The internal laryngeal nerve and the superior laryngeal artery are closely associated with each other. The superior laryngeal artery travels alongside the internal laryngeal branch of the superior laryngeal nerve, beneath the thyrohyoid muscle. It originates from the superior thyroid artery near its separation from the external carotid artery.

If the internal laryngeal nerve is damaged, it can result in a loss of sensation to the laryngeal mucosa. The nerve is situated beneath the mucous membrane of the piriform recess, making it vulnerable to injury from sharp objects like fish and chicken bones that may become stuck in the recess.

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.

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.

Cerebral vasodilation is a common result of hypercapnia, which can be problematic for patients with cranial trauma due to the potential increase in intracranial pressure.

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.

The raised transfer factor suggests that the patient is experiencing an exacerbation of asthma. This condition can cause obstructive patterns on pulmonary function tests, leading to reduced FEV1 and FEV1/FVC, as well as hypoxia and wheezing. However, other conditions such as COPD exacerbation, idiopathic pulmonary fibrosis, and pulmonary embolism would result in a low transfer factor, and are therefore unlikely explanations for the patient’s symptoms.

Understanding Transfer Factor in Lung Function Testing

The transfer factor is a measure of how quickly a gas diffuses from the alveoli into the bloodstream. This is typically tested using carbon monoxide, and the results can be given as either the total gas transfer (TLCO) or the transfer coefficient corrected for lung volume (KCO). A raised TLCO may be caused by conditions such as asthma, pulmonary haemorrhage, left-to-right cardiac shunts, polycythaemia, hyperkinetic states, male gender, or exercise. On the other hand, a lower TLCO may be indicative of pulmonary fibrosis, pneumonia, pulmonary emboli, pulmonary oedema, emphysema, anaemia, or low cardiac output.

KCO tends to increase with age, and certain conditions may cause an increased KCO with a normal or reduced TLCO. These conditions include pneumonectomy/lobectomy, scoliosis/kyphosis, neuromuscular weakness, and ankylosis of costovertebral joints (such as in ankylosing spondylitis). Understanding transfer factor is important in lung function testing, as it can provide valuable information about a patient’s respiratory health and help guide treatment decisions.

The signs are indicative of sialolithiasis, which usually involves the formation of stones in the submandibular gland and can block Wharton’s duct. Stensen’s duct, on the other hand, is responsible for draining the parotid gland.

Diseases of the Submandibular Glands

The submandibular glands are responsible for producing mixed seromucinous secretions, which can range from more serous to more mucinous depending on parasympathetic activity. These glands secrete approximately 800-1000ml of saliva per day, with parasympathetic fibers derived from the chorda tympani nerves and the submandibular ganglion. However, several conditions can affect the submandibular glands.

One such condition is sialolithiasis, which occurs when salivary gland calculi form in the submandibular gland. These stones are usually composed of calcium phosphate or calcium carbonate and can cause colicky pain and postprandial swelling of the gland. Sialography is used to investigate the site of obstruction and associated stones, with impacted stones in the distal aspect of Wharton’s duct potentially removed orally. However, other stones and chronic inflammation may require gland excision.

Sialadenitis is another condition that can affect the submandibular glands, usually as a result of Staphylococcus aureus infection. This can cause pus to leak from the duct and erythema to be noted. A submandibular abscess may develop, which is a serious complication as it can spread through other deep fascial spaces and occlude the airway.

Finally, submandibular tumors can also affect these glands, with only 8% of salivary gland tumors affecting the submandibular gland. Of these, 50% are malignant, usually adenoid cystic carcinoma. Diagnosis usually involves fine needle aspiration cytology, with imaging using CT and MRI. Due to the high prevalence of malignancy, all masses of the submandibular glands should generally be excised.

Hypoxia causes vasoconstriction in the pulmonary arteries, which can lead to pulmonary artery hypertension in patients with chronic lung disease and chronic hypoxia. Diffuse bronchoconstriction is not a response to hypoxia, but may cause hypoxia in conditions such as acute asthma exacerbation. Hypersecretion of mucus from goblet cells is a characteristic finding in chronic inflammatory lung diseases, but is not a response to hypoxia. Pulmonary artery vasodilation occurs around well-ventilated alveoli to optimize oxygen uptake into the blood.

The Effects of Hypoxia on Pulmonary Arteries

When the partial pressure of oxygen in the blood decreases, the pulmonary arteries undergo vasoconstriction. This means that the blood vessels narrow, allowing blood to be redirected to areas of the lung that are better aerated. This response is a natural mechanism that helps to improve the efficiency of gaseous exchange in the lungs. By diverting blood to areas with more oxygen, the body can ensure that the tissues receive the oxygen they need to function properly. Overall, hypoxia triggers a physiological response that helps to maintain homeostasis in the body.

Glomerulonephritis is a condition that affects the kidneys and can present with various pathological changes. In rapidly progressive glomerulonephritis, patients may present with respiratory tract symptoms and cutaneous manifestations of vasculitis. Renal biopsy will show epithelial crescents in Bowman’s capsule, indicating severe glomerular injury. Mesangioproliferative glomerulonephritis is characterized by a diffuse increase in mesangial cells and is not associated with respiratory tract symptoms or cutaneous manifestations of vasculitis. Membranoproliferative glomerulonephritis involves deposits in the intraglomerular mesangium and is associated with activation of the complement pathway and glomerular damage. It is unlikely to be the diagnosis in the scenario as it is not associated with vasculitis symptoms. A normal nephron architecture would not explain the patient’s symptoms and is an incorrect answer.

Granulomatosis with Polyangiitis: An Autoimmune Condition

Granulomatosis with polyangiitis, previously known as Wegener’s granulomatosis, is an autoimmune condition that affects the upper and lower respiratory tract as well as the kidneys. It is characterized by a necrotizing granulomatous vasculitis. The condition presents with various symptoms such as epistaxis, sinusitis, nasal crusting, dyspnoea, haemoptysis, and rapidly progressive glomerulonephritis. Other symptoms include a saddle-shape nose deformity, vasculitic rash, eye involvement, and cranial nerve lesions.

To diagnose granulomatosis with polyangiitis, doctors perform various investigations such as cANCA and pANCA tests, chest x-rays, and renal biopsies. The cANCA test is positive in more than 90% of cases, while the pANCA test is positive in 25% of cases. Chest x-rays show a wide variety of presentations, including cavitating lesions. Renal biopsies reveal epithelial crescents in Bowman’s capsule.

The management of granulomatosis with polyangiitis involves the use of steroids, cyclophosphamide, and plasma exchange. Cyclophosphamide has a 90% response rate. The median survival rate for patients with this condition is 8-9 years.

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.

As a junior doctor, you will often encounter patients who retain carbon dioxide and depend on their hypoxic drive to breathe. When using Venturi masks to deliver controlled oxygen, it is important to set a target that balances the patient’s need for oxygen with their reliance on hypoxia to stimulate breathing. Answer 4 is the correct choice in this scenario. Providing too much oxygen, as in answers 2 and 3, can cause the patient to lose their hypoxic drive and become drowsy or confused. Answer 5 does not provide enough oxygen to properly perfuse the tissues. Failing to set a target for these patients is not good clinical practice.

Guidelines for Oxygen Therapy in Emergency Situations

In 2017, the British Thoracic Society updated its guidelines for emergency oxygen therapy. The guidelines state that in critically ill patients, such as those experiencing anaphylaxis or shock, oxygen should be administered through a reservoir mask at a rate of 15 liters per minute. However, certain conditions, such as stable myocardial infarction, are excluded from this recommendation.

The guidelines also provide specific oxygen saturation targets for different patient populations. Acutely ill patients should have a saturation level between 94-98%, while patients at risk of hypercapnia, such as those with COPD, should have a saturation level between 88-92%. Oxygen levels should be reduced in stable patients with satisfactory oxygen saturation.

For COPD patients, a 28% Venturi mask at 4 liters per minute should be used prior to the availability of blood gases. The target oxygen saturation level for these patients should be 88-92% if they have risk factors for hypercapnia but no prior history of respiratory acidosis. If the patient’s pCO2 is normal, the target range should be adjusted to 94-98%.

The guidelines also state that oxygen therapy should not be used routinely in certain situations where there is no evidence of hypoxia, such as in cases of myocardial infarction, acute coronary syndromes, stroke, obstetric emergencies, and anxiety-related hyperventilation.

Overall, these guidelines provide important recommendations for the appropriate use of oxygen therapy in emergency situations, taking into account the specific needs of different patient populations.

Arterial carbon dioxide stimulates them, but it takes longer to reach equilibrium compared to the carotid peripheral chemoreceptors. They are not as responsive to acidity because of the blood-brain barrier.

The Control of Ventilation in the Human Body

The control of ventilation in the human body is a complex process that involves various components working together to regulate the respiratory rate and depth of respiration. The respiratory centres, chemoreceptors, lung receptors, and muscles all play a role in this process. The automatic, involuntary control of respiration occurs from the medulla, which is responsible for controlling the respiratory rate and depth of respiration.

The respiratory centres consist of the medullary respiratory centre, apneustic centre, and pneumotaxic centre. The medullary respiratory centre has two groups of neurons, the ventral group, which controls forced voluntary expiration, and the dorsal group, which controls inspiration. The apneustic centre, located in the lower pons, stimulates inspiration and activates and prolongs inhalation. The pneumotaxic centre, located in the upper pons, inhibits inspiration at a certain point and fine-tunes the respiratory rate.

Ventilatory variables, such as the levels of pCO2, are the most important factors in ventilation control, while levels of O2 are less important. Peripheral chemoreceptors, located in the bifurcation of carotid arteries and arch of the aorta, respond to changes in reduced pO2, increased H+, and increased pCO2 in arterial blood. Central chemoreceptors, located in the medulla, respond to increased H+ in brain interstitial fluid to increase ventilation. It is important to note that the central receptors are not influenced by O2 levels.

Lung receptors also play a role in the control of ventilation. Stretch receptors respond to lung stretching, causing a reduced respiratory rate, while irritant receptors respond to smoke, causing bronchospasm. J (juxtacapillary) receptors are also involved in the control of ventilation. Overall, the control of ventilation is a complex process that involves various components working together to regulate the respiratory rate and depth of respiration.

In acidosis, the oxyhaemoglobin dissociation curve shifts to the right, indicating a decrease in affinity of haemoglobin for oxygen. This is due to an increase in the number of [H+] ions, reflecting greater metabolic activity. Low [H+] levels cause a shift to the left. The low HCO3- in this patient can be explained by metabolic acidosis, but it does not cause a shift in the oxyhaemoglobin dissociation curve. Hypokalaemia may be a result of treatment for diabetic ketoacidosis, but it does not cause a shift in the oxygen dissociation curve. When temperature increases, the oxyhaemoglobin dissociation curve also shifts to the right, causing a decrease in haemoglobin affinity for oxygen. Hypothermia causes a shift to the left, indicating an increased affinity of haemoglobin for oxygen.

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 hila of the kidneys are at the level of the transpyloric plane, with the left kidney slightly higher than the right. The adrenal glands sit just above the kidneys at the level of T12. The neck of the pancreas, not the body, is at the level of the transpyloric plane. The coeliac trunk originates at the level of T12 and the inferior mesenteric artery originates at L3.

The Transpyloric Plane and its Anatomical Landmarks

The transpyloric plane is an imaginary horizontal line that passes through the body of the first lumbar vertebrae (L1) and the pylorus of the stomach. It is an important anatomical landmark used in clinical practice to locate various organs and structures in the abdomen.

Some of the structures that lie on the transpyloric plane include the left and right kidney hilum (with the left one being at the same level as L1), the fundus of the gallbladder, the neck of the pancreas, the duodenojejunal flexure, the superior mesenteric artery, and the portal vein. The left and right colic flexure, the root of the transverse mesocolon, and the second part of the duodenum also lie on this plane.

In addition, the upper part of the conus medullaris (the tapered end of the spinal cord) and the spleen are also located on the transpyloric plane. Knowing the location of these structures is important for various medical procedures, such as abdominal surgeries and diagnostic imaging.

Overall, the transpyloric plane serves as a useful reference point for clinicians to locate important anatomical structures in the abdomen.

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.

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 most likely diagnosis for this patient is granulomatosis with polyangiitis, as indicated by the presence of cANCA and the involvement of multiple organs including the lungs, skin, kidneys, and upper respiratory tract. This condition is known to cause inflammation in the glomeruli, leading to renal impairment. Churg-Strauss disease and Alport’s syndrome are unlikely due to normal eosinophil levels and cANCA positivity, respectively. Goodpasture’s syndrome is also unlikely as the patient does not present with haematuria or haemoptysis.

Granulomatosis with Polyangiitis: An Autoimmune Condition

Granulomatosis with polyangiitis, previously known as Wegener’s granulomatosis, is an autoimmune condition that affects the upper and lower respiratory tract as well as the kidneys. It is characterized by a necrotizing granulomatous vasculitis. The condition presents with various symptoms such as epistaxis, sinusitis, nasal crusting, dyspnoea, haemoptysis, and rapidly progressive glomerulonephritis. Other symptoms include a saddle-shape nose deformity, vasculitic rash, eye involvement, and cranial nerve lesions.

To diagnose granulomatosis with polyangiitis, doctors perform various investigations such as cANCA and pANCA tests, chest x-rays, and renal biopsies. The cANCA test is positive in more than 90% of cases, while the pANCA test is positive in 25% of cases. Chest x-rays show a wide variety of presentations, including cavitating lesions. Renal biopsies reveal epithelial crescents in Bowman’s capsule.

The management of granulomatosis with polyangiitis involves the use of steroids, cyclophosphamide, and plasma exchange. Cyclophosphamide has a 90% response rate. The median survival rate for patients with this condition is 8-9 years.

Both the lungs and vertebral bodies are located outside of the mediastinum.

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 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.

The temporal bone is the correct answer. It contains the bony external auditory canal and middle ear, which are composed of a cartilaginous outer third and a bony inner two-thirds. The temporal bone articulates with the parietal, occipital, sphenoid, zygomatic, and mandible bones.

The sphenoid bone is a complex bone that articulates with 12 other bones. It is divided into four parts: the body, greater wings, lesser wings, and pterygoid plates.

The zygomatic bone is located on the anterior and lateral aspects of the face and articulates with the frontal, sphenoid, temporal, and maxilla bones.

The parietal bone forms the sides and roof of the cranium and articulates with the parietal on the opposite side, as well as the frontal, temporal, occipital, and sphenoid bones.

The occipital bone is situated at the rear of the cranium and articulates with the temporal, sphenoid, parietals, and the first cervical vertebrae.

The patient’s symptoms of ear pain, erythematous pinna and external auditory canal, and tender tragus on palpation are consistent with otitis externa, which has numerous possible causes. The patient is not febrile and has no loss of hearing or dizziness.

Anatomy of the Ear

The ear is divided into three distinct regions: the external ear, middle ear, and internal ear. The external ear consists of the auricle and external auditory meatus, which are innervated by the greater auricular nerve and auriculotemporal branch of the trigeminal nerve. The middle ear is the space between the tympanic membrane and cochlea, and is connected to the nasopharynx by the eustachian tube. The tympanic membrane is composed of three layers and is approximately 1 cm in diameter. The middle ear is innervated by the glossopharyngeal nerve. The ossicles, consisting of the malleus, incus, and stapes, transmit sound vibrations from the tympanic membrane to the inner ear. The internal ear contains the cochlea, which houses the organ of corti, the sense organ of hearing. The vestibule accommodates the utricule and saccule, which contain endolymph and are surrounded by perilymph. The semicircular canals, which share a common opening into the vestibule, lie at various angles to the petrous temporal bone.

The process of lung expansion relies on the negative pressure in the intrapleural space between the visceral and parietal pleura, which is present throughout respiration. This negative pressure pulls the lung towards the chest wall, allowing it to expand. However, if air enters the intrapleural space, the negative pressure is lost and the lung cannot fully reinflate. It is important to note that the intrapleural space is a potential space between the pleural surfaces, and there is typically no actual space present under normal circumstances.

Management of Pneumothorax: BTS Guidelines

Pneumothorax is a condition where air accumulates in the pleural space, causing the lung to collapse. The British Thoracic Society (BTS) has published guidelines for the management of spontaneous pneumothorax, which can be primary or secondary. Primary pneumothorax occurs without any underlying lung disease, while secondary pneumothorax is associated with lung disease.

The BTS recommends that patients with a rim of air less than 2 cm and no shortness of breath may be discharged, while those with a larger rim of air or shortness of breath should undergo aspiration or chest drain insertion. For secondary pneumothorax, patients over 50 years old with a rim of air greater than 2 cm or shortness of breath should undergo chest drain insertion. Aspiration may be attempted for those with a rim of air between 1-2 cm, but chest drain insertion is recommended if aspiration fails.

Patients with iatrogenic pneumothorax, which is caused by medical procedures, have a lower likelihood of recurrence than those with spontaneous pneumothorax. Observation is usually sufficient, but chest drain insertion may be required in some cases. Ventilated patients and those with chronic obstructive pulmonary disease (COPD) may require chest drain insertion.

Patients with pneumothorax should be advised to avoid smoking to reduce the risk of further episodes. They should also be aware of restrictions on air travel and scuba diving. The CAA recommends a waiting period of two weeks after successful drainage before air travel, while the BTS advises against scuba diving unless the patient has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively.

In summary, the BTS guidelines provide a comprehensive approach to the management of pneumothorax, taking into account the type of pneumothorax and the patient’s individual circumstances. Early intervention and appropriate follow-up can help prevent complications and improve outcomes.

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.

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.

Acute Treatment of Asthma

When dealing with acute asthma, the initial approach should be SOS, which stands for Salbutamol, Oxygen, and Steroids (IV). It is also important to organize a CXR to rule out pneumothorax. If the patient is experiencing bronchoconstriction, further efforts to treat it should be considered. If the patient is tiring or has a silent chest, ITU review may be necessary. Magnesium is recommended at a dose of 2 g over 30 minutes to promote bronchodilation, as low magnesium levels in bronchial smooth muscle can favor bronchoconstriction. IV theophylline may also be considered, but magnesium is typically preferred. While IV antibiotics may be necessary, promoting bronchodilation should be the initial focus. IV potassium may also be required as beta agonists can push down potassium levels. Oral prednisolone can wait, as IV hydrocortisone is already part of the SOS approach. Non-invasive ventilation is not recommended for the acute management of asthma.

The medullary rhythmicity area in the medullary oblongata controls the basic rhythm of breathing through its inspiratory and expiratory neurons. During quiet breathing, the inspiratory area is active for approximately 2 seconds, causing the diaphragm and external intercostals to contract, followed by a period of inactivity lasting around 3 seconds as the muscles relax and there is elastic recoil. Additional brainstem regions can be stimulated to regulate various aspects of breathing, such as extending inspiration in the apneustic area (refer to the table below).

The Control of Ventilation in the Human Body

The control of ventilation in the human body is a complex process that involves various components working together to regulate the respiratory rate and depth of respiration. The respiratory centres, chemoreceptors, lung receptors, and muscles all play a role in this process. The automatic, involuntary control of respiration occurs from the medulla, which is responsible for controlling the respiratory rate and depth of respiration.

The respiratory centres consist of the medullary respiratory centre, apneustic centre, and pneumotaxic centre. The medullary respiratory centre has two groups of neurons, the ventral group, which controls forced voluntary expiration, and the dorsal group, which controls inspiration. The apneustic centre, located in the lower pons, stimulates inspiration and activates and prolongs inhalation. The pneumotaxic centre, located in the upper pons, inhibits inspiration at a certain point and fine-tunes the respiratory rate.

Ventilatory variables, such as the levels of pCO2, are the most important factors in ventilation control, while levels of O2 are less important. Peripheral chemoreceptors, located in the bifurcation of carotid arteries and arch of the aorta, respond to changes in reduced pO2, increased H+, and increased pCO2 in arterial blood. Central chemoreceptors, located in the medulla, respond to increased H+ in brain interstitial fluid to increase ventilation. It is important to note that the central receptors are not influenced by O2 levels.

Lung receptors also play a role in the control of ventilation. Stretch receptors respond to lung stretching, causing a reduced respiratory rate, while irritant receptors respond to smoke, causing bronchospasm. J (juxtacapillary) receptors are also involved in the control of ventilation. Overall, the control of ventilation is a complex process that involves various components working together to regulate the respiratory rate and depth of respiration.

The superior laryngeal nerve, a branch of the vagus nerve, has two branches: the external laryngeal nerve, which is a motor nerve, and the internal laryngeal nerve, which is a sensory nerve. The recurrent laryngeal nerve, also a branch of the vagus nerve, supplies all intrinsic muscles of the larynx except for the cricothyroid muscles.

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 patient’s oxygen dissociation curve has shifted to the left, indicating respiratory alkalosis. This is likely due to the patient experiencing a panic attack and hyperventilating, leading to a decrease in carbon dioxide levels and an increase in the affinity of haemoglobin for oxygen. Respiratory acidosis, hypercapnia, and a right shift of the curve are not appropriate explanations for this patient’s condition.

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.

Hypercapnia causes a shift in the oxygen dissociation curve to the right. This means that for the same partial pressure of oxygen, the hemoglobin saturation will be less. Other factors that can cause a right shift in the curve include high altitudes, anaerobic metabolism resulting in the production of lactic acid, physical activity, and an increase in temperature. These shifts allow the body tissues to extract more oxygen from the blood, resulting in a lower hemoglobin saturation of the blood leaving the body tissues. Carbon dioxide is also known to produce a right shift in the curve, further contributing to this effect.

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 superior mesenteric artery originates from the abdominal aorta at the transpyloric plane, which is an imaginary axial plane located at the level of the L1 vertebral body and midway between the jugular notch and superior border of the pubic symphysis. Another transverse plane commonly used in anatomy is the subcostal plane, which passes through the 10th costal margin and the vertebral body L3. Additionally, the trans-tubercular plane, which is a horizontal plane passing through the iliac tubercles and in line with the 5th lumbar vertebrae, is often used to delineate abdominal regions in surface anatomy.

The Transpyloric Plane and its Anatomical Landmarks

The transpyloric plane is an imaginary horizontal line that passes through the body of the first lumbar vertebrae (L1) and the pylorus of the stomach. It is an important anatomical landmark used in clinical practice to locate various organs and structures in the abdomen.

Some of the structures that lie on the transpyloric plane include the left and right kidney hilum (with the left one being at the same level as L1), the fundus of the gallbladder, the neck of the pancreas, the duodenojejunal flexure, the superior mesenteric artery, and the portal vein. The left and right colic flexure, the root of the transverse mesocolon, and the second part of the duodenum also lie on this plane.

In addition, the upper part of the conus medullaris (the tapered end of the spinal cord) and the spleen are also located on the transpyloric plane. Knowing the location of these structures is important for various medical procedures, such as abdominal surgeries and diagnostic imaging.

Overall, the transpyloric plane serves as a useful reference point for clinicians to locate important anatomical structures in the abdomen.

Bronchiectasis can be diagnosed through various methods, including chest radiography, histopathology, and pulmonary function tests.

Chest radiography can reveal thickened bronchial walls, cystic lesions with fluid levels, collapsed areas with crowded pulmonary vasculature, and scarring, which are characteristic features of bronchiectasis.

Histopathology, which is a more invasive investigation often done through autopsy or surgery, can show irreversible dilation of bronchial airways and bronchial wall thickening.

However, high-resolution computerised tomography is a more favorable imaging technique as it is less invasive than histopathology.

Pulmonary function tests are commonly used to diagnose bronchiectasis, but they should be used in conjunction with other investigations as they are not sensitive or specific enough to provide sufficient diagnostic evidence on their own. An obstructive pattern is the most common pattern encountered, but a restrictive pattern is also possible.

Understanding the Causes of Bronchiectasis

Bronchiectasis is a condition characterized by the permanent dilation of the airways due to chronic inflammation or infection. There are various factors that can lead to this condition, including post-infective causes such as tuberculosis, measles, pertussis, and pneumonia. Cystic fibrosis, bronchial obstruction caused by lung cancer or foreign bodies, and immune deficiencies like selective IgA and hypogammaglobulinaemia can also contribute to bronchiectasis. Additionally, allergic bronchopulmonary aspergillosis (ABPA), ciliary dyskinetic syndromes like Kartagener’s syndrome and Young’s syndrome, and yellow nail syndrome are other potential causes. Understanding the underlying causes of bronchiectasis is crucial in developing effective treatment plans for patients.

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.

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.