Located on chromosome 17, p53 is a gene that suppresses tumours by inducing neoplastic cells to undergo apoptosis.

Oncogenes are genes that promote cancer and are derived from normal genes called proto-oncogenes. Proto-oncogenes play a crucial role in cellular growth and differentiation. However, a gain of function in oncogenes increases the risk of cancer. Only one mutated copy of the gene is needed for cancer to occur, making it a dominant effect. Oncogenes are responsible for up to 20% of human cancers and can become oncogenes through mutation, chromosomal translocation, or increased protein expression.

In contrast, tumor suppressor genes restrict or repress cellular proliferation in normal cells. Their inactivation through mutation or germ line incorporation is implicated in various cancers, including renal, colonic, breast, and bladder cancer. Tumor suppressor genes, such as p53, offer protection by causing apoptosis of damaged cells. Other well-known genes include BRCA1 and BRCA2. Loss of function in tumor suppressor genes results in an increased risk of cancer, while gain of function in oncogenes increases the risk of cancer.

Cranial nerves are a set of 12 nerves that emerge from the brain and control various functions of the head and neck. Each nerve has a specific function, such as smell, sight, eye movement, facial sensation, and tongue movement. Some nerves are sensory, some are motor, and some are both. A useful mnemonic to remember the order of the nerves is Some Say Marry Money But My Brother Says Big Brains Matter Most, with S representing sensory, M representing motor, and B representing both.

In addition to their specific functions, cranial nerves also play a role in various reflexes. These reflexes involve an afferent limb, which carries sensory information to the brain, and an efferent limb, which carries motor information from the brain to the muscles. Examples of cranial nerve reflexes include the corneal reflex, jaw jerk, gag reflex, carotid sinus reflex, pupillary light reflex, and lacrimation reflex. Understanding the functions and reflexes of the cranial nerves is important in diagnosing and treating neurological disorders.

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.

Absorption of Fat-Soluble Vitamins

Fat-soluble vitamins, namely A, D, E, and K, have a different absorption process compared to water-soluble vitamins. In the gut, these vitamins are combined with other fat-soluble substances such as monoacylglycerols and cholesterol to form micelles. These micelles are then transported to the lymphatic system and eventually enter the bloodstream through the subclavian vein.

However, any issues that affect the absorption of fats will also impact the absorption of fat-soluble vitamins. This means that individuals with conditions that affect fat absorption, such as cystic fibrosis or celiac disease, may have difficulty absorbing these vitamins. It is important to ensure adequate intake of fat-soluble vitamins through a balanced diet or supplements to prevent deficiencies and associated health problems.

The renal reabsorption of phosphate is increased by calcitriol.

Hormones Controlling Calcium Metabolism

Calcium metabolism is primarily controlled by two hormones, parathyroid hormone (PTH) and 1,25-dihydroxycholecalciferol (calcitriol). Other hormones such as calcitonin, thyroxine, and growth hormone also play a role. PTH increases plasma calcium levels and decreases plasma phosphate levels. It also increases renal tubular reabsorption of calcium, osteoclastic activity, and renal conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol. On the other hand, 1,25-dihydroxycholecalciferol increases plasma calcium and plasma phosphate levels, renal tubular reabsorption and gut absorption of calcium, osteoclastic activity, and renal phosphate reabsorption. It is important to note that osteoclastic activity is increased indirectly by PTH as osteoclasts do not have PTH receptors. Understanding the actions of these hormones is crucial in maintaining proper calcium metabolism in the body.

Polycystic ovary syndrome leads to anovulation with normal levels of FSH and estrogen, known as normogonadotropic normoestrogenic anovulation. LH levels may be elevated or normal in this condition.

Hypogonadotropic hypogonadal anovulation is caused by hypopituitarism or hyperprolactinemia, resulting in low levels of gonadotropins and estrogen. However, hyperprolactinemia can be ruled out based on gonadotropin and estrogen levels alone.

Hypothalamic amenorrhea is a functional cause of hypogonadotropic hypogonadal anovulation, often due to factors such as low BMI, stress, or excessive exercise.

Understanding Ovulation Induction and Its Categories

Ovulation induction is a common treatment for couples who have difficulty conceiving naturally due to ovulation disorders. The process of ovulation requires a balance of hormones and feedback loops between the hypothalamus, pituitary gland, and ovaries. Anovulation can occur due to alterations in this balance, which can be classified into three categories: hypogonadotropic hypogonadal anovulation, normogonadotropic normoestrogenic anovulation, and hypergonadotropic hypoestrogenic anovulation. The goal of ovulation induction is to induce mono-follicular development and subsequent ovulation, leading to a singleton pregnancy.

There are various forms of ovulation induction, starting with the least invasive and simplest management option first. Exercise and weight loss are typically the first-line treatment for patients with polycystic ovarian syndrome, as ovulation can spontaneously return with even a modest 5% weight loss. Letrozole is now considered the first-line medical therapy for patients with PCOS due to its reduced risk of adverse effects on endometrial and cervical mucous compared to clomiphene citrate. Clomiphene citrate is a selective estrogen receptor modulator that acts primarily at the hypothalamus, blocking the negative feedback effect of estrogens. Gonadotropin therapy tends to be the treatment used mostly for women with hypogonadotropic hypogonadism.

One potential side effect of ovulation induction is ovarian hyperstimulation syndrome (OHSS), which can be life-threatening if not identified and managed promptly. OHSS occurs when ovarian enlargement with multiple cystic spaces form, and an increase in the permeability of capillaries leads to a fluid shift from the intravascular to the extra-vascular space. The severity of OHSS varies, with the risk of severe OHSS occurring in less than 1% of all women undergoing ovarian induction. Management includes fluid and electrolyte replacement, anticoagulation therapy, abdominal ascitic paracentesis, and pregnancy termination to prevent further hormonal imbalances.

When the ulnar nerve is injured in the mid to distal forearm, it can result in a claw hand. This means that the 4th and 5th interphalangeal joints will flex while the metacarpophalangeal joints will extend. The severity of the clawing can be increased if the flexor digitorum profundus is not affected. However, if the ulnar nerve lesion is more proximal, the clinical picture will be milder due to the simultaneous paralysis of the ulnar half of the flexor digitorum profundus. This is known as the ‘ulnar paradox’. In this case, the hand may not have a claw-like appearance that is typically seen in more distal injuries. The ulnar nerve also supplies the first dorsal interosseous muscle, which will be affected by the injury.

The ulnar nerve originates from the medial cord of the brachial plexus, specifically from the C8 and T1 nerve roots. It provides motor innervation to various muscles in the hand, including the medial two lumbricals, adductor pollicis, interossei, hypothenar muscles (abductor digiti minimi, flexor digiti minimi), and flexor carpi ulnaris. Sensory innervation is also provided to the medial 1 1/2 fingers on both the palmar and dorsal aspects. The nerve travels through the posteromedial aspect of the upper arm and enters the palm of the hand via Guyon’s canal, which is located superficial to the flexor retinaculum and lateral to the pisiform bone.

The ulnar nerve has several branches that supply different muscles and areas of the hand. The muscular branch provides innervation to the flexor carpi ulnaris and the medial half of the flexor digitorum profundus. The palmar cutaneous branch arises near the middle of the forearm and supplies the skin on the medial part of the palm, while the dorsal cutaneous branch supplies the dorsal surface of the medial part of the hand. The superficial branch provides cutaneous fibers to the anterior surfaces of the medial one and one-half digits, and the deep branch supplies the hypothenar muscles, all the interosseous muscles, the third and fourth lumbricals, the adductor pollicis, and the medial head of the flexor pollicis brevis.

Damage to the ulnar nerve at the wrist can result in a claw hand deformity, where there is hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits. There may also be wasting and paralysis of intrinsic hand muscles (except for the lateral two lumbricals), hypothenar muscles, and sensory loss to the medial 1 1/2 fingers on both the palmar and dorsal aspects. Damage to the nerve at the elbow can result in similar symptoms, but with the addition of radial deviation of the wrist. It is important to diagnose and treat ulnar nerve damage promptly to prevent long-term complications.

Lithium use in patients can lead to diabetes insipidus by desensitizing the kidney’s response to ADH in the collecting ducts. This is likely the cause of diabetes insipidus in the patient described, as they are on lithium and have no signs of cranial diabetes insipidus. Cranial diabetes insipidus typically results from head trauma or pituitary surgery, while nephrogenic diabetes insipidus is caused by kidney dysfunction.

The posterior pituitary gland releases ADH, and dysfunction at this site can cause cranial diabetes insipidus. An anterior pituitary tumor may present with bilateral hemianopia, as this gland secretes several hormones.

Thiazide diuretics act on the distal convoluted tubule and are used to treat diabetes insipidus. Gitelman syndrome is caused by a mutation in the Na+-Cl− co-transporter, while Fanconi syndrome results from dysfunction in the proximal renal tubule, leading to an inability to absorb certain substances.

Diabetes insipidus is a medical condition that can be caused by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary gland (cranial DI) or an insensitivity to ADH (nephrogenic DI). Cranial DI can be caused by various factors such as head injury, pituitary surgery, and infiltrative diseases like sarcoidosis. On the other hand, nephrogenic DI can be caused by genetic factors, electrolyte imbalances, and certain medications like lithium and demeclocycline. The common symptoms of DI are excessive urination and thirst. Diagnosis is made through a water deprivation test and checking the osmolality of the urine. Treatment options include thiazides and a low salt/protein diet for nephrogenic DI, while central DI can be treated with desmopressin.

According to the 2021 NICE guidelines on preventing stroke in individuals with atrial fibrillation, DOACs should be the first-line anticoagulant therapy offered. The correct answer is ‘edoxaban’. ‘Aspirin’ is not appropriate for managing atrial fibrillation as it is an antiplatelet agent. ‘Low molecular weight heparin’ and ‘unfractionated heparin’ are not recommended for long-term anticoagulation in this case as they require subcutaneous injections.

Atrial fibrillation (AF) is a condition that requires careful management, including the use of anticoagulation therapy. The latest guidelines from NICE recommend assessing the need for anticoagulation in all patients with a history of AF, regardless of whether they are currently experiencing symptoms. The CHA2DS2-VASc scoring system is used to determine the most appropriate anticoagulation strategy, with a score of 2 or more indicating the need for anticoagulation. However, it is important to ensure a transthoracic echocardiogram has been done to exclude valvular heart disease, which is an absolute indication for anticoagulation.

When considering anticoagulation therapy, doctors must also assess the patient’s bleeding risk. NICE recommends using the ORBIT scoring system to formalize this risk assessment, taking into account factors such as haemoglobin levels, age, bleeding history, renal impairment, and treatment with antiplatelet agents. While there are no formal rules on how to act on the ORBIT score, individual patient factors should be considered. The risk of bleeding increases with a higher ORBIT score, with a score of 4-7 indicating a high risk of bleeding.

For many years, warfarin was the anticoagulant of choice for AF. However, the development of direct oral anticoagulants (DOACs) has changed this. DOACs have the advantage of not requiring regular blood tests to check the INR and are now recommended as the first-line anticoagulant for patients with AF. The recommended DOACs for reducing stroke risk in AF are apixaban, dabigatran, edoxaban, and rivaroxaban. Warfarin is now used second-line, in patients where a DOAC is contraindicated or not tolerated. Aspirin is not recommended for reducing stroke risk in patients with AF.

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 two end branches of the lateral cord of the brachial plexus are the lateral root of the median nerve and the musculocutaneous nerve. If the musculocutaneous nerve is damaged, it can result in weakened elbow flexion. The posterior cord has two end branches, the axillary nerve and radial nerve. The lateral pectoral nerve is a branch of the lateral cord but not an end branch. The medial cord has two end branches, the medial root of the median nerve and the ulnar nerve.

Brachial Plexus Cords and their Origins

The brachial plexus cords are categorized based on their position in relation to the axillary artery. These cords pass over the first rib near the lung’s dome and under the clavicle, just behind the subclavian artery. The lateral cord is formed by the anterior divisions of the upper and middle trunks and gives rise to the lateral pectoral nerve, which originates from C5, C6, and C7. The medial cord is formed by the anterior division of the lower trunk and gives rise to the medial pectoral nerve, the medial brachial cutaneous nerve, and the medial antebrachial cutaneous nerve, which originate from C8, T1, and C8, T1, respectively. The posterior cord is formed by the posterior divisions of the three trunks (C5-T1) and gives rise to the upper and lower subscapular nerves, the thoracodorsal nerve to the latissimus dorsi (also known as the middle subscapular nerve), and the axillary and radial nerves.

The macroscopic features of this condition typically involve ulcers, fibrosis, and a granulomatous process. It is more commonly a primary occurrence rather than a consequence of acute inflammation.

Chronic inflammation can occur as a result of acute inflammation or as a primary process. There are three main processes that can lead to chronic inflammation: persisting infection with certain organisms, prolonged exposure to non-biodegradable substances, and autoimmune conditions involving antibodies formed against host antigens. Acute inflammation involves changes to existing vascular structure and increased permeability of endothelial cells, as well as infiltration of neutrophils. In contrast, chronic inflammation is characterized by angiogenesis and the predominance of macrophages, plasma cells, and lymphocytes. The process may resolve with suppuration, complete resolution, abscess formation, or progression to chronic inflammation. Healing by fibrosis is the main result of chronic inflammation. Granulomas, which consist of a microscopic aggregation of macrophages, are pathognomonic of chronic inflammation and can be found in conditions such as colonic Crohn’s disease. Growth factors released by activated macrophages, such as interferon and fibroblast growth factor, may have systemic features resulting in systemic symptoms and signs in individuals with long-standing chronic inflammation.

Pericarditis is inflammation of the pericardium, a sac surrounding the heart. It can be caused by various factors, including viral infections. The typical symptom of pericarditis is central chest pain that is relieved by sitting up or leaning forward. ST-segment depression on a 12-lead ECG is not a sign of pericarditis, but rather a sign of subendocardial tissue ischemia. A pansystolic cardiac murmur heard on auscultation is also not associated with pericarditis, as it is caused by valve defects. Additionally, pericarditis is not typically associated with bradycardia, but rather tachycardia.

Acute Pericarditis: Causes, Features, Investigations, and Management

Acute pericarditis is a possible diagnosis for patients presenting with chest pain. The condition is characterized by chest pain, which may be pleuritic and relieved by sitting forwards. Other symptoms include non-productive cough, dyspnoea, and flu-like symptoms. Tachypnoea and tachycardia may also be present, along with a pericardial rub.

The causes of acute pericarditis include viral infections, tuberculosis, uraemia, trauma, post-myocardial infarction, Dressler’s syndrome, connective tissue disease, hypothyroidism, and malignancy.

Investigations for acute pericarditis include ECG changes, which are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events. The ECG may show ‘saddle-shaped’ ST elevation and PR depression, which is the most specific ECG marker for pericarditis. All patients with suspected acute pericarditis should have transthoracic echocardiography.

Management of acute pericarditis involves treating the underlying cause. A combination of NSAIDs and colchicine is now generally used as first-line treatment for patients with acute idiopathic or viral pericarditis.

In summary, acute pericarditis is a possible diagnosis for patients presenting with chest pain. The condition is characterized by chest pain, which may be pleuritic and relieved by sitting forwards, along with other symptoms. The causes of acute pericarditis are varied, and investigations include ECG changes and transthoracic echocardiography. Management involves treating the underlying cause and using a combination of NSAIDs and colchicine as first-line treatment.

The breakdown of long chain fatty acids is primarily carried out by peroxisomes. However, this patient is exhibiting symptoms of Zellweger syndrome, a genetic disorder that impairs peroxisome function.

The rough endoplasmic reticulum plays a crucial role in the translation and folding of newly synthesized proteins. The nucleus is responsible for housing and regulating DNA, as well as facilitating RNA transcription. Meanwhile, proteasomes are responsible for breaking down proteins that have been marked with ubiquitin.

Functions of Cell Organelles

The functions of major cell organelles can be summarized in a table. The rough endoplasmic reticulum (RER) is responsible for the translation and folding of new proteins, as well as the manufacture of lysosomal enzymes. It is also the site of N-linked glycosylation. Cells such as pancreatic cells, goblet cells, and plasma cells have extensive RER. On the other hand, the smooth endoplasmic reticulum (SER) is involved in steroid and lipid synthesis. Cells of the adrenal cortex, hepatocytes, and reproductive organs have extensive SER.

The Golgi apparatus modifies, sorts, and packages molecules that are destined for cell secretion. The addition of mannose-6-phosphate to proteins designates transport to lysosome. The mitochondrion is responsible for aerobic respiration and contains mitochondrial genome as circular DNA. The nucleus is involved in DNA maintenance, RNA transcription, and RNA splicing, which removes the non-coding sequences of genes (introns) from pre-mRNA and joins the protein-coding sequences (exons).

The lysosome is responsible for the breakdown of large molecules such as proteins and polysaccharides. The nucleolus produces ribosomes, while the ribosome translates RNA into proteins. The peroxisome is involved in the catabolism of very long chain fatty acids and amino acids, resulting in the formation of hydrogen peroxide. Lastly, the proteasome, along with the lysosome pathway, is involved in the degradation of protein molecules that have been tagged with ubiquitin.

Enzymes Involved in Glycogen Degradation and Production

Glycogen degradation is a process that requires several enzymes. One of these enzymes is glycogen phosphorylase, which plays a role in releasing glucose molecules from the polysaccharide chain by removing α1-4 glycosidic linkages. Another enzyme required for glycogen degradation is the debranching enzyme, which removes the α1-6 glycosidic linkages that occur only at the branch points. This enzyme accomplishes this by removing a short row of glucose molecules near a branch point and attaching it to the end of a glucose chain. Once this is done, glucose phosphorylase can remove the glucose units one by one.

It is important to note that the debranching enzyme and glycogen phosphorylase are both used in the breakdown of glycogen, while the branching enzyme and glycogen synthase are involved in glycogen production. Additionally, phosphofructokinase is an enzyme in the glycolysis pathway, while pyruvate carboxylase is required for gluconeogenesis. the roles of these enzymes is crucial in the complex processes involved in glycogen metabolism.

The radial nerve is the nerve most commonly associated with injury in mid-shaft humeral fractures. This is because the nerve runs along the posterior of the humeral shaft in the radial groove, making it vulnerable to injury in this area.

In contrast, the axillary nerve is less likely to be injured in mid-shaft humeral fractures as it is located more proximally in the arm. Fractures of the surgical neck of the humerus or shoulder dislocations are more commonly associated with axillary nerve injury.

The median nerve is situated along the medial side of the arm and is not typically at risk of injury in mid-shaft humeral fractures. Instead, it is more commonly affected in supracondylar fractures of the humerus.

The musculocutaneous nerve is relatively well protected as it travels between the biceps brachii and brachialis muscles, and is therefore unlikely to be injured in mid-shaft humeral fractures.

Finally, the ulnar nerve is most commonly associated with injury at the elbow, either due to a fracture of the medial epicondyle of the humerus or as part of cubital tunnel syndrome.

The Radial Nerve: Anatomy, Innervation, and Patterns of Damage

The radial nerve is a continuation of the posterior cord of the brachial plexus, with root values ranging from C5 to T1. It travels through the axilla, posterior to the axillary artery, and enters the arm between the brachial artery and the long head of triceps. From there, it spirals around the posterior surface of the humerus in the groove for the radial nerve before piercing the intermuscular septum and descending in front of the lateral epicondyle. At the lateral epicondyle, it divides into a superficial and deep terminal branch, with the deep branch crossing the supinator to become the posterior interosseous nerve.

The radial nerve innervates several muscles, including triceps, anconeus, brachioradialis, and extensor carpi radialis. The posterior interosseous branch innervates supinator, extensor carpi ulnaris, extensor digitorum, and other muscles. Denervation of these muscles can lead to weakness or paralysis, with effects ranging from minor effects on shoulder stability to loss of elbow extension and weakening of supination of prone hand and elbow flexion in mid prone position.

Damage to the radial nerve can result in wrist drop and sensory loss to a small area between the dorsal aspect of the 1st and 2nd metacarpals. Axillary damage can also cause paralysis of triceps. Understanding the anatomy, innervation, and patterns of damage of the radial nerve is important for diagnosing and treating conditions that affect this nerve.

When the baby has Rh-positive blood and the mother has Rh-negative blood, their blood supplies can mix during pregnancy. This can lead to the mother producing antibodies that may harm the baby by passing through the placenta and causing conditions like hydrops fetalis. Additionally, subsequent pregnancies may also be impacted.

Rhesus negative mothers can develop anti-D IgG antibodies if they deliver a Rh +ve child, which can cause haemolysis in future pregnancies. Prevention involves testing for D antibodies and giving anti-D prophylaxis at 28 and 34 weeks. Anti-D should also be given in various situations, such as delivery of a Rh +ve infant or amniocentesis. Tests include cord blood FBC, blood group, direct Coombs test, and Kleihauer test. Affected fetuses may experience oedema, jaundice, anaemia, hepatosplenomegaly, heart failure, and kernicterus, and may require transfusions and UV phototherapy.

Haematuria is a common symptom of Schistosoma haematobium infection.

Schistosomiasis is a disease that is caused by parasitic blood flukes and is most prevalent in sub-Saharan Africa. The parasites responsible for schistosomiasis live in freshwater snails, and the infectious form of the parasite, known as cercariae, contaminates water. People can become infected with schistosomiasis when their skin comes into contact with cercariae. While most people with schistosomiasis are asymptomatic, acute infection can cause an itchy rash (known as swimmer’s itch) or acute schistosomiasis syndrome, which includes symptoms such as fever, urticaria, chills, myalgias, arthralgia, headache, and abdominal pain.

Chronic infection with Schistosoma haematobium can lead to inflammation of the bladder, resulting in symptoms such as dysuria, frequency, haematuria, fibrosis, and bladder calcification. Schistosoma intercalatum is another type of blood fluke that can cause schistosomiasis.

Schistosomiasis, also known as bilharzia, is a type of parasitic flatworm infection caused by three main species of schistosome: S. mansoni, S. japonicum, and S. haematobium. Acute symptoms usually occur in individuals who travel to endemic areas and have no immunity to the worms. These symptoms may include fever, cough, urticaria/angioedema, eosinophilia, and acute schistosomiasis syndrome (Katayama fever). Chronic infections caused by S. haematobium can lead to bladder inflammation and calcification, which can cause an obstructive uropathy and kidney damage. Schistosoma mansoni and Schistosoma japonicum can lead to progressive hepatomegaly and splenomegaly due to portal vein congestion, as well as complications of liver cirrhosis, variceal disease, and cor pulmonale. Schistosoma intercalatum and Schistosoma mekongi are less common but can cause intestinal schistosomiasis. Diagnosis is typically done through urine or stool microscopy to look for eggs, and treatment involves a single oral dose of praziquantel.

Statin Therapy for Hypercholesterolemia in Acute Coronary Syndrome

Hypercholesterolemia is a common condition in patients with acute coronary syndrome. The initial treatment approach for such patients is statin therapy, which includes drugs like simvastatin, atorvastatin, and rosuvastatin. Statins have been proven to reduce mortality in both primary and secondary prevention studies. The target cholesterol concentration for patients with hypercholesterolemia and acute coronary syndrome is less than 5 mmol/L.

According to NICE guidance, statins should be used more widely in conjunction with a QRISK2 score to stratify risk. This will help prevent cardiovascular disease and improve patient outcomes. The guidance recommends that statins be used in patients with a 10% or greater risk of developing cardiovascular disease within the next 10 years. By using statins in conjunction with risk stratification, healthcare professionals can provide more targeted and effective treatment for patients with hypercholesterolemia and acute coronary syndrome.

Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis are common bacterial organisms that can cause bacterial otitis media. Pseudomonas aeruginosa can also be a common cause in patients with cystic fibrosis.

The patient’s symptoms are typical of acute otitis media (AOM), which can cause ear pain, fever, and temporary hearing loss. AOM is more common in children due to their short, horizontal eustachian tubes that allow for easier movement of organisms from the upper respiratory tract to the middle ear.

AOM can be caused by either bacteria or viruses, and it can be difficult to distinguish between the two. However, features that may suggest a bacterial cause include the absence of upper respiratory tract infection symptoms and conditions that predispose to bacterial infections. In some cases, viral AOM can increase the risk of bacterial superinfection. Antibiotics may be prescribed for prolonged cases of AOM that do not appear to be resolving within a few days or in patients with immunosuppression.

Escherichia coli and Enterococcus faecalis are not the correct answers as they are not commonly associated with AOM. Haemophilus influenzae is more likely due to the proximity of the middle ear to the upper respiratory tract. Staphylococcus aureus is also an unlikely cause of bacterial AOM.

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.