/hour, or 300 mcg/kg/hour for elderly patients. It is important to monitor plasma theophylline concentrations.

Otitis media is primarily caused by bacteria, with viral URTIs often preceding the infection. The majority of cases are secondary to bacterial infections, with the most common culprit being…

Acute otitis media is a common condition in young children, often caused by bacterial infections following viral upper respiratory tract infections. Symptoms include ear pain, fever, and hearing loss, and diagnosis is based on criteria such as the presence of a middle ear effusion and inflammation of the tympanic membrane. Antibiotics may be prescribed in certain cases, and complications can include perforation of the tympanic membrane, hearing loss, and more serious conditions such as meningitis and brain abscess.

The typical range for intracranial pressure is 7 to 15 mm Hg, with the brain able to tolerate increases up to 24 mm Hg before displaying noticeable clinical symptoms.

Understanding the Monro-Kelly Doctrine and Autoregulation in the CNS

The Monro-Kelly doctrine governs the pressure within the cranium by considering the skull as a closed box. The loss of cerebrospinal fluid (CSF) can accommodate increases in mass until a critical point is reached, usually at 100-120ml of CSF lost. Beyond this point, intracranial pressure (ICP) rises sharply, and pressure will eventually equate with mean arterial pressure (MAP), leading to neuronal death and herniation.

The central nervous system (CNS) has the ability to autoregulate its own blood supply through vasoconstriction and dilation of cerebral blood vessels. However, extreme blood pressure levels can exceed this capacity, increasing the risk of stroke. Additionally, metabolic factors such as hypercapnia can cause vasodilation, which is crucial in ventilating head-injured patients.

It is important to note that the brain can only metabolize glucose, and a decrease in glucose levels can lead to impaired consciousness. Understanding the Monro-Kelly doctrine and autoregulation in the CNS is crucial in managing intracranial pressure and preventing neurological damage.

During pregnancy, a woman’s increased tidal volume leads to a decrease in carbon dioxide levels, resulting in alkalosis. This is because carbon dioxide generates acid, and reduced levels of it lead to a decrease in acid. The kidneys eventually adapt to this change by reducing the amount of alkaline bicarbonate in the body. Therefore, pregnancy causes a compensated respiratory alkalosis.

If a woman’s bicarbonate levels remain normal, she would have simple respiratory alkalosis.

On the other hand, if a woman produces excess acid, she would have metabolic acidosis, which is the opposite of what occurs during pregnancy.

Arterial Blood Gas Interpretation: A 5-Step Approach

Arterial blood gas interpretation is a crucial aspect of patient care, particularly in critical care settings. The Resuscitation Council (UK) recommends a 5-step approach to interpreting arterial blood gas results. The first step is to assess the patient’s overall condition. The second step is to determine if the patient is hypoxaemic, with a PaO2 on air of less than 10 kPa. The third step is to assess if the patient is acidaemic (pH <7.35) or alkalaemic (pH >7.45).

The fourth step is to evaluate the respiratory component of the arterial blood gas results. A PaCO2 level greater than 6.0 kPa suggests respiratory acidosis, while a PaCO2 level less than 4.7 kPa suggests respiratory alkalosis. The fifth step is to assess the metabolic component of the arterial blood gas results. A bicarbonate level less than 22 mmol/l or a base excess less than -2mmol/l suggests metabolic acidosis, while a bicarbonate level greater than 26 mmol/l or a base excess greater than +2mmol/l suggests metabolic alkalosis.

To remember the relationship between pH, PaCO2, and bicarbonate, the acronym ROME can be used. Respiratory acidosis or alkalosis is opposite to the pH level, while metabolic acidosis or alkalosis is equal to the pH level. This 5-step approach and the ROME acronym can aid healthcare professionals in interpreting arterial blood gas results accurately and efficiently.

Ramsay Hunt syndrome is characterized by a combination of Bell’s palsy facial paralysis, along with symptoms such as a herpetic rash, deafness, tinnitus, and vertigo. It is important to note that the rash may not always be visible, despite being present.

While Bell’s palsy may present with facial paralysis, it does not typically involve the presence of herpetic rashes.

Understanding Ramsay Hunt Syndrome

Ramsay Hunt syndrome, also known as herpes zoster oticus, is a condition that occurs when the varicella zoster virus reactivates in the geniculate ganglion of the seventh cranial nerve. The first symptom of this syndrome is often auricular pain, followed by facial nerve palsy and a vesicular rash around the ear. Other symptoms may include vertigo and tinnitus.

To manage Ramsay Hunt syndrome, doctors typically prescribe oral acyclovir and corticosteroids. These medications can help reduce the severity of symptoms and prevent complications.

The bronchioles’ lining inflammation obstructs the outflow of air from the lungs, leading to asthma symptoms that may come and go. Additionally, there could be heightened mucus production and constriction of bronchial muscles.

Asthma is a common respiratory disorder that affects both children and adults. It is characterized by chronic inflammation of the airways, resulting in reversible bronchospasm and airway obstruction. While asthma can develop at any age, it typically presents in childhood and may improve or resolve with age. However, it can also persist into adulthood and cause significant morbidity, with around 1,000 deaths per year in the UK.

Several risk factors can increase the likelihood of developing asthma, including a personal or family history of atopy, antenatal factors such as maternal smoking or viral infections, low birth weight, not being breastfed, exposure to allergens and air pollution, and the hygiene hypothesis. Patients with asthma may also suffer from other atopic conditions such as eczema and hay fever, and some may be sensitive to aspirin. Occupational asthma is also a concern for those exposed to allergens in the workplace.

Symptoms of asthma include coughing, dyspnea, wheezing, and chest tightness, with coughing often worse at night. Signs may include expiratory wheezing on auscultation and reduced peak expiratory flow rate. Diagnosis is typically made through spirometry, which measures the volume and speed of air during exhalation and inhalation.

Management of asthma typically involves the use of inhalers to deliver drug therapy directly to the airways. Short-acting beta-agonists such as salbutamol are the first-line treatment for relieving symptoms, while inhaled corticosteroids like beclometasone dipropionate and fluticasone propionate are used for daily maintenance therapy. Long-acting beta-agonists like salmeterol and leukotriene receptor antagonists like montelukast may also be used in combination with other medications. Maintenance and reliever therapy (MART) is a newer approach that combines ICS and a fast-acting LABA in a single inhaler for both daily maintenance and symptom relief. Recent guidelines recommend offering a leukotriene receptor antagonist instead of a LABA for patients on SABA + ICS whose asthma is not well controlled, and considering MART for those with poorly controlled asthma.

The function of alpha-1 antitrypsin is to inhibit elastase. However, smoke has a negative impact on this protein in the lungs, resulting in increased activity of elastases and the breakdown of elastic tissue, which leads to emphysema.

Contrary to popular belief, smoke actually activates polymorphonuclear leucocytes, which contributes to the development of emphysema.

Mucous gland hyperplasia, basal cell metaplasia, and basement membrane thickening are all examples of how smoke affects the lungs to cause chronic bronchitis, not emphysema.

COPD, or chronic obstructive pulmonary disease, can be caused by a variety of factors. The most common cause is smoking, which can lead to inflammation and damage in the lungs over time. Another potential cause is alpha-1 antitrypsin deficiency, a genetic condition that can result in lung damage. Additionally, exposure to certain substances such as cadmium (used in smelting), coal, cotton, cement, and grain can also contribute to the development of COPD. It is important to identify and address these underlying causes in order to effectively manage and treat COPD.

The most crucial step to enhance the patient’s prognosis is to assist them in quitting smoking. While lung reduction surgery and long-term oxygen therapy may benefit certain patient groups, smoking cessation remains the top priority. Proper inhaler technique and adherence, as well as the use of home nebulizers, can provide symptomatic relief for the patient.

The National Institute for Health and Care Excellence (NICE) updated its guidelines on the management of chronic obstructive pulmonary disease (COPD) in 2018. The guidelines recommend general management strategies such as smoking cessation advice, annual influenzae vaccination, and one-off pneumococcal vaccination. Pulmonary rehabilitation is also recommended for patients who view themselves as functionally disabled by COPD.

Bronchodilator therapy is the first-line treatment for patients who remain breathless or have exacerbations despite using short-acting bronchodilators. The next step is determined by whether the patient has asthmatic features or features suggesting steroid responsiveness. NICE suggests several criteria to determine this, including a previous diagnosis of asthma or atopy, a higher blood eosinophil count, substantial variation in FEV1 over time, and substantial diurnal variation in peak expiratory flow.

If the patient does not have asthmatic features or features suggesting steroid responsiveness, a long-acting beta2-agonist (LABA) and long-acting muscarinic antagonist (LAMA) should be added. If the patient is already taking a short-acting muscarinic antagonist (SAMA), it should be discontinued and switched to a short-acting beta2-agonist (SABA). If the patient has asthmatic features or features suggesting steroid responsiveness, a LABA and inhaled corticosteroid (ICS) should be added. If the patient remains breathless or has exacerbations, triple therapy (LAMA + LABA + ICS) should be offered.

NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot use inhaled therapy. Azithromycin prophylaxis is recommended in select patients who have optimised standard treatments and continue to have exacerbations. Mucolytics should be considered in patients with a chronic productive cough and continued if symptoms improve.

Cor pulmonale features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, and loud P2. Loop diuretics should be used for oedema, and long-term oxygen therapy should be considered. Smoking cessation, long-term oxygen therapy in eligible patients, and lung volume reduction surgery in selected patients may improve survival in patients with stable COPD. NICE does not recommend the use of ACE-inhibitors, calcium channel blockers, or alpha blockers

The Rinne and Weber tests are used to diagnose hearing loss. The Rinne test involves comparing air and bone conduction, with a positive result indicating a healthy or sensorineural loss and a negative result indicating a conductive loss. The Weber test involves placing a tuning fork on the forehead and determining if the sound is symmetrical or louder on one side, with a conductive loss resulting in louder sound on the affected side and a sensorineural loss resulting in louder sound on the non-affected side. When used together, these tests can provide more information about the type and affected side of hearing loss.

Rinne’s and Weber’s Test for Differentiating Conductive and Sensorineural Deafness

Rinne’s and Weber’s tests are used to differentiate between conductive and sensorineural deafness. Rinne’s test involves placing a tuning fork over the mastoid process until the sound is no longer heard, then repositioning it just over the external acoustic meatus. A positive test indicates that air conduction (AC) is better than bone conduction (BC), while a negative test indicates that BC is better than AC, suggesting conductive deafness.

Weber’s test involves placing a tuning fork in the middle of the forehead equidistant from the patient’s ears and asking the patient which side is loudest. In unilateral sensorineural deafness, sound is localized to the unaffected side, while in unilateral conductive deafness, sound is localized to the affected side.

The table below summarizes the interpretation of Rinne and Weber tests. A normal result indicates that AC is greater than BC bilaterally and the sound is midline. Conductive hearing loss is indicated by BC being greater than AC in the affected ear and AC being greater than BC in the unaffected ear, with the sound lateralizing to the affected ear. Sensorineural hearing loss is indicated by AC being greater than BC bilaterally, with the sound lateralizing to the unaffected ear.

Overall, Rinne’s and Weber’s tests are useful tools for differentiating between conductive and sensorineural deafness, allowing for appropriate management and treatment.

Chronic bronchitis is characterized by a persistent cough with sputum production for a minimum of 3 months in two consecutive years, after excluding other causes of chronic cough. Emphysema, on the other hand, is defined by the enlargement of air spaces beyond the terminal bronchioles. None of the remaining options are considered as definitions of COPD.

COPD, or chronic obstructive pulmonary disease, can be caused by a variety of factors. The most common cause is smoking, which can lead to inflammation and damage in the lungs over time. Another potential cause is alpha-1 antitrypsin deficiency, a genetic condition that can result in lung damage. Additionally, exposure to certain substances such as cadmium (used in smelting), coal, cotton, cement, and grain can also contribute to the development of COPD. It is important to identify and address these underlying causes in order to effectively manage and treat COPD.

Nasopharyngeal carcinoma is typically diagnosed through Trotter’s triad, which includes unilateral conductive hearing loss, ipsilateral facial and ear pain, and ipsilateral paralysis of the soft palate. This condition is commonly associated with previous Epstein Barr Virus infection, but there is no known link between the development of nasopharyngeal carcinoma and the other viruses mentioned.

Understanding Nasopharyngeal Carcinoma

Nasopharyngeal carcinoma is a type of squamous cell carcinoma that affects the nasopharynx. It is a rare form of cancer that is more common in individuals from Southern China and is associated with Epstein Barr virus infection. The presenting features of nasopharyngeal carcinoma include cervical lymphadenopathy, otalgia, unilateral serous otitis media, nasal obstruction, discharge, and/or epistaxis, and cranial nerve palsies such as III-VI.

To diagnose nasopharyngeal carcinoma, a combined CT and MRI scan is typically used. The first line of treatment for this type of cancer is radiotherapy. It is important to catch nasopharyngeal carcinoma early to increase the chances of successful treatment.

Asthma is linked to type 1 hypersensitivity, which is caused by the binding of IgE to Mast cells, resulting in an inflammatory reaction. Other types of hypersensitivity include type 2, which involves the binding of IgG or IgM to cell surface antigens, type 3, which is immune complex-mediated, and type 4, which is T-cell mediated.

Asthma is a common respiratory disorder that affects both children and adults. It is characterized by chronic inflammation of the airways, resulting in reversible bronchospasm and airway obstruction. While asthma can develop at any age, it typically presents in childhood and may improve or resolve with age. However, it can also persist into adulthood and cause significant morbidity, with around 1,000 deaths per year in the UK.

Several risk factors can increase the likelihood of developing asthma, including a personal or family history of atopy, antenatal factors such as maternal smoking or viral infections, low birth weight, not being breastfed, exposure to allergens and air pollution, and the hygiene hypothesis. Patients with asthma may also suffer from other atopic conditions such as eczema and hay fever, and some may be sensitive to aspirin. Occupational asthma is also a concern for those exposed to allergens in the workplace.

Symptoms of asthma include coughing, dyspnea, wheezing, and chest tightness, with coughing often worse at night. Signs may include expiratory wheezing on auscultation and reduced peak expiratory flow rate. Diagnosis is typically made through spirometry, which measures the volume and speed of air during exhalation and inhalation.

Management of asthma typically involves the use of inhalers to deliver drug therapy directly to the airways. Short-acting beta-agonists such as salbutamol are the first-line treatment for relieving symptoms, while inhaled corticosteroids like beclometasone dipropionate and fluticasone propionate are used for daily maintenance therapy. Long-acting beta-agonists like salmeterol and leukotriene receptor antagonists like montelukast may also be used in combination with other medications. Maintenance and reliever therapy (MART) is a newer approach that combines ICS and a fast-acting LABA in a single inhaler for both daily maintenance and symptom relief. Recent guidelines recommend offering a leukotriene receptor antagonist instead of a LABA for patients on SABA + ICS whose asthma is not well controlled, and considering MART for those with poorly controlled asthma.

The Relationship between Alveolar Size and Surface Tension in Respiratory Physiology

In respiratory physiology, the alveolus is often represented as a perfect sphere to apply Laplace’s law. According to this law, there is an inverse relationship between the size of the alveolus and the surface tension. This means that smaller alveoli experience greater force than larger alveoli for a given surface tension, and they will collapse first. This phenomenon explains why, when two balloons are attached together by their ends, the smaller balloon will empty into the bigger balloon.

In the lungs, this same principle applies to lung units, causing atelectasis and collapse when surfactant is not present. Surfactant is a substance that reduces surface tension, making it easier to expand the alveoli and preventing smaller alveoli from collapsing. Therefore, surfactant plays a crucial role in maintaining the proper functioning of the lungs and preventing respiratory distress. the relationship between alveolar size and surface tension is essential in respiratory physiology and can help in the development of treatments for lung diseases.

Prochlorperazine belongs to a class of drugs known as dopamine receptor antagonists, which work by inhibiting stimulation of the chemoreceptor trigger zone (CTZ) through D2 receptors. Other drugs in this class include domperidone, metoclopramide, and olanzapine.

Antihistamine antiemetics, such as cyclizine and promethazine, are H1 histamine receptor antagonists.

5-HT3 receptor antagonists, such as ondansetron and granisetron, are effective both centrally and peripherally. They work by blocking serotonin receptors in the central nervous system and gastrointestinal tract.

Antimuscarinic antiemetics are anticholinergic drugs, with hyoscine (scopolamine) being a common example.

Vertigo is a condition characterized by a false sensation of movement in the body or environment. There are various causes of vertigo, each with its own unique characteristics. Viral labyrinthitis, for example, is typically associated with a recent viral infection, sudden onset, nausea and vomiting, and possible hearing loss. Vestibular neuronitis, on the other hand, is characterized by recurrent vertigo attacks lasting hours or days, but with no hearing loss. Benign paroxysmal positional vertigo is triggered by changes in head position and lasts for only a few seconds. Meniere’s disease, meanwhile, is associated with hearing loss, tinnitus, and a feeling of fullness or pressure in the ears. Elderly patients with vertigo may be experiencing vertebrobasilar ischaemia, which is accompanied by dizziness upon neck extension. Acoustic neuroma, which is associated with hearing loss, vertigo, and tinnitus, is also a possible cause of vertigo. Other causes include posterior circulation stroke, trauma, multiple sclerosis, and ototoxicity from medications like gentamicin.

The posterior and superior mediastinum contain the thoracic duct.

The mediastinum is the area located between the two pulmonary cavities and is covered by the mediastinal pleura. It extends from the thoracic inlet at the top to the diaphragm at the bottom. The mediastinum is divided into four regions: the superior mediastinum, middle mediastinum, posterior mediastinum, and anterior mediastinum.

The superior mediastinum is the area between the manubriosternal angle and T4/5. It contains important structures such as the superior vena cava, brachiocephalic veins, arch of aorta, thoracic duct, trachea, oesophagus, thymus, vagus nerve, left recurrent laryngeal nerve, and phrenic nerve. The anterior mediastinum contains thymic remnants, lymph nodes, and fat. The middle mediastinum contains the pericardium, heart, aortic root, arch of azygos vein, and main bronchi. The posterior mediastinum contains the oesophagus, thoracic aorta, azygos vein, thoracic duct, vagus nerve, sympathetic nerve trunks, and splanchnic nerves.

In summary, the mediastinum is a crucial area in the thorax that contains many important structures and is divided into four regions. Each region contains different structures that are essential for the proper functioning of the body.

The most likely cause of a pleural transudate is heart failure. This is due to the congestion of blood into the systemic venous circulation, which can result from long-standing COPD and increase in pulmonary vascular resistance leading to right-sided heart failure or cor pulmonale. Other options such as infective exacerbation of COPD or pulmonary edema secondary to heart failure are less likely to explain the clinical signs. Pleural exudate effusion secondary to cor pulmonale is also not the most appropriate answer as it would cause a transudate pleural effusion, not an exudate.

Understanding the Causes and Features of Pleural Effusion

Pleural effusion is a medical condition characterized by the accumulation of fluid in the pleural space, which is the area between the lungs and the chest wall. The causes of pleural effusion can be classified into two types: transudate and exudate. Transudate is characterized by a protein concentration of less than 30g/L and is commonly caused by heart failure, hypoalbuminemia, liver disease, and other conditions. On the other hand, exudate is characterized by a protein concentration of more than 30g/L and is commonly caused by infections, pneumonia, tuberculosis, and other conditions.

The symptoms of pleural effusion may include dyspnea, non-productive cough, and chest pain. Upon examination, patients may exhibit dullness to percussion, reduced breath sounds, and reduced chest expansion. It is important to identify the underlying cause of pleural effusion to determine the appropriate treatment plan. Early diagnosis and treatment can help prevent complications and improve the patient’s overall health.

Understanding Lung Volumes in Respiratory Physiology

In respiratory physiology, lung volumes can be measured to determine the amount of air that moves in and out of the lungs during breathing. The diagram above shows the different lung volumes that can be measured.

Tidal volume (TV) refers to the amount of air that is inspired or expired with each breath at rest. In males, the TV is 500ml while in females, it is 350ml.

Inspiratory reserve volume (IRV) is the maximum volume of air that can be inspired at the end of a normal tidal inspiration. The inspiratory capacity is the sum of TV and IRV. On the other hand, expiratory reserve volume (ERV) is the maximum volume of air that can be expired at the end of a normal tidal expiration.

Residual volume (RV) is the volume of air that remains in the lungs after maximal expiration. It increases with age and can be calculated by subtracting ERV from FRC. Speaking of FRC, it is the volume in the lungs at the end-expiratory position and is equal to the sum of ERV and RV.

Vital capacity (VC) is the maximum volume of air that can be expired after a maximal inspiration. It decreases with age and can be calculated by adding inspiratory capacity and ERV. Lastly, total lung capacity (TLC) is the sum of vital capacity and residual volume.

Physiological dead space (VD) is calculated by multiplying tidal volume by the difference between arterial carbon dioxide pressure (PaCO2) and end-tidal carbon dioxide pressure (PeCO2) and then dividing the result by PaCO2.

Acidosis shifts the oxygen dissociation curve to the right, which enhances oxygen delivery to the tissues by causing more oxygen to dissociate from Hb. postictal lactic acidosis is a common occurrence in patients with tonic-clonic seizures, and it is typically managed by monitoring for spontaneous resolution. During a seizure, tissue hypoxia can cause lactic acidosis. Therefore, a venous blood gas test for this patient should show low pH, high lactate, and low SaO2.

If the venous blood gas test shows a high pH, normal lactate, and low SaO2, it would not be consistent with postictal lactic acidosis. This result indicates alkalosis, which can be caused by gastrointestinal losses, renal losses, or Cushing syndrome.

A high pH, normal lactate, and normal SaO2 would also be inconsistent with postictal lactic acidosis because tissue hypoxia would cause an increase in lactate levels.

Similarly, low pH, high lactate, and normal SaO2 would not be expected in postictal lactic acidosis because acidosis would shift the oxygen dissociation curve to the right, decreasing the oxygen saturation of haemoglobin.

Finally, normal pH, normal lactate, and normal SaO2 are unlikely to be found in this patient shortly after a seizure. However, if the venous blood gas test was taken days after the seizure following an uncomplicated clinical course, these findings would be more plausible.

Understanding the Oxygen Dissociation Curve

The oxygen dissociation curve is a graphical representation of the relationship between the percentage of saturated haemoglobin and the partial pressure of oxygen in the blood. It is not influenced by the concentration of haemoglobin. The curve can shift to the left or right, indicating changes in oxygen delivery to tissues. When the curve shifts to the left, there is increased saturation of haemoglobin with oxygen, resulting in decreased oxygen delivery to tissues. Conversely, when the curve shifts to the right, there is reduced saturation of haemoglobin with oxygen, leading to enhanced oxygen delivery to tissues.

The L rule is a helpful mnemonic to remember the factors that cause a shift to the left, resulting in lower oxygen delivery. These factors include low levels of hydrogen ions (alkali), low partial pressure of carbon dioxide, low levels of 2,3-diphosphoglycerate, and low temperature. On the other hand, the mnemonic ‘CADET, face Right!’ can be used to remember the factors that cause a shift to the right, leading to raised oxygen delivery. These factors include carbon dioxide, acid, 2,3-diphosphoglycerate, exercise, and temperature.

Understanding the oxygen dissociation curve is crucial in assessing the oxygen-carrying capacity of the blood and the delivery of oxygen to tissues. By knowing the factors that can shift the curve to the left or right, healthcare professionals can make informed decisions in managing patients with respiratory and cardiovascular diseases.

Adenocarcinoma has become the most prevalent form of lung cancer, as per the given scenario. This type of cancer accounts for approximately one-third of all cases and can occur in both smokers and non-smokers. Therefore, the most probable answer to the question is adenocarcinoma. Mesothelioma, on the other hand, is a rare and incurable cancer that is almost exclusively linked to asbestos exposure and affects the pleura. It would not present as an upper lobe mass, but rather as a loss of lung volume or pleural opacity. Alveolar cell carcinoma, which is less common than adenocarcinoma, would likely cause significant sputum production.

Lung cancer can be classified into two main types: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). SCLC is less common, accounting for only 15% of cases, but has a worse prognosis. NSCLC, on the other hand, is more prevalent and can be further broken down into different subtypes. Adenocarcinoma is now the most common type of lung cancer, likely due to the increased use of low-tar cigarettes. It is often seen in non-smokers and accounts for 62% of cases in ‘never’ smokers. Squamous cell carcinoma is another subtype, and cavitating lesions are more common in this type of lung cancer. Large cell carcinoma, alveolar cell carcinoma, bronchial adenoma, and carcinoid are other subtypes of NSCLC. Differentiating between these subtypes is crucial as different drugs are available to treat each subtype.

The internal laryngeal nerve is responsible for providing sensory information to the supraglottis and branches off from the superior laryngeal nerve. It is important to note that the cervical plexus, external laryngeal nerve, recurrent laryngeal nerve, and superior laryngeal nerve do not perform the same function as the internal laryngeal nerve.

Anatomy of the Larynx

The larynx is located in the front of the neck, between the third and sixth cervical vertebrae. It is made up of several cartilaginous segments, including the paired arytenoid, corniculate, and cuneiform cartilages, as well as the single thyroid, cricoid, and epiglottic cartilages. The cricoid cartilage forms a complete ring. The laryngeal cavity extends from the laryngeal inlet to the inferior border of the cricoid cartilage and is divided into three parts: the laryngeal vestibule, the laryngeal ventricle, and the infraglottic cavity.

The vocal folds, also known as the true vocal cords, control sound production. They consist of the vocal ligament and the vocalis muscle, which is the most medial part of the thyroarytenoid muscle. The glottis is composed of the vocal folds, processes, and rima glottidis, which is the narrowest potential site within the larynx.

The larynx is also home to several muscles, including the posterior cricoarytenoid, lateral cricoarytenoid, thyroarytenoid, transverse and oblique arytenoids, vocalis, and cricothyroid muscles. These muscles are responsible for various actions, such as abducting or adducting the vocal folds and relaxing or tensing the vocal ligament.

The larynx receives its arterial supply from the laryngeal arteries, which are branches of the superior and inferior thyroid arteries. Venous drainage is via the superior and inferior laryngeal veins. Lymphatic drainage varies depending on the location within the larynx, with the vocal cords having no lymphatic drainage and the supraglottic and subglottic parts draining into different lymph nodes.

Overall, understanding the anatomy of the larynx is important for proper diagnosis and treatment of various conditions affecting this structure.

Based on the results of the Weber and Rinne tests, the patient in the question is likely experiencing conductive hearing loss on the left side. The Weber test revealed that the patient hears sound better on the left side, which could indicate a conductive hearing loss or sensorineural hearing loss on the right side. However, the Rinne test was negative on the left side, indicating a conductive hearing loss. This is further supported by the patient’s reported symptoms of hearing loss in the left ear. This presentation, along with a family history of hearing loss, suggests a possible diagnosis of otosclerosis, a condition that affects the stapes bone and can lead to severe or total hearing loss.

Understanding the Different Causes of Deafness

Deafness can be caused by various factors, with ear wax, otitis media, and otitis externa being the most common. However, there are other conditions that can lead to hearing loss, each with its own characteristic features. Presbycusis, for instance, is age-related sensorineural hearing loss that often makes it difficult for patients to follow conversations. Otosclerosis, on the other hand, is an autosomal dominant condition that replaces normal bone with vascular spongy bone, causing conductive deafness, tinnitus, and a flamingo tinge in the tympanic membrane. Glue ear, also known as otitis media with effusion, is the most common cause of conductive hearing loss in children, while Meniere’s disease is characterized by recurrent episodes of vertigo, tinnitus, and sensorineural hearing loss. Drug ototoxicity, noise damage, and acoustic neuroma are other factors that can lead to deafness.

Understanding the different causes of deafness is crucial in diagnosing and treating the condition. By knowing the characteristic features of each condition, healthcare professionals can determine the appropriate interventions to help patients manage their hearing loss. It is also important for individuals to protect their hearing by avoiding exposure to loud noises and seeking medical attention when they experience any symptoms of hearing loss. With proper care and management, people with deafness can still lead fulfilling lives.